StemCell Therapy

California is one of the most receptive states in the country for folks who want to enter surrogacy agreements, according to Wright, who practices law in Marin County. Court support through case law for surrogacy in California goes back some 20 years, she said.

In California, a pre-birth court order can grant parental rights in-utero, whether or not the intended parents have any biological connection to the embryo. When the birth certificate comes out, theres no mention of surrogacy, Kimborough said.

Many surrogate mothers report that the most rewarding part of the process is handing over the baby to new parents, who often view the surrogate as angelic. Anyone who knows me knows Im not an angel, Kimborough said, laughing. Surrogates feel that they gain. Its not that we give so much.

Emotional business

The business has powerful emotional underpinnings. There is an altruism that is unparalleled, Wright said.

Intended parents usually come into the process from a place of loss, Wright said. Unfortunately, my husband and I struggled with fertility issues over nearly seven years, she said. She had both miscarriage and late-term pregnancy loss. Through in vitro fertilization with her egg and her husbands sperm, they were able to eventually have a son, now age 6. Along the way, they considered both adoption and surrogacy. Infertility is statistically about a third of the time tracked to the woman, a third to the man and a third inexplicable.

Its a difficult, traumatic thing, Wright said of fertility issues. You hope and then you lose, hope and then you lose internal battles. Surrogates come from the other side. Pregnancy has been easy, fun, family-building. They come together this incredible meeting.

Adoption and surrogacy rarely cross paths, Kimborough said. We dont compete with adoption agencies. Most intended parents choose one route or the other. It has to do with who you are as a person. Adoption contains more unknowns, with no biological connection or history on the mother or pregnancy. Adoption through foster care can be invasive, she said.

Some women in heterosexual couples who cannot have children on their own struggle with allowing another woman to be a surrogate.

Can I watch somebody else carry my child, have another woman in my life who can do something I cant do, Kimborough said, and give my husband something I could not give very emotional parts of being a woman insecurity or hurt thats so deep she cant get past it.

State laws vary on surrogacy

The American Society for Reproductive Medicine issued guidelines for gestational carriers in surrogacy, Kimborough said.

In many states, those receiving a child must go through an adoption process after the child is born, Wright said.

California Assembly Bill 1217, which became law in 2013, amended the Family Code to require a surrogate mother and intended parents to be represented by independent counsel before entering an assisted-reproduction agreement for gestational carriers. The law required that such an agreement include certain information and be notarized or witnessed. Parties to a surrogacy arrangement cannot undergo an embryo transfer or injectable medication for assisted reproduction until such an agreement has been properly executed.

Traditional surrogacy agreements, where the surrogate is the source of the egg, may be structured as pre-planned adoption agreements. Gestational surrogacy, such as the pregnancy of Gamble, is not allowed in some states but is common in California.

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California law supports surrogacy for gay and straight couples with fertility issues - North Bay Business Journal

Dog Bites: A Multidisciplinary Perspective is the most comprehensive book ever assembled on all aspects of dog bites. Thirty-two original essays by 39 authors tell it all.

Why dogs bite, the medical, legal, and other consequencesof humans being bitten by dogs, and how to manage them, are"hot" topics globally. (Note 1) I'm very interested in the general topic ofdog biting,but when I go to the web to learn about specific studies there are numerous hits and it's often difficult to make sense of the data and to separate fact from fiction. So, I was thrilled to learn of a new book edited by Daniel Mills and Carri Westgarth calledDog Bites: A Multidisciplinary Perspective. To say this volume is encyclopedic is amajor understatement, and each time I go back to it I learna lot of new information. Its description reads:

Dog Bites is organized into nine sections titled Fundamental Principles, Perceptions of Dogs that Bite, Dog Bites and Risk, Investigative and Legal Issues, Health Issues, Handling the Aggressive Dog, Managing Future Risk, Prevention, and Concluding Comments. Thirty-nine contributors wrote its 32 chapters.

I reached out to Dr. Mills,Europe's first professor of veterinary behavioural medicine,and Dr. Westgarth,a Research Fellow at the University of Liverpool where she completed her Ph.D. in Veterinary Epidemiology and Masters degree in Public Health, and they agreed to answer a few questions about their landmark book. Dr. Mills' answers are in italics and Dr. Westgarth's are in plain text. Our interview went as follows.

Why did you decide to compile the essays for Dog Bites: A Multidisciplinary Perspective?

Dr. Mills: It has been clear that so many people are stakeholders in this and its implications and many people see to use the data for their own agenda by being both selective and over simplifying things. There was however no single authoritative point of reference and so this what we decided to set about addressing.

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Dr. Westgarth: I have always been a very multidisciplinary person, perhaps a jack of all trades, master of none type so to speak, and this extends to my research. But this enabled me to see that different disciplines I was viewing the subject of dog bites from were seeing the problem and the solutions quite differently. For example, dog behaviour counselling (people do stupid things to dogs and simply need to stop) compared to human public health (people do what they do because their environment sets them up to do that and its very difficult to do any different). A broad reference point was needed in order to challenge our personal thinking.

Why is it essential to take a broad and multidisciplinary perspective on the problems at hand?

Its a bit about the three blind men and the elephant- one has the trunk, one the ear and one the leg, they all perceive the animal very differently and so it is with aggressive behaviour we need people to at least appreciate that its complex and that we need to be critical of simple solutions- if they existed it would be solved by now. Only with us coming together can we make real difference.

Even experts in one particular area of dog bites make a lot of assumptions. This was really apparent in reading the manuscript drafts, where authors of one chapter were stating background assumptions to introduce their specialist area whereas another author (who was the specialist in that area) was busting that myth in their chapter. We have to think more broadly and put the pieces of the puzzle together if we are going to effectively prevent and treat dog bites.

Can you briefly summarize some of your findings, noting general trends and surprises?

Oh thats a hard one -- to me, the main thing to appreciate is that we know very little with much confidence generally the data is very poor, but that does not mean that all solutions are equally valid. I think if we can be more critical we can perhaps at least have better pragmatic solutions until the research catches up.

I think people will be surprised at how little we actually know, especially when it comes to risk factors for aggression. Its very easy to read one research paper and think their results are great and must hold true but it is only when you look at a whole body of work and really critically engage with it, which we gave our authors liberty to do (and we did of them), that you start to really see the contrasting findings and gaps. We actually dont know for sure how many dog bites there are, who is at most risk, or how to effectively prevent them. I am also excited by the new data that this book contributes, including breed variations in jaw structure and bite strength, media and societal perceptions of aggressive dogs, and my own data on deep reaching impacts of even minor dog bites on victims.

Who is your intended audience?

Anyone with a serious interest in this, but especially the professions covered by the authorship as well as academics

I hope that there is something for everyone who is interested in dog bites, even if someone is already at the top of the game in their own discipline. For example, dog trainers can learn about statistics, epidemiological risk factors and bacterial infections caused by dog bites. Surgeons can learn about best practice aggressive dog rehabilitation methods and educational initiatives for prevention of bites to children. Vets can learn about societal constructions of aggressive breeds and forensic investigation of human fatalities. It will hopefully open up new worlds for everyone.

Do you have hope that there are solutions to reduce the incredible number reported dog bites and how might this be done? What role can veterinarians play?

It think we can -- but we also need to abandon the idea that all bites are preventable- living with dogs caries an inevitable risk the first question is to educate people about what these risks are and what as a society we think is acceptable- bearing in mind the enormous benefits dog ownership brings. Vets have a role to play (I am a vet) but its relatively small, as they are not well trained in behaviour it needs cross-disciplinary collaboration.

In my mind we definitely have to abandon the blame the victim or owner approach and we cannot rely on education. Education alone does not work in any other health promotion topic, why would it work for dog bites? People often know that they are at risk of being bitten but carry on anyway! We also need to challenge the perceptions that dog bites are just one of those things that cant be prevented. I think many of them can, but there is no one solution, prevention has to happen at a number of levels. The swiss cheese model is one way to think about it: Think of slices of swiss cheese lined up against each other. Each hole is a potential point in the barrier through which failure to prevent the risk could occur. When all these holes align a dog bite occurs. For example, a puppy from a sire with a nervous disposition, the pup went to socialisation classes, but was attacked by another dog a few years later and developed back pain that made him suspicious of being handled, one day a parcel delivery man comes and the dog is usually shut away during these situations but he managed to push on the door and it sprang open and the dog ran to the front of the house, the delivery man reached to stroke him on his back, and was bitten. Hypothetical but you can see where there area number of events and contexts which contributed to this one dog bite event. Each one alone may not have.

