Just because you've watched Jurassic Park doesn't mean you know that gene editing is bad

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Gene editing is an important area for further research.

Gene editing is the future and we should embrace it. I dont mean a wholehearted approval of the technique but to recognize that its here. We must be thoughtful about its applications and aware of its potential.

Weve been gene editing all throughout history. Selectively breeding animals and crops to promote the traits that are desirable or helpful to us. But todays gene editing is much different.

We use CRISPR-Cas9, which can target specific gene sequences to edit, said Samantha Noll, a bioethicist with the Functional Genomics Initiative.

CRISPR, a gene editing tool taken from bacterial defenses against viruses, allows molecular biologists here at WSU to alter specific genes in big animals. Compared to CRISPR, selective breeding is crude and inaccurate, only using phenotypic traits, such as eye or hair color, as the roadmap for which animal to breed or not. Selective breeding attempts to manipulate the genome by prioritizing expressed traits whereas CRISPR allows the manipulation of the genome by access to the entire gene pool.

Charlie Powell, the public information officer for WSUs school of Veterinary Medicine, mentioned multiple ways this gene editing technique can be applied positively.

At any given moment here in the US there are a million pigs in transit. A certain percentage of those animals will develop upper respiratory diseases as a result of the stress, Powell said. If we could make those pigs resistant instead of vaccinating them then we have the possibility of limiting those losses in the industry. This involves adding back the wild-type genes that they originated with.

This suggests ethical solutions by way of medical intervention. Lingering just on livestock application, how much animal suffering could be eliminated by well-applied selective gene editing? Instead of injecting tons of antibiotics, genetic immunity may be the way to go.

Fostering the path to healthier and happier livestock could be inroads to alleviating human challenges such as hunger and poverty. Abundance of sustainable and ethically produced meats could ease food demand, and resilient healthy livestock could be a valuable investment for underprivileged individuals.

Being a land-grant university, WSU research is primarily aimed at helping the local community, hence the focus on big animals and local agriculture. One of the research programs seeks to knock out the genes responsible for horns in cattle. This avoids the painful horn removal process for the animals and prevents accidental injury between cattle, which cost time and money.

Though these are promising initiatives, we cant be short-sighted either. William Kabasenche, a bioethicist focusing on the therapeutic applications of CRISPR, described what he called off-target effects.

Its called pleiotropy, when one gene influences multiple phenotypes, Kabasenche said.

Phenotypes are just the expressed traits. The information for those traits is stored in the gene. Off-target effects occur when a gene has unaccounted phenotypes, meaning that the manipulation of that gene produced an unforeseen or undesirable change in a phenotype.

This is why we have to be very careful when gene editing. Yes, the potential is huge both for scientific discovery as well as the well-being of conscious entities but we must guard against a utopic vision of the technology. There are trade-offs involved. Changing one gene may produce the desired effects, but drastically impact an unrelated but necessary function.

This stresses the need for research and the role of ethics in research. We should all want this work to be done, but we cannot simply focus on positive outcomes and draw the conclusion that it justifies its good. We must also consider how these outcomes are achieved.

We must also consider the harmful potential of gene editing. How we choose to engage our resources, the decisions and norms we set in research will in some part determine how well apply this technology. These norms are being born at research institutions like WSU.

Its a promising start that WSU includes ethicists, educators and biologists to tackle these difficult issues.

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OPINION: Support gene researchers - The Daily Evergreen

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Chicago, United States: The global CRISPR Technology Market is expected to surge at a steady CAGR in the coming years, states the latest Report Hive Research. The publication offers an insightful take on the historical data of the market and the milestones it has achieved. The report also includes an assessment of current market trends and dynamics, which helps in mapping the trajectory of the global CRISPR Technology market. Analysts have used Porters five forces analysis and SWOT analysis to explain the various elements of the market in absolute detail. Furthermore, it also studies the socio-economic factors, political changes, and environmental norms that are likely to affect the global CRISPR Technology market.

The CRISPR Technology market study published in the report is in a chapter-wise format to ease of the readability and complexity of the data covered. Each chapter is further categorized into its respective segments containing well-structured data. The competitive scenario displayed includes major market player details such as, company profile, end-user demand, import/export volume, sales data, etc. The report also covers the business strategies applied by different players, which will be a great addition for smart business decisions.

Get a Sample PDF Report: https://www.reporthive.com/request_sample/2243315

Top Key players cited in the report:

Thermo Fisher ScientificMerck KGaAGenScriptIntegrated DNA Technologies (IDT)Horizon Discovery GroupAgilent TechnologiesCellecta, Inc.GeneCopoeia, Inc.New England BiolabsOrigene Technologies, Inc.Synthego CorporationToolgen, Inc.

In this report, we analyze the CRISPR Technology industry from two aspects. One part is about its production and the other part is about its consumption. In terms of its production, we analyze the production, revenue, gross margin of its main manufacturers and the unit price that they offer in different regions from 2020 to 2025. In terms of its consumption, we analyze the consumption volume, consumption value, sale price, import and export in different regions from 2020 to 2025. We also make a prediction of its production and consumption in coming 2019-2024.At the same time, we classify different CRISPR Technology based on their definitions. Upstream raw materials, equipment and downstream consumers analysis is also carried out. What is more, the CRISPR Technology industry development trends and marketing channels are analyzed.

The research report is committed to giving its readers an unbiased point of view of the global CRISPR Technology market. Thus, along with statistics, it includes opinions and recommendation of market experts. This allows the readers to acquire a holistic view of the global market and the segments therein. The research report includes the study of the market segments on the basis of type, application, and region. This helps in identifying segment-specific drivers, restraints, threats, and opportunities.

The scope of the Report:The research report on the global CRISPR Technology market is a comprehensive publication that aims to identify the financial outlook of the market. For the same reason it offers a detailed understanding of the competitive landscape. It studies some of the leading players, their management styles, their research and development statuses, and their expansion strategies.

The report also includes product portfolios and the list of products in the pipeline. It includes a through explanation of the cutting-edging technologies and investments being made to upgrade the existing ones.

Global CRISPR Technology Market: Competitive RivalryThe chapter on company profiles studies the various companies operating in the global CRISPR Technology market. It evaluates the financial outlooks of these companies, their research and development statuses, and their expansion strategies for the coming years. Analysts have also provided a detailed list of the strategic initiatives taken by the CRISPR Technology market participants in the past few years to remain ahead of the competition.

Global CRISPR Technology Market: Regional Segments

The chapter on regional segmentation details the regional aspects of the global CRISPR Technology market. This chapter explains the regulatory framework that is likely to impact the overall market. It highlights the political scenario in the market and the anticipates its influence on the global CRISPR Technology market.

CRISPR Technology Segmentation by Product

EnzymesKitsgRNALibrariesDesign Tools

CRISPR Technology Segmentation by Application

BiomedicalAgricultural

Get Customized PDF template of this report: https://www.reporthive.com/request_customization/2243315

Strategic Points Covered in TOC:

Chapter 1: Introduction, market driving force product scope, market risk, market overview, and market opportunities of the global CRISPR Technology market

Chapter 2: Evaluating the leading manufacturers of the global CRISPR Technology marketwhich consists of its revenue, sales, and price of the products

Chapter 3: Displaying the competitive nature among key manufacturers, with market share, revenue, and sales

Chapter 4: Presenting global CRISPR Technology marketby regions, market share and with revenue and sales for the projected period

Chapter 5, 6, 7, 8 and 9: To evaluate the market by segments, by countries and by manufacturers with revenue share and sales by key countries in these various regions

Speak to Research Analyst: +1-312-604-7084

About Us:Report Hive Research delivers strategic market research reports, statistical survey, and Industry analysis and forecast data on products and services, markets and companies. Our clientele ranges mix of United States Business Leaders, Government Organizations, SMEs, Individual and Start-ups, Management Consulting Firms, and Universities etc. Our library of 600,000+ market reports covers industries like Chemical, Healthcare, IT, Telecom, Semiconductor, etc. in the USA, Europe Middle East, Africa, Asia Pacific. We help in business decision-making on aspects such as market entry strategies, market sizing, market share analysis, sales and revenue, technology trends, competitive analysis, product portfolio and application analysis etc.

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CRISPR Technology Market 2020 Sales and Revenue Analysis by Region, 2020-2025 | Thermo Fisher Scientific, Merck KGaA, GenScript, Integrated DNA...

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Potbelly.Beer belly. Muffin top. Spare tire. Regardless of what you call it, excessbelly fat is frustrating.

Cleveland Clinic is a non-profit academic medical center. Advertising on our site helps support our mission. We do not endorse non-Cleveland Clinic products or services.Policy

For most people, the appearance of excess weight around the midsection is their biggest concern. But obesity medicine specialist W. Scott Butsch, MD, says the bigger issue is the increased health risks that come with belly fat.

Abdominalfat is visceral fat, stubborn fat that surrounds the organs deep within theabdomen. Researchers have proved that excess visceral fat increases a personsrisk of metabolic diseases, including:

Dr.Butsch says belly fat affects men and women differently: Men are more likelyto havemore belly fat (orvisceral fat) than premenopausal women. But aftermenopause, women begin to gain more weight in their abdominal area.

An easy wayto gauge abdominal weight gain is to just pay attention to how your pants fitor the notch on your belt, says Dr. Butsch. If things are tight, then thatmay be an early warning sign of potential health problems.

Waistcircumference correlates to visceral fat. For men, a waist circumferenceapproaching 40 inches indicates increased risk. For women, 35 inches raises ared flag.

Patientswant to know why they cant just do sit-ups to melt away the fat, says Dr.Butsch. When you do sit-ups, youre increasing muscles in the abdomen, butthat doesnt specificallytarget the visceral fat that is around the organsdeeper in the body. Instead, Dr. Butsch recommends these strategies to trim thebelly fat:

Weight lossalone can effectively reduce visceral fat, says Dr. Butsch. By losing 10% ofyour body weight, you may lose up to 30% of your body fat.

Talk to your doctor about a weight-loss method that is right for you. While there are lots of options to choose from, Dr. Butsch recommends you avoid fasting for long periods. Prolonged fasts cause the body to hold onto the visceral fat, making it tougher to lose. If fasting is your jam, an intermittent or time-restricted fasting approach may be more effective for losing belly fat.

Exercises that increase the heart rate and make you sweat help you lose weight in general both visceral fat and the subcutaneous fat under the skin. Aerobic exercise burns overall calories and helps you reduce total body fat.

Dr. Butsch says the key to losing abdominal visceral fat seems to lie in a combination approach. He suggests trying 20 minutes of whole-body strength training plus a cardio routine to strengthen muscle cells and increase fat burn.

Fructose, or sugar, causes fat cells to mature faster, specifically in the visceral fat. A diet filled with fructose-containing sodas or drinks not only increases your calorie intake, but it impacts how the belly fat develops.

If youre feeling stressed out, especially right now that were in the middle of a pandemic, your body is likely releasing the stress hormone, cortisol, into the bloodstream. This can not only lead to weight gain, but theres also a strong link between an increase in cortisol and higher amounts of visceral fat.

Do your best tode-stress if you want to whittle your middle. Dr. Butsch states yoga,meditation, therapy and physical activity as ways to dial down your stresslevel.

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Want to Lose the Belly Fat? - Health Essentials from Cleveland Clinic

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From weird dreams and nightmares to increased insomnia, the coronavirus pandemic has stimulated some unusual sleep issues for many people.

As a behavioral sleep researcher at theUniversity of Alabama at Birmingham, a number of patients have been asking: "Why is this happening, and what can I do to stop it?"

We do most of our dreaming during a stage of sleep called "rapid eye movement." This is when the brain grows more active and revs up the amygdala and hippocampus (regions of the brain that deal with emotions and memories).

In this time of heightened fear and distress, the brain has even more emotional demands to process. And because our brain likes order, the frontal lobes attempt to process, organize and integrate our thoughts to make sense of the chaos of REM neural signals (which is what produces those dreams).

In other words, our colorful yet strange dreams may be a reflection of the negative emotions invited by Covid-19.

Like so many others, I've also had my fair share of weird and memorable dreams since the pandemic.

In one dream, I boarded a cruise ship, dressed head to toe in bubble wrap and carrying nothing but a roll of toilet paper. In another, I slept through my shift at the telemedicine clinic and missed all my patients.

Luckily, I've been able to get those unwanted dreams under control. Here's what I've been doing to sleep better at night:

1. I wake up at the same time every day.

We tend to keep a consistent sleep schedule mostly during the weekdays. But I'm now waking up at 5:30 a.m., seven days a week.

This helps because the body rewards regularity: People who wake up at the same time experience more metabolic health, improved cognition and enhanced emotion regulation.

To keep myself accountable, I place my alarm clock across the room so that I have to get out of bed to turn it off. I've also created an enjoyable morning routine that involves coffee and gratitude journaling outside, where I can bask in the morning light.

Having something pleasant to look forward to makes waking up easier, while the natural light helps entrain my circadian rhythm.

2.I do everything I can to stay active during the day.

This can be a difficult task during a time of social distancing and quarantining. It now feels nearly impossible to get in as much physical movement as I did before the pandemic.

But it's still important to try.Vigorous, moderate or even mild cardiovascular exercise (i.e., walking or doing household chores) stimulates adenosine, which helps build sleep pressure or the body's "hunger" for sleep. And an increased sleep pressure means less likelihood of anxiety or insomnia.

However, I avoid exercising too much in the evenings.Research has shown that intense physical activity within one hour of bedtime can reduce sleep time, while also making it harder to wake up.

3. I use my bed for three things: Sleep,sex and rest (if I'm sick).

Everything else watching, reading or anxiously scrolling through my phone for news about Covid-19 happens out of the bed.

With more time spent inside, people may start adopting the habit of eating, working or binge-watching Netflix in bed. This can be disruptive to our sleep, because it trains the brain to associate the bed with daytime activities, rather than a place for resting.

Even on nights when I find myself unable to sleep, I'll get out of bed and go to another room. Keeping a dim light on, I'll do something relaxing, like guided meditation or fold the laundry. When I'm finally sleepy again, I'll return to bed.

4.I take a bath before bedtime and avoid devices.

Darkness facilitates healthy production of melatonin, a hormone that promotes drowsiness; whereas light interrupts it. So at least one hour before bedtime, I try to reduce my exposure to light-emitting devices, such as my phone, laptop and TV.

Instead, I take hot bath or shower.According to studies, our core body temperature needs to drop by about2 to 3 degrees Fahrenheit to maintain deep sleep and soaking yourself in warm water can help.

Most people think it's easier to fall asleep after a bath because your body is nice and toasty.But the opposite happens: It actually brings the heat from the core of your body to the surface, thus naturally cooling the body andpromoting a more peaceful sleep.

Christina Pierpaoli Parker is a behavioral sleep researcher and clinical psychology resident at the University of Alabama at Birmingham. She writes about sleep forPsychology Today and HealthDay, and her work has been published in the Journals of Aging & Health, Geriatric Psychiatryand The Clinical Gerontologist.

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This sleep expert also had 'weird dreams and nightmares' since Covid-19. Here's what she does now to sleep better - CNBC

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Connectus Health is donating nonperishable food items, hygiene products and diapers at two of its Middle Tennessee clinics for those dealing with hardships brought about by the coronavirus pandemic. (Courtesy Connectus Health)

At Connectus, we strive to serve as a healthcare home for every single Nashvillian in need, and Second Harvests mission aligns perfectly with ours, Connectus Health Co-CEO Suzanne Hurley said in a release. We feel so lucky to have this partnership with them and do our part in alleviating food insecurity in our community.

The clinics pantries are stocked with food items, such as soup, rice, cereal and pasta, along with hygiene products, such as toothpaste, soap and deodorant.

For those wishing to pick up supplies or visit the clinics, Connectus asks that they call ahead at 615-292-9770 to ensure that a staff member is able to meet them.

Supplies are available for pick up Mon.-Thu. 8 a.m.- 5 p.m. and Friday from 8 a.m.-2 p.m. at the Vine Hill clinic, located at 601 Benton Ave., Nashville, or the clinic at Priest Lake, located at 2637 Murfreesboro Pike, Nashville.

In addition to food and hygienic products, Connectus Health is also accepting new patients for pediatrics, midwifery, primary care, behavioral health services, hormone replacement therapy and transgender care, with financial counselors available to assist with securing health insurance coverage.

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Connectus Health providing food, supplies to Middle Tennessee during coronavirus pandemic - Community Impact Newspaper

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Even if youve been staying mostly inside during the COVID-19 outbreak and laying off heavy makeup, your skin may be acting out.

Reports of increased acne and dry skin are not uncommon, even for people who previously had their skin under control.

For many people, stress can be a trigger for acne and we are certainly living in stressful times, said Dr. Julia Carroll, a Toronto-based dermatologist at Compass Dermatology.

But stress is only one culprit.

Here are some reasons why you may be experiencing acne or overly dry skin during coronavirus isolation.

Stress

Like Carroll said, the outbreak of the novel coronavirus is understandably causing a lot of people stress. From job loss to health concerns, many Canadians are experiencing a pique in anxiety.

Unfortunately, stress can wreak havoc on our skin and the stress hormone, cortisol, can lead to acne flare-ups. Theres also stress-related habits that we develop.

With so many people working from home all day in isolation, Ive had a lot of my patients confess to touching and picking at their face, Carroll said.

Its a common habit when people are stressed, bored or procrastinating.

Carroll said people should try to keep their hands off their face, which is not only important for acne, but for preventing the transmission of COVID-19.

To help lower stress levels, try to find ways to relax, like exercising, deep breathing, meditation or doing something creative.

New skincare routines

With more free time on our hands, some people are experimenting with their skincare routine, Carroll said. This can include using different and new products, like cleansers and leave-on face masks.

Many of the patients I have been seeing virtually are trying new routines while isolating and this has caused some breakouts, she said.

Others are abandoning their routine all together, which is also causing changes in the skin.

Carroll suggests people take a look at their skincare routine and make modifications accordingly. If you tend to have breakouts, she said to add products with either salicylic or glycolic acid.

This could be in the form of a cleanser or a medicated cream, she added.

For people who are wearing masks, their skin may also see a change.

Carroll said shes seeing a lot of acne-like breakouts due to the humidity in closed-off masks, like the N95 model.

Stress may also be a factor here, she said.

Others are reacting to the mask material with contact dermatitis. This could be a true allergy or just an irritation. The mask marks are another common complaint.

To treat mask irritation, Carroll suggests people use a gentle cleanser before putting on the mask and after they remove it.

Moisturizer can also be used, but she cautions against over-applying as it can affect the masks material, she said.

Lifestyle and environment

Because health officials urge people to stay at home to help curb the spread of COVID-19, many of us are not getting the same amount of fresh air we are used to.

Im seeing a lot of patients with dry skin, Carroll said. This comes from low humidity in some of our dwellings.

Theres also lifestyle changes, including diet and exercise, that many of us are experiencing.

Research shows exercise can help reduce inflammation, which can be a culprit of acne. Exercise also helps reduce stress, and might even lead to younger-looking skin, according to research out of McMaster University.

Our eating patterns may also be out of whack, and what we eat might affect our complexion.

While this varies from person to person, Carroll said, some people do have specific triggers to certain foods.

According to the Canadian Dermatology Association, if a certain kind of food seems to aggravate your acne, its best to avoid it.

There is evidence that avoiding dairy products or having a diet with a low glycemic index may reduce symptoms for some people, the association said on its website.

Treatment

If you have dry skin, Carroll suggests adding a hydrating wash to your routine, as well as moisturizers or serums with ceramides and hyaluronic acid.

If your acne does not get better with a consistent skincare routine and lifestyle changes, you might want to see a dermatologist, Carroll said.

Whatever you do, do not pop your pimples or pick at your skin. Squeezing pimples only leaves behind holes, or worse, acne scars.

Once scars are on your face, you cant do anything, Dr. Faisal Al-Mohammadi, a Mississauga, Ont.-based dermatologist and pathologist at Dermcare clinic, previously told Global News.

He said that for for some adults, laser scar removal treatments only improve scars by 40 to 50 per cent.

We will not be able to bring your skin back, he said.

Questions about COVID-19? Here are some things you need to know:

Health officials caution against all international travel. Returning travellers are legally obligated to self-isolate for 14 days, beginning March 26, in case they develop symptoms and to prevent spreading the virus to others. Some provinces and territories have also implemented additional recommendations or enforcement measures to ensure those returning to the area self-isolate.

Symptoms can include fever, cough and difficulty breathing very similar to a cold or flu. Some people can develop a more severe illness. People most at risk of this include older adults and people with severe chronic medical conditions like heart, lung or kidney disease. If you develop symptoms, contact public health authorities.

To prevent the virus from spreading, experts recommend frequent handwashing and coughing into your sleeve. They also recommend minimizing contact with others, staying home as much as possible and maintaining a distance of two metres from other people if you go out.

For full COVID-19 coverage from Global News, click here.

Laura.Hensley@globalnews.ca

- Global News

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COVID-19: Here's how isolation might be impacting your skin - ThoroldNews.com

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Welcome to the T List, a newsletter from the editors of T Magazine. Each week, were sharing things were eating, wearing, listening to or coveting now. Sign up here to find us in your inbox every Wednesday. You can always reach us at tlist@nytimes.com.

