Contents
13 December 2017
Vol 9, Issue 420
Vol 9, Issue 420
Research Articles
- Targeted apoptosis of myofibroblasts with the BH3 mimetic ABT-263 reverses established fibrosis
ABT-263 blocks BCL-XL to induce apoptosis in human dermal fibroblasts from patients with scleroderma and in myofibroblasts in mice, reversing dermal fibrosis.
- Urine lipoarabinomannan glycan in HIV-negative patients with pulmonary tuberculosis correlates with disease severity
The Mycobacterium tuberculosis–specific antigen lipoarabinomannan measured in the urine of HIV-negative, pulmonary TB-infected patients correlates with disease severity.
- Effect of population viral load on prospective HIV incidence in a hyperendemic rural African community
We propose HIV population viral load indices, which we demonstrate predict future risk of acquiring HIV in a rural South African population.
- Durability and correlates of vaccine protection against Zika virus in rhesus monkeys
Not all vaccines afford robust protection against ZIKV challenge in rhesus monkeys at 1 year after vaccination.
Report
- Thorase variants are associated with defects in glutamatergic neurotransmission that can be rescued by Perampanel
Rare variants in the enzyme Thorase increase AMPAR expression, resulting in behavioral abnormalities in mice that can be rescued with Perampanel.
Editors' Choice
- A diet pill for critical illness weakness?
The serotoninergic drug Lorcaserin rescued motor neuron electrophysiological abnormalities in an animal model of critical illness–induced weakness.
- Running interference on hemorrhagic fever
A siRNA-based therapy for Marburg viruses shows promise.
- Myc heals all (tumor) wounds
The activation of Myc in Ras-driven lung adenomas causes profound immune/stromal remodeling to support tumor growth.
- NRF2 much of a good thing
Chronic hyperglycemia induces hypertension and renal injury through nuclear factor erythroid 2–related factor 2 (NRF2)–stimulation of the renin-angiotensin system.
Erratum
About The Cover
ONLINE COVER Primed to Perish. This image shows human dermal myofibroblasts from a patient with scleroderma, a fibrotic disorder. Myofibroblasts produce large amounts of collagen and contribute to the extracellular matrix stiffening that is a hallmark of fibrosis. Lagares et al. determined that damaged mitochondria (magenta) within these activated cells (stress fibers, cyan) become dependent upon antiapoptotic proteins for survival. Fibrosis could be reversed by treating cells from patients with scleroderma or mouse models of dermal fibrosis with ABT-263, a drug that inhibits an antiapoptotic protein. Evaluating the state of mitochondria within myofibroblasts could help identify effective drug targets for fibrosis. [CREDIT: A. SANTOS, D. LAGARES/MASSACHUSETTS GENERAL HOSPITAL]