Is there anything else you'd like to share with readers?

Not that springs to mind,other than its not a self help book it is a point of reference I actually like your conceptualisation of it as a series of essays in a moreencyclopedicway -- hadnt thought about it like that.

We hope readers find it useful, and to expect some myth-busting and conflicting points of view!

What are some of your current and future projects?

In relation to dog aggression I have on-going work on cultural factors altering perception and how we communicate better interventions, work Im writing up on when the aggressive behaviour becomes seen to be a problem and what that means, and then on-going work on medical issues affecting dogs that show aggressive behaviour.

I have a Ph.D. student investigating in detail perceptions and beliefs regarding risk and safety around dogs, using detailed interviews and field observations, in particular of work places at risk of dog bites. Ive been working closely with Royal Mail on their dog bite prevention initiatives over 7000 postal workers in the UK are bitten each year. We need to better understand how high risk people such as this can be protected from bites. My other research is regarding peoples motivations for walking their dogs, and beneficial effects on human wellbeing. We need to balance the risks and benefits of dogs to society.

Thank you Drs. Mills and Westgarth for compiling this much-needed and timely volume, and thanks to your 39 contributors as well. I find myself picking it up and randomly going to chapters and to the tables and graphs to absorb what you and your authors have written.

All in all,Dog Bites: A Multidisciplinary Perspectiveis extremely comprehensive and a most valuable addition to a scattered and difficult to interpret literature.I hope itreceives a broad global audience, because dog bites know no geographical boundaries. As we learn more and more about why dogs bite, it'll be a win-win for them and for us. And, our companions need all the help they can get (for more on this topic please see "Companion Animals Need Much More Than We Give Them," "Dogs Want and Need Much More Than They Usually Get From Us," and links therein).

Please stay tuned for more information on dogs and other nonhuman companions with whom share our lives. There's no shortage of new studies coming our way.

Note 1: The World health Organization (WHO) reports "There are no global estimates of dog bite incidence, however studies suggest that dog bites account for tens of millions of injuries annually. In the United States of America for example, approximately 4.5 million people are bitten by dogs every year. Of these, nearly 885 000 seek medical care; 30 000 have reconstructive procedures; 318% develop infections and between 10 and 20 fatalities occur. Other high-income countries such as Australia, Canada and France have comparable incidence and fatality rates." According to DogsBite.org, "Each day about 1,000 U.S. citizens require emergency care treatment for serious dog bite injuries. Annually, about 9,500 citizens are hospitalized due to dog bite injuries.1The below statistics and studies examine injury occurrence and the breeds of dogs most likely to inflict severe and fatal injuries. For those new to this area,Quick Statisticsand recentDog Bite Studiesare good starting points. Also see our October report that reviewslevel 1 trauma center studies from 2009 to 2016. More graphics can be seen here.

Marc Bekoffs latest books areJaspers Story: Saving Moon Bears(with Jill Robinson);IgnoringNatureNo More: The Case for Compassionate Conservation;Why Dogs Hump and Bees Get Depressed: The Fascinating Science of AnimalIntelligence, Emotions,Friendship, and Conservation;Rewilding Our Hearts: Building Pathways of Compassion and Coexistence;The Jane Effect: Celebrating Jane Goodall(edited with Dale Peterson);andThe Animals Agenda: Freedom, Compassion, and Coexistence in the Human Age(with Jessica Pierce).Canine Confidential: Why Dogs Do What They Dowill be published in early 2018. Learn more atmarcbekoff.com.

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Dog Bites: A New Book Offers Comprehensive Data and Cross-Disciplinary Analyses - HuffPost

AUGUST 23, 2017

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

The commentary made four recommendations about human germline editing:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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CRISPR, Patents, and Nobel Prizes - lareviewofbooks

Theres a lot to be said for being in the right place at the right time, but could Air Supplys long-time success be the result or a chance meeting or was the cosmos working overtime on a little something called destiny? Maybe, but one thing is for surenone of it would have been possible at all without their hard work and tenacity to make it happen.The two Russells, Graham Russell and Russell Hitchcock, happened to be cast in the same Sydney, Australian production of Jesus Christ Superstar in 1975, and everything changed after that.

Many an audience member has probably asked himself if a fine looking group of ladies about to take the stage could possibly do justice to one of the most popular rock bands in the world. Its a legitimate question considering its not easy music to play, so a person cant help but wonder if the music will be taken as seriously as the people in the audience do. However, once the guitars are plugged in and the girls dig into those first few chords, the obvious answer to that question is, oh, hell, yes.

Many a cook tries their hand at duplicating foods they love in restaurants and specialty shops, telling themselves, it cant be that difficult. Often times, theyre right. It can be doneand its pretty simple. However, sometimes, its not as easy as it looks.Mexican food for example looks easy because ingredients are simple, sauces are often slow-cooked and meat is marinated, making this comfort food one of Americas favorite. Recipes are often handed down and each time theyre prepared, a spice might be tweaked or flavor added, depending on taste and preference.

Its been 40 years since Elvis Presley died (August 16, 1977) and millions of people still have the date circled in red on their calendars. People still remember and they still mourn. Some internet sites have gone to the extent of estimating what he would look like now, if he were still here in the physical.This time of year Memphis fills up with more people than usual as crowds in large numbers make their pilgrimages to Graceland for visits to his home while tribute shows pop up all around the country to remember the huge icon that he was.

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A human stem cell replicating itself.

Hal X. Nguyen and Aileen J. Anderson

But when it comes to spinal cord injuries, the healing process goes awry.

Immune cells rush in and cause a scar that blocks the ability of neurons to regrow and reconnect. However, recent studies have shown that the immune system can also aid regeneration.

The immune system has both positive and a negative impact what it does is really context specific, says Jan Kaslin, who studies neural regeneration in zebrafish at the Australian Regenerative Institute of Medicine in Melbourne, Australia.

Stem cells provide a great hope for damaged spinal cords and brain injury but it has not been clear on how the immune system may affect the regrowth.

Now a new study has taken a look at how stem cells and the immune system interact in the repair of the spinal cord. Led by Aileen Anderson from the University of California, Irvine and published in the Journal of Neuroscience, the study suggests that whether or not the immune system hinders or helps transplanted stem cells to regrow lost tissue may be influenced by the presence of certain kinds of immune cells.

The study used stem cells derived from human foetal brain tissue and transplanted them into mice with a wound in their spinal cord. They then blocked the invasion of a specific population of immune cells called neutrophils and observed how well the wound was repaired by transplanted stem cells.

In contrast to earlier research, Andersons team found with that with neutrophils out of the way the transplanted stem cells behaved differently and were more able to repair the damage.

This is the first data to show that the immune environment can be altered to allow stem cell populations to perform better in terms of restoring function, according to Anderson.

Can other immune cells be manipulated to increase the effectiveness of stem cell transplantation in spinal cord regeneration?

These findings are an important of piece of the puzzle, says Kaslin, that may significantly improve future stem cell transplantation approaches.

Originally posted here:
Immune cells may prevent stem cell growth in spinal cord repair - Cosmos

Agents acting on behalf of the Food and Drug Administration have seized what they said are unproven, and "potentially dangerous" stem cell treatments at two California clinics.

The seizures took place at the California Stem Cell Treatment Centers in Rancho Mirage and Beverly Hills, California, where U.S. Marshals said they confiscated five vials of Vaccinia Virus Vaccine (Live) a vaccine the FDA said belonged to StemImmune Inc. of San Diego. The vaccine has been given to people at high risk for smallpox, such as some members of the U.S. military, but in this case was reportedly being used to treat cancer.

The FDA says Vaccinia Virus Vaccine (Live) is not commercially available, and therefore it is concerned about its origin. The FDA said an active investigation is underway to determine how the company obtained the vaccine.

"StemImmune, a biopharmaceutical company engaged in cutting edge R&D of adult human stem-cell based therapies for the treatment of cancer, is fully cooperating with the FDA about the development of its stem cell-based investigational cancer therapy," the company said in a statement to ConsumerAffairs. "We look forward to continuing our dialogue with the FDA as we seek to bring this important cancer therapy to cancer patients."

"Speaking as a cancer survivor, I know all too well the fear and anxiety the diagnosis of cancer can have on a patient and their loved ones and how tempting it can be to believe the audacious but ultimately hollow claims made by these kinds of unscrupulous clinics or others selling so-called cures," said FDA Commissioner Dr. Scott Gottlieb.

Gottlieb said the agency is concerned that potential cures are being offered vulnerable patients without offering any proof they actually work.

