StemCell Therapy

This week in Paris, companies in the diabetes managment space came together at theAdvanced Technologies and Treatments for Diabetes conference to share news and, mostly, a lot of efficacy data. It's an exciting time for the space as closed-loop systems that allow people with diabetes to monitor their glucose continuously and automatically manage their insulin dosing get closer and closer to becoming a validated, regulated reality for people with Type 1 diabetes. We didn't make it out to Paris ourselves, but we're covering the news. We've written up some of the bigger stories from the conference earlier this week. Look below for a roundup of other digital health news from the show.

Nonprofit organizationT1D Exchangepublished a major study in Diabetes Care yesterday (and presented the research at the conference).The data re-affirmsthe FDA's recent clearance ofDexcom's CGM for insulin dosing. The study looked at 226 adult CGM users for six months. Of those, 149 dosed their insulin using the CGM and 77 used a fingerstick glucometer in addition, as is currently required for most CGMs. There was no difference in outcomes between the two groups.

"This study is an important step to support regulatory pathways for the automation of insulin delivery for people with type 1 diabetes, Dana Ball, executive director and co-founder of T1D Exchange, said in a statement. These data are supportive of the recent FDA decision to approve the Dexcom G5 indication for insulin dosing and removes a key obstacle that has prevented reimbursement of CGM by Medicare.

Integrity Applications, makers of GlucoTrak, a novel non-invasive glucose monitor that clips onto the ear lobe, presented data showing that their device has improved in accuracy from previous generations. The data shows GlucoTrak has increased its tracking consistency, with different devices on opposite earlobes of the same subject returning the same results. They've also corrected for previous inaccuracies in readings before and after meals.

Aspire Ventures announced that its portfolio company Tempo Health's Rhythm system, based on Aspire's A2I adaptive artifical intelligence platform, performed well in an observational study at Diabeter, a specialized treatment center in Europe. Rhythm uses A2I toforecast and manage blood glucose levels of people with diabetes, based on data from non-invasive biometric sensors. In seven out of eight patients in the study, Rhythm would have helped them to achieve a 20 percent increase in time in range, and a 9 percent reduction in low glucose ratings, as compared to the actual results achieved by active monitoring by Diabeter doctors and their diabetes teams using patient-activated remote monitoring.

Waltham, Massachusetts-based Glytec,which makes a personalized therapy and decision support module for patients with diabetes, presented two studies about its Glucommander system. One study sawA1C levels drop from a baseline average of 10.2 percent to 7.7 percent at three months and 7.6 percent at six months. Another study looked at the use of Glucommander for patients prescribed subcutaneous insulin.Among 5,718 patients, the median time to prescribed glucose target was 0.8 days. Once in the target range, 67.9 percent of all blood glucose readings remained between 70 and 180 mg/dL.

Insulet, maker of the Omnipod line of tubeless insulin pumps, presented data about its own closed-loop system, a hybrid system called OmniPod Horizon.The 36-hour, 24-person study used a modified version of Omnipod, a Dexcom CGM sensor, and Insulets personalized model predictive control algorithm. Use of the system was associated with significantly less time spent in hypoglycemic blood glucose range compared to ranges prior to the study, the company said. Additionally, patients stayed in the target blood glucose control range 69 percent of the time over the course of the study, including staying in range 90 percent of the time at night.

Valeritas, which makes a wearable, disposable insulin-delivery device called V-Go, shared data showing the device helped lower A1c and insulin dosage better than insulin pens for people with type 2 diabetes. In a retrospective study of 107 people, split roughly in half by use of V-Go versus insulin pens, V-Go users had their A1c levels down by 1.96 percent to insulin pen users 1.23 percent reduction. V-Go users also had fewer insulin doses than insulin pen users, with 56 units per day versus 77, respectively, and insulin pen users had to go through 3.6 needle sticks per day while V-Go users only required one.

UK-based device company Nemaura Medicalshowcased sugarBEAT, its still-in-development continuous glucose-monitoring patch. In a poster session, the company demonstrated the needle-free disposable patch, which is about 1 millimeter thick and uses a small electronic sensor to measure blood sugar levels and streams the data via Bluetooth to a companion smartphone app. They expect to launch at a "cost-competitive" price point next year.

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Roundup: News from the Advanced Technologies & Treatments for ... - MobiHealthNews

A small pilot study in which researchers attempted to slow attacks mounted by the immune system on insulin-producing cells in type 1 diabetes has given promising results. The study by researchers at Linkping University in Sweden has been published in the scientific journal New England Journal of Medicine.

Type 1 diabetes is an autoimmune disease in which the body loses its ability to produce insulin. During the development of the disease, the body's own immune system attacks the insulin-producing beta cells in the pancreas. This often gives rise to the presence of antibodies against the body's own proteins in the beta cells. One of these proteins is GAD65 (glutamic acid decarboxylase), and several clinical trials are underway of a drug known as GAD-alum, based on GAD65.

In the study reported here, DIAGNODE, researchers from Linkping University have injected GAD-alum directly into lymph nodes in the groin, rather than under the skin, in order to determine whether this causes the immune response to become more tolerant towards the body's own GAD protein. This method is similar to one known as "allergen immunotherapy" used in certain treatments for allergy, where it induces tolerance against an allergenic substance.

Six patients aged 20-22 years who had been diagnosed with type 1 diabetes up to 6 months previously were included in the study. They were injected with a small dose of GAD-alum on three occasions, and took vitamin D supplements during the period of the study. The latter can reduce the inflammatory response of the immune system.

"The results for these six patients are very promising. Type 1 diabetes usually progresses gradually as the patient loses the ability to produce insulin, but this has not happened in these patients. We must follow them for a longer period and we must include more patients before we can say anything about the effectiveness of the treatment, but the results so far are extremely exciting," says Johnny Ludvigsson, senior professor at Linkping University and principal investigator for the study.

The pilot study does not contain a control group of patients who do not receive the treatment being tested. The report instead compares the results with those from other studies of untreated patients. The long-term blood sugar level (HbA1c) and the need to inject extra insulin both fell in the patients in the current study. Their natural production of insulin remained at a stable level. The six patients were followed for at least six months; four of them for more than 15 months.

The researchers are now planning to continue the study by increasing the number of participants, and including younger patients.

"If these results are confirmed when we test more patients, it would be an extremely important advance. The way in which type 1 diabetes progresses differs between individuals for many reasons, and this means that it is not necessary to find a treatment that has excellent effects for everyone. Even if it helps only half of patients, this would be a major step forward," says Johnny Ludvigsson.

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Materials provided by Linkping Universitet. Note: Content may be edited for style and length.

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Pilot study shows stable insulin production in type 1 diabetes - Science Daily

By Robert Preidt

HealthDay Reporter

THURSDAY, Feb. 16, 2017 (HealthDay News) -- Diabetes that develops during pregnancy -- known as gestational diabetes -- carries health risks for both the mom-to-be and her baby, new research confirms.

A team of French researchers analyzed data from more than 700,000 births in France occurring after 28 weeks of pregnancy in 2012.

Compared to other pregnant women, those with gestational diabetes were 30 percent more likely to experience preterm birth, 40 percent more likely to require a C-section, and 70 percent more likely to have preeclampsia/eclampsia, a dangerous spike in blood pressure.

Risks weren't confined to the mother, however. Babies born to women with gestational diabetes were 80 percent more likely to be of significantly larger-than-average size at birth; 10 percent more likely to suffer respiratory issues; 30 percent more likely to experience a traumatic birth, and 30 percent more likely to have heart defects, the study found.

Babies born after 37 weeks to women with gestational diabetes also had an increased risk of death, compared to babies born to women without the condition, the study authors said.

The study clearly shows that gestational diabetes "is a disease related to adverse pregnancy outcomes," concluded a team led by Dr. Sophie Jacqueminet, of the Pitie-Salpetriere Hospital in Paris.

