Category Archives: Wisconsin Stem Cells

Stem Cell Assay Market: Snapshot

Stem cell assay refers to the procedure of measuring the potency of antineoplastic drugs, on the basis of their capability of retarding the growth of human tumor cells. The assay consists of qualitative or quantitative analysis or testing of affected tissues andtumors, wherein their toxicity, impurity, and other aspects are studied.

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With the growing number of successfulstem cell therapytreatment cases, the global market for stem cell assays will gain substantial momentum. A number of research and development projects are lending a hand to the growth of the market. For instance, the University of Washingtons Institute for Stem Cell and Regenerative Medicine (ISCRM) has attempted to manipulate stem cells to heal eye, kidney, and heart injuries. A number of diseases such as Alzheimers, spinal cord injury, Parkinsons, diabetes, stroke, retinal disease, cancer, rheumatoid arthritis, and neurological diseases can be successfully treated via stem cell therapy. Therefore, stem cell assays will exhibit growing demand.

Another key development in the stem cell assay market is the development of innovative stem cell therapies. In April 2017, for instance, the first participant in an innovative clinical trial at the University of Wisconsin School of Medicine and Public Health was successfully treated with stem cell therapy. CardiAMP, the investigational therapy, has been designed to direct a large dose of the patients own bone-marrow cells to the point of cardiac injury, stimulating the natural healing response of the body.

Newer areas of application in medicine are being explored constantly. Consequently, stem cell assays are likely to play a key role in the formulation of treatments of a number of diseases.

Global Stem Cell Assay Market: Overview

The increasing investment in research and development of novel therapeutics owing to the rising incidence of chronic diseases has led to immense growth in the global stem cell assay market. In the next couple of years, the market is expected to spawn into a multi-billion dollar industry as healthcare sector and governments around the world increase their research spending.

The report analyzes the prevalent opportunities for the markets growth and those that companies should capitalize in the near future to strengthen their position in the market. It presents insights into the growth drivers and lists down the major restraints. Additionally, the report gauges the effect of Porters five forces on the overall stem cell assay market.

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Global Stem Cell Assay Market: Key Market Segments

For the purpose of the study, the report segments the global stem cell assay market based on various parameters. For instance, in terms of assay type, the market can be segmented into isolation and purification, viability, cell identification, differentiation, proliferation, apoptosis, and function. By kit, the market can be bifurcated into human embryonic stem cell kits and adult stem cell kits. Based on instruments, flow cytometer, cell imaging systems, automated cell counter, and micro electrode arrays could be the key market segments.

In terms of application, the market can be segmented into drug discovery and development, clinical research, and regenerative medicine and therapy. The growth witnessed across the aforementioned application segments will be influenced by the increasing incidence of chronic ailments which will translate into the rising demand for regenerative medicines. Finally, based on end users, research institutes and industry research constitute the key market segments.

The report includes a detailed assessment of the various factors influencing the markets expansion across its key segments. The ones holding the most lucrative prospects are analyzed, and the factors restraining its trajectory across key segments are also discussed at length.

Global Stem Cell Assay Market: Regional Analysis

Regionally, the market is expected to witness heightened demand in the developed countries across Europe and North America. The increasing incidence of chronic ailments and the subsequently expanding patient population are the chief drivers of the stem cell assay market in North America. Besides this, the market is also expected to witness lucrative opportunities in Asia Pacific and Rest of the World.

Global Stem Cell Assay Market: Vendor Landscape

A major inclusion in the report is the detailed assessment of the markets vendor landscape. For the purpose of the study the report therefore profiles some of the leading players having influence on the overall market dynamics. It also conducts SWOT analysis to study the strengths and weaknesses of the companies profiled and identify threats and opportunities that these enterprises are forecast to witness over the course of the reports forecast period.

Some of the most prominent enterprises operating in the global stem cell assay market are Bio-Rad Laboratories, Inc (U.S.), Thermo Fisher Scientific Inc. (U.S.), GE Healthcare (U.K.), Hemogenix Inc. (U.S.), Promega Corporation (U.S.), Bio-Techne Corporation (U.S.), Merck KGaA (Germany), STEMCELL Technologies Inc. (CA), Cell Biolabs, Inc. (U.S.), and Cellular Dynamics International, Inc. (U.S.).

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Stem Cell Assay Market to Witness Growth Acceleration During 2017-2025 - Cole of Duty

Twenty years after the University of WisconsinMadisons James Thomson derived the first human embryonic stem cell lines (ESC), his revolutionary discovery is just beginning to emerge on the clinical landscape.

To date, a handful of clinical trials of embryonic stem cell-derived therapies have been completed, withabout16 more now underway worldwide.

From a patients perspective, 20 years may seem like a frustratingly long time for an important discovery to get from bench to bedside. For physicians and researchers, however, the strong desire to give hope to patients is balanced with realism about the path forward. Responsible science is almost always a slow, grueling process. But experts in the field of stem cell and regenerative medicine feel more optimistic than ever, due to a critical mass of small successes.

Perhaps no field of medicine has as much reason to be hopeful about stem cell therapy as ophthalmology. Of the human trials underway, all but two involve therapies for eye disorders. David Gamm, MD, PhD, associate professor of ophthalmology and visual sciences at the UW School of Medicine and Public Health, attributes this to three factors: practicality, safety and cost.

Most new stem cell therapies require new surgical techniques and devices, but not always for the eye, Gamm explains. That reduces the cost of development and quickens the pace of getting new therapies through the FDA and into patients.

But Gamm, who also directs UWMadisons McPherson Eye Research Institute, understands patients frustrations. He likens the process of developing stem cell therapies to the first attempts at human flight.

If the Wright brothers claimed they could build a plane that would fly across the Atlantic, they would have been laughed at, Gamm says. What they were really trying to do was glide off a hill safely, with the hope of greater things to come. And thats where this field is right now.

Most of the advances in the field to date have involved the development of human embryonic stem cell-derived retinal pigment epithelium (RPE). Theretinal pigment epithelium is a single layer of cells that regulates the transport of nutrients and waste products to and from the retina and is considered to be the part of the eye where macular degeneration begins. In 2012, 18 adults with severe eye disease received transplants created from human embryonic stem cells and continue to have no apparent complications.

Thirteen of those patients had an increase in pigmentation, suggesting that the transplanted cells were still alive. The results of the study, reported by researchers at Advanced Cell Technology in Massachusetts, provided the first evidence of the medium- to long-term safety and graft survival, and possible biological activity of pluripotent stem cells in individuals with any disease.

Gamm says the numerous stem cell experts at UWMadison work together, often across disparate disciplines, from cell biology to engineering to ethics.

This is where Jamie Thomson and UW have led the way. We have a very strong sense of integrity and ethics here, and because we have this multidisciplinary approach to stem cells we also have a sense of realism, Gamm says. So, while we may not have flown that far yet, what we have done has allowed us to land safely. And that has allowed us to dust ourselves off, re-evaluate, climb back up that hill and try again.

Gamms own company, Opsis Therapeutics, is working with Cellular Dynamics International, founded by Thomson and now owned by Fujifilm, toward clinical trials for retinitis pigmentosa, a group of genetic diseases that lead to blindness at an early age. Currently, there are no treatments for these debilitating diseases.

