RT-nPCR Assays for Amplification and Sequencing of VP1 Genes in Human Enterovirus A-D from Clinical Specimens

ObjectiveTo develop RT-nPCR assays for amplifying partial and complete VP1 genes of human enteroviruses (HEVs) from clinical samples and to contribute to etiological surveillance of HEV-related diseases.MethodsA panel of RT-nPCR assays, consisting of published combined primer pairs for VP1 genes of HEV A–C and in-house designed primers for HEV-D, was established in this study. The sensitivity of each RT-nPCR assay was evaluated with serially diluted virus stocks of five serotypes expressed as CCID₅₀ per μL and copies per μL, and the newly established methods were tested in clinical specimens collected in recent years.ResultsThe sensitivity of RT-nPCR assays for amplifying partial VP1 gene of HEVs was 0.1 CCID₅₀ per μL and 10 virus copies per μL, and for the complete VP1 gene was 1 CCID₅₀ per μL and 100 virus copies per μL, using serially-diluted virus stocks of five serotypes. As a proof-of-concept, 25 serotypes were identified and complete VP1 sequences of 23 serotypes were obtained by this system among 858 clinical specimens positive for HEVs during the past eight surveillance seasons.ConclusionThis RT-nPCR system is capable of amplifying the partial and complete VP1 gene of HEV A–D, providing rapid, sensitive, and reliable options for molecular typing and molecular epidemiology of HEVs in clinical specimens.     

"肌少-骨质疏松症"的共同发病机制

"肌少-骨质疏松症"(sarco-osteopenia)的提出是基于两者共同的病理生理学基础,其中涉及八类主要影响因素.简要概括为机械因素作用于骨细胞构成的机械支架和肌管;肌肉-骨骼系统相互影响彼此化学因子的释放;甲基转移酶样蛋白21C(METTL21C)和肌肉生长抑制素(myostatin,MSTN,简称肌抑素)以及硬骨抑素(sclerostin,SOST)作为共同的遗传因素调控肌肉-骨骼系统;肌肉和骨骼在旁分泌和内分泌水平上的串扰、脂肪浸润因素导致肌力的下降和骨折发生率增加;炎性反应、糖尿病和糖皮质激素过量影响肌肉的丢失以及骨丢失;营养缺乏加速骨丢失和肌肉蛋白质合成减少;个体运动量的减少和神经-肌肉功能减弱间接影响肌肉和骨骼的合成代谢.深入研究"肌少-骨质疏松症"共同的致病机制,以推动生物检测特异性指标的确定、临床疾病的评估和诊断以及有效治疗药物和设备开发工作,最终目标是有效地治疗和预防"肌少-骨质疏松症".本文对"肌少-骨质疏松症"共同病理生理学机制研究现状与进展进行系统综述.     

两种局灶性脑缺血大鼠模型的影像及超微结构比较

目的比较大鼠大脑中动脉闭塞（MCAO）模型和光化学诱导局灶性脑缺血模型的磁共振影像及超微结构的差异。方法分别建立大鼠MCAO和光化学诱导局灶性脑缺血模型,利用小动物磁共振成像系统观察脑缺血区域及周边血管分布,结合透射电镜技术比较两种模型缺血区超微结构的变化。结果MCAO模型缺血区范围较大且不稳定,细胞结构破坏严重,血管变形显著,新生血管较少。光化学诱导模型缺血区范围较小且稳定,细胞结构损伤区域较小,新生血管较多。结论两种模型方法各有优缺点,均为脑缺血后血管损伤保护及溶栓治疗的研究提供实用性工具,可根据科研需求选取适合的造模方法     

论中医“症状性病名”的合理性

症状性病名是病名演变过程中的必然阶段,也是以症状为纲目编撰医籍的需要,虽然症状性病名因症病概念混淆饱受诟病,但基于症状性病名仍有其存在的合理性和必要性,当前临床的关键问题是如何在继续继承及发展症状性病名同时,综合应用中医诊断基本要素、西医病名诊断与客观检查指标,弥补症状性病名应用短板。     

论中医“症”描述的准确性与规范化

“症”是中医诊断体系中最具体的要素,症状信息规范化其关键在于明确“症”的认识和理解,文章系统分析中医“症”的内涵,分析目前“症”规范化中存在的主要问题,如缺乏统一标准、各家之言迥异、中西医“症”的混杂等,这些一定程度上阻碍了中医临床与科研,不利于中医学术的交流及中医诊断学的现代化研究。因此提出从明确症名定义、统一规范症名、拆分复合症名、区分症状轻重、避免诊断性症名、纳入客观指征等几个方面对中医“症”的描述进行规范,通过建立系统标准体系,进行“症”的量化分级,规范信息采集过程,借助微观指标辨证等开展中医“症”的规范化研究。     

腹壁下动脉穿支皮瓣在全舌癌缺损修复中的应用效果评价

目的: 评价游离腹壁下动脉穿支皮瓣（deep inferior epigastric perforator,DIEP）用于舌癌术后全舌缺损修复的效果。方法: 2018年1月—2018年7月应用游离DIEP修复13例舌癌患者,手术缺损部位均为全舌或近全舌缺损。术中将腹壁下动脉与甲状腺上动脉或面动脉吻合,伴行静脉与颈外静脉或颈内静脉属支吻合。结果: l3例DIEP皮瓣均修复成功,皮瓣外观满意。术后随访舌形态良好,功能满意。供区直接闭合,其中1例患者皮瓣供区出现感染,经换药后愈合。所有腹部伤口均为线性瘢痕,腹直肌功能未受明显影响,未发现腹壁疝和腹壁隆起等手术并发症。结论: 腹壁下动脉穿支皮瓣组织量丰富、血供可靠、质地柔软,再造舌外形及功能良好,且供区保留了腹直肌和前鞘,损伤小,将供区并发症降到最低限度,是舌癌术后全舌缺损修复新的可靠技术。     

