Health & Wellness
© Natural Society
Researchers at North Carolina State University found that
bisphenol-A (BPA) exposure in early life stages can actually cause gene expression changes. These effects are seen in a part of the brain called the amygdala, which can lead to increased levels of anxiety. What may surprise you is that soy - which has been accused of mimicking estrogen, as has BPA - prevented the behavioral changes.
BPA and Genetic Changes
Lead author of
the study as published in the journal
PLOS ONE, Dr. Heather Patisaul is an NC State associate professor of biology. For the research, she and other researchers divided rats into four groups:
- Group I was fed only soy.
- Group II was fed a soy-free diet.
- Group III was fed only soy ad exposed to BPA.
- Group IV was fed a soy-free diet and exposed to BPA.
Rats exposed to BPA were given low doses during gestation, lactation, and throughout puberty. When administered blood tests, the rats dosed with BPA showed levels comparable to those found in humans. The same was true of rats fed a soy diet, which displayed comparable levels of genistein the estrogen-mimicking chemical much abhorred in soy.
Group IV - rats fed no soy and exposed to BPA - showed markedly higher levels of anxiety than the other groups. Their genes had changed, specifically where expressed in the amygdala (a region of the brain that deals with responses to fear and stress, also associated with behavior). The affected genes - estrogen receptor beta and melanocortin receptor 4 - both deal with the process of releasing oxytocin, a hormone and neurotransmitter linked to social behavior. Researchers therefore believe that the increased anxiety must have to do with BPA's ability to change the oxytocin/vasopressin signaling pathway.
The abstract of the study states:
"Early life exposure to Bisphenol A (BPA), a component of polycarbonate plastics and epoxy resins, alters sociosexual behavior in numerous species including humans. The present study focused on the ontogeny of these behavioral effects beginning in adolescence and assessed the underlying molecular changes in the amygdala."
Pharmaceutical company GlaxoSmithKline will open a new research unit in China to look at traditional Chinese medicine.
According to the company, Innovative TCM will be one of GSK's R&D programs in China, aiming to transform TCM from an experience-based practice to evidence-based medicines through innovation and differentiation.
"Traditional chinese medicine is a well-established system of medical practice developed through thousands of years of empirical testing and refinement of herbal mixtures, and relies generally on clinical experience," said Zang Jingwu, senior vice president and head of R&D China.
"Western medicines, on the other hand, are generally target-based small molecules or biologics, and their approvals for clinical use are based on clinical evidence of safety and efficacy by staged clinical trials," he said.
He said the newly formed unit is working with academic TCM experts in China to develop new TCM products for the benefits of patients in China and the rest of the world.
The strategy is to integrate the existing TCM knowledge of diseases with modern drug discovery technology and clinical trial methodology.
"We are developing novel therapeutic TCM mixtures as prescription medicines through innovative extraction methods and combinations, and we use clinical data/evidence to differentiate from existing TCM products on the market," he said.
The company's R&D China center was founded in 2007 with a focus on neurosciences. So far, the center has developed into a fully integrated global R&D organization in China to deliver medicine globally and for China.
A study carried out by Dr. Louis Bherer, PhD (Psychology), Laboratory Director and Researcher at the Institut universitaire de gériatrie de Montréal (IUGM), an institution affiliated with Université de Montréal, has shown that all seniors, even those considered frail, can enjoy the benefits of exercise in terms of their physical and cognitive faculties and quality of life and that these benefits appear after only three months.
This discovery is excellent news, as increased life expectancy has also increased the number of frail seniors in our communities. In geriatrics, frailness is characterized by decreased functional reserves in an individual, which increases vulnerability to stressors and the risk of adverse health effects. Frailty is associated with a higher risk of falls, hospitalizations, cognitive decline and psychological distress. Currently, 7% of seniors aged 65 to 74, 18% of those aged 75 to 84, and 37% of seniors over the age of 85 are considered frail.
There has been an outbreak of an adult-onset immunodeficiency syndrome in Southeast Asia. The autoimmune disease causes AIDS-like symptoms but is not associated with HIV and is not contagious.
