Proxomed Tergumed用于椎间孔镜术后早期康复的临床效果分析

目的:探讨Proxomed Tergumed系统用于腰椎间盘突出症椎间孔镜术后早期康复的治疗效果。方法:按照纳入和排除标准,选择2016年6月至2017年6月在我科明确诊断为腰椎间盘突出症并进行腰椎间孔镜手术的63例患者进行回顾性分析。按照是否进行系统的Proxomed Tergumed脊柱功能训练,将其分为功能训练组实验组(28例)与对照组(35例)。比较两组患者在术前、术后1周、术后3月及术后6月的疼痛(VAS)、功能评分(ODI)、相关肌肉力量及术后并发症的发生情况。结果:两组患者术后的VAS评分及ODI评分均较术前明显降低(P0.05)。术后1周时,两组VAS评分及ODI评分比较差异无统计学意义(P0.05)。术后3月及6月,实验组VAS评分和ODI评分均显著低于对照组(P0.05)。术后6个月,实验组肌力恢复显著优于对照组(P0.05)。术后6月,实验组各肌肉群力量与术前相比均无显著差异(P0.05),而对照组肌肉群力量仍较术前显著降低(P0.05)。结论:Proxomed Tergumed系统在腰椎间盘突出症椎间孔镜术后的康复中可以有效的降低患者的术后疼痛,改善患者的腰椎功能,相对于传统的术后康复训练而言有其明显的优势,且并无显著的安全性差异。     

经皮激光汽化术联合杜仲腰痛丸治疗腰椎间盘突出症的效果观察

目的:研究经皮激光汽化术联合杜仲腰痛丸治疗腰椎间盘突出症的临床效果。方法:选择2016年4月~2018年4月我院脊柱骨科收治的106例腰椎间盘突出症患者,随机分为两组。对照组单独采用经皮激光汽化术治疗,观察组联合口服杜仲腰痛丸治疗,每次8粒,每天3次。比较两组的治疗有效率,治疗前后的VAS评分、JOA评分,血清白介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)水平的改变情况。结果:治疗后,观察组的治疗有效率为88.68%(47/53),明显高于对照组[73.58%(39/53)](P0.05)。两组治疗后的VAS评分值均较治疗前明显降低(P0.05),JOA评分值均较对照组明显升高(P0.05),且观察组VAS评分值明显低于对照组,JOA评分值显著高于对照组(P0.05)。两组治疗后的血清IL-1β、TNF-α水平均较治疗前明显降低(P0.05),且观察组血清IL-1β、TNF-α水平明显低于对照组(P0.05)。两组均未发生神经损伤和无椎间盘炎等并发症。结论:经皮激光汽化术联合杜仲腰痛丸治疗腰椎间盘突出症的临床效果明显优于单独采用经皮激光汽化术治疗,其可以显著改善患者的生活质量,降低疼痛程度,其作用机制可能与有降低患者血清炎症介质IL-1β、TNF-α的表达有关。     

独活寄生汤加减治疗对风寒湿痹型腰椎间盘突出症患者生活质量、自由基代谢及睡眠质量的影响

目的:探讨独活寄生汤加减治疗对风寒湿痹型腰椎间盘突出症(LIDP)患者生活质量、自由基代谢及睡眠质量的影响。方法:选取2012年1月～2017年12月期间海南省中医院骨一科收治的风寒湿痹型LIDP患者286例。采用随机数字表法将患者分为对照组(n=143)和研究组(n=143),对照组给予常规治疗,研究组在对照组基础上联合独活寄生汤加减治疗,比较两组临床疗效,比较两组治疗前、治疗30 d后生活质量、自由基代谢及睡眠质量情况,记录两组治疗期间不良反应情况。结果:研究组临床总有效率为93.71%,显著高于对照组的66.43%(P0.05)。治疗30 d后,两组患者超氧化物歧化酶(SOD)水平升高,且研究组高于对照组(P0.05),丙二醛(MDA)水平降低,且研究组低于对照组(P0.05)。两组患者治疗前、治疗30d后活力(VT)、社会功能(SF)评分比较无差异(P0.05),两组患者治疗30d后躯体功能(PF)、躯体疼痛(BP)、躯体角色(RP)、心理健康(MH)、总体健康(GH)以及情感角色(RE)评分均较治疗前升高,且研究组较对照组升高(P0.05)。两组患者治疗30 d后匹兹堡睡眠质量指数(PSQI)评分均较治疗前降低,且研究组低于对照组(P0.05)。两组患者治疗期间不良反应发生率比较无统计学差异(P0.05)。结论:独活寄生汤加减治疗风寒湿痹型LIDP患者疗效确切,其可有效改善患者生活质量、自由基代谢及睡眠质量,且安全性较好,具有一定的临床应用价值。     

