StemCell Therapy

With the usual mix of anticipation and apprehension, Kaitlyn Johnson is getting ready to go to her first summer camp. She's looking forward to meeting new friends and being able to ride horses, swim and host tea parties. She's also a little nervous and a little scared, like any 7-year-old facing her first sleepaway camp.

But the wonder is that Kaitlyn is leaving the house for anything but a medical facility. Diagnosed with leukemia when she was 18 months old, her life has been consumed with cancer treatments, doctors' visits and hospital stays.

Acute lymphoblastic leukemia is the most common cancer among young children, accounting for a quarter of all cancer cases in kids, and it has no cure. For about 85% to 90% of children, the leukemia can, however, be effectively treated through chemotherapy.

If it is not eliminated and comes back, it is, more often than not, fatal. Rounds of chemotherapy can buy patients time, but as the disease progresses, the periods of remission get shorter and shorter. "The options for these patients are not very good at all," says Dr. Theodore Laetsch, a pediatrician at the University of Texas Southwestern Medical Center.

When Kaitlyn's cancer wasn't controlled after three years and round after round of chemotherapy drugs, her doctors had little else to offer. "They said, 'This did nothing, it didn't touch it,'" says Kaitlyn's mother Mandy, a dental assistant from Royce City, Texas. "My stomach just dropped." Kaitlyn could receive a bone-marrow transplant, but only about half of those procedures are successful, and there was a good chance that she would reject the donor cells. If that happened, her chances of surviving were very small.

In a calculated gamble, her doctors suggested a radical new option: becoming a test subject in a trial of an experimental therapy that would, for the first time, use gene therapy to train a patient's immune system to recognize and destroy their cancer in the same way it dispatches bacteria and viruses. The strategy is the latest development in immunotherapy, a revolutionary approach to cancer treatment that uses a series of precision strikes to disintegrate cancer from within the body itself. Joining the trial was risky, since other attempts to activate the immune system hadn't really worked in the past. Mandy, her husband James and Kaitlyn traveled from their home in Texas to Children's Hospital of Philadelphia (CHOP), where they stayed in a hotel for eight weeks while Kaitlyn received the therapy and recovered. "The thought crossed my mind that Kaitlyn might not come home again," says Mandy. "I couldn't tell you how many times I would be in the bathroom at the hospital, spending an hour in the shower just crying, thinking, What are we going to do if this doesn't help her?"

But it did. After receiving the therapy in 2015, the cancer cells in Kaitlyn's body melted away. Test after test, including one that picks up one cancer cell in a million, still can't detect any malignant cells lurking in Kaitlyn's blood. What saved Kaitlyn was an infusion of her own immune cells that were genetically modified to destroy her leukemia. "You take someone who essentially has no possibility for a cure--almost every single one of these patients dies--and with [this] therapy, 90% go into remission," says Dr. David Porter, director of blood and bone-marrow transplantation at the University of Pennsylvania. Such radical immune-based approaches were launched in 2011 with the success of intravenous drugs that loosen the brakes on the immune system so it can see cancer cells and destroy them with the same vigor with which they attack bacteria and viruses. Now, with the genetically engineered immune cells known as chimeric antigen receptor (CAR) T cells that were used in Kaitlyn's study, doctors are crippling cancer in more precise and targeted ways than surgery, chemotherapy and radiation ever could. While the first cancer immunotherapies were broadly aimed at any cancer, experts are now repurposing the immune system into a personalized precision treatment that can not only recognize but also eliminate the cancer cells unique to each individual patient.

What makes immune-based therapies like CAR T cell therapy so promising--and so powerful--is that they are a living drug churned out by the patients themselves. The treatment isn't a pill or a liquid that has to be taken regularly, but a one-hit wonder that, when given a single time, trains the body to keep on treating, ideally for a lifetime.

"This therapy is utterly transformative for this kind of leukemia and also lymphoma," says Stephan Grupp, director of the cancer immunotherapy program at CHOP and one of the lead doctors treating patients in the study in which Kaitlyn participated.

Eager to bring this groundbreaking option to more patients, including those with other types of cancers, an advisory panel for the Food and Drug Administration voted unanimously in July to move the therapy beyond the testing phase, during which several hundred people have been able to take advantage of it, to become a standard therapy for children with certain leukemias if all other treatments have failed. While the FDA isn't obligated to follow the panel's advice, it often does, and it is expected to announce its decision in a matter of weeks.

Across the country, doctors are racing to enroll people with other cancers--breast, prostate, pancreatic, ovarian, sarcoma and brain, including the kind diagnosed in Senator John McCain--in hundreds of trials to see if they, too, will benefit from this novel approach. They are even cautiously allowing themselves to entertain the idea that this living drug may even lead to a cure for some of these patients. Curing cancers, rather than treating them, would result in a significant drop in the more than $120 billion currently spent each year on cancer care in the U.S., as well as untold suffering.

This revolutionary therapy, however, almost didn't happen. While the idea of using the body's immune cells against cancer has been around for a long time, the practical reality had proved daunting. Unlike infection-causing bacteria and viruses that are distinctly foreign to the body, cancer cells start out as healthy cells that mutate and grow out of control, and the immune system is loath to target its own cells.

"Only a handful of people were doing the research," says Dr. Carl June, director of the Center for Cellular Immunotherapy at the University of Pennsylvania's Abramson Cancer Center and the scientist who pioneered the therapy. A graduate of the U.S. Naval Academy, June is all too familiar with the devastating effects of cancer, having lost his first wife to ovarian cancer and battled skin cancer himself. Trial after trial failed as reinfusions of immune cells turned out to be more of a hit-or-miss endeavor than a reliable road to remission.

After spending nearly three decades on the problem, June zeroed in on a malignant fingerprint that could be exploited to stack the deck of a cancer patient's immune system with the right destructive cells to destroy the cancer.

In the case of leukemias, that marker turned out to be CD19, a protein that all cancerous blood cells sprout on their surface. June repurposed immune cells to carry a protein that would stick to CD19, along with another marker that would activate the immune cells to start attacking the cancer more aggressively once they found their malignant marks. Using a design initially developed by researchers at St. Jude Children's Research Hospital for such a combination, June and his colleague Bruce Levine perfected a way to genetically modify and grow these cancer-fighting cells in abundance in the lab and to test them in animals with leukemia. The resulting immune platoon of CAR T cells is uniquely equipped to ferret out and destroy cancer cells. But getting them into patients is a complex process. Doctors first remove a patient's immune cells from the blood, genetically tweak them in the lab to carry June's cancer-targeting combination and then infuse the modified cells back into the patient using an IV.

Because these repurposed immune cells continue to survive and divide, the therapy continues to work for months, years and, doctors hope, perhaps a lifetime. Similar to the way vaccines prompt the body to produce immune cells that can provide lifelong protection against viruses and bacteria, CAR T cell therapy could be a way to immunize against cancer. "The word vaccination would not be inappropriate," says Dr. Otis Brawley, chief medical officer of the American Cancer Society.

June's therapy worked surprisingly well in mice, shrinking tumors and, in some cases, eliminating them altogether. He applied for a grant at the National Cancer Institute at the National Institutes of Health to study the therapy in people from 2010 to 2011. But the idea was still so new that many scientists believed that testing it in people was too risky. In 1999, a teenager died days after receiving an experimental dose of genes to correct an inherited disorder, and anything involving gene therapy was viewed suspiciously. While such deaths aren't entirely unusual in experimental studies, there were ethical questions about whether the teenager and his family were adequately informed of the risks and concerns that the doctor in charge of the study had a financial conflict of interest in seeing the therapy develop. Officials in charge of the program acknowledged that important questions were raised by the trial and said they took the questions and concerns very seriously. But the entire gene-therapy program was shut down. All of that occurred at the University of Pennsylvania--where June was. His grant application was rejected.

It would take two more years before private funders--the Leukemia and Lymphoma Society and an alumnus of the university who was eager to support new cancer treatments--donated $5 million to give June the chance to bring his therapy to the first human patients.

The date July 31 has always been a milestone for Bill Ludwig, a retired corrections officer in New Jersey. It's the day that he joined the Marines as an 18-year-old, and the day, 30 years later, that he married his wife Darla.

It was also the day he went to the hospital to become the first person ever to receive the combination gene and CAR T cell therapy, in 2010. For Ludwig, the experimental therapy was his only remaining option. Like many people with leukemia, Ludwig had been living on borrowed time for a decade, counting the days between the chemotherapy treatments that would hold the cancer in his blood cells at bay for a time. Inevitably, like weeds in an untended garden, the leukemia cells would grow and take over his blood system again.

