Anemia also known as iron-poor blood is a condition that develops when either the blood doesn't have enough red blood cells or the concentration of hemoglobin in red blood cells is very low. Hemoglobin is the iron-containing protein in red blood cells that carries oxygen from the lungs to the rest of the body. When there are fewer red blood cells than normal or low levels of hemoglobin, the body doesn't get enough oxygen-rich blood for healthy functioning, which is what causes the symptoms of anemia.

Anemia is the most common blood disorder in the United States, affecting nearly 3 million Americans, according to the Centers for Disease Control and Prevention (CDC).

The term anemia is a broad one that represents several hundred different conditions some of them mild and treatable, others that are quite serious, said Dr. Nancy Berliner, chief of hematology at Brigham and Women's Hospital in Boston. There are three reasons that people are anemic, Berliner said: Either their body can't make enough red blood cells, something is destroying the red blood cells faster than their body can make news ones or blood loss (from menstrual periods, colon polyps or a stomach ulcer, for example) is greater than blood cell production.

There are more than 400 different types of anemia, according to the Pacific Heart, Lung & Blood Institute. Here are a few of the more common and better understood types:

Iron-deficiency anemia: The most common form of anemia is caused by low-iron levels in the body. Humans need iron to make hemoglobin, and most of that iron comes from dietary sources. Iron-deficiency anemia can result from a poor diet or from blood loss through menstruation, surgery or internal bleeding.

Pregnancy also increases the body's need for iron because more blood is needed to supply oxygen to the developing fetus, which may quickly drain the body's available iron stores, leading to a deficit. Problems absorbing iron from food because of Crohn's disease or celiac disease can also result in anemia.

Vitamin deficiency anemia: Besides iron, the body also needs two different B-vitamins folate and B12 to make enough red blood cells. Not consuming enough B12 or folate in the diet or an inability to absorb enough of these vitamins can lead to deficient red blood cell production.

Sickle cell anemia or sickle cell disease (SDC): This inherited disease causes red blood cells to become crescent-shaped rather than round. Abnormally shaped red cells can break apart easily and clog small blood vessels, resulting in a shortage of red blood cells and episodes of pain, according to the Mayo Clinic. People become chronically anemic because the sickle-shaped red cells are not pliable and can't get through blood vessels to deliver oxygen, Berliner said.

SDC occurs most often in people from parts of the world where malaria is or was common, according to the CDC; the sickle cell trait may provide protection against severe forms of malaria. In the U.S., SDC affects an estimated 100,000 Americans.

Thalassemia: Thalassemia is an inherited blood disorder that results in lower-than-normal levels of hemoglobin. This type of anemia is caused by genetic mutations in one or more of the genes that control the production of hemoglobin, according to the National Heart, Lung & Blood Institute (NHLBI).

Aplastic anemia: Aplastic anemia is a rare, life-threatening condition that develops when bone marrow stops making enough new blood cells, including red cells, white cells and platelets.

Aplastic anemia may be caused by radiation and chemotherapy treatments, which can damage stem cells in bone marrow that produce blood cells. Some medications, exposure to toxic chemicals like pesticides, viral infections and autoimmune disorders can also affect bone marrow and slow blood cell production.

Hemolytic anemias: This disorder causes red blood cells to be destroyed faster than bone marrow can replace them. Hemolytic anemias may be caused by infections, leaky heart valves, autoimmune disorders or inherited abnormalities in red blood cells, according to the American Society of Hematology.

Anemia of inflammation: Also called anemia of chronic disease, anemia of inflammation commonly occurs in people with chronic conditions that cause inflammation. This includes people with infections, rheumatoid arthritis, inflammatory bowel disease, chronic kidney disease, HIV/AIDS and certain cancers, according to the National Institute of Diabetes and Digestive and Kidney Diseases.

When a person has a disease or infection that causes inflammation, the immune system responds in a way that changes how the body works, resulting in anemia. For example, inflammation suppresses the availability of iron, so the body may not use and store the mineral normally for healthy red blood cell production, Berliner said. Inflammation may also stop the kidneys from producing a hormone that promotes red blood cell production.

The risk for anemia is higher in people with a poor diet, intestinal disorders, chronic diseases and infections. Women who are menstruating or pregnant are also prone to the disorder.

The risk of anemia increases with age, and about 10% to 12% of people over 65 are anemic, Berliner said. But the condition is not a normal part of aging, so the cause should be investigated when it's diagnosed, she said. Older adults may develop anemia from chronic diseases, such as cancer, or iron-deficiency anemia from abnormal bleeding.

According to NHLBI, the following types of people have an increased risk of developing anemia:

Mild forms of anemia may not cause any symptoms. When signs and symptoms of anemia do occur, they may include the following, according to the NHLBI:

The first test used to diagnose anemia is a complete blood count, which measures different parts and features of the blood: It shows the number and average size of red blood cells, as well as the amount of hemoglobin. A lower-than-normal red blood cell count or low levels of hemoglobin indicate anemia is present.

If more testing is needed to determine the type of anemia, a blood sample can be examined under a microscope to check for abnormalities in the size and shape of the red cells, white cells and platelets.

Related: This man's taste buds disappeared because of a blood condition

The treatment of anemia depends on the specific type of anemia, Berliner said, and anemias caused by nutritional deficiencies respond well to changes in diet. People with iron-deficiency anemia may need to take supplemental iron for several months or longer to replenish blood levels of the mineral. Some people, especially pregnant women, may find it hard to take iron because it causes side effects, such as an upset stomach or constipation, Berliner said.

For vitamin-deficiency anemias, treatment with B12 or folate from supplements (or a B12 shot) and foods, can improve levels of these nutrients in the blood, Berliner said.

Serious problems, such as aplastic anemia, which involves bone marrow failure, may be treated with medications and blood transfusions. Severe forms of thalassemia might need frequent blood transfusions.

Treatment for sickle cell anemia may include pain medications, blood transfusions or a bone marrow transplant.

Additional resources:

This article is for informational purposes only, and is not meant to offer medical advice.

See the article here:
Anemia: Causes, symptoms and treatment - Livescience.com

Recommendation and review posted by Bethany Smith

Mesoblast Tenders Completed Biologics License Application

Mesoblast Limited (MESO) announced that it has filed a completed Biologics License Application (BLA) with the United States Food and Drug Administration for its lead allogeneic cell therapy Ryoncil. The therapy is aimed at treating children with steroid-refractory acute graft versus host disease (SR-aGVHD).

Mesoblast submitted the final module of its rolling BLA submission on January 31, 2020. This module covers various aspects related to manufacturing and quality control. The drug candidate currently has Fast Track designation assigned to it and on the basis of this tag, the company is now seeking the FDA to carry out Priority Review of its BLA.

Subject to the approval of the therapy, the company is looking to launch it in the US markets in 2020. CEO Dr. Silviu Itescu said, "This is a major corporate milestone for Mesoblast." The company is expected to use the insights gained from its Temcell product in Japan for the marketing of Ryoncil.

Acute Graft versus Host disease affects nearly 50 percent of patients given an allogeneic Bone Marrow transplant. It is estimated that nearly 30,000 patients undergo bone marrow transplants worldwide. The mortality rate for patients suffering from actual GVHD is close to 90 percent. Currently, there is no FDA approved treatment for this in the United States for children under 12.

Ryoncil has been tested on 309 children suffering from SR-aGVHD during three different studies. It was employed as salvage therapy on 241 children with SR-aGVHD (80% Grade C/D) who failed institutional standard of care. It has also been tested as first line therapy for an open label Phase 3 trial in 55 children with SR-aGVHD. RYONCIL, is an investigational therapy comprising culture-expanded mesenchymal stem cells. These stem cells are taken from the bone marrow of an unrelated donor. The drug is administered to patients as intravenous infusions.

Mesoblast specializes in developing allogeneic cellular medicines. The company uses its proprietary cell therapy technology platform for research and development purpose. It has strong drug pipeline with products such as Remestemcel-L, Revascor, MPC-06-ID and MPC-300-IV. Revascor and MPC-06-ID have completed patient enrollment for its Phase 3 trials. The former drug candidate is aimed at treating advanced chronic heart failure while the latter is targeted at treating chronic low back pain caused by degenerative disc disease. The companys Temcell and Alofisel drugs are already approved in Japan and Europe, respectively.

Mesoblast has posted strong operative results as well. The company had reported 46 percent growth in its revenue during the first quarter of 2020. Mesoblast ended the quarter with $34.5 million in cash while its pro forma cash in hand stood at $100 million. The company also reported its strategic partnership with Grunenthal, which entitles Mesoblast to receive up to $150 million in upfront and milestone payments. The collaboration will also result in commercialization milestone payments. Such milestone payments have the potential to cross $1 billion mark.

Mesoblast stock has performed strongly in the market. The stock has charted over 200 percent in the past 12 months. Currently, it is trading close to its 52-week high of $10.88 and has potential to maintain its positive trajectory as the company forges ahead with its research and development activities and marketing efforts.

Waters Corporation (WAT) reported its fourth-quarter earnings and provided guidance for 2020. The company registered $716 million in revenue for the fourth quarter, in line with the revenue of $715 million it had reported for the corresponding quarter of the previous year. Its GAAP diluted earnings per share stood at $3.12 per share, up from $2.46 on year-on-year basis.

For the full fiscal year 2019, the companys revenue stood at $2.4 billion, down 1 percent from $2.42 billion in revenue it had earned in fiscal year 2018. The EPS for the fiscal year stood at $8.69, up from $7.65 for the previous year. The non GAAP EPS also increased from $8.29 to $8.99 for fiscal year 2019.

The company reported that its sales in both the pharmaceuticals and industrial market declined by 1 percent. However, its sales into the government and academic market grew 8 percent. Chris OConnell, Chairman and Chief Executive Officer of Waters Corporation, said, We were encouraged by the increasing impact in the fourth quarter of our new products launched during 2019.

While its full-year and fourth-quarter numbers were strong, the company provided rather lackluster guidance for fiscal year 2020. Waters Corporation expects its full-year revenue to increase by 1 percent to 3 percent. Its non GAAP EPS will likely remain between $9.15 and $9.40, lower than consensus estimate of $1.75. For its first quarter, Waters Corporations non GAAP EPS for the first quarter is expected to be in the range of $1.55 and $1.65. The consensus estimate for non GAAP EPS guidance was at $1.75.

EyePoint Pharmaceuticals (EYPT) reported its new exclusive licensing deal with Equinox Science. The deal involves the development of vorolanib for treating wet age-related macular degeneration, retinal vein occlusion and diabetic retinopathy. Vorolanib is a tyrosine kinase inhibitor.

EyePoint elaborated that its drug candidate EYP 1901, which incorporates vorolanib, uses a miniaturized, sustained release and injectable intravitreal drug delivery system offering six months duration. The company has used its bioerodible Durasert technology for this purpose. EyePoint is optimistic about the combination of vorolanib with Durasert technology for delivering superior results.

Under the terms of the agreement, EyePoint will take care of development and global commercialization of the treatment. However, the global commercialization will exclude China, Hong Kong, Taiwan and Macau regions. For this purpose, EyePoint will pay $1 million to Equinox Science as upfront payment. It will also pay development and regulatory milestones and post commercialization royalties.

EyePoint recently concluded a positive Type B pre investigational New Drug meeting with the FDA. The meeting clarified the pathway for a Phase 1 clinical trial. The company expects to present the data from Phase 1 trial during the second half of 2021. Nancy Lurker, President and Chief Executive Officer of EyePoint Pharmaceuticals, said, We are encouraged by the potential of vorolanib, as it demonstrated a promising Phase 1 and Phase 2 efficacy signal in prior human wAMD studies as an oral therapy and in preclinical animal studies as intravitreal EYP-1901.

EyePoint is a biopharma company specializing in developing novel ophthalmic products. The company currently has two products available in the market which are Dexycu and Yutiqu. The former is the first approved intraocular treatment for postoperative inflammation while the latter is a three-year treatment of chronic non-infectious uveitis affecting the posterior segment of the eye.

Thanks for reading. At the Total Pharma Tracker, we do more than follow biotech news. Using our IOMachine, our team of analysts work to be ahead of the curve.

That means that when the catalyst comes that will make or break a stock, weve positioned ourselves for success. And we share that positioning and all the analysis behind it with our members.

Disclosure: I am/we are long MESO. I wrote this article myself, and it expresses my own opinions. I am not receiving compensation for it (other than from Seeking Alpha). I have no business relationship with any company whose stock is mentioned in this article.

See the rest here:
Mesoblast Submits BLA, And Other News: The Good, Bad And Ugly Of Biopharma - Seeking Alpha

Recommendation and review posted by Bethany Smith

Stem Cell Therapy Market: Snapshot

Of late, there has been an increasing awareness regarding the therapeutic potential of stem cells for management of diseases which is boosting the growth of the stem cell therapy market. The development of advanced genome based cell analysis techniques, identification of new stem cell lines, increasing investments in research and development as well as infrastructure development for the processing and banking of stem cell are encouraging the growth of the global stem cell therapy market.

To know Untapped Opportunities in the MarketCLICK HERE NOW

One of the key factors boosting the growth of this market is the limitations of traditional organ transplantation such as the risk of infection, rejection, and immunosuppression risk. Another drawback of conventional organ transplantation is that doctors have to depend on organ donors completely. All these issues can be eliminated, by the application of stem cell therapy. Another factor which is helping the growth in this market is the growing pipeline and development of drugs for emerging applications. Increased research studies aiming to widen the scope of stem cell will also fuel the growth of the market. Scientists are constantly engaged in trying to find out novel methods for creating human stem cells in response to the growing demand for stem cell production to be used for disease management.

It is estimated that the dermatology application will contribute significantly the growth of the global stem cell therapy market. This is because stem cell therapy can help decrease the after effects of general treatments for burns such as infections, scars, and adhesion. The increasing number of patients suffering from diabetes and growing cases of trauma surgery will fuel the adoption of stem cell therapy in the dermatology segment.

Global Stem Cell Therapy Market: Overview

Also called regenerative medicine, stem cell therapy encourages the reparative response of damaged, diseased, or dysfunctional tissue via the use of stem cells and their derivatives. Replacing the practice of organ transplantations, stem cell therapies have eliminated the dependence on availability of donors. Bone marrow transplant is perhaps the most commonly employed stem cell therapy.

Osteoarthritis, cerebral palsy, heart failure, multiple sclerosis and even hearing loss could be treated using stem cell therapies. Doctors have successfully performed stem cell transplants that significantly aid patients fight cancers such as leukemia and other blood-related diseases.

Get Discount on Latest Report @CLICK HERE NOW

Global Stem Cell Therapy Market: Key Trends

The key factors influencing the growth of the global stem cell therapy market are increasing funds in the development of new stem lines, the advent of advanced genomic procedures used in stem cell analysis, and greater emphasis on human embryonic stem cells. As the traditional organ transplantations are associated with limitations such as infection, rejection, and immunosuppression along with high reliance on organ donors, the demand for stem cell therapy is likely to soar. The growing deployment of stem cells in the treatment of wounds and damaged skin, scarring, and grafts is another prominent catalyst of the market.

On the contrary, inadequate infrastructural facilities coupled with ethical issues related to embryonic stem cells might impede the growth of the market. However, the ongoing research for the manipulation of stem cells from cord blood cells, bone marrow, and skin for the treatment of ailments including cardiovascular and diabetes will open up new doors for the advancement of the market.

Global Stem Cell Therapy Market: Market Potential

A number of new studies, research projects, and development of novel therapies have come forth in the global market for stem cell therapy. Several of these treatments are in the pipeline, while many others have received approvals by regulatory bodies.

In March 2017, Belgian biotech company TiGenix announced that its cardiac stem cell therapy, AlloCSC-01 has successfully reached its phase I/II with positive results. Subsequently, it has been approved by the U.S. FDA. If this therapy is well- received by the market, nearly 1.9 million AMI patients could be treated through this stem cell therapy.

Another significant development is the granting of a patent to Israel-based Kadimastem Ltd. for its novel stem-cell based technology to be used in the treatment of multiple sclerosis (MS) and other similar conditions of the nervous system. The companys technology used for producing supporting cells in the central nervous system, taken from human stem cells such as myelin-producing cells is also covered in the patent.

Global Stem Cell Therapy Market: Regional Outlook

The global market for stem cell therapy can be segmented into Asia Pacific, North America, Latin America, Europe, and the Middle East and Africa. North America emerged as the leading regional market, triggered by the rising incidence of chronic health conditions and government support. Europe also displays significant growth potential, as the benefits of this therapy are increasingly acknowledged.

Asia Pacific is slated for maximum growth, thanks to the massive patient pool, bulk of investments in stem cell therapy projects, and the increasing recognition of growth opportunities in countries such as China, Japan, and India by the leading market players.

Request TOC of the Reportfor more Industry Insights @CLICK HERE NOW

Global Stem Cell Therapy Market: Competitive Analysis

Several firms are adopting strategies such as mergers and acquisitions, collaborations, and partnerships, apart from product development with a view to attain a strong foothold in the global market for stem cell therapy.

Some of the major companies operating in the global market for stem cell therapy are RTI Surgical, Inc., MEDIPOST Co., Ltd., Osiris Therapeutics, Inc., NuVasive, Inc., Pharmicell Co., Ltd., Anterogen Co., Ltd., JCR Pharmaceuticals Co., Ltd., and Holostem Terapie Avanzate S.r.l.

About TMR Research:

TMR Research is a premier provider of customized market research and consulting services to business entities keen on succeeding in todays supercharged economic climate. Armed with an experienced, dedicated, and dynamic team of analysts, we are redefining the way our clients conduct business by providing them with authoritative and trusted research studies in tune with the latest methodologies and market trends.

Read the rest here:
Stem Cell Therapy Market Trends and Growth, Outlook, Research, Trends and Forecast to 2025 - Instant Tech News

Recommendation and review posted by Bethany Smith

Latest Research Report on Stem Cell Treatments Market size | Industry Segment by Applications (Nerve Diseases, Immunological Diseases, Musculoskeletal Disorders, Cardiovascular Diseases, Gastrointestinal Diseases and Other), by Type (Adipose Tissue-Derived Mesenchymal Stem Cells, Bone Marrow-Derived Mesenchymal Stem Cells, Cord Blood/Embryonic Stem Cells and Other Cell Sources), Regional Outlook, Market Demand, Latest Trends, Stem Cell Treatments Industry Growth, Share & Revenue by Manufacturers, Company Profiles, Forecasts 2025.Analyzes current market size and upcoming 5 years growth of this industry.

New research report to its expanding repository. The research report, titled Stem Cell Treatments Market, mainly includes a detailed segmentation of this sector, which is expected to generate massive returns by the end of the forecast period, thus showing an appreciable rate of growth over the coming years on an annual basis. The research study also looks specifically at the need for Stem Cell Treatments Market.

Our Report Offerings Include:

Request Sample Copy of this Report @ https://www.aeresearch.net/request-sample/72554

Report Scope:

The study includes the profiles of key players in the Stem Cell Treatments market with a significant global and/or regional presence. The Stem Cell Treatments market competition by Top Manufacturers Covers:

By Product:

By Application:

Points Covered in The Report:

Recent Industry Trend:

The report contains the profiles of various prominent players in the Global Stem Cell Treatments Market. Different strategies implemented by these vendors have been analyzed and studied to gain a competitive edge, create unique product portfolios and increase their market share. The study also sheds light on major global industry vendors. Such essential vendors consist of both new and well-known players. Besides, the business report contains important data relating to the launch of new products on the market, specific licenses, domestic scenarios and the strategies of the organization implemented on the market.

