手法整复经皮导入空心加压螺纹钉内固定治疗肱骨近端骨折脱位

目的：介绍一种治疗新鲜肱骨近端骨折脱位的闭合整复和半开放手术方法,并对其疗效进行评价。方法：对43例肱骨近端骨折合并肩关节前脱位患者应用反“？”手法整复骨折,经皮导入空心螺纹钉内固定后按单纯肩关节前脱位整复治疗。术后2年进行肩关节Neer评分。结果：术后针眼无感染,均工期愈合。螺纹钉无折断。骨折均在术后2个月内愈合。经24～52个月的随访,无肱骨头坏死发生。疗效优35例,良7例,可1例,优良率为97．7％。结论：反“？”手法设计合理,复位率高。经皮导入内固定可靠,无须外固定,术后可早期活动肩关节,有效预防了关节粘连,较好地保护了肱骨头的血供,避免了肱骨头缺血性坏死的发生。     

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.     

改良Uhl闭合穿针技术治疗Colles骨折回顾性研究

目的:回顾性分析中国接骨学(Chinese osteosynthesis,CO)理念指导下改良Uhl技术治疗Colles骨折的优势。方法:回顾性研究2016年1月至2021年6月采用改良Uhl闭合穿针技术治疗Colles骨折358例,符合条件的纳入120例,按照手术方法不同分为两组:闭合穿针组和切开复位组。闭合穿针组68例,采用CO接骨理念指导下改良Uhl闭合复位经皮穿针技术;切开复位组52例,采用切开复位钢板内固定技术。术后6个月比较两组腕关节改良的Sarmiento影像学评分、Gartland-Werley腕关节评分及手术时间、住院时间、治疗费用。结果:两组患者均获得6个月以上随访。两组在Sarmiento影像学评分、Gartland-Werley腕关节评分方面比较,差异无统计学意义(P>0.05)。闭合穿针组手术时间(35.88±14.11) min、住院时间(9.78±2.48) d、治疗费用(16 074.91±1 964.48)元,与切开复位组手术时间(65.48±14.26) min、住院时间(15.88±2.00) d、治疗费用(20 451.27±1 760.2...