During a recent with interview with Business Innovators, Skin Care Expert Eti Elison of Skin By Eti Elison discussed advancements in stem cell technology for skin care and how she helps her clients improve their skin with the technology.

Eti Elison, Skin Care Expert, was recently interviewed by Business Innovators Magazine about how she helps her clients improve the look of their skin using stem cell therapy.

Eti has mastered the art of healthy, vibrant, glowing skin. As a licensed skin therapist in three different countries: Israel, Switzerland and USA, she has been immersed in the skin care industry for over 25 years. She provides cutting edge treatments, the result of many years of experience in clinical skincare. Her facials are meticulously customized to each patients individual needs.

During the interview Elison stated, When it comes to skin care there are many products on the market that mention stem cells in their labeling, but in most cases, those stem cells function as antioxidants, growth factors or peptides. But they are not actually effecting the stem cells that are in the skin.

When asked about how she uses stem cell technology Elison Stated: in my skin care procedures I use a product called Tensage Stem Cell Cream formulated with Cellpro technology. It is the only product that I know of that increases the skins ability to turn stem cells into new skin cells.

Eti Elison is based in Los Angeles, CA and can be contacted to for help for improving skin conditions or the appearance of aging.

To read the full interview, visithttp://businessinnovatorsmagazine.com/skin-care-expert-eti-elison-talks-about-new-stem-cell-technology-for-skin-care/

To learn more about Eti Elison please visit: https://www.skinbyetielison.com

Media ContactCompany Name: Skin By Eti ElisonContact Person: Eti ElisonEmail: etigelison@yahoo.comPhone: (310) 922-5110Country: United StatesWebsite: https://www.skinbyetielison.com/

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Eti Elison, Skin Care Expert, Talks About Stem Cell Therapy in New Interview with Business Innovators Magazine - Digital Journal

Recommendation and review posted by simmons

Unlike most flowering plants, cannabis is unique in that it requires both a male and female plant to reproduce. While hermaphroditic (self-pollinating) cannabis does exist, the plant most commonly expresses male- or female-specific sex organs.

Female cannabis plants produce the large, resinous buds that are dried, cured, and consumed. For this reason, females are typically the only plants youll find in someones cannabis garden.

Male plants are commonly regarded as useless and discarded.While pollination by males is essential for producing more cannabis plants (unless working from clones), its a process that is generally best left to breeders so growers can focus on producing consumable seedless buds calledsinsemilla.

Do male plants truly belong in a compost bin, or could they serve a more beneficial purpose to gardeners? Surprisingly, there are more uses for male plants than one might think.

The obvious function of male cannabis plants is for breeding seeds. When pollinating females, males provide half of the genetic makeup inherited by seeds. Because of this, its important to look into the genetics of the male plants. Their shape, rate of growth, pest and mold resistance, and climate resilience can all be passed on to increase the quality of future generations.

When it comes to hemp fiber, the male cannabis plants produce a softer material while females are responsible for producing a coarse, stronger fiber. The soft fiber from the male plants make them more desirable for products like clothing, tablecloths, and other household items.

It may come as a surprise that male plants can be psychoactive in naturethough much less potent than females. The plants do not produce buds, but small amounts of THC can be found in the leaves, stems, and sacs, which can be extracted to produce hash or other oils.

Cannabis plants offer more benefits in the garden beyond bud production. Both male and female cannabis plants produce aromatic oils called terpenes, which are associated with pest and disease control. Since males also produce terpenes, you may consider including your males in a vegetable or flower garden (as long as theyre well separated from any female cannabis plants). Dried material from cannabis plants have also been used to produce terpene-rich oils that are applied to repel insects and pests as natural bug sprays.

Additionally, cannabis plants are deep rooting plants with long taproots. Taproots are known for their ability to dive deep into the ground and break apart low-quality soil, allowing for moisture and nutrients to infiltrate and improve the soil quality. These taproots also help keep the soil in place, thereby preventing nutrient runoff and loss of soil during heavy rains.

Humans are largely focused on female cannabis plants, and rightly so. But its important to acknowledge and cherish the characteristics of the male cannabis plants as well. Females may produce the buds we know and love, but by limiting diversity of the males, we could be losing out on potential benefits we do not yet understand. Specific males could have compounds we are unaware of that might play significant roles in how females develop, or how cannabis as a whole develops in the future.

If attempting to capitalize on any of the above benefits without the intent to breed, keep in mind that cannabis pollen is extremely good at traveling long distances, determined to find a female. It helps to have a solid understanding of how pollen works and travels before you embark on any of these alternative uses so as not to accidentally pollinate your own plants or a neighbors.

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4 Ways to Make Use of Male Cannabis Plants - Leafly

Recommendation and review posted by sam

Men, and especially male smokers, appear to be more likely to develop lung cancer if they take high doses of vitamins B6 and B12, new research suggests.

For men taking these vitamin supplements, the risk of lung cancer was nearly doubled. For men who smoked, the risk was between three and four times higher, the study found.

"High-dose B6 and B12 supplements should not be taken for lung cancer prevention, especially in men, and they may cause harm in male smokers," said study lead author Theodore Brasky. He is a research assistant professor at Ohio State University.

However, the study wasn't designed to prove cause-and-effect between the vitamins and lung cancer; it only showed an association.

It's also not clear why only men and current male smokers seem to face an extra risk.

And a trade organization representing the vitamin industry cautioned against reading too much into the study.

Most people in the United States get enough vitamin B6 through their diets, according to the U.S. National Institutes of Health (NIH). Some people with certain health conditions may need supplements.

As for vitamin B12, the NIH reports that most Americans get enough from their diet. But some groups -- such as older people and vegetarians -- may be deficient and need supplements. The vitamin may also cause interactions with medications.

Dietary sources of vitamin B6 and B12 include fortified cereals and foods that are high in protein.

The new study included more than 77,000 adults, aged 50 to 76, in Washington state. The participants were recruited from 2000 to 2002, and answered questions about their vitamin use over the previous 10 years.

The researchers found that just over 800 of the study volunteers developed lung cancer over an average follow-up of six years.

The study found no sign of a link between folate (a type of B vitamin) and lung cancer risk. And vitamin B6 and B12 supplements didn't seem to affect risk in women.

However, "we found that men who took more than 20 milligrams per day of B6 averaged over 10 years had an 82 percent increased risk of lung cancer relative to men who did not take supplemental B vitamins from any source," Brasky said.

"Men who took more than 55 micrograms per day of B12 had a 98 percent increased lung cancer risk relative to men who did not take B vitamins," he noted.

Men who smoked at the beginning of the study period and consumed high levels of the B vitamins were three to four times more likely to develop lung cancer, he added.

"B6 is typically sold in 100 mg (milligram) tablets. B12 is often sold between 500 mcg (microgram) and 3,000 mcg tablets," Brasky said.

"In contrast, most multivitamins include 100 percent of the U.S. Recommended Dietary Allowance, which is under 2 mg per day for B6 and 2.4 mcg per day for B12. People should really ask themselves if they need over 1,200 times the RDA (recommended daily allowance) of a substance. There's simply no scientific backing for these doses," he said.

The study doesn't conclusively link higher doses of the vitamins to higher rates of lung cancer. If there is a connection, it's not clear how the vitamins might influence the cancer risk, Brasky said, although it may have something to do with how the vitamins interact with male sex hormones.

Paul Brennan, head of the genetics section with the International Agency for Research on Cancer, said the study appears to be valid.

However, the findings conflict with his group's recent research, published July 22 in theJournal of the National Cancer Institute, which didn't find any links between high blood levels of vitamin B6 and lung cancer in people at large, or men specifically.

"If anything," Brennan said, "we found a small protective effect that was more apparent among men."

Still, Brennan added that "there is clearly no evidence that these vitamins have any substantial protective effect. Smokers taking these vitamins should quit smoking."

Dr. Eric Bernicker, a thoracic oncologist with Houston Methodist Hospital, agreed with that advice and said the study points to a higher risk of lung cancer from higher doses.

"There's a strong belief that vitamins would never harm you. As in much of nutrition, the story is more complicated than that," Bernicker said.

In a statement, Duffy MacKay, a senior vice president of the Council for Responsible Nutrition, a trade group for the vitamin industry, urged consumers "to resist the temptation to allow sensational headlines from this new study to alter their use of B vitamins."

According to MacKay, "The numerous benefits of B vitamins from food and dietary supplements -- including supporting cognition, heart health and energy levels -- are well-established."

In addition, McKay said, the study has limitations. Among other things, it required participants to remember what they consumed over 10 years.

The study was published Aug. 22 in theJournal of Clinical Oncology.

See more here:
Could high doses of vitamin B supplements raise lung cancer risk? - CBS News

Recommendation and review posted by Bethany Smith

Countries have to maintain a large number of operational naval assets in order to build deterrence, protect sovereignty, and secure Sea Lines of Communication (SLOC). Operators are initiating comprehensive midlife upgrades and life extension programs in order to field adequate operational assets. The naval ship modernization market will grow at a compound annual growth rate (CAGR) of 4.3% during 20162026 and result in a total valuation of $49.10 billion. The market will be dominated by upgrades for surface combatant and submarine segments (92.5% of the total market).

Through this research service, Frost & Sullivan provides an assessment of global naval ship modernization programs, opportunities, forecasts, and technology trends from a macro level and also from a comprehensive micro-level countrywise assessment.

Key Target Audience

The key target audience includes: Defense OEMs and Integrators (especially their marketing and sales teams) Tier 1/ Tier 2/Tier 3 Suppliers Defense Consultants and Researchers Educational Bodies Personnel Working with Ministry/Department of Defense

Research ScopeThe market trends are analyzed for the study period 2016 to 2026, with the base year being 2016. The scope of the study is global, covering most nations which field a naval force.

The market is segmented across surface combatants, submarines, support ships, and patrol boats. Each segment is broken up into different vessel types and classes for granularity in information. Companies mentioned in the study include Lockheed Martin, Terma, Atlas Electronick, Raytheon, STM, TKMS, Kongsberg Marine, HII, and DCNS among others.

Country-specific modernization, life extension, and upgrade programs are arrived at using a combination of data including vessel acquisition and commissioning time frames, defense contract data, previous upgrades, defense spending patterns, and geopolitical exigencies.

Key Questions This Study Will Answer What are the committed, planned, and upcoming opportunities in the naval ship modernization market over the next 10 years? Which geographical markets and segments are growing? What are the key success factors that OEMs should consider in the market? What drives the need for modernizing naval ships in different nations and how do their procurement preferences and market dynamics differ? What are the major programs underway and planned within these markets and what opportunities do they open up for OEMs/contractors?Read the full report: http://www.reportlinker.com/p05075872/Global-Naval-Ship-Modernization-Assessment-Forecast-to.html

About Reportlinker ReportLinker is an award-winning market research solution. Reportlinker finds and organizes the latest industry data so you get all the market research you need - instantly, in one place.

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Global Naval Ship Modernization Assessment, Forecast to 2026 - PR Newswire (press release)

Recommendation and review posted by sam

CRISPR keeps cancer in check

SPL

By Michael Le Page

The CRISPR genome editing revolution continues to advance at an astounding pace. As many as 20 human trials will be under way soon, mostly in China, New Scientist has learned.

One of these trials will involve the first-ever attempt to use CRISPR to edit cells while they are inside the body. The aim is to prevent cervical cancers by targeting and destroying the genes of the human papillomavirus (HPV) that cause tumour growth. This study is due to begin in July at the First Affiliated Hospital of Sun Yat-Sen University in China.

Gene therapy, which involves adding extra genes to cells, was first used to cure people in 1990, but it is mainly useful for treating rare genetic disorders. In contrast, gene-editing, which involves altering existing genes inside cells, promises to treat or cure a much wider range of conditions, from HIV infection to high blood cholesterol.

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One of these trials will involve the first-ever attempt to edit cells insidethe body

The first gene-editing trial in humans started in 2009. Doctors removed immune cells from people with HIV, disabled the gene for the CCR5 receptor which the virus uses to get into cells and returned the HIV-resistant cells to the body. The treatment appears to keep HIV in check.

But subsequent progress in gene editing was slow because developing a way to target each particular sequence is costly and time consuming. All that changed in 2012 when CRISPR genome editing was developed, making it cheap and easy to target almost any sequence.

The first clinical trial involving CRISPR began at the West China Hospital in Chengdu in October 2016. Doctors removed immune cells from the blood of a person with lung cancer, used CRISPR to disable a gene called PD-1 and then returned the cells to the body.

