System Assimilation of E-Skills in Tertiary Institutions to Empower Graduates in South Africa

The value of system assimilation is to improve working relationships between tutors and learners while increasing workflow efficiency among tertiary institutions with low operational costs. E-skills could be described as electronic education development, to assist ICT professionals to reach their future career goals and aim to help users boost their ICT skills. In a society that is expanding, it is also a crucial issue to take into account. Researchers have turned their attention to this topic because of its significance and contribution to the empowerment of graduates in digital education. Many scholars have proposed many methods for integrating e-skills into society with impressive results, but the rising rate of graduate unemployment in South Africa is gradually becoming a big worry in our society. A model based on Activity Theory (AT) and e-skills will be developed in our tertiary institution to equip graduates with skills that will increase their employability and provide more individualized work opportunities as part of this study’s effort to solve this issue. With the use of the Statistical Package for the Social Sciences (SPSS) and Cronbach’s Alpha for validity and reliability testing, the study will create an experimental performance to assess the approach taken to measure e-skills in tertiary institutions to empower graduates in South Africa. The study established that system development and e-skilled models for tertiary institutions are growing gradually, especially in South African institutions, that empower graduates with profitable employability with experiences to improve work operation in the industries. In conclusion, system development and e-skills are very demanding but important to empower graduate employability to determine competency in the professional workforce.

Exercise-induced modulation of miR-149-5p and MMP9 in LPS-triggered diabetic myoblast ER stress: licorice glycoside E as a potential therapeutic target

Background:This study explores the relationship between endoplasmic reticulum(ER)stress and diabetes,particularly focusing on the impact of physical exercise on ER stress mechanisms and identifying potential therapeutic drugs and targets for diabetes-related sepsis.The research also incorporates traditional physical therapy perspectives,emphasizing the genomic insights gained from exercise therapy in disease management and prevention.Methods:Gene analysis was conducted on the GSE168796 and GSE94717 datasets to identify ER stress-related genes.Gene interactions and immune cell correlations were mapped using GeneCard and STRING databases.A screening of 2,456 compounds from the TCMSP database was performed to identify potential therapeutic agents,with a focus on their docking potential.Techniques such as luciferase reporter gene assay and RNA interference were used to examine the interactions between microRNA-149-5p and MMP9.Results:The study identified 2,006 differentially expressed genes and 616 miRNAs.Key genes like MMP9,TNF-α,and IL1B were linked to an immunosuppressive state.Licorice glycoside E demonstrated high affinity for MMP9,suggesting its potential effectiveness in treating diabetes.The constructed miRNA network highlighted the regulatory roles of MMP9,IL1B,IFNG,and TNF-α.Experimental evidence confirmed the binding of microRNA-149-5p to MMP9,impacting apoptosis in diabetic cells.Conclusion:The findings highlight the regulatory role of microRNA-149-5p in managing MMP9,a crucial gene in diabetes pathophysiology.Licorice glycoside E emerges as a promising treatment option for diabetes,especially targeting MMP9 affected by ER stress.The study also underscores the significance of physical exercise in modulating ER stress pathways in diabetes management,bridging traditional physical therapy and modern scientific understanding.Our study has limitations.It focuses on the microRNA-149-5p-MMP9 network in sepsis,using cell-based methods without animal or clinical trials.Despite strong in vitro findings,in vivo studies are needed to confirm licorice glycoside E’s therapeutic potential and understand the microRNA-149-5p-MMP9 dynamics in real conditions.