Clinical trials for other diseases, including Parkinsons, diabetes, spinal cord injury and heart disease, will likely use induced pluripotent stem cells (iPSCs), adult cells genetically reprogrammed to behave like embryonic stem cells.

CardiologistTim Kamp, MD, PhD, a UWMadison professor of medicine and director of theUW Stem Cell and Regenerative Medicine Center, shares Gamms cautious optimism.

Stem cell biology is a dynamic landscape; things are constantly evolving, Kamp says. With every new legitimate effort, though, itll get easier for the rest of us to get approval from the FDA and our therapies into patients.

Kamp cites Geron, the first company to get a stem cell trial approved by the FDA, as an example of how each success helps accelerate progress.

Gerons final FDA application was more than 20,000 pages, Kamp explains. It took them many years and millions of dollars, but that initial process educated the FDA and provided answers to some previously unanswered questions. And that was great news for the rest of us.

Kamp is conducting preclinical work with colleagues from Duke University and the University of Alabama on a patch made of contracting heart muscle derived from induced pluripotent stem cells. He and his collaborators hope one day these cells can be used to treat patients who lose heart muscle after a heart attack.

Another of Kamps collaborators, French researcher Philippe Menasch, recently completed a phase 1 trial that transplanted embryonic stem cell-derived cardiac progenitor cells into patients with severe heart failure. That therapy seems to be safe, but its too early to tell how effective it was in re-muscularizing damaged parts of the heart.

Diabetes is another cell-based disease in the crosshairs of UW School of Medicine and Public Health researchers. Earlier this year, results of the first human trial of a stem cell-derived beta cell replacement therapy were published. Professor of Surgery Jon Odorico, MD, who organized the conference at which the results of the trial were presented, says while the findings were not a home run, the trial helped blaze an important trail through the FDA. Conducted by the company Viacyte, the trial was the first involving stem cells and a macroencapsulation device designed to protect the transplanted cells from a patients immune system.

A second trial is underway in the same patient population (adult patients with type 1 diabetes and hypoglycemia unawareness) and a handful of others are planned, including one through Odoricos own company Regenerative Medical Solutions. He hopes to have a product in clinical trials within the next few years.

There is now a critical mass of experts involved in this field and things are moving a lot faster, with more money and more industry involvement, Odorico says. Wisconsin has played a leading role in getting the field to this point and we are poised to take an even more prominent role, both nationally and internationally.

As for Gamm and his patients, the conversation has begun to shift from one of resignation to one that allows for guarded optimism. He recalls a time when there wasnt much he could offer patients, and while there are still no approved and proven stem cell therapies on the market, his message in the clinic has changed dramatically:

Its great to be able to tell my patients that they are not forgotten, Gamm says. I can finally tell them that the hope is real.

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Clinical prospects for stem cells begin to emerge

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A reader left a voicemail asking: "Where can I get some good sweet onions that are not bitter ... like ones like you get at McDonald's."

The short answer to finding onions short on bitterness is to buysweet onion varieties with names like Vidalia and Walla Walla.

As far as finding McDonald's onions at the local grocery storewell, you don't become a global restaurant powerhouse by broadcasting trade secrets.However, there are plenty of online posts on how to replicate McDonald's onions at home by hydratingminced onions.

I tried a method that callsfor 1 tablespoon of minced onions mixed with an cup of water mixed in a bowl. Microwavethe soaked onion bits for 30 seconds and let sit for 15 minutes.

It worked. The onions were sweet and plumped up but no larger than the minced onions on McDonald's burgers.

Hydrating dried minced onions creates tiny pieces that add onion flavor with minimal bitterness.(Photo: Daniel Higgins/USA TODAY NETWORK-Wisconsin)

Still, there's no need to reconstitute dried onions to satisfy your sweet onion tooth. Sweet onions are available nearly year-round in Wisconsin.

University of Wisconsinhorticulture professor Irwin Goldman wrote in an email response to my onion inquiries that most sweet onions are grown in the southern United States, Mexico, and both Central and South America. A smaller amount are grown in the Pacific Northwest.

When it comes to onions, Goldman has many layers of knowledge. Since joining the UW faculty in 1992 he's headed up the Goldman Lab that focuses on research, breeding and genetics of table beets, carrotsand onions.

Goldman explains the science of why onions make us cry and the varying bitterness as follows:

Before being cut, compartments in the onion's cells isolate a specific enzymefrom a sulfur-based substrate a substrate is a substance acted upon by an enzyme.

When the onion is cut,the cells are ruptured,allowing the enzyme and substrate to combine and produce propanethial sulfoxidethatacts a little like sulfuric acid on the nerve cell membrane of the eye and causes tearing.

The substrate concentration levels vary based on the onion variety and where and how the onion is grown. Higher substrateconcentrations and a more activeenzyme can lead to larger amounts of propanethial sulfoxide.

Variety, growing conditions and how long onions have been stored all impact their flavor.(Photo: Daniel Higgins/USA TODAY NETWORK-Wisconsin)

Onions grown in soil with lower levels of sulfur produce substrates with lower sulfur concentrations and therefore result in a milder flavor. Soil with lower levels of sulfur is more widely found in states like Georgia, Floridaand Texas. This is why sweeter, milder onions typically come from the southern states, whereas stronger flavored onions come from northern regions.

Stored onion bulbs generally increase in pungency up to about 90 days after harvest,and some continue to increase up to 120 days. There are a few that get milder with storage, but most onions simply lose water and further concentrate the substrate, which in turn makes the onion a bit more pungent with time. Also, the onion bulb goes dormantafter harvest, but its dormancy is broken after a few months. Onions that are a few months old may be producing green sprouts because their dormancy has been broken and the sulfur compounds in the substrate are being mobilized into the new leaves.

The greatest pungency of the onion is found in the tissues at the base of the bulb. Cutting through that part of a bulb releases the most pungency and would make you tear up faster than if you kept the basal portion intact and cut other parts of the onion.(Photo: Daniel Higgins/USA TODAY NETWORK-Wisconsin)

The greatest pungency of the onion is found in the tissues at the base of the bulb, near where the stem is located. If you were holding an onion in the palm of your hand with the roots at the bottom, the base would be the centimeter or so of tissue closest to your palm. Disrupting this part of a bulb releases the most pungency and would make you tear up faster than if you kept the basal portion or the onion bulb intact and cut other parts.

My thanks to professor Irwin Goldman for answering our onion questions. If you have a food question, send it my way via email or leave a voicemail message. I can't promise every answer will come from an expert of Goldman's stature, but I will get your questions answered.

More: Higgins Eats ingestigative report: These five frozen pizzas have surprisingly distinct flavor profiles

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Contact Daniel at (920) 996-7214or dphiggin@gannett.com. Follow himon Twitter and Instagram at @HigginsEats.

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Answering your sweet onion question and the science of why onions make you cry - Green Bay Press Gazette

Parkinsons disease researchers have used gene-editing tools to introduce the disorders most common genetic mutation into marmoset monkey stem cells and to successfully tamp down cellular chemistry that often goes awry in Parkinsons patients.

The edited cells are a step toward studying the degenerative neurological disorder in a primate model, which has proven elusive. Parkinsons, which affects more than 10 million people worldwide, progressively degrades the nervous system, causing characteristic tremors, dangerous loss of muscle control, cardiac and gastrointestinal dysfunction and other issues.

