甲状腺乳头状癌伴发桥本甲状腺炎的临床研究

背景与目的：甲状腺乳头状癌（papillary thyroid carcinoma，PTC）和桥本甲状腺炎（Hashimoto’s thyroiditis，HT）的发病率均呈上升趋势，两者之间的关系已成为目前研究的热点。探讨PTC和HT之间的关系。方法：回顾性分析2014—2015年期间在中国科学院大学附属肿瘤医院头颈肿瘤外科行甲状腺癌手术治疗的首诊患者306例，术后病理学检查均明确诊断为PTC，其中术后病理学确诊伴发HT者42例，比较伴发HT与未伴发HT患者的临床病理学特征。结果：PTC患者女性发病年龄高于男性（46.2岁 vs 41.9岁）。相较于与未伴发HT的PTC患者，伴发HT的患者中女性比例更高（93% vs77%），中央区淋巴结数目较多［（5.0±3.4）枚 vs （2.5±2.7）枚］，术前促甲状腺激素（thyroid-stimulating hormone，TSH）水平较高［（3.28±1.91）μU/mL vs （2.12±1.29）μU/mL］，术前抗甲状腺过氧化物酶抗体（thyroid peroxidaseantibody，TPOAb）阳性率较高（55% vs 14%），术前甲状腺球蛋白抗体（thyroglobulin antibodies，TgAb）阳性率较高（69% vs 13%）。发生中央区淋巴结转移的患者中，中央区淋巴结转移数目与中央区淋巴结总数显著相关（Pearson相关系数=0.582）。多因素logistic回归分析发现，男性、低龄、被膜侵犯是PTC患者中央区淋巴结转移的独立危险因素。结论：伴发HT对PTC患者的预后无显著影响。伴发HT的PTC患者TSH水平显著偏高，提示HT可能是PTC发病风险因素之一。中央区淋巴结转移数目与中央区淋巴结总数相关，推测PTC淋巴结转移可能与淋巴结炎症反应相关。     

改良单图像法手工测量髌骨不稳患者胫骨结节-股骨滑车沟间距的可行性分析

目的 探讨改良单图像法手工测量髌骨不稳患者胫骨结节-股骨滑车沟（tibial tuberosity-trochlear groove，TT-TG）间距的可行性。 方法 选取髌骨不稳患者30例。高年资手术医师A、B，使用改良单图像法手工测量髌骨不稳患者TT-TG间距，对比高资年影像学医师C，使用双图法测量髌骨不稳患者TT-TG间距。应用Cronbach′s alpha系数评价结果的可信度。应用组内相关系数（intraclass correlation coefficient，ICC）评价结果的可重复性。使用Bland-Altman分析图评价结果的一致性。 结果 高年资手术医师A、B使用改良单图像法手工测量髌骨不稳患者TT-TG间距分别和高年资影像学医师C使用双图法测量髌骨不稳患者TT-TG间距比较，Cronbach′s alpha系数分别为0.913和0.959，组内相关系数分别为0.913和0.958。Bland-Altman分析图显示，TT-TG间距差值（mm）的均值为-0.276（95%CI：-3.526~2.974）和0.143（95%CI：-3.110~3.397）。A、B医师之间使用改良单图像法手工测量髌骨不稳患者TT-TG间距比较，Cronbach′s alpha系数为0.891，组内相关系数为0.891。Bland-Altman分析图显示TT-TG间距差值（mm）的均值为-0.276（95%CI：-3.526~2.974）。 结论 改良单图像法手工测量髌骨不稳患者TT-TG间距操作简单，可以准确测量出髌骨不稳患者的TT-TG间距，该方法和双图法可以相互替换使用。     