"I especially won't allow cases such as this one to go unchallenged, where we have good medical reasons to believe these purported treatments can actually harm patients and make their conditions worse," he said.

According to the FDA, clinics were using the product by injecting it directly into patents' tumors. The danger, the agency says, is when unvaccinated people are in close contact with someone who has been vaccinated, and are accidentally infected.

For its part, Steminnune notes on its website it provides "a potent new class of immunotherapies to wage a targeted, stealth attack on cancer."

See the rest here:
US Marshals seize 'unapproved' cancer treatment - ConsumerAffairs

Researchers from several Russian institutes, including MIPT, have found out how prolonged exposure to ionizing radiation affects human stem cells. They discovered that it causes a cell cycle delay, which leads to faster repairs of radiation-induced DNA double-strand breaks, with fewer errors. It is unclear what the health implications are, particularly how this affects the risk of developing cancer.

When statistics is no good

To a physicist, an ordinary flashlight or a portable radio is, among other things, radiation sources, and ionizing radiation is the proper scientific name of the high-energy rays that an ordinary person thinks of when they hear the word radiation. It comes in different types, including X-rays, gamma rays, and streams of various particles. Ionizing radiation is capable of turning neutral atoms and molecules into charged ions. The human body is inevitably exposed to radiation, with an average person receiving about 3 milligrays of natural background radiation annually. Moreover, one X-ray exam amounts to anywhere from 0.001 to 10 milligrays of additional exposure, depending on the exact procedure. That said, overexposure is dangerous: A dose of more than 1,000 milligrays received within a brief period of time causes acute radiation sickness.

To ensure radiation security, it is vital that we can accurately assess the risks posed by ionizing radiation. Studies of people that were exposed to radiation have only conclusively established the increased risk of cancer as a result of receiving a high dose of radiation. This led the regulating authorities to accept a linear model, under which low doses of radiation, too, increase the risk of cancer. However, experiments showed that low-dose radiation exposure either had no adverse biological effect or even was beneficial, as evidenced by prolonged life spans and less frequent cancer occurrence. Apart from that, the importance of the so-called dose rate should not be overlooked. Exposure to equal doses of radiation over shorter or longer time intervals has a different effect, with slow irradiation causing less harm. The extent to which dose rate affects the biological outcomes has been a cause of much debate. Because in a real-life setting, people are more likely to face prolonged exposure to low-dose radiation, it is crucial that we understand its effects.

DNA double-strand breaks

One of the negative effects of radiation is the formation of the so-called DNA double-strand breaks, in which both strands of the double helix are severed. Fortunately, the cell is capable of repairing damaged DNA. If one of the two strands is damaged, the other can be used to reverse this. However, in the case of a double-strand break, other more error-prone mechanisms have to be employed. Left unrepaired or misrepaired, such lesions can give rise to oncological diseases. This explains why research into the effects of radiation on living cells tends to focus on double-strand breaks. Not long ago, it was found that stem cells functionally undifferentiated cells play a major part in the formation of tumors by accumulating mutations and passing them on to the specialized cells that are their descendants. However, stem cell response to prolonged irradiation remains poorly understood.

The scientists conducted several experiments using stem cells derived from gingivae, or the gums. They treated the cells with identical radiation doses administered over long and short time spans. The formation of double-strand breaks was monitored using stained H2AX and 53BP1 proteins as markers. With brief but intense radiation exposure, the incidence of both markers was found to increase linearly with the dose. But in the case of prolonged irradiation, the response was linear only up to a certain point, followed by a plateau at 1,000 milligrays. In other words, after reaching a certain number, the lesion count does not continue to rise. A balance of sorts is achieved between break formation and repair.

DNA repair

The cell comes equipped with repair systems capable of mending DNA double-strand breaks. However, following intense irradiation, the cell has to resort to a mechanism known as end joining a quick but faulty procedure in eight out of 10 double-strand breaks. This often leads to chromosomal aberrations. Such misrepairs of DNA breaks can potentially result in cell death, oncogene activation, and anti-oncogene suppression. But there is an alternative mechanism of DNA repair, called homologous recombination. It uses a similar or identical DNA molecule as a template and produces much fewer errors, but it is only available during certain phases of the cell cycle. The researchers monitored homologous recombination using Rad51, another protein marker. During a two-hour long exposure, the amount of Rad51 remained roughly constant, followed by a linear growth afterward. The team hypothesized that prolonged irradiation might activate homologous recombination.

Cell division

Stem cells can be divided into two groups, called proliferating and quiescent, where the former undergo division and the latter have ceased reproducing, and there is a balance between the two types of cells. The researchers counted up the DNA double-strand breaks in proliferating and quiescent cells separately. This is made possible by a certain protein that is only found in cells undergoing division. It turned out, in both types of cells, the number of DNA breaks grew, eventually reaching a constant value.

It was also observed that exposure to radiation did not change the roughly 4-1 ratio between proliferating and quiescent cells. However, a more detailed investigation revealed that four hours of slow irradiation result in a considerably increased number of cells in the S and G2 phases of the cycle, that is DNA synthesis and final preparation for division, respectively. It is during these phases that a copy of the cells DNA is available for the sake of division, but also to be used as a template in homologous recombination. This fact is a likely explanation for the detection of increased amounts of the Rad51 marker. To put it another way, irradiation causes a delay in the cell cycle with the consequence that, at any given time, there are more cells in those phases which enable homologous recombination. This means it is possible to repair DNA double-strand breaks correctly.

We have shown that prolonged irradiation of mesenchymal stem cells leads to cell cycle redistribution. This might influence the biological response to radiation, says Sergey Leonov, the director of the Phystech School of Biological and Medical Physics. Our findings could become the basis of further research into double breaks in stem cells and their effect on tumor formation.

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

Reference:

Tsvetkova, A., Ozerov, I. V., Pustovalova, M., Grekhova, A., Eremin, P., Vorobyeva, N., . . . Osipov, A. N. (2017). H2AX, 53BP1 and Rad51 protein foci changes in mesenchymal stem cells during prolonged X-ray irradiation. Oncotarget. doi:10.18632/oncotarget.19203

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Upon Prolonged Irradiation, Human Stem Cells' Defenses Are ... - Technology Networks

Thirty million American women and men will struggle with eating disorders in their lifetime, and these life-threatening conditions have a higher mortality rate than any other psychiatric illness. For example, someone struggling with anorexia for five years has a 5 per cent, or one in20 chance, of dying.

While more and more people have come to understand that eating disorders are diseases of the brain, there's still awidespreadbeliefthat people with these devastating conditionsare vain, attention-seeking, or lacking in will power. But apaperjust published in Plos One makes it clear that this isn't true. The studyevaluated the genomes of95 individuals with diagnosed eating disorders andidentified 430 genes, clustered into two large groups, that are more likely to be damaged than in people without those disorders.

This adds to a growing body of research shows that eating disorders are powerful, biologically-driven illnesses. The new studysupports previous findings that the risk of developing an eating disorder is 50-80 per cent geneticthatpatientshave inherited damaged copies of genes that increase their risk of developing disordered eating. And understanding which genes are damaged can practitioners create better treatment treatment protocols.

In the PlosOne study, patients with eating disorders were clustered into two main groups. In the first, the damaged genes fell into a class of gut neuropeptides affecting that control appetite,food intakeand digestion/absorption of nutrients, making patients more likely to binge. Roughly half of this group struggled with restricted eating patterns, and the other half were binge eaters. The research confirms reports by our patients who believe their behavior is biologically driven.

The second group of patients had a cluster of genes involved in the function of the immune system and inflammation, which has long been known to suppress appetite. Patients with damaging mutations in the inflammation cluster are much more likely to have restricted-eating patterns. More research is needed to test a possible connection between eating disorders and auto-immune conditions like irritable bowel disease.

The new findings are consistent with known environmental eating disorder triggers. Faddieting, excessive exercise, or medical illness, are examples of negative energy states that have long been seen as possible eating disorder triggers. Negative energy states can set up behavioral changes like food binges or restricted food intake, triggering preexisting genetic drivers for eating disorders. Based on these findings, we argue that eating disorders are biologically driven illnesses that alter mood and behavior, similar to how the lack of thyroid hormone can result in depression in a patient with hypothyroidism.

Failure to understand the underlying causes of eating disorders creates stigma, making it less likely for those who struggle to get treatment. People with any medical condition deserve support and access to the best treatment. Someone with cancer wouldnt be denied treatment for their illness. Likewise, patients with eating disorders shouldnt feel guilty about their illness and they should have access to safe, effective treatment.

