• Skovbjerg Boisen posted an update 6 months ago

    To explore the role of prostacyclin (PGI2) and thromboxane A2 (TXA2) in lung hyper-permeability induced by mechanical ventilation (MV) in rabbits.

    Forty-eight healthy Japanese white rabbits were randomly allocated to vehicle treatment group (group V), tranylcypromine (a PGI2 synthase inhibitor) treatment group (group T), dazoxiben (a TXA2 synthase inhibitor) treatment group (group D), vehicle-treated MV group (group VM), tranylcyprominetreated MV group (group TM) and dazoxiben-treated MV group (group DM). The contents of PGI2 and TXA2 in the lung tissues and TNF-α level in BALF and lung tissues were measured by ELISA. The lung wet/dry weight (W/D) ratio, lung permeability index and pulmonary expressions of myosin light chain kinase (MLCK) protein and mRNA were detected to evaluate the pulmonary permeability. The severities of lung injury were assessed by lung histological scores.

    The measured parameters did not differ significantly among the rabbits receiving different treatments without MV. selleck inhibitor In rabbits regulating TNF-α/MLCK signaling pathway, while TXA2 can exacerbate MV-induced lung hyperpermeability in rabbits by up-regulating TNF-α/ MLCK signaling pathway.

    PGI2 plays a protective role against MV-induced lung hyper-permeability and lung injury by downregulating TNF-α/MLCK signaling pathway, while TXA2 can exacerbate MV-induced lung hyperpermeability in rabbits by up-regulating TNF-α/ MLCK signaling pathway.

    To assess the effect and timing of human menopausal gonadotropin (HMG) supplementation in advancedage patients with diminished ovarian reserve (DOR) receiving gonadotropin-releasing hormone antagonist protocol.

    A total of 682 patients with DOR aged over 35 years undergoing IVF-ET treatment were included in this study. All the patients underwent a GnRH antagonist protocol, and controlled ovarian stimulation was initiated on day 2-3 of the menstrual cycle with follicle stimulation hormone (FSH). According to the timing of HMG supplementation, the patients were divided into no supplementation group (

    =371) without HMG supplementation; early supplementation group (

    =139), in which daily HMG supplementation started on the first day till the trigger day; and late supplementation group (

    =172), in which HMG supplementation started when the leading follicle reached 10-14 mm in diameter and lasted until the trigger day. The pregnancy outcomes of the patients were compared among the 3 groups.

    The 3 groups show pregnancy rate or live birth rate of the first frozen-thawed embryo transfer cycle with a freeze-all strategy (

    >0.05).

    HMG supplementation in the middle and late follicular phase can improve the outcomes of controlled ovarian hyperstimulation and increase the clinical pregnancy rate of fresh embryo transfer cycle in advanced-age patients with DOR undergoing GnRH antagonist protocol.

    HMG supplementation in the middle and late follicular phase can improve the outcomes of controlled ovarian hyperstimulation and increase the clinical pregnancy rate of fresh embryo transfer cycle in advanced-age patients with DOR undergoing GnRH antagonist protocol.

    To investigate the injury types of atrial myocytes induced by heat exposure and the effect of amiodarone on heat-induced injuries in atrial myocytes.

    The optimal temperature for heat exposure and optimal concentration of amiodarone were determined by measuring the cell viability exposed to different temperatures and different concentrations of amiodarone. Heat exposure of HL1 atrial myocytes was conducted using a water bath, and the effect of amiodarone on cell viability was assessed with MTS method; cell apoptosis was detected using flow cytometry, and the levels of IL-1β, IL-6, TNF-α, SOD and MDA were detected with enzyme-linked immunosorbent assay (ELISA).

    Compared with the blank control cells, the cells exposed to a temperature of 52 ℃ showed a significantly decreased survival rate and a lowered SOD activity (

    < 0.001) with increased IL-1β and MDA levels (

    < 0.01) and markedly increased apoptosis rate and IL-6 level (

    < 0.001). Compared with the heat exposure group, amiodarone resulted in significantly decreased survival rate of the atrial myocytes (

    < 0.01), obviously decreased SOD activity (

    < 0.05), and increased cell apoptosis rate (

    < 0.05) and IL-1β, IL-6, MDA and TNF-α levels (

    < 0.01 or 0.001).

    Heat exposure induces apoptosis, inflammation and oxidative stress in mouse HL1 atrial myocytes, and amiodarone can enhance the effects of heat exposure to aggravate the cell injuries.

    Heat exposure induces apoptosis, inflammation and oxidative stress in mouse HL1 atrial myocytes, and amiodarone can enhance the effects of heat exposure to aggravate the cell injuries.

    To investigate the mechanism of the antidepressant-like effects of

    decoction (CGD).

    Chaihu Guizhi decoction at the daily dose of 17 g/kg and solvent vehicle were administered by gavage in 12 and 14 male C57BL/6J mice for 7 consecutive days, respectively. Forced swimming test (FST), elevated plus maze (EPM) test, open field test (OFT) and novelty-suppressed feeding test (NSF) were performed to assess the depression- and anxiety-like behaviors and motor ability of the mice. We further used chronic social defeat stress (CSDS) and social interaction test to evaluate the antidepressant-like effects of CGD in comparison with the solvent vehicle. Western blotting and RT-qPCR were performed to detect the expressions of sirt1, p53, acetylated p53, and the neuron plasticity-related genes including synapsin I (Syn1), Rab4B, SNAP25 and tubulin beta4b in the hippocampus of the mice.

    In FST, the immobility time of CGDtreated mice was decreased significantly (

    < 0.05); no significant differences were found in the performances in EPM, NSF and OFT tests between the two groups. In social interaction test, the mouse models of CSDS treated with CGD showed significantly increased time in the interaction zone (

    < 0.05). Compared with those in the vehicle group, the CGD-treated mouse models exhibited significantly increased protein level of SIRT1 and decreased p53 acetylation (

    < 0.05) with up-regulated synapsin I mRNA expression in the hippocampus (

    < 0.05); no significant difference were found in Rab (

    =0.813), SNAP (

    =0.820), or Tubb mRNA expressions (

    =0.864) between the two groups.

    CGD produces antidepressant-like effects in mice possibly through the sirt1-p53 signaling pathway and synaptic plasticity.

    CGD produces antidepressant-like effects in mice possibly through the sirt1-p53 signaling pathway and synaptic plasticity.

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