HOUSTON -- (March 31, 2008) -- When it comes to the latest celebrity blunder, parents should tune in rather than tune out.

It could give parents an opportunity to talk with their children about making good decisions, said an expert at Baylor College of Medicine in Houston.

Youngsters can be exposed to drugs, alcohol and other unhealthy activities simply by reading about their favorite celebrity.

Start a conversation

"Rather than avoiding the topic, parents should do their research and be sure they have their facts straight about the situation," said Dr. John Sargent, professor of psychiatry and behavioral sciences and pediatrics at BCM and director of child and adolescent psychiatry at Ben Taub General Hospital. "It's important to know what your kids are being exposed to."

Since children may already be talking about the issues with friends, the first step is to talk with them about what they've heard and what they think about the situation.

"Be sure to make it an open conversation," said Sargent.

Choices, behaviors

Parents should discuss their own feelings about the situation and remind their youngsters that privacy is difficult to maintain as a celebrity. There are always two sides to a story, and this can relate back to a situation the youngsters might face with gossip in their own lives.

Another important point to make is that there are a number of successful celebrities who live physically and emotionally healthy lives, and that there are various ways for celebrities and others to get help when facing situations such as drug and alcohol abuse.

"Use these opportunities to talk about choices, behaviors and friends," said Sargent.

Just as any other type of news, parents should do their research about celebrity news and be prepared for an open conversation. Parents can use these same tips to talk to their children about world news, politics and other topics.

HOUSTON -- (March 31, 2008) -- A mutation in a gene controlling calcium flux in skeletal muscle cells links the rare condition malignant hyperthermia to enhanced susceptibility to heat stroke and sudden death, said a consortium of researchers led by Baylor College of Medicine in a report in the current issue of the journal Cell.

"We created our mouse to be a model for malignant hyperthermia," said Dr. Susan Hamilton, chair of molecular physiology and biophysics at BCM and senior author of the report. Coincidentally, they found that the mouse model demonstrated a link to a condition similar to heat stroke – when the mice were exposed to warm conditions and stressed.

Rare but deadly

Malignant hyperthermia occurs because a gene mutation – often in a gene called RyR1 (http://ghr.nlm.nih.gov/gene=ryr1) – causes the body to react violently to certain drugs used as anesthetics or paralytics during surgery. The drugs trigger a chain reaction affecting the skeletal muscles. The heart beats too fast, the metabolism speeds up, muscle contracts violently and temperatures exceed 110 degrees F. Without prompt treatment, patients can die. Malignant hyperthermia is rare, but no one knows how often it occurs.

RyR1 refers to ryanodine receptor (the channel through which skeletal muscle releases calcium ions when contracting). The RyR1 mutation Hamilton and her colleagues engineered in the mice makes the channel leaky. As the calcium leaks out, it activates an enzyme called nitric oxide synthase, which stimulates production of nitric oxide. The nitric oxide then interacts with cysteines (amino acids) in RyR1, making it more temperature sensitive and starting a vicious cycle in which the response just gets worse.

Vulnerabilities exposed

When they initially tested the mouse, they found that the animal did not respond negatively to the anesthetics, probably because the body temperatures of mice regularly drop when they are under anesthesia. However, if they tried to control the animal's temperature to more normal levels under the anesthesia, its muscles contracted and it had malignant hyperthermic episodes. Later, they found that if the animal was frightened or stressed in a warm room, it had the same response.

"One day, we were in a closed off room that was really warm. All of the animals seized while running on the treadmill," she said. "We found that they were vulnerable to increased temperature. After careful analysis, we realized that the muscle was contracting at temperatures that are normally well tolerated."

The situation was similar to a marathon where the temperature is not unduly warm but 1 in 1,000 people might have heat stroke.

"This is likely to be a similar thing," she said. "They are stressed, warm and exercising."

She found that under very warm conditions, the mice die of something similar to classic heat stroke.
"The important next step is to determine if this underlies enhanced susceptibility to heat stroke in humans," she said.

Triggers

In addition, she said, they found that the leaky calcium channels in the muscles of the mice led to weakening as the animals aged.

"With these mutations, the muscles get weaker," she said. "In mice, you can prevent this with low doses of a weak antioxidant called n-acetylcysteine given over a long term."

Hamilton said there are human medical implications from the study. "There are documented cases of temperature sensitivity in some families with histories of malignant hyperthermia. I think this is telling us something really important."