MAJOR TOC OF THE REPORT:

Request Customization on This Report @ https://www.aeresearch.net/request-for-customization/72554

Read the original here:
Stem Cell Treatments Market to Exhibit Impressive Growth of CAGR during the per - News by aeresearch

Recommendation and review posted by Bethany Smith

By Michael Le Page

Vchal/Getty Images

CRISPR gene-edited immune cells have been injected into threepeople with advanced cancer without any serious side effects, the first trial of its kind in the US. It is also the first CRISPR cancer trial in the world to publish its findings, and the encouraging results will pave the way for many more trials.

Its an important milestone, says Waseem Qasim at theUCLGreat Ormond Street Institute of Child Health in the UK, who is carrying out a similar trial there.

The US trial was intended only to assess safety. The threeparticipants had tumours that hadnt responded to other treatments, and were given only one dose of gene-edited cells.

Advertisement

Is it safe and feasible? says team member Edward Stadtmauer at the University of Pennsylvania. I think thats what we demonstrated.

Many cancers involving blood cells are now treated by removing immune cells from individuals, adding a gene that makes them target cancer cells and putting them back in the body.

But this treatment doesnt work for everyone, says Stadtmauer. And in some, it works at first but they later relapse.

The hope is that using gene editing to delete genes in addition to adding the targeting gene will make this approach even more effective. For instance, immune cells have a safety switch, called PD-1, that other cells can flip to say dont hurt me. Many cancers exploit this to avoid immune attacks.

In this trial, the team removed immune cells from three peoplewho hadtumours with the same protein on their surface. A virus was used to add a gene to make the immune cells target this protein.

Next, three genes, including PD-1, were deleted using CRISPR. After six weeks, the cells were put back in the individuals, where they survived for at least 9 months.

There were two big safety concerns. Firstly, CRISPR can cause unintended changes to genomes that could turn cells cancerous. Deleting three genes means cutting around each one in three spots in the genome, for instance, and the wrong ends can be joined up. This did happen in some cells, but there was no sign of any turning cancerous.

The other worry was that lingering traces of the CRISPR protein used for gene editing might trigger an immune reaction, since it is a bacterial protein. There was no sign of this.

The trial wont continue because its 2016 gene-editing technology is already outdated, says Carl June, also at the University of Pennsylvania. In particular, a new form of CRISPR called base editing can be used to inactivate genes without cutting DNA, which should reduce the cancer risk even further. We are very attracted to that, says June.

There are also many other ways to edit immune cells to make them more effective, says Stadtmauer. The possibilities are limitless based on our imagination and scientific focus.

In particular, Stadtmauer wants to create off-the-shelf cells that could be given to any patient, rather than modifying each patients own cells. This would speed up treatments and greatly reduce costs.

Qasims team has already saved lives in an ongoing trial at Great Ormond Street using off-the-shelf cells created by an older form of gene editing called TALEN. But these cells have to be given as part of a drastic treatment, which is followed by a bone marrow transplant that kills off the edited cells. Stadtmauer wants to create cells that can survive indefinitely in peoples bodies.

The risk of edited cells turning cancerous or starting to attack healthy cells would be higher if they survive longer. But it is also possible to add a self-destruct mechanism triggered by a specific drug to kill them off if necessary.

There have been a number of trials of CRISPR-edited immune cells for treating cancer in China, but no results have yet been published.

Journal reference: Science, DOI: 10.1126/science.aba7365

More on these topics:

See the original post here:
CRISPR cancer trial finds that gene-edited immune cells are safe - New Scientist News

Recommendation and review posted by Bethany Smith

The lottery that began this week was not about money, or about choosing a school, or about obtaining a visa. It was about a childs life.

In this case, the children selected would receive a drug that otherwise was not available. Jamie Clarkson, an electrician in Queensland, Australia, entered his 18-month-old daughter, Wynter.

We applied for it because we desperately want this drug for our daughter, but youre putting your daughters well-being and longevity in the hands of a lottery, Clarkson said. I guess its the fairest way to decide who gets the drug and who doesnt, but yeah, its not a great feeling.

advertisement

The treatment, a gene therapy called Zolgensma, is designed for children like Wynter who have a neuromuscular disease called spinal muscular atrophy, or SMA. Without it or other treatments, those with the most serious type are likely to die as babies. It was first approved by U.S. regulators only last year, and is not yet available in other countries.

The lottery was devised by the drugs manufacturer, Novartis, to give families in those places a chance to get it through a novel form of compassionate use a way to get medications that have not been approved while they wait. Fifty doses are slotted to be given away for free in the first half of the year, with up to 100 total.

The first drawing occurred Monday.

Ethicists and advocates have debated the merits and the design of the unusual arrangement. Parents said that it was uncomfortable to cast their childs fate into what felt like a sweepstakes a kind of bizarre Willy Wonka contest in which, as Maura Blair, a Canadian mother of a child with SMA put it, were talking about lives. But if it was a chance to get the drug, it was worth trying.

Zolgensma costs $2.1 million in the United States the worlds most expensive drug. And even if it is to cost less in other countries, even if it is to be covered by insurance, infants at this point are not eligible for it after turning 2. Some families have even tried to fundraise in hopes of buying the drug themselves and getting it injected by doctors in the United States.

Shes 7 months, Laura Silva, who lives north of Toronto, said about her daughter, Rebecca. Do we rely on their word and wait it out? Or do we take action ourselves? Because the sooner she can get it, the better for her.

Some parents said they had taken issue with news coverage of the lottery, which has framed the eventual recipients of the drugs as lucky winners. If that were the case, what did that say about everyone else?

The kids appeared healthy at birth. But soon, their parents recalled, it became clear that something was wrong. They couldnt raise or control their arms and legs. They would choke on their milk.

Jamie Clarkson, in Australia, said he and his wife, Kellee, had a friend with a daughter around Wynters age. When laid face down (tummy time, in parental parlance), the girl had no problem lifting her head.

The difference was chalk and cheese, he said. Our girl sort of laid there and didnt do anything.

Sometimes the parents were told their kids just needed more time, but eventually, a clinical evaluation and genetic test would confirm the SMA diagnosis. The most serious form, called type 1, is estimated to affect 1 in 15,000 babies.

Children with the disease have a mutation in a gene called SMN1 (or a missing gene) that meant cells dont produce sufficient SMN protein. The dearth of the protein debilitates motor neurons, which are responsible for relaying messages to muscles, and creates a cascade of issues that culminates in muscle weakness.

Without treatment, babies with type 1 SMA might never be able to lift their heads or arms or legs, and struggle to regulate their swallowing and breathing. Most die by 2, typically because of respiratory issues.

Zolgensma works by ferrying a healthy copy of an SMN gene into motor neurons restoring production of the protein and the health of the neurons. It is a one-time treatment with lasting benefits like reigniting a pilot light.

When Zolgensma won approval from the U.S. Food and Drug Administration in May, it was hailed a monumental victory for families and an achievement in genetic medicine one of the first gene therapies to make it to the market. But it also created a divide between haves and have-nots American parents, assuming insurance companies would cover the treatment, and parents anywhere else in the world.

It is not uncommon for a drug to be available in the United States before other countries; drug makers routinely apply for and receive regulatory clearance from agencies around the world at different times. But the FDAs approval drove global appeals for a drug that offered babies a chance.

Beyond the issue of regulatory approval, supplies of Zolgensma are tight, Novartis has said. Gene therapies are complex to manufacture, and the company only has one facility producing the drug right now, with plans for two more to come online this year. It also needs to have doses available for U.S. patients and for patients in other countries where the drug could become available in the coming months. (European regulators are expected to decide on Zolgensma this quarter, and Japanese officials before the middle of the year, the company has said. Decisions in Canada and Australia may not come until 2021.)

Novartis saw a lottery as the answer.

Random lotteries are an accepted way to mete out resources when there is a limited amount, some ethicists have argued. They establish an equal playing field and remove the possibility that those with money or connections can maneuver to jump the line.

But experts have also questioned whether Novartis has done enough to try to overcome the scarcity issues. Some have also said that favoring those with the greatest need meaning the sickest children would be a more ethical approach; patients who are healthier could potentially wait until the drug is approved in their home countries or until more supply is available.

If it is really not possible to help all who are in need of help, then a lottery with priority to patients who are worst off is not a bad approach and definitely fairer than other things a company could do, said Holly Fernandez Lynch, a bioethicist at University of Pennsylvanias Perelman School of Medicine. The key is to first do everything possible to minimize the need for a lottery at all and its not obvious to me that Novartis has done that here.

The fact that the lottery created a situation in which there are, for lack of better descriptors, winners and losers also left some people uneasy.

You cant do anything to improve your chances, said Genevieve Kanter, also a bioethicist at Penn. But it does become a zero-sum game, which is what bothers some people about the mechanism, even if at the end of the day, more kids get treated than in the alternate scenario where theres no lottery.

Its the price we have to pay to have some kids treated.

In an interview with STAT, the president of AveXis, the Novartis unit that developed Zolgensma, said the company considered prioritizing the patients who were sickest or those for whom another SMA treatment did not help. But the company, which is using an outside party to handle the selection and brought in ethicists to consult on the system, did not want to put a finger on the scale in any way, he said. Instead, selections would be random.

Its the only fair way to allocate, the official, Dave Lennon, said, even as he acknowledged, its not an ideal situation.

The alternative is not do anything, which we didnt feel like was a good option, he added.

He said if the supply was sufficient, Novartis hoped to expand the program.

Novartis would not say how many people were being selected each time. Drawings are set to take place every two weeks.

And that means families in desperate need have a chance to obtain the medicine just as often.

For them, they try every possible way to get this Zolgensma, said Csilla Galik, a friend of the family of Noel lys, who has type 1 SMA and whose family lives in Romania near the Hungarian border. They need to try every possibility because this medicines price is incredible.

Beyond Zolgensma, there is another treatment for SMA: Spinraza, manufactured by the drug maker Biogen and more widely available globally. Injected into the spinal fluid every few weeks and then every four months, it promotes the production of the SMN protein by boosting the activity of another gene similar to SMN1.

Many of the children waiting for Zolgensma are already receiving Spinraza, and their parents say it appears to be helping, to an extent.

Wynter Clarksons motor function has improved, though not as much as her parents had hoped it would. She can move her head and raise her arms, and can sit up with a back brace. She can rock from side to side, but not quite roll over. Each treatment requires the family to travel about two and a half hours from their home in Toowoomba to Brisbane.

Spinraza and Zolgensma have not been compared in a head-to-head study, and how long the benefits of Zolgensma last is not yet known. But parents said they see a one-time infusion of Zolgensma which replaces the faulty gene at the root of the disease, instead of just building a workaround as the best option for their children.

Even when children are on Spinraza, their disease can progress, if at a slower rate, parents said.

Blair said her daughter, Lennon, has more control over her head and limbs since starting Spinraza. But after three doses, the girl still needed a feeding tube inserted; she lost her ability to swallow. Thats on top of other care required by Blair and other parents of infants with the disease. Oxygen levels needed to be checked, sleeping sometimes requires a mask and machines to aid breathing, physical therapy exercises are done to try to coax some muscle activity.

You basically repeat that all day, all day until bed time, said Blair, of St. Catharines, Ontario. And everything takes so long.

There is another wrinkle to having a child with the disease: Its inherited, and some parents though not all said they felt responsible for having passed on a mutation that made their child so sick.

To have the disease, a child needs to inherit two mutated copies of the gene, one from each parent who can go through life not knowing they are carrying the mutation until they have a child with the disease.

The parents who have struggled with a sense of guilt know they shouldnt blame themselves, but they still catch themselves wondering if there was something they could have done differently.

Its something we technically gave to her, not even knowing that we could, said Laura Silva, the mother who lives near Toronto. And thats the hardest part.

When it came time for the lottery drawing this week, her daughter Rebeccas name wasnt in the pool she hadnt yet gotten the necessary approval from a Candian health authority to try an experimental drug. Its not clear how many Canadian children found themselves in similar circumstances, or how many were successfully entered by their doctors. Some parents said they were still waiting for that approval.

Noel, the boy in Romania, was entered by his doctor. But his family had not heard anything following the initial drawing. Neither had the Clarksons in Australia:

No word from our neurologist about the free Zolgensma dose, Jamie wrote in an email Tuesday, so Im assuming Wynter wasnt picked this time around, unfortunately.

Winnie Luk-Taylor and Cory Taylor, who live outside Toronto, were once hopeful that Zolgensma could help their daughter, Skye.

She was born in June. Her motor skills werent developing as they should have, and her breath had a rattle to it, as if she were congested. At around 4 months, Skye was diagnosed with SMA and, with a cough, her parents were told to take her to the hospital. She was also started on Spinraza.

She spent a month and a half at the hospital with respiratory infections and complications. She died Dec. 21.

Skye took it all in and smiled at every one and didnt seem to realize she was experiencing some very, I guess, major medical procedures, her mom said. She was a very good-natured girl.

Luk-Taylor said she sometimes wondered what might have happened if Skye had been born one year later June 24, 2020, not 2019. Ontario, the province where they live, started testing for SMA this year as part of its newborn screening, meaning Skye might have been diagnosed earlier in her life and started on Spinraza sooner. Maybe it could have had more of an effect. And maybe Zolgensma would have become available to Canadian babies not long after that.

Instead, at Christmas, Luk-Taylor wrote her daughter a poem.

We will never let you go, it reads in part.

Your spirit will live onIt lives in everything I doI will always fight for youI will always care for youI will always dream of youI got to see who you were to becomeAnd I am blessed and proud of youI am blessed and proud of youI hope you see and hear me nowAnd know that I love you.

Read more:
Lottery like no other offers a cutting-edge medicine with lives on the line - STAT

Recommendation and review posted by Bethany Smith

Dr. Thomas Lynch in Seattle on Monday, his first day as the new president and director of the Fred Hutchinson Cancer Research Center. (GeekWire Photo / Todd Bishop)

Dr. Thomas Lynch is in his first week as the new leader of the Fred Hutchinson Cancer Research Center, but he already has a four-point plan to help guide the Seattle-based institute in its quest to treat and ultimately cure cancer.

Given his new home, in the middle of one of the countrys hottest tech hubs, its no coincidence that one of those points heavily involves the technology industry.

The intersection between tech and data and science is something we are really well-poised to be able to understand and exploit here in the Seattle ecosystem, Lynch said in an interview with GeekWire this week. He cited the quest to look at very large data sets of electronic medical records, genomic data, proteomic data, and begin to understand who gets cancer, and why do they get it.

For example, Fred Hutch currently collaborates with Amazon to mine and decode medical records using artificial intelligence, and reduce the processing time needed to analyz the microbiome. It partners with Microsoft on a Pacific Northwest data discovery program, and a new $40 million initiative to address global health challenges with AI. A collaboration with Pattern Computer for analyzing genetic variations is an example of the institutes work with smaller tech companies.

Dr. Lynch, a veteran physician and scientist, is the sixth president in the 44-year history of the Seattle-based cancer research institution, which employs more than 3,000 people and is ranked first in National Institutes of Health funding among all U.S. independent research centers.

Hes a scientist and oncologist who was part of the first research team to discover how targeted therapies could help lung cancer patients with a specific genetic mutation. Lynch was most recently chief scientific officer of Bristol-Myers Squibb. Prior to that he held leadership roles as CEO of Massachusetts General Physicians Organization, director of the Yale Cancer Center, physician-in-chief at Yales Smilow Cancer Hospital, chief of hematology-oncology at Massachusetts General Hospital and professor of medicine at Harvard Medical School.

Listen to our conversation above, or subscribe to GeekWire Health Tech in your favorite podcast app. Continue reading for an edited transcript.

Todd Bishop: You said in the announcement that you were becoming the new Fred Hutch president that as soon as you saw the opening, you knew this is where you wanted to be. This is what you wanted to do. Why?

Dr. Lynch: The excitement about whats happening in Seattle and at the Hutch in terms of cancer, in terms of technology, in terms of how were moving society forward in this kind of integration, this is a dynamic place to be. My whole career has been about approaching cancer, from the treatment of cancer, prevention of cancer, understanding what populations of people get cancer, and how we can understand it better. And I couldnt think of a better place to be than the Hutch. The combination of a focus on cancer prevention, as well as the integration of understanding how viruses and microbial species can impact cancer, plus the focus on cancer treatment, with the fact that this is the birthplace of bone marrow transplant and the home of cellular immunotherapy. This is just an extraordinary place to be and the opportunity here is perfect.

TB: Among other things, youre a scientist and an oncologist. You were part of the first research team to discover how targeted therapies could help lung cancer patients with a specific genetic mutation. And I do want to talk in part about what role genes will play, and specifically, genetic analysis will play. But most recently, you were the chief scientific officer at Bristol Myers Squibb. Im curious, after your career in research and academia, what perspective youre bringing from Bristol Myers Squibb to this new role and how that job changed your viewpoint, if at all, of the entire cancer research sphere.

Dr. Lynch: One of the reasons that actually I really enjoyed my time at Bristol Myers Squibb is that the way that cancer is going to be defeated, its an ecosystem. Its a large number of people coming at it from a number of different areas. And you need doctors who are able to deliver therapy and were also able to make important observations about the types of diseases we have. You need fundamental scientists who are working in laboratories like the Hutch, who are discovering why cancers occur.

And then you need people who develop medicines and treatments based on those scientific understandings. And some of those are biotechs. And one of the things at the Hutch were very proud of is that weve had approximately 40 biotechs that have come out of science at the Hutch, where new therapies are based on some of the things that happened there. But then big pharma can take the findings of smaller biotechs and the laboratories within big pharma and create medicines and create products. So that exposure to me was priceless in terms of understanding how crucial it is to bring new drugs to patients.

However, I think at the heart of the cancer ecosystem is the comprehensive cancer center, such as the Hutch. And the Hutch is one of approximately 45 comprehensive cancer centers in the United States, and I think its the very best.

It is an independent research center, but I think its important to remember our important partners that are part of the consortium. So the University of Washington is a fantastic university and hospital system. They are incredibly important as a partner. Childrens Hospital in Seattle, incredibly important as a partner to the Hutch. And together, the three institutions have formed the Seattle Cancer Care Alliance. While the Hutch is an independent cancer research institute, I think its also important to know that were approaching cancer utilizing many of the other key partners here in Seattle.

TB: You mentioned the spin-offs and there have been many notable ones from the Fred Hutchinson Cancer Research Center, such as Adaptive Biotechnologies, Juno Therapeutics. Theres a long list, as you said. Can you explain the significance, the importance of developing therapies and technologies that can be spun off into other companies?

Dr. Lynch: Well, I think if you look at the model of how we develop new products now, I think its changing. I think products now are often discovered in academia by scientists who are unconstrained. One of the things I love about the Hutch is the independence of the faculty. The idea that scientists come to work everyday at the Hutch arent coming to work with an agenda thats being driven by shareholders. Theyre coming to work with an agenda thats being driven by science and knowledge.

