Triptolide potentiates the cytoskeleton-stabilizing activity of cyclosporine A in glomerular podocytes a GSK3β dependent mechanism.

Tripterygium wilfordii Hook F. (TwHF) is a traditional Chinese herb and has a broad spectrum of biological functions including immunosuppression and anti-inflammatory effects. When used in combination with other standard of care medications, such as glucocorticoids and calcineurin inhibitors like cyclosporine A, for treating glomerular diseases, TwHF demonstrates a remarkable dose-sparing effect, the molecular mechanism for which remains largely unknown.

Brain natriuretic peptide mitigates TIMP2 induction and reinstates extracellular matrix catabolic activity GSK3β inhibition in glomerular podocytes exposed to a profibrogenic milieu.

Brain natriuretic peptide (BNP) has a demonstrable anti-fibrotic effect on diverse organ systems, including the kidney. To understand the molecular mechanism underlying this renoprotective effect, the efficacy of BNP was examined in an model of glomerular sclerosis by exposing glomerular podocytes to transforming growth factor (TGF)β1-containing media that recapitulates the profibrogenic milieu in chronic glomerular disease. BNP mitigates extracellular matrix (ECM) accumulation in TGFβ1-treated podocytes, as evidenced by Sirius red assay and staining, concomitant with a restoration of the ECM catabolizing activity, as assessed by pulse chase analysis.

Expression, regulation and functional assessment of the 80 amino acid Small Adipocyte Factor 1 (Smaf1) protein in adipocytes.

The gene for Small Adipocyte Factor 1, Smaf1 (also known as adipogenin, ADIG), encodes a ∼600 base transcript that is highly upregulated during 3T3-L1 in vitro adipogenesis and markedly enriched in adipose tissues. Based on the lack of an obvious open reading frame in the Smaf1 transcript, it is not known if the Smaf1 gene is protein coding or non-coding RNA. Using a peptide from a putative open reading frame of Smaf1 as antigen, we generated antibodies for western analysis.

Methamphetamine effects on blood-brain barrier structure and function.

Methamphetamine (Meth) is a widely abuse psychostimulant. Traditionally, studies have focused on the neurotoxic effects of Meth on monoaminergic neurotransmitter terminals. Recently, both in vitro and in vivo studies have investigated the effects of Meth on the BBB and found that Meth produces a decrease in BBB structural proteins and an increase in BBB permeability to various molecules.

Analysis of FK506, timcodar (VX-853) and FKBP51 and FKBP52 chaperones in control of glucocorticoid receptor activity and phosphorylation.

The immunosuppressive ligand FK506 and the FK506-binding protein FKBP52 are stimulatory to glucocorticoid receptor (GR) activity. Here, we explore the underlying mechanism by comparing GR activity and phosphorylation status in response to FK506 and the novel nonimmunosuppressive ligand timcodar (VX-853) and in the presence and absence of FKBP52 and the closely related protein FKBP51. Using mouse embryonic fibroblast cells (MEFs) deficient knockout (KO) in FKBP51 or FKBP52, we show decreased GR activity at endogenous genes in 52KO cells, but increased activity in 51KO cells.

Elevated hemoglobin A1c is associated with readmission but not complications.

Background: studies have shown that elevated hemoglobin A1c levels are associated with worse short-term outcomes after cardiac surgery. However, the effect on readmission has not been studied. The primary purpose of this study was to determine the independent effect of hemoglobin A1c level on the readmission rate after cardiac surgery.

The Basal Ganglia as a Substrate for the Multiple Actions of Amphetamines.

Amphetamines are psychostimulant drugs with high abuse potential. Acute and chronic doses of amphetamines affect dopamine (DA) neurotransmission in the basal ganglia. The basal ganglia are a group of subcortical nuclei that are anatomically positioned to integrate cognitive, motor and sensorimotor inputs from the cortex.

Molecular and functional characterization of non voltage-operated Ca entry in gastrointestinal neuroendocrine tumor cells.

Ca(2+) entry through non-voltage operated channels serves as a key signaling component for tumor progression in a variety of cancers including prostate, colon and breast. As a starting point for an inquiry into the role of Ca(2+) signaling pathways in gastroenteropancreatic neuroendocrine cancers, including carcinoid, we characterized Ca(2+) entry in a set of human carcinoid cell lines originating in the foregut, midgut and hindgut. In the current study, we provide molecular and functional evidence for store-operated and other non-voltage operated Ca(2+) permeable channels in carcinoid tumor cell lines.