But the periods of reprieve were getting dangerously short. "I was running out of treatments," says Ludwig. So when his doctor mentioned the trial conducted by June and Porter at the University of Pennsylvania, he didn't hesitate. "I never thought that the clinical trial was going to cure me," he says. "I just wanted to live and to continue to fight. If there was something that would put me into the next month, still breathing, then that's what I was looking for."

When Ludwig signed the consent form for the treatment, he wasn't even told what to expect in terms of side effects or adverse reactions. The scientists had no way of predicting what would happen. "They explained that I was the first and that they obviously had no case law, so to speak," he says. So when he was hit with a severe fever, had difficulty breathing, showed signs of kidney failure and was admitted to the intensive care unit, he assumed that the treatment wasn't working.

His condition deteriorated so quickly and so intensely that doctors told him to call his family to his bedside, just four days after he received the modified cells. "I told my family I loved them and that I knew why they were there," he says. "I had already gone and had a cemetery plot, and already paid for my funeral."

Rather than signaling the end, Ludwig's severe illness turned out to be evidence that the immune cells he received were furiously at work, eliminating and sweeping away the huge burden of cancer cells choking up his bloodstream. But his doctors did not realize it at the time.

It wasn't until the second patient, Doug Olson, who received his CAR T cells about six weeks after Ludwig, that Porter had a eureka moment. When he received the call that Olson was also running a high fever, having trouble breathing and showing abnormal lab results, Porter realized that these were signs that the treatment was working. "It happens when you kill huge amounts of cancer cells all at the same time," Porter says. What threw him off initially is that it's rare for anything to wipe out that much cancer in people with Ludwig's and Olson's disease. June and Porter have since calculated that the T cells obliterated anywhere from 2.5 lb. to 7 lb. of cancer in Ludwig's and Olson's bodies. "I couldn't fathom that this is why they both were so sick," says Porter. "But I realized this is the cells: they were working, and working rapidly. It was not something we see with chemotherapy or anything else we have to treat this cancer."

Ludwig has now been in remission for seven years, and his success led to the larger study of CAR T cell therapy in children like Kaitlyn, who no longer respond to existing treatments for their cancer. The only side effect Ludwig has is a weakened immune system; because the treatment wipes out a category of his immune cells--the ones that turned cancerous--he returns to the University of Pennsylvania every seven weeks for an infusion of immunoglobulins to protect him from pneumonia and colds. Olson, too, is still cancer-free.

While the number of people who have received CAR T cell therapy is still small, the majority are in remission. That's especially encouraging for children, whose lives are permanently disrupted by the repeated cycles of treatments that currently are their only option. "It's a chance for these kids to have a normal life and a normal childhood that doesn't involve constant infusions, transfusions, infections and being away from their home, family and school," says Dr. Gwen Nichols, chief medical officer of the Leukemia and Lymphoma Society.

The hope is that while CAR T cell therapy will at first be reserved for people who have failed to respond to all standard treatments, eventually they won't have to wait that long. As doctors learn from pioneers like Kaitlyn, Ludwig and Olson, they will have more confidence in pushing the therapy earlier, when patients are stronger and the cancer is less advanced--perhaps as a replacement for or in combination with other treatments.

The severe immune reaction triggered by the therapy remains a big concern. While it can be monitored in the hospital and managed with steroids or antibodies that fight inflammation, there have been deaths in other trials involving CAR T cells. One drug company put one of its studies on hold due to the toxic side effects. "I am excited by CAR T therapy, but I'm also worried that some people might get too excited," says the American Cancer Society's Brawley. "It's important that we proceed slowly and do this meticulously so that we develop this in the right way."

For now, CAR T cells are expensive--some analysts estimate that each patient's batch of cells would cost hundreds of thousands of dollars--because they require a bespoke production process. If approved, Novartis, which licensed the technology from the University of Pennsylvania, will provide the therapy in about 35 cancer centers in the U.S. by the end of the year. Other companies are already working toward universal T cells that could be created for off-the-shelf use in any patient with cancer. "This is just the beginning," says June.

Since Ludwig's cancer has been in remission, he and his wife have packed their RV and taken the vacations they missed while he was a slave to his cancer and chemotherapy schedule. This year, they're visiting Mount Rushmore, Grand Teton National Park and Yellowstone National Park before taking their granddaughter to Disney World in the fall. "When they told me I was cancer-free, it was just like someone said, 'You won the lottery,'" he says. "If somebody else with this disease has the chance to walk in my shoes and live past it, that would be the greatest gift for me."

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Cancer's Newest Miracle Cure - TIME

For patients with severe and end-stage heart failure there are few treatment options left apart from transplants and stem-cell therapy. But a new Israeli study finds that stem-cell therapy may harm heart-disease patients.

The research, led by Prof. Jonathan Leor of Tel Aviv Universitys Sackler Faculty of Medicineand Sheba Medical Center and conducted by TAUs Dr. Nili Naftali-Shani, explores the current practice of using cells from the host patient to repair tissue and contends that this can prove toxic for patients.

We found that, contrary to popular belief, tissue stem cells derived from sick hearts do not contribute to heart healing after injury, said Leor. Furthermore, we found that these cells are affected by the inflammatory environment and develop inflammatory properties. The affected stem cells may even exacerbate damage to the already diseased heart muscle.

Tissue or adult stem cells blank cells that can act as a repair kit for the body by replacing damaged tissue encourage the regeneration of blood vessel cells and new heart muscle tissue. Faced with a worse survival rate than many cancers, many heart-failure patients have turned to stem-cell therapy as a last resort.

But our findings suggest that stem cells, like any drug, can have adverse effects, said Leor. We concluded that stem cells used in cardiac therapy should be drawn from healthy donors or be better genetically engineered for the patient.

The researchers, who published their study in the journal Circulation, also discovered the molecular pathway involved in the negative interaction between stem cells and the immune system as they isolated stem cells in mouse models of heart disease. Afterward, they focused on cardiac stem cells in patients with heart disease.

The results could help improve the use of autologous stem cells those drawn from the patients themselves in cardiac therapy, Leor said.

We showed that the deletion of the gene responsible for this pathway can restore the original therapeutic function of the cells, said Leor. Our findings determine the potential negative effects of inflammation on stem-cell function as theyre currently used. The use of autologous stem cells from patients with heart disease should be modified. Only stem cells from healthy donors or genetically engineered cells should be used in treating cardiac conditions.

The researchers are currently testing a gene editing technique (CRISPER) to inhibit the gene responsible for the negative inflammatory properties of the cardiac stem cells of heart disease patients. We hope our engineered stem cells will be resistant to the negative effects of the immune system, said Leor.

Read the rest here:
Stem-cell treatment may harm heart disease patients - ISRAEL21c

August 10, 2017 - By Louis Casey

Investors sentiment decreased to 0.3 in Q4 2016. Its down 0.37, from 0.67 in 2016Q3. It turned negative, as 16 investors sold Neuralstem, Inc. shares while 11 reduced holdings. 2 funds opened positions while 6 raised stakes. 6.88 million shares or 44.05% less from 12.30 million shares in 2016Q3 were reported.Fifth Third Bank & Trust accumulated 120,000 shares. Moreover, Northern has 0% invested in Neuralstem, Inc. (NASDAQ:CUR). Geode Capital Mgmt Limited Liability Company, Massachusetts-based fund reported 1.03 million shares. Blair William Il holds 0% or 418,942 shares. National Bank Of Mellon Corp owns 0% invested in Neuralstem, Inc. (NASDAQ:CUR) for 91,969 shares. California Public Employees Retirement invested in 155,700 shares. Wells Fargo And Mn stated it has 0% in Neuralstem, Inc. (NASDAQ:CUR). Vanguard Group Incorporated Inc invested in 3.09 million shares or 0% of the stock. The California-based Blackrock Institutional Na has invested 0% in Neuralstem, Inc. (NASDAQ:CUR). National Asset Mgmt Incorporated invested in 0.01% or 167,500 shares. Natl Bank Of America Corp De, North Carolina-based fund reported 8,400 shares. Blackrock Advisors reported 17,361 shares. First Heartland Consultants accumulated 10,000 shares. Kcg Holding reported 0% in Neuralstem, Inc. (NASDAQ:CUR). Gru One Trading L P accumulated 4,349 shares.