However, once youve found a lead that can turn into a potential drug, then the kind of focused resources that biotech can bring becomes really important. And you have two options. You can either start a biotech and develop that technology or you can license that technology to a bigger pharma company. I think one of the things that were seeing in the world of drug development is increasingly, good ideas are going from universities to biotech and then from biotech to big pharma as the way things get developed.

It doesnt mean it always has to be that way, but Im just saying that I think were seeing that that model is far more likely to produce new drugs. It allows people who want to invest earlier in a biotech to bring funds and resources rapidly to be able to develop these ideas quicker. And so, I think theres a big advantage in terms of speed and bringing capital to be able to make these decisions and to be able to find out if the idea from the laboratory really works in patients or has the potential to work in patients.

TB: I was digging through the Fred Hutch financials and one thing really stood out to me and that was that back in 2014, one and a half percent of revenues came from royalties and five years later, just this past year in 2019, 10% of revenue came from IP licensing. So in the same general category. What role do you see startups, tech investments, your stake as Fred Hutch in spin-offs playing in the overall growth of the institution and the quest for cures for cancer?

Dr. Lynch: Licensing will continue to be a very important place that cancer centers around the country look to be able to diversify their funding base. Research funding from the National Cancer Institute and National Institutes of Health is incredibly important. And the Hutch, as you mentioned earlier in the interview, the Hutch is the leading independent, freestanding research institute in terms of NIH funding. Thats very important. And then, therell be other sources of revenue, philanthropy and generosity of patients and of people in the community. Really important to the institute.

But then when you think about other sources, licensing becomes a very natural place to look for ways of supporting our research and supporting the mission of the Hutch itself. And I think that thats something, its not just located here. If you go to Cambridge and you look at Harvard and MIT, you look at Yale, you look at Penn, you look at Stanford, you look at UCSF. All of these places are working hard to be able to find ways to support their cancer research, and that intellectual property becomes an important way to think about that as a way of funding was.

I think it also indicates the quality of the research thats happening when you have a venture community and investment community thats able to see the value in very early stage research thats coming out of the Hutch.

TB: Your predecessor as the president of Fred Hutch, Dr. Gary Gilliland, made a bold proclamation about five years ago that he believed, within the next 10 years from then, so five years from now, there would be therapies, if not cures, for most, if not all, forms of cancer. And it got lots of attention at the time. I know youve also spoken publicly about the possibility of curing cancer in our lifetime. Give us a state of the union on the fight against cancer.

Dr. Lynch: So Id say this, I think that Gary was right. I think there are cancers now that are curable in 2025 or theyre curable 2020 that werent curable in 2015. When I took over as the head of the Yale Cancer Center in 2009, I talked about curing cancer in 2020. And I think there are cancers that are curable today that werent when I started in 2009. I know that when I started at Yale. And I think Gary was correct in saying the same thing.

And I will hold that, that by 2025 and 2030, there have to be more types of cancer were curing. It doesnt mean that were going to cure every single type of cancer by 2025 or 2030, but we need to make progress in a number of different cancers.

One of the things that I feel is really important for the Hutch, and not just the Hutch, but Id say American cancer in general, is this concept of urgency. Okay? There are patients who are being diagnosed with cancer every day that need hope and need options, and thats what a cancer center is there for. Thats what the Hutch is there for. Cures start here is not just a corporate logo. Its actually true. And if you think about people whove got lymphoma or people whove got leukemia, theyre alive today because of the things that have happened at the Hutch. And so, I think that bringing that sense of urgency to solid tumors, I think is incredibly important.

TB: A lot of times, in cases of lymphoma and other blood cancers, the immunotherapy has worked well and its in part because of the characteristics of those cancers. Youre able to essentially take the red blood cells correct me if Im wrong on this, I am not a scientist but take the T-cells, reprogram them and essentially put them back in in a way that the cells that would normally go after an illness instead go after the cancer. But as you said, solid tumors have been much more difficult. This is in part your specialty. Whats the prognosis there?

Dr. Lynch: So Id say solid tumors is my specialty, and I think one of the things that I cant wait to work with people at the Hutch on. Theres two big problems I would say right now with cellular therapy for solid tumors. One is that we want to have a cellular therapy approach that can be used on more than one patient, what we would call an allogeneic T-cell therapy. Thats going to become incredibly important.

I think the second key thing is understanding what are the specific targets on the cancer cell of a solid tumor that you can go after that would distinguish it from normal tumors. I mean, one of the reasons this has been successful in leukemias, lymphomas, and even in myelomas is that they have antigens on their surface that allow the T-cell to go after them, specifically.

The good news is I think were beginning to get some insights into what these could like. And at the Hutch, more than half of our trials that were starting now in cellular therapies are for patients with solid tumor. Now, there are enormous engineering problems that have to be overcome to be able to figure out how to safely unleash the immune system. Because if you unleash the immune system against an antigen which is present throughout the entire body on other normal tissues, like lung cells or liver cells, you could end up with a lot of side effects that youd like to not see. So its a major challenge, but one that certainly needs to be addressed.

TB: Is that one of the key ingredients to the broader effort to cure cancers of all different forms, the effort to take immunotherapy and apply it to solid tumors?

Dr. Lynch: Absolutely. Ive been asked a lot in the last day, this is my first day at the Hutch. And Ive been asked a lot today, what do you want to do here? And I would say there are four areas I want to really look at.

TB: Matt McIlwain from Madrona Venture Group is the board chair of the Fred Hutchinson Cancer Research Center, and Satya Nadella, the Microsoft CEO, is also on your board. So its natural that you would see intersections with tech being here in the Seattle area. What kinds of ways might you work differently with tech and the tech industry to expand those kinds of partnerships and accelerate that kind of innovation?

Dr. Lynch: So I think thats a great question. I think one of the things thats great is you want to build teams. You want to build teams that have scientists, doctors and engineers working together. And its interesting, I was talking to a friend of mine who started a tech company thats at the influence of data and medicine. And he said to me, he said, the one thing hes been so impressed with at his company is how engineers really start to shine when they begin to realize the impact that their understanding of coding can have on patients, and that it really makes for an incredible partnership between an engineer, a doctor, and a scientist. And we think thats going to be something that were obviously going to look at.

I think one of the things you want to be a little careful of, and I have to be very careful how I say this, is to realize that some of this will take a little bit of time. For example, we look now at artificial intelligence and AI-enabled cancer research and is it all there yet? I think its still going to take a little bit of time for us to be able to apply some of these tools to able to get these answers, but I couldnt think of a better place to be in trying to get there.

TB: This cuts both ways in a market like Seattle. Youve got the existence of high level technology companies, but you also have the competition for talent among engineers. And then, of course, physicians and researchers. How do you attract and retain the best talent in both of those areas, because youve got one of the most difficult jobs around in both fronts?

Dr. Lynch: Well, Id say this. I think your point about talent is incredibly important. Id say this. I think people want to be places where the culture is great. They want to be places where the mission is real, where the energy is high and, lets face it, life is short and people want to enjoy their work and get meaning from their work. I couldnt imagine a better place to be than the Hutch to get meaning for your work.

TB: Youve had a long career in this field, but it actually dates back to your childhood, right?

Dr. Lynch: It does, yes.

TB: Tell that story if you would.

Dr. Lynch: I grew up in Hackensack, N.J., and my dad was a hematologist, a blood doctor, one of the first blood doctors in the United States. And he was actually one of the first in New Jersey, for sure. And back then, his office was attached to our house. And it sounds kind of crazy, but as a little kid, I remember playing in the yard and watching patients walk into his office.

And I remember him saying to me, he said, Tommy, he said, These patients who have leukemia, and he said, I cant do much. He said, Most of my patients with leukemia, in fact, all of his patients with leukemia, would die from their disease. And that included children, it included young adults, as well as adult patients. And weve come so far just in treating leukemia in his career, and certainly, in my lifetime as well. So its something I would say, Ive stayed in the family business to a certain extent.

TB: To what extent did your dad inspire that?

Dr. Lynch: So I think he did. I think I knew all along I wanted to be a doctor. It was something that in my family, I knew this was something that was motivating to me. And I think, he of course said, you can do whatever you want to do. He said, whatever type of medicine you want to do, but he was extremely supportive as was the remainder of my family.

And I do think one of the things though thats interesting that, you mentioned this, one of the things Im interested in is I want to make sure at the Hutch and at UW that were recruiting people into medicine who might not have had that advantage that I had of growing up in a medical family. I think one of our problems in medicine is that 30% or 35% of the people, I have a daughter whos in medical school, but 35% of people who become doctors come from medical families.

And I think we have a tremendous amount of talent out there that were missing because they dont come from medical families and they dont know the steps necessary to get there. And I think when you look at particularly trying to increase the diversity of the people who become physicians, we as a society need to do a better job of that. And I can tell you thats something were very much dedicated to at the Hutch is increasing the diversity of our physician workforce, our engineering workforce, and certainly, our scientific workforce.

TB: A lot of times when we sit down with leaders of major institutions, we talk about competitors, but your competitor in many ways is the ultimate foe, cancer. Obviously, you compete against other institutions for funding, but what is it about cancer that drove you to get into this as a career, and how would you describe this as something that youre trying to tackle day to day?

Dr. Lynch: So I think thats a great question, about the idea of cancer being the ultimate competitor. Id say the one thing that Ive been attracted to are hard problems. Okay? And when I went into cancer, I had to make a decision about what type of cancer to become most interested in. And I chose lung cancer. And the reason I chose lung cancer is because it was the leading cancer cause of death in the United States. Still is the leading cause of cancer death in the United States.

And I wanted to do something where nobody else was. I wanted to go into something which is relatively untapped as an area. Now weve made a lot of progress in lung cancer, but there is still way more progress that needs to be made to change the outcome from this disease. And so, I do think that working on hard problems is particularly rewarding. And its one of the things thats driven me.

TB: So there has been some progress, as youve been saying, especially since the days when you were watching your dads patients go into the office there attached to your house. The American Association of Cancer Research reports that the age-adjusted overall U.S. cancer death rate declined by 27% from 1991 to 2016. So thats about 2.6 million cancer deaths avoided. Yet, it sounds like based on the trends in the global population, this threat is bigger than ever. How do you look at this today?

Dr. Lynch: Well, Id say two things. So a couple things. So first, I think one of the policy decisions that we can be very happy about thats led to reducing deaths from cancer is the the emphasis on smoking cessation. So smoking cessation is really important. Understanding other behaviors for prevention, incredibly important. One of the things Im very proud of at the Hutch is the focus on cancer prevention and epidemiology, both in terms of who we should screen earlier and maybe screen differently for the emergence of early cancers, but also how can we instill behaviors that could reduce the risk of developing cancer down the road.

So I think thats also incredibly important as a means of being able to control cancer. Its not just about coming up with treatments that you can use later in the stage of a disease. Another good example is understanding the role that viruses play and the vaccinations against viruses can make. So the whole story with HPV and the advent of the HPV vaccine will prevent men and women from developing certain HPV-related cancers. And so, those kinds of things I think will make a big difference in terms of what we do now.

Now you asked the question, well isnt cancer still a major scourge? It is a major scourge. And I would say that one of the things, one of the reasons for that is our populations aging. And cancer still remains a disease of older people. And the average age of patients with cancer in the United States is about 69 to 72 years old, so its still a disease of aging. So as the population ages, the total amount of cancer continues to be substantial.

TB: What do you say to someone when they say, when will cancer be cured and how is it going to happen?

Dr. Lynch: I think one of the issues there is that its not just one disease. Cancer isnt just one disease. Cancer is hundreds of diseases defined by unique genetic abnormalities in the cancer, as well as differences between the patients in terms of how each of us have our immune system and our ability to recognize foreign cells. So I actually think that we are so much further and so much closer now than we were in terms of being able to fight cancer and understand cancer than we were 20 years ago.

If you think about the fact that we can now sequence the genome of a cancer cell and we can do that in about two days, three days to be able to get an answer. Second, were able to edit genomes incredibly well, and I think thats really important. And finally, some work that is happening at the Hutch and other major centers in terms of understanding structural biology, were able to actually look at these mutated proteins and understand what they look like and come up with ways of trying to make drugs against them that are really important.

And so, I think that those kinds of developments have accelerated where we are in cancer research and bring us closer. I would be wrong to say though, that cancer is going to be cured completely in five to seven to 10 years. I think it will happen. I just think its going to take a little bit of time, given the complexity of cancer itself.

And once we finally do cure cancer, then were going to be looking at viral diseases, which will continue to be a problem, because they can mutate and change. And were seeing that with the Wuhan coronavirus right now in terms of what can happen when viruses change. I just say that to emphasize how important virology is to the Hutch as well. We have a very large group thats working on various different, not only HIV, but other types of viruses as well.

TB: There was just a new story today about an HIV vaccine trial that the Hutch and the Gates Foundation were coordinating on that was halted because it had been shown to be ineffective. I know youre on day one on the job, literally, but to what extent can you address that and are there any lessons to be learned from it?

Dr. Lynch: Thats an important point, is number one, you have to remember that the Hutch is one of the major centers for HIV research in the world. And weve been committed to looking for HIV vaccines. Now what we know about HIV is that HIV is a disease where we have medications, antiretroviral medications that can certainly control the disease. Okay? But we havent been able to show that we can cure the disease in the way that would allow someone whos got HIV to be able to take medicine and then not need to take something else or to prevent it from happening.

So right now, youre still looking at a lifetime of medication for many, many patients. The vast majority of patients who are HIV positive have to stay on medication for quite some time. It would be terrific to come up with vaccine strategies that could prevent it.

And so, I think that one of the things that we tried was the HIV vaccine that was developed between the Gates Foundation and the Hutch. It did not meet its endpoint in the trial this morning. It doesnt mean that we dont keep trying. It doesnt mean we cant learn from that study as well. And it doesnt mean that were not going to be remain incredibly focused with that same urgency to bring to HIV that we would bring to cancer itself.

So there will be stumbles. Not every approach is going to work, and in the field of cancer there are many, many approaches that dont work. It doesnt mean you dont try things, but you want to learn as much as you can, even from the studies that dont work. Sometimes you learn the key things that lead the next study to be successful.

TB: Tying a couple things together, Dr. Gilliland, when he made that comment about curing cancer or finding therapies within 10 years, one criticism was that the funding of all forms would be attracted to that kind of statement and people felt that he might be overstating it. I guess a couple of different things here. How do you balance the need to be optimistic and pragmatic to make sure that youre speaking the truth, and yet, also encouraging donors and finding different forms of funding?

Dr. Lynch: In this, I come back to my roots as a physician. When I had a large practice at Mass General Hospital back in Boston, I took care of a lot of patients, thousands of patients with non-small cell lung cancer. And there might be a development about cancer thered be described in the media as being a breakthrough. And I would know that it probably was never going to make a difference for my patients. And I know the rollercoaster that people who are on, that people who are listening to this podcast whove recently been diagnosed with cancer, who are looking for nuggets and colonels that might be able to help them in their fight against their disease.

I think its important that we are as factual and clear as we can be. It doesnt mean though that we shouldnt be optimistic that we might find things. And I think Gary was absolutely right in saying hes optimistic. Were going to find ways to cure some cancers by 2025. And I feel the same way about 2025 and 2030, that were going to try to find ways to cure more and more cancers at that point. And thats going to be important for us to get there.

I do think that as long as cancer remains such a major public health threat, there will still be a lot of people who want to get behind the funding, both from a philanthropy standpoint, want to be able to give money to the Hutch. I think philanthropy for all cancer centers around the entire country is crucial. And just look at something like Obliteride, which is our big bike ride. You dont have to be somebody whos giving an entire building to the Hutch, although thats certainly great, but people who just ride their bike and raise money or people who do things in their community to help support cancer care and cancer research. Its incredibly important in the way we approach this disease.

And I think you just have to be balanced in how you describe it. One of the things that I think allows me to stay balanced as I think about the perspective of my patients and how they would react to a press report based on a paper in Nature that was done using a lung cancer model in mice. And I know that my patients would come in, theyd bring the paper to me just in case I didnt see it, and Id have six copies of it in my office the next day. You know, Dr. Lynch, have you seen this? What does it mean for me? And it just, the frustrating thing is its years before the finding in mice translates necessarily into outcomes for patients.

TB: Speaking of newspapers, a story in the Boston Globe was pivotal in one of your discoveries. Am I right?

Dr. Lynch: Youre absolutely right. And I think from your perspective, as someone in the science and technology media, you should feel very good that your profession led to this discovery. So this is an interesting story. I was a somewhat younger physician at the MGH at the time. It was back in 2003, 2002, and I was contacted by people who worked at the Mass General Hospital and public affairs. And they called me up and they said, Tom, they said, the holidays are coming up. The Boston Globe always likes to write motivating stories about the holidays and about peoples challenges with health. Do you have any patients whove had great examples of great outcomes? And I had this one patient and her name was Kate Robbins, and she had a fabulous response to this experimental drug that we were using in a clinical trial.

And I told the story to the Globe. They went out and they took her picture. She was on the front page of the paper. And to show you how serendipity can happen, that morning when the paper came out, there was a scientist named Daniel Haber who was in Chestnut Hill, Mass., eating cereal that morning. And he was having his breakfast, and thats back when there was a paper. Everything wasnt always on a website, but he actually opened up the paper, read her story, and he had the Eureka moment. Called me up and said, Tom, I am pretty certain your patient has a mutation in the tyrosine kinase domain of her EGFR gene. And Dan was 100% right, and that led to development of new therapies for patients with lung cancer.

TB: And this was the genetic mutation that I was referring to earlier.

Dr. Lynch: And thats the genetic mutation you were referring to earlier. Exactly.

TB: Right, and so, isnt it amazing how this was something you could have talked about, but instead he read it in the paper about one of your patients.

Dr. Lynch: He read about it in the paper. Yeah.

TB: Thats great. Any bigger lessons from that, other than talk to the press?

Dr. Lynch: Exactly.

TB: Thats great.What else should people know about you personally that I havent dug up in five-year-old YouTube videos or bios of yourself?

Dr. Lynch: So Im a very enthusiastic person in terms of thinking about what the future can bring in terms of cancer research. I am passionate about sports. I like to run and bike and play tennis. I love to follow sports teams, which is why Im delighted to be coming to Seattle. Im going to hope to make it to the first Seattle Dragons game this weekend, because I like watching sports, like playing sports. And I love Bruce Springsteen.

TB: Well, of course you love Bruce Springsteen.

Dr. Lynch: Of course I do. Im from Jersey. I mean, come on.

TB: Now wait, I got to ask you, maybe the toughest question that you might answer. Are you a Patriots fan?

Dr. Lynch: Okay. So, I do like the Patriots. Okay? And so, I had to think about this. When I get asked this in Seattle, how do I answer this question? So to say Im not a Patriots fan would be a huge problem for me. It would be denying a important part of who I am, and I love Tom Brady. But what do we have in common? Seattle has a fantastic quarterback in Russell Wilson. Everybody loves Russell Wilson. And Pete Carroll was the coach of both the Seahawks and the Patriots.

TB: There you go. So, okay. I think youre stretching there, but I will say, youre totally safe with the Celtics at this point, because theres no competitor.

