互动式歌唱表演对轻中度阿尔茨海默病患者抑郁、精神行为和运动训练参与率的影响

目的 观察互动式歌唱表演对轻中度阿尔茨海默病（AD）患者抑郁、精神行为症状及运动训练参与率的影响。方法 选取符合入组条件≥60周岁AD患者63例，随机分为研究组（31例）和对照组（32例）。所有受试患者常规药物治疗及常规运动训练，对照组接受被动性音乐治疗，研究组接受以互动歌唱为主的主动性音乐治疗，1次/d，每次1小时，每周训练5天，持续干预6个月。于治疗前、治疗1个月后、治疗3个月后、治疗6个月后分别采用康奈尔痴呆抑郁量表（CSDD）评分、阿尔茨海默病病理行为（BEHAVE AD）评分、参与率进行评估。结果 治疗1个月、3个月后，研究组CSDD评分较治疗前均降低（P<0.05）；治疗6个月后，研究组患者CSDD评分较治疗前、治疗1个月、3个月后均显著降低（P<0.05），且与对照组比较差异有统计学意义（P<0.05）。治疗1个月、3个月后，研究组BEHAVE AD评分较治疗前均降低（P<0.05）；治疗6个月后，研究组患者BEHAVE AD评分较治疗前、治疗1个月、3个月后均显著降低（P<0.05），且与对照组比较差异有统计学意义（P<0.05）。治疗6个月后，两组运动训练参与率组间比较差异有统计学意义（P<0.05）。结论 互动式歌唱表演可能对改善轻中度AD患者的抑郁和精神行为症状有着积极的疗效，同时对提高受试者运动训练的参与率可能有着更积极的疗效。     

葫芦素B固体分散体的制备

目的制备葫芦素B固体分散体。方法溶剂法制备固体分散体后,以溶出度为评价指标筛选药物-载体(PVP K30)比例。扫描电子显微镜(SEM)、傅里叶变换红外光谱(FTIR)、差示扫描量热(DSC)、X射线衍射(XRD)进行表征。结果药载比为1∶11时,60 min内溶出度为62.01%。葫芦素B可能以无定形状态分散于载体中。结论该方法简便可行,葫芦素B制成固体分散体后体外溶出度明显提高。     

H型高血压患者舌面诊图像颜色特征参数分析＊

目的 分析H型高血压患者的舌面诊图像颜色参数特征，探讨H型高血压患者的舌诊、面诊变化规律。方法 运用上海中医药大学自行研制的Smart TCM-1型中医舌面一体仪，采集高血压患者舌面诊图像，提取特征参数，分析健康对照组、H型高血压组与非H型高血压组患者舌面颜色参数特征。结果 ①在舌色各项参数中，H型高血压组舌尖部R值、B值、V值均显著小于健康对照组（P < 0.01）；非H型高血压组舌尖部B值显著小于健康对照组（P < 0.01），S值较健康对照组显著增大（P < 0.05）；H型高血压组舌尖部R、V值均明显小于非H型高血压组（P < 0.05）。在舌苔各项参数中，H型高血压组舌中H值、V值均明显小于健康对照组（P < 0.05）；非H型高血压组舌中V值、舌右V值均显著小于健康对照组（P < 0.01）；H型高血压组舌中H值明显小于非H型高血压组（P < 0.05），右侧舌苔S值明显大于非H型高血压组（P < 0.05）。②H型高血压组面色参数鼻G值、下颌G值、口唇R值、口唇V值均明显小于健康对照组（P < 0.05）；非H型高血压组前额H值、目眶H值、脸颊H值、鼻H值、下颌H值、整体H值均明显大于健康对照组（P < 0.05）；H型高血压组前额H值、目眶G值、目眶H值、脸颊H值、鼻G值、鼻H值、下颌R值、下颌G值、下颌H值、下颌V值、口唇R值、口唇G值、口唇V值、整体R值、整体G值、整体H值、整体V值均明显小于非H型高血压组（P < 0.05）。结论 H型高血压患者苔色偏黄，以舌中部为主，且舌右侧黄苔积聚较明显；H型高血压患者面色为黄中带红，口唇、下颌部更为晦暗。H型高血压患者的舌、面诊特征参数的变化，与高血压病阳亢湿盛病机相符。     