The disease causes patients' bodies to produce antibodies that attack their own immune systems. Dr. Sarah Browne, a clinical investigator at the National Institute of Allergy and Infectious Diseases at NIH and the lead author on the study, says that we all have molecules and proteins that tell different immune cells when to start fighting infection. A large number of the patients studied with serious opportunistic infections make an antibody that blocks the function of one of these molecules. The molecule is called interferon-gamma. Without functioning interferon-gamma, people become more susceptible to certain types of infections -- infections people with working immune systems normally don't get. Interferon-gamma is a protein that helps the body fight off infections. In those diagnosed, the immune system has begun treating interferon-gamma as an enemy and makes an autoantibody against it, thus making it an autoimmune condition.
Researchers at the Walter and Eliza Hall Institute have discovered that a pair of molecules work together to kill so-called 'self-reactive' immune cells that are programmed to attack the body's own organs. The finding is helping to explain how autoimmune diseases develop.
© The Walter and Eliza Hall Institute, Australia
Dr Daniel Gray and colleagues have discovered that immune cell death is an important safeguard against autoimmune diseases.
Dr Daniel Gray and colleagues from the institute's Molecular Genetics of Cancer division and the University of Ballarat discovered that the absence of two related proteins, called Puma and Bim, led to self-reactive immune cells accumulating and attacking many different body organs, causing illness. The research is published online today in the journal
Immunity.
Autoimmune diseases, such as type 1 diabetes, rheumatoid arthritis, inflammatory bowel disease and multiple sclerosis, develop when immune cells launch an attack on the body's own cells, destroying important body organs or structures. Around one in 20 Australians is affected by autoimmune conditions, most of which are chronic illnesses with no cure.
Puma and Bim are so-called 'BH3-only' proteins that make cells die by a process called apoptosis. Defects in apoptosis proteins have been linked to many human diseases, including cancer and neurodegenerative disorders.
When mice are born lacking the master gene Atoh1, none breathe well and all die in the newborn period. Why and how this occurs could provide new answers about sudden infant death syndrome (SIDS), but the solution has remained elusive until now.
Research led by Baylor College of Medicine and the Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital demonstrates that when the gene is lacking in a special population of neurons called RTN (retrotrapezoid nucleus), roughly half the young mice die at birth. Those who survive are less likely to respond to excess levels of carbon dioxide as adults. A report of their work appears online in the journal Neuron.
"The death of mice at birth clued us in that Atoh1 must be needed for the function of some neurons critical for neonatal breathing, so we set out to define these neurons," said Dr. Huda Zoghbi, senior author of the report and director of the Neurological Research Institute and a professor of molecular and human genetics, neuroscience, neurology and pediatrics at BCM. Zoghbi is also a Howard Hughes Medical Institute investigator.
A team of neuroscientists and informatics experts at Cold Spring Harbor Laboratory (CSHL) reports important progress in an effort to understand the relationship between transposons -- sequences of DNA that can jump around within the genome, potentially causing great damage -- and mechanisms involved in serious neurodegenerative disorders including ALS (amyotrophic lateral sclerosis, also known as Lou Gehrig's disease), FTLD (frontotemporal lobar degeneration) and Alzheimer's disease.
A close analysis of previously unanalyzed genome data has led CSHL Associate Professor Joshua Dubnau, Ph.D., and colleagues to discover a signature of disease that may help explain these and other neural pathologies. As reported by the team September 6 in the journal PLoS ONE, this signature leads them to hypothesize that dormant transposons awaken in the genome, setting off the equivalent of a transposon storm in some brain cells, capable of causing cell death.
Transposons -- often called transposable elements, or TEs, by scientists -- are understood collectively to occupy a large fraction (~40%) of the genetic material of multicellular organisms, including humans. Most TEs are genomic fossils, effectively inactive. A minority of TEs capable of activation are ordinarily suppressed by a variety of cellular defense mechanisms that have evolved along with life over eons of time to prevent sudden rearrangements (i.e., mutations) of the genetic material.
