ScienceDaily (May 15, 2012) — Child abuse or neglect are strong predictors of major health and emotional problems, but little is known about how the chronicity of the maltreatment may increase future harm apart from other risk factors in a child’s life.

This chart illustrates the individual childhood and adult outcomes according to the number of reports that occurred before the event of interest. Because it was possible for some children to enter the study period with a pre-existing condition, these are indicated as gray or black bars with the legend indicating the outcome occurred “before the study.” Chronicity is associated with increasing risk for all but child maltreatment perpetration, violent delinquency, and head or brain injury. In these cases, there is a slight decline in prevalence for the highest category compared with middle categories, but in all cases having reports was associated with higher rates of outcomes. (Credit: Image courtesy of Washington University in St. Louis)

In a new study published in the current issue of the journal Pediatrics, Melissa Jonson-Reid, PhD, child welfare expert and a professor at the Brown School at Washington University in St. Louis, looked at how chronic maltreatment impacted the future health and behavior of children and adults.

The study tracked children by number of child maltreatment reports (zero to four or more) and followed the children into early adulthood, by which time some of the children had become parents.

The study sought to determine how well the number of child maltreatment reports predicted poor outcomes in adolescence, such as delinquency, substance abuse in the teen years or getting a sexually transmitted disease.

"For every measure studied, a more chronic history of child maltreatment reports was powerfully predictive of worse outcomes," Jonson-Reid says.

"For most outcomes, having a single maltreatment report put children at a 20 percent to 50 percent higher risk than non-maltreated comparison children.

In addition, a series of adult outcomes were tracked to see if the chronicity of maltreatment still mattered after controlling for the poor outcomes in adolescence. Adult outcomes included adult substance abuse or growing up and having children whom they then maltreated.

"In models of adult outcomes, children with four or more reports were about least twice as likely to later abuse their own children and have contact with the mental health system, even when controlling for the negative outcomes during adolescence." Jonson-Reid says that there appears to be good reason to put resources into preventing ongoing maltreatment.

"Successfully interrupting chronic child maltreatment may well reduce risk of a wide range of other costly child and adolescent health and behavioral problems," she says.

Jonson-Reid cites a recently published Centers for Disease Control and Prevention study estimating lifetime costs for a single year’s worth of children reported for maltreatment at $242 billion.

"What our study illustrates is that these costs are even more likely to accrue for children who continue to be re-reported," she says.

The study also found that maltreatment predicts a range of negative adolescent outcomes, and those adolescent outcomes then predict poor adult outcomes.

"If the poor outcomes in adolescence can be dealt with effectively, then later adult outcomes may also be forestalled," Jonson-Reid says.

"Our findings could therefore be interpreted as supporting many current evidence-based interventions that seek to improve behavioral and social functioning among children and adolescents who have experienced trauma like abuse or neglect."

Source: Science Daily

ScienceDaily (May 15, 2012) — A novel mechanism for anxiety behaviors, including a previously unrecognized inhibitory brain signal, may inspire new strategies for treating psychiatric disorders, University of Chicago researchers report.

By testing the controversial role of a gene called Glo1 in anxiety, scientists uncovered a new inhibitory factor in the brain: the metabolic by-product methylglyoxal. The system offers a tantalizing new target for drugs designed to treat conditions such as anxiety disorder, epilepsy, and sleep disorders.

The study, published in the Journal of Clinical Investigation, found that animals with multiple copies of the Glo1 gene were more likely to exhibit anxiety-like behavior in laboratory tests. Further experiments showed that Glo1 increased anxiety-like behavior by lowering levels of methylglyoxal (MG). Conversely, inhibiting Glo1 or raising MG levels reduced anxiety behaviors.

"Animals transgenic for Glo1 had different levels of anxiety-like behavior, and more copies made them more anxious," said Abraham Palmer, PhD, assistant professor of human genetics at the University of Chicago Medicine and senior author of the study. "We showed that Glo1 was causally related to anxiety-like behavior, rather than merely correlated."

In 2005, a comparison of different mouse strains found a link between anxiety-like behaviors and Glo1, the gene encoding the metabolic enzyme glyoxylase 1. However, subsequent studies questioned the link, and the lack of an obvious connection between glyoxylase 1 and brain function or behavior made some scientists skeptical.

