Each Hour Of Television Viewing Associated With 144 Fewer Steps

A study of low-income housing residents has documented that the more television people say they watched, the less active they were, researchers from Dana-Farber Cancer Institute and colleagues report.

The findings of television's effects on physical activity are the first to be based on objective measurements using pedometers, rather than the study subjects' memories of their physical activity, say the researchers. The study was published online by the American Journal of Public Health on July 27 and later in the Journal's September 2006 issue.

"Clearly the more time a person spends watching television the less time they have to be physically active, and in many lower income communities, other factors might have influenced the study participants' decisions to spend time watching television," said the paper's lead author, Gary Bennett, PhD, of Dana-Farber's Center for Community-Based Research and the Harvard School of Public Health.

These factors may include fear of street crime and poor maintenance of parks and playground equipment, which create barriers to outdoor activities. Older people were particularly prone to staying indoors and watching television, which reflects their increasing isolation in society today, Bennett said.

The study involved 486 low-income housing residents in Boston. The study participants tended to be black or Hispanic, older, and female. Two-thirds were overweight or obese, 37 percent had less than a high-school education.

To avoid the potential inaccuracies associated with self-reported physical activity, the researchers arranged to have the study participants wear pedometers during their waking hours to count the number of steps they took every day for five days. The pedometers were "blinded" to prevent the participants from knowing how many steps they had taken and possibly altering their normal patterns of activity. The participants also reported the number of hours they watched television.

Results showed that the participants watched an average of 3.6 hours a day of television, with some reporting spending no time watching television while others watched as much as 14.5 hours on weekdays and 19 hours on weekend days.

Researchers have estimated that 10,000 steps a day measured with a pedometer roughly approximates recommended daily activity levels. In the current study, on an average day, each hour of television viewing was associated with 144 fewer steps walked - or an average of 520 fewer steps a day for those who spent 3.6 hours in front of the television.

In addition, for each hour of television they watched, participants were 16 percent less likely to achieve the 10,000-step-per-day goal. For those who watched the 3.6-hour-a-day mean value, their odds of walking 10,000 steps a day were 47 percent less than non-television-watchers.

The study findings represent "a piece of a larger puzzle for us - how do we help people to become more active?" said Bennett. Simply telling people not to watch television "doesn't work terribly well," he explained, and often leads to substituting other sedentary activities like reading and computer use.

Going forward, "we need to do a better Job of understanding the factors that lead people to be physically active," Bennett said. "This is an important area of research, particularly because the impact of physical inactivity disproportionately affects the health of lower income Americans."

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Co-authors of the report are from Dana-Farber, the Harvard School of Public Health, Northwestern University Feinberg School of Medicine, and the University of Massachusetts at Amherst.

The research was funded by grants from the National Cancer Institute, Liberty Mutual, National Colorectal Cancer Research Alliance, and the Patterson Fellowship Fund.

Dana-Farber Cancer Institute (http://www.Dana-farber.org/) is a principal teaching affiliate of the Harvard Medical School and is among the leading cancer research and care centers in the United States. It is a founding member of the Dana-Farber/Harvard Cancer Center (DF/HCC), designated a comprehensive cancer Center by the National Cancer Institute.

Contact: Janet Haley Dubow
Dana-Farber Cancer Institute



Enviado por

Dr. José Manuel Ferrer Guerra

REM Sleep Behavior Disorder At Young Age Linked To Antidepressant Use

A Mayo Clinic study has shown that the onset of REM Sleep Behavior Disorder (RBD) at a younger age appears to be connected to antidepressant use.

RBD is a sleep disorder where patients act out their dreams, which are often unpleasant and violent, according to Maja Tippmann-Peikert, M.D., sleep medicine specialist, neurologist and study investigator. This acting out results from a loss of normal muscle paralysis in REM (rapid eye movement) sleep, the dream stage of sleep, which normally prevents enacting one's dreams. RBD patients generally act out their dreams in a defensive posture, as if fending off an attacker, says R. Robert Auger, M.D., Mayo Clinic sleep medicine specialist, psychiatrist and primary investigator. The disorder is often recognized by a bed partner.

Although previously published case reports and a more recently published study have suggested the association between antidepressants and RBD, this study represents the first systematic demonstration of the relationship. Findings will be presented June 19 at the Associated Professional Sleep Societies' SLEEP 2006 meeting in Salt Lake City.

"Our findings suggest that RBD in younger patients -- in the 30s instead of the usual age of the 50s or older -- is frequently linked to antidepressant use," says Dr. Auger. "I'd interpret this to mean one of three things: 1) in younger patients, antidepressants can cause RBD, or 2) in younger patients, RBD results in psychiatric diagnoses that then result in antidepressant prescriptions, or 3) a common factor is causing both the RBD and the psychiatric diagnoses, which in turn results in antidepressant prescriptions. If medications are implicated in a direct manner, it may be an idiosyncratic effect, it could be related to the dose of medication, or the medications simply may be unmasking an underlying predisposition to RBD."

To conduct this study, investigators reviewed records of patients consecutively diagnosed with RBD at Mayo Clinic between 2002 and 2005, removing those with neurodegenerative diseases such as Parkinson's disease or dementia at the time of RBD diagnosis. Twenty patients diagnosed when they were less than 50 years old (average age 34) were age- and gender-matched for comparison to a group of patients without RBD. Equivalent comparisons were performed in patients diagnosed with RBD over age 50. After looking at all groups, the investigators found that the younger RBD patients were unique with respect to greater use of antidepressants than those without RBD (80 percent versus 15 percent use). Antidepressants prescribed for these patients spanned all types: selective serotonin reuptake inhibitors (SSRIs), venlafaxine, mirtazapine and tricyclic antidepressants. The investigators also found a higher prevalence of females in the early-onset group of RBD (45 percent female) patients than in older-onset RBD (13 percent female). RBD is known to be largely a Male disease.

A link between antidepressants and RBD is not completely surprising, according to Dr. Auger, as the neurotransmitters affected by these medications are involved in REM sleep regulation, and a recent study shows that they diminish the muscle paralysis associated with normal REM sleep.

Dr. Auger says that due to the retrospective Nature of the study, correlation but not direct causality between antidepressants and RBD can be inferred.

"From the results of our study, it appears that young-onset RBD is frequently associated with antidepressants," says Dr. Auger. "It nevertheless appears to be a relatively rare phenomenon, so I don't think one should hesitate to take an antidepressant based on this particular risk. Physicians should be aware of this potential side effect, however, particularly in patients who complain of sleep disturbances. I'm hoping these findings will create a greater awareness, as practitioners generally would not link medications with RBD."

There are no treatments available for those prescribed antidepressants to prevent them from later developing RBD, but the condition is generally quite treatable once identified, he says. It is uncertain whether this younger group of patients possesses the same risk of developing a neurodegenerative disease later in life, as has been described in previous studies involving patients with older-onset RBD.

Currently, 10 million Americans take antidepressants.

###

Other investigators involved in this study include: Paul Teman, M.D.; Timothy Young, M.D.; Michael Silber, M.B.Ch.B; and Nancy Slocumb. This research was supported through a philanthropic gift to Mayo Clinic.

To obtain the latest news releases from Mayo Clinic, go to http://www.mayoclinic.org/news. MayoClinic.com (http://www.mayoclinic.com/) is available as a resource for your health stories.

Contact: Lisa Lucier
Mayo Clinic



Saludos Cordiales
Dr. José Manuel Ferrer Guerra

Key To Early Diagnosis Of Autism May Be In The Placenta

Researchers at Yale School of Medicine have discovered in the placenta what may be the earliest marker for autism, possibly helping physicians diagnose the condition at birth, rather than the standard age of two or older.

The findings are reported in the June 26 online issue of Biological Psychiatry. Autism is a developmental disorder that has a profound effect on socialization, communication, learning and other behaviors. In most cases, onset is early in infancy. Information on the earliest development aspects of autism in children has been limited even though approximately one in every 200 children is diagnosed with an Autism Spectrum Disorder (ASD). The earlier the diagnosis is made, the greater the treatment impact.

Current studies are searching for characteristics in children at risk for ASD so that the diagnosis can be made prior to age one. The ideal time for diagnosis would be at birth, according to senior author on the study Harvey J. Kliman, M.D., research Scientist in the Department of Obstetrics, Gynecology & Reproductive Sciences at the Yale School of Medicine.

In previous work, Kliman had observed an unusual pathologic finding in the placentas from children with Asperger Syndrome, an ASD condition which, like autism, impairs the ability to relate to others.

"By serendipity, at a dinner party I happened to sit next to George M. Anderson, a research Scientist in the Yale Child Study Center who had access to many cases of children with ASD," said Kliman. "We realized that by working together we might be able to determine if this placental abnormality could be a useful clinical marker."

With the help of Andrea Jacobs-Stannard, a student in Kliman's laboratory, and Katarzyna Chawarska and Fred R. Volkmar of the Yale Child Study Center, the group designed a study to see if the placental abnormality, specifically the presence of trophoblast inclusions, was a marker for ASD. The multidisciplinary team of Yale researchers compared placentas from 13 children with ASD to those from 61 unaffected children for the presence of trophoblast inclusions.

