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macular edema

FDA Approves New Treatment for Diabetic Retinopathy in Patients

Diabetic retinopathy (DR) is the most common diabetic eye disease and is a leading cause of blindness in adults in the United States. According to the Centers for Disease Control and Prevention, diabetes (type 1 and type 2) affects more than 29 million people in the United States and is the leading cause of new blindness among people ages 20 to 74 years. In 2008, 33 percent of adults with diabetes aged 40 years or older had some form of DR. In some cases of DR with diabetic macular edema (DME), abnormal new blood vessels grow on the surface of the retina. Severe vision loss or blindness can occur if the new blood vessels break.

“Diabetes is a serious public health crisis, affecting more patients every year…”

“Diabetes is a serious public health crisis, affecting more patients every year,” said Edward Cox, M.D., M.P.H, director of the Office of Antimicrobial Products in the FDA’s Center for Drug Evaluation and Research. “Today’s approval gives patients with diabetic retinopathy and diabetic macular edema another therapy to treat this vision-impairing complication.”

In February, the FDA approved Lucentis (ranibizumab injection) 0.3 mg to treat DR in patients with DME.

Eylea is administered by a physician as an injection into the eye once a month for the first five injections and then once every two months. It is intended to be used along with appropriate interventions to control blood sugar, blood pressure and cholesterol.

The safety and efficacy of Eylea to treat DR in patients with DME were evaluated in 679 participants in two clinical studies where participants were randomly assigned to receive Eylea or macular laser photocoagulation, a laser-based treatment used to burn small areas of the retina. At week 100, participants being treated with Eylea showed significant improvement in the severity of their DR, compared to patients who did not receive Eylea.

The most common side effects associated with Eylea include bleeding of the conjunctiva (the tissue that lines the inside of the eyelids and covers the white part of the eye); eye pain; cataracts; floaters; increased pressure inside the eye (increased intraocular pressure); and separation of the interior jelly of the eye from the retina (vitreous detachment). Serious adverse reactions include infection within the eye (endophthalmitis) and retinal detachments.

The FDA granted breakthrough therapy designation to Eylea for the treatment of DR with DME. The FDA can designate a drug a breakthrough therapy at the request of the sponsor if preliminary clinical evidence indicates the drug may demonstrate a substantial improvement over available therapies for patients with serious or life-threatening conditions. The FDA also reviewed the new use for Eylea under the agency’s priority review program, which provides for an expedited review of drugs that demonstrate the potential to be a significant improvement in safety or effectiveness in the treatment of a serious condition.

The FDA previously approved Eylea to treat wet (neovascular) age-related macular degeneration, a condition in which abnormal blood vessels grow and leak fluid into the macula. Eylea is also approved to treat DME and macular edema secondary to retinal vein occlusions, both of which cause fluid to leak into the macula resulting in blurred vision.

Eylea is marketed by Tarrytown, N.Y.-based Regeneron Pharmaceuticals Inc. Lucentis is marketed by South San Francisco, California-based Genentech, a subsidiary of Roche Pharmaceuticals.


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air pollution

Traffic-Related Air Pollution Linked to Type 1 Diabetes in Children

Several studiesTraffic- Air Pollution have already linked the likelihood of death by respiratory and circulatory illness to the level of fine dust particles present in the air. A Munich study now shows that high levels of fine dust pollution could possibly increase the risk of type 1 diabetes among children.

Fine dust pollution leads to earlier instances of type 1 diabetes in small children, according to a study by the Institute for Diabetes Research at the Helmholtz Centre in Munich. Environmental factors, the researchers found, also have an effect on the development of the illness.

“Our results indicate that exposure to traffic-related pollutants accelerates the development of type 1 diabetes…”

“Our results indicate that exposure to traffic-related pollutants accelerates the development of type 1 diabetes,” the authors of the study, Andreas Beyerlein, Miriam Krasmann and their colleagues indicated. But their data suggests this result only applies to very young children.

The researchers analysed data from 671 young patients with type 1 diabetes, recorded between April 2009 and May 2013 in the Bavarian diabetes register DiMelli (Diabetes Incidence Cohort Registry).

The focus of the analysis was to compare the time of diagnosis in small children with contact to certain air pollutants around their homes. Blood samples from patients were also tested for various inflammatory markers at the time of diagnosis.