Read more …

May 15, 2012

A drug made from the saliva of the Gila monster lizard is effective in reducing the craving for food. Researchers at the Sahlgrenska Academy, University of Gothenburg, have tested the drug on rats, who after treatment ceased their cravings for both food and chocolate.

In a study with rats published in the Journal of Neuroscience, Assistant Professor Karolina Skibicka and her colleagues show that exendin-4 effectively reduces the cravings for food. Credit: Photo: University of Gothenburg

An increasing number of patients suffering from type 2 diabetes are offered a pharmaceutical preparation called Exenatide, which helps them to control their blood sugar. The drug is a synthetic version of a natural substance called exendin-4, which is obtained from a rather unusual source – the saliva of the Gila monster lizard (Heloderma suspectum), North America’s largest lizard.

Researchers at the Sahlgrenska Academy at the University of Gothenburg, have now found an entirely new and unexpected effect of the lizard substance.

In a study with rats published in the Journal of Neuroscience, Assistant Professor Karolina Skibicka and her colleagues show that exendin-4 effectively reduces the cravings for food.

"This is both unknown and quite unexpected effect," comments an enthusiastic Karolina Skibicka:

" Our decision to eat is linked to the same mechanisms in the brain which control addictive behaviours. We have shown that exendin-4 affects the reward and motivation regions of the brain"

The implications of the findings are significant” states Suzanne Dickson, Professor of Physiology at the Sahlgrenska Academy: “Most dieting fails because we are obsessed with the desire to eat, especially tempting foods like sweets. As exendin-4 suppresses the cravings for food, it can help obese people to take control of their weight,” suggests Professor Dickson.

Research on exendin-4 also gives hope for new ways to treat diseases related to eating disorders, for example, compulsive overeating.

Another hypothesis for the Gothenburg researchers’ continuing studies is that exendin-4 may be used to reduce the craving for alcohol.

"It is the same brain regions which are involved in food cravings and alcohol cravings, so it would be very interesting to test whether exendin-4 also reduces the cravings for alcohol,” suggests Assistant Professor Skibicka.

Provided by University of Gothenburg

Source: medicalxpress.com

May 15, 2012

(Medical Xpress) — New research from Uppsala University, Sweden, suggests that an active lifestyle in late life protects grey matter and cognitive functions in humans. The findings are now published in the scientific journal Neurobiology of Aging.

In a new study, a multidisciplinary research team from the Uppsala University has systematically studied 331 men and women at the age of 75 years. The researchers examined whether an active lifestyle is tied to brain health in seniors living in Uppsala, Sweden. The brain structure of each participant was measured using magnetic imaging technology, so-called MRT, and various memory tests were administered in order to monitor the seniors’ cognitive status.

“We found that those elderly who reported to be more active in daily routine had larger grey and white matter and showed better performances on various memory tests, compared to those who had a sedentary lifestyle. Interestingly, active elderly had also more grey matter in the precuneus, a brain region that typically shrinks at the beginning of Alzheimer’s disease. Our findings suggest that an active lifestyle is a promising strategy for counteracting cognitive aging late in life,” says Christian Benedict.

The data for the study were taken from the major epidemiological study Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS). http://www.medsci.uu.se/pivus/

More information: Benedict C et al., Association between physical activity and brain health in older adults, Neurobiology of Aging, in press. http://www.sciencedirect.com/science/article/pii/S0197458012002618

Provided by Uppsala University

Source: medicalxpress.com

ScienceDaily (May 14, 2012) — A new study consisting of inducing cells to express telomerase, the enzyme which — metaphorically — slows down the biological clock — was successful. The research provides a “proof-of-principle” that this “feasible and safe” approach can effectively “improve health span.”

Pictured are Maria A. Blasco and Bruno M. Bernardes de Jesús (co-author) in the CNIO building in Madrid. (Credit: CNIO)

A number of studies have shown that it is possible to lengthen the average life of individuals of many species, including mammals, by acting on specific genes. To date, however, this has meant altering the animals’ genes permanently from the embryonic stage — an approach impracticable in humans. Researchers at the Spanish National Cancer Research Centre (CNIO), led by its director María Blasco, have demonstrated that the mouse lifespan can be extended by the application in adult life of a single treatment acting directly on the animal’s genes. And they have done so using gene therapy, a strategy never before employed to combat aging. The therapy has been found to be safe and effective in mice.