Two experts in diabetes care weren't surprised by the findings, and they noted that while a woman's weight isn't always a factor, the odds for gestational diabetes go up in the obese.

"Gestational diabetes is a dangerous entity, and the child is at risk," said Dr. Robert Courgi, an endocrinologist at Northwell Health's Southside Hospital, in Bay Shore, N.Y.

"As obesity increases, so does [the risk of] diabetes," he added. "We need to do a better job at diagnosing and treating gestational diabetes."

The study also found that the risk of death was 30 percent higher among babies born to women whose gestational diabetes was treated with a special diet. There was no increased risk of death among babies born to women whose gestational diabetes was treated with insulin, however.

This difference in death risk could be because women with diet-treated gestational diabetes tend to give birth later than those who are insulin-treated, the research team said.

Outcomes were worse for mothers with gestational diabetes "who gave birth later because the baby was exposed to higher blood sugar levels for a longer period of time," Courgi explained.

Dr. Gerald Bernstein coordinates the diabetes program at Lenox Hill Hospital in New York City. He stressed that gestational diabetes requires prompt and proper treatment.

"Once diagnosed, treatment is geared to maintain normal blood sugar but without the risk of hypoglycemia [low blood sugar]," Bernstein explained. "This may range from nutritional and other lifestyle changes to the addition of insulin. The goal is to give the baby a maximum opportunity for growth and development without an unusual early delivery, so that key organs are as mature as possible.

"Most patients are followed by an endocrinologist, a high-risk ob-gyn and diabetes educators in various disciplines," Bernstein added. "To reduce birth complications, early diagnosis along with aggressive therapy with a full health care team is essential."

The study was published Feb. 15 in the journal Diabetologia.

WebMD News from HealthDay

SOURCES: Robert Courgi, M.D., endocrinologist, Northwell Health's Southside Hospital, Bay Shore, N.Y.; Gerald Bernstein, M.D., endocrinologist and coordinator, Friedman Diabetes Program, Lenox Hill Hospital, New York City; Dibatetologia, news release, Feb. 15, 2017

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Gestational Diabetes Poses Risks for Mom, Baby - WebMD - WebMD

Fat cells can regulate genes in distant organs like the liver by sending out molecular messengers.

Steve Gschmeissner/Science Source

By Emma HiolskiFeb. 16, 2017 , 6:00 PM

Theres more to those love handles than meets the eye. Fat tissue can communicate with other organs from afar, sending out tiny molecules that control gene activity in other parts of the body, according to a new study. This novel route of cell-to-cell communication could indicate fat plays a much bigger role in regulating metabolism than previously thought. It could also mean new treatment options for diseases such as obesity and diabetes.

I found this very interesting and, frankly, very exciting, says Robert Freishtat of Childrens National Health System in Washington, D.C., a pediatrician and researcher who has worked with metabolic conditions like obesity and diabetes. Scientists have long known that fat is associated with all sorts of disease processes, he says, but they dont fully understand how the much-reviled tissue affects distant organs and their functions. Scientists have identified hormones made by fat that signal the brain to regulate eating, but this new studyin which Freishtat was not involvedtakes a fresh look at another possible messenger: small snippets of genetic material called microRNAs, or miRNAs.

MiRNAs, tiny pieces of RNA made inside cells, help control the expression of genes and, consequently, protein production throughout the body. But some tumble freely through the bloodstream, bundled into tiny packets called exomes. There, high levels of some miRNAs have been associated with obesity, diabetes, cancer, and cardiovascular disease.

To understand how miRNAs function in fat, a team of researchers led by Thomas Thomou, a diabetes researcher at Joslin Diabetes Center and Harvard Medical School in Boston, studied a genetically engineered strain of mice in which fat cells lacked a critical miRNA-processing enzyme. These rodents had less fat tissue, and they couldnt process glucose as effectively as nonengineered mice. They also had low circulating miRNA levels overall, suggesting that most of the miRNAs in exosomes come from fat tissue, the researchers reported this week in Nature.

By transplanting fat from normal mice, the researchers restored the previously low miRNA levels in the modified mice. Transplants of brown fatspecialized energy-burning fat that regulates temperaturehelped restore glucose processing in the genetically modified mice, whereas white fatenergy-storing fattransplants did not.

In a previous study with the mice whose fat had impaired miRNA production, the researchers also noticed that other organsincluding the heart and liverwere affected, even though the genetic modification didnt alter those tissues directly. So they decided to investigate whether fat uses miRNAs to communicate with other tissues, Thomou says. They developed a method to measure cross-talk using a human miRNA. In one group of mice, they engineered brown fat cells to produce the human miRNA and package it in exosomes; in another, they engineered liver cells to produce a fluorescent molecular target for the miRNA. Injecting exosomes from the first group of mice into mice from the second group caused a drastic drop in liver cell fluorescence, because the miRNA bound to the fluorescent target and suppressed its production. This confirmed that fat tissue, through exosomes, can communicate with the liver and regulate gene expression. Exosomal miRNAs from brown fat were also found to regulate expression of an important metabolism gene, Fgf21, in liver cells.

This finding will provide not only insights into new pathways of tissue communication, but also pathways that can be altered in disease states, says study co-author C. Ronald Kahn, a diabetes researcher and physician at Harvard University. If researchers can figure out how to engineer exomes to target specific cell types, adds Thomou, they might one day use the vesicles to deliver drugs and other therapies. But its far from clear, he notes, whether exomes target specific cell typesusing a kind of molecular ZIP code that could help them travel from point A to point B.

Thomou and his team plan to continue identifying specific miRNA signatures from different tissues to determine what other factors, besides miRNAs, are bundled into exosomes. For Freishtat, the new work offers an exciting way to begin filling a gap between mouse models and human patient studies. This is a big deal, he says. Were just beginning to scratch the surface of exosomes and how they regulate processes in the body.

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Fat tissue can 'talk' to other organs, paving way for possible treatments for diabetes, obesity - Science Magazine

HUNTINGTON A health professor and researcher at the Department of Family and Community Health at Marshall University has received a $1.3 million grant to support health care work for high-risk diabetes patients.

Dr. Richard Crespo said the funds from the Appalachian Regional Commission will aid community health workers in Kentucky, West Virginia, and Ohio. He said the grant supports the creation of care coordination teams, which work with patients in their homes and communities.

What community health workers can do is invaluable, especially with patients with chronic conditions who are at high risk, Crespo said. What we are doing with this project is engaging the health insurance companies in coming up with a system for reimbursing the health care agencies who are doing this care coordination for the high-risk patients.

Crespo said community health workers rely on grants for much of their funding, so the project is important to the continued care of patients.

The critical outcome of this grant is sustainable employment for the community health workers, he said.

Crespo estimated the funds will support approximately 25 community health workers care for about 625 high-risk diabetes patients with the goal of providing them with self-management skills to control their condition.

In Kentucky, he is working with Big Sandy Healthcare, which operates in Magoffin, Martin and Pike counties.

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Marshall researcher lands grant for diabetes - The Independent

People who undergo gastric bypass surgery are more likely to experience a remission of their diabetes than patients who receive a gastric sleeve or intensive management of diet and exercise, according to a new study. Bypass surgery had already shown better results for diabetes than other weight-loss methods in the short term, but the new research followed patients for five years.

We knew that surgery had a powerful effect on diabetes, says Philip Schauer of the Bariatric & Metabolic Institute at the Cleveland Clinic. What this study says is that the effect of surgery is durable. The results were published online February 15 in the New England Journal of Medicine.

The study followed 134 people with type 2 diabetes for five years in a head-to-head comparison of weight-loss methods. At the end of that time, two of 38 patients who only followed intensive diet and exercise plans were no longer in need of insulin to manage blood sugar levels. For comparison, 11 of 47 patients who had a gastric sleeve, which reduces the size of the stomach, and 14 of 49 who underwent gastric bypass, a procedure that both makes the stomach smaller and shortens digestion time, did not need the insulin anymore. In general, patients who had been diabetic for fewer than eight years were more likely to be cured, Schauer says.