"Malignant hyperthermia syndrome a potentially fatal inherited disorder is most often 'triggered' by certain gas anesthetics and the paralyzing drug succinylcholine. In the naturally occurring animal model, certain breeds of swine, the syndrome is also precipitated by environmental conditions, said Dr. Henry Rosenberg, president of the Malignant Hyperthermia Association of the United States (http://www.mhaus.org/) and professor of anesthesiology at Mount Sinai School of Medicine, N.Y. "It has long been debated as to whether some cases of heat stroke and exercise-induced muscle breakdown in humans are related to malignant hyperthermia as well. This study defines a biochemical pathway that might very well clarify the relationship between anesthesia-induced malignant hyperthermia and heat stroke. This elegant study, using modern molecular techniques, opens new avenues for the study of the not-uncommon problem of heat stroke and exercise-induced muscle breakdown and the risk for malignant hyperthermia."

"Given the frequency of the mutations in the ryanodine receptor, I suspect that malignant hyperthermia is underdiagnosed or diagnosed as something else," Hamilton said. "Some people receive the volatile anesthetics, and can die on the operating table or even die a day or so later."

Their muscles undergo sustained contractions causing them to deteriorate, releasing potassium and proteins that are toxic to the heart and kidneys.

More knowledge, better treatment

Sudden death in young athletes and soldiers is frequently associated with cardiac defects, but Hamilton and her colleagues propose that some cases of sudden death at elevated environmental temperatures are secondary to the abnormal skeletal muscle response associated with RyR1 mutations. Some people may never have the classic malignant hyperthermia response but develop a disorder of the muscles when they get too hot.

"Along with cardiac abnormalities, heat stroke is a major culprit in unexpected sudden deaths of otherwise fit, young athletes and soldiers," said Robert T. Dirksen, Ph.D., associate professor of pharmacology and physiology at the University of Rochester Medical Center. "With a better knowledge of these mechanisms, we can begin to better diagnose and treat both disorders, and hopefully, save some lives," said Dirksen, a co-author on the study.

Another factor is the muscle weakness and abnormal temperature sensitivity associated with these mutations.

"An affected individual may never have a diagnosed malignant hyperthermia episode but could have quality of life issues such as muscle weakness or poor ability to tolerate warmer temperatures," Hamilton said. "No one has looked at the myopathy (muscle deterioration) component of them because it is subtle. But by the time our mice were a year old, their muscle strength had decreased by half."

This research was performed by an interdisciplinary team including William J. Durham, Paula Aracena Parks, Cheng Long, Daniel L. Galvan, Charles P. Gilman and Mariah Baker, all of BCM; Ann E. Rossi, Sanjeewa A. Goonasekera and Robert Dirksen of the University of Rochester Medical Center in New York and Simona Boncompagni and and Feliciano Protasi of Università degli Studi G. d'Annunzio in Chieti, Italy and Natalia Shirokova of the New Jersey Medical School in Newark.

Funding for this work came from National Institute of Arthritis, Musculoskeletal, and Skin Diseases of the National Institutes of Health, the Muscular Dystrophy Association to the Italian Telethon Foundation and a NIH Dental and Craniofacial training grant.

The paper can be found at www.cell.com.

HOUSTON -- (March 28, 2008) -- Treatment with the potent cholesterol-lowering drug rosuvastatin (Crestor®) reversed, or at least halted the narrowing of the coronary arteries that take blood to heart – the first time that treatment with one type of drug has achieved this effect, said a Baylor College of Medicine researcher in a presentation today at the 57th annual scientific sessions of the American College of Cardiology in Chicago. The results also appear online in the journal Circulation.

In A Study to Evaluate the Effect of Rosuvastatin on Intravascular Ultrasound-Derived Coronary Atheroma Burden (ASTEROID), Dr. Christie Ballantyne, professor of medicine-cardiology, chief of the Section of Atherosclerosis and Vascular Medicine at BCM, and colleagues from the Cleveland Clinic, the University Clinic Essen and the Montreal Heart Institute treated 507 patients with narrowed coronary arteries with 40 milligrams of rosuvastatin daily for two years. The treatment lowered the patients "bad" or low-density lipoprotein cholesterol levels on average by 53 percent and increased their "good" or high density lipoprotein levels by 13 percent.