They found that the placentas from ASD children were three times more likely to have the inclusions. Kliman and the team identified trophoblast inclusions by performing microscopic examinations of placental tissues.

"We knew that trophoblast inclusions were increased in cases of chromosome abnormalities and genetic diseases, but we had no idea whether they would be significantly increased in cases of ASD," said Kliman. "These results are consistent with studies by others who have shown that ASD has a clear genetic basis."

Trophoblast inclusions reflect abnormal folding of microscopic layers in the placenta and appear to result from altered cell growth. Kliman likened the presence of trophoblast inclusions to an automobile check-engine-light. "When the light goes on it simply means that something is not right," said Kliman. "If the light is on and there is, for example, steam coming from under the hood, then it is likely that the radiator is leaking. However, if the check engine light is on and there is nothing obviously wrong, then the car should be carefully checked."

The Yale team plans to replicate the evaluation with larger multi-Center and prospective studies. They will examine the placentas of the children in the study in greater detail to gain insight into the biological basis of the inclusions in ASD.

Volkmar said, "If the work is confirmed by the next series of studies, then the finding of trophoblast inclusions at the time of birth in the absence of any obvious genetic abnormalities would be an indication to have a child examined by a specialist to determine the presence of ASD."

Citation: Biological Psychiatry, Published online (June 26, 2006)

Yale News Releases are available via the World Wide Web at http://www.yale.edu/opa



Saludos Cordiales
Dr. José Manuel Ferrer Guerra

Prozac saves thousands of lives

A New study should help alleviate any concern over a link between the use of certain antidepressants and suicide.
A New class of drugs called selective serotonin reuptake inhibitors (SSRI) have been increasingly used to treat depression and have undoubtedly saved thousands of lives, despite concerns of a possible link with an increased suicide risk.

Antidepressants such as Zoloft (Pfizer), Paxil (GlaxoSmithKline) and Prozac (Eli Lilly) are used by millions of Americans.

The Food and Drug Administration insisted on "black box warnings" on the most popular SSRIs in 2004 amid rising concerns in the United States and United Kingdom concerning the relationship between suicide and antidepressant use in children and adults.

The New study was conducted by Dr. Julio Licinio, while he was the director of the Center for Pharmacogenomics and Clinical Pharmacology at the Semel Institute for Neuroscience and Human Behavior, UCLA.

He is now the New chairman of the Department of Psychiatry and Behavioral Sciences at the University of Miami Leonard M. Miller School of Medicine.

The study analyzed federal data on overall suicide rates since the early 1960s along with sales of Prozac since the antidepressant's introduction in 1988 through to 2002.

The researchers found that the U.S. Suicide rate remained steady for 15 years prior to the introduction of fluoxetine, then dropped steadily over 14 years as sales of the antidepressant rose; the strongest effect was among women.

Licinio says the findings suggest that the introduction of SSRIs has contributed to the reduction of suicide rates in the United States.

Licinio also says the psychiatric community fears that the absence of such treatment may prove more harmful to depressed individuals than the effects of the drugs themselves, and most people who commit suicide suffer from untreated depression.

Major depressive disorder affects approximately 10 percent of American men and 20 percent of women over their lifetimes.

Because the prevalence is so high and treatment lasts several months or years, antidepressant medications are the most common form of treatment.

Prozac is the most widely prescribed antidepressant medication in the world and the only antidepressant that is FDA-approved for treatment of depression in children.

The research was funded by the National Institutes of Health and the Dana Foundation and is published in the June 2006 edition of the peer-reviewed Journal PLoS Medicine.




Saludos Cordiales
Dr. José Manuel Ferrer Guerra

Incorrect Condom Use Prevalent Among Teens

By Crystal Phend, MedPage Today Staff Writer
Reviewed by Robert Jasmer, MD; Assistant Professor of Medicine, University of California, San Francisco
August 10, 2006
Also covered by: BBC News, Forbes
Explain to interested patients that incorrect condom use is prevalent among teens.


Explain to interested patients that this study found good early family relationships promote safer sex practices later in the teenage years.


Note that the American Academy of Pediatrics recommends that physicians encourage abstinence in adolescent patients as well as correct and consistent use of reliable contraception and condoms when teens are contemplating or already sexually active.
SOUTHAMPTON, England, Aug. 10 -- Teens appear to have problems using condoms properly, found investigators here.

Up to a third of surveyed British teens had used a condom improperly, putting it on too late or removing it too soon, according to a study published online in Sexually Transmitted Infections.


"If we are to see a reduction in [sexually transmitted infection] prevalence, it is essential that young people understand the importance of using condoms consistently and correctly, and are also equipped with the skills and knowledge to do so," wrote psychologist Nicole Stone, Ph.D., of the Centre for Sexual Health Research at the University of Southampton.


Other Australian and American studies have found that 38% to 51% of teens reported applying a condom after initial penetration on at least one recent occasion and 14% to 15% reported removing it early.


"We should not simply assume that adolescents know how to do this," said David S. Rosen, M.D., M.P.H., of the University of Michigan in Ann Arbor, who commented on the British study. "When physicians talk with sexually active Male patients it's probably not enough to encourage them to use a condom but to be very specific in how to use condoms."


The British study surveyed 1,373 young people at 21 schools and colleges across England about their condom use at the most recent occasion of vaginal sex. Most participants were 16 to 18 years old. Of these, 108 were selected to participate in a second phase of the study in which they kept a diary for six months.


A little less than half of the surveyed teens reported having ever engaged in vaginal sex. A little more than 60% of these sexually active teens had used a condom on the most recent occasion.


Of those 375 survey participants who reported using a condom, 12% had used it incorrectly. Six percent applied the condom after penetration and another 6% continued engaging in sex after condom removal.


About 55% of the diary entries indicated condom use during sex. However, 7% of all condoms used during the diary phase were applied late and 2% were removed early. The most common responses for applying a condom late were intimacy, better sensation, use of another contraception method, and that they got carried away.


Only one diary entry indicated that the teen applied the condom, although penetration had already occurred, in order to prevent sexually transmitted diseases. Others replied that they used it in this circumstance to avoid pregnancy, to avoid making a mess, and to make sex last longer.


Overall, 31% of diary respondents applied a condom late and 9% removed it early at least once during the six-month diary phase of the study.


Teens who reported consistent condom use, confidence in correct condom use, not using another contraception method, and desire to use a condom were significantly less likely to use condoms incorrectly (P<0.05).


Survey respondents who reported having an unavailable mother or a poor relationship with her during their early teen years were 2.66 times more likely to improperly use condoms (P<0.05). Interestingly, this correlation was highly significant for men only (P<0.0001).


The reason may be that good early family relationships give teens an advantage in communication skills, less motivation to begin sexual relations at an early age, and different gender attitudes in general, the authors suggested.


Other studies have shown that age, primary partner, lack of partner support, multiple partners, and using condoms for contraceptive purposes only (rather than for protection against sexually transmitted diseases as well) increase the odds of delayed condom application.


The American Academy of Pediatrics recommends that physicians encourage abstinence in adolescent patients as well as correct and consistent use of reliable contraception and condoms when teens are contemplating or already sexually active.

Primary source: Sexually Transmitted Infections
Source reference:
Bethan Hatherall, et al "How, not just if, condoms are used: the timing of condom application and removal during vaginal sex among young people in England" Sex Transm Infect 2006;000:1-3.



Enviado por Dr. José Manuel Ferrer Guerra

Children's Health Tip of the Day - August 21, 2006

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Say the words “road trip” to most kids, and it means a visit to a theme park, day at the beach or jaunt to the mall. Say the words “road trip” to kids who suffer from motion sickness, and it means dizziness, nausea and vomiting.



Who gets motion sickness and why

About 90 percent of Americans suffer from motion sickness at some time in their life; toddlers and preschoolers are most susceptible.



Motion sickness results from a conflict between the eye and ear: the inner ears detect that the car is moving, but the eyes – which are focused within the car – do not. The brain gets conflicting signals, and nausea results. For example, if you are reading while riding in a car, your sight is detecting little movement because it is concentrating on the printed page, but your balance Center can still feel the larger movement of the car.



Any type of transportation can cause motion sickness – riding on an airplane, in a boat, a train, or a car. Even amusement park rides can bring on the uncomfortable symptoms.



How to spot motion sickness

The symptoms of motion sickness usually start with a slight feeling of queasiness, a cold sweat, fatigue and loss of appetite. A young child may not be able to describe the nausea, but will show signs by becoming pale and sweaty, and eventually, vomiting.



Protect your child from motion sickness

The best way to deal with motion sickness is to prevent it. Try the following tips to keep your children motion sickness free on your next “road trip”:


- Have him sit in the middle of the vehicle, and facing forward
- Have her look out the front window in the distance
- Don’t let him read or play with hand-held video games
- Feed her a small, nutritious snack, not a big meal, before the trip
- Avoid spicy or greasy foods
- Avoid strong odors such as cigarette smoke and smelly foods
- Open the window for fresh air
- Distract him by listening to a CD, the radio, or by talking
- Ask your pediatrician about motion sickness drugs and the appropriate dosage for children
- Plan your trip with enough stops to allow your child to get out and walk around if she needs to do so


When traveling by plane, request a seat over the front edge of a wing, and direct the air vent toward the child’s face. If going on a cruise, request a cabin in the middle of the ship near the water line. When riding on a train, seat your child near a window in a forward-facing seat.



