Analysis of the reasons and costs of hospitalization for epilepsy patients in East China.

PURPOSE: This study aimed to assess the cause and cause-specific risks of hospitalization for epilepsy patients in East China. Further analysis was performed for inpatient hospitalization days, hospital mortality and costs. METHOD: This study was performed on epilepsy patients admitted to our hospital including 21 community health centers in East China from January 2011 to April 2017. Case records including patient data, length of hospitalization, reasons for admission, hospital mortality, and the costs incurred for hospitalization of epilepsy patients were reviewed. RESULTS: The three principal reasons for admission were: 1) cerebral vascular disease (CVD), 2) newly diagnosed epilepsy with unknown etiology; and 3) frequent seizures including status epilepticus. The median length of hospitalization was 13 days. The three major reasons regarding inpatient days were: 1) Parkinson's Disease (PD), 2) dementia, 3) trauma. The average hospital mortality was 14.81‰ (17/1148) with 1) lung infection (mainly pneumonia), 2) depression (deaths occurred by suicide) and 3) frequent seizures including status epilepticus being the three top reasons. The three major financial cost incurred for in-patients with epilepsy were: 1) PD, 2) arteriovenous malformation and 3) trauma. CONCLUSIONS: The most common hospitalized reasons for epilepsy patients were CVD, PD and dementia, which all were common diseases in the elderly. Consequently, the hospitalization days of these patients were longer and their financial burden was heavier. Epilepsy patients with comorbid depression should be closely monitored to prevent suicide from the onset of epilepsy.

Neuroprotective effect of angiotensin-(1-7) against rotenone-induced oxidative damage in CATH.a neurons.

There is evidence to support that ROSs are increased in Parkinson's disease (PD). Our recent research showed that angiotensin II (Ang II) participated in the pathogenesis of PD by triggering oxidative stress. Angiotensin-(1-7)[Ang-(1-7)] has been shown to moderate the adverse effects of the Ang II in many diseases. The purpose of the present study was to determine whether the Ang-(1-7) could have similar effects in CATH.a neurons. We used rotenone-induced neuron injury models to evaluate changes in cultured CATH.a cell lines levels of SOD, GSH and ROS. We also evaluated the expression of AT1, AT2, Mas receptors and Nox1, Nox2, P47phox, Hsp70 in treated with PBS, rotenone, Ang-(1-7), or Mas receptor antagonist A-779, alone and combined. The qRT-PCR and western blot were used to detect mRNA and protein levels of the AT1, AT2, Mas receptors and Nox1, Nox2, P47phox, Hsp70. The levels of SOD and GSH were determined by using commercial kits. The ROS generation was measured by the fluorescent probe assay. Ang-(1-7) in our current study significantly decreased rotenone-induced oxidative damage and increased the SOD and GSH generation. In addition, Ang-(1-7) significantly elevated Mas receptor expression and reduced NADPH oxidase activation, and these effects were completely eliminated by the A-779. Our findings suggest that Ang-(1-7) attenuates rotenone-induced oxidative damage in CATH.a neurons by activating the Mas receptor expression and inhibiting NADPH oxidase.

Indirubin-3'-monoxime suppresses amyloid-beta-induced apoptosis by inhibiting tau hyperphosphorylation.

Indirubin-3'-monoxime is an effective inhibitor of cyclin-dependent protein kinases, and may play an obligate role in neuronal apoptosis in Alzheimer's disease. Here, we found that indirubin-3'-monoxime improved the morphology and increased the survival rate of SH-SY5Y cells exposed to amyloid-beta 25-35 (Aß25-35), and also suppressed apoptosis by reducing tau phosphorylation at Ser199 and Thr205. Furthermore, indirubin-3'-monoxime inhibited phosphorylation of glycogen synthase kinase-3ß (GSK-3ß). Our results suggest that indirubin-3'-monoxime reduced Aß25-35-induced apoptosis by suppressing tau hyperphosphorylation via a GSK-3ß-mediated mechanism. Indirubin-3'-monoxime is a promising drug candidate for Alzheimer's disease.

Paralytic shellfish toxin profiles and toxin variability of the genus Alexandrium (Dinophyceae) isolated from the Southeast China Sea.

Paralytic shellfish toxin (PST) profiles of 16 Alexandrium isolates from the Southeast China Sea were analyzed by high-pressure liquid chromatography. Toxin content and composition of three A. tamarense isolates, ATDH01, ATGX02 and ATMJ02, were also investigated at different growth phases and under various culture conditions. Our results showed that six strains of A. affine were non-toxic, while 10 strains of A. tamarense and A. catenella were toxic. These toxic isolates grown in the same culture conditions consistently produced an unusually high proportion of the N-sulfocarbamoyl toxin C1/2 (around 60-80% of total toxins) and medium amounts of gonyautoxin GTX5 (around 15-30% of total) with only trace quantities (<5% of total) of other saxitoxin derivatives (i.e. GTX1, GTX3, GTX4 and neoSTX). The toxin composition of three A. tamarense isolates did not vary with the growth phases, although higher toxin contents (Qt, fmolcell(-1)) were found in the exponential phase. Variations in temperature, salinity and nutrient levels affected toxin content of three A. tamarense isolates but they did not have pronounced effects on the toxin composition (mole %). These results indicate that toxin composition remained relatively constant under various culture conditions, suggesting that toxin composition could be used as a stable biomarker for the Alexandrium species in this region. However, comparison of toxin profiles between isolates from different localities require special caution since isolates even from the same region can have distinct toxin profiles.

Blockade of L-type voltage-gated Ca channel inhibits ischemia-induced neurogenesis by down-regulating iNOS expression in adult mouse.

Neurogenesis in the adult mammalian hippocampus may contribute to repairing the brain after injury. The signals that regulate neurogenesis in the dentate gyrus following ischemic stroke insult are not well known. We have previously reported that inducible nitric oxide synthase (iNOS) expression is necessary for ischemia-stimulated neurogenesis in the adult dentate gyrus. Here, we show that mice subjected to 90 min of middle cerebral artery occlusion (MCAO) significantly increased the number of new neurons and up-regulated iNOS expression in the dentate gyrus. Blockade of the L-type voltage-gated Ca(2+) channel (L-VGCC) prevented neurogenesis in the dentate gyrus and subventricular zone (SVZ), and down-regulated iNOS expression in the dentate gyrus after cerebral ischemia. This study suggests that Ca(2+) influx through L-VGCC is involved in ischemia-induced neurogenesis by up-regulating iNOS expression.