Traumatic middle meningeal artery pseudoaneurysm: Case report and review of literature.

Traumatic aneurysms represent less than 1 percent of intracranial aneurysms and middle meningeal artery pseudoaneurysms are even rare. Traumatic aneurysms are usually pseudoaneurysms formed by the rupture of all the layers of the vessel wall. They are associated with high mortality as they can present as epidural, subdural, and rarely intraparenchymal hematoma.

Humanin alone and in combination with GnRHa therapy attenuates ovarian dysfunction induced by prepubertal cyclophosphamide chemotherapy in female mice.

Prepubertal chemotherapy induced ovarian damage poses a significant threat to female fertility, particularly following cyclophosphamide (CP) treatment. Humanin (HNG), a small molecule polypeptide encoded by mitochondrial DNA, has a variety of effects, this study aimed to investigate the protective effects of HNG and its combination with conventional Gonadotropin Releasing Hormone Agonist (GnRHa) on ovarian function in a CP-induced damage model. The 21-day-old C57BL/6 J female mice were randomly assigned to six groups: Control, CP model, HNG, HNG+CP, GnRHa+CP, and HNG+GnRHa+CP.

Evolution of interspecific interactions underlying the nonlinear relationship between active biomass and pollutant degradation capacity in bioelectrochemical systems.

This study proposes a switching operating mode that alternates between microbial fuel cell (MFC) and microbial electrolysis cell (MEC) to restore the biofilm activity and organic pollutant degradation capacity in bioelectrochemical systems (BESs) during prolonged operation. After the model switching, the toluene degradation kinetics in BESs equipped with graphite sheet (GS) and polyaniline@carbon nanotubes (PANI@CNTs) bioanodes were elevated by 2.10 and 3.

S6K1 is a Targetable Vulnerability in Tumors Exhibiting Plasticity and Therapy Resistance.

Most tumors initially respond to treatment, yet refractory clones subsequently develop owing to resistance mechanisms associated with cancer cell plasticity and heterogeneity. We used a chemical biology approach to identify protein targets in cancer cells exhibiting diverse driver mutations and representing models of tumor lineage plasticity and therapy resistance. An unbiased screen of a drug library was performed against cancer cells followed by synthesis of chemical analogs of the most effective drug.