Volume 22 Issue 3, March 2016

In the digital age, biomedical scientists are frequently contacted by lay individuals seeking medical help, but they still receive little, if any, training in how to respond. Researchers need to reach back to these patients, but in a way that steers clear of giving medical advice.

Altered microbial colonization associated with cesarean section (C-section) birth could potentially have adverse effects on host development. The first interventional study of its kind attempts to reconfigure the early microbiota composition in C-section–delivered newborns to resemble that associated with vaginal birth.

Two new studies show that mechanisms of acquired resistance to targeted therapy in lung cancer do not necessarily pre-exist in resistant subclones. Instead, some cancers may harbor the potential to acquire a variety of drug-resistance mechanisms after response to targeted therapy.

In a recent study, beige adipocytes were derived from the capillaries of human subcutaneous adipose tissue. When implanted into mice, these cells enhanced glucose tolerance, thus providing evidence for their potential therapeutic use.

A study has demonstrated that transplanting human embryonic stem cell–derived, insulin-producing cells shielded in capsules made with an optimized biomaterial can achieve long-term cure of diabetes in mice without the need for any immunosuppression.

Ron Duman and colleagues discuss recent insights into a role for circuit disruption in the mechanisms of stress-induced depression. Furthermore they discuss the potential for rapid-acting antidepressants to alleviate these defects.

The microbiota of cesarean-born infants can be partially restored to that of vaginally born infants immediately after birth.

Dysregulated GABA-GIRK signaling drives lateral habenula hyperactivity in mouse models of depression. Restoring GABA-GIRK signaling by treatment with a PP2A inhibitor alleviates depression-like phenotypes.

Drug-tolerant but initially EGFR^T790M-negative tumor cells that undergo genetic evolution to acquire resistance to EGFR inhibitors are more resistant than pre-existing EGFR^T790M -positive clones to subsequent therapy.

Transcriptional profiling of Kras-driven early lesions—aimed at identifying founder events—reveals DDR1 as a therapeutic target relevant to adenocarcinoma.

Expression of HNF1A and KRT81 stratifies pancreatic ductal adenocarcinoma tumors into different subtypes, and expression of cytochrome P450 3A5 mediates basal and/or drug-induced therapy resistance in each subtype.

In a mouse model of the 5q- subtype of myelodysplastic syndrome, haploinsufficiency of the ribosomal protein gene Rps14 leads to anemia through a mechanism involving innate immune signaling and the Tlr4 ligand S100A8, which induces a p53-dependent block to erythroid differentiation.

Genome-wide DNA methylation analysis of metastatic biopsies from patients with castration-resistant prostate cancer reveals marked epigenetic differences between samples with adenocarcinoma and neuroendocrine histologies.

When encapsulated with alginate derivatives that resist the foreign-body response, human embryonic stem cell–derived beta cells restore long-term normoglycemia in immunocompetent mice without the need for immunosuppression.

Human beige adipocyte precursors associated with capillary networks proliferate in response to angiocrines, and when activated in vitro and transplanted into mice, they improve glucose intolerance.

Inhibition of ROR-γt impairs T_H17 responses, but not innate lymphoid cells, and is therapeutically effective in mouse models of intestinal inflammation.