The molecular events involved in oligodendrocyte precursor cell proliferation induced by the conditioned medium from b104 neuroblastoma cells.

The conditioned medium from B104 neuroblastoma cells (B104CM) induces proliferation of oligodendrocyte progenitor cells (OPCs) in vitro. However, the molecular events that occur during B104CM-induced proliferation of OPCs has not been well clarified. In the present study, using OPCs immunopanned from embryonic day 14 Sprague-Dawley rat spinal cords, we explored the activation of several signaling pathways and the expression of several important immediate early genes (IEGs) and cyclins in OPCs in response to B104CM.

Protective effects of the delta opioid peptide [D-Ala2, D-Leu5]enkephalin in an ex vivo model of ischemia/reperfusion in brain slices.

Introduction: The delta opioid peptide [D-Ala2, D-Leu5]enkephalin (DADLE) plays a key role in neuronal protection against both hypoxic and ischemic conditions. However, the cellular mechanisms of action of DADLE under these conditions remain unclear.

Methods: Ischemia was simulated with perfusing the brain slices with glucose-free artificial cerebrospinal fluid.

PDGF-AA and bFGF mediate B104CM-induced proliferation of oligodendrocyte precursor cells.

The conditioned medium from B104 neuroblastoma cells (B104CM) induces proliferation of οligodendrocyte precursor cells (OPCs) in vitro, which indicates that certain factors contained within B104CM give instructional signals that direct the proliferation of OPCs. However, the OPC-proliferative factors present in B104CM have yet to be identified. Platelet-derived growth factor AA (PDGF-AA), basic fibroblast growth factor (bFGF) and insulin-like growth factor-1 (IGF-1) have been reported to act as potent mitogens for OPC proliferation.

Comparative study on transcatheter arterial chemoembolization, portal vein embolization and high intensity focused ultrasound sequential therapy for patients.

Objective: To investigate the safety and efficacy of transcatheter arterial chemoembolization (TACE), combined with portal vein embolization (PVE), and high intensity focused ultrasound (HIFU) sequential therapy in treating patients with hepatocellular carcinoma (HCC).

Methods: Patients with inoperative HCC were treated by two methods: in the study group with TACE first, then PVE a week later, and then TACE+PVE every two months as a cycle, after 2~3 cycles finally HIFU was given; in the control group only TACE+PVE was given. Response (CR+PR), and disease control rate (CR+PR+SD), side effects, overall survival and time to progress were calculated.

Propofol attenuates oxidative stress-induced PC12 cell injury via p38 MAP kinase dependent pathway.

Aim: To investigate the neuroprotective effect of propofol and its intracellular mechanism on neurons in vitro.

Methods: Cell viability was determined with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide reduction. Apoptotic cell death was determined by Hoechst 33258 staining and a fluorescence-activated cell sorter.

Aceclidine and pilocarpine interact differently with muscarinic receptor in isolated rabbit iris muscle.

The relationship between muscarinic receptor affinity states and the contractile response to the muscarinic agonists carbachol, aceclidine, and pilocarpine, has been examined in the isolated rabbit iris muscle. Contraction of the iris muscle by carbachol and aceclidine was more potent and/or more efficacious than the response to pilocarpine. Analysis of [3H]-Quinuclidinyl benzilate (QNB) binding showed that while both carbachol and aceclidine bound to high- and low-affinity forms of the muscarinic receptor, pilocarpine bound to one affinity state.

Phosphorylated heat shock protein 27 is involved in enhanced heart tolerance to ischemia in short-term type 1 diabetic rats.

Aim: To examine the tolerance of type 1 diabetic hearts to ischemia and reperfusion injury. Myocardial contents of 27-kDa and 70-kDa heat shock proteins (hsp) as well as phosphorylated hsp27 were also determined.

Methods: Hearts from hyperglycemic rats 3 weeks after streptozocin injection and age-matched normal rats were subjected to ischemia and reperfusion in vitro.

Up-regulation of M1 muscarinic receptors expressed in CHOm1 cells by panaxynol via cAMP pathway.

Loss of cholinergic neurons along with muscarinic acetylcholine receptors (mAChRs) in cerebral cortex and hippocampus is closely associated with Alzheimer's disease (AD). Recent drug development for AD treatment focuses heavily on identifying M(1) receptor agonists. However, mAChRs undergo down-regulation in response to agonist-induced sustained activation.

Simultaneous changes in secretory amyloid precursor protein and beta-amyloid peptide release from rat hippocampus by activation of muscarinic receptors.

Amyloid deposits in Alzheimer's disease (AD) are composed of beta-amyloid peptides (Abeta) that are derived from the larger amyloid precursor protein (APP). A number of studies with various transfected cell lines demonstrated that either APP secretion or Abeta production could be modulated by specific muscarinic receptor activation. In the present study, we investigated the simultaneous changes of neurotrophic secretory APP (APPs) and neurotoxic Abeta release from rat hippocampus by activation of muscarinic receptors.

6beta-acetoxy nortropane regulated processing of amyloid precursor protein in CHOm1 cells and rat brain.

The effects of the muscarinic receptor agonist 6beta-acetoxy nortropane on amyloid precursor protein (APP) processing were studied in both transfected Chinese hamster ovary cells stably expressing muscarinic M(1) receptors (denoted as CHOm(1) cell line) and in cerebral cortical and hippocampal slices. Exposure of CHOm(1) cells to 6beta-acetoxy nortropane for 1 h significantly increased the secretion of secretory amyloid precursor protein (derived from alpha-secretase cleavage) in a concentration-dependent manner. In the same system, 6beta-acetoxy nortropane reduced the beta-amyloid peptide production.