清肾颗粒对大鼠NRK-52E细胞转分化模型miR-23b和PINK1/Parkin通路的影响

目的 探讨TGF-β1诱导大鼠NRK-52E细胞转分化模型中miR-23b对PINK1/Parkin通路的靶向调节机制,并阐明清肾颗粒含药血清对NRK-52E细胞转分化的干预机理。方法 采用超高效液相色谱(UPLC)指纹图谱法对清肾颗粒进行全指纹图谱分析。构建TGF-β1诱导大鼠NRK-52E细胞转分化模型,转染siRNA后分为模拟物空载对照组、miR-23b-5p模拟物组、抑制剂空载对照组、miR-23b-5p抑制剂组,观察miR-23b-5p对PINK1表达量的影响。再将NRK-52E细胞分组为正常组、TGF-β1组、清肾颗粒组、miR-23b-mimic-NC组、miR-23b-mimic组、miR-23b-mimic+清肾颗粒组,Western blot法检测NRK-52E细胞中Pink1、Parkin、LC3Ⅱ、Beclin-1、P62、α-SMA蛋白表达,RT-qPCR法检测NRK-52E细胞中miR-23b-5p、Pink1、Parkin、Beclin-1、α-SMA mRNA的表达,双荧光素酶报告基因实验检测miR-23b-5p与PINK1的靶向关系。结果 UPLC指纹图谱法鉴定出清肾颗粒中11个活性成分。miR-23b-5p过表达后,PINK1 mRNA表达量也显著增加(P<0.05);而miR-23b-5p表达沉默后,PINK1 mRNA表达量也显著减少(P<0.05)。双荧光素酶报告显示,Rno-miR-23b-5p能显著下调Rno-PINK1-WT荧光素酶活性(P<0.05),但未能下调突变Rno-PINK1-mut荧光素酶活性(P>0.05)。清肾颗粒含药血清干预实验发现,TGF-β1组的miR-23b-5p、Pink1、Parkin、Beclin-1、LC3Ⅱ表达及LC3Ⅱ/Ⅰ比值均明显低于正常组,P62和α-SMA表达明显高于正常组(P<0.05)。清肾颗粒组和miR-23b-mimic组的miR-23b-5p、Pink1、Parkin、Beclin-1、LC3Ⅱ表达及LC3Ⅱ/Ⅰ比值均明显高于TGF-β1组,P62和α-SMA表达明显低于TGF-β1组(P<0.05)。miR-23b-mimic+清肾颗粒组的表现更优于miR-23b-mimic组(P<0.05)。结论 清肾颗粒能够上调NRK-52E细胞内miR-23b-5p表达,并通过增强PINK1/Parkin通路介导的线粒体自噬活性,抑制NRK-52E细胞转分化进程。

Factors Affecting the Adoption of E-Learning Systems in Public Higher Learning Institutions in Tanzania: A Case of Institute of Accountancy Arusha (IAA)

In most developing countries, governments attempt to enforce the movement from analogue to digital for all their sectors, from public to private. These technological advancements have been noted to bring necessary and unavoidable changes to businesses and learning environments. Higher learning institutions have adopted various e-learning systems to support learning, research, and publication activities to stay competitive in global academic systems. However, most public higher learning institutions in Tanzania lag behind in the adoption of these systems. Thus, research shows a failure of these institutions in utilising the full benefit that today’s Information and Communication Technology (ICT) can offer in learning environments. Thus, this study examines factors affecting the adoption of such a system in developing countries like Tanzania, taking the Institute of Accountancy Arusha (IAA) as a case study. The study used a mixed methodology where thematic and descriptive analysis was used to analyse both qualitative and quantitative research data. The study population was 187 teaching staff, a sample size of 126 was obtained, and 157 study participants were involved in the study. The study found that factors affecting the adoption of e-learning systems in public higher learning institutions in Tanzania include lack of ICT infrastructure, lack of technical and managerial support and lack of computers and e-learning knowledge among facilitators. Thus, the study recommended investments in adequate and reliable ICT facilities, high intermate speed and bandwidth, and policies that support e-learning and training programs about e-learning knowledge and use. Also, this study recommends the use of the Multi-Factors Adoption Model (MFAM11) for the successful adoption of an e-learning system in public higher learning institutions in Tanzania.

Linc01419调控miR-34a-5p/E2F3轴促进膀胱癌细胞增殖与侵袭

目的:探讨长链非编码RNA Linc01419对膀胱癌细胞增殖和侵袭的影响及作用机制。方法:通过UALCAN软件(https://ualcan.path.uab.edu/)分析TCGA数据库中Linc01419在膀胱癌组织与正常膀胱组织中的表达差异;采用实时荧光定量聚合酶链反应(real-time fluorescence quantitative polymerase chain reaction,RT-qPCR)检测Linc01419在不同膀胱癌细胞系、22例经病理证实为膀胱癌的手术患者的肿瘤组织及癌旁正常膀胱组织中的表达水平;应用细胞增殖/毒性检测(cell counting kit-8,CCK-8)实验和Transwell小室侵袭实验检测敲低Linc01419表达对膀胱癌细胞增殖与侵袭的影响;采用双荧光素酶报告基因检测法分析Linc01419与miR-34a-5p及miR-34a-5p与E2F3之间的靶向调控关系。结果:UALCAN数据库分析显示相较正常膀胱组织,Linc01419在膀胱癌组织中显著高表达(P<0.001);RT-qPCR分析结果显示相较癌旁正常膀胱组织,Linc01419在22例膀胱癌组织中表达明显上调(P<0.001),与UALCAN数据库分析结果一致;Linc01419在4株膀胱癌细胞中的表达明显高于正常膀胱上皮细胞(P<0.01);敲低Linc01419表达,可显著抑制膀胱癌细胞的增殖、侵袭及N-cadherin、PCNA蛋白的表达,而显著促进E-cadherin的蛋白表达(P<0.05);miR-34a-5p过表达对膀胱癌细胞具有类似的抑制作用;双荧光素酶报告基因实验、RIP及Pull-down实验证实Linc01419可靶向结合miR-34a-5p,而后者进一步介导了对E2F3的靶向调控;抑制miR-34a-5p表达,可显著削弱Linc01419沉默对膀胱癌细胞生物学行为及E-cadherin、N-cadherin、PCNA、E2F3表达的影响。结论:Linc01419在膀胱癌中异常高表达,其通过调控miR-34a-5p/E2F3轴促进膀胱癌细胞增殖和侵袭,很可能是膀胱癌发生、发展过程中的一个重要环节。

