甲状腺疾病患者血清 Tg-CIC 中 Tg-Ab 水平检测及相关临床研究

目的　对血清甲状腺球蛋白免疫复合物 (thyroglobulin circulating immune complex, Tg-CIC) 中抗甲状腺球蛋白抗体 (anti-thyroglobulin antibody, Tg-Ab) 含量检测，探讨 Tg-CIC 在甲状腺疾病中的临床以及流行病学意义。方法　收集甲状腺疾病患者血清标本 187 例，每例血清标本分为两组 ( 实验组和空白对照组 )，采用免疫复合物解离专利技术对甲状腺疾病患者血清标本 Tg-CIC 进行分离、解离，通过检测 Tg-CIC 解离后的 Tg-Ab 含量来间接反映甲状腺疾病患者血清中Tg-CIC 水平，按照不同的甲状腺疾病进行分组并对实验结果分析讨论。结果　不同甲状腺患者血清中 Tg-CIC 总阳性率达 92.51%，不同甲状腺疾病血清中 Tg-CIC 的阳性率差异无统计学意义 (χ?=2.917, P>0.05)。不同甲状腺疾病患者间血清游离 Tg-Ab 含量差异无统计学意义 (H=3.882, P>0.05)，不同甲状腺疾病患者间血清 CIC 中 Tg-Ab 含量差异无统计学意义(H=5.5842, P>0.05)。不同甲状腺疾病患者中，甲状腺功能亢进、甲状腺炎以及甲状腺结节患者血清游离 Tg-Ab 的含量与血清 CIC 中的 Tg-Ab 含量呈正相关 (P<0.05)，甲状腺功能减退、甲状腺肿瘤患者血清游离 Tg-Ab 的含量与血清 CIC 中的Tg-Ab 含量不相关 (P>0.05)。结论　在甲状腺疾病患者血清中，大部分可检出 Tg-CIC，与疾病类型无关。而甲状腺疾病患者中，甲状腺功能亢进、甲状腺炎以及甲状腺结节患者血清游离 Tg-Ab 含量与血清 CIC 中 Tg-Ab 含量存在相关性，为我们进一步了解 Tg-CIC 与甲状腺疾病的发生、发展的相关性研究奠定了基础，提供了新的研究视角。     

柴芍四金汤预防ERCP术后胆总管结石复发的临床观察

目的 研究柴芍四金汤预防ERCP术后胆总管结石复发的临床疗效。方法 选取昆山市中医医院脾胃肝胆科2014年1月至2016年12月因胆总管结石行ERCP取石病例120例，按随机数字表法将120例病例随机分为治疗组和对照组，每组各60例，治疗组口服自拟柴芍四金汤，每日1剂，水煎400 mL，分早晚两次温服，随证加减；对照组口服熊去氧胆酸250 mg/次，3次/d，2组均连续药物治疗6月，观察术后2周血清中总胆红素（Tbil）、直接胆红素（Dbil）、碱性磷酸酶（ALP）、谷氨酰转肽酶（GGT）指标、术后半年临床症状（包括腹痛、腹胀、恶心、纳差）及术后6月、12月、18月胆总管结石复发情况。结果 治疗组术后6月、12月及18月结石复发率略低于对照组，但两者差异无统计学意义（ P >0.05）；治疗组在改善腹痛、腹胀、恶心、纳差症状方面优于对照组（ P <0.05）；治疗组在改善血清Tbil、Dbil、ALP、GGT水平方面优于对照组（ P <0.01）。结论 柴芍四金汤能有效预防ERCP术后胆总管结石的复发，且能改善胆总管结石引起的临床症状及血清生化指标。      

不同波形低频率电刺激对小鼠海马电点燃癫痫的作用比较

目的观察比较不同脉冲波形的低频率电刺激对海马电点燃癫痫模型小鼠的作用差异。方法采用电点燃刺激法建立小鼠癫痫模型, 观察正弦波、单相方波、双相方波低频率电刺激对模型小鼠癫痫行为发作及后放电持续时间的影响, 并比较不同时间点给予正弦波低频率电刺激的抗癫痫作用。结果与对照组比较, 正弦波低频率电刺激30 s能降低小鼠海马电点燃癫痫发作等级(2.85 ± 0.27 vs 4.75 ±0.12, P < 0.05)、减少大发作概率(53.6% vs 96.5%, P < 0.01) 和缩短后放电持续时间[(16.22 ± 1.69) s vs (30.29 ± 1.12) s, P < 0.01], 而单相方波和双相方波低频率电刺激30 s没有明显的抗癫痫作用。常用的单相方波低频率电刺激15 min能降低小鼠海马电点燃发作等级(3.58 ± 0.16, P < 0.05)、减少大发作概率(66.7%, P < 0.01);但对海马后放电持续时间及大发作持续时间无影响(均 P>0.05)。此外, 电点燃刺激前预先给予或结束后3 s内给予正弦波低频率电刺激具有明显的抗癫痫作用( P < 0.05或 P < 0.01), 而电点燃刺激结束10 s给予正弦波低频率电刺激则无上述抗癫痫作用。 结论低频率电刺激抗癫痫作用受波形参数的影响, 其中正弦波低频率电刺激能有效抑制小鼠海马电点燃癫痫的发作。     