Dr. Lynch: There will be. We got to get the Sonics back. Okay?

TB: Yes.

Dr. Lynch: Its really important to get the Seattle Supersonics back to Seattle.

TB: I think youll find a lot of people agreeing with that point and perhaps not the prior.

Dr. Lynch: Not the prior. OK.

TB: Whats the biggest challenge that youre going to face in this new role at Fred Hutch?

Dr. Lynch: So I think the biggest challenge that we look at is how can we create teams across diseases and centers that work really well together. Okay? Because I think to be able to cure cancer, its not going to happen just with two doctors in a room together, or two scientists in a room together, or two data people in a room together. Its going to come from six to eight people, with all those different backgrounds working together. And creating high quality, high functioning teams is going to be a big part of what we need to do here at the Hutch, and I would say across cancer research in America today.

Read more:
Interview: New Fred Hutch president on the fight against cancer, and the tech industrys central role - GeekWire

Recommendation and review posted by Bethany Smith

Some of the first biological evidence of the incongruence transgender individuals experience, because their brain indicates they are one sex and their body another, may have been found in estrogen receptor pathways in the brain of 30 transgender individuals.

Twenty-one variants in 19 genes have been found in estrogen signaling pathways of the brain critical to establishing whether the brain is masculine or feminine, saysDr. J. Graham Theisen, obstetrician/gynecologist and National Institutes of Health Womens Reproductive Health Research Scholar at theMedical College of GeorgiaatAugusta University.

Basically and perhaps counterintuitively these genes are primarily involved in estrogens critical sprinkling of the brain right before or after birth, which is essential to masculinization of the brain.

Variants investigators identified may mean that in natal males (people whose birth sex is male) this critical estrogen exposure doesnt happen or the pathway is altered so the brain does not get masculinized. In natal females, it may mean that estrogen exposure happens when it normally wouldnt, leading to masculinization.

Both could result in an incongruence between a persons internal gender and their external sex. The negative emotional experience associated with this incongruence is called gender dysphoria.

They are experiencing dysphoria because the gender they feel on the inside does not match their external sex, Theisen says. Once someone has a male or female brain, they have it and you are not going to change it. The goal of treatments like hormone therapy and surgery is to help their body more closely match where their brain already is.

It doesnt matter which sex organs you have, its whether estrogen, or androgen, which is converted to estrogen in the brain, masculinizes the brain during this critical period, saysDr. Lawrence C. Layman, chief of the MCG Section of Reproductive Endocrinology, Infertility and Genetics in theDepartment of Obstetrics and Gynecology. We have found variants in genes that are important in some of these different areas of the brain.

These brain pathways are involved in regions of the brain where the number of neurons and how connected the neurons are typically differ between males and females.

They note that while this critical period for masculinizing the brain may seem late, brain development actually continues well after birth and these key pathways and receptors already need to be established when estrogen arrives.

While its too early to definitively say the gene variants in these pathways result in the brain-body incongruence called gender dysphoria, it is interesting that they are in pathways of hormone involvement in the brain and whether it gets exposed to estrogen or not, says Layman.

He and Theisen are co-corresponding authors of the study in the journalScientific Reports.

This is the first study to lay out this framework of sex-specific development as a means to better understand gender identity, Theisen says. We are saying that looking into these pathways is the approach we are going to be taking in the years ahead to explore the genetic contribution to gender dysphoria in humans.

In fact, they already are exploring the pathways further and in a larger number of transgender individuals.

For this study, they looked at the DNA of 13 transgender males, individuals born female and transitioning

to male, and 17 transgender females, born male and transitioning to female. The extensive whole exome analysis, which sequences all the protein-coding regions of a gene (protein expression determines gene and cell function) was performed at the Yale Center for Genome Analysis. The analysis was confirmed by Sanger sequencing, another method used for detecting gene variants.

The variants they found were not present in a group of 88 control exome studies in nontransgender individuals also done at Yale. They also were rare or absent in large control DNA databases.

Reproductive endocrinologist/geneticist Layman says his experience with taking care of transgender patients for about 20 years, made him think there was a biological basis. We certainly think that for the majority of people who are experiencing gender dysphoria there is a biologic component, says Theisen. We want to understand what the genetic component of gender identity is.

While genetics have been suggested as a factor in gender dysphoria, proposed candidate genes to date have not been verified, the investigators say. Most gene or gene variants previously explored have been associated with receptors for androgens, hormones more traditionally thought to play a role in male traits but, like estrogen in males, also are present in females.

MCG investigators and their colleagues decided instead to take what little is known about sex-specific brain development that estrogen bath needed in early life to ensure masculinization of the brain to hone in on potential sites for relevant genetic variances. Extensive DNA testing initially revealed more than 120,000 variants, 21 of which were associated with these estrogen-associated pathways in the brain.

Animal studies have helped identify four areas of the brain with pathways leading to development of a male or female brain, and the investigators focused on those likely also present in humans. Laboratory studies have indicated that disrupting these brain pathways in males and females during this critical period results in cross sex behavior, like female rodents mounting and thrusting and males taking on a more traditional female posture when mating. These cross sex behaviors, which also have been documented in non-human primates, emerge during the natural sex hormone surge of puberty.

While sex specific brain development has not been thoroughly evaluated in humans, as with animals, the effects typically play out most at the time of puberty, a time when sex hormones naturally surge, when the general awareness of our sexuality really begins to awaken and when the complex state of gender dysphoria may become easier for adolescents to articulate, the investigators say. Layman notes that many individuals will report experiencing gender incongruent feelings as early as age 5.

Theisen notes that we all are full of genetic variants, including ones that give us blue eyes versus brown or green, and the majority do not cause disease rather help make us individuals. I think gender is as unique and as varied as every other trait that we have, Theisen says.

The investigators suggest modification of the current system for classifying variants that would not imply that a variant means pathogenic, or disease causing.

Last year, the World Health Organization said that genderincongruenceis not a mental health disorder and six years before thatThe Diagnostic and Statistical Manual of Mental Disorders, replaced gender identity disorder with general dysphoria.

About 0.5 to 1.4% of individuals born male and 0.2 to 0.3 % of individuals born female meet criteria for gender dysphoria. Identical twins are more likely than fraternal twins to both report gender dysphoria.

Gender affirming therapies, like hormone therapies and surgeries along with mental health evaluation and support, help these individuals better align their bodies and brains, the physician-scientists say.

Transgender individuals experience increased rates of discrimination, sexual violence and are at increased risk of depression, substance abuse and attempted suicide. About 26% report use of alcohol or other drugs to help cope; 19% have been denied medical care by a physician or other provider, some report verbal harassment in a medical environment and insurance companies do not consistently cover the cost of gender affirming hormone or surgical therapies.

A problem, the investigators say, is an overall lack of understanding of the biologic basis of gender dysphoria.

While their study of 30 individuals they now have data on more than 30 others appears to be the largest to date, the sample size prompted them to classify the published findings as preliminary.

Reference: Theisen et al. (2019).The Use of Whole Exome Sequencing in a Cohort of Transgender Individuals to Identify Rare Genetic Variants. Scientific Reports.DOI: https://doi.org/10.1038/s41598-019-53500-y.

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

View post:
Genetic Variants Linked to Disparity Between a Persons Internal Gender and Their External Sex - Technology Networks

Recommendation and review posted by Bethany Smith

Adapted from the cover of Human Diversity(Twelve)Human Diversity: The Biology of Gender, Race, and Class, by Charles Murray (Twelve, 528 pp., $35)

The dumb kids at Middlebury College had no idea what they were setting in motion when they stopped Charles Murray from speaking. At an instantly infamous 2017 lecture, students shouted down his speech, waited through a livestreamed discussion between him and a faculty member given from a private location, and swarmed him after the event, injuring the faculty member.

Murray, you see, had been thinking about swimming back toward the fraught waters he and the late Richard Herrnstein had explored in 1994s The Bell Curve notions that traits such as intelligence are hugely important in determining who gets ahead in modern societies, and that gaps on those traits among social groups, including racial groups, could be partly genetic in origin. His wife had been telling him not to.

Confound it! he recalls her saying after the Middlebury affair (. . . or two syllables to that effect). If theyre going to do this kind of thing anyway, go ahead and write it. And now, three years later, we have Human Diversity: The Biology of Gender, Race, and Class.

This isnt an intemperate screed meant to trigger oversensitive 19-year-olds, however. Instead, its a patient and generally cautious explanation of where the science stands in the three highly contentious areas mentioned in the subtitle: the biological underpinnings of sex differences, social-class differences, and racial differences.

Those whove been following developments in these areas will find little thats surprising. But those new to the topics will learn a lot, so long as they understand basic statistical concepts well enough to follow Murrays often-a-bit-technical prose. Murray provides some of his own entry-level instruction, but its a little scattershot in terms of what concepts get an explanation in the text, which definitions are relegated to an appendix, and what terms the reader is simply expected to know.

Murray begins with sex differences because theyre the most obvious and hard to deny, so Ill do the same. Men and women have measurably different abilities, preferences, and behaviors; many of those differences do not seem to be shrinking in societies that strive for gender egalitarianism; and new research is establishing some connections between the sexes behaviors and their brains.

Theres a long list of sex differences that researchers have found repeatedly, and they go well beyond physical size. Men are more likely to have autism, women depression. Women are more concerned with the well-being of others; men are more assertive. Men have stronger visuospatial skills, women better verbal ability. Men tend to have higher variation in ability; for example, the sexes have the same average IQ, but men are overrepresented among people with very high or very low IQs. Men and women also have markedly different interests, especially in that men are more likely to prefer working with things, women with people.

These gaps are no doubt at least partly due to socialization and culture, but at least some almost certainly have a biological component. One way of seeing this is to look at what happens when societies adopt stronger norms in favor of gender equity: Do the gaps shrink, as would be expected if socially enforced gender norms caused the gaps to begin with?

Sometimes, sometimes not. Murray goes through a long list of different trends. Male overrepresentation among high scorers on the math portion of the SAT, for example, has shrunk steadily for decades. Womens movement into jobs that involve working with things rather than people, though, happened speedily in the 1970s and 1980s and stopped thereafter, with women still underrepresented in things jobs. (This Murray shows through a fascinating original analysis of federal job classifications and survey data.) Meanwhile, the most gender-egalitarian countries actually have bigger gaps in certain outcomes, such as the share of women who score highly in STEM (science, tech, engineering, and math) tests but choose not to go into those fields. Some theorize that living in an advanced country allows talented women to do what they want rather than what pays most. Another important fact is that women who score highly in STEM tend to have better language skills, and thus more non-STEM job options, than do men who score highly in STEM.

Theres also a growing body of research that looks directly at the effects of male and female hormones and differences in the brains of men and women. Changes in hormone levels tend to exaggerate or reduce sex differences in exactly the direction youd expect people injected with testosterone become more impulsive; prenatal exposure to testosterone predicts a childs future visuospatial ability, autism risk, empathy, and interest in children. As for brains, women have stronger functional connectivity in regions involved in emotion processing and social cognition, and there are sex differences in the sizes of numerous brain regions as well.

Murrays discussion of class differences, meanwhile, relies heavily on a much older body of evidence: the research of behavioral genetics, especially twin studies. Over a period of decades this work has shown that genes are incredibly powerful, though hardly all-powerful, in shaping how a person turns out within a given society whether its his personality, health, intelligence, or education while the shared environment, which is to say the effect of being raised in the same home (with the same income, neighborhood, parenting philosophy, etc.), is generally weak. Newer methods, involving the DNA sequencing of thousands of subjects, actually pinpoint some of the specific genes that affect important traits, and these methods can even be used to generate a polygenic score that predicts from DNA (very imprecisely, but far better than chance) how strongly a person will exhibit a trait.

The clear role of genes in life outcomes, coupled with a weak role for the home environment, implies that social class is not just a matter of privilege and oppression and public policy, and not just a matter of personal responsibility and effort, but also heavily a function of natural abilities. This is not exactly a shocking conclusion, though it does challenge some of the more extreme narratives put forth by both Left and Right.

One criticism Ill make of Murray here, though, is that in noting the limits of public policy he could have dealt more thoroughly with various strains of research showing that environments do matter, sometimes a lot, including Raj Chettys work on how neighborhoods affect social mobility and Susan Dynarskis recent study showing that something as simple as promising financial aid up front, rather than later in the process, can make poor kids much more likely to go to a top-tier college. Educational attainment, by the way, is an important trait that is affected by the shared environment quite a bit: 25 percent in a table presented here, though its also 50 percent genetic.

Lastly, theres race the topic that attracted nearly all of the controversy associated with The Bell Curve despite taking up only a minority of its pages. Interestingly, Murray is more circumspect now than he was in that tome a quarter century ago, when he and Herrnstein wrote that it was highly likely that part of the gap between blacks and whites IQ scores was genetic. Here he is more interested in debunking the notion that race is nothing more than a social construct that has nothing to do with genes at all.

Even on that front hes pretty timid. Indeed, he begins by agreeing to dispense with the word race when talking about genetics, because the word carries so much baggage and the professional geneticists have mostly abandoned it. Instead he goes with population, while noting that the ancestral populations that geneticists distinguish from one another overlap heavily with commonly used racial categories.

Yes, these groups can be identified using nothing but DNA, and yes, there are some important genetic differences among populations: Some less controversial ones affect skin color, malaria resistance, and adaptations for living at high altitudes. In other words, humans have continued to evolve in lots of ways since they spread out across the globe, and different changes have taken hold in different environments. But what about hot-button psychological characteristics such as intelligence?

Youd think wed be getting close to answering that question by now. Recall that weve actually identified a lot of genes that affect these traits, and even developed scoring systems that roughly predict from someones DNA how hell turn out. One imagines you could just apply these techniques to the average DNA profile of each racial group excuse me, population and get a simple answer, albeit a tentative one that would become more precise as methods improved and additional influential genes were discovered.

But its not that easy. For a variety of technical reasons, you cant apply a single scoring system across multiple populations, at least with current methods. Murray notes that the genetic variants weve singled out as playing a role in assorted traits often show up more frequently in some populations than others a point he makes more painstakingly than he probably needs to, with a series of scatterplots and tabulations but he admits these gaps are only grist for future, more sophisticated research. His bottom line is not much different from the point made by the prominent Harvard geneticist David Reich in a 2018 New York Times piece: Human populations differ at the genetic level, and we have to prepare for the possibility that these genetic differences substantively affect traits wed rather they didnt, but we dont know the specifics yet.

In 1994, Herrnstein and Murray lit the world on fire with a book that made highly controversial claims about IQ, class, and race. Human Diversitys publicists no doubt hope for a repeat performance; I had to sign a nondisclosure agreement to see the text before the release date. But the result is actually, as Murray himself promises early on, pretty boring for those already familiar with the topics it covers. What it is, is an excellent primer for the uninitiated at least for a few years, by which point new science will likely have superseded much of the research discussed here.

Hopefully the Middlebury kids and their ilk will bother to read it before denouncing it.

This article appears as The Power of Genes in the February 24, 2020, print edition of National Review.

If you enjoyed this article, we have a proposition for you: Join NRPLUS. Members getallof our content (including the magazine), no paywalls or content meters, an advertising-minimal experience, and unique access to our writers and editors (conference calls, social-media groups, etc.). And importantly, NRPLUS members help keep NR going. Consider it?

If you enjoyed this article, and were stimulated by its contents, we have a proposition for you: Join NRPLUS.

The rest is here:
'Human Diversity: The Biology of Gender, Race, and Class' Book Review - National Review

Recommendation and review posted by Bethany Smith

Following is a transcript of the video.

Graham Flanagan: Look at that beautiful bald man. He's oozing swagger and confidence. He owns it. But it wasn't always like this. This is Rob. He's 33. This is also Rob. He started to lose his hair when he was about 20. So, what happened? Why did Rob go bald, and what does it mean? There's something about being bald and owning it. I mean, look at all these bald icons. Michael Jordan, Jason Statham, his sidekick, The Rock. But losing your hair is not something you aspire to.

Commercial: If you're concerned about your thinning hair, call Hair Club for Men and receive our free brochure.

Flanagan: In fact, there's an entire industry built around fighting it.

Man: And remember: I'm not only the Hair Club president, but I'm also a client.

Flanagan: I asked a dermatologist about why some men lose their hair and if going bald is my destiny as well.

Jennifer Chwalek: So, when we say "baldness," we're usually referring to male-pattern baldness, or androgenetic alopecia. The hair follicle is slowly, over time, becoming smaller and smaller, to the point when it stops producing a full hair. Testosterone is becoming converted to dihydrotestosterone in the hair follicle by an enzyme called 5-alpha-reductase, and when it attaches to the androgen receptor in the hair follicle, it causes the follicle to produce a smaller hair.

Flanagan: So, I want to show you my friend Rob here. Rob started losing his hair in his early 20s, and, as you can see, there's little to...well, there's none left. So what is going on with Rob?

Chwalek: Well, Rob has what we call androgenetic alopecia, or male-pattern baldness. This is due to several genes. And some of the genes are early expressing, and some susceptible individuals, they start to lose their hair very young, usually by age 30.

Flanagan: The fact that Rob is bald, does that make him any less virile?

Chwalek: No. So, it's a myth that hair loss or balding is associated with virility in men. Men who go bald don't have abnormal levels of testosterone. It's really that the hair follicle becomes sensitized to the effects of testosterone or androgens, and it starts to create a smaller hair, and eventually it stops producing hair.

Flanagan: So, what role do genetics play, and is it true that baldness is inherited from your mom's side?

Chwalek: The genetics of male-pattern thinning and baldness is complicated. We know that the androgen receptor gene is on the X chromosome, which is inherited from your maternal side, typically. So, there are some studies showing that having a brother who expresses male-pattern baldness might be more predictive than if your father has male-pattern thinning.

Flanagan: Let's talk about me.

Chwalek: Mm-hmm.

Flanagan: I'm 37. I've still got some hair.

Chwalek: Yeah.

Flanagan: But can you tell me what's going on? Am I gonna go bald?

Chwalek: Well, do you have a family history of any thinning?

Flanagan: Yes, I do, on my dad's side. My dad, pretty much bald, his brother is bald. I have a brother who has a very thick head of hair.

Chwalek: Do you think your hair has been thinning?

Flanagan: I think it might be, like, in the front a little bit. I don't really know what's going up top there.

Chwalek: Yeah, maybe a little.

Flanagan: Really?

Chwalek: Maybe a little. So, androgenetic alopecia is actually not an uncommon trait. About 40% of the population has some degree of thinning, usually between the ages of, like, 20 to 40.

Flanagan: My wife, Janet, she really likes my blond hair, and if it were to go, that could be a problem. So, how long do you think I've got to keep some semblance of this?

Chwalek: I think you probably have a while to go. I think you're gonna be OK. The men who tend to go bald-bald tend to do so by age 30, usually.

Flanagan: Based on what you see, my age, what I've described about my family, you don't expect my hair to just fall out in the next, like, five years?

Chwalek: No, it would be unusual, but you may notice, you know, as you get a little bit older, it may continue to thin slightly.

Flanagan: OK, that's a relief. Fantastic. That's great!

Excerpt from:
The reason some men go bald, according to a dermatologist - Business Insider - Business Insider

Recommendation and review posted by Bethany Smith

Following is a transcript of this movie.

