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THURSDAY, June 29, 2017 (HealthDay News) -- A high IQ might do more than help you garner good grades: New research suggests it might also lengthen your life.

Scottish researchers analyzed data on nearly 66,000 people who were born in that country in 1936, took an IQ test at age 11, and were followed up to age 79 or death. The investigators discovered that children with high IQs were more likely to live longer than their less intelligent peers.

Specifically, a higher IQ test score in childhood was associated with a 28 percent reduced risk of death from respiratory disease, a 25 percent lower risk of death from heart disease and a 24 percent reduced risk of death from stroke.

But the study didn't prove that high IQ caused this reduced risk, just that an association existed.

A higher IQ in childhood was also significantly associated with a lower risk of death from injury, smoking-related cancers (particularly lung and stomach), digestive disease and dementia. There was no evidence of a link between childhood intelligence and death from cancers not related to smoking.

The findings suggest that lifestyle -- especially smoking -- plays a major role in how intelligence affects the risk of death, according to the University of Edinburgh team. It was led by Ian Deary, a professor of differential psychology.

The findings were published June 28 in the journal BMJ.

In an editorial accompanying the study, Swedish researchers wrote that "childhood IQ is strongly associated with causes of death that are, to a great extent, dependent on already known risk factors."

But according to Daniel Falkstedt, an assistant professor, and Anton Lager, head of the department of public health sciences at Karolinska Institute in Stockholm, "It remains to be seen if this is the full story or if IQ signals something deeper, and possibly genetic, in its relation to longevity."

Senior study author Deary agreed, telling The New York Times, "We don't know yet why intelligence from childhood and longevity are related, and we are keeping an open mind. Lifestyles, education, deprivation and genetics may all play a part."

The U.S. National Institute on Aging has more about longevity.

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Could a High IQ Mean a Longer Life? - Sioux City Journal

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Last October, scientists made a splash when they determined that on average, people can only live for about 115 years . That was the magic age at which the human body and brain just petered out; it wasnt designed to chug along much longer than that, they said.

That conclusion, published in the journal Nature , sparked hot debate among longevity researchers. Some felt the results vindicated what they felt to be the case, while others took issue with pinpointing a limitand such a specific one, at that.

Now, in the new issue of Nature , the editors invited scientists who criticized the original authors methods to lay out their arguments for why there isn't necessarily a limit to human aging. In the five resulting critiques, researchers tease apart the original authors methods, noting that they made assumptions that weren't warranted and overreached in their conclusions. (The researchers who concluded that human lifespan maxes out at 115 years stand by their findings, and they responded to each of the current authors criticisms.)

The new papers dont argue that human lifespan is limitless. But they note that its premature to accept that a maximum lifespan for humans exists. Its equally possible, they say, that humans will continue to live longer, and therefore might survive beyond 115 years. It was reasonable that when everybody lived to 50 that the very long lived, for whatever reasongenetics or luckwould make it to 80," says Siegfried Hekimi, professor of genetics at McGill University in Canada and one of the authors of a criticism. "If people live on average to 80 or 90, like they do now, then the very long lived make it to 110 or 120. So if the average lifespan keeps expanding, that would mean the long-lived would live even longer, beyond 115 years."

Overall, trends in longevity have been going up, and average lifespan has inched upward since even the 1990s. Back then, life expectancy in the U.S. was just around 50 years, while babies born today live to about 79 years on average. In any given year, however, if you look at the longest-lived, or the age at which the oldest person died, there may be considerable variation. There may be several years in which the maximum lifespan drops a bit, and other years in which it jumps.

MORE: How Silicon Valley Is Trying to Hack Its Way Into a Longer Life

The maximum lifespan in a population varies so much year to year that if you take the wrong snapshot of dataas Hekimi contends the original authors didit may look like there is a flattening of the age at which the longest lived die. If you throw a die several times every year that represents maximum lifespan, by chance alone you will see a lot of spread," he says. "Sometimes it will be low, sometimes it will be high.

For example, in coming up with the maximum lifespan of 115 years, the original papers researchers divided their population data into two groups: from 1968 to 1994 and 1995 to 2006. They determined that maximum lifespan peaked in the first era and started to plateau in the next. However, that coincides with the years in which Jeanne Calment, the oldest-lived human, was alive. She passed away in 1997 at age 122, so the plateau in maximum lifespan that the original researchers saw could be wholly attributed to her, Hekimi says. He and the other authors argue that the conclusion that human lifespan stops at 115 years was based on misinterpreting the data by seeing a plateau at 115 years where there was none.

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There's No Known Limit To How Long Humans Can Live | Time.com - TIME

Smart children tend to live longer than their less intelligent peers, a new study suggests.

The analysis by Scottish researchers, published by medical journal BMJ, tracked 75,252 men and women born in 1936 who had taken standardized intelligence tests in 1947.

By 2015, researchers confirmed a cause of death for 25,979 of them; 30,464 were still living in Britain.

"In a whole national population year of birth cohort followed over the life course from age 11 to age 79, higher scores on a well validated childhood intelligence test were associated with lower risk of mortality ascribed to coronary heart disease and stroke, cancers related to smoking (particularly lung and stomach), respiratory diseases, digestive diseases, injury, and dementia," the researchers wrote.

According to The New York Times, even after controlling for smoking, the link to lower scores on the intelligence testsdidn't disappear. The study found no association of lower intelligence with cancers unrelated to smoking or with suicide, but there was a strong association with death by accidental injury.

"We dont know yet why intelligence from childhood and longevity are related, and we are keeping an open mind," senior author, Ian Deary of the University of Edinburgh told the Times.

"Lifestyles, education, deprivation and genetics may all play a part."

2017 Newsmax. All rights reserved.

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68-Year Study: Childhood Intelligence and Longevity Related - Newsmax

Rudrapur, Uttrakhand, India (PRWEB) July 02, 2017

Revita Life Sciences, (http://revitalife.co.in) a biotechnology company focused on translational regenerative therapeutic applications, has announced that it is continuing to advance their novel, multi-modality clinical intervention in the state of brain death in humans.

We have proactively continued to advance our multi-modality protocol, as an extended treatment before extubation, in an attempt to reverse the state of brain death said Mr.Pranjal Agrawal, CEO Revita Life Sciences. This treatment approach has yielded some very encouraging initial outcome signs, ranging from minor observations on blood pressure changes with response to painful stimuli, to eye opening and finger movements, with corresponding transient to permanent reversal changes in EEG patterns.

This first exploratory study, entitled Non-randomized, Open-labelled, Interventional, Single Group, and Proof of Concept Study with Multi-modality Approach in Cases of Brain Death Due to Traumatic Brain Injury Having Diffuse Axonal Injury is ongoing at Anupam Hospital, Rudrapur, Uttrakhand. The intervention primarily involves intrathecal administration of minimal manipulated (processed at point of care) autologous stem cells derived from patients fat and bone marrow twice a week.

This study was inappropriately removed from the Indian Council of Medical Research (ICMR) database. ICMR has no regulatory oversight on such research in India.

The Central Drugs Standard Control Organization (CDSCO), Drug Controller General of India, had no objection to the program progressing. Regulatory approval as needed for new drugs, is currently not required when research is conducted on the recently deceased, although IRB and family consent is definitely required. CDSCO, the regulator of such studies, clearly states that no regulatory requirements are needed for any study with minimal manipulated autologous stem cells in brain death subjects.