Even those surgical patients who still needed to take insulin had greater weight loss and lower median glucose levels than others in the study. This study was also one of the few to show that bariatric surgery could help those with only mild obesity, defined as a body mass index between 27 and 34. How bariatric surgery might improve diabetes is still unknown, but scientists have pointed to effects on the bodys metabolism (SN: 8/24/13, p. 14) and gut microbes (SN: 9/5/15, p. 16).

Over five years, gastric bypass patients showed bettercontrol ofblood sugar levels than patients whoused a gastric sleeve or medical management such as intensive diet and exercise plans.

The same research team had published similar results at one and three years after surgery, but few studies looked further, says Kristoffel Dumon, a bariatric surgeon with the University of Pennsylvania Health System in Philadelphia. The criticism of bariatric research has been that there are no good long-term results. With weight-loss surgery, you often see rapid initial results, but you want to see that to a five-year time point.

Dumon also notes that the patients who received only intensive medical therapy did not report an improvement in their quality of life, and their emotional well-being worsened. People in the surgical group reported improvements in quality of life, but not in emotional well-being, a finding that Schauer says has more to do with stress management and other characteristics that wouldnt necessarily be affected by surgery.

Schauer hopes to have even longer-term data in the future. His team will combine their results with those from similar research at three other U.S. sites with the goal of following patients for up to 10 years.

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Gastric bypass controls diabetes long term better than other methods - Science News

It may be possible to slow the progression of type 1 diabetes, according to a new pilot study that used an experimental therapy that centers on the immune system.

In the new study, researchers in Sweden tested a new method to train the immune system to stop attacking the body's own insulin-producing cells, according to the findings published today (Feb. 15) in the New England Journal of Medicine. With only six participants, the study was small, but experts called these early results exciting.

In people with type I diabetes, the immune system mistakenly recognizes certain proteins in beta cellsas foreign invaders and wages a war against them. Once the beta cells have been killed, the pancreas produces little or no insulin, the hormone that regulates how the body absorbs sugar from the blood to use for energy. As a result, patients need to follow lifelong treatments such as insulin injections to keep their blood sugar levels at normal ranges. [9 Healthy Habits You Can Do in 1 Minute (Or Less)]

This destruction of beta cells doesn't happen overnight, however. Although the majority of them are gone by the time someone is diagnosed, some cells manage to dodge the attacks and continue to produce some insulin. That's why several research teams have been working on finding ways to rescue the remaining cells, or delay their destruction in people who have been recently diagnosed with the condition.

In the new study, the researchers injected a protein normally found on beta cells directly into the patients' lymph nodes.

"This method has shown the best efficacy so far," at slowing the disease's progression, said Dr. Johnny Ludvigsson, senior professor of pediatrics at Linkping University and the study's lead investigator. "But we have to be cautious. The number of patients is small."

If confirmed in larger trials, the therapy could bring a number of benefits to patients. The ability to make insulin secretion, even if only at very low levels, dramatically decreases people's risk of complications, such as episodes of dangerously low blood sugar levels, Ludvigsson told Live Science.

The small amount of insulin that the patients in the study could produce would also make it easier for the patients to maintain a good blood sugar balance, improving their quality of life. It would also reduce their risk of long-term complications of the disease, such as heart attack, stroke, neuropathy, kidney problems and eye disease.

"These are exciting results," said Dr. Lawrence Steinman, a professor of pediatrics and neurological sciences at Stanford University, who was not involved with the study. Steinman echoed Ludvigsson's warning that the study is small, and said that trials with more people and which include a control group of patients who are given a placebo are needed to confirm the findings.

The injections that the researchers gave to the patients in the study contained a protein called GAD, which is normally found in the beta cells. Ludvigsson and his colleagues injected this protein into the patients' lymph nodes near the groin. Lymph nodes contain many immune cells, and the idea behind the treatment is that exposing the body's immune cells to larger amounts of GAD than they normally encounter will cause the immune cells to become more tolerant of GAD, and halt their attack on it.

The participants in the study were ages 20 to 22, and all had been diagnosed with type 1 diabetes within the last six months. The researchers followed up with the patients six to 15 months after the treatment, and found that the functioning of the pancreas had not declined, as expected in the typical course of the disease, but remained stable.

Previously, Ludvigsson's team had tried the same treatment, but had injected the protein under the skin. The new results suggest that an injection directly into the lymph nodes better exposes immune cells to the self-antigen.

"With a much lower dose, we got a very strong desired effect on the immune system," Ludvigsson said.

The team is now planning to repeat the study in a larger number of people, which would take a few years, Ludvigsson said.

Although these results are far too early to be applied to patients, they lend promising evidence to a relatively new line of research that aims to modify the immune system with high precision to treat or perhaps even cure type 1 diabetes.

"A few approaches are in clinical trials, but nothing is yet on the market," Steinman said. "Antigen-based therapy [which was used in the new study] is a sought-after approach, but only a few in the world are attempting this."

In his own work, Steinman has focused on another protein, called proinsulin, which also becomes a target of the immune system in people with type 1 diabetes.

In a 2012 clinical trial with 80 people, Steinman and his team injected participants with a chunk of DNA-encoding proinsulin, in an attempt to desensitize the immune system to proinsulin. The researchers found that the function of the pancreas not only stabilized, but actually improved. It is possible, Steinman said, that some beta cells somehow hide from the immune attacks by going into hibernation, and that once the attacks are eased, they recover and resume function. Plans for the next trial are ongoing, Steinman said.

An immune therapy for type 1 diabetes in the future might combine some of the various approaches that different research teams have tried.

"So far, almost all studies have been performed testing one drug at a time, and they have not been effective enough," Ludvigsson said. "My opinion is that we need a combination of different approaches. For example, different drugs, given in a planned scheme, as is done in oncology. And not until just recently has that idea started to become accepted."

Originally published on Live Science.

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Experimental Therapy May Slow Type 1 Diabetes - Live Science

(THE CONVERSATION) In 1997 Dolly the sheep was introduced to the world by biologists Keith Campbell, Ian Wilmut and colleagues. Not just any lamb, Dolly was a clone. Rather than being made from a sperm and an egg, she originated from a mammary gland cell of another, no-longer-living, six-year-old Fynn Dorset ewe.

With her birth, a scientific and societal revolution was also born.

Some prominent scientists raised doubts; it was too good to be true. But more animals were cloned: first the laboratory mouse, then cows, goats, pigs, horses, even dogs, ferrets and camels. By early 2000, the issue was settled: Dolly was real and cloning adults was possible.

The implications of cloning animals in our society were self-evident from the start. Our advancing ability to reprogram adult, already specialized cells and start them over as something new may one day be the key to creating cells and organs that match the immune system of each individual patient in need of replacements.

But what somehow got lost was the fact that a clone was born at day zero created from the cell of another animal that was six years old. Researchers have spent the past 20 years trying to untangle the mysteries of how clones age. How old, biologically, are these animals born from other adult animals cells?

Dolly became an international celebrity, but she was not the first vertebrate to be cloned from a cell taken from the body of another animal. In 1962, developmental biologist John Gurdoncloned the first adult animal by taking a cell from the intestine of one frog and injecting it into an egg of another. Gurdons work did not go unnoticed he went on to share the 2012 Nobel Prize in Physiology or Medicine. But it was Dolly who had captured our imagination. Was it because she was a warm-blooded animal, a mammal, much closer to human? If you could do it in a sheep, you could do it on us!

