Sleep Disorders Common Among Police Officers

A survey of police officers indicated that about 40 percent have a sleep disorder, which was associated with an increased risk of adverse health, safety and performance outcomes, according to a study in the December 21 issue of JAMA.

Sleep disorders, such as obstructive sleep apnea, insomnia, and shift work disorder, affect 50 to 70 million U.S. residents. Most are undiagnosed and remain untreated. "Police officers frequently work extended shifts and long work weeks, which in other occupations are associated with increased risk of errors, unintended injuries, and motor vehicle crashes. According to data through the year 2003, more officers are killed by unintended adverse events than during the commission of felonies. It has been hypothesized that fatigue- likely due to reduced duration and quality of sleep and untreated sleep disorders-may play an important role in police officer unintentional injuries and fatalities. To date, the effect of sleep disorders on police officer health, safety, and performance has not been systematically investigated," the authors write.

Shantha M. W. Rajaratnam, Ph.D., of Brigham and Women's Hospital, Boston, and colleagues examined the risk of major sleep disorders and associated adverse outcomes among North American police officers. The study consisted of police officers participating in either an online or an on-site screening (n = 4,957) and monthly follow-up surveys (n = 3,545 officers) between July 2005 and December 2007. A total of 3,693 officers in the United States and Canada participated in the online screening survey, and 1,264 officers from a municipal police department and a state police department participated in the on-site survey. The average age of the officers was 38.5 years, with an average of 12.7 years of police service.

A total of 2,003 of 4,957 participants (40.4 percent) screened positive for at least 1 sleep disorder. Of the total group, 1,666 (33.6 percent) screened positive for obstructive sleep apnea (OSA), the most common disorder, followed by 281 (6.5 percent) with moderate to severe insomnia; and 269 (5.4 percent) with shift work disorder (14.5 percent of those who worked the night shift). Positive screening for any sleep disorder was associated with increased risk of self-reported health- and safety-related outcomes: 203 (10.7 percent) of those who tested positive for a sleep disorder reported having depression vs. 37 (4.4 percent) of those who did not screen positive; 399 (34.1 percent) of the positive- screen group reported burnout (emotional exhaustion) vs. 89 (17.9 percent) in the negative-screen group, and 388 (20.0 percent) in the positive-screen group reported falling asleep while driving vs. 66 (7.9 percent) in the negative-screen group. Positive OSA screening was also associated with a diagnosis of diabetes; cardiovascular disease; and high caffeine consumption.

The researchers also found that 28.5 percent of participants had screening scores that indicated that they experienced excessive sleepiness. Of the survey respondents, 45.9 percent reported having nodded off or fallen asleep while driving; 56.9 percent of these reported falling asleep while driving at least 1 to 2 times a month; and 307 (13.5 percent, representing 6.2 percent of the total group) reported falling asleep while driving at least 1 to 2 times a week.

Compared to those who screened negative, participants who screened positive for any sleep disorder were more likely to report making important administrative errors; falling asleep while driving; making errors or committing safety violations due to fatigue; having uncontrolled anger toward a citizen or suspect; incurring citizen complaints; having absenteeism; or falling asleep during meetings.

"In conclusion, a large proportion of police officers in our sample showed a positive sleep disorder screening result, which was associated with adverse health, safety, and performance outcomes. Further research is needed to determine whether sleep disorder prevention, screening, and treatment programs in occupational settings will reduce these risks," the authors write.

Read more: http://www.sciencedaily.com/releases/2011/12/111220172618

New Sugar Land Office 2012

ADHD Genetic Variant Found, May Enable Doctors to Individualize Treatment

Attention-Deficit/Hyperactivity Disorder is a complex neurological condition that is known to have a strong genetic component. However, several factors could go into causing the disorder which leads to symptoms such as inattention, hyperactivity, and impulsivity. This is the reason why finding the best treatment option for patients can sometimes be a challenge. Researchers at The Children’s Hospital of Philadelphia have located a specific genetic variation that may affect about 10% of ADHD patients, and the finding could enable doctors to individualize treatment.

Study leader Hakon Hakonarson MD PhD, the director of the Center for Applied Genomics at The Children’s Hospital, and a team of researchers completed a whole-genome analysis of 1,000 children with ADHD and compared them to 4,100 children without the disorder. The scientists were particularly interested in locating copy number variations, or CNVs, which are deletions or duplications of DNA sequences.

Glutamate Nerve Transmission Pathway Affected
The team identified four genes with a significantly higher number of CNVs in children with ADHD. All were members of the glutamate receptor gene family, with the strongest result in GMR5 which affects nerve transmission.