Buy This

Until last month, I had been a proud but distant observer of the small citrus tree in my apartment. The three-foot-tall semi-dwarf calamondin a plant native to the Philippines that produces sour, compact orange fruit thought to be a hybrid of a kumquat and a mandarin has always thrived despite, rather than because of, my attempts at care. But on my first day of working from home, the small white buds that had spread slowly along its wispy green branches throughout February suddenly burst into constellations of white, star-shaped flowers and its success became the focus of my newly confined existence. In return for more regular waterings, it has filled my apartment with the sweet, subtle, powdery scent of orange blossom for a month. And last week, when its petals finally began to fall, they left behind small green orbs that will soon become new fruit, making it not only the perfect houseplant colorful, fragrant and forgivingly resilient but an ideal houseguest. From $29, fourwindsgrowers.com

In our 2020 Culture issue, out April 19, T celebrates various groups of creative people who, whether united by outlook or identity, happenstance or choice, built communities that have shaped the larger cultural landscape including the now renowned black artists who showed at one or all of three black-owned galleries in the 70s and 80s, the butches and studs whose identity is both its own aesthetic and a repudiation of the male gaze, and the foreign correspondents explaining America to the world. Here, an excerpt from the editors letter by Hanya Yanagihara: Every magazine is by its nature retrospective, a time capsule from the near past. A magazine such as this takes months to photograph, write, edit and research, and a few weeks to print; this means that the things that were true at its conception are sometimes no longer so when its published. Yet while the world around us has changed in ways that were just a few weeks ago once reserved for the realm of fiction, the spirit and thesis of this issue has not. One of the things that has defined our age has been the rise and dominance of what we can colloquially call tribes, groups of people bound not by blood or genetics or law, but by something more profound and just as durable call it an affinity, if you will. Sometimes that affinity has its roots in race, or gender, or sexuality, but its just as often based in something not innate, but developed: taste, say, or sensibility, or experience, or history. These are assemblages of people not born unto one another, but who find one another, and as a result, their bond is more charged, more powerful, more intimate. To see the issue come alive, head to tmagazine.com.

Eat This

Molly Goddard and Joel Jeffery met in 2011, when she was 19 and he was 23, while skiing in Canada; when she returned to Brisbane, Australia, and he to London, they started a long-distance romance. On Sundays, they would Skype. Because of the time difference, one of us would always be in pajamas, Jeffery says. Thus, the seed was planted for their now five-year-old brand, Desmond & Dempsey, which sells womens, mens and childrens cotton pajamas that are joyfully splashed with brightly colored, vaguely nostalgic prints and retail for $180 a set. The two, who married in 2016, now often eat breakfast together at their Brixton apartment before walking to work. Goddard usually oversees the cooking, favoring a recipe she inherited from her mother, which she has lovingly called spiffy eggs. She makes it regularly on Sunday mornings, and would occasionally make it at the Desmond & Dempsey offices for lunch with their 10-person team. Not long after starting the company, when we didnt know what the rules were, Goddard says, the couple invited an interested buyer from the department store Fortnum & Mason to their apartment and served her Goddards special eggs. It was an unconventional approach, but it worked the buyer picked up the brand. For Goddard, the baked egg dish which includes pumpkin, Parma ham and crumbled feta is appealing not only because it is delicious and filling but also because its made in a single pot and easy to clean up. For the recipe, visit tmagazine.com.

Try This

Like many of you, Ive been spending a lot more time on my couch, a dark gray chenille-tweed settee that was my first big furniture purchase. This fact, along with increased scrolling through design-minded Instagram accounts, has left me wanting a cozy, colorful throw to can get me through springs brisker days and refresh my living room. The Hudson Valley-based brand Alicia Adams Alpaca, which makes ready-to-wear and home goods using wool from its own Alpaca farm, just released a super-soft rainbow-hued throw to celebrate its 10 years in business; 10 percent of the proceeds from each sale will be donated to Glsen, a nonprofit organization that supports the L.G.B.T.Q. community. The Spanish fashion house Loewe offers a vibrantly striped blanket in fuzzy mohair thats also available in solid colors, like this bright pink; one could also turn to Missoni, whose home collection includes an array of throws in the Italian fashion houses familiar chevron motif, like this lightweight polyester version, which is perfect for warmer temperatures. And for a more affordable option, check out Mantas Ezcaray, a small, family-owned business that offers a range of textiles made from luscious mohair in La Rioja, Spain; or these cotton blankets from the lifestyle brand VISO that feature abstract, arty shapes.

Last fall, Sara Gernsbacher and Patrick Walsh accidentally started a candle company: The Los Angeles-based artist couple both are painters and sculptors had been experimenting with folding colorful oil-pastel paintings into rectangular molds, pouring in wax from melted-down thrift-store candles, sticking in wicks and giving the results away to friends. I liked the idea of making sculpture for everyone and stepping outside the commerce of the gallery system, Gernsbacher told me. Then, thanks to Instagram (which is where I spotted their creations), the pair started getting proper sales requests from stores like the womens wear boutique Scout in Los Angeles and the cafe-slash-design-shop Relationships in Brooklyn; thus, Crying Clover Candles was born. Named for a dream Walsh had that featured a tattoo of a sad four-leaf clover, the project has continued to gain momentum, and made an appearance at last months Object & Thing show in New York, which is part of the Independent Art Fair. The allure is no doubt thanks to the candles eye-catching patterns imperfect checkerboards that Gernsbacher likens to skyscraper windows and only heightened now that most of us are stuck inside and in need of calming energy. From $36, cryingclovercandles.org

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We are living in stressful times.

For some the mask wearing, hand washing, food hoarding and job uncertainty will cause sleepless nights, for others it might trigger, or exacerbate existing, hair loss.

Its well established that hair loss can be related to emotional stress or anxiety, award-winning trichologist Dr. Serkan Aygin tells theStandard. When youre stressed or anxious, your body produces whats known as the fight or flight response. This is when your body is making extra hormones to prepare it to deal with whatever it thinks of as being a potential threat. This change in your hormone levels can have effects all around your body. When these extra hormones are made, they can affect the growth patterns of the hair follicles on your scalp.

Theres usually about a three-month delay between the stressful event or time period and the moment your hair starts falling out. So anyone feeling the Covid-19 anxiety, might not actually notice any hair loss until the end of summer.

The good news though, is that hair loss due to stress tends to be temporary. Unless theres another underlying medical reason for your hair loss, it should only last for as long as youre going through that particular period of stress or anxiety, says Dr. Aygin, who has treated over 10,000 patients for hair loss at his eponymous specialist hair clinic.

During the period of hair loss, more hairs on your head are in whats known as the resting stage. This doesnt mean your hair follicles are dead or that your hair will stop growing permanently. Your usual hair growth and regrowth pattern should return to normal a few months after your stress levels go back down to normal.

How to stop WFH getting in the way of your sleep

If youve lost hair as a result of stress or anxiety, theres every chance it will start to grow back once your stress levels are back to normal. Try working on reducing your stress levels as well as improving your general health and wellbeing. Any hair loss due to stress should grow back on its own in a few months.

So, if youre experiencing hair loss due to stress, the best thing to do is to stay calm, stay healthy and try not to panic. But how do you know if your hair loss is due to stress? And if its hair loss of a more permanent variety, what are the best methods of prevention, detection and treatment?

We asked Dr Aygin to provide some further clarification on the varying causes of hair loss and his preferred methods of treatment.

What causes hair loss?

Possible causes of hair loss include:

1. Genetics

The most common cause of hair loss is a hereditary condition called male-pattern baldness or female-pattern baldness. It usually occurs gradually with ageing and in predictable patterns a receding hairline and bald spots in men and thinning hair in women. Dihydrotestosterone or DHT, a breakdown product of the hormone testosterone, generally triggers male pattern baldness. Hair follicles exposed to DHT begin to shrink and the growth stage becomes shorter. The end result is thinner and shorter hair strands. Over a period of time, hair follicles will reach a phase where they are no longer capable of producing hair.

2. Hormonal Imbalance

A hormonal imbalance can lead to a multitude of annoying health and beauty issues, from adult acne to weight gain. If your hormones are out of balance, the effects will radiate throughout the whole body (and of course, that includes your hair). Hormones play a huge role in regulating the hair growth cycle. "Oestrogens (female hormones) are 'hair friendly' and help to keep hairs in their growth phase for the optimal length of time. Androgens (male hormones) are not very hair friendly, and can shorten the hair growth cycle. An excess of androgens (which could be caused by an endocrine disorder, such as Polycystic Ovarian Syndrome) can cause hair loss. The extent of this is often down to genes - If you have a genetic predisposition to follicle sensitivity, a hormonal imbalance can affect your hair more than it would someone who does not have a predisposition.

3. Medications and supplements

Hair loss can be a side effect of certain drugs, such as those used for cancer, arthritis, depression, heart problems, gout and high blood pressure.

4. Iron Deficiency and Anaemia

One of the most common causes of hair loss in women is an iron deficiency. Iron is essential for producing hair cell protein, without it, your strands will suffer.

5. Thyroid imbalance

The thyroid gland helps to regulate the body's metabolism by controlling the production of proteins and tissue use of oxygen. Any thyroid imbalance can therefore affect hair follicles. Also, if hypothyroidism is left untreated it may result in anaemia, which - as we've just discussed - is another condition that can impact the hair.

6. Vitamin B12 Deficiency

Vitamin B12 deficiency often causes hair loss as it can affect the health of red blood cells, which carry oxygen to your tissues. It's most common in vegans as you can primarily only obtain B12 through animal proteins.

7. Dramatic Weight Loss

A steep drop on the scales can impact your tresses,6-12 weeks after dramatic weight loss, whether it be intentional or unintentional, hair commonly comes out in excess. While our hair is incredibly important to us psychologically, physiologically it is non-essential; we could survive without it with no detriment to our physical health. This means that any nutritional deficiency often first shows up in our hair. Yet another reason to avoid crash dieting and instead try to adopt a healthy, balanced lifestyle.

8. Stress

Many people experience a general thinning of hair several months after a physical or emotional shock. Stress may also trigger scalp problems such as dandruff, disrupt eating habits and mess with the digestive system all of which can have a negative impact on hair. This type of hair loss is generally temporary.

9. Age

For women who are about to enter menopause, changes in their body may also have an effect on their hair. Hair loss becomes more prevalent leading up to and after the menopause. That being said, it's important to realize that our hair ages, and as we get older, hair naturally gets finer. It's a totally normal part of the ageing process.

Is hair loss more common in men?

Although both men and women experience hair loss, it is more common in men.

Androgenetic alopecia, also known as male pattern baldness, is a hereditary condition that is the most common type of hair loss among men. According to the American Hair Loss Association, 95 per centof hair loss in men is caused by androgenetic alopecia. It affects roughly 30 per cent of men by the age of 30, 40 per cent by 40, 50 per cent by 50, and 60 per cent by 60.

This inherited trait that tends to result as a receding hairline and a thinning crown in men, is caused by genetic sensitivity to a by-product of testosterone called dihydrotestosterone (DHT). Because men are constantly producing testosterone throughout their lives, they are also constantly producing DHT. This makes men more likely to lose hair than women, who do not have a similar genetic disposition to hair loss.

The early signs of male pattern baldness are as follows:

Noticeable change in your hairline

Male pattern baldness generally begins in the hairline, when you notice that your mildly receded hairline has turned into a more obvious M-shaped hairline. For most men this begins around the temples and the crown and often starts with thinning rather than total hair loss.

Noticeable thinning of your hair

Not all men experience baldness in their hairline. Some men experience what is defined as diffuse thinning; a type of hair loss that either affects the entire scalp or specific areas like the crown that results in hair loss that starts from the back or top, rather than from the hairline.

Excessive hair loss after showering or brushing

On average, people lose round 50-100 hairs a day, meaning that the five to 10 hairs you notice between your hands after shampooing aren't anything to be concerned about. However, if you start noticing an excessive amount of hair falling out throughout the day, then there is a risk that it could be the result of male pattern baldness.

In general the early signs of hair loss show up in the following ways;

Gradual thinning of the hair on the head

Receding hairline that becomes more visible with each passing year

For women, the first noticeable sign of hair loss is often a widening part or less fullness to their ponytail.

Are there effective preventative measures that can be taken?

Treating hair loss in its early stages can help minimise overall hair loss and increase the treatments efficacy. There are a few ways to control hair loss, but what to do depends on the cause of why you are losing your hair.

Some hair loss conditions such as hair loss experienced after pregnancy (telogen effluvium) are temporary and may resolve on their own. However if your hair loss is persistent you may want to schedule an appointment with your local dermatologist so as to diagnose if your hair loss is caused by conditions such as male pattern baldness, thyroid issues, scalp infections, nutrient deficiencies, stress or simply ageing.

I would recommendfour main hair-loss prevention treatments to consider, all of whichwork to stimulate regrowth on dormant follicles.

1. Finasteride

Finasteride, also sold under the brand name Propecia, is an FDA-approved prescription medication for hair loss prevention in men. Finasteride can be an effective way to prevent your hair from thinning because it prohibits the conversion of testosterone into dihydrotestosterone (DHT). DHT is a powerful hormone that is thought to cause hair follicles to miniaturise and eventually stop growing hair. To get this benefit of finasteride, you need to take it properly and consistently as prescribed by your doctor.

2. Minoxidil

Minoxidil is a vasodilator, meaning its designed to widen blood vessels and improve the flow of blood to certain areas of your body. When applied topically in the form of a serum or foam, Minoxidil increases blood flow to the parts of your scalp where hair grows. By increasing blood flow, more oxygen and nutrients can be transported into each hair follicle, promoting growth and hair health.

3. PRP (Platelet Rich Plasma)

PRP involves taking a small sample of blood and spinning it in a centrifuge to concentrate and separate the platelets and plasma from the other components of your blood, which is then injected back into the scalp. Platelets are the source of growth factors that have the power to promote hair growth and also thicken your existing hair. Growth factor generates new formation of blood vessels in the scalp, which in turn, increases the amount of oxygen and nutrients that are delivered to the hair follicles with subcutaneous blood flow.

The role of PRP is to strengthen the hair and prevent hair loss. PRP aims to promote and enhance tissue repair as well as to stimulate new hair growth.

4. LLLT (Low Level Laser Therapy) or LED Light Therapy

LED light therapy, which is actually known as Low Level Laser Therapy, is a clinically proven, effective treatment for men and women who have mild to moderate hereditary pattern hair loss. Laser hair therapy increases the production of adenosine triphosphate (ATP), which induces the release of nitric oxide. This in turn leads to enhanced hair growth. Additionally, it has been also observed that laser therapy was capable of reducing scalp tissue DHT, which may help slow, or even stop hair loss and improve hair growth.

Can hair grow back after it falls out?

Some forms of hair loss can be naturally reversed, without treatment. Reversible conditions mainly include hair loss caused by medications, prolonged stress, temporary illnesses, inadequate nutrition and improper hair care. In addition to this, hair loss caused by hormonal changes related to pregnancy and deficiencies in the function of the immune system can also be reversible.

What products would you recommend to slow the process of hair loss? And how do they work?

The important criterion to consider for controlling and/or slowing the hair loss process is to always have your hair follicles supplied with additional nutrient substances which, in turn, are requirements for healthy hair growth and hair regeneration. Hair growth can be stimulated as well as enhanced by products aimed at dermatological anti-hair loss care which:

Improve blood supply to the scalp

Serve as an additional source of energy for the hair

Promote hair strengthening

Increase hair resistance

Usinganti-hair loss products depends on the severity of the hair loss condition. For individuals with more defined hair loss patterns it is recommended to use a combination of different products such as shampoo, lotion and capsules for providing the hair with the necessary biological nutrition. At our clinic we recommendPriorin capsules (shop them here) and Sebamed Repair Shampoo (shop it here) to all our clients.

It is important to acknowledge that before trying out any recommendation that has been provided here, you should always first schedule a consultation session with your local dermatologist.

Dr. Serkan Aygin is a hair transplant specialist andmember of the International Society of Dermatology. Currently operating from his eponymous clinic in Turkey, he is due to open a second specialist hair clinic in London in August 2020.

Read the rest here:
Hair loss prevention: How to stop it falling out and thinning with stress - Evening Standard

Recommendation and review posted by Bethany Smith

The ensuing gold rush was catastrophic for fish and porpoise alike. At first, the totoabas were so plentiful that they could be harpooned from the beach, butchered for their mawswhich, when dried, resemble colossal potato chips with unappetizing tendrilsand left to rot. But as the population dwindled, fisherman turned to new methods. Near the Colorado River estuary, they laid gill nets, aquatic weapons of mass destruction designed to hang in the water column and ensnare passing prey. Vaquitas have the fatal misfortune of being nearly the same size as totoabas, so the nets were disastrous for them.

Lorenzo Rojas-Bracho, head of the International Committee for the Recovery of the Vaquita, at his home in Ensenada, Mexico.

The Mexican government banned totoaba fishing in the 1970s, but the killing never really stopped. By 2017, Rojas-Bracho and Taylor faced a difficult decision. With vaquitas stuck in critical decline, what else could be done? They'd talked about setting up a captive breeding program for years, but the expense and complexity had never seemed worth the risk. Now, though, it was time for a Hail Mary. That summer, Rojas-Bracho's boss, the Mexican environment minister, gave him the go-ahead to assemble his armada.

The team had four weeks to pull it all off. Early on in the effort, the vaquitas showed a knack for slipping past the researchers' nets, or just disappearing altogether. Then, with one week remaining, everything changed. It was a gorgeous day, Rojas-Bracho recalled, sinking into his sofa. I was far away from the action, but I could follow by radio. They were saying, We have the vaquita, it's behaving very nicely, it's coming to the net. We've got it on board, it's a female, it's a great animal, it's very calm. Rojas-Bracho motored over to take a look. It was the closest he'd ever been to a live vaquita. I could see my eyes in her eyes, he said.

As the sun set and the sea darkened, the team introduced the vaquita to its temporary home, el Nido. At first, it swam erratically, taking the measure of its new surroundings. Then it started to adapt. Rojas-Bracho was seated on deck, taking it all in. He heard one of the vets say to the vaquita, You're doing well, baby, so he stood up and walked away to call the environment minister. By the time he hung up, the situation had changed dramatically.

The animal started behaving wildly, and then it stopped breathing and it started to kind of sink, he said. Then there was a decision to take it out of the water and do CPR for three hours until it died, and that was painful. Jesus, it was painful. Seeing the best vets in the world trying to prevent the vaquita from dying, saying, Come on sweetie, you can do it, you can do it, it was He sighed quietly and lifted his glasses to wipe his eyes.

Conservationists must ask unpleasant questions: How to triage so many at-risk creatures? How to decide what lives and what dies?

The scientists' terrible night wasn't over. They took the vaquita onshore and performed a necropsy. Rojas-Bracho didn't sleep. The next morning, everyone agreed to shelve the captivity project.

The rest is here:
How a Pudgy Porpoise May Save Other Animals From Extinction - WIRED

Recommendation and review posted by Bethany Smith

The US Department of Agriculture recently reached out to stakeholders in the dietary supplement industry to measure the toll coronavirus has taken on businesses. In response, the Council for Responsible Nutrition (CRN) surveyed their members on disruptions they may be experiencing. CRN identified a number of supply chain challenges such as shipment delays, shortages and increased pricing.

CRN gathered and summarized member responses and responded to officials at USDA and FEMA to the potential and existing supply chain disruptions related to coronavirus. According to their report, CRN members identified biotin in China in short supply, high in price and a long lead time due to the shutdown.

NutraIngredients-USA spoke with several firms in the industry, who weighed in on how their biotin supply has been impacted. The impact has affected everyone differently, ranging from little to no disruption to heavy impacts on business.

Vincent Tian, chief executive officer & founder at NutriVitaShop, didnt go into detail, but said they are seeing a shortage of several ingredients, including biotin.

A number of companies reported that theyre seeing higher price tags, including Connie Richter, VP of purchasing for Life Extension. Biotin supply seems to be okay for now, but the price is increasing, apparently dramatically. Since this comes from China, most of the delays, if any, are on the transportation side, not necessarily the production side. Along with manufacturer price increases, the cost of freight has increased as well.

Rhodora Amazan-Gutierrez, Global Purchasing Manager, NOW, is also seeing higher prices. She shared that her company's biotin supply, which comes from China by way of sea, has been in short supply and at a significantly higher price. Our purchasing team has worked to ensure that we have plenty of stock.She said that NOW was fortune in highing inked their supply contracts before they saw prices jump.

According to Tony Xue, China General Manager at ingredientsonline.com, said the supply picture for biotin has been a chaotic one: Biotin has been unstable for years. Sometimes production is slow, and prices are stagnant, but sometimes prices skyrocket for the same reason. Xue added that one possible reason for this is because one of the main producers in China shut down production last year and no date to resume production has been announced.

Companies such as Lycored who rely on local ingredients may be better positioned to respond to the coronavirus situation as it evolves.

Tamie Green, Lycoreds customer experience director, reports the company has had a much different experience than many.

We are not anticipating any issues supplying our partners with Biotin. Our supply chain is fully back integrated and we are closely monitoring our levels of raw materials to ensure timely and smooth supply. Our production facility in the US is where we manufacture our vitamins and minerals, including Biotin. It is designated as an Essential Supplier and continues to operate in-line with personnel safety guidelines.

While China is beginning to get back on its feet, the backlash of the pandemic may be enough to push many American companies to restructure their supply chains so that if and when, they are prepared to withstand the impact of another pandemic.

Continued here:
Coronavirus: Spotlight on the biotin supply chain - NutraIngredients-usa.com

Recommendation and review posted by Bethany Smith

The Decadent Society:How We Became the Victimsof Our Own SuccessBy Ross DouthatAvid Reader Press,272 pagesReviewed by Wilfred M. McClay

Ross Douthats interesting but frustrating new book, The Decadent Society, puts me in mind of a famous Jewish joke. The scene opens with the wise and beloved old rabbi, lying on his deathbed. He is attended by a dozen or so of his students and disciples, all of whom are dutifully lined up in order of seniority, somberly awaiting the rabbis last words. Finally, the moment arrives. The rabbi opens his eyes, leans over to his side, and grants to his first and best student his parting declaration: Life isa river. Quickly, the first student passes the word along to the next student in line. The rabbi says life is a river. And then it is passed to the next: The rabbi says life is a river. And so it goes on down the line, until the message reaches the youngest of the entourage. He receives the news, ponders it for a moment, then naively responds, But what does the rabbi mean, life is a river? And so back up the line his question comes, one by one, until it reaches the most senior student, who feels obliged to pose the question, on behalf of the others. Rabbi, he asks, his voice nervous with apprehension, what do you mean, Life is a river? The rabbi closes his eyes to think.

He opens them. He looks over at his beloved student, shrugs his shoulders, raises his palms, and admits:

OK, so its not a river!

