Clinical Outcomes in Patients With Hypocontractile Bladders Undergoing Holmium Laser Enucleation of the Prostate.

Objective: To compare post-operative outcomes in patients who underwent holmium laser enucleation of the prostate (HoLEP) for benign prostatic hyperplasia (BPH) and had urodynamic evidence of bladder hypocontractility versus those with normocontractile bladders.

Methods: We retrospectively reviewed HoLEP patients with pre-operative urodynamic studies at a single institution, categorizing them into normocontractile and hypocontractile groups based on the bladder contractility index (BCI) (hypocontractile defined as BCI < 100). Post-void residual (PVR) volume was measured at 6 weeks and 6 months.

Estrogen-Induced hsa-miR-10b-5p Is Elevated in T Cells From Patients With Systemic Lupus Erythematosus and Down-Regulates Serine/Arginine-Rich Splicing Factor 1.

Objective: Autoimmune diseases affect women disproportionately more than men. Estrogen is implicated in immune cell dysfunction, yet its precise molecular roles are not fully known. We recently identified new roles for serine/arginine-rich splicing factor 1 (SRSF1) in T cell function and autoimmunity.

Oxaloacetate enhances neuronal cell bioenergetic fluxes and infrastructure.

We tested how the addition of oxaloacetate (OAA) to SH-SY5Y cells affected bioenergetic fluxes and infrastructure, and compared the effects of OAA to malate, pyruvate, and glucose deprivation. OAA displayed pro-glycolysis and pro-respiration effects. OAA pro-glycolysis effects were not a consequence of decarboxylation to pyruvate because unlike OAA, pyruvate lowered the glycolysis flux.

Mitochondrial lysates induce inflammation and Alzheimer's disease-relevant changes in microglial and neuronal cells.

Neuroinflammation occurs in Alzheimer's disease (AD). While AD genetic studies implicate inflammation-relevant genes and fibrillar amyloid-β protein promotes inflammation, our understanding of AD neuroinflammation nevertheless remains incomplete. In this study we hypothesized damage-associated molecular pattern (DAMP) molecules arising from mitochondria, intracellular organelles that resemble bacteria, could contribute to AD neuroinflammation.