右美托咪定复合罗哌卡因对膝关节置换术后镇痛镇静效果、睡眠质量及应激反应的影响

目的:探讨右美托咪定复合罗哌卡因对膝关节置换术后的临床效果。方法:选取2015年2月～2018年12月期间在武警陕西省总队医院择期行膝关节置换术患者103例,根据随机数字表将患者分成对照组(n=51)和研究组(n=52),对照组股神经阻滞时给予罗哌卡因,研究组在对照组基础上联合右美托咪定。比较两组患者镇痛镇静效果、睡眠质量、应激反应以及不良反应。结果:研究组术后12 h、术后24 h、术后48 h视觉模拟评分(VAS)低于对照组(P0.05),Ramsay镇静评分则高于对照组(P0.05)。研究组术后24 h、术后48 h阿森斯失眠量表(AIS)评分均低于术前,且呈先降低后升高趋势(P0.05)。研究组术后24 h、术后48 h AIS评分低于对照组(P0.05)。两组患者手术开始即刻、术毕的去甲肾上腺素(NE)、肾上腺素(E)水平均上升,且呈先升高后降低趋势(P0.05);研究组手术开始即刻、术毕的NE、E水平低于对照组(P0.05)。两组不良反应发生率对比无统计学差异(P0.05)。结论:右美托咪定复合罗哌卡因方案应用于膝关节置换术,镇痛镇静效果确切,可减轻术中应激反应,有效改善睡眠质量,且不增加不良反应发生率,临床应用价值较高。     

妇科盆腔恶性肿瘤血常规检测结果分析

目的:了解妇科盆腔恶性肿瘤血常规变化及其临床意义。方法:以无锡市人民医院2018年1月～2019年3月收治的90例妇科盆腔恶性肿瘤患者作为病例组,同期住院的243例确诊为盆腔良性病变或妊娠状态的患者作为良性对照组,选取同期717名接受体检的成年女性作为健康对照组,对三组研究对象的血常规指标进行回顾性分析。结果:与健康对照组比较,良性对照组和病例组患者的嗜酸性粒细胞百分比(EO)、嗜酸性粒细胞计数(EO#)、红细胞压积(HCT)、血红蛋白水平(HGB)、淋巴细胞百分比(LY)、淋巴细胞计数(LY#)、红细胞平均血红蛋白浓度(MCHC)、血小板分布宽度(PDW)、红细胞计数(RBC)水平降低,单核细胞计数(MO#)、血小板平均体积(MPV)、中性粒细胞百分比(NE)、中性粒细胞计数(NE#)、红细胞分布宽度(RDW)、白细胞计数(WBC)水平升高;病例组患者EO、EO#、LY、LY#、MO#、MPV水平低于良性对照组,HCT、HBG、MCHC、PDW、NE、NE#、RDW水平高于良性对照组,同时,病例组患者的红细胞平均血红蛋白含量(MCH)、红细胞平均体积(MCV)水平高于健康对照组,健康对照组的MCH、MCV水平高于良性对照组,良性对照组患者的单核细胞百分比(MO)、血小板压积(PCT)水平高于健康对照组,健康对照组的MO、PCT水平高于病例组,差异均有统计学意义(P0.05)。Logistic多元回归分析结果显示,LY#、MO#、MCHC、RDW、MCH、MCV与盆腔恶性肿瘤的发生具有相关性(P0.05)。ROC曲线分析结果显示,在各项血常规指标中,MCV诊断妇产科盆腔恶性肿瘤的曲线下面积(AUC)最高,为0.683。结论:盆腔恶性肿瘤患者的血常规指标与良性病变患者和健康人群均存在差异,部分指标与恶性肿瘤的发生具有独立相关性。     