miR-155对人椎间盘退变髓核细胞凋亡的作用及机制研究

目的:探讨mi R-155对人椎间盘退变髓核细胞凋亡的影响及其作用机制。方法:首先构建慢病毒表达载体,在293T细胞中获得重组慢病毒,然后感染椎间盘退变髓核细胞得到稳定过表达细胞系,同时设置空载体和空白细胞组对照。用荧光显微镜观察慢病毒载体的标签蛋白GFP的表达,分别提取三组细胞总RNA,采用RT-q PCR方法检测mi R-155的表达;通过流式细胞术检测细胞凋亡,Western-Blot检测细胞中凋亡相关蛋白FADD、Caspase-3、Bcl-2及Bax的表达,JC-1试剂盒检测细胞线粒体膜电位的变化情况。结果:在荧光显微镜下,经慢病毒感染的过表达细胞系和空载体细胞系均出现绿色荧光,而空白细胞组未见绿色荧光;RT-qPCR结果显示构建的稳定过表达细胞系(GV369-miR-155-NP)中mi R-155的表达水平较高,且与空载体细胞系及空白细胞对照组均呈显著性差异(P0.05);与空载体组(GV369-NP)及空白细胞对照组相比,过表达组(GV369-miR-155-NP)细胞凋亡率显著降低(P0.05),FADD、Caspase-3、Bax的表达水平均明显下降,而Bcl-2表达水平显著增加(P0.05)。结论:mi R-155可能通过靶向结合Caspase-3和FADD阻止FasL-Fas途径或通过线粒体途径抑制人椎间盘退变髓核细胞凋亡。     

几种椎间盘退变动物模型的建立和应用

椎间盘退变是一种年龄相关的退行性疾病,是引起下腰痛的主要因素,严重影响病人的生活质量,并显著增加家庭的经济负担。目前,缺少椎间盘退变的有效干预和治疗手段,部分原因是其发病机制尚未阐明。椎间盘退变动物模型的构建对于阐明该疾病的病理机制至关重要。椎间盘退变是一个复杂的过程,受机械应力、结构损伤、生物化学与基因表达等多种因素的影响。本文总结了应用异常机械应力、结构损伤、生物化学或化学诱导和基因敲除等方式构建的椎间盘退变动物模型。生物力学是维持椎间盘稳态的重要因素,异常的机械应力会导致椎间盘退变。同时,椎间盘退变常伴随结构性损伤,椎间盘结构破坏也会导致椎间盘发生退变。此外,生物化学或化学诱导和关键基因敲除也会导致椎间盘退变。本文按照造成异常机械应力的因素将机械应力模型分为加压模型和失稳模型;按照椎间盘结构将结构损伤模型分为髓核与纤维环损伤模型和软骨终板损伤模型。总结了生物化学或化学诱导模型以及新型的基因敲除模型。讨论了不同类型椎间盘退变动物模型的可能应用和局限性。     

龙虎交战针法联合悬吊训练对腰椎间盘突出症患者腰背伸肌群功能、神经传导速度和血清炎症因子的影响

摘要 目的：观察龙虎交战针法联合悬吊训练对腰椎间盘突出症（LDH）患者腰背伸肌群功能、神经传导速度和血清炎症因子的影响。方法：纳入我院2018年4月-2021年8月期间接收的LDH患者82例。按照随机数字表法将患者分为对照组（悬吊训练,n=41）和实验组（龙虎交战针法联合悬吊训练,n=41）。观察两组患者腰椎功能恢复情况、疼痛症状改善情况以及腰背伸肌群功能、神经传导速度和血清炎症因子的变化情况。结果：实验组的临床总有效率高于对照组（P<0.05）。治疗后,两组日本骨科协会下腰痛评价表（JOA）评分升高,且实验组高于对照组（P<0.05）。治疗后,两组Oswestry功能障碍指数（ODI）、视觉疼痛模拟评分法（VAS）评分下降,且实验组低于对照组（P<0.05）。治疗后,两组平均功率、腰背伸状态下峰力矩升高,且实验组高于对照组（P<0.05）。治疗后,两组腰背屈伸比下降,且实验组较对照组低（P<0.05）。治疗后,两组腓总神经和胫神经的传导速度均升高,且实验组较对照组高（P<0.05）。治疗后,两组血清白细胞介素-1β（IL-1β）、白介素-1（IL-1）、基质金属蛋白酶 3（MMP-3）、肿瘤坏死因子-α（TNF-α）水平均下降,且实验组低于对照组（P<0.05）。结论：龙虎交战针法联合悬吊训练可促进LDH患者腰椎功能改善,减轻疼痛症状,改善腰背伸肌群功能和腓总神经、胫神经的神经传导速度,降低机体血清炎症因子水平,具有较好的临床应用价值。     

Structural and Functional Insight into the Carbohydrate Receptor Binding of F4 Fimbriae-producing Enterotoxigenic Escherichia coli

