Health & Wellness
Because our knowledge of the mind's afflictions remains so limited, psychologists - even when writing in academic publications - still deploy metaphors to understand difficult disorders. And possibly the most difficult of all to fathom - and thus one of the most creatively named - is the mysterious-sounding borderline personality disorder (BPD). University of Washington psychologist Marsha Linehan, one of the world's leading experts on BPD, describes it this way: "Borderline individuals are the psychological equivalent of third-degree-burn patients. They simply have, so to speak, no emotional skin. Even the slightest touch or movement can create immense suffering."

Imaging techniques help scientists look at the basis for principles of social psychology in the brain.
Decades of research show people tend to go along with the majority view, even if that view is objectively incorrect. Now, scientists are supporting those theories with brain images.
A new study in the journal Neuron shows when people hold an opinion differing from others in a group, their brains produce an error signal. A zone of the brain popularly called the "oops area" becomes extra active, while the "reward area" slows down, making us think we are too different.
In the worst cases, an age-related delay in healing keeps the two sides of a fractured bone from ever rejoining (non-union), leaving many confined to wheelchairs, unable to walk or to live independently. Of the estimated 5.6 million fractures in the United States each year, between five and ten percent (up to 560,000) will heal slowly or incompletely. Researchers have known for 30 years that aging interferes with fracture healing, and have been filling in the details since on the complex web of biochemicals, stem cells and genes that bring about healing. The field is now reaching the point where precision designed drugs are in different stages of animal and human trials.
The current study is focused on cyclooxygenase 2 (COX-2), an enzyme known from past studies to drive stem cells to differentiate into cartilage, which then matures into bone. Researchers at the University of Rochester Medical Center 20 years ago discovered the gene in humans that is responsible for producing the COX-2 enzyme and revealed the enzyme's role in causing inflammation, the reason drugs like the painkiller Vioxx were developed to shut down its action. Then about seven years ago another research team here determined that COX-2 also plays an essential role in bone formation during skeletal repair.
In 2002, a group of scientists at the University of Toronto was able to identify a gene which they dubbed DREAM (downstream regulatory element antagonistic modulator). The gene's function was highly interesting: it obviously served as a key regulator in the perception of pain. Mice who lacked the gene showed clear signs of markedly reduced sensitivity to all kinds of pain, whether chronic or acute. Otherwise, the mice appeared perfectly normal.
The work leading to these findings was carried out in the lab of Josef Penninger, then principal investigator at the Amgen Institute in Toronto. The publication describing the gene's function was received with great interest (Cell, Vol. 108, 31-43, 11.1.2002) and DREAM was subsequently termed the "Master-Gene of pain perception".
Why be miserable? OK, so it's January and you're feeling fat and broke after the excesses of the holiday season, but there's really no need. Misery is inconvenient, unpleasant, and in a society where personal happiness is prized above all else, there is little tolerance for wallowing in despair. Especially now we've got drugs for it.
Antidepressants can help banish sad feelings - not just the life-sapping black dog of clinical depression, but the rough patches that most people go through sometimes, whether it's after losing a job, the break-up of a relationship or the death of a loved one. So it's no surprise that more and more people are taking them.
But is this really such a good idea? A growing number of cautionary voices from the world of mental health research are saying it isn't. They fear that the increasing tendency to treat normal sadness as if it were a disease is playing fast and loose with a crucial part of our biology. Sadness, they argue, serves an evolutionary purpose - and if we lose it, we lose out.
"When you find something this deeply in us biologically, you presume that it was selected because it had some advantage, otherwise we wouldn't have been burdened with it," says Jerome Wakefield, a clinical social worker at New York University and co-author of The Loss of Sadness: How psychiatry transformed normal sorrow into depressive disorder (with Allan Horwitz, Oxford University Press, 2007). "We're fooling around with part of our biological make-up."

Expression of a small fragment of p115 (green) leads to Cytochrome C (red) release in cells causing cell death.
In response to stress or as a natural part of aging, many cells undergo programmed suicide, also known as apoptosis. Cancer cells often become immortal and dangerous by developing the ability to suppress apoptosis.
A decade ago apoptosis was thought to be directed solely by the nucleus and mitochondria of cells. Dr. Shields' laboratory was the first to show that a cellular organelle known as the Golgi apparatus also plays a role in apoptosis.
The finding is the latest in a succession of recent reports contradicting the long-held assumption that the new drugs, which include Risperdal, Zyprexa and Seroquel, are safer than the older and much less expensive medications that they replaced.
The risk of death from the drugs is not high, on average about 3 percent in a person being treated at least 10 years, according to the study, published today in The New England Journal of Medicine. Nor was the risk different from that of the older antipsychotic drugs.
Graffiti was not the only misdemeanor that fostered a cavalier attitude toward theft. When the ground near the mailbox was covered in litter, 25 percent of the subjects stole the envelope. These results are significant for both social and statistical reasons. Is a disorderly environment responsible for disorderly conduct?
Surprising new research by University of Calgary, Faculty of Kinesiology researcher Dr. Raylene Reimer, published in an international journal, indicates a direct connection between an adult's propensity to put on weight and our early childhood diet.
Reimer is a leader in a growing field of study that examines the developmental origins of health and disease. Researchers in this area believe our pre-natal and early childhood environment influences our future risk of developing conditions like cardio vascular disease, obesity and diabetes.
Many studies have demonstrated the profound effect of group opinion on individual judgments, and there is no doubt that we look to the behavior and judgment of others for information about what will be considered expected and acceptable behavior.
"We often change our decisions and judgments to conform with normative group behavior," says lead study author Dr. Vasily Klucharev from the F.C. Donders Center for Cognitive Neuroimaging in The Netherlands. "However, the neural mechanisms of social conformity remain unclear."