Marina Emborg

We know now how to insert a single mutation, a point mutation, into the marmoset stem cell, says Marina Emborg, professor of medical physics and leader of University of WisconsinMadison scientists who published their findings Feb. 26 in the journal Scientific Reports. This is an exquisite model of Parkinsons. For testing therapies, this is the perfect platform.

The researchers used a version of the gene-editing technology CRISPR to change a single nucleotide one molecule among more than 2.8 billion pairs of them found in a common marmosets DNA in the cells genetic code and give them a mutation called G2019S.

In human Parkinsons patients, the mutation causes abnormal over-activity of an enzyme, a kinase called LRRK2, involved in a cells metabolism. Other gene-editing studies have employed methods in which the cells produced both normal and mutated enzymes at the same time. The new study is the first to result in cells that make only enzymes with the G2019S mutation, which makes it easier to study what role this mutation plays in the disease.

The metabolism inside our stem cells with the mutation was not as efficient as a normal cell, just as we see in Parkinsons, says Emborg, whose work is supported by the National Institutes of Health. Our cells had a shorter life in a dish. And when they were exposed to oxidative stress, they were less resilient to that.

The mutated cells shared another shortcoming of Parkinsons: lackluster connections to other cells. Stem cells are an especially powerful research tool because they can develop into many different types of cells found throughout the body. When the researchers spurred their mutated stem cells to differentiate into neurons, they developed fewer branches to connect and communicate with neighboring neurons.

We can see the impact of these mutations on the cells in the dish, and that gives us a glimpse of what we could see if we used the same genetic principles to introduce the mutation into a marmoset, says Jenna Kropp Schmidt, a Wisconsin National Primate Research Center scientist and co-author of the study. A precisely genetically-modified monkey would allow us to monitor disease progression and test new therapeutics to affect the course of the disease.

The concept has applications in research beyond Parkinsons.

We can use some of the same genetic techniques and apply it to create other primate models of human diseases, Schmidt says.

The researchers also used marmoset stem cells to test a genetic treatment for Parkinsons. They shortened part of a gene to block LRRK2 production, which made positive changes in cellular metabolism.

We found no differences in viability between the cells with the truncated kinase and normal cells, which is a big thing. And when we made neurons from these cells, we actually found an increased number of branches, Emborg says. This kinase gene target is a good candidate to explore as a potential Parkinsons therapy.

This research was supported by grants from the National Institutes of Health (R24OD019803, P51OD011106 and UL1TR000427).

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Cells carrying Parkinson's mutation could lead to new model for studying disease - University of Wisconsin-Madison

There is new hope for patients with a rare autoimmune disorder. In mild cases, scleroderma causes areas of hardened skin. But in severe cases, it can also cause deadly hardening of internal organs like the lungs.

A transplant typically used to treat cancer is having remarkable results for patients who had little hope of surviving.

A year ago, Chuck Beschta couldn't walk more than a few minutes without stopping to rest.

"Just going out and doing normal activities outside raking the lawn, mowing the grass, shoveling the driveway, whatever, snow blowing those became impossible," he said.

After months of testing, he was diagnosed with severe scleroderma, which was hardening his skin. But even worse, it was hardening his lungs, making it hard to breathe.

"He was getting worse despite the best therapy we had to offer," University of Wisconsin rheumatologist Dr. Kevin McKown said.

McKown recommended a stem cell transplant newly approved for scleroderma to reboot Beschta's immune system.

"There's a process by which they try to remove the autoreactive immune cells, the cells that are caught in the immune process, and then they infuse that back in and hope that the body will basically take up and graft that immune system," McKown said.

Beschta saw almost immediate results. His skin was softer and his breathing improved. He hopes his scleroderma has been cured.

"I think we can be optimistic, and so far the people who have been followed out as far as 10 years out don't seem to be getting it back," McKown said.

Without a transplant, less than half the patients who have diffuse scleroderma and severe lung disease live 10 years past diagnosis.

Stem cell transplants are commonly used to treat leukemia and lymphoma, cancers that affect the blood and lymphatic system.

MEDICAL BREAKTHROUGHSRESEARCH SUMMARYTOPIC: NEW THERAPY FOR SCLERODERMAREPORT: MB #4698

BACKGROUND: Scleroderma is an autoimmune rheumatic disease where an overproduction of collagen produced in the body tissues causes the skin and internal organs to harden. The symptoms and effects range by person, but some common symptoms include hardened patches of skin (locations on the body vary,) painful and numb-feeling fingers and toes, and sharp internal pain in the esophagus, intestines, heart, lungs, or kidneys. Women are four times as likely to have scleroderma and the onset is between 30 and 50 years of age. However, anyone from infants to the elderly can have scleroderma. Possible risk factors include having certain gene variations as other family members, ethnic groups, exposure to certain medications or drugs, and already having another autoimmune disease, like rheumatoid arthritis, lupus or Sjogren's syndrome. (Source: https://www.scleroderma.org/site/SPageNavigator/patients_whatis.html;jsessionid=00000000.app30132b?NONCE_TOKEN=9B76519DF6B5819859319F0B63B805C9#.XheCGVVKhaQ , https://www.mayoclinic.org/diseases-conditions/scleroderma/symptoms-causes/syc-20351952 )

DIAGNOSING: A physical exam will be conducted as well as a blood test to check for elevated levels of antibodies the immune system produced. The doctor will also take a sample of skin to be tested in the lab. If there are complaints about internal pain, the doctor may run other tests, including imaging, organ function, and other blood tests. (Source: https://www.mayoclinic.org/diseases-conditions/scleroderma/diagnosis-treatment/drc-20351957 )

NEW TECHNOLOGY: A new stem cell transplant that's commonly known to treat cancer is improving the quality and quantity of life for those with scleroderma. Rheumatologists at University of Wisconsin Health tested the treatment since they have already been conducting bone marrow transplants for decades. Surgeons take out a sample of the patient's bone marrow, isolate the stem cells, and use radiation and chemotherapy to clean out their immune system. The same stem cells are later injected back into the patient's immune system with the hope that new cells will grow and the system is rid of the bad ones. The process is dangerous when the cells are taken out because the patient's immune system is more vulnerable, making infections more likely to occur. However, after four and a half years, 79% of patients that underwent the treatment were alive without serious complications compared to 50% that were treated with the original drugs. (Source: https://madison.com/wsj/news/local/health-med-fit/man-with-severe-autoimmune-disease-gets-stem-cell-transplant-at/article_7e8e17a5-21da-52f8-b728-fe584dab2b77.html)

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New technique developed to treat hardening of internal organs - WNDU-TV

At several labs across the US, researchers use fetal tissue from humans to investigate everything from viral infections to the developing brain. Such studies have been ongoing for decades, as have politically fraught debates about this research, because it primarily relies on tissue donated after terminated pregnancies.

Last summer, President Donald Trumps administration announced that it would be placing restrictions on experiments involving fetal tissue obtained from elective abortions, which included banning government scientists from using this material for research and applying increased scrutiny for National Institutes of Health (NIH) grant proposals from nongovernmental scientists.

Researchers say that the new restrictions on fetal tissue research have required them to change their plans for future work or to search for alternative sources of funding. Its impacted almost all of the facets of the lab, says Carolyn Coyne, a microbiologist at the University of Pittsburgh who uses fetal tissue to study how viruses penetrate the placenta.