从“木郁克土”角度探讨围绝经期综合征肝郁证大鼠胃肠动力的改变

目的从“木郁克土”角度探讨围绝经期综合征(PPS)肝郁证大鼠胃肠动力的改变。方法选择3月龄SPF级SD雌性大鼠,分为假手术组、PPS组、PPS肝郁组和柴胡疏肝散组,采用去势法结合慢性不可预知性温和应激建立PPS肝郁证大鼠模型,用柴疏疏肝散进行干预,观察大鼠体重增长率、饲料消耗量、胃残留率及肠推进率变化。结果在体重增长率方面,PPS组显著高于假手术组(P<0.01);PPS肝郁组显著低PPS组(P<0.01);柴胡疏肝散组显著高于PPS肝郁组(P<0.01)。在饲料消耗方面,PPS组高于假手术组,PPS肝郁组低于PPS组;柴胡疏肝散组高于PPS肝郁组。在胃残留率方面,PPS肝郁组显著高于假手术组和PPS组(P<0.01);柴胡疏肝散组显著低于PPS肝郁组(P<0.01)。在肠推进率方面,PPS肝郁组显著低于假手术组和PPS组(P<0.01);柴胡疏肝散组显著高于PPS肝郁组(P<0.01)。结论PPS肝郁大鼠的体重和饲料消耗量发生了改变,体重的增长与饲料的消耗量存在一定的联系,且与大鼠胃肠动力有关。从“木郁克土”角度提示其机制可能是肝郁状态影响到了脾胃功能的正常运行。     

Research progress in rehabilitation treatment of stroke patients A bibliometric analysis

BACKGROUND: Stroke presents as a transient or chronic brain dysfunction and is associated with high morbidity and high mortality. The doctors and scientists would like to argue how to enhance the validity of the rehabilitation treatment and how to further improve the level of treatment on stroke. OBJECTIVE: The aim of this study was to quantitatively analyze the current worldwide progress in research on stroke rehabilitation treatment based on Web of Science database and ClinicalTrial.gov in the past 10 years. METHODS: We conducted a quantitative analysis of clinical trial articles regarding stroke rehabilitation published in English from 2003 to 2013 and indexed in the National Institutes of Health Clinical Trials registry and Web of Science databases. Data were downloaded on March 15, 2013. RESULTS: (1) From 2003 to 2013, 2 654 clinical trials investigating stroke were indexed in ClinicalTrials.gov. There were only 58 clinical trials registered in 2003, and there was a marked increase from 2005. A total of 605 clinical trials on the rehabilitation of stroke were conducted in the past 10 years. (2) The analysis showed that most of the trials in the field were registered by North American institutions. With respect to the Asian countries, China and Taiwan area of China also published a reasonable proportion of the trials, but comparatively speaking, the number of trials is really rare. Most of the interventions were drugs, followed by the devices, and behavioral interventions were ranked third. (3) In the past 10 years, there were 4 052 studies on stroke indexed by Web of Science database. CONCLUSION: From perspective of research progress, we found that the number of clinical trials and papers on stroke rehabilitation has increased significantly in the past 10 years, between them a remarkable positive correlation exists.     

芍药苷干预阿尔茨海默病作用机制研究进展

阿尔茨海默病(Alzheimer’sdisease,AD)是造成老龄人口认知能力减退的主要疾病之一。芍药苷是毛茛科(Ranunculaceae)植物芍药Paeonia lactiflora或牡丹Paeonia suffruticosa根皮中提取出的水溶性单萜苷,具有改善认知能力、镇静、抗炎、镇痛、解痉等作用,可以有效调节AD动物及细胞模型异常磷酸化的Tau蛋白和过度沉积的β-淀粉样蛋白(Aβ)水平,恢复乙酰胆碱、神经生长因子、Ca2+、α7烟碱样乙酰胆碱受体和腺苷受体等神经递质及神经受体的平衡状态,降低组织炎症反应和氧化应激反应并减少细胞凋亡的发生。对近10年来国内外有关芍药苷干预AD的研究进展进行综述,为探索中药防治AD研究提供理论依据。     

金铁锁根中2个新的麦芽酚苷类化合物

目的研究金铁锁Psammosilene tunicoides根的化学成分。方法经硅胶、Sephadex LH-20凝胶、ODS反相硅胶等柱色谱方法进行分离,并运用NMR、HR-ESI-MS等波谱学方法进行化合物的结构鉴定。结果从金铁锁根80%乙醇水提取物中分离得到2个麦芽酚苷类化合物,分别鉴定为麦芽酚-3-O-[6-O-(4-O-α-L-吡喃鼠李糖基)-Z-p-香豆酰基]-β-D-吡喃葡萄糖苷(1)和麦芽酚-3-O-[6-O-(4-O-α-L-吡喃鼠李糖基)-E-p-香豆酰基]-β-D-吡喃葡萄糖苷(2)。结论化合物1和2为新的麦芽酚苷类化合物,分别命名为金铁锁酚苷A和B。