关节镜下同期行冻结肩松解术对肩袖损伤患者的治疗效果评估

目的:评估关节镜下同期行冻结肩松解术对肩袖损伤患者的治疗效果。方法:选择2015年3月到2018年3月在我院诊治的肩袖损伤患者70例进行研究,按随机数表法将其分为观察组(n=36)和对照组(n=34)。对照组采用传统小切口肩袖修复术治疗,观察组采用关节镜下同期行冻结肩松解术进行治疗。比较两组治疗后疗效、手术时间、术中出血量、住院时间、疼痛减轻时间、治疗前后VAS、美国肩肘外科协会评分(ASES)、Contant-Muley评分的变化情况。结果:治疗后,观察组总有效率为94.44%,显著高于对照组(73.53%,P0.05);观察组手术时间、术中出血量、住院时间及疼痛减轻时间均显著低于对照组(P0.05);两组VAS、ASES、Contant-Muley评分较治疗前均显著改善(P0.05),且观察组VAS评分明显低于对照组,ASES及Contant-Muley评分显著高于对照组(P0.05)。结论:关节镜下同期行冻结肩松解术治疗肩袖损伤的临床疗效显著优于传统小切口肩袖修复术治疗,其可显著促进关节功能恢复,并减轻患者痛苦。     

单孔、两孔及三孔胸腔镜下早期非小细胞肺癌根治术的效果比较研究

目的:通过比较不同胸腔镜手术方式治疗早期非小细胞肺癌根治术术后的相关临床指标,为临床手术方式提供经验。方法:收集我院2017年1月～2019年12月收治的行肺癌根治术的早期非小细胞肺癌病例共100例,分别采用单孔胸腔镜(40例),两孔胸腔镜(32例)及三孔胸腔镜(28例)手术方式,比较三组手术术中及术后的相关指标。结果:单孔胸腔镜组术中出血量、术后引流量明显少于两孔胸腔镜组和三孔胸腔镜组(P0.05),而两孔胸腔镜组明显少于三孔胸腔镜组(P0.05);单孔胸腔镜组术后胸管留置时间和术后住院时间均短于两孔胸腔镜组和三孔胸腔镜组(P0.05),而两孔胸腔镜组明显短于三孔胸腔镜组(P0.05)。三组组内疼痛评分术后24h低于术后12h,术后48h低于术后24h,差异均有统计学意义(P0.05)。三组组间不同时间点疼痛评分比较发现,单孔胸腔镜组疼痛评分低于两孔胸腔镜组和三孔胸腔镜组(P0.05),而两孔胸腔镜组低于三孔胸腔镜组(P0.05)。三组清扫淋巴结数目、淋巴结站数和术后并发症发生率差异均无统计学意义(P0.05)。结论:单孔胸腔镜早期非小细胞肺癌根治术与两孔、三孔胸腔镜手术相比优势明显,且不会显著增加术后并发症,可作为临床首选。     

食管癌调强放射治疗的初期疗效及急性放射性肺损伤的影响因素分析

摘要 目的：探讨食管癌调强放射治疗的初期疗效及急性放射性肺损伤的影响因素。方法：选取2015年1月-2019年1月在我院进行调强放射治疗的食管癌患者322例,评价食管癌调强放射治疗后一个月的疗效;按照是否发生急性放射性肺损伤（RILI）分为急性RILI组和无急性RILI组,采用多因素Logistic回归分析分析急性RILI的影响因素。结果：调强放射治疗的完全缓解和部分缓解的患者占98.45%;322例患者中90例（27.95%）出现急性RILI,其中36例（11.18%）出现2级及以上的急性RILI;急性RILI组和无急性RILI组间卡氏（KPS）评分、淋巴结转移、基础肺疾病、V5、V10、V20、V30和全肺平均剂量（MLD）差异有统计学意义（P<0.05）;多因素Logistic回归分析显示,KPS评分<80分、有淋巴结转移、有基础肺疾病,V5≥60%、V10≥40%、V20≥28%、V30≥20%和MLD≥10Gy是食管癌调强放射治疗后急性放射性肺损伤的危险因素（P<0.05）。结论：使用调强放射治疗技术治疗食管癌的初期疗效较好,治疗过程中,应充分考虑病患的临床特征,优化放疗方案和靶区,减少急性RILI的发生,提高食管癌患者放疗后的生存质量。     