PD-1 codes for an immune cell off switch. Tumours can flip this switch to prevent immune cells attacking so if immune cells lack the PD-1 switch then cancer cells cannot manipulate them. However, there is a risk that the always on immune cells could begin attacking healthy cells.

The lung cancer trial isnt due to finish until 2018, but other teams are forging ahead. Clinical trial registries show that a dozen more trials that will disable PD-1 with CRISPR are planned in China. These target conditions including breast, prostate, bladder, oesophageal, kidney, colorectal and Epstein-Barr virus-associated cancers.

The HPV trial, meanwhile, will break new ground. Instead of editing cells outside the body, a gel containing DNA coding for the CRISPR machinery will be applied to the cervix. The CRISPR machinery should leave the DNA of normal cells untouched, but in cells infected by HPV, it should destroy the viral genes, preventing them from turning cancerous.

Targeting HPVs seems a sensible approach if they can deliver the genome-editing components to sufficient numbers of cells, says Robin Lovell-Badge of the Crick Institute in the UK.

It is tricky to do these experiments in animals as they are not infectable by HPV, says Bryan Cullen of Duke University Medical Center in North Carolina, whose group also hopes to use gene editing to get rid of HPV. But there is a risk of off-target mutations leading to cancer, he warns.

If these trials are successful, it could benefit millions of people. Vaccination against HPV is now possible, but there is no way to get rid of the virus in people who have it already. It can cause mouth, throat and anal cancers in both sexes, as well as being the main cause of cervical cancer.

While the HPV trial looks set to be the first to use CRISPR to edit cells inside the body, it may not be the first ever such use of genome editing. Three trials getting underway in the US will use another genome editing method known as zinc finger nucleases to add genes to liver cells to try to treat haemophilia B, and Hurler and Hunter syndromes.

A further four planned CRISPR trials involve changing immune cells to make them better at killing cancers. First, a virus will be used to add a gene to immune cells that makes them attack specific tumours creating so-called CAR-T cells. Then two or more genes usually including PD-1 will be disabled with CRISPR to make the cells even more effective.

Such UCART19 cells have already saved the lives of two girls, but these cells were created with an older gene-editing method. Now a clinical trial is due to start in the UK. Our lab is moving over to CRISPR, team leader Waseem Qasim of University College London told a meeting in February.

Two similar UCART19 trials areplanned in China, with another in the US. Trials are also planned for Duchenne muscular dystrophy, says Lovell-Badge, butthese are probably some way from starting.

This article will appear in print under the headline Boom in gene-editing clinical trials

We clarified what is unique about the reported trials.

More on these topics:

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Boom in human gene editing as 20 CRISPR trials gear up | New ...

Recommendation and review posted by sam

In BriefCRISPR Therapeutics has teamed up with General Hospital of Massachusetts to further-widen CRISPR's near-ubiquitous applications. Within this two-year collaboration, CRISPR/Cal9 will also be used in T cell cancer therapies.

In a recent development, CRISPR Therapeutics, the subsidiary of CRISPR AG, has signed onto a two-year research collaboration with Massachusetts General Hospital (MGH), to research the use of CRISPR/Cas9 in T cell cancer therapies.

This comes on the heels of a seemingly-endless list of advances. Two weeks ago, the CRISPR/Cas9 gene editing tool successfully removed genetic disorders from human embryos and additionally,successfully extracted HIV from a living organism. It was used to develop semi-synthetic organisms, targeted the command center of cancer, and even coerced superbugs to kill themselves on the genetic level.

The application of CRISPR/Cas9 to T cell therapies is expected to address unmet needs in hematologic and solid tumors, masses which from the cells are typically extracted and programmed to recognize and attach to. Leading the scientific work at MGH is the director of the Cellular Immunotherapy Program, Marcela V. Maus, MD, Ph.D. Anticipating the benefits of the collaboration, head of Immuno-oncology Research and Translation at CRISPR Therapeutics, Jon Terrett, Ph.D., told GlobeNewswire:

It is becoming increasingly clear that CRISPR/Cas9 can play a major role in enabling the next generation of T cell therapies in oncology. By combining our gene editing capabilities with Dr. Maus pioneering expertise in T cell therapy, we hope to accelerate our progress toward making these therapies a reality for patients suffering from cancer.

This partnership is CRISPR Therapeutics latest step toward advancing immuno-oncology. Terrett was brought aboard in February of this year as the companys leader in this regard.

Mausadded:

We have already seen the profound benefit that T cell therapies can have for certain patients with a specific set of tumor types. Now the potential with gene editing, and specifically CRISPR/Cas9, exists to create improved versions of these cells that may work for a wider variety of patients with a more diverse set of tumor types. Im glad to see the commitment CRISPR Therapeutics is making to this area, and am excited to collaborate with them.

Expect to see CRISPR/Cas9 expand its applications to include a more diverse spectrum of tumor types and molecular targets, as the revolutionary medical technology carries on.

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CRISPR Therapeutics Joins Hospital For Cancer Treatment Tests - Futurism

Recommendation and review posted by sam

AUGUST 23, 2017

A CRACK IN CREATION is not The Double Helix. They are both stories of revolutionary biological advances, told by one of the discoverers, but The Double Helix feels like a novel. And, like a historical novel, it was eventually understood to be based on real events but not always reliable history.

A Crack in Creation is also not a history that is, a detailed and precise explanation of who did what and when to produce CRISPR/Cas9, this centurys biggest biological discovery to date. That history awaits its Horace Freeland Judson, whose magisterial The Eighth Day of Creation provided a gripping blow-by-blow account of the birth and adolescence of molecular biology, or its Robert Cook-Deegan, whose The Gene Wars illuminated the beginnings of the Human Genome Project.

Nor is this a how to book for aspiring do-it-yourself CRISPR users; or a deep analysis of the ethical, legal, and social issues CRISPR and its progeny will raise; or a legal analysis of the already (in)famous CRISPR patent fight; or a look at the unresolved Nobel Prize race. And it is not a gossipy inside look at the people intimately involved in CRISPRs invention.

So what is A Crack in Creation? It is an essential start to educating the public.

Humans use of the bacterial defense mechanism called clustered regularly interspaced short palindromic repeats (CRISPR), with or without CRISPR associated protein 9 (Cas 9) along with the technologies that eventually will modify or displace it is of vast importance. Thats not because it is the first way we have found to edit DNA. It misses that distinction by over 40 years. But it is the first truly fast, cheap, easy, and accurate way to do so. It is biotechnologys Model T. The Model T was not, by several decades, the first automobile, but it transformed cars from expensive, unreliable, inconvenient, and rare objects to something everyone could, and soon did, own. It is the change in degree, not in kind, that has transformed the world we live in (nowhere more than California). Similarly, humans have been manipulating living organisms, including ourselves, at least since the dawn of modern man, but CRISPR is the change in degree that turns gene editing from expensive, unreliable, inconvenient, and rare to ubiquitous. It vastly increases our powers to edit all life, including our own.

A Crack in Creation tells the story of CRISPR through the eyes and in the voice of Jennifer Doudna, the UC Berkeley biochemist who was a central figure in harnessing it. (The co-author, Samuel Sternberg, is Doudnas former graduate student.) It divides elegantly into two four-chapter parts, plus prologue and epilogue. The first part describes what CRISPR is and how it was discovered; and the second sets out CRISPRs possible uses in the environment and medicine, and in editing humankind.

It is not, however, the first publication to recount the origins of CRISPR. Indeed, as with the double helix, the identity of the originators is contested. In January 2016, Eric Lander, director of the Cambridge, Massachusettsbased Broad Institute (jointly owned by Harvard and MIT), published a 7,200-word essay titled The Heroes of CRISPR in Cell, one of three leading journals for bioscience publications. It was widely criticized for minimizing the contributions of Doudna and one of her key collaborators, Emmanuelle Charpentier, and highlighting instead the work of Feng Zhang, a researcher at the Broad (and hence Landers employee). As well as triggering, fairly or not, debate over the issue of sexism in science, Landers piece was particularly controversial in that the publication never mentioned its authors conflicts of interest, not just in promoting Zhang as CRISPRs hero, but because of the very expensive patent fight over CRISPR between the Broad Institute and Doudnas employer, the University of California (UC).

This said, what both Lander and Doudna do well is reveal the complex, interlocking, and thoroughly international nature of todays bioscience. They acknowledge the work of a dizzying number of contributors to CRISPR. The first publication to show that CRISPR could be used to edit bacterial DNA was Doudna and Charpentiers Science article in June 2012 but, by that time, scores of researchers had already been exploring what was regarded as a tantalizing bacterial curiosity.

In his Cell article, Lander writes that [t]he story starts in the Mediterranean port of Santa Pola, on Spains Costa Brava, with Francisco Mojica who published a report in 2005 on the existence of, and possible immune system function of, certain odd, largely palindromic, DNA repeats in several bacterial species. Researchers at a yogurt company, Danisco, also played important roles, as did Sylvain Moineau in Quebec and John van der Oost from the Netherlands. Even before her first meeting with Doudna in March 2011, Charpentier and her lab at the University of Ume in Sweden had also contributed to the development of the CRISPR system.

Virginijus iknys, a Lithuanian researcher, greatly improved researchers understanding of the proteins bacteria used with CRISPR. He saw some of the possibilities of CRISPR as a tool and submitted a paper to Cell on the topic on April 6, 2012. Cell rejected his paper, which was eventually published on September 4, 2012, in the Proceedings of the National Academy of Sciences. In the meantime, Doudna and Charpentiers paper was submitted to Science on June 8 and published 20 days later.

But if this is more or less the beginning of the CRISPR discovery story, it is certainly not the end.

Feng Zhang, a brilliant young researcher at the Broad, had spent much of 2011 and 2012 working on a way to use CRISPR in mammalian cells. Zhang submitted his first CRISPR publication on October 5, 2012. Later that month, George Church, an exceptionally wide-ranging and creative Harvard researcher, submitted a paper on using CRISPR in human cells, which Science published in the same issue as Zhangs on January 3, 2013.

This summary does not come close to mentioning all the laboratories involved in discovering and developing CRISPR and does not even begin to talk about the vital contributions of the post-docs and graduate students in those labs, all of them highlighted in A Crack in Creation.

Whose version is closest to the true history of CRISPR? Landers history was widely attacked and A Crack in Creation has already been criticized in a review in Nature for downplaying Zhangs role (though it mentions him more than Lander mentioned Doudna). I suspect neither Lander nor Doudna and Sternberg could tell the full story for at least one sad reason lawyers probably wouldnt let them. Their employers are locked in a patent struggle. The details of who did, said, or knew what when could be crucial to its outcome. How many changes in the manuscripts came as a result of lawyers comments? Probably more than a few.

In fairness, A Crack in Creation never promises to be the definitive history of CRISPR much less a story of all its heroes. It tells Doudnas CRISPR story, as well as the authors thoughts on its potential uses and implications. These uses and implications make up the books second part, The Task. It begins with the use of CRISPR in the non-human world for agricultural purposes and beyond, including the ongoing development of gene drives, an important adaptation of CRISPR that can speed the spread of desired genetic changes in sexually reproducing species, as well as plausible speculation about future unicorns (in this case, the mythical animal). It then addresses the medical applications of CRISPR to living people in the form of so-called somatic gene editing, intended to heal their bodies without changing their eggs or sperm and so not affecting future generations. The authors rightly view this as the least controversial use of CRISPR. The last chapters address what has become the stickiest question for most people: the use of CRISPR to make changes in the genome of the human germline (eggs and sperm) that can be inherited from generation to generation.

Doudnas interest in these last issues is neither new nor shallow. In October 2014, I was invited to a small meeting she was organizing in Napa Valley the following January to discuss the ethical issues of CRISPR. (Coincidentally, this was almost exactly 40 years after the famous 1975 Asilomar meeting to assess safety issues of the first gene editing, recombinant DNA.) The Napa meeting involved about a dozen prominent scientists including Paul Berg and David Baltimore, the two Nobel Prize winners who helped organize the Asilomar meeting and two law professors who work in the field, Alta Charo from the University of Wisconsin and myself. Doudnas genuine concern was evident, not just in calling the meeting but in her active and thoughtful participation in it. And human germline genome editing was clearly the focus of that concern.

The Napa meeting reached consensus surprisingly quickly: the somatic cell uses of CRISPR should be pursued actively, but human germline modifications needed more thought. Doudna took the lead in drafting a commentary, signed by the meetings participants and several others, which Science published in March 2015.

The commentary made four recommendations about human germline editing:

The Science article was not alone. Nature had published a commentary on human gene editing the week before, endorsing somatic cell uses of genome editing, but rejecting germline changes. And two weeks later, an obscure journal published an article in which Chinese scientists reported their (slightly) successful efforts using CRISPR to edit human embryos.