Biology isnt destiny. Eating disorders treatment is most effective if its accompanied by a general understanding that eating illnesses are biologically driven.

Lasting recovery from an eating disorder is possibleand those who struggle deserve understanding and support without guilt or judgment.

See more here:
The Genetics of Eating Disorders - Scientific American (blog)

White women whose genetic makeup puts them at higher risk for Alzheimers disease are more likely than white men to develop the disease during a critical 10-year span in their lives, according to a study headed by Keck School of Medicine of USC researchers.

The findings from one of the worlds largest big-data studies on Alzheimers counter long-held beliefs about who is at greatest risk for the disease and when, suggesting new avenues for clinical trials.

Study results show genetically vulnerable 55- to 85-year-old white men and women have the same odds of developing the memory-erasing disease. One exception: From their mid-60s to mid-70s, these women still face significantly higher risk. That may provide clues to disease causes and potential interventions among these women.

Our discovery is important because it highlights how clinical trials could be weighted toward women a susceptible part of the population to help scientists more rapidly identify effective drug interventions to slow or cure Alzheimers, said Arthur Toga, director of the USC Stevens Neuroimaging and Informatics Institute at the Keck School of Medicine among the nations leaders in innovative scientific discovery.

The study was published Aug. 28 in the Journal of the American Medical Association Neurology. It included data from 57,979 North Americans and Europeans in the Global Alzheimers Association Interactive Network (GAAIN). This big-data project provides scientists around the world with shared data and sophisticated analysis tools to address a disease that makes up about 65 percent of the 47 million cases of dementia worldwide.

The results contradict a seminal 20-year-old study that found women with one copy of ApoE4, a gene variant linked to Alzheimers, were diagnosed with the disease 50 percent more often than men with the same genetic profile.

The findings presented in the USC-led study expand the number of participant data by ninefold and indicate the critical decade falls between 65 and 75, more than 10 years after the start of menopause. Previous studies in animals and humans have reported a relationship between ApoE4, menopause and cognitive decline.

So much work has been dependent on one 1997 finding, but with tools like GAAIN, we now have the ability to reinvestigate with increased statistical power, Toga said.

The new findings are significant because almost two-thirds of the more than 5 million Americans now with Alzheimers disease today are women.

The new findings are significant because almost two-thirds of the more than 5 million Americans now living with Alzheimers disease are women, according to the Alzheimers Association.

Many attribute the imbalance in disease risk to the fact that women, on average, live longer than men. However, a growing body of evidence suggests other reasons also contribute to the difference. For instance, men have higher rates of heart disease and stroke. So, men who live longer may be healthier than women of the same age and may face less risk of developing Alzheimers, according to the USC-led study.

In the future, doctors who want to prevent Alzheimers may intervene at different ages for men and women, said Judy Pa, co-author of the study and an assistant professor of neurology at the USC Stevens Neuroimaging and Informatics Institute.

Menopause and plummeting estrogen levels, which on average begins at 51, may account for the difference, Pa said. However, scientists still dont know what is responsible. Researchers need to study women 10, 15 or even 20 years before their most vulnerable period to see if there are any detectable signals to suggest increased risk for Alzheimers in 15 years.

Only some women are at increased risk of developing Alzheimers in their mid-60s to mid-70s compared to men. To find out, women could have their DNA analyzed. However, Pa cautions that genetic testing for the ApoE4 variant is no crystal ball.

There is controversy in terms of whether people should know their ApoE status because it is just a risk factor, Pa said. It doesnt mean youre going to get Alzheimers disease. Even if you carry two copies of ApoE4, your chances are greatly increased, but you could still live a long life and never have symptoms.

Even if some women discover they are at heightened risk, they can improve their odds by making life changes.

Get more exercise. Work out your mind, especially in old age.

Judy Pa

Get more exercise. Work out your mind, especially in old age, Pa said. Pick up hobbies that are cognitively or physically challenging. Reduce processed sugar intake because its linked to obesity, which is associated with many chronic diseases.

Alzheimers disease is the fifth-leading cause of death for Americans 65 and older, but it may one day outpace the nations top two killers heart disease and cancer. Alzheimers-related deaths increased by nearly 39 percent between 2000 and 2010 while heart disease-related deaths declined 31 percent and cancer deaths fell 32 percent, according to the Centers for Disease Control and Prevention.

Because Alzheimers disease has a huge impact on lifelong health, USC has more than 70 researchers dedicated to the prevention, treatment and potential cure of the memory-erasing disease. Big data projects like this require experts across disciplines computer science, biology, pathophysiology, imaging and genetics to coordinate.

For this study, the researchers examined data from 27 different studies that assessed participants ApoE gene variation, as well as characteristics such as sex, race, ethnicity, diagnosis (normal, mild cognitive impairment or Alzheimers disease) and age at diagnosis.

The records of nearly 58,000 people were scrutinized. Meta-analyses were performed on 31,340 whites who received clinical diagnoses sometime between ages 55 and 85.

The proportion of minorities was so small that analysts could not draw statistically significant conclusions about their disease risk. Because of this, the study focused on whites only.

Most of the archives around the world have insufficient numbers of underrepresented groups, Toga said. One of the take-home messages from our study is people of all races and ethnicities need to be involved in Alzheimers clinical trials because this disease is a problem that affects all of us.

The current findings need to be confirmed in more diverse study populations.

USC is working to build more diverse population studies related to Alzheimers. Established in 1984, the Alzheimer Disease Research Center at the Keck School of Medicine reaches out to communities in the greater Los Angeles area to educate the citys diverse population about Alzheimers and the clinical trials they might be interested in joining. Previous studies, for example, have focused on Latinos.

Historically, women have not been adequately represented in clinical trials, especially in studies on heart disease. Women need to be represented equally to men or even overrepresented, Pa said.

The bottom line is women are not little men, Pa said. A lot more research needs to target women because gender-specific variations can be so subtle that scientists often miss them when they control for gender or use models to rule out gender differences. Most research today is ignoring a big part of the equation.

The study was made possible because of lead author Scott Neu, a leader in the development of a federated approach to analyzing metadata and assistant professor of research at the Laboratory of Neuro Imaging at the Keck School of Medicine.

GAAIN the free resource we created in conjunction with the Alzheimers Association allows anyone to explore data sets around the world and conduct preliminary analyses to test scientific hypotheses, Neu said. Our goal is to connect scientists with those who have collected data to create new collaborations to further research and understanding of Alzheimers disease.

Analysts excluded people with a history of stroke, cerebrovascular disease, abnormal proteins that contribute to Parkinsons disease and dementia, gene mutations leading to higher levels of toxic amyloid brain plaques and any known neurological diseases.

Scientists did not adjust for known Alzheimers risk factors such as education, family history of Alzheimers or dementia because that information was not provided in all data sets. They also were unable to adjust for sex-dependent differences such as cigarette smoking, hormonal changes with age and alcohol usage.

The study was supported by the Alzheimers Association through the Global Alzheimers Association Interactive Network initiative (GAAIN-14-244631) via a $5 million grant and a portion of two National Institutes of Health grants: $12 million from Big Data to Knowledge (U54-EB020406) and $5 million from neuroimaging and genetics (P41-EB015922).

More stories about: Alzheimer's Disease, Research

Original post:
Genetics put some older women at higher risk than men for Alzheimer's - USC News

Hospital to boost genetic testing for newborn babies

BelfastTelegraph.co.uk

One of the UK's largest women's hospitals is to increase its ability to genetically test newborn babies 12-fold.

http://www.belfasttelegraph.co.uk/news/northern-ireland/hospital-to-boost-genetic-testing-for-newborn-babies-36079324.html

http://www.belfasttelegraph.co.uk/news/northern-ireland/article36079323.ece/c3338/AUTOCROP/h342/PANews%20BT_P-013b5e7c-4e66-4b0a-b8d6-04b3c11abd37_I1.jpg

One of the UK's largest women's hospitals is to increase its ability to genetically test newborn babies 12-fold.

Liverpool Women's NHS Foundation Trust will be able to screen all infants for inherited conditions or illnesses and plan for early treatment as part of a major new IT project.

It will also contribute to a major population health programme in Liverpool analysing genetic information by location, identifying and enabling work to prevent localised health issues.

IT firm Novosco will introduce the computing system.

Novosco managing director Patrick McAliskey said: "We are delighted to secure this contract which will enable the trust to take genetic testing to the next level and play an important role in the identification and prevention of conditions and illnesses in new-born babies and the wider population."

