Rd significantly suppressed the accumulations of DNA, protein and lipid peroxidation products at 24 h post-ischemia. Rd also protected mitochondria at 4 and 24 h after reperfusion as indicated by preserved respiratory chain complex activities and check details aconitase activity, lowered mitochondrial hydrogen peroxide

production, and hyperpolarized mitochondrial membrane potential. Furthermore, Rd partly enhanced endogenous antioxidant activities following MCAO. Collectively, these findings demonstrated that Rd exerts neuroprotection against transient focal ischemia in the aged brain, which may be associated with the attenuation of redox imbalance. (C) 2011 Elsevier Ltd. All rights reserved.”
“Cyclical neutropenia (CN) is a rare hematopoietic disorder in which the patient’s neutrophil level drops to extremely low levels for a few days approximately every three weeks. CN is effectively treated with granulocyte

colony stimulating factor (G-CSF), which is known to interfere with apoptosis in neutrophil precursors and to consequently increase the circulating neutrophil level. However, G-CSF treatment usually fails to eliminate the oscillation. In this study, we establish an age-structured model of hematopoiesis, which reduces to a set of four delay differential equations with specific forms of initial functions. We numerically investigate the see more possible stable solutions of the model equations with respect to changes in the parameters as well as the initial conditions. The results show that the hematopoietic system possesses Aspartate multistability for parameters typical of the normal healthy state. From our numerical results, decreasing the proliferation rate of neutrophil precursors or increasing the stem cell death rate are two possible mechanisms to induce cyclical neutropenia, and the periods of the resulting oscillations are independent of the changing parameters. We also discuss the dependence of the model solution on the initial condition at normal parameter values corresponding to a healthy state. Using insight from our results we design a hybrid

treatment method that is able to abolish the oscillations in CN. (C) 2010 Elsevier Ltd. All rights reserved.”
“It has recently been shown that clonidine suppresses itch-related responses via its action on alpha(2)-adrenoceptors in the spinal cord, raising the possibility that the descending noradrenergic system regulates itch signaling in the spinal cord. In this study, we investigated whether the transmission of itch signals in the spinal cord is under tonic inhibition by the descending noradrenergic system. An intraplantar injection of serotonin in mice induced biting of the treated paw (an itch-related response). An intrathecal injection of 6-hydroxydopamine (catecholaminergic neurotoxin) enhanced the itch-related response.