The results were recently published in the journal EMBO Molecular Medicine. The CNIO team, in collaboration with Eduard Ayuso and Fátima Bosch of the Centre of Animal Biotechnology and Gene Therapy at the Universitat Autònoma de Barcelona (UAB), treated adult (one-­‐year-­‐old) and aged (two-­‐year-­‐old) mice, with the gene therapy delivering a “rejuvenating” effect in both cases, according to the authors.

Mice treated at the age of one lived longer by 24% on average, and those treated at the age of two, by 13%. The therapy, furthermore, produced an appreciable improvement in the animals’ health, delaying the onset of age-­‐related diseases — like osteoporosis and insulin resistance — and achieving improved readings on aging indicators like neuromuscular coordination.

The gene therapy consisted of treating the animals with a DNA-­modified virus, the viral genes having been replaced by those of the telomerase enzyme, with a key role in aging. Telomerase repairs the extreme ends or tips of chromosomes, known as telomeres, and in doing so slows the cell’s and therefore the body’s biological clock. When the animal is infected, the virus acts as a vehicle depositing the telomerase gene in the cells.

This study “shows that it is possible to develop a telomerase-­based anti-­aging gene therapy without increasing the incidence of cancer,” the authors affirm. “Aged organisms accumulate damage in their DNA due to telomere shortening, [this study] finds that a gene therapy based on telomerase production can repair or delay this kind of damage,” they add.

'Resetting' the biological clock

Telomeres are the caps that protect the end of chromosomes, but they cannot do so indefinitely: each time the cell divides the telomeres get shorter, until they are so short that they lose all functionality. The cell, as a result, stops dividing and ages or dies. Telomerase gets around this by preventing telomeres from shortening or even rebuilding them. What it does, in essence, is stop or reset the cell’s biological clock.

But in most cells the telomerase gene is only active before birth; the cells of an adult organism, with few exceptions, have no telomerase. The exceptions in question are adult stem cells and cancer cells, which divide limitlessly and are therefore immortal — in fact several studies have shown that telomerase expression is the key to the immortality of tumour cells.

It is precisely this risk of promoting tumour development that has set back the investigation of telomerase-­‐based anti-­‐aging therapies.

In 2007, Blasco’s group demonstrated that it was feasible to prolong the lives of transgenic mice, whose genome had been permanently altered at the embryonic stage, by causing their cells to express telomerase and, also, extra copies of cancer-­‐resistant genes. These animals live 40% longer than is normal and do not develop cancer.

The mice subjected to the gene therapy now under test are likewise free of cancer. Researchers believe this is because the therapy begins when the animals are adult so do not have time to accumulate sufficient number of aberrant divisions for tumours to appear.

Also important is the kind of virus employed to carry the telomerase gene to the cells. The authors selected demonstrably safe viruses that have been successfully used in gene therapy treatment of hemophilia and eye disease. Specifically, they are non-­‐replicating viruses derived from others that are non-­‐pathogenic in humans.

This study is viewed primarily as “a proof-­‐of-­‐principle that telomerase gene therapy is a feasible and generally safe approach to improve healthspan and treat disorders associated with short telomeres,” state Virginia Boccardi (Second University of Naples) and Utz Herbig (New Jersey Medical School-­‐University Hospital Cancer Centre) in a commentary published in the same journal.

Although this therapy may not find application as an anti-­‐aging treatment in humans, in the short term at least, it could open up a new treatment option for ailments linked with the presence in tissue of abnormally short telomeres, as in some cases of human pulmonary fibrosis.

More healthy years

As Blasco says, “aging is not currently regarded as a disease, but researchers tend increasingly to view it as the common origin of conditions like insulin resistance or cardiovascular disease, whose incidence rises with age. In treating cell aging, we could prevent these diseases.”