During the analysis, the researchers also took other factors into consideration, such as the history of diabetes in a child’s family, the education level of parents and a child’s body mass index.

Air pollution from exhaust emissions increase risk in urban areas.

The researchers found that small children from residential environments with high levels of ambient air pollution developed type 1 diabetes three years earlier on average than children in the same age group from areas with low levels of pollution.

The correlation was found for concentrations of fine dust particles with an aerodynamic diameter of <10µm and nitrogen dioxide. Both substances are categorised as traffic-related pollutants.

Further, the researchers consider it unlikely that other typical occurrences related to city life could also be contributing to the correlation between diabetes and place of residence.

“Our results were independent from the level of urbanisation in the areas analysed,” the researchers said. This indicates that pollutants are responsible for the correlation observed and not a different lifestyle in cities or higher temperatures in urban areas.

Type 1 diabetes is the most common chronic illness in children and youth. 65,000 new cases are diagnosed worldwide each year, with an estimated 3% annual rate of increase. In Germany alone, 2,100 to 2,300 new cases are registered annually among children and teens up to 14 years of age.

Studies indicate a yearly 3-4% increase in the rate of new cases for type 1 diabetes. Now, the Helmholtz Centre study suggests a correlation between the increase in new cases and growing urbanisation.

Air pollution poses biggest environment-related health risk.

The fact that smog and traffic-related air pollution considerably increase the risk for numerous diseases, including cancer, lung diseases as well as heart and circulatory conditions, is nothing new. The European Environment Agency (EEA) presented its progress report in early March.

According to the agency, fine particulates in the air are to blame for around 430,000 premature deaths in the European Union. Despite measures to introduce a driving ban, and stricter guidelines for industry, the report does not consider the danger to be over.

The World Health Organisation (WHO) classifies air pollution as the largest environment-related health risk worldwide and estimates the number of deaths due to air pollution at 7 million per year.

In 2013, the US Environmental Protection Agency responded to the dramatic increase in evidence of adverse health effects related to fine dust particles by adjusting threshold values for the pollutants. The long-term threshold values for respirable fine dust particles with an aerodynamic diameter under 2.5µm was decreased from 15 to 12 µg per cubic metre. In the EU, the roughly comparable value is currently still at 25µg per cubic metre.

In Germany, especially large episodes of smog have become a rare occurrence. Still, the country’s limit values for air quality are often exceeded. Though filtration of more coarse particles has been mostly effective, the amount of smaller, respirable particles – so-called fine dust particles – in emissions has increased. The main sources of fine dust particles are industry, furnace heating, motors and agriculture.


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cell regeneration

Novel Drug Candidate Regenerates Pancreatic Cells Lost in Diabetes

cell-regenrationIn a screen of more than 100,000 potential drugs, only one, harmine, drove human insulin-producing beta cells to multiply, according to a study led by researchers at the Icahn School of Medicine at Mount Sinai, funded by JDRF and the National Institutes of Health, and published online in Nature Medicine.

Diabetes results from too few insulin-producing “beta cells” in the pancreas secreting too little insulin, the hormone required to keep blood sugar levels in the normal range. The disease affects 380 million people worldwide, and leads to major medical complications: heart attackstroke, kidney failure, blindness and limb amputation.

The Mount Sinai study found that harmine drove the sustained division and multiplication of adult human beta cells in culture, a feat that had eluded the field for years. In addition, harmine treatment tripled the number of beta cells and led to better control of blood sugar in three groups of mice engineered to mimic human diabetes.

“…we believe these results represent a key step toward more effective future treatment of diabetes”

“Our results provide a large body of evidence demonstrating that the harmine drug class can make human beta cells proliferate at levels that may be relevant for diabetes treatment,” said senior study author Andrew Stewart, MD, Director of the Diabetes, Obesity and Metabolism Institute at the Icahn School of Medicine. “While we still have a lot of work to do in improving the specificity and potency of the harmine and related compounds, we believe these results represent a key step toward more effective future treatment of diabetes.”

