NASA has lost the tapes of the Moon landing. All of the Moon landings.
And in better news:
Cure For Diabetes: Researchers permanently reverse diabetes in mice.
By Dave Mosher
April 24, 2006 | Medicine
Since the first insulin injection in 1922, a long-term cure for type 1 (insulin-dependent) diabetes has been a number-one priority among researchers. It may soon be reality, thanks to a collaboration of investigators at the La Jolla Institute for Allergy and Immunology in San Diego, according to a study published April 20 in the Journal of Clinical Investigation.
Dr. Matthias von Herrath says his team combined short-term therapies for type 1 diabetes and cured around half of the mice used in the study.
In a type 1 diabetic, symptoms begin to appear when the body loses roughly 80 percent of its beta cells - the pancreatic tissue responsible for producing insulin and enabling the body to use glucose for energy. The culprit of the disease is a diabetic's own immune system, specifically T cells known as CD4+ and CD8+. Like a tag-team, the CD4+ T cells detect a threat and then instruct CD8+ T cells to launch an attack. For reasons still not fully understood, these cells can become aggressive toward beta cells.
Curing type 1 diabetes, von Herrath says, requires blocking the activity of aggressive T cells with their counterparts: Regulatory T cells, or Tregs. "As long as they're around, they're endogenous peacekeeping machines," von Herrath says.
Previous researchers, von Herrath says, used human proinsulin to stimulate pancreatic Treg production. In a specific way, these Tregs protect beta cells by suppressing aggressive T cells that attack pancreatic tissue.
"Tregs can somehow talk to the aggressive cells and say 'you have to stop destroying beta cells because they're good for the body,'" says Damien Bresson, another member of the research team. But simply boosting their numbers does not reverse type 1 diabetes in the long run.
Two clinical studies published in 2005 show vaccination with anti-CD3 antibodies, which suppresses the immune system, is the most effective way to combat the disease. "The cool thing is that (anti-CD3) treatment … halts beta cell destruction not only in mice, but also in humans," von Herrath says.
According to the studies, 10 days of anti-CD3 treatment slowed beta cell destruction in humans for 18 months, but not without side effects such as "fever, nausea, and muscle aches, much like you have the flu," von Herrath says. And reversal is not permanent.
Experimenting with a more long-term treatment, von Herrath's team combined anti-CD3 with the vaccination and observed something exciting: Beta cells began to regenerate and permanently reverse type 1 diabetes in half of the mice - almost twice as much as using anti-CD3 alone. "Once we applied the therapy to diabetic mice, those that reversed stayed non-diabetic for the rest of their lives," von Herrath said.
One possible explanation for the effectiveness of the combined therapy, von Herrath says, is that an auto-destructive immune system tips in favor of saving beta cells instead of destroying them. Anti-CD3 suppresses aggressive T cells, creating a "window of opportunity" for the vaccine to boost pancreatic protection and permit beta cell regeneration. Because some beta cells are still destroyed in the process, antigens are continuously released, Treg production is maintained, and protection continues for the remainder of a mouse's two-year life.
and, while that might take a while to become a reality, this is far closer to fruition:
No More Nerve Damage: A new drug could reverse nerve damage in diabetics.
By Eva Gladek
May 26, 2006 | Medicine
Mark Kipnes, MD, from the Diabetes & Glandular Disease Research Clinic, is leading the first human testing of the diabetes nerve drug. Photo: ScienCentral
It could be the first treatment for a terrifying problem faced by people with diabetes – the nerve damage that's a leading cause of amputations. A new drug being tested in people with diabetic nerve damage uses a patient's own genes to treat them.
Diabetic neuropathy nerve damage, which causes a loss of sensation in the hands and feet, can allow small injuries to go unnoticed and become severely infected, to the point where amputation is the only option. Tight control of blood sugar can keep neuropathy at bay, but there is no cure.
"There are a variety of medications that are available now that can help with the pain but unfortunately, there's nothing available to help with numbness or prevention of nerve damage," says diabetes specialist Mark Kipnes, MD, director of the Diabetes and Glandular Disease Research Clinic in San Antonio, Texas.
But now Kipnes is leading the first human testing of a new drug that might prevent or even reverse such damage. Designed by researchers at Sangamo Biosciences, the drug uses a natural protein that turns on the patient's own gene for helping nerve growth. As the researchers wrote in the journal, "Diabetes," tests on diabetic rats showed that repeated treatments with the drug led to increasingly improved nerve function.
Sangamo biochemist Philip Gregory notes that this Phase 1 clinical trial is the first human test of an entirely new class of drug that could turn any gene on or off, depending on the disease. "These proteins are natural proteins that exist in essentially every human cell, there are thousands of them, they naturally regulate genes in cells," Gregory explains.
These gene-regulating proteins have an important feature called a zinc finger domain. The zinc finger region, whose structure was discovered by Nobel laureate Aaron Klug, is a finger-shaped structure containing a zinc atom. Unlike most proteins, those with these special domains can actually bind to DNA and act as transcription factors – telling specific genes to turn on or off.
"So what we're able to do is to engineer these proteins so that they can bind to different genes of our choice," says Gregory. In this case, the gene targeted by the Sangamo team was one encoding a protein called VEGF-A, a natural growth factor.
"In diabetes, patients have significant blood sugar changes that give rise to the production of toxic byproducts in tissues that drive, essentially, a poisoning of the nerves," says Gregory. He explains that because VEGF-A naturally stimulates regeneration of nerves and the blood vessels that nourish them, it can reverse the damage caused by the glucose-driven degeneration.
"It's not that diabetic patients lack the gene for VEGF-A," explains Gregory. "They continue to have the gene and they produce VEGF-A, but it's like the patient's cells don't realize they could be more protected or suffer from the disease much less if the cells produce more of this particular protective factor."
While patients in the Phase 1 trial tolerated the drug well it needs to be tested for longer time periods to prove its safety – particularly since this treatment would need repeated administration. As Gregory explains, "Obviously this is a chronic disease and we need to have a chronic treatment, if you like, for such a disease." More than half of the 185,000 amputations in the U.S. each year are a result of diabetes, a disease that plagues an estimated 20.8 million Americans -- seven percent of the population -- and is on the rise.
Kipnes is excited about the prospect of having a treatment to offer people with diabetic neuropathy, but he points out that there may be some risks. As he points out, injecting a growth factor into the body could theoretically encourage other, unwanted things to grow. "So these patients are very carefully screened for any kinds of cancers and tumors," he says.
The researchers report there's been no evidence of carcinogenesis in their extensive animal studies. They also say that some patients in the safety trial showed some anecdotal improvement in their nerve function.
Kipnes is currently recruiting patients for a second safety trial as well as a larger Phase 2 trial of the drug's effectiveness. Both are scheduled to begin later this year.
Both from Discover magazine.
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