With regard to the therapy under testing, Bosch explains: “Because the vector we use expresses the target gene (telomerase) over a long period, we were able to apply a single treatment. This might be the only practical solution for an anti-­‐aging therapy, since other strategies would require the drug to be administered over the patient’s lifetime, multiplying the risk of adverse effects.”

Source: Science Daily

May 14th, 2012

Controlled trial shows improved spasticity, reduced pain after smoking medical marijuana.

A clinical study of 30 adult patients with multiple sclerosis (MS) at the University of California, San Diego School of Medicine has shown that smoked cannabis may be an effective treatment for spasticity – a common and disabling symptom of this neurological disease.

The placebo-controlled trial also resulted in reduced perception of pain, although participants also reported short-term, adverse cognitive effects and increased fatigue. The study will be published in the Canadian Medical Association Journal on May 14.

Principal investigator Jody Corey-Bloom, MD, PhD, professor of neurosciences and director of the Multiple Sclerosis Center at UC San Diego, and colleagues randomly assigned participants to either the intervention group (which smoked cannabis once daily for three days) or the control group (which smoked identical placebo cigarettes, also once a day for three days). After an 11-day interval, the participants crossed over to the other group.

“We found that smoked cannabis was superior to placebo in reducing symptoms and pain in patients with treatment-resistant spasticity, or excessive muscle contractions,” said Corey-Bloom.

Earlier reports suggested that the active compounds of medical marijuana were potentially effective in treating neurologic conditions, but most studies focused on orally administered cannabinoids. There were also anecdotal reports of MS patients that endorsed smoking marijuana to relieve symptoms of spasticity.

However, this trial used a more objective measurement, a modified Ashford scale which graded the intensity of muscle tone by measuring such things as resistance in range of motion and rigidity. The secondary outcome, pain, was measured using a visual analogue scale. The researchers also looked at physical performance (using a timed walk) and cognitive function and – at the end of each visit – asked patients to assess their feeling of “highness.”

Although generally well tolerated, smoking cannabis did have mild effects on attention and concentration. The researchers noted that larger, long-terms studies are needed to confirm their findings and determine whether lower doses can result in beneficial effects with less cognitive impact.

The current study is the fifth clinical test of the possible efficacy of cannabis for clinical use reported by the University of California Center for Medicinal Cannabis Research (CMCR). Four other human studies on control of neuropathic pain also reported positive results.

Source: Neuroscience News

May 14th, 2012

Using tiny solar-panel-like cells surgically placed underneath the retina, scientists at the Stanford University School of Medicine have devised a system that may someday restore sight to people who have lost vision because of certain types of degenerative eye diseases.

This device — a new type of retinal prosthesis — involves a specially designed pair of goggles, which are equipped with a miniature camera and a pocket PC that is designed to process the visual data stream. The resulting images would be displayed on a liquid crystal microdisplay embedded in the goggles, similar to what’s used in video goggles for gaming. Unlike the regular video goggles, though, the images would be beamed from the LCD using laser pulses of near-infrared light to a photovoltaic silicon chip — one-third as thin as a strand of hair — implanted beneath the retina.

Electric currents from the photodiodes on the chip would then trigger signals in the retina, which then flow to the brain, enabling a patient to regain vision.

A study, to be published online May 13 in Nature Photonics, discusses how scientists tested the photovoltaic stimulation using the prosthetic device’s diode arrays in rat retinas in vitro and how they elicited electric responses, which are widely accepted indicators of visual activity, from retinal cells . The scientists are now testing the system in live rats, taking both physiological and behavioral measurements, and are hoping to find a sponsor to support tests in humans.

“It works like the solar panels on your roof, converting light into electric current,” said Daniel Palanker, PhD, associate professor of ophthalmology and one of the paper’s senior authors. “But instead of the current flowing to your refrigerator, it flows into your retina.” Palanker is also a member of the Hansen Experimental Physics Laboratory at Stanford and of the interdisciplinary Stanford research program, Bio-X. The study’s other senior author is Alexander Sher, PhD, of the Santa Cruz Institute of Particle Physics at UC Santa Cruz; its co-first authors are Keith Mathieson, PhD, a visiting scholar in Palanker’s lab, and James Loudin, PhD, a postdoctoral scholar. Palanker and Loudin jointly conceived and designed the prosthesis system and the photovoltaic arrays.