Loss of insulin-producing beta cells has long been recognized as a cause of type 1 diabetes, in which the immune system mistakenly attacks and destroys beta cells. In recent years, researchers have concluded that a deficiency of functioning beta cells also contributes importantly to type 2 diabetes. Thus, developing drugs that can increase the numbers of healthy beta cells is a major priority in diabetes research.

Re-Creating a Burst

As humans develop, each cell divides into two, leading to many more cells in subsequent generations as organs form. In the case of beta cells in the pancreas, most of this multiplication comes in a burst during the first year of life and then declines during childhood, leaving a limited supply to last a lifetime. During this burst, about two percent of a child’s beta cells are dividing at any one time. The current study found that harmine re-creates roughly the same amount of beta cell division, both in cell and animal tests.

While increasing the supply of beta cells seems an obvious approach, past attempts to do so have been met with limited success. Perhaps as a result of their unique genetic program, adult beta cells strongly resist attempts to nudge them into cell division.

Over several years, Dr. Stewart and colleagues unraveled genes and signaling pathways that drive multiplication (proliferation) of beta cells, and then confirmed proposed mechanisms with gene therapy. Based on the current study results, the team believes a particular enzyme, “dual specificity tyrosine-regulated kinase-1a (DYRK1A),” is the likely target of harmine. With this discovery, DYRK1A, known from past studies to drive cell division in other cell types, becomes a drug development target.

“We found that harmine, likely by interacting with DYRK1A, increases levels of other known drivers of cell division,” said Peng Wang, PhD, Assistant Professor of Medicine, Endocrinology, Diabetes, and Bone Disease at the Icahn School of Medicine and first author of the paper. “These drivers include the protein c-MYC, the gene for which was the basis of the screen we used to identify harmine as a potential treatment.”

Dr. Wang said the team designed a sensor to glow (thanks to a firefly gene) when any compound activated the promoter DNA snippet responsible for turning on the c-MYC gene. Of more than 100,000 compounds analyzed in a high-speed robotic screen, harmine was among 86 that caused the brightest glow, and was the only one of these that caused beta cell proliferation. The c-MYC pathway appeared to some researchers to be an unlikely therapeutic target for beta cell regeneration because past studies had found it to cause beta cell death when activated in high doses. However, the current study found that harmine causes only modest increases in c-MYC levels, and no beta cell death.

The research team will now focus on making changes to the harmine and its relatives (harmalogs) to find drug candidates that target only beta cells.

Harmine is derived from a flowering plant called Harmal (peganum Harmala) found in the Middle East, and from some South American vines. Drug development efforts based on harmine will need to grapple with its known psychoactive effects on the brain, which may explain its traditional use in spiritual ceremonies and as medicine.

The study was funded by grants from JDRF, the leading research and advocacy organization funding type 1 diabetes research (17-2011-598 and 1-2011-603).

“We believe that beta cell regeneration will play a key role in ultimately curing type 1 diabetes, and JDRF is pleased to support Dr. Stewart’s research into renewing these cells in humans,” said Patricia Kilian, PhD, director of the JDRF Regeneration Research Program. “If successful, this early research could lead to drugs that restore beta cells in people with type 1 diabetes, realizing the vision of a future free from insulin therapy.”

Adapted by MNT from original media release




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Genes associated with T1D

Genes That Increase the Risk of Type 1 Diabetes Have Lost Their Hiding Place

Newswise — TheGenes That Increase the Risk of Type 1 Diabetes genes that increase the risk of type 1 diabetes have lost their hiding place. A research group that includes a University of Florida genetics expert has located and narrowed down the number of genes that play a role in the disease, according to a study published Monday in the journal Nature Genetics. Knowing the identities and location of causative genes is a crucial development: Other researchers can use this information to better predict who might develop type 1 diabetes and how to prevent it.

“It’s a game-changer for type 1 diabetes,” said Patrick Concannon, director of the University of Florida Genetics Institute.

Researchers gathered information about the genetic makeup of 27,000 people, including those who had type 1 diabetes and others who did not. They then began looking for individual differences in DNA that raise the risk of type 1 diabetes. Starting with 200,000 possible locations in the genome, researchers used a technique known as fine mapping to pinpoint DNA sequence variations that can lead to diabetes. In some genomic regions, they narrowed the number of disease-causing DNA variations — known as single nucleotide polymorphisms or SNPs — from the thousands down to five or less.

