葛根素联合复方樟柳碱注射液对眼底病患者的治疗效果及对血液流变学指标的影响

目的研究葛根素联合复方樟柳碱注射液对眼底病患者的治疗效果及对血液流变学指标的影响。方法选择2013年4月至2014年4月在绵阳市第三人民医院眼科进行眼底病治疗的患者100例,并按入院顺序抽签随机分为观察组和对照组,各50例。对照组进行葛根素常规治疗(葛根素注射液0.4 g加入生理盐水250 m L中静脉滴注,每日1次,1个疗程14 d,1个疗程后停药3 d,再进行下一疗程),观察组在此基础上联合复方樟柳碱注射液进行治疗(采用复方樟柳碱2 m L在患者颞浅动脉旁行皮下注射,每日1次,1个疗程14 d,完成1个疗程后停药3 d,再换肾俞穴进行注射,1个疗程后停药3 d,再进行第一个疗程的用药)。3个疗程后,比较两组患者治疗前后血液流变学的变化、术后复发率和不良反应情况及患者的治疗效果。结果治疗后,观察组全血黏度为(4.82±0.41)m Pa·s明显低于对照组的(5.56±0.39)m Pa·s,红细胞聚集指数(3.80±0.41)明显低于对照组(4.77±0.55),纤维蛋白原(4.20±0.24)g/L明显低于对照组(5.25±0.43)g/L,差异均有统计学意义(t=9.247,9.998,15.077,P<0.01);观察组患者治疗后复发率为2.0%(1/50),不良反应的总发生率为4.0%(2/50),分别低于对照组14.0%(7/50)和18.0%(9/50)(P<0.01);观察组患者的总有效率为98.0%(49/50),显著高于对照组的82.0%(41/50)(P<0.05)。结论葛根素和复方樟柳碱注射液联合治疗眼底病患者,可改善患者血液流变学,并提高临床治疗效果。     

甲状旁腺激素对大鼠牵张成骨过程中O NC、OPN、C-FOS、COL1、VEGF、RUNX2、ALP基因表达的影响

目的：探讨甲状旁腺激素（PTH）对大鼠牵张成骨（DO）过程中ONC、OPN、C-FOS、COL1、VEGF、RUNX2、ALP基因表达的影响。方法30只雄性大鼠制备大鼠下颌骨DO模型。随机分5组，每组6只。第1组（只有牵张无PTH），术后8周取材，应用HE染色及微CT检测，以确定成骨情况。第2组（有牵张无PTH），第3组（有牵张有PTH），第4组（无牵张有PTH），第5组（对照组：无牵张无PTH）。2、3、4组及对照组术后1周取材，RT-PCR测定ONC、OPN、C-FOS、COL1、VEGF、RUNX2、ALP基因的表达。结果第1组，新骨形成，骨质充满牵张区，骨质连续，大鼠建模成功。RT-PCR检测结果显示，2、3、4组与对照组比较，OPN、COL1、RUNX2、ALP基因表达有明显提高（P＜0．05），其中第3组最为明显。ONC、C-FOS、VEGF基因2、3、4组与对照组比较差异无统计学意义（P＞0．05）。结论 PTH在 DO 过程中，间歇性给以 PTH的作用只有在牵张期发挥作用，其对 OPN、COL1、RUNX2、ALP基因表达能够获得理想的协同作用。     

高乳酸血症-卒中样发作综合征型线粒体脑肌病一家系两代四例报告

线粒体脑肌病属于罕见性母系遗传病，本文回顾性分析了1家4例高乳酸血症-卒中样发作综合征（MELAS）型线粒体脑肌病患者，其主要表现为卒中样发作、头痛、癫痫、高乳酸血症、肌肉不耐受疲劳、高级智能下降、听力下降和身材矮小等，结合特征性影像学变化、基因检测及肌肉活检明确诊断，并结合文献对只有女儿能将其线粒体DNA（mt-DNA）传递给下一代的母系遗传MELAS型线粒体脑肌病临床特点进行了总结分析，旨在帮助临床认识此病，进一步提高MELAS型线粒体脑肌病的临床诊断率。     

