纹牙弧轨钉板系统在微创通道下腰椎融合术中的应用

目的:观察自行设计的纹牙弧轨钉板系统在可扩张通道下行腰椎固定融合术中应用的有效性、可靠性.方法:2008年2月～2011年2月,对132例腰椎失稳性疾病患者经可扩张通道行微创固定融合手术,随机分成观察组和对照组,观察组应用自行设计的纹牙弧轨钉板系统固定,对照组采用椎弓根钉棒系统固定,分别于术后1周、3个月和1年时复查.比较两组的总手术时间、钉板(钉棒)置入时问、总出血量;各时问点VAS评分、ODI及改善率;术前和术后3个月、1年时的椎问隙高度;术后1年的融合率结果:所有患者均在微创通下完成手术,切口均Ⅰ期愈合,无严重并发症出现.观察组的手术时间、钉板置入时间较对照组短,术中及术后总失血量少于对照组.两组术后1周、3个月和1年时的VAS评分与术前比较均有显著性差异,两组同一时间点比较无显著性差异;术后3个月ODI明显改善,与术前比较有显著性差异,术后1年进一步改善,与术后3个月比较有显著性差异,观察组改善率为(79.46±6.34)％,对照组改善率为(76.73±4.49)％,两组问差异有统计学意义(P＜0.05).术后椎问高度明显改善,1年时两组椎问隙高度均有丢失,但仍显著高于术前,观察组椎问隙高度丢失大于对照组.术后1年时,观察组融合率为98.48％,对照组融合率为87.88％,两组差异有显著性(P＜0.05).结论:纹牙弧轨钉板系统在微创通道下行腰椎固定融合术安装方便,固定可靠,适合在可扩张通道下使用.     

通用脊柱椎弓根钉棒矫形固定系统治疗胸腰椎失稳性伤病的生物力学测试

目的：评价通用脊柱椎弓根钉棒矫形固定系统（GSPS）治疗脊柱失稳性伤病的生物力学性能。方法：用新鲜猪胸腰段脊柱标本（T10-L3）制成失稳模型和骨折模型各4具,分别用自行研制的GSPS模拟手术固定。对试件进行轴向和弯曲扭转加载测试,观察GSPS的应力、应变关系特点。测试GSPS连接棒从弹性夹块中的拔出力。结果：在0～600N轴向加载范围内,GSPS各点应变与应力呈线性关系;弯曲扭转实验中,试件两端之间相对扭转角与弯扭矩呈线性关系,当弯扭矩达到300N.cm时,扭转角不到6°;GSPS的连接棒从弹性夹块中拔出的最小拔出力大于3300N。结论：GSPS具有较高的抗轴向和弯扭载荷的能力,显示出高弹性。采用弹簧垫连接钉棒具有很高的可靠性。     

Alpha-Mangostin suppresses interleukin-1β-induced apoptosis in rat chondrocytes by inhibiting the NF-κB signaling pathway and delays the progression of osteoarthritis in a rat model

Osteoarthritis (OA) is a chronic degenerative joint disease that is characterized by progressive joint dysfunction and pain. Apoptosis and catabolism in chondrocytes play critical roles in the development of OA. Alpha-Mangostin (α-MG), one of the main components of the mangosteen, has been reported to have anti-apoptotic, anti-inflammatory and antioxidant effects. We investigated the therapeutic effects of α-MG on OA through experiments on rat chondrocytes in vitro and in a rat model of OA induced by destabilization of the medial meniscus (DMM). In vitro, we provided experimental evidence that α-MG inhibits the expression of MMP-13 and ADAMTs-5, and promotes the expression of SOX-9 in rat chondrocytes stimulated with interleukin-1β (IL-1β). In addition, we also found that α-MG can inhibit the expression of pro-apoptotic proteins such as Bax, Cyto-c, and C-caspase3, and increase the expression of the anti-apoptotic protein Bcl-2. These changes may be related to an α-MG induced inhibition of the IL-1β-induced activation of the NF-kB signaling pathway. In vivo, we also found that α-MG can limit the development of OA in rat models. The above results show that α-MG has a potential therapeutic effect on OA, and that this effect may be achieved by inhibiting the mitochondrial apoptosis of chondrocytes induced by an activation of the NF-kB pathway.     