That will make diabetes researchers’ work more effective and efficient by giving them the most detailed directions yet about where to look for the genetic variations that cause type 1 diabetes and perhaps other autoimmune diseases such as arthritis, Concannon said. Now that the group of geneticists has identified the important genes and SNPs, diabetes researchers will reap the benefits, according to Concannon.

“We’ve taken this genetic data which was interesting but hard to work with, and we’ve condensed it down into something that people can actually use to begin to explore the mechanism of the disease. It moves it out of the realm of genetics to being broadly applicable to type 1 diabetes research,” he said.

Type 1 diabetes occurs when the body’s immune system kills off insulin-producing cells in the pancreas. Some 3 million people in the United States have the disease, according to the JDRF, a group that funds type 1 diabetes research and education. Experts don’t know exactly what causes the disease but suspect that genetics and environmental factors may play a role.

The researchers’ findings are the most comprehensive yet in the effort to locate and identify the genetic risk variants for type 1 diabetes and other autoimmune diseases, said Todd Brusko, a member of the UF Diabetes Institute and an assistant professor in the UF College of Medicine’s department of pathology, immunology and laboratory medicine, part of UF Health.

Researchers can now shift away from trying to determine which genes heighten the risk for diseases like type 1 diabetes, Brusko said. Instead, researchers can focus on how genetic changes alter immune cell activity. That, he said, could eventually lead to new treatments that prevent or stop type 1 diabetes and other automimmune diseases.

“Ultimately, this information will allow researchers and clinicians to tailor treatments…”

“Ultimately, this information will allow researchers and clinicians to tailor treatments to correct underlying defects in the immune system that allow for autoimmune disease development,” Brusko said.

The findings are significant because certain interactions within the genome can now be analyzed to identify which genes and regulatory sequences cause the disease, said Stephen S. Rich, the study’s lead author and the director of the Center for Public Health Genomics at the University of Virginia. Defining the variants that cause type 1 diabetes may lead to new therapeutic targets and treatments, he said.

The study also included work by researchers from the Massachusetts Institute of Technology, the Eli and Edythe L. Broad Institute of MIT and Harvard, and the University of Cambridge in England. The current study was part of the type 1 diabetes Genetics Consortium, which was established in 2001 to enhance scientists’ ability to detect genes and variants that are relevant to the disease. The Genetics Consortium has received about $50 million in funding from the JDRF and the National Institute of Diabetes and Digestive and Kidney Diseases, Rich said.



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Type 1 Diabetes Baby

Type 1 Diabetes Originates in the Gut But Probiotics Could Offer Cure

Two separatType 1 Diabetes Babye pieces of research have found that the development of type 1 diabetes is likely caused by the gut, and therefore, a type of probiotic could be the cure.

Scientists from several European and US institutions studied 33 Finnish infants over three years from birth who were genetically predisposed to type 1 diabetes.

Their study, entitled “The Dynamics of the Human Infant Gut Microbiome in Development and in Progression toward Type 1 Diabetes” is published in the journal Cell Host & Microbe.

They discovered that four children in the group that developed type 1 diabetes had 25% less types of bacteria in their guts than other children.

The same four infants were also found to have more amounts of a specific bacteria that is known to trigger gut inflammation. This could be a prelude to type 1 diabetes as the bacteria causes the immune system to mistakenly attack and destroy beta cells in the pancreas that usually make insulin and monitor glucose levels.

“We know from previous human studies that changes in gut bacterial composition correlate with the early development of type 1 diabetes, and that the interactions between bacterial networks may be a contributing factor in why some people at risk for the disease develop type 1 diabetes and others don’t,” said Jessica Dunne, Director of Discovery Research at Juvenile Diabetes Research Foundation (JDRF), a UK charity which funded the study.

“This is the first study to show how specific changes in the microbiome are affecting the progression to symptomatic T1D.”

By being able to understand how the community of microorganisms in our guts (known as a microbiome) and which species are absent in the gastrointestinal tracts of children, the researchers believe they can slow down the progression of type 1 diabetes.

Probiotics could be the cure for type 1 diabetes

Cornell University researchers have a similar idea, but they have been working on a treatment that involves regulating insulin by engineering the bacteria found in our guts.

