Heart disease hits people with diabetes twice as often as people without diabetes. In those with diabetes, cardiovascular complications occur at an earlier age and often result in premature death, making heart disease the major killer of diabetic people. But why is heart disease so prevalent among diabetics?

To help answer that question, researchers at Washington University School of Medicine in St. Louis have been analyzing the fat (lipid) composition of heart tissue from laboratory mice with diabetes. They have found that heart cells of diabetic mice lose an important lipid from cellular components that generate energy for the heart, and their latest research shows this happens at the very earliest stages of diabetes.

Alcohol and smoking can be harmful, if not deadly. While the desire for these substances can be due to environmental cues, genomic factors also play an important role. The etiology of these desires is multifactorial and a result of complex interactions with the environment. Adoption and twin studies have shown that the use of these substances is likely to be inherited. Such studies have provided evidence that one’s sex can influence the genetic factors for alcohol and tobacco use.

In an attempt to find the genomic determinants underlying alcohol and tobacco use, researchers examined 120 families (approximately 900 individuals). The researchers identified an area relating to alcohol and tobacco use on chromosome 1. They found another area relating to alcohol on chromosome 3.

More than a mile beneath the Atlantic’s surface, roughly halfway between New York and Portugal, seawater rushing through the narrow gullies of an underwater mountain range much as winds gust between a city’s tall buildings is generating one of the most turbulent areas ever observed in the deep ocean.

In fact, the turbulence packs an energy wallop equal to about five million watts -- comparable to output from a small nuclear reactor, according to a landmark study led by Florida State University researcher Louis St. Laurent.

The study -- an international collaboration of scientists from the United States and France -- documents for the first time the turbulent conditions in an undersea mountain range known as the Mid-Atlantic Ridge.

When molecular disaster strikes, causing structural damage to DNA, players in two important pathways talk to each other to help contain the wreckage, scientists at The University of Texas M. D. Anderson Cancer Center report in the August edition of Cell.

This connection between a signaling pathway crucial to DNA damage control and a pathway known as chromatin remodeling "opens an entirely new category of targets for potentially attacking cancer," says senior author Xuetong "Snow" Shen, Ph.D., an assistant professor in M. D. Anderson's Department of Carcinogenesis at the Science Park - Research Division in Smithville, Texas.

In a study published in the August 17 issue of the Journal of Biological Chemistry, Amanda J. Law, Associate Professor at the University of Oxford and colleagues at NIH describe for the first time a genetic variation that causes a gene to be overexpressed in the human brain. These results may provide a new way to design better drugs to treat schizophrenia.

“Although the exact causes of schizophrenia are yet to be determined, scientists agree that the disease is in part due to genetic variations,” Law says. “These variations are not simple to understand because they don’t directly disturb the function of proteins.

Scientists have discovered that leptin, one of the key hormones responsible for reducing hunger and increasing the feeling of fullness, also controls our fondness for food.

A University of Cambridge team, headed by Dr Sadaf Farooqi and Dr Paul Fletcher, have discovered that the appetising properties of food have strong effects on the same key brain regions responsible for rewarding emotions and desires. Using brain imaging technology, they show that these areas of the brain “light up” when individuals deficient in leptin are shown images of food.

Hunger influences what and how much we eat, but is not the only determinant of our eating behaviour.