RPN2与肝癌患者预后及对肝癌细胞生长的作用

目的:探讨核糖蛋白2(ribophorin II,RPN2)在肝细胞肝癌(HCC)组织中的表达和对HCC患者生存的影响,同时分析RPN2对肝癌HepG2细胞生长和克隆形成的作用。方法:应用免疫组化方法和HCC公共芯片数据,从蛋白和m RNA水平检测HCC组织中RPN2的表达,同时分析RPN2与HCC患者临床参数的关系及预后相关性;进一步利用MTS法和克隆形成实验在肝癌HepG2细胞中检测RPN2对细胞生长的作用。结果:98例肝癌组织中,RPN2阳性表达率88.78%,对应癌旁肝组织中,RPN2阳性表达率74.49%;癌组织中RPN2染色评分为5.80±3.15,癌旁肝组织RPN2染色评分为2.13±1.59,肝癌组织中RPN2表达显著上调(P0.001)。3个肝癌公共芯片数据(共522例肝癌)中RPN2的m RNA表达水平同样显著升高(均P0.001)。98例肝癌患者RPN2表达水平与肿瘤直径(P=0.004)、门脉侵袭(P=0.012)和TNM分期(P=0.009)相关;RPN2高表达的患者总体生存期(OS)和无复发生存期(RFS)较RPN2低表达的患者短(OS:P=0.027;RFS:P=0.036)。肝癌HepG2细胞转染RPN2小干扰RNA后,细胞生长能力显著受抑制。结论:RPN2在肝癌中表达显著升高,RPN2的表达与肝癌的恶性进展有关,RPN2显著促进肝癌细胞生长。     

miR-195通过靶向调控趋化因子5促进胃癌细胞增殖、转移及侵袭的实验研究

目的:研究miR-195通过靶向调控趋化因子5促进胃癌细胞增殖、转移及侵袭的分子机制。方法:选取MGC803及NCI-N87细胞,根据转染不同分为:miR-NC组(空质粒),miR-195-mimics组(模拟序列)。实时荧光定量PCR法检测miR-195表达;MTT检测细胞增殖能力;Transwell侵袭实验检测细胞侵袭力;细胞划痕实验检测细胞转移能力;流式细胞术检测细胞凋亡情况;Western blot检测chemokine 5表达水平;Spearman相关分析miR-195及chemokine 5相关性。荧光素酶实验验证miR-195与chemokine 5的靶向关系。结果:miR-195-mimics组细胞miR-195水平高于miR-NC组(P0.05);miR-195 mimics组第1、2、3、4 d细胞活力低于miR-NC组(P0.05);miR-195 mimics组G1细胞高于miR-NC组,G2期、S期细胞低于miR-NC组,G2/S期细胞比值低于miR-NC组(P0.05);miR-195 mimics组划痕距离大于miR-NC组(P0.05);miR-195 mimics组细胞侵袭数低于miR-NC组(P0.05);miR-195-mimics组细chemokine 5蛋白含量低于miR-NC组(P0.05);miR-195 m RNA水平与chemokine 5蛋白含量负相关(r=-0.398,P=0.00);miR-195可直接靶向chemokine 5。结论:miR-195可通过靶向chemokine 5促进胃癌MGC803及NCI-N87细胞的增殖、转移及侵袭。     

Could urinary ACE2 protein level help identify individuals susceptible to SARS-CoV-2 infection and complication?

Science China Life Sciences -     

Diverse Roles of the Salicylic Acid Receptors NPR1 and NPR3/NPR4 in Plant Immunity

The plant defense hormone salicylic acid (SA) is perceived by two classes of receptors, NPR1 and NPR3/NPR4. They function in two parallel pathways to regulate SA-induced defense gene expression. To better understand the roles of the SA receptors in plant defense, we systematically analyzed their contributions to different aspects of Arabidopsis (Arabidopsis thaliana) plant immunity using the SA-insensitive npr1-1 npr4-4D double mutant. We found that perception of SA by NPR1 and NPR4 is required for activation of N-hydroxypipecolic acid biosynthesis, which is essential for inducing systemic acquired resistance. In addition, both pattern-triggered immunity (PTI) and effector-triggered immunity (ETI) are severely compromised in the npr1-1 npr4-4D double mutant. Interestingly, the PTI and ETI attenuation in npr1-1 npr4-4D is more dramatic compared with the SA-induction deficient2-1 (sid2-1) mutant, suggesting that the perception of residual levels of SA in sid2-1 also contributes to immunity. Furthermore, NPR1 and NPR4 are involved in positive feedback amplification of SA biosynthesis and regulation of SA homeostasis through modifications including 5-hydroxylation and glycosylation. Thus, the SA receptors NPR1 and NPR4 play broad roles in plant immunity.     