Their study, entitled “Engineered Commensal Bacteria Reprogram Intestinal Cells Into Glucose-Responsive Insulin-Secreting Cells for the Treatment of Diabetes” is published in the journal Diabetes.

The scientists took a strain of bacteria known as Lactobacillus gasseri – a type of bacteria found in probiotic yoghurts – and engineered the bacteria to be able to secrete a hormone called glucagon-like peptide-1 (GLP-1).

When they fed this engineered probiotic to a group of diabetic rats for 90 days, they discovered that the bacteria triggered the upper intestinal epithelial cells in the rats to convert into cells that acted a lot like the pancreatic beta cells.

The rats had up to 30% lower high blood glucose than diabetic rats that did not receive the probiotic, and the probiotic was shown to reduce glucose levels in diabetic rats the same way the levels would be reduced in normal rats.

“The amount of time to reduce glucose levels following a meal is the same as in a normal rat… and it is matched to the amount of glucose in the blood. It’s moving the centre of glucose control from the pancreas to the upper intestine,” said John March, professor of biological and environmental engineering at Cornell University and the paper’s senior author.

The next step for March and his team is to prove that their method of engineering bacteria to move insulin production to the intestine will work in humans too.

They aim to develop a pill that patients suffering from both type 1 and type 2 diabetes can take daily, that will be available within the next two years.


To learn how you can get more involved in the DRC’s research projects visit: Support a Diabetes Research Project





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Child Getting Blood Pressure Checked

Children in UK: Alarming Rise in Type 1 Diabetes Among Youth

A substantially high numberChild Getting Blood Pressure Checked of children in the UK have been found to exhibit long-term health implications associated with type 1 diabetes, a report from the Royal College of Paediatrics and Child Health (RCPCH) says.

It looked at figures from diabetes units across England and Wales in 2013-14 and found that more than 27 percent of young people had high blood pressure, while around 7 percent had markers of future kidney disease.

Over 14 percent had early signs of eye disease putting them at risk of blindness in later years.

More than 25 percent were classed as obese. Obesity is one of the risk factors for developing diabetes.

The analysis shows that 26,867 children and young people with diabetes were recorded last year, compared with 25,221 in 2012/13.

While the overall blood sugar control in the group has improved, just 16 percent underwent all seven annual health checks recommended to monitor their blood sugar control and complications, reports BBC.

With some patients showing early markers of eye, heart and kidney disease, the findings raise concern for their future health.

Barbara Young, Diabetes UK chief executive, said there was evidence that children were experiencing problems with their eyesight or kidneys before they reached their 18th birthday.

She said: “There is an urgent need for the NHS to make the pace of improvement quicker.”

The data revealed more than 1,000 new cases recorded in people under-25 last year.

Dr Justin Warner, of the RCPCH, said: “This is the first time we have been able to collect and analyse the data on early warning signs and levels are higher than we would expect.”

Health implications
Type 1 diabetes that appears in childhood is caused by the immune system destroying cells in the pancreas, leading to high blood sugar levels.

The more common type 2 diabetes is largely due to an unhealthy lifestyle.

Persistently high blood sugar levels can lead to serious problems, including heart disease and kidney disorders.

The study also looked at type 2 diabetes, which accounts for 5 percent of all cases of diabetes in children and young people.

Similar rise in type 1 diabetes has been recorded by many other countries. The cause is not known, but it is thought to be the result of a combination of genetic and environmental factors, says the World Health Organization.



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Empty Beakers in Science Lab

Young Scientists Face The Worst Research Funding In 50 Years

WASHINGTON Empty Beakers in Science Lab— Young scientists entering biomedical research find themselves in the worst financial environment in half a century, the head of the National Institutes of Health says.

In an appearance before the House of Representatives Committee on Appropriations, Dr. Francis Collins offered a familiar warning to lawmakers considering future appropriations for scientific research. Investments are falling relative to inflation, he said, forcing changes likely to snowball into the future.

“Given international trends,” Collins said, citing a recent article in the medical journal JAMA, “the United States will relinquish its historical international lead in biomedical research in the next decade unless certain measures are undertaken.”

Collins warned that these trends would convince a future generation of researchers that their field was inhospitable. Fewer young scientists would mean fewer scientific discoveries, making it more difficult for companies to profit and for public health authorities to guard against diseases.

