Researchers at the Mayo Clinic say a common condition called leukoaraiosis, made up of tiny areas in the brain that have been deprived of oxygen and appear as bright white dots on MRI scans, is not a harmless part of the aging process, but rather a disease that alters brain function in the elderly. Results of their study are published online in the journal Radiology.
"There has been a lot of controversy over these commonly identified abnormalities on MRI scans and their clinical impact," said Kirk M. Welker, M.D., assistant professor of radiology in the College of Medicine at Mayo Clinic in Rochester, Minn. "In the past, leukoaraiosis has been considered a benign part of the aging process, like gray hair and wrinkles."
Leukoaraiosis, also called small vessel ischemia and often referred to as unidentified bright objects or "UBOs" on brain scans, is a condition in which diseased blood vessels lead to small areas of damage in the white matter of the brain. The lesions are common in the brains of people over the age of 60, although the amount of disease varies among individuals.
"We know that aging is a risk factor for leukoaraiosis, and we suspect that high blood pressure may also play a role," Dr. Welker said.
Dr. Welker's team performed functional MRI (fMRI) scans on cognitively normal elderly participants recruited from the Mayo Clinic Study of Aging between 2006 and 2010. In 18 participants, the amount of leukoaraiosis was a moderate 25 milliliters, and in 18 age-matched control participants, the amount of disease was less than five milliliters.
© Gary MeekResearch led by Manu Platt, an assistant professor in the Wallace H. Coulter Department of Biomedical Engineering at Georgia Tech and Emory University, has shown for the first time that members of the cathepsin family of proteases can attack one another -- instead of the protein substrates they normally degrade.
Researchers for the first time have shown that members of a family of enzymes known as cathepsins -- which are implicated in many disease processes -- may attack one another instead of the bodily proteins they normally degrade. Dubbed "cathepsin cannibalism," the phenomenon may help explain problems with drugs that have been developed to inhibit the effects of these powerful proteases.
Cathepsins are involved in disease processes as varied as cancer metastasis, atherosclerosis, cardiovascular disease, osteoporosis and arthritis. Because cathepsins have harmful effects on critical proteins such as collagen and elastin, pharmaceutical companies have been developing drugs to inhibit activity of the enzymes, but so far these compounds have had too many side effects to be useful and have failed clinical trials.
Using a combination of modeling and experiments, researchers from the Georgia Institute of Technology and Emory University have shown that one type of cathepsin preferentially attacks another, reducing the enzyme's degradation of collagen. The work could affect not only the development of drugs to inhibit cathepsin activity, but could also lead to a better understanding of how the enzymes work together.
An international team of scientists led by researchers at Mount Sinai School Medicine have discovered that a drug that had previously yielded conflicting results in clinical trials for Alzheimer's disease effectively stopped the progression of memory deterioration and brain pathology in mouse models of early stage Alzheimer's disease.
The findings, published July 31, 2012 in Molecular Psychiatry, demonstrate renewed potential for this compound and could lead to clinical trials in patients with early stages of the disease.
Latrepirdine, known commercially as Dimebon, was initially sold as an antihistamine in Russia, approved for use there in 1983. In the 1990s, researchers at the Institute of Physiologically Active Compounds in Moscow determined that the compound appeared effective in treating Alzheimer's disease in animals. They continued their research in humans and performed several studies, including Phase I and II trials, all of which showed significant and sustained improvement in cognitive behavior with minimal side effects. The Phase II trials, performed in Russia, were overseen by U.S. Alzheimer's researchers, including Mary Sano, PhD, Director of the Mount Sinai Alzheimer's Disease Research Center.
A popular class of diabetes drugs increases patients' risk of bladder cancer, according to a new study published online this month in the Journal of the National Cancer Institute. Researchers from the Perelman School of Medicine at the University of Pennsylvania found that patients taking thiazolidinedione (TZDs) drugs -- which account for up to 20 percent of the drugs prescribed to diabetics in the United States -- are two to three times more likely to develop bladder cancer than those who took a sulfonylurea drug, another common class of medications for diabetes.
The authors say the findings are especially important since diabetic patients are known to already be at a slightly increased risk of this type of cancer as compared to the generation population, in which about 30 in 100,000 people develop bladder cancer. Among diabetes patients overall, the incidence of this cancer is typically about 40 out of 100,000.
The authors of the new study analyzed 60,000 Type 2 diabetes patients from the Health Improvement Network (THIN) database in the United Kingdom. They found that patients treated with the TZD drugs pioglitazone (Actos) or rosiglitzaone (Avandia) for five or more years had a two-to-three-fold increase in risk of developing bladder cancer when compared to those who took sulfonylurea drugs. Among patients taking TZDs for that length of time, the team's analysis indicates that 170 patients per 100,000 would be expected to develop the disease. About 60 in 100,000 of those who take sulfonylurea drugs -- such as glipizide (Glucotrol) -- would be expected to develop bladder cancer.
The commonly used broad-spectrum antibiotics moxifloxacin and levofloxacin are associated with an increased risk of severe liver injury in older people, according to a new study published in CMAJ (Canadian Medical Association Journal).
Moxifloxacin and levofloxacin are commonly prescribed "fluoroquinolone" antibiotics often used for bacterial infections such as respiratory infections, sinus infections and others. However, both the European Medicines Agency and Health Canada have issued warnings about the risk of liver injury from moxifloxacin, although there are few published studies on the safety of fluoroquinolones, especially related to liver damage.
