36 research outputs found

    Effect of melatonin in reducing second-generation antipsychotic metabolic effects: A double blind controlled clinical trial

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    Introduction The use of second-generation atypical antipsychotics has an increasing role in the development of metabolic syndrome. However, these medications due to metabolic disorders can lead to an increased risk of cardiovascular disease and subsequently mortality as well as reduced adherence to treatment. The main objective of current study was to determine the ability of melatonin to reduce the metabolic effects of second-generation antipsychotics. Methods This double blind controlled clinical trial was conducted on 100 patients aged 18–64 years old were treated with the second-generation antipsychotics for the first time. The patients were divided randomly into two groups of 50. The case group received slow-release melatonin at a dose of 3 mg and the control group was given oral placebo at 8 p.m. Results The findings in melatonin group indicated significantly increase of HDL and decreased fasting blood sugar and systolic blood pressure, as well as had statistically significant increase in waist circumference, weight and BMI compared with placebo group. Conclusion According to the findings, it can be claimed that the addition of melatonin to atypical antipsychotics has led to a reduction in some of the metabolic effects of these drugs. In this study, HDL level was increased, and the mean systolic blood pressure and FBS were decreased in the melatonin group. Considering that these factors are contributing to cardiovascular disease as a leading cause of mortality in psychiatric patients, so the use of melatonin can reduce some of the medical effects of long-term treatment of atypical antipsychotics. © 2017 Diabetes Indi

    Thickness mode high frequency MEMS piezoelectric micro ultrasound transducers

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    Thickness mode piezoelectric micro-electromechanical system (MEMS) ultrasound transducers, operating in the 50–75 MHz range, have been fabricated using a composite sol gel technique in combination with wet etching. The composite sol gel technique involves producing a PZT powder/sol composite slurry, which when spun down yields films a few micrometers thick. Repeated layering, and infiltration, has been used to produce PZT films between 20 and 40 μm thick. Due to the low firing temperature (<720°C) it has also been possible to integrate these PZT films with a micro-machined silicon support wafer. These PZT thick films have been structured using a wet etching technique to create free standing pillars that have been shown to resonate in thickness mode in the frequency range of 50–75 MHz. Examples of these structures and their resonant behaviour are pre

    Epicortical Brevetoxin Treatment Promotes Neural Repair and Functional Recovery after Ischemic Stroke

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    Emerging literature suggests that after a stroke, the peri-infarct region exhibits dynamic changes in excitability. In rodent stroke models, treatments that enhance excitability in the peri-infarct cerebral cortex promote motor recovery. This increase in cortical excitability and plasticity is opposed by increases in tonic GABAergic inhibition in the peri-infarct zone beginning three days after a stroke in a mouse model. Maintenance of a favorable excitatory&ndash;inhibitory balance promoting cerebrocortical excitability could potentially improve recovery. Brevetoxin-2 (PbTx-2) is a voltage-gated sodium channel (VGSC) gating modifier that increases intracellular sodium ([Na+]i), upregulates N-methyl-D-aspartate receptor (NMDAR) channel activity and engages downstream calcium (Ca2+) signaling pathways. In immature cerebrocortical neurons, PbTx-2 promoted neuronal structural plasticity by increasing neurite outgrowth, dendritogenesis and synaptogenesis. We hypothesized that PbTx-2 may promote excitability and structural remodeling in the peri-infarct region, leading to improved functional outcomes following a stroke. We tested this hypothesis using epicortical application of PbTx-2 after a photothrombotic stroke in mice. We show that PbTx-2 enhanced the dendritic arborization and synapse density of cortical layer V pyramidal neurons in the peri-infarct cortex. PbTx-2 also produced a robust improvement of motor recovery. These results suggest a novel pharmacologic approach to mimic activity-dependent recovery from stroke
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