Lifestyle Intervention Improves High Schoolers’ Health, Social Skills, Grades
A teacher-delivered intervention program promoting healthy lifestyles improved health behaviors, social skills, severe depression and academic performance in high school adolescents, a study has found. Routine integration of such programs into health education curricula in high school settings may be an effective way to prevent high-risk teen populations from becoming overweight or obese and could lead to improved physical health, psychosocial skills and academic outcomes, according to the study.
The study, supported by the National Institute of Nursing Research, appears in the online September issue of the American Journal of Preventive Medicine. It is one of the first studies to report multiple immediate improvements that were sustained over time using a teacher-delivered, cognitive-behavioral skills-building intervention program incorporated into a high school health education class. Cognitive-behavioral skills training teaches coping techniques, social functioning skills and problem-solving skills.
“Nutrition and physical activity-based interventions are often tested when it comes to preventing obesity, but mental and psychosocial health can also be contributing factors,” said NINR director Dr. Patricia Grady. “This NINR-supported study highlights the importance of an evidence-based lifestyle intervention that addresses the complex interplay of these factors.”
Fishing for New Epilepsy Model, Scientists Reel In Potential Drug
According to new research on epilepsy, zebra-fish have certainly earned their stripes. Results of a study in Nature Communications suggest that zebrafish carrying a specific mutation may help researchers discover treatments for Dravet syndrome (DS), a severe form of pediatric epilepsy that results in drug-resistant seizures and developmental delays.
Dr. Scott Baraban and his colleagues at the University of California, San Francisco, assessed whether the mutated zebrafish could serve as a model for DS and then developed a new screening method to quickly identify potential treatments for DS using these fish. The study was supported by the National Institute of Neurological Disorders and Stroke and builds on pioneering epilepsy zebrafish models first described by the Baraban laboratory in 2005.
Wild-type and larval zebrafish carrying a mutation in the Scn1a gene (mimicking a severe form of pediatric epilepsy) were used for drug screening.
Photo: Scott Baraban/UCSF
Dravet syndrome is commonly caused by a mutation in the Scn1a gene, which encodes for Nav1.1, a specific sodium ion channel found in the brain. Sodium ion channels are critical for communication between brain cells and proper brain functioning.
The researchers found that the zebrafish that were engineered to have the Scn1a mutation that causes DS in humans exhibited some of the same characteristics, such as spontaneous seizures, commonly seen in children with DS. Unprovoked seizure activity in the mutant fish resulted in hyperactivity and whole-body convulsions associated with very fast swimming. These types of behaviors are not seen in normal healthy zebrafish.
The findings suggest that Scn1a mutant zebrafish may serve as a good model of DS and that a drug screen created by the researchers may be effective in quickly identifying novel therapies for epilepsy.
Researchers Help ID New Metabolic Disorder Caused by Faulty Gene Expression
National Human Genome Research Institute researchers participating in an international study with colleagues at the University of Colorado in Denver, McGill University in Montreal and University Children’s Hospital in Zurich have described a new disease involving a defect in the body’s ability to process vitamin B12, or cobalamin. The rare inherited disorder that has only been found in boys, can cause severe neurological symptoms, including developmental delay, epilepsy and brain malformations.
Newborns are screened for cobalamin metabolic defects but the new disorder had not previously been distinguished from a related condition, known as cobalamin C deficiency, or cblC. With their discovery, published Sept. 5 in the American Journal of Human Genetics, the researchers located a gene alteration on the X chromosome that regulates expression of a critical enzyme in the metabolism of cobalamin. The new disorder is called cobalamin X deficiency (cblX).
“CblX is a new class of metabolic error that derives from transcriptional dysregulation,” said co-author Dr. Charles Venditti, investigator in NHGRI’s Genetic and Molecular Biology Branch. “This mechanism has not been observed in any other inborn error of metabolism.”