微创治疗方法在输尿管上段结石中应用进展

输尿管上段结石为临床中常见泌尿系结石类型之一,如不能及时诊治,可引起重度积水、泌尿系感染,甚至脓毒血症,对患者肾功能、健康造成严重影响。随着微创治疗技术在泌尿系结石中应用,微创治疗方法能降低对患者造成治疗性创伤,降低相关并发症发生率,促进患者康复,了解临床中微创治疗输尿管上段结石方法,对临床中合理治疗输尿管上段结石有重要价值。     

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。     

阿戈美拉汀联合乙哌立松治疗青年慢性紧张性头痛的疗效分析

目的 探讨阿戈美拉汀联合乙哌立松治疗青年慢性紧张性头痛(Chronictention-typeheadache,CTTH)的疗效及安全性.方法 80例青年慢性紧张性头痛患者依据是否倒班随机分为对照组和治疗组,对照组口服乙哌立松治疗,治疗组在对照组基础上联合阿戈美拉汀治疗,评估2组患者治疗前匹兹堡睡眠量表评分(PSQI)评估治疗6周后两组的头痛疗效以及不良反应.结果 倒班人员的入组前PSQI的总评分、睡眠质量、入睡时间、催眠药物及睡眠障碍因子分高于非倒班人员;治疗组的疗效优于对照组,有统计学意义(P＜0.05);治疗组内,倒班患者疗效优于非倒班患者(P＜0.05).两组不良反应无明显差异.结论 阿戈美拉汀联合乙哌立松治疗慢性紧张性头痛的的疗效确切,安全性高.     

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。     

超脉冲CO2点阵激光联合PRP治疗面部痤疮凹陷性瘢痕疗效分析

目的:探究超脉冲CO2点阵激光联合富血小板血浆(PRP)治疗面部痤疮凹陷性瘢痕的疗效。方法:72例面部痤疮凹陷性瘢痕患者,随机分为观察组(36例)和对照组(36例)。对照组采用超脉冲CO2点阵激光治疗,观察组采用超脉冲CO2点阵激光联合PRP治疗。比较两组患者的灰度差异、时间指标、瘢痕程度、疼痛、不良反应及视觉评估。结果:观察组的并发症发生率为11.11%,低于对照组的36.11%,差异具有统计学意义(P<0.05)。治疗后,两组患者的灰度差异率均减小,且观察组患者的灰度差异率显著低于对照组,差异具有统计学意义(P<0.05)。治疗后,观察组的炎性渗出时间、红肿时间、愈合时间、停工时间及瘢痕程度评分均低于对照组,差异均具有统计学意义(P<0.05);但疼痛度评分组间比较,差异无统计学意义(P>0.05)。结论:超脉冲CO2点阵激光联合PRP治疗面部痤疮凹陷性瘢痕效果较好,可有效降低瘢痕程度,减少治疗时间及并发症的发生,帮助患者迅速回归正常工作与生活,值得临床推广使用。     

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.     

缺血修饰性白蛋白在急性缺血性胸痛中的诊断价值

目的 评价缺血修饰性白蛋白（ischemia modified albumin，IMA）对急性缺血性胸痛（ICP）的早期诊断价值。方法 时206例发病〈12h、表现为急性胸痛的患者立即行12导联心电图（ECG）检查，并抽血进行IMA、肌钙蛋白I（cTnI）、肌酸激酶同工酶MB（CK-MB）测定。将ECG、IMA、cTnI、CK-MB的结果单独或结合与最终诊断为非缺血性胸痛（NICP）及ICP的相互关系进行比较。结果 最后诊断为ICP98例，NICP108例，ICP发病〈3h和3-6h组IMA水平明显升高，与NICP组比较差异有统计学意义（P〈0．001）；ICP发病〉6h组IMA水平与NICP组比较差异无统计学意义（P〉0．05）。IMA诊断发病〈3hICP的敏感性和阴性预测值（NPV）为89．1％和88．8％，明显高于ECG、cTnI和CK-MB，四者结合为97．6％和96．9％；IMA诊断发病3～6hICP的敏感性和NPV为71．7％和74．5％，也高于ECG、cTnI、CK-MB，四者结合为95．5％和94．2％；但IMA对于发病〉6h的ICP则无诊断作用。结论 IMA是诊断ICP的早期敏感生化指标，对于发病〈6h（尤其是〈3h）的ICP诊断具有较高的敏感性和NPV，优于ECG、CK-MB、cTnI；将IMA与其他指标结合，可进一步提高对ICP的诊断价值。     

以失用为主要表现的胼胝体梗死

目的探讨胼胝体梗死的临床表现、病因及鉴别诊断特点。方法对2005年7月收治的1例53岁男性胼胝体梗死患者的临床表现、影像学特点、病因机制及其治疗过程进行回顾分析。结果临床主要表现为发作性黑蒙、言语不利,既往有高血压、糖尿病、脑梗死、吸烟、饮酒史,体格检查以失用为主要表现。头部MRI检查可见左侧脑室旁、胼胝体梗死,右侧基底节、脑桥陈旧性腔隙性梗死;脑血管造影检查显示为多发性血管狭窄,其中以左侧大脑中动脉、右侧颈内动脉及基底动脉最为严重。经颈内动脉内膜剥离术及颈内动脉支架植入术治疗,临床症状缓解。结论失用可以是胼胝体梗死的主要表现,其病因是在脑动脉粥样硬化基础上的血流动力学改变,患者预后良好。