(PHILADELPHIA) -- About 5.7 million Americans have heart failure, half of whom will die from the disease within 5 years, according to the Centers for Disease Control and Prevention (CDC). Two processes help drive the disease: a weakened heart muscle that is less able to pump, and the death of heart cells that irreparably damage the heart. Beta-blockers, commonly used to treat heart disease, work by blocking the beta-adrenergic receptors in the heart, saving heart cells from cell death. But beta-adrenergic receptors also help keep the heart pumping, a function that this medication also blocks.

Inflammatory myofibroblastic tumors (IMTs) -- masses of immune cells-- are benign, but poorly understood. Current IMT treatments often have side effects and surgery is sometimes not an option due to the tumor's proximity to vital organs. A better understanding of how IMTs form could spur the development of more effective therapeutics. Researchers at University of California San Diego School of Medicine have now found that a likely cause of IMT is deficiency in nonsense-mediated RNA decay (NMD), a system cells use to control which genes are activated.

The study is published June 27 by the Journal of Clinical Investigation.

LA JOLLA, CA - June 27, 2016 - Scientists at The Scripps Research Institute (TSRI) have identified a protein that launches cancer growth and appears to contribute to higher mortality in breast cancer patients.

The new findings, published June 27, 2016 in the journal Nature Structural & Molecular Biology, suggest that future therapies might target this protein, called GlyRS, to halt cancer growth.

"We have potentially found an important target for anti-cancer treatment," said TSRI Professor Xiang-Lei Yang, who led the study.

Japan -- What goes on inside the brain when we learn new things? Much still remains wrapped in mystery, but scientists have found a way to examine this at the molecular level.

Researchers in Japan have engineered an artificial switch that could let scientists turn individual neurotransmitter receptors on and off. Shedding light on these receptors' role in memory formation could contribute to the development of new drugs for neurological diseases, including Alzheimer's, Parkinson's, and ALS.

Scientists have discovered that the malaria parasite Plasmodium vivax is evolving rapidly to adapt to conditions in different geographical locations, in particular to defend itself against widely-used antimalarial drugs. The study, published in Nature Genetics today, provides a foundation for using genomic surveillance to guide effective strategies for malaria control and elimination.

P. vivax is mainly found in Asia and South America, and 2.5 billion people are at risk of infection worldwide. This species of malaria parasite is notoriously difficult to work with and the new study has created one of the largest genomic data sets of this species to date, which is available to all researchers.

Progressive neurodegeneration in Parkinson's disease is linked to toxic accumulation of α-synuclein aggregates in neurons. Although mutations in the gene encoding α-synuclein are associated with inherited forms of Parkinson's disease, the identification of other factors that contribute to α-synuclein aggregation may lead to more effective approaches for slowing disease advancement. In this month's issue of the JCI, a team led by Ted Dawson and Han Seok Ko at Johns Hopkins School of Medicine determined that activation of a protein called c-Abl exacerbates α-synuclein accumulation and the appearance of behavioral hallmarks of Parkinson's disease in mice.