跗骨窦入路切开复位内固定与外侧"L"形入路切开复位内固定治疗跟骨骨折的疗效比较研究

目的:比较跗骨窦入路切开复位内固定与外侧"L"形入路切开复位内固定治疗跟骨骨折的疗效。方法:选取2016年10月到2017年6月期间川北医学院附属医院收治的86例跟骨骨折患者,根据随机数字表法分为对照组和观察组,两组均为43例。对照组采用外侧"L"形入路切开复位内固定进行治疗,观察组采用跗骨窦入路切开复位内固定进行治疗。比较两组患者的手术时间、住院时间、骨折愈合时间、踝-后足功能优良率、视觉模拟评分法(VAS)、B?hler角、Gissane角和术后并发症发生率。结果:两组患者的手术时间和骨折愈合时间比较无统计学差异(P0.05),而观察组患者的住院时间短于对照组(P0.05)。观察组患者术后踝-后足功能优良率高于对照组(P0.05)。在术前和术后12个月时,两组患者的VAS评分、Gissane角、B?hler角比较无统计学差异(P0.05),术后12个月时两组患者的VAS评分均明显低于术前,B?hler角及Gissane角明显高于术前(P0.05)。观察组患者术后并发症发生率低于对照组(P0.05)。结论:跗骨窦入路和外侧"L"形入路切开复位内固定均可有效治疗跟骨骨折,但跗骨窦入路可更有效地改善踝-后足功能,且住院时间短、术后并发症发生率更低。     

高血压患者颈动脉粥样硬化与血脂、血压和血尿酸水平的相关性分析

目的:探讨高血压患者颈动脉粥样硬化(CAS)与血脂、血压以及血尿酸水平的相关性。方法:选择2017年2月至2018年8月在我院就诊的高血压患者117例作为研究组,另选择同期在我院进行体检的健康志愿者50例作为对照组。采用彩色多普勒超声诊断仪测定所有受试者的颈动脉内中膜厚度(IMT),并根据研究组患者的颈动脉IMT将其分为斑块组(IMT≥1.3 mm,33例)、IMT增厚组(1.0 mm≤IMT1.3 mm,49例)和IMT正常组(IMT1.0 mm,35例)。比较研究组与对照组受试者IMT,同时分别比较研究组与对照组受试者以及不同IMT高血压患者平均收缩压(SBP)、平均舒张压(DBP)、血清总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)以及尿酸水平,并采用Pearson相关性分析法分析高血压患者IMT与各指标的相关性。结果:与对照组比较,研究组IMT、SBP、DBP、TC、TG、LDL-C、血尿酸水平升高,HDL-C水平降低,差异均有统计学意义(P0.05)。斑块组患者SBP、DBP、TC、TG、LDL-C、血尿酸水平高于IMT增厚组和IMT正常组,HDL-C水平低于IMT增厚组和IMT正常组,差异均有统计学意义(P0.05);IMT增厚组患者SBP、DBP、TC、TG、LDL-C、血尿酸水平高于IMT正常组,HDL-C水平低于IMT正常组,差异均有统计学意义(P0.05)。Pearson相关性分析显示,高血压患者的IMT与SBP、DBP、TC、TG、LDL-C、血尿酸均呈正相关,与HDL-C呈负相关(P0.05)。结论:高血压患者IMT与血脂、血压和血尿酸水平均有明显相关性,血压、血脂、血尿酸参与了高血压患者CAS的发生与发展。     

湖北地区健康成人网织红细胞相关参数参考区间的建立

目的:建立湖北地区健康成人网织红细胞相关参数的参考区间,以便更准确为临床提供服务。方法:选取我院体检中心751例健康体检者进行空腹静脉采血,采用迈瑞BC-6800血液分析仪进行网织红细胞相关参数检测,建立网织红细胞百分比(RET%)、网织红细胞绝对值(RET#)、低荧光网织红细胞百分比(LFR%)、中荧光网织红细胞百分比(MFR%)、高荧光网织红细胞百分比(HFR%)和幼稚网织红细胞百分比(IFR%)的参考区间。结果:RET%、RET#、LFR%、MFR%、HFR%和IFR%均呈非正态分布,建立的参考区间分别为:RET%:0.54～1.80;RET#:男0.029～0.098、女0.024～0.093;LFR%:男89.9～98.7、女92.4～98.8;MFR%:男1.3～9.6、女1.2～7.3;HFR%:男0～0.5、女0～0.1;IFR%:男1.3～10.3、女1.2～7.4。健康成人男性LFR%、MFR%、IFR%结果存在年龄组间显著性差异,女性未发现年龄组间存在差异性。结论:湖北地区健康成人网织红细胞6项相关参数的参考区间存在地区特异性、性别差异性以及年龄差异性。不同地区实验室应根据当地调查情况,适当的调整网织红细胞相关参数的参考区间,以便更准确的为临床提供判断标准。     