Its affected pretty much every grant application that that weve written.

Mana Parast, University of California, San Deigo

One of the main concerns, according to several researchers who spoke to The Scientist,is the lack of clarity regarding what the NIH will require in grant applications for this work. The Department of Health and Human Services (HHS), which oversees the NIH, has stated that it would put together a new ethics advisory board to review such proposals. Last week (February 20), HHS posted a notice indicating its intent to convene the NIHs fetal tissue ethics advisory board in 2020. In a written statement to The Scientist,the NIH states that it is in the process of setting up the Ethics Advisory Board for the purpose of evaluating research proposing the use of human fetal tissue from elective abortion.

Scientists are waiting to find out who will be appointed to the board and how it will evaluate proposals once it convenes. [Well] see whether the administration is going to act in good faith and appoint a decent ethics review committee, or if theyre going to ignore the value of the scientific and medical research that needs to be done in this area and let ideology weigh out over logic, says Lawrence Goldstein, a stem cell scientist at the University of California, San Diego, whose lab has worked with fetal cells in the past. The fetal tissue that were talking aboutif we dont use it for research, it will be discarded. Thats the choice. Discard the fetal tissue in the in the trash, or use it for valuable research.

This is not the first time such a ban has been put in place. In 1988, former US President Ronald Reagan placed similar restrictions on federal funding for fetal tissue studies, which stayed in place until President Bill Clinton overturned them during the first year of his term in 1993.

Fetal tissue used for research is primarily obtained from elective abortions, which women can consent to donate after deciding to terminate a pregnancy. This is because there are some major limitations to tissue obtained through other means, such as miscarriages, according to Anita Bhattacharyya, a stem cell scientist at the University of Wisconsin-Madisons Waisman Center. Supply is limited and the underlying factors that lead to pregnancy loss can complicate experiments. On top of that, such events often happen unexpectedly, meaning that the collected tissue is not always intact. We would worry about using poor quality tissue as a foundation for the work we do, says Bhattacharyya, who uses donated fetal brain tissue to study brain development and disorders such as Down syndrome and fragile X syndrome.

Bhattacharyya says that although her lab currently has the tissue it needs to complete experiments from a prior grant, shes not comfortable submitting proposals for studies that require obtaining new fetal tissue. Its because I dont know whats going to happen. If I spend hours writing a grant that I think is really good science, and I send it to NIH . . . its going to get stuck there, Bhattacharyya explains. Were so busy as scientists that to just write a grant that isnt going to go anywhere is a waste of our time.

As such, her projects may suffer. According to Bhattacharyya, not only is brain development difficult to study in model organisms such as rodents, but fragile X and Down syndrome in particular are difficult, if not impossible, to model in animals. Induced pluripotent stem cells (iPSCs), which can be generated by reprogramming cells from skin or blood in adults, have offered an alternative means of studying the development and disorders of the brain, yet researchers still need to validate the results they obtain, Bhattacharyya says. Really, the only way to do that is using fetal tissue.

In addition to cells and tissue from the fetus itself, the restrictions on NIH funding were also applied to other biological materials obtained in the process of abortions, such as umbilical cord, placenta, and amniotic fluid. While some of these can be useful to scientists when collected after birth, placental tissue obtained in this way has limitations. Full term placentas are actually aged tissues, explains Coyne. If were studying a full-term placenta post-delivery, the gnawing question is: Has that placenta changed from the placenta that exists in the first or second trimester?

Mana Parast, a stem cell and placental biologist at the University of California, San Diego, who studies placental development and disorders, tells The Scientist that while the policy change has left ongoing projects unscathed, its affected pretty much every grant application that that weve written since then. While Parasts team has used fetal tissue in the past, they are now focusing on using iPSC-based models. However, like Bhattacharyya, she notes that this isnt the perfect solutionas these models are fairly new and not yet broadly accepted, it is still necessary to validate them with cells from human placentas.

Coyne says that in addition to limiting access to grants for her research, the restrictions have also made it more difficult to procure tissue. A lot of major medical schools have federally funded tissue banks, Coyne explains. Our institutional tissue bank has been affected by this such that we cant obtain tissue from elective terminations anymore.

For researchers who have been able to obtain funding from alternative sources, such as philanthropists or private foundations, the effects of the restrictions have been minimal. Thomas Reh, a biologist at the University of Washington whose team uses fetal tissue to study the developing retina, says that his groups work is currently supported by a grant from the Open Philanthropy Project, a nonprofit organization. When the political climate gets more restrictive, private donors will often step in, Reh says. I wont say that works for everybody, or that it works all the time. At least in my own case, this is whats allowed me to sort of fill these gaps when [restrictions on fetal tissue] happen.

Its the next generation of trainees that are going to be most impacted, not just because they cant get funding, but if I were one of them, I would think to myself, is this really an area that I want to specialize in?

Carolyn Coyne, University of Pittsburgh

Andrew McMahon, a stem cell scientist at the University of Southern California, still has about a year left before he needs to apply for more funding, and hes started looking into potential alternatives to NIH. My understanding is that its not entirely clear at the moment what that process is going to be, McMahon says. Ive been using the time to obtain non-NIH funding to support aspects of the research that I would have tried to get NIH funding [for] in the future.

Private funds are not available to everyone, and can be more difficult for researchers in some fields to obtain than others. For some of the disorders that I work on, the major private funding foundation does not allow fetal tissue research, Bhattacharyya says. And sometimes the foundation funding can be quite a bit less than NIH funding.

For researchers in some states, nonprofits are not the only option. In California, the states stem cell agency, the California Institute for Regenerative Medicine (CIRM) has provided funding for stem cell studies using fetal tissue since it was founded in 2004. That fund is about to run out, but a bill that would provide $5.5 billion in funding to CIRM will come before voters in November.

That will hopefully provide funding for areas of fetal tissue research that involves stem cells, Goldstein says. But . . . its ridiculous to rely on one or two states to self-fund, because we dont have all of the best and brightest [scientists], and it means lots of students and postdocs will train in areas where federal training support will be unavailable to them.

Goldstein isnt the only one concerned that the most profound effect of the governments restrictions will be on early-career investigators and trainees. While established researchers may be able to circumvent the effects of the restrictions in the short term, the ramifications for trainees in this field will likely be much longer-lasting, Coyne says. Its the next generation of trainees that are going to be most impacted, not just because they cant get funding, but if I were one of them, I would think to myself, is this really an area that I want to specialize in and get into?

One scientist, who asked to remain anonymous for fear of being harassed by anti-abortion activists, tells The Scientist that the restrictions have been a source of huge stress and anxiety for his lab, which he only established a few years ago. He adds that while his team has pivoted to using animal models and organoids generated from iPSCs, these are imperfect models of the developing human brain, which is the focus of his work.

It makes no sense to limit this research, given that the tissue from abortions will get discarded now that donation is not an option, Parast says. Were not talking about encouraging this procedurewere trying to use the material from patients who have already decided to undergo this procedure in order to be able to help other women.

Diana Kwon is a Berlin-based freelance journalist. Follow her on Twitter@DianaMKwon.

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Scientists Grapple with US Restrictions on Fetal Tissue Research - The Scientist

By Don Doc Sanders

I can still remember as a 12-year-old seeing live deer for the first time, in the field near my childhood home in Auglaize County. With his Super-8 movie camera my uncle captured four deer jumping a fence after they scouted the field for several minutes. It was an awesome experience for our whole family; none of us had ever seen deer in the wild.