The Chinese group had carefully used human embryos that were not viable and thus could never become babies, but the article still set off a firestorm. One of its results was a US National Academies of Sciences, Engineering, and Medicine initiative to study genome editing. A major part of that initiative was an International Summit on Human Gene Editing held in Washington, DC in December 2015, with additional sponsorship from the Chinese Academy of Sciences and the UK Royal Society. At its end, the summits planning committee (not the sponsoring academies) issued its conclusions, roughly echoing the March Science commentary.

As A Crack in Creation usefully points out, the debate over germline modification is not new. The issue was discussed in print at least 30 years before CRISPR was imagined. But a sense of urgency and some specificity about both the likely intervention and the societies into which it will be launched helps focus discussions. Since the International Summit (and submission of the last manuscript of the book), the National Academies alone have published at least three relevant reports two concerning non-human uses of CRISPR in October 2016 and March 2017, and the third, issued in February 2017 on Valentines Day, on CRISPR and humans, endorsing somatic cell uses of CRISPR and opening the door for possible germline editing for medical reasons.

A Crack in Creation hints that the discussions thus far have modified Doudnas views. Like the February 2017 report, the book shows some openness to human germline modification, at least for addressing clearly genetic diseases.

Personally, I think we focus too much on human germline genome modification. There is no human germline genome there are over seven billion of them, each changing slightly by mutation in every generation. Editing out rare, disease-causing DNA variations or replacing them with the more common safe variants hardly seems radical. The real concerns for germline or somatic human gene editing should be about enhancements (as opposed to disease), but that is just one part of a much wider conversation about all kinds of biological, electronic, and mechanical enhancements. The combination of our great concern about the safety of babies and our ignorance regarding enhancing genetic variants, however, means we have time to get this right. But were way behind in regulating the use of CRISPR in non-humans. The medical, practical, and political constraints around human babies do not exist for mosquito babies, let alone genetically modified microbes or plants. For the moment, we need to concentrate on this much less constrained use of CRISPR, which is already beginning.

Doudna called for discussions about the uses of CRISPR in Napa in January 2015 and A Crack in Creation amplifies that plea, providing the interested public with the background critical to such discussions. But CRISPR has raised two other interesting questions, which, though not discussed in the book, are worth mentioning: the Nobel Prize and the patent fight.

A Crack in Creation says nothing about the likely Nobel Prize for CRISPR, but CRISPR junkies regularly discuss it. A Nobel Prize in either Chemistry or in Medicine and Physiology seems almost certain, and will likely be granted soon. But who will receive it?

Scores of people in many countries contributed to its discovery, but Nobel Prizes in the sciences are limited to not more than three people. Doudna and Charpentier should be shoo-ins, for their own insights, for the work of their labs, and for their first publication. Plausible other candidates include at least Mojica, iknys, Zhang, and Church but four into one wont go.

Many have read Landers Cell article as an effort to tilt the third spot toward his faculty member, Zhang, but the fight over the patent rights for CRISPR could also influence who wins the prize. A Crack in Creation mentions the patent fight only once, as a disheartening twist to what had begun as collegial interactions and genuine shared excitement about the implications of the research. But the patent cases over CRISPR have been unusual, and unusually fascinating, from the beginning. (For more details see various pieces by Jacob Sherkow, the law professor who has followed this most closely.)

In December 2012, Zhang and others (meaning the Broad Institute on behalf of Zhang and others) filed a patent application on the use of CRISPR in any cells from complex organisms, called eukaryotic cells, which include everything from algae to us, as opposed to prokaryotic cells (bacteria and archaebacteria) and viruses. Doudna and Charpentiers patent application had been filed seven months earlier, claiming the use of CRISPR in all cells. But the Broad paid for and got a special expedited patent procedure so that its patent application, though filed after the UCs, was granted in April 2014, before the UCs was decided.

A year later, in April 2015, the UC invoked an interference proceeding, asking the Patent and Trademark Office (PTO) to resolve an apparent inconsistency in patent applications and determine who was the first inventor. In February 2017, the PTO ruled in favor of Zhang and the Broad. But the UC has appealed this decision, and even if it stands, it is possible that the Doudna and Charpentier patent and the Zhang patent will be held valid, in which case someone who wanted to use CRISPR in eukaryotic cells, including human cells, would need licenses from both UC and the Broad.

Furthermore, all patents are limited to the jurisdiction that granted them. US patents have no force outside the United States. This past March, the European Patent Organization granted CRISPR patents to UC, as have the patent authorities in China and the United Kingdom. So we could have a world where the Broad seems to control important US uses and the UC the European, British, and Chinese uses. The rest of the world is, at this point, up for grabs.

What does all this mean? In terms of the ultimate ownership of the most basic CRISPR patent rights, stay tuned. It is too soon to tell. But, in a larger sense, I dont think it matters.

This is mainly a fight about money: about which American universities will make money, and how much of it, off some uses of CRISPR. If the money goes to the UC system, as a Californian I would be pleased. But the question of who profits shouldnt change the adoption of CRISPR. That is, as long as either entity uses a good licensing strategy. Of course, even that may not matter. The CRISPR patents will give the players ownership of some approaches, but they will be of little value if novel approaches are developed. Already various inventors have come up with alternatives to Cas9 as part of the CRISPR complex. Bacteria invented CRISPR billions of years ago and have had time, and selective pressure, to invent variations on it. The harder the Broad or UC try to enforce rigorous patent terms, the more they encourage researchers to invent around their patents. The more they tighten their grip, the sooner the money will slip through their hands.

This raises the more fundamental question of why the CRISPR patent fight is happening at all. Like many people, I initially thought the UC and the Broad would settle their patent dispute quickly. Each would take a certain percent of the royalties for their combined patents and be happy not least because they would avoid tens of millions of dollars of expense, months of distraction for their researchers, and years of uncertainty. If one of the institutions involved were a novice in technology licensing, then it might get greedy and seek a complete victory, but neither the UC system nor the Broad (and certainly not the Broads owners, Harvard and MIT) are novices. They have some of the most experienced and sophisticated technology licensing offices in the world.

So why are they spending so much money on this fight? It might, in part, relate to the Nobel Prize. If Lander really wants to bolster Feng Zhangs case for winning a CRISPR Nobel Prize, then he may think that having Feng win some or all of the patents will be helpful. That seems a bit far-fetched, and yet it could be one factor in the Broads litigation strategy. If so, it is not clear whether it will succeed, even if the Broad patents eventually sweep the field. The Nobel Prize decision-makers need not follow the patent office of any country.

In the end, the history, the prizes, and the patents dont really matter. The structure of DNA would have been discovered without Watson and Crick, and CRISPR did not require Doudna and Charpentier (or Zhang). The discoveries, not those who make them, are important and those discoveries are only important as they affect people. CRISPR heralds a new era of massively increased human control over life, one that will affect every person on Earth, directly or indirectly, and much of the rest of our planets biosphere. If humans are to have any chance of harnessing its benefits, avoiding its risks, and using it in ways consistent with our values and cultures, then we all not just the scientists, ethicists, and patent lawyers need to understand something about CRISPR and its implications. A Crack in Creation is a great place to start.

In the interest of full disclosure, the author has met, been on panels with, and likes Doudna, Charpentier, Zhang, Church, and many of the other scientists discussed in the review. He also has lectured the last three summers in a CRISPR program held by the Innovative Genomics Institute at UC Berkeley for modest honoraria.

Henry T. Greely is a professor of Law, and professor by courtesy of Genetics, at Stanford University, where he directs its Center for Law and the Biosciences and Program in Neuroscience and Society. He is an expert on the ethical, legal, and social implications of advances in the biosciences.

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CRISPR, Patents, and Nobel Prizes - lareviewofbooks

Recommendation and review posted by sam

The first test-tube baby made headlines around the world in 1978, setting off intense debate on the ethics of researching human embryos and reproductive technologies. Every breakthrough since then has raised the same questions about designer babies and playing God but public response has grown more subdued rather than more engaged as assisted reproductive technologies have become increasingly sophisticated and powerful.

As the science has advanced, doctors are able to perform more complex procedures with better-than-ever success rates. This progress has made in vitro fertilization and associated assisted reproductive technologies relatively commonplace. Over one million babies have been born in the U.S. using IVF since 1985.

And Americans acceptance of these technologies has evolved alongside their increased usage, as weve gotten used to the idea of physicians manipulating embryos.

But the ethical challenges posed by these procedures remain and in fact are increasing along with our capabilities. While still a long way from clinical use, the recent news that scientists in Oregon had successfully edited genes in a human embryo brings us one step closer to changing the DNA that we pass along to our descendants. As the state of the science continues to advance, ethical issues need to be addressed before the next big breakthrough.

Louise Brown was born in the U.K. on July 25, 1978. Known as the first test-tube baby, she was a product of IVF, a process where an egg is fertilized by sperm outside of the body before being implanted into the womb. IVF opened up the possibility for infertile parents to have their own biologically related children. But Browns family was also subjected to vicious hate mail, and groups opposed to IVF warned it would be used for eugenic experiments leading to a dystopian future where all babies would be genetically engineered.

The reaction in the U.S. had another layer to it when compared to other developed countries. Here, research on embryos has historically been linked to the debate on abortion. The 1973 Supreme Court decision to make abortion legal in Roe v. Wade fueled anti-abortion groups, who also oppose research on human embryos.

Embryonic research and procedures offer the hope of eliminating devastating diseases, but scientists also destroy embryos in the process. Under pressure from these groups over the ethical implications of embryo creation and destruction, Congress issued a moratorium in 1974 on federally funded clinical research on embryos and embryonic tissue, including on IVF, infertility and prenatal diagnosis. To this day, federal funds are still not available for this type of work.

In hindsight, the sharp media attention and negative response from anti-abortion groups to IVF didnt accurately represent overall public opinion. The majority of Americans (60 percent) were in favor of IVF when polled in August 1978, and 53 percent of those polled said they would be willing to try IVF if they were unable to have a child.

So while the intense media coverage at the time helped inform the public of this new development, the insensitive labeling of Louise Brown as a test-tube baby and warnings about dystopian results didnt stop Americans from forming positive opinions of IVF.

In the nearly 40 years since IVF was introduced for use in humans, scientists have developed several new technologies from freezing eggs to genetically testing embryos before implantation that have improved patient experience as well as the chances that IVF will result in the birth of a baby. The announcement of each of these breakthroughs has resulted in flurries of media attention to the ethical challenges raised by this type of research, but there has been no consensus social, political or scientific on how to proceed.

Americans general opinion of assisted reproductive technologies has remained positive. Despite opposition groups efforts, surveys show that Americans have separated out the issue of abortion from embryonic research. A Pew Research Center poll from 2013 revealed that only 12 percent of Americans say they personally consider using IVF to be morally wrong. Thats a significant decrease from the 28 percent of respondents in 1978 who replied that they opposed the procedure for being not natural. In addition, the 2013 poll showed that twice as many Americans (46 percent) said they do not personally consider using IVF to be a moral issue compared to the number of Americans (23 percent) who said they personally do not consider having an abortion to be a moral issue.

Although most Americans dont think of embryonic research and procedures like IVF as a moral issue or morally wrong, the introduction of new technologies is outpacing Americans understanding of what they actually do.

Polls from 2007-2008 showed that only 17 percent of respondents reported that they were very familiar with stem cell research, and that there was a relative absence of knowledge about even the most prominent of the embryo-research issues. When Americans are asked more specific questions that explain IVF, they show less support for certain procedures, like freezing and storing eggs or using embryos for scientific research.

In light of recent developments, surveys show that nearly 69 percent of Americans have not heard or read much or know nothing at all about gene editing. Additionally, support for gene editing depends on how the technology will be used. A majority of Americans generally accept gene editing if the purpose is to improve the health of a person, or if it will prevent a child from inheriting certain diseases. The scientists in Oregon used a gene-editing technique that allowed them to correct a genetic defect in human embryos that causes heart disease. This type of progress falls into the category that most Americans would support.

But the technique thats used to make this correction, known as CRISPR-Cas9, can potentially be used for editing genes in other ways, not just to eliminate diseases. The success of the Oregon team opens the door to many possibilities in gene editing, including ones unrelated to health, such as changes to appearance or other physical characteristics.