Death is defined as the termination of all biological functions that sustain a living organism. Brain death, the complete and irreversible loss of brain function (including involuntary activity necessary to sustain life) as defined in the 1968 report of the Ad Hoc Committee of the Harvard Medical School, is the legal definition of human death in most countries around the world. Either directly through trauma, or indirectly through secondary disease indications, brain death is the final pathological state that over 60 million people globally transfer through each year.

We are in process of publishing our initial retrospective results, as well ongoing early results, in a peer reviewed journal. These initial findings will prove invaluable to the future evolution of the program, as well as in progressing the development multi-modality regenerative therapeutics for the full range of the severe disorders of consciousness, including coma, PVS, the minimally conscious state, and a range of other degenerative CNS conditions in humans, said Dr. Himanshu Bansal, Chief Scientific Officer, Revita Life Sciences and Director of Mother Cell.

With the maturation of the tools of medical science in the 21st century, especially cell therapies and regenerative medicines, tissues once considered irretrievable, may finally be able to be revived or rejuvenated. Hence many scientists believe that brain death, as presently defined, may one day be reversed. While the very long term goal is to find a solution for re-infusing life, the short term purpose of these types of studies is much less dramatic, which is to confirm if the current definition of brain irreversibility still holds true. There have been many anecdotal reports of brain death reversal across the world over the past decades in the scientific literature. Studies of this nature serve to verify and establish this very fact in a scientific and controlled manner. It will also one day give a fair chance to individuals, who are declared brain dead, especially after trauma.

About Revita Life Sciences

Revita Life Sciences is a biotechnology company focused on the development of stem cell therapies and regenerative medicine interventions that target areas of significant unmet medical need. Revita is led by Dr. Himanshu Bansal MD, who has spent over two decades developing novel MRI based classifications of spinal cord injuries as well as comprehensive treatment protocols with autologous tissues including bone marrow stem cells, Dural nerve grafts, nasal olfactory tissues, and omental transposition.

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Revita Life Sciences Continues to Advance Multi-Modality Protocol ... - PR Web (press release)

TAMPA (FOX 13) - In 2014, at the age of 41, Barbara Popoli was diagnosed with inflammatory breast cancer,or IBC.

"The first doctor that saw me actually went pale and he excused himself from the room," she remembered. "It was already inoperable and it had spread to 20 lymph nodes."

It was a shock since Barbara had never heard of IBC. It began with swelling in her breast and arm.

"And the skin started to get pink and the texture of my skin started to change and instead of feeling smooth like a tomato it started to feel rough and dimply like the outside of an orange," she continued.

Even more dismal were her odds of survival.

"I have never met so many people who have passed so quickly. Anywhere from 60 to 80 percent pass away within just a couple of years after having it," she said.

After a year and a half of traditional treatments including chemo, immunotherapy, and radiation, she joined a clinical trial at Moffitt Cancer Center in Tampa. The experimental therapy helps restore immune cells that fight the cancer.

"I think this is a big deal for patients because we've identified that there is a deficit in this cell type so we're actually offering a specific therapy to correct that particular defect," explainedDr. Brian Czerniecki, who is heading up the study at Moffitt.

The defect that may also be present in other breast cancers, including DCIS, lies in T-cells called CD-4'S.

"We identified people who didn't have a complete response to therapy, have a loss of a particular type of immune cell called the CD4 cell, the same cell that the AIDS virus attacks," he said.

To fix the problem, a large catheter inserted in the neck is connected to a blood-filtering machine. A bag collects white blood cells that are then transformed and multiplied into over a hundred million cancer-fighting cells.

Treatments consist of injections of 20 million cells into a lymph node in the groin. So far, results are promising.

"Everyone to date, so far, their immune response has boosted up to where almost to the point where healthy women are walking around," Dr. Czerniecki said.

Side effects are flu-like symptoms, usually lasting about 24 hours. The side effect means the immune system is responding to the therapy.

Barbara hopes it's enough to keep her cancer from coming back.

"There's not a lot of options for us except chemo," she continued. "If we can stop it and let people get back to a healthy life, it's going to be amazing."

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Experimental therapy uses immune system to fight breast cancer - FOX 13 News, Tampa Bay

June 29, 2017 Killer T cells surround a cancer cell. Credit: NIH

Cancer hides in plain sight of the immune system. The body's natural tumor surveillance programs should be able to detect and attack rogue cancer cells when they arise, and yet when cancer thrives, it does so because these defense systems have failed. A team of investigators led by Niroshana Anandasabapathy, MD, PhD, at Brigham and Women's Hospital have uncovered a critical strategy that some cancers may be using to cloak themselves - they find evidence of this genetic program across 30 human cancers of the peripheral tissue, including melanoma skin cancer. Their results are published June 29 in Cell.

"Our study reveals a new immunotherapy target and provides an evolutionary basis for why the immune system may fail to detect cancers arising in tissues," said corresponding author Anandasabapathy, of BWH's Department of Dermatology. "The genetic program we report on helps the immune system balance itself. Parts of this program prevent the immune system from destroying healthy organs or tissues, but might also leave a blind spot for detecting and fighting cancer."

The authors studied immune mononuclear phagocytes - a group of disparate cells that act as the "Pac man" of the immune system. When these cells detect foreign invaders and dying normal tissues, they devour or engulf their components. These cells then present these components on their surface teach T cells to maintain tolerance to healthy tissues, or to fight infections and pathogens. Despite differences in function, all immune mononuclear phagocytes found in the skin- (a peripheral tissue like lung and gut) share a common set of genetic programming, which is further enhanced when they enter the tissue. This program is conserved in fetal and adult development, and across species. And, the research team reports, is co-opted by multiple human cancers of tissue.

The team finds that this program is prompted by an "instructive cue" from interferon gamma - a molecule that plays a critical role in regulating immunity. The authors find IFN-gamma for mononuclear phagocytes in development but that IFN-gamma and tissue immune signatures are much higher in skin cancer than in healthy skin. Having an immune response measured by IFN-gamma and tissue signatures correlated with improved metastatic melanoma survival outcomes, making these signatures potential biomarkers for cancer survival.

The authors reasoned such a program might contain key molecules that help the immune system reduce inflammation, but that might also leave a blind spot to cancer detection. One of the key genes the researchers detected is suppressor of cytokine signaling 2 (SOCS2). When this gene was turned off in a mouse model, the immune system was able to robustly detect and reject cancer in models of melanoma and thymoma (cancer of the thymus). They also observed improved vaccination responses, and heightened auto-inflammation suggesting this gene normally dampens auto-inflammatory responses and contracts protective immunity.

"Our research suggests that these cancers are co-opting tissue-specific immune development to escape detection, but we see that turning off SOCS2 unmasks them," said Anandasabapathy. "This sheds new light on our understanding of how the immune system is programed to see cancers and also points the way toward new therapeutic targets for treating cancers that have these signatures."

Explore further: Researchers identify key mutation that suppresses the immune system in melanoma

More information: Nirschl CJ et al. "IFN-gamma-dependent tissue immune homeostasis is co-opted in the tumor microenvironment" Cell DOI: 10.1016/j.cell.2017.06.016

Journal reference: Cell

Provided by: Brigham and Women's Hospital

University of California, Irvine researchers have identified a specific mutation that allows melanoma tumor cells to remain undetected by the immune system. The finding may lead to the development of better immunotherapies ...

