Scientists’ Findings May Lead to New Drug-abuse Treatments
Increased connections among brain cells caused by excessive drug use may represent the body’s defense mechanism to combat addiction and related behaviors, scientists at UT Southwestern Medical Center have found.
Previous studies have shown that repeated use of drugs such as cocaine, amphetamines and nicotine increase the number of anatomical structures called dendritic spines in brain regions associated with pleasure and reward. These dendritic spines represent sites where brain cells communicate with one another. Many scientists believe that this long-lasting brain rewiring underlies the similarly persistent behaviors of drug-taking and drug-seeking associated with addiction and relapse. The mechanism that controls this brain rewiring, however, and its relationship to addiction-related behaviors were previously unknown.
In a study appearing in the Aug. 28 issue of Neuron, researchers found that cocaine suppresses the activity of the protein MEF2 in mice. Because MEF2 normally reduces the number of brain connections, suppressing MEF2 leads to an increase in dendritic spine density. The researchers also found that when they enhanced MEF2 activity in the brain this blocked the drug-induced increase in dendritic spine density and increased addiction-related behavioral responses to cocaine.
New role for Natural Killers!
Scientists at the University of York have discovered a new role for a population of white blood cells, which may lead to improved treatments for chronic infections and cancer.
Natural Killer (or NK) cells are abundant white blood cells that were recognised over 30 years ago as being able to kill cancer cells in the test tube. Since that time, a role for NK cells in activating other white blood cells (including ‘T’ lymphocytes and phagocytes) and in directing how the immune system responds to a wide range of infections has also been established.
Because of these properties, NK have been widely regarded as being of benefit in the fight against cancer and infection, and methods to increase NK cell activity underpin a range of new experimental anti-cancer drugs and anti-infectives.
Heart attack patients who stop statin risk death, say McGill researchers
Patients discontinuing statin medication following an acute myocardial infarction (AMI) increase their risk of dying over the next year, say researchers at McGill University and the McGill University Health Centre (MUHC). Their study was published in a recent issue of the European Heart Journal.
Using data on British patients who survived an AMI and were still alive three months later, Dr. Stella Daskalopoulou and colleagues found that those who discontinued their statin medication were 88% more likely to die during the following year compared to those who had never been on the medication.
“Statins were found to be beneficial drugs,” said Dr. Daskalopoulou, of McGill’s Faculty of Medicine and the Department of Medicine and the Division of Clinical Epidemiology at the MUHC. “Patients who used statins before an AMI and continued to take them after were 16% less likely to die over the next year than those who never used them. So even if it appears that the statins failed to prevent your AMI, it is beneficial to continue taking them and potentially quite harmful to stop.”
Health risk behaviors associated with lower prostate specific antigen awareness
According to a study conducted at Columbia University Mailman School of Public Health, health risk behaviors such as smoking and obesity are associated with lower awareness of the Prostate Specific Antigen (PSA), which could lead to a lower likelihood of undergoing actual prostate cancer screening. Although previous studies have explored predictors of PSA test awareness, this is the first research to focus on health risk behaviors, such as smoking, physical inactivity, obesity, and excessive alcohol consumption. The study findings were reported in the August issue of The Journal of Urology.
Awareness of PSA testing is considered an important cognitive precursor of prostate cancer screening and it was found to contribute to differences in prostate cancer screening rates. Earlier studies have suggested that persons who seek out cancer information are more likely to acquire knowledge, demonstrate healthy behaviors, and undergo cancer screening. According to the Mailman School study, a quarter of the men older than 50 years without a history of prostate cancer who were among the population of 7,000 men studied, remain unaware of the PSA test.
“Our primary findings suggested that smoking, physical inactivity and obesity are inversely associated with awareness of the PSA test. These risk behaviors are linked with higher prostate cancer morbidity and mortality,” said Firas S. Ahmed, MD, MPH, Mailman School of Public Health, and first author. This finding may be due to a general lack of concern about health maintenance or less interactions with health care providers by smokers, according to Dr. Ahmed.
History of nonmelanoma skin cancer is associated with increased risk for subsequent malignancies
Individuals with a history of nonmelanoma skin cancer (NMSC) are at increased risk for other cancers, according to a study published in the August 26 online issue of the Journal of the National Cancer Institute.
Previous studies have documented that people who have had nonmelanoma skin cancer were at increased risk for developing melanoma, but it is less well-established whether they were also at risk for cancers that do not involve the skin.
In the current study, Anthony Alberg, Ph.D., of the Medical University of South Carolina and colleagues analyzed data from a prospective cohort study called CLUE II, which was established in Washington County, Md., in 1989. Alberg’s team compared the risk of malignancies in 769 individuals who had been diagnosed with nonmelanoma skin cancer and 18,405 individuals with no history of the disease during a 16-year follow-up period.
Chronic stress alters our genetic immune response
Most people would agree that stress increases your risk for illness and this is particularly true for severe long-term stresses, such as caring for a family member with a chronic medical illness. However, we still have a relatively limited understanding of exactly how stress contributes to the risk for illness. In the August 15th issue of Biological Psychiatry, researchers shed new light on one link between stress and illness by describing a mechanism through which stress alters immune function.
In a very promising preliminary study, Miller and colleagues found that the pattern of gene expression differed between caregivers of family members with cancer relative to a matched group of individuals who did not have this type of life stress. They found that among the caregivers, even though they had normal cortisol levels in their blood, the pattern of gene expression in the monocytes, a type of white blood cell involved in the body’s immune response, was altered so that they were relatively less responsive to the anti-inflammatory actions of cortisol, but relatively more responsive to pro-inflammatory actions of a transcription factor called nuclear factor-kappa B, or NF-κB. Gregory Miller, Ph.D., corresponding author, explains more simply that, although “caregivers have similar cortisol levels as controls, their cells seem to be ‘hearing’ less of this signal. In other words, something goes awry in caregivers’ white blood cells so they are not able to ‘receive’ the signal from cortisol that tells them to shut down inflammation.”
Thus, the current findings might help to explain why the caregivers would seem to be in a chronic pro-inflammatory state, a condition of immunologic activation. This activated state could contribute to the risk for a number of medical illnesses, such as depression, heart disease, and diabetes. Dr. Miller remarks that part of the importance of these findings is “because people have traditionally thought that higher cortisol is the reason that stress contributes to disease, but this work shows that, at least in caregivers, it’s actually the opposite - there’s too little cortisol signal being heard by the cells, rather than too much.”