Advancements in assisted reproductive technologies have happened rapidly over the last few decades, leading to over five million births worldwide. But as common as these procedures have become, scientists are not yet in agreement over how to integrate CRISPR and gene editing to the IVF toolkit. There are concerns about changing the genomes of human embryos destined to be babies, particularly since any modifications would be passed on to future generations. Scientific committees have noted that decisions on whether and how to use gene editing should be revisited on a regular basis. The newest breakthrough with CRISPR is providing us with one of those opportunities.

We should focus our attention on answering the ethical questions that have long gone unanswered: What are the boundaries to this type of research? Who decides what is an ethical use of CRISPR? What responsibility do we have to people affected by genetic conditions? Who pays for these medical procedures? How will this research and potential clinical use be regulated?

The successful use of assisted reproductive technologies has skyrocketed in the last decade, making Americans complacent about some of the ethical concerns that these procedures raise. Its important that we engage with these issues now, before gene editing becomes as familiar to us as IVF.

Read more from the original source:
Will CRISPR fears fade with familiarity? - The Conversation US

Recommendation and review posted by Bethany Smith

Next-Generation Immunotherapies

CRISPR Therapeutics interest in next-generation T-cell cancer immunotherapies comes as both Kite Pharma and Novartis await FDA decisions on their CAR-T immuno-oncology treatments, with the companies emerging as leading developers of CAR-T therapies. Last month, Novartis won an FDA advisory committees unanimous recommendation of approval for Novartis leukemia-fighting treatment CTL019 (tisagenlecleucel), a CAR-T therapy developed through a collaboration between the pharma giant and researchers from the University of Pennsylvania launched in 2012.

CRISPR Therapeutics drug development efforts also include partnerships with Bayer and Vertex Pharmaceuticals intended to develop CRISPR-based therapeutics in diseases with high unmet need. CRISPR Therapeutics and Bayer have formed a $335 million-plus joint venture, Casebia Therapeutics, to develop treatments aimed at curing blood disorders, blindness, and congenital heart disease.

CRISPR Therapeutics is among four companies to have licensed CRISPR technology for which a European patent was granted in March to the Regents of the University of California (UC), the University of Vienna, and Emmanuelle Charpentier, Ph.D., a director at the Max-Planck Institute in Berlin.

The European patent holders are appealing a February 15 decision by the Patent Trial and Appeal Board (PTAB), which sided with the Broad Institute of MIT and Harvard in the bitter legal battle over who invented the gene-editing platform. The PTAB found no interference in fact between 12 patents related to CRISPR technology that list as inventor Feng Zhang, Ph.D., of the Broad, and a patent application by Dr. Charpentier and Jennifer Doudna, Ph.D., of UC Berkeley.

The European patent holders have cited decisions by other countries to grant them patents for CRISPR/Cas9 in all settings, including eukaryotic cellsincluding the U.K., nearly 40 other countries that are members of the European Patent Convention, and Asia-Pacific nations such as Australia, New Zealand, Singapore, and China.

Joining CRISPR Therapeutics in licensing the European-patented CRISPR technology are Caribou Biosciences, ERS Genomics, and Intellia Therapeutics.

Also last month, the European Patent office granted Cellectis a patent to use CRISPR in T cells, to be issued in August and valid until 2034. Were not a company thats here to block the other [companies], Cellectis chairman and CEO Andre Choulika, Ph.D., told GEN. Were here to develop products on our sidebut, if there are people that are interested in using CRISPR in T cells, were definitely open to talk to them.

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CRISPR Therapeutics, MGH Partner to Develop T-Cell Cancer Therapies - Genetic Engineering & Biotechnology News

Recommendation and review posted by simmons

(Reuters Health) - Black men with riskier prostate cancers may be less likely than their white counterparts to get aggressive treatment that can give them the best survival odds, a recent U.S. study suggests.

Researchers focused on men with medium- and high-risk localized prostate tumors likely to benefit from aggressive treatment like surgery or radiation, rather than the conservative approaches of watchful waiting or hormone therapy often used for men with low-risk tumors.

While 83% of white men received aggressive treatment, just 74% of black men did, the study found.

Given the evidence suggesting a benefit for treatment in men diagnosed with intermediate- and high-risk prostate cancer, our findings may explain, to some degree, the differences in survival odds between black and white men diagnosed with prostate cancer," said lead study author Dr. Quoc-Dien Trinh, co-director of the Dana-Farber/Brigham and Women's Prostate Cancer Center in Boston.

Black men are more likely to develop prostate cancer and to die from it than white men, the researchers note in European Urology, online August 2. Black patients are also more likely to be diagnosed when tumors are more advanced and more difficult to treat.

For the current study, researchers examined national cancer registry data on 223,873 white men and 59,262 black men aged 40 or older diagnosed with prostate tumors in the U.S. between 2004 and 2013.

Half of the white men in the study were at least 65 years old, while half of the black men were at least 63.

Black men were more likely to be low-income and uninsured or covered by Medicaid, the U.S. health program for the poor.

During the study period, the proportion of white men receiving aggressive treatment rose from 81% to 83%, while for black men it increased from 73% to 75%.

Overall, 39% of the 356 facilities in the study were significantly more likely to give aggressive therapy to white men than to black men with similar tumors. Only 1% of facilities were more likely to give aggressive treatment to black men.

Geography also played a role. For example, in the southeastern U.S., white men were 69% more likely to receive aggressive treatment than black men, the study found.

From a system-level perspective, we need to do a better job to (standardize) prostate cancer counseling and recommendations, Trinh said by email. There is no reason why there would be such a variation in how black men are treated from one institution to another.

One limitation of the study is that researchers lacked data on patient preferences that may have driven treatment decisions. Researchers also lacked data on patients treated at smaller facilities and places that treated fewer than 50 men a year for prostate cancer.

Its also hard to say how many patients may have opted against aggressive treatment because they didnt trust their physician or worried about side effects like urinary incontinence or erectile dysfunction, said Dr. Simpa Salami, a urologist at the University of Michigan in Ann Arbor who wasnt involved in the study.

We do not know if black men were offered definitive therapy at the same rate as white men but chose other options instead, or if black men were simply not offered the same treatment options as white men, Salami said by email.

Differences in income and insurance may also help explain the disparities in how men were treated, said Dr. Brian Chapin of the University of Texas MD Anderson Cancer Center in Houston.

I would expect that if a comparison was made between whites and blacks within the same income bracket and equivalent insurances, the findings may not have been as significantly different, Chapin, who wasnt involved in the study, said by email.

Even so, the findings suggest that men should speak to more than one doctor before deciding how to proceed, Chapin said.

I would encourage any newly diagnosed prostate cancer patient to obtain a second opinion regarding their cancer care, and meet with both a radiation oncologist and a urologist to be presented with all available options and make sure they are fully informed before making a treatment decision, Chapin advised.

SOURCE: bit.ly/2voWkvq

Eur Urol 2017.

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Blacks with prostate cancer less likely to get ideal treatment - Reuters

Recommendation and review posted by sam

PUBLISHED: 14:42 23 August 2017 | UPDATED: 16:02 23 August 2017

Taz Ali

Free fertility roadshow in Kings Lynn on Thursday, August 31 could help improve your chances of having a baby. Picture: Bourn Hall

Bourn Hall

A free event hosted by fertility experts will give couples a chance to find out how they can get fertility fit and boost their chances of conceiving.

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The Bourn Hall Clinic based in Kings Lynn will provide visitors with the opportunity to have an informal chat about their current situation and plans on moving forward.

Specialists from the clinic will offer advice on how a change of lifestyle can enable women to get pregnant without the need for IVF.

Simples measures such as keeping a diary to track ovulation, leading a healthy lifestyle, drinking less alcohol and caffeine and getting more sleep can help couples improve their fertility.

Experts also advise couples to take some time to wind down and enjoy each others company as emotional stress has profound effects on fertility.

Of the 800 couples that have been referred to the clinic since it opened two years ago, almost half have successfully conceived.

Carol Steel, lead specialist fertility nurse at Bourn Hall Clinic, said: 80pc of couples will become pregnant within one year of actively trying to conceive, so if you are still not pregnant after this length of time you should seek advice.

The good news, however, is that there are many things which you can do to improve your chances of conceiving.

The event will be of benefit to anyone who is trying to get pregnant, or thinking about it, whether they are struggling to conceive or not. Couples can also find out about the more common reasons for infertility such as low sperm count, failure to release eggs (ovulate) regularly, fibroids and endometriosis and how to treat them.

The event will take place on Thursday, August 31 at the Knights Hill Hotel, in South Wootton at 6pm.

The evening will include expert presentations and an opportunity to have a private, free mini consultation with a Bourn Hall Clinic fertility nurse specialist.

Norfolk was one of the first counties to provide an integrated fertility service. GPs can refer couples to the Bourn Hall Clinic, in Kings Lynn and Wymondham, for treatment on the NHS.

For more information, visit the Bourn Hall Clinic website.

Simple measures can help couples improve their fertility:

Calculate when you are ovulating and keep a diary - Many people are unaware that there are only around six days each month when you can get pregnant. Your best chance of conceiving is on the day of ovulation, when one of the ovaries releases a ripe egg.

For a woman on a regular 28-day cycle the day of ovulation will be around 14 days after the start of her period but this can vary so it helps to keep a diary.

There are also a number of ovulation prediction kits available which might help.

Drink less alcohol and caffeine and cut out smoking altogether - Smoking harms sperm and can reduce a mans sex drive; in women it affects ovulation and reduces fertility. The best thing would be to to stop completely.

Heavy drinking (more than six units per day) can lower a mans sperm count and affect the health of the sperm so men should really watch their alcohol intake.

Women should ideally avoid alcohol altogether when they are trying to conceive as it can affect a developing foetus and cause birth defects.

In addition it is thought that caffeine affects the fertility level of both men and women so cutting back is a sensible precaution. Caffeine is not just found in tea and coffee but in chocolate and some soft drinks too.

Keep to a healthy weight, eat well and do more exercise - Eating a healthy, balanced diet is good news all round. It helps maintain an ideal body weight, helps to regulate hormones and improves the health of the reproductive system. Excess body fat in men is also a significant cause of low sperm count.

Vitamins C and E and zinc may play key roles in fertility, increasing sperm count and motility (movement) and supporting the female reproductive organs. Foods such as green leafy vegetables, eggs and dairy, nuts, seeds and citrus fruits provide key nutrients.

Doing some exercise every day is key to maintaining a healthy body, helping to burn off excess body fat and reducing the effect of stress on hormone levels. For men it can boost the fertility hormone testosterone, but it is important that women avoid excessive exercise as this can result in irregular periods. Try low-impact activities that you enjoy such as walking, swimming, cycling, pilates and yoga.

Ditch the hard bike seats and keep your cool - For men, overheated testicles can temporarily lower sperm counts, so it is important to avoid saunas, hot baths, sunbathing and tight underwear.

In addition, cycling regularly and for long periods of time on hard bike seats can also reduce fertility through pressure on the perineum, potentially damaging nerves and blood vessels to the genital area. Think about buying yourself a gel seat for your bike to provide more cushioning.

Consider your health - Get some advice about any treatments you might be taking to see if they are affecting your fertility. As well as over-the-counter medicines, some herbal remedies such as St Johns Wort, ginko biloba and Echinacea might have an adverse effect on your fertility.

Take it easy and get more sleep - Getting a good nights sleep of about eight hours a day or more can help men and women optimise their fertility. Not getting enough sleep can have a negative impact on hormone levels and studies of female professionals with sleep deprivation have shown an increase in irregular periods.

Couples should not forget to take the time to wind down and enjoy each others company. Emotional stress has profound effects on fertility, including interfering with the hormones responsible for egg and sperm production.

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Free fertility roadshow in West Norfolk could help improve your chances of having a baby - Norfolk Eastern Daily Press

Recommendation and review posted by sam

Cryonics is the practice in which a body is frozen shortly after death with the hope, when technology catches up, they will be able to be revived.

Zhan Wenlian, who died of lung cancer aged 49 earlier this year, became the first person in China to be cryogenically frozen.

Ms Wenlians remains are currently in a giant tank filled with 2,000 litres of liquid nitrogen at Yinfeng Biological Group in Jinan, capital of East China's Shandong Province.

The deceased was volunteered for the procedure by her husband Gui Junmin, who said that his late wife wanted to donate her body to science to "give back to society, according to The Mirror.

The project was a collaboration between the Yinfeng Biological Group and from US firm Alcor Life Extension Foundation.

In cryonics, as soon as a persons heart stops beating, they must be rapidly cooled but not technically frozen.

If the person is frozen, their cells form ice crystals which is irreversible damage.

A cocktail of chemicals like glycerol and propandiol, as well as antifreeze agents, are commonly used in the procedure so the body can be cooled without freezing.