Two techniques

"In this sub-study, we broadened our assessment of patients by determining the effect of rosuvastatin on the narrowing in coronary arteries, using sophisticated measurements," said Ballantyne, who is also the director of the Center for Cardiovascular Disease Prevention at the Methodist DeBakey Heart & Vascular Center and lead author of the study. "Both measurements showed improvement in the measurements of the diameter of the arteries and the amount of narrowing with intensive statin therapy."

They used two techniques – intravascular ultrasound and quantitative coronary angiography – to measure the effect of the drug on the diameter and the clogging of the coronary arteries.

The amount of stenosis or narrowing of the coronary arteries decreased from an average of 37.73 percent to 36 percent. (This figure represents an average taken from 10 segments of coronary artery.)

The median diameter of the coronary arteries increased from 1.65 millimeter to 1.68 mm.

What is regression?

Doctors define regression as greater than a 10 percent reduction in coronary artery narrowing. By this criterion, 22 patients or 7.5 percent showed improvement. Another 261 patients or 89.4 percent saw an improvement of less than 10 percent. The disease progressed in nine patients. (The tests results were evaluable for only some of the patients in the study.)

Doctors consider that a disease has progressed or regressed if the average diameter of the artery has changed by 0.2 mm as measured by ultrasound. In this study, the diameter increased by at least 0.2mm in 34 patients. It increased less than that in 230 patients. The disease got worse in 17 patients.

Other researchers who took part in the study are Drs. Joel S. Raichlen and Valerie A. Cain both of AstraZeneca; Raimund Erbel, University Clinic Essen in Germany; Jean-Claude Tardif, Montreal Heart Institute, and Stephen J. Nicholls, Sorin J. Brener, and Steven E. Nissen of the Cleveland Clinic Foundation in Ohio.

This study was funded by AstraZeneca. It can be found online at http://circ.ahajournals.org/.

If identical twins eat and exercise equally, must they have the same body weight" By analyzing the fundamental equations of body weight change, NIH researchers Carson Chow and Kevin Hall find that identical twins with identical lifestyles can have different body weights and different amounts of body fat.

The study, published March 28th in the open-access journal PLoS Computational Biology, uses a branch of mathematics called dynamical systems theory to demonstrate that a class of model equations has an infinite number of body weight solutions, even if the food intake and energy expenditure rates are identical. However, the work also shows that another class of models directly refutes this, predicting that food intake and energy expenditure rates uniquely determine body weight. Existing data are insufficient to tell which is closer to reality, since both models can make the same predictions for a given alteration of food intake or energy expenditure.

Given the ongoing obesity epidemic, Drs. Chow and Hall are interested in what factors determine human body weight and its stability. Of particular importance is whether a therapy for obesity would have to be administered repeatedly over a lifetime or could be given only until a target body weight is reached. As a particular example, the study considers whether weight lost from a liposuction procedure is permanent. For the class of equations with an infinite number of body weight solutions, fat removal through liposuction could lead to permanent results. However, the opposing models predict that the body would eventually return to its original weight.

Chow and Hall note that neither class of models accounts for the a number of variables affecting how much a person tends to eat, an important factor determining bodyweight. Nevertheless, for any food intake rate this latest research suggests that an individual may have an infinite number of possible body weights. The study outlines the mathematical conditions underlying this possibility and suggests how future experiments could determine if it is true.


Posted by: Evelyn    Source

New Haven, Conn.Discrimination against overweight peopleespecially womenis as common as racial discrimination, as per a research studyby the Rudd Center for Food Policy & Obesity at Yale University.

These results show the need to treat weight discrimination as a legitimate form of prejudice, comparable to other characteristics like race or gender that already receive legal protection, said Rebecca Puhl, research scientist and lead author.

The study documented the prevalence of self-reported weight discrimination and compared it to experiences of discrimination based on race and gender among a nationally representative sample of adults aged 25- to 74-years-old. The data was obtained from the National Survey of Midlife Development in the United States.

The study also revealed that women are twice as likely as men to report weight discrimination and that weight discrimination in the workplace and interpersonal mistreatment due to obesity is common.

The scientists observed that men are not at serious risk for weight bias until their body mass index (BMI) reaches 35 or higher, while women begin experiencing a notable increase in weight discrimination risk at a BMI level of 27. BMI is the measure of body fat based on height and weight.

Co-author Tatiana Andreyava of Yale said weight discrimination is more prevalent than discrimination based on sexual orientation, nationality/ethnicity, physical disability, and religious beliefs. However, despite its high prevalence, it continues to remain socially acceptable, she said.


Posted by: Evelyn    Source