Enterotoxigenic Escherichia coli (ETEC) strains are important causes of intestinal disease in humans and lead to severe production losses in animal farming. A range of fimbrial adhesins in ETEC strains determines host and tissue tropism. ETEC strains expressing F4 fimbriae are associated with neonatal and post-weaning diarrhea in piglets. Three naturally occurring variants of F4 fimbriae (F4_ab, F4_ac, and F4_ad) exist that differ in the primary sequence of their major adhesive subunit FaeG, and each features a related yet distinct receptor binding profile. Here the x-ray structure of FaeG_ad bound to lactose provides the first structural insight into the receptor specificity and mode of binding by the poly-adhesive F4 fimbriae. A small D′-D″-α1-α2 subdomain grafted on the immunoglobulin-like core of FaeG hosts the carbohydrate binding site. Two short amino acid stretches Phe¹⁵⁰–Glu¹⁵² and Val¹⁶⁶–Glu¹⁷⁰ of FaeG_ad bind the terminal galactose in the lactosyl unit and provide affinity and specificity to the interaction. A hemagglutination-based assay with E. coli expressing mutant F4_ad fimbriae confirmed the elucidated co-complex structure. Interestingly, the crucial D′-α1 loop that borders the FaeG_ad binding site adopts a different conformation in the two other FaeG variants and hints at a heterogeneous binding pocket among the FaeG serotypes.     

Insights into the dynamics of hind leg development in honey bee (Apis mellifera L.) queen and worker larvae - A morphology/differential gene expression analysis

Phenotypic plasticity is a hallmark of the caste systems of social insects, expressed in their life history and morphological traits. These are best studied in bees. In their co-evolution with angiosperm plants, the females of corbiculate bees have acquired a specialized structure on their hind legs for collecting pollen. In the highly eusocial bees (Apini and Meliponini), this structure is however only present in workers and absent in queens. By means of histological sections and cell proliferation analysis we followed the developmental dynamics of the hind legs of queens and workers in the fourth and fifth larval instars. In parallel, we generated subtractive cDNA libraries for hind leg discs of queen and worker larvae by means of a Representational Difference Analysis (RDA). From the total of 135 unique sequences we selected 19 for RT-qPCR analysis, where six of these were confirmed as differing significantly in their expression between the two castes in the larval spinning stage. The development of complex structures such as the bees’ hind legs, requires diverse patterning mechanisms and signaling modules, as indicated by the set of differentially expressed genes related with cell adhesion and signaling pathways.     

Adipose-Derived Stromal Cells Protect Intervertebral Disc Cells in Compression: Implications for Stem Cell Regenerative Disc Therapy

Introduction: Abnormal biomechanics plays a role in intervertebral disc degeneration. Adipose-derived stromal cells (ADSCs) have been implicated in disc integrity; however, their role in the setting of mechanical stimuli upon the disc''s nucleus pulposus (NP) remains unknown. As such, the present study aimed to evaluate the influence of ADSCs upon NP cells in compressive load culture.Methods: Human NP cells were cultured in compressive load at 3.0MPa for 48 hours with or without ADSCs co-culture (the ratio was 50:50). We used flow cytometry, live/dead staining and scanning electron microscopy (SEM) to evaluate cell death, and determined the expression of specific apoptotic pathways by characterizing the expression of activated caspases-3, -8 and -9. We further used real-time (RT-) PCR and immunostaining to determine the expression of the extracellular matrix (ECM), mediators of matrix degradation (e.g. MMPs, TIMPs and ADAMTSs), pro-inflammatory factors and NP cell phenotype markers.Results: ADSCs inhibited human NP cell apoptosis via suppression of activated caspase-9 and caspase-3. Furthermore, ADSCs protected NP cells from the degradative effects of compressive load by significantly up-regulating the expression of ECM genes (SOX9, COL2A1 and ACAN), tissue inhibitors of metalloproteinases (TIMPs) genes (TIMP-1 and TIMP-2) and cytokeratin 8 (CK8) protein expression. Alternatively, ADSCs showed protective effect by inhibiting compressive load mediated increase of matrix metalloproteinases (MMPs; MMP-3 and MMP-13), disintegrin and metalloproteinase with thrombospondin motifs (ADAMTSs; ADAMTS-1 and 5), and pro-inflammatory factors (IL-1beta, IL-6, TGF-beta1 and TNF-alpha).Conclusions: Our study is the first in vitro study assessing the impact of ADSCs on NP cells in an un-physiological mechanical stimulation culture environment. Our study noted that ADSCs protect compressive load induced NP cell death and degradation by inhibition of activated caspase-9 and -3 activity; regulating ECM and modulator genes, suppressing pro-inflammatory factors and preserving CK8. Consequently, the protective impact of ADSCs found in this study provides an essential understanding and expands our knowledge as to the utility of ADSCs therapy for intervertebral disc regeneration.