However, there is no evidence that people will one day be able to be revived.

Director Jia Chusheng of Yinfeng Biological Group said that although there is a chance the procedure will not work, it gives the husband and wife hope for the future.

She said: [Zhan] and her family are clear about the risks and the possibility that the procedure might ultimately fail.

"But as someone who has donated her body to science, she also gains hope of being revived one day.

Her husband is extremely hopeful, however, and even plans to have himself preserved when he dies so that he can be reunited with his wife.

Mr Junmin said: "I tend to believe in new and emerging technologies, so I think it will be completely possible to revive her.

"If my wife wakes up, she might be lonely. I need to keep her company."

Read the original:
Chinese woman cryogenically frozen with 'COMPLETE possibility' of ... - Express.co.uk

Recommendation and review posted by sam

Cryonics is the practice ofdeep-freezing recently deceased bodies(or even justthe brains of thosewho have recently died)in the hopes of one day reviving them.

It has been the subject of serious scientific exploration and study as well as a fair share of pseudoscience, lore, and myth. Fictional accounts like Batmans Iceman, and the (untrue) rumours of Walt Disney being cryogenically frozen have cast a speculative shadow over the field of cryonics.

Butrecently, for the first time ever in China,a woman has been cryogenically frozen. Zhan Wenlian died at the age of 49 from lung cancer and her husband, Gui Junmin, volunteered her for the cryonic procedure.

Bothhe and his late wife wanted to donate her body to science to give back to society. He told TheMirror UKthat hewas initially pitchedthe idea of cryonicswith it being described as a life preservation project.

This procedure which has Wenlians body restingface downin 2,000 litres of liquid nitrogen was completed at theYinfeng Biological Group in Jinan.

This project is the collaborative effortof the Yinfeng Biological Group, Qilu Hospital Shandong University and consultants fromAlcor Life Extension Foundation, a nonprofit cryonics company based in the United States.

Even with all the faith many have in the procedure, the question remains: how scientifically possible is a project like this? Is this just an experiment to allow us to better understand human biology, orcould cryonics one day become a feasible option?

Cryonics isall about timing.The bodies of the deceased arecryogenically frozenimmediately after the heartstops beating.Freezing is a bit of a misleading term, because cryonic freezing is actually very specifically trying toavoidice crystal formation which damages the cells of the bodys tissues.

Rapid cooling, rather than freezing, is a more accuratedescription of the process.

A chemical cocktail of preservatives likeglycerol andpropandiol, in addition to antifreeze agents, are commonly used to get the body into a stable state where it wont be decaying, but also wont suffer damage from being stored at low temperatures for, conceivably, a very long time.

From there, the bodiesare given specific care that caters to the idea that death is a continuing process; one that can ultimately be reversed.

The aim of cryonic preservation would be to one day be able to thaw the bodies and reanimate them at a cellular level preferably without too many epigenetic changes.

I tend to believe in new and emerging technologies, so I think it will be completely possible to revive her.

With ourcurrent understanding and technology, this process of reversingdeath so completely is just not possible. The closest kind of revival we have are themoments after clinical death where patients are revived by something such as cardiac defibrillation.

Cryonics acts within this critical, albeit brief, period as well but works within the belief that death is a grey area. More of a processrather than a definite, final, event.

Just because we havent succeeded in reviving the dead yetdoesnt mean the field of cryonics isunnecessary or unimportant.This case inChina is a step forward for everyone researchingthe field of cryonics and those of us who hope to benefit from advancements in it.

We may not be able to reverse death just yet,but it doesnt seem outof the realm of possibility to imagine that, withsuch wild scientific advancements underway, technology could one day allow it to be possible.

Whether or not it does in our lifetimes, this most recent development is certainly an interesting one.

This article was originally published by Futurism. Read the original article.

Continued here:
For The First Time Ever, a Woman in China Has Been Cryogenically ... - DeathRattleSports.com

Recommendation and review posted by simmons

A high-powerered magnification of chronic lymphocytic leukemia cells (stained in blue). A new treatment may offer better outcomes for patients who suffer from another kind of leukemia. Photo by Mary Ann Thompson

published on August 22, 2017 - 11:57 AMWritten by Donald A. Promnitz

Valley oncologists and groups devoted to fighting cancer are optimistic about a new leukemia treatment that was recently recommended for approval by the US Food and Drug Administration.

CTL019, a CAR T-cell therapy from the pharmaceutical company Novartis, was recommended unanimously last month, and doctors in the Central Valley have taken notice. One person to welcome the therapy is Saint Agnes Cancer Center oncologist Dr. Ravi Rao who stated that it was a profound development comparable to going to the moon and coming back.

I think its an exceptionally good idea. This is something thats been talked about for many, many decadeseven in the 1960s, 70s scientists were trying to figure out how to get your immune system to wake up and attack the cancer, Rao said. And so finally, the fact that its happened, to me, is like science fiction.

I think its groundbreaking for sure, said Valley Childrens Hospital oncologist and hematologist Dr. Vinod Balasa. If it is approved of by the FDA, it would be the first gene therapy in the United States.

CAR T-cell therapy involves the removal of a patients T cells (an immune cell) and introducing chimeric antigen receptors or CARs to the cell that will cause them to attack their cancer. These modified cells are then reintroduced to the patient. CARs are receptors that have been engineered to graft onto the T cells.

When the CAR T cell is put back in to the patient, it makes the T cells bind to the tumor cells and this in turn activates the T-cell to kill the tumor cell as well as force the T-cell to divide, said Lee Greenberger, the Leukemia & Lymphoma Societys New York-based chief scientific officer. So in essence, a genetically engineered, tumor-killing factory has been created in the patient.

The concept of introducing cells to fight blood cancer dates back to the early 1950s and in the 60s and 70s, researchers conceived the idea of introducing immune cells from donors to kill tumor cells in patients. In the 80s, the receptor was discovered and the first CAR was made.

In the 90s and 2000s, the CAR T cell was further researched and optimized. Dr. Carl H. June pioneered the immunotherapy at the University of Pennsylvania.

It doesnt just come out of the blue, Greenberger said. Theres a lot of manipulation to find out what works.

Over the last two decades, the Leukemia & Lymphoma Society has spent $40 million on CAR T-cell research. This includes $20 million to the University of Pennsylvania.

Currently, CAR T-cell therapy is approved for only one type of cancer B-cell acute lymphoblastic leukemia (ALL). Leukemia is the most common form of cancer in children, with ALL being the most prevalent form. The therapy is intended for use as a last-ditch effort to kill the cancer when all other treatments have failed.

Right now, its approved for just one subtype of leukemia, but the technology is scalable in that it can be scaled to other kinds of cancers, Dr. Rao said. So I think time will tell us how far this will go.

Of 63 patients treated with CAR T-cell therapy in a 2015-16 trial, 82.5 percent went into remission. It is also being tested for treating chronic lymphocytic leukemia and non-Hodgkin lymphoma.

Getting the treatment into the Valley, however, will present its own challenges. While effective against leukemia, the treatment includes a number of adverse side effects, including cytokine-release syndrome (or CRS). CRS occurs when cytokines chemical messengers that stimulate and direct immune response are rapidly released into the bloodstream. High fevers and dangerous falls in blood pressure are the common result.

It really requires a lot of supervision from a highly specialized team at this time, so having this treatment in the Valley is years away, said Bethanie Mills, Leukemia & Lymphoma Societys Central California senior manager of patient access. However, that doesnt mean that our Valley patients would not have access to it.

In order to receive the treatment, a Valley patient would have to be taken to a cancer specialty hospital, where staff would be better equipped to administer the therapy and care for them as it takes effect.

Despite this, Dr. Rao said that he hopes that he will himself be able to use this treatment on his patients in time.

I dont really think we need more staff I think we just need staff to be trained. We already have good cardiologists, good kidney specialists we just need them to be on board, Dr. Rao said. Its a really new branch of medicine. Theres no way people who have been trained in cardiology or infectious diseases they have never seen the kinds of side effects and complications that happen with this. Neither have I for that matter.

Dr. Balasa expressed his own optimism that Valley Childrens Hospital would be able to administer the treatment within a few years.

We already do manage those kinds of problems with other kinds of treatments, Dr. Balasa said, so I feel that being able to treat children with CAR T-cell therapy in the future is more than likely a reality.

See original here:
Doctor on new cancer treatment: 'genetically engineered, tumor-killing factory' - The Business Journal

Recommendation and review posted by simmons

Dr. Alexandre R. Colas is an assistant professor at SBP. Credit: James Short

Researchers from Sanford Burnham Prebys Medical Discovery Institute (SBP), the Cardiovascular Institute at Stanford University and other institutions were surprised to discover that the four genes in the Id family play a crucial role in heart development, telling undifferentiated stem cells to form heart tubes and eventually muscle. While Id genes have long been known for their activity in neurons and blood cells, this is the first time they've been linked to heart development. These findings give scientists a new tool to create large numbers of cardiac cells to regenerate damaged heart tissue. The study was published in the journal Genes & Development.

"It has always been unclear what intra-cellular mechanism initiates cardiac cell fate from undifferentiated cells," says Alexandre Colas, Ph.D., assistant professor in the Development, Aging and Regeneration Program at SBP and corresponding author on the paper. "These genes are the earliest determinants of cardiac cell fate. This enables us to generate unlimited amounts of bona fide cardiac progenitors for regenerative purposes, disease modeling and drug discovery."

The international team, which included researchers from the International Centre for Genetic Engineering and Biotechnology in Italy, University Pierre and Marie Curie in France and the University of Coimbra in Portugal, combined CRISPR-Cas9 gene editing, high-throughput microRNA screening and other techniques to identify the role Id genes play in heart development.

In particular, CRISPR played a crucial role, allowing them to knock out all four Id genes. Previous studies had knocked out some of these genes, which led to damaged hearts. However, removing all four genes created mouse embryos with no hearts at all. This discovery comes after a decades-long effort to identify the genes responsible for heart development.

"This is a completely unanticipated pathway in making the heart," says co-author Mark Mercola, Ph.D., professor of Medicine at Stanford and adjunct professor at SBP. "People have been working for a hundred years to figure out how the heart is specified during development. Nobody in all that time had ever implicated the Id protein."

Further study showed Id genes enable heart formation by turning down the Tcf3 and Foxa2 proteins, which inhibit the process, and turning up Evx1, Grrp1 and Mesp1, which support the process.

In addition to contributing a new chapter in the understanding of heart development, this study illuminates a powerful technique to screen for protein function in complex phenotypical assays, which was previously co-developed by Colas and Mercola. This technology could have wide-spread impact throughout biology.

"On a technical level, this project succeeded because it combined high-throughput approaches with stem cells to functionally scan the entire proteome for individual proteins involved in making heart tissue," says Mercola. "It shows that we can effectively walk through the genome to find genes that control complex biology, like making heart cells or causing disease."

Understanding this pathway could ultimately jumpstart efforts to use stem cells to generate heart muscle and replace damaged tissue. In addition, because Id proteins are the earliest known mechanism to control cardiac cell fate, this work is an important milestone in understanding cardiovascular developmental biology.

"We've been influenced by the skeletal muscle development field, which found the regulator of myogenic lineage, or myoD," says Colas. "For decades, we have been trying to find the cardiac equivalent. The fact that Id genes are sufficient to direct stem cells to differentiate towards the cardiac lineage, and that you don't have a heart when you ablate them from the genome, suggests the Id family collectively is a candidate for cardioD."

Explore further: Discovery of a key regulatory gene in cardiac valve formation

More information: Thomas J. Cunningham et al, Id genes are essential for early heart formation, Genes & Development (2017). DOI: 10.1101/gad.300400.117

Read more from the original source:
Id genes play surprise role in cardiac development - Medical Xpress - Medical Xpress

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VistaGen Therapeutics has received a notice of allowance for a stem cell production patent, which the firm says could be used in autoimmune disorder and cancer treatments.

The US Patent and Trademark Office (USPTO) issued VistaStem a subsidiary of VistaGen the notice for patent no. 14/359,517, which covers methods for producing hematopoietic precursor stem cells usually found in red blood marrow.

These are stem cells that give rise to all of the blood cells and most of the bone marrow cells in the body, with potential to impact both direct and supportive therapy for autoimmune disorders and cancer, said VistaGen VP Mark McPartland.

With CAR-T cell applications and foundational technology, McPartland said he believed the technology will provide approaches for producing bone marrow stem cells for bone marrow transfusions.

Business opportunities

In December last year, VistaGen signed an exclusive sublicense agreement with stem cell research firm BlueRock Therapeutics, under which the latter paid VistaGen $1.25m (1.06m) upfront for its cardiac stem cell production technologies.

