Early proteome analysis of rat pancreatic acinar AR42J cells treated with taurolithocholic acid 3-sulfate

BackgroundBile acids are the initiating factors of biliary acute pancreatitis. Bile acids can induce the activation of intracellular zymogen, thus leading injury in pancreatic acinar cells. Pathological zymogen activation in pancreatic acinar cells is a common feature of all types of acute pancreatitis. The proteins expressed in pancreatic acinar cells during the activation of zymogen may determine the severity of acute pancreatitis. The present study aims to determine the differentially expressed proteins in taurolithocholic acid 3-sulfate-stimulated pancreatic acinar cells as an in vitro model for acute pancreatitis.MethodsRat pancreatic acinar AR42J cells were treated with taurolithocholic acid 3-sulfate for 20 min. Laser confocal scanning microscopy and flow cytometry were used to detect activated trypsinogen in pancreatic acinar AR42J cells. After the determination of trypsinogen activation, proteome analysis was performed to identify the proteins differentially expressed in taurolithocholic acid 3-sulfate-treated cells and non-treated cells.ResultsAfter treatment with taurolithocholic acid 3-sulfate for 20 min, the activation of trypsinogen in AR42J cells was concurrent with changes in the protein expression profile. Thirty-nine differentially expressed proteins were detected; among these, 23 proteins were up-regulated and 16 proteins were down-regulated. KEGG analysis indicated that these proteins are involved in cellular metabolic pathways, cellular defensive mechanisms, intracellular calcium regulation and cytoskeletal changes.ConclusionThe expression of proteins in the pancreatic acinar cell changes at the early stage of biliary acute pancreatitis. These differentially expressed proteins will provide valuable information to understand the pathophysiologic mechanism biliary acute pancreatitis and may be useful for prognostic indices of acute pancreatitis.     

儿童复发性分泌性中耳炎致病因素meta分析

目的明确儿童复发性分泌性中耳炎(OME)的高危致病因素,为指导复发性OME的治疗提供依据。方法检索英文PubMed、MEDLINE和EMBASE及中文中国期刊全文数据库(CNKI)、中国科技期刊全文数据库(VIP)、万方数据库,收集各个数据库建库至2020年5月1日已发表的文献。检索策略:英文检索(pediatric or children)AND(recurrent otitis media with effusion or refractory otitis media with effusion or recurrent OME or refractory OME);中文检索(儿童)AND(复发性分泌性中耳炎OR难治性分泌性中耳炎)。结果共纳入符合检索策略的文献15篇,总研究例数1867例,反复上呼吸道感染合并OR值为4.67(95%CI为2.97~7.36),性别合并OR值为1.18(95%CI为0.80~1.73),吸烟环境合并OR值为0.91(95%CI为0.67~1.22),腭裂合并OR值为3.80(95%CI为2.50~5.79)。结论儿童复发性OME的高危因素主要包括反复上呼吸道感染和腭裂2类。对于有高危因素的复发性OME患儿,建议延长鼓膜置管留置时间至12个月以上,以最大程度降低复发率。     

HMGA1在葡萄膜黑色素瘤中的表达及对细胞增殖和侵袭的影响

目的：探讨高迁移率族蛋白A1(HMGA1)蛋白在葡萄膜黑色素瘤(UM)组织中的表达,以及抑制该基因表达对细胞增殖和侵袭的影响。

方法：选取2014-02/2019-08在我院接受手术治疗的UM患者53例53眼,同期留取因外伤摘除眼球的正常葡萄膜组织34例34眼。采用免疫组织化学法检测组织中HMGA1蛋白表达。将体外培养的人UM细胞系M23分为HMGA1下调组、阴性对照组和空白组,分别转染HMGA1干扰序列、阴性对照序列和不作任何处理,采用实时荧光定量PCR术检测HMGA1 mRNA表达,CCK-8法检测细胞增殖能力,Transwell法检测细胞迁移和侵袭能力。

结果：UM组织中HMGA1蛋白阳性表达率为77%,高于正常葡萄膜组织中的29%(P<0.001); 与未发生巩膜浸润、未累及睫状体和未发生眼外生长相比,HMGA1蛋白在发生巩膜浸润、累及睫状体和发生眼外生长的组织中阳性表达率升高(均P<0.05)。与阴性对照组和空白组相比,HMGA1 mRNA在HMGA1下调组细胞中相对表达量降低,且HMGA1下调组细胞培养24、48、72、96h时吸光度OD值降低,迁移细胞数和侵袭细胞数均明显减少(均P<0.05)。

结论：UM组织中HMGA1蛋白阳性表达率升高,下调M23细胞中HMGA1表达可减少细胞增殖,抑制细胞迁移和侵袭。     

Secular trends in the etiology and comorbidity of hospitalized patients with congestive heart failure: A single-center retrospective study