Tripartite motif protein 52 (TRIM52) promoted fibrosis in LX‐2 cells through PPM1A‐mediated Smad2/3 pathway

To investigate the roles of tripartite motif containing 52 (TRIM52) in human hepatic fibrosis in vitro, human hepatic stellate cell line LX‐2 cells were transfected with hepatitis B virus (HBV) replicon to establish HBV‐induced fibrosis in LX‐2 cells, and then treated with small interfering RNA‐mediated knockdown of TRIM52 (siTRIM52). LX‐2 cells without HBV replicon transfection were treated with lentiviruses‐mediated overexpression of TRIM52 and phosphatase magnesium dependent 1A (PPM1A). Fibrosis response of LX‐2 cells were assessed by the production of hydroxyproline (Hyp) and collagen I/III, as well as protein levels of α‐smooth muscle actin (α‐SMA). PPM1A and phosphorylated (p)‐Smad2/3 were measured to assess the mechanism. The correlation between TRIM52 and PPM1A was determined using co‐immunoprecipitation, and whether and how TRIM52 regulated the degradation of PPM1A were determined by ubiquitination assay. Our data confirmed HBV‐induced fibrogenesis of LX‐2 cells, as evidenced by significant increase in Hyp and collagen I/III and α‐SMA, which was associated with reduction of PPM1A and elevation of transforming growth factor‐β (TGF‐β), p‐Smad2/3, and p‐Smad3L. However, those changes induced by HBV were significantly attenuated with additional siTRIM52 treatment. Similar to HBV, overexpression of TRIM52 exerted promoted effect in the fibrosis of LX‐2 cells. Interestingly, TRIM52 induced the fibrogenesis of LX‐2 cells and the activation of TGF‐β/Smad pathway were significantly reversed by PPM1A overexpression. Furthermore, our data confirmed TRIM52 as a deubiquitinase that influenced the accumulation of PPM1A protein, and subsequently regulated the fibrogenesis of LX‐2 cells. TRIM52 was a fibrosis promoter in hepatic fibrosis in vitro, likely through PPM1A‐mediated TGF‐β/Smad pathway.     

MicroRNA‐93‐5p expression in tumor tissue and its tumor suppressor function via targeting programmed death ligand‐1 in colorectal cancer

This work aimed to investigate miR‐93‐5p expression in tumor tissue and its in vitro effects in colorectal cancer (CRC) by targeting programmed death ligand‐1 (PD‐L1). MiR‐93‐5p and PD‐L1 expression was detected in CRC and adjacent normal tissues by quantitative real‐time polymerase chain reaction and immunohistochemistry. The correlation between miR‐93‐5p and PD‐L1 was validated by a dual‐luciferase reporter assay. HCT116 and SW480 cells were divided into blank, miR‐NC, miR‐93‐5p mimics, miR‐93‐5p inhibitor, PD‐L1 small interfering RNA (siRNA) and miR‐93‐5p inhibitor + PD‐L1 siRNA groups, and wound‐healing and transwell assays were performed to detect cell migration and invasion, respectively. Protein expression was measured by western blotting. The secretion of cytokines was detected in the CRC cell/T coculture models. MiR‐93‐5p was downregulated in CRC tissues with upregulated PD‐L1. In PD‐L1‐negative patients, miR‐93‐5p expression was increased compared with that in PD‐L1‐positive patients. MiR‐93‐5p and PD‐L1 expression levels were associated with the tumor differentiation, lymphatic metastasis, TNM, Duke's stage, and prognosis of CRC. PD‐L1 siRNA weakened the migration and invasion abilities via decreased expression of matrix metalloproteinase‐1 (MMP‐1), ‐2, and ‐9, and these effects were abolished by the miR‐93‐5p inhibitor. Additionally, anti‐PD‐L1 upregulated the expressions of interleukin‐2 (IL‐2), tumor necrosis factor‐α (TNF‐α), and interferon γ (IFN‐γ) in the coculture of T cells with CRC cells, but downregulated the expressions of IL‐1β, IL‐10, and TGF‐β. However, these changes were partially reversed by miR‐93‐5p inhibition. miR‐93‐5p is expected to be a novel target for CRC treatment since it decreases the migration and invasion, as well as the immune evasion, of CRC cells via targeting PD‐L1.