Background and Purpose-Ethyl pyruvate (EP) is a pyruvate derivative that has been reported recently to prevent lethality in mice with established lethal sepsis and systemic inflammation. In this study, we examined the neuroprotective effect of EP in a rat cerebral ischemia model of middle cerebral artery occlusion (MCAO). Methods-Male Sprague-Dawley rats were subjected to 1 hour of MCAO, and EP was administered at various time points before or after MCAO. The changes in the brain infarction, neurological deficits, microglia activation, and proinflammatory cytokine expression were evaluated. BV2 microglial cells were also used to access the anti-inflammatory effect of EP.
The JNK interacting protein, JSAP1, has been identified as a scaffold protein for mitogen-activated protein kinase (MAPK) signaling pathways and as a linker protein for the cargo transport along the axons. To investigate the physiological function of JSAP1 in vivo, we generated mice lacking JSAP1. The JSAP1 null mutation produced various developmental deficits in the brain, including an axon guidance defect of the corpus callosum, in which phospho-FAK and phospho-JNK were distributed at reduced levels. The axon guidance defect of the corpus callosum in the jsap1-/- brain was correlated with the misplacement of glial sling cells, which reverted to their normal position after the transgenic expression of JNK interacting protein 1(JIP1). The transgenic JIP1 partially rescued the axon guidance defect of the corpus callosum and the anterior commissure of the jsap1-/- brain. The JSAP1 null mutation impaired the normal distribution of the Ca+2 regulating protein, calretinin, but not the synaptic vesicle marker, SNAP-25, along the axons of the thalamocortical tract. These results suggest that JSAP1 is required for the axon guidance of the telencephalic commissures and the distribution of cellular protein(s) along axons in vivo, and that the signaling network organized commonly by JIP1 and JSAP1 regulates the axon guidance in the developing brain.
Despite medical progress, high morbidity and mortality rates, due primarily to cardiovascular diseases, have persisted in patients with end-stage renal disease (ESRD). Recently, nontraditional risk factors, such as inflammation and malnutrition, have been emphasized in the development or progression of atherosclerosis in ESRD patients. Depression, the most common psychological problem in the ESRD population, is also known to be associated with inflammation and malnutrition, suggesting a possible link between depression with inflammation and cardiovascular diseases. The purpose of this study was to investigate the relationship between depression with cardiovascular risk factors and inflammation in patients undergoing continuous ambulatory peritoneal dialysis (CAPD). Eighty-one stable CAPD patients were enrolled. Depressive symptoms were assessed with the Beck Depression Inventory. Various cardiovascular risk factors and inflammatory markers were measured. Forty-three patients had depressive symptoms (53.8%). Patients with depressive symptoms showed significantly lower levels of albumin and IL-10, but higher levels of inflammatory markers than patients without depressive symptoms. Left ventricular hypertrophy was also found more frequently and pulse wave velocity and asymmetric dimethylarginine were all significantly increased in patients with depressive symptoms. Depression in CAPD patients was associated with inflammation and cardiovascular risk factors, and might be used as a predictor of cardiovascular diseases.
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