A transport mechanism is uncovered in the major drug-efflux system in E. coli involving two remote alternating-access conformational cycles, which could provide the basis for the development of allosteric inhibitors against multidrug resistance.

Polycystic ovary syndrome (PCOS) is a highly prevalent disorder of women, with significant reproductive, endocrine, and metabolic morbidities and a total healthcare-related economic burden exceeding $15 billion (2021 USD) for the U.S. alone, $4 billion due to mental health disorders.

Elevated levels of ectopic fat and a decreased number of oxidative insulin-sensitive type I muscle fibers in skeletal muscle could lead to insulin resistance in women with polycystic ovary syndrome.

Infection with Mycobacterium tuberculosis triggers de novo synthesis of polyunsaturated fatty acids by host macrophages, which promote their antimicrobial responses but feed the intracellular pathogen.

Androgen receptor activation modifies B cell frequencies and functionality, accompanied by weight gain in female mice exposed to human PCOS IgG, highlighting the unrecognized involvement of B cells in PCOS autoimmune comorbidities despite their absence not preventing PCOS phenotype development.

Common mouse models of polycystic ovary syndrome (PCOS) have variable ability to recapitulate the increased GnRH pulse generator frequency thought to exist in women with PCOS.

Evidence for a largely unexplored radiation of squamates (lizards, snakes, and amphisbaenians) in the Middle to Late Jurassic is revealed by analyses of morphospace expansion, disparity, and evolutionary rates.

TCR and CD40L microclusters are linked in synaptic ectosomes (extracellular vesicles) and released in the immunological synapse by helper T cells and induce dendritic cell maturation and cytokine production.

The regulation of tfap2α expression by adam13 is essential during cranial neural crest cell migration in Xenopus laevis.

Pathological TNF-α-producing B cells are involved in the pathological process of polycystic ovary syndrome, and metformin inhibits mTOR phosphorylation, affects metabolic reprogramming, and further inhibits TNF-α expression in pathological B cells.