The climate crisis in the time of COVID-19 illustrates the difference between the important and the urgent. There is, of course, no alternative to focusing on the current pandemic. But at the same time, the SARS-CoV-2 coronavirus has not changed the fact that the climate crisis is a coming wave whose health consequences will ultimately dwarf those of any single infectious agent.
BioWorld looks at translational medicine, including: Neutralizing RSV; Insulin cuts both ways in vasculature; Transcriptomic insights into Parkinson’s disease; Restoring synaptic transmission for rare neurodevelopmental disease; Polymerase k and drug resistance; Sphingolipids accumulate in neurodegeneration; How does innate immunity remember? Not via polycomb; Antibiotics affect oxycodone effects; Cabo as next annual shot?
The activity of many proteins is controlled through phosphorylation by kinases and dephosphorylation by phosphatases. Overactive kinases are one of the major drivers of tumors and, as a result, kinase inhibitors are a mainstay of oncology drug development. But “activation of the brakes, the phosphatases, could be equally therapeutically viable for the treatment of a broad range of cancers” to kinase inhibition, Goutham Narla told the audience at the 2020 American Association for Cancer Research (AACR) meeting.
A multi-institutional group led by the University of California at San Francisco’s Quantitative Biosciences Institute (QBI) has identified more than 200 host proteins that interacted with SARS-CoV-2 viral proteins during infection, creating “a blueprint of how SARS-CoV-2 hijacks human cells,” QBI Director Nevan Krogan told reporters. They then used that blueprint to identify 10 drugs, some FDA approved and some in clinical trials, that were able to inhibit viral growth in cell culture assays, marking them for further study as potential antivirals. The work also identified one compound, dextromethorphan, that appeared to facilitate viral growth.
BioWorld looks at translational medicine, including: Edited stem cells reverse mouse diabetes; Noncoding TET2 variants affect neurodegeneration risk; Pancreatic cancer uses autophagy to hide from immune system; Heart failure hormone has role in sepsis; NRF2 wakes sleeping tumor cells; Oral drug can wake up telomerase; Cheating cell death improves infarct outcomes; Older siblings’ example turns stem cells into heart cells; Lung changes from PD drug hopeful are reversible; Platelets play role in Tylenol toxicity.
By analyzing the antibody response of a survivor of Marburg virus infection, researchers at the University of Texas Medical Branch and Vanderbilt University Medical Center have gained new insights into the function of non-neutralizing antibodies in fighting infections.
Chinese scientists have shown for the first time that the down-regulation of a single RNA-binding protein, polypyrimidine tract-binding protein 1 (Ptbp1), locally converted glial cells to neurons and showed promise for treating the symptoms of neurodegenerative diseases in mice.
BioWorld looks at translational medicine, including: Engineering better bacterial backstabbers; Targeting bystander protein improves sepsis outcome; Long noncoding RNA has sex-specific role in depression; Targeted IL-12 heats up cold tumors; Fast route from fibroblasts to photoreceptors; Eating pro-inflammatory IgG helps prevent liver failure; Depression’s structural problem; Modeling the post-infarct heart; Interleukins rile each other up in reaction to implants; Complement links high BMI to dementia.
The largest study to date on hypermutated gliomas has delivered new insights into their origin, as well as their response to several different treatments. Specifically, even though they are hypermutated, such tumors are unlikely to respond to PD-1 blockers.
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