Gapless assembly of NVSL348.

We are reporting a genome containing four nuclear chromosomes, a mitochondrial genome, and an apicoplast from reference isolate NVSL348. This report includes a gapless assembly consisting of all six genetic molecules.

Complete Genome Sequence of Theileria equi NVSL354.

We are reporting the nearly complete genome of Theileria equi (Piroplasmida, Apicomplexa), which contains four nuclear chromosomes, a mitochondrial genome, and an apicoplast from the NVSL354 reference isolate. This report includes all six genetic molecules.

Attenuation of Blood-Brain Barrier Breakdown and Hyperpermeability by Calpain Inhibition.

Blood-brain barrier (BBB) breakdown and the associated microvascular hyperpermeability followed by brain edema are hallmark features of several brain pathologies, including traumatic brain injuries (TBI). Recent studies indicate that pro-inflammatory cytokine interleukin-1β (IL-1β) that is up-regulated following traumatic injuries also promotes BBB dysfunction and hyperpermeability, but the underlying mechanisms are not clearly known. The objective of this study was to determine the role of calpains in mediating BBB dysfunction and hyperpermeability and to test the effect of calpain inhibition on the BBB following traumatic insults to the brain.

Tumor necrosis factor-α disruption of brain endothelial cell barrier is mediated through matrix metalloproteinase-9.

Traumatic brain injuries cause vascular hyperpermeability. Tumor necrosis factor-α (TNF-α), matrix metalloproteinase-9 (MMP-9), and caspase-3 may be important in these processes but the relationship between them has not been investigated. We hypothesized that TNF-α regulates caspase-3-mediated hyperpermeability and blood brain barrier damage and hyperpermeability directly or indirectly via activation of MMP-9.

Insulin--carcinogen or mitogen? Preclinical and clinical evidence from prostate, breast, pancreatic, and colorectal cancer research.

Diabetes mellitus is a chronic disease that affects > 23.6 million Americans, and occurs when the body is unable to produce or becomes resistant to endogenous insulin. This alteration of insulin's action reduces adequate utilization of glucose transporter type 4 (GLUT4) receptors, which are responsible for cellular glucose uptake.