A Family of High_order Accuracy Explicit Difference Schemes for Solving 2-D Parabolic Partial Differential Equation

A family of high_order accuracy explicit difference schemes for solving 2_dimension parabolic P.D.E. are constructed. Th e stability condition is r=Δt/Δx 2=Δt/Δy 2【1/2 and the truncation err or is O(Δt 3+Δx 4).

p16/Ki-67双染检测、HPVE6/E7mRNA检测在宫颈病变诊断中的价值研究

目的:探讨p16/Ki-67双染检测、HPVE6/E7mRNA检测在宫颈病变诊断中的价值。方法:选择2021年4月至2023年2月我院收治的605例高危型HPV阳性患者为研究对象,所有患者入院后均进行阴道镜检查与病理活检,取患者细胞学样本分别进行p16/Ki-67双染检测、HPVE6/E7mRNA检测。比较两种方法单独检查与联合检测对宫颈病变阳性检出率的差异;比较三种检查方法对宫颈病变诊断效能的差异。结果:联合检测检出CIN1~3阳性率均高于p16/Ki-67双标记、HPVE6/E7mRNA检测(P<0.05);三种检测方式的浸润癌阳性检出率比较无明显差异(P>0.05)。Kappa检验分析结果显示,p16/Ki-67双标记与HPVE6/E7mRNA检查结果与病理诊断结果具有较好的一致性(Kappa值=0.719,P<0.05);联合检测结果与病理诊断结果具有高度的一致性(Kappa值=0.894,P<0.05)。联合检测对宫颈病变的诊断灵敏度、特异性与准确率高于p16/Ki-67双标记与HPVE6/E7mRNA检查(P<0.05)。结论:p16Ki-67双染与HPVE6/E7mRNA联合检测可准确检出宫颈病变程度,对宫颈病变疾病类型的鉴别可提供充足可靠的数据支持,联合检查的诊断效能较好,对患者后续相关治疗开展有积极指导意义。

miR-150-5p靶向ZEB1调控EMT对子宫内膜癌细胞恶性生物学行为的影响

目的探讨微小RNA-150-5p(miR-150-5p)是否可靶向锌指E盒结合蛋白1(ZEB1)调控子宫内膜癌(EC)细胞上皮间质转化(EMT)进而影响癌细胞的恶性生物学行为。方法RT-qPCR技术检测正常子宫内膜和EC组织中、子宫内膜上皮细胞系hEEC及EC细胞系Ishikawa和HEC-1-A中miR-150-5p相对表达量。过表达miR-150-5p,MTT法、菌落形成实验、伤口愈合实验和Transwell实验分别评估Ishikawa细胞活力、克隆形成、迁移及侵袭能力;双荧光素酶报告基因实验验证miR-150-5p与ZEB1的靶向关系;RT-qPCR检测miR-150-5p及ZEB1 mRNA相对表达量;Western blot技术检测ZEB1、E-钙黏蛋白(E-cadherin)、N-钙黏蛋白(N-cadherin)、波形蛋白(Vimentin)及基质金属蛋白酶9(MMP-9)蛋白表达量。结果与正常子宫内膜组织比较,EC组织中miR-150-5p相对表达量降低(P<0.05);与hEEC细胞比较,HEC-1-A细胞和Ishikawa细胞中miR-150-5p相对表达量降低(P<0.05),Ishikawa细胞中最低(P<0.05)。与空白组比较,miR-150-5p mimics组细胞490 nm处吸光度值、细胞菌落数、迁移数和侵袭数、ZEB1 mRNA和蛋白相对表达量及N-cadherin、Vimentin和MMP-9蛋白相对表达量显著降低,miR-150-5p相对表达量、E-cadherin蛋白相对表达量显著升高(P<0.05)。经生物信息学分析,ZEB1被预测为miR-150-5p的潜在靶基因。结论miR-150-5p可靶向ZEB1抑制癌细胞的恶性生物学行为,其作用机制可能与调控EC细胞EMT进展有关。