最大等速离心运动诱发肌肉损伤程度与肌酸激酶水平的关系

为探讨人体进行最大等速离心运动(ECC)诱发血液肌酸激酶(CK)水平变化、血清肌酸激酶水平与肌肉损伤(EIMD)的关系,本研究筛选出150名"缺乏运动"的健康大学生为受试者,进行血样采集,进行前测包括血清肌酸激酶(CK)、最大等长肌力(MVC)、肘关节活动角度(ROM)、上臂围(CIR)、肌肉感受(VAS)。受试者进行5组×12次最大等速离心运动,运动后恢复期,将全部受试者血清肌酸激酶值进行排序:血清肌酸激酶值最高和最低20%样本,高肌酸激酶水平组(HCK组)和低肌酸激酶水平组(low LCK组),利用SPSS18.0统计学软件,以方差分析和多元回归分析进行统计分析。本研究发现全部受试者、高肌酸激酶水平组、低肌酸激酶水平组在最大等速离心运动后各评估指标均显著高于比前测结果,p<0.05。全部受试者、高肌酸激酶水平组受试者在最大等速离心运动后各指标变化皆明显大于低肌酸激酶水平组受试者,p<0.05。受试者血清肌酸激酶峰值与最大等长肌力、肘关节活动角度、上臂围、肌肉感受最大变化值有相关,p<0.05。本研究认为肌肉损伤程度与肌酸激酶水平具有显著相关,尤其高血清肌酸激酶水平者肌酸激酶水平较大程度反映肌肉损伤程度趋势。本研究表明,肘关节活动角度、上臂围具有预测肌酸激酶峰值的效果。     

血栓通注射液对暂时性和永久性大鼠脑缺血模型的神经保护作用

血栓通注射液(冻干)(XST)是一种从三七中提取的中草药标准化产品,广泛用于临床治疗急性脑梗塞等脑血管疾病。本研究评估了XST在不同大鼠脑缺血模型中的急性和延长保护作用,并探讨了其对过氧化物酶(Prx) 6-toll样受体(TLR) 4信号通路的影响。用XST处理抑制过氧化物酶(Prx) 6-toll样受体(TLR) 4的蛋白质表达和p38的磷酸化水平,并且上调STAT3的磷酸化水平。XST治疗3 d可显著降低暂时性大脑中动脉阻塞(MCAO)诱导的梗死体积和肿胀百分比,并调节白细胞介素-1β(IL-1β)、IL-17、IL-23p19、肿瘤坏死因子-α(TNFα)和诱导型一氧化氮合酶(iNOS)。在永久MCAO大鼠中,XST可以减少梗死体积和肿胀百分比。XST治疗还可以增加大鼠的体重并改善一批功能结果。XST可以保护暂时性和永久性MCAO大鼠的缺血性损伤可能与Prx6-TLR4途径有关。     

RHCG基因在非小细胞肺癌中的表达及对细胞增殖的影响

为了探讨Rh type C glycoprotein (RHCG)对非小细胞肺癌(non-small cell lung cancer,NSCLC)细胞增殖的影响及可能的作用机制,本研究使用荧光定量PCR法检测12对NSCLC及癌旁组织样本中RHCG mRNA的表达水平及pcDNA3.1-RHCG质粒对A549细胞RHCG m RNA的表达;采用CCK-8法检测细胞增殖能力;运用PI染色法检测细胞周期;使用免疫印迹法检p-PI3K、PI3K、p-AKT以及AKT蛋白表达水平。本研究发现,与癌旁组织比较,NSCLC中RHCG m RNA表达水平明显降低。RHCG过表达能抑制NSCLC细胞系A549细胞增殖能力。此外,RHCG过表达使A549细胞周期G1/S期转化发生阻滞。本研究还发现,RHCG过表达可下调A549细胞p-PI3K/PI3K和p-AKT/AKT水平。本研究表明,RHCG抑制NSCLC细胞增殖的作用与其抑制PI3K/AKT信号通路有关。     