经可扩张通道纹牙弧轨钉板系统治疗腰椎失稳性疾病的病例对照研究

目的:评价纹牙弧轨钉板系统在经可扩张通道固定融合术中的有效性和可靠性。方法:自2007年8月至2010年8月,采用外科手术治疗108例腰椎失稳性疾病患者,其中男61例,女47例;年龄26～57岁,平均41岁;腰椎间盘突出症23例,腰椎间盘突出症术后复发4例,腰椎管狭窄症49例,腰椎滑脱症32例。采用随机数字表法分成微创组与开放组,每组54例。微创组应用自行设计的纹牙弧轨钉板系统经可扩张通道行微创椎弓根钉固定椎间融合术,开放组采用传统开放入路椎弓根钉固定椎间融合术。对两组的手术时间、内置物置入时间、出血量进行观察;分别于术后1周、3个月、1年对两组患者的VAS评分、ODI评分及改善率进行比较;通过X线对手术前后不同时期的椎间隙高度、术后融合率进行观察。结果:所有患者切口Ⅰ期愈合,无硬脊膜撕裂、神经根或马尾损伤及椎间隙感染等并发症出现。微创组的手术时间较开放组长,术中及术后失血量明显少于开放组,椎弓根钉系统置入时间比开放组短。VAS评分:术后1周、3个月、1年两组患者的VAS评分均比术前明显下降;术后3个月开放组VAS评分比术后1周明显增加,而微创组变化不明显;术后1年两组VAS评分比术后1周、3个月均降低。ODI评分:术后3个月、1年两组患者ODI评分比术前均明显下降。术后1年两组ODI评分比术后3个月均降低。术后1周、3个月、1年,两组间VAS、ODI评分比较,微创组均低于开放组。术后1年,微创组的改善率为(77.46±6.34)%,开放组的改善率为(72.73±4.49)%,两组间差异有统计学意义(P<0.01)。术后两组椎间隙高度有明显增加。术后3个月,两组椎间隙高度差异无统计学意义;术后1年,两组椎间隙高度均有丢失,但微创组椎间隙高度大于开放组。术后1年所有患者获融合。结论:经可扩张通道微创固定融合术具有创伤小、术中出血少、术后疼痛轻、术后恢复快等特点,椎间融合率与开放手术疗效相似,是治疗腰椎失稳性疾病的一种有效方法。纹牙弧轨钉板系统设计合理,安装方便,复位效果好,固定可靠,适合可扩张通道下使用。     

弧轨自锁椎弓根矫形固定器Ⅱ(ALPFⅡ)治疗脊柱疾病临床应用研究

目的：探讨弧轨自锁椎弓根矫形固定器Ⅱ（ALPFⅡ）治疗脊柱疾病的临床疗效。方法：86例脊柱疾病患者,其中男49例,女37例;年龄18～69岁,平均36.8岁。应用ALPFⅡ治疗,并随访。结果：86例获随访,时间9～30个月,平均12个月。患者神经功能、脊柱活动、腰背痛和下肢痛的改善率分别为94.1%、65.9%、92.1%和87.4%,术前后椎体前、后缘高度恢复均明显（P〈0.01,P〈0.05）,后凸角得到满意矫正（P〈0.01）。未发现钉棒松动、断裂。结论：ALPFⅡ治疗脊柱疾病是一种操作安全简便、容易掌握、复位良好、疗效可靠、并发症少的治疗方法。     

Highlighting the interaction between immunomodulatory properties of mesenchymal stem cells and signaling pathways contribute to Graft Versus Host Disease management

BackgroundAllogeneic hematopoietic stem cell transplantation (Allo-HSCT) has been increasingly used as a therapeutic approach for hematological malignancies. Several potential strategies have been developed for treating or preventing allo-HSCT complications, specifically graft-versus-host disease (GVHD). GVHD could significantly affect the morbidity and mortality of patients after allo-HSCT. Curative treatment and prophylaxis regimens for GVHD could reduce GVHD incidence and improve survival rate. Among these therapeutic strategies, mesenchymal stem cell (MSCs) mediated immunomodulation has been explored widely in clinical trials. MSCs immunomodulation ability in GVHD correlates with the interactions of MSCs with innate and adaptive immune cells. However, signaling pathways responsible for MSCs' impact on GVHD regulation, like JAK/STAT, NOTCH, MAPK/ERK, and NFκβ signaling pathways, have not been clearly described yet. This review aims to illuminate the effect of MSCs-mediated immunomodulation in GVHD management after allo-HSCT representing the role of MSCs therapy on signaling pathways in GVHD.ConclusionMSCs could potentially modulate immune responses, prevent GVHD, and improve survival after allo-HSCT. Previous studies have investigated different signaling pathways' contributions to MSCs immunoregulatory ability. Accordingly, targeting signaling pathways components involved in MSCs related GVHD regulation is proven to be beneficial.     

Risk factors of early liver dysfunction after liver transplantation using grafts from donation after citizen death donors

