Monthly Archives: December 2016
Folks who walk to work or school while listening to music via headphones may want to unplug, with a new U.S. study finding injuries to this group of people tripling since 2004.
The reason, University of Maryland researchers say, is that use of iPods and other MP3 players makes people much less aware of their environment, including oncoming traffic.
“MP3 usage is common in young adults and teenagers and we found that people wearing headphones are at risk of getting hit and having injury or death,” said lead researcher Dr. Richard Lichenstein, an associate professor of pediatrics in Pediatric Emergency Medicine Research at the University of Maryland Children’s Hospital.
“These are pedestrians getting hit by cars, trains, trucks, vans, buses and things like that,” he said. “About 70 percent of the injuries were fatal and more than 50 percent of the victims were hit by trains.”
The report was published in the Jan. 16 online edition of Injury Prevention.
For the study, Lichenstein’s team used the U.S. National Electronic Injury Surveillance System, the U.S. Consumer Product Safety Commission and Google to find data on deaths and injuries among pedestrians wearing headphones from January 2004 through June 2011.
During this time, they found 116 such events reported. In 2004-05 just 16 such cases were noted, but that rate rose nearly three-fold to 47 during 2010-2011, the researchers report.
About two-thirds of victims were under 30 years of age, and the most common accident (55 percent) was being hit by a train. Most such accidents happened in cities, with only 12 percent occurring in rural areas.
In 70 percent of cases the accident proved fatal, and in three out of four, bystanders had actually seen the victim wearing headphones just prior to the accident. The sound coming from those headphones likely masked outside noise, because in 29 percent of the accidents, horns or sirens had been sounded just before the victim was hit.
“People wearing headphones need to be conscious of the outside environment and risk of moving vehicles, because not only are you distracted by the music, but also the sounds of traffic or horns or sirens are blocked,” Lichenstein said. Experts label this type of distraction “inattentional blindness.”
Commenting on the study, Dr. Carl Schulman, director of Injury Prevention Education at the University of Miami Miller School of Medicine, pointed to an earlier study suggesting that any form of impaired hearing can raise a person’s injury risk.
In a 1995 New Zealand study involving almost 200 children, those with (natural) hearing problems had an increased risk of being hit by a car, compared with children with normal hearing, Schulman noted.
This is similar to having one’s hearing intentionally blocked by music coming from headphones, so it is not surprising that the new study saw a similar pattern among people plugged into MP3 players, Schulman said.
Lichenstein said the way to reduce the risk is simple. “Be cognizant of the environment. Know there is risk out there. It’s not a great idea to be distracted and it’s not a great idea to shut out those sounds that may help you live another day,” he said.
Tall or short, it’s long been known that genes account for much of a person’s height. Now, scientists have found that short people actually might be missing copies of certain genes, which can leave them significantly smaller than average.
Studying DNA from more than 11,000 children and adults, an international team of researchers learned that those of short stature — defined roughly as falling into the shortest 2.5 percent of their peer group — had an excess number of rare deletions, or missing copies, of specific genes. Thus far, most research into genes and height has centered on identifying variations in common genes instead of an absence of others, study author Dr. Joel Hirschhorn said.
“We were a little bit surprised, since we didn’t really know what we would find going in [to the study] and whether we would see enough of an effect,” said Hirschhorn, a professor of genetics at Children’s Hospital Boston. “We were trying to figure out what’s the underlying genetics of height and things like it, and this is a class of variation less well studied.”
The study is published in the December issue of the American Journal of Human Genetics.
Common gene variants linked to height explain only about 10 percent of the variation in adult height, Hirschhorn said, but perhaps half of such variation might eventually be explained by some of the differences his team studied.
First analyzing the DNA of more than 4,400 children whose genetic material was collected for other purposes, the researchers observed that many more CNVs or “copy-number variants” — in this case, fewer copies of a gene — were present in those of short stature.
Extending the findings to a larger, population-based group of nearly 6,900 African Americans, the scientists again found that shorter participants had an excess of such missing gene copies. These deletions would typically be inherited from one’s parents, but not always, Hirschhorn said.
“Usually [researchers] look at variants one at a time, but this is a cumulative-effect type of variation,” said Hirschhorn, also a senior associate at the Broad Institute, a biomedical research organization in Cambridge, Mass.