The experience of reading The Decadent Society is a bit like that. Its an engaging book by a smart and well-read journalist that ventures a considerable number of observations, generalizations, and predictions relating to our current condition and our civilizational prospects. It has moments of interpretive boldness. But it is also much too willing to back away from those assertions, and in fact often does so almost preemptively, even before we have a chance to challenge them. Like the rabbi in the joke, Douthat manages to do this with charm and a certain modesty. But what were left with is a book that, despite its many strengths, does not quite come off. The smart observations never expand into something broader. At almost every turn, where what one wants from a book of this kind are wise conclusions and plausible visions for the future, what one gets instead is a profusion of plausible scenarios and clever alternative plot outcomes.

The problem begins very early on. One comes to this book primed to read about our societys decadence, a word that may be hard to define with precision, but that is forever associated with moral decay and falling apart (it derives from the Latin decadere). Since we are surrounded these days by clear signs of late-Roman moral decay, it seems reasonable to expect that Douthat would talk about them. That expectation is reinforced by the books jacket design, a grotesque depiction of Rabelaiss Gargantua, who is gorging himself on the various delicacies of a sumptuous table while being attended by a retinue of servants, including a smiling man who is merrily defecating into a bowl on the tables corner.

But you cant judge a book by its cover, and it turns out that decadence in this book is defined as something far tamer and more respectable than the lurid jacket art would suggest. Douthat defines it as a condition of slowing growth or stasis, a pause or interlude in the flow of material and cultural innovation and expansive energy that has hitherto characterized the history of the West in general and the United States in particular. He defines the term this way, he explains, partly so that he can point to quantitative measures of decline, such as economic or demographic data, rather than speaking only in glittering and impressionistic generalities or cherry-picked examples. But such an approach may have the effect of defining out of consideration the most interesting questions about our decadence.

The book is carried along by a large but loose interpretive framework. Douthat draws upon the historian Frederick Jackson Turners claim that the existence of an unbroken frontier called the American national character into beingand goes on to extend this logic, as John F. Kennedy did, to the new frontier of space, whose conquest would ensure the persistence of the classic American traits. But with the effective end of the American space program after the triumphant Apollo moon landing in July 1969, Douthat writes, there began a closing of the frontiera shrinking of American horizons that would also entail a steady loss of inventiveness, creativity, productivity gains, population growth, and confidence in the future.

As an admirer of both Turner and the space program (in which my father worked, and through which my best friend from childhood became an astronaut), Im drawn toward this framing of history. But Im afraid that it is a bit too fanciful and forced, neglecting the inconvenient truth that much of the nation had other troubles on its mind in the summer of 1969 and was therefore not as enchanted with the moon landing as I was, partly because it had trouble envisioning the highly technocratic space programs search for frontiers as something it could claim as its own. Many my age took the contrary view articulated by Lewis Mumford, who dismissed the moon landing as the hasty exploration of a barren satellite. They regarded the chief value of our space exploration as the photographic glimpses it had given us, for the first time in human history, of our fragile blue planet as a lonely and stunning exception to the vast and hollow impersonality of space, and an eloquent rebuke to the delusion that modern technics would soon replace Mother Earth with a more perfect, scientifically organized, electronically controlled habitat.

Moving to the present day, it is not always clear whether or not Douthat regards our current condition as something to be seriously concerned about. To be sure, he organizes the book around the four horsemen of stagnation, sterility, sclerosis, and repetition, which sounds pretty apocalyptic. But he does not want the book to be morally judgmental, or to fall victim to the excesses of either catastrophic doom-saying or Panglossian optimism. Its not his style to get too hot under the collar. If there is a Jeremiah inside him struggling to get out, that fact is kept well concealed.

Perhaps our problems are merely the result of our success, and we are currently in a pause that refreshes. Or maybe not. Maybe we are in a state of sustainable decadence, something that could go on for years and years without serious interruption. Or maybe not. Maybe the election of Donald Trump has revealed the underlying instability of our decadence and opened the path to authoritarian doom. Or maybe Trump is more farcical that threatening, a feature of our decadence we can easily absorb. Whatever.

In his chapter entitled Stagnation, Douthat deals with the question of whether the Silicon Valley economy is real. Adducing examples like Elizabeth Holmess Theranos fraud and, a bit more speculatively, the lighter-than-air success of the universal but as yet unprofitable ride-sharing company Uber, the answer seems to be no. These two are prime examples of economic decadencewhat it looks like when an extraordinarily rich society cant find enough new ideas that justify investing all its stockpiled wealth. You might imagine from this description that Uber is in the pet-rock business, instead of a company providing complex, innovative, and immensely valuable services. But then were told that despite the stories Ive just told [about Theranos and Uber]many Silicon Valley institutions deserve their success, many tech companies have real customers and real revenue and a solid structure underneath. So which is it? Is the economy a river? Or not a river?

Some of the best parts of Douthats book come with his analysis of culture, and with the pattern of endless repetition that seems to characterize the world of ideas and the arts in recent years. About this, he is largely on target. In film, on Broadway, in popular music, in literature, in academia, and in a dozen other arenas, things seem to him to be stuck in what he calls a pattern of recurrence. We seem unable to imagine or produce fresh and innovative things, a fact that is surely connected, as is the chicken to the egg, to an inability of stodgy, incurious audiences to appreciate those fresh things when they come alongand also connected to the transformed economics of cultural production, which makes endless streaming of the same-old-same-old more attractive and profitable than the risk and expense of nurturing and embracing something new.

Hes also largely right that there seem to be very few new ideas in circulation, but instead a great deal of rehashing of the same-old intractable arguments about race, class, feminism, sexuality, poverty, environmentalism, socialism, capitalism, and so on, debates that were already running down well-worn tracks in the 1980s. He calls this the eternal return to 1975, and while there is some oversimplification involved, it is striking how often what he says turns out to be true. Those of us in academic life who look back to Yales Woodward Reportwhich happened to be issued in 1975as one of the most enduring defenses of free speech and free inquiry in the academy, have forgotten that the report concludes with a dissenting statement. It was written by a student committee member who objected to all the arguments the historian C. Vann Woodward had adduced for free inquiry, and offered a clear statement of the very same justifications for suppressing unwanted speech and shouting down of disagreeable ideas that increasingly prevail today. Add a few new buzz words, such as intersectionality, marginalization, and privilege, and the document would be right up to date.

So all the arguments and counterarguments were already out there. What has changed, though, is that today it is our university presidents who mouth the dissenters lines to appease their student protesters, while Woodwards ringing words, and the handful of faculty who still believe in them, are being ignored or forgotten. So plus a change is not quite the right maxim to apply here. About such developments, Douthat is characteristically ambiguous. Maybe, he speculates, woke progressivism will carry all before it in a way that the new left failed to do. Maybe the current recycling of New Age impulseswill deliver the West to some new post-Christian religious moment. Or maybe all these trends give an illusion of forward movement and momentum, when theyre actually bearing us ceaselessly back, back toward 1975. Or maybe something else. If you dont like these scenarios, he has others.

Douthat is insightful on the growing substitution of the virtual for the real, and how that substitution feeds a comfortable passivity, insulated from the requirements of action in the world. Hence the sense that we are polarized as never before coexists quite easily with the fact of our relative inactivity. He offers a withering passage that encompasses that paradox: If you want to feel like Western society is convulsing, theres an app for that, a convincing simulation waiting. But in the real world, nothing much is actually happening. Western society is really leaning back in an easy chair, hooked up to a drip of something soothing, playing and replaying an ideological greatest-hits tape from its wild and crazy youth, all riled up in its own imagination and yet, in reality, comfortably numb.

It is hard not to see in his description of such a condition an accusation of decadence in the familiar, morally charged sense of the word. And Douthat comes close to issuing a charged warning, a rude intrusion of actual reality, when he asks, How can a decadent society hope to avoid being challenged by more vigorous rivals, and ultimatelybeing subverted, dismantled, overthrown? His answer: It cant, and therefore were doomed, unless our enemies are even weaker and more decadent than we are. One wishes the book had more of that kind of realism.

The books concluding chapters, which explore possibilities of rebirth and renewal, continue to offer a multitude of possible avenues for us to follow. Perhaps the infusion of African cultural vitality into the moribund cultures of Europe will uplift and enliven them both, together. Perhaps some fabulous technological innovations, in energy, robotics, biotechnology, life extension, and of course space travel, Martian colonization, etc., will change everything. Perhaps there will be a revolution of localism, a disaggregation of the global grid. Perhaps there will be a worldwide religious revival, facilitated by a growing dissatisfaction with the limitations of secularism. Perhaps there will be a new paganism, or an unprecedented westernization of Islam. Perhaps there will be some hybridized version of some or all of these things, going on all at the same time!

In the end, Douthat seems to opt, albeit with his usual casualness, for a combination of scientific-technological advance and revitalized religious faith, concluding the book with, in its final sentence, what is probably its only command: So down on your kneesand start working on that warp drive. This is not a deliberately incoherent directive, since Douthat wants to insist that there can be a mysterious alchemy between science and religion, and he is not wrong to do so. The cultural power of that alchemy was well expressed when the three Apollo 8 astronauts read the text of Genesis 1:110 to the nation from space at Christmas of 1968. That such a crew would never be allowed to read such a thing today, and might not even want to do so, is surely a sign of our cultural decline, and in light of the space programs subsequent demise, perhaps indirect evidence of Douthats alchemy, too.

But there are reasons to be cautious about combining kneeling with that warp drive. Earlier in the book, Douthat mentions in passing Henry Adamss famous encounter with the great hall of dynamos, at the Paris Exposition of 1900. He reads Adamss description as an example of the technological sublime, the tendency of Americans to invest divine properties in certain technological achievements, such as the construction of the transcontinental railroad, the Hoover Dam, and the Golden Gate Bridge. But the passage itself, in which Adams writes of himself in the third person, gave voice to a far darker view of technologys religious claims:

To [an inventor of the day], the dynamo itself was but an ingenious channel for conveying somewhere the heat latent in a few tons of poor coal hidden in a dirty engine-house carefully kept out of sight; but to Adams the dynamo became a symbol of infinity. As he grew accustomed to the great gallery of machines, he began to feel the forty-foot dynamos as a moral force, much as the early Christians felt the Cross. The planet itself seemed less impressive, in its old-fashioned, deliberate, annual or daily revolution, than this huge wheel, revolving within arms-length at some vertiginous speed, and barely murmuring,scarcely humming an audible warning to stand a hairs-breadth further for respect of power,while it would not wake the baby lying close against its frame. Before the end, one began to pray to it; inherited instinct taught the natural expression of man before silent and infinite force.

Adams struggled for years to understand the conflicting pull of these alternative moral forces and never succeeded. But he did come away with one insight that endures: All the steam in the world could not, like the Virgin, build Chartres. I suspect that the same could be said of all the rocketry in the world. Particularly if one were to begin to pray to it.

Read more here:
Wilfred M. McClay :The Ambiguities of Ross Douthat - : :Commentary - Commentary Magazine

Recommendation and review posted by Bethany Smith

The statistical surveying report on the global cryonics technology market has been prepared by using professional or expert knowledge through standard and modified research approaches and forecasts. The report carefully examines the cryonics technology market, with a focus on most of the major players and their business strategies, geographical scope, market segments, product landscape, price and cost structure. The study not only analyses the business profile of key suppliers but also analyses their winning strategies to give business owners, stakeholders and field marketing staff a competitive advantage over others operating in the same space. Cryonics Technology Market applies the best of primary and secondary research to weigh on the competitive landscape and the main market players expected to dominate this global market with forecast period, 2020-2029. Through qualitative and quantitative analysis, we support you in a comprehensive analysis of the cryonics technology market.

The Cryonics Technology Market research focuses on the market structure and various factors (positive and negative) affecting the growth of the market. The report mainly studies the size, recent trends and development status of the cryonics technology market, as well as investment opportunities, government policy, market dynamics (drivers, restraints, opportunities), supply chain and competitive landscape. This report studies and presents the process of manufacturing and product specifications. Different facts and figures are included in cryonics technology report for a basic understanding of the businesses. Different global key players of cryonics technology market are listed in the report, which provides a detailed description of higher-level industries. It focuses on the elaboration of the development trend and client survey, which helps in decision making. Technological innovation and advancement will further optimize the performance of the product, making it more widely used in downstream applications.

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Technological advancements and increasing applications in software and services sectors would provide growth opportunities to the cryonics technology industry during the forecast period 2020-2029. New emerging markets, emerging consumer demographics, and technological advancements would accelerate the growth of this market in the coming years. Consequently, Slow freezing, Vitrification, Ultra-rapid are playing a vital role in driving the growth of cryonics technology market. The use of cryonics technology in wide applications such as Animal husbandry, Fishery science, Medical science, Preservation of microbiology culture, Conserving plant biodiversity majorly drives the growth of the market.

Factors Covered For Cryonics Technology Market Penetration

1. Market Entry and Top Winning Strategies Cryonics Technology Market Report adopted by Top Leading Players.

2. Geographical Analysis of the Cryonics Technology Market with respect to Product and Services.

3. Potential Countries to Grasp for Investment.

4. Prospective Risk for Suppliers and Manufacturers.

5. Key Performance Indicators of Global Executive Players based on Financial Positioning Identify In The Whole Market.

6. Market Dynamics in the Cryonics Technology Industry and Its Impact on Worldwide Market.

Scope of the Report

The research on the Cryonics Technology market concentrates on extracting valuable data on swelling investment pockets, significant growth opportunities, and major market vendors to help understand business owners what their competitors are doing best to stay ahead in the competition. Detailed analysis of critical aspects such as impacting factors and competitive landscape are showcased with the help of vital resources, which include charts, tables, and infographics.

Additionally, the report offers an in-depth analysis of key market players functioning in the global cryonics technology industry. The key players profiled in this report include Sigma-Aldrich, Thermo Fisher Scientific, Cryotherm, Oregon Cryonics, Alcor Life Extension Foundation, Praxair, Osiris Cryonics, Cellulis, VWR, Cryologics, Custom Biogenic Systems, Southern Cryonics and KrioRus.

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Most important key Products Type [Outlook(Revenue, USD Million, 20192029)] of Cryonics Technology covered in this report are:

Slow freezingVitrificationUltra-rapid

Based on end-user/application [Outlook(Revenue, USD Million, 20192029)], this report focuses on the status and outlook for major applications:

Animal husbandryFishery scienceMedical sciencePreservation of microbiology cultureConserving plant biodiversity

Geographically, this report focuses on product sales, value, market share, and growth opportunity in key regions such as,

North America (United States, Canada), Market Size, Y-O-Y Growth Market size, Y-O-Y Growth and Opportunity Analysis, Future Forecast

Latin America (Brazil, Mexico, Argentina, Rest of LATAM), Market Size, Y-O-Y Growth, Future Forecast

Europe (U.K., Germany, France, Italy, Spain, Hungary, BENELUX (Belgium, Netherlands, Luxembourg), NORDIC (Norway, Denmark, Sweden, Finland), Poland, Russia, Rest of Europe), Market Size, Y-O-Y Growth, Future Forecast

Asia-Pacific (China, India, Japan, South Korea, Malaysia, Indonesia, Taiwan, Hong Kong, Australia, New Zealand, Rest of Asia-Pacific), Market Size, Y-O-Y Growth, Future Forecast

The Middle East and Africa (Israel, GCC (Saudi Arabia, UAE, Bahrain, Kuwait, Qatar, Oman), North Africa, South Africa, Rest of the Middle East and Africa), Market size, Y-O-Y Growth, Future Forecast

You can also get individual chapter wise section or region wise report versions like North America, Europe or Asia or Country like US, UK, China and others. Click Here to Get Customized Report inquiry.

The Cryonics Technology market study answers critical questions including:

What tactics are being utilized by the cryonics technology market players to expand their production footprint in the region?

What are the possibilities and threats faced by players in the global cryonics technology market mutually?

Why the key region scale holds the majority of share in the global cryonics technology market?

Why segment has the largest consumption in the region?

Which industries remain the leading consumers of the cryonics technology across the globe?

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Table Of Content

Chapter 1 Cryonics Technology Market Introduction (Taxonomy and Market Definition)

Chapter 2 Research Methodology verified by Market.us

Chapter 3 Players Profiles and Pipeline Analysis

Chapter 4 Cryonics Technology Production, Revenue (Value), Price Trend by Type

Chapter 5 Cryonics Technology Market Analysis by Application

Chapter 6 Cryonics Technology Production, Consumption, Export, Import by Region (2020-2029)

Chapter 7 Cryonics Technology Production, Revenue (Value) by Region (2020-2029)

Chapter 8 Cryonics Technology Manufacturing Analysis

Chapter 9 Industrial Chain, Sourcing Strategy and Downstream Buyers

Chapter 10 Market Dynamics

Chapter 11 Cryonics Technology Market Forecast (2020-2029)

Chapter 12 Research Findings and Conclusion

Chapter 13 Appendix

Click to View Figures, TOC, and Companies Mentioned in the Cryonics Technology Market Report at: https://market.us/report/cryonics-technology-market/#toc

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See more here:
Cryonics Technology Market | Business Revenue Forecast and Geography Analysis Based on Growth Factors, Demand and Trends by 2029 - TechnoVally

Recommendation and review posted by Bethany Smith

More men are dying from COVID-19 worldwide than women, and the potential reasons run the gamut from biology to bad habits.

The World Health Organization (WHO) reports that 68 percent of deaths related to COVID-19 in Europe have been among men.

A study by the Higher Health Institute of Rome found that among Italians hospitalized for the novel coronavirus, 8 percent of men died compared to 5 percent of women.

In New York City, men have been dying of coronavirus at almost twice the rate of women. The citys health department reports 43 COVID-19 deaths for every 100,000 men, compared with 23 deaths for every 100,000 women.

The Centers for Disease Control and Prevention (CDC) currently isnt reporting COVID-19 deaths by gender, but experts see no reason the trend would differ elsewhere in the country.

Some of the underlying reasons why COVID-19 may be more deadly for men than women may include the fact that heart disease is more common in elderly men than in elderly women, Dr. Stephen Berger, an infectious disease expert and co-founder of the Global Infectious Diseases and Epidemiology Network (GIDEON), told Healthline. Studies also find that high blood pressure and liver disease are more prevalent in men and these all contribute to more negative outcomes with COVID-19.

Genetics may also play a big role, Berger said. Women, because of their extra X chromosome, have a stronger immune system and response to infections than men.

You cant get away from biology and genetics, agreed Salvatore J. Giorgianni, PharmD, a pharmacist and senior science advisor for the Mens Health Network, which advocates for the health of men and boys.

Males are culturally conditioned to think of themselves as strong, Giorgianni told Healthline, but women are not the weaker sex when it comes to immunity.

Moreover, he noted, men have higher rates in 9 out of 10 of the leading causes of death in the United States.

That means theyre more likely to have preexisting conditions that can make COVID-19 more dangerous.

Behaviors that impact lung health, such as smoking, also may play a role in the diseases deadly impact on men.

In China, for example, smoking is largely a male habit, resulting in many men suffering from chronic lung disease, Berger said. This puts men at a much greater disadvantage should they get COVID-19.

The WHO estimates that air pollution kills more than 4 million people annually by contributing to illnesses such as asthma, bronchitis, emphysema, lung and heart diseases, and respiratory allergies.

A recent study from the Harvard T.H. Chan School of Public Health in Massachusetts reported that people who live in areas with high levels of air pollution are also more likely to die of COVID-19 than those in less polluted areas.

Pollution could also be playing a role in elevated COVID-19 mortality rates among men.

In most cultures, men are more likely to be engaged in outdoor work, exposing them to conditions associated with extreme climate and pollution, Berger said. This could directly impact their response to an infection like COVID-19.

High-risk occupations deemed essential under pandemic emergency orders notably first responders also may be disproportionately jobs men traditionally do, Derek M. Griffith, PhD, director of the Institute for Research on Mens Health at Vanderbilt University in Tennessee, told Healthline.

Higher rates of death among men in pandemics is not new.

Research on the worldwide flu of 1918, for example, found that non-elderly adult males died at a much higher rate than women, possibly because more men had a history of lung-damaging tuberculosis.

Male behavior during the pandemic also could be increasing their exposure to the novel coronavirus.

A Gallup poll taken between March 2 and 13 found that women were more concerned about COVID-19 than men were (by a 62 to 58 percent margin).

Its possible that men are more at risk because they tend to expose themselves more to larger crowds and social exchanges, including things like handshaking and sporting events, Berger said.

There are men with invincibility syndrome that underpins a lot of behaviors, and they tend to be less compliant with pandemic-related restrictions such as physical distancing, Giorgianni said.

For other men, he said, the issue isnt so much a cavalier attitude as simply being conditioned to think of health as not their job.

COVID-19 prevention messages aimed at men should focus on these traditional male roles, not ignore millions of year of biology and natural selection, Giorgianni said.

Guys are very concerned for their families, so tell them dont do it for yourself, do it for those who love you, he said. Even if they feel like theyre in good shape and can fight it off, they can still be a carrier can cause the death of their spouse or daughter or their dad.

Griffith cautioned, however, that much remains unknown about COVID-19, including its different impact on men and women.

Its worth considering these factors, but its a little premature, he said. Most of these statements seem to assume we know more about this disease than we do.

One thing that is well-proven, however, is that men tend to delay seeking healthcare and ignore or dismiss symptoms of illness.

Many men see self-care as an admission of weakness, David Ezell, chief executive officer of Darien Wellness, a mental health group in Connecticut, told Healthline. We are taught to be self-sufficient and there for everyone but ourselves. That results in ignoring telltale symptoms of not only COVID but any life-threatening condition.

Dr. Deborah Birx, the COVID-19 response coordinator for the Trump administration, noted at an April 9 briefing that 56 percent of people who have been tested for the illness are male compared to 44 percent female.

Of the men who were tested, 23 percent were positive for COVID-19, compared to 16 percent of women.

It gives you an idea about how men often dont present in the healthcare delivery system until they have greater symptomatology, Birx said. This is to all of our men out there, no matter what age group: If you have symptoms, you should make sure that you are tested.

