1 gene lost = 1 limb regained? Scientists demonstrate mammalian regeneration through single gene deletion

From PhysOrg.com:

A quest that began over a decade ago with a chance observation has reached a milestone: the identification of a gene that may regulate regeneration in mammals. The absence of this single gene, called p21, confers a healing potential in mice long thought to have been lost through evolution and reserved for creatures like flatworms, sponges, and some species of salamander. In a report published today in the Proceedings of the National Academy of Sciences, researchers from The Wistar Institute demonstrate that mice that lack the p21 gene gain the ability to regenerate lost or damaged tissue.

Full article

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First automated carbohydrate 'assembly line' opens door to new field of medicine

From PhysOrg.com:

Scientists from Germany today reported a major advance toward opening the doors of a carbohydrate-based medicine chest for the 21st Century. Much more than just potatoes and pasta, these carbohydrates may form the basis of revolutionary new vaccines and drugs to battle malaria, HIV, and a bevy of other diseases.

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U.S. military researchers grow new limbs, organs

From OttowaCitizen.com:

American military researchers say they have unlocked the secret to regrowing limbs and recreating organs in humans who have sustained major injuries.

Using "nanoscaffolding," the researchers have regrown a man's fingertip and the internal organs of several test subjects.

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Aussies crack cancer secret

Aussies crack cancer secret (from the Daily Telegraph):

AUSTRALIAN scientists are hoping to cure leukaemia, asthma and rheumatoid arthritis after their breakthrough discovery of how to stop killer blood cells growing.

The team has unlocked the secrets behind the protein which controls the way the blood cancer cells spread when it is damaged - and have found a way to stop its deadly process.

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Waistline Growth On High-carb Diets Linked To Liver Gene

From the Science Daily article "Waistline Growth On High-carb Diets Linked To Liver Gene":

Experts have been warning for years that foods loaded with high-fructose corn syrup and other processed carbohydrates are making us fatter. Now, a University of Wisconsin-Madison study has uncovered the genetic basis for why this is so.

Basically, a gene in liver cells (named "SCD-1") produces the enzyme SCD, which synthesizes fatty acids (a major component of fat.) When the SCD-1 gene is present and active, so that the SCD enzyme is produced in liver cells, the SCD enzyne converts any excess carbohydrates into fatty acids, which end up stored as fat by fat cells.

To get and/or stay thin, you have to avoid carbohydrates. Eat protein and fat instead. Instead of "you are what you eat," it's "you are what your body does with what you eat."

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Low-carb Diet Reduces Inflammation And Blood Saturated Fat In Metabolic Syndrome

According to the Science Daily article "Low-carb Diet Reduces Inflammation And Blood Saturated Fat In Metabolic Syndrome," a low-carbohydrate diet is much more effective than is a low-fat diet at reducing both inflammation and blood-levels of saturated fatty acids for people who suffer from metabolic syndrome.

The facts are that:

• A low-carb diet lowers blood levels of triglycerides much more effectively then does a low-fat diet
• Even when one's diet is low in fat, carbohydrate-induced lipogenesis caused by a high-carbohydrate diet (which cannot be avoided if one's diet is low in fat) more than overrides the low fat content of the diet
• Carbohydrates stimulate insulin secretion which biases fat metabolism towards storage rather than oxidation

The above facts are the reason why a low-carb diet, such as the Atkins Diet, not only works for losing weight, but is healthier than a low fat diet. It also explains why the idea that dietary cholesterol is a significant cause of heart disease is nothing but a myth.

If you suffer from either metabolic syndrome, or are overweight, then sugar and flour are deadly poisons. They will kill you at a relatively early age.

Link to full article

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Scientists transform human skin cells into stem cells

Scientists transform human skin cells into stem cells from PhysOrg.com

Two groups of scientists have successfully transformed human skin cells into stem cells, potentially granting unlimited access to the foundation cells which can replace diseased or damaged tissues and organs, it was announced Tuesday.

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Mass Spectrometry of Living Subjects

Mass Spectrometry of Living Subjects from PhysOrg.com

In science fiction movies, it happens all the time: A small device is briefly held against the skin of a sick crewmember and seconds later the monitor displays what ails him. This futuristic image could someday be real.

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Insulin Resistance: The Problem May Be "Bone Deep"

According the the article Skeletal Discovery: Bone cells affect metabolism:

If your blood glucose is out of whack, the problem may be in your bones. New research in mice shows that bone cells exert a surprising influence on how the body regulates sugar, energy, and fat.