“This is the issue that wakes me up at night when I try to contemplate the future of where biomedical research can go in the United States,” Collins said. “They are finding themselves in a situation that is the least supportive of that vision in 50 years. They look ahead of them and see the more senior scientists struggling to keep their labs going and suffering rejection after rejection of grants that previously would have been supportive. And they wonder, ‘Do we really want to sign up for that?’ And many of them, regrettably, are making the decision to walk away.”

Sobering budgetary assessments are nothing new from Collins, who heads the federal government’s main funder of biomedical research. He has been preaching the need for stable NIH budgeting for years, and has amplified those warnings since the spending cuts brought about by sequestration went into effect in 2013. NIH has lost about 22 percent of its purchasing power since 2003. In fiscal 2014, it was appropriated $30.1 billion.

A two-year bipartisan budget agreement brought a temporary reprieve. But that agreement runs out in September.

Collins’ appearance in the House on Tuesday is likely the first prong in a months-long campaign arguing that the days of sequestration shouldn’t return. The budget situation for NIH, like every other federal agency, is uncertain come September. Under current law, non-defense discretionary spending would be $493 billion in fiscal 2016, up just $1 billion from fiscal 2015., according to a document put together by House Democrats. Without a change, appropriators will have little discretion to provide more funding. If they did increase the NIH budget, it would come at the harm of other domestic programs.

A recent  report by the group United for Medical Research made clear the high stakes of stagnant scientific research funding. Compared with countries that have “made long-term commitments to increase their support of biomedical sciences,” the report said, federal funding cuts are leading to “an erosion of America’s preeminence in biomedicine.”

“China is filing more patents in biomedicine than the U.S. — not just as a portion of GDP, but absolutely more patents,” Collins said. “And the consequences, I think you can imagine, are going to be significant.”

Members of Congress from both parties have tried innovations to funnel funds to NIH. Proposals have included creating an incentive fund to encourage appropriators to make steady financial commitments; a biomedical research private-public bank; to remove the NIH from the discretionary budget; to generate money by penalizing big pharmaceutical companies that break the law; and to certify that the sequester no longer applies to NIH.

None of these have gained significant traction in the new Congress, where some conservative members have criticized NIH for funding quixotic-sounding projects at the expense of critical short-term needs.

Collins wasn’t asked about this critique (though in the past, he has argued that science funding decisions are best made through peer review and that even funny-sounding ideas may bear great fruit). He also didn’t address any new funding proposals during his two-hour appearance on Tuesday morning. Instead, he offered a broad pitch for lawmakers to fund NIH in a way that “that keeps up with inflation, plus a little bit.”

The reception he received underscores the difficulty and frustration of his objective.

Rep. Tom Cole (R-Okla.) called the hearing “the most popular panel we will see all session long.” Rep. Rosa DeLauro (D-Conn.) called for a “group hug” among attendees. Rep. Nita Lowey (D-N.Y.) said the discussion was “so very exciting” and happily offered enthusiasm for doubling NIH funding, which happened during the Clinton and Bush administrations. And Rep. Mike Simpson (R-Idaho) noted that, “the bipartisan nature of this subject with this committee is pretty obvious.”

Then Simpson delivered a bitter pill. Everyone on the committee would like to “substantially increase the research we’re doing,” he said, “if we didn’t have an $18 trillion debt and $500 billion deficit that we are having to deal with at the same time, which makes it more difficult.”


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DRC Logo for News

New Crowdfunding Hub to Choose and Follow Your Donations

Written by Mike Hoskins on April 20, 2015 via Healthline


Each time I donate to diabetes research in recent years, I get this sinking feeling that I’m throwing money into a bottomless pit, and may never know exactly what my donation is going toward or whether it’s making any difference. I just have to go on faith.

Now a new non-profit called the Diabetes Research Connection aims to change that, by creating an online crowdfunding hub for type 1 diabetes research where you can pinpoint a particular scientist and project to fund, watch your money be assigned to that research, and get regular updates on what’s happening inside the research lab.

Think of it as a Kickstarter orIndiegogo hub set up specifically for diabetes research.