Fast forward to today: We see deer everywhere. We also see the consequences of their presence, like damaged crops, deer-vehicle collisions and trampled flower beds. Deer seem to take a special liking to the security of residential areas, within city limits, safe from hunters. As a plus for the city deer, some people delight in putting out food, apparently in case the moochers are still hungry after plundering their neighbors gardens.

With deer as plentiful as they are, were constantly on edge as we drive on highways and country roads, especially at dusk, fearful one might run out at any moment into our path or the side of our car or truck. The deer are probably on edge, too.

Now they have an additional concern, besides becoming roadkill or getting bagged by a hunter: chronic wasting disease, or CWD. With CWD, as the diseases name implies, an infected deers musculature and flesh waste away over time until the animal dies from emaciation.

But CWD isnt just another infection like Strep, Staph or E. coli. CWD is believed to be caused by abnormally folded brain proteins called prions.

Scientists are still trying to learn why brain proteins become misfolded, but they recently learned that copper ions bind to the tail of prion proteins. They dont know how copper binding causes the misfolding, but they do know that it seems to lead to misfolding of proteins in adjacent brain cells, which clump together.

These clumped, misfolded brain proteins become dangerous pathogens that lead to widespread destruction of an infected brain.

Prion diseases are categorized, as a group, as transmissible spongiform encephalopathy (TSE). TSE diseases are known by different names in different species Creutzfeldt-Jakob disease in humans, scrapie in sheep and mad cow disease in cattle (so called due to the bizarre, aggressive behavior of infected cows that endangers caretakers). By the way, cannibalistic tribes in New Guinea also have a TSE disease known commonly as kuru, which spreads when people eat the brains of misfolded-prion-infected dead family members. It appears that all TSE diseases are spread by consuming infected brain tissue or by inheriting it from the dam.

Hot off the press while I was writing this column a scientific report published by Texas Life Sciences, Colorado State and the USDA has reported that the CWD misfolded prions to also occur in deer semen and other reproductive organs. Researchers arent certain, but believe there may also be other causes.

There is some evidence that Alzheimers disease has prion-like lesions similar to those in CWD and mad cow disease. In Alzheimers, amyloid beta proteins malform and clump together in the brain. This suggests a link to prion diseases in animals more than previously speculated though amyloid beta proteins are different than prions.

Mad cow disease became epidemic in Britain during the 90s when carcasses of sheep that died from scrapie were processed into a protein source for cattle feed. At one point, Britain had 800,000 cases of mad cow disease, apparently as a result of this. Mad cow disease disappeared gradually in Britain once the cause was discovered and the processing of scrapie-infected sheep was stopped.

To prevent the spread of TSE diseases, packing plants under state or USDA inspection are required to remove brain and nerve tissue from food animal sources. Custom slaughter plants that process meat for individual customers must also follow inspection guidelines established by state veterinary and agricultural officials.

And to prevent the spread of CWD, Ohio state laws require that deer killed during a hunting season must have the head submitted for testing, to check for misfolded prions before the meat is processed. Checking for misfolded prions in the brain stem and mandibular lymph nodes is a reliable method for determining if a deer has CWD. Any deer carcass testing positive is immediately destroyed.

Ohios regulations require testing of any bagged deer a year old or older but will test younger harvested deer when requested. Ohio officials report that no deer have tested positive in the past few years. Prior to this, in 2014 multiple cases were diagnosed in one herd on a private Ohio deer farm. That herd was immediately destroyed. And several years ago, individual deer on three private farms tested positive. There have not been positive cases reported for CWD in deer since then.

CWD-infected deer have also been reported being harvested in the wild in Minnesota, Wisconsin, Pennsylvania and Indiana. We are living in an interesting new era as scientists work to discover the cause of all prion diseases, CWD included.

And even more hopeful for us humans are scientists continuing efforts to determine the causes of Alzheimers and dementia, to identify ways to prevent and treat this brain pathology.

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Deer hunter or Bambi lover: What you should know about chronic wasting disease - Ohio's Country Journal and Ohio Ag Net

Most often cord tissue is donated or set aside as medical waste after a child is born and doctors use that tissue to isolate regenerative cells for use in Cord Tissue Cell Therapy treatments. These donations are made with the permission of the parents and under careful ethical restrictions. The process is safe for all parties involved and poses no risk of pain or damage to the mother and child. Cord tissue donations are meticulously audited for healthy, high-quality regenerative cells to be used for Cord Tissue Cell Therapy. The application of Cord Tissue Cell Therapy will vary patient to patient after your doctor has had time to assess your needs and decide on the most effective therapy to provide positive results.

Harvested cord tissue cells used for this procedure have a low possibility of malignant transformation and adverse immune response, making Cord Tissue Cell Therapy a safe option for patients. These cells are unlikely to be rejected by your immune system and careful, sterile laboratory processes eliminate the potential for contamination or infection. Cord Tissue Cell Therapy resists against any production of antibodies or T-cell responses, ensuring protection against any adverse reactions to the procedure.

As with any medical treatment, each patients response will vary so discussing options for your specific needs is key.

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Cord Tissue Cell Therapy | Wisconsin Stem Cell Therapy

In 2017, Bennet Omalu traveled the globe to accept a series of honors and promote his autobiography, "Truth Doesn't Have A Side."

In a visit to an Irish medical school, he told students he was a "nobody" who "discovered a disease in America's most popular sport."

In an appearance on a religious cable TV show, he said he named the disease chronic traumatic encephalopathy, or CTE, because "it sounded intellectually sophisticated, with a very good acronym."

And since his discovery, Omalu told "Sports Illustrated," researchers have uncovered evidence that shows adolescents who participate in football, hockey, wrestling and mixed martial arts are more likely to drop out of school, become addicted to drugs, struggle with mental illness, commit violent crimes and kill themselves.

A Nigerian American pathologist portrayed by Will Smith in the 2015 film, "Concussion," Omalu is partly responsible for the most important sports story of the 21st century. Since 2005, when Omalu first reported finding widespread brain damage in a former NFL player, concerns about CTE have inspired a global revolution in concussion safety and fueled an ongoing existential crisis for America's most popular sport. Omalu's discovery initially ignored and then attacked by NFL-allied doctors inspired an avalanche of scientific research that forced the league to acknowledge a link between football and brain disease.

Nearly 15 years later, Omalu has withdrawn from the CTE research community and remade himself as an evangelist, traveling the world selling his frightening version of what scientists know about CTE and contact sports. In paid speaking engagements, expert witness testimony and in several books he has authored, Omalu portrays CTE as an epidemic and himself as a crusader, fighting against not just the NFL but also the medical science community, which he claims is too corrupted to acknowledge clear-cut evidence that contact sports destroy lives.

After more than a decade of intensive research by scientists from around the globe, the state of scientific knowledge of CTE remains one of uncertainty. Among CTE experts, many important aspects of the disease from what symptoms it causes, to how prevalent or rare it is remain the subject of research and debate.

But across the brain science community, there is wide consensus on one thing: Omalu, the man considered by many the public face of CTE research, routinely exaggerates his accomplishments and dramatically overstates the known risks of CTE and contact sports, fueling misconceptions about the disease, according to interviews with more than 50 experts in neurodegenerative disease and brain injuries, and a review of more than 100 papers from peer-reviewed medical journals.