This role of genetics in healthcare is one of the most rapidly expanding areas of development for Liverpool Women's.

It provides a regional clinical genetics service based at Alder Hey Hospital, covering a population of around 2.8 million people from across Merseyside, Cheshire and the Isle of Man, chief executive Kathryn Thomson posted on the trust's website.

She added: "To discover that you or any child you have or plan to have may be at risk of a genetic disorder which could cause disability or a rare condition is traumatic.

"People are sometimes shocked and anxious and wonder what the future might hold.

"They need as much information and support as possible to help them cope.

"That is why the often unsung work of our clinical genetics team is so important, providing diagnosis and supporting families when they need it most."

Liverpool Women's NHS Foundation Trust specialises in the health of women and their babies - both within the hospital and in the community. It is one of only two such specialist trusts in the UK - and the largest women's hospital of its kind.

Novosco is an IT infrastructure and managed cloud computing company and employs over 150 people. It has its headquarters in Belfast, with offices in Manchester, Dublin, and Cork.

Here is the original post:
Hospital to boost genetic testing for newborn babies - Belfast Telegraph

Adult stem cells can be extracted from human fat. Patrick T. Fallon /The Washington Post/Getty Images hide caption

Adult stem cells can be extracted from human fat.

The Food and Drug Administration is cracking down on "unscrupulous" clinics selling unproven and potentially dangerous treatments involving stem cells.

Hundreds of clinics around the country have started selling stem cell therapies that supposedly use stem cells but have not been approved as safe and effective by the FDA, according to the agency.

"There are a small number of unscrupulous actors who have seized on the clinical promise of regenerative medicine, while exploiting the uncertainty, in order to make deceptive, and sometimes corrupt assurances to patients based on unproven and, in some cases, dangerously dubious products," FDA Commissioner Scott Gottlieb said in a statement Monday.

The FDA has taken action against clinics in California and Florida.

The agency sent a warning letter to the US Stem Cell Clinic of Sunrise, Fla., and its chief scientific officer, Kristin Comella, for "marketing stem cell products without FDA approval and significant deviations from current good manufacturing practice requirements."

The clinic is one of many around the country that claim to use stem cells derived from a person's own fat to treat a variety of conditions, including Parkinson's disease, amyotrophic lateral sclerosis (ALS), and lung and heart diseases, the FDA says.

The Florida clinic had been previously linked to several cases of blindness caused by attempts to use fat stem cells to treat macular degeneration.

The FDA also said it has taken "decisive action" to "prevent the use of a potentially dangerous and unproven treatment" offered by StemImmune Inc. of San Diego, Calif., and administered to patients at California Stem Cell Treatment Centers in Rancho Mirage and Beverly Hills, Calif.

As part of that action, the U.S. Marshals Service seized five vials of live vaccinia virus vaccine that is supposed to be reserved for people at high risk for smallpox but was being used as part of a stem-cell treatment for cancer, according to the FDA. "The unproven and potentially dangerous treatment was being injected intravenously and directly into patients' tumors," according to an FDA statement.

Smallpox essentially has been eradicated from the planet, but samples are kept in reserve in the U.S. and Russia, and vaccines are kept on hand as a result.

But Elliot Lander, medical director of the California Stem Cell Treatment Centers, denounced the FDA's actions in an interview with Shots.

"I think it's egregious," Lander says. "I think they made a mistake. I'm really baffled by this."

While his clinics do charge some patients for treatments that use stem cells derived from fat, Lander says, none of the cancer patients were charged and the treatments were administered as part of a carefully designed research study.

"Nobody was charged a single penny," Lander says. "We're just trying to move the field forward."

In a written statement, U.S. Stem Cell also defended its activities.

"The safety and health of our patients are our number one priority and the strict standards that we have in place follow the laws of the Food and Drug Administration," according to the statement.

"We have helped thousands of patients harness their own healing potential," the statement says. "It would be a mistake to limit these therapies from patients who need them when we are adhering to top industry standards."

But stem-cell researchers praised the FDA's actions.

"This is spectacular," says George Daley, dean of the Harvard Medical School and a leading stem-cell researcher. "This is the right thing to do."

Daley praised the FDA's promise to provide clear guidance soon for vetting legitimate stem-cell therapies while cracking down on "snake-oil salesmen" marketing unproven treatments.

Stem-cell research is "a major revolution in medicine. It's bound to ultimately deliver cures," Daley says. "But it's so early in the field," he adds. "Unfortunately, there are unscrupulous practitioners and clinics that are marketing therapies to patients, often at great expense, that haven't been proven to work and may be unsafe."

Others agreed.

"I see this is a major, positive step by the FDA," says Paul Knoepfler, a professor of cell biology at the University of of California, Davis, who has documented the proliferation of stem-cell clinics.

"I'm hoping that this signals a historic shift by the FDA to tackle the big problem of stem-cell clinics selling unapproved and sometimes dangerous stem cell "treatments" that may not be real treatments," Knoepfler says.

Read the original here:
FDA Cracks Down On Stem-Cell Clinics Selling Unapproved Treatments - NPR

Scientists at Kazan Federal University's Institute of Fundamental Medicine and Biology, led by Professor Albert Rizvanov, have shown that artificial membrane vesicles generated by Cytochalasin B treatment of human cells retain angiogenic activity.

Vesicles are small packages of material released from cells and act to deliver cargo and messages to adjacent and distant cells. Vesicles are known to be important regulators of normal physiology and have also been implicated in disease, notably cancer. Extracellular vesicles exhibit the biological activity of the cell from which they originate. For example, extracellular vesicles of stem cells are able to promote angiogenesis and regeneration. For this reason, extracellular vesicles represent a promising tool for cell-free therapy to deliver biologically active molecules.

However, the yield of naturally occurring vesicles is too low for practical purposes. Recently, several studies demonstrated the ability to generate a large number of membrane vesicles from cultured cells treated with a drug, Cytochalasin B. This cost-effective approach permits the generation of large quantities of extracellular vesicles. However, it remained unknown whether these Cytochalasin B-induced micro-vesicle (CIMVs) retained characteristic biological properties of their parental cells.

To address this, an international team of investigators, led from Kazan Federal University, Russia by Professor Albert Rizvanov, with international collaborators, characterized the biological activity of membrane vesicles.

The study was published in Oncotarget. The lead author, Dr. Marina Gomzikova, and colleagues described the morphology, molecular composition, fusion capacity and biological activity of Cytochalasin B-induced membrane vesicles (CIMVs). This data suggests that the biophysical, molecular and size distribution properties of CIMVs are similar to natural vesicles. Furthermore, they demonstrated that CIMVs retain the biological properties of the donor cells, as they can stimulate angiogenesis in vitro and in vivo.

CIMVs can now be produced in large quantities and scaled to an industrial production level; potential therapeutic applications to deliver biologically active molecules of CIMVs are now possible.

Explore further: Insulin release is controlled by the amount of Epac2A at the secretory vesicles

More information: Cytochalasin B-induced membrane vesicles convey angiogenic activity of parental cells. Oncotarget. doi.org/10.18632/oncotarget.19723

Read more:
New tool for cell-free therapy based on artificial membrane vesicles - Medical Xpress

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When I see patients with rheumatoid arthritis, Im often asked about diet. Are there foods that can help? Should I avoid certain foods?

Whenever Im asked about diet for arthritis, my short answer is that with a few exceptions, there is no proven role for making dietary changes. In the case of rheumatoid arthritis, there is no clear evidence that eating more (or less) of any particular food will improve (or worsen) their symptoms or protect their joints. Of course, new research could change my answer.

And what about the exceptions? The most important is probably gout. Certain foods and beverages (such as organ meats and alcohol) can predispose to the condition or make it worse. Most people with gout are told to modify their diets, although for most the impact is small.

There is enormous interest now in the role of the microbiome the vast numbers of microorganisms living within us in health and disease. And we know that diet affects the microbiome within the intestinal tract. It could turn out that what you eat may cause certain populations of bacteria in the intestinal tract to rise or fall. Since these bacteria may affect immune function, and since rheumatoid arthritis is an autoimmune condition, its possible that changes in the microbiome will affect the activity and severity of rheumatoid arthritis. Researchers are working hard to understand how the microbiome might affect autoimmune diseases, and how this new perspective could lead to better control of conditions such as rheumatoid arthritis.