Targeting a molecule called B7-H4which blocks T-cells from destroying tumor cellscould lead to the development of new therapies that boost the immune system's ability to fight cancer, according to a review published ...

(HealthDay) -- Growth of the deadly skin cancer melanoma may be triggered by the immune system turning on itself, according to a new study that also identified the mechanism that causes this to happen.

Internal conflict between cell types explains why the immune system struggles to recognize and attack pancreatic cancer. Curbing this infighting has the potential to make treatment more effective, according to a study led ...

Researchers from Mayo Clinic have quantified the numbers of various types of immune cells associated with the risk of developing breast cancer. The findings are published in a study in Clinical Cancer Research.

A new step in cancer immunotherapy: researchers from the Netherlands Cancer Institute and University of Oslo/Oslo University Hospital show that even if one's own immune cells cannot recognize and fight their tumors, someone ...

Cancer hides in plain sight of the immune system. The body's natural tumor surveillance programs should be able to detect and attack rogue cancer cells when they arise, and yet when cancer thrives, it does so because these ...

An immune-related protein deployed between neighboring cells in Drosophila plays an essential role in the cell degradation process known as autophagy, according to new research by Eric H. Baehrecke, PhD, at UMass Medical ...

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Investigators at the National Institutes of Health (NIH) and international colleagues have discovered a genetic cause and potential treatment strategy for a rare immune disorder called CHAPLE disease. Children with the condition ...

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New insights into why the immune system fails to see cancer - Medical Xpress

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Mavenclad Reduces MS Relapses by Reseting the Immune System - Multiple Sclerosis News Today

Two researchers from the National University of Singapore have developed a sour beer that is infused with a probiotic strain of bacteria, Lactobacillus paracasei L26.

L. paracasei is known to neutralize toxins and viruses, and help regulate the human immune system. It is already incorporated into a variety of dairy products to help improve gut-health.

Chan Mei Zhi Alcine, a student in the Food Science and Technology Program at NUS said she regularly consumes dairy-based probiotic beverages, and wanted to apply similar techniques to brewing a gut-friendly beer flavor.

The health benefits of probiotics are well known. While good bacteria are often present in foods that have been fermented, there are currently no beers in the market that contain probiotics, said Alcine in a university release.

With the help of Associate Professor Liu Shao Quan, the duo spent nine months perfecting their recipe and ensuring they had the optimal amount of live probiotics in the beer.

They isolated the L. paracasei bacterium from human intestines and grew the probiotic, as well as the yeast, in pure cultures.

The team altered some aspects of the conventional brewing and fermentation processes to successfully create the beer with the live probiotic.

The final result was a sour beer with an alcohol content of 3.5 percent. It takes about a month before it is ready to drink.

For this beer, we used a lactic acid bacterium as a probiotic micro-organism. It will utilize sugars present in the wort to produce sour-tasting lactic acid, resulting in a beer with sharp and tart flavors, said Alcine.

But, as she also explained, developing sufficient counts of live probiotics in beer proved to be challenging because the hop acids in beer prevent probiotics from growing and surviving.

Alcine and Shao Quan have filed for a patent to protect the sour beer recipe. The duo believes they hit a sort of sweet spot in the market according to Shao Quan, food and beverage products containing probiotics have increased in recent years, and a similar trend has been seen with a boost in craft and specialty beer flavors. The sour beer they developed could be an attractive option for consumers in both groups.

But further researcher may be needed to test how effective the live probiotics in the beer are for gut and immune health before they can market it as a gut-friendly beer.

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Probiotic Beer Aims to Boost Immune System - Laboratory Equipment

Two new studies suggest that one in five seemingly healthy people hasDNA mutations that puts him or herat increased risk for genetic disease.

BlackJack3D/iStockPhoto

By Ryan CrossJun. 26, 2017 , 6:15 PM

Some doctors dream of diagnosing diseasesor at least predicting disease riskwith a simple DNA scan. But others have said the practice, which could soon be the foundation of preventative medicine, isnt worth the economic or emotional cost. Now, a new pair of studies puts numbers to the debate, and one is the first ever randomized clinical trial evaluating whole genome sequencing in healthy people. Together, they suggest that sequencing the genomes of otherwise healthy adults can for about one in five people turn up risk markers for rare diseases or genetic mutations associated with cancers.

What that means for those people and any health care system considering genome screening remains uncertain, but some watching for these studies welcomed the results nonetheless. It's terrific that we are studying implementation of this new technology rather than ringing our hands and fretting about it without evidence, says Barbara Biesecker, a social and behavioral researcher at the National Human Genome Research Institute in Bethesda, Maryland.

The first genome screening study looked at 100 healthy adults who initially reported their family history to their own primary care physician. Then half were randomly assigned to undergo an additional full genomic workup, which cost about $5000 each and examined some 5 million subtle DNA sequence changes, known as single-nucleotide variants, across 4600 genessuch genome screening goes far beyond that currently recommended by the American College of Medical Genetics and Genomics (ACMG), which suggests informing people of results forjust 59 genes known or strongly expected to cause disease.

Of the 50 participants whose genomes were sequenced, 11 had alterations in at least one letter of DNA suspected to causeusually rarediseases, researchers report today in The Annals of Internal Medicine. But only two exhibited clear symptoms. One was a patient with extreme sensitivity to the sun. Their DNA revealed a skin condition called variegate porphyria. Now that patient knows they will be much less likely to get bad sunburns or rashes if they avoid the sun and certain medications, says Jason Vassy, a primary care clinician-investigator at Veteran Affairs Boston Healthcare System and lead author of the study.

The team also found that every sequenced patient carried at least one recessive mutation linked to a diseasea single copy of a mutant gene that could cause an illness if two copies are present. That knowledge can be used to make reproductive decisionsa partner may get tested to see if they have a matching mutationand prompt family members to test themselves for carrier status. And in what Vassy calls a slightly more controversial result, the team examined participants chances of developing eight polygenic diseases, conditions that are rarely attributed to a single genetic mutation. Here, they compiled the collective effects of multiple genesup to 70 for type II diabetes and 60 for coronary heart diseaseto predict a patients relative risk of developing the disease.

Just 16% of study volunteers who only reported their family history were referred to genetic counselors or got follow-up laboratory tests. In the genome sequencing group, the number was 34%.

Some researchers have expressed concern that such whole genome screening will skyrocket medical costs or cause undue psychological harm. Aside from the initial cost of sequencing (which was covered by the study), patients who underwent the genomic screen paid an average of $350 additional in healthcare costs over the next 6 months, Vassy and colleagues reported. But contrary to fears of emotional trauma, neither the sequencing group nor the control group showed any changes in anxiety or depression 6 months after the study.

Vassy stresses that their study was small and needs follow-up, but it still impressed Christa Martin, a geneticist at Geisinger Health System, in Danville, Pennsylvania, who worked on the ACMGs recommendations for genome sequencing. I almost feel like the authors undersold themselves, she says. Many of their patients are making health behavioral changes, so they are using the information in a positive way.

The study was extremely well designed and very appropriately run, adds Barbara Koenig, a medical anthropologist who directs the University of CaliforniaSan Francisco Bioethics Program. But she still questions the assumption by many physicians, ethicists, and patient advocates that more information is always beneficial. It is just hard to know how all this information is going to be brought together in our pretty dysfunctional healthcare system.