利伐沙班用于急性肺栓塞的抗凝效果及对血清Hcy、BNP、TnI与D-D水平的影响

目的:探讨利伐沙班用于急性肺栓塞的抗凝效果及对血清脑钠肽(Brain natriuretic peptide,BNP)、肌钙蛋白I (Troponin I,TnI)、D-二聚体(D-Dimer,D-D)、同型半胱氨酸(homocysteine,Hcy)水平的影响。方法:选择2014年2月至2017年12月在我院进行治疗的(高)中危组急性肺栓塞患者106例,并将其随机分为观察组和对照组。对照组皮下注射低分子肝素钙搭配华法林治疗,观察组予以利伐沙班治疗,观察和比较两组患者的临床疗效、治疗前后血清BNP、TnI、D-D、Hcy水平的变化及不良反应的发生情况。结果:治疗后,观察组患者总有效率为94.37%,显著高于对照组(42.10%,P0.05);观察组患者血清BNP、TnI、D-D、Hcy及肺动脉收缩压水平均显著低于对照组(P0.05),而动脉收缩压、动脉血氧分压水平较对照组水平显著升高(P0.05)。结论:利伐沙班应用于治疗急性肺栓塞的抗凝效果显著优于低分子肝素钙搭配华法林治疗,其可有效降低患者血清BNP、TnI、D-D、Hcy水平以及肺动脉收缩压。     

分泌性中耳炎患者外周血Th1Th2细胞及T淋巴细胞亚群水平的表达及临床意义

目的:探讨分泌性中耳炎(SOM)患者外周血T辅助细胞1(Th1)、T辅助细胞2(Th2)细胞因子及T淋巴细胞亚群水平的表达及其临床意义。方法:选取我院于2015年1月至2018年1月期间收治的SOM患者135例记为SOM组,根据病程将患者分为急性组(病程14d,49例)、亚急性组(病程14-30d,53例)、慢性组(病程30d,33例)。另外选择同期于我院进行体检的100例健康者为对照组。分别对比SOM组和对照组受试者、不同病程SOM患者外周血Th1细胞因子[干扰素(INF-γ)、白细胞介素-2(IL-2)]、Th2细胞因子[白细胞介素-4(IL-4)、白细胞介素-10(IL-10)]以及T淋巴细胞亚群[CD3~+、CD4~+、CD8~+、CD4~+/CD8~+]水平。采用Pearson相关性分析INF-γ、IL-2、IL-4、IL-10与CD3~+、CD4~+、CD8~+、CD4~+/CD8~+的相关性。结果:SOM组患者外周血INF-γ、IL-2、IL-4、IL-10水平高于对照组(P0.05);急性组患者外周血INF-γ、IL-2、IL-4、IL-10水平低于亚急性组、慢性组,亚急性组患者外周血INF-γ、IL-2、IL-4、IL-10水平低于慢性组(P0.05)。SOM组患者外周血CD3~+、CD4~+、CD4~+/CD8~+水平低于对照组,CD8~+水平高于对照组(P0.05);急性组患者外周血CD3~+、CD4~+、CD4~+/CD8~+水平高于亚急性组、慢性组,CD8~+水平低于亚急性组、慢性组,亚急性组患者外周血CD3~+、CD4~+、CD4~+/CD8~+水平高于慢性组,CD8~+水平低于慢性组(P0.05)。Pearson相关性分析结果显示,SOM患者外周血INF-γ、IL-4与CD8~+呈正相关(P0.05),IL-4与CD3~+、CD4~+呈负相关(P0.05)。结论:SOM患者外周血Th1Th2细胞因子、T淋巴细胞亚群水平均表现异常,且其水平与疾病发生和发展存在一定联系,通过监测Th1Th2细胞因子、T淋巴细胞亚群有助于评估SOM患者病情。     