磁锚定技术辅助腹腔镜阑尾切除术的实验研究

目的:验证自行设计加工的磁锚定装置在减戳孔腹腔镜阑尾切除术中应用的可行性。方法:设计加工适用于辅助减戳孔腹腔镜阑尾切除术的磁锚定装置,该装置包括内置抓钳和锚定磁体2个部分。以6只健康雄性Beagle犬为模型,用磁锚定装置代替传统腹腔镜阑尾切除术中的副操作孔抓钳,经主操作孔置入磁锚定内置抓钳并钳夹于阑尾尖部,体外放置锚定磁体,锚定磁体与内置抓钳的靶磁体相吸,移动锚定磁体即可改变内置抓钳的牵拉方向,从而有效牵拉暴露手术术野,完成减戳孔腹腔镜阑尾切除手术。记录手术操作时间、术中出血量,评价利用磁锚定装置进行阑尾切除时操作的安全性和可行性。结果:6只Beagle犬均顺利完成磁锚定技术辅助减戳孔腹腔镜阑尾切除,手术时间27~38 min,出血量均小于10 ml,术后实验犬状态良好,未出现并发症。结论:磁锚定装置用于减戳孔腹腔镜阑尾切除手术操作简单、安全可行,在相关设计进一步优化基础上,可尝试或试验性用于临床。     

INAUGURAL ARTICLE by a Recently Elected Academy Member:Functional redundancy of type I and type II receptors in the regulation of skeletal muscle growth by myostatin and activin A

Myostatin (MSTN) is a transforming growth factor-β (TGF-β) family member that normally acts to limit muscle growth. The function of MSTN is partially redundant with that of another TGF-β family member, activin A. MSTN and activin A are capable of signaling through a complex of type II and type I receptors. Here, we investigated the roles of two type II receptors (ACVR2 and ACVR2B) and two type I receptors (ALK4 and ALK5) in the regulation of muscle mass by these ligands by genetically targeting these receptors either alone or in combination specifically in myofibers in mice. We show that targeting signaling in myofibers is sufficient to cause significant increases in muscle mass, showing that myofibers are the direct target for signaling by these ligands in the regulation of muscle growth. Moreover, we show that there is functional redundancy between the two type II receptors as well as between the two type I receptors and that all four type II/type I receptor combinations are utilized in vivo. Targeting signaling specifically in myofibers also led to reductions in overall body fat content and improved glucose metabolism in mice fed either regular chow or a high-fat diet, demonstrating that these metabolic effects are the result of enhanced muscling. We observed no effect, however, on either bone density or muscle regeneration in mice in which signaling was targeted in myofibers. The latter finding implies that MSTN likely signals to other cells, such as satellite cells, in addition to myofibers to regulate muscle homeostasis.