BackgroundAs an early complication after liver transplantation, early allograft dysfunction (EAD) indicates a poor prognosis. This study analyzes the risk factors related to early allograft dysfunction (EAD) after liver transplantation using grafts from donation after citizen death (DCD) to provide a reference for the prevention of EAD after DCD liver transplantation.MethodsA total of 32 patients who underwent DCD liver transplantation in the organ transplantation center of our hospital from September 2013 to January 2021 were enrolled in this study. The patients were divided into the EAD group and non-EAD group according to whether they developed EAD after transplantation. The general data of the donors and recipients before transplantation, intraoperative conditions, and clinical data within one week after transplantation were compared between the two groups, and related complications were statistically analyzed. The follow-up time was one week postoperatively or, if they died within the first week postoperatively, until the patient died.ResultsThe subjects included 10 females and 22 males, and the incidence of postoperative EAD was 25% (8/32). Four patients (12%) had primary malignant tumors (primary liver cancer and cholangiocarcinoma), and five donors (15%) had fatty liver. The univariate analysis revealed that the donor BMI (P = 0.005), degree of fatty liver (P = 0.025), aspartate aminotransferase (P = 0.001), alanine aminotransferase (P < 0.001), and total bilirubin (P = 0.009) were related to the occurrence of EAD after DCD liver transplantation. By analyzing the correlation between the incidence EAD and postoperative complications after liver transplantation using grafts from DCD donors, it was shown that the incidence of primary nonfunction (PNF) is related to EAD (P = 0.024).ConclusionDonor BMI, the degree of fatty liver, and preoperative liver function are risk factors for EAD after DCD liver transplantation, and the occurrence of EAD after DCD liver transplantation significantly increases the probability of PNF.     

LncRNA H19 modulates neuropathic pain through miR-141/GLI2 axis in chronic constriction injury (CCI) rats

BackgroundThe participation of long non-coding RNAs (lncRNAs) in progressions of chronic pain has been evaluated. We explored mechanisms of lncRNA H19 in chronic constriction injury (CCI)-induced neuropathic pain model in vivo.MethodsThe expressions of lncRNA H19, microRNA-141, and GLI Family Zinc Finger 2 (GLI2) in CCI rats were determined by using RT-qPCR. Paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) were used as neuropathic pain index implying mechanical allodynia and thermal hyperalgesia. The protein concentrations of IL-1β, IL-6 and TNF-α in rats were examined by ELISA assay. RT-qPCR analyzed gene expression changes of lncRNA H19, miR-141 and GLI2. Online bioinformatics predictions supported that the bindings between miR-141 and GLI2 and dual luciferase reporter method, and RNA pull-down assays determined connections within lncRNA H19, miR-141 and GLI2 in HEK 293 cells.ResultsLncRNA H19 was upregulated in the tissues of rats. Also, thermal hyperalgesia and mechanical allodynia were inhibited by lncRNA H19 suppression in rats. Moreover, IL-1β, IL-6 and TNF-α protein concentrations were suppressed by the downregulation of lncRNA H19 in rats. Furthermore, miR-141 was reduced in CCI rats and restored by the lncRNA H19 knockdown, suggesting the potential negative associations of miR-141 with lncRNA H19. GLI2 targeted miR-141 and GLI2 was increased in CCI rats. Additionally, the neuropathic pain was inhibited by the inhibition of GLI2 in rats, which was reversed by the miR-141 inhibitors.ConclusionLncRNA H19 aggravated the neuropathic pain of CCI rats through miR-141/GLI2 axis, implying that lncRNA H19 might be a biomarker for the inflammation-related neuropathic pain.     

Andrographolide suppresses osteoarthritis progression by regulating circ_Rapgef1/miR-383-3p/NLRP3 signaling axis

BackgroundAndrographolide (AD) has been reported to play a potential anti-arthritic role by facilitating the proliferation and inhibiting the apoptosis of chondrocytes. However, the molecular mechanism underlying the protective role of AD in osteoarthritis (OA) remains to be elucidated.MethodsOA mice model was established via anterior cruciate ligament transection (ACLT) operation. OA cell model was established through treating mice primary chondrocytes with LPS (1 μg/mL, 24 h). Enzyme-linked immunosorbent assay (ELISA) was performed to measure the concentrations of inflammatory cytokines in the supernatant. Cell proliferation was assessed by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and 5-Ethynyl-2′-deoxyuridine (EdU) assay. Cell apoptosis was evaluated by flow cytometry. The intermolecular interaction was verified by dual-luciferase reporter assay.ResultsAD administration reduced the infiltration of inflammatory cells in the synovial tissues of ankle joint and suppressed the inflammatory response in OA mice model in vivo. Lipopolysaccharide (LPS) stimulation suppressed the proliferation and induced the apoptosis and inflammation of chondrocytes, and AD treatment protected chondrocytes from LPS-induced dysfunction. Circular RNA (circRNA) Rap guanine nucleotide exchange factor 1 (circ_Rapgef1) overexpression attenuated AD-mediated protective effects in OA cell model. Circ_Rapgef1/microRNA-383-3p (miR-383-3p)/Nod-like receptor pyrin domain 3 (NLRP3) axis was identified in this study for the first time. Circ_Rapgef1 overexpression-mediated effects were partly reversed by the overexpression of miR-383-3p in chondrocytes. NLRP3 silencing partly overturned miR-383-3p knockdown-mediated effects in chondrocytes. Circ_Rapgef1 overexpression up-regulated the expression of NLRP3 partly by targeting miR-383-3p in chondrocytes.ConclusionCirc_Rapgef1 suppressed AD-mediated protective effects in OA partly by regulating miR-383-3p/NLRP3 signaling.