Objective To assess the secular trends in the etiology and comorbidity of patients hospitalized with congestive heart failure (CHF)．Methods Data of 7319 patients (mean age 59.6 years, 62.1% male) with a primary discharge diagnosis of CHF, hospitalized from January 1, 1993, to December 31, 2007, at the Chinese People’s Liberation Army (PLA) General Hospital were extracted and analyzed. These patients were divided into three groups according to hospitalization period: 1993–1997 (n = 1623), 1998–2002 (n = 2444), and 2003–2007 (n = 3252). The etiological characteristics and comorbidities were assessed. Results　Over the study period, the proportion of patients with ischemic heart disease (IHD) increased from 37.2% during the period 1993–1997 to 46.8% during the period 2003–2007, while that with valvular heart disease (VHD) decreased (from 35.2% during the period 1993–1997 to 16.6% during the period 2003–2007, both P < 0.05); Atrial fibrillation (AF) was the most common comorbidity of heart failure (23.2%, 23.0% and 20.6%, respectively, in the three periods); Compared to that of the period of 1993–1997 with that of, the proportion of patients with myocardial infarction, pneumonia, renal function impairment and hepatic cirrhosis of the period of 2003–2007 increased significantly (P < 0.05) and the proportion of patients with chronic obstructive pulmonary disease and atrial fibrillation decreased significantly (P < 0.05). Conclusions This study implies that IHD has became a more common etiology of CHF, while VHD has deceased as an etiology of CHF in Chinese patients during the last two decades.     

儿童近视进展与眼底血流及脉络膜厚度的关系

目的：探讨儿童近视进展过程中眼底血流及脉络膜厚度的变化。方法：前瞻性研究。招募2018 年 7—9月就诊于温州医科大学附属眼视光医院的低中度近视儿童,随访观察其1年的屈光度数及眼轴 长度（AL）变化,以评估其近视进展。同期采用扫频源光学相干断层扫描血流成像（SS-OCTA）技术 进行黄斑区3 mm×3 mm扫描。采用扫频光学相干断层成像（SS-OCT）技术进行黄斑区6 mm×6 mm 放射状扫描,并采集随访观察1年前后受检者右眼黄斑中心凹,中心凹上、下、鼻、颞侧的脉络膜厚 度以及浅层和深层视网膜及脉络膜毛细血管层的血流密度。取受检者右眼数据进行统计分析。采 用配对t检验、Pearson相关性及简单线性回归进行统计学分析。结果：共纳入47例（47眼）受检儿童, 男21例,女26例,年龄为（11.1±1.3）岁。1年后随访,平均等效球镜度（SE）由（-2.59±0.93）D增至 （-3.09±0.96）D（t=11.12,P<0.001）;AL由（24.75±0.86）mm增长至（24.91±0.84）mm（t=12.25, P<0.001）;脉络膜厚度由（238±54）μm减小至（231±55）μm（t=2.67,P=0.011）;视网膜浅层、深层及 脉络膜毛细血管层血流密度均出现明显下降（t=6.66,P<0.001;t=3.38,P=0.002;t=3.18,P=0.003）。 视网膜浅层、深层血流密度变化量与近视度数增加量之间存在线性相关（r=0.35,P=0.02;r=0.37, P=0.01）。结论：近视儿童在近视进展过程中,脉络膜厚度变薄,视网膜及脉络膜血流密度降低,推 测此类眼底变化可能在近视进展过程中起到一定作用。     

Deterioration of Avellino corneal dystrophy in a Chinese family after LASIK

AIM: To evaluate macular microvasculature changes in eyes after pars plana vitrectomy (PPV) and intraocular silicone oil (SO) tamponade for macula-off rhegmatogenous retinal detachment (RRD) using optical coherence tomography angiography (OCTA). METHODS: Totally 19 eyes (19 patients) with macula-off RRD who underwent PPV and intraocular SO tamponade were retrospectively reviewed. The parafoveal superficial capillary plexus (SCP) vessel density (VD), deep capillary plexus (DCP) VD, choriocapillaris plexus (CCP) VD, and foveal macular thickness were evaluated using OCTA throughout 16wk postoperatively. The values of healthy fellow eyes were used as control. RESULTS: The parafoveal SCP, DCP, and CCP VDs were significant increased over time in RRD eyes during the 12wk postoperatively, then decreased at 16wk postoperatively (all P<0.001). The ratios of RRD eyes and fellow healthy eyes (r/f ratios) of the SCP and DCP VDs were lower than those of the CCP VD postoperatively (all P<0.05). There were not significant differences in the r/f ratios between SCP and DCP VDs postoperatively (all P>0.05). CONCLUSION: The parafoveal SCP, DCP, and CCP VDs gradually recover over time after PPV surgery with SO tamponade. Long-time SO tamponade might decrease postoperative macular VDs. Compared to parafoveal CCP VD, the parafoveal SCP and DCP VDs were more vulnerable in RRD eyes postoperatively.