“Members of the GMR gene family, along with genes they interact with, affect nerve transmission, the formation of neurons, and interconnections in the brain, so the fact that children with ADHD are more likely to have alterations in these genes reinforces previous evidence that the GRM pathway is important in ADHD,” said Hakonarson. “Our findings get to the cause of the ADHD symptoms in a subset of children with the disease.”

Hakonarson notes that about 10% of their sample cohort had the genetic condition, so the findings could potentially benefit about half a million US children.

Co-author Josephine Elia MD, a child psychiatrist, was also excited about the “robust finding.” She said that the research may allow for new therapies to be developed that are tailored toward the glutamate brain signaling pathway and would be a step toward individualizing treatment to a child’s genetic profile.

Read more: http://www.emaxhealth.com/1506/adhd-genetic-variant-found-may-enable-doctors-individualize-treatment

Depression drug may help insomniacs

Montreal psychiatrist Gabriella Gobbi was testing a new drug on depression in her laboratory when a curious thing happened. The mice fell asleep.

It wasn't the kind induced by sleeping pills but the deep, restorative slumber of childhood.

Conducted in collaboration with scientists in Italy, the discovery of a novel drug called UCM765 is expected to pave the way for new treatment for sleep disorders, which afflict millions worldwide.

Published in the Journal of Neuroscience, the research on rats and mice found the drug administered under the skin or directly into the brain had two distinct effects on sleep.

Rats fell asleep 60 per cent faster than the control group that did not have the drug, and they slept longer, increasing non-REM sleep, also known as "deep sleep" by 45 per cent, said Gobbi, an associate professor of psychiatry in the Faculty of Medicine at McGill University.

"It was like opening a dark box, a totally unknown world. We found it by serendipity," said Gobbi, who led a team from the Research Institute of the McGill University Health Centre on a multi-experiment, seven-year study of melatonin receptors.

Gobbi said she often treats people with sleep disorders and depression and the research was driven by her feelings of great sympathy for insomniacs.

Chemists in Italy who developed the drug from the hormone melatonin in 2005 initially had aimed to try to alleviate depression and anxiety.

It also was believed melatonin could alter the circadian rhythm or body clock.

"But its main effect was on sleep," said Gobbi, whose discovery unveiled the inner workings of melatonin on two receptors in the brain called MT1 and MT2. These are localized in one area of the brain, the reticular thalamic nucleus, which is a "powerhouse of [restorative] sleep," Gobbi said.

Read more: http://www.vancouversun.com/health/Depression+drug+help+insomniacs/5864354/story.html

Model to Foster New Drug Development to Treat Pain and Epilepsy Developed

Drawing on X-ray crystallography and experimental data, as well as a software suite for predicting and designing protein structures, a UC Davis School of Medicine researcher has developed an algorithm that predicts what has been impossible to generate in the laboratory: the conformational changes in voltage-gated sodium channels when they are at rest or actively transmitting a signal in muscle and nerve cells.

Structural modeling of the voltage-sensing mechanism is important because it allows researchers to generate testable hypotheses and design new, highly specific drugs to treat a wide range of disorders, from chronic pain to epilepsy. The study is published in the Dec. 12 early edition of the Proceedings of the National Academy of Sciences.

Voltage-gated sodium channels are embedded in the plasma membranes of nerve and muscle cells. The channel consists of a large protein that allows sodium ions to pass when a change in voltage occurs across the cell membrane. While high-resolution structures of the voltage sensors that control ion-gate activation have been identified in an activated state, scientists need to know all of the conformational changes that occur throughout the cycle of activation and rest to develop better treatments for disease.

"Sodium channels transmit pain and are the sites of action of local anesthetics," said Vladimir Yarov-Yarovoy, an assistant professor of physiology and membrane biology at the UC Davis School of Medicine who developed the models in collaboration with researchers from the University of Washington in Seattle. "They are critical targets for new drug development for the treatment of chronic pain, epilepsy and other conditions caused by gain or loss-of-function mutations in voltage-gated sodium channels, which hyperexcite sensory neurons or attenuate action-potential firing causing pain or seizures."

Serious chronic pain affects at least 116 million Americans each year, and epilepsy affects nearly 3 million Americans and 50 million people worldwide. Yet, the treatment of chronic pain and epilepsy remains a major unmet medical need.

"Currently available drugs for these conditions have limited effectiveness and significant side effects," said Yarov-Yarovoy. "While the research community has focused on identifying selective inhibitors of sodium-channel subtypes in nerve, heart and muscle cells, no new therapies have advanced to clinical trials. The algorithm is an innovative approach that fosters the design of novel subtype-selective sodium channel blocking drugs that have high efficacy and minimal side effects to treat these disorders."