Myostatin (MSTN) is a secreted signaling molecule that normally acts to limit skeletal muscle growth (for review, see ref. 1). Mice lacking MSTN exhibit dramatic increases in muscle mass throughout the body, with individual muscles growing to about twice the normal size (2). MSTN appears to play two distinct roles in regulating muscle size, one to regulate the number of muscle fibers that are formed during development and a second to regulate the growth of those fibers postnatally. The sequence of MSTN has been highly conserved through evolution, with the mature MSTN peptide being identical in species as divergent as humans and turkeys (3). The function of MSTN has also been conserved, and targeted or naturally occurring mutations in MSTN have been shown to cause increased muscling in numerous species, including cattle (3–5), sheep (6), dogs (7), rabbits (8), rats (9), swine (10), goats (11), and humans (12). Numerous pharmaceutical and biotechnology companies have developed biologic agents capable of blocking MSTN activity, and these have been tested in clinical trials for a wide range of indications, including Duchenne and facioscapulohumeral muscular dystrophy, inclusion body myositis, muscle atrophy following falls and hip fracture surgery, age-related sarcopenia, Charcot–Marie–Tooth disease, and cachexia due to chronic obstructive pulmonary disease, end-stage kidney disease, and cancer.The finding that certain inhibitors of MSTN signaling can increase muscle mass even in Mstn^−/− mice revealed that the function of MSTN as a negative regulator of muscle mass is partially redundant with at least one other TGF-β family member (13, 14), and subsequent studies have identified activin A as one of these cooperating ligands (15, 16). MSTN and activin A share many key regulatory and signaling components. For example, the activities of both MSTN and activin A can be modulated extracellularly by naturally occurring inhibitory binding proteins, including follistatin (17, 18) and the follistatin-related protein, FSTL-3 or FLRG (19, 20). Moreover, MSTN and activin A also appear to share receptor components. Based on in vitro studies, MSTN is capable of binding initially to the activin type II receptors, ACVR2 and ACVR2B (also called ActRIIA and ActRIIB) (18) followed by engagement of the type I receptors, ALK4 and ALK5 (21). In previous studies, we presented genetic evidence supporting a role for both ACVR2 and ACVR2B in mediating MSTN signaling and regulating muscle mass in vivo. Specifically, we showed that mice expressing a truncated, dominant-negative form of ACVR2B in skeletal muscle (18) or carrying deletion mutations in Acvr2 and/or Acvr2b (13) have significantly increased muscle mass. One limitation of the latter study, however, was that we could not examine the consequence of complete loss of both receptors using the deletion alleles, as double homozygous mutants die early during embryogenesis (22). Moreover, the roles that the two type I receptors, ALK4 and ALK5, play in regulating MSTN and activin A signaling in muscle in vivo have not yet been documented using genetic approaches. Here, we present the results of studies in which we used floxed alleles for each of the type II and type I receptor genes in order to target these receptors alone and in combination in muscle fibers. We show that these receptors are functionally redundant and that signaling through each of these receptors contributes to the overall control of muscle mass.     

六西格玛在肿瘤标志物质量目标选择上的应用

目的应用6σ理论对肿瘤标志物项目的分析性能进行评价，并初步确定各项目的质量目标。 方法收集本实验室2018年1至12月室内质控数据和国家卫生健康委临床检验中心室间质量评价结果，以生物学变异导出的质量规范和国家室间质量评价标准作为允许总误差(TEa)计算6项肿瘤标志物的σ水平，并依据质量目标选择流程图和肿瘤标志物分析性能验证图评价肿瘤标志物的分析性能，进而为肿瘤标志物选择合适的质量目标。 结果应用不同层级的生物学变异导出的质量规范和国家室间质量评价标准，肿瘤标志物项目的σ水平存在显著差异；依据质量目标选择流程图：选择生物学变异导出的"适当的"质量规范作为CA125项目的质量目标，选择生物学变异导出的"最低的"质量规范作为t-PSA、CEA、AFP、CA199和CA153项目的质量目标。 结论6σ能够客观评价肿瘤标志物的分析性能，并为实验室质量目标的选择提供重要的参考价值。     

对《脉经》脏腑讨论的初步认识

历代医家一直重视脏腑相关问题,本文从中医发展之初对脏腑问题的两种视角(联系视角与解剖视角)开始思考,基于《脉经》前后的经典文献梳理《脉经》文本,得出《脉经》脏腑讨论的初步认识,即王叔和讨论了传统藏象视角认识下的脏腑生理、病理、诊断与经脉腧穴的联系,而各种古代文献的重组、编排、归纳则提示藏象理论的系统构建在此时发生,并且已经纳入经脉的相关内容;《脉经》卷六集中体现了王叔和对“脏腑-经脉一体化”的理论构建和临床观察,《脉经》对于脏腑病候进行了仔细梳理,并注重病候、诊脉、脏腑与腧穴的联系。