Graham Flanagan: Look at this gorgeous bald guy. He has oozing swagger and confidence. He possesses it. Nevertheless, it was not always like this. That is Rob. He is 33. This can also be Rob. He began to lose his hair when he was going 20. So, what happened? Why did Rob go hairless, and what exactly does it mean? There is something about being owning it. I mean, look at these bald icons. Michael Jordan, Jason Statham, his sidekick, The Rock. However losing your hair isnt something you aspire to.

Commercial: In case you are worried about your thinning hair, telephone Hair Club for Men and get our free brochure.

Flanagan: In actuality, there is an whole industry built around battling it.

Person: And remember: I am not the Hair Club president, however I am also a customer.

Flanagan: I requested a dermatologist about why some men lose their hair and when moving bald is my fate too.

Jennifer Chwalek: Therefore, once we sayhair thinning, we are generally referring to male-pattern baldness, or androgenetic alopecia. The hair follicle is gradually, with time, getting smaller and smaller, to this stage when it ceases producing a complete hair. Testosterone has turned into to dihydrotestosterone in the hair follicle via an enzyme known as 5-alpha-reductase, and once it attaches to the androgen receptor from the hair follicle, it causes the follicle to create a more compact hair.

Flanagan: Therefore, I wish to reveal my buddy Rob here. Rob began losing his hair in his ancient 20s, and, as you may see, there is little . . .well, there is none left. So whats happening with Rob?

Chwalek: Well, Rob has that which we call androgenetic alopecia, or male-pattern hair loss. This can be due to many genes. And a few of the genes have been ancient expressing, and a few vulnerable people, they begin to lose their own hair really young, typically by era 30.

Flanagan: The very fact that Rob is hairless, does this make him less virile?

Chwalek: No. Thus, it is a fantasy that hair balding or loss is connected with virility in men. Men who go bald do not have abnormal levels of testosterone. It is really the hair follicle becomes more sensitized to the effects of testosterone or androgens, and it begins to make a more compact hair, and finally it stops generating hair.

Flanagan: So, what part do genetics play, and can it be accurate that hair loss is inherited from the mothers side?

Chwalek: The genetics of male-pattern thinning and hair loss is complex. We are aware that the androgen receptor gene is on the X chromosome, which is inherited from the maternal side, generally. So, there are a number of studies showing that with a brother that expresses male-pattern baldness may be more predictive than if your dad has male-pattern thinning.

Flanagan: Lets talk about me.

Chwalek: Mm-hmm.

Flanagan: I am 37. I have still got a few hair.

Chwalek: Yeah.

Flanagan: But can you tell me what is happening? Am I gonna go bald?

Chwalek: Well, have you got a family history of any thinning?

Flanagan: Yes, I really do, in my fathers side. My father, pretty much bald, and his brother is hairless. Ive a brother with quite a thick head of hair.

Chwalek: Can you believe that your hair was thinning?

Flanagan: I think that it could be, for example, at front just a little bit. I do not know what is going up .

Chwalek: Yeah, perhaps just a bit.

Flanagan: Really?

Chwalek: Perhaps a bit. Thus, androgenetic alopecia is really not an unusual trait. Approximately 40percent of the populace has some level of thinning, normally between the ages of, for example, 20 to 40.

Flanagan: My wife, Janet, she actually likes my blonde hair, and if it were to proceed, that might be an issue. So, how long do you believe I have to maintain some semblance of the?

Chwalek: I believe you most likely have some time to go. I believe you are gont be OK. The guys who are inclined to go bald-bald often do this by era 30, generally.

Flanagan: According to what you see, my era, what I have described about my loved ones, you do not expect my hair to simply fall out at another, for example, five decades?

Chwalek: It would be odd, but you could notice, you understand, as you get a little bit old, it might continue to lean slightly.

Flanagan: OK, that is a relief. Excellent. That is fantastic!

See original here:
The reason some guys go hairless, as reported by a dermatologist - BingePost

Recommendation and review posted by Bethany Smith

If you look up the word "chin" in the encyclopedia, you will read about Kirk Douglas. This isn't an exaggeration or a figure of speech: Douglas is literally named as an example of someone with a chin in the Oxford University Press entry for the mandibular arch.

It makes sense: there have been few chins in human history as noteworthy as Douglas'. When the actor died at the extraordinary age of 103 on Wednesday, obituaries seemed to mourn the loss of his dimple as much as his talent. "That famously dimpled chin, which you'd never believe on a statue, nonetheless gave the Hollywood icon a granite jaw that served him well as a leading man for more than 60 years," wrote Vanity Fair. "When you hear his name, so crisp and ramrod strong (Kirk!), you think, at first, of how he looked: the jutting chin with a dimple that made it unlike all other jutting chins," gushed Variety. The Los Angeles Times chose to describe the actor as a "dimple-chinned screen icon who was known for bringing an explosive, clenched-jawed intensity to a memorable array of heroes and heels."

Embed from Getty Images

Of course chins, being at the lower center of our faces, have an outsized effect on perceived attractiveness, for better or worse. Curiously, humans are actually the only animal that have jutting lower jaws; "even chimpanzees and gorillas, our closest genetic cousins, lack chins," writes The Smithsonian, noting that the great apes' jaws slope down and back from their teeth instead of protruding forward. While researchers aren't sure why exactly humans have chins in the first place even Neanderthals didn't have them one hypothesis is that they were possibly a sexually selective feature that factored unconsciously into our choice of mates. These days, though, it's not so unconscious: Vulture has ranked Batmans by their chins, and BuzzFeed once ran a list of the Most Important Jawlines of 2014.

Despite being best known for portraying a rakish Spartacus in Stanley Kubrick's 1960 epic of the same name, Douglas' bullseye on his jaw wouldn't have been considered attractive 2,000-odd years ago. "In images whose beauties were of a lofty cast, the Greek artists never allowed a dimple to break the uniformity of the chin's surface," claimed Johann Joachim Winckelmann in The History of Ancient Art Among the Greeks in 1764, adding that "when, in drawings made from them, the lower part of [the chin] seems, as it were, to be pinched in ... it may justly be suspected that some modern ignorant hand has been attempting to improve upon them." In other words, dimples like Douglas', while left up to the mercy of genetics, have come and gone in popularity; the screen actor just happened to be born at the right time for his maximalist jawline to be in fashion.

Story continues

Even by the standards of the time, though, when masculine icons from Batman to Clark Gable boasted clefts, Douglas was an extreme. "When I made my first picture [The Strange Love of Martha Ivers in 1946] with Barbara Stanwyck, the director wanted me to fill it in and I said 'listen, this is what you get.' I didn't cave," Douglas told The Telegraph in 2016. It was a decision that would have a lasting impact; as Douglas began to collect more on-screen roles, directors and agents realized they could use his dimple to their advantage, alternating between emphasizing it as a trait of a classical (if anachronistic) hero, or to accentuate the look of a tougher sort, like his character in Champion. As the Financial Times put it, regardless of if he was playing a good guy or a bad guy, "the Kirk jaw was made for clenching."

Embed from Getty Images

It was also made for exaggerating. Artists leaned into depicting Douglas' distinctive jaw, but the actor never minded; in addition to the customary hand and foot prints outside the TCL Chinese Theater in Hollywood, he jokingly left behind an imprint of his chin as well. The body part was also a favorite topic of conversation in interviews: "It's not really a dimple, it's a hole in the chin," a bearded Douglas once told Dick Cavett, who quipped in response, "well I know if we could see it, it'd be the most cleavage we've had on the show in a long time." Seemingly everyone had questions about how he navigated shaving the thing. Later, when Douglas' grandson, Dylan, was born in 2000, The New York Post announced "NEWBORN HAS THE DOUGLAS DIMPLE" with the same drama as Rafiki holding up Simba to the savannah. Subsequent male actors with head-turning chins rode on the coattails of his success, from John Travolta to Simon Cowell. Nevertheless, on the occasion of Douglas' 100th birthday in 2016, The New Yorker declared that "the cleft in the Douglas chin is, with the exception of the Grand Canyon, the most popular natural rift in America."

Embed from Getty Images

But physical trends come and go; just as Douglas' passing marks the loss of one of the last remaining legends of the Golden Age of Hollywood, so too do we lose one of the great chins of history. These days, plastic surgery websites advertise procedures to smooth out one's jawline: "Although chins with a dimple were once more popular, these have largely gone out of fashion, and some patients have preferred to have their dimple reduced, often with the use of fillers," cosmetic surgeon Dr. Julian De Silva told The Daily Mail in 2017.

Douglas, though, was nothing if not a titan of the industry, and he didn't make over 90 movies, many of them masterpieces of classic Hollywood cinema, by relying on his facial structure alone. To quote Angelo Dundee, a boxing instructor who coached Muhammad Ali, "You can't train a chin." The mandible, just like stardom, is elusive, innate, impossible to capture with words. You either have it or you don't.

More stories from theweek.comFox News warns Fox News about spreading pro-Trump 'disinformation' on UkraineTrump's wall-building now involves blowing up mountains in Organ Pipe Cactus National MonumentThe real State of the Union

Read more from the original source:
Kirk Douglas was the best thing to ever happen to chins - Yahoo News

Recommendation and review posted by Bethany Smith

Olive Fertility Centre in Vancouver has seen an exponential increase in the number of women coming into the clinic interested in social egg freezing. According to fertility expert and Olive co-director, Dr. Niamh Tallon, We are seeing more women in their early to mid-thirties who are not yet in a position to have a family, because of finances, career, or most often they just havent found the right partner, deciding to take control of their fertility by freezing their eggs.

Dr Tallon will be giving a free information talk on egg freezing at Olive Fertility Centre on Feb 26th for women who want to find out more about the process.

While egg freezing has been around for several years, the use of a technology called vitrification, which involves flash freezing the eggs, has significantly increased the odds of pregnancy for women using frozen eggs. With vitrification, the eggs are frozen so quickly that damaging ice crystals dont get a chance to form.

This makes them much more likely to survive thawing later.

We continue to see excellent results with high egg survival rates and pregnancy rates mirroring what is expected for the age of the egg. says Dr. Tallon.

The egg freezing process is the same as traditional IVF. It involves a woman injecting medications that stimulate egg growth to the point they can be harvested. However, instead of fertilizing the eggs with sperm, the eggs are frozen unfertilized and stored until a woman is ready to conceive sometime in the future. At that point, the eggs are thawed and fertilized to hopefully result in viable embryos that can then be transferred into the uterus.

According to the latest Statistics Canada report in 2016, more babies were born to Canadian women over the age of 35 than women in their early 20s. Deferring starting a family until later in life comes with the increased risk of infertility. A 2012 study shows that infertility rates in Canada have almost doubled in the last two decades due, in part, to the fact that on average women are starting their families later in life.

Fertility in women is directly associated with the age of a womans eggs. Not only does the quantity of eggs decline as a woman ages, but the genetic quality declines as well. Poor egg quality leads to a longer time to achieving a pregnancy, infertility, more frequent miscarriages, and a greater risk of chromosomal disorders in the offspring. Egg freezing halts that ongoing genetic decline in quality associated with the biological clock. In addition, a woman who freezes her eggs at a younger age tends to have more eggs than if she froze them later in life.

However, many women still underestimate the effects of age on fertility. A survey conducted by UBCs counselling psychology department found that many women believe that overall health and fitness levels are better indicators of fertility than age.

The fact is that, despite how fit you are or how young you look, 40 is not the new 30 when it comes to our fertility. Our eggs are exactly as old as we are, says Dr Tallon.

The egg freezing process allows women to safeguard some of their best eggs for potential future use. Most women express feeling empowered and, even though pregnancy is not a guarantee, they understand this is the best outcome they could expect using this technology. At least it offers an opportunity to act today. Egg freezing is one of many options for someone wanting or needing to defer pregnancy to a later time.

While a few American companies like Google, Facebook, and Amazon cover egg freezing in their medical plans, social egg freezing is not covered by government health plans in Canada. The cost for an egg freezing cycle is approximately $7,000 for an egg freezing cycle, plus the cost of drugs, which can range from $3,000 to $5,000. The entire procedure, including hormone injections, takes about three weeks.

Lets Talk Egg Freezing

Feb 26th, 6:30 to 8:00 pm

OLIVE FERTILITY CENTRE / 4thFloor

400 East Tower, 555 West 12th Avenue.

Spaces are limited. To register, go to http://www.olivefertility.com/egg-freezing-social or e-mail info@olivefertility.com.

Olive Fertility Centre is one of Canadas largest fertility clinics, offering an advanced IVF lab, personal care teams and innovative programs that include the PGT-A, specialized genetic testing, egg freezing, and prenatal NIPT testing.

See the original post here:
More single women choosing to freeze their eggs - The Asian Pacific Post

Recommendation and review posted by Bethany Smith

Excitement in the consumer genetic testing market continues to show signs of slowing down.

In the past two weeks layoffs have hit two of the biggest consumer genetic testing services 23andme and Ancestry with the latter announcing that it would slash its staff by 6% earlier today, in a blog post.

CNBC first reported the news.

In her blogpost announcing the layoffs, Ancestry chief executive Margo Georgiadis wrote:

over the last 18 months, we have seen a slowdown in consumer demand across the entire DNA category. The DNA market is at an inflection point now that most early adopters have entered the category. Future growth will require a continued focus on building consumer trust and innovative new offerings that deliver even greater value to people. Ancestry is well positioned to lead that innovation to inspire additional discoveries in both Family History and Health.

Today we made targeted changes to better position our business to these marketplace realities. These are difficult decisions and impact 6 percent of our workforce. Any changes that affect our people are made with the utmost care. Weve done so in service to sharpening our focus and investment on our core Family History business and the long-term opportunity with AncestryHealth.

The move from Ancestry follows job cuts at 23andMe in late January, which saw 100 staffers lose their jobs (or roughly 14% of its workforce.

The genetic testing company Illumina has been warning of softness in the direct to consumer genetic testing market, as Business Insider reported last August.

We have previously based our DTC expectations on customer forecasts, but given unanticipated market softness, we are taking an even more cautious view of the opportunity in the near-term, the companys chief executive Francis deSouza said in a second quarter earnings call.

Consumers seem to be waking up to the privacy concerns over how genetic tests can be used.

You can cancel your credit card. You cant change your DNA, Matt Mitchell, the director of digital safety and privacy for the advocacy organization Tactical Tech, told Business Insider earlier in the year.

And privacy laws in the U.S. have not caught up with the reality of how DNA testing is being used (and could potentially be abused), according to privacy experts and legal scholars.

In the US we have taken to protecting genetic information separately rather than using more general privacy laws, and most of the people whove looked at it have concluded thats a really bad idea, Mark Rothstein, a law professor at Brandeis and the director of the University of Louisvilles Institute for Bioethics, Health Policy and Law, told Wired in May.

The investigation into the Golden State Killer and the eventual arrest of Joseph James DeAngelo thanks to DNA evidence collected from an open source genealogy site called GEDMatch likely helped focus consumers thinking on the issue.

In that case a relative of DeAngelos had uploaded their information onto the site and investigators found a close match with DNA at the crime scene. That information was then correlated with other details to eventually center on DeAngelo as a suspect in the crimes.

While consumer genetic testing services may be struggling, investors still see increasing promise in clinical genetics testing, with companies like the publicly traded InVitae seeing its share price rally and the privately held company, Color, raising roughly $75 million in new capital from investors led by T. Rowe Price.

Read more:
Ancestry lays off 6% of staff as consumer genetic testing market continues to decline - TechCrunch

Recommendation and review posted by Bethany Smith

Genetic cancer testing is a whole new world for cancer survivors, newly diagnosed patients with cancer and their family members.

Barbara Tako is a breast cancer survivor (2010), melanoma survivor (2014) and author of Cancer Survivorship Coping ToolsWe'll Get You Through This. She is a cancer coping advocate, speaker and published writer for television, radio and other venues across the country. She lives, survives, and thrives in Minnesota with her husband, children and dog. See more at http://www.cancersurvivorshipcopingtools.com,or http://www.clutterclearingchoices.com.

It still rattles my cage to think that my initially diagnosed generic (not genetic) breast cancer almost ten years ago was recently determined to have been caused by the PALB2 genetic mutation found in my redone genetic tests a couple of years back. Thank goodness my oncologist urged me to test for the newly discovered genetic mutations years out from my breast cancer treatments!

With a cancer diagnosis, most of us want two things to catch it early and to have it be a common kind of cancer where everyone agrees on the best treatment. What happens when we start to learn early on what is likely to kill us? Genetic cancer testing has a psychological impact as well as possible monitoring and/or treatment consequences. What does all of that mean as a patient?

Internal Stress

It is scary to discover you are one of the "special" fish in the lake. If you have not yet had cancer, does it mean extra frequent monitoring, special tests, or even prophylactic surgery? Does knowing you have a genetic cancer mutation increase your fear and anxiety? Even removing my breasts does not make me immune to metastatic breast cancer or a lump developing in an area near where my breasts were.

Social Stress

Who are you going to tell for support? Who are you not going to tell for fear of employment or insurance consequences? Plus, how do you tell other family members who may be at risk because of your genetic findings? No one really wishes other people to have the specter of cancer looming over them too. Friends may not understand prophylactic surgery treatment choices. Family members will have to then make their own testing and treatment choices.

Personal Decisions

Decide. How much do you want to know? What will you do if something is found? What will you do if something is not found? I remind myself that each of us can only do our best at any given moment in time. We do not know the long-term impact of PALB2 yet. Data across five to ten years is not available yet for some of these more recent genetic cancer mutations. Looking regretfully back or worrying forward are pretty darn futile.

Ongoing Concern

This part is not fun, but it is necessary. Put the appointments or appointment reminders into your calendar and try to get on with living the rest of your life. That is my advice. It is easier said than done. Genetic testing is exciting, new, and preventative, and it does create ongoing stress, decisions and concerns.

It was the best of times, it was the worst of times, it was the age of wisdom, it was the age of foolishness, it was the epoch of belief, it was the epoch of incredulity, it was the season of Light, it was the season of Darkness - from A Tale of Two Cities by Charles Dickens. Does it sound like the world of genetic cancer testing today? You bet. We each may face some difficult yet hopeful choices. Hang in there and let's talk.

Original post:
The Good, The Bad, And The Unknown Of Genetic Testing - Curetoday.com

Recommendation and review posted by Bethany Smith

BETHESDA, Md., Feb. 5, 2020 /PRNewswire/ --Prenatal genetic screening is a complex and rapidly evolving field of medicine.In an effort to help promote consensus recommendations and strive for consistency among various medical societies that issue recommendations and guidelines in the area of prenatal genetic testing, six national organizations have partnered to create the Reproductive Genetics Technology Consortium. (http://rgtc.perinatalquality.org)

Member organizations include the American College of Medical Genetics and Genomics; American Society for Reproductive Medicine; International Society of Prenatal Diagnosis; National Society of Genetic Counselors; Perinatal Quality Foundation; and Society for Maternal-Fetal Medicine. Representatives from each organization will meet regularly and as needed to facilitate group discussion and/or consensus.

The new Consortium aims to facilitate communication between professional organizations in their development of practice guidelines and to provide a forum for different societies to discuss appropriate utilization of reproductive genetic testing. It will also provide a forum through which commercial laboratories or other entities developing new technologies can proactively communicate to obtain input and guidance regarding new testing and will provide consensus expert opinions about the clinical utility and application of emerging genetic tests.

