SIMPLE is greatly facilitated by the use of a whole-slide scanner, which can capture the results of each sequential stain without any information loss. (J Histochem Cytochem 57:899-905, 2009)”
“Hyperglycemia is common after acute stroke. In the acute phase of stroke (within 24 h), rats

with permanent cerebral ischemia developed higher fasting blood glucose and insulin levels in association with up-regulation of hepatic gluconeogenic gene expression, including phosphoenolpyruvate carboxykinase, glucose-6-phosphatase, and fructose-1,6-bisphosphatase. In addition, hepatic gluconeogenesis-associated positive regulators, such as FoxO1, CAATT/enhancer-binding proteins (C/EBPs), and cAMP responsive Crenolanib in vitro element-binding protein (CREB), were up-regulated. Dinaciclib inhibitor For insulin signaling transduction, phosphorylation of insulin receptor (IR), insulin receptor substrate-1 (IRS1) at the tyrosine residue, Akt, and AMP-activated protein kinase (AMPK), were attenuated in the liver, while negative regulators of insulin action, including phosphorylation of p38, c-Jun N-terminal kinase (JNK), and insulin receptor substrate-1 (IRS1)

at the serine residue, were increased. In addition, the brains of rats with stroke exhibited a reduction in phosphorylation of IRS1 at the tyrosine residue and Akt. Circulating cortisol, glucagon, C-reactive protein (CRP), monocyte chemoattractant protein 1 (MCP-1), and resistin levels were elevated, but adiponectin was reduced. Our data suggest that cerebral ischemic insults might modify intracellular and extracellular environments, favoring hepatic gluconeogenesis and the consequences of hyperglycemia. (C) 2013 Published by Elsevier Ireland Ltd.”
“Neuromuscular electrical stimulation (NMES) can be used to activate paralyzed or paretic muscles to generate functional or therapeutic movements. The goal of this research was to develop a rodent model of NMES-assisted movement therapy after spinal cord injury (SCI) that will enable investigation of mechanisms of NMES-induced plasticity, Pinometostat from the molecular

to systems level. Development of the model requires accurate mapping of electrode and muscle stimulation sites, the capability to selectively activate muscles to produce graded contractions of sufficient strength, stable anchoring of the implanted electrode within the muscles and stable performance with functional reliability over several weeks of the therapy window. Custom designed electrodes were implanted chronically in hindlimb muscles of spinal cord transected rats. Mechanical and electrical stability of electrodes and the ability to achieve appropriate muscle recruitment and joint angle excursion were assessed by characterizing the strength duration curves, isometric torque recruitment curves and kinematics of joint angle excursion over 6-8 weeks post implantation.