HCN4 Gene Variations in Sudden Unexplained Nocturnal Death Syndrome in the Southern Han Chinese Population,

Sudden unexplained nocturnal death syndrome (SUNDS) is widely considered to be related to hereditary fatal arrhythmias. Hyperpolarization‐activated cyclic nucleotide‐gated channel 4 (HCN4) channels are widely distributed in sinus myocytes and play a profound role in generating pacemaker electro‐activity in cardiomyocytes. In the present study, the potential correlation between HCN4 gene variations and the occurrence of SUNDS was investigated. Genomic DNA was extracted from blood samples of both 119 unrelated SUNDS patients and 184 healthy individuals and screened for candidate HCN4 gene variants. One missense heterozygous variant c.1578C>T (Ala195Val) and four synonymous heterozygous variants c.1552C>T, c.2833C>T, c.3823C>T, and c.4189C>A were discovered in the SUNDS cases. The missense variant c.1578C>T (Ala195Val) was absent in 163 recruited controls and 105 persons of the Southern Han Chinese population, had in‐silico prediction indications as damaging, and was reported prevalent in sudden infant death, and is thus likely to be involved in SUNDS.     

Experimental Study on the Postmortem Redistribution of the Substituted Phenethylamine, 25B‐NBOMe

2‐(4‐Bromo‐2,5‐dimethoxyphenyl)‐N‐(2‐methoxybenzyl)ethanamine (25B‐NBOMe) is a substituted phenethylamine, which has become highly prevalent worldwide since 2014. Recently, in an autopsy case involving fatal 25B‐NBOMe intoxication, we found the postmortem increase of 25B‐NBOMe concentration in the cardiac blood approximately 2 days after death. The aim of this study was to investigate the distribution of 25B‐NBOMe and reproduce the postmortem redistribution using a rat model. Sprague‐Dawley rats were killed 30 min after intraperitoneal injection of 25B‐NBOMe (0.5 mg/kg) and left for 0, 3, 6, 9, 15, or 24 h (six rats at each time point). Postmortem 25B‐NBOMe concentrations in the cardiac blood increased by more than 10‐fold at 6‐h postmortem. 25B‐NBOMe accumulated primarily in the lung. Moreover, this postmortem redistribution occurred even in rats that had died 1 week following the 25B‐NBOMe administration. These findings indicate that attention should be paid to sample collection and data interpretation in the toxicological analysis of 25B‐NBOMe.     

行气调神针刺疗法对缺血性卒中后抑郁大鼠左前皮质及海马CREB和PDE4 mRNA表达的影响

目的 观察cAMP反应元件结合蛋白(cAMP response element binding protein,CREB)和磷酸二酯酶4(phosphodiesterase 4,PDE4)在缺血性卒中后抑郁(post stroke depression,PSD)发病中的作用及行气调神针刺疗法对其的影响。方法 将SD大鼠随机分为正常组、模型组、行气调神针刺组、西药组,每组各20只。采用大脑中动脉电凝结合应激和孤养的方法复制PSD模型。针刺组取“人中”、双侧“合谷”和双侧“太冲”,针刺治疗6周,西药组予以盐酸氟西汀灌胃治疗6周。采用RT-PCR检测左前皮质及海马CREB mRNA和PDE4 mRNA的表达水平。结果 最终各组样本量为11。与正常组比较,模型组大鼠左前皮质及海马CREB mRNA表达水平显著下调(P<0.01),PDE4 mRNA表达水平显著上调(P<0.01);与模型组比较,西药组及针刺组大鼠左前皮质及海马CREB mRNA表达水平显著上调(P<0.01),PDE4 mRNA表达水平显著下调(P<0.01)。结论 行气调神针刺疗法治疗PSD的机制与上调脑组织CREB mRNA的表达和下调PDE4 mRNA的表达有关。     

灸预处理对乙醇诱导胃黏膜损伤大鼠TLR4、MyD88、NF-κB p65蛋白的影响

目的 观察灸预处理对乙醇诱导大鼠胃黏膜损伤的影响,探讨灸法对胃黏膜损伤“未病先防”的作用机制。方法 将大鼠随机分为正常组、模型组和灸预处理组,每组10只,先对灸预处理组大鼠进行艾灸“足三里”“中脘”,再对模型组和灸预处理组大鼠进行乙醇灌胃制备胃黏膜损伤模型。比较各组大鼠胃黏膜溃疡指数(ulcer index, UI)和病理学变化,ELISA法检测大鼠血清肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)和白细胞介素-6 (interleukin-6,IL-6)水平,免疫组织化学法和Western blot法检测胃黏膜组织Toll样受体4(Toll-like receptor 4,TLR4)、髓样分化因子88(myeloid differentiation factor 88,MyD88)、核转录因子-κB(nuclear factor kappa B,NF-κB)p65蛋白表达水平。结果 模型组大鼠UI显著高于正常组,灸预处理组UI显著低于模型组(P<0.05),模型组大鼠胃黏膜上皮结构破坏严重,有出血灶和炎症细胞浸润;灸预处理组大鼠胃黏膜病理损伤低于...     

化瘀温经利湿法治疗慢性盆腔炎20例临床观察

目的观察化瘀温经利湿中药对慢性盆腔炎患者的疗效及对外周血CD4^＋CD25^＋CD127^lo调节性T细胞（regulative Tcells，Treg）的影响。方法将40例慢性盆腔炎患者按随机数字表法分为化瘀温经利湿中药治疗组20例和西药对照组20例，两组均以1个月为1个疗程，均治疗1个疗程，观察临床疗效及对症状出现率的影响；采用流式细胞术检测患者治疗前后外周血CD4^＋CD25^＋CD127^loTreg的数量及其在CD4^＋T淋巴细胞中所占的比例；并检测治疗前后血沉（erythrocyte sedimentation rate，ESR）和C反应蛋白（C—reactive peptide，CRP）水平。结果与对照组比较，治疗组总有效率和CD4^＋CD25^＋CD127^loTreg表达水平显著升高，ESR、CRP及症状出现率显著降低（P〈0．05）。结论化瘀温经利湿中药治疗慢性盆腔炎的作用机制，可能与其上调CD4^＋CD25^＋CD127^loTreg表达水平，促进免疫调节，降低炎症反应有关。     

Lipidic compounds found in soils surrounding human decomposing bodies and its use in forensic investigations – A narrative review

Following decomposition of a human body, a variety of decomposition products, such as lipids, are released into the surrounding environment, e.g. soils. The long-lasting preservation in soils and their high diagnostic potential have been neglected in forensic research. Furthermore, little is known about the preservation, chemical transformation, or degradation of those human derived lipids in soils. To date, several studies identified various lipids such as long-chain free fatty acids and steroids in soils that contained decomposition fluids. Those lipids are preserved in soils over time and could serve as markers of human decomposition in forensic investigations, e.g. for estimating the post-mortem interval or identifying the burial location of a human body. Therefore, this review focuses on the current literature regarding fatty acid and steroid that have been detected in soils and associated with human body decomposition. After a short introduction about human decomposition processes, this review summarises fatty acid and steroid analysis applied in current case studies and studies related to taphonomic research. This review provides an overview of the available studies that have used fatty acids and steroids as identifiers of human decomposition fluid in soils in a forensic context and discusses the potential for developing this innovative field of research with direct application in a forensic context.