Crowdfunding is of course nothing new in our world; Diabetes Research Connectionwe’ve seen many campaigns to fund the creation of a new product or educational resource, as well as a wave of crowdfunding to help individuals with everything from a visit to D-camp, paying for needed diabetes supplies, or supporting walks or charity efforts. We’ve also reported on another non-profit that aims to act as a consumer watchdog for diabetes donations by publishing independent reports on how organizations are allocating their resources: the Juvenile Diabetes Cure Alliance (JDCA).

But this new DRC website in unique, in that it creates a kind of one-stop shop for donors to find some T1D research they might be interested in funding and becoming involved with. This seems to come at a critical time, with calls for change in the diabetes research paradigm and more emphasis on transparency from scientists beyond just publishing in scientific journals.

As explained by D-blogger Joshua Levy, the DRC currently has six projects on their site right now, one of which is fully funded, and one being a sort of “internal project” to fund the web site itself. The other projects are all in the process of aiming to raise the the max allowed funding of $50,000,

We looked into the backstory of this new, creative funding effort.

The Origins

The concept was first created about five years ago, the brainchild of endocrinologist and researcher Dr. Alberto Hayek in San Diego, CA, who saw the need to do better in diabetes research funding. He retired a couple of years ago, after a quarter-century of diabetes research at Scripps Whittier Diabetes Institute and UCSD.

Hayek says that the level of diabetes research funding in general has dipped in recent years; in today’s dollars the National Institutes of Health (NIH) is funding much less than it did five years ago, and less than 4% of of the investigators getting money are younger than 40, since most of the money goes toward older, more established scientists.

“I was increasingly aware of how difficult it is for young scientist to get funding in their initial research activities, so I felt that there ought to be a novel way to do so by developing a new source of funding that will connect early career investigators in type 1 diabetes with donors who wanted to be more involved in the research,” Hayek tells us.

He connected with David Winkler, an attorney, real estate investor and VC entrepreneur who was diagnosed with type 1 diabetes at the age of six. Winkler shared his vision of more personalized research funding and the need to help support those early-career scientists who aren’t typically getting support from larger organizations and grant-giving sources. They also brought on fellow UCSD board members and renowned diabetes experts, Dr. Nigel Calcutt and Charles C. “C.C.” King, in those early days; these four now make up the board of directors.

“These four believe there can really be some innovative, breakthrough research from these early-career scientists, but we’re missing that opportunity because of how the funding model is setup,” says DRC executive director Christina Kalberg. “Funding for these younger scientists is scarce in recent years, and as a result they’ve been leaving the field. And that’s alarming. So what we’re trying to do is be innovative to help these early-career researchers who need to get themselves and their research out there for funding, to help them connect with people and get that exposure to hopefully unlock breakthroughs in diabetes.”

Their idea didn’t immediately materialize, though, and although the DRC received official non-profit status in 2012, it wasn’t until November 2014 that it finally launched online. That was a soft-launch, the leaders say, and they are planning a “hard-launch” with more national publicity in late May or early June of 2015 — just in time for the big ADA Scientific Sessions in Boston this year, where the diabetes world sets its sights on diabetes science.

The Connection’s Crowdfunding Model

As of now, the projects listed fall under four categories: Cure, Care, Complications, and Prevention.

Kalberg says the organization would certainly welcome diabetes technology research that would fit into the “care” category, but as of now they haven’t received any projects along those lines, and most fall under the “cure” or “prevention” monikers. A total of five projects (other than the DRC itself) have been submitted, with $120,000 raised so far in total. One project based at the University of Florida studying the autoimmune attack behind T1D has already completely funded at $50,000, the maximum level allowed for the three months a campaign is active online.

The overall goal is to fund at least 10 projects a year, to the tune of $500,000 donated annually.

If a particular project doesn’t get sufficient funding to move ahead, donors can choose to have the money they already donated either be returned to them, or reallocated within the same crowdfunding category to support other projects.

Once a project is funded and the study begins, the scientists send out ongoing updates to donors and answer questions, to give insight into what the money is actually paying for.

“This is very different from what’s out there — we want people to connect with the researchers, to know if research is a success or failure, and what the stumbling blocks may be. We are trying to personalize the research, and want to make this a transparent and very visible process,” Kalberg says.