How to respond to motion sickness

If your child starts to feel motion sickness:


- If possible, stop the activity immediately. Pull the car over and allow the child to get out and walk around.
- Place a cool damp cloth on the forehead.
- Feed her some dry crackers and a carbonated beverage.


Reviewed by: Patrick S. Pasquariello Jr., MD

Date: May 2005


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Enviado por Dr. José Manuel Ferrer Guerra

Study Provides Evidence That Autism Affects Functioning of Entire Brain

A recent study provides evidence that autism affects the functioning of virtually the entire brain, and is not limited to the brain areas involved with social interactions, communication behaviors, and reasoning abilities, as had been previously thought. The study, conducted by scientists in a research network supported by the National Institutes of Health (NIH), found that autism also affects a broad array of skills and abilities, including those involved with sensory perception, movement, and memory.

The findings, appearing in the August Child Neuropsychology, strongly suggest that autism is a disorder in which the various parts of the brain have difficulty working together to accomplish complex tasks.

The study was conducted by researchers in the Collaborative Program of Excellence in Autism (CPEA), a research network funded by two components of the NIH, the National Institute of Child Health and Human Development and the National Institute on Deafness and Other Communication Disorders.

“These findings suggest that further understanding of autism will likely come not from the study of factors affecting one brain area or system, but from studying factors affecting many systems,” said the director of NICHD, Duane Alexander, M.D.

People with autism tend to display 3 characteristic behaviors, which are the basis of the diagnosis of autism, explained the study’s senior author, Nancy Minshew, M.D., Professor of Psychiatry and Neurology at the University of Pittsburgh School of Medicine. These behaviors involve difficulty interacting socially, problems with verbal and non-verbal communications, and repetitive behaviors or narrow, obsessive interests. Traditionally, Dr. Minshew said, researchers studying autism have concentrated on these behavioral areas.

Within the last 20 years, however, researchers began studying other aspects of thinking and brain functioning in autism, discovering that people with autism have difficulty in many other areas, including balance, movement, memory, and visual perception skills.

In the current study, Dr. Minshew and her colleagues administered a comprehensive array of neuropsychological tests to a group of children with autism. The researchers tested 56 autistic children, and compared their responses to those of 56 children who did not have autism. The children with autism were classified as having higher functioning autism — an I.Q. Of 80 or above, and the ability to speak, read, and write. All of the children in the study ranged in age from 8 to 15 years. The purpose of the test array, Dr. Minshew said, was to determine whether there were any patterns in mental functioning unique to autism.

“We set out to find commonalities across a broad range of measures, so that we could make inferences about what’s going on in the brain,” Dr. Minshew said.

The researchers found that, across the entire series of tests, the children with autism performed as well as — and in some instances even better than — the other children on measures of basic functioning. Uniformly, however, they had trouble with complex tasks.

For example, regarding visual and spatial skills, the children with autism were very good at finding small objects in a cluttered visual field, on tasks like finding Waldo in the “Where’s Waldo” picture books series. However, when asked to perform a complex task, like telling the difference between the faces of similar looking people, they had great difficulty.

Although their memory for the detail in a story was phenomenal, the children with autism had great difficulty comprehending the story. Many were highly proficient at spelling and had a good command of grammar, but had difficulty understanding complex figures of speech, like idioms and metaphors.

“We see this with our patients,” Dr. Minshew said. “If you use an expression like ‘hop to it,’ a child with autism may literally hop.”

Other complex tasks were also difficult for them. The children with autism either had poor handwriting, or wrote very slowly. Many had difficulty tying their shoes and with using scissors.

“These findings show that you can’t compartmentalize autism under three basic areas,” Dr. Minshew said. “It’s much more complex than that.”

Dr. Minshew explained that the major implication of the finding is that when seeking to understand autism, researchers need to look for a cause or causes that affect multiple brain areas, rather than limiting their search to brain areas dealing with the three characteristic behaviors involving social interactions, communication, and repetitive behaviors or obsessive interests.

“Our paper strongly suggests that autism is not primarily a disorder of social interaction, but a global disorder affecting how the brain processes the information it receives — especially when the information becomes complicated.”

In previous research with an imaging technology known as functional magnetic resonance imaging, or fMRI, Dr. Minshew and her coworkers determined that adults with autism have abnormalities in the neurological wiring through which brain areas communicate. In those studies, the researchers found that people with autism had difficulty performing certain complex tasks that involved brain areas working together. (This research is described in previous releases, http://www.nichd.nih.gov/new/releases/final_autism.cfm, and http://www.nichd.nih.gov/new/releases/autism_brain_structure.cfm.)

Dr. Minshew said that such abnormalities in brain circuitry provide the most likely explanation for why the children with autism in the current study have difficulty with complex tasks that require coordination among brain regions but do well on tasks that require only one region of the brain at a time.

The researchers undertook the current study as a follow up to an earlier study they did of adults with autism. The researchers studied children to determine if the features of autism were consistent throughout life, or changed as people with autism grow older. For the most part, the current study revealed that both adults and children with autism experience the same kinds of difficulties with complex tasks.

One difference is that adults with autism appear to score higher on tests involving sensory interpretation than do children with autism. Such tests would involve identifying a number traced on a finger tip, or identifying an object placed in one’s hand without looking at it. Dr. Minshew said that as people with autism grow older, they may have less sensory difficulty than they did as children.

Still, adults with autism fare much worse on tests of complex language and reasoning than do other adults. This gap in complex language and reasoning ability between the two groups is not as pronounced when children with autism are compared to other children. This is because children’s brains have not yet developed these skills, Dr. Minshew said. However, the gap widens with time. As typical children get older, they develop these higher order language and reasoning skills while adolescents and adults with autism do not.

The NICHD sponsors research on development, before and after birth; maternal, child, and family health; reproductive biology and population issues; and medical rehabilitation. For more information, visit the Institute’s Web site at http://www.nichd.nih.gov/.

The National Institutes of Health (NIH) — The Nation's Medical Research Agency — includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.


Enviado por Dr. José Manuel Ferrer Guerra

FDA Approvals: Solodyn and Dacogen

News Author: Yael Waknine
CME Author: Yael Waknine

The US Food and Drug Administration (FDA) has approved minocycline HCl extended-release tablets for the once-daily treatment of inflammatory lesions of nonnodular moderate to severe acne vulgaris in patients aged 12 years and older; and decitabine injection for the treatment of patients with myelodysplastic syndromes.
Minocycline Extended-Release Tablets (Solodyn) for Acne in Adolescents and Adults
On May 8, the FDA approved an extended-release formulation of minocycline HCl tablets (Solodyn, made by Medicis Pharmaceutical Corp) for the treatment of inflammatory lesions of nonnodular moderate to severe acne vulgaris in patients aged 12 years and older.

According to a company news release, the lipid-soluble formulation exerts its action in the skin and sebum. It is not bioequivalent to any other previously approved minocycline products and is in no way interchangeable with other forms of the drug. Minocycline extended-release tablets have not been evaluated in the treatment of infections.

The approval was based on data from two 12-week multicenter, randomized, double-blind, clinical trials in 924 patients. Result showed that extended-release minocycline was associated with a greater mean percent change in inflammatory lesion counts from baseline, relative to placebo (study 1, 43.1% vs 31.7%; study 2, 45.8% vs 30.8%).

Moreover, a greater number of patients receiving minocycline therapy were clear or almost clear at 12 weeks, as rated using the Evaluator's Global Severity Assessment scale (study 1, 17.3% vs 7.9%; study 2, 15.9% vs 9.5%).

The most commonly reported adverse events related to use of the study drug included headache, fatigue, dizziness, and pruritus. Although central nervous system adverse effects, such as light-headedness, dizziness, and vertigo, have been reported with other minocycline therapies, these were not significant in patients receiving extended-release tablets. Photosensitivity was reported rarely.

The recommended dosage for minocycline extended-release tablets is 1 mg/kg daily for 12 weeks; no loading dose is required. According to FDA-approved labeling, higher doses have not conferred additional benefit in the treatment of inflammatory acne lesions and may be linked with more acute vestibular adverse effects. The tablets are supplied in 45-, 90-, and 135-mg strengths.

Minocycline extended-release tablets should not be used by individuals attempting to conceive a child nor should they be taken during pregnancy; concurrent use of minocycline may reduce the efficacy of oral contraceptives.

Decitabine Injection (Dacogen) for Patients With Precancerous Myelodysplastic Syndromes
On May 2, the FDA approved decitabine injection (Dacogen, made by MGI Pharma, Inc) for the treatment of patients with myelodysplastic syndromes (MDS). It is intended for use in previously treated and untreated, de novo, and secondary MDS of all French-American-British subtypes (refractory anemia, refractory anemia with ringed sideroblasts, refractory anemia with excess blasts, refractory anemia with excess blasts in transformation, and chronic myelomonocytic leukemia), and intermediate-1, intermediate-2, and high-risk International Prognostic Scoring System groups.