Another paper published last week on the preprint server bioRxiv, which has not yet undergone peer review, yields similar results. Using whole-exome sequencing, which looks only at the protein-coding regions of the genome, Michael Snyder, director of the Stanford Center for Genomics and Personalized Medicine in Palo Alto, California, and colleagues found that 12 out of 70 healthy adults, or 17%, unknowingly had one or more DNA mutations that increased the risk for genetic diseases for which there are treatment or preventative options.

Both studies suggest that physicians should look at genes beyond the ACMGs 59 top priorities, Snyder says. He argues that whole-genome sequencing should be automatically incorporated into primary care. You may have some super-worriers, but I would argue that the information is still useful for a physician to have. Vassy, however, says that there isnt yet enough evidence to ask insurance companies to reimburse whole genome sequencing of healthy patients.

We like a quick fix and the gene is an important cultural icon right now, so we probably give it more power than it really has, Koenig says. But these are still really early days for these technologies to be useful in the clinic.

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One in five 'healthy' adults may carry disease-related genetic mutations - Science Magazine

Patients who underwent genetic screenings now fear that documentation of the results in their medical records could lead to problems if a new health law is enacted. Sam Edwards/Caiaimage/Getty Images hide caption

Patients who underwent genetic screenings now fear that documentation of the results in their medical records could lead to problems if a new health law is enacted.

Two years ago, Cheasanee Huette, a 20-year-old college student in Northern California, decided to find out if she was a carrier of the genetic mutation that gave rise to a disease that killed her mother. She took comfort in knowing that whatever the result, she'd be protected by the Affordable Care Act's guarantees of insurance coverage for pre-existing conditions.

Her results came back positive. Like her mother, she's a carrier of one of the mutations known as Lynch syndrome. The term refers to a cluster of mutations that can boost the risk of a wide range of cancers, particularly colon and rectal.

As Republican lawmakers advance proposals to overhaul the ACA's consumer protections, Huette frets that her future health coverage and employment options will be defined by that test.

She even wonders if documentation of the mutation in her medical records and related screenings could rule out individual insurance plans. She's currently covered under her father's policy. "Once I move to my own health care plan, I'm concerned about who is going to be willing to cover me, and how much will that cost," she says.

In recent years, doctors have urged patients to be screened for a variety of diseases and predisposition to illness, confident it would not affect their future insurability. Being predisposed to an illness such as carrying the BRCA gene mutations associated with breast and ovarian cancer does not mean a patient will come down with the illness. But knowing they could be at risk may allow patients to take steps to prevent its development.

Under the current health law, many screening tests for widespread conditions such as prediabetes are covered in full by insurance. The Centers for Disease Control and Prevention and the American Medical Association have urged primary care doctors to test patients at risk for prediabetes. But doctors, genetic counselors and patient advocacy groups now worry that people will shy away from testing as the ACA's future becomes more uncertain.

Dr. Kenneth Lin, a family physician at Georgetown University School of Medicine in Washington, D.C., says if the changes proposed by the GOP become law, "you can bet that I'll be even more reluctant to test patients or record the diagnosis of prediabetes in their charts." He thinks such a notation could mean hundreds of dollars a month more in premiums for individuals in some states under the new bill.

Huette says she's sharing her story publicly since her genetic mutation is already on her medical record.

But elsewhere, there have been "panicked expressions of concern," says Lisa Schlager of the patient advocacy group Facing Our Risk of Cancer Empowered (FORCE). "Somebody who had cancer even saying, 'I don't want my daughter to test now.' Or 'I'm going to be dropped from my insurance because I have the BRCA mutation.' There's a lot of fear."

Those fears, which come in an era of accelerating genetics-driven medicine, rest upon whether a gap that was closed by the ACA will be reopened. That remains unclear.

A law passed in 2008, the Genetic Information Nondiscrimination Act, bans health insurance discrimination if someone tests positive for a mutation. But that protection stops once the mutation causes "manifest disease" essentially, a diagnosable health condition.

That means "when you become symptomatic," although it's not clear how severe the symptoms must be to constitute having the disease, says Mark Rothstein, an attorney and bioethicist at the University of Louisville School of Medicine in Kentucky, who has written extensively about GINA.

The ACA, passed two years after GINA, closed that gap by barring health insurance discrimination based on pre-existing conditions, Rothstein says.

On paper, the legislation unveiled by Senate Majority Leader Mitch McConnell last week wouldn't let insurers set higher rates for people with pre-existing conditions, but it could effectively exclude such patients from coverage by allowing states to offer insurance plans that don't cover certain maladies, health analysts say. Meanwhile, the bill that passed the House last month does have a provision that allows states to waive protections for people with pre-existing conditions, if they have a gap in coverage of 63 days or longer in the prior year.

When members of a Lynch Syndrome social media group were asked for their views on genetic testing amid the current health care debate, about two dozen men and women responded. Nearly all said they were delaying action for themselves or suggesting that family members, particularly children, hold off.

Huette was the only one who agreed to speak for attribution. She says before the ACA was enacted, she witnessed the impact that fears about insurance coverage had on patients. Her mother, a veterinarian, had wanted to run her own practice but instead took a federal government job for the guarantee of health insurance. She died at the age of 57 of pancreatic cancer, one of six malignancies she had been diagnosed with over the years.

Huette says she doesn't regret getting tested. Without the result, Huette points out, how would she have persuaded a doctor to give her a colonoscopy in her 20s?

"Ultimately, my health is more important than my bank account," she says.

Kaiser Health News, a nonprofit health newsroom whose stories appear in news outlets nationwide, is an editorially independent part of the Kaiser Family Foundation.

Continued here:
Patients Who Tested Positive For Genetic Mutations Fear Bias ... - NPR - NPR

June 30, 2017

Uncovering rare susceptibility variants that contribute to the causes of complex diseases requires large sample sizes and massively parallel sequencing technologies. These sample sizes, often made up of exome and genome data from tens to hundreds of thousands of individuals, are often too large for current analytical tools to process. A team at Baylor College of Medicine, led by Dr. Suzanne Leal, professor of molecular and human genetics, has developed new software called SEQSpark to overcome this processing obstacle. A study on the new technology appears in The American Journal of Human Genetics.

"To handle these large data sets, we built the SEQSpark tool based on the commonly used Spark program, which allows SEQSpark to utilize multiple processing platforms to increase the speed and efficiency of performing data quality control, annotation and rare variant association analysis," Leal said.

To test and validate the versatility and speed of SEQSpark, Leal and her team analyzed benchmarks from the whole genome sequence data from the UK10K, testing specifically for waist-to-hip ratios.

"The analysis and related tasks took about one and a half hours to complete, in total. This includes loading the data, annotation, principal components analysis and single and rare variant aggregate association analysis for the more than 9 million variants present in this sample set," explained Di Zhang, a postdoctoral associate in the Leal lab at Baylor and first author on the paper.

To evaluate SEQSpark's performance in a larger data set, Leal and the research team generated 50,000 simulated exomes. The SEQSprak program ran the analysis for a quantitative trait using several variant aggregate association methods in an hour and forty-five minutes.

When compared to other variant association tools, SEQSpark was consistently faster, reducing computation to a hundredth of the time in some cases.