More here:
Why COVID-19 Is Hitting Men Harder Than Women - Healthline

Recommendation and review posted by Bethany Smith

INTRODUCTION

Interplanetary space is populated by densely ionizing particle radiation not naturally present on Earth (1). Life on Earth has evolved under the protection of a geomagnetic field, which deflects high-charge, high-energy (HZE) ions; however, the constant flux of HZE ions in deep space is essentially impossible to shield, making astronaut exposures inevitable (2).

In the absence of human epidemiological data for exposures to HZE radiation, uncertainties surround the cancer risk estimates for space flight crews that venture beyond low Earth orbit. The current NASA space radiation cancer risk model is built largely upon epidemiological data from the survivors of the Hiroshima and Nagasaki atomic bombings, a cohort of individuals exposed predominantly to -rays (35), a form of photon radiation. One key assumption in this NASA model is that the spectra of tumor types, and their biologic behaviors, will be similar for individuals exposed to ionizing radiation, whether particle or photon. However, notable physical differences exist between ionizing photon and particle radiation, and these physical differences translate to unique ionization and damage patterns at the molecular, cellular, and tissue levels. HZE ion exposures produce spatially clustered DNA double-strand breaks, along with other DNA lesions in close proximity to break sites (6). In contrast, -rays produce sparse ionization events that are random in spatial distribution and less likely to have additional DNA lesions immediately adjacent to the break sites. Other assumptions in the model are that radiogenic tumors are no more lethal than their sporadic counterparts and that females are at greater risk for radiogenic cancers than males (7).

In assessing cancer risks to astronauts, the premise that HZE ion exposures increase the risk for the same types of tumors that arise in human populations exposed to -rays is supported by the few animal studies of HZE ion carcinogenesis conducted to date (8). These studies, conducted on genetically homogeneous animals, have demonstrated that tumor types arising in HZE ionirradiated animals are the same as those that occur spontaneously in these animals or following exposure to photon radiation (8). However, all previous data are from either inbred mice (9, 10) or rats (11), F1 hybrid mice (12, 13), or rat stocks with limited genetic heterogeneity (11, 1416), and the tumor types that arise in inbred rodents are determined, in very large part, by their genetic background. Therefore, the spectrum of tumors that might arise in a genetically diverse population exposed to HZE ions is unknown.

With the emergence of multiparent outbreeding strategies that produce highly recombinant mouse populations with allelic variants from multiple founder strains (1719), it is possible to model the effects of population diversity in carcinogenesis studies by minimizing the overwhelming effects of genetic background and increasing the phenotypic repertoire available within a test population. These populations also allow for high-precision genetic mapping (18, 20). Quantitative trait locus (QTL) mapping is a powerful forward-genetics approach that allows for unbiased testing of genetic variants that may influence gene-environment interactions for radiation effects (21, 22). Highly recombinant populations were constructed for the purpose of mapping complex traits, and QTL can often be resolved to megabase resolution (1820). In addition, complete sequence information can be used on genotyped individuals by imputing the substantial genomic resources available for the founder strains.

Studying tumors that arise in irradiated, genetically diverse mouse populations presents a unique opportunity to test key assumptions of the NASA risk model, particularly whether HZE ions induce the same tumors by the same mechanisms as -rays. If so, the current practice of extrapolating human epidemiological data from individuals exposed to -rays to astronauts exposed to HZE ions would be a valid approach for risk calculation in the space radiation environment.

To study the effects of HZE ion irradiation in a genetically heterogeneous population, 1850 HS/Npt stock mice (23) of both sexes were genotyped for 77,808 single-nucleotide polymorphism (SNPs) and exposed to (i) 0.4 gray (Gy) of 28Si ions (240 MeV/n) [linear energy transfer (LET), 80 keV/m; = 0.031 particles/m2] or (ii) 56Fe ions (600 MeV/n) (LET, 181 keV/m; = 0.014 particles/m2), (iii) 3 Gy of 137Cs -rays, or (iv) sham irradiation. We chose 56Fe ions because of their high abundance in galactic cosmic radiation (GCR) and because their high charge (Z = +26) makes them particularly damaging (24). The 28Si ions were selected because their LET more closely approximates the dose average LET of secondary fragments generated by GCR penetrating an aluminum spacecraft hull (25). The mice were monitored daily until they reached 800 days of age or became moribund. Comprehensive necropsies were performed on each mouse and involved all organ systems. Each detected lesion was characterized histologically by a board-certified veterinary pathologist. Tumors were the predominant cause of morbidity and mortality for both HZE ionirradiated (n = 622) and -rayirradiated (n = 615) populations as well as for the population of unirradiated mice (n = 613). Overall life span was significantly reduced for irradiated populations (Fig. 1A), which can be attributed to the increased incidence and decreased median survival for radiation-induced tumors. For irradiated mice, populations exposed to 0.4-Gy HZE ions had increased survival times compared to mice exposed to 3.0 Gy of -rays (Fig. 1A). Although these doses seem disparate, their selection is based on preliminary dose-response studies (26), which reveal that 0.4 Gy of HZE ions and 3.0-Gy -rays are each maximally tumorigenic.

Overall survival for HS/Npt mice, plotted as Kaplan-Meier survival, is presented for each exposure group (A). The incidence of specific tumor histotypes (B) and median survival times for these tumors (C) are plotted for each exposure group, which demonstrates that certain tumor types occur at an increased frequency following exposures to radiation of specific qualities and survival times in irradiated mice are decreased for some tumor types. The incidence of specific tumor histotypes within HS/Npt families is plotted for unirradiated (D), -rayirradiated (E), and HZE ionirradiated families (F) and demonstrates that specific tumor types often occur at very high incidence within some families and not at all in others, indicating heritability of tumor susceptibility. Furthermore, adjacent families are more closely related, and tumor incidences, for example, family 23 and adjacent families, have a high incidence of B cell lymphoma. The 47 HS/Npt families are arranged along the x axis (D to F).

A wide variety of tumor diagnoses [82 distinct tumor histotypes (table S1)] were observed in HS/Npt mice. Although most of these tumor types were rare, 18 histotypes were observed at incidences greater than 1%. Overall, the spectra of tumor histotypes produced in genetically diverse populations exposed to HZE ions and -rays were similar (Fig. 1B). Furthermore, tumor types induced by radiation were generally similar to those arising spontaneously in HS/Npt mice; however, radiation-exposed populations demonstrated decreased median survival times associated with tumor development (Fig. 1C and figs. S7 to S22) and increased incidences for specific tumor types, such as leukemias and Harderian gland adenocarcinomas, following radiation (Fig. 1B). The structure of the HS/Npt population can be divided into families that consist of mice more closely related to one another. Many tumor histotypes show high incidences within some families but are absent or rare in others (Fig. 1, D to F), which is consistent with genetic susceptibility to certain tumor types. Furthermore, certain tumorsparticularly lymphomas, pulmonary adenocarcinomas, hepatocellular carcinomas, Harderian gland tumors, and myeloid leukemiasdemonstrate a periodicity in tumor incidence (Fig. 1, D to F) where adjacent families often display similar incidences, which could be predicted on the basis of the circular breeding design used to generate HS/Npt, in which adjacent families are more related to one another than families further removed.

Although the tumor spectra are similar for each irradiated population, the different radiation qualities demonstrate varied efficiencies for producing specific tumor histotypes. -rayirradiated mice were at greater risk for myeloid leukemia, T cell lymphoma, pituitary tumors, and ovarian granulosa cell tumors than unirradiated mice; HZE ionirradiated mice demonstrated an intermediate susceptibility to these histotypes (Fig. 1B). For Harderian gland tumors, thyroid tumors, hepatocellular carcinomas, and sarcomas, HZE ion and -rayirradiated mice were at a similarly and significantly increased risk compared to unirradiated controls (fig. S7 to S22).

NASA permissible exposure limits for radiation limit the number of days an astronaut can spend in space based on modeled cancer risk. These limits are different for men and women (27) due primarily to epidemiological data that indicate that women are at greater risk for radiogenic cancers than men due to their longer life spans and susceptibility to specific cancer types, such as lung, ovarian, and breast carcinomas. Female HS/Npt mice have longer life spans than males (P = 2.7 106, log-rank test), with unirradiated females living 43 days longer (686.1 days), on average, than males (643.2 days) (fig. S1A). In contrast, no survival difference is observed between -rayirradiated females and males (P = 0.51) or HZE ionirradiated females and males (P = 0.06), indicating that female HS/Npt mice are more susceptible to radiation-induced morbidities and mortalities than males (fig. S1, B and C). Irradiated female mice had increased incidences of (i) ovarian tumors, (ii) mammary tumors, (iii) central nervous system tumors (pituitary adenomas, choroid plexus tumors, and ependymomas), (iv) diffuse large B cell and lymphoblastic B cell lymphomas, (v) osteosarcomas, and (vi) leiomyosarcomas (fig. S1D). Female mice were at lower risk for radiogenic lung cancer (fig. S1D and table S1), which is a major contributor to limiting flight time for female astronauts. Modeling risk by sex in humans has been confounded by different smoking rates between men and women in the atomic bomb survivor cohort (28).

To determine whether the genetic variants that increase tumor susceptibility following -ray irradiation also increase tumor susceptibility following HZE ion irradiation, genome-wide association mapping was performed for 18 tumor types in which there was an incidence of greater than 1%. Genomes were reconstructed for each mouse using a probabilistic model to predict founder haplotypes from high-density genotype data (18). Reconstructed genomes represent the unique accumulation of meiotic events for each individual and form a scaffold for the imputation of known sequencing information from the eight parental inbred strains. Polygenic covariance among related individuals is of significant concern in multiparent crosses and was corrected for during QTL mapping with a kinship term (18, 29). Mapping was performed for each phenotype using both a generalized linear mixed-effects model and proportional hazards regression model with the aforementioned kinship to adjust for polygenic covariance between related mice. To determine the significance thresholds for a model in which no QTL is present, the phenotypes were permuted, the regression model was run, and the maximum statistic was retained from each permutation (30). The 95% significance threshold was minimally variable between phenotypes with a mean threshold of log(P) > 5.8, and this value was used to identify significant associations. This is consistent with the estimated 0.05 Bonferroni genome-wide corrected threshold of log(P) > 6.0, which is considered overly conservative for QTL mapping (30).

At least one QTL was identified for 13 of the 18 tumor phenotypes examined. For tumor incidence, 35 QTL were identified with an average confidence interval of 3.4 Mb (table S2). For QTL at the 95% confidence threshold, effect sizes average 3.7% of the phenotypic variance with a range of 0.75 to 7.46%. For most of the tumors, the genetic architecture was complex with multiple QTL individually explaining a small proportion of the total variance. Although loci with moderate effects on the phenotype were most common, 11 large effect QTL were observed for seven tumor histotypes, with effect sizes greater than 5% (table S2).

To determine potential effects of genetic variants on tumor latency following irradiation, mapping was also performed using proportional hazards regression model (table S3) and 38 QTL were identified for 12 tumor types. QTL associated with tumor survival times mirrored those identified for tumor incidence, indicating that the genetic variants that control susceptibility to radiation-induced tumors also determine latencies.

Neoplasia is a binomially distributed trait, and therefore, the power to detect significant associations is primarily dependent on tumor incidence and QTL effect size. This leads to important considerations for the ultimate goal of this analysis, which is to determine similarities between QTL for specific neoplasms in populations exposed to different qualities of radiation. For some tumor types, a significant peak was observed in one exposure group with a suggestive peak present at the same locus in the alternative exposure group. We speculate that the reason certain radiation qualities produce only suggestive QTL for certain tumor phenotypes is likely due to decreased mapping power as a result of the variation in incidence between groups. In these cases, if the peak was more significant when combining radiation groups, the QTL was considered significant for all irradiated animals regardless of radiation quality.

Thyroid tumors are a well-known radiation-induced entity for both humans and mice; however, relatively little is known about genetic variants that increase susceptibility to this disease in mice. In HS/Npt mice, spontaneous thyroid adenomas occurred at relatively low frequencies and had a uniformly late onset, with tumors occurring between 700 and 800 days of age (Fig. 2A). In contrast, thyroid tumors arising in HZE ion or -rayexposed mice occur with significantly earlier onsets, with tumors arising as early as 250 days of age (Fig. 2A).

Thyroid follicular adenoma Kaplan-Meier survival estimate (A) along with genome-wide association plots for thyroid adenoma in HZE ionirradiated, -rayirradiated, HZE ion and -rayirradiated, and unirradiated mice (B) and an expanded plot for chromosome 2 (C), which contains the most significant association locus; gray lines indicate 95% (upper line) and 90% confidence (lower line) for log10(P values). Genome-wide association results reveal significant results in HZE ion and -rayirradiated mice that are further bolstered by combining the groups. The top panel of (D) shows strains that contribute the reference allele for the SNPs highlighted in red in the middle panel, indicated by vertical lines (D); the C57BL/6J strain contributes an allele that differs significantly from the other seven strains. The middle panel shows the log10(P value) of each SNP in the interval (D); the most significant SNPs are highlighted in red, and the bottom panel lists genes within the QTL interval. Genes that contain splice site, missense, or stop-related SNPs are colored red (D). Resample model averaging was performed within chromosome 2 to compare the distribution of peak log10(P values) for each exposure group (E); there is broad overlap for HZE- and -rayirradiated mice, and grouping all irradiated mice together further narrows the distribution of peak log10(P values). Mbp, megabase pair.

Association mapping reveals a significant 3.4-Mb interval on chromosome 2 for HZE ionexposed animals (Fig. 2, B and C). The same locus is identified in the -rayirradiated population if the significance threshold is decreased to a level at which 30% of identified QTL will be false positives. Combining both irradiated populations markedly increases the significance of the QTL identified on chromosome 2. The QTL interval (119 to 125 Mb) contains 39,179 SNPs (Sanger Mouse Genomes, REL-1505) and 142 genes (Ensembl version 85) (Fig. 2D). Within the QTL region, the C57BL/6J parental strain contains an introgression from the Mus musculus musculus genome (31); we found that HS/Npt mice carrying the C57BL/6J haplotype at the QTL have increased thyroid tumor incidence regardless of whether they are exposed to HZE ions or -rays.

To further explore the possibility that the QTL identified on chromosome 2 controls susceptibility following -ray and HZE ion exposures, we used a nonparametric resample model averaging procedure (32) across the entire chromosome to identify genomic loci that consistently reappear in resampled populations. Briefly, genome scans are repeated for each new dataset created, in which some individuals may be sampled more than once and some not at all (32). Resample model averaging consistently identifies the same locus for all groups of mice, regardless of radiation exposure (Fig. 2E). Furthermore, the resample model averaging procedure identifies the same locus for tumors arising spontaneously (Fig. 2E). Data from this tumor phenotype indicate that the same inheritable genetic variants contribute to an individuals risk of developing thyroid cancer, regardless of radiation exposure.

Acute myeloid leukemia (AML) is another common radiation-induced tumor in both mice and humans (33, 34). In concordance with previous studies conducted with inbred mice (26), -ray exposures in HS/Npt mice are more efficient at inducing AML than HZE ion exposures. In our -irradiated mice, 15.6% (96 of 615) developed AML compared to 2.9% (18 of 622) of those exposed to HZE ions and 1.6% (10 of 613) of unirradiated mice. AML median survival times were similar for all groups (Fig. 3A). Association mapping revealed a significant QTL for the -irradiated population on chromosome 2 that reached the 95% confidence threshold (Fig. 3, B and C), but no QTL was observed for the HZE ionexposed population, in which the incidence of AML was much lower. However, when grouping HZE ion and -rayirradiated mice together, the same QTL was significantly bolstered (Fig. 3B). If the susceptibility alleles identified at this locus were only contributing to disease following -ray irradiation and were, therefore, randomly distributed among the affected mice in the HZE ionexposed group, then we would expect the log10(P values) to decrease when combining -irradiated mice; however, the log10(P value) for this locus significantly increases when repeating the mapping procedure included all irradiated mice.

(A) Kaplan-Meier plots for myeloid leukemia demonstrate similar median survival estimates for myeloid leukemia between groups. (B) Genome-wide association procedures identify a narrow QTL on chromosome 2; two gray lines indicate 95% (upper line) and 90% confidence (lower line) for log10(P values). Expanded mapping results are depicted in (C) along with contributing strains for the reference allele. The A/J, AKR/J, C57BL/6J, DBA/2J, and LP/J strains contribute alleles that differ from the other strains, indicated by vertical lines in the top panel (C). The middle panel shows the log10(P value) of each SNP in the interval. The most significant SNPs are highlighted in red. The bottom panel shows the genes in the QTL interval. Genes that contain splice site, missense, or stop-related SNPs are indicated in red. Copy number results for Spi1 and Asxl1 in splenic samples from mice diagnosed with myeloid leukemia are plotted by exposure group (D).

Radiation-induced AML is a well-characterized disease in mice (10, 35, 36) and is most commonly the result of a radiation-induced minimally deleted region on chromosome 2 containing the PU.1 gene (current murine nomenclature, Spi1) and a recurrent point mutation that inactivates the remaining Spi1 allele (37). Figure 3C depicts mouse chromosome 2 with the positions of the QTL identified in our irradiated mice and the Spi1 gene. To test the hypothesis that AMLs occurring in HZE ionexposed animals will contain the same molecular aberrations know to occur in AML arising in -rayexposed mice, the copy number for Spi1 was investigated in leukemia samples to assess for deletions. As expected, most of the leukemias occurring in -rayexposed mice had a deletion in one copy of Spi1. In contrast, Spi1 deletions in spontaneously occurring AML were less common (Fig. 3D). Similar to -rayirradiated mice, leukemias that developed in mice exposed to HZE ions, although fewer in number, also have an increased incidence of Spi1 deletion. This finding indicates that AML arises by similar molecular mechanisms following exposures to HZE ions or -rays.

Because the QTL identified on chromosome 2 is approximately 60 Mb from the commonly deleted region containing Spi1 and because radiation-induced deletions can be notoriously large, we considered the possibility that the identified QTL was also deleted in these leukemias, resulting in loss of one copy of the QTL region. To test this hypothesis, we determined the copy number for a gene located at distal to the QTL support interval, Asxl1. As expected, we found that Asxl1 was not deleted in any sample in which Spi1 was not deleted; however, in 69% of cases with a Spi1 deletion, Asxl1and presumably the entire QTL regionwas also deleted (Fig. 3D). This demonstrates that most of the radiation-induced AML cases arose from progenitor cells haploinsufficient for the entire QTL region.

HZE ion and, to a lesser extent, -ray irradiation were particularly effective in inducing Harderian gland tumors at the doses used in this study, which was expected on the basis of extensive published radiation quality data on these tumors (8, 38). In the HZE ionirradiated group, Harderian gland tumors were observed in 22.7% (221 of 622) of mice and 3.2% (20 of 622) were malignant. In the -irradiated group, 15.3% (94 of 615) of mice developed Harderian gland tumors and 2.7% (17 of 615) were malignant. In contrast, spontaneous Harderian gland tumors occurred in only 4.1% (25 of 613) of unirradiated mice and 0.7% (4 of 613) were malignant. Despite the differences in tumor incidences following irradiation, median survival times for Harderian gland adenocarcinoma were similar for all groups (HZE ion, 582 days; -ray, 571 days; and unirradiated mice, 571 days).

Two QTL were observed for Harderian gland adenocarcinomas in HZE ionirradiated mice, one on chromosome 4 and another on chromosome 9 (Fig. 4A). The 1.7-Mb interval identified on chromosome 4 (Fig. 4B) is similar to previously discussed QTL regions in that combining both irradiated populations markedly increases the significance of this locus, which suggests that this QTL is associated with Harderian gland adenocarcinoma susceptibility in both HZE ion and -rayirradiated mice. In contrast, a 2.3-Mb QTL interval on chromosome 9 is observed only in HZE ionirradiated mice, and the locus is absent when combining all irradiated mice and repeating the mapping procedure (Fig. 4C). To further evaluate these QTL, resample model averaging was performed within chromosomes 4 and 9 to determine the distribution of peak log10(P values) along each chromosome. For chromosome 4, there is substantial spatial overlap identified in peak log10(P value) associations in the HZE ionexposed population and the -rayirradiated population, and the HZE ion and -rayirradiated population yields the most consistent identification of the QTL region (Fig. 4D). In contrast, although nearly all identified peak log10(P values) were identified in the 2.3-Mb QTL interval on chromosome 9 for HZE ionirradiated mice, the distributions of peak log10(P values) for other exposure groups do not substantially overlap and are widely distributed along the chromosome (Fig. 4E). The resample model averaging results indicate that while the chromosome 4 QTL contributes to susceptibility to Harderian gland adenocarcinomas in both HZE ion and -rayirradiated populations, the QTL identified on chromosome 9 appears to only be involved in Harderian adenocarcinoma susceptibility following HZE ion exposures.

Genome-wide association plots for Harderian gland adenocarcinoma (A) for HZE ionirradiated, -rayirradiated, HZE ion and -rayirradiated, and unirradiated mice; two gray lines indicate 95% (upper line) and 90% confidence (lower line) for log10(P values). Chromosome 4, which is expanded in (B), reveals a significant QTL associated with HZE ion irradiation, which is further increased significantly when grouping all irradiated mice (HZE ion and -ray irradiated) together, which indicated that the genetic variants in this location are important for Harderian gland adenocarcinoma following exposures to either HZE ion or -ray irradiation. In contrast, chromosome 9, which is expanded in (C), reveals a significant QTL associated only with HZE ion irradiation; this locus is absent when grouping all irradiated mice (HZE ion and -ray irradiated) together, which suggests that the allele(s) present in this region may only play a role for HZE ioninduced tumors. Resample model averaging was performed within chromosomes containing significant QTL. There is significant spatial overlap identified on chromosome 4 for peak log10(P value) associations in the HZE ionexposed population, the -rayirradiated population, and the HZE ion and -rayirradiated population that demonstrates the most consistent identification of the QTL region (D). In contrast, although nearly all identified peak log10(P values) were identified in the chromosome 9 QTL interval for HZE ion irradiated mice, the peak log10(P values) for other exposure groups are widely distributed along the chromosome (E).