Dolly, along with Gurdons frogs from 35 years earlier and all the other experiments in between, redirected our scientific studies. It was amazing to see a differentiated cell an adult cell specialized to do its particular job transform into an embryonic one that could go on to give rise to all the other cells of a normal body. We researchers wondered if we could go further: Could we in the lab make an adult cell once again undifferentiated, without needing to make a cloned embryo?

A decade after Dolly was announced, stem cell researcher Shynia Yamanakas team did just that. He went on to be the Nobel corecipient with Gurdon for showing that mature cells could be reprogrammed to become pluripotent: able to develop into any specialized adult cell.

Now we have the possibility of making individualized replacement cells potentially any kind to replace tissue damaged due to injury, genetic disorders and degeneration. Not only cells; we may soon be able to have our own organs grown in a nonhuman host, ready to be transplanted when needed.

If Dolly was responsible for unleashing the events that culminate with new methods of making fully compatible cells and organs, then her legacy would be to improve the health of practically all human beings on this planet. And yet, I am convinced that there are even better things to come.

In the winter of 2013, I found myself driving on the wrong side of the road through the Nottingham countryside. In contrast to the luscious landscape, I was in a state gloom; I was on my way to see Keith Campbells family after his sudden death a few weeks earlier. Keith was a smart, fun, loving friend who, along with Ian Wilmut and colleagues at the Roslin Institute, had brought us Dolly 15 years earlier. We had met at a conference in the early 1990s, when we were both budding scientists playing around with cloning, Keith with sheep, me with cows. An extrovert by nature, he quickly dazzled me with his wit, self-deprecating humor and nonstop chat, all delivered in a thick West Midlands accent. Our friendship that began then continued until his death.

When I knocked at the door of his quaint farmhouse, my plan was to stay just a few minutes, pay my respects to his wife and leave. Five hours and several Guinnesses later, I left feeling grateful. Keith could do that to you, but this time it wasnt him, it was his latest work speaking for him. Thats because his wife very generously told me the project Keith was working on at the time of his death. I couldnt hide my excitement: Could it be possible that after 20 years, the most striking aspect of Dollys legacy was not yet revealed?

See, when Dolly was cloned, she was created using a cell from a six-year-old sheep. And she died at age six and a half, a premature death for a breed that lives an average of nine years or more. People assumed that an offspring cloned from an adult was starting at an age disadvantage; rather than truly being a newborn, it seemed like a clones internal age would be more advanced that the length of its own life would suggest. Thus the notion that clones biological age and their chronological one were out of sync, and that cloned animals will die young.

Some of us were convinced that if the cloning procedure was done properly, the biological clock should be reset a newborn clone would truly start at zero. We worked very hard to prove our point. We were not convinced by a single DNA analysis done in Dolly showing slightly shorter telomeres the repetitive DNA sequences at the end of chromosomes that count how many times a cell divides. We presented strong scientific evidence showing that cloned cows had all the same molecular signs of aging as a nonclone, predicting a normal lifespan. Others showed the same in cloned mice. But we couldnt ignore reports from colleagues interpreting biological signs in cloned animals that they attributed to incomplete resetting of the biological clock. So the jury was out.

Aging studies are very hard to do because there are only two data points that really count: date of birth and date of death. If you want to know the lifespan of an individual you have to wait until its natural death. Little did I know, that is what Keith was doing back in 2012.

That Saturday afternoon I spent in Keiths house in Nottingham, I saw a photo of the animals in Keiths latest study: several cloned Dollies, all much older than Dolly at the time she had died, and they looked terrific. I was in awe.

The data were confidential, so I had to remain silent until late last year when the work was posthumously published. Keiths coauthors humbly said: For those clones that survive beyond the perinatal period [] the emerging consensus, supported by the current data, is that they are healthy and seem to age normally.

These findings became even more relevant when last December researchers at the Scripps Research Institute found that induced pluripotent stem cells reprogrammed using the Yamanaka factors retain the aging epigenetic signature of the donor individual. In other words, using these four genes to attempt to reprogram the cells does not seem to reset the biological clock.

The new Dollies are now telling us that if we take a cell from an animal of any age, and we introduce its nucleus into a nonfertilized mature egg, we can have an individual born with its lifespan fully restored. They confirmed that all signs of biological and chronological age matched between cloned and noncloned sheep.

There seems to be a natural built-in mechanism in the eggs that can rejuvenate a cell. We dont know what it is yet, but it is there. Our group as well as others are hard at work, and as soon as someone finds it, the most astonishing legacy of Dolly will be realized.

This article was originally published on The Conversation. Read the original article here: http://theconversation.com/more-lessons-from-dolly-the-sheep-is-a-clone-really-born-at-age-zero-73031.

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More lessons from Dolly the sheep: Is a clone really born at age zero? - San Francisco Chronicle

It is estimated that almost one in every ten people over 65 has some signs of age-related macular degeneration (AMD), and its prevalence is likely to increase as a consequence of the aging population. AMD is a form of blindness, common in Caucasians, which causes distorted vision and blind spots. Scientists at the Center for Genome Engineering, within the Institute for Basic Science (IBS) report the use of CRISPR-Cas9 in performing "gene surgery" in the layer of tissue that supports the retina of living mice. Published in Genome Research, this study combines basic research and mouse model applications.

The most common retinopathies causing blindness are 'retinopathy of prematurity' in children, 'diabetic retinopathy' and 'AMD' in older adults. In these diseases, abnormally high levels of the Vascular Endothelial Growth Factor (VEGF) are secreted. In AMD, VEGF causes the formation of new blood vessels in the eyes but also leads to leakages of blood and fluid into the eye, damaging an area at the center of the retina called macula.

Injections of anti-VEGF drugs are the most common treatment against AMD, but at least seven injections per year are required, because VEGF is continuously overexpressed by the cells of the diseased retinal pigment epithelium. Instead of such invasive treatments, IBS scientists believe that gene therapy with the third generation gene editing tool CRISPR-Cas9 could improve the situation. "The injections tackle the effects, but not the main cause of the problem. By editing the VEGF gene, we can achieve a longer-term cure," explains KIM Jin-Soo, Director of the Center for Genome Engineering.

CRISPR-Cas9 can precisely cut and correct DNA at the desired site in the genome. The CRISPR-Cas9 system works by cutting DNA at a target site, in this case, inside the VEGF gene. Two year ago, IBS scientists proved that a pre-assembled version of CRISPR-Cas9, a.k.a, Cas9 ribonucleoprotein (RNP), can be delivered to cells and stem cells to modify target genes. The pre-assembled complex works rapidly and degrades before the body has time to build up an immune response against it. Despite these advantages and previous successes, the difficulty in delivering pre-assembled CRISPR-Cas9 has limited its use in therapeutic applications.

In this study, the research team successfully injected CRISPR-Cas9 into the eyes of a mice model with wet AMD and locally modified the VEGF gene. Initially they found that the delivery of the pre-assembled CRISPR-Cas9 complex is more efficient that the delivery of the same components in a plasmid form. Secondly, the complex disappeared after just 72 hours. Scientists assessed the whole genome of the animals and found the CRISPR-Cas9 complex modified only the VEGF gene and did not affect other genes. The progression of the eye disease was monitored by looking at choroidal neovascularization (CNV), the creation of new blood vessels between the retina and the sclera -- a common problem of 'wet' macular degeneration -- and researchers found the CNV area reduced by 58%. Moreover, a likely side effect, namely cone dysfunction, that takes only 3 days to show in these mice, did not occur a week after the treatment.

"We have developed a treatment to suppress CNV by inactivating the VEGF gene, one of the causes of AMD. We envision that, in the future, surgeons will be able to cut and paste disease-causing genetic elements in patients," explains Kim Jin-Soo.

While CRISPR-Cas9 is conventionally used to correct mutations causing hereditary diseases or cancer, this study suggests a new therapy for non-hereditary degenerative disease."We believe that this is a new therapeutic modality for the treatment of non-hereditary degenerative diseases," points out Professor KIM Jeong Hun (Seoul National University), "We confirmed the effect on the animal models of the disease and now we wish to continue with preclinical trials."