In Vivo Kinematics of Functional Ankle Instability Patients and Lateral Ankle Sprain Copers During Stair Descent

Patients with mechanic ankle instability experience increased tibiotalar and subtalar joint laxity. However, in vivo joint kinematics in functional ankle instability (FAI) patients and lateral ankle sprain (LAS) copers, especially during dynamic activities, are poorly understood. Ten FAI patients, 10 LAS copers, and 10 healthy controls were included in this study. A dual fluoroscopic imaging system was used to analyze the tibiotalar and subtalar joint kinematics during stair descent. Five key poses of stair descent were analyzed. Kinematic data from six degrees of freedom were calculated utilizing a solid modeling software. The range of motion and joint positions in each degree of freedom were compared among the three groups. The tibiotalar joints of FAI patients and LAS copers were significantly more inverted than those of healthy controls during the foot strike (p = 0.016, = 0.264). The subtalar joints of FAI patients were significantly more anteriorly translated (pose 2, p = 0.003, = 0.352; pose 3, p < 0.001, = 0.454; pose 4, p = 0.004, = 0.334), inverted (pose 4, p = 0.027, = 0.234; pose 5,p = 0.034, = 0.221), and externally rotated (pose 4, p = 0.037, = 0.217; pose 5; p = 0.004, = 0.331) than those of healthy controls during the mid‐stance and the heel off. The FAI patients showed excessive tibiotalar inversion and subtalar joint hypermobility during stair descent. Meanwhile, the LAS copers maintained subtalar joint stability, and only showed excessive tibiotalar inversion in foot strike. These data provide insight into the mechanisms behind the development of FAI after initial LAS. © 2019 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 37:1860–1867, 2019     

Hyodeoxycholic acid protects the neurovascular unit against oxygen-glucose deprivation and reoxygenation-induced injury in vitro

Calculus bovis is commonly used for the treatment of stroke in traditional Chinese medicine. Hyodeoxycholic acid(HDCA) is a bioactive compound extracted from calculus bovis. When combined with cholic acid, baicalin and jas-minoidin, HDCA prevents hypoxia-reoxygenation-induced brain injury by suppressing endoplasmic reticulum stress-mediated apoptotic signaling. However, the effects of HDCA in ischemic stroke injury have not yet been studied. Neurovascular unit(NVU) dysfunction occurs in ischemic stroke. Therefore, in this study, we investigated the effects of HDCA on the NVU under ischemic conditions in vitro. We co-cultured primary brain microvascular endothelial cells, neurons and astrocytes using a transwell chamber co-culture system. The NVU was pre-treated with 10.16 or 2.54 μg/mL HDCA for 24 hours before exposure to oxygen-glucose deprivation for 1 hour. The cell counting kit-8 assay was used to detect cell activity. Flow cytometry and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling were used to assess apoptosis. Enzyme-linked immunosorbent assay was used to measure the expression levels of inflammatory cytokines, including interleukin-1β, interleukin-6 and tumor necrosis factor-α, and neurotrophic factors, including brain-derived neurotrophic factor and glial cell line-derived neurotrophic factor. Oxidative stress-related factors, such as superoxide dismutase, nitric oxide, malondialdehyde and γ-glutamyltransferase, were measured using kits. Pretreatment with HDCA significantly decreased blood-brain barrier permeability and neuronal apoptosis, significantly increased transendothelial electrical resistance and γ-glutamyltransferase activity, attenuated oxidative stress damage and the release of inflammatory cytokines, and increased brain-derived neurotrophic factor and glial cell line-derived neurotrophic factor expression. Our findings suggest that HDCA maintains NVU morphological integrity and function by modulating inflammation, oxidation stress, apoptosis, and the expression of neurotrophic factors. Therefore, HDCA may have therapeutic potential in the clinical management of ischemic stroke. This study was approved by the Ethics Committee of Experimental Animals of Beijing University of Chinese Medicine(approval No. BUCM-3-2016040201-2003) in April 2016.     

完全型雄激素不敏感综合征2例临床特点及处理

雄激素不敏感综合征(androgen insensitivity syndrome,AIS)又称为睾丸女性化综合征(testicular feminization syndrome,TFS),是一种X连锁遗传病,是男性假两性畸形中较常见的类型,可分为完全型AIS和不完全型AIS,其原因主要是雄激素受体(androgen receptor,AR)基因的突变导致其对雄激素产生抵抗和不应答。本文回顾南京医科大学附属妇产医院2例CAIS患者的临床资料及诊疗过程,以期能进一步提高对该病的认知及诊治水平。