Omalu did not discover CTE, nor did he name the disease. The alarming statistics he recites about contact sports are distorted, according to the author of the studies that produced those figures. And while Omalu cultivates a reputation as the global authority on CTE, it's unclear whether he is diagnosing it correctly, according to several experts on the disease.

Omalu's definition for CTE, as described in his published papers, is incredibly broad and all-encompassing, describing characteristics that can be found in normal, healthy brains, as well as in other diseases, according to experts including Ann McKee, lead neuropathologist for Boston University's CTE Center.

"His criteria don't make sense to me," McKee said. "I don't know what he's doing."

McKee's assessment was supported by three neuropathologists who worked with her to develop guidelines for diagnosing CTE used by researchers around the world.

"My God, if people were actually following [Omalu's] criteria, the prevalence of this disease would be enormous, and there's absolutely no evidence to support that," said Dan Perl, one of those experts and professor of pathology at the Uniformed Services University.

McKee and other experts confirmed, in interviews, something that long has been an open secret in the CTE research community: Omalu's paper on Mike Webster the former Pittsburgh Steelers great who was the first NFL player discovered to have CTE does not depict or describe the disease as the medical science community defines it.

McKee and other experts believe Webster had CTE, based on his history of head trauma and his mental disorders. But the paper Omalu published shows images that are not CTE and could have come from the brain of a healthy 50-year-old man, they said.

"This is the problem," McKee said. "People lump me with him, and they lump my work with him, and my work is nothing like this."

Omalu declined several requests for an interview and refused to answer any questions for this report. In an email, he dismissed questions raised by experts as coming from "a minority of doctors who are seeking very cheap and bogus popularity ... who work directly or indirectly with these sports organizations."

"Your paper engaging in such bogus controversies will bolster some people's allegations of 'Fake News,' " Omalu wrote.

This is typically how Omalu responds to criticism: by claiming it comes from scientists corrupted by relationships with sports leagues. But his depiction of the science of CTE and his prominence in the CTE research community have yielded his own financial benefits.

Billing himself as the man who discovered CTE, Omalu has built a lucrative business as an expert witness for hire in lawsuits including in the growing CTE-related litigation field charging a minimum of $10,000 per case, according to his testimony. He also maintains a busy schedule of paid speaking engagements, charging $27,500 per appearance, records show, as he delivers his sermon against contact sports.

A deeply religious man, Omalu has said he believes he is on a mission from God, and he views scientists who question him with suspicion and hostility.

"As a Christian, I believe after death there is judgment," Omalu told a lawyer in a deposition once, when asked about experts who raised doubts about his theories. "They will all answer for this on judgment day."

***

Omalu first drew national news attention in 2007 as the diminutive, quirky local coroner in Pittsburgh declaring he had identified a new brain disease in former NFL players.

"We are calling it football-induced chronic traumatic encephalopathy," Omalu told ESPN.

Contrary to Omalu's claims, doctors have been studying what we now call CTE since 1928, when New Jersey pathologist Harrison Martland described a phenomenon he observed among several boxers that he termed "punch drunk."

Over the next 70 years, doctors around the globe encountered similar ailments in boxers, and the syndrome became commonly known as "dementia pugilistica." In 1949, British neurologist MacDonald Critchley was the first to use the term chronic traumatic encephalopathy. By the early 2000s, the term CTE was in common usage among the then-small community of experts who researched the disease.

In 2005, Omalu published his first paper, in collaboration with doctors at University of Pittsburgh Medical Center, reporting he found CTE in Webster, who had died of a heart attack after enduring an array of behavioral disturbances for years after his retirement.

To the medical science community, the significance of Omalu's paper was that CTE had been found for the first time in a former NFL player. But over the years, Omalu has repeatedly claimed that he discovered CTE.

"I said to myself ... you need to give it a sexy name," Omalu said in 2013. "You need to give it a name that has a good acronym that people would remember. ... That was how CTE came about."

In 2009, McKee and her colleagues at BU published their first CTE paper, describing what they found in the brains of two former boxers and a former NFL player John Grimsley, a linebacker for the Houston Oilers and Miami Dolphins. McKee's paper described the long history of CTE research and referenced Omalu's Webster paper.

In "Truth Doesn't Have A Side," Omalu falsely accused McKee of trying to take credit for his discovery, referring to her as "the blonde white woman who claimed she discovered CTE."

Asked by email whether she ever has claimed to have discovered CTE, McKee replied: "Ha. No."

Steven DeKosky, a neurologist and deputy director of the McKnight Brain Institute at the University of Florida, was one of Omalu's early collaborators. In a phone interview, DeKosky said he and Omalu knew in 2005 they had not discovered a new disease. DeKosky knew the disease as dementia pugilistica, however, and agreed with Omalu that they should rename it because Webster hadn't been a boxer. Omalu suggested CTE.

DeKosky believed then that Omalu had come up with the name, he said, until he later learned researchers had been using the term for years.

"I was a bit embarrassed," DeKosky said. He said he has no idea why Omalu continues to claim he discovered and named the disease.

"Maybe, like me, he just didn't realize that it had been called by that same name before," DeKosky said. "He's a complex guy. All of us are."

In a 2018 deposition in a CTE-related lawsuit against the NCAA, Omalu acknowledged he did not discover CTE.

"Some people who give me credit of discovering CTE, that is not true, really," he said. Later, Omalu said he had only been "successful in rebranding this disease concept."

***

CTE became a national news story in 2009 as Omalu and McKee diagnosed the disease in several former NFL players who died young, prompting congressional hearings.

As Omalu and McKee publicized their findings, they dealt with attacks from NFL-allied doctors. Scientists who wanted to conduct their own CTE research, meanwhile, dealt with another problem: Omalu and McKee had different definitions for what CTE looked like and how to diagnose it, a disagreement they have never resolved.

Omalu often uses the phrase "tested positive for CTE," implying the diagnostic process is black and white, akin to a pregnancy test. In reality, diagnosing CTE is far more complicated, more like looking out into a starry night and spotting a constellation.

There is no reliable technology to detect CTE in the living; the disease can be diagnosed only after someone dies and their brain can be dissected and analyzed.

CTE is marked by accumulations of an abnormal or defective form of a protein called tau in the brain. Tau is a normal protein found in the brain and the central nervous system that has a stabilizing effect on cells.

Tau can become abnormal, however, and clump into formations called tangles.

This can happen as people get older, and small amounts of abnormal tau in the brain are thought by some experts to be benign and part of the aging process. In significant amounts, however, abnormal tau is a sign of brain damage or disease, such as Alzheimer's disease, as well as CTE.

Even under the microscope, diagnosing CTE is complicated by another factor: Abnormal tau is also found in more than a dozen other diseases. Tau also accumulates in healthy brains as people age, with no apparent effect on brain function or behavior.

Scientists can distinguish brains with benign accumulations of abnormal tau from brains with damage and disease based on the amount, pattern and location of the tau, among several factors.

In 2014, the National Institutes of Health stepped in to answer the question of how to diagnose CTE by funding a study overseen by McKee and seven other neuropathologists from around the world. They concluded that CTE's unique characteristic its signature, essentially is clusters of tau around blood vessels deep in the folds of the cortex, the brain's outermost region. CTE experts around the globe use this definition in their research.