Since February 24, 2017, it had 3 buys, and 0 insider sales for $70,004 activity. LLOYD JONES JONATHAN BRIAN had bought 5,455 shares worth $30,003. 7,500 shares were bought by Daly Richard J, worth $30,000.

The stock of Neuralstem Incorporated (NASDAQ:CUR) registered an increase of 0.98% in short interest. CURs total short interest was 942,000 shares in August as published by FINRA. Its up 0.98% from 932,900 shares, reported previously. With 90,000 shares average volume, it will take short sellers 11 days to cover their CURs short positions. The short interest to Neuralstem Incorporateds float is 11.11%.

It closed at $1.08 lastly. It is down 3.35% since August 10, 2016 and is uptrending. It has underperformed by 13.35% the S&P500.

Neuralstem, Inc. is a clinical-stage biopharmaceutical company. The company has market cap of $13.09 million. The Firm is engaged in research, development and commercialization of central nervous system therapies based on its human neuronal stem cells and its stem-cell derived small molecule compounds. It currently has negative earnings. The Firm has approximately three assets: its NSI-189 small molecule program, its NSI-566 stem cell therapy program and its chemical entity screening platform.

More notable recent Neuralstem, Inc. (NASDAQ:CUR) news were published by: Globenewswire.com which released: Neuralstem Reports Second Quarter 2017 Fiscal Results and Provides Clinical on August 08, 2017, also Seekingalpha.com with their article: Neuralstem Is Doomed published on August 03, 2017, Globenewswire.com published: Neuralstem Announces Pricing of Public Offering of Common Stock and Warrants on July 27, 2017. More interesting news about Neuralstem, Inc. (NASDAQ:CUR) were released by: Globenewswire.com and their article: Neuralstem Awarded $~1MM Grant by NIH to Continue Preclinical Research into published on August 02, 2017 as well as Benzinga.coms news article titled: Mid-Day Market Update: ShoreTel Gains On Acquisition News; Neuralstem Shares with publication date: July 27, 2017.

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What Will Happen to Neuralstem Incorporated (NASDAQ:CUR) Next? The Stock Has Increase in Shorts - BZ Weekly

In fact, people reported more knee and hip pain when the weather was good, suggesting it is activity, not cold or rain that affects sufferers most.

Arthritis, causing achy joints affects ten million Britons and is said to be fuelled by the damp climate.

But people's activity levels, which rise with the temperature, are likelier than the weather to trigger online searches for knee and hip pain, say scientists.

Google hits for arthritis over a period of five years had no discernible link with the elements, said Professor Scott Telfer.

He said: "You hear people with arthritis say they can tell when the weather is changing.

"But with past studies there's only been vague associations, nothing very concrete, and our findings align with those."

In fact searches for knee-and-hip-pain increased in tandem with temperatures - until it got uncomfortably hot.

And rainy days tended to slightly reduce internet traffic for both conditions. This inferred "changes in physical activity levels" were primarily responsible.

Prof Telfer, a researcher in orthopaedics and sports medicine at Washington University in St Louis, said: "We haven't found any direct mechanism that links ambient temperature with pain."

His interest in using internet data stems from the fact web searches are increasingly people's first response to experiencing adverse health symptoms.

He said some people with achy joints and arthritis swear weather influences their pain.

So in the first study of its kind across 45 major US cities he found sunshine, rainfall and temperature are indeed associated with joint pain, but not in the way you'd expect.

Within the study's focus span of 23 to 86 degrees Fahrenheit searches rose steadily. Knee-pain peaked at 73 degrees and were less frequent at higher temperatures.

Hip-pain searches peaked at 83 degrees and then tailed off. Rain actually dampened search volumes for both.

The findings published in PLOS ONE show people's activity level is a bigger risk than the weather to cause pain that spurs online searches.

Prof Telfer said: "We were surprised by how consistent the results were throughout the range of temperatures in cities across the country."

His team used Google Trends for how the number of searchers for arthritis or hip and knee pain fluctuated with the weather. Searches related to stomach pain were also calculated as a control.

Daily summaries of local weather data from 1 January 2011 to 31 December 2015 included temperature, rainfall, relative humidity and barometric pressure.

These are factors previously suggested as associated with increases in musculoskeletal pain.

Among all the variables only temperature and rainfall were found to have statistically significant associations for knee-and-hip-pain but not arthritis.

Prof Telfer said:

"What we think is a much more likely explanation is the fact people are more active on nice days - so more prone to have overuse and acute injuries from that and to search online for relevant information.

"That's our hypothesis for what we'll explore next."

The stomach-pain searches rose at low and high temperature extremes and ebbed in mild temperatures.

This was a very different pattern from the knee-and-hip-pain searches - backing the findings.

Excerpt from:
Does the rain affect arthritis pain? Bad weather linked to joint pain could be a MYTH - Express.co.uk

Atascadero resident Jenn Foss was scrolling through her Facebook feed when she first learned of the California Coast Classic, a 525-mile bike ride along Highway 1 that benefits the Arthritis Foundation.

Its a cause that carries extra weight with Foss, a nurse at Wilshire Hospice in San Luis Obispo who sees the debilitating effects of arthritis on a daily basis. The 30-year-old Foss even deals with her own arthritis, stemming from a dirt bike crash when she was a teenager.

My mom also had to have knee surgeries on both knees when she was fairly young, Foss said in an email to The Tribune. And now working in hospice, geriatric arthritis pain is something that is a very real discomfort that many of the patients struggle with.

The 17th annual California Coast Classic which begins Sept. 9 in San Francisco and ends Sept. 16 in Los Angeles offered Foss and hundreds of others the opportunity to help raise funds needed to find a cure for arthritis.

Each rider must pay a registration fee and raise a minimum of $3,500 to join the tour. Foss has her own donation page set up online (donations are tax deductible) and had raised more than $1,400 as of Aug. 5 42 days before the race begins.

Foss also has two local fundraisers planned this month.

On Aug. 12, Foss will host a hotdog BBQ fundraiser and silent auction in the Grocery Outlet parking lot in Atascadero.

And from 8 a.m. until noon on Aug. 27, the Foss family plans to host a yard sale at their farm, located at 3300 Traffic Way in Atascadero.

As far as training and preparation for the bike ride, Foss said she fits in as much as she can while keeping an extremely tight schedule.

All I can say is thank goodness this is not a race everyone can do this in their own pace, Foss said. So far my mileage and timing is good. Im just working on a good diet, staying strong, keeping up with my cardio and being kind to my body.

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SLO County woman to bike 525 miles to raise money for Arthritis Foundation - The San Luis Obispo Tribune

It affects more than 690,000 people in the UK, of which over 500,000 are women and around three-quarters are of working age.

People with rheumatoid arthritis experience a range of symptoms, including pain and swelling in the joints, tiredness and depression which can affect their daily lives.

The condition cannot be cured but can be treated.

Experts have revealed patients who smoke or are overweight however see fewer improvements in their symptoms.

A study by American and Canadian researchers found smoking and being overweight is more difficult for patients with rheumatoid arthritis to achieve optimal control of inflammation and symptoms.

Researchers from collected data on more than 1,100 patients.

"Early, aggressive treatment to achieve remission is the primary goal of therapy and can be best achieved early on when treating patients with newly diagnosed rheumatoid arthritis, as early disease control is associated with improved long-term outcomes," said Vivian Bykerk, senior investigator and director of the Inflammatory Arthritis Centre of Excellence at Hospital for Special Surgery.

"We have previously shown that individuals with excess weight are less likely to achieve sustained remission in the first three years after diagnosis.

Here we explore the impact of smoking and being overweight or obese on the ability to achieve good control of symptoms and inflammation in men and women with rheumatoid arthritis."

Researchers at the Hospital for Special Surgery in New York analysed more than 1,109 patients who were being treated with methotrexate and other arthritis drugs.

The majority of patients were female, but among the women, 31 per cent were overweight, 32 per cent were obese and 15 per cent smoked. Among the males, 44 per cent were overweight and 35 per cent were obese and 22 per cent currently smoked.

Experts found less symptom improvement was also seen in patients who were overnight or obese compared with those of a healthy weight.

Current smokers also saw less symptom relief compared to nonsmoker over time.

The finding revealed the most dramatic differences in patients were seen in those who were overweight, or obese and smoked.

These patients had considerably worse outcomes over time compared to nonsmoking patients with a healthy weight.