Several limitations might affect the validity of the study results, the authors acknowledged. One is the fact that children whose DNA was evaluated had initially undergone genetic analysis for other reasons such as developmental delays, autism spectrum disorders and multiple birth defects. So it’s possible that those with many missing gene copies are likelier to have conditions leading to poor growth, the study said, but the replication of results in a more representative population suggests the findings can be generalized to others.
Estrogen therapy has already been credited with helping women manage an array of menopause-related issues, including reducing hot flashes, improving heart health and bone density, and maintaining levels of sexual satisfaction. Now a new study suggests that the same estrogen therapy used to treat osteoporosis can actually lead to healthier teeth and gums. The study outcomes are being published online today in Menopause, the journal of The North American Menopause Society (NAMS).
As estrogen levels fall during menopause, women become more vulnerable to numerous health issues, including loss of bone mineral density which can lead to osteoporosis. Around the same time, changes in oral health also are common as teeth and gums become more susceptible to disease, which can lead to inflammation, pain, bleeding, and eventually loose or missing teeth.
In the Menopause article “Association between osteoporosis treatment and severe periodontitis in postmenopausal women,” 492 postmenopausal Brazilian women aged 50 to 87 years, 113 in osteoporosis treatment and 379 not treated, were evaluated to determine whether osteoporosis treatment could help increase the bone mineral density in their jaws and, subsequently, improve overall oral health.
The study found that the rate of occurrence of severe periodontitis was 44% lower in the postmenopausal osteoporosis-treatment group than in the untreated group. Treatment consisted of systemic estrogen alone or estrogen plus progestin, as well as calcium and vitamin D supplements, for a minimum of six months.
“Osteoporosis can occur throughout the body, including the jaw, and lead to an increased risk of periodontal disease,” says Dr. JoAnn Pinkerton, NAMS executive director. “This study demonstrates that estrogen therapy, which has proven to be effective in preventing bone loss, may also prevent the worsening of tooth and gum disease. All women, but especially those with low estrogen or on bisphosphonate treatment for osteoporosis, should make good dental care a part of their healthy lifestyles.”
Now a team led by researchers at the Duke Cancer Institute have identified a cellular process that cancer cells hijack to hoard cholesterol and fuel their growth. Identifying this process could inform the development of better ways to control cholesterol accumulation in tumors, potentially leading to improved survival for prostate cancer patients.
The findings are published online this month in the journal Cancer Research.
“Prostate cancer cells, as well as some other solid tumors, have been shown to contain higher cholesterol levels than normal cells,” said senior author Donald McDonnell, Ph.D., chairman of the Department of Pharmacology and Cancer Biology at Duke. “All cells need cholesterol to grow, and too much of it can stimulate uncontrolled growth.
“Prostate cancer cells somehow bypass the cellular control switch that regulates the levels of cholesterol allowing them to accumulate this fat,” McDonnell said. “This process has not been well understood. In this study, we show how prostate cancer cells accomplish this.”
McDonnell and colleagues began by identifying genes involved in cholesterol regulation in prostate tumors. They homed in on a specific gene, CYP27A1, which is a key component of the machinery that governs the level of cholesterol within cells.
In patients with prostate cancer, the expression of the CYP27A1 gene in tumors is significantly lower, and this is especially true for men with aggressive cancers compared to the tumors in men with more benign disease. Downregulation of this gene basically shuts off the sensor that cells use to gauge when they have taken up enough cholesterol. This in turn allows accumulation of this fat in tumor cells. Access to more cholesterol gives prostate cancer cells a selective growth advantage.
“It remains to be determined how this regulatory activity can be restored and/or whether it’s possible to mitigate the effects of the increased cholesterol uptake that result from the loss of CYP27A1 expression,” McDonnell said.
He said statin use alone might help, but perhaps not enough, since tumors could simply rev up the regulation of the cholesterol manufacturing process in tumors to compensate.
McDonnell said is lab is continuing the research, including finding ways to induce cells to eject cholesterol, reverse the inhibition of CYP27A1 activity, or introduce compounds that interfere with cholesterol-production in the tumor.