According to a company news release, the agent is thought to exert its antineoplastic effects via incorporation into DNA and inhibition of DNA methyltransferase. Decitabine-induced hypomethylation in neoplastic cells may restore normal function to genes previously silenced by abnormal methylation, thereby reestablishing control of cellular differentiation and proliferation.

The approval was based in part on data from an open-label, multicenter, phase 3 controlled clinical trial of 170 MDS patients at medium to high risk of developing acute myeloid leukemia.

Results showed that the addition of decitabine to supportive therapy yielded a significant increase in overall response rate compared with supportive therapy alone (17% vs 0%; P < .001; complete response, 9%; partial response, 8%). The median time to response was 93 days (range, 55 - 272 days), with a median duration of 288 days (range, 116 - 388 days).

Among decitabine-treated patients who had undergone 2 or more treatment cycles, the overall response rate was 21%. Benefit in the form of hematologic improvement was observed in an additional 13% of patients compared with 7% in the supportive care group. Treatment with decitabine did not significantly delay the median time to acute myeloid leukemia or death.

These findings were supported by results from 2 open-label, single-group, multicenter phase 2 studies, showing that decitabine induced overall response rates of 26% (n = 66) and 24% (n = 98), respectively.

Decitabine-related adverse events in the studies most commonly included neutropenia (90%), thrombocytopenia (89%), anemia (82%), pyrexia (53%), fatigue (48%), nausea (42%), cough (40%), petechiae (39%), constipation (35%), and diarrhea (34%).

The recommended dose of decitabine for the initial treatment cycle is 15 mg/m2 administered by continuous intravenous infusion for 3 hours and repeated every 8 hours for 3 days. Premedication with standard antiemetic therapy may be considered.

The cycle should be repeated every 6 weeks for a minimum of 4 cycles. The FDA notes that a complete or partial response may take longer than 4 cycles and that treatment may be continued as long as the patient continues to benefit.

If hematologic recovery (elevated neutrophil and platelet counts) from a previous treatment cycle requires longer than 6 weeks but less than 8 weeks, the next decitabine cycle should be delayed for up to 2 weeks. On resumption of therapy, the dose should be temporarily reduced to 11 mg/m2 every 8 hours (33 mg/m2/day, 99-mg/m2/cycle).

If recovery requires more than 8 but less than 10 weeks, the patient should be assessed for disease progression (bone marrow aspirates). In the absence of progression, the next decitabine cycle should be delayed for up to 2 more weeks, and the dose temporarily reduced as above.

Decitabine should be discontinued permanently pending resolution of certain nonhematologic toxicities, such as serum creatinine levels of 2 mg/dL or greater; serum glutamic pyruvic transaminase or total bilirubin levels 2 or more times the upper limit of normal; and active or uncontrolled infection.

Because of the risk for fetal harm, women of childbearing potential should take measures to avoid becoming pregnant during decitabine therapy. Also, men should not father children during treatment and for 2 months after receiving their last dose of decitabine.

Decitabine is supplied in vials containing 50 mg of the lyophilized product for reconstitution to a 0.1- to 1.0-mg/mL solution. If possible, it should be administered within 15 minutes of reconstitution. Alternatively, the injection can be reconstituted using cold fluid and stored for up to 7 hours at 2 to 8°C.

The product previously was granted orphan drug status by the FDA for this indication and the treatment of chronic myelogous leukemia and by the European Commission as an orphan drug for MDS. Its use for acute myeloid leukemia is currently being investigated in a phase 3 trial.

Learning Objectives for This Educational Activity
Upon completion of this activity, participants will be able to:
Identify a new formulation of minocycline for the treatment of acne.
Describe the appropriate use of minocycline extended-release tablets.
Evaluate the benefits of decitabine therapy for the treatment of MDS.
Pearls for Practice
The FDA has approved an extended-release formulation of minocycline tablets for the treatment of inflammatory lesions of nonnodular moderate to severe acne vulgaris in patients aged 12 years and older. The product is not bioequivalent to any other minocycline products nor is it interchangeable with any other forms of the drug.
The recommended dosage for minocycline extended-release tablets is 1 mg/kg daily for 12 weeks; no loading dose is required. The tablets are supplied in 45-, 90-, and 135-mg strengths. Adverse events may include headache, fatigue, dizziness, and pruritus. Pregnant patients and those of both sexes attempting to conceive a child should not receive minocycline therapy; treatment may also reduce the efficacy of oral contraceptives.
The FDA has approved decitabine injection for the treatment of myelodysplastic syndromes. In clinical trials, decitabine induced overall response rates ranging from 17% to 26% vs 0% for supportive therapy alone. Decitabine is administered by continuous infusion (15 mg/m2 for 3 hours), repeated every 8 hours for 3 days. The cycle should be repeated every 6 weeks for a minimum of 4 cycles. Pretreatment with standard antiemetic therapy should be considered.

Saludos Cordiales
Dr. José Manuel Ferrer Guerra

New Extension website offers recipes for people with diabetes

University of Illinois Extension has a New resource on diabetes -- "Recipes for Diabetes" to assist people with diabetes in preparing healthy foods..

Karen Chapman-Novakofski, Associate Professor and Nutrition Specialist developed this New site with recipes on main dishes, side dishes and desserts. The site is at: http://www.urbanext.uiuc.edu/diabetesrecipes.

The recipes have been either part of Illinois Extension's Dining with Diabetes or Living Well with Diabetes programs, or have been featured in the Illinois Extension newsletter, "Diabetes Lifelines."


Each recipe also contains an approximate nutritional analysis for calories, protein, carbohydrate, fat, saturated fat, fiber, sodium, and cholesterol. Exchanges have been calculated based on the exchange list of the American Diabetes Association and the American Dietetic Association. For those using the carbohydrate counting method of meal planning carbohydrate units are also provided.

A link to this website can be found on the main page of the Fulton County Extension website at www.extension.uiuc.edu/fulton. The site provides a calendar of upcoming Extension programs, online registrations to meetings and workshops, news releases, newsletters, and information on ag and natural resources; children, families, and seniors; community and economic development; horticulture and environment; money management; nutrition and health; 4-H and youth; and a special section just for kids.




If you do not know me, do not judge me
CERTIFICADO CONTRA VIRUS POR BIT DEFENDER PROFESSIONAL PLUS 8


http://groups.yahoo.com/group/DaisyDoodlesStats-n-Songs
DaisyDoodles
Graphics From WWW
No Copyright Infringement Intended



Saludos Cordiales
Dr. José Manuel Ferrer Guerra

IAC: Dyslipidemia in Children Abated by Switched Regimens

By Ed Susman, MedPage Today Staff Writer
Reviewed by Robert Jasmer, MD; Assistant Professor of Medicine, University of California, San Francisco
August 14, 2006

Explain to parents that side effects with antiretroviral drugs impact children's lipid profiles as well as adults being treated with those drugs.


Note that body changes in children are difficult to observe because of the on-going Nature of their development.


This study was published as an abstract and presented at an industry-sponsored symposium conference. These data were not peer-reviewed.
TORONTO, Aug. 14 -- Children treated for HIV infection are at increased risk of dyslipidemia, but a switch in regimens may dampen the impact of those metabolic changes.

In a mini-satellite symposium held in conjunction with the 16th International AIDS Conference, Alessandra Vigano, M.D., chief of pediatrics infectious disease at the University of Milan in Italy reviewed studies that involved long-term treatment of children with highly active antiretroviral therapy (HAART).


"This population is particularly vulnerable because children are growing and are likely to have long-term exposure to highly active antiretroviral therapy," Dr. Vigano said during the Bristol-Myers Squibb Canada-sponsored symposium, Metabolic Complications: New Insights and Evolving Management Strategies.


Various studies have shown that abnormalities in lipids occur 13% to 52% of the time in all patients taking combination antiretroviral therapy. Dr. Vigano suggested that these abnormalities occur more frequently in children with lipodystrophy and that the phenomenon is associated with protease inhibitors.


She cited one European study in which 280 children ages three to 18 underwent lipid testing. The median age of the children was nine. She said that study found that 27% of those children had hypercholesterolemia with levels of cholesterol greater than 200 mg/dl. She also said the study found that 21% of the children had elevated triglycerides, and 10% of them had both high cholesterol and high triglycerides.


In a study that Dr. Vigano reported in 2005, 14 children were switched from a regimen of Zerit (stavudine), Epivir (lamivudine), and a protease inhibitor to a New regimen of Viread (tenofovir), Epivir and Sustiva (efavirenz) in a 48-week randomized trial.


At the start of the trial nearly half the children were in the 95th percentile of cholesterol level. After 48 weeks, none of the children was in the 95th percentile. After 12 weeks on the New regimen, there were less than 10% of the children in the 95th percentile.


