A modality-specific somatosensory evoked potential test protocol for clinical evaluation: A feasibility study

ObjectiveWe aimed to establish an objective neurophysiological test protocol that can be used to assess the somatosensory nervous system.MethodsIn order to assess most fiber subtypes of the somatosensory nervous system, repetitive stimuli of seven different modalities (touch, vibration, pinprick, cold, contact heat, laser, and warmth) were synchronized with the electroencephalogram (EEG) and applied on the cheek and dorsum of the hand and dorsum of the foot in 21 healthy subjects and three polyneuropathy (PNP) patients. Latencies and amplitudes of the modalities were assessed and compared. Patients received quantitative sensory testing (QST) as reference.ResultsWe found reproducible evoked potentials recordings for touch, vibration, pinprick, contact-heat, and laser stimuli. The recording of warm-evoked potentials was challenging in young healthy subjects and not applicable in patients. Latencies were shortest within Aβ-fiber-mediated signals and longest within C-fibers. The test protocol detected function loss within the Aβ-fiber and Aδ-fiber-range in PNP patients. This function loss corresponded with QST findings.ConclusionIn this pilot study, we developed a neurophysiological test protocol that can specifically assess most of the somatosensory modalities. Despite technical challenges, initial patient data appear promising regarding a possible future clinical application.SignificanceEstablished and custom-made stimulators were combined to assess different fiber subtypes of the somatosensory nervous system using modality-specific evoked potentials.     

骨填充网袋椎体成形术与经皮椎体后凸成形术治疗Kümmell病的疗效比较

目的比较骨填充网袋椎体成形术（Vesselplasty）与经皮椎体后凸成形术（percutaneous kyphoplasty，PKP）治疗 Kümmell 病的临床疗效。方法2015 年 1 月—2018 年 12 月收治 63 例 Kümmell 病患者，其中 28 例采用 Vesselplasty 治疗（Vesselplasty 组），35 例采用 PKP 治疗（PKP 组）。两组患者性别、年龄、病程、骨密度 T 值、骨折节段及术前疼痛视觉模拟评分（VAS）、Oswestry 功能障碍指数（ODI）、伤椎前缘高度、后凸 Cobb 角等一般资料比较，差异均无统计学意义（P>0.05），具有可比性。记录两组手术时间、术中透视时间、骨水泥注射量、骨水泥渗漏率、骨水泥弥散面积率和随访期间并发症发生情况，以及术前、术后 1 d、末次随访时 VAS 评分、ODI、伤椎前缘高度、后凸 Cobb 角。 结果两组患者均获随访，随访时间 12～36 个月，平均 24.2 个月。Vesselplasty 组手术时间、术中透视时间、骨水泥注射量、骨水泥弥散面积率均明显小于 PKP 组（P<0.05）。Vesselplasty 组骨水泥渗漏率（7.14%）明显低于 PKP 组（34.29%）（χ²=5.153，P=0.023）。两组患者术后 1 d 及末次随访时 VAS 评分、ODI、伤椎前缘高度、后凸 Cobb 角均较术前显著改善（P<0.05），术后两组间比较差异均无统计学意义（P>0.05）。随访期间两组均未见术椎再塌陷，Vesselplasty 组邻椎骨折发生率（7.14%）与 PKP 组（14.29%）比较，差异无统计学意义（χ²=0.243，P=0.622）。 结论Vesselplasty 和 PKP 治疗 Kümmell 病疗效相似，均能有效缓解患者疼痛症状，改善生活质量，部分恢复伤椎高度，矫正椎体后凸。但前者具有手术时间短、术中透视时间少、骨水泥渗漏少等优势。     

Valvular heart disease in Antiphospholipid antibody syndrome: Isolated Tricuspid stenosis

Antiphospholipid antibody syndrome (APLS) is a rare disorder characterized by a hypercoagulable state. Manifestations include arterial or venous thrombosis, recurrent fetal wastage, coronary artery disease, valvular heart disease, dilated cardiomyopathy, pulmonary artery hypertension, and intracardiac thrombus. Most commonly mitral valve is affected followed by aortic and then tricuspid valve. In this report, a rare case of spontaneous aortic thrombosis with tricuspid stenosis uncomplicated by other valve lesions is presented with clinical and echocardiographic studies and computed tomographic images.     