"These results contribute to growing evidence of how lifestyle impacts how well patients may respond to treatment and the potential value of referring them to proven community-based smoking cessation and weight management programs," said Dr Bykerk.

DOES ARTHRITIS GET WORSE IN WINTER?

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Rheumatoid arthritis - symptoms will not improve if patients do THIS - Express.co.uk

COLUMBUS, Ga. 1 in 5 people over age 18 has doctor-diagnosed arthritis or more than 50 million adults. Arthritis wears down the cartilage, giving the bones in certain joints nothing to cushion them so they rub together and cause a lot of pain. Doctors can replace these arthritic joints in the fingers as well as the knees and hips.

Dr. Sean Blake is the director of the Hand Center at St. Francis Orthopaedic Institute. He says arthritis can make common everyday tasks painful.

Folding laundry, doing dishes, opening jars, shaking hands, opening the car door, turning the key. All those things are things people think they just have to deal with. Its just aging. But actually, we can actually help them with some good relief of pain, said Dr. Blake.

Those painful joints can be replaced.

Most common spots that well put joints in are what we call the Metatarsal Phalangea ljoints, your knuckles , or the middle knuckle which is the Proximal Interphalangeal Joint, said Dr. Blake.

Only regional anesthesia is used for the surgery, paralyzing the arm for about 12 hours.

We go on the back of the hand and make an incision, a Curvilinear incision so its curved so it actually doesnt scar as much and we literally have to cut out the piece of bone.

And insert the implant. The patient goes home the same day, wearing a splint. Physical therapy is required. Healing takes about 10 TO 12 weeks.

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Arthritic joints can be replaced in the hands - WRBL

DETROIT - Lauren Reed is a pretty typical 23 year old woman. She very active and she loves to travel and explore, but just a few years ago she had trouble even getting up and out of bed.

"I totally shut down at one point and I wasnt motivated at all to do anything," explains Reed.

The problems started when she was injured playing basketball when she was 11 years old.

"That just sparked everything up. All my joints inflamed and I knew there was a bigger problem," she says.

After years of pain and few answers, Dr. Bernard Rubin diagnosed her with juvenile arthritis.

"She had developed severe arthritis and we needed to treat her aggressively," explains Dr. Rubin.

They used pills and injections, and less than a year ago Reed had not one, but two hip replacements.

"About three weeks in between and I was back to work in 7 weeks," says Reed. Her case is a very rare one.

Dr. Rubin explains, Its unusual to have arthritis as a child. There are only a few hundred thousand cases in the United States."

Surgery is scary, but it also brought reed the relief shes been looking for almost half her life

"It was terrible. I'd say nine out of ten pains. I couldn't stand for long periods of time. I couldnt play sports. Now I'm doing whatever, waking up feeling fantastic, going to work being more active. The surgeries just changed my life totally."

Now she plays basketball and works out at the gym, all while balancing work and school.

Reed is scheduled for another surgery -- a knee replacement -- in the next six months or so.

More here:
23-year-old Lauren Reed not letting juvenile arthritis, two hip replacements slow her down - WXYZ

A dad-of-two has a spring in his step after being one of the first people in Yorkshire to have a space-age jelly bean fitted to his big toe to end his arthritis agony.

Mick Wood, 53, found himself at the cutting-edge of medical science when his toe was fitted with a Cartiva implant a spacer made of slippery, organic polymer.

It was fitted at Spire Elland by consultant orthopaedic surgeon Mr Kurt Haendlmayer who said: I call it a jelly bean for the big toe because that is what it looks and feels like.

It is just a squidgy bean-type thing that functions in a similar way to natural cartilage and allows much more movement in the toe than a traditional fusion operation would.

Mick had previously had a conventional fusion operation on his left big toe three years ago, so when he found himself in a similar situation with the right toe he thought the same procedure would be on the cards.

However, Mr Haendlmayer suggested that for someone fit and active, the new implant would produce better results.

I was a bit apprehensive at first it all seemed a bit Tomorrows World-ish for me, said Mick.

But Mr Haendlmayer gave me lots of information about the success of similar operations in America and it didnt take me long to decide I was happy with the whole thing.

It was obviously a new procedure because when I went in for the operation there were a load of other people in there simply to observe it taking place I felt like I was a bit of a celebrity!

In a conventional fusion procedure, the additional bone build-up around the joint (osteophytes) and the usually very ragged, degenerated joint surfaces, are scraped away before the toe joint is secured with screws and a plate, making it immobile. Up until recently that was the gold standard of toe surgery.

Mr Haendlmayer added: This does alleviate the pain caused by the arthritis but, on the down-side, it means the toe is now held rigid by the metalwork which, in turn, limits the amount of movement possible by the toe.

With the Cartiva implant the extra bone is also cleared, but instead of making the joint immobile, we fix metal rods in both the toe and the socket and introduce the implant which cushions the area where the toe and the foot meet, just as normal cartilage would.

Mick, from Pontefract, is delighted with the results, saying he was now virtually pain-free and able to run, kneel and even drive for long distances.

To be honest, I wasnt unhappy with the previous fusion operation it certainly relieved a lot of the pain but this one seems much, much better and the movement I have in the toe is unbelievable.

I might be one of the first in this area to have a jelly bean toe but I dont think I will be the last.

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How a 'space-age jelly bean' cured my arthritis - Huddersfield Examiner

CHARLOTTESVILLE, Va. (WVIR) -

The University of Virginia School of Medicine is using a $50,000 donation to further research for an un-named, rare genetic disorder.

The money comes from the Bow Foundation which works to help people affected by the disease. Right now the disease is fairly new; it was only discovered in the past year and has only 50 known patients.

The disorder has mainly been targeting children, and can cause seizures, severe development delays, and movement disorders.

"By making the cells that we're making from the first patients, we'll then be able to compare those cells with other researchers and really broaden the research in this field. In a way that wouldn't be possible without this initial funding, Mike McConnell, UVA professor and researcher, said.

The hospital says they still know very little about this disease, but the funding is a step in the right direction.

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UVA School of Medicine Using Grant to Research Rare Genetic Disorder - NBC 29 News

On August 2nd, scientists achieved a milestone on the path to human genetic engineering. For the first time in the United States, scientists successfully edited the genes of a human embryo. A transpacific team of researchers used CRISPR-Cas9 to correct a mutation that leads to an often devastating heart condition. Responses to this feat followed well-trodden trails. Hype over designer babies. Hope over new tools to cure and curb disease. Some spin, some substance and a good dose of science-speak. But for me, this breakthrough is not just about science or medicine or the future of humankind. Its about faith and family, love and loss. Most of all, its about the life and memory of my brother.

Jason was born with muscle-eye-brain disease. In his case, this included muscular dystrophy, cerebral palsy, severe nearsightedness, hydrocephalus and intellectual disability. He lived past his first year thanks to marvels of modern medicine. A shunt surgery to drain excess cerebrospinal fluid building up around his brain took six attempts, but the seventh succeeded. Aside from those surgeries complications and intermittent illnesses due to a less-than-robust immune system, Jason was healthy. Healthy and happy very happy. His smile could light up a room. Yet, that didnt stop people from thinking that his disability made him worse off. My family and those in our religious community prayed for Jason. Strangers regularly came up to test their fervor. Prayer circles frequently had his name on their lists. We wanted him to be healed. But I now wonder: What, precisely, were we praying for?

Jasons disabilities fundamentally shaped his experience of the world. If praying for his healing meant praying for him to be normal, we were praying for Jason to become someone else entirely. We were praying for a paradox. If I could travel back in time, Id walk up to young, devout Joel and ask: How will Jason still be Jason if God flips a switch and makes him walk and talk and think like you? The answer to that question is hard. Yes, some just prayed for his seizures to stop. Some for his continued well-being. But is that true of most? Is that what I was praying for?

The ableist conflation of disability with disease and suffering is age-old. Just peruse the history of medicine. Decades of eugenic practices. Sanctioned torture of people with intellectual disability. The mutilation of otherwise healthy bodies in the name of functional or aesthetic normality. These stories demonstrate over and over again how easily biomedical research and practice can mask atrocity with benevolence and injustice with progress. Which leads me to ask: What, precisely, are we editing for?

Although muscle-eye-brain disease does not result from a single genetic variant, researchers agree that a single gene, named POMGNT1, plays a large role. Perhaps scientists will soon find a way to correct mutations in that and related genes. Perhaps people will no longer be born with it. But that means there would never be someone like Jason. Those prayers I mentioned above? Science will have retroactively answered them. That thought brings me to tears.