The story was similar for triglycerides with the percentage of children in the 95th percentile falling from 42% at baseline to less than 10% after 48 weeks.


In a 96-week study, 24 children were switched from Zerit to Viread and from a protease inhibitor to Sustiva. "Switching from Zerit to Viread was associated with restoration of physiological fat accrual and a lack of lipoatrophy progression." Dr. Vigano said.


"These changes may well yield possible positive effects on pubertal development, fertility, psychological wellness and normal lipid and glucose metabolism," she said.


While the studies indicate that treatment changes can alter unhealthy lipid abnormalities in children, Dr. Vigano noted that there has been little research on the subject. "Data on the long-term consequences of these metabolic complications are lacking," she said. "An important goal in treating pediatric HIV-infection will be to design drugs with fewer side effects or to better mange those of the current drugs."

Primary source: 16th International AIDS Conference


Enviado por Dr. José Manuel Ferrer Guerra

Topics in Diabetic Retinopathy

Hans-Peter Hammes, MD, PhD


The symposium entitled "Diabetic Retinopathy -- Diagnostic and Treatment Novelties[1]" centered on 2 important areas of research: (1) the retina as an additional independent risk indicator of cardiovascular morbidity and mortality and (2) clinical treatments.

Insulin-like Growth Factor-1 Antagonists in the Treatment of Retinopathy
Maria Grant, MD,[2] University of Florida, Gainesville, reported on 2 large, as yet unpublished studies in which patients with preexisting diabetic retinopathy were treated with an insulin-like growth factor (IGF) antagonist. With the report of Poulsen (1953) that patients with spontaneous destruction of the pituitary gland experienced resolution of proliferative diabetic retinopathy, a long series of experimental and clinical studies assessed whether the growth hormone (GH)-IGF-1 axis had a role in the initiation and/or progression of diabetic retinopathy. It was demonstrated by several groups that (1) patients with diabetic retinopathy had elevated serum IGF-1 levels; (2) patients with proliferative diabetic retinopathy had elevated IGF-1 levels in their vitreous; and (3) IGF-1 was acting with the other important retinal growth factor, vascular endothelial growth factor (VEGF), to induce retinal neovascularizations.

Experimental inhibition of the GH-IGF-1 axis in a model of acute proliferative retinopathy prevented New vessel formation, and small clinical trials by Dr. Grant[3] and researchers in Europe indicated that the Administration of the somatostatin analog octreotide was beneficial. However, the need for frequent Administration of the drug prevented wider therapeutic application. With the development of a long-acting release form of octreotide (Sandostatin LAR, Novartis), the groundwork was established for larger clinical trials.

Dr. Grant reported the results of two of these trials, known as the 802 study and the 804 study. In the 802 study, 61 centers in 15 European countries recruited 585 patients who had moderate-to-severe nonproliferative to non-high-risk proliferative diabetic retinopathy (Early Treatment Diabetic Retinopathy Study [ETDRS] levels 47-61). The primary endpoints of the study were to assess the effect of 2 doses of octreotide long-acting release injection (20 mg and 30 mg once per month) on the progression of preexisting diabetic retinopathy, i.e., prevention of a 3-step progression on the ETDRS retinopathy scale or a more than 2-step progression in an individual eye. Secondary endpoints were the time to development of macular edema and the loss of visual acuity. Safety and tolerability also were assessed.

In the 804 study, 313 patients from sites in the United States, Canada, and Brazil received 30 mg octreotide long-acting release injection once per month; primary endpoints were the same as the 802 study. (Patient characteristics will be described in detail soon in a full paper.) The most important finding was the significant delay in time to progression of retinopathy with the Administration of 30 mg of octreotide in the 804 study (hazard ratio [HR], 0.6; P < .043). No effect was observed for visual acuity and progression to macular edema. Safety and tolerability were within margins of previous studies, the most frequent side effects being diarrhea, development of cholelithiasis, and mild hypoglycemia.

The 802 study failed to confirm these results. When comparing serum IGF-1 levels in the 2 studies as parameters of the efficacy of octreotide treatment, there was a difference in the level of suppression, indicating that the 804 trial had better patient compliance and study monitoring than the 802 study. Together, these data are consistent with the concept that the GH-IGF-1 system plays an important role in the propagation of retinal neovascularization, and that treatment with somatostatin analogs can significantly inhibit the clinically relevant progression to more severe stages of diabetic retinopathy.

Lipids and Retinopathy
There is an ongoing debate about whether elevated lipids are important in the pathogenesis of diabetic retinopathy. Several historical anecdotal reports have shown that diabetic patients with elevated lipids were more prone to diabetic macular edema, and that treatment with lipid-lowering drugs resolved these deposits. Because elevated lipids are involved in atherosclerosis and vessel stenosis, including stenosis of the carotid artery, an indirect relationship may exist between hyperlipidemia and diabetic retinopathy, given that moderate carotid artery stenosis protects from diabetic retinopathy, whereas more severe stenosis leads to ischemic retinopathy. The Atherosclerosis Risk in Communities (ARIC) study showed a weak but significant correlation between thickening of the carotid artery intima-media wall and diabetic retinopathy.[4] In that light, Paul Dodson, MBBS, MD, FRCP, FRCOphth,[5] Birmingham Heartlands Hospital, Birmingham, United Kingdom, summarized studies on the effect of statins and fibrates in the treatment of diabetic retinopathy.

In the Collaborative Atorvastatin Diabetes Study (CARDS),[6] approximately 1400 patients with type 2 diabetes received 10 mg of atorvastatin for primary prevention of coronary heart disease, which resulted in a 26% drop in total cholesterol and a 40% drop in low-density lipoprotein (LDL) cholesterol. Treatment duration was 4-4.5 years. At baseline and at annual follow-up, the investigators reported whether any fundal examination record from the previous year showed "no retinopathy," "nonproliferative retinopathy," "preproliferative retinopathy," or "proliferative retinopathy." Whether the patient had received photocoagulation in the past year was also noted, but the type or purpose of any photocoagulation was not recorded. Retinal photographs were not obtained. The investigators used accelerated failure time models with interval censoring to examine whether there was any treatment effect on retinopathy over a median 4-year follow-up.

The study's main problem was that there were considerable data missing, both at baseline and during follow-up. Of 2838 patients enrolled in CARDS, only 65% had retinopathy status recorded at baseline, and 39% of these patients had some retinopathy. There was no effect of treatment on progression of retinopathy severity by at least 1 step (6% lower rate in the atorvastatin group; P = .5). At least 1 follow-up recording of photocoagulation status was available in 2298 (81%) participants. Baseline status was available in just 1729 of these (61% overall). The incidence of photocoagulation was 6.03/100 person-years at risk (95% confidence interval [CI]: 5.28, 6.90) in the placebo group and 5.50/100 person-years at risk (95% CI: 4.81, 6.30) in the atorvastatin group. This 13% reduction in coagulation with atorvastatin treatment (P = .4) increased to a 21% reduction on adjusting for baseline status but remained nonsignificant (P = .1).

Firm conclusions about the effect of atorvastatin on retinal outcomes in CARDS are hindered by the lack of photographs and considerable missing data. Although there was no clear evidence of a treatment effect, the results, although nonsignificant, are consistent with some protective effect.

The Eye as a Risk Marker for Cardiovascular Morbidity and Mortality: Yes and No
The retinal circulation has long been considered a window to the systemic circulation. Studies by Gunn (1898) had already demonstrated retinal changes in patients with hypertension. However, ophthalmoscopy as a routine diagnostic procedure had been found too imprecise to allow for assessments of retinal vessel changes as a risk indicator of increased cardiovascular morbidity and mortality. Gabrielle Tikellis, PhD,[7] Center of Eye Research Australia, Melbourne, Australia, summarized data from the 6 studies over the past few years that have demonstrated clearly that vessel changes in the eye serve as a risk marker: ARIC, the Cardiovascular Health Study (CHS), the Beaver Dam Eye Study, the Blue Mountain Eye Study, the Wisconsin Epidemiologic Study of Diabetic Retinopathy Study (WESD), and the Rotterdam study.

Two distinct groups of lesions were analyzed with novel technologies to digitize and quantitatively analyze retinal photographs: (1) focal lesions, including arteriolar narrowing, arteriovenous nicking, microaneurysms/dot hemorrhages, cotton-wool spots, retinal arteriolar wall opacification; and (2) diffuse lesions, such as generalized arteriolar narrowing and changes in the arteriovenous ratio of vessel width (AVR). The overall prevalence of retinal signs of damage was 3% to 14%. A decrease in retinal arteriolar diameter was observed with increasing blood pressure, and a reduced AVR (meaning a progressive generalized narrowing of retinal arterioles) was associated with higher risk of developing metabolic syndrome or overt diabetes. Isolated venular dilatation was associated with developing proteinuria. Cotton-wool spots indicated a 6.4-fold greater risk for stroke, and microaneurysms indicated a 4-fold greater risk for stroke. These lesions were even more predictive for congestive heart failure. In persons with diabetes, a 4.5-fold greater increased risk for congestive heart failure was observed when retinopathy was present. In the Beaver Dam Eye Study, a reduction in AVR was significantly associated with hypertension, increased intima-media thickness, stroke, congestive heart failure, and cardiovascular mortality. With the improved precision of novel methods of analysis, the retina provides independent information on cardiovascular morbidity and mortality.