This pinpoint-sized photovoltaic chip (upper right corner) is implanted under the retina in a blind rat to restore sight. The center image shows how the chip is comprised of an array of photodiodes, which can be activated by pulsed near-infrared light to stimulate neural signals in the eye that propagate then to the brain. A higher magnification view (lower left corner) shows a single pixel of the implant, which has three diodes around the perimeter and an electrode in the center. The diodes turn light into an electric current which flows from the chip into the inner layer of retinal cells. Adapted from Stanford image courtesy of the Daniel Palanker lab.

Read more …

May 14, 2012

What goes bump in the night? In many U.S. households: people. That’s according to new Stanford University School of Medicine research, which found that about 3.6 percent of U.S. adults are prone to sleepwalking. The work also showed an association between nocturnal wanderings and certain psychiatric disorders, such as depression and anxiety.

The study, the researchers noted, “underscores the fact that sleepwalking is much more prevalent in adults than previously appreciated.”

Maurice Ohayon, MD, DSc, PhD, professor of psychiatry and behavioral sciences, is the lead author of the paper, which will appear in the May 15 issue of Neurology, the medical journal of the American Academy of Neurology.

Sleepwalking is a disorder “of arousal from non-REM sleep.” While wandering around at night can be harmless and is often played for laughs — anyone remember the Simpsons episode where Homer began wandering around and doing silly things in his sleep? — sleepwalking can have serious consequences. Episodes can result in injuries to the wanderer or others and lead to impaired psychosocial functioning.

It is thought that medication use and certain psychological and psychiatric conditions can trigger sleepwalking, but the exact causes are unknown. Also unclear to experts in the field is the prevalence.

"Apart from a study we did 10 years ago in the European general population, where we reported a prevalence of 2 percent of sleepwalking," the researchers wrote in their paper, "there are nearly no data regarding the prevalence of nocturnal wanderings in the adult general population. In the United States, the only prevalence rate was published 30 years ago."

For this study, the first to use a large, representative sample of the U.S. general population to demonstrate the number of sleepwalkers, the researchers also aimed to evaluate the importance of medication use and mental disorders associated with sleepwalking. Ohayon and his colleagues secured a sample of 19,136 individuals from 15 states and then used phone surveys to gather information on participants’ mental health, medical history and medication use.

Participants were asked specific questions related to sleepwalking, including frequency of episodes during sleep, duration of the sleep disorder and any inappropriate or potentially dangerous behaviors during sleep. Those who didn’t report any episodes in the last year were asked if they had sleepwalked during their childhood. Participants were also queried about whether there was a family history of sleepwalking and whether they had other parasomnia symptoms, such as sleep terrors and violent behaviors during sleep.

The researchers determined that as many as 3.6 percent of the sample reported at least one episode of sleepwalking in the previous year, with 1 percent saying they had two or more episodes in a month. Because of the number of respondents who reported having episodes during childhood or adolescence, lifetime prevalence of sleepwalking was found to be 29.2 percent.

The study also showed that people with depression were 3.5 times more likely to sleepwalk than those without, and people with alcohol abuse/dependence or obsessive-compulsive disorder were also significantly more likely to have sleepwalking episodes. In addition, individuals taking SSRI antidepressants were three times more likely to sleepwalk twice a month or more than those who didn’t.

"There is no doubt an association between nocturnal wanderings and certain conditions, but we don’t know the direction of the causality," said Ohayon. "Are the medical conditions provoking sleepwalking, or is it vice versa? Or perhaps it’s the treatment that is responsible."

Although more research is needed, the work could help raise awareness of this association among primary care physicians. “We’re not expecting them to diagnose sleepwalking, but they might detect symptoms that could be indices of sleepwalking,” said Ohayon.

Among the researchers’ other findings:

• The duration of sleepwalking was mostly chronic, with just over 80 percent of those who have sleepwalked reporting they’ve done so for more than five years.
• Sleepwalking was not associated with gender and seemed to decrease with age.
• Nearly one-third of individuals with nocturnal wandering had a family history of the disorder.
• People using over-the-counter sleeping pills had a higher likelihood of reporting sleepwalking episodes at least two times per month. (Indeed, a sleeping pill was the trigger for Homer Simpson’s middle-of-the-night shenanigans.)