"What is unique about SEQSpark is that it is scalable, and smaller labs can run it without super specific hardware, and it can also be run in a multi-server environment to increase its speed and capacity for large genetic data sets," Zhang said. "It is ideal for large-scale genetic epidemiological studies and is highly efficient from a computational standpoint."

"We see this software as being very useful as the demand for the analysis of massively parallel sequence data grows. SEQSpark is highly versatile, and as we analyze increasingly large sets of rare variant data, it has the potential to play a key role in furthering personalized medicine," Leal said.

In the future, Leal and her team will continue to test and increase SEQSpark's capabilities and will be analyzing soon data sets that have 500,000 samples or more.

Explore further: Genetic test for familial data improves detection genes causing complex diseases such as Alzheimer's

More information: Di Zhang et al. SEQSpark: A Complete Analysis Tool for Large-Scale Rare Variant Association Studies using Whole-Genome and Exome Sequence Data, The American Journal of Human Genetics (2017). DOI: 10.1016/j.ajhg.2017.05.017

A team of researchers at Baylor College of Medicine has developed a family-based association test that improves the detection in families of rare disease-causing variants of genes involved in complex conditions such as Alzheimer's. ...

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Researchers build SEQSpark to analyze massive genetic data sets - Medical Xpress

June 26, 2017 Credit: CC0 Public Domain

Between 15 and 20 percent of black people carry a genetic mutation that puts them at risk for certain chronic kidney disease, but only about half of them develop the illness - a variance that long has puzzled researchers. Now a study has found that the gene mutation's toxic effects require higher than normal levels of a protein called suPAR to trigger the onset and progression of the disease.

The results of the study, published in a research article in the journal Nature Medicine today, could lead soon to new treatments for chronic kidney disease that target these risk factors, according to Dr. Jochen Reiser, the senior author of the paper. Reiser is the chairperson of the Department of Internal Medicine and Ralph C. Brown MD Professor of Medicine at Rush University Medical Center, Chicago.

Chronic kidney disease - or CKD for short - is a progressive failure of function that prevents kidneys from fulfilling their role filtering waste from the blood stream. Nearly 17 percent of people in the U.S. have chronic kidney disease, and approximately 4 percent require dialysis and/or a kidney transplant due to kidney failure. Currently, there are no drugs that can treat CKD in an effective way.

Study analyzed samples from more than 1,000 people with genetic risk for CKD

For the study recounted in the Nature Medicine paper, Reiser worked with a team that included researchers at Emory University, Harvard University, Johns Hopkins University, the National Institute of Health, Ruprecht Karls University of Heidelberg, the Israel Institute of Technology and others. Together, they looked at two well-known genetic risk factors for CKD in black people, the mutated G1 or G2 variations in the gene known as apolipoprotein L1 (APOL1). To be at risk for developing CKD, an individual must have inherited two of these gene variants, one from each parent.

The study analyzed blood samples for suPAR levels, screened for APOL1 gene mutations and measured kidney function from two separate cohorts of black patients - 487 people from the Emory Cardiovascular Biobank, 15 percent of whom had a high-risk APOL1 genotype; and 607 from the multi-center African American Study of Kidney Disease and Hypertension, including 24 percent with the high-risk mutation.

Using these two large, unrelated cohorts, the researchers found that plasma suPAR levelsindependently predict renal function decline in individuals with two copies of APOL1 risk variants. APOL1-related risk is reduced by lower levels of plasma suPAR and strengthened by higher levels.

The team then went on and used purified proteins to study if suPAR and APOL1 bind to each other. They found that the mutated G1 and G2 variant did so particularly well on what's known as a receptor on the surface of kidney cells, in this case the suPAR activated receptor alphavbeta3 integrin. "This binding appears to be a key step in the disease onset" adds Dr. Kwi Hye Ko, a scientist at Rush and the study's co-first author.

This binding causes kidney cells to change their structure and function, permitting disease onset. Using cell models and genetically engineered mice, the authors then could reproduce kidney disease changes upon expression of APOL1 gene variants, but the disease required the presence suPAR.

Without elevated suPAR levels, genetic mutation much less likely to trigger disease

Everybody has suPAR, which is produced by bone marrow cells, in their blood, with normal levels around 2400 picogram per milliliter (pg/ml). As levels of suPAR rise, risk for kidney disease rises in turn.

Patients with levels above 3000 picogram per milliliter carry a much higher risk for kidney disease in the general population. Black people are particularly at risk, given the study's finding that suPAR activates its receptor on kidney cells that then attract the APOL1 risk proteins. Over time, these assaults can damage and eventually destroy the kidney.

On the other hand, without high levels of suPAR, the ability of the genetic mutation of APOL1 to exert its damaging effects is impaired, which helps identify patients in most need of suPAR lowering or future anti-suPAR therapy.

"Patients with APOL1 mutations who don't get kidney disease have more commonly low suPAR levels," said Dr. Salim Hayek, co-first author of the paper and a cardiologist at Emory University School of Medicine. "The suPAR level needs to be high to activate the mechanism in the kidney that enables APOL1 proteins" and set off the chain of events the genetic mutation can trigger.

suPAR 'is to the kidneys as cholesterol is to the heart'

Like some other pathological gene mutations, the APOL1 variations may have persisted in the population, in this case in Africa, because they could protect people from infection with the parasites known as trypanosome. explained Sanja Sever, PhD, co-correspondent author of the paper and associate professor of medicine at Harvard Medical School. In the United States, however, fighting parasitic trypanosomes isn't a significant concern, while lifestyle and environmental pressures such as obesity promote the rise in suPAR levels. This scenario sets up people for high risk of kidney disease.

Reiser has spent his career studying a scarring type of chronic kidney disease, focal segmental glomerulosclerosis. In past studies, he discovered that suPAR not only is a marker for kidney disease, but also a likely cause.

"What we are learning today is that suPAR in a general way is to kidneys what cholesterol is to the heart, a substance that can cause damage if levels rise too high, or a substance that can likely make many forms of kidney disease worse," Reiser says. "Based on these fundamental insights, suPAR level testing may become a routine test at many institutions around the world."

Like cholesterol, suPAR levels vary from person to person. Some environmental factors can contribute significantly to elevated suPAR levels. "Lifestyle is a big factor, bigger than we thought," Reiser says.

Smoking, weight gain and even frequent infections can add up and send suPAR to dangerous heights. Weight loss and smoking cessation can help bring levels down, but once elevated, suPAR may not recede to a healthy level again, said Dr. Melissa Tracy, co-author of the study and an associate professor of cardiology at Rush. People at genetic risk for kidney disease should aim to live a healthy life to keep suPAR levels low.

Explore further: Circulating blood factor linked with a leading cause of kidney failure

More information: A tripartite complex of suPAR, APOL1 risk variants and v3 integrin on podocytes mediates chronic kidney disease, Nature Medicine (2017). DOI: 10.1038/nm.4362

Patients with a disease that is a leading cause of kidney failure tend to have high levels of a particular factor circulating in their blood, according to a study appearing in an upcoming issue of the Journal of the American ...

A protein known as suPAR has been identified in recent years as both a reliable marker for chronic kidney disease and a pathogen of the often deadly condition. Its place of origin in the human body, however, has been a mysteryuntil ...

Make room, cholesterol. A new disease marker is entering the medical lexicon: suPAR, or soluble urokinase-type plasminogen activator receptor. A study in the New England Journal of Medicine shows that suPAR, a circulating ...