In addition to looking for similarities between individual, selected QTL for HZE ion and -rayexposed populations, we also sought a more holistic method in which entire genome-wide association results could be compared between groups in an unsupervised process. We used hierarchical clustering to create cluster dendrograms using entire genome-wide scans for a given phenotype. By considering results from genome-wide associations, rather than individualized peaks observed within genome-wide associations, we submit for comparison not only highly significant QTL regions but also the numerous loci detected with lower confidence.

Unsupervised hierarchical clustering of genome scans creates significant clustering events that often occur for the same histotype regardless of radiation exposure (Fig. 5A). Multiple tumor histotypesincluding mammary adenocarcinoma, thyroid adenoma, and hepatocellular carcinomacluster by histotype, regardless of radiation exposure. To demonstrate and validate the methodology of QTL clustering, genome-wide scans for coat colors in each treatment group are evaluated and coat color genome-wide scans cluster together, as expected (Fig. 5B). These results further support the hypothesis that host genetic factors are highly important in determining risk of radiation carcinogenesis, whether following HZE ion or -ray exposures.

(A) Unsupervised hierarchical clustering of genome-wide association scans for tumor phenotypes reveals that the most significant clustering events often occur for the same histotype regardless of radiation exposure; these include mammary adenocarcinoma, thyroid adenoma, and hepatocellular carcinoma. (B) As expected, clustering genome scans for coat color demonstrates the expected results: that genome scans cluster together despite exposure group. The green line represents the 99% confidence level of the most significant dendrogram heights by permutations (log10 values permuted with genetic markers) to determine a distribution of dendrogram heights under the null hypothesis that no associations exist (C), demonstrating that the observed clusters are highly unlikely to occur randomly.

Permissible exposure limits for astronauts are based on the risk of death from cancer rather than cancer development, and the incidence to mortality conversion used in the risk calculation uses spontaneously occurring cancers in the U.S. population. Thus, there is an assumption that radiogenic tumors are no more lethal than spontaneous tumors. To determine whether tumors that arise following HZE ion exposure are more malignant than their counterparts arising in unirradiated or -rayirradiated mice, metastatic disease was characterized for each group. Pulmonary metastases were consistently observed in cases of hepatocellular carcinoma, Harderian gland adenocarcinoma, osteosarcoma, and ovarian granulosa cell tumor. Metastases were no more frequent in irradiated animals than in controls, and there was no significant difference in metastatic incidence between HZE ionirradiated mice and -rayirradiated mice (fig. S5A), and pulmonary metastatic density is similar between groups (fig. S5, B to D).

Tumor latency following irradiation was compared between exposure groups using survival statistics. Differences in tumor latency in this context indicate a decrease in time for tumor initiation or promotion. Since radiation is efficient at both initiation and promotion, decreased latencies are expected for irradiated population. Tumor progression is not evaluated, and our results therefore do not demonstrate whether tumors arising in irradiated individuals are more likely to progress rapidly than those arising spontaneously. As expected, tumors arising in both HZE ion and -rayirradiated mice show significantly decreased latencies in comparison to the unirradiated population (fig. S7 to S22). However, HZE ions did not further decrease latencies when compared to -rayirradiated mice.

Carcinogenesis as a result of space radiation exposure is considered the primary impediment to human space exploration (2). Compared to forms of radiation found naturally on Earth, including x-rays, -rays, and particles, HZE ions in space are much more difficult to shield (2) and have a distinct ionization pattern that aligns along dense track structures, resulting in clustered damage to chromatin (6). Because HZE ions, a highly penetrating component of GCRs, are not amenable to shielding (28, 29), exposure risks are inherent to manned missions in interplanetary space, but estimating the risk associated with this unique form of particle radiation is complicated by the essential lack of data for human exposures (28). As a substitute, human exposure data from other forms of ionizing radiation, primarily -ray (35) photon radiation, are used in cancer risk models with the assumption that photon and particle radiation have qualitatively comparable biological effects.

Animal models are a vital component in determining the validity of the extrapolation of human terrestrial radiation exposure data to exposures that will occur in astronauts in the space radiation environment. To date, carcinogenesis studies designed to evaluate the effects of HZE ions have used rodents with limited genetic heterogeneity (916). The advantage of removing genetic variability in animal models is the consequent decrease in phenotypic variability, which allows for fewer individuals to detect potential environmental effects on phenotype; the disadvantage is that strain-specific responses in genetically identical populations are significant and can obscure the variability that one might expect in a diverse population, such as humans. By using a genetically diverse population with a wide range of tumor susceptibilities, the spectra of tumors that occur following exposures to particle and photon radiation can be compared. The results of this study indicate that the spectrum of tumor histotypes observed in a genetically diverse population exposed to particle radiation is not unique to that observed in a population exposed to photon radiation or to the tumor spectrum observed in an unirradiated population. Despite the similarities observed in tumor spectra following radiation exposures, the radiation qualities and doses used for this study have unique efficiencies at producing specific tumor types, and while this work demonstrates that the underlying genetics of susceptibility can be similar for tumorigenesis following both high- and low-LET radiation, further work is necessary to define risks for specific tumor histotypes based on exposures.

This study uses a highly recombinant mouse population (HS/Npt stock) that is genetically diverse and designed for genome mapping (1921, 23), a forward-genetics approach that allows for an unbiased search of the entire genome for genetic associations. In contrast, genetically engineered mouse models rely on a reverse-genetics approach in which a given gene is first altered and the resulting phenotypes are then characterized. Studies using forward-genetics are most informative in populations that contain abundant genetic and phenotypic diversity. HS/Npt mice are a multiparent cross derived from eight inbred strains (A/J, AKR/J, BALBc/J, CBA/J, C3H/HeJ, C57BL/6J, DBA/2J, and LP/J); each individual contains a unique mosaic of founder haplotypes and a high degree of heterozygosity, and recombination events become increasingly dense with each generation. Our population of HS/Npt mice was obtained from generation 71 of circular outbreeding. Creating these populations is not trivial and has been a central goal of communities involved in genetics research over the past few decades, resulting in the creation of rodent populations ideal for genome mapping (1820, 3942).

Genome mapping allows the discovery of QTL associated with susceptibility to complex traits, such as radiogenic cancers; this approach is uniquely suited to comparing inheritable risk factors for cancers following exposures to unique carcinogens, such as particle and photon radiation. In broader terms, this work demonstrates the utility of highly recombinant mouse models created for genetic mapping in carcinogenesis studies, an application that has not been previously attempted. Mapping QTL in carcinogenesis studies provides inherent challenges due to the structure of binomial data, potential confounding causes of death following irradiation and aging, the fundamental stochastic nature of radiation tumorigenesis, and incomplete penetrance of potential allelic variants. Despite these challenges, we were able to map QTL for 13 neoplastic subtypes and many of these identified loci are previously unidentified.

At the doses used in this study, HZE ions appear to be less effective than -rays in inducing precursor T cell lymphoblastic lymphoma (pre-T LL) and ovarian tubulostromal adenomas and granulosa cell tumors. This may be due to a combination of dose inhomogeneity in HZE ionirradiated tissues and the major role cell killing plays in the etiology of these specific tumors. pre-T LL can be prevented by transplanting irradiated mice with unirradiated syngeneic bone marrow cells or by shielding some of their bone marrow during irradiation (43, 44). The underlying mechanism by which unirradiated bone marrow cells suppress lymphomagenesis may involve a cell competition process by which older T cell progenitors resident in the thymus are normally replaced by fresh progenitors that immigrate from the bone marrow. Radiation kills these fresh bone marrow cells or reduces their fitness, which, in turn, prolongs the time that older T cell progenitors already in the thymus survive and self-renew. This, along with the increased proliferative cycles of the older T cell progenitors needed to maintain production of mature T cells, results in a corresponding increase in the oncogenic mutations that they accumulate and a concomitant increase in lymphomagenesis (45). Replenishing dead or damaged bone marrow cells by transplantation or preventing their damage through shielding suppresses lymphomagenesis.

At the 3-Gy dose of -rays used in this study, all of the bone marrow cells are uniformly irradiated. This is not the case for HZE particle radiation. The average diameter of a murine bone marrow cell nucleus is around 6 m (46). At the fluence of HZE ions used in this study, the probability that a 6-m-diameter nucleus will be traversed by a 28Si ion and a 56Fe particle is 0.88 and 0.40, respectively. On the basis of a Poisson distribution, the probabilities of a nucleus not being traversed at all are 0.41 and 0.67 for 28Si and 56Fe irradiation, respectively. Thus, many of the T cell progenitors in the bone marrow are not irradiated (although they receive a small dose from -rays). These cells should exert a protective effect similar to transplanting unirradiated bone marrow cells or shielding some of the bone marrow during irradiation, rendering HZE ions less efficient for lymphomagenesis. Given that most of the pre-T LL in the HZE ionirradiated group are likely spontaneous, it is expected that they cluster more closely to spontaneous pre-T LL than to -rayinduced pre-T LL.

The mechanism leading to murine tumors of ovarian surface epithelium origin is well understood. Loss of primordial follicle oocytes by radiation-induced apoptosis results in a decrease in estrogen production, which, in turn, leads to elevated levels of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) in the circulation. FSH and LH drive proliferation of ovarian surface epithelium cells (47). Ovarian tumors can be induced in some animal models by artificially manipulating levels of these hormones (4749). Irradiated mice can be protected from tubulostromal adenomas and granulosa cell tumors by shielding one ovary during irradiation or by transplanting the mice with an unirradiated ovary (50, 51); these interventions protect some oocytes and thereby maintain proper regulation of FSH and LH levels.

Assuming that the target cells are primordial follicle oocytes with a diameter of 12 m, the probabilities of no traversals are 0.2 for 56Fe and 0.03 for 28Si at the 0.4-Gy dose used here. The probabilities for one or fewer traversals are 0.52 for 56Fe and 0.14 for 28Si. Whether a sufficient number of follicles survive at 0.4 Gy to account for the observed ovarian tumor sparing is unknown. Mishra and colleagues (52) observed a dose-dependent decrease in primordial stage follicles in C57BL/6 mice 8 weeks after irradiation with 56Fe ions (600 MeV/n). Sixteen percent of the follicles survived at the 0.3-Gy dose, and normal levels of serum FSH and LH were present; at 0.5 Gy, only 1% of the follicles survived and an increase in serum FSH was observed. Caution is needed in using Mishras results in interpreting our own since we used mice with different genetic backgrounds and the FSH and LH levels in the 0.3 Gyirradiated mice may increase relative to unirradiated controls if time points beyond 8 weeks are assayed. In any event, microdosimetric effects should be incorporated into any risk model for tumors in which cell killing plays a prominent role.

The location of the chromosome 2 QTL in a region frequently deleted in radiogenic AMLs may be happenstance, but there are scenarios in which its chromosomal location would be crucial to its function. One possibility is that the polymorphism increases the frequency of AML-associated chromosome 2 deletions in irradiated hematopoietic cells by controlling the spatial confirmation of the chromosome such that the proximal and distal deletion breakpoints are in close proximity to one another (46). This type of proximity mechanism has been evoked to explain recurrent chromosomal rearrangements seen in radiation-induced papillary thyroid carcinoma and some spontaneous cancers (53, 54). In this scenario, the QTL could be a structural polymorphism (e.g., segmental duplication or interstitial telomeric sequence), which would affect chromosomal conformation, yielding a different conformation in susceptible mouse strains than resistant strains. Structural polymorphisms are easily missed in the assembly of the strain-specific genomic sequences used for mapping studies, so we would be unaware of its existence. A second possibility is that the polymorphism is in a gene needed for myeloid progenitor cell survival. Mouse strains resistant to myeloid leukemia would have a hypomorphic allele of this gene. If one copy is lost (i.e., through radiation-induced deletion), then the remaining copy would be insufficient for cell survival. Thus, in mouse strains resistant to radiogenic AML, a chromosome 2 deletion, which is the first step in radiation leukemogenesis, is a lethal event and leukemogenesis is thereby halted. Susceptible strains would have a fully functional allele of the gene, so that if one copy is deleted, the remaining copy maintains cell viability, allowing further leukemogenic events to occur (46). A caveat to both the chromosome conformation and haploinsufficiency scenarios is that the chromosome 2 deletions mapped in radiogenic AMLs from the F1 progeny of AML-susceptible CBA/H mice and AML-resistant C57BL/6 mice do not occur preferentially in the CBA/H origin chromosome (55). However, in that study, only 10 tumors were informative. In addition, susceptibility to radiogenic AML is multigenic, so it is possible that the difference in susceptibility between the CBA/H and C57BL/6 strains is not due to the chromosome 2 QTL.

HZE ions seem particularly effective in inducing Harderian gland tumors at the doses used in this study. This result was expected on the basis of extensive published radiation quality data on these tumors (8, 38). The mechanism responsible for higher tumorigenic efficacy of HZE ions relative to -rays is unknown; however, we have identified a QTL associated with Harderian gland adenocarcinoma following HZE ion exposures that does not appear to lend susceptibility to the same tumor following -ray exposures (Fig. 4C). Furthermore, HZE ioninduced Harderian gland adenomas and adenocarcinomas cluster away from spontaneous and -rayinduced Harderian gland tumors (Fig. 5), indicating non-overlap of some of the susceptibility loci. There are data that suggest that HZE ion irradiation has an effect on tumor promotion that -ray irradiation lacks. The observation is that pituitary isografts, which result in elevated levels of pituitary hormones, enhance the induction of Harderian gland tumors and decrease their latency in mice irradiated with -rays or fission neutrons but do not increase tumor prevalence in mice irradiated with 56Fe ions (600 MeV/n) (12). This would explain the high relative biological effectiveness (RBE) for 56Fe ions. It would also render QTLs that act in the promotion of -ray and spontaneous tumors irrelevant to HZE ioninduced tumors.

The use of unsupervised clustering on genome-wide association results is a novel approach to search for shared tumorigenic mechanisms between radiogenic and spontaneous tumors or between tumors induced by different radiation qualities. Potentially, the results could be used to inform risk modeling. For example, using the 99% confidence interval as a cutoff, thyroid adenomas, pituitary tumors, osteosarcomas, B cell lymphoblastic leukemia, mammary tumors, and hepatocellular carcinomas cluster by histotypes regardless of whether they arose in HZE ionirradiated or -rayirradiated mice. Of these, the incidences of thyroid tumors, pituitary tumors, and osteosarcomas are significantly increased following exposures to either HZE ions or -rays. Taking pituitary adenoma as an example, these findings suggest that it would be reasonable to extrapolate the risk of HZE ioninduced pituitary adenoma as a multiple of -rayinduced pituitary adenoma risk (i.e., using a relative risk model). Because there were too few spontaneous pituitary adenomas to position them on the dendrogram, we cannot determine whether the risk of HZE ioninduced pituitary adenoma could reasonably be modeled on the basis of the incidence of the spontaneous tumor. Another pattern of association is observed for Harderian gland adenoma and follicular B cell lymphoma in which, at the 99% confidence interval, spontaneous tumors cluster with -rayinduced tumors but not with HZE ioninduced tumors. There are a number of ways that this could occur. Three possibilities are as follows: (i) HZE ions act through a tumorigenic mechanism different from that of spontaneous and -rayinduced tumors. (2) HZE ions bypass the need for one or more of the genetically controlled steps required for spontaneous and -rayinduced tumors, and (iii) there are multiple pathways to tumor formation, and HZE ion irradiation forces tumorigenesis through only one (or a subset) of them. Harderian gland tumors may fall into the second possibility. As described earlier, observations on mice receiving pituitary isografts before irradiation suggest that HZE ions may have Harderian gland tumor promotion effects that -rays lack. If so, the QTL controlling those effects would be inconsequential in the tumorigenesis of HZE ioninduced Harderian gland tumors, and those tumors would cluster away from their spontaneous and -rayinduced counterparts. Whether a relative risk model, an absolute risk model, or a combination of the two would be most appropriate in Harderian gland tumor risk calculations would depend on which of the above possibilities is most accurate.

NASA seeks to limit the risk of exposure-induced death (REID) from radiogenic cancer to below 3% (56). For multiple missions aboard the International Space Station (flown in solar minimum conditions), the model projects that males will exceed permissible exposure limits at 24 months and females, at 18 months; women are considered at greater risk for radiogenic cancers than men because of longer life spans and increased susceptibility to specific cancer types, including lung, ovarian, and breast carcinomas. Because the 3% REID is derived from the upper 95% confidence interval for the risk estimate (57), decreasing the uncertainty for space radiationinduced cancers can significantly increase the flight time allowed for astronauts. The 95% confidence interval surrounding the risk estimates not only primarily reflects uncertainties in our understanding of HZE ions but also includes uncertainties surrounding dose-rate effects, transfer of risk between human populations, space dosimetry, and errors in the existing human epidemiology data. Concerning sex predilections, our results also demonstrate a sex difference in carcinogenesis risk, where female mice are at greater risk for radiogenic cancers than males, following either HZE ion or -ray exposures. These results are consistent with the current NASA model to calculate cancer risk from space radiation exposures (5).

Whether genotypic assays of radiosensitivity can improve the precision of risk assessment in humans will depend on a number of factors. One is the extent to which heritable sequence variants determine cancer risk from HZE ion exposures. HZE ion radiation exposures result in more complex molecular lesions that are less amenable to repair (58). Thus, it could be argued that sequence variants that result in subtle differences in DNA repair and damage response pathways would have a lesser impact on HZE ion radiation carcinogenesis. However, this work demonstrates that genetic susceptibility does indeed have a significant role in tumorigenesis following HZE ion exposures. Personalized approaches to cancer risk assessments may eventually allow for greater reductions in uncertainties when generating space radiation cancer risk estimates (28).

There are limitations to a mouse carcinogenesis study comparing acute -ray and HZE ion exposures. First, for cost efficiency and logistics reasons, a single dose was used for each radiation quality: 3.0 Gy for -ray exposures and 0.4 Gy for HZE ion exposures. Preliminary studies have demonstrated that these doses produce the maximum tumor incidence in inbred strains (24). Because tumor susceptibility and association mapping were the primary goals of this study, doses were chosen with the goal of generating the greatest tumor incidences and, therefore, the greatest power to detect significant QTL. However, caution must be taken when comparing the two single-dose groups, as it is impossible to untangle dose responses in such a study. An additional benefit of the selected doses is that 0.4 Gy of HZE ions represents a realistic dose, received over 20 to 30 months, for a flight crew traveling to Mars. Second, the applicability of these findings to human populations is limited, as rodents serve only as models of carcinogenesis.

The results presented here indicate that host genetic factors dictate risk for tumor development following radiation exposures, regardless of radiation quality. Therefore, at a population level, risks can be extrapolated from terrestrial exposures to the space radiation environment and at an individual level, and humans harboring susceptibility alleles for radiation-induced tumors developed on Earth are also likely at increased risk in space.

Male and female HS/Npt mice (n = 1850) were generated from breeding pairs obtained from Oregon Health and Sciences University (Portland, OR). The mice were group-housed (five mice of the same sex per cage) in a climate-controlled facility at 70F (21.1C) with free access to food (Teklad global rodent diet 2918) and sterile water and a 12-hour light cycle. Mice were shipped to Brookhaven National Laboratories (Upton, NY) where they were exposed to accelerator-produced HZE ions at the NASA Space Radiation Laboratory at 7 to 12 weeks of age. HS/Npt stock mice of both sexes were exposed to 0.4 Gy of 28Si ions (240 MeV/n) (n = 308) or 56Fe ions (600 MeV/n) (n = 314), 3 Gy of 137Cs -rays (n = 615), or sham irradiated (n = 622). Following irradiation exposure or sham irradiations, mice were returned to Colorado State University (Fort Collins, CO) and monitored twice daily for the duration of the study. The mice were evaluated for cancer development until they reached 800 days of age or became moribund. All animal procedures were approved by the Colorado State University Institutional Animal Use and Care Committee.

This study uses a highly recombinant mouse population (HS/Npt stock) that is genetically diverse and designed for genome mapping (1921, 23). HS/Npt mice are a multiparent cross derived from eight inbred strains (A/J, AKR/J, BALBc/J, CBA/J, C3H/HeJ, C57BL/6J, DBA/2J, and LP/J); each individual contains a unique mosaic of founder haplotypes and a high degree of heterozygosity, and recombination events become increasingly dense with each generation. Our population of HS/Npt mice was obtained from generation 71 of circular outbreeding.

DNA was isolated from tail biopsies taken from each mouse at 9 to 10 weeks of age. DNA was extracted and purified (QIAGEN, catalog no. 69506) according to the manufacturers instructions. GeneSeek (Lincoln, NE) performed genotyping assays using the Mega Mouse Universal Genotyping Array (MegaMUGA) (59) for a total of 1878 mice (including 28 inbred mice representing the founder strains). The MegaMUGA is built on the Illumina Infinium platform and consists of 77,808 single-nucleotide polymorphic markers that are distributed throughout the genome with an average spacing of 33 kb.

The heterogeneous stock mice are descendants of eight inbred founder strains. For each mouse, allele calls from the MegaMUGA array were used to calculate descent probabilities using a hidden Markov model (HMM), in which the hidden states were the founder strains and the observed data were the genotypes. The HMM generates probabilistic estimates of the diplotype state(s) for each marker locus and produces a unique founder haplotype mosaic for each mouse (18).

For this lifetime carcinogenesis study, all disease states were interpreted within the context of a systematic pathologic evaluation directed by board-certified veterinary pathologists (E.F.E. and D.A.K.). Structured necropsy and tissue collection protocols were followed for each mouse and involved photodocumentation of all gross lesions, collection of frozen tumor material, and preservation of tumor material in RNAlater. All tissues were grossly evaluated for all mice. To evaluate brain tissues and Harderian glands, craniums were decalcified for 48 hours in Formical-4 (StatLab, McKinney, TX 75069, product 1214) and five coronal sections of the skull were reviewed for each mouse. All gross lesions were evaluated microscopically and fixed in 10% neutral-buffered formalin and paraffin-embedded, and 5-m sections were stained with hematoxylin and eosin (H&E) and evaluated by a veterinary pathologist. For mice with solid tumors, all lung fields were examined histologically to detect the presence or absence of micrometastases. Tumor nomenclature was based on consensus statements produced by the Society of Toxicologic Pathology for mouse tumors (www.toxpath.org/inhand.asp). Representative histologic images routinely stained with H&E are presented in figs. S2 (A to E) and S3 (A and B).