Providing a contrary view, Manon van Hecke, MD, PhD,[8] VU University Medical Center, Amsterdam, The Netherlands, pointed out that several of the above studies did not consistently find associations between focal and generalized changes in the eye and cardiovascular events, indicating that the issue may be much more complex than when viewed at first glance. Depending on the type of study and the parameters assessed, retinal vessel changes did not always reflect cardiovascular prognosis. For example, in the Hoorn Study,[9] a population-based cohort study of over 600 patients with type 2 diabetes, there was a significant association of retinopathy with all-cause and cardiovascular mortality. However, after controlling for diabetes duration, body mass index, and prior cardiovascular disease, this association was no longer found.

The mechanisms explaining why retinal vessels may not exactly mirror what happens to the macrovascular systems are, however, not clear. The Hoorn study addressed the following question: If microvascular dysfunction affects the risk for atherosclerosis, by which mechanism(s) does this occur? For that purpose, a cohort of 256 patients with type 2 diabetes was studied. Retinal photographs were taken and related to flow-mediated dilatation of forearm blood flow (endothelial-dependent) and to nitroglycerin-dependent vasodilatation (endothelial-independent). No difference was found in flow-mediated vasodilatation, nitroglycerin-dependent vasodilatation, and intima-media thickness for those with and without retinal abnormalities. The only retinal parameter that showed a significant association with intima-media thickness was retinal venular dilatation. Thus, retinal microvascular disease was not associated with large artery endothelial dysfunction in the established type 2 diabetes group.

Ruboxistaurin and Retinopathy
An oral presentation session on diabetic retinopathy was entitled "More than VEGF and PKC"; however, the most important paper in this session actually was about protein kinase C (PKC). Lloyd Paul Aiello, MD, PhD,[10] Joslin Diabetes Center, Harvard Medical School, Boston, Massachusetts, reported on a combined analysis of the trials with the PKC inhibitor ruboxistaurin in diabetic patients. The final analysis was done on 608 patients with the following characteristics: 59 years of age (SD 11); 85% had type 2 diabetes, with an average duration of 15 years; mean glycated hemoglobin (A1C) was 8.2%; 10% had retinopathy ETDRS level < 47, and 60% had ETDRS level of 47. The primary aim was prevention of retinopathy progression; the secondary aim was the prevention of vision loss. Although the primary target was not met, the reduction in sustained moderate vision loss was 4.2% (relative risk reduction, 41%; P = .011). Safety and tolerability were shown to be excellent in light of the need for long-term administration.

Calculating the Risk for Diabetic Retinopathy
Data from the United Kingdom Prospective Diabetes Study (UKPDS) have been used to calculate the risk for fatal and nonfatal macrovascular complications in patients with type 2 diabetes, and a downloadable version (UKPDS Risk Engine 2.0) is available online.[11] At the American Diabetes Association (ADA) meeting, Ruth L. Coleman,[12] Diabetes Trials Unit, University of Oxford, Oxford, United Kingdom, presented a risk calculator for diabetic retinopathy. UKPDS data were used to construct a model on the basis of 1949 patients for whom complete data were available. Their baseline characteristics (mean age, 54; A1C 7.1%; systolic blood pressure, 136 mm Hg; total cholesterol 210 mg/dL; HDL 43 mg/dL; body mass index [BMI] 28) did not differ from the original cohort of 5100 patients. After 12 years, a total of 50% of the patients had developed at least mild nonproliferative diabetic retinopathy. Univariate risk-factor analysis revealed macroalbuminuria, microalbuminuria, prior cardiovascular events, and metabolic control as the most important risk factors. In a multivariate analysis, macroalbuminuria and metabolic control were retained. Increasing age and smoking reduced the risk, whereas diabetes duration and systolic blood pressure contributed stepwise. Risk of developing diabetic retinopathy over t years in patients without diabetic retinopathy is:

Risk (t) = 1 - exp(-0.038 x 0.950AGE-55 x 0.793CURRENT SMOKER x 1.251HbA1c-6.8 x 1.111(SBP - 135.5)/10 x 2.800MACROALBUMINURIA x 1.046DIABETES DURATION x Sigmas0.174
Thus, the likelihood of developing diabetic retinopathy in patients with type 2 diabetes can be calculated from available clinical information with sufficient precision. Internal validation of the system has been performed successfully, whereas external validation awaits.

Enviado por Dr. José Manuel Ferrer Guerra

Grow Fast, Learn Slow

In a New study of zebra finches, scientists at Glasgow University have found that accelerated growth following an initial diet of poor quality food can result in slower learning in adulthood.

Professor Pat Monaghan of Glasgow University, said: “ If environmental conditions improve for animals that have previously experienced a poor quality diet, their growth can accelerate to catch up in body size. We have found that this very rapid growth can carry long term costs - in our study on birds the greater the growth spurt in the chick, the poorer the learning performance of the adult.”

The findings of this research, funded by the Natural Environment Research Council, appear to be common across other species. Studies of humans and early nutrition have also found that low birth weight babies who grow quickly when fed an enriched diet have a similarly lower performance when tested at nine months compared with babies given a normal diet. Unlike the finches ‘though, this effect seems not to be so long lasting in humans.

In the zebra finches study, the scientists provided siblings with unlimited amounts of different quality food for a short period after hatching. Those that got the lower quality diet, which had less protein and vitamins, were then switched to the normal food. To test the long-term effect on learning abilities, the scientists gave all the birds a simple learning task involving finding food behind colour screens once they reached adulthood. Although all the birds eventually learned the task, how fast they did so was related to the rate of compensatory growth they had undergone as chicks. Birds that had grown fastest when switched to the normal diet were slowest to learn the task

The results suggest that accelerating growth can have long lasting negative consequences for learning ability. What is not clear at this point is whether the learning defects stem from behavioural, hormonal or neural changes. It is possible that resources normally dedicated to these pathways are diverted to support the accelerated growth. But in the harsh competitive world of Nature, being big may be more important than being bright.

About the NATURAL ENVIRONMENT RESEARCH COUNCIL (NERC)

The mission of the Natural Environment Research Council is to promote and support, by any means, high quality basic, strategic and applied research, survey, long-term environmental monitoring and related postgraduate training in terrestrial, marine and freshwater biology and Earth, atmospheric, hydrological, oceanographic and polar sciences and Earth observation.

NATURAL ENVIRONMENT RESEARCH COUNCIL (NERC)
Polaris House
North Star Avenue
Swindon

http://www.nerc.ac.uk

Saludos Cordiales
Dr. José Manuel Ferrer Guerra

Children's Health Tip of the Day - August 08, 2006

As they grow, your children will reach many milestones: their first tooth, first steps, first words – and first “big kid” bed.

Saying goodbye to the crib

Generally, children are ready to make the move from crib to bed somewhere between the ages of 2 and 3. Signs of “readiness” include:


- When the child is about 35 inches tall.
- If she is able to stand up and climb out of the crib with the mattress at the lowest setting.
- When he is able to put himself back to sleep when he wakes up in the middle of the night.
- When she is potty trained.


Making the big step easier

Experts agree that the move from crib to bed is a big step for children, and offer the following tips to ease the transition:


- Allow your child to help pick out her New bed and blanket.

- Move as many things from his crib to his bed, such as a favorite quilt or toy.

- If space allows, set up the bed in the same room with the crib to allow her to get used to it.

- Let him take his daytime naps in the bed.

- Don’t try moving your child during a stressful time, such as after the arrival of a New sibling, moving to a New home, starting a New daycare, beginning potty training, etc.

- Stick to the bedtime routine to which she is accustomed.


If your child is resistant to sleeping in her New bed, it may be better to wait a few months. As long as she isn’t climbing out of the crib, you can continue to “talk up” the idea of a “big kid” bed until she is ready.



Reviewed by: Patrick S. Pasquariello Jr., MD

Date: March 2005


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The word "first" is inextricably linked with The Children's Hospital of Philadelphia. Since we opened our doors in 1855 as the nation's first hospital devoted exclusively to the care of children, Children's Hospital has been the setting for many dramatic firsts. Our remarkable institution and its staff and physicians have fostered Medical discoveries, innovations and breakthroughs that have benefited children throughout the world.

Today, The Children's Hospital of Philadelphia is ranked among the leading pediatric hospitals and research facilities in the world, and was recently rated the number one children's hospital in the U.S. By Child magazine.. Our resources are committed to providing exceptional patient care, training New generations of pediatric healthcare providers and pioneering major research initiatives.

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Enviado por Dr. José Manuel Ferrer Guerra

Researchers Discover Mutations In The Progranulin Gene Cause Frontotemporal Dementia

Researchers at Mayo Clinic and colleagues at the University of British Columbia and the University of Manchester have discovered mutations in the progranulin gene cause frontotemporal dementia (FTD). Their work, which will be published in the July 16 online edition of the Journal Nature, indicates that progranulin function plays an important but previously unrecognized role in neuronal survival.