African Americans have a heightened risk of developing chronic and end-stage kidney disease. This association has been attributed to two common genetic variants - named G1 and G2in APOL1, a gene that codes for a human-specific ...

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Catalyst for genetic kidney disease in black people identified - Medical Xpress

June 29, 2017 Micrograph showing prostatic acinar adenocarcinoma (the most common form of prostate cancer) Credit: Wikipedia

Scientists have had limited success at identifying specific inherited genes associated with prostate cancer, despite the fact that it is one of the most common non-skin cancers among men. Researchers at University of Utah Health studied prostate cancer patients with multiple cancer diagnoses, many who would not be recommended for genetic tests following current guidelines, to identify genetic mutations that may influence cancer treatment and cancer risk assessment for family members. Their findings are reported in the June issue of the journal Cancer.

"We commonly use a combination of a patient's personal and family cancer histories to identify those individuals who may have a mutation in a gene that predisposes that individual to developing cancers," said Patrick Pili, M.D., medical oncology fellow at the University of Texas MD Anderson Cancer Center. "Testing for hereditary cancers impacts not only the patient with cancer but also potentially the cancer screening and health outcomes of their entire family, but many prostate cancer patients do not meet the current guidelines to test for genetic cancer heritability."

Pili was part of a research team led by Kathleen Cooney, M.D., chair of the Department of Internal Medicine at U of U Health and a Huntsman Cancer Institute investigator, who proposed a strategy to identify germline mutations in men selected for the study based on their clinical history not their family history.

The study was highly selective, including 102 patients who had been diagnosed with prostate cancer and at least one additional primary cancer, like melanoma, pancreatic cancer, testicular cancer, or Hodgkin lymphoma.

The researchers examined the frequency of harmful germline mutations in this group of men. These mutations originate on either the egg or sperm and become incorporated into the DNA of every cell in the body of the resulting offspring.

Using next generation sequencing, the researchers found that 11 percent of the patients had a disease-causing mutation in at least one cancer-predisposing gene, which suggests these genetic variations contributed to their prostate cancer. Cooney found no difference in cancer aggressiveness or age of diagnosis compared to patients without these mutations.

In addition, a certified genetic counselor and co-investigator Elena Stoffel, M.D., University of Michigan Comprehensive Cancer Center, reviewed personal and family histories from each patient to determine whether they would meet clinical genetic testing guidelines. The majority of the men in the study, 64 percent, did not meet current criteria to test for hereditary cancer based on personal and/or family history.

The findings suggest that there are men with heritable prostate cancer-predisposing mutations that are not eligible for genetic screening under current guidelines.

"This is the first paper in which we can show the potential of using a clinical history of multiple cancers, including prostate cancer, in a single individual to identify inherited germline mutations," Cooney said.

The majority of harmful mutations identified were in genes involved in DNA repair.

"These mutations prevent the DNA from healing itself, which can lead to a predisposition for cancer," Cooney said.

This result is also beneficial because drugs like PARP [poly ADP ribose polymerase] inhibitors have a better success rate in treating cancers with the underlying gene mutation associated with DNA repair.

Cooney cautions that this is a small pilot study rather than a broader epidemiological survey, and it consists of a highly specific subset of patients.

"We cannot generalize these findings to the broader population, because we used highly selective criteria to tip us off to patients that may have mutations outside typical hereditary genetic patterns," she said.

The 102 patients included in the study were identified from the University of Michigan's Prostate Cancer Genetics Project, which registers patients who are diagnosed with prostate cancer before age 55 or who have a first- or second-degree relative with prostate cancer. In addition, the research team identified patients from the University of Michigan's Cancer Genetics Registry, which includes individuals with personal or family history suggestive of a hereditary risk of cancer.

"Our findings are in line with those of other studies, suggesting that approximately 1 in 10 men with advanced prostate cancer harbors a genetic variant associated with increased cancer risk," said Stoffel. "While family history is an important tool, there may be better ways to identify patients with genetic risk."

Future studies with larger sample sizes will include sequencing of tumors that will allow investigators to more carefully explore the different features associated with tumors that arise in individuals with germline mutations.

"This approach will help us identify patients at greater risk for aggressive prostate cancer so they can seek earlier screening while pre-symptomatic," Cooney said.

Explore further: Are men with a family history of prostate cancer eligible for active surveillance?

More information: Patrick G. Pili et al. Germline genetic variants in men with prostate cancer and one or more additional cancers, Cancer (2017). DOI: 10.1002/cncr.30817

Journal reference: Cancer

Provided by: University of Utah

Active surveillancecareful monitoring to determine if or when a cancer warrants treatmentis an increasingly prevalent choice for prostate cancer, but it's unclear if the strategy is appropriate for men with a family ...

Inherited mutations in genes that function to repair DNA may contribute to metastatic prostate cancer more than previously recognized, according to a study out today in the New England Journal of Medicine. Though infrequent ...

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Born in August, Charlie Gard has a rare genetic disorder known as mitochondrial DNA depletion syndrome. Caused by a genetic mutation, it leads to weakened muscles and organ dysfunction, among other symptoms, with a poor prognosis for most patients.

Charlie is on life support and has been in the intensive care unit at the Great Ormond Street Hospital for Children in London since October. His doctors wish to take him off life support, but his parents disagree.

"The domestic courts concluded that it would be lawful for the hospital to withdraw life sustaining treatment because it was likely that Charlie would suffer significant harm if his present suffering was prolonged without any realistic prospect of improvement, and the experimental therapy would be of no effective benefit," a press release from the court announcing the decision said.

Charlie's parents appealed to the UK Supreme Court to decide the best interests of their child. After they lost that appeal, the 10-month-old was due to have his life support switched off at the end of the day June 13.

Gard and Yates then filed a request with the European Court of Human Rights, an international court based in Strasbourg, France, to consider the case.

The original ruling to provide life support until June 13 was extended by European Court of Human Rights initially for one week, until June 19. Rather than making a decision then, the court granted a three week-extension, until July 10, to allow for a more informed decision by the court. That extension ended Tuesday with the courts decision.

However, parental rights are not absolute, and in cases in which doctors and parents disagree, the courts may exercise objective judgment in a child's best interest.

In April, a judge tasked with ruling on the impasse between doctors and parents decided in favor of the Great Ormond Street Hospital doctors. In his decision, Justice Francis said life support treatment should end so Charlie could die with dignity.

The boy's parents challenged this ruling in May, yet it was upheld by a Court of Appeal. Three Supreme Court justices later dismissed another challenge from the couple.

Since Charlie's birth, "his condition has deteriorated seriously," the UK Supreme Court stated in a decision June 8; his brain is severely affected, and "he cannot move his arms or legs or breathe unaided."

On this basis, the court ruled that the child's life support should be switched off June 13, but the family appealed to the European court.

Charlie's parents argued that the UK courts gave insufficient weight to their own human rights, and some of Charlie's human rights, in their decision-making, Wilson said.

After the European court's ruling to extend the deadline while judges considered the case further, the Supreme Court told doctors it "would not be unlawful" to continue to provide life support.

After the extension, a Supreme Court hearing was requested by the government and the Great Ormond Street Hospital for Children, which did not know whether the Strasbourg court order was legally binding in the UK, Wilson explained.