Omalu's definition for CTE, described in his published papers, is different than the NIH's definition. Omalu has identified four types of CTE. In interviews with The Washington Post, experts said two of Omalu's types could be CTE. The other two types, however, experts found problematic.

Omalu's third CTE type is marked by "moderate to frequent" tau tangles in the brain stem, and "none to sparse" tau tangles in the cerebral cortex. Brains can develop tau in these areas through normal aging, experts said, as well as through other diseases.

Omalu's fourth CTE type, which he called "incipient CTE," is marked by "a combination of none to sparse" tau tangles in the cerebral cortex, brainstem and basal ganglia. Tau also can accumulate, in small amounts, in these areas through normal aging and other diseases.

Experts found Omalu's fourth type nonsensical, noting that, as written, it suggested he would diagnose CTE in a brain with no tau.

"It sort of sounds like he's saying, if you had someone who had a history of playing contact sports, it's OK to diagnose them with CTE even if you don't have any" tau, said Perl, an internationally known expert in brain diseases. "That doesn't make any sense."

In a deposition in 2018, Omalu displayed ambivalence when asked whether he followed the NIH guidelines.

"The final decision is still with the doctor who is examining," Omalu said. "Not every CTE case will have all those guidelines."

McKee said she does not believe what Omalu calls "incipient CTE" is actually CTE.

"His criteria for diagnosing CTE are all over the map," McKee said.

McKee and other experts in brain disease have held doubts about Omalu's diagnostic methods since his first, and most famous, CTE paper.

***

The tragic decline of the man known around Pittsburgh as "Iron Mike" has been told and retold over the years, in magazine articles, books and in the opening scenes of "Concussion."

Before he died in 2002, at 50, Webster had struggled for years with depression, paranoia and chronic pain so agonizing that he sometimes needed to shock himself unconscious with a stun gun just to get some sleep.

CTE experts, in interviews, did not dispute football damaged Webster's brain. He probably played through many concussions, and the NFL's retirement board acknowledged Webster suffered from football-related brain damage in 1999.

But whether the man who was essentially "Patient Zero" for CTE in football actually had the disease, according to experts, is an unanswered question.

In medical research papers, it is customary to publish, as photos, the most compelling, striking images that depict the paper's subject. The images Omalu published in the Webster paper do not show CTE, nor do they show alarming amounts of tau for a 50-year-old man, experts said.

The images show tau in formations called tangles. One image shows a single tangle, highly magnified, and another shows a similarly magnified image of two tangles, according to the paper. Both images come from the cortex.

McKee and other experts said one or two tangles can be found in the cortexes of otherwise healthy 50-year-olds. If surrounded by several other tangles, they could be part of a disease. But in isolation, they could be benign. It was as if Omalu had claimed to have found a rare species of bird and then, as proof, published a paper that included only a few close-up images of the tip of the beak.

In the text of the paper, Omalu described more tau than doctors would expect to find in the brain of a 50-year-old, experts said, but for reasons he has never explained, he selected images that could have come from the brain of a healthy 50-year-old man.

"What Omalu described is just some tau ... [with] not enough details to know what kind of tau it was or what the disease was. ... From reading that paper, I would have no idea the guy had CTE," McKee said.

"I'm 50. I would expect my brain would have a few tangles here and there," said Willie Stewart, Britain's leading CTE researcher, a neuropathologist and honorary clinical associate professor at the University of Glasgow. "The images that Bennet has in that paper, they don't show CTE."

In interviews, two of Omalu's co-authors had conflicting memories about what they saw in Webster's brain.

DeKosky, the Florida neurology professor, said he recalls seeing the signature CTE pattern but was unsure why the correct images weren't selected for the paper. Ronald Hamilton, a retired former Pittsburgh neuropathologist, said he does not recall seeing the signature pattern and no longer has his research material from the case.

"There's a 100 percent chance" Webster had CTE, Hamilton said. "But, yes, I can't prove it."

There is one other person who examined Webster's brain tissue in the 2000s. But his recollection of what he saw only deepens the mystery.

In 2008, Peter Davies, an Alzheimer's researcher and professor at the Albert Einstein College of Medicine in New York, met with Omalu, who let him take some tissue from Webster's brain, as well as from five of his other early CTE cases, back to his lab.

Davies said Omalu was right; Webster did have a disease he had never seen, with "buckets of tau." Tissue from two of the other brains one from another former NFL player, the other from a former professional wrestler also had the same widespread tau.

Davies believes, however, that the disease he saw in Webster's brain and the two others was "extremely rare" and different from the CTE described by other researchers, because of the overwhelming amount of tau he saw under the microscope.

"In my mind, it's a separate disease," Davies said.

The reason Omalu picked the wrong images, Davies said, was that Omalu "was not any kind of an expert."

"He would be very upset to hear me say something like that," Davies said.

BU's McKee has never examined Webster's brain, but she said she has asked doctors at Pittsburgh labs where Omalu worked if they know where the tissue is, with no success.

In "Truth Doesn't Have A Side," Omalu wrote that he confiscated the Webster tissue and other CTE brains from the coroner's office in Pittsburgh because of an attempt by "detractors" to destroy them. DeKosky said he believes Omalu still has Webster's brain, either at his home or in his private lab outside Sacramento, California.

Omalu has not published a paper describing refinements to his definition for CTE since 2011. He continues to examine brains of suspected CTE cases, however, and his diagnoses prompt lawsuits and news coverage.

***

In Omalu's words, CTE is an epidemic, a risk for anyone who plays any contact sport, at any level, and likely affecting every former NFL player.

"No single concussion is safe regarding the risk of developing gridiron dementia," Omalu wrote in his first book, "Play Hard, Die Young."

"I believe there is a very good chance that every person who plays (or has played or will play) in the NFL will suffer from some degree of CTE," he wrote in "Truth Doesn't Have A Side."

In recorded medical literature, there are no documented cases of someone developing CTE from a single concussion. And while mounting scientific evidence suggests CTE is a significant risk for NFL players, studies examining groups of athletes who played other sports suggest it remains possible, if not likely, that Omalu is significantly overestimating the population potentially afflicted with CTE.

Several studies have found former NFL players die with brain disease at significantly higher rates than comparison populations, but nothing approaching 100%, with figures ranging from 5% to 8%. There have been no published studies examining rates of brain disease among former college football players, but one sizable research project, overseen by the NCAA and the Department of Defense, is underway. Three studies of former high school football players who played in Minnesota and Wisconsin between 1946 and 1970 found they had no higher rates of brain disease than their classmates.

Studies examining the rates of brain disease among athletes who played other sports have produced mixed results. A study published late last year of thousands of former professional soccer players in Scotland found higher rates of players dying with brain disease 11.4% among soccer players, compared with 3.2% among the general population. But smaller studies examining groups of former NHL players and professional rugby players found no signs of higher rates of brain disease.

At BU, McKee and her colleagues focus criticism on football, which they believe has a relationship with CTE similar to smoking and cancer. They support banning tackle football before age 12 and rules changes in other sports to reduce head hits. They have not echoed Omalu's call for the abolition of youth wrestling, hockey and mixed martial arts.

"I don't know where he's coming up with those recommendations," McKee said. "I don't think he is basing them on any data."