Tissue microarrays were constructed to immunophenotype and subcategorize lymphoid neoplasms, which were the most commonly diagnosed tumors in irradiated and unirradiated HS/Npt mice. Identification of tissue sampling regions was performed by a veterinary pathologist. For each case, duplicate cores were taken from multiple anatomic locations (lymph nodes, spleen, thymus, etc.). Thirteen tissue microarrays were created, each of which contained six cores of control tissue at one corner of the array (haired skin, spleen, thymus, or liver); these control tissues were present in a unique combination and allowed for (i) orientation of the resulting sections, (ii) verification that the slide matched the block, and (iii) positive controls for immunohistochemistry. Figure S3D illustrates one tissue microarray as well as the resulting immunohistochemistry results for one thymic lymphoma (fig. S3E) and a core containing normal spleen (fig. S3F). Immunohistochemistry for T cell identification was performed using a rabbit monoclonal, anti-CD3 (SP7) antibody obtained from Abcam (ab16669; 1:300). Immunohistochemistry for B cell identification was performed using two rabbit monoclonal antibodies: an anti-CD45 antibody (ab10558; 1:1000) and an anti-PAX5 antibody (ab140341; 1:50). All immunohistochemistry was performed on a Leica BOND-MAX autostainer with the Leica BOND Polymer Refine Red Detection system (Leica DS9390, Newcastle Upon Tyne, UK). In addition to defining the immunophenotype, lymphomas were characterized according to the Mouse Model of Human Cancer Consortiums Bethesda protocols (60). For these protocols, anatomic location is important for the final diagnosis, and therefore, lymph node involvement was used from necropsy reports when necessary. Additional features included cell size, nuclear size, chromatic organization, and mitotic figure frequency, and the presence or absence of a leukemic phase was defined by bone marrow involvement within the sternum or femur. The most common lymphoma subtypes (fig. S4A) were evaluated for survival (fig. S4B), and pre-T LL typically presented with early-onset and large thymic masses.

Droplet digital polymerase chain reaction (ddPCR) was performed on cases of AML to assess deletion status via copy number variation for two genes: Spi1 and Asxl1. These genes are both located on chromosome 2 at base pair locations 91,082,390 to 91,115,756 for Spi1 and 153,345,845 to 153,404,007 for Asxl1. To establish a reference for normal diploid copy number in each AML sample, the copy number of H2afx was also determined. H2afx is located on chromosome 9, and deletions in this region have not been reported in murine AML. Bio-Rad PrimePCR probes were used for all assays as follows: Asxl1 ddPCR probe (dMmuCPE5100268), Spi1 ddPCR probe (dMmuCPE5094900), and H2afx ddPCR probe (dMmuCPE5104287). Ratios were created between the test gene and the reference gene (Spi1:H2afx and Asxl1:H2afx) to determine copy number with the assumption that the reference gene would not be deleted or amplified. Ideally, ratios of 1:1 represent equal copy numbers for both the test gene and the reference gene, and ratios of 1:2 represent a deletion in one copy of the test gene. However, since the tumor samples contained neoplastic cells as well as stromal cells and other cells, the ideal 1:2 ratio was not commonly observed. This is because stromal cells, which occur at unknown proportions in each tumor and which should not have chromosomal deletions, artificially increase ratios for tumor samples in which a deletion is indeed present. To account for stromal cell contamination, a cutoff ratio of 3:4 was established. Tumor samples with ratios below 3:4 were considered to have a deletion in one copy of the test gene.

For cases in which a solid tumor was identified, a standard section containing all lung lobes was processed and evaluated histologically. In cases where pulmonary metastases were observed, whole-slide scanning was performed at 200 magnification using an Olympus VS120-S5 and the OlyVIA software suite (www.olympusamerica.com/) to generate images for quantification of metastatic density (fig. S5). An analysis software, ImageJ (https://imagej.nih.gov/ij/), was used to quantify the total area of normal lung and the total area of metastatic foci (fig. S5). Metastatic density is reported as a percentage of the total metastasis area divided by the total lung area.

Association mapping was performed using a mixed-effects regression model with sex and cohort as fixed effects and a random-effects term to adjust for relatedness between mice by computing a matrix of expected allele sharing of founder haplotypes for each pair of mice (22). Three statistical models were fit to account for the wide range of trait distributions in this study. A generalized linear regression model was fit for binomial distributions, such as neoplasia. Cox regression analysis was incorporated to model time-to-event distributions to evaluate genetic contributions to tumor latency. Following genome-wide association analyses, resample model averaging methods were used to identify QTL that are consistently reproduced within subsamples of the mapping population.

Thresholds were determined using a permutation procedure in which the genotypes were fixed and the phenotype values were rearranged randomly within each sex. The distribution of the maximum negative log(P value) of association under the null hypothesis that no associations exist (null model) was determined for each genome scan with permuted data. One thousand permutations were performed for each phenotype in each radiation exposure group, simulating effects arising from covariates, the linkage disequilibrium structure of the genome, and effects due to phenotype distribution. A threshold was defined as an estimate of the genome-wide significance for which a type I statistical error will occur at a given frequency (29). Confidence intervals for each QTL were determined by nonparametric resample model averaging procedures using bootstrap aggregation with replacement. In this procedure, the mapping population is sampled to create a new dataset in which some individuals may be omitted and some may appear multiple times (30), and the locus with peak significance is recorded. Resampling is repeated 200 times for each phenotype to determine a 95% confidence interval for a given QTL. Effect sizes were calculated using the Tjur method for association mapping with logistic regression and pseudo-R2 for mapping with Cox proportional hazard regression. Statistical significance for each model was assessed using a permutation strategy to randomize genotypes via resampling without replacement and maintaining covariates. Permutation analysis was performed (1000 tests) for each trait and exposure group to generate estimations of genome-wide significance thresholds. As genome scans with hundreds of thousands of imputed SNPs are computationally intensive, parallel computing was essential and accomplished using spot instances of resizable Elastic Compute Cloud hosting resources.

Comparisons were made between whole-genome scans using Pearson correlations as a similarity measure with clustering based on average linkage. Significance of clustering results was estimated with 10,000 random permutations of the dataset (log10 values permuted with genetic markers) to determine a distribution of dendrogram heights under the null hypothesis that no associations exist. Each permutated dataset simulates a null distribution of the maximally significant clustering based on a randomly assorted set of P values for each genomic locus.

Bootstrap aggregation is a resample model averaging procedure that has been demonstrated to produce highly accurate estimates of QTL in structured populations (32). The procedure is relatively simple: for a genome-wide association study (GWAS) of n individuals, a sampling of n draws is obtained, with replacement, from the observed individuals to form a new dataset in which some individuals are omitted and some appear multiple times. For each new dataset created this way, an estimate of the QTL location is calculated. This process is repeated many times and is the basis for determining a confidence interval for a given result. The use of bootstrap procedures is commonly used this way to estimate QTL support intervals in experimental crosses; however, this statistical method can potentially be applied to other areas of QTL research, including comparative QTL mapping.

When an identical QTL is observed for two distinct traits, one explanation is that a single gene is involved for two distinct biologic processes, also known as pleiotropy. This was sometimes assumed in early mouse QTL studies that resulted in coincident loci for distinct traits. Another possibility, however, is that two distinct genetic variants are present in close proximity, each independently contributing to the two phenotypes. Because the two hypothetical genetic variants happen to be in close proximity, they are difficult to distinguish in low-resolution mapping studies. Using resample model averaging in highly recombinant mice is proposed to best differentiate precise locations of the QTL; if the same markers were repeatedly identified, then the case for pleiotropy was strengthened. For comparative QTL mapping in tumorigenesis studies, nonparametric resample model averaging could similarly be leveraged to identify whether the same QTL renders an individual susceptible to distinct environmental carcinogens. One significant advantage to using bootstrap procedures to detect potential coincident loci is that comparisons can be made between groups based on the identification of a highly significant QTL identified in only one exposure group (e.g., at a false-positive rate of 1 per 20 scans). This QTL may be present in the alternative exposure group, but at lower confidence (e.g., at a false-positive rate of 1 per 10 scans), and therefore discarded in a typical GWAS. A diagrammatic representation of the comparative QTL bootstrap procedure is presented in fig. S6. Because the resultant genetic positions derived from bootstrapping are composed of the most significant locus for each resampling regardless of the significance level for the mapping procedure, comparisons can be drawn between QTL that might have been discarded on the basis of the stringent statistical demands of an assay involving hundreds of thousands of independent tests. Using this procedure on thyroid tumors demonstrates that the same loci are consistently identified whether exposed to particle or photon irradiation (Fig. 2E). Using the comparative QTL procedure described, it can be determined whether an individuals cancer risk from one carcinogen will be predictive of that individuals cancer risk to another carcinogen. The application of this procedure is well illustrated by the space radiation problem, where much is known about -ray exposures and little is known about space radiation exposures.

In addition to looking for similarities between individual selected QTL for HZE ion and -rayexposed populations, we also sought a more holistic method in which entire genome scans could be compared between groups in an unsupervised process. By using entire genome scans, we submit for comparison not only highly significant regions but also the numerous loci detected with lower confidence. To determine similarity of genetic association profiles for all phenotypes and to detect possible coincident QTL, clustering procedures were used to compare genome-wide association scans between different radiation exposure groups. To demonstrate and validate the methodology of QTL clustering, genome-wide scans for coat colors in each treatment group are evaluated (Fig. 5B). As expected, genome-wide scans for coat color are unaffected by radiation exposures, and therefore, clustering is based entirely on coat phenotype rather than radiation exposure group. Using the same procedure for neoplasia indicates that tumor types often clustered together as well, regardless of radiation exposure (Fig. 5A). Genome scans for thyroid tumors and mammary adenocarcinomas in radiation-exposed groups and all hepatocellular carcinoma genome scans cluster together. This finding supports the hypothesis that host genetic factors are more important in determining neoplasm incidence than radiation exposure type. Unlike other statistic procedures, such as regression models, clustering lacks a response variable and is not routinely performed as a formal hypothesis test. Therefore, determining the significance of a clustering result can be problematic, as no consensus method exists for cluster validation. Permutation analysis provides the distribution of clustering results that will randomly occur from a given dataset; this can then be used as a baseline from which to determine a significance level on a given dendrogram tree [green line in Fig. 5 (A to C)]. While the overall validity of a given cluster can be accomplished by cluster permutation analysis, no method is identified to estimate the number of clusters that should be present in a dataset. Furthermore, methods to determine the significance of specific subset of objects clustering together do not exist; in such cases, the permutation threshold is likely overly stringent.

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Genomic mapping in outbred mice reveals overlap in genetic susceptibility for HZE ion and -rayinduced tumors - Science Advances

Recommendation and review posted by Bethany Smith

As the global death toll from the novel coronavirus mounts, evidence is growing that more men than women are becoming seriously ill and dying from the virus. In New York state as of April 9, for example, more than 60 percent of over 6,200 total deaths have been men.

From the early days of the first coronavirus outbreak in China, men were turning up severely ill at a higher rate than women. And this pattern seems to be largely repeating itself if in slightly different numbers in country after country.

Researchers are still not entirely sure why this is. But there are already some intriguing clues.

Could it be higher rates of smoking among men? A higher likelihood of delaying medical care? Or do the answers lie among the genes and sex hormones in our bodies that are setting men on a riskier course if they encounter the virus?

As Marcia Stefanick, a professor of medicine at Stanford University School of Medicine, told the Wall Street Journal, There are profound sex differences in immune systems, and this pandemic is revealing them. But, she noted, What is biology versus what are our social norms and gender behaviors confounds our ability to understand whats going on.

Finding answers could help develop more effective treatment protocols and prevention measures, as well as lead to a more successful vaccine.

One key piece of context for these questions is that there are, in general, a variety of key biological differences in the way men and women fight off infections. Women, for example, tend to mount a stronger immune response. Researchers think this is in part because most women have two X chromosomes, and the X chromosome happens to contain most of the genes related to the immune system (and those with two X chromosomes instead of one also have a wider diversity of immune responses). This extra immune functioning, however, also seems to put women more at risk for autoimmune diseases, such as rheumatoid arthritis and Crohns disease.

Hormones might also help provide women with a more effective defense. Some important immune cells have estrogen receptors, and an estrogen supplement has been shown to increase general immune responses in mice.

A 2017 study in the Journal of Immunology specifically looked into sex differences from the coronavirus that causes SARS (which seems to have killed more men than women during an outbreak in 2003). In that study, researchers found that male mice were more susceptible to the virus. But when they blocked estrogen from working normally in the female mice, the females fell ill at higher rates.

Women might also be more likely to launch an earlier attack on infections in general, saving the body from needing to use all of its virus-fighting might later an event that can skyrocket inflammation and often do more damage to key organs.

These sex patterns are not universal among infections. And data from other viruses, including influenza, sometimes even skews in the other direction, with more women dying than men. Theres still a lot to learn about the novel coronavirus, and so far there arent any studies on it looking specifically at these biological factors. We dont yet know how these biological differences play out for Covid-19, if they do at all. But theyre definitely possibilities.

There are also clues that differences in behavior could be putting men at higher risk for severe Covid-19. It can be a difficult (and time-consuming) endeavor for epidemiologists to untangle behavioral risk factors from one another, so its important to remember that at this point, what we have are correlations that suggest possible risks, not hard proof.

One factor could be smoking rates. A review of existing research as of March 17 concluded that smoking is most likely associated with the negative progression and adverse outcomes of Covid-19. There are a couple of reasons this could be the case, the World Health Organization notes. One is that smokers are more likely to have lung disease, which is an established risk factor for severe infection. The other is that when smoking, a person is more likely to touch their mouth or face, possibly allowing the virus an easy path in.

And smoking is often more common among men than women. According to a 2017 analysis in the Journal of Epidemiology & Community Health, 54 percent of Chinese adult men smoked tobacco, compared with just 2.6 percent of Chinese women. The World Bank reports that, as of 2016, about 41 percent of South Korean men smoked versus about 6 percent of women. (Spain also shows the same general trend, as does the US, but the sex difference isnt as large as it is for China and South Korea.)

Because the research on all of this is so new, it will still probably be some time before we have a clear understanding of what role smoking might play.

Other broad social and cultural variations among genders (that, to be sure, are not universal) might be further exacerbating this trend. For example, in the US, various studies show that men wash their hands less often and are less likely to seek care earlier in an illness. A March 24 poll from Reuters revealed that a smaller percentage of men than women were taking warnings about the coronavirus seriously including changing their behavior.

In this pandemic, the information being reported around the world varies widely. And due to continued lack of testing and increasing concern about deaths being underreported, we still do not have a complete picture of how sex is playing out as a risk factor for the disease and how that might be different in different countries. (Some governments, including the US, are not even reporting cases by sex.) Despite the fuzzy details, however, the pattern is holding steady.

Analysis of data from about 2,000 patients during Chinas main outbreak, from December through February, showed that about 60 percent of patients were men. And Chinas Center for Disease Control reported a fatality rate of 2.8 percent for men versus 1.7 percent for women.

In South Korea, men were actually far less likely to be confirmed to have Covid-19, according to a March 31 paper in Clinical Infectious Diseases. There, just 38 percent of patients were male. But, according to that analysis, men were about twice as likely to die from the disease (1.19 percent for men versus 0.52 percent for women).

In Spain, men and women comprise about an equal number of Covid-19 cases, as the countrys Health Ministry reported on April 3. But men were more than twice as likely to wind up in the ICU and more likely to die (making up almost two-thirds of deaths).

An April 6 study of the hard-hit region of Lombardy, Italy, found that 82 percent of patients admitted to the ICU were men. And in Italy overall, about 70 percent of people dying from coronavirus have been male.

The US CDC isnt releasing coronavirus case breakdowns by sex at this time (it also doesnt prominently feature this data for other infectious diseases, like influenza). This is an additional blow to those who are trying to understand this rapidly spreading illness because the US now has by far the largest number of cases.

Some US states have released sex breakdowns, however. A Washington Post report found that of 13 states that have substantial outbreaks and are reporting these details, men make up a larger number of deaths. As an emergency department nurse told the Post, In general, Ive seen more male patients. And when they do come in, they are at a sicker state. (Recent US data also shows concerning patterns of racial disparities.)

Learning more about how the virus impacts men and women could help determine the most effective treatment for individual patients. For example, it might point to different or earlier interventions in men, or more targeted public health messaging for people who might be more likely to delay seeking care.

Better understanding the nuances of mens and womens immune response to the virus could also be crucial to developing a good vaccine. There are well-documented differences in vaccine effectiveness among men and women, with women tending to be better protected after vaccination. So it will be especially important to ensure that sex is taken into account when designing and analyzing vaccine trials in both animal studies and human ones.

Although men seem to be dying at slightly higher rates than women, everyone is at risk even the young.

There are also some factors that might put some women more at risk. For example, in the US, 76 percent of health care workers are women, according to the US Census Bureau. That means they are at the forefront of this pandemic, coming into contact with potentially infected people on a daily basis.

Additionally, digging deeper into the data reveals other emerging trends in subpopulations. For example, according to an April 2 report from the Italian government, in those 90 and older, women were more likely to die from Covid-19 than men. And, although the overall numbers are small, it seems as though women with certain risk factors (including heart failure, hypertension, and dementia) were more likely to die from Covid-19 than the men who had those conditions.

What has become clear from all this data is that we still have a lot to learn about why some cases of Covid-19 end in respiratory failure or death, or severe illness, and some dont regardless of a persons sex. And we all still have the responsibility to reduce our own odds of getting the virus, and of it spreading to others. It remains crucial for everyone to do their part (washing hands, maintaining social distancing, etc.) to keep the virus from spreading.

Support Voxs explanatory journalism

Every day at Vox, we aim to answer your most important questions and provide you, and our audience around the world, with information that has the power to save lives. Our mission has never been more vital than it is in this moment: to empower you through understanding. Voxs work is reaching more people than ever, but our distinctive brand of explanatory journalism takes resources particularly during a pandemic and an economic downturn. Your financial contribution will not constitute a donation, but it will enable our staff to continue to offer free articles, videos, and podcasts at the quality and volume that this moment requires. Please consider making a contribution to Vox today.

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Coronavirus deaths: Why is the virus killing more men than women? - Vox.com

Recommendation and review posted by Bethany Smith

Scientists have created a mathematical model that can help explain why so many pregnancies and in vitro fertilization attempts fail.

The Rutgers-led study, which may help to improve fertility, is published in the journalProceedings of the National Academy of Sciences.

Mistakes in female meiosis, the cell division process that creates egg cells, result in eggs with an abnormal number of chromosomes (too many or too few). This phenomenon is strongly associated with the repeated loss of pregnancies and the failure of in vitro fertilization (IVF) procedures, as well as developmental disorders such as Down syndrome.

"Our study demonstrates that in the future, mathematical models can be powerful tools for predicting the outcomes of in vitro fertilization for infertility patients and/or provide the basis for considering alternative family planning options, such as adoption," said senior authorJinchuan Xing, an associate professor in theDepartment of Geneticsin theSchool of Arts and Sciencesand at theHuman Genetics Institute of New JerseyatRutgers University-New Brunswick.

"Modeling efforts such as ours can provide guidelines on, for instance, how many eggs must be collected during a single IVF cycle to ensure there will be at least one chromosomally normal conception," said co-authorKaren Schindler, an associate professor in the Department of Genetics and at the Human Genetics Institute of New Jersey.

Pregnancy loss is extremely common, with nearly 20 percent of clinically recognized pregnancies resulting in miscarriage, and many more unrecognized pregnancies end earlier, the study notes.

A leading cause of early miscarriage is called aneuploidy, when eggs have the wrong number of chromosomes, and it's also the main cause of IVF failure. The vast majority of eggs with chromosome problems are linked to errors in female cell division that increase as women age. Understanding how that happens is crucial because the average age at conception is rising in developed countries.

"Such basic knowledge is required to pave the way for future diagnostic and therapeutic innovations to improve human fertility," the study says.

The scientists developed a mathematical model describing all possible abnormal chromosome count issues in eggs due to cell division errors. Using data on 11,157 early stage human embryos (blastocysts), the model revealed previously unknown patterns of errors.

The model can be used to identify IVF patients who produce an extreme number of abnormal embryos. It's also a powerful tool for understanding why abnormal numbers of chromosomes arise when cells divide and for predicting the outcomes of IVF reproduction. The model potentially could provide guidance for clinicians on the expected number of IVF cycles needed to get a normal conception for each patient. The modeling framework can also be expanded and adapted to address other processes, such as predicting errors in sperm.

Original post:
Why do so many pregnancies and in vitro fertilization attempts fail? - Jill Lopez

Recommendation and review posted by Bethany Smith

THE number of people dying from coronavirus across the world is continuing to rise every day - with just under 130,000 deaths in 210 countries.

And in the UK alone,the total of deathspushed past the 12,000 barrier yesterday - with the grim total expected to be 15 per cent higher than reported due to people dying outside of hospital.

4

However, scientists have now revealed that there are some key factorsthat people who pass away from Covid-19have in common.

A team of researchers from eight institutions in China and the United States including the Chinese Peoples Liberation Army General Hospital in Beijing, and the University of California Davis recently looked at the data of 85 patients who died of multiple organ failure after having received care for severe Covid-19.

All individuals whose data the study used received care at either the Hanan Hospital or the Wuhan Union Hospital between January 9 and February 15, 2020.

And the researchers who conducted the study,that appears in the American Journal of Respiratory and Critical Care Medicine,uncovered a series of factors that the majority of these patients shared.

Here, we outline these key factors...

The killer new coronavirus appears to be posing a particular threat to men.

The researchers found that 72.9 per cent of those who died from the new coronavirus - Sars-Cov-2 - were male.