McPartland said he expects this recent notice of allowance to also create potential opportunities for additional regenerative medicine transactions.

IP portfolio growth

VistaGen told us it plans to secure IP protection in multiple domains and international jurisdictions.

We intend to grow our IP portfolio in a manner that emphasises platform protection and maximises opportunities for commercialisation and out-licensing, McPartland said.

The rest is here:
VistaGen's cell production methods receive US patent boost - BioPharma-Reporter.com

Recommendation and review posted by Bethany Smith

Newswise La Jolla, Calif., August 22, 2017 Researchers from Sanford Burnham Prebys Medical Discovery Institute (SBP), the Cardiovascular Institute at Stanford University and other institutions were surprised to discover that the four genes in the Id family play a crucial role in heart development, telling undifferentiated stem cells to form heart tubes and eventually muscle. While Id genes have long been known for their activity in neurons and blood cells, this is the first time theyve been linked to heart development. These findings give scientists a new tool to create large numbers of cardiac cells to regenerate damaged heart tissue. The study was published in the journal Genes & Development.

It has always been unclear what intra-cellular mechanism initiates cardiac cell fate from undifferentiated cells, says Alexandre Colas, Ph.D., assistant professor in the Development, Aging and Regeneration Program at SBP and corresponding author on the paper. These genes are the earliest determinants of cardiac cell fate. This enables us to generate unlimited amounts of bona fide cardiac progenitors for regenerative purposes, disease modeling and drug discovery.

The international team, which included researchers from the International Centre for Genetic Engineering and Biotechnology in Italy, University Pierre and Marie Curie in France and the University of Coimbra in Portugal, combined CRISPR-Cas9 gene editing, high-throughput microRNA screening and other techniques to identify the role Id genes play in heart development.

In particular, CRISPR played a crucial role, allowing them to knock out all four Id genes. Previous studies had knocked out some of these genes, which led to damaged hearts. However, removing all four genes created mouse embryos with no hearts at all. This discovery comes after a decades-long effort to identify the genes responsible for heart development.

This is a completely unanticipated pathway in making the heart, says co-author Mark Mercola, Ph.D., professor of Medicine at Stanford and adjunct professor at SBP. People have been working for a hundred years to figure out how the heart is specified during development. Nobody in all that time had ever implicated the Id protein.

Further study showed Id genes enable heart formation by turning down the Tcf3 and Foxa2 proteins, which inhibit the process, and turning up Evx1, Grrp1 and Mesp1, which support the process.

In addition to contributing a new chapter in the understanding of heart development, this study illuminates a powerful technique to screen for protein function in complex phenotypical assays, which was previously co-developed by Colas and Mercola. This technology could have widespread impact throughout biology.

On a technical level, this project succeeded because it combined high-throughput approaches with stem cells to functionally scan the entire proteome for individual proteins involved in making heart tissue, says Mercola. It shows that we can effectively walk through the genome to find genes that control complex biology, like making heart cells or causing disease.

Understanding this pathway could ultimately jumpstart efforts to use stem cells to generate heart muscle and replace damaged tissue. In addition, because Id proteins are the earliest known mechanism to control cardiac cell fate, this work is an important milestone in understanding cardiovascular developmental biology.

Weve been influenced by the skeletal muscle development field, which found the regulator of myogenic lineage, or myoD, says Colas. For decades, we have been trying to find the cardiac equivalent. The fact that Id genes are sufficient to direct stem cells to differentiate towards the cardiac lineage, and that you dont have a heart when you ablate them from the genome, suggests the Id family collectively is a candidate for cardioD.

About SBPSanford Burnham Prebys Medical Discovery Institute (SBP) is an independent nonprofit medical research organization that conducts world-class, collaborative, biological research and translates its discoveries for the benefit of patients. SBP focuses its research on cancer, immunity, neurodegeneration, metabolic disorders and rare childrens diseases. The Institute invests in talent, technology and partnerships to accelerate the translation of laboratory discoveries that will have the greatest impact on patients. Recognized for its world-class NCI-designated Cancer Center and the Conrad Prebys Center for Chemical Genomics, SBP employs about 1,100 scientists and staff in San Diego (La Jolla), Calif., and Orlando (Lake Nona), Fla. For more information, visit us at SBPdiscovery.org or on Facebook at facebook.com/SBPdiscovery and on Twitter @SBPdiscovery.

View post:
Where Do Heart Cells Come From? - Newswise (press release)

Recommendation and review posted by Bethany Smith

Whether you are a social butterfly or more of a shy homebody may at least in part be attributable to your genes.

A new study by researchers at the National University of Singapore reports that two specific genes play a role in young adults social skills and the number of close friends they have.

The study, published in Psychoneuroendocrinology focused on the CD38 gene and the CD157 gene sequence both of which regulate oxytocin, the human social hormone.

Oxytocin is involved with behaviors such as pair-bonding, mating and child-rearing. It is also linked with more complex emotions and traits like empathy, trust and generosity.

The NUS study included 1,300 Chinese participants living in Singapore. The researchers examined how the expression of CD38 and the sequence changes of CD517 related to the participants social skills.

Their social behaviors were evaluated through questionnaires that asked about participants ability to engage in social relationships, the quality of friendships they have and the value they place on those friendships.

The team found that a higher expression of the CD38 gene and the presence of differences in the CD157 gene sequence correlated with a participant having more close friends and better social skills.

According to study leader Richard Ebstein, professor with NUS Psychology, this study was unique because many other gene studies focus on just structural changes in gene sequences, and how that affects a particular characteristic or disease. But by studying gene expression, Ebstein and fellow researchers were able capture more information than simple structural studies.

The higher expression and changes in the genes accounted for 14 percent of the variance in social skills in the general population. Typically, less than two percent of findings in behavioral genetic association studies rely on genetic variations alone.

The researchers also noted that the results were even more profound in the male participants.

Male participants with the higher gene expressions displayed greater sociality such as preferring activities involving other people over being alone, better communication and empathy-related skills compared to the other participants. Meanwhile, participants with lower CD38 expression reported less social skills such as difficulty in reading between the lines or engaging less in social chitchat, and tend to have fewer friends, said Anne Chong, PhD graduate who conducted the research with Ebstein.

Moreover, while expressed genes can influence behaviors, our own experiences can influence the expression of genes in return. So, whether the genes are expressed to impact our behaviors or not, depend a lot on our social environments. For most people, being in healthy social environments such as having loving and supportive families, friends and colleagues would most likely lessen the effects from disadvantageous genes, added Chong.

Another interesting find the team reported was that a variation in the CD157 gene sequence, which was found to be more common in autism cases in a previous Japanese study, was also associated with the participants innate interest in socializing and building relationships.

Ebstein and Chong believe these results could be useful in developing future intervention therapies or targeted treatments that would help achieve desired results for individuals with special needs. For example, they note that treatments based on new drugs that mimic of enhance the functions of the CD38 and CD157 genes could be one potential approach.

The researchers are now conducting several behavioral economics and molecular genetics studies to investigate the impact of oxytocin on human traits like creativity and openness to exposure.

Originally posted here:
Two Genes May Dictate How Social, Friendly You Are - Laboratory Equipment

Recommendation and review posted by sam

Mike VIIs official welcome was rained out Tuesday, which allowed LSU to discuss how the new live mascot underscores the need to protect the endangered predator in the wild and to improve the plight of privately owned tigers in this country.

We now have a new mission and that mission is to play a role in conservation, LSU President F. King Alexander told reporters who gathered for the official welcome. The schools welcome party will be rescheduled for Wednesday or Thursday.

Were going to utilize our research expertise and our educational mission as an institution to perhaps save one of the worlds best known and most regal creatures on earth, Alexander said.

LSU officials have tacked towards conservation as some critics raised questions about the propriety of a public university housing a wild animal as a mascot. The number of tigers that are not in a zoo but owned as pets or as marketing tools or have been abandoned in facilities, far exceeds the number of cats in the wild.

This is a refuge tiger, one we have saved, Alexander said.

The tiger announced early Monday as LSUs new mascot, Mike VII, was something of child star

As a cub named Harvey, the new Mike the Tiger was used to make money by letting tourists feed and pet him for $100 a shot. When he grew too old and too large, the tiger ended up in a facility that lost its license. New owners were brought in by Florida authorities to upgrade the facility and find new homes for the tigers, lions, leopards and other cats.

He is here, Alexander said, as a tiger who was facing impending doom.

We wanted to find a tiger that wasnt wanted, could no longer be cared for and was in need of a permanent home, said Dr. David Baker, the LSU professor who serves as Mike the Tigers veterinarian.

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He and Dr. Gordon Pirie, the veterinarian for the Baton Rouge Zoo, went to Florida to look at a tiger named Rocky. Almost as an aside, we were also shown a younger cub named Harvey. It was quickly apparent to me that Harvey had all the characteristics that we were looking for.

Baker wanted certain anatomical traits, such as a double stripe that makes the tiger look bold. But he also was interested in the beasts behavior.

Harvey was very confident, very interactive, very affectionate. He was up at the front of his little enclosure, which was little dirt lot, chuffing at us, which is a happy sound, greeting us, obviously wanting to play, Baker said.

Baker said laws and procedures are much more stringent now than when he searched for Mike VI in 2007. He received hundreds of unsolicited notices from people about tigers, including those from breeders who offered to provide a tiger to LSU. He didnt want to promote breeding of the tigers in captivity, so crossed off any that were purposely bred.

Instead, Baker said he relied on tiger sanctuaries as well as state and federal captive wildlife inspectors to point him towards possibles.

Mike VII will live alone, a situation some have criticized. But Baker says thats natural, particularly for males. In the wild the only time tigers come together are to mate and thats not in the cards for this animal.

Mike VII is not among the six subspecies whose genetics are being protected by conservationists, veterinarians and zoos. He will not be bred.

He is what is called a gray tiger, a mix. But he is fine for us, Baker said. I am certain he will do fine on his own.

Baker said Mike VII will be a very visible mascot, often in his yard, but for his own protection and well-being, he won't be paraded around Tiger Stadium before games.

The LSU Senate faculty passed a resolution asking to add $1 to sports tickets to raise money for conservation efforts.

Alexander said he appreciates the faculty wanting to raise money, but he hasnt discussed the idea with them and right now hes not sure LSU would include a surcharge.

Right now, its a Pandoras box, Alexander said.

Before he was Mike VII, he was Harvey, a young tiger cub growing up at a Florida wildlife sa

Follow Mark Ballard on Twitter, @MarkBallardCnb.

Read more from the original source:
LSU needed a tiger; Harvey needed a home: Officials say new Mike VII a great choice for mascot - The Advocate

Recommendation and review posted by Bethany Smith

The competition to replace America's 1970s-era nuclear-tipped intercontinental ballistic missile program is now down to two large defense companies in a contract that the Air Force originally estimated would cost about $62 billion.

Yet there's still a lot of uncertainty about the project, and its acquisition costs for taxpayers could go up to as much as $140 billion. Also, some critics of the program suggest we should just continue maintaining the current nuclear missiles as a deterrent for another decade to save money.

Regardless, the Air Force announced late Monday that Boeing and Northrop Grumman each won three-year contracts for the "technology maturation and risk reduction," or essentially the preliminary design phase, of the Ground-Based Strategic Deterrent intercontinental ballistic missile weapon system program.

Lockheed Martin had been in the running, but it didn't prevail.

GBSD is a modernization planned for the land-based Minuteman III, one leg of the nation's nuclear triad land, sea and air-based capabilities.

Boeing was the prime contractor on the Minuteman III system, which dates back to 1970s and has been undergoing continued maintenance to keep it in service.

"It was an important win for Boeing," Jefferies analyst Howard Rubel said in an interview. The analyst said Boeing's defense business has suffered several setbacks in recent years, including losing the long-range strike bomber contact to Northrop and having problems with its aerial tanker program.

However, he said Boeing and Northrop each are now "competing to be the eventual prime contractor" on the GBSD program. "You went from three competitors to two. You went from what I call broad concepts to now, two competing designers, who will come up with an industrialization concept that will...probably have some testing done to prove certain points along the way."

Boeing has yet to announce all of its partners in the GBSD program, and Northrop has announced some but not all.

Rubel said in a research note that he expects Orbital ATK and Aerjet Rocketdyne to also eventually get some work from the GBSD "as producers of large solid rocket motors. We expect the two companies to split the propulsion work in some fashion."

This is the first of several phases in the contract process for the GBSD program, although the Pentagon isn't expected to settle on a sole contractor for another few years. Production and then deployment aren't expected until the late 2020s.

