A new class of treatment, PTC124, has been shown to restore muscle function in a mouse model of Duchenne muscular dystrophy by targeting a specific genetic defect. The drug allows the ribosome to read through a mutation and produce full-length dystrophin protein, enabling enough protein to be made to correct defects in the muscles.
A study by Ugandan researchers found that interruptions in antiretroviral medication supply due to financial or logistical issues led to the development of drug resistance in HIV-infected patients. Despite near-perfect adherence, treatment interruptions created opportunities for resistance to develop.
A new survey by Duke University Medical Center and Johns Hopkins University found that 41% of clinical trial coordinators have experience disclosing financial conflicts of interest, but many feel uncomfortable doing so. The researchers suggest that additional education and training are needed to address these concerns.
Researchers at Salk Institute discovered a 2-step mechanism for cilia to agree on direction, enabling directional fluid flow. Cilia refinement phase ensures coordinated movement of up to 200 cilia per cell.
Researchers found that a miscue in the body's genetic repair system may cause Huntington's disease, a fatal condition that destroys the nervous system. The study revealed that repeated tracts of replacement repair segments become toxic and accelerate cell death.
A new study reveals that serotonin and neuropeptide F regulate aggression in fruit flies, similar to their effects on mammals. The findings suggest that the molecular and neural roots for complex social behavior are of ancient evolutionary origin.
UCSF scientists have discovered that chitin triggers an allergic inflammatory response in the lungs of mice, leading to increased production of the anti-chitin enzyme. The researchers suggest that people with less-effective versions of this enzyme may be more prone to asthma due to their inability to control exposure to inhaled chitin.
Researchers at Johns Hopkins created a publicly available database on phosphorylation events in proteins, known as PhosphoMotif Finder. The database contains nearly all chemical changes nature makes by adding phosphate to proteins manufactured in human cells.
Researchers have discovered that faulty DNA repair contributes to the onset of Huntington's disease. The study suggests that targeting a key enzyme in oxidative lesion repair may offer a way to slow or stop the disease.