Experts believe there are a few reasons for more men dying than women, including some biological and other lifestyle choices.

Hand washing is one of the best ways to prevent infection - but multiple studies show that women are much more likely to wash their hands and use soap than men.

4

Akiko Iwasaki, a professor of immunology at Yale University, told the New York Times that men may have a "false sense of security" about coronavirus.

Meanwhile, Chinese men are much more likely to smoke than women, which can lead to a weaker immune system.

China has the largest population of smokers in the world - accounting for nearly a third of the world's smokers - but just two per cent of them are women.

Meanwhile, in the UK 16.5 per cent of men - around 3.9 million - and 13 per cent of women - around 3.2 million - reported being current smokers.

Chinese men also have higher rates of high blood pressure, type 2 diabetes and chronic obstructive pulmonary disease than women.

All of these conditions can increase the risk of complications following infection of coronavirus.

Meanwhile, some experts believe that oestrogen, the female sex hormone, may also play a role in protecting women.

The new strain of deadly coronavirus doesn't discriminate and can infect anyone of any age.

However, it's older adults - aged 60 and upwards - who are more likely to get seriously ill from it - with the scientists discoveringthat those who died from Covid-19 had amedian age of 65.8 years.

Medics say it's because our immune systems weaken with age, meaning an older person's body is less able to fight Covid-19.

Dr Sarah Jarvis, GP and Clinical Director of Patient Access, told The Sun: "We know that as you get older, your immune system becomes less efficient thats why older people are at higher risk of serious complications of coronavirus infection.

4

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"If your immune system isnt strong, its more likely that the virus can multiply deep inside your lung, causing inflammation and scarring.

"Your immune system will try and fight it off, and will often destroy healthy lung tissue in the process.

"This makes you more prone to get secondary infections like pneumococcal pneumonia."

In fact, evidence from China, where the deadly virus originated, shows one in seven of those over 80 known to have contracted coronavirus have died.

Those who died from Covid-19 in the study mostly had underlying chronic conditions, such as heart problems or diabetes.

The greatest number of deaths in our cohort were in males over 50 with noncommunicable chronic diseases, the researchers said.

We hope that this study conveys the seriousness of Covid-19 and emphasises the risk groups of males over 50 with chronic comorbid conditions, including hypertension (high blood pressure), coronary heart disease, and diabetes," they added.

4

In fact, another study recently revealed that your risk of dying from coronavirus is 80 per cent higher if you have just one underlying health issue.

For those with two pre-existing conditions or more, the chances of being admitted to intensive care are even higher, experts warned.

Some of the chronic conditions said to heighten the risk among patients are asthma, cancer, cystic fibrosis, chronic obstructive pulmonary disease (COPD), diabetes and HIV and AIDS.

People who are obese or seriously overweightfall into the high risk category for coronavirus.

This is because being overweight or obese can weaken the bodys immune system which could make people more likely to catch coronavirus and makes it harder for the body to fight the bug.

The NHS has said people with a BMI of 40 or above have a greater risk of developing complications if they catch the virus.

More than 60 per cent of patients in intensive care with the virus were overweight or classed as morbidly obese, arecent NHS survey found.

Those who were overweight, with a BMI of 25 to 40, made up 64 per cent of the 194 coronavirus patients who were in ICU at the time, while seven per cent were classed as obese with a BMI over 40.

BMI is a measure of whether youre a healthy weight for your height, you can calculate yours on the NHS website.

In the past, studies have shown overweight and obese people are at greater risk of serious complications or death from infections, like flu.

The extra weight on obese people's diaphragms puts pressure on lungs and makes it harder to breathe, starving them of oxygen.

Clogged up arteries can also make it harder for blood carrying immune cells to circulate and travel to fight infection around the body.

In terms of other potentially relevant information, the research team found that 81.2 per cent of those who died from Covid-19 in the study had very low eosinophil counts on admission to the hospital."

This is a type of white blood cells, which are specialised immune cells that help fight infection.

The medics suggested that having abnormally low levels of eosinophils a condition known as eosinophilopenia may correlate with a greater risk of severe outcomes in people who have contracted Covid-19.

While the scientists hope that their current findings may help other doctors better understand and prepare for fighting coronavirus, the researchers nevertheless urge other experts to keep on recording all possible information about people receiving care for this new illness.

Our study, which investigated patients from Wuhan, China, who died in the early phases of this pandemic, identified certain characteristics, the researchers said.

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"Yet as the disease has spread to other regions, the observations from these areas may be the same, or different.

They added: Genetics may play a role in the response to the infection, and the course of the pandemic may change as the virus mutates, as well.

"Since this is a new pandemic that is constantly shifting, we think the medical community needs to keep an open mind as more and more studies are conducted.

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The 5 factors that increase your risk of dying from coronavirus - The Sun

Recommendation and review posted by Bethany Smith

News Release

Wednesday, April 15, 2020

NIH-funded study offers new path to modeling eye disease, advancing therapies

Researchers have discovered a technique for directly reprogramming skin cells into light-sensing rod photoreceptors used for vision. The lab-made rods enabled blind mice to detect light after the cells were transplanted into the animals eyes. The work, funded by the National Eye Institute (NEI), published April 15 in Nature. The NEI is part of the National Institutes of Health.

Up until now, researchers have replaced dying photoreceptors in animal models by creating stem cells from skin or blood cells, programming those stem cells to become photoreceptors, which are then transplanted into the back of the eye. In the new study, scientists show that it is possible to skip the stem-cell intermediary step and directly reprogram skins cells into photoreceptors for transplantation into the retina.

This is the first study to show that direct, chemical reprogramming can produce retinal-like cells, which gives us a new and faster strategy for developing therapies for age-related macular degeneration and other retinal disorders caused by the loss of photoreceptors, said Anand Swaroop, Ph.D., senior investigator in the NEI Neurobiology, Neurodegeneration, and Repair Laboratory, which characterized the reprogrammed rod photoreceptor cells by gene expression analysis.

Of immediate benefit will be the ability to quickly develop disease models so we can study mechanisms of disease. The new strategy will also help us design better cell replacement approaches, he said.

Scientists have studied induced pluripotent stem (iPS) cells with intense interest over the past decade. IPSCs are developed in a lab from adult cells rather than fetal tissue and can be used to make nearly any type of replacement cell or tissue. But iPS cell reprogramming protocols can take six months before cells or tissues are ready for transplantation. By contrast, the direct reprogramming described in the current study coaxed skin cells into functional photoreceptors ready for transplantation in only 10 days. The researchers demonstrated their technique in mouse eyes, using both mouse- and human-derived skin cells.

Our technique goes directly from skin cell to photoreceptor without the need for stem cells in between, said the studys lead investigator, Sai Chavala, M.D., CEO and president of CIRC Therapeutics and the Center for Retina Innovation. Chavala is also director of retina services at KE Eye Centers of Texas and a professor of surgery at Texas Christian University and University of North Texas Health Science Center (UNTHSC) School of Medicine, Fort Worth.

Direct reprogramming involves bathing the skin cells in a cocktail of five small molecule compounds that together chemically mediate the molecular pathways relevant for rod photoreceptor cell fate. The result are rod photoreceptors that mimic native rods in appearance and function.

The researchers performed gene expression profiling, which showed that the genes expressed by the new cells were similar to those expressed by real rod photoreceptors. At the same time, genes relevant to skin cell function had been downregulated.

The researchers transplanted the cells into mice with retinal degeneration and then tested their pupillary reflexes, which is a measure of photoreceptor function after transplantation. Under low-light conditions, constriction of the pupil is dependent on rod photoreceptor function. Within a month of transplantation, six of 14 (43%) animals showed robust pupil constriction under low light compared to none of the untreated controls.

Moreover, treated mice with pupil constriction were significantly more likely to seek out and spend time in dark spaces compared with treated mice with no pupil response and untreated controls. Preference for dark spaces is a behavior that requires vision and reflects the mouses natural tendency to seek out safe, dark locations as opposed to light ones.

Even mice with severely advanced retinal degeneration, with little chance of having living photoreceptors remaining, responded to transplantation. Such findings suggest that the observed improvements were due to the lab-made photoreceptors rather than to an ancillary effect that supported the health of the hosts existing photoreceptors, said the studys first author Biraj Mahato, Ph.D., research scientist, UNTHSC.

Three months after transplantation, immunofluorescence studies confirmed the survival of the lab-made photoreceptors, as well as their synaptic connections to neurons in the inner retina.

Further research is needed to optimize the protocol to increase the number of functional transplanted photoreceptors.

Importantly, the researchers worked out how this direct reprogramming is mediated at the cellular level. These insights will help researchers apply the technique not only to the retina, but to many other cell types, Swaroop said.

If efficiency of this direct conversion can be improved, this may significantly reduce the time it takes to develop a potential cell therapy product or disease model, said Kapil Bharti, Ph.D., senior investigator and head of the Ocular and Stem Cell Translational Research Section at NEI.

Chavala and his colleagues are planning a clinical trial to test the therapy in humans for degenerative retinal diseases, such as retinitis pigmentosa.

The work was supported by grants EY021171, EY025667, EY025905, and EY025717 and NEI Intramural Research Program grants ZIAEY000450, ZIAEY000474 and ZIAEY000546.

The University of North Texas has a patent pending on the chemical reprogramming method reported in this paper. CIRC Therapeutics is a start-up company that plans to commercialize treatments using the technology.

This press release describes a basic research finding. Basic research increases our understanding of human behavior and biology, which is foundational to advancing new and better ways to prevent, diagnose, and treat disease. Science is an unpredictable and incremental process each research advance builds on past discoveries, often in unexpected ways. Most clinical advances would not be possible without the knowledge of fundamental basic research.

NEI leads the federal governments research on the visual system and eye diseases. NEI supports basic and clinical science programs to develop sight-saving treatments and address special needs of people with vision loss. For more information, visit https://www.nei.nih.gov.

About the National Institutes of Health (NIH):NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.

NIHTurning Discovery Into Health

Mahato B, Kaya KD , Fan Y, Sumien N, Shetty RA, Zhang W, Davis D, Mock T , Batabyal S, Ni A, Mohanty S, Han Z, Farjo R, Forster M, Swaroop A and Chavala SH. Pharmacologic fibroblast reprogramming into photoreceptors restores vision. Published online April 15, 2020 in Nature.http://dx.doi.org/10.1038/s41586-020-2201-4

###

See the original post:
Researchers restore sight in mice by turning skin cells into light-sensing eye cells - National Institutes of Health

Recommendation and review posted by Bethany Smith

DUBLIN--(BUSINESS WIRE)--The "Hormone Replacement Therapy Market Size, Share & Trends Analysis Report by Product (Estrogen, Human Growth), by Route Of Administration (Oral, Parenteral), by Type Of Disease, by Region, and Segment Forecasts, 2020 - 2027" report has been added to ResearchAndMarkets.com's offering.

The global hormone replacement therapy market size is expected to reach USD 39.6 billion by 2027, expanding at a CAGR of 7.7%. A significant rise in the incidence rate of hormonal disorders in the newborns, adults, and elderly and populations is driving the market. The Prader-Willi syndrome (PWS) affects one in every 15,000 newborns, thereby boosting the demand for the therapy.

Estrogen replacement hormone therapy helps in reducing the vaginal indications of menopause, such as dryness, burning, itching, and pain during intercourse. Estrogen is available in the forms of pill, gel, skin patch, cream or spray form. It is highly successful for treating problematic menopausal night sweats and hot flashes. Around 45% of women between the ages of 40 to 60 years of age were reported taking counseling sessions from a physician regarding the advantages and disadvantages of using hormone replacement therapy (HRT) after menopause.

Growing awareness about menopausal signs and the treatment options is growing the HRT market. Owing to the significant development for ERT, there has been an initiation of very safe treatment options for the patients situated in various geographies of the world. For example, augmentation of innovative drug delivery systems like transdermal estrogen patches and vaginal estrogen drugs.

Further key findings from the report suggest:

Key Topics Covered:

1. Methodology and Scope

2. Executive Summary

2.1 Market Outlook

2.2 Segment Outlook

2.2.1 Product

2.2.2 Route of Administration

2.2.3 Type of Disease

2.2.4 Region

2.3 Competitive Insights

3. Market Variables, Trends & Scope

3.1 Market Segmentation

3.2 Penetration & Growth Prospect Mapping

3.2.1 Market Driver Analysis

3.2.2 Market Restraint Analysis

3.3 Hormone Replacement Therapy Market: Business Environment Analysis Tools

3.3.1 Porter's Five Forces Analysis

3.3.2 PESTEL Analysis

4. Hormone Replacement Therapy Market: Product Analysis

4.1 Hormone Replacement Therapy Product Market Share Analysis, 2019 & 2027

4.2 Hormone Replacement Therapy Product Market: Segment Dashboard

4.3 Market Size & Forecasts and Trend Analyses, 2016 to 2027 for the Product Segment

4.3.1 Estrogen Hormone Replacement Therapy

4.3.2 HGH Replacement Therapy

4.3.3 Thyroid Hormone Replacement Therapy

4.3.4 Testosterone Hormone Replacement Therapy

5. Hormone Replacement Therapy Market: Route of Administration Analysis

5.1 Hormone Replacement Therapy Route of Administration Market Share Analysis, 2019 & 2027

5.2 Hormone Replacement Therapy Route of Administration Market: Segment Dashboard

5.3 Market Size & Forecasts and Trend Analyses, 2016 to 2027 for the Route of Administration Segment

5.3.1 Oral

5.3.2 Parenteral

5.3.3 Transdermal

5.3.4 Others

6. Hormone Replacement Therapy Market: Type of Disease Analysis

6.1 Hormone Replacement Therapy Type of Disease Market Share Analysis, 2019 & 2027

6.2 Hormone Replacement Therapy Type of Disease Market: Segment Dashboard

6.3 Market Size & Forecasts and Trend Analyses, 2016 to 2027 for the Type of Disease Segment

6.3.1 Menopause

6.3.2 Hypothyroidism

6.3.3 Male Hypogonadism

6.3.4 Growth Hormone Deficiency

6.3.5 Others

7. Hormone Replacement Therapy Market: Regional Analysis

7.1 Hormone Replacement Therapy Regional Market Share Analysis, 2019 & 2027

7.2 Hormone Replacement Therapy Regional Market: Segment Dashboard

7.3 Regional Market Snapshot (Market Size, CAGR, Top Verticals, Key Players, Top Trends)

7.4 Market Size, & Forecasts, and Trend Analysis, 2016 to 2027

7.4.1 North America

7.4.2 Europe

7.4.3 Asia Pacific

7.4.4 Latin America

7.4.5 Middle East and Africa (MEA)

8. Competitive Analysis

8.1 Strategic Framework/ Competition Categorization (Key innovators, Market leaders, emerging players

8.2 Vendor Landscape

8.3 Company market position analysis (Geographic Presence, Product Portfolio, Strategic Initiatives, Employee Strength)

8.4 Company Profiles

Companies Mentioned

For more information about this report visit https://www.researchandmarkets.com/r/rowxnu

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Insights into the Worldwide HRT Industry to 2027 - Featuring Abbott Laboratories, Novartis & Pfizer Among Others - ResearchAndMarkets.com -...

Recommendation and review posted by Bethany Smith

As scientists around the world race toward finding an effective treatment and cure for COVID-19, health officials in China have started encouraging an alternative type of medicine to help those who get sick with the respiratory infection traditional herbal remedies.

Using herbs for illness isnt a novel idea. For thousands of years, herbs like licorice, ginger, and ephedra have been used to treat respiratory infections like the flu and pneumonia.

Some remedies, like forsythia, were put to the test for SARS and found to be somewhat effective in laboratory studies.

Anecdotally, people have claimed herbal medicines have kept them healthy or improved their symptoms, but the bulk of research on herbs is inconclusive. Health experts warn that we dont have enough data to support the use of herbal remedies for COVID-19.

Though we may eventually find that certain herbs may be beneficial for the coronavirus, the science is scarce and now is not the time to start experimenting with herbal remedies on your own if you contract COVID-19.

Everything has to be taken with an understanding that we dont have any data with the coronavirus, Dr. Felicia Gersh, the founder and director of the Integrative Medical Group of Irvine in Irvine, California, told Healthline. Who knows what the future may bring.

Herbal remedies have long been used to treat infections and viruses, such as the common cold, influenza, fever, and even herpes.

Some are thought to enhance the immune system and put the body in a healthier position to fight infections. Others are believed to be powerful antivirals that block certain viruses from replicating in the body.

But just because weve seen some promise with other illnesses does not mean people should assume herbal remedies provide the same benefit with COVID-19.

Every virus is unique in its structure and behavior. The herbs that seem to work for other viral infections will need to be tested to see if they also hold up against COVID-19.

This ones a little bit more of a dangerous virus, said Jeffrey Langland, PhD, an assistant research professor at Arizona State Universitys Biodesign Center for Immunotherapy, Vaccines and Virotherapy and associate professor of medical microbiology at the Southwest College of Naturopathic Medicine in Tempe.

Historically, theres been a major lack of evidence surrounding natural medicines.

For one, its been difficult to secure the necessary funding to study the health effects of plants and herbs. The United States is a very pharmaceutical-driven society, so thats where the priority has historically been.

Research has also been somewhat inconsistent. There are so many parts of a plant the root, stem, leaf, flower and its hard to get studies that consistently analyze the same portion of a plant.

Langland has been leading up a team of researchers who have been studying if and how certain herbs could potentially be used to treat COVID-19.

His team is testing over 30 herbs, and looking at each plants antiviral and immune-supportive properties.

Langland is hopeful theyll find a treatment, but says it will take time to get the results and put the science behind botanicals.

Even for those herbs we find effective, we want to go through and make sure we look at any sort of toxicity, and sort of side effects that may be associated with them, look at quality of extracts, and start to move that forward, Langland said.

Were not going to jump and throw this out there for people to start using without regarding things like safety, Langland added. Just like any pharmaceutical, we cannot rush this.

Just like any other medicine, herbal remedies could cause adverse side effects.

Take licorice, one of the remedies that officials in China have recommended for COVID-19.

According to Gersh, licorice is thought to be an effective treatment for herpes viruses.

Licorice paste, when applied to a herpes sore, can prevent the virus from replicating and stop it in its tracks, says Gersh. But it also has a major downside.

It can activate a hormone in the body called aldosterone which causes fluids retention and can actually induce hypertension, Gersh said.

Because hypertension is a huge risk factor for COVID-19 complications, Gersh said she would be concerned about using licorice, especially in high quantities, in someone with coronavirus.

St Johns wort is a widely available supplement but it can cause issues if a person is on medication.

It can interact with other medications that a patients on and block their absorption in the body and prevent them from acting, Langland said.

Furthermore, some peoples immune systems are overreacting to COVID-19, triggering widespread inflammation that can be even more problematic than the infection itself.

Certain herbs, if misused, could boost the immune system even more and lead to a cytokine storm, or a fatal overactive immune response, according to Gersh.

One of the biggest problems, according to Langland, is that many herbal and natural remedies are low quality.

There is so much herbal medicine that is adulterated, which means the product youre buying has been spiked with other botanicals or doesnt contain any of the botanicals that are labeled on the bottle, Langland said.

If you are getting the product from a local health store, theres a good chance you arent getting a high quality product, he added.

You cant assume every herb is safe. It may have some properties that could be potentially harmful, Gersh said.

If you are considering trying herbal remedies for COVID-19, keep in mind that we dont fully understand the risks and benefits.

How a botanical works in one persons body may be drastically different from how it behaves in another, depending on their health, age, and symptoms.

With botanicals, you want to treat people individually, Langland said, noting how the type of herb and dosage would likely vary from person to person.

If people are curious about herbal remedies, its best to consult a physician or naturopathic doctor who is well versed in various herbs and their properties.

I wouldnt advocate that people willy-nilly start taking all kinds of herbal products and not have a clue whats in it, Gersh said.

You want to have data, and be aware of any potential side effects before you take herbal products for an infection as potentially life threatening as COVID-19.

Health officials in China are recommending traditional herbal remedies for COVID-19, but many experts warn that we dont have enough data on COVID-19 to understand how different herbs may affect peoples health.

Though herbal remedies may seem harmless, if misused, they could increase a persons risk for COVID-19. We may find that certain herbs are effective in preventing and treating COVID-19 in some people, but there currently isnt enough data regarding the use of herbal remedies for the new coronavirus.

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Herbal Remedies and COVID-19: What to Know - Healthline

Recommendation and review posted by Bethany Smith

Infertility is a disease that affects millions of people in the United States but is rarely discussed openly. Twelve percent of married women between the ages of 15 and 44 experienced infertility, along with just over nine percent of men in that age group, according to a 2013 report from the Centers for Disease Control and Prevention. Those numbers translate to about one in eight couples who have trouble getting or staying pregnant. There are a variety of treatments for infertility, but they can be costly and are not accessible to everyone.

Guest host Anita Rao talks about infertility with Dr. Steven Young of UNC fertility, associate professor Belle Boggs, fertility advocate Nichelle Sublett, reproductive endocrinologist and infertility specialist Dr. Desire McCarthy-Keith, and Liberty Barnes, medical sociologist and ethnographer.

On this episode of Embodied, a series about sex, relationships and your heath, guest host Anita Rao talked to doctors, experts and those with firsthand knowledge about the issues surrounding infertility in American culture. Dr. Steven L. Young joined Rao to talk about who is affected by infertility, what causes it and what treatments are available. He is a professor of obstetrics and gynecology at the University of North Carolina School of Medicine and a physician at UNC Fertility.

Dr. Young also talked about the technology available today that is advancing fertility treatments.

Preimplantation genetic testing allows looking at all the chromosomes with a pretty good accuracy now say 98 to 99 percent accuracy, he explained. And so one can choose among many embryos the best one by finding which ones have normal chromosomal complement.

CDC statistics show African American women are more likely to be infertile than white women, but they are almost half as likely to seek treatment as white women. Dr. Desire McCarthy-Keith explored the reasons why black women are more likely to experience problems with fertility and why they are less likely to seek treatment. McCarthy-Keith is a reproductive endocrinologist and infertility specialist at Shady Grove Fertility Atlanta.