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Genome surgery with CRISPR-Cas9 to prevent blindness - Science Daily

Wilson Ring, Associated Press

Non-profit seeking to cure blindness up for $100M grant

WATERBURY, Vt. (AP) A Vermont-based nonprofit group that works to cure blindness in Nepal and other developing countries is one of eight semifinalists for a $100 million grant from the John D. and Catherine T. MacArthur Foundation.

The Waterbury-based Himalayan Cataract Project, based out of a rented office in a church parsonage, has been working for years to train local health care providers to perform cataract and laser surgery in Nepal and other countries.

The organization was co-founded in 1995 by Nepalese Dr. Sanduk Ruit and Dr. Geoff Tabin, formerly of the University of Vermont Medical Center and now at the University of Utah.

"They had a shared motivation that the right to sight is a human right and that no one anywhere in the world should receive care of a different or lower quality," said Job Heintz, the chief executive officer of the nonprofit, formed in 2003 to carry out the vision of the doctors. It now has 10 employees and an annual budget of about $9 million.

Over the years the organization has provided eye care for thousands of patients by training health care providers and providing equipment and other infrastructure.

"The quality of eye health care has dramatically risen, nowhere better than in Nepal," Heintz said on Thursday.

The Chicago-based MacArthur Foundation announced Wednesday that the Cataract Project was one of eight organizations chosen as semifinalists from among 1,904 proposals, for the $100 million grant program. The foundation says the competition is for "proposals promising real progress toward solving a critical problem of our time in any field or any location."

The winner would receive the entire $100 million.

Other semifinalists include Catholic Relief Services in Baltimore, which is working to change the way children are cared for in orphanages, and The Carter Center in Atlanta, which is working to eliminate river blindness in Nigeria.

The winner will be chosen in December.

The Cataract Project got its start at the Tilganga Eye Centre in Kathmandu, Nepal, which performed its first outpatient cataract surgery in 1994. Ruit and Tabin started the Cataract Project a year later.

At the Tilganga Centre providers now see about 1,000 patients a day for a variety of eye care needs.

Tabin worked at what is now the University of Vermont Medical Center from 1995 to 2005. The project opened Vermont offices in Waterbury and Norwich in 2003

The Cataract Project already has expanded its operations to a number of other countries, but the grant would be to expand operations in Nepal, Ethiopia and Ghana.

If they win the grant, the organization would increase the work it currently does, such as training doctors and support staff in their home countries and at other locations, including the United States.

"We know what we would do with every dollar," Heintz said.

More here:
Non-profit seeking to cure blindness up for $100M grant - SFGate

Jaitleys attempt to underplay the damage caused by demonetisation contrasts with the somewhat more sober assessment of the Economic Survey prepared by his Ministry.

THE Union Budget is only one of several instruments of economic policy available to the government. It must necessarily take into account not just the national context and the prevailing distribution of economic and political power among the various social classes in the country, but also the international context, more than ever before, given that the sum of Indias exports and imports amounts to a substantial share of the countrys gross domestic product (GDP). This years Budget, which was presented a few months after the shock and awe of demonetisation, had to contend with that move as well. Notwithstanding these constraints and taking into account the fact that the media hype over the Budget is possibly a bit over the top, the Union Budget is nonetheless very important as the total expenditure of the Union government accounts for between one-eighths and one-sevenths of the countrys GDP.

The Union Budget for 2017-18 was presented in Parliament on the first day of February instead of the last day of that month, as had been the practice for many years. The other distinctive feature this year was that the Railway Budget was subsumed within the Union Budget and not presented separately. Both these features have some negative implications. The database for the Budget is weakened somewhat by its advancement. The subsuming of the Railway Budget within the Union Budget weakens the special attention that the Railways, with its truly all-India character, deserves. Some read this subsuming as a prelude to the privatisation of the Railways.

Be these as they may, Arun Jaitleys fourth Budget as Union Finance Minister is wilfully blind to the serious negative economic impact of the demonetisation exercise imposed on the country by the Central government.

In a Budget speech that was true to form in terms of being long on rhetoric and short on substance, Jaitley hailed demonetisation as a momentous initiative and claimed that it would produce great benefits in the long run. The Minister presented little evidence to back his claim. His attempt to underplay the damage caused by demonetisation contrasts with the somewhat more sober, even if still wishful, assessment of the Economic Survey prepared by his Ministry.

The fact of the matter is that the demonetisation measure inflicted on an economy that was already showing some evidence of decline in momentum has caused considerable economic harm already, not to mention the tragic and entirely avoidable loss of more than a hundred lives. Estimates by various sources, including the Centre for Monitoring the Indian Economy (CMIE) and the All India Manufacturers Organisation (AIMO) and several independent economists, suggest substantial monetary loss and a decline of between 1 and 2 percentage points in the rate of economic growth.

Economists of widely different persuasions have shown a rare unanimity in highlighting the serious negative impact of the measure on aggregate demand in the economy. Given the damage caused by demonetisation and the consequent decline in aggregate demand, there was a general expectation that the Union Budget would provide a substantial stimulus to the economy to counteract the deflationary impact of demonetisation. However, an examination of the tax and expenditure proposals, which constitute the core of any budget, shows a failure to recognise the need for a substantial stimulus to the economy.

The Budget Estimate (B.E.) of total expenditure for 2017-18 is Rs.21.47 lakh crore as against a Revised Estimate (R.E.) for 2016-17 of Rs.20.14 lakh crore. This works out to a less-than-7 per cent increase in nominal terms. Taking inflation into account and viewed against a GDP growth estimated at 6.5-6.75 per cent, this is no stimulus at all. The total budgeted expenditure of the Union government for 2017-18 is 12.7 per cent of the GDP as against 13.4 per cent in 2016-17, a reduction in relative terms.

There is a great deal of rhetoric in the Budget speech on large increases in allocations for agriculture and farmers welfare, rural development, education and health. There is also the claim of significantly enlarged spending on infrastructure. The Budget speech suggests a thrust towards agriculture and allied activities and rural development. But the allocation for these two sectors taken together rises from Rs.167,768 crore in R.E. 2016-17 to Rs.187,223 crore in B.E. 2017-18, an increase of 11.5 per cent in nominal terms, implying only a modest increase in real terms. The allocation for education and health was Rs.114,806 crore in R.E. 2016-17. It has risen to Rs.130,215 crore in B.E. 2017-18, again a rather modest increase given the countrys overall low spending on these key sectors. The total expenditure on infrastructure as a share of Budget outlay is also marginally lower in B.E. 2017-18 compared with R.E. 2016-17.

An especially important negative impact of demonetisation has been on employment in the informal sector. There was widespread expectation that the Budget would address this issue by substantially increasing allocation for the rural employment guarantee scheme and possibly initiating a similar urban employment guarantee scheme. However, the allocation for the Mahatma Gandhi National Rural Employment Guarantee Scheme (MGNREGS) in B.E. 2017-18, at Rs.48,000 crore, is barely more than the R.E. 2016-17 figure of Rs.47,499 crore. Given the increase in wages for MGNREGS work, there will be a decline in the number of days of employment per household registered in the scheme. A larger point also needs to be made. As data from the Labour Bureau surveys remind us, job creation has nosedived over the past year, and this was a key issue for the Budget to take into account. However, it has made no serious effort in that direction.

Turning to receipts, the tax proposals in the Budget are estimated to result in a loss of Rs.20,000 crore in direct tax revenues. This continues the trend under the present government of persistent tax giveaways in respect of direct taxes even while the rhetoric is about widening the tax base and increasing the share of direct taxes. What is happening is that the indirect tax burden, a large share of which is borne by ordinary working people, is rising steadily. For instance, the revised excise duty collection in 2015-16 was Rs.2.88 lakh crore as against a B.E. of Rs.2.29 lakh crore. In 2016-17, the excise duty collection was Rs.3.87 lakh crore as against a B.E. of Rs.3.19 lakh crore.