A Double Peer-Review Process

But, hey: Can we really trust these crowdfunded research projects?

Yes, we’re told, because what’s also unique about DRC is that it has a very large and respected scientific review committee, made up of more than 80 D-experts from across the country and globe. Those individuals review the submitted proposals and decide if they have merit, and then vote on them before sending to the so-called layperson committee made up of patient advocates to “translate” the science-heavy explanations into something that regular folk can better understand.

Current Diabetes Research Projects

A big advantage of this DRC model is that this peer-based scientific review takes just roughly 12 weeks, compared to the six months or a year it can take through bigger organizations and funding mechanisms. Of course, scientists who go through this DRC application and review process can also go on to leverage results from crowdfunded studies to submit applications for larger grants from the ADA, JDRF, and NIH if they choose.

We connected with D-Mom Amy Adams in Chicago, who’s part of the DRC layperson review committee and has a 28-year-old son Matt, diagnosed at age 5. She tells us she had reached out to Dr. Hayek many years ago and they became friends, so the DRC founders in turn reached out to her a couple of years ago to get involved based on that relationship as well as Amy’s long history supporting the JDRF on a national and local level.

“I’ve given my time to other diabetes and non-diabetes organizations in the past, and still do, and while I appreciate them all, I see how the money I’m giving for research is going to party planning and other things that aren’t research,” she said. “This is the first organization where I feel like I am in control and can make the most difference.”

For Adams, a huge advantage of the DRC model is that research results are shared within and beyond the scientific community regardless of whether a project is funded or succeeds.

“The proprietary way of thinking about disease research is outdated, and all the secrecy is limiting our progress,” she said. “I feel strongly that we need to change our focus, to one in which researchers are rewarded for sharing their work.”

Very interesting idea, one that will surely catch on, given many folks’ reservations about donating and then rarely being able to see any tangible impact from our hard-earned dollars. We’re interesting to see the community’s reaction when DRC re-launches just prior to the ADA Scientific Sessions in June. Meanwhile, more and more people will learn the details of this crowdfunding channel from events like the Children with Diabetes Focus on Technology forum in Anaheim, CA, in September.

Hopefully, this does make a difference and inspires more established funding entities to think outside the box and recognize the importance of early-career scientists, as well as the interactive updates we donors really want to see. How great to have a channel to watch our money at work in the research lab!


Click here to read the originally published article on Healthline

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Role of the integrated stress response in type 1 diabetes pathogenesis
In individuals with type 1 diabetes (T1D), the insulin-producing beta cells are spontaneously destroyed by their own immune system. The trigger that provokes the immune system to destroy the beta cells is unknown. However, accumulating evidence suggest that signals are perhaps first sent out by the stressed beta cells that eventually attracts the immune cells. Stressed cells adapt different stress mitigation systems as an adaptive response. However, when these adaptive responses go awry, it results in cell death. One of the stress response mechanisms, namely the integrated stress response (ISR) is activated under a variety of stressful stimuli to promote cell survival. However, when ISR is chronically activated, it can be damaging to the cells and can lead to cell death. The role of the ISR in the context of T1D is unknown. Therefore, in this DRC funded study, we propose to study the ISR in the beta cells to determine its role in propagating T1D.
Wearable Skin Fluorescence Imaging Patch for the Detection of Blood Glucose Level on an Engineered Skin Platform
A Potential Second Cure for T1D by Re-Educating the Patient’s Immune System
L Ferreira
Validating the Hypothesis to Cure T1D by Eliminating the Rejection of Cells From Another Person by Farming Beta Cells From a Patient’s Own Stem Cells
Han Zhu
Taming a Particularly Lethal Category of Cells May Reduce/Eliminate the Onset of T1D
JRDwyer 2022 Lab 1
Can the Inhibition of One Specific Body Gene Prevent Type 1 Diabetes?
Is Cholesterol Exacerbating T1D by Reducing the Functionality and Regeneration Ability of Residual Beta Cells?
Regeneration Ability of Residual Beta Cells
A Call to Question… Is T1D Caused by Dysfunctionality of Two Pancreatic Cells (β and α)?
Xin Tong
Novel therapy initiative with potential path to preventing T1D by targeting TWO components of T1D development (autoimmune response and beta-cell survival)
flavia pecanha