"There was also a secondary issue, which was that (Great Ormond Street Hospital's) legal representatives were concerned that at present, doctors did not have sufficient legal clarity about what they can and can't do if Charlie's condition deteriorates," Wilson said. "So this court was also invited to consider whether any UK court, and if so which court, should handle that matter."

In fact, it has never been used to treat this form of mitochondrial DNA depletion syndrome, according to the British ruling, though it has proved beneficial to patients with a different form of the disease.

"He literally has nothing to lose but potentially a healthier, happier life to gain," they said.

Parents are rightly at the "heart" of decisions made about life-sustaining treatment for critically ill children, noted Dominic Wilkinson, director of medical ethics at the Oxford Uehiro Centre.

"Sadly, reluctantly, doctors and judges do sometimes conclude -- and are justified in concluding -- that slim chances of life are not always better than dying." Sometimes, the "best that medicine can do" -- and the most ethical decision -- is to provide comfort and to avoid painful and unhelpful medical treatments, he wrote.

The court said the decision was meticulous, noting that they spoke with Charlie's health care providers, independent experts, experts recommended by the family, and Charlie's parents to inform the ruling. In the end, the press released said they determined, "it was most likely Charlie was being exposed to continued pain, suffering and distress and that undergoing experimental treatment with no prospects of success would offer no benefit, and continue to cause him significant harm."

CNN's Stephanie Halasz, Debra Goldschmidt and Judith Vonberg contributed to this report.

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Court rules hospital can withdraw life support for sick baby Charlie Gard - CNN International

June 30, 2017 Size switchable nano-theranostics constructed with decomposable inorganic nanomaterials for acidic TME targeted cancer therapy. (a) A scheme showing the preparation of HSA-MnO2-Ce6&Pt (HMCP) nanoparticles, and (b) their tumor microenvironment responsive dissociation to enable efficient intra-tumoral penetration of therapeutic albumin complexes. (c) A scheme showing the preparation of Ce6(Mn)@CaCO3-PEG, and (d) its acidic TME responsive dissociation for enhanced MR imaging and synergistic cancer therapy. Credit: Science China Press

Cancer is one of leading causes of human mortality around the world. The current mainstream cancer treatment modalities (e.g. surgery, chemotherapy and radiotherapy) only show limited treatment outcomes, partly owing to the complexities and heterogeneity of tumor biology. In recent decades, with the rapid advance of nanotechnology, nanomedicine has attracted increasing attention as promising for personalized medicine to enable more efficient and reliable cancer diagnosis and treatment.

Unlike normal cells energized via oxidative phosphorylation, tumor cells utilize the energy produced from oxygen-independent glycolysis for survival by adapting to insufficient tumor oxygen supply resulting from the heterogeneously distributed tumor vasculatures (also known as the Warburg effect). Via such oncogenic metabolism, tumor cells would produce a large amount of lactate along with excess protons and carbon dioxide, which collectively contribute to enhanced acidification of the extracellular TME with pH, often in the range of 6.5 to 6.8, leading to increased tumor metastasis and treatment resistance.

With rapid advances in nanotechnology, several catalogs of nanomaterials have been widely explored for the design of cancer-targeted nano-theranostics. In a new overview published in the Beijing-based National Science Review, co-authors Liangzhu Feng, Ziliang Dong, Danlei Tao, Yicheng Zhang and Zhuang Liu at the Institute of Functional Nano & Soft Materials (FUNSOM), Soochow University in Suzhou, China present new developments in the design of novel multifunctional nano-theranostics for precision cancer nanomedicine by targeting the acidic TME and outline the potential development directions of future acidic tumor microenvironment-responsive nano-theranostics.

"Various types of pH-responsive nanoprobes have been developed to enable great signal amplification under slightly reduced pH within solid tumors. By taking the acidic TME as the target, smart imaging nanoprobes with excellent pH-responsive signal amplification would be promising to enable more sensitive and accurate tumor diagnosis," they state in the published study.

"As far as nano-therapeutics are concerned, it has been found that the acidic TME responsive surface charge reverse, PEG corona detachment and size shrinkage (or decomposition) of nanoparticles would facilitate the efficient tumor accumulation, intra-tumoral diffusion and tumor cellular uptake of therapeutics, leading to significantly improved cancer treatment. Therefore, the rational development of novel cancer-targeted nano-theranostics with sequential patterns of size switch from large to small, and surface charge reverse from neutral or slightly negative to positive within the tumor, would be more preferred for efficient tumor-targeted drug delivery."

The scientists also write, "For the translation of those interesting smart pH-responsive nano-therapeutics from bench to bedside, the formulation of those nanoscale systems should be relatively simple, reliable and with great biocompatibility, since many of those currently developed nano-theranostics were may be too complicated for clinical translation."

Explore further: Treatment with Alk5 inhibitor improves tumor uptake of imaging agents

More information: Liangzhu Feng et al, The acidic tumor microenvironment: a target for smart cancer nano-theranostics, National Science Review (2017). DOI: 10.1093/nsr/nwx062

A form of genetic variation, called differential RNA splicing, may have a role in tumor aggressiveness and drug resistance in African American men with prostate cancer. Researchers at the George Washington University (GW) ...

While mutations in protein-coding genes have held the limelight in cancer genomics, those in the noncoding genome (home to the regulatory elements that control gene activity) may also have powerful roles in driving tumor ...

A molecular test can pinpoint which patients will have a very low risk of death from breast cancer even 20 years after diagnosis and tumor removal, according to a new clinical study led by UC San Francisco in collaboration ...

Scientists have had limited success at identifying specific inherited genes associated with prostate cancer, despite the fact that it is one of the most common non-skin cancers among men. Researchers at University of Utah ...

Cancerous tumors are formidable enemies, recruiting blood vessels to aid their voracious growth, damaging nearby tissues, and deploying numerous strategies to evade the body's defense systems. But even more malicious are ...

Leukemia researchers led by Dr. John Dick have traced the origins of relapse in acute myeloid leukemia (AML) to rare therapy-resistant leukemia stem cells that are already present at diagnosis and before chemotherapy begins.

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Exploiting acidic tumor microenvironment for the development of novel cancer nano-theranostics - Medical Xpress

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Our Colorado regenerative medicine specialists are skilled in the areas of helping you heal from chronic pain. Using state-of-the-art technologies, such as amniotic, adipose, or bone marrow stem cell injections, PRP therapy, A2M, or hormone therapies, we have found great success for patients suffering from joint, back, musculoskeletal, or tissue damage.

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To provide people with non-surgical treatment options that bring relief from pain, harness the bodys ability to heal itself, and restore hope for a healthier active future.

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5280 Stem Cell | Colorado Stem Cell Therapy

Regenerative medicine combines the latest advances in stem cell biology, embryology, tissue engineering and medicine to develop products for the replacement, restoration or regeneration of damaged or diseased cells and tissues. Tools used in regenerative medicine include biomaterials and extracellular matrices, lab-generated cells and tissues, and new biological molecules. These powerful technologies and tools are allowing clinical scientists to engineer and provide healthy cells, tissues and organs to patients with chronic degenerative diseases. This revolution in medical science changes the focus from treating symptoms of chronic and degenerative diseases to providing cures, and directly addresses costs that constitute approximately 83% of the 2.5 trillion dollar annual healthcare budget in the U.S. and are growing due to an aging population.