A number of studies have found that fish oil supplements or a diet rich in fish oils may be helpful in controlling the inflammation of rheumatoid arthritis. In addition, its possible higher intake of fish oil actually reduces the likelihood of developing the disease. Some studies have found that rheumatoid arthritis is less common in places where fish consumption is highest. However, fish oil is not routinely recommended, because its effect is modest and medications tend to be much more effective.

A new study resurrects the idea that fish oil (or at least fish consumption) might suppress the joint inflammation of rheumatoid arthritis. Researchers publishing in the medical journal Arthritis Care & Research report that the more fish a person consumes, the better the control of their arthritis. In this study, researchers analyzed data from 176 people with rheumatoid arthritis, comparing their reported intake of non-fried fish with the results of their joint examinations and blood tests. Heres what they found:

This was a small study that found an association between fish consumption and control of rheumatoid arthritis. Thats not the same as finding that fish intake actually caused the improvement in arthritis. This is an important point because factors other than diet could explain the findings. For instance, its possible that people who eat fish regularly are generally more attuned to their health and take their medications more reliably than people who eat fish less often. Thats why the authors of this study do not conclude that everyone with rheumatoid arthritis should start eating more fish. What they do say is that additional research is needed.

One other point: the improvement in arthritis control noted among those who ate the most fish was modest, and so small that most patients probably wouldnt notice. Still, small improvements can add up, so even a small effect from a natural remedy that poses minimal risk is worth consideration.

Im hopeful that in the near future well have more definitive, larger, and long-term studies that examine the role of diet on rheumatoid arthritis and other types of joint disease. Until then, I think people with rheumatoid arthritis should consider increasing their intake of non-fried fish. It might be good for the joints. And eating fish may have other health benefits as well, especially if it replaces less healthy choices.

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Fish consumption and rheumatoid arthritis: Natural remedy or just another fish tale? - Harvard Health (blog)

Almost every drug on the market for heart disease targets cholesterol. So it was major news on Aug. 27 when a group of cardiologists from around the world announced theyd discovered a drug that reduces inflammationand currently used to treat juvenile arthritissuccessfully prevented heart attacks, strokes, and other kinds of cardiac death in a recent trial.

The drug is called canakinumab and sold under the brand name Ilaris by the Swiss company Novartis, which funded the study. It works to treat juvenile arthritis by reducing the number of inflammatory chemicals in the blood called interleukin-1.

The new study, published in the New England Journal of Medicine, involved over 10,000 patients living in 39 countries who were at a higher risk of heart disease. Each had a history of heart attacks and high levels of interleukin-1 in their blood; 40% of the patients also had diabetes. Patients were randomly put in four groups and received either a placebo, 50 milligrams, 150 milligrams, or 300 milligrams of canakinumab every two weeks of the first month, and then once every three months through an injection for up to four years after.

Throughout the study, researchers also kept track of heart attacks, strokes, and death resulting from heart failure. By the end of the study, there were just over 1,400 reported incidents of these events; the patients receiving the highest dose of canakinumab had 14% fewer of them than the placebo group.

For years, cholesterol was thought to be the hormonal villain associated with heart disease. The idea was that it would clog up arteries by clumping against the sides of blood vessels, making it impossible for blood to squeeze through. Doctors were hugely excited when cholesterol-lowering statins were invented back in 1994; these drugs are now prescribed to tens of thousands of Americans with the hope that they will keep heart disease at bay.

But lowering cholesterol doesnt seem to prevent heart disease in every patient. So now experts believe high interleukin-1 blood levels can also be responsible for raising heart attack risk. The general thinking is that these inflammatory chemicals end up preventing the heart from healing from damage from previous heart heart attacks. This extra stiffening and swelling may put an extra strain on it in the future, too.

Interleukin-1 isnt all bad; we need it to survive injury or other infections. The chemical works by forcing damaged tissue to swell up with extra fluid from blood vessels, in order to isolate potential pathogens before they make their way all over the body. But interleukin-1 tends to be a little trigger-happy, and can sometimes cause inflammatory reactions that are more harmful than helpful, especially in certain chronic diseases like arthritis, and now, possibly, heart disease.

Interestingly, different results from the same trial suggesting that this therapy may even work to extend the lives of patients living with lung cancer were published in a paper the same day in The Lancet. That said, Barnett Kramer, the director of the Division of Cancer Prevention at the National Cancer Institute who was not associated with the work, told the Washington Post that these effects may be coincidental.

The drug itself is not likely to be a miracle cure. In both papers, those taking canakinumab were at a higher risk of dying from infectionssuggesting that there are risks associated with decreasing the bodys immune response. Canakinumab is also really expensive: a years supply for heart disease treatment would cost $64,000. But, this trial opens the door for future treatments for patients for whom controlling cholesterol isnt enough to improve heart health.

Read this article:
In a first, scientists may have found a treatment for heart disease that doesn't target cholesterol - Quartz

Arthritis is an unforgiving condition that doesnt just cause physical pain; for many people it impacts so dramatically on their quality of life that it also causes emotional pain. A study conducted by Revealing Reality for the charity Arthritis Research UK found that a quarter of people with arthritis say they often or frequently feel low or depressed on account of their condition. This comes as no surprise to Dr Tom Margham, who works closely with the charity.

Given that mental health and arthritis are so closely linked, healthcare professionals should not just be treating the physical impact of the condition, but also the knock-on effect on mental health, he says.

The invisibility of arthritis means its often misunderstood, making it harder for people living with the condition to find support.

Olivia Belle, Arthritis Research UKs director of external affairs, agrees: Most people underestimate the effects arthritis can have on a persons life. We are working to lift the lid on the reality of living with the condition so that people can live better lives and get the help they need whether that be empathy, treatments or support with their mental health.

The classic symptoms a swollen knee, painful ankles, burning pains in my joints started when I was 17. For the next three years, while studying to be a nurse, I suffered painful flare-ups every few weeks. When I was given a diagnosis of rheumatoid arthritis (RA) in 2010, damage to my joints had already occurred. I went through three knee operations in as many years, all of which left me housebound and in a cast for months.

By 2014, I was working as a clinical assistant at a hospital in London. When I had to resign a year later after taking yet more time off for surgery and recuperation, I was and still am devastated. I got another job as a receptionist but I had to leave that, too. Whenever I thought things were going OK, Id need another operation and then Id be back home again, stuck in bed recuperating. Ive had a total of eight operations and Im awaiting a date for my ninth surgery.

Every day, I wear an ankle and foot brace, and my palms are blistered from using crutches. It upsets me that friends arent supportive. When I say Im in too much pain to meet up, they just go out without me; I would really love it if they came over, and we ordered a takeaway and watched a movie together. It doesnt seem fair that Im in my bedroom clutching a knee full of fluid that feels like molten lava, trying to make some kind of sense out of whats happening to me, while everyone else is out having fun and getting on with their lives.

I live at home with my dad; I dont think hes really grasped the seriousness of my illness and my mum is in India looking after my grandmother. I havent even told the rest of my family how bad things are.

I recently flew to America to visit relatives. I had to get away from the four walls of my bedroom and the endless trips to hospital. I did struggle with the travel and Im paying the price for my adventure now with a huge flare up of RA but it was worth it to feel like I had a life again, albeit it only for a few weeks.

To find out how arthritis affects us all, please visit: arthritisresearchuk.org/jointproblem

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Arthritis: the hidden impact on mental health - The Guardian

The warning was issued yesterday by scientists during a conference in Barcelona on cardiovascular disease.

Delegates were told new research has revealed that ibuprofen one of the most widely prescribed drugs in the world increased blood pressure more than other non-steroidal antiinflammatory drugs (NSAIDs).

The over-the-counter tablet is often the choice for millions in the UK who suffer from the agony of arthritic pain every day.

Researchers at the University Heart Centre in Zurich studied a number of pain relief drugs, which included ibuprofen, naproxen and celecoxib and found a pronounced risk of increased blood pressure in the ibuprofen users, adding to the risk of heart disease and stroke.

The study clearly demonstrates that NSAIDs, particularly ibuprofen, may be not as safe as previously thought

Frank Ruschitzka - Professor of cardiology

Investigator Frank Ruschitzka, professor of cardiology and head of the department at the centre in Switzerland, warned: The study clearly demonstrates that NSAIDs, particularly ibuprofen, may be not as safe as previously thought.

Patients receiving ibuprofen had a 61 per cent higher incidence of de novo hypertension [high blood pressure] compared to those receiving celecoxib.

Researchers had found that celecoxib produced a slight decrease in blood pressure while naproxen caused a relatively small increase.

They warned the findings would have the greatest clinical significance for the elderly, who have a high prevalence of arthritis and hypertension.