The discovery could lead to new ways to treat type 2 diabetes, a disease involving poor regulation of blood glucose. It also means that skeletons act as endocrine organs, which affect other body tissues by releasing hormones into the bloodstream.
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"This could also have important ramifications for cardiovascular disease because of the effect on metabolic syndrome," a condition related to diabetes, comments Dana T. Graves of Boston University. "The fact that bone cells regulate energy metabolism, and that they do it through osteocalcin, is a major finding," he says.

Full Article

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Drug Protects Against Diabetes And Atherosclerosis In Mice

From Science Daily:

Blocking a single protein with an experimental drug prevented and treated both type 2 diabetes and atherosclerosis in laboratory mice that had been fed unhealthy diets and were genetically predisposed to these common killers, according to an article published online at Nature on June 6, 2007.
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In one experiment, mice genetically engineered to be highly susceptible to atherosclerosis were fed high-fat diets and assigned to receive the drug or an inert substance. One set of mice was put on a high-fat “western” diet at five weeks of age; half received the inhibitor drug. A second group of animals ate the western diet for eight weeks, at which time they developed severe atherosclerosis. Then they were started on the drug to determine whether the drug could halt or reverse the disease process.

In both experiments, the drug treatment reduced the size of fatty plaques in the animals’ aortas by more than 50 percent compared to control mice.

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Common genetic variation is linked to substantial risk for heart attack

Researchers at the Icelandic genomics company deCODE Genetics, along with U.S. researchers at Emory University School of Medicine, Duke University, and the University of Pennsylvania, published an article in Science today announcing the discovery of a common genetic variation on the 9p21 chromosomal region that significantly raises the risk of developing heart disease independent of other recognized risk factors, such as weight, diet or cholesterol levels.

The stretch of DNA (called 9p21) that carries the mutation is in an area of the chromosome that had not previously been identified as a gene. The 9p21 region is not associated with inherited tendencies to have high cholesterol or high blood pressure. But 9p21 is found near two genes called CDKN2A and CDKN2B, which four international teams of researchers last week reported they had identified in their own genome-wide association study looking for genetic causes of diabetes.

The researchers found that, were the gene variant not present, there would be 21 percent fewer heart attacks overall in the population and 31 percent fewer early onset heart attacks.

The medical establishment is slowly coming to the realization that cholesterol does not cause heart disease. Inflammation causes heart disease (which is why statin drugs prevent heart attacks: because they inhibit arterial inflammation.) And lots of things cause inflammation (such as homecysteine.) Perhaps the mutation in the 9p21 chromosomal region either causes inflammation, or makes an individual more susceptible to inflammation-induced arterial blockage.

References:

[1] Common genetic variation is linked to substantial risk for heart attack | PhysOrg.com

[2] DNA mutation causes heart disease in whites | Yahoo | Reuters

[3] The Cholesterol Myths

[4] Inflammation and atherosclerosis

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To Treat the Dead

In the article To Treat the Dead, Newsweek highlights the implications of research that shows that cells don't die after a mere 5 minutes without oxygen. Cells will continue to live for hours without oxygen. The reason that 5-minutes (approximately) of oxygen deprivation usually leads to cell death is that, after about 5 minutes, oxygen actually becomes toxic to the cells.

It's the reperfusion with oxygen-carrying blood that causes cell death, not the 5-minute lack of oxygen itself.

One implication is that it may be possible to develop drugs and/or treatment protocols that will allow the revival of heart attack, stroke or trauma patients after an hour or more without blood flow, instead of the current 5-minute limit. Another implication is that cryonic suspension is far more likely to work than most would have believed.

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Discovery of new family of pseudo-metallic chemicals

Discovery of new family of pseudo-metallic chemicals from PhysOrg.com

The periodic table of elements, all 111 of them, just got a little competition. A new discovery by a University of Missouri-Columbia research team, published in Angewandte Chemie allows scientists to manipulate a molecule discovered 50 years ago in such as way as to give the molecule metal-like properties, creating a new, "pseudo" element. The pseudo-metal properties can be adjusted for a wide range of uses and might change the way scientists think about attacking disease or even building electronics.

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Scientists make major breakthrough in regenerative medicine

Scientists make major breakthrough in regenerative medicine from PhysOrg.com

Findings described in a new study by Stanford scientists may be the first step toward a major revolution in human regenerative medicine—a future where advanced organ damage can be repaired by the body itself. In the May 2007 issue of The FASEB Journal, researchers show that a human evolutionary ancestor, the sea squirt, can correct abnormalities over a series of generations, suggesting that a similar regenerative process might be possible in people.

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