Progranulin is a type of protein known as a growth factor. Production of too much progranulin has been associated with cancer. So the gene that codes for progranulin was not an obvious one to sequence in order to look for mutations that cause neurodegenerative disease. However, researchers solved a ten-year genetic puzzle when they found mutations in the gene explain a large number of FTD cases in North America and Europe.

Although researchers found the age of onset in people carrying one of these mutations can come as early as their 50s or as late as their 90s, it is almost certain that anyone with an identified progranulin gene mutation will develop FTD at some point in life if they live long enough.

FTD, the second most common form of dementia after Alzheimer's disease, is a group of brain disorders that affect the frontal and temporal lobes of the brain, which control personality and speech. One or both of these functions may be affected. Patients may exhibit apathetic or uninhibited behavior and increasing lack of self-awareness. Patients may also lose the ability to put words together to form intelligible sentences. Speech decreases, and patients may become mute. However, patients usually retain memory until later in the disease course. This differentiates FTD from Alzheimer's disease, where memory function is affected early on.

In 1996 researchers first linked a genetic cause for FTD to chromosome 17. In 1998 Mayo Clinic neurobiologist, Michael Hutton, Ph.D., and others discovered mutations in a gene on chromosome 17 that codes for a protein called tau. Investigators discovered mutations in this gene cause the disease in patients from a number of families with a history of FTD. However, many FTD-affected families with genetic linkage to chromosome 17 lacked these mutations, so researchers continued to hunt for an additional culprit gene or genes. "It was like looking for two needles in the same haystack, and you didn't know you were looking for the second one until you found the first one," Hutton says.

Hutton led a group of collaborators within Mayo Clinic, the University of British Columbia and Vancouver Coastal Health Research Institute in Vancouver, Canada, and the University of Manchester in the United Kingdom. They analyzed over 80 genes close to the tau gene in FTD-affected and unaffected individuals from a large Canadian family with linkage to chromosome 17, but they failed to find any disease-causing mutations. However, when they sequenced the progranulin gene, located in the same genetic region, they found the first mutation. Subsequent analysis of 42 more FTD families identified a total of nine different mutations in the progranulin gene. All of the mutations effectively knock out one copy of the gene, and therefore its ability to direct production of progranulin. (Gene sequencing is the process of determining the order of the four DNA bases. Each of the approximately 30,000 human genes has its own unique order.)

"What we've found is a little bit different than what we've found in other common neurodegenerative diseases," Hutton says. "What we're looking at here is simply the loss of progranulin that is causing the disease." Other neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease and even FTD caused by mutations in the tau gene, are characterized by the accumulation of disease-specific proteins within surviving brain cells. "Here it's the other way around," Hutton says. "One copy of the progranulin gene has been knocked out by the mutation, and therefore we have less progranulin produced, which is enough on its own to cause the disease."

The mutations not only reveal the mechanism that causes the disease, they point to potential for a cure. "Replacing progranulin is the obvious therapeutic approach," Hutton says. That might be possible through gene therapy. Or by understanding the process that regulates progranulin expression, researchers may find ways to increase progranulin production from the surviving copy of the gene.

There are many growth factors required for neuronal function, and although Hutton and his colleagues don't yet know what role progranulin plays in the normal function of these brain cells, he says this discovery implies there may be other brain disorders, such as Lou Gehrig's disease (amyotrophic lateral sclerosis) in which the loss of certain growth factor-type proteins can actually give rise to the disease.

Because of its apparent role in neuronal function, Hutton's lab has begun to investigate whether normal variability in the progranulin gene influences the risk of developing Alzheimer's disease or Parkinson's disease. He asks, "If you have a particular, common variant in the progranulin gene, does that mean you are protected from getting Alzheimer's disease or a lower risk, because your neurons are better able to withstand the kind of damage they get from accumulation of amyloid beta?" (The amyloid beta protein is the principal component of the senile plaques that develop in brain cells of people with Alzheimer's disease.)

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Authors contributing to the paper to be published by Nature are: Matt Baker, Jennifer Gass, Rosa Rademakers, Jennifer Adamson, Ashley Cannon, Stacey Melquist, Dennis Dickson, Zdenek Berger, Jason Eriksen, Todd Robinson, Cynthia Zehr, Chad A. Dickey, Richard Crook, Eileen McGowan, Mike Hutton, Department of Neurosciences, Mayo Clinic College of Medicine; Bradley Boeve, Department of Neurology, Mayo Clinic College of Medicine; Ian R. Mackenzie, Department of Pathology, University of British Columbia; Caroline Lindholm, A. Dessa Sadovnick, Howard Feldman, Division of Neurology, University of British Columbia; Emily Dwosh, Department of Medical Genetics, University of British Columbia; Stuart M. Pickering-Brown, Sara Rollinson, Division of Laboratory and Regenerative Medicine, Department of Medicine, University of Manchester; Julie Snowden, Anna Richardson, David Neary, David Mann, Centre for Clinical Neurosciences, University of Manchester.

A second paper, from researchers at the University of Antwerp in Belgium, describing similar findings, will be published at the same time in Nature.

This research was funded by the National Institute on Aging, Mayo Foundation and the Robert and Clarice Smith Fellow program.

Contact: Erik Kaldor
Mayo Clinic, Jacksonville




Saludos Cordiales
Dr. José Manuel Ferrer Guerra

Fear of Snakes May Have Driven Pre-Human Evolution

The idea, proposed by Lynne Isbell, an anthropologist at the University of California, Davis, suggests that snakes and primates share a long and intimate history, one that forced both groups to evolve New strategies as each attempted to gain the upper hand.

To avoid becoming snake food, early mammals had to develop ways to detect and avoid the reptiles before they could strike. Some animals evolved better snake sniffers, while others developed immunities to serpent venom when it evolved.

Early primates developed a better eye for color, detail and movement and the ability to see in three dimensions — traits that are important for detecting threats at close range.

Humans are descended from those same primates.

Scientists had previously thought that these traits evolved together as primates used their hands and eyes to grab insects, or pick fruit or to swing through trees, but recent discoveries from Neuroscience are casting doubt on these theories.

Primates went a particular route," Isbell told LiveScience. "They focused on improving their vision to keep away from [snakes]. Other mammals couldn't do that. Primates had the pre-adaptations to go that way."

Harry Greene, an evolutionary biologist and snake expert at Cornell University in New York, says Isbell's New idea is very exciting.

"It strikes me as a very special piece of scholarship and I think it's going to provoke a lot of thought," Greene said.

Isbell's work is detailed in the July issue of the Journal of Human Evolution.

A New weapon

Fossil and DNA evidence suggests that snakes were already around when the first mammals evolved some 100 million years ago. The reptiles were thus among the first serious predators mammals faced.

Today, the only other threats faced by primates are raptors, such as eagles and hawks, and large carnivores, such as bears, large cats and wolves, but these animals evolved long after snakes did.

Furthermore, these other predators can be safely detected from a distance. For snakes, the opposite is true.

"If you see them close to you, you still have time to avoid them," Isbell said. "Primate vision is particularly good at close range."

Early snakes killed their prey using surprise attacks and by suffocating them to death — the method of boa constrictors.

But the improved vision of primates, combined with other snake-coping strategies developed by other animals, forced snakes to evolve a New weapon: venom. This important milestone in snake evolution occurred about 60 million years ago.

"The [snakes] had to do something to get better at finding their prey, so that's where venom comes in," Isbell said. "The snakes upped the ante and then the primates had to respond by developing even better vision."

Once primates developed specialized vision and enlarged brains, these traits became useful for other purposes, such as social interactions in groups.

Seeing in 3D

Isbell's New theory could explain how a number of primate-defining traits evolved.

For example, primates are among the few animals whose eyes face forward (most animals have eyes located on the sides of their heads).

This so-called orbital convergence improves depth perception and allows monkeys and apes, including humans, to see in three dimensions.

Primates also have better color vision than most animals and are also unique in relying heavily on vision when reaching and grasping for objects.

One of the most popular ideas for explaining how these traits evolved is called the "visual predation hypothesis."

It proposes that our early ancestors were small, insect-eating mammals and that the need to stalk and grab insects at close range was the driving force behind the evolution of improved vision.

Another popular idea, called the "leaping hypothesis," argues that orbital convergence is not only important for 3D vision, but also for breaking through camouflage.

Thus, it would have been useful not only for capturing insects and finding small fruits, but also for aiming at small, hard-to-see branches during mid-leaps through trees.

But there are problems with both hypotheses, Isbell says.

First, there is no solid evidence that early primates were committed insectivores. It's possible that like many primates today, they were generalists, eating a variety of plant foods, such as leaves, fruit and nectar as well as insects.

More importantly, recent Neuroscience studies do not support the idea that vision evolved alongside the ability to reach and grasp. Rather, the data suggest that the reaching-and-grasping abilities of primates actually evolved before they learned to leap and before they developed stereoscopic, or 3D, vision.