I wish we could cure cancer, relieve undue pain and heal each break and bruise. But I also wish for a world with Jason and people like him in it. I want a world accessible and habitable for people full stop not just the people we design. I worry that in our haste to make people healthy, we are in fact making people we want. We, who say we pray for healing, but in fact pray for others to be like us. We, who say were for reducing disease and promoting health, but support policies and practices aimed instead at being normal. We, who are often still unable to distinguish between positive, world-creating forms of disability and negative, world-destroying forms between Deafness, short stature or certain types of neurodiversity and chronic pain, Tay-Sachs or Alzheimers. It is with great responsibility that we as a society balance along the tightrope of biomedical progress. I long for us to find that balance. Ive certainly not found it for myself. Lest I forget how often weve lost it and how easy it is to fall, I hold dearly onto the living memory of Jason. I no longer pray for paradoxes, but for parity for the promise of a world engineered not for normality, but equality.

But that world will never come if we edit it away.

Go here to see the original:
Gene Editing Might Mean My Brother Would've Never Existed - TIME

The chip has not been tested in humans, but it has been used to heal wounds in mice. Wexner Medical Center/The Ohio State University hide caption

The chip has not been tested in humans, but it has been used to heal wounds in mice.

Scientists have created an electronic wafer that reprogrammed damaged skin cells on a mouse's leg to grow new blood vessels and help a wound heal.

One day, creator Chandan Sen hopes, it could be used to be used to treat wounds on humans. But that day is a long way off as are many other regeneration technologies in the works. Like Sen, some scientists have begun trying to directly reprogram one cell type into another for healing, while others are attempting to build organs or tissues from stem cells and organ-shaped scaffolding.

But other scientists have greeted Sen's mouse experiment, published in Nature Nanotechnology on Monday, with extreme skepticism. "My impression is that there's a lot of hyperbole here," says Sean Morrison, a stem cell researcher at the University of Texas Southwestern Medical Center. "The idea you can [reprogram] a limited number of cells in the skin and improve blood flow to an entire limb I think it's a pretty fantastic claim. I find it hard to believe."

When the device is placed on live skin and activated, it sends a small electrical pulse onto the skin cells' membrane, which opens a tiny window on the cell surface. "It's about 2 percent of the cell membrane," says Sen, who is a researcher in regenerative medicine at Ohio State University. Then, using a microscopic chute, the chip shoots new genetic code through that window and into the cell where it can begin reprogramming the cell for a new fate.

Sen says the whole process takes less than 0.1 seconds and can reprogram the cells resting underneath the device, which is about the size of a big toenail. The best part is that it's able to successfully deliver its genetic payload almost 100 percent of the time, he says. "No other gene delivery technique can deliver over 98 percent efficiency. That is our triumph."

Chandan Sen, a researcher at Ohio State University, holds a chip his lab created that has reprogrammed cells in mice. Wexner Medical Center/The Ohio State University hide caption

Chandan Sen, a researcher at Ohio State University, holds a chip his lab created that has reprogrammed cells in mice.

To test the device's healing capabilities, Sen and his colleagues took a few mice with damaged leg arteries and placed the chip on the skin near the damaged artery. That reprogrammed a centimeter or two of skin to turn into blood vessel cells. Sen says the cells that received the reprogramming genes actually started replicating the reprogramming code that the researchers originally inserted in the chip, repackaging it and sending it out to other nearby cells. And that initiated the growth of a new network of blood vessels in the leg that replaced the function of the original, damaged artery, the researchers say. "Not only did we make new cells, but those cells reorganized to make functional blood vessels that plumb with the existing vasculature and carry blood," Sen says. That was enough for the leg to fully recover. Injured mice that didn't get the chip never healed.

When the researchers used the chip on healthy legs, no new blood vessels formed. Sen says because injured mouse legs were was able to incorporate the chip's reprogramming code into the ongoing attempt to heal.

That idea hasn't quite been accepted by other researchers, however. "It's just a hand waving argument," Morrison says. "It could be true, but there's no evidence that reprogramming works differently in an injured tissue versus a non-injured tissue."

What's more, the role of exosomes, the vesicles that supposedly transmit the reprogramming command to other cells, has been contentious in medical science. "There are all manners of claims of these vesicles. It's not clear what these things are, and if it's a real biological process or if it's debris," Morrison says. "In my lab, we would want to do a lot more characterization of these exosomes before we make any claims like this."

Sen says that the theory that introduced reprogramming code from the chip or any other gene delivery method does need more work, but he isn't deterred by the criticism. "This clearly is a new conceptual development, and skepticism is understandable," he says. But he is steadfast in his confidence about the role of reprogrammed exosomes. When the researchers extracted the vesicles and injected them into skin cells in the lab, Sen says those cells converted into blood vessel cells in the petri dish. "I believe this is definitive evidence supporting that [these exosomes] may induce cell conversion."

Even if the device works as well as Sen and his colleagues hope it does, they only tested it on mice. Repairing deeper injuries, like vital organ damage, would also require inserting the chip into the body to reach the wound site. It has a long way to go before it can ever be considered for use on humans. Right now, scientists can only directly reprogram adult cells into a limited selection of other cell types like muscle, neurons and blood vessel cells. It'll be many years before scientists understand how to reprogram one cell type to become part of any of our other, many tissues.

Still, Morrison says the chip is an interesting bit of technology. "It's a cool idea, being able to release [genetic code] through nano channels," he says. "There may be applications where that's advantageous in some way in the future."

The rest is here:
A Chip That Reprograms Cells Helps Healing, At Least In Mice - NPR

The father of a boy with a rare genetic mutation has accused a scientist of exploiting his child by proclaiming the defect a genetic syndrome and naming it after herself.

At an impasse with scientists investigating, publicizing, and interpreting his sons condition, the father seems willing to use any leverage he can muster to remove the syndrome entry in an online genetic disease database. Based solely on an email he obtained from the database director, the father became convinced that if the paper underpinning the entry were retracted, the syndrome would go down with it. So earlier this year, he withdrew his consent and asked the journal that published the paper for a retraction, based on improper patient consent. He has also threatened to lob accusations of research misconduct at the papers last author.

Marc Pieterse, of The Netherlands, is the father of Vincent, a teenager who has a mutation in the RPS23 gene that has only been found in one other person, so far. In March, an international team of researchers published a paper on Vincents RPS23 mutation in the American Journal of Human Genetics (AJHG), linking it to defective ribosomes, organelles involved in protein synthesis.

One of the scientists Pieterse engaged several years ago is Alyson MacInnes, a rare disease researcher at the University of Amsterdams Academic Medical Center. She is last author of the AJHG paper and the person whose name is now connected to an entry in the Online Mendelian Inheritance in Man (OMIM) database. MacInnes told Retraction Watch that, contrary to what Pieterse claims, she played no direct role in naming the syndrome; OMIM confirmed this account.

The OMIM entry for MacInnes Syndrome, which links the RPS23 mutation with a collection of features that resemble Vincents hearing loss, issues with the hands was created on March 29, weeks after the paper was published. Pieterse said he was shocked when he found it in April as he was browsing the database.

Pieterse told us he feels used and fears that the designation will stigmatize his sons mutation. A syndrome is a disease, he said. Now, he wants the database entry either changed he prefers the umbrella term ribosomopathy, which is used in the paper or taken down.

Believing MacInnes submitted Vincents condition for consideration, Pieterse demanded she find a way to remove it. When she didnt respond, he went directly to AJHG and OMIM to get the paper and syndrome entry removed.

So far, nothing has worked.

A campaign begins

The Pieterses found out about Vincents mutation after a long diagnostic odyssey that ultimately resorted to sequencing all the protein-coding regions of Vincents genome. In 2015, the Journal of the American Medical Association published a news feature on Vincents diagnosis, saying it heralded a new era of clinical genomics.

Marc is a former telecommunications engineer and entrepreneur who has shifted his focus to raising his four children. He told Retraction Watch that although hes not a scientist, in the years since receiving Vincents diagnosis he has committed himself to advocating for further study of the mutation and has even co-authored a paper on RPS23. Marc claims he played a role in connecting MacInnes, Baserga, and several other European scientists, who eventually published the AJHG paper together.

