In a recent paper in Nature Neuroscience, two researchers at the Scripps Research Institute in Florida report that obese rats with extended access to what they deemed “palatable food” — bacon, sausage, cheesecake, pound cake, frosting and chocolate — exhibited compulsive like eating behavior, much like rats with extended access to cocaine or heroin . This compulsive eating meant that they continued eating despite negative ramifications, in this case a flash of light signaling an oncoming electric shock administered to their foot. This lack of control over behavior with known negative consequences is a hallmark of both drug addiction and obesity. The investigators found that just like drug addicted rats, these obese rats had fewer striatal (a region of the forebrain) dopamine D2 receptors; this is responsible for the observed dampening of their neural reward responses to the food, which caused them to continue to eat, seeking that elusive high.
Although the root cause(s) of stuttering remain unknown, evidence has accumulated from twin and adoption studies that genetics plays a role. Dennis Drayna, a geneticist at the National Institute on Deafness and other Communication Disorders (NIDCD), undertook a study to identify the genes involved in the disorder with the ultimate goal to elucidate poorly defined neural structures and functions regulating human speech. Results from the study were reported recently in the New England Journal of Medicine .
The study focused on a Pakistani family in whom previous work had determined that stuttering was linked to the long arm of chromosome 12 (chromosome 12q). In addition to the affected and unaffected members of these families, the study also included 123 Pakistani stutterers who were unrelated and 270 stutterers from the United States and England. Children under the age of eight were excluded, as they often recover from stuttering, as were people with neurologic or psychiatric symptoms. The control group (non-stutterers) consisted of 96 Pakistanis and 276 North American whites.
The gene Granulocyte-Macrophage Colony Stimulating Factor (GM-CSF) encodes a cytokine, a signaling molecule secreted by immune cells that has an effect on other cells and is involved in inflammation. A recent report in Cell Host and Microbe reveals that in the gut, GM-CSF helps protect against infection by a bacterial pathogen .
GM-CSF has long been known to promote the survival and differentiation of dendritic cells, immune cells that are present in small quantities in tissues that are in contact with the external environment, including the skin and the inner lining of the nose, lungs, stomach and intestines. Dendritic cells are immune modulators that originate in the bone marrow and travel through the blood and lymph to the peripheral tissues in an immature state. Once they arrive, they differentiate and function as professional “antigen presenting cells”: they alert T cells and B cells to the presence of any foreign invaders. The T and B cells then mount an immune response.
Personalized Medicine Approach Provides More Benefit for Patients with High Cholesterol than Current Guidelines
Statins are a class of drugs that lower cholesterol and thereby reduce the risk of heart disease and stroke. They work by preventing the synthesis of low-density lipoprotein (LDL or “bad cholesterol”) in the liver and promoting its clearance from the blood. They are the most effective cholesterol-lowering drugs currently available and are the cornerstone of the National Heart, Lung, and Blood Institute’s National Cholesterol Education Program (NCEP) treatment guidelines.
The NCEP recommends a “treat-to-target” strategy, in which patients are given specific statin doses to achieve a desired level of LDL cholesterol in the blood. In this case, low LDL cholesterol is the “target.” Yet some physicians are questioning whether treating to any target is the best approach to fighting disease. A recent study in the Annals of Internal Medicine suggests that “tailored treatment”, an approach attempts to practice personalized medicine by estimating three factors, is more effective than a treat-to-target strategy .
A new study published in The American Journal of Medicine highlights another reason not to light up that cigarette — smokers (current and former) are more likely to suffer from low back pain than people who have never smoked . Although the association is moderate, it is strongest for chronic back pain and for adolescents.
By now, the vast majority of us know that smoking is bad for you. A number of health risks are associated with smoking. Indeed, many women are not aware that smoking is a risk factor for breast cancer . However, there are other conditions associated with smoking besides the key conditions of cancer and heart disease. Previous research has looked at the link between the experience of low back pain and the potential risk factor of smoking [3-6]. The experience of back pain is widespread . “Chronic” back pain is often of particular interest as it is associated with days lost from work and healthcare costs, in addition to the impact on the patient’s quality of life. In the UK, “persistent” back pain is that which has lasted more than 6 weeks . In the US, “chronic” back pain is pain lasting more than 3 months . The causes of back pain are often complex and unclear. In the present study, the association between back pain and smoking was assessed.