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Prof Ruschitzka advised: Patients with osteoarthritis and arthritis should continue to consult their doctor before taking NSAIDs and clinicians need to weigh the potential hazards of worsening blood pressure control when considering the use of these agents.

He said that since decreasing blood pressure by a small amount could lower both stroke and heart mortality by 10 per cent and seven per cent respectively, the findings were particularly significant.

In the UK, 10 million people suffer from arthritis with 8.5 million of these with the most common form, osteoarthritis, caused when the cartilage that cushions movement in the joints is worn away.

Currently around 400,000 people in Britain suffer from rheumatoid arthritis, an autoimmune disease in which the bodys own immune system attacks the bodys joints.

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The often crippling condition, which has no cure, causes pain, swelling, stiffness and loss of function in the joints.

It is typically diagnosed in people aged 40 to 70 and affects three times as many women as men.

Arthritis Research UK confirmed ibuprofen was taken by many sufferers but warned them of the dangers.

A spokesman said: Longterm use of NSAIDs, including ibuprofen, can increase the risk of problems with your heart or circulation, especially if you have other risk factors for these conditions.

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Common health myths and old wives' tales

Therefore you shouldnt take ibuprofen for long-term pain relief without seeing your doctor first and you shouldnt take ibuprofen if youre also being prescribed another type of NSAID tablet.

Experts in heart disease, which remains Britains biggest killer and claims the lives of 155,000 people a year, also welcomed the new study.

Professor Jeremy Pearson, associate medical director at the British Heart Foundation, said last night: Patients and doctors must weigh up the risks and benefits of NSAIDs, particularly if you have another long-term health condition such as arthritis.

Although not all of these drugs raise your blood pressure significantly, its important to have a discussion with your doctor about the best treatment for you.

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Whether you are being prescribed painkillers like ibuprofen, or buying them over the counter, its important to be aware of the risks and you should always talk to your GP or specialist before you start taking any new medication.

NSAID labels include warnings about potential increases in blood pressure but there is little data on the effects of individual drugs.

Researchers found that achieving blood pressure control in patients with arthritis could avoid thousands of deaths from stroke and coronary heart disease each year.

The findings were yesterday presented to the European Society of Cardiology conference in Barcelona.

Read the original here:
New Ibuprofen health ALERT: Painkiller raises blood pressure in arthritis sufferers - Express.co.uk

People talk about arthritis being an invisible condition, says Liam OToole, chief executive of Arthritis Research UK. If you cant see the pain, you cant understand the impact. A study for the charity backs him up: it found eight out of 10 people with arthritis felt society didnt understand their condition because it doesnt look serious.

Yet the scale of the problem is huge. Lives, not just of individuals but of families too, are devastated by the pain, isolation and fatigue wrought by arthritis. Meanwhile, the cost to the NHS and the economy, via lost working days, runs to billions of pounds. Arthritis affects everybody, either directly or indirectly, and yet nobody talks about it, OToole says. While other hidden health problems are frequently discussed, arthritis lags behind in the public consciousness.

Arthritis Research UK wants to change that lifting the lid on arthritis is a crucial part of its overall mission: to create a world free from the impact of the condition. The charity believes that once society understands the true impact of arthritis, people will start working together to find solutions. And with its heritage and expertise, its in a strong position to lead the way.

Each strand of Arthritis Research UKs work plays a key role in its overarching objective. As one of the top five medical research charities in the UK in terms of spending, its currently funding more than 300 active projects up and down the country to develop new treatments, so people with arthritis dont have to live in pain. Its working with politicians, doctors, designers and employers, to ensure the NHS, public services, public spaces and workplaces are better equipped to support those struggling with the condition. And with its constantly evolving information and advice services, it works to assist and reassure them and their loved ones.

Last year alone, the charity spent 21.62m on research. Its focus is threefold: finding a cure for arthritis; prevention of the condition in the first place; and transforming the daily existence of those living with the pain of it. Its renowned for its groundbreaking discoveries, including anti-tumour necrosis factor (TNF) therapy a whole new class of drugs that have changed the lives of people with inflammatory arthritis over the past 15 years, since Arthritis Research UK funded research into the activities of TNF in the 1990s.

Pain itself is a key area for research. We think there is a significant subgroup probably 4 million people who are really struggling, OToole says. This is not the sort of pain most of us experience for a couple of weeks. This is chronic, long-term pain for months, years, decades.

But the problem has been neglected, he believes, because the health service is organised around diseases and disciplines: There isnt much research into pain because it doesnt fit into that [structure], and there wasnt enough funding. We want to be strategic: we need to get clever scientists together to get them interested in pain.

In recent years, the 81-year-old organisation has sought the views of 10,000 people living with arthritis to help shape its work and ensure their voices are heard by the people with the power to make change. Everything we do is informed by people with arthritis, OToole says.

Arthritis Research UK works closely with healthcare professionals and provides them with advice and support on caring for people with arthritis. For example, together with the Royal College of General Practitioners, the charity has developed a free online programme that teaches GPs core skills in arthritis care.

Its also working with the design community to give people with arthritis more opportunities to live independently, creating the inclusively designed products and public spaces that are so desperately needed. A funding and support programme to help budding designers turn their ideas into commercial products, delivered with the Design Council, has already discovered Handy-Fasteners magnetic fasteners to replace fiddly buttons, which can be added to peoples existing clothes. And with the Helen Hamlyn Centre for Design, it has developed kitchen products such as a kitchen anchor to support peeling, grating and chopping, and a cook book that encourages hand exercise through recipes involving techniques like kneading.

Arthritis Research UK wants people with arthritis and their families to feel supported to live well with arthritis, which is why it provides a huge range of free information on its website tailored to the needs of those living with arthritis.

Theres an enormous unmet need for advice and support, OToole says. Arthritis Research UK is now using cognitive computing and the input of 500 people with arthritis to develop an online virtual assistant that will learn to answer hundreds of questions people living with arthritis might have.

The virtual assistant is available 24 hours a day which is important, given that pain often keeps people awake at night, says OToole. So is the fact they may have personal questions theyd be embarrassed to ask a doctor. Sometimes people are in so much pain they cant hold their partners hand, he says. You can imagine what that does to a healthy love life.

For OToole, the way arthritis is overlooked has been brought home most starkly by the interviews the charity has carried out. In all the conversations, weve almost needed to take the lid off and give people permission to talk about it and say: Its not OK, he says. The emotional outpouring you then get is enormous.

To find out how arthritis affects us all, please visit: arthritisresearchuk.org/jointproblem

Read more:
The UK's 'hidden' disease: 'Arthritis affects everybody, yet nobody talks about it' - The Guardian

A study conducted by Keele University shows that patients with rheumatoid arthritis who are also suffering with anxiety or depression may avoid talking to their GP about their mental health symptoms.

Rheumatoid arthritis is a long-term inflammatory condition which causes joint pain, swelling and deformity. Although 1 in 5 people with rheumatoid arthritis experience anxiety or depression, the study (funded by the Haywood Hospital) found that healthcare providers may not recognise mental health problems; instead prioritising physical health concerns. The research showed that this negative experience of care can lead to patients feeling unable to raise their mood problems in future consultations.

The Haywood Foundation funded the set-up of nurse-led clinics in two North Staffordshire community hospitals, as part of a rheumatoid arthritis annual review. Dr Annabelle Machin, a National Institute for Health Research (NIHR) funded researcher, interviewed patients about their previous experiences of care, understanding of anxiety and depression, and preferences for the management of mood problems.

Some patients interpreted their mood problems as normal because of their rheumatoid arthritis, which prevented them from seeking help. Others reported GP appointments to be anxiety-provoking, or felt that their GP prioritised physical over mental health concerns. Patients felt these potential barriers to the discussion of their mood problems could be overcome through continuity of care, provision of time, and encouragement to attend follow-up appointments by a named GP. Patients experiencing severe anxiety and depression felt that mood problems themselves could be a barrier to self-referral for psychological therapy, suggesting that a GP referral could improve access to care.

There was key input from a patient group, who not only assisted with study design and analysis of the interview transcripts, but also helped to develop an information leaflet, which educates patients about mental health problems and treatments in rheumatoid arthritis. The leaflet is now readily available in the Patient Information and Education Resource Centre (PIER) at the Haywood Hospital.

Lead researcher and academic GP, Dr Annabelle Machin, said, "I would like to thank the NIHR for funding this study, which I hope will promote future discussion of mood problems within rheumatoid arthritis annual reviews, as this could have a great impact on both physical and mental health outcomes for patients".