When Pieterse found the OMIM entry for MacInnes syndrome, he believed that MacInnes had created it to boost her career. He told us that after he found it, he tried asking her to take it down. However, their relationship had at that point already suffered a communication breakdown and he didnt hear back. This further upset him and he began a campaign to bring down the entry by any means possible.

But MacInnes told us she had nothing to do with either the OMIM entrys creation or its naming:

I did not submit this paper to OMIM or in any way initiate this entry as a syndrome. This was independently picked up by OMIM and registered as such; apparently such registrations are made upon their decision only.

OMIM director Ada Hamosh confirmed this to Retraction Watch:

Dr. Macinnes did not ask for this to be named after herself and did not bring it to our attention.

We are dealing with this gene-phenotype relationship exactly as we would any other. We did this because this is what we do.

Hamosh, a geneticist at Johns Hopkins University, told us that the term syndrome is for a constellation of features and that the naming was done in accordance with policies that have long been in place at OMIM:

Sometimes something has too many features to be described succinctly. In that case, the default way to name something is to use the first authors last name and last authors last name.

Indeed, Hamosh told us that at first the syndrome was called Paolini-MacInnes syndrome, after first author Nahuel Paolini, of the University of Amsterdam. However, Hamosh said OMIM later realized there were four co-first authors. OMIM never adds more than three names to a syndrome, so Hamosh simply named it after MacInnes:

Given how little we know about it, it makes more sense to name it eponymously than after some features I cant put my hands on, especially since we have a policy on not ever naming something after a gene.

Its stigmatizing

Part of Pieterses issue with dubbing the condition a new syndrome is the early and ongoing nature of RPS23 research, and he isnt alone. In an email to Hamosh, MacInnes co-author Susan Baserga, a professor at the Yale School of Medicine, said:

I was very surprised that you are so pressed to name the phenotype as a new syndrome, especially since the clinical findings are so non-specific. I find this very odd indeed, and worry that it muddles the medical and genetic literature instead of providing clarity. This is so new that I am not even sure that it is a syndrome, and worry that it is presumptuous at best and wrong at worst.

Baserga, who did not respond to our requests for comment, also suggested that OMIM simply call the condition a ribosomopathy, as the AJHG paper does. But Hamosh told Retraction Watch:

We never, ever, ever, name a disease after a gene.

Gene symbols are not stable. More fundamentally, many, many, many genes have more than one condition associated with them. It is not a good idea to put a gene name into a disease name. Thats why we wont call it RPS23 ribosomopathy. Its not personal, we wont do this for any gene.

Pieterse told us that neither Hamosh, nor anybody else from OMIM, has ever informed him that OMIM itself created the entry and that MacInnes Syndrome is the result of standard naming procedures.

Like MacInnes, Hamosh wont respond to his attempt at contact. But Pieterse has obtained an email chain, from late April, between those two scientists, as well as Baserga. In it, Hamosh wrote:

Are you planning to retract or correct the paper to indicate the apparent uncertainty regarding its conclusions? If so, we will remove the phenotype and reclassify the variants.

Niether MacInnes nor Baserga thought a retraction was necessary, but this exchange convinced Pieterse that a retraction would force OMIM to remove the entry. So he wrote MacInnes to inform her he was withdrawing his parental consent and asked AJHG to retract the paper. Pieterse told Retraction Watch that the consent form he submitted to the University of Freiburgs medical center, in Germany (cells used in the study were created there) was very broad and that he believed it would allow him get the paper pulled.

Readers may recall some of the cases weve covered in which patient consent issues have led to papers being retracted. Pieterses situation most closely resembles a story we covered in 2015, where the authors requested a retraction from the Journal of Medical Case Reports after a legal guardian withdrew permission after publication.

But his attempt to trigger retraction didnt work. AJHG editor David Nelson, of the Baylor College of Medicine, told Pieterse the journal had looked into the situation but found nothing improper. According to an email shared by Pieterse, Nelson wrote:

Because there was no reason to retract the article due to misrepresentation of scientific content, we investigated the issues around withdrawal of patient consent. We have been in communication with the [University of Amsterdam Academic Medical Center] Biobank Committee and Medical Ethics Committee and they have confirmed that withdrawal from the study is not relevant to the article and data that have been published already.

Given the serious implications of a retraction on the journal, the authors of the article, and the scientific record, we have therefore decided that the American Journal of Human Genetics will not retract the article.

In an email to Retraction Watch, Nelson expanded on what he told Pieterse:

Our understanding from the authors and their institutions who obtained and approved consent for this study is that it is possible for research subjects to withdraw their consent at any time and that samples and information should be destroyed upon withdrawal. However, published scientific articles deriving from the studies are not subject to the consent withdrawal and this was confirmed by individuals familiar with European Union Regulations relating to personal data.

Pieterse told us that knows a retraction would be counterproductive to his long-term goal, which is to see the research around Vincents mutation grow. But he still wants to see the OMIM entry come down:

At a certain moment, people are going to cite OMIM in genetics papers and its going to spread. If you want to correct something, you should correct it fast. Once the internet is soaked, you cannot do that.

Like Retraction Watch? Consider making atax-deductible contribution to support our growth. You can also follow uson Twitter, like uson Facebook, add us to yourRSS reader, sign up on ourhomepagefor an email every time theres a new post, or subscribe to ourdaily digest. Clickhere to review our Comments Policy. For a sneak peek at what were working on,click here.

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Fearing stigmatization, patient's father seeks retraction of paper on rare genetic mutation - Retraction Watch (blog)

Dr. Shigeaki Hinohara died last month at age 105. Over his long life, he helped many others achieve long lives by popularizing annual medical checkups and by sharing what he knew, which was one of his tips for longer living:

He also wrote a musical for children when he was 88 and a best-selling book when he was 101. He recently took up golf. Until a few months ago he was still treating patients and kept a date book with space for five more years of appointments.

Here's the short and sweet version based on this list:

He also suggested finding a job where you never want to retire, and taking the time to enjoy music and animals.

10 Longevity Tips from Dr. Shigeaki Hinohara, Japans 105-Year-Old Longevity Expert (Open Culture via NYT)

Oriental Rat Flea (Xenopsylla cheopis) SIZE: Up to 1/6 in (4 mm) FAMILY: Pulicidae HABITAT: Near rats, their primary food source DISTRIBUTION: Worldwide, particularly tropical and subtropical climates, but some temperate zones as well MEET THE RELATIVES: The cat flea, Ctenocephalides felis, is a relative, as is the dog flea C. can isbut in the []

The establishment wing of the Democratic Party has spent decades receiving dump-trucks full of money from the insurance industry and then, totally coincidentally, explaining that the time isnt right for single-payer for completely unrelated reasons.

Once big data systems agglomerate enough data about you to predict whether you are likely to get sick or badly injured, insurers will be able to deny coverage (or charge so much for it that it amounts to the same thing) to anyone who is likely to get sick, forcing everyone who might ever need []

You dont always have to pay out the nose for household items, everyday accessories, or memorable gifts. If youre searching for something unexpected that can be had for less than two sawbucks, take a look at the following goods:20oz Insulated Water Bottle ($18.99)This stainless steel water bottle is double-walled with vacuum-sealed insulation to keep drinks []

For anyone thats always travelling between their home, office, storage unit, art studio, or any other location thats behind a locked door, you probably have more keys than you know what to do with. Fortunately, the Extended KeySmart keeps them all in a single, compact place that mitigates the need for a huge janitor key []

Working remotely often means using a full-size laptop, or forcing a tablet to do things it was never intended to do. Depending on your job, each may be a reasonable, if somewhat compromising solution, or an impossibly frustrating one. Either way, youll be stuck with a tiny screen and a form factor that will destroy []

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Lifehacks from a longevity expert who just died at age 105 / Boing ... - Boing Boing

New study finds that the exceptionally long lifespan of the Greenland shark may provide clues to extending human lifespan.

About Greenland Sharks

Greenland sharks are considered the longest living vertebrates. A team of scientists led by Julius Nielson, a marine biologist from the University of Copenhagen, used radiocarbon dating on 28 Greenland sharks. They established that one of the female sharks was approximately 392 years.

Research Surrounding the Greenland Sharks

The longevity of the Greenland sharks has stirred interest in the research world. Scientists have worked towards identifying the genes responsible for this unique trait.

Could these genes be used to extend the lifespan of human beings? Scientists believe that a successful identification and extraction of the genes could be a major milestone in achieving longevity among human beings.

