Contents
26 September 2018
Vol 10, Issue 460
Vol 10, Issue 460
Research Articles
- Disrupting the LINC complex in smooth muscle cells reduces aortic disease in a mouse model of Hutchinson-Gilford progeria syndrome
Disrupting the LINC complex reduces aortic disease in a mouse model of Hutchinson-Gilford progeria syndrome.
- Gallium disrupts bacterial iron metabolism and has therapeutic effects in mice and humans with lung infections
Gallium disrupts bacterial iron metabolism and treats infections in mice and patients with chronic airway infections.
- Prime and target immunization protects against liver-stage malaria in mice
A prime and target vaccine for liver-stage malaria results in sterile protection in mouse disease models and appears safe for human use.
- PD-1 up-regulation on CD4+ T cells promotes pulmonary fibrosis through STAT3-mediated IL-17A and TGF-β1 production
PD-1+TH17 cells enhance collagen-1 production from human lung fibroblasts.
Report
- Reconstitution of the gut microbiota of antibiotic-treated patients by autologous fecal microbiota transplant
A randomized clinical trial demonstrates that autologous fecal microbiota transplant can reconstitute the gut microbiota of patients undergoing intensive antibiotic treatment.
Editors' Choice
- Cannabis use and schizophrenia: Chicken or egg?
A genome-wide association study identifies risk genes for cannabis use and examines direction of causality for its association with schizophrenia.
- Dissolving microneedle vaccination—No magic needled
Amphiphilic polymeric microneedles dissolve into nanomicelles that inhibit tumor growth.
- It takes two to tango: IDH mutation and glutaminase inhibition in glioma
IDH1 mutant gliomas show increased radiation sensitivity in combination with a glutaminase inhibitor.
Erratum
About The Cover
ONLINE COVER Mechanism of Malady. Progeria is a disease of premature aging caused by the production of a truncated form of prelamin A (progerin). Shown here is a colored transmission electron microscopy image of an aortic smooth muscle cell (SMC) from a mouse with progeria. Kim et al. studied vascular dysfunction in progeria, revealing that progerin expression and mechanical strain induced cell death in SMCs. Disrupting the link between the cytoskeleton and nuclear lamina in progerin-expressing SMCs improved aortic pathology by reducing shear stress transmission. This study helps identify the mechanism of arterial pathology in Hutchinson-Gilford progeria syndrome.[CREDIT: KIM ET AL./UNIVERSITY OF CALIFORNIA, LOS ANGELES]