基于虚实辨证的补泻平衡手法治疗膝骨关节炎临床研究

目的观察补泻平衡手法治疗膝骨关节炎的疗效及对患者临床症状、体征的影响。方法采用随机数字表法将220例单膝骨关节炎患者分为治疗组和对照组各110例。治疗组予补泻平衡手法,对照组予常规推拿手法,均每次20 min,每日2次,1周为1个疗程,连续治疗2个疗程。观察2组治疗前后及治疗后3、6个月全身临床症状、体征及中医证候评分,比较2组临床疗效及不良反应。结果与本组治疗前比较,2组治疗后全身临床症状、体征评分明显降低(P<0.05),治疗组中医证候评分明显降低(P<0.05);2组治疗后比较,治疗组全身临床症状、体征改善程度优于对照组(P<0.05);与本组治疗后比较,2组治疗后3、6个月全身临床症状、体征评分升高。治疗组治疗后3、6个月中医证候评分升高,仍低于治疗前(P<0.05)。治疗组总有效率为91.8%(101/110),对照组为78.2%(86/110),2组比较差异有统计学意义(P<0.05)。2组均未见不良反应。结论补泻平衡手法与常规推拿手法治疗膝骨关节炎均有效,前者疗效优于后者,且中远期疗效更佳。     

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.     

天麻研究进展及产业发展建议

天麻为传统名贵中药材，具有增智、健脑、延缓衰老、预防和治疗阿尔兹海默病等作用，越来越受到人们的关注。本研究对已经发表的有关天麻成分及分析、天麻栽培及分子生物学的研究文章进行归纳、总结，结合对国内主要天麻产区调研，提出了天麻产业发展目前存在的问题，并给出天麻产业发展建议，旨在为今后天麻深入开发利用提供参考。     

骶骨肿瘤切除ISOLA重建骨盆环稳定

目的探讨骶骨肿瘤切除术后应用ISOLA重建骨盆环稳定的疗效。方法手术治疗32例骶骨肿瘤患者。肿瘤切除后均应用ISOLA行腰骶部内固定植骨融合,其中24例行前后联合入路,结扎双侧髂内动脉;8例行单纯后路肿瘤切除植骨融合内固定。结果术后经过6个月～5年的随访,术后感染去除内固定1例,因肿瘤复发死亡3例,再手术3例,失访5例,余患者术后症状均明显改善,植骨融合好,骨盆环稳定,内固定物无松动,未发现断钉断棒现象。结论骶骨肿瘤切除术后应用ISOLA重建下腰椎及骨盆环稳定,疗效满意。     

术中电生理动态监护下显微手术切除椎管神经鞘瘤（附65例报告）

目的 探讨术中电生理监护对椎管神经鞘瘤显微手术中的作用及意义，提高对椎管内神经鞘瘤的治疗水平。方法 回顾性分析65例术中电生理动态监护下，显微手术切除椎管内神经鞘瘤。结果 治愈60例（占92．3％），好转5例（占7．7％），无死亡；肿瘤全切62例，次全切除3例，全切率95．4％。结论 常规动态电生理监测下显微手术切除椎管神经鞘瘤，能保全脊髓神经的功能，减少副损伤，提高手术安全性；显微手术有助于提高肿瘤全切率，可有效减少术后复发。对影响脊柱稳定性的行脊柱融合内固定。     

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。     

64层CT下肢动脉成像技术研究

目的探讨64层CT下肢动脉成像强化质量的对比剂注射方式。方法前瞻性地选择60例疑诊下肢动脉病变的病人,利用64层螺旋CT行下肢动脉CT血管成像。采用不同的扫描和重建参数,应用370mgI/100ml浓度的对比剂100ml团注或采用先70ml的对比剂后50ml的0.9%生理盐水用双筒高压注射器分别以4.0ml/s的注射速度团注入肘静脉,应用对比剂追踪触发扫描方式待腹主动脉CT阈值达120HU时延迟7s开始扫描;利用MIP和VR方式重建CTA图像;对比不同参数和不同对比剂应用方式的CT血管成像图像质量。结果最佳的扫描与重建参数为准直64×0.6mm,螺距1.5,层厚1.0,重建间隔50%;最佳的对比剂应用方式为(浓度为370mgI/100ml)对比剂70ml、生理盐水50ml以4.0ml/s注射速度按先后顺序团注。结论选择合适的准直、螺距以保证适当的扫描速度,选择合适的对比剂浓度、用量和注射速度以保证血管内足够的对比剂峰值浓度及峰值持续时间,此二者是64层CT下肢动脉成像成功的关键。