Yarov-Yarovy developed his high-resolution structural models using the Rosetta computational methods along with available X-ray crystallography and experimental data. The models sidestep a significant challenge to researchers -- the inability to obtain X-ray crystallography structures for the resting and intermediate states of the sodium channel because of their instability and the limitations of current X-ray crystallization techniques.

"To fully grasp the mechanism of voltage activation, we need to know more than one conformation of the voltage-sensing domain," said Benoít Roux, professor of biochemistry and molecular biophysics at the University of Chicago. "So far, X-ray crystallography has provided only the structure of the channel in the activated-state. The careful computational modeling developed by Yarov-Yarovoy is a powerful technique that is absolutely critical to advance our understanding of these systems."

Read more: http://www.sciencedaily.com/releases/2011/12/111212153133

Teaching Children With Autism to Imitate Others May Improve Social Skills

Teaching young children with autism to imitate others may improve a broader range of social skills, according to a new study by a Michigan State University scholar.

The findings come at a pivotal time in autism research. In the past several years, researchers have begun to detect behaviors and symptoms of autism that could make earlier diagnosis and even intervention like this possible, said Brooke Ingersoll, MSU assistant professor of psychology.

"It's pretty exciting," Ingersoll said. "I think we, as a field, are getting a much better idea of what autism looks like in infants and toddlers than we did even five years ago."

In the current study, Ingersoll found that toddlers and preschoolers with autism who were taught imitation skills made more attempts to draw the examiner's attention to an object through gestures and eye contact, a key area of deficit in autism.

Imitation is an important development skill that allows infants and young children to interact and learn from others. However, children with autism often show a lack of ability to imitate.

The study, which appears in the Journal of Autism and Developmental Disorders, analyzed children with autism who were 27 months to 47 months old.

The findings come on the heels of a paper Ingersoll published in the journal Current Directions in Psychological Science that highlighted recent findings in autism research by U.S. scientists.

Read more: http://www.sciencedaily.com/releases/2011/12/111212124518

Blood Test Might Predict How Well a Depressed Patient Responds to Antidepressants

Loyola University Medical Center researchers are reporting what could become the first reliable method to predict whether an antidepressant will work on a depressed patient.

The method would involve a blood test for a protein called vascular endothelial growth factor (VEGF). A Loyola study found that among depressed patients who had higher than normal blood levels of VEGF, more than 85 percent experienced partial or complete relief from depression after taking escitalopram (brand name Lexapro®). By comparison, fewer than 10 percent of depressed patients who had low levels of VEGF responded to the drug.

"This would be the first time we would have a predictor for how well a patient would respond to an antidepressant," said Angelos Halaris, MD, PhD, first author of the study. Halaris presented results during the 2011 annual meeting of the Society of Biological Psychiatry and the 4th Annual Illinois Brain, Behavior and Immunity Meeting.

About 60 percent of depressed patients do not respond fully to the first prescribed medication. Consequently, doctors often must prescribe a different medication again and again before finding one that works. "It would greatly benefit our patients if we could predict ahead of time whether a given medication would be effective for a certain patient," Halaris said.

The Loyola study involved 35 patients who took escitalopram for major depressive disorder. Escitalopram belongs to a class of antidepressants called selective serotonin reuptake inhibitors (SSRIs). Other common SSRIs are Prozac®, Paxil® and Zoloft®.
Scientists aren't certain why SSRIs work in some patients but not in others. One possible mechanism is that SSRIs help restore a chemical balance in the brain. Some scientists recently have proposed a second possible mechanism, called neurogenesis -- SSRIs help to regenerate brain cells in specific parts of the brain that have atrophied in depressed patients.

The Loyola study supports the neurogenesis theory. It appears that escitalopram, the SSRI used in the Loyola study, jump-starts brain cells that have become inactive. This regeneration is fueled by VEGF. In the brain, VEGF stimulates the growth of blood vessels and works in other ways to keep brain cells healthy and active.

It appears that in patients with higher levels of VEGF, there was more regeneration, helping to reduce depression. Conversely, in patients with lower VEGF levels, there was less regeneration of brain cells and less relief from depression.

If the finding is confirmed by further studies, it could lead to a blood test that would help physicians tailor treatment. If, for example, a patient had low levels of VEGF, the physician might skip SSRIs and try alternative classes of antidepressants, such as bupropion, or alternative therapies, such as psychotherapy or Transcranial Magnetic Stimulation (TMG). These treatments are all available at Loyola University Medical Center.

Read more: http://www.sciencedaily.com/releases/2011/12/111215135853