"Each member of the new Consortium has a goal of optimizing the health of women and infants," said SMFM representative, Mary Norton, MD. "Bringing our organizations together will establish an opportunity for dialogue between stakeholders and provide a stronger voice on these important issues."

ACMG President Anthony R. Gregg, MD, MBA, FACOG, FACMG said, "ACMG is confident that collaborations among the RGTC member organizations will ensure patients receive high quality care as innovative genetic technologies move from the laboratory to the bedside."

To contact the Consortium, contact Jean Spitz, MPH, CAE, RDMS at jspitz@perinatalquality.org.

About the American College of Medical Genetics and Genomics (ACMG) and ACMG Foundation

Founded in 1991, the American College of Medical Genetics and Genomics (ACMG) is the only nationally recognized medical society dedicated to improving health through the clinical practice of medical genetics and genomics and the only medical specialty society in the US that represents the full spectrum of medical genetics disciplines in a single organization. The ACMG is the largest membership organization specifically for medical geneticists, providing education, resources and a voice for more than 2,400 clinical and laboratory geneticists, genetic counselors and other healthcare professionals, nearly 80% of whom are board certified in the medical genetics specialties. ACMG's mission is to improve health through the clinical and laboratory practice of medical genetics as well as through advocacy, education and clinical research, and to guide the safe and effective integration of genetics and genomics into all of medicine and healthcare, resulting in improved personal and public health. Four overarching strategies guide ACMG's work: 1) to reinforce and expand ACMG's position as the leader and prominent authority in the field of medical genetics and genomics, including clinical research, while educating the medical community on the significant role that genetics and genomics will continue to play in understanding, preventing, treating and curing disease; 2) to secure and expand the professional workforce for medical genetics and genomics; 3) to advocate for the specialty; and 4) to provide best-in-class education to members and nonmembers. Genetics in Medicine, published monthly, is the official ACMG journal. ACMG's website (www.acmg.net) offers resources including policy statements, practice guidelines, educational programs and a 'Find a Genetic Service' tool. The educational and public health programs of the ACMG are dependent upon charitable gifts from corporations, foundations and individuals through the ACMG Foundation for Genetic and Genomic Medicine.

Raye Alford, PhDralford@acmg.net

View original content to download multimedia:http://www.prnewswire.com/news-releases/leading-experts-in-genetics-and-pregnancy-announce-the-creation-of-a-new-consortium-300999484.html

SOURCE American College of Medical Genetics and Genomics

Continue reading here:
Leading Experts in Genetics and Pregnancy Announce the Creation of a New Consortium - Yahoo Finance

Recommendation and review posted by Bethany Smith

MADISON, WI Wisconsin Gov. Tony Evers signed 16 bills into law. The governor acted on the following bills:

Act 85: School Report Cards

Requires the Department of Public Instruction to include in the annual school report card the percentage of students participating in music, dance, drama, and visual arts for each high school and school district, and the statewide percentage of participation.

Act 86: Dyslexia Guide For Educators

Requires the Department of Public Instruction to establish an advisory committee to develop a guidebook related to dyslexia and related conditions for parents, guardians, teachers, and school administrators.

Act 87: Nonlethal Weapons

Allows private detectives, investigators, or private security personnel licensed to carry firearms by the Department of Safety and Professional Services to carry electric weapons while on duty to provide a nonlethal alternative.

Act 88: Medicaid Reimbursement

Ensures reimbursement for clinical consultations with a parent on behalf of a student under the age of 21 in the Medicaid program.

Act 89: Driver School Offices

Prohibits any Department of Transportation requirements for driver school offices located in residences from applying if students and the public have no access to the office.

Act 90: Medical and End-Of-Life Considerations

Allows a physician and a physician assistant or nurse practitioner to make findings of incapacity for a health care power of attorney to become effective and for admission to a hospice; andAllows a physician assistant or an advanced practice registered nurse to certify that a patient is afflicted with a terminal condition or is in a persistent vegetative state and would allow an attending physician assistant or an attending advanced practice registered nurse to issue do-not-resuscitate orders.

Act 91: Historic Churches

Permits a church over 100 years old to install a stairway chair lift to assist individuals and improve accessibility for congregational activities.

Act 92: Special Needs Definition

Expands the definition of children with special needs who are eligible for adoption assistance to include a child who is seven years or older, if age is the only factor in determining eligibility, or a child who is a member of a sibling group of two or more children that must be placed together; and Allows the Department of Children and Families to submit a request to the Joint Committee on Finance to transfer money from another appropriation to fund the increased assistance payments.

Act 93: Water Infrastructure Projects

Requires the Department of Natural Resources to direct up to $5.2 million in funds from the Stewardship 2000 Program to fund high-priority water infrastructure projects in state parks; andIncreases the amount appropriated to the department for state park operations by $300,000 SEG in fiscal year 2019-20.

Act 94: Certifications For Retired Professionals

Allows retired architects, landscape architects, professional engineers, designers and professional land surveyor credential holders to maintain their title by applying to renew the credential in a retired status classification and paying half of the credential application renewal fee.

Act 95: Genetic Testing in Paternity Actions

Creates a new presumption of paternity through genetic testing and generally requires the court in a paternity action to order genetic testing.

Act 96: Open Meeting Notices

Allows school board members to provide notice of special meetings by e-mail, text message, phone call, in-person, or by mail.

Act 97: Assault Cases

Makes battery to a nurse or health care professional who is working in a hospital a Class H felony.

Act 98: Hunting Weapons

Allows bows and crossbows to be possessed in or on a stationary vehicle, all-terrain vehicle or utility terrain vehicle.

Act 99: Election Rules

Creates election and recount procedures for lake protection and rehabilitation district board elections.

Act 100: Physical Therapy Licensure Compact

Ratifies and enters Wisconsin into the Physical Therapy Licensure Compact.

Read more from the original source:
Wisconsin Governor Signs 16 Bills Into Law: How They Affect You - Milwaukee, WI Patch

Recommendation and review posted by Bethany Smith

Industrial hempcannabis with a low level of THC, the compound that provides marijuanas highis legal nationwide, thanks to the 2018 Farm Bill. But due to a long period of prohibition, scientists, farmers, and consumers know very little about the plant. One of the biggest mysteries, one rife with anecdotal evidence and theories, was what causes a hemp plant to go hot, or have illegally high levels of THC. A new study from Cornell University researchers finds that the conventional wisdom is way off.

Industrial hemp has boatloads of uses; Senator Mitch McConnell used a hemp pen to sign the 2018 Farm Bill legalizing hemp, for example. But whats looking like the big cash reason for growing hemp, at least right now, is cannabidiol, or CBD. CBD is a compound in the hemp plant, and while it is very poorly understood, the CBD industry has become massive, with claimed uses ranging from anti-anxiety to cancer prevention. (The FDA has had to stop companies from claiming most of these effects, as none of them are proven.)

Currently, the law states that industrial hemp is legal if it tests with a THC level of less than 0.3 percent. Growers do their best to breed low-THC varieties of hemp, but sometimes plants still go hot, exhibiting higher THC percentages than that, and those plants cannot be sold and must be disposed of. That can be expensive, depending on how often it happens, and it can also be concerning for consumers who want to make sure they wont get accidentally stoned. So its in everyones best interest to figure out exactly what causes a hemp plant to go hot.

There had been some conventional wisdom that geography and environmentterroir, reallymight play a role in a hemp plant unexpectedly going hot. Different temperatures, amounts of water, soil makeup, the location it was grown in, all of that stuff was believed to be a possible cause of a hemp plant going hot.

New research from Cornell, though, says thats not the case. Our evidence from this paper is that fields go hot because of genetics, not because of environmental conditions, says Larry Smart, the lead author of the study, in a press release.

The study involved testing two different hemp fields, comparing genetic makeup and environmental differences. The researchers found that environment conditions had no significant effect on THC levels, but did discover that the hemp plants had different genes that seem to trigger whether theyll produce THC, CBD, or both.

This could be incredibly valuable; the researchers note that genetic testing of hemp plants can be done while the plants are still seedlings, dramatically reducing the penalty for discovering high THC levels in a mature plant. Their research indicates that THC and CBD are all based on genetics, and could provide a pathway for much easier, cheaper, and more conclusive testing. And thats good news for hemp farmers, who are finding the hemp industry to be a bit less lucrative than expected.

Go here to read the rest:
What Makes Industrial Hemp Spike to Illegal Levels of THC? - Modern Farmer

Recommendation and review posted by Bethany Smith

When Anna Lambert and Joey Lapointe decided to have a baby, they knew any child they conceived had a 50-50 chance of inheriting a debilitating genetic disease.

Lapointe carries the mutation for Huntington's disease, passed on by his father.

Huntington's is a hereditary and fatal neurological illness which typically sets in in middle age, destroying a person's mental and physical abilities. Early symptoms include involuntary movements, cognitive decline and mood disturbances.

There is no cure.

To rule out the possibility of bearing a child with the mutation, Lambert had prenatal testing around the 12-week mark of her pregnancy.

The result was positive, but the couple was encouraged by genetic markers that showed the fetus could be carrying the mutation for late-onset Huntington's, which typically develops after the age of 60.

They chose not to terminate the pregnancy. However, last summer, the baby was stillborn.

Her voice catching, Lambert described the stillbirth, 24 weeks into her pregnancy, as "traumatic." She and her husband only had a week to grieve before they both had to return to work.

"It's something that no one should have to go through," Lapointe said.

Still wanting a child but hoping to avoid reliving such a painful experience, the couple discussed their options. One of them is in-vitro fertilization (IVF).

Embryos conceived through IVF can be screened for genetic mutations such as Huntington's, and only disease-free embryos are then transferred to the mother's uterus. That procedure is known as pre-implantation genetic diagnosis.

However, since cost overruns led the former Liberal government to cut public funding of IVF in 2015, there's no financial assistance for couples in Lambert and Lapointe's situation.

To cover it themselves would be a huge financial hit: a single cycle of IVF, plus the genetic testing of the embryos, could set them back by as much as $15,000.

Although Quebec now offers a one-time tax credit based on household income to help cover fertility treatments, the couple doesn't qualify.

The rules state that neither potential parent can have children already. Lapointe has two daughters from a previous marriage.

Lambert said she's always wanted to be a parent and doesn't think she should be penalized because her partner has children.

She calls the exclusions to the tax credit unfair and short-sighted. In the long run, paying for the treatment could save the health care system tens of thousands of dollars.

"It might only take one round in order to get a child that's Huntington's disease-free," said Lambert. "We would never have to worry about the disease being passed on again."

When IVF was publicly funded in Quebec between 2010 and 2015, the McGill University Health Centre's reproductive centre performed thousands of IVF cycles.

Dr. William Buckett, the centre's director, said of those, only 60 or 70 cases a year involved testing embryos for hereditary genetic diseases.

"It really is a drop in the ocean," he said.

The low volume of cases is also reflected in statistics from countries such as the United Kingdom, which covers up to three full IVF cycles for parents who risk passing on Huntington's disease, said Buckett.

A round of IVF plus pre-implantation genetic testing is much less costly than caring for someone with Huntington's disease or even a late termination of a pregnancy and the psychological costs associated with that, he said.

"Reducing the amount of suffering by offering it is, I think, far and away more cost-effective," said Buckett.

Buckett said if the government is concerned about costs spiralling out of control, it could follow the example set by the U.K., which has a regulated central agency which approves which conditions it will cover.

During the 2018 election campaign, Coalition Avenir Qubec promised to reinstate a public IVF program and offer at least one cycle at no cost to would-be parents by 2020.

This week, a spokesperson for the Health Ministry told CBC the program's criteria arestill being developed, and it's too early to say what will be covered.

The Huntington Society of Qubec said it plans to send a letter to Health Minister Danielle McCann, outlining the advantages of covering the procedure for people who suffer from genetic disorders.

Danile Bouret, a social worker at the society, said people who have Huntington's typically develop symptoms between the ages of 30 and 50 what should be the most productive years of their lives. Eventually, an afflicted person is not able to work, drive or look after themselves.

"Every part of that person is affected," said Bouret.

Once the symptoms set in, most people die within 15 to 20 years.

Bouret, too, believes that in the long term, it's cheaper for the government to help ensure a child isn't born with Huntington's in the first place.

Having IVF funding available would give potential parents peace of mind.

"It would be taking a very difficult load off of their shoulders because knowing you might have given that faulty gene to your child is devastating," said Bouret.

The testing also has a lasting benefit. If a child doesn't have the faulty gene, it can't pass on Huntington's to future offspring.

Removing such a devastating disease from their family tree is important to Lambert and Lapointe.

Lapointe's father's Huntington's disease has advanced to the stage where he is bedridden and living in a long-term care institution.

Lambert knows at some point, her husband will also develop symptoms. If they can help it, they don't want a child of theirs to ever have to go through that, she said.

"They don't need to watch their dad going through that decline, then thinking, 'That could be me.'"

View original post here:
Quebec couple pleads for IVF funding to help them conceive a baby without Huntington's disease - CBC.ca

Recommendation and review posted by Bethany Smith

SUDBURY -- Health Sciences North in Sudbury is hoping to keep its littlest patients closer to home with a newly acquired chloridometer.

The instrument is used in the HSN laboratories to diagnose children, as young as newborns, with cystic fibrosis by measuring the amount of the chloride in their sweat.

Children with the genetic disorder can have elevated amounts of chloride in their sweat.

Dr. Vijay Kumar has been a pediatrician in the city for 35 years and says this new equipment has been on the NEO Kids & Family Program wish list for some time.

"We currently do genetic testing for newborns, but the sweat chloride test helps to confirm the diagnosis," said Dr. Kumar.

The pediatrician adds that now that testing is available locally, patients no longer have to travel to Toronto or Ottawa.

Previously when patients were referred to southern Ontario, they often would continue their treatment with the specialist who confirmed their diagnosis.

The HSN lab is also able to do the testing for samples provided by other hospitals in the northeast including North Bay, Timmins, Kapuskasing and Matheson.

The chloridometer was purchased by the NEO Kids Foundation through funds raised in the community.

View post:
It's all in the sweat: new equipment helps detect cystic fibrosis - CTV News

Recommendation and review posted by Bethany Smith

Spurred by promising clinical results in an important trial, each of the three major CRISPR stocks had a great performance in the second half of 2019. Unfortunately, they didn't keep the momentum going in the first month of 2020.

Shares of Intellia Therapeutics (NASDAQ:NTLA) fell 18.8% in January, according to data provided by S&P Global Market Intelligence. That was followed by a 14.7% loss for shares of CRISPR Therapeutics (NASDAQ:CRSP) and a 10.7% tumble for shares of Editas Medicine (NASDAQ:EDIT).

While each has recovered some ground in the first week of February, this trio of pharma stocks is no stranger to volatility. Investors should probably expect that to continue as clinical programs advance in 2020.

Image source: Getty Images.

In November, CRISPR Therapeutics reported data for the first two individuals in the trial, one with sickle cell disease (SCD) and one with transfusion-dependent beta thalassemia (TDT), treated with its lead drug candidate CTX001. Both enjoyed significant benefits in their standard of living, which investors interpreted as a sign that CRISPR gene editing might actually live up to the hype.

That fueled annual gains of 113% for CRISPR Therapeutics last year. While Editas Medicine and Intellia Therapeutics gained only 30% and 7%, respectively, each had been sitting at a year-to-date loss in October.

What relevance does that have for the tumbles taken in January? First, it's not unusual for stocks to regress to the mean. Stocks that are red hot eventually cool off, while those that tumble without good reason eventually recover some ground.

Second, and the more important consideration for investors, is that the early stage results for CTX001 mean relatively little for the industry's pipeline of CRISPR-based gene editing drug candidates.

Consider that CTX001 is an ex vivo tool. Researchers harvest bone marrow from patients, extract specific types of stem cells, and engineer those with CTX001. The engineered stem cells are then grown in the lab before being reinjected into the patient.

Many other CRISPR-based drug candidates are designed as in vivo tools. That means the gene editing payloads are designed to engineer a patient's DNA while inside the body. An in vivo approach is inherently more complex and will be more difficult to control compared to an ex vivo approach.

Put another way, investors cannot take the promising, early stage results from CTX001 and extrapolate it broadly across all first-generation CRISPR tools. Wall Street certainly isn't, if the correlation between technical approach and stock performance is any guide.

Consider that the two most advanced drug candidates from CRISPR Therapeutics rely on ex vivo engineering. By contrast, the lead drug candidate from Editas Medicine relies on in vivo methods.

The lead pipeline asset from Intellia Therapeutics is also an in vivo tool, though unlike the lead assets from its peers, it has yet to advance to clinical trials.

Investors should expect 2020 to be a busy year for these CRISPR stocks. CRISPR Therapeutics will have more clinical data from CTX001 and the first set of data for its lead oncology asset CTX110.

Similarly, Editas Medicine should have results for EDIT101 and progress additional assets, while Intellia Therapeutics is preparing to finally enter the clinic with NTLA-2001 in the second half of the year.

Investors cannot know if the next batch of results will be as rosy as the initial data for CTX001, but they can probably expect another year of volatile stock movements.

Go here to read the rest:
Here's Why CRISPR Stocks Fell in January - The Motley Fool

Recommendation and review posted by Bethany Smith

The first targets of trials in humans are serious diseases we know are caused by a single gene, but as we understand more about combinations of genes increasing risk factors for other diseases, Crispr could be used more widely

BL PREMIUM

01 February 2020 - 06:17 Hannah Kuchler

Jennifer Doudna wears her responsibility lightly. The scientist who co-discovered Crispr (clustered regularly interspaced short palindromic repeats) does not appear to be weighed down by the burden of her creation: the revolutionary gene-editing technology that promises to empower humans to control our own genome. She waves and smiles as she bypasses the hostess stand at Gather, an organic, farm-to-table restaurant in Berkeley. Its the sort of place that wears its principles on its sleeve a fitting venue for a discussion of the ethical conundrums that Crispr has unleashed.

Doudna appears to have thrown on her blazer in a rush, squashing down one side of her shirt collar. Since news of her scientific breakthrough was published in 2012, she has learnt to toggle between the white coat of her lab work, building on that initial discovery, and her suited-and-booted role pushing politicians and lawmakers to contemplate the consequences of changing the human genome.

Continued here:
LUNCH WITH THE FT: Jennifer Doudna, scientist and gene editor at the heart of the Crispr maelstrom - Business Day

Recommendation and review posted by Bethany Smith

The recent performance of Fastly (NYSE:FSLY) stock in the market spoke loud and clear to investors as FSLY saw more than 1.51M shares in trading volumes in the last trading session, way higher than the average trading volume of 1.51M shares by far recorded in the movement of Fastly (FSLY). At the time the stock opened at the value of $22.60, making it a high for the given period, the value of the stock jumped by 1.43%. After the increase, FSLY touched a low price of $22.10, calling it a day with a closing price of $22.43, which means that the price of FSLY went 22.75 below the opening price on the mentioned day.