Over the last three years, we have seen the abolition of wealth tax in a country characterised by obscene wealth inequality. We have also seen repeated overtures to tax evaders even while the rhetoric around demonetisation was on wiping out black money. These steps do not enhance the credibility of the governments morality plays. In respect of corporate income taxes, there is reasonable ground for eliminating numerous exemptions. The clamour for lower tax rates on corporate profits is to be assessed against the reality of effective tax rates of hardly 25 per cent on profits accruing to large corporate entities. The several lakh crores in revenue foregone on account of concessions to robust corporate and individual entities does not speak of equity in budget-making.

The economic philosophy underlying the Budget is one which sees the state as, at best, a necessary evil, and believes that the sole path to rapid growth and social well-being is through incentivising corporate investment. It also places exclusive emphasis on so-called fiscal prudence, which is interpreted to mean minimising fiscal deficits essentially through expenditure reduction. The self-serving argument that a lowering of tax rates will lead to an improvement in compliance is not sustained by evidence from across the world. The reason is simple enough: if the marginal costs of tax evasion are perceived to be lower than the benefits from such evasion, compliance need not improve at all.

Excerpt from:
Stubborn blindness | Frontline - Frontline

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Hello, again, Dolly - The Economist

Market Summary Follow

Puma Biotechnology Inc is a A biopharmaceutical company

PBYI - Market Data & News

PBYI - Stock Valuation Report

Puma Biotechnology Inc (PBYI) had a good day on the market for Friday February 17 as shares jumped 7.76% to close at $40.25. About 1.37 million shares traded hands on 9,969 trades for the day, compared with an average daily volume of 928,303 shares out of a total float of 36.82 million. After opening the trading day at $37.25, shares of Puma Biotechnology Inc stayed within a range of $40.50 to $36.70.

With today's gains, Puma Biotechnology Inc now has a market cap of $1.48 billion. Shares of Puma Biotechnology Inc have been trading within a range of $73.27 and $19.74 over the last year, and it had a 50-day SMA of $34.47 and a 200-day SMA of $41.58.

Puma Biotechnology Inc is a biopharmaceutical company. It is engaged in the acquisition, development and commercialization of products to enhance cancer care.

Puma Biotechnology Inc is based out of Los Angeles, CA and has some 156 employees. Its CEO is Alan H. Auerbach.

For a complete fundamental analysis of Puma Biotechnology Inc, check out Equities.coms Stock Valuation Analysis report for PBYI.

Want to invest with the experts? Subscribe to Equities Premium newsletters today! Visit http://www.equitiespremium.com/ to learn more about Guild Investments Market Commentary and Adam Sarhans Find Leading Stocks today.

Puma Biotechnology Inc is also a component of the Russell 2000. The Russell 2000 is one of the leading indices tracking small-cap companies in the United States. It's maintained by Russell Investments, an industry leader in creating and maintaining indices, and consists of the smallest 2000 stocks from the broader Russell 3000 index.

Russell's indices differ from traditional indices like the Dow Jones Industrial Average (DJIA) or S&P 500, whose members are selected by committee, because they base membership entirely on an objective, rules based methodology. The 3,000 largest companies by market cap make up the Russell 3000, with the 2,000 smaller companies making up the Russell 2000. It's a simple approach that gives a broad, unbiased look at the small-cap market as a whole.

To get more information on Puma Biotechnology Inc and to follow the companys latest updates, you can visit the companys profile page here: PBYIs Profile. For more news on the financial markets and emerging growth companies, be sure to visit Equities.coms Newsdesk. Also, dont forget to sign-up for our daily email newsletter to ensure you dont miss out on any of our best stories.

All data provided by QuoteMedia and was accurate as of 4:30PM ET.

DISCLOSURE: The views and opinions expressed in this article are those of the authors, and do not represent the views of equities.com. Readers should not consider statements made by the author as formal recommendations and should consult their financial advisor before making any investment decisions. To read our full disclosure, please go to: http://www.equities.com/disclaimer

Continued here:
Puma Biotechnology Inc (PBYI) Soars 7.76% on February 17 ... - Equities.com

February 17, 2017 6:33am NASDAQ:IBB NYSE:XLV

From Taki Tsaklanos: Biotechnology was once the darling of stock market investors. Not so anymore, since the summer of 2015 the sector collapsed from 400 points to 250 points in the IBB ETF.

Likewise, the health stock market sector lost its status of outperformer as the XLV ETF went from 75 points to 62 points. Note that biotech is part of the health sector (XLV).

Biotechnology is now showing the first signs of life. The IBB ETF is up 3 percent on the week.

We warned readers to watch closely the 250 level in this alert: Biotechnology and Health Sector Testing Long Time Support. Later on, we noticed that biotech refused to break down, and started to show a pattern of higher lows. Right now, the biotech stock market sector is testing a breakout level. Things will really get bullish once 300 points in the IBB ETF is cleared.

The iShares NASDAQ Biotechnology Index ETF (NASDAQ:IBB) fell $1.78 (-0.61%) in premarket trading Friday. Year-to-date, IBB has gained 10.40%, versus a 5.01% rise in the benchmark S&P 500 index during the same period.

IBB currently has an ETF Daily News SMART Grade of A (Strong Buy), and is ranked #2 of 36 ETFs in the Health & Biotech ETFs category.

The broader healthcare sector (XLV ETF) looks even more interesting. It recovered its losses, and is now ready to test all-time highs. Make no mistake, 75 points is a very important price level. A triple-test is significant as, mostly, three tests are sufficient for a breakout. However, a failure to breakout, after 3 tests, is bearish to say the least.

The Health Care SPDR ETF (NYSE:XLV) was unchanged in premarket trading Friday. Year-to-date, XLV has gained 6.70%, versus a 5.01% rise in the benchmark S&P 500 index during the same period.

XLV currently has an ETF Daily News SMART Grade of A (Strong Buy), and is ranked #1 of 36 ETFs in the Health & Biotech ETFs category.

This article is brought to you courtesy of Investing Haven.

Tags: biotech Health Care NASDAQ:IBB NYSE:XLV

Categories: NASDAQ:IBB NYSE:XLV

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iShares NASDAQ Biotechnology Index (ETF)(NASDAQ:IBB),Health ... - ETF Daily News (blog)

Experts have said inflammation could be addressed by what people eat, adding that every day foods including sugar and saturated fat can dramatically affect the conditions.

One of the everyday foods people could benefit from cutting out, they suggest, is vegetable oil - found in many processed foods - as too much Omega 6 in the diet can trigger inflammation.

Chronic low grade inflammation is linked to all the common diseases out there, said Philip Calder, Professor of Nutritional Immunology at Southampton University.

Understandably this is why there has been such a huge focus in the last decade on understanding it and trying to find ways to reduce it.

Think of inflammation as essentially a sign something is wrong and the body is try to find a way to resolve it.

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For example, a thumb will become swollen, heat up and painful if you hit it with a hammer this inflammation response warns your body something is amiss and then can kick start the healing process.

But significantly it is short-lived. What is different is when we experience intermittent or recurrent inflammation.

Where it is not turned off it becomes chronic, says Professor Calder.

Chronic inflammation - that persists and serves no purpose damages the body and is a key factor in causing illness and is now recognised as the underlying basis of a significant number of diseases.

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Chronic low grade inflammation is linked to all the common diseases out there

Professor Philip Calder

Professor Calder added: Many of the factors of a modern Western lifestyle - like taking little or no exercise and a diet often high in sugar and bad fats appear to make it easier for the body to become inflamed.

He said there is no magical food group which can reduce inflammation but components of some foods may be able to regulate or dampen down the inflammatory response.