Researchers from the Institute for Clinical Evaluative Sciences (ICES), Toronto; the University of Toronto and McMaster University, Hamilton, Ont., examined the risk of acute liver injury in patients taking moxifloxacin compared with those taking other antibiotics commonly used to treat respiratory tract infections. They looked at 9 years of data from Ontario to identify people aged 66 years or older with no history of liver disease who were admitted to hospital for liver injury within 30 days after receiving a prescription for these antibiotics. Excluding patients admitted for previous liver disease or recent hospitalization, 144 patients were admitted for acute liver injury, with the median time from the dispensing of the antibiotic to admission to hospital being 9 days. Eighty-eight (61.1%) of patients died during their index admission to hospital for liver injury.
Burkitt lymphoma is a malignant, fast-growing tumor that originates from a subtype of white blood cells called B lymphocytes of the immune system and often affects internal organs and the central nervous system. Now Dr. Sandrine Sander and Professor Klaus Rajewsky of the Max Delbrück Center for Molecular Medicine (MDC) Berlin-Buch have identified a key element that transforms the immune cells into malignant lymphoma cells. They developed a mouse model that closely resembles Burkitt lymphoma in humans and that may help to test new treatment strategies.
Burkitt lymphoma typically develops in childhood and occurs most frequently in equatorial Africa and South America. This tumor originates from germinal centers of the lymphoid organs (Peyer's patches in the small intestine, lymph nodes and spleen). The germinal center reaction is initiated by mature B cells upon detection of a foreign substance (antigen). These B cells modify their DNA in the course of the reaction, resulting finally in a highly specific antibody response against the antigen.
The B cell receptor (BCR), an antibody presented on the surface of mature B cells, plays a crucial role in the germinal center reaction. In order to optimally recognize the respective antigen and initiate an appropriate immune response, the DNA segments encoding the antibody need to be modified and rearranged. While the processes are complex, DNA breaks occur and error-prone repair mechanisms may lead to genetic mutations associated with cancer development.
Scientists at Albert Einstein College of Medicine of Yeshiva University have made a discovery involving mice and humans that could mean that people with acute myeloid leukemia (AML), a rare and usually fatal cancer, are a step closer to new treatment options.
Their study results were published online August 13 in Cancer Cell.
Ulrich Steidl, M.D., Ph.D."We have discovered that a gene called HLX is expressed at abnormally high levels in leukemia stem cells in a mouse model of AML," said Ulrich Steidl, M.D., Ph.D., assistant professor of cell biology and of medicine at Einstein and senior author of the paper. (Gene expression is the process by which a gene synthesizes the molecule that it codes for; an "over-expressed" gene makes its product in abnormally high amounts.)
According to the National Cancer Institute, AML will be diagnosed in one of every 254 people during their lifetime. Most die within a few years of diagnosis. For the last several decades there has been little improvement in the survival rate for AML patients.
A research team at the University of California, Davis, has found that important and resourceful bacteria in the baby microbiome can ferret out nourishment from a previously unknown source, possibly helping at-risk infants break down components of breast milk.
Breast milk is amazingly intricate, providing all of the nutrients necessary to sustain and strengthen infants in the first months of life. Moreover, this natural source of nutrition provides protection from infections, allergies and many other illnesses.
Breast milk also promotes the growth of protective bacteria in an infant's intestine. Because breast milk contains glycans (complex sugars) that infants cannot breakdown, it promotes the growth a specific type of bacteria, called bifidobacteria, that can process these glycans. While it is known that bifidobacteria avail themselves of the free glycans in breast milk, it was not known whether these bacteria could also obtain glycans that were linked to proteins. Such proteins are called glycoproteins, and they are abundant in breast milk.
The research team led by David A. Mills at the UC-Davis investigated the ability of bifidobacteria to remove glycans from milk glycoproteins. Their work was recently published in the journal Molecular & Cellular Proteomics.
A team of researchers at Case Western Reserve University School of Medicine, led by Dr. Mark W. Jackson, have developed a novel method to identify genes that, when overexpressed, make normal cells behave like cancer cells. Using this method, the Jackson laboratory has identified a new oncogene, which is a gene that contributes to the development of cancer, named FAM83B.
"We made our discovery in a model of breast cancer," said Mark W. Jackson, Ph.D., Assistant Professor, Department of Pathology, Case Western Reserve University School of Medicine, Case Comprehensive Cancer Center. "Using an unbiased screening approach, we let the biology of cancer formation tell us what genes are important and FAM83B was one of the genes that came out of our screen. When FAM83B was overproduced in normal breast cells, it transformed the normal cells, causing them to behave like breast cancer," stated Jackson.
There are relatively few oncogenes that are critical to breast cancer growth, and only one other breast cancer oncogene has been identified in the last 6 years. Breast cancers are classified clinically into subgroups based on the presence of specific proteins, including estrogen receptor (ER), progesterone receptor (PR), and HER2.
When it comes to college-age individuals taking care of their bodies, appearance is more important than health, research conducted at the University of Missouri suggests. María Len-Ríos, an associate professor of strategic communication, Suzanne Burgoyne, a professor of theater, and a team of undergraduate researchers studied how college-age women view their bodies and how they feel about media messages aimed at women. Based on focus group research findings, the MU team developed an interactive play about body image to encourage frank discussions about conflicting societal messages regarding weight, values and healthful choices.
"During our focus group conversations, we learned that young people don't think about nutrition when it comes to eating," Len-Ríos said. "They think more about calorie-counting, which isn't necessarily related to a balanced diet."
The focus groups included college-age women, college-age men and mothers of college-age women, who discussed how body image is associated with engaging in restrictive diets, irregular sleep patterns and over-exercising.
"We receive so many conflicting media messages from news reports and advertising about how we should eat, how we should live and how we should look," Len-Ríos said. "Some participants said they realize images of models are digitally enhanced, but it doesn't necessarily keep them from wanting to achieve these unattainable figures -- this is because they see how society rewards women for 'looking good.'"