Given the most recent momentum in the market in the price movement of FSLY stock, some strong opinions on the matter of investing in the companys stock started to take shape, which is how analysts are predicting an estimated price of $26.11 for FSLY within consensus. The estimated price would demand a set of gains in total of 8.5%, which goes higher than the most recent closing price, indicating that the stock is in for bullish trends. Other indicators are hinting that the stock could reach an outstanding figure in the market share, which is currently set at 38.62M in the public float and 2.21B US dollars in market capitalization.

When it comes to the technical analysis of FSLY stock, there are more than several important indicators on the companys success in the market, one of those being the Relative Strength Indicator (RSI), which can show, just as Stochastic measures, what is going on with the value of the stock beneath the data. This value may also indicate that the stock will go sideways rather than up or down, also indicating that the price could stay where it is for quite some time. When it comes to Stochastic reading, FSLY stock are showing 19.29% in results, indicating that the stock is neither overbought or oversold at the moment, providing it with a neutral within Stochastic reading as well. Additionally, FSLY with the present state of 200 MA appear to be indicating bullish trends within the movement of the stock in the market. While other metrics within the technical analysis are due to provide an outline into the value of FSLY, the general sentiment in the market is inclined toward positive trends.

With the previous 100-day trading volume average of 964502 shares, CRISPR Therapeutics AG (CRSP) recorded a trading volume of 902880 shares, as the stock started the trading session at the value of $52.71, in the end touching the price of $53.48 after jumping by 1.46%.

CRSP stock seem to be going ahead the lowest price in the last 52 weeks with the latest change of 82.28%.Then price of CRSP also went backward in oppose to its average movements recorded in the previous 20 days. The price volatility of CRSP stock during the period of the last months recorded 4.09%, whilst it changed for the week, now showing 3.21% of volatility in the last seven days. The trading distance for this period is set at -6.90% and is presently away from its moving average by -14.88% in the last 50 days. During the period of the last 5 days, CRSP stock lost around -3.36% of its value, now recording a sink by 8.63% reaching an average $49.32 in the period of the last 200 days.During the period of the last 12 months, CRISPR Therapeutics AG (CRSP) dropped by -12.19%.

According to the Barcharts scale, the companys consensus rating fall to 4.27 from 4.40, showing an overall improvement during the course of a single month. Based on the latest results, analysts are suggesting that the target price for CRSP stock should be $53.48 per share in the course of the next 12 months. To achieve the target price as suggested by analysts, CRSP should have a spike by 0% in oppose to its present value in the market. Additionally, the current price showcases a discount of 48.58% when compared to the high consensus price target predicted by analysts.

CRSP shares recorded a trading volume of 857794 shares, compared to the volume of 1.21M shares before the last close, presented as its trading average. With the approaching 3.21% during the last seven days, the volatility of CRSP stock remained at 4.09%. During the last trading session, the lost value that CRSP stock recorded was set at the price of $53.48, while the lowest value in the last 52 weeks was set at $29.34. The recovery of the stock in the market has notably added 82.28% of gains since its low value, also recording -10.03% in the period of the last 1 month.

Read more:
Stocks That Are Finally Turning The Corner: Fastly (FSLY), CRISPR Therapeutics AG (CRSP) - US Post News

Recommendation and review posted by Bethany Smith

INTRODUCTION

The date palm (Phoenix dactylifera), a dioecious species in the Arecaceae (formerly Palmae) family has a historical distribution stretching from Mauritania in the west to the Indus Valley in the east (1). A major fruit crop in hot and arid regions of North Africa and the Middle East and one of the earliest domesticated tree crops, archaeobotanical records suggest that the earliest exploitation and consumption of dates is from the Arabian Neolithic some 7000 years before the present (yr B.P.) (1). Evidence of cultivation in Mesopotamia and Upper Arabian Gulf approximately 6700 to 6000 yr B.P. support these centers as the ancient origin of date palm domestication in this region, with a later establishment of oasis agriculture in North Africa (1, 2).

The current date palm germplasm is constituted by two highly differentiated gene pools: an eastern population, consisting of cultivars extending from the Middle East and Arabian Peninsula to northwest India and Pakistan and a western population covering North Africa and sub-Saharan Africa (3, 4). Introgressive hybridization by a wild relative in North African date palms has been proposed as a source of this differentiation (2).

Date palms in the southern Levant (modern-day Israel, Palestine, and Jordan), situated between eastern and western domestication areas, have historically played an important economic role in the region and were also of symbolic and religious significance (5). The Kingdom of Judah (Judea) that arose in the southern part of the historic Land of Israel in the 11th century BCE was particularly renowned for the quality and quantity of its dates. These so-called Judean dates grown in plantations around Jericho and the Dead Sea were recognized by classical writers for their large size, sweet taste, extended storage, and medicinal properties (5). While evidence suggests that Judean date culture continued during the Byzantine and Arab periods (4th to 11th century CE), further waves of conquest proved so destructive that by the 19th century, no traces of these historic plantations remained (5).

In 2008, we reported the germination of a 1900-year-old date seed (6) recovered from the historical site of Masada overlooking the Dead Sea. In the current study, six additional ancient date seeds from archaeological sites in the Judean desert were germinated, bringing to seven the number of ancient genotypes genetically analyzed using molecular markers. In addition, morphometric analysis was used to compare the size and shape of ungerminated ancient date seeds with modern varieties and wild dates.

This study, which confirms the long-term survival of date palm seeds, provides a unique opportunity to rediscover the origins of a historic date palm population that existed in Judea 2000 years ago. The characteristics of the Judean date palm may shed light on aspects of ancient cultivation that contributed to the quality of its fruit and is thus of potential relevance to the agronomic improvement of modern dates.

Of the hundreds of ancient date seeds and other botanical material recovered from excavations carried out in the Judean desert between 1963 and 1991 (7, 8) (fig. S1), 32 well-preserved date seeds from the archaeological sites of Masada, Qumran, Wadi Makukh, and Wadi Kelt were planted in a quarantine site at Kibbutz Ketura (table S1). Of these, six ancient seeds germinated and were further identified by the following monikers: Masada: Adam; Qumran: Jonah, Uriel, Boaz, and Judith; and Wadi Makukh: Hannah (Figs. 1 and 2).

(A) Adam, (B) Jonah, (C) Uriel, (D) Boaz, (E) Judith, (F) Hannah, and (G) HU37A11, an unplanted ancient date seed from Qumran (Cave FQ37) used as a control. Scale bars, 0.5 cm (A, no bar size as unmeasured before planting). Photo credit: Guy Eisner.

Ages in months at time of photograph (A to C) Adam (110 months), Jonah (63 months), and Uriel (54 months). (D to F) Boaz (54 months), Judith (47 months), and Hannah (88 months). Photo credit: Guy Eisner.

On visual inspection, no specific observation linked the ability of these seeds to germinate compared with those that failed to germinate. Before planting, the ancient date seeds had been weighted, and their length was measured, with the exception of those seeds from Masada, (including Adam, the germinated seed), which unfortunately were not measured (table S1). No statistically significant differences were found between germinated and ungerminated seeds in either weight {1.67 0.55 and 1.61 0.29 g, respectively [Students t test (t) = 0.348, degree of freedom (df) = 24, P = 0.731]} or length [27.60 3.7 and 26.8 3.7 mm, respectively (t = 0.455, df = 24, P = 0.653)].

Radiocarbon ages are shown (Fig. 3 and table S2) for ancient date seeds germinated in the current study and also for the date seed (seed 3/Methuselah) germinated in our previous work (6). These ages were obtained from seed shell fragments found clinging to the rootlets of germinated seedlings during their transfer into larger pots (3 to 17 months of age). The values were recalculated to take into account contamination by modern carbon incorporated during seedling growth previously shown to reduce measured radiocarbon age by approximately 250 to 300 years, equivalent to 2 to 3% modern carbon (table S2) (6). On the basis of these calculations, Methuselah germinated in our previous study (6) and Hannah and Adam in the current study are the oldest samples (first to fourth centuries BCE), Uriel and Jonah are the youngest (first to second centuries CE), and Judith and Boaz are intermediate (mid-second century BCE to mid-first century CE) (Fig. 3).

Eighteen ancient date seeds that failed to germinate were recovered from the potting soil and compared with modern seeds derived from 57 current date palms of which 48 are cultivated varieties and 9 are wild individuals (9, 10). Ancient seeds were significantly larger in terms of both length and width (length, 27.62 3.96 mm; width, 10.38 0.71 mm) than both current cultivar (length, 20.60 4.70 mm; width, 8.33 1.02 mm) and wild date palm seeds (length, 16.69 3.39 mm; width, 7.08 0.46 mm) (Fig. 4). Ancient seeds were, on average, 27.69% wider (t = 11.923, df = 18.391, P = 2.157 1010) and 38.37% longer than the combined current samples (wild and cultivated) (t = 7.422, df = 17.952, P = 3.564 107).

Length (millimeters) (left) and width (millimeters) (right) of ancient date seeds that failed to germinate (n = 18), 9 current wild individuals (n = 180), and 48 cultivated P. dactylifera varieties (n = 928). Letters a, b, and c above boxes indicate Tukeys groups derived from HSD.test function and R package agricolae.

When only compared to the cultivars, the ancient date seeds were still larger: 24.55% wider (t = 11.923, df = 18.391, P = 2.157 1010) and 34.06% longer (t = 7.422, df = 17.952, P = 3.564 107). However, the contrast in seed size is even more marked when comparing ancient seeds and current wild date palms: The Judean date palm seeds were, on average, 39.55% wider (t = 19.185, df = 18.471, P = 5.943 1014) and 65.48% longer than current wild samples (t = 11.311, df = 19.574, P = 2.472 1010) (tables S3 and S4).

Analysis of seed shape diversity in current and ancient date seeds using principal components analysis (PCA) (dudi.pca function) performed on seed outlines confirmed visual observation that modern cultivated seeds were more diverse in size than ancient ones but did not differentiate between the two groups [multivariate analysis of variance (MANOVA), P > 0.05]. Ancient seeds displayed an elongated shape similar to current cultivated samples (fig. S2).

The sex of the six germinated ancient date seedlings in the current study identified using three sex-linked simple sequence repeats (SSR) (11) were as follows: Judith and Hannah are female genotypes and Uriel, Jonah, Boaz, Adam, and Methuselah (seed 3) from the previous study (6) are male genotypes. Through microsatellite genotyping, three levels of genetic inheritance were investigated to highlight geographic origins (Fig. 5, A and B): (i) inheritance transmitted by both parents to progeny, obtained by microsatellite markers showing western and eastern patterns of the ancient seeds genomes (4), as presented in structure analysis and pie charts (Fig. 5A); (ii) inheritance transmitted from mother to progeny through the chloroplast genome, reflecting maternal lineage origin by reporting chloroplastic minisatellite eastern or western alleles (Fig. 5B, arrow) (12); and (iii) inheritance transmitted from father to son through the Y chromosome, reflecting paternal lineage origin by reporting male specific sex-linked eastern or western alleles (Fig. 5B, arrow) (11).

(A) Structure analysis results are shown for modern and ancient western (green) and eastern (orange) genotype contributions. Pie charts highlight eastern (orange) and western (green) ancient seeds nuclear genomes contributions. (B) Ancient seeds maternal and paternal lineages origin. Arrows represent clonally transmitted parental information, with maternal (chloroplastic) and paternal (Y chromosome) from western (green) and eastern (orange) origins.

Structure analysis revealed that distribution of the germinated ancient date seeds was within previously described eastern and western date palm gene pools (Fig. 5A). Methuselah, Hannah, and Adam are the most eastern genotypes, although they also show ancient western contributions requiring numerous generations and highlighting ancient crosses. Boaz and Judith are the most admixed, with almost equal eastern and western contributions reflecting more recent crossings. Jonah and Uriel are the most western genotypes with the most western parental lineages (Fig. 5B).

To shed light on genetic diversity of the ancient dates, basic population genetic parameters were estimated and compared to modern reference collections (tables S5 and S6). The ancient genotypes showed an allelic richness value (Ar) (i.e., the number of alleles) of 3.59, a relatively high diversity for such a small sample size (seven genotypes) compared to values of other countries sampled (table S6). Genetic relationships between the ancient date and current varieties (Fig. 6 and table S7) show Methuselah and Adam close to eastern modern varieties Fardh4 and Khalass, respectively, assigned to current Arabian Gulf varieties; Hannah and Judith related to modern Iraqi varieties Khastawi and Khyara, respectively; and Uriel, Boaz, and Jonah, the most western genotypes, related to modern Moroccan varieties, Mahalbit, Jihel, and Medjool, respectively.

Modern varieties from United Arab Emirates (light orange), Iraq (red), Tunisia (blue), Morocco (light green), Egypt (dark green), and ancient genotypes (purple).

In the current study, six ancient date seeds, in addition to the seedling obtained in our previous study (6), were germinated. All the seeds were approximately 2000 years old and had been previously recovered from archaeological sites in the Judean desert, a rain shadow desert of ca. 1500 km2 located between the maquis-covered Judean Hills and the Dead Sea (fig. S1).

Little is known about the mechanisms determining seed longevity; however, it has been related to the ability to remain in a dry quiescent state (13). In the current study, low precipitation and very low humidity around the Dead Sea could have contributed to the longevity of the ancient date seeds, which may be an adaptation of date palms to extreme desert conditions fostering seed dispersion. Their remarkable durability, however, may also be connected to other extreme environmental conditions in this area; at 415 m below mean sea level, the Dead Sea and its surroundings have the thickest atmosphere on Earth, leading to a unique radiation regime and a complex haze layer associated with the chemical composition of the Dead Sea water (14). However, since no visible evidence in the current study was linked to seed germination and, accordingly, to their long term survival, further investigations are needed to understand the basis of date palm seed longevity.

Among the worlds oldest cultivated fruit trees, P. dactylifera is the emblematic of oasis agriculture and highly symbolic in Muslim, Christian, and Jewish religions (5). Closely connected to the history of human migrations, the first cultivated varieties of P. dactylifera are thought to have originated around Mesopotamia and the Upper Arabian Gulf some 6700 to 6000 yr B.P. (1, 2, 10). In Judea, an ancient geopolitical region that arose during the 11th century BCE in the southern part of the historic Land of Israel, and situated at the cross roads of Africa, Asia, and Europe, the origins of date palm cultivation are unknown. However, from historical records, a thriving Judean date culture was present around Jericho, the Dead Sea, and Jordan Valley from the fifth century BCE onward, benefitting from an optimal oasis agriculture environment of freshwater sources and subtropical climate (5).

Described by classical writers including Theophrastus, Herodotus, Galen, Strabo, Pliny the Elder, and Josephus, these valuable plantations produced dates attributed with various qualities including large size, nutritional and medicinal benefits, sweetness, and a long storage life, enabling them to be exported throughout the Roman Empire (5, 15, 16). Several types of Judean dates are also described in antiquity including the exceptionally large Nicolai variety measuring up to 11 cm (5, 15, 16).

In the current study, ancient seeds were significantly longer and wider than both modern date varieties and wild date palms. Previous research has established that both fruits and seeds are larger in domesticated fruit crops compared with their wild ancestors (17), suggesting that the ancient seeds were of cultivated origin (9, 18), most likely originating from the regions date plantations. Furthermore, an increase in seed size has been linked allometrically to an increase in fruit size (19), corroborating the historical descriptions of the large fruits grown in this region.

Genotypes of the germinated ancient date seedlings cover a large part of present-day date palm distribution area, findings that reflect the variety, richness, and probable influences of the historic Judean date groves. Microsatellite genotyping shows a relatively high diversity, with eastern and western gene pool contributions, allelic richness, and genetic proximity to current varieties cultivated in the Arabian Peninsula, Iraq, and North Africa. Although the sample size is small, a predominance of eastern female lineages (six of seven) indicates that eastern female varieties grown from local germplasm were probably clonally propagated from offshoots to maintain desirable fruit qualities. Male lineages, mainly western (four of five), suggest that genetically different or foreign males were used for pollination. This assumption is supported by first century texts, indicating that substantial knowledge existed in ancient Judea 2000 years ago regarding the most suitable males for pollination of female date palms (20).

Our results reinforce the historical narrative that a highly sophisticated domestication culture existed in ancient Judea. Local farmers with an interest in maintaining genetic diversity in their date plantations and anthropogenic pressures leading to selection on fruit dimension and other desirable traits used cross-breeding with foreign (genetically different) males to develop a rich collection of varieties.

These findings suggest that Judean date culture was influenced by a variety of migratory, economic, and cultural exchanges that took place in this area over several millennia.

In Israel, the oldest remains of P. dactylifera are wood specimens 19,000 yr B.P. from Ohalo II site on the Sea of Galilee (21). Recovery of carbonized date seeds from Chalcolithic and Early Bronze Age sites (4500 to 2900 BCE) in the Judean desert, Jordan Valley, and Jericho (22, 23) and early Iron Age sites in Israel (12th to 11th century BCE) (24) suggest that human exploitation and consumption of dates occurred at this time. However, it is unclear whether these samples, which are relatively few in number and of very small size (22, 25, 26), are derived from ancient wild populations, as suggested by morphometric studies of modern wild date populations (18) or represent an early stage of the domestication process.

In the current study, although the sample size is too small to claim a trend, on a gradient from east to west genetic contributions, the older the germinated seeds are on radiocarbon dating (Fig. 3), the more eastern is the nuclear genome (Fig. 5, A and B ). In this respect, Methuselah, Adam, and Hannah (first to fourth centuries BCE) have a predominantly eastern nuclear genome and eastern maternal lineage, their relationship to modern varieties from the Arabian Gulf and Iraq suggesting that they belong to the same eastern genetic background.

The P. dactylifera cultivated by the inhabitants of Judea at that time therefore appears to be from the eastern gene pool, possibly growing locally and related to oasis populations, of which relict populations were recently found in Oman (9).

Elite female cultivars may also have been introduced to ancient Israel from these regions, consistent with a pattern of human intervention and possibly active acquisition of date palm varieties. Established trade links are documented with Arabia and the Persian Gulf from at least the 12th century BCE (27). Babylonian date palm cultivation in southern Mesopotamia (most of modern Iraq), originating some 6000 yr B.P. (1, 2), used deportees from ancient Judea following its conquest in the sixth century BCE (28). After the collapse of the Neo-Babylonian Empire, returning exiles may have brought this specialized knowledge and selected cultivars back to Judea; a date variety Taali cultivated in both Judea and Babylon is mentioned in the Talmud (29).

Western genetic admixtures in the germinated seedlings and their proximity to current cultivated date varieties from Morocco also suggest that ancient Judean date palms were the result of germplasm exchanges with this area and of multiple crosses. Introgression of eastern genomes into western ones are common, detected in varieties from Algeria, Morocco, Mauritania, and particularly east-west junction areas like Egypt (1, 2, 4, 30). In the latter, eastern contributions from the Persian Gulf, detected in ancient Egypt date seeds from 1400 BCE to 800 CE, reveal a chronological pattern of change in agrobiodiversity and the possible emergence of a western form in the Roman period (10).

Introgression of date palm western genomes into eastern ones, however, is far lower (1, 2, 4, 12), their presence in the current study reflecting west to east exchanges.

The origins of these exchanges are unclear; however, archaeological evidence indicates that North Africa, Near East, and Mediterranean cultures were clearly linked during the Neolithic in the southern Levant (approximately 11,700 to 7300 B.P.) and were associated in Jericho with the earliest origins of food production and fundamental changes in human subsistence strategies (31).