BioTime is led by Michael West, PhD., who pioneered the regenerative medicine industry. He founded Geron Corporation in the early 90s which funded the first studies of cultured hESC to realize their potential to cure intractable human degenerative diseases. Dr. West has since built BioTime around key technologies and intellectual property that constitute major pillars of regenerative medicine.

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Regenerative Medicine - BioTime, Inc.

A regenerative medicine startup led by a Mayo Clinic cardiologist is setting up shop in a downtown Rochesters Minnesota BioBusiness Center, according to newly filed city documents. The filing indicated Rion LLC, a Minnesota company registered to Dr. Atta Behfar of the Mayo Clinic Center for Regenerative Medicine, has signed a three-year lease for just over 2,000 square feet at the city-owned BioBusiness Center. The lease begins July 1. The nine-story BioBusiness Center opened in downtown Rochester in 2007 as a center for innovation in biotechnology, promoting the linkages between the researchers and practitioners at Mayo Clinic; instructors and students at the University of Minnesota Rochester, and the biotechnology business community. It houses the Mayo Clinic Business Accelerator among other tenants. Behfar is an assistant medical professor and leads a laboratory at Mayo concentrating on applying regenerative medicine the practice of using stem cells to regenerate damaged or missing tissue to prevent and cure chronic heart conditions. Specifically, his group focuses on development and use of both stem cells and protein-based therapies to reverse injury caused by lack of blood flow to the heart. The business direction of Rion, meanwhile, appears to be specifically geared toward a cutting-edge development in the field of regenerative medicine the use of extracellular vesicles (EVs) in speeding and directing the growth of regenerating tissues in the heart and elsewhere in the body. EVs, long brushed off by researchers as mere debris in the bloodstream, are membrane-enclosed spheres that break off from the surfaces of nearly all living cells when disturbed. They transport lipids, proteins and nucleic acids, and have now been found to be important players in cell-to-cell communication, influencing the behavior and even the identity of cells. Their emerging role in regenerative medicine could potentially be huge. For instance, by bioengineering them to transport protein payloads from stem cells, they can be used to signal the bodys own cells to regenerate tissue instead of transplanting the stem cells themselves, thus eliminating the chance of host immune system rejection. A patent application filed last year by Rion, Behfar, Mayo Center for Regenerative Medicine Director Dr. Andre Terzic and two other local inventors is aimed at adapting the healing properties of a specific type of EV into a unique kind of product that could have wide applications. It focuses on EVs derived from blood platelets, which are well known to stop bleeding, promote the growth of new tissues and blood vessels, relieve inflammation and provide a host of other benefits. The patent describes a system of encapsulating platelet EVs derived from human or animal blood into a platelet honey and delivering it to target areas of the body, such as damaged tissues or organs. Its purported effect is to regenerate, repair and restore damaged tissue, with possible uses including treating heart disease; healing damaged bones or joints; wound treatment; and cosmetic skin applications. A brief business description provided by Rion to Rochester city officials stated the company is focused on the delivery of cutting edge regenerative technologies to patients at low cost and in off-the-shelf fashion. Building on initial research at Mayo Clinic, Rion LLC aims to develop and bring to practice products in the space of wound healing, orthopedics and cardiac disease. The statement also added the company is an enthusiastic backer of Rochesters efforts to develop a local biotech business cluster, and is seeking to participate in the realization of the Destination Medical Center initiative.

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Mayo-Connected Regenerative Medicine Startup Inks Downtown Rochester Lease - Twin Cities Business Magazine

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Why it matters to you

The new finding could help scientists unlock the secrets to regenerative medicine in humans.

In the future, artificial and transplanted organs may be things of the past as regenerative medicine becomes so advancedthat a damaged heart or lung is simply regrown from cells already present.

That possibility is still far in the distance, but a new study out of the University of Floridacould help pave the way. While examining the genes of the starlet sea anemone an invertebrate capable of regenerating itself a research team led by Mark Martindale discovered genes that are known to grow heart cells in humans.

The finding was surprising in part because anemones dont have hearts or muscles, and yet Martindale knew they shared more in common with humans than might be expected.

A group of us sequenced the genome of the anemone about 10 years ago, he told Digital Trends. One of the super cool things we found was that this little sea anemone had more genes in common with human beings than all of the other so-called model systems that 99 percent of the people in my field work on.

Since these model systems including fruit flies and nematodes are nearer to humans on the evolutionary timescale, that finding suggested that theyve lost genes along the way.

It turns out that the number of genes you have does not seem to be a very good predictor of organismal complexity as we have traditionally interpreted it, Martindale said.

Rather of the number of genes, the deciding factor may be the way they communicate with each other.

One of the most important findings in this paper is not necessarily how many genes are involved in heart formation, but how they are wired-up. Martindale explained. Genes control other genes in very complicated networks. Many people focus on genes that are involved in cell division but not as many people have studied the differences in how these genes talk to each other in animals that can regenerate versus those that can not regenerate.

By understanding how genes communicate, the researchers hope that they can someday stimulate regenerative healing in the human body.

But theres a lot of work to be done first. One of the big challenges will be determining whether certain mechanisms are species-specific or if they can be adapted. In vertebrates, for example, heart genes create lockdown loops that require them to perform functions related to their location in the body. Anemone genes dont lockdown in such a way. Its unclear whether this feature is fixed to anemone or if it can be activated in humans as well.

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Sea anemone genes could spur advancements in regenerative medicine - Digital Trends

sea anemone heart gene regeneration regenerative medicine

In the future, artificial and transplanted organs may be things of the past as regenerative medicine becomes so advancedthat a damaged heart or lung is simply regrown from cells already present.

That possibility is still far in the distance, but a new study out of the University of Floridacould help pave the way. While examining the genes of the starlet sea anemone an invertebrate capable of regenerating itself a research team led by Mark Martindale discovered genes that are known to grow heart cells in humans.

The finding was surprising in part because anemones dont have hearts or muscles, and yet Martindale knew they shared more in common with humans than might be expected.

A group of us sequenced the genome of the anemone about 10 years ago, he told Digital Trends. One of the super cool things we found was that this little sea anemone had more genes in common with human beings than all of the other so-called model systems that 99 percent of the people in my field work on.

Since these model systems including fruit flies and nematodes are nearer to humans on the evolutionary timescale, that finding suggested that theyve lost genes along the way.

It turns out that the number of genes you have does not seem to be a very good predictor of organismal complexity as we have traditionally interpreted it, Martindale said.

Rather of the number of genes, the deciding factor may be the way they communicate with each other.

One of the most important findings in this paper is not necessarily how many genes are involved in heart formation, but how they are wired-up. Martindale explained. Genes control other genes in very complicated networks. Many people focus on genes that are involved in cell division but not as many people have studied the differences in how these genes talk to each other in animals that can regenerate versus those that can not regenerate.

By understanding how genes communicate, the researchers hope that they can someday stimulate regenerative healing in the human body.

But theres a lot of work to be done first. One of the big challenges will be determining whether certain mechanisms are species-specific or if they can be adapted. In vertebrates, for example, heart genes create lockdown loops that require them to perform functions related to their location in the body. Anemone genes dont lockdown in such a way. Its unclear whether this feature is fixed to anemone or if it can be activated in humans as well.

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New study on anemone genes could pave way for regenerative ... - Yahoo News