She said knowledge is power and recommends that women who would like to have children investigate their ovarian reserve.

Women need to understand that we are on a timeline with our fertility from birth. - Dr. Desiree' McCarthy-Keith

You can have an ultrasound at the beginning of a menstrual cycle to look at the ovaries and see how many follicles or little egg sacs are developing in the ovaries. There's a hormone test that can be done called AMH, which stands for anti-mllerian hormone. It's a simple blood draw that will measure this hormone level in your blood. And that level is a reflection of how much activity and follicle development there is in the ovary, she said.

Nichelle Sublett and Belle Boggs share their personal journeys with infertility. Sublett had five miscarriages over five years. She is a fertility advocate and Mrs. North Carolina 2018. She discussed the emotional and psychological impacts of pregnancy loss.

It really is a death. I know some people may not understand that, but this is a child that you hoped and dreamed for, and you had plans for. And you've probably mapped out half their lives by the time you see your positive pregnancy test, Sublett said.

It's absolutely the hardest thing my husband and I have ever been through, was going through those five miscarriages. - Nichelle Sublett

Boggs is an associate professor in the department of English and director of the Master of Fine Arts program in creative writing at North Carolina State University. She struggled with fertility for five years, and during that time wrote the memoir and cultural history The Art of Waiting: On Fertility, Medicine and Motherhood (Graywolf Press/2016).

Cost was a big factor for Boggs and her husband when it came to fertility treatments.

Only 16 states in the whole country have laws requiring health insurance companies to write fertility care into their policies. And North Carolina is not one of those states, she explained.

Medical sociologist and ethnographer Liberty Barnes digs into how cultural stereotypes play into who receives fertility treatment. She also discusses the financial barriers to fertility treatment, LGBTQ couples and her book, Conceiving Masculinity: Male Infertility, Medicine, and Identity (Temple University Press/2014).

There was a lot of care in the medical system around protecting these men's masculine identities, I would argue, and that it was about making sure that men felt comfortable in the clinic. - Liberty Barnes

Barnes also described the historically inaccurate statistics used in the United States when it comes to fertility.

We were looking at the statistics that we use in the United States to track infertility and the statistics we've used since 1955 The study is reproduced every five to 10 years in waves. Women of color were not included in the study until the fourth wave, which wasn't until 1970. Men were not included until this century until 2002. And there were no questions asking about the sexual orientations of the respondents until 2002.

Note: This program originally aired July 18, 2019.

Read more here:
Fertile Ground: The Silent Struggle Of Infertility - WUNC

Recommendation and review posted by Bethany Smith

In this Autologous Stem Cell And Non Stem Cell Based Therapies Market report, industry trends have been explained on the macro level which makes it possible to summarize the market landscape and probable future issues. The report analyses and estimates general market drivers in the form of consumer demand, government policy and demand which are related to consumer buying pattern and thereby market growth and development. This market research report contains thorough analysis of market and numerous related factors that range from market drivers, market restraints, market segmentation, opportunities, challenges, and market revenues to competitive analysis. This report is also useful when launching a new product or expanding the business regionally or globally.

Key Market Competitors:

Few of the major market competitors currently working in the europe autologous stem cell and non-stem cell based therapies market are Takeda Pharmaceutical Company Limited, Cytori Therapeutics Inc., General Electric Spiegelberg GmbH & Co. KG ., Medtronic, Natus Medical Incorporated., Integra LifeSciences Corporation, RAUMEDIC AG, Abbott., Endotronix, Inc. among others.

Click Here To Get Global Autologous Stem Cell And Non Stem Cell Based Therapies Market Research Sample PDF Copy @https://www.databridgemarketresearch.com/request-a-sample/?dbmr=europe-autologous-stem-cell-and-non-stem-cell-based-therapies-market&skp

Market Analysis: EuropeAutologous Stem Cell and Non-Stem Cell Based Therapies Market

Europe autologous stem cell and non-stem cell based therapies market is registering a substantial CAGR in the forecast period of 2019-2026. The report contains data from the base year of 2018 and the historic year of 2017. The rise in the market can be attributed growing awareness of the therapeutic potential of stem cells in effective disease management and increased public-private investment in the development of stem cell therapies.

Market Definition: EuropeAutologous Stem Cell and Non-Stem Cell Based Therapies Market

Autologous stem cell transplantation, the individuals own undivided cells or stem cells are collected and transplanted back to the person after intensive therapy. These therapies are performed using hematopoietic stem cells, in some cases, cardiac cells are used to correct the damage caused by heart attacks. Autologous and non-systemic stem cell therapies are used to treat different diseases, for example neurodegenerative diseases, cardiovascular diseases, cancer and autoimmune diseases, parasitic diseases.

Market Drivers

Market Restraints

Segmentation:EuropeAutologous Stem Cell and Non-Stem Cell Based Therapies Market

By Product Type

By Application

By End-User

By Country

Key Developments in the Market:

Competitive Analysis:

Europe Autologous Stem Cell and Non-Stem Cell Based therapies market is highly fragmented and the major players have used various strategies such as new product launches, expansions, agreements, joint ventures, partnerships, acquisitions, and others to increase their footprints in this market. The report includes market shares of autologous stem cell and non-stem cell based therapies market for Europe.

Autologous Stem Cell And Non Stem Cell Based Therapies reports includes the following deliverable

This report scope includes a holistic study of the current dynamics of the market, industry growth and restraints of the Global Autologous Stem Cell And Non Stem Cell Based Therapies Market. It provides the market forecast to 2025, recent developments in the market and pipeline analysis of the major players. The report also includes a review of micro and macro forecasts, new entrant strategies, and market penetration strategies with a comprehensive value chain analysis.

Table Of Contents: Global Autologous Stem Cell And Non Stem Cell Based Therapies MarketPart 01: Executive Summary

Part 02: Scope Of The Report

Part 03: Research Methodology

Part 04: Market Landscape

Part 05: Pipeline Analysis

Part 06: Market Sizing

Part 07: Five Forces Analysis

Part 08: Market Segmentation

Part 09: Customer Landscape

Part 10: Regional Landscape

Part 11: Decision Framework

Part 12: Drivers And Challenges

Part 13: Market Trends

Part 14: Vendor Landscape

Part 15: Vendor Analysis

Part 16: Appendix

Browse TOC with selected illustrations and example pages of Global Autologous Stem Cell And Non Stem Cell Based Therapies Market @https://www.databridgemarketresearch.com/toc/?dbmr=europe-autologous-stem-cell-and-non-stem-cell-based-therapies-market&skp

Key Questions Answered in Autologous Stem Cell And Non Stem Cell Based Therapies Report

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Key focus of the Autologous Stem Cell And Non Stem Cell Based Therapies report

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Autologous Stem Cell And Non Stem Cell Based Therapies Market Insight, Present Scenario & Growth Prospect 2020-2026 - Science In Me

Recommendation and review posted by Bethany Smith

Advance Market Analyticsreleased the research report ofGlobal Liver CirrhosisMarket, offers a detailed overview of the factors influencing the global business scope.Global Liver Cirrhosis Market research report shows the latest market insights with upcoming trends and breakdown of the products and services.The report provides key statistics on the market status, size, share, growth factors of the Global Liver Cirrhosis.This Report covers the emerging players data, including: competitive situation, sales, revenue and global market share of top manufacturers are F. Hoffmann-La Roche AG (Switzerland), Merck & Co., Inc (United States), Abbott Laboratories (United States), Novartis International AG (Switzerland), Bristol Myers Squibb Company (United States), Gilead Sciences, Inc (United States), Conatus Pharmaceuticals (United States), GlaxoSmithKline plc (United Kingdom), Grifols, S.A. (Spain), GWOXI Stem Cell Applied Technology Co., Ltd (China), Hepion Pharmaceuticals (United States), Intercept Pharmaceuticals, Inc. (United States) and Lepu Medical Technology (Beijing) Co., Ltd. (China).

Free Sample Report + All Related Graphs & Charts @ https://www.advancemarketanalytics.com/sample-report/63193-global-liver-cirrhosis-market

The liver cirrhosis means the condition that causes scar tissue of the liver to replace healthy liver tissue cells, it happens over the period due to the chronic infection or alcohol addiction. It is diagnosed by various radiology tests such as computed tomography (CT), ultrasound, magnetic resonance imaging (MRI), needle biopsy of the liver. A new imaging technique called elastography, which can be performed with ultrasound or MRI, can also diagnosis cirrhosis.

Market Trend

Market Drivers

Opportunities

Restraints

Challenges

The Global Liver Cirrhosisis segmented by following Product Types:

Type (Alcoholic Cirrhosis, Atrophic Cirrhosis, Biliary Cirrhosis, Cardiac Cirrhosis, Cryptogenic Cirrhosis), Application (Hospitals, Specialty Clinics, Others), Treatment (Self-care, Medications {Diuretic, Ammonia Reducer, Beta Blocker, Antibiotics, Antiviral Drug}, Medical procedure {Rubber Band Ligation, Therapeutic Endoscopy, and Transjugular Intrahepatic Portosystemic Shunt}, Surgery {Liver transplantation}), Stages (Stage 1, Stage 2, Stage 3, Stage 4), Tests (Computed Tomography (CT), Ultrasound, Magnetic Resonance Imaging (MRI), Needle Biopsy)

Region Included are: North America, Europe, Asia Pacific, Oceania, South America, Middle East & Africa

Country Level Break-Up: United States, Canada, Mexico, Brazil, Argentina, Colombia, Chile, South Africa, Nigeria, Tunisia, Morocco, Germany, United Kingdom (UK), the Netherlands, Spain, Italy, Belgium, Austria, Turkey, Russia, France, Poland, Israel, United Arab Emirates, Qatar, Saudi Arabia, China, Japan, Taiwan, South Korea, Singapore, India, Australia and New Zealand etc.Enquire for customization in Report @:https://www.advancemarketanalytics.com/enquiry-before-buy/63193-global-liver-cirrhosis-market

Strategic Points Covered in Table of Content of Global Liver Cirrhosis Market:

Chapter 1: Introduction, market driving force product Objective of Study and Research Scope the Global Liver Cirrhosis market

Chapter 2: Exclusive Summary the basic information of the Global Liver Cirrhosis Market.

Chapter 3: Displayingthe Market Dynamics- Drivers, Trends and Challenges of the Global Liver Cirrhosis

Chapter 4: Presenting the Global Liver Cirrhosis Market Factor Analysis Porters Five Forces, Supply/Value Chain, PESTEL analysis, Market Entropy, Patent/Trademark Analysis.

Chapter 5: Displaying the by Type, End User and Region 2013-2018

Chapter 6: Evaluating the leading manufacturers of the Global Liver Cirrhosis market which consists of its Competitive Landscape, Peer Group Analysis, BCG Matrix & Company Profile

Chapter 7: To evaluate the market by segments, by countries and by manufacturers with revenue share and sales by key countries in these various regions.

Chapter 8 & 9: Displaying the Appendix, Methodology and Data Source

Finally, Global Liver Cirrhosis Market is a valuable source of guidance for individuals and companies.

Data Sources & Methodology

The primary sources involves the industry experts from the Global Liver Cirrhosis Market including the management organizations, processing organizations, analytics service providers of the industrys value chain. All primary sources were interviewed to gather and authenticate qualitative & quantitative information and determine the future prospects.

In the extensive primary research process undertaken for this study, the primary sources Postal Surveys, telephone, Online & Face-to-Face Survey were considered to obtain and verify both qualitative and quantitative aspects of this research study. When it comes to secondary sources Companys Annual reports, press Releases, Websites, Investor Presentation, Conference Call transcripts, Webinar, Journals, Regulators, National Customs and Industry Associations were given primary weight-age.

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Advance Market Analytics is Global leaders of Market Research Industry provides the quantified B2B research to Fortune 500 companies on high growth emerging opportunities which will impact more than 80% of worldwide companies revenues.

Our Analyst is tracking high growth study with detailed statistical and in-depth analysis of market trends & dynamics that provide a complete overview of the industry. We follow an extensive research methodology coupled with critical insights related industry factors and market forces to generate the best value for our clients. We Provides reliable primary and secondary data sources, our analysts and consultants derive informative and usable data suited for our clients business needs. The research study enable clients to meet varied market objectives a from global footprint expansion to supply chain optimization and from competitor profiling to M&As.

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Liver Cirrhosis Market Projected to Gain Significant Value by 2024 - Science In Me

Recommendation and review posted by Bethany Smith

In the early 1980s, a deadly epidemic was gaining momentum. Caused by a virus dubbed HIV, AIDs has infected and killed millions of people around the world. But not everyone who was exposed to HIV got sick. In the mid-90s, researchers found that a variation of a gene called CCR5 made some people resistant to the virus.

When it comes to how viral infections interact with our bodies, genes matter.

Now, scientists are turning to DNA to solve a mystery at the heart of the Covid-19 pandemic. Why do some young and otherwise healthy people get gravely ill, while others have only mild symptoms or no symptoms at all? Might the answer be in our genes?

A host of studies aims to tap the genetic information of thousands of people to find out.

Itll take time to tease answers from the data, and the story will have to account for the complicated dance of genes, body, environment, and behavior. But scientists hope new discoveries can help us identify those most at riskeven if they dont seem itbetter trace the diseases course in the body, and hopefully, more effectively treat patients.

From the earliest days of the pandemic, reports have noted Covid-19 was most severe for the elderly and ill. The CDC says theres still not enough information to fully outline risk factors. But older people with pre-existing health conditions, including asthma and lung disease, cardiac disease, diabetes, and immune conditions are most at risk.

In the general population, however, theres a wide range of how sick people get.

There are accounts of young and seemingly healthy people admitted to the ICU, while othersscientists dont know how many yethave no symptoms at all. Theres even some variation between the extremes. Some people get moderately sick with a dry cough, fever, fatigue, and shortness of breath. Some lose their sense of taste. Others have diarrhea.

Epidemiologists are already digging through a trove of information to better understand the disease. How do demographics, behavior, medications, or availability of care affect outcomes? Answers to these questions will likely be most helpful in coming weeks and months, just as soap, water, communication, and planning are our most effective short-term weapons for halting its spread.

New capabilitiesmaybe for this pandemic, maybe the next oneare emerging too though. While studies into how genes bend the course of a disease would have once taken years, were nearing a time when they can yield answers faster to bring more targeted care.

But first, how might DNA play a role in how sick Covid-19 makes people?

Viruses break into our cells and commandeer cellular machinery to reproduce. Like a thief whos copied the key to your front door, they carry proteins that fit complementary receptor proteins on a cells surface. If theres a match, presto, theyre in.

The CCR5 mutation, for example, codes for a variant of the surface protein HIV uses to invade immune cells. As the key no longer fits the lock, the virus is left out in the cold. Unable to replicate on its own, it cant spread. The would-be invasion hits a wall.

The virus behind Covid-19 also uses a protein receptor, ACE2, to enter respiratory cells. It may be that some peoples genes produce protein locks that are harder for Covid-19 to pick, or that regulatory genes are slowing the production of ACE2. Depending on our DNA, then, some of us may have cells that are more open to infectionand so suffer more serious illnesswhile others offer fewer viral targets and escape relatively unscathed.

Another possibility is that genetic variants are tuning our immune systems differently. Perhaps its a combination, or some other cog in the machine still waiting to be discovered.

At the moment, we just dont know.

Mainstream genetic testing and whole genome sequencing are tools we havent had in the past. Not long ago, DNA testing kits for ancestry or general health were some of the most popular holiday gifts. Meanwhile, the cost of sequencing a whole human genome has been at or under $1,000 for years, leading to a number of very large sequencing projects.

In the former case, companies like 23andMe have assembled huge DNA databases. Though such tests look at only a fraction of a genomeusing a process called genotyping23andMe has the genetic data of over 10 million people on file. Eighty percent of these have authorized the company to use their data for research, and to that end, they recently sent customers a survey to collect information for a potential Covid-19 study.

If they get enough responses, theyll combine survey answers with each persons genetic profile and conduct a genome-wide association study to link genetic similarities and differences to particular traits and outcomes. This approach would most likely find common gene variants shared by many people, but it may miss less common variants that more complete gene sequences would capture. And such rarities may be key, according to Stephen Chapman, a University of Oxford respiratory physician and researcher.

This is where collections of more complete genomic data may prove powerful.

Many such studies already exist, and new ones are popping up. To gather the work under one banner, the University of Helsinkis Andrea Ganna and Mark Daly started the Covid-19 Host Genetics Initiative. Over 100 studies are participating in the project, according to their site, and a dozen large biobanks have shown interest.

There are long-standing studies, involving hundreds of thousands of people, and other smaller ones collecting data on patients who test positive, Ganna told the BBC. Its such a huge diversity and there are a lot of countries involved, and we will try to centralize it.

The UK Biobank is an example of one of those bigger existing studies.

The biobank has biological samples and health information for 500,000 people and plans to collect and add Covid-19 information to the database. Over 15,000 scientists have access to the data. Similarly, DeCODE Genetics, an Icelandic company, has the genetic and health data of over half of Icelands population and is also testing people for Covid-19.

The Personal Genome Project, founded in 2005 by Harvards George Church, is hoping to add Covid-19 data from thousands of participants to its database too. And a team led by Jean-Laurent Casanova, a Rockefeller University professor, will tap sequencing hubs around the world to record the genomes of young, healthy patients sent to the ICU with Covid-19.

Its unclear what these projects will find, or how long it will take. What is clear is that large collections of genetic and health information are making it possible to quickly begin serious genetic studies of the diseasesometimes with little more needed than a new survey.

Scientists have never so willingly shared information or singularly focused on one problem. Add to that a flood of clinical and scientific information gathering and a digital highway to deliver it worldwide, and you have the recipe for scientific collaboration of epic proportions.

Well know more tomorrow, in two weeks, and in two months than we do today. Faced with so much uncertainty, thats a hopeful thought.

Image Credit: Fusion Medical Animation /Unsplash

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Is the Reason Coronavirus Seriously Sickens Some and Spares Others in Our Genes? - Singularity Hub

Recommendation and review posted by Bethany Smith

Even before Texas first case of the novel coronavirus landed in March in Fort Bend County, Mrudula Rakhade was preparing how her clinical laboratory in a northwest Houston business park could accommodate the testing to come.

Anticipating the need in February to test for the rapidly-spreading virus back when international travel was the leading source Rakhade took the lead in ordering COVID-19 supplies for Altru Diagnostics, where she works as the chief scientific officer. She also made the lab one of the few statewide to be registered with the U.S. Food and Drug Administration to identify positive traces of the virus.

By the time her boss of two years, Dr. Jesse Howard, suggested the lab take on COVID-19 testing in March she had news for him.

I told him, Youre going to get COVID testing in a week because I had already been working on it, Rakhade proudly said.

As Howard, who opened the lab with his late father in 2016, walked by her office Monday afternoon, he said I trust her blindly.

CORONAVIRUS UPDATES: Stay informed with accurate reporting you can trust

Now, the 25-employee operation off the Katy Freeway is analyzing more than 1,000 specimens a day, mostly for local medical providers, including four United Memorial Medical Center drive thru-testing sites. Increases in testing have doubled the number of specimens they started with on March 19. Since then, they have analyzed an estimated 20,000 tests or more, Howard said.

Rakhade and her team of molecular technologists are pulling 12-hour shifts in cramped rooms to meet the growing demand. Social distancing is not an option. Some workers wear N-95 masks, while others, like Rakhade, choose at times not to.

I havent gotten anything yet, she said, adding that employees are tested every week for the novel coronavirus out of precaution. We dont go and touch anything without gloves on.

A meticulous assembly line starts the moment a courier arrives and couriers with coolers packed with tests routinely pop into the lab.

Specimens are packed into one-time use plastic plates designed to hold 96 biological samples which are then injected with a magnetic solution to isolate any trace of the coronavirus ribonucleic acid, also known as RNA.

Another machine identifies how much novel coronavirus if any is in a sample, using a predetermined range for a positive result. A lower range of a positive could mean the nasal swab was not administered properly.

Some people dont go that deep, she said.

Undetermined values mean the sample is negative.

For each batch, the process can take up to four hours. As of Monday, the turnaround time, which includes contacting patients with their results, can be anywhere from 24 to 48 hours.

It is difficult to fulfill everyones expectations at this point, she continued.

And then the patients themselves start calling.

We just have to be patient with them, Rakhade said. Sometimes they get frustrated wondering why their results are not yet in. What can I do, they ask. Im quarantined.

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On Sunday, for the first time in a month, Rakhade took the day off.

Up until then, she had spent several sleepless nights at the lab. She worked exhaustively in mid-March to finalize their COVID-19 certification with a positive patient sample supplied by the Centers for Disease Control to base their review.

I stayed up two nights continuously getting that done, Rakhade said. The night before I finished, we went home around 2 a.m. and I came back at 6 a.m. to finish.

During their research for certification, the lab stumbled across what appeared to be Laredos first case, she said. Without federal registration, which she finalized on March 18, the lab was unable to consider it official and recommended the patient an elementary school teacher be retested. According to Laredo officials, the San Antonio Metro Laboratory handled her test and her case was confirmed on March 17. Two days later, Altru Diagnostics first official positive arrived amid an estimated batch of 500 samples. That lone specimen was followed by about three more positives.

It was very rare to see a positive. It had just started, Rakhade said. After that it became routine because we had been testing so many samples.

Despite all her preparation, the lab ran into a similar problem plaguing hospitals and the Houston and Harris County-operated drive-thru testing sites: supply shortages.

On Friday, the lab used up all its plastic plates designed to hold COVID-19 samples. The plates can only be used once and the manufacturer was also out.

Rakhade resorted to old-school bartering to get what they needed. Another lab in Houston, which does not do COVID-19 testing, had a stash of unused plates. And she had what they needed micro fluiditcs chips for genetic testing.

All the manufacturers are focusing on COVID-19 supplies, she said. They needed something they couldnt get because its not COVID-19.

nicole.hensley@chron.com

Read more:
Inside the Houston lab tackling thousands of COVID-19 tests and its familiar problem - Houston Chronicle

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