Agents of evolutionary change

Isbell thinks proto-primates — the early mammals that eventually evolved into primates — were in a better position compared to other mammals to evolve specialized vision and enlarged brains because of the foods they ate.

"They were eating foods high in sugar, and glucose is required for metabolizing energy," Isbell said. "Vision is a part of the brain, and messing with the brain takes a lot of energy, so you're going to need a diet that allows you to do that."

Modern primates are among the most frugivorous, or "fruit-loving," of all mammals, and this trend might have started with the proto-primates.

"Today there are primates that focus on leaves and things like that, but the earliest primates may have had a generalized diet that included fruits, nectar, flowers and insects," she said.

Thus, early primates not only had a good incentive for developing better vision, they might have already been eating the high-energy foods needed to do so.

Testing the theory

Isbell says her theory can be tested. For example, scientists could look at whether primates can visually detect snakes more quickly or more reliably than other mammals. Scientists could also examine whether there are differences in the snake-detecting abilities of primates from around the world.

"You could see whether there is any difference between Malagasy lemurs, South American primates and the African and Asian primates," Isbell said.

Anthropologists have tended to stress things like hunting to explain the special adaptations of primates, and particularly humans, said Greene, the Cornell snake expert, but scientists are starting to warm to the idea that predators likely played a large role in human evolution as well.

"Getting away from things is a big deal, too," Greene said in a telephone interview.

If snake and primate history are as intimately connected as Isbell suggests, then it might account for other things as well, Greene added.

"Snakes and people have had a long history; it goes back to long before we were people, in fact," he said. "That might sort of explain why we have such extreme attitudes towards snakes, varying from deification to ophidiphobia, or fear of snakes."

Copyright © 2006 Imaginova Corp. All Rights Reserved. This material may not be published, broadcast, rewritten or redistributed.




Saludos Cordiales
Dr. José Manuel Ferrer Guerra

12.5% Of Babies Born Premature In USA

12.5% of babies are born premature in the USA, that is a total of half a million babies each year - an increase of over 30% during the last twenty-five years, according to two New reports, one by the Institute of Medicine and the other by the National Institutes of Health. Helping premature babies survive is costing the USA $26 billion each year. Doctors say there should be more ultrasound exams during pregnancy. Others are calling for stricter fertility treatment guidelines.

The good news is that more pre-term babies are surviving and fewer teenagers are giving birth. However, the USA ranks 23rd in infant mortality when compared to other developed nations. Even though infant mortality is going down in America - in 2003, 6.8 babies of every 1,000 died during their first year, down from 7 per 1,000 in 2002 - other developed nations have been surging ahead at a much faster rate. The average infant mortality rate in the European Union, which includes its New Eastern European members, is 5 per 1,000.

8.1% of babies were born with a low birthweight in 2004, up from 7.9% in 2003 in the USA. A baby is considered to be of low birthweight when he/she is under 5.5lbs (2.5 kilos).

Dr. Jay Iams, Ohio State University, co-author of one of the New reports, says it is virtually impossible for health care professionals to predict who is going to give birth early. He says we urgently need to carry out research into better predicting pre-term births.

The authors say many pregnant mothers live under the illusion that a pre-term birth is no big deal. They believe modern medicine will sort everything out and their bouncing baby will thrive, even is he/she is born premature.

Dr. Iams states that having a pre-term baby is a big deal. It is a problem that is not appreciated by the US public.

A premature baby is one that is born before 38-42 weeks of pregnancy, before the 37th week is complete. The earlier the baby is born the greater is his/her risk of having devastating disabilities, such as cerebral palsy and mental retardation.

There are some indications which may point towards a higher risk of giving birth prematurely. For example:

-- If the mother gave birth prematurely before

-- If the mother is going to give birth to twins or triplets

-- Afro-American women are much more likely to give birth early than white or Hispanic women - even when the women have similar incomes, education and access to good health care.

-- Women who have become pregnant as a result of fertility treatment. Even if they are carrying just one child.

-- Extremely young mothers and mothers over 35

-- Women who are poor

-- Women who smoke

-- Women who do not have access to prenatal care

-- Women who are under a lot of stress

-- Women who are obese

However, most health care experts agree that it is very hard to predict who is going to give birth too early.

Infant Mortality Rates, 2006

Lithuania - 6.78
Croatia - 6.72
United States - 6.43
Taiwan - 6.29
Cuba - 6.22
Korea, South - 6.16
Faroe Islands - 6.12
Italy - 5.83
Isle of Man - 5.82
Aruba - 5.79
New Zealand - 5.76
San Marino - 5.63
Greece - 5.43
Monaco - 5.35
Ireland - 5.31
Jersey - 5.16
European Union - 5.10
United Kingdom - 5.08
Gibraltar - 5.06
Portugal - 4.98
Netherlands - 4.96
Luxembourg - 4.74
Canada - 4.69
Guernsey - 4.65
Liechtenstein - 4.64
Australia - 4.63
Belgium - 4.62
Austria - 4.60
Denmark - 4.51
Slovenia - 4.40
Spain - 4.37
Macau - 4.35
Switzerland - 4.34
France - 4.21
Germany - 4.12
Andorra - 4.04
Czech Republic - 3.89
Malta - 3.86
Norway - 3.67
Finland - 3.55
Iceland - 3.29
Japan - 3.24
Hong Kong - 2.95
Sweden - 2.76
Singapore - 2.29

Written by: Christian Nordqvist
Editor: Medical News Today


Saludos Cordiales
Dr. José Manuel Ferrer Guerra

Weight Loss Reduces Physical Disability In Patients With Knee Osteoarthritis

Results from a comprehensive meta-analysis, presented today at the 2006 EULAR congress suggest weight reduction in patients with knee osteoarthritis significantly reduces physical disability and has an impact on pain.

Osteoarthritis is the most common form of joint disease, and it is often associated with significant disability and an impaired quality of life. A number of trials have suggested a relationship between weight loss and clinical benefit in patients diagnosed particularly with knee osteoarthritis, prompting a Danish study team to assess and quantify whether clinical benefits are evident when overweight patients achieve a weight loss.

A total of 23 clinical trials were identified by the study team. Among these, 4 trials met pre-determined inclusion criteria and provided data suitable for further analysis. Three randomized controlled trials (4 intervention/control groups, n=417) reported changes in pain and disability, with 2 trials reporting changes in the Lequesne index, assessing pain, walking and function (n=117).

The association between improvement in physical disability and weight reduction was convincing, and showed that disability reduction could be predicted with great certainty from weight loss.

Whilst the team were not able to predict the clinical efficacy of pain reduction (owing to contradictory results from published trials), meta-regression evidence shows that osteoarthritis patients will experience at least a moderate clinical effect in their physical disability (ES>0.5) with a moderate dietary regime following more than 7.6% weight reduction. In addition, statistical models predicted that even a modest weight loss of more than 5.02% and an intensity of at least 0.25% per week, respectively - would result in a significant disability reduction.

"Based on the pooled analysis from 3 randomised controlled trials, we can provide category 1a evidence that weight reduction does reduce the pain and physical disability in knee OA patients. As such, weight reduction therapy in overweight osteoarthritic patients is a very appealing goal, both with regards to disease specific pain and disability reduction as well as for overall health benefits such as cardiovascular risk reduction" explained study author Robin Christensen, The Parker Institute, HS Frederiksberg Hospital, Copenhagen. "Weight loss is quite possible in these patients in spite of the lack of mobility and physical exercise, often associated with progression of osteoarthritis. A 10% reduction in body weight results in a moderate to large improvement in self reported physical disability; attention from the health care providers is necessary in support of patients learning to cope with a 'double chronic disease' - I.e. Both knee osteoarthritis and obesity" he concluded.

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For further information on this study, or to request an interview with the study lead, please do not hesitate to contact the EULAR congress press office on:

Email: eularpressoffice@uk.cohnwolfe.com

Jim Baxter
Jo Spadaccino
Mia Gannedahl

Abstract number: OP0194

About EULAR

* The European League Against Rheumatism (EULAR) is the organization which represents the patient, health professional and scientific societies of rheumatology of all the European nations.

* The aims of EULAR are to reduce the burden of rheumatic diseases on the individual and society and to improve the treatment, prevention and rehabilitation of musculoskeletal diseases. To this end, EULAR fosters excellence in education and research in the field of rheumatology. It promotes the translation of research advances into daily care and fights for the recognition of the needs of people with musculoskeletal diseases by the governing bodies in Europe.

* Diseases of bones and joints, such as rheumatoid arthritis and osteoarthritis cause disability in 4 - 5 % of the adult population and are predicted to rise as people live longer.

* As New treatments emerge and cellular mechanisms are discovered, the 7th Annual European Congress of Rheumatology in Amsterdam (EULAR 2006) brings together more than 10,000 experts - scientists, clinicians, healthcare workers, pharmaceutical companies and patients - to share their knowledge in a global endeavour to challenge the pain and disability caused by musculo-skeletal disorders.

* To find out more information about the activities of EULAR, visit: http://www.eular.org/.

Contact: Mia Gannedahl

European League Against Rheumatism




Saludos Cordiales
Dr. José Manuel Ferrer Guerra