Omalu repeatedly has cited data that he claims show children who play these sports are at increased risk to see their lives unravel from mental illness, substance abuse or other struggles.

"Studies have shown that if a child plays a high-impact, high-contact sport," Omalu wrote in "Truth Doesn't Have A Side," "that child stands a higher risk of dropping out of high school, not attending college, not doing well in life . . . developing psychiatric and psychological problems ... and even dying at a younger age."

No studies have found that merely playing a contact sport increases the risk of the tragic life outcomes Omalu has described. In some settings, when citing these figures, he has mentioned "a paper that came out of Sweden." This appears to be a reference to research led by Seena Fazel, professor of forensic psychiatry at the University of Oxford, examining what happened to more than 1.1 million people in Sweden who suffered brain injuries before turning 25.

Fazel was unaware of how Omalu had been interpreting his studies until contacted by a reporter last year.

"That's definitely not what we said. ... You can't extrapolate that from our work," Fazel said in a phone interview.

Fazel's research examined a population that included people who had suffered concussions in sports but also people who had survived much more severe injuries, such as head impacts during car crashes that resulted in lengthy hospitalizations.

"We're not just talking about someone who's had a bang on the head at a sports match. ... We're talking about the more severe end of the spectrum," Fazel said. "These papers don't say, 'Don't play sports.' ... They support good [head safety] policies in sports."

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The selling of CTE: How the 'Concussion' doctor has built a career on distorted science - Stars and Stripes

Delta plane slides off icy taxiway at the Green Bay airport

GREEN BAY, Wis. (AP) A Delta Air Lines plane slid off a taxiway amid icy conditions Saturday morning at an airport in Green Bay, Wisconsin.

Airport officials said Flight 1770 was headed for Atlanta when it left the taxiway around 6:15 a.m. No injuries were reported, nor was there any damage to the plane.

Conditions were icy at the time of the incident, but Airport Director Marty Piette told the Green Bay Press-Gazette that he wasnt sure if thats what caused the plane to slide off the taxiway. He said airport staff were aware of the icy conditions and treated the taxiway with sand and alerted pilots of the icy and slippery conditions.

Freezing drizzle was blamed for several crashes on northeastern Wisconsin roads Saturday morning.

The 107 passengers were bused back to the airport for rebooking on other flights and were given meal vouchers.

Passenger Kent Maxwell, of Green Bay, told the newspaper that people on the plane were calm and respectful as the airline dealt with the issue.

I fly a lot and usually problems cause infrequent passengers to really get excited, Maxwell said. That didnt happen on this flight. I think most people can relate to sliding off the road into a ditch.

NASHVILLE, Tenn. (AP) One African American defendant was forced by a judge to represent himself at trial. Another was shackled in front of an all white jury during a sentencing hearing. And a third black defendant facing the death penalty is intellectually disabled.

Those are some of the arguments made by defense attorneys in documents filed this week with the state Supreme Court in an attempt to stem the pace of executions in Tennessee, which has surged to the forefront nationally in its application of the death penalty. They also argue Tennessees use of capital punishment is rooted in a racist past and is still plagued with inherent racism.

Attorney General Herbert Slatery is seeking to set dates for the nine death row inmates, all men, to die. Four of the nine are African American. Attorneys for the inmates point out that the justices could keep Tennessee moving in the opposite direction of the country as a whole or could join the ranks of most states in trending away from executions.

While the standards of decency of the nation as a whole have evolved towards rejection of the death penalty, Tennessee has fallen out of step with the rest of the country particularly in the last eighteen months, during which the State has executed six of its citizens at a rate not seen since before 1960, attorneys for the inmates wrote.

One of the inmates facing a possible execution date, Tony Carruthers, would be the first person in about a century to be put to death after being forced to represent himself at trial, supervisory assistant federal public defender Kelley Henry wrote in a filing.

Carruthers and another man were convicted of the 1994 killing of three people in an attempt to corner the illegal drug trade in their Memphis neighborhood.

The trial judge refused to appoint another attorney after Carruthers, whose attorneys describe him as severely mentally ill, ran off about a half-dozen lawyers with threats or lack of cooperation, the filing said. A court has never weighed in on whether Carruthers self-representation was constitutionally adequate, Henry wrote.

Farris Morris, an African American man convicted of a 1994 double murder and rape, was shackled during his sentencing trial in sight of an all-white panel of jurors, according to the filing that seeks to block an execution date for him. Two jurors noted the shackles in affidavits, but a court said after his conviction that nothing in the trial record showed he was visibly shackled in front of jurors, the filing states.

BISMARCK, N.D. (AP) Tommy Fisher peered into a Fox News camera and talked up his North Dakota-based companys ability to build a border wall faster and cheaper than others could, with technology so revolutionary, its like comparing the iPhone to a pay phone. Fisher Sand and Gravel, he said, was eager to help President Donald Trump deliver on a key campaign promise.

Hopefully the president will see this, Fisher said during the April appearance on Fox & Friends First, part of a blitz on conservative media over several months as the construction executive took a well-worn path to the presidents ear. Fishers company ultimately won a $400 million contract, though the contract is now being audited over concern it may not meet operational requirements.

That Fisher, 49, was able to land the contract came as no surprise in North Dakota, where people who know him describe a man with a get-it-done attitude, a knack for self-promotion and a strong belief in the company he took over from his father when he was just 25.

U.S. Rep. Kelly Armstrong, who grew up with Fisher, called him a gung-ho, hardworking, smart guy. Though Fisher long ago moved to Arizona he runs the company from a distance Armstrong said he remains well known in his hometown.

Go sit in a coffee shop in Dickinson and try to find someone who doesnt like Tommy, Armstrong said. Hes a great corporate citizen.

Kurt Robinson, who worked in the companys IT department from 1996 to 2005, said he left to start his own business in part because he wasnt happy with leadership in Dickinson. He said the company would have tanked if not for Fisher, who was managing it from Arizona.

Tommy is the driving force of the company and he is a very good businessman, Robinson said.

Fisher, who said last month that he expected the audit to find nothing amiss, didnt respond to a request for an interview.

Mississippi authorities were searching for two prisoners believed to have escaped Saturday from one of several prisons rocked by violence that has left at least five inmates dead in the past week.

Gov. Phil Bryant on Saturday said via Twitter that he has directed the use of all necessary assets and personnel to find the two inmates who escaped from the Mississippi State Penitentiary at Parchman.

The state Department of Public Safety has deployed state troopers and the highway patrols special operations group to help the Department of Corrections find the two inmates and to help restore order at the troubled facility that they escaped from, Bryant said.

The Corrections Department said in a Facebook posting that David May, 42, and Dillion Williams, 27, were discovered missing from Parchman during an emergency count about 1:45 a.m. May is serving a life sentence for two aggravated assault convictions in Harrison County, and Williams is serving a 40-year sentence for residential burglary and aggravated assault in Marshall County.

The department said via Twitter Saturday afternoon that there were no major disturbances occurring at Parchman.

There was a minor fire at Unit 30 earlier this week. That fire, set by an inmate, was immediately extinguished. Like other facilities in the prison system, the prison has limited movement, the department tweeted.

Five inmates have died in prison violence since Sunday; three of those deaths have occurred at Parchman. The prison is a series of cell blocks scattered across thousands of acres of farmland in Mississippis Delta region. Inmates who escape their cells sometimes dont make it off the property.

Associated Press

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