These components can be found in a typical Mediterranean diet, one that has been shown to lower cholesterol and reduce symptoms of inflammatory conditions like rheumatoid arthritis.

Rob Hobson Head of Nutrition at Healthspan said people should be eating oily fish - rich in omega 3, fibrous pulses, berries, nuts, dark green and other brightly coloured vegetables, which contain antioxidants and other polyphenols to help quell inflammation in the body.

Processed foods rich in refined carbohydrates - including sugar - and saturated fats can exacerbate the inflammatory process, he said.

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Foods to avoid if you are suffering with Gout

Both experts said having too much omega 6 in the diet - found in vegetable oils like sunflower and safflower and found in many processed foods.

These fats oxidise easily, depleting the body of antioxidants and potentially causing inflammation and mutation in cells.

Switch to extra virgin olive oil and avoid margarine and too much meat, said Rob.

There is also increasing evidence that overeating leads to an inflammatory response in the body.

If you measure the blood of an obese person you will find higher levels of inflammatory chemicals than in someone who is not overweight, said Professor Calder.

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And heres the interesting thing: lose weight and those levels of inflammatory cells return to normal.

Experts also state there are herbs and spices which can help people reduce inflammation, including ginger and tumeric.

The active components of the ginger root known as gingerols are potent antioxidants and exhibit anti-inflammatory effects that have been proven to help reduce migraines and period pain.

People who dont get much turmeric or ginger in their diet can consider taking a supplement like Healthspans OptiTurmeric, 15.95 or Ginger Extract, 13.95.

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Diet to cure your arthritis: THIS everyday food could be making symptoms WORSE - Express.co.uk

Dividing mesenchymal stem cells

Its the kind of the data the field has worked towards for years.

Rheumatoid arthritis (RA) patients given a single intravenous dose ofMesoblastsnovel stem cell therapy were still demonstrating therapeutic benefits nine months later, according to new Phase 2 data from the Melbourne, Australia-based company.

While much larger Phase 3 studies are needed to validate the results, the data offer a tantalizing look at what optimized and targeted regenerative medicines could do as the field moves closer to an approval.

The study involved 48 patients that were resistant to frontline TNF-alpha therapies, such as Enbrel, Remicade, and Humira.

While these drugs have revolutionized the field and generated billions in revenue around20-40 percent of patients treated with a TNF inhibitor dont achieve a significant reduction in symptoms. Theyre non-responders. Others become resistant over time or experience adverse events.

When TNF inhibitors are off the table, patients are typically prescribed second-line drugs such as Rituxan. These, however, are not as effective and come with a range of serious side effects.

CEOSilviu Itescu said Mesoblasts mesenchymal precursor cells (MPCs) have demonstrated virtually no toxicity. The immune system doesnt register them as foreign so theres no negative immune response.The cells also appear targeted, intrinsically moving towards sites of inflammation and embedding themselves in the tissue.

The way the cells work is, they have receptors on their surface that are activated by every major cytokine that is important in progressive rheumatoid arthritis, including TNF, IL-1, IL-6, IL-17, Itescu explained. Those cytokines drive the disease and also bind to receptors on our cells. And when they bind to our cells they activate the cells to release other factors that switch off the very cells that made those cytokines.

In other words, MPCs interfere with the feed forward production of inflammatory molecules. Because the cells are addressing multiple pathways, he believes the therapy has an edge on the biologics inhibiting TNF-alpha or others key targets. It is also getting to the heart of the inflammation and disease, not simply knocking the immune system back.

Listed on both the NASDAQ and the Australian Stock Exchange (ASX), Mesoblast is evaluating its platform to a wide range of diseases. For each indication, the cells are delineated and optimized. Mesoblasts portfolio, Itescu said, is the most advanced in the stem cell field.

At the front of the pack is MSC-100-IV, a Phase 3 therapy for pediatric graft-versus-host disease (GvHD). MSC-100-IV secured orphan drug designation in the U.S., paving the way for an accelerated approval. The company is expecting a data readout in the third-quarter of this year.

Two other product candidates, MPC-150-IM and MPC-06-ID, are in late-stage development for advanced chronic heart failure and chronic low back pain due to degenerative disc disease.

In late December, U.S.-based MallinckrodtPharmaceuticals took an option on the GvHD and lower back pain programs.

When it comes to manufacturing, Itescu said the cells are designed to scale. The foundation for the supply chain is the allogeneic nature of the cells they can be administered to any patient.

Its not a problem for us, its an advantage, Itsecu said about the production logistics.Weve been at this for ten years and weve focused the entire thing on a scalable manufacturing platform using a unique subtype that can be used off-the-shelf and that can be industrially manufactured.

There are plenty of potential customers if the therapy is approved.

Rheumatoid arthritis is particularly lucrative. As Global Business Intelligencenotes, in 2013, three TNF-a-targeting biologics Humira, Remicade, and Enbrel were ranked among the top-10 best-selling drugs in the world, with global revenues of $11.1 billion, $9.9 billion, and $8.9 billion respectively.

Photo: Mesoblast

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Nine months of rheumatoid arthritis suppression with one stem cell dose? - MedCity News

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The New England Journal of Medicine published supplementary data, which show that people with moderate-to-severe rheumatoid arthritis (RA) who took the oral Janus kinase inhibitor baricitinib had better outcomes through 52 weeks compared to adalimumab (Humira).

This is an exciting time for rheumatology, with potential new treatments for rheumatoid arthritis on the horizon. The RA-BEAM study of baricitinib is the first phase 3 trial showing that a once-daily, oral treatment significantly improved clinical outcomes compared with a current standard of care, injectable adalimumab used with background methotrexate therapy, said Peter Taylor, M.A., Ph.D., F.R.C.P., study author and Norman Collisson chair of Musculoskeletal Sciences in the Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences at the University of Oxford.

In the RA-BEAM study, researchers studies more than 1,300 people who did not have an adequate response to methotrexate, but continued the use of methotrexate throughout the duration of the study. Participants were randomized to placebo once daily (n=488), baricitinib 4 mg once daily (n=487) or adalimumab 40 mg biweekly (n=330). At the 24th week, participants taking placebo crossed over to the baricitinib treatment group. The design of the head-to-head study and statistical analysis plan included prespecified and controlled for multiple testing for both non-inferiority and superiority of baricitinib compared with adalimumab.

A higher proportion of participants taking baricitinib achieved ACR50 and ACR70 response composite scores that represent at least 50 percent and 70 percent improvement, respectively, in multiple components of RA disease activity compared to adalimumab. This was observed as early as week 8 and continued through week 52.

These improvements were statistically significant compared to adalimumab at weeks 12, 20, 28, 32 and 40. At week 52, both ACR50 and ACR70 rates were higher in the baricitinib group compared to adalimumab, although only ACR50 was statistically significant.

Serious adverse events were observed in 8% for baricitinib and 4% for Adalimumab. Major adverse cardiovascular events (MACE) were reported in less than 1% of patients in both the baricitinib and adalimumab groups (baseline through 52 weeks). A total of 5 deaths were reported in the study (1 placebo, 2 baricitinib, 1 adalimumab and 1 placebo rescued to baricitinib).

These data demonstrate that baricitinib could provide another treatment option for people with rheumatoid arthritis, Taylor added.

Read the original here:
Baricitinib Better for Rheumatoid Arthritis than Humira - National Pain Report

Finding the right treatment to keep your psoriatic arthritis under control can take time. The first, second, or even third may not work for managing your particular condition.

Treatment change would come about in two different situations for psoriatic arthritis, says Reshma Marri-Gottam, MD, a rheumatologist at St. John Providence health system in Detroit. One would be theyre not tolerating the medication or they have an adverse effect or reaction to the medication, or the risk outweighs the benefits. The other is theyre just not responding to the medication.