Explore further: Study examines opioid use in patients with rheumatoid arthritis

More information: Annabelle Machin et al. Improving recognition of anxiety and depression in rheumatoid arthritis: a qualitative study in a community clinic, British Journal of General Practice (2017). DOI: 10.3399/bjgp17X691877

More:
Improving the recognition of anxiety and depression in rheumatoid arthritis - Medical Xpress

Clipped from the sports section of the Oct. 4, 1996, some of the first coverage Clodys One Eye Golf Scramble received in the Banner Graphic still adorns the wall of tournament namesake Terry Clody Clodfelter. Old Hickory Golf Course will host the tournaments final round on Saturday, Sept. 9.

Banner Graphic archive

After 25 years and nearly $200,000 in fundraising, a unique Putnam County tradition is coming to an end.

Clodys One Eye, still touting itself as the worlds only one-eye golf tournament, is set for one last round on Saturday, Sept. 9 at Old Hickory Golf Course.

For the final go-round, organizers are planning a single flight set for 11 a.m.

This is gonna be the final 25 years, organizer and tournament namesake Terry Clody Clodfelter told the Banner Graphic recently.

The rules are straightforward: A four-man best-ball scramble with one mulligan per player available for $5 per person.

The cost is $200 per four-man team. First prize is $300, followed by $200 for second and $100 for third.

The tournament will be followed by a 5 p.m. reception at Greencastle Elks Lodge 1077, 202 S. Indiana St.

All proceeds go to the Riley Childrens Hospital opthalmology department. Through the 2016 scramble, $182,000 has been donated by Clodys One Eye so far.

Oh yes, and there is the little matter of those pesky, little eye patches that make golf so much more challenging.

For a quarter century now, those patches have been teaching otherwise competent golfers how difficult the game can be without depth perception.

It was a lesson that Clodys friends needed 25 years ago when they couldnt stop razzing him for his golfing skills.

When Clody, who has no sight in one eye following a childhood accident, challenged these friends to try golfing with just one eye, a tradition was born.

One of the participants who shall remain nameless borrowed the original set of eye patches from the infirmary at the Putnamville State Farm.

Then, as now, even Clody donned an eye patch, noting that the discomfort of the patch is itself a handicap to comfortably playing the game.

Eight of us started it, Clody noted recently. Threw money in the hat, winner takes all. Five buck winner, five buck loser.

It took a few years for the fundraising for Riley to start. The first three years were for sh**s and grins, as Clody puts it.

During the third year, Tony Sparks said to Clody, You ought to do this for charity.

And so Clody reached out to Dr. Eugene Helveston, who had performed his surgery back in 1972, and the partnership between Clodys One Eye and Riley was born.

Dr. Helveston was the surgeon performing in 1972, Clody said. Between the two of us, we got this all started. He was on the ground floor of the One Eye and hes coming back this year.

Now into his 80s, Helveston has not been at the tournament in several years, so his former patient will be glad to see him.

Im glad hes coming, Clody said. Ive had a lot of conversations with that man over the years.

Itll probably be an emotional, humbling day.

Their 45-year relationship began with a freak accident by a 13-year-old boy. Clody was cutting down a thorn tree and got a thorn in his eye.

Five days later he suffered a cataract.

Five or six months later, his retina detached.

Dr. Helveston performed the surgery that kept Clody from further injury, but he has had no sight in the eye since he was 14.

Clody noted how much has changed since his own accident and surgery.

I think I was there at Riley for six or eight days after the retina surgery, he said. Now they do the retina surgery and send you home that afternoon.

While the general advancement of medicine is certainly a part of such positive changes, Clodys own tournament has helped Riley keep up with those changes.

They have opened their own digital diagnosis eye laboratory with the funds that we produced for them, Clody said.

Here in Putnam County, the funds have also provided juvenile vision screening kits to local schools and even funded eye surgeries for kids in Putnam and Clay counties.

Weve taken care of 10 or 12 kids over the years in unfortunate situations, Clody said. The families would get ahold of me and Id contact Riley. It would take care of 100 percent of the cost.

Even as the tournaments run winds to a close, the Riley connection remains strong. Current ophthalmology chief of staff Dr. David Plager will be in attendance, as will others from Riley.

Clody even recently learned that the One Eye is notable in its long-running support of Riley.

We are the longest-running charitable group to have supported any one department that Rileys ever had, Clody said. I didnt know it.

Brad Alspaugh, who has played in the tournament from the beginning and still serves as a co-organizer, hopes to go out with a bang. While it would be departure from recent years, hes hoping to raise $18,000 to bring the total money to $200,000 over the tournaments history.

To do so, the tournament not only needs participants, but sponsors. All donations are tax deductible.

Anyone interested in playing or a sponsorship may contact Clody at 653-9322, Alspaugh at 653-7273 or Jo Corbitt at 247-9426.

Its not for lack of passion that theyll be calling it quits. Clody still keeps a 1996 Banner Graphic clipping of the fourth-annual event tacked up at his house and can recall how Alspaughs team edged his for the tournament title.

With the teams tied for low score, it went to a chip-off and E.J. Rosengarten placed his just inside of Clodys to give a team that also included Barb Young and Mike Cherry the title.

Its the task of organizing the tournament and subsequent reception at Greencastle Elks Lodge 1077 thats become taxing on organizers.

Its run its course, I think, Clody said. And whos to say it may never kick off again? I know Im tired and the other guys are tired. Maybe somebody will get energetic and start it up again.

He also knows that the tradition of golfing with one eye wont be going anywhere just yet.

Brad and I were talking and we know therell be eight or so of us go out and throw money in the hat, Clody said.

For now, theres still the fun of watching some fool put on an eye patch and try to hit a ball with one eye for the very first time. Clody will be playing this time with his son and 13-year-old grandson, who got his first taste of the One Eye last year.

He was saying, How do you do it? This is stupid, Clody said with a grin. But I know he enjoyed it.

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One Eye, once more: Final Clody's scramble set Sept. 9 - The Banner-Graphic

Dr. Jon Pederson, the president of the Colorado Optometric Association, is here to answer your eclipse damage questions.

Josh Hafner, USA TODAY , WXIA 7:29 AM. MDT August 22, 2017

A composite image of the total solar eclipse seen from the Lowell Observatory Solar Eclipse Experience August 21, 2017 in Madras, Oregon. / AFP PHOTO / STAN HONDA (Photo credit should read STAN HONDA/AFP/Getty Images)

If you,like our nation's president, looked directly into Monday's eclipse, you might wonder: Did I just damage my eyes?

Whether by accident or disregard, untold masses looked at the sun with unshielded eyes during the must-see-safely event. By Monday afternoon,peoplewere alreadyfreaking outabouttheir eyesonline.

The sun isn't more damaging to your eyes during asolar eclipse than on any other day. But asOhio optometristMichael Schectertold USA TODAY, the moon's covering makes it a lot less painful to look at it for a lot longer. That makes it tempting for folks to peer over their cardboard eclipse glasses to see "what's really going on," Schecter said.

So how long can you look before getting hurt?Not long,says Jacob Chung, Chief of Opthalmology at New Jersey's Englewood Hospital.

"If you look at it for a second or two, nothing will happen," he said."Five seconds, I'm not sure, but 10 seconds is probably too long, and 20 seconds is definitely too long."

You won't feel any pain if your eyes suffer damage, Chung said, because ourretinas lackpain fibers. Retinas can't heal themselves, either, he said, making permanent damage a possibility.

Any blurry vision won't kick in for a day or two, after the affected area swells "like an egg yolk" Schecter said. It can take months, even a year, for eyes to return to normal, he said if it they do at all.

You would basically get a burn on your central vision," Schecter said.

A2001 studylooked at 45 British patients who viewed the 1999 solar eclipse. While 20 patients claimedsymptoms of affected vision, just five showed damage on their retinas. All five looked at the eclipse for 18 seconds or longer,Slate's Will Oremusnoted.

One way to testat home whether you've damaged your eyes is to print offan Amsler Grid, Schecter said, a tool usedto detect vision problems. Closing each eye separately, focus on the center dot and see whether the surrounding grid appears wavy, splotchy or distorted, he said.

An eye doctor, of course, can properly diagnosewhether you've indeed damaged your eyes.

Contributing: Elyse Toribio of The (Bergen County, N.J.) Record.

Follow Josh Hafner on Twitter:@joshhafner

2017 USATODAY.COM

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How to know if you damaged your eyes during the eclipse | 9news ... - 9NEWS.com