Haemophilus parasuis infection in 3D4/21 cells induces autophagy through the AMPK pathway

Haemophilus parasuis (H. parasuis) is a common commensal in the upper respiratory tract of pigs, but causes Glässer's disease in stress conditions. To date, many studies focused on the immune evasion and virulence of H. parasuis; very few have focused on the role autophagy played in H. parasuis infection, particularly in porcine alveolar macrophages (PAMs). In this study, a PAM cell line, 3D4/21 cells were used to study the role of autophagy in H. parasuis infection. 3D4/21 cells tandemly expressing GFP, mCherry, and LC3 were infected with H. parasuis serovar 5 (Hps5). Western blot analysis and confocal and transmission electron microscopy showed that H. parasuis infection effectively induces autophagy. Using Hps strains of varying virulence (Hps4, Hps5, and Hps7) and UV‐inactivated Hps5, we demonstrated that autophagy is associated with the internalisation of living virulent strains into cells. In 3D4/21 cells pretreated with rapamycin and 3‐MA then infected by Hps4, Hps5, and Hps7, we demonstrated that autophagy affects invasion of H. parasuis in cells. AMPK signal results showed that Hps5 infection can upregulate the phosphorylation level of AMPK, which is consistent with the autophagy development. 3D4/21 cells pretreated with AICAR or Compound C then infected by Hps5 revealed that the autophagy induced by Hps5 infection is associated with the AMPK pathway. Our study contributes to the theoretical basis for the study of H. parasuis pathogenesis and development of novel drugs target for prevention Glässer's disease.     

Dysregulated haemolysin promotes bacterial outer membrane vesicles‐induced pyroptotic‐like cell death in zebrafish

Inflammasomes are important innate immune components in mammals. However, the bacterial factors modulating inflammasome activation in fish, and the mechanisms by which they alter fish immune defences, remain to be investigated. In this work, a mutant of the fish pathogen Edwardsiella piscicida (E. piscicida), called 0909I, was shown to overexpress haemolysin, which could induce a robust pyroptotic‐like cell death dependent on caspase‐5‐like activity during infection in fish nonphagocyte cells. E. piscicida haemolysin was found to mainly associate with bacterial outer membrane vesicles (OMVs), which were internalised into the fish cells via a dynamin‐dependent endocytosis and induced pyroptotic‐like cell death. Importantly, bacterial immersion infection of both larvae and adult zebrafish suggested that dysregulated expression of haemolysin alerts the innate immune system and induces intestinal inflammation to restrict bacterial colonisation in vivo. Taken together, these results suggest a critical role of zebrafish innate immunity in monitoring invaded pathogens via detecting the bacterial haemolysin‐associated OMVs and initiating pyroptotic‐like cell death. These new additions to the understanding of haemolysin‐mediated pathogenesis in vivo provide evidence for the existence of noncanonical inflammasome signalling in lower vertebrates.     

Perivascular adipose tissue‐derived stromal cells contribute to vascular remodeling during aging

Aging is an independent risk factor for vascular diseases. Perivascular adipose tissue (PVAT), an active component of the vasculature, contributes to vascular dysfunction during aging. Identification of underlying cell types and their changes during aging may provide meaningful insights regarding the clinical relevance of aging‐related vascular diseases. Here, we take advantage of single‐cell RNA sequence to characterize the resident stromal cells in the PVAT (PVASCs) and identified different clusters between young and aged PVASCs. Bioinformatics analysis revealed decreased endothelial and brown adipogenic differentiation capacities of PVASCs during aging, which contributed to neointimal hyperplasia after perivascular delivery to ligated carotid arteries. Mechanistically, in vitro and in vivo studies both suggested that aging‐induced loss of peroxisome proliferator‐activated receptor‐γ coactivator‐1 α (PGC1α) was a key regulator of decreased brown adipogenic differentiation in senescent PVASCs. We further demonstrated the existence of human PVASCs (hPVASCs) and overexpression of PGC1α improved hPVASC delivery‐induced vascular remodeling. Our finding emphasizes that differentiation capacities of PVASCs alter during aging and loss of PGC1α in aged PVASCs contributes to vascular remodeling via decreased brown adipogenic differentiation.