Men who experienced childhood sexual abuse are three times more likely to have a heart attack than men who were not sexually abused as children, according to a new study from researchers at the University of Toronto. The researchers found no association between childhood sexual abuse and heart attacks among women.
In a paper published online this week in the journal Child Abuse & Neglect, investigators examined gender-specific differences in a representative sample of 5095 men and 7768 women aged 18 and over, drawn from the Center for Disease Control's 2010 Behavioral Risk Factor Surveillance Survey. A total of 57 men and 154 women reported being sexually abused by someone close to them before they turned 18 and 377 men and 285 women said that a doctor, nurse or other health professional had diagnosed them with a heart attack or myocardial infarction. The study was co-authored by four graduate students at the University of Toronto, Raluca Bejan, John Hunter, Tamara Grundland and Sarah Brennenstuhl.
"Men who reported they were sexually abused during childhood were particularly vulnerable to having a heart attack later in life," says lead author Esme Fuller-Thomson, Professor and Sandra Rotman Chair at University of Toronto's Factor-Inwentash Faculty of Social Work. "We had expected that the abuse-heart attack link would be due to unhealthy behaviors in sexual abuse survivors, such as higher rates of alcohol use or smoking, or increased levels of general stress and poverty in adulthood when compared to non-abused males. However, we adjusted statistically for 15 potential risk factors for heart attack, including age, race, obesity, smoking, physical inactivity, diabetes mellitus, education level and household income, and still found a three-fold risk of heart attack."
© Hiroyuki Miyoshi
Scientists have identified a protein that is critical to repairing glands in the intestine’s inner lining. The glands appear as dark green spots above and are rebuilt every two to four weeks as the inner lining of the gut is continually renewed.
Scientists at Washington University School of Medicine in St. Louis have identified a protein essential to repairing the intestine's inner lining.
That lining is among the body's busiest highways, trod not only by the food we ingest but also by trillions of microorganisms that aid digestion. Because the intestine plays key roles in absorbing nutrients and containing the microbes, any damage must be fixed promptly.
The researchers report Sept. 6 in
Science Express that a protein called
Wnt5a is essential for reconstructing glands in the intestinal lining. The glands, called crypts of Lieberkühn, contain stem cells that continually pump out other cells that renew the gut lining, which is replaced every two to four weeks. The crypts look like dimples in the gut lining and are vulnerable to damage and loss from infection and inflammation.
"For example, inflammatory bowel disease can destroy huge stretches of the lining, including the crypts," says senior author Thaddeus Stappenbeck, MD, PhD, associate professor of pathology and immunology. "If crypts can't be repaired as the lining is rebuilt, their absence would place substantial stresses on crypts in healthy portions of the gut. So it's important to better understand how the crypts are replaced."
Untreated severe obstructive sleep apnea (OSA) is associated with an increased risk of cardiovascular mortality in the elderly, and adequate treatment with continuous positive airway pressure (CPAP) may significantly reduce this risk, according to a new study from researchers in Spain.
"Although the link between OSA and cardiovascular mortality is well established in younger patients, evidence on this relationship in the elderly has been conflicting," said lead author Miguel Ángel Martínez-García, MD, of La Fe University and Polytechnic Hospital in Valencia, Spain. "In our study of 939 elderly patients, severe OSA not treated with CPAP was associated with an increased risk of cardiovascular mortality especially from stroke and heart failure, and CPAP treatment reduced this excess of cardiovascular mortality to levels similar to those seen in patients without OSA."
The findings were published online ahead of print publication in the American Thoracic Society's American Journal of Respiratory and Critical Care Medicine.
All subjects in this prospective, observational study were 65 years of age or older. Median follow-up was 69 months. Sleep studies were conducted with either full standard polysomnography or respiratory polygraphy following Spanish guidelines. OSA was defined as mild-to-moderate (apnea-hypopnea index [AHI] 15-29) or severe (AHI ≥30). Patients with AHI (less than) 15 acted as controls. CPAP use ≥4 hours daily was considered as good adherence to treatment.