D. Le’ger, MD, PhD, from the Universite Paris Descartes in France, was senior author of the study. Researchers from the University of Minnesota Medical School, the Hopital Gui-de-Chauliac in Montpellier, France, and Duke University School of Medicine were also involved.

Provided by Stanford University Medical Center

Source: medicalxpress.com

May 14, 2012

Why does one person become anorexic and another obese? A study recently published by a University of Colorado School of Medicine researcher shows that reward circuits in the brain are sensitized in anorexic women and desensitized in obese women. The findings also suggest that eating behavior is related to brain dopamine pathways involved in addictions.

Guido Frank, MD, assistant professor director of the Developmental Brain Research Program at the CU School of Medicine and his colleagues used functional magnetic resonance imaging (fMRI) to examine brain activity in 63 women who were either anorexic or obese. Scientists compared them to women considered “normal” weight. The participants were visually conditioned to associate certain shapes with either a sweet or a non-sweet solution and then received the taste solutions expectedly or unexpectedly. This task has been associated with brain dopamine function in the past.

The authors found that during these fMRI sessions, an unexpected sweet-tasting solution resulted in increased neural activation of reward systems in the anorexic patients and diminished activation in obese individuals. In rodents, food restriction and weight loss have been associated with greater dopamine-related reward responses in the brain.

"It is clear that in humans the brain’s reward system helps to regulate food intake" said Frank. "The specific role of these networks in eating disorders such as anorexia nervosa and, conversely, obesity, remains unclear.”

Scientists agree that more research is needed in this area. The study was published in Neuropsychopharmacology.

Provided by University of Colorado Denver

Source: medicalxpress.com

May 14, 2012

Following a stroke, factors as varied as blood sugar, body temperature and position in bed can affect patient outcomes, Loyola University Medical Center researchers report.

In a review article in the journal MedLink Neurology, first author Murray Flaster, MD, PhD and colleagues summarize the latest research on caring for ischemic stroke patients. (Most strokes are ischemic, meaning they are caused by blood clots.)

"The period immediately following an acute ischemic stroke is a time of significant risk,” the Loyola neurologists write. “Meticulous attention to the care of the stroke patient during this time can prevent further neurologic injury and minimize common complications, optimizing the chance of functional recovery.”

Stroke care has two main objectives – minimizing injury to brain tissue and preventing and treating the many neurologic and medical complications that can occur just after a stroke.

The authors discuss the many complex factors that affect outcomes. For example, there is considerable evidence of a link between hyperglycemia (high blood sugar) and poor outcomes after stroke. The authors recommend strict blood sugar control, using frequent finger-stick glucose checks and aggressive insulin treatment.

For each 1 degree C increase in the body temperature of stroke patients, the risk of death or severe disability more than doubles. Therapeutic cooling has been shown to help cardiac arrest patients, and clinical trials are underway to determine whether such cooling could also help stroke patients. Until those trials are completed, the goal should be to keep normal temperatures (between 95.9 and 99.5 degrees F).

Position in bed also is important, because sitting upright decreases blood flow in the brain. A common practice is to keep the patient lying flat for 24 hours. If a patient has orthopnea (difficulty breathing while lying flat), the head of the bed should be kept at the lowest elevation the patient can tolerate.

The authors discuss many other issues in stroke care, including blood pressure management; blood volume; statin therapy; management of complications such as pneumonia and sepsis; heart attack and other cardiac problems; blood clots; infection; malnutrition and aspiration; brain swelling; seizures; recurrent stroke; and brain hemorrhages.

Studies have shown that hospital units that specialize in stroke care decrease mortality, increase the likelihood of being discharged to home and improve functional status and quality of life.

All patients should receive supportive care — including those who suffer major strokes and the elderly. “Even in these populations, the majority of patients will survive their stroke,” the authors write. “The degree of functional recovery, however, may be dramatically impacted by the intensity and appropriateness of supportive care.”

Provided by Loyola University Health System

Source: medicalxpress.com