Researchers at the University of Exeter have studied almost 100 Greenland sharks. They have sequenced their mitochondrial genome. The achievement set an excellent stage for researchers to scrutinize the sequence and understand the reason behind the shark's longevity.

Prof Kim Praebel, the lead scientist of the research, explained why the research is vital. He noted that unraveling the secrets behind the Green shark's longevity may tremendously boost the efforts on the improvement of humans' lifespan.

Why is the Study of Greenland Sharks Important?

Discovery of the genes responsible for longevity in Greenland sharks would be a vital achievement in the research world. It would explain the limited life spans in almost all the vertebrates. Additionally, the discovery would allow the scientists to study whether the genes can be used to prolong the life of the human beings.

The research at the University of Exeter found out that the Greenland sharks swim long distances across the Atlantic Ocean. They discovered that they mate in the deeply hidden fjords of the Arctic. This realization is instrumental in uncovering the negative effects of the activities of human beings on aquatic life. The study of the tissues and the bones of the animal forms genetic data that is crucial in determining when contaminants and chemicals from industries started affecting the marine. The findings would be of considerable benefit to the environment and marine life protection.

The findings of this research have been presented in various forums including the Fisheries Society of the British Isles symposium. The scientists hope that the findings will boost the conservation efforts of the Greenland shark species and other wildlife in the ecosystem.

Read the rest here:
Do Sharks Hold the Secret to Longevity? - Anti Aging News

The police departments number one priorityreducing gun violenceis being achieved and the crime stats prove it: Five homicides compared to seven last year, and a shining achievement compared to the states comparable big cities, where to date Hartford has 19 homicides and Bridgeport 18.

But would a diminishing of resources due to the ongoing state budget crisis put the brakes on that positive momentum?

No, and, yes. Possibly.

Those achievements, combined with a touch of low-grade anxiety about the resources to continue to advance them, emerged in a candid discussion at Tuesday nights regular meeting of the Board of Police Commissioners.

Commissioner Donald Walker asked about the departments plans for the continuing [state] fiscal crisis.

Mayor Harp is committed to not cutting public safety, Chief Anthony Campbell replied. He said the department is not anticipating the need to cut any officers.

However, if things dont change soon, I can see our going to zero overtime. Were not there yet and we hope and pray we dont, and we have a plan [in place] for that, he added.

That zero overtime plan would affect the configuration of the shifts and other deployments, but it should not affect public safety.

One area, where the states fiscal woes are already being felt: Project Longevity.

That project launched here in November 2012 by the city, the U.S. attorney, and the governor, identifies the small number of gang-related young men most involved in violence. It brings them to carefully choreographed call-ins to hear from law enforcement officials and community leaders. They hear a plea to stop the violence. Then they get a choice: Take advantage of immediate help in finding jobs, housing, medical care or earning degrees to straighten out their lives. Or go back to shooting in which case local, state and federal agents will come down on their entire groups to put them behind bars for decades under federal mandatory minimum sentencing laws. (Click here for a story on how the project helped fell one deadly gang.)

New Havens project has been successful. (An example was announced on Wednesday, with the arrests of six alleged New Haven gang members, affiliated with the Goodrich Street Boys gang, on federal attempted murder, firearms, narcotics, and racketeering charges.)

Assistant Chief Archie Generoso, who also presented at the commissioners meeting, attributed much of the reduction in gun violence to the project: Between 2003 and 2012 there were 126 shootings. However, since the advent of Project Longevity in November 2012, only 64 shootings have been logged in. We cut it in half, said Generoso.

That was one reason why already eight cities have come to study New Havens approach, including, Generoso added, officials from Honduras arriving in town next week for that purpose.

The anxiety centered on the paycheck of the exceptional former police officer who runs Project Longevity, Stacy Spell. Only he and an assistant are paid all the other officers who participate do it on their own time and they are paid by the cash-strapped and budget-stalled state. The state faces a $5-plus billion two-year deficit and is already more than a month late in trying to pass a new budget.

He hasnt received a pay check in a month, due to the state budget stalemate, Generoso reported.

Commissioner Stephen Garcia asked how the department is supporting Spell.

Stacy is doing an unbelievable job, said Genoroso.

Despite not being paid, Chief Campbell added.

Commission Chair Anthony Dawson said he has some ideas to address the situation, which will be discussed at another time.

The chiefs also reported that 29 new officers recently completed their field training and are ready to be deployed. They will reduce our overtime by $15,000 a day, said Campbell.

After presenting the crime stats, Generoso concluded: Well not be satisfied until zero [homicides]. We are bucking national trends. Our numbers are going down, while nationally the numbers are going up. Were making it happen. Its due to the support from you, the alders, the mayor. They have not cut back on money and resources. This city invests in the safety of its citizens.

Following the tragic shooting of 14-year-old Tyriek Keyes on July 16, not only are more police patrolling Newhallville. There are more crews of tree-trimmers at work there as well.

That news emerged in a report by Assistant Chief Generoso at Tuesday nights commissioners meeting.

For the last eight days two of the Department of Parks, Recreation and Trees four contract tree-trimming crews have been assigned to the streets around the Lincoln-Bassett School, the neighborhood where Tyriek was killed.

While tree-trimming is part of an ongoing citywide program, the Department Director Rebecca Bombero said that for the first time we did a ride-along with the police to scope some of their requested safety trim, which resulted in a larger scope of work. The focus was in Newhallville around Lincoln Bassett.

That scope includes raising trees to improve site lines for cameras, traffic signals, and lighting, she added.

At Tuesday nights meeting, Assistant Chief Generoso reported to the commissioners that the stepped up police patrolling was being accompanied by this important arboreal work, with an aim to cut some of the trees around some of our cameras and lights.

The city is in the process of putting up more cameras in Newhallville and elsewhere, he added. Cutting trees that obscure lights and camera views is work Generoso described as essential to enhance safety and crime-solving.

He said that officers indicated areas where the branch trimming is a priority and that the parks and rec crews should be finishing up in Newhallville this week.

Bombero wrote in an email that her department has over 2,000 open issues, or trimming requests, at any given time. The staff to respond to all that consists of two internal crews, along with contract crews funded through a capital allocation centered around hurricane season.

This year the funding has allowed for four crew, with the priorities being immediate hazards, safety trimming as requested by police, engineering or [the department of] Transportation, Traffic & Parking for site lines and secruity and then by level of hazard by date reported, she wrote.

Call your state legislators. They are doing nothing but waiting to be told how to vote. They demand more and higher taxes. They dont cut costs. They are bankrupt of ideas and they are hiding from this entire budget issue. This issue has been around since fxxking February - It is not August. The budget is late, the excuses are lame and plentiful. Meanwhile, they all pose for selfies, go live and one even went to Boston for a conference on Being Ready from the Inside. lol - you just cant make this stuff up. Meanwhile, this program suffers; schools are laying off teachers and others; not one community can do anything. Even well run East Haven has a hiring and spending freeze on except for the basic stuff.

The stupidity of not having a budget this late in the yar; of operating on a day to day basis by executive order, causing non-profits to close, of homeless shelters for women and kids to close - these nitwits couldnt even pass a mini-budget while they traveled and played golf. Oh, and collected their nice paychecks, perks and accumulated their retirement benefits. Amazing.

Read more from the original source:
State Budget Woes Threaten Project Longevity - New Haven Independent

First-half operating profits at Legal & General climbed 27% year-on-year to 988m ($1.28bn), with more than half of the increase arising from a review of longevity assumptions in its annuity book.

Decades of sustained improvement in longevity in the UK appears to have reversed in recent years, in particular among older age groups. Commentators have attributed this to a variety of causes, such as less government spending on health and old-age care, and virulent winter flu outbreaks.

The trend towards lower longevity improvements means that annuity underwriters may have to set aside fewer reserves, and has led some analysts to consider how much reserve could be released and returned to shareholders.

In todays half-year results announcement, L&G revealed it had released 126m of reserves. But this was based on a review of its base mortality assumptions the current levels of mortality being experienced by pensioners not the mortality trends.

In preparing the half-year results, we have not adjusted our assumptions for the rate of future longevity improvement; they remain consistent with those disclosed last year.

L&G said it will review its longevity improvement assumptions at the year end, including the appropriateness of using theContinuous Mortality Investigation (CMI) 2015 model.

There is increasing evidence that the higher than expected level of recent mortality is in part due to medium or long-term influences rather than short-term events. In performing this review, consideration will be given as to whether, and over what period, to move to newer versions of the CMI model.