秋葵籽油对高强度运动所致肝损伤的保护作用

本研究考察了秋葵籽油对高强度运动所致肝损伤的保护作用及机制。研究显示,对昆明小鼠灌胃不同剂量(10 mg/kg,20 mg/kg和50 mg/kg)的秋葵籽油4周后,秋葵籽油以剂量依赖性方式提高了小鼠的力竭游泳时间(p<0.05)。秋葵籽油降低了小鼠血清乳酸和尿素氮水平,并升高了血清游离脂肪酸和肝糖原水平(p<0.05)。秋葵籽油以剂量依赖性方式提高了小鼠肝脏组织中SOD、CAT和GSH-Px活性,并抑制了MDA的合成(p<0.05)。秋葵籽油抑制了力竭游泳诱导的小鼠血清CK、AST和ALT水平及肝脏组织NO水平的升高(p<0.05)。此外,苏木精和伊红(HE)染色证实了秋葵籽油减轻了力竭游泳诱导的肝脏病理改变。因此,本研究初步结论表明,在高强度运动过程中,秋葵籽油可通过抑制乳酸和尿素氮的积累、增加脂肪动员、降低糖原消耗、减弱氧化应激损伤等多种途径来对肝脏发挥保护作用。     

Hepatoprotective effect of pyrroloquinoline quinone against alcoholic liver injury through activating Nrf2-mediated antioxidant and inhibiting TLR4-mediated inflammation responses

The present study was aimed at investigating the hepatoprotective effect of pyrroloquinoline quinone (PQQ) against acute alcoholic liver injury in mice. Acute alcoholic liver injury model was established in mice, and they were administrated with PQQ to investigate its hepatoprotective effect. Our results shows that PQQ can significantly ameliorate acute alcoholic liver injury by decreasing the hepatic marker enzymes, including serum alanine transaminase (ALT) and aspartate transaminase (AST), and increasing the levels of alcohol dehydrogenase (ADH), aldehyde dehydrogenase (ALDH), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) in the liver. And PQQ can also significantly reduce the content of hepatic triglyceride (TG) and malondialdehyde (MDA). Moreover, PQQ attenuated alcohol-induced oxidative damage by activating NF-E2-related factor 2 (Nrf2)-mediated signaling pathway, and inhibiting Toll-like receptor 4 (TLR4)-mediated nuclear factor-kappa B (NF-κB) signaling pathway. Our findings have elucidated the liver protection mechanism of PQQ, which would encourage the further exploitation of PQQ as a hepatoprotective functional food.     

Cell senescence contributes to tissue regeneration in zebrafish

Cellular senescence is a stress response that limits the proliferation of damaged cells by establishing a permanent cell cycle arrest. Different stimuli can trigger senescence but excessive production or impaired clearance of these cells can lead to their accumulation during aging with deleterious effects. Despite this potential negative side of cell senescence, its physiological role as a pro‐regenerative and morphogenetic force has emerged recently after the identification of programmed cell senescence during embryogenesis and during wound healing and limb regeneration. Here, we explored the conservation of tissue injury‐induced senescence in a model of complex regeneration, the zebrafish. Fin amputation in adult fish led to the appearance of senescent cells at the site of damage, and their removal impaired tissue regeneration. Despite many conceptual similarities, this tissue repair response is different from developmental senescence. Our results lend support to the notion that cell senescence is a positive response promoting tissue repair and homeostasis.     

Intrinsically altered lung‐resident γδT cells control lung melanoma by producing interleukin‐17A in the elderly

Cancer is an age‐associated disease, potentially related to the altered immune system of elderly individuals. However, cancer has gradually decreased incidence in the eldest globally such as the most common lung cancer, the mechanisms of which remain to be elucidated. In this study, it was found that the number of lung‐resident γδT cells was significantly increased with altered gene expression in aged mice (20–24 months) versus young mice (10–16 weeks). Aged lung Vγ4⁺ and Vγ6⁺ γδT cells predominantly produced interleukin‐17A (IL‐17A), resulting in increased levels in the serum and lungs. Moreover, the aged mice exhibited smaller tumors and reduced numbers of tumor foci in the lungs after challenge with intravenous injection of B16/F10 melanoma cells compared with the young mice. Aged lung Vγ4⁺ and Vγ6⁺ γδT cells were highly cytotoxic to B16/F10 melanoma cells with higher expression levels of CD103. The markedly longer survival of the challenged aged mice was dependent on γδT17 cells, since neutralization of IL‐17A or depletion of indicated γδT cells significantly shortened the survival time. Consistently, supplementation of IL‐17A significantly enhanced the survival time of young mice with lung melanoma. Furthermore, the anti‐tumor activity of aged lung γδT17 cells was not affected by alterations in the load and composition of commensal microbiota, as demonstrated through co‐housing of the aged and young mice. Intrinsically altered lung γδT17 cells underlying age‐dependent changes control lung melanoma, which will help to better understand the lung cancer progression in the elderly and the potential use of γδT17 cells in anti‐tumor immunotherapy.