The two contracts announced Monday, valued at no more than $359 million apiece, are just a small portion of what the overall program will cost. The Pentagon's independent cost assessment and program evaluation office last year upped the estimated acquisition cost to between $85 billion and about $140 billion.

"We are moving forward with modernization of the ground-based leg of the nuclear triad," Secretary of the Air Force Heather Wilson said in a statement. "Our missiles were built in the 1970s. Things just wear out, and it becomes more expensive to maintain them than to replace them. We need to cost-effectively modernize."

The modernization of the nation's nuclear comes at a time when superpowers such as Russia and China are modernizing their weapons. Also there are rogue countries such as North Korea that also are a nuclear threat with missile development programs.

Even so, some have suggested that the nuclear weapon capability using bombers and submarines is a more effective deterrent because they are harder to detect and can be dispersed. The Trump administration is conducting a nuclear posture review that will debate whether the U.S. should maintain the triad.

Also, some critics of the GBSD program believe the Pentagon should keep the current Minuteman III missiles as a deterrent for at least another decade rather than replacing it right away.

"Sustaining the Minuteman III for a period of time (say 10-15 years) beyond 2030 would be cheaper than GBSD over that period," said Reif Kingston, director of disarmament and threat reduction policy for the ACA. "The case for deferring a decision on GBSD and pursuing another life extension of the Minuteman III is strong."

To be clear, Kingston said deferring the modernization would require a reduction, but not elimination, in the size of the current force of land-based nuclear ICBMs. "A smaller force would not diminish the overall strength and credibility of the U.S. nuclear deterrent," he said.

Added Kingston, "We haven't built a new intercontinental ballistic missile in decades. As the program proceeds, they will have start to get a better sense of the costs. But at this point, there's a lot of uncertainty, and the Air Force's estimate ($62 billion) by all accounts is unrealistically low."

According to Kingston, a good portion of the data that the Air Force and others in the Pentagon had to work with to get an acquisition estimate on the Minuteman III replacement is "old and incomplete."

Read the rest here:
Competition to replace US nuclear missiles is down to 2 companies, but uncertainties remain - CNBC

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It sounds like science fiction: with a light zap of electricity, a tiny stamp-like device transforms your skin cells into reservoirs of blood vessels or brain cells, ready to heal you from within.

Recently, a team of medical mavericks at the Ohio State University introduced a device that does just that. The technology, dubbed tissue nanotransfection (TNT), is set to blow up the field of organ regeneration.

When zapped with a light electrical jolt, the device shoots extra bits of DNA code from its nanotube arrays directly into tiny pores in the skin. There, the DNA triggers the cells to shed their identity and reprograms them into other cell types that can be harvested to repair damaged organs.

Remarkably, the effect spreads with time. The rebooted cells release tiny membrane bubbles onto their neighboring skin cells, coaxing them to undergo transformation. Like zombies, but for good.

So far, the device has already been used to generate neurons to protect the brains of mice with experimental stroke. The team also successfully healed the legs of injured mice by turning the skin cells on their hind limbs into a forest of blood vessels.

While still a ways from human use, scientists believe future iterations of the technology could perform a myriad of medical wonders: repairing damaged organs, relieving brain degeneration, or even restoring aged tissue back to a youthful state.

By using our novel nanochip technology, injured or compromised organs can be replaced. We have shown that skin is a fertile land where we can grow the elements of any organ that is declining, says lead author Dr. Chandan Sen, who published the result in Nature Nanotechnology.

In my lab, we have ongoing research trying to understand the mechanism and do even better, adds Dr. L. James Lee, who co-led the study with Sen. So, this is the beginning, more to come.

The Ohio teams research builds on an age-old idea in regenerative medicine: that even aged bodies have the ability to produce and integrate healthy, youthful cellsgiven the right set of cues.

While some controversy remains on whether replacement cells survive in an injured body, scientistsand some rather dubious clinicsare readily exploring the potential of cell-based therapies.

All cells harbor the same set of DNA; whether they turn into heart cells, neurons, or back into stem cells depend on which genes are activated. The gatekeeper of gene expression is a set of specialized proteins. Scientists can stick the DNA code for these proteins into cells, where they hijack its DNA machinery with orders to produce the protein switchesand the cell transforms into another cell type.

The actual process works like this: scientists harvest mature cells from patients, reprogram them into stem cells inside a Petri dish, inject those cells back into the patients and wait for them to develop into the needed cell types.

Its a cumbersome process packed with landmines. Researchers often use viruses to deliver the genetic payload into cells. In some animal studies, this has led to unwanted mutations and cancer. Its also unclear whether the reprogrammed stem cells survive inside the patients. Whether they actually turn into healthy tissue is even more up for debate.

The Ohio teams device tackles many of these problems head on.

Eschewing the need for viruses, the team manufactured a stamp-sized device out of silicon that serves as a reservoir and injector for DNA. Microetched onto each device are arrays of nanochannels that connect to microscopic dents. Scientists can load DNA material into these tiny holding spots, where they sit stably until a ten-millisecond zap shoots them into the recipients tissue.

We based TNT on a bulk transfection, which is often used in the lab to deliver genes into cells, the authors explain. Like its bulk counterpart, the electrical zap opens up tiny, transient pores on the cell membrane, which allows the DNA instructions to get it.

The problem with bulk transfection is that not all genes get into each cell. Some cells may get more than they bargained for and take up more than one copy, which increases the chance of random mutations.

We found that TNT is extremely focused, with each cell receiving ample DNA, the authors say.

The device also skips an intermediary step in cell conversion: rather than turning cells back into stem cells, the team pushed mouse skin cells directly into other mature cell types using different sets of previously-discovered protein factors.

In one early experiment, the team successfully generated neurons from skin cells that seem indistinguishable from their natural counterparts: they shot off electrical pulses and had similar gene expression profiles.

Surprisingly, the team found that even non-zapped cells in the skins deeper layers transformed. Further testing found that the newly reprogrammed neurons released tiny fatty bubbles that contained the molecular instructions for transformation.

When the team harvested these bubbles and injected them into mice subjected to experimental stroke, the bubbles triggered the brain to generate new neurons and repair itself.

We dont know if the bubbles are somehow transforming other brain cell types into neurons, but they do seem to be loaded with molecules that protect the brain, the researchers say.

In an ultimate test of the devices healing potential, the researchers placed it onto the injured hind leg of a handful of mice. Three days prior, their leg arteries had been experimentally severed, whichwhen left untreatedleads to tissue decay.

The team loaded the device with factors that convert skin cells into blood vessel cells. Within a week of conversion, the team watched as new blood vessels sprouted and grew beyond the local treatment area. In the end, TNT-zapped mice had fewer signs of tissue injury and higher leg muscle metabolism compared to non-treated controls.

This is difficult to imagine, but it is achievable, successfully working about 98 percent of the time, says Sen.

A major draw of the device is that its one-touch-and-go.

There are no expensive cell isolation procedures and no finicky lab manipulations. The conversion happens right on the skin, essentially transforming patients bodies into their own prolific bioreactors.

This process only takes less than a second and is non-invasive, and then youre off. The chip does not stay with you, and the reprogramming of the cell starts,says Sen.

Because the converted cells come directly from the patient, theyre in an immune-privileged position, which reduces the chance of rejection.

This means that in the future, if the technology is used to manufacture organs immune suppression is not necessary, says Sen.

While the team plans to test the device in humans as early as next year, Sen acknowledges that theyll likely run into problems.

For one, because the device needs to be in direct contact with tissue, the skin is the only easily-accessible body part to do these conversions. Repairing deeper tissue would require surgery to insert the device into wounded areas. And to many, growing other organ cell types is a pretty creepy thought, especially because the transformation isnt completely localnon-targeted cells are also reprogrammed.

That could be because the body is trying to heal itself, the authors hypothesize. Using the chip on healthy legs didnt sprout new blood vessels, suggesting that the widespread conversion is because of injury, though (for now) there isnt much evidence supporting the idea.

For another, scientists are still working out the specialized factors required to directly convert between cell types. So far, theyve only had limited success.

But Sen and his team are optimistic.

When these things come out for the first time, its basically crossing the chasm from impossible to possible, he says. We have established feasibility.

Image Credit: Researchers demonstrate tissue nanotransfection,courtesy of The Ohio State University Wexner Medical Center.

Go here to see the original:
This Chip Uses Electricity to Reprogram Cells for Healing - Singularity Hub

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Chaster Skin Care Ltd., a leading manufacturer of high-quality anti-aging skincare solutions, recently announced the launch of its highly anticipated EGA Antiaging Cream, a lightweight, fast absorbing anti-aging cream features auto-adapting technology to provide the ultimate comfort and protection in all climates and EGA Antiaging Serum, a revolutionary new product that fights inflammation by soothing irritated skin and reducing skin sensitivity using Probiotics to restore the skin's self-renewal to reduce moisture loss and boost skin immunity.

St. Petersburg, FL (PRWEB) August 23, 2017

Chaster Skin Care Ltd., a leading manufacturer of high-quality anti-aging skincare solutions, recently announced the launch of its highly anticipated EGA Antiaging Cream, a lightweight, fast absorbing anti-aging cream features auto-adapting technology to provide the ultimate comfort and protection in all climates and EGA Antiaging Serum, a revolutionary new product that fights inflammation by soothing irritated skin and reducing skin sensitivity using Probiotics to restore the skin's self-renewal to reduce moisture loss and boost skin immunity.

"This new product launch is the culmination of years of clinical research and testing," explains Charles Brown, Vice President of Marketing, "EGA Antiaging Cream and EGA Antiaging Serum can visibly reduce fine lines and wrinkles for anyone interested in reversing the signs of aging."

EGA Antiaging Cream is a lightweight, fast-absorbing cream provides the hydrating benefits of a moisturizer with the power of an anti-aging concentrate. Anogeissus Leiocarpa Bark Extract and Vitamin C work synergistically to increase the incorporation of Vitamin C in the skin, significantly boosting antioxidant capability and collagen synthesis. EGA Antiaging Cream contains powerful, bioavailable peptides rebuild and restore skin from the inside out to lift, fill, and smooth out wrinkles. The cream features comfrey stem cells and a probiotic to speed skin renewal and turnover while tomato-derived carotenoids fight UV damage and lighten skin. Sandalwood and Barley Extract reduce water loss and stimulates lipids found naturally in skin. EGA Antiaging Cream addresses signs of aging caused by UV damage, glycation, gravity, and dryness. This rich, luxurious cream "turns back the clock" to reveal smooth, supple and healthy skin.

EGA Antiaging Serum is a lightweight, fast absorbing anti-aging serum features auto-adapting technology to provide the ultimate comfort and protection in all climates. The serum's marine-based neuro-soother addresses one of the root causes of aging and wrinkles -- inflammation. EGA Antiaging Serum fights inflammation by soothing irritated skin and reducing skin sensitivity. Probiotics restores skin's self-renewal to increase skin thickness, reduce moisture loss, and boost skin immunity. EGA Antiaging Serum counteracts photoaging with soybean seed extract and olive fruit revealing an increase in skin smoothness, firmness, hydration, and elasticity while decreasing wrinkle depth. Anogeissus Leiocarpa Bark Extract increases the incorporation of Vitamin C in the skin, significantly boosting antioxidant capability and collagen synthesis.

"We have gotten tremendous feedback from our earliest adopters some saying these incredible creams are like a facelift in a box or Botox in bottle, we are very excited to bring these new products to market for our customers," says Brown.

About Chaster Skin Care Ltd.

Chaster Skin Care Ltd., based in St. Petersburg, Florida is one of the world's leading manufacturers and marketers of high-quality anti-aging skincare solutions. To learn more about Chaster Skin Care Ltd., visit https://www.chasterskincareltd.com or learn more about the products at https://www.egaskin.com.

For the original version on PRWeb visit: http://www.prweb.com/releases/EGA-Antiaging-Cream/EGA-Antiaging-Serum/prweb14617279.htm

Link:
New Launch of EGA Antiaging Cream and EGA Antiaging Serum to Change the Face of OTC Cosmetics - Benzinga

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In 2013, University of Virginia researcher Michael McConnell published research that would forever change how scientists study brain cells.

McConnell and a team of nationwide collaborators discovered a genetic mosaic in the brains neurons, proving that brain cells are not exact replicas of each other, and that each individual neuron contains a slightly different genetic makeup.

McConnell, an assistant professor in the School of Medicines Department of Biochemistry and Molecular Genetics, has been using this new information to investigate how variations in individual neurons impact neuropsychiatric disorders like schizophrenia and epilepsy. With a recent $50,000 grant from the Bow Foundation, McConnell will expand his research to explore the cause of a rare genetic disorder known as GNAO1 so named for the faulty protein-coding gene that is its likely source.