L&Gs Retirement division responsible for writing individual and bulk annuities, longevity insurance and equity-release mortgages has a gross longevity exposure of 61.4bn across its annuity and longevity insurance business. The firm has reinsured 15.9bn of longevity risk with 11 reinsurance counterparties, leaving a net exposure of 45.5bn. Going forward, the firm plans to reinsure 80-90% of longevity risk from new bulk annuity business.

L&Gs Solvency II ratio climbed by 15 percentage points over the six months to 30 June, to reach 180%. The figure incorporates an estimated impact from recalculating the transitional measures for technical provisions (TMTP) as at 30 June.

Christopher Cundy

Continue reading here:
Longevity review boosts L&G's half year profits - insuranceERM

A shot of klotho, a hormone associated with longevity, seems to make mice smarter. Klotho is a naturally occurring hormone in the body. More than two decades ago, Japanese researchers discovered that this hormone plays a role in aging. People with more klotho in their body, tend to live longer and to retain more of their facultiesthat is to stay sharpwell into old age.

Researchers injected three types of mice with a portion of the protein. They injected young mice, aged mice, and mice genetically altered to have brains similar to that which we would see in Alzheimers or Parkinsons patients in humans.

Within hours they showed better cognitive function, says Dubal.

Since you cant exactly administer a mouse an IQ test, they assessed brain power based on the mices ability to navigate a series of water mazes, in an experiment that sounds on par with human a trip to Wisconsins famed waterslide park, The Dells.

They found that mice that had daily injections and were better able to navigate the maze (as measured by the distance traveled to find a hidden platform) than their control group peers. In a classic example of work smarter, not harder, the klotho mice were just much more efficient seekers.

We tested them two weeks later in a different cognitive test and they were still smarter, says Dubal, which suggested that getting the klotho protein into their bodies combined with brain training and stimulation had a long-lasting effect in their brain. Because the half-life of the protein is only seven and a half hours long, any of the protein should have been long out of their system.

Cell Reports Peripheral Elevation of a Klotho Fragment Enhances Brain Function and Resilience in Young, Aging, and -Synuclein Transgenic Mice

Highlights

A klotho fragment (KL-F) enhances cognition in young and aging mice KL-F counters deficits in -synuclein mice without altering pathogenic protein levels KL-F induces GluN2B cleavage and increases NMDAR-dependent synaptic plasticity Selective NMDAR blockade of GluN2B subunits abolishes acute KL-F effects

Summary

Cognitive dysfunction and decreased mobility from aging and neurodegenerative conditions, such as Parkinson and Alzheimer diseases, are major biomedical challenges in need of more effective therapies. Increasing brain resilience may represent a new treatment strategy. Klotho, a longevity factor, enhances cognition when genetically and broadly overexpressed in its full, wild-type form over the mouse lifespan. Whether acute klotho treatment can rapidly enhance cognitive and motor functions or induce resilience is a gap in our knowledge of its therapeutic potential. Here, we show that an -klotho protein fragment (KL-F), administered peripherally, surprisingly induced cognitive enhancement and neural resilience despite impermeability to the blood-brain barrier in young, aging, and transgenic -synuclein mice. KL-F treatment induced cleavage of the NMDAR subunit GluN2B and also enhanced NMDAR-dependent synaptic plasticity. GluN2B blockade abolished KL-F-mediated effects. Peripheral KL-F treatment is sufficient to induce neural enhancement and resilience in mice and may prove therapeutic in humans.

Introduction

Cognitive dysfunction and decreased mobility from aging and age-related neurodegenerative conditions such as Alzheimer disease (AD) and Parkinson disease (PD) are major biomedical challenges. Because more effective treatments are needed, and clinical trials targeting putative pathogenic proteins have failed, it is critical to develop alternate or complimentary therapeutic strategies. In light of this urgent medical need for our rapidly aging populations, delaying aging itself or increasing the function and resilience of the brain (Bennett, 2017, McEwen and Morrison, 2013) may represent new treatment strategies.

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Klotho longevity hormone helped make mice smarter - Next Big Future

Wayne Gretzky knows a thing or two about being the best in his discipline, and it comes as no surprise to the hockey legend that Rafael Nadal and Roger Federer are currently battling for No. 1 in the Emirates ATP Rankings, more than a decade after the pair first dominated the ATP World Tour.

Oh yeah, when youre that good and that dedicated, anything is possible, Gretzky exclusively told ATPWorldTour.com in Montreal on the opening day of main draw action at the Coupe Rogers.

Gretzky hung up his skates at the age of 38, finishing his career with four Stanley Cups, an all-time best 894 goals and countless records in 20 NHL seasons. Federer, a five-time year-end World No. 1, celebrates his 36th birthday on Tuesday. The 31-year-old Nadal finished World No. 1 in 2008, 10 and 13 and this week has a chance to return to the top spot for the first time since July 2014.

Together this season, the rivals and friends have swept three Grand Slam titles and four of the five ATP World Tour Masters 1000 tournaments. They have faced off three times, including a memorable five-set win for Federer at the Australian Open.

As a sports fan, I admire when a player can be at an elite level, said Gretzky. To get to an elite level is really hard, but to stay there for a long period of time obviously Roger has been there a little bit longer, is a little bit older than Nadal but it really is incredible for sports and its really fascinating to see two players of that caliber compete as hard as they do against each other, yet have so much respect for each other.

If you have a passion for what youre doing, you go to another level, he added. I think the thing that separates stars from superstars is that superstars want to be under pressure. They want to be under the microscope. They want to play in the finals. They want to be 2-2 going into the fifth set. Thats where theyre comfortable. You see players like Nadal and players like Djokovic and obviously Federer, and going back to guys like Bjorn and McEnroe, they want to be under the gun. It makes them play that much better, the bigger the game the more relaxed they seem to be and the more inspired they are and the better they play.

On Monday, The Great One strolled around the Stade Uniprix grounds, making his rounds of the practice courts to show his support for the home favourites. After greeting top Canadian Milos Raonic, Gretzky headed over to Court 8 to watch up-and-coming Canadian Denis Shapovalov during a practice session with another #NextGenATP star, Korean Hyeon Chung. Gretzkys 14-year-old daughter Emma, who has been playing tennis for a year, also had an opportunity to hit with the Bryans as they wrapped up practice on the adjacent court.

Thats the great thing with sports, theres always the next person that comes along Guys like Milos and Daniel Nestor have opened doors for the young guys to come along, and years from now hopefully theyll open doors for the new generation of kids that come along 10-15 years from now, said Gretzky.

The Brantford, Ontario native, who also frequents the BNP Paribas Open in Indian Wells, said he enjoyed the level of competition at the ATP World Tour Masters 1000 tournaments and planned to be back on site throughout the week to watch some matches.

Its always fun to have a big event like this in Canada, he said. Everyone enjoys seeing the best players compete against each other. In our country, we rally around supporting our local favourites, whether its Milos, Denis this year now, Genie Bouchard in Toronto. Were very proud of our kids who compete against the best in the world and thats what makes it fun for Canadians to watch.

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Gretzky Calls Federer & Nadal's Longevity On Top 'Incredible' - ATP World Tour

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A lab technician at Myriad Genetics in Salt Lake City, Utah.

Thousands of people are getting genetic tests, for everything from their cancer risk to their likelihood of passing on a disease to a child.

But many doctors aren't adequately trained to interpret these results, or tell patients how to act on them. And genetic counselors -- who do have that knowledge -- are in short supply. There are only about 4,000 genetic counselors in the country today. That's one for every 80,000 Americans. That means some patients have to wait months to get a consultation.

Start-up Clear Genetics, which launches this week after raising $2.5 million in financing, is trying to make genetic expertise more widely available.

The start-up has developed a conversational chatbot to guide a user through their results, collect information and review options for genetic testing, and answer questions about things like whether the test will be covered by insurance. If there's a need for additional support, the patient can then schedule a consultation with a human expert via video or in-person.

"We're finding that it's working really well with patients," said Moran Snir, Clear Genetics' CEO, who was previously a software engineer with the Israeli military.

Clear Genetics is working with several large health systems in the United States to test out a beta version of its product.

"I think this is a very good use for AI," said David Ledbetter, executive vice president and chief scientific officer at hospital network Geisinger Health System, in an interview with CNBC.

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You're getting a DNA test start-up Clear Genetics is building chatbots to help you understand the results - CNBC