It may be that your body has built up a resistance to one drug or that the disease itself is ramping up, especially if youve only been managing the symptoms rather than the source of the symptoms.

Usually we are adjusting medications due to active joint inflammation and active skin disease, explains Kelly Weselman, MD, a rheumatologist at Wellstar Rheumatology in Atlanta and chair of the American College of Rheumatology communications and marketing committee. Sometimes we change a medication because it is not effective at all, she says. Sometimes the medication shows partial benefit, but the patient and I might decide we can do better with an alternative medication strategy.

The right treatment plan can make all the difference in controlling your symptoms and allowing you to continue your daily activities.

Although this is not a curable disease, it can often be put into remission, Dr. Weselman says. There are certainly patients who we just cannot get into complete remission, but usually we can find a treatment regimen that improves their quality of life.

Here are the questions you should ask to determine whether its time to change treatment and what to expect.

Every drug comes with side effects and risks, and these can be the reason some patients want to stop taking a drug. The most important thing is to be open with your doctor about what you can and cannot handle.

Be honest with your physician about ongoing symptoms that are bothersome. Your appointment is the best time to discuss changes, so arrive prepared, Weselman says. Recognize that every treatment carries some degree of risk, and lack of appropriate treatment also carries risk. Many decisions must be made in person, either due to a need for the doctor to examine a particular area or to have effective discussions about the available options.

I explain to patients our ladder of treatment options as well as the risks, benefits, and potency of each agent, Weselman says. We discuss costs as well.The options are finite, so we need to discuss all options to avoid running out of treatments.

The first drug most people use to treat psoriatic arthritis is a nonsteroidal anti-inflammatory drug (NSAID). These over-the-counter drugs, such as ibuprofen(Advil, Motrin) or naproxen(Aleve), treat the pain and inflammation but not the underlying cause of the disease.

The next step up from NSAIDs are disease-modifying anti-rheumatic drugs (DMARDs). These drugs, such as methotrexate, do not actually modify psoriatic arthritis disease but can prevent its progression.

Biologics, which are made from living organisms, work by targeting specific proteins or cells in the immune system.

Patients may receive a temporary course of corticosteroids during any of their treatment plans to stop a particularly bad flare-up.

We discuss guidelines in treatment and standards of care and how that applies to their specific situation, Weselman says. Spending a few minutes giving the patient information helps us to make decisions together.

Its only human to want instant relief, but some drugs take time to really kick in. Weselman and Dr. Marri-Gottam recommend allowing three months for a new medication to begin working.

It can be frustrating for patients waiting to see if a medication is effective, but if we give up on a treatment too quickly, we risk losing potentially effective treatments, Weselman says.

The most current framework for thinking about psoriatic arthritis treatment today is that combination therapy is better than monotherapy, Marri-Gottam says. That means that using two drugs simultaneously can often achieve better results than just one.

Usually methotrexate is combined with a biologic agent, Weselman says.Sometimes sulfasalazine is a part of the combination.

Sometimes doctors have to try one treatment before another simply to make sure you dont end up paying out of pocket.

We tend to use the medications that have been out on the market the longest, and we try to do what we think is right for the patient. But sometimes the insurance company dictates what we can and cant use, Marri-Gottam says.

One company might require a patient to try adalimumab(Humira) before etancercept(Embrel), for example; while another company may require a different protocol. Insurance companies often require patients try a DMARD before moving on to biologics.

Methotrexate is the first med I usually start with, even if theyre a good candidate for a biologic, Marri-Gottam says. With DMARDs, if theres any dose changes that can happen, you try to give a fair chance to that medication before you say, Hey, this isnt going to work anymore.

Some drugs restrict the activities you can engage in or delay goals you may want to achieve, such as starting a family. Its important to discuss with your doctor what youre willing to do and give up.

Younger patients should definitely think about whether they want to have kids, Marri-Gottam says. I advise patients that they need to be on birth control if taking methotrexate because it is known to be harmful to the fetus.

Not enough data exists about biologics to know if they can cause harm, so its currently recommended not to take biologics while pregnant or trying to conceive either.

Alcohol is another big one for methotrexate, Marri-Gottam says. If youre on methotrexate, you shouldnt drink at all. Methotrexate is heavy on the liver, so if youre taking that and drinking alcohol, which is processed by the liver, its too much for the liver to handle for some patients.

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6 Things You Need to Know About Switching Psoriatic Arthritis Treatments - Everyday Health (blog)

Arthrogen will start a Phase Ib trial for a gene therapy aiming to treat rheumatoid arthritis with a single injection and reduce costs for patients.

Arthrogen,based in Amsterdam, is developing local gene therapies for inflammatory diseases. The biotech company has now announced it has received approval to start a Phase Ib trial with its lead candidate, ART-I02, in patients with rheumatoid arthritis who still suffer from inflamed joints despitemultiple treatments.

The clinical trial will be conducted by the Centre for Human Drug Research (CHDR) in Leiden, with collaboration from other University Medical Centers in the Netherlands. Patients will start to be recruited in the first quarter of this year and results are expected by the end of 2018.

ART-I02 consists of a recombinant adeno-associatedviral vector (rAAV) genetically engineered to encode the human interferon (hIFN-) protein, which has anti-inflammatory activity.By including an inflammation-inducible promoter in the genetic construct, the gene is only expressed when the patient suffers flares of acute pain and inflammation.

Founded in 2005 as a joint venture between the Dubai Bone & Joint Center (DBAJ) in the United Arab Emirates and the Academic Medical Center (AMC) in Amsterdam, Arthrogen has managed to raise almost 15M so far to support its pipeline for inflammatory disease.

One of the advantages of ART-I02 is that its delivered locallyin the rheumatic joint, only affecting the target area to minimize side effects. In addition, gene therapy offers a long-lasting treatment with a single injection, which can significantly reduce costs for patients in the long term. However, Arthrogen will have to be careful to not follow the steps of its neighboruniQure, whose firstcommercial gene therapy was a failure because of pricing issues.

Rheumatoid arthritis is a big market, expected to generate 32.5B ($34.6B) by 2020. The space is crowded, but by then blockbusters like top-seller Humira will no longer be protected by patents in both the US and Europe, leading the way for biosimilars and other options affordable in the long term such as gene therapy.

Images byMidas Anim; Tefi /Shutterstock

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Gene Therapy for Rheumatoid Arthritis gets Approval to Start ... - Labiotech.eu (blog)

Knee Pain

Knee pain, often caused by sport injuries, is incredibly common. If your knee pain is getting worse learn how you can stay out of surgery with Stem Cell Therapy.

The hip joint is the largest joint in the human body but this joint isn't indestructible. Over time and overuse joint pain can occur. Click to learn how you can be treated with Stem Cell Therapy.

Shoulder pain is typically a result from previous injury to the shoulder joint or tendons. Click to see how Stems Cell Therapy can help.

Plantar Fasciitis is one of the most common types of heel pain. The pain you experience during plantar fasciitis is actually inflammation in a ligament in your foot. This inflammation is commonly treated with stem cell therapy.

The lower back is a problematic area for many older adults. This part of the body is a very complex and interconnected network of muscles, discs, nerves and bones that can cause a number of problems that range from arthritis to muscle spasms.

Elbow joints are much less prone to wear and tear as other joints but pain is typically a result from years of repetitive motion. Click to see how we can help with Stem Cell Therapy.

Wrist pain is a common complaint. It's typically caused by sudden impacts and repetitive stress. Check out how Stem Cell therapy can alleviate your pain.

Like other joints injury and overuse are the typical causes of ankle pain. However, gout and joint space are among other causes. Click to see how you can benefit from Stem Cells.

Your neck or cervical spine is another problem area for many people. Like the lower back the neck is made up of discs, bones, muscles and ligaments which can cause people to experience many painful symptoms.

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Stem Cell Professionals: Stem Cell Therapy in York, Pa