Phoenicia, a maritime trading nation occupying the coastal areas of modern northern Israel, Lebanon, and Syria (1500 to 300 BCE), was also historically associated with cultivation and trade of date palms (32). We can speculate that later west to east germplasm exchanges to this region may have been associated with domesticated varieties originating in Phoenician City States in North African (e.g., Carthage in present-day Tunisia) (32), where oasis agriculture appeared relatively late in the archaeological record (3).

The most western genotypes in the current study (Uriel and Jonah) are also the youngest seeds (mid-first to mid-second CE), coinciding with established trade routes linking this region to North Africa and supporting evidence for date consumption in the latter 2000 years ago (2, 3). This period coincides with Judeas well-documented wars against Rome (66 to 73 CE and 132 to 136 CE) and deportation and displacement of its population (16). The ancient seeds in the current study were found in the Judean desert, historically a place of refuge due to its steep cliffs and inaccessible caves (16, 23). The loss of political autonomy and the final collapse of Judea have been postulated as causing major disruption to labor intensive practices associated with date cultivation (33). Elite cultivars no longer conserved by vegetative propagation (offshoots) were gradually replaced by seedling date palms producing fruits displaying considerable variation within the progeny. Although P. dactylifera can live for more than 100 years (33) and date groves in this region are thought to have persisted for several more centuries, they were already rare by the 11th century and had been entirely replaced by seedling populations or feral, wild trees producing only low-quality fruit (5, 33), by the 19th century.

The current study sheds light on the origins of the Judean date palm, suggesting that its cultivation, benefitting from genetically distinct eastern and western populations, arose from local or introduced eastern varieties, which only later were crossed with western varieties. These findings are consistent with Judeas location between east-west date palm diversification areas, ancient centers of date palm cultivation, and the impact of human dispersal routes at this crossroads of continents.

Given its exceptional storage potentialities, the date palm is a remarkable model for seed longevity research. Investigations on the molecular mechanisms involved in long-term protection in the dried state have important implications on plant adaptation to changing environments and for biodiversity conservation and seed banking. As new information on specific gene-associated traits (e.g., fruit color and texture) (3) is found, we hope to reconstruct the phenotypes of this historic date palm, identify genomic regions associated with selection pressures over recent evolutionary history, and study the properties of dates produced by using ancient male seedlings to pollinate ancient females. In doing so, we will more fully understand the genetics and physiology of the ancient Judean date palm once cultivated in this region.

The objectives of this study and its design were as follows:

1) The origin and selection of ancient date seeds derived from archaeological sites in the Judean desert.

2) The germination of ancient date seeds in a quarantine site following a preparatory process.

3) Radiocarbon dating and recalculation of calendar ages of germinated ancient date seeds based on seed shell fragments and selected controls.

4) Seed morphometric studies: Comparing ungerminated ancient date seeds with seeds from modern date varieties and wild date palms.

5) Microsatellite analysis of seven germinated date seedlings.

(statistical methods are included in the respective sections)

The ancient date seeds in the current study were obtained from botanical material recovered from archaeological excavations and surveys carried out at the following sites in the Judean desert between 1963 and 1991 and stored at room temperature since their discovery (fig. S1).

1) Masada: An ancient fortress/palace complex built by King Herod the Great (37 to 4 BCE) at the southern end of the Dead Sea on the site of an earlier Hasmonean fortification (141 to 37 BCE) (7). The site, built on a plateau approximately 400 m above the Dead Sea, was first excavated by the late Y. Yadin (Institute of Archaeology, Hebrew University, Jerusalem, Israel) from 1963 to 1965 (7). Bioarchaeological material found at this time included large numbers of date seeds buried under rubble close to the remains of an area identified as a food storage site.

2) Qumran: An archaeological site situated at the northern end of the Dead Sea including an ancient settlement dating from the second century BCE destroyed in 68 CE and a number of caves located in the surrounding cliffs and marl terrace associated with the 1947 discovery of the Dead Sea Scrolls. Later excavations and surveys of caves in this area, carried out from 1986 to 1989, by J. Patrich and B. Arubas (The Institute of Archaeology, The Hebrew University, Jerusalem, Israel) (8) included the following: Qumran Cave 13: artifacts found included potsherds from period 1b Qumran (until 31 BCE), numerous date stones and dried dates in a pit, and a pottery juglet dated to approximately 67 to 79 CE containing an unknown viscid substance and wrapped in palm fibers (used as a control in radiocarbon analysis in the current study) (see below); and Qumran Cave FQ37: containing a number of date stones and first to second CE century artifacts from the late Second Temple period (60 to 70 CE) and Roman period.

3) Wadi Makukh: A winter water channel in the Judean desert surrounded by high cliffs and containing a number of caves, which were surveyed from 1986 to 1989 (above). Date seeds found in caves 1, 3, 6, and 24 in this area were included in the current study; Cave 1 was found to include a Chalcolithic burial site (fifth millennium B.P.) containing human skeletons as well as Roman period artifacts but with signs of considerable disturbance by grave robbers (8).

4) Wadi Kelt: A winter water channel running from Jerusalem to the Dead Sea containing a number of caves (8). Date seeds from Masada were provided to S.S. by M. Kislev (Faculty of Life Sciences, Bar Ilan University), initially in 2005 (6) and again in 2007 (germinated in the current study), following permission by the late E. Netzer (Department of Archaeology, Hebrew University of Jerusalem). Date seeds from Qumran, Wadi Makukh, and Wadi Kelt were provided to S.S. by J. Patrich in 2009.

Out of a collection of many hundreds of ancient date seeds, a total of 34 were selected for the current study based on the specimens appearing visually to be intact whole seeds, in good condition, and without holes. They included Masada (8 seeds), Qumran (18 seeds), Wadi Makukh (7 seeds), and Wadi Kelt (1 seed). Ancient date seeds selected above were identified by code numbers and photographed, and measurements of weight and length were made before planting (with the exception of Masada seeds, which unfortunately were not measured) (table S1). One date seed, from the Qumran excavations (HU 37 A11), was selected as a control and left unplanted (table S1).

The remaining 33 seeds were subjected to a preparatory process to increase the likelihood of seed germination using the following established methods to sprout delicate germplasm (34): seeds were initially soaked in water for 24 hours and in gibberellic acid (5.19 mM) (OrthoGrow, USA) for 6 hours to encourage embryonic growth. This was followed by Hormoril T8 solution (5 g/liter) (Asia-Riesel, Israel) for 6 hours to encourage rooting and KF-20 organic fertilizer (10 ml/liter) (VGI, Israel) for 12 hours. All solutions were maintained at 35C.

Following the above procedure, one seed was found to be damaged and not planted. The remaining 32 seeds were separately potted in fresh sterile potting soil, 1 cm below the surface, and placed in a locked quarantine site at the Arava Institute of Environmental Sciences, Kibbutz Ketura, located in the southern Israel. Eight weeks after germination and periodically afterward, KF-20 (10 ml/liter) and iron chelate (10 g/liter) were added to the seedlings. Irrigation used desalinated water, as our previous study on germinating the first ancient date seed (6) indicated that using the regions highly mineralized water produced tip burn (darkening and drying of leaves).

Radiocarbon ages in the current study were obtained for the following bioarchaeological material: (i) fragments of seed shell coat found clinging to the rootlets of six germinated ancient date seeds when these seedlings were transferred into larger pots, (ii) an unplanted ancient date seed from cave 37 Qumran (HU37 A11) (used as a control), and (iii) part of an ancient palm frond surrounding an oil juglet found in Qumran Cave 13 (used as a control). Radiocarbon ages of seed shell fragments from the germinated seedlings were recalculated to take into account modern carbon incorporated during seedling growth (6).

1) Methodology: Nonorganic carbon (carbonates) were removed from all samples with 10% HCl under reduced pressure followed by repeated washes in deionized water until neutral (pH 7). Organic acids formed during the rotting process were removed with 10% NaOH followed by repeated washes (as above). To prevent absorption of atmospheric CO2, all samples were placed again in 10% HCl and then washed in deionized water until neutral. To remove chemicals used in the germination process, a 7-mm-long shell fragment from the germinated date seed weighing 80 mg was cut into six cubes of 8 mm3 and subjected to an additional series of four boil washes. All samples were heated in an evacuated sealed quartz tube with CuO as an oxygen source. The resulting CO2 was mixed with hydrogen in the ratio 2.5:1 and catalytically reduced over cobalt powder at 550C to elemental carbon (graphite). This mixture was pressed into a target and the 14C:12C ratio (for radiocarbon age) measured by accelerator mass spectrometry at the Institute for Particle Physics of the Swiss Federal Institute of Technology Zurich (ETHZ).

2) Calendar age: Calendar age was obtained using the OxCal 4.3 calibration program based on the latest IntCal 13 calibration curve (35). Calibrated calendar ages can be found with a probability of 68.3% in the 1-range and with a probability of 95.4% in the 2-range (table S2). The probability distribution P of individual ages is given for each sigma range. The 14C activity is reported as pMC (percentage of modern carbon) and corresponds to the ratio of the activity of the sample to the corrected activity of the oxalic acid standard, which has an age of 0 yr B.P.

3) Calculation of correction for pMC: The effect of contamination by modern carbon incorporated during seedling growth previously shown in our first germination of an ancient date seed to reduce measured age by 250 to 300 years (equivalent to 2 to 3% pMC) (6) was calculated using the following three groups based on the source of the ancient seeds in both the current and previous studies:

(i) Masada: Adam (current study), Methuselah (seed 3), and seed 1 [both from previous study (6) in which seed 1 was used as a control].

(ii) Qumran Cave 13: Judith and an ancient palm frond (used as a control)

(iii) Qumran Cave 37: Boaz, Jonah, Uriel, and seed HU37A11 (used as a control)

The germinated ancient seed Hannah from Wadi Makhukh was not assigned to a group due to the absence of a suitable control and considerable disruption to the site.

Using as age-controls the ancient palm frond (Qumran Cave 13), seed HU37A11 (Qumran Cave 37) from the current study and seed 1 (Masada) from the previous study (6), we assumed that a positive pMC difference between the germinated seeds and control sample could be attributed to modern carbon that was absorbed during germination. Ages of the germinated seeds were therefore recalculated (assuming that the measurement error remains unchanged) by adjusting the measured age to the control sample. For Hannah since no control exists, an average deviation (derived from the other samples) was taken into account.

Comparison of ancient date seeds that failed to germinate with modern date seeds. This was performed on the following groups:

1) Modern date seed (P. dactylifera) samples (n = 56): Being either from cultivated varieties (n = 47) or uncultivated and possibly wild individuals (n = 9) (9). Seeds from these sources (total n = 1108) were used as a current referential for seed morphometric analysis. The cultivated modern samples originated from 11 countries spanning date palm distribution from Spain to North Africa to the Middle-East. The candidate wild date palms originated from Oman and have been hypothesized as wild date palms based on seed shape, seed size (18), and genetic studies based on microsatellite and whole-genome resequencing data (9).

2) Ancient date seeds (n = 18): Of 26 ancient date seeds obtained from Qumran, Wadi Makukh, and Wadi Kelt archaeological sites (described above) that had been planted in the quarantine site, 21 failed to germinate and were retrieved from the potting soil. Of these, three were discarded as they had fragmented and were in poor condition. The remaining 18 retrieved ancient date seeds together with modern reference seeds (described above) were rephotographed on dorsal and lateral sides, and measurements of length and width were remade (table S3) [Neither current or previous (6) ancient date seeds from Masada that failed to germinate were used in the morphometric study as these seeds were not retrieved from the potting soil].

The following statistical analyses were performed using R software (36).

1) Size analysis of modern seeds: The length and width of a total of 1108 seeds obtained from 47 current cultivated varieties (928 seeds) and 9 current wild individuals (180 seeds) were measured using ImageJ (37) following the protocol previously established by Gros-Balthazard et al. (18). The thickness was not measured since it is highly correlated with width (18).

2) Comparison of seed size between current and ancient samples: Measurements for current varieties were compared with those measured for the ancient date seeds using boxplots and Students and Tukeys tests (table S4).

3) Analysis of seed shape diversity in current and ancient date seeds: PCA (dudi.pca function) was performed on seed outlines assessed by Fourier coefficients, a morphometric method applied to outline analysis.

DNA preparation. DNA of six ancient date seedlings from the current study and one (Methuselah) from the previous study (6) was analyzed. A set of 19 SSR was used for genotyping as described by Zehdi-Azouzi et al. (4). Gender was determined using date palm sex-linked microsatellite markers (11). Maternal lineages were traced back using the plastid intergenic spacer psbZ-trnf minisatellite (12, 38). Paternal lineages were studied through Y haplotypes using the three sex-linked SSRs (mPdIRDP80, mPdIRDP50, and mPdIRDP52) (11).

Total cellular DNA was extracted from lyophilized leaves using the TissueLyser and the DNeasy Plant Mini Kit (QIAGEN SA, Courtaboeuf, France) according to the manufacturers instructions. After purification, DNA concentrations were determined using a GeneQuant spectrometer (Amersham Pharmacia Biotech, France). The quality was checked by agarose minigel electrophoresis. The resulting DNA solutions were stored at 20C.

Amplification and genotyping. Polymerase chain reactions were performed in an Eppendorf (AG, Hamburg, Germany) thermocycler. Reaction was performed in 20 l and contained 10 ng of genomic DNA, 10 reaction buffer, 2 mM MgCl2, 200 M deoxynucleotide triphosphates, 0.5 U polymerase, and 0.4 pmol of the forward primer labeled with a 5M13 tail, 2 pmol of the reverse primer, and 2 pmol of the fluorochrome-marked M13 tail and MilliQ water. A touchdown polymerase chain reaction (PCR) was carried out with following parameters: denaturation for 2 min at 94C, followed by six cycles of 94C for 45 s, 60C for 1 min, and 72C for 1 min; then 30 cycles of 94C for 45 s, 55C for 1 min, and 72C for 1.5 min; then 10 cycles of 94C for 45 min, 53C for 1 min, 72C for 1.5 min; and a final elongation step at 72C for 10 min. PCR products were analyzed using an ABI 3130XL Genetic Analyzer (Applied Biosystems, Foster City, CA, USA). Allele size scoring was performed with GeneMapper software v3.7 (Applied Biosystems).

Genetic analyses. The ancient genotypes were compared to a reference matrix (90 genotypes) containing genotyping data on current date palm varieties covering the two genetic pools defined by Zehdi-Azouzi et al. (4) and including 35 samples from the eastern pool and 55 samples from the western pool (table S5). The number of alleles per group (NA), the number of alleles with a frequency higher than 5% (NA,P), and the observed (Ho), the expected (He) heterozygosities, and the fixation index values (FIS) were estimated using the GenAlEx 6.5 program (table S6). The allelic richness of each group was also calculated via the divBasic function implemented in the R package diversity (table S6) (39).

The hierarchical classifications were generated using PHYLIP package by calculating Cavalli-Sforza and Edwards distances (40) between ancient genotypes and current varieties (table S7). The obtained distance was used to construct the dendrogram using the neighbor-joining algorithm (41). The tree was drawn using DARwin software (42).

The membership probabilities of the ancient genotypes were identified by using a model-based clustering algorithm implemented in the computer program STRUCTURE v.2.3.4 (43). This algorithm identifies clusters (K) with different allele frequencies and assigns portions of individual genotypes to these clusters. It assumes the Hardy-Weinberg equilibrium and linkage equilibrium within clusters. The STRUCTURE algorithm was run without previous information on the geographic origin of the accessions using a model with admixture and correlated allele frequencies with 10 independent replicate runs for each K value (K value ranging from 1 to 6). For each run, we used a burn period of 10,000 iterations followed by 1 million iterations. The optimal number of clusters was assigned by using the run with the maximum likelihood validated with an ad hoc quantity based on the second-order rate of change in the log probability of data between different K values (fig. S3).The optimal alignment of the independent iterations was obtained by CLUMPP v.1.1 implemented in the Pophelper software v.1.0.10 (44); Pophelper v.1.0.10 (44) was also used to plot the results for the optimal K.

Acknowledgments: We thank J. Patrich and the late E. Netzer for making available ancient date seeds from Judean desert excavations; R. Krueger (USDA-ARS, USA) for providing some current date palm varieties; and S. Zehdi (Faculty of Sciences, University of Tunis El Manar, Tunisia), A. Lemansour (UAEU, DPDRUD, United Arab Emirates), M. A. Elhoumaizi (Sciences Faculty, Morocco), and C. Newton for allowing the use of genotyping data on current date palm varieties in the reference matrix. M. Collin is acknowledged for the help in the figure preparation and T. Bdolah Abraham for the help in statistics. O. Fragman-Sapir is acknowledged for identification of ancient date seeds and C. Yeres and A. Rifkin for information on Midrashic and Talmudic Jewish source material. Funding: The study was supported by donations to NMRC from The Charles Wolfson Charitable Trust (UK), G. Gartner and the Louise Gartner Philanthropic Fund (USA), and the Morris Family Foundation (UK). Author contributions: S.S. initiated, designed, and coordinated the study, procured ancient date samples, researched historical and archaeological information and integrated it with scientific findings, and wrote the paper. E.C. and N.C. performed genetic analyses on germinated seedlings. E.S. germinated ancient date seeds. M.E. performed radiocarbon analysis. M.G.-B., S.I., and J.-F.T. performed morphometric analysis. F.A. supervised genetic analyses and with E.C., M.G.-B., and M.E. helped write the manuscript. Competing interests: The authors declare that they have no competing interests. Data and materials availability: All data needed to evaluate the conclusions in the paper are present in the paper and/or the Supplementary Materials. Additional data related to this paper may be requested from the authors.

Read this article:
Origins and insights into the historic Judean date palm based on genetic analysis of germinated ancient seeds and morphometric studies - Science...

Recommendation and review posted by Bethany Smith

You want hair so healthythat it shines. But can anything other than good genes turn you into a walking shampooad?

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

Yes, says dermatologist Shilpi Khetarpal, MD, with the help of some nutrients and products.

Coloring, blow-drying and overwashing can all harm your hair, but there are also some other landmines to watch out for, such as:

A well-balanced diet is the first key to top-notch tresses. But you may still need extra help to kick-start your hair restoration.

Yourprimary care doctor or dermatologist can help you safely determine which hairgrowth shampoos and supplements would be the most appropriate, Dr. Khetarpalsays.

Here are six to consider for a full head of luxuriouslocks:

Dr. Khetarpalsays that success depends more on the duration of hair loss than anything else.People who have been losing hair for only two or three years are more likely tosee noticeable results than those losing it for 10 or 20 years, she explains.

You may be able to restore your hair to what it was likefive years ago, but not much beyond that. Those are the hair follicles that canbe woken up with nutritional supplementation and medical treatments, she says.Hair that has become too thin and fine can no longer penetrate and exit thesurface of the scalp. You have to be reasonable with your expectations.

And, always talk to your doctor if you start shedding morehair than is normal for you.

Originally posted here:
The Best Vitamins, Supplements and Products for Healthier Hair - Health Essentials from Cleveland Clinic

Recommendation and review posted by Bethany Smith