Research advances from the National Institutes of Health (NIH) Intramural Research Program (IRP) often make headlines. Read the news releases that describe our most recent findings:
The act of cooking offers the chance to unwind and create something special, whether you’re planning to feed a crowd or just yourself. And while you may have noticed feeling good after whipping up that perfect pie or braise, there’s actually a lot of scientific data to suggest that cooking can have a positive impact on mental health.
One meta-analysis (a report of pre-existing research) from the National Institutes of Health looked at 11 studies and found that “cooking interventions” — encouraging people to follow certain recipes or giving people cooking classes — can improve a person’s mental well-being. It specifically found that people who participated in cooking interventions reported having better self-esteem and quality of life, as well as a more positive emotional state after the fact. Another study even discovered that baking can help raise a person’s confidence level.
Scientists have demonstrated how an investigational drug works against a rare, fatal genetic disease, Niemann-Pick type C1 (NPC1). They found that a closely related compound will activate an enzyme, AMPK, triggering a cellular “recycling” system that helps reduce elevated cholesterol and other accumulated fats in the brains and livers of NPC1 patients, which are hallmarks associated with severe neurological problems. The research was led by scientists at the National Center for Advancing Translational Sciences (NCATS), part of the National Institutes of Health, and their colleagues.
The work could lead to a new generation of potential therapies for NPC1 and other similar disorders, as well as neurodegenerative diseases such as Parkinson’s and Alzheimer’s diseases. The scientists reported their findings online on July 17, 2017 in the journal Autophagy.
Vaccines protect against Zika-related congenital damage.
Two experimental vaccines can restrict Zika virus transmission from pregnant mice to their fetuses and can prevent Zika virus-induced placental damage and fetal demise, according to new findings published July 13 in Cell. Scientists from the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health (NIH); Washington University School of Medicine in St. Louis; the University of Texas Medical Branch (UTMB); and other partners conducted the research. They tested a live-attenuated vaccine candidate developed by UTMB and an mRNA vaccine candidate developed by the biotechnology company Moderna.
NIH discovery could lead to new drugs to prevent HIV infection.
Researchers at the National Institutes of Health have discovered a key step in the process that HIV uses to inject its genetic material into cells. Working with cultures of cells and tissues, the researchers prevented the invasion process by chemically blocking this step, preventing HIV genetic material from entering cells. The findings could lead to the eventual development of new drugs to prevent HIV infection.
NIH study shows microbe living on the surface of the eye protects cornea from infection.
Bugs in your eyes may be a good thing. Resident microbes living on the eye are essential for immune responses that protect the eye from infection, new research shows. The study, which appears in the journal Immunity on June 27, demonstrates the existence of a resident ocular microbiome that trains the developing immune system to fend off pathogens. The research was conducted at the National Eye Institute (NEI), part of the National Institutes of Health.
“This is the first evidence that a bacterium lives on the ocular surface long-term,” explained Rachel Caspi, Ph.D., senior investigator in NEI’s Laboratory of Immunology. “This work addresses a longstanding question about whether there is a resident ocular microbiome.”
Rare disease research uncovers new mechanism underlying muscle development.
An international team of researchers has identified genomic mutations for Carey-Fineman-Ziter (CFZS) syndrome, a very rare congenital myopathy (inherited muscle disorder) characterized by facial weakness, a small or retracted chin, a cleft palate and curvature of the spine (scoliosis), among other symptoms. The researchers determined that CFZS is caused by mutations in the gene MYMK that encodes for the protein myomaker. This protein is necessary for the fusion of muscle cells (myoblasts) into muscle fibers (myotubes) during the development of an embryo and the regeneration of muscle cells after injury. The study was published July 6, 2017, in Nature Communications.
Investigators at the National Institutes of Health and international colleagues have discovered a genetic cause and potential treatment strategy for a rare immune disorder called CHAPLE disease. Children with the condition can experience severe gastrointestinal distress and deep vein blood clots. No effective treatments are available to ameliorate or prevent these life-threatening symptoms.
Findings in mouse models reveal inflammatory factors that promote liver scarring
New findings from mouse models reveal that the type of immune response that helps maintain healthy metabolism in fatty tissues, called type 2 immunity, also drives obesity-induced nonalcoholic fatty liver disease (NAFLD). The work, led by scientists at the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, shows that the inflammatory environment in the fatty liver is more complex than previously thought. These insights may inform the development of new NAFLD treatments as well as immune-altering therapies for obesity and related health issues in people with NAFLD.
Research led by IRP investigators suggests potential treatment strategy.
Researchers have identified mutations in a gene called CARD11 that lead to atopic dermatitis, or eczema, an allergic skin disease. Scientists from the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, and other institutions discovered the mutations in four unrelated families with severe atopic dermatitis and studied the resulting cell-signaling defects that contribute to allergic disease. Their findings, reported in Nature Genetics, also suggest that some of these defects potentially could be corrected by supplementation with the amino acid glutamine.
Glutamine supplements can suppress reactivation of herpes simplex virus (HSV) in mice and guinea pigs, according to findings recently published in the Journal of Clinical Investigation. The research was conducted by scientists at the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, and at the U.S. Food and Drug Administration.
There is no cure for infection with HSV-1 and HSV2, viruses that can cause recurrent outbreaks of cold sores and genital sores in humans. Although antiviral medications can help shorten outbreaks, the virus persists in the body and can reactivate, which underscores the need for new treatment approaches. Prior research demonstrated the importance of HSV-specific T cells for controlling recurrent HSV outbreaks, and that activated T cells require increased metabolism of glutamine (an amino acid produced by the body and found in food). Therefore, the authors speculated that glutamine supplementation might increase T-cell function and improve infection control.
Duchenne muscular dystrophy is caused by a faulty gene that leads to progressive muscle weakness.
Researchers at the National Institutes of Health’s National Center for Advancing Translational Sciences (NCATS) and the University of Nevada, Reno School of Medicine (UNR Med) have demonstrated that a drug originally targeted unsuccessfully to treat cancer may have new life as a potential treatment for Duchenne muscular dystrophy (DMD).
The candidate drug, SU9516, represents a different kind of approach for treating DMD, a degenerative muscle disease that usually begins in childhood and has no known cure. It is caused by a faulty gene that leads to progressive muscle weakness, with death often occurring around age 25. Rather than trying to fix or replace the broken gene, SU9516 ramps up the muscle repair process, helping reinforce muscle structure.
