醒脑静注射液治疗急性缺血性中风的临床与实验研究

目的观察醒脑静注射液治疗急性缺血性中风的临床疗效及其可能作用机理.方法临床研究用随机分组单盲对照观察256例急性缺血性中风;实验研究用埋线法造成大鼠大脑中动脉梗塞模型,观察大鼠大脑中动脉梗塞模型对下丘脑-垂体-肾上腺皮质轴的影响.结果醒脑静注射液能降低急性脑梗塞患者的神经功能缺损积分及MCAO大鼠神经功能缺损积分,降低MCAO大鼠下丘脑CRH、血浆ACTH、CORT水平,改善下丘脑-垂体-肾上腺皮质轴形态学异常.结论醒脑静注射液对急性脑梗塞有较好的治疗作用,其作用机理可能与改善下丘脑-垂体-肾上腺皮质轴功能有关.     

Epidemiology of stillbirths based on different gestational thresholds at a tertiary hospital

INTRODUCTIONThe stillbirth rate (SBR) is an important public health indicator. We studied the distribution of maternal and fetal characteristics and time trends of the SBR at KK Women’s and Children’s Hospital (KKH), Singapore, from 2004 to 2016 based on various definitions of stillbirth.METHODSData was obtained from the Data Warehouse and Stillbirth Reporting System of KKH from 2004 to 2016. SBRs were calculated based on three definitions (fetal deaths at ≥ 20 weeks, 24 weeks or 28 weeks of gestation per 1,000 total births) and were described with maternal and fetal characteristics, and by year.RESULTSFrom 2004 to 2016, the SBR declined by 44.7%, 25.5% and 18.9% based on Definitions I, II and III, respectively. The SBR at KKH in 2016 was 5.2 (Definition I), 4.1 (Definition II) and 3.0 (Definition III) per 1,000 total births. The SBR was significantly higher in women aged ≥ 35 years, nulliparas and female fetuses. The number of live births at 24–27⁺⁶ weeks of gestation was more than four times higher than that of stillbirths (822 vs. 176). There were 104 (12.7%) neonatal deaths during this gestation period, giving a high survival rate of 87.3%.CONCLUSIONThe SBR in KKH is relatively lower than that in other developed countries. There is a need to consider revising our hospital and national definitions of the stillbirth lower boundary from 28 weeks to 24 weeks of gestation. This would allow us to make better comparisons with other developed countries, in line with improvements in healthcare.     

Triptolide induced cell death through apoptosis and autophagy in murine leukemia WEHI‐3 cells in vitro and promoting immune responses in WEHI‐3 generated leukemia mice in vivo

Triptolide, a traditional Chinese medicine, obtained from Tripterygium wilfordii Hook F, has anti‐inflammatory, antiproliferative, and proapoptotic properties. We investigated the potential efficacy of triptolide on murine leukemia by measuring the triptolide‐induced cytotoxicity in murine leukemia WEHI‐3 cells in vitro. Results indicated that triptolide induced cell morphological changes and induced cytotoxic effects through G0/G1 phase arrest, induction of apoptosis. Flow cytometric assays showed that triptolide increased the production of reactive oxygen species, Ca²⁺ release and mitochondrial membrane potential (ΔΨ_m), and activations of caspase‐8, ‐9, and ‐3. Triptolide increased protein levels of Fas, Fas‐L, Bax, cytochrome c, caspase‐9, Endo G, Apaf‐1, PARP, caspase‐3 but reduced levels of AIF, ATF6α, ATF6β, and GRP78 in WEHI‐3 cells. Triptolide stimulated autophagy based on an increase in acidic vacuoles, monodansylcadaverine staining for LC‐3 expression and increased protein levels of ATG 5, ATG 7, and ATG 12. The in vitro data suggest that the cytotoxic effects of triptolide may involve cross‐talk between cross‐interaction of apoptosis and autophagy. Normal BALB/c mice were i.p. injected with WEHI‐3 cells to generate leukemia and were oral treatment with triptolide at 0, 0.02, and 0.2 mg/kg for 3 weeks then animals were weighted and blood, liver, spleen samples were collected. Results indicated that triptolide did not significantly affect the weights of animal body, spleen and liver of leukemia mice, however, triptolide significant increased the cell populations of T cells (CD3), B cells (CD19), monocytes (CD11b), and macrophage (Mac‐3). Furthermore, triptolide increased the phagocytosis of macrophage from peripheral blood mononuclear cells (PBMC) but not effects from peritoneum. Triptolide promoted T and B cell proliferation at 0.02 and 0.2 mg/kg treatment when cells were pretreated with Con A and LPS stimulation, respectively; however, triptolide did not significant affect NK cell activities in vivo. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 550–568, 2017.