中医药调控IL-1治疗肿瘤机制的研究进展

炎症已成为影响肿瘤细胞增殖转移的第七大因素,而白细胞介素-1(IL-1)是炎性微环境的重要因子之一。中医药在治疗肿瘤时具有多途径、多靶点的优势,同时炎性微环境致病特点与现代中医学"癌毒"的理论相吻合。查阅近年中医药调控IL-1家族分子治疗肿瘤机制的文献,对其进行梳理,并做出概括及评价,从中医药主要调控IL-1α、IL-1β和IL-18因子治疗肿瘤展开综述,为中医药更系统化治疗肿瘤提供参考。     

人肠道病毒71型及柯萨奇病毒A组16型VP1蛋白的真核表达

目的：克隆人肠道病毒71型（EV71）及柯萨奇病毒A组16型（CA16）的VP1蛋白编码基因，构建相应真核表达质粒在体外进行重组表达，检测其细胞内定位，为EV71及CA16的疫苗研究提供基础。方法：通过PCR扩增分别获取EV71及CA16的VP1编码序列，插入pcFlag载体，分别构建EV71及CA16 VP1与FLAG标签融合的真核表达质粒；瞬时转染人胚肾293T细胞及横纹肌肉瘤RD细胞，Western blot法检测融合蛋白的表达，免疫荧光检测融合蛋白的细胞内定位情况。结果：测序表明两种来源VP1蛋白的重组表达质粒构建正确；分别转染两种不同的细胞后，均可通过Western blot检测到相应蛋白表达；免疫荧光检测显示两种毒株的VP1均表达在细胞质中。结论：外源融合表达EV71或CA16 VP1蛋白的真核表达质粒构建成功；所构建质粒分别转染细胞后，均可在细胞质内检测到VP1融合蛋白的表达。     

维生素D与多囊卵巢患者胰岛素抵抗相关性及其机制研究

目的:探讨维生素D对多囊卵巢综合征(PCOS)患者胰岛素抵抗(IR)的影响及其机制研究.方法:选取自2013年2月～2014年2月在该院就诊的48例PCOS患者作为PCOS组,另选30例健康育龄期妇女作为对照组,测量研究者身高、体质量参数,计算体质指数(BMI),采用全自动生化分析仪葡萄糖氧化酶检测空腹血糖浓度(FBG)、化学发光法检测血清空腹胰岛素(FI)及胰岛素样生长因子-1(IGF-1)水平、ELISA方法测定血清25-(OH)D3浓度,计算稳态胰岛素评价指数(HOMA-IR)用于评价胰岛素抵抗性,量化胰岛素敏感指数(QUICKI)用于评价胰岛素敏感度,并分析FI、HOMA-IR、QUICKI及IGF-1与血清25-(OH)D3浓度的相关性.结果:PCOS组BMI及FBG与对照组相比,差异无统计学差异(P＞0.05),而FI、HOMA-IR、QUICKI、25-(OH) D3及IGF-1与对照组比较,差异均有统计学差异(P＜0.05);并且PCOS组FI和HOMA-IR与血清25-(OH)D3浓度呈显著负相关,差异有统计学意义(P＜0.05),QUICKI和IGF-1水平与血清25-(OH)D3浓度呈显著正相关,差异有统计学意义(P＜0.05).结论:PCOS患者IR可能与血清中维生素D缺乏有关,而IGF-1分泌减少又可能是导致PCOS患者维生素D缺乏的重要原因.     

Genome wide identification of new genes and pathways in patients with both autoimmune thyroiditis and type 1 diabetes

Autoimmune thyroid diseases (AITD) and Type 1 diabetes (T1D) frequently occur in the same individual pointing to a strong shared genetic susceptibility. Indeed, the co-occurrence of T1D and AITD in the same individual is classified as a variant of the autoimmune polyglandular syndrome type 3 (designated APS3v). Our aim was to identify new genes and mechanisms causing the co-occurrence of T1D + AITD (APS3v) in the same individual using a genome-wide approach. For our discovery set we analyzed 346 Caucasian APS3v patients and 727 gender and ethnicity matched healthy controls. Genotyping was performed using the Illumina Human660W-Quad.v1. The replication set included 185 APS3v patients and 340 controls. Association analyses were performed using the PLINK program, and pathway analyses were performed using the MAGENTA software. We identified multiple signals within the HLA region and conditioning studies suggested that a few of them contributed independently to the strong association of the HLA locus with APS3v. Outside the HLA region, variants in GPR103, a gene not suggested by previous studies of APS3v, T1D, or AITD, showed genome-wide significance (p < 5 × 10⁻⁸). In addition, a locus on 1p13 containing the PTPN22 gene showed genome-wide significant associations. Pathway analysis demonstrated that cell cycle, B-cell development, CD40, and CTLA-4 signaling were the major pathways contributing to the pathogenesis of APS3v. These findings suggest that complex mechanisms involving T-cell and B-cell pathways are involved in the strong genetic association between AITD and T1D.