GNAO1 causes seizures, movement disorders and developmental delays. Currently, only 50 people worldwide are known to have the disease. The Bow Foundation seeks to increase awareness so that other probable victims of the disorder can be properly diagnosed and to raise funds for further research and treatment.

UVA Today recently sat down with McConnell to find out more about how GNAO1 fits into his broader research and what his continued work means for all neuropsychiatric disorders.

Q. Can you explain the general goals of your lab?

A. My lab has two general directions. One is brain somatic mosaicism, which is a finding that different neurons in the brain have different genomes from one another. We usually think every cell in a single persons body has the same blueprint for how they develop and what they become. It turns out that blueprint changes a little bit in the neurons from neuron to neuron. So you have slightly different versions of the same blueprint and we want to know what that means.

The second area of our work focuses on a new technology called induced pluripotent stem cells, or iPSCs. The technology permits us to make stem cell from skin cells. We can do this with patients, and use the stem cells to make specific cell types with same genetic mutations that are in the patients. That lets us create and study the persons brain cells in a dish. So now, if that person has a neurological disease, we can in a dish study that persons disease and identify drugs that alter the disease. Its a very personalized medicine approach to that disease.

Q. Does cell-level genomic variety exist in other areas of the body outside the central nervous system?

A. Every cell in your body has mutations of one kind or another, but brain cells are there for your whole life, so the differences have a bigger impact there. A skin cell is gone in a month. An intestinal cell is gone in a week. Any changes in those cells will rarely have an opportunity to cause a problem unless they cause a tumor.

Q. How does your research intersect with the goals of the Bow Foundation?

A. Let me back up to a little bit of history on that. When I got to UVA four years ago, I started talking quite a lot with Howard Goodkin and Mark Beenhakker. Mark is an assistant professor in pharmacology. Howard is a pediatric neurologist and works with children with epilepsy. I had this interest in epilepsy and UVA has a historic and current strength in epilepsy research.

We started talking about how to use iPSCs the technology that we use to study mosaicism to help Howards patients. As we talked about it and I learned more about epilepsy, we quickly realized that there are a substantial number of patients with epilepsy or seizure disorders where we cant do a genetic test to figure out what drug to use on those patients.

Clinical guidance, like Howards expertise, allows him to make a pretty good diagnosis and know what drugs to try first and second and third. But around 30 percent of children that come in with epilepsy never find the drug that works, and theyre in for a lifetime of trial-and-error. We realized that we could use iPSC-derived neurons to test drugs in the dish instead of going through all of the trial-and-error with patients. Thats the bigger project that weve been moving toward.

The Bow Foundation was formed by patient advocates after this rare genetic mutation in GNAO1 was identified. GNAO1 is a subunit of a G protein-coupled receptor; some mutations in this receptor can lead to epilepsy while others lead to movement disorders.

Were still trying to learn about these patients, and the biggest thing the Bow Foundation is doing is trying to address that by creating a patient registry. At the same time, the foundation has provided funds for us to start making and testing iPSCs and launch this approach to personalized medicine for epilepsy.

In the GNAO1 patients, we expect to be able to study their neurons in a dish and understand why they behave differently, why the electrical activity in their brain is different or why they develop differently.

Q. What other more widespread disorders, in addition to schizophrenia and epilepsy, are likely to benefit from your research?

A. Im part of a broader project called the Brain Somatic Mosaicism Network that is conducting research on diseases that span the neuropsychiatric field. Our lab covers schizophrenia, but other nodes within that network are researching autism, bipolar disorder, Tourette syndrome and other psychiatric diseases where the genetic cause is difficult to identify. Thats the underlying theme.

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Researcher Seeks to Unravel the Brain's Genetic Tapestry to Tackle Rare Disorder - University of Virginia

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Credit: Martha Sexton/public domain

A type of mouse widely used to assess how the human immune system responds to transplanted stem cells does not reflect what is likely to occur in patients, according to a study by researchers at the Stanford University School of Medicine. The researchers urge further optimization of this animal model before making decisions about whether and when to begin wide-scale stem cell transplants in humans.

Known as "humanized" mice, the animals have been engineered to have a human, rather than a murine, immune system. Researchers have relied upon the animals for decades to study, among other things, the immune response to the transplantation of pancreatic islet cells for diabetes and skin grafts for burn victims.

However, the Stanford researchers found that, unlike what would occur in a human patient, the humanized mice are unable to robustly reject the transplantation of genetically mismatched human stem cells. As a result, they can't be used to study the immunosuppressive drugs that patients will likely require after transplant. The researchers conclude that the humanized mouse model is not suitable for studying the human immune response to transplanted stem cells or cells derived from them.

"In an ideal situation, these humanized mice would reject foreign stem cells just as a human patient would," said Joseph Wu, MD, PhD, director of Stanford's Cardiovascular Institute and professor of cardiovascular medicine and of radiology. "We could then test a variety of immunosuppressive drugs to learn which might work best in patients, or to screen for new drugs that could inhibit this rejection. We can't do that with these animals."

Wu shares senior authorship of the research, which will be published Aug. 22 in Cell Reports, with Dale Greiner, PhD, professor in the Program in Molecular Medicine at the University of Massachusetts Medical School, and Leonard Shultz, PhD, professor at the Jackson Laboratory. Former postdoctoral scholars Nigel Kooreman, MD, and Patricia de Almeida, PhD, and graduate student Jonathan Stack, DVM, share lead authorship of the study.

"Although these mice are fully functional in their immune response to HIV infection or after transplantation of other tissues, they are unable to completely reject the stem cells," said Kooreman. "Understanding why this is, and whether we can overcome this deficiency, is a critical step in advancing stem cell therapies in humans."

"Humanized mice are critical preclinical models in many biomedical fields helping to bring basic science into the clinic, but as this work shows, it is critical to frame the question properly," said Greiner. "Multiple laboratories remain committed to advancing our understanding and enhancing the function of engrafted human immune systems."

Greiner and Shultz helped to pioneer the use of humanized mice in the 1990s to model human diseases and they provided the mice used in the study.

Understanding stem cell transplants

The researchers were studying pluripotent stem cells, which can become any tissue in the body. They tested the animals' immune response to human embryonic stem cells, which are naturally pluripotent, and to induced pluripotent stem cells. Although iPS cells can be made from a patient's own tissues, future clinical applications will likely rely on pre-screened, FDA-approved banks of stem cell-derived products developed for specific clinical situations, such as heart muscle cells to repair tissue damaged by a heart attack, or endothelial cells to stimulate new blood vessel growth. Unlike patient-specific iPS cells, these cells would be reliable and immediately available for clinical use. But because they won't genetically match each patient, it's likely that they would be rejected without giving the recipients immunosuppressive drugs.

Humanized mice were first developed in the 1980s. Researchers genetically engineered the mice to be unable to develop their own immune system. They then used human immune and bone marrow precursor cells to reconstitute the animals' immune system. Over the years subsequent studies have shown that the human immune cells survive better when fragments of the human thymus and liver are also implanted into the animals.

Kooreman and his colleagues found that two varieties of humanized mice were unable to completely reject unrelated human embryonic stem cells or iPS cells, despite the fact that some human immune cells homed to and were active in the transplanted stem cell grafts. In some cases, the cells not only thrived, but grew rapidly to form cancers called teratomas. In contrast, mice with unaltered immune systems quickly dispatched both forms of human pluripotent stem cells.

The researchers obtained similar results when they transplanted endothelial cells derived from the pluripotent stem cells.

A new mouse model

To understand more about what was happening, Kooreman and his colleagues created a new mouse model similar to the humanized mice. Instead of reconstituting the animals' nonexistent immune systems with human cells, however, they used immune and bone marrow cells from a different strain of mice. They then performed the same set of experiments again.

Unlike the humanized mice, these new mice robustly rejected human pluripotent stem cells as well as mouse stem cells from a genetically mismatched strain of mice. In other words, their newly acquired immune systems appeared to be in much better working order.

Although more research needs to be done to identify the cause of the discrepancy between the two types of animals, the researchers speculate it may have something to do with the complexity of the immune system and the need to further optimize the humanized mouse model to perhaps include other types of cells or signaling molecules. In the meantime, they are warning other researchers of potential pitfalls in using this model to screen for immunosuppressive drugs that could be effective after human stem cell transplants.

"Many in the fields of pluripotent stem cell research and regenerative medicine are pushing the use of the humanized mice to study the human immune response," said Kooreman. "But if we start to make claims using this model, assuming that these cells won't be rejected by patients, it could be worrisome. Our work clearly shows that, although there is some human immune cell activity, these animals don't fully reconstitute the human immune system."

The researchers are hopeful that recent advances may overcome some of the current model's limitations.

"The immune system is highly complex and there still remains much we need to learn," said Shultz. "Each roadblock we identify will only serve as a landmark as we navigate the future. Already, we've seen recent improvements in humanized mouse models that foster enhancement of human immune function."

Explore further: Study provides hope for some human stem cell therapies

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Mouse model of human immune system inadequate for stem cell ... - Medical Xpress

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CAMBRIDGE, Mass.--(BUSINESS WIRE)--Apic Bio, Inc., a pre-clinical stage gene therapy company leveraging its proprietary platform to advance therapies to treat rare diseases with complex mechanisms, in particular Alpha-1 Antitrypsin Deficiency (Alpha 1), launched today with an initial investment led by the venture philanthropy arm of the Alpha-1 Foundation and a private investor with the disease.

Its lead product, APB-101, targets the liver via an AAV delivered Dual Function Vector (df-AAV) whereby the Z-AAT protein is silenced and M-AAT protein is augmented. APB-101 has achieved a pre-clinical proof of concept with efficacy demonstrated in vitro and in vivo. It is currently undergoing pre-clinical GLP toxicology studies in non-human primates. Patients living with Alpha 1 lack sufficient levels of circulating AAT protein to protect lung tissue against damage from proteases, and experience the accumulation of mutant AAT polymers in the liver. Clinically, the deficiency is manifested by progressive emphysema and the accumulation presents a significant risk of liver cirrhosis.

John Reilly, Co-Founder & President said: We are grateful to TAP and A1AT Investors, LLC who have supported the successful start of Apic Bio by providing the first tranche of our seed financing round allowing us to secure key intellectual property rights and operational support. With such strong support from the advocacy and patient community, we are confident that we will identify the right corporate partners to help us achieve our business development goals and bring this exciting new therapy to patients.

The df-AAV platform allows treatment of other diseases with complex mechanisms where the mutant gene product must be reduced and the normal gene product must be augmented.

Dr. Chris Mueller, Co-founder and Chief Scientific Officer of Apic Bio said: We are encouraged by the feedback that we have received during our pre-IND meeting with the FDA that there is a clear path for us to conduct a first-in-human Phase 1/2 clinical study. Furthermore, we are very much looking forward to demonstrating the benefit of APB-101 to patients that have been living with alpha-1 and have had very little hope for a cure. Our data suggests this is a liver sparing approach for gene augmentation which may exceed the therapeutic and safety margins when compared to a strict gene augmentation without gene silencing that may exacerbate the underlying liver disease.

TAP is very pleased to provide this funding to Apic Bio. Their cutting-edge work on a therapy that addresses both the liver and lung disease brings us closer to finding a cure for Alpha-1 Antitrypsin Deficiency, thus fulfilling our mission, said Jean-Marc Quach, CEO for The Alpha-1 Project.

Todays launch of Apic Bio has been a long time coming for the hundreds of thousands of people who are challenged by Alpha 1, said Ed Krapels, who has been living with Alpha 1 and is the new companys first individual investor. Now that we are moving forward, we hope to work with patients, their advocates and researchers to make a cure readily available. Krapels added.

About Apic Bio: Apic Bio, Inc. is a spin-off from the University of Massachusetts Medical School (UMMS) and is based upon nearly 30 years of gene therapy research by its scientific founders Christian Mueller, PhD, Associate Professor of Pediatrics and a member of the Horae Gene Therapy Center at the University of Massachusetts Medical School, Terence R. Flotte, MD, the Celia and Isaac Haidak Professor in Medical Education, dean of the School of Medicine and provost and executive deputy chancellor of the University of Massachusetts Medical School; and colleagues at the Horae Gene Therapy Center. Their research is funded in part by an $11M grant from the National Heart, Lung, and Blood Institute (NHLBI).

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Apic Bio Launches to Advance First-in-Class Gene Therapy for ... - Business Wire (press release)

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