抑郁症康复技能训练程式在基层医院推广应用的价值研究

背景　抑郁症的康复技能训练是一种很好的辅助治疗方法，本课题通过引进成熟的抑郁症康复技术，使基层医务人员熟练掌握，为辖区内广大抑郁症患者开展康复训练，以期提高抑郁症患者的疗效，降低自杀风险。目的　探讨抑郁症康复技能训练程式在基层医院推广应用的价值。方法　选取门头沟区龙泉医院2018年1-9月门诊就诊的65例抑郁症患者为研究对象。入选患者全部接受康复训练，分别于训练前和训练结束3个月后采用汉密尔顿抑郁量表（HAMD）、社会功能缺陷筛选量表（SDSS）、服药依从性、自杀风险评估量表（nurses' global assessment of suicide risk，NGASR）和自杀风险问卷对患者进行评估。结果　共61例患者完成研究，与训练前比较，训练结束3个月后患者HAMD、SDSS评分明显降低，服药依从性除自行停药外均明显提高，自杀风险明显降低，差异有统计学意义（P<0.05）。结论　抑郁症康复训练程式能有效提高患者服药依从性，改善抑郁症状，减少自杀观念，在基层医院有推广价值。     

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.     

华细辛和北细辛HPLC特征图谱识别与抗炎靶点及抗炎成分分析

建立华细辛和北细辛HPLC特征图谱并结合聚类分析研究2种来源细辛的识别方法;应用网络药理学方法预测细辛潜在抗炎靶点并寻找潜在抗炎成分。对89批细辛药材(12批华细辛和77批北细辛)的数据进行分析确定了11个特征峰,用对照品、紫外光谱和LC-MS指认了11个特征成分。特征峰面积聚类分析显示华细辛和北细辛被分为2类,且利用特征峰面积比值可实现两者区分,当特征峰9(细辛素)/参照峰S(卡枯醇)峰面积比值大于5时为华细辛,小于2时为北细辛。对119种细辛成分进行网络药理学分析的结果表明细辛抗炎作用可能与COX-2,COX-1,iNOS,MAPK14,LAT4H,NR3C1,PPARG和TNF等8个靶点相关,其中COX-2最为关键,与5种特征成分细辛脂素、芝麻脂素、细辛素、甲基丁香酚和黄樟醚均存在相互作用。此外,细辛脂素、芝麻脂素与iNOS,MAPK14也存在相互作用关系,黄樟醚和细辛素可作用于iNOS,COX-1,LAT4H,甲基丁香酚可作用于COX-1,LAT4H。细辛脂素与芝麻脂素均可作用在COX-2,iNOS和MAPK143个靶点上,提示它们是细辛发挥抗炎作用的活性成分;COX-2分子对接结果和COX-2活性实验结果验证了细辛脂素、芝麻脂素可抑制COX-2活性,为细辛抗炎作用活性成分。基于HPLC特征图谱的华细辛和北细辛识别方法简便易行;预测到的细辛抗炎靶点和抗炎成分为完善细辛质量评价体系奠定了基础。     

无偿献血宣传招募工作的实践和思考

该文总结该市2017年1月-2018年12月之间,在无偿献血宣传招募方面工作内容。结果显示2018年较2017年献血总量有所提升,其中团体献血所占比例逐渐上升,街头献血所占比例逐渐下降。通过大力宣传无偿献血工作,扩大无偿献血团体招募工作,完善并深化无偿献血各项制度,使得普通群众的无偿献血认知度不断提高。     

人体感染西里伯瑞列绦虫1例报告

为深入宣传我国血吸虫病防治工作取得的成就，培养和锻炼我国血防队伍的新生力量，激励更多的有志青年投身血防事业，为我国血防事业培养人才，由卫生部血吸虫病专家咨询委员会、中华预防医学会主办的全国血吸虫病防治研究青年学术交流会将于2006年第4季度召开，届时将邀请国际及我国血吸虫病科研和防治领域著名专家和学者作专题报告。现将有关事事宜通知如下。