Microbes are everywhere and we are host to trillions -- many of them in our gut. These experiments illustrate how gut bacteria transplanted from mice that had received gastric bypass helped other mice lose weight too. Below is a summary of the research:

Obese people considering gastric bypass surgery to help trim their fat might one day have another option: swallowing a new supply of gut bacteria. A study in mice suggests that weight loss after bypass surgery is caused not by the operation itself, but at least in part by a change in the amounts of various species of microbes in the gut. A bypass operation separates off a small part of the stomach and connects that directly to the intestines. Recipients tend to feel less hungry, fill up more quickly and burn more calories at rest, and they often lose up to 75% of their excess fat. Counter-intuitively, this is thought to be caused by a change in metabolism, rather than by the reduced size of the stomach. Gut microbes are thought to be part of this picture. People who have had bypasses are known to experience changes in the selection of microbes in their guts. Fat people have been shown to host a different selection of gut bacteria from people who are obese, and transferring the gut bacteria of fat mice into thin ones can cause the thin mice to pack on extra weight. But no one knew whether the microbes in bypass patients changed because they got thin, or if the patients got thin because the microbes changed. To investigate, Lee Kaplan, director of the Obesity, Metabolism and Nutrition Institute at Massachusetts General Hospital in Boston, and his colleagues gave about a dozen obese mice bypass surgery. As expected, the mice lost about 29% of their body weight, and kept it off despite a high-fat diet. New conditions in their bodies — such as a change in bile acids — allowed a different set of gut bacteria to thrive. The results are promising for obesity treatments, but there are still hurdles to overcome. “You can’t just take a pill of the right bacteria and have them stick around,” says Seeley. If the gut’s environmental conditions don’t change, then the original microbes come back, he says. Kaplan says that the next steps are to isolate the four bacteria types that the study found to be at play and introduce them into obese mice or people. Antibiotic treatments might help the new bacteria to stick. “I believe it’s possible,” says Kaplan.

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Circular RNAs can act like molecular 'sponges' binding to and blocking tiny gene modulators called microRNAs. These circular RNA molecules comprise "a hidden parallel universe" of unexplored RNAs that control gene expression. Typical RNA-sequencing methods did not detect this molecules unless they had a molecular 'tail'.

Erik Sontheimer, a molecular biologist at Northwestern University in Evanston, Illinois said: “It’s yet another terrific example of an important RNA that has flown under the radar,” you just wonder when these surprises are going to stop.” Previous accounts of circular RNAs in plants and animals were generally dismissed as genetic accidents or experimental artefacts. Nikolaus Rajewsky, the lead author of one of the studies and a systems biologist at the Max Delbrück Center for Molecular Medicine in Berlin focused on a circular behemoth, some 1,500 nucleotides around, that is expressed in the brains of mice and humans. They found that it contains about 70 binding sites for a microRNA that can block gene expression linked to cancer and Parkinson’s disease.

Circular RNAs could also be sponges for microRNA from outside the cell, notes Rajewsky. Some have possible binding sites for viral microRNAs, which can subvert immune responses. He hypothesizes that circular RNA could even interact with RNA-binding proteins. “They are so abundant, there are probably a multitude of functional roles.”

This discovery goes further to illustrate that life is such a rich tapestry of interconnecting elements that it truly challenges our ability to fathom its complexity.

Reference: Nature vol: 494, pg 415 (28 February, 2013)

Aubrey de Grey, a British researcher on aging, has drawn a roadmap of how we can defeat biological aging.

Normal metabolism leads to cell damage -- the goal of Gerontology is to prevent the damage before it happens. Geriatric medicine is about ameliorating the pathology of the damage.

The focus of damage control is on the long-lived molecules. Also there is possible control of genes by the FOXO protein -- the activation of the latent ability of the cell for self-repair.

Using a mouse model some of the targets for damage control have been successful.

For more here is Aubrey ...