Two New Species of Freshwater Shrimps from Hunan Province,China (Decapoda:Atyidae:Caridina)

Two new freshwater atyid shrimps, Caridina angustipes sp nov.and C clavipes sp nov.from Hunan Province,China are described. C angustipes sp nov.is similar to C baojingensis Guo,He et Bai,1992,but with longer rostrum,15-27 dorsal teeth,3-6 ventral teeth,and straighter inner margin of endopods in male 1st pleopods. C clavipes sp nov.is similar to C angustipes ,but with narrower distal and fewer spines on inner margin of endopds in male 1st pleopods,and shorter and thinner appendix masculina in male 2nd pleopods with only 1 spine on inner lateral margin and 4 spines in apex.The holotypes are deposited in Shanghai Fisheries University.Some representative paratypes are deposited in Foshan Science and Technology College.

The Prognostic Value of Pathological and Molecular Margins Marked by p53 and eIF4E in Laryngeal Carcinoma

Objective: To study the prognostic value of the pathological margin and molecular margin marked by eIF4E and P53 protein in laryngeal carcinoma. Methods: The prognostic value of pathological and molecular margin was studied in 253 cases and 67 cases respectively, the latter were pathological negative margin chosen from the former. Immunohistochemisty was used to detect the expression of eIF4E and p53 proteins. Results: The rate of pathological, p53 and eIF4E positive margins was 20.2%, 19.4% and 32.8% respectively. The recurrent rate of those with positive margins was higher than that of negative margins, which including pathological margin (70.6% vs 35.1%, P =0.0000), p53 margin (69.2% vs 33.3%, P =0.018) and eIF4E margin (63.6% vs 28.9%, P =0.018); The survival rate of those with negative margins was higher than those with positive margins, including pathological margin (the 5-year cumulative survival rate was 37.52% and 64.37% respectively, P =0.0023), p53 margin (the 5-year cumulative survival rate was 24.62% and 75.69% respectively, P =0.0012) and eIF4E margin (the 5-year cumulative survival rate was 43.31% and 77.52% respectively, P =0.0006). Conclusion: The prognosis of those with both pathological and molecular positive margins was worse than that of the negative margins; Both the eIF4E and p53 were useful markers to pick out the poor prognostic patients from those with pathological negative margin, and the former seemed to be more potential.

Introduction of Internet P.E News Reporter

Consistent with previous research, results showed men get more paragraphs and photography coverage. Interestingly, women's factual information is always associated with relevant men report, including P.E relevant with personal information.

Development Characteristics of Private P.E Economy

The regional policy in the innovation development of private P.E economy plays better role in management according to law,guidance and escort;increase the macro quality of main body of private P.E entrepreneurs and the overall staff quality,develop P.E vocational P.E to provide P.E talents for private P.E economy.

清胆利肝方治疗肝经郁热型带状疱疹临床疗效及对患者T淋巴细胞亚群、血清疼痛物质P、PGE2的影响

目的 探讨清胆利肝方治疗肝经郁热型带状疱疹临床疗效及对患者血清疼痛物质(S)P、前列腺素(PG)E2的影响。方法 收集肝经郁热型带状疱疹患者144例,根据随机数字表法随机分为对照组及观察组,每组72例,对照组给予阿昔洛韦及甲钴胺进行常规治疗,观察组在对照组用药基础上给予清胆利肝方进行治疗,两组均治疗2 w。对比两组临床疗效,检测治疗前后T淋巴细胞亚群、血清SP、PGE2水平的变化情况,同时记录并比较两组疼痛视觉模拟评分(VAS)及不良反应;治疗后随访2个月,观察后遗神经痛(PHN)的发生情况。结果 治疗后,观察组临床总体有效率显著高于对照组(P<0.05);观察组疱疹结痂消退时间及疼痛缓解时间显著短于对照组(P<0.05)。随访2个月,观察组PHN发生率显著低于对照组(P<0.05)。治疗后,两组血清白细胞介素(IL)-4,IL-6,肿瘤坏死因子(TNF)-α及CD8^(+)水平与治疗前相比明显降低,且观察组上述指标显著低于对照组(P<0.05);治疗后,两组血清CD4^(+)及CD4^(+)/CD8^(+)与治疗前相比显著增加,且观察组升高水平显著高于对照组(P<0.05);治疗后与对照组相比,观察组血清中SP、PGE2显著降低(P<0.05)。结论 清胆利肝方可提高肝经郁热型带状疱疹患者T淋巴细胞亚群水平,降低患者血清中PGE2水平及SP含量,有效减少炎症反应并缓解疼痛。

长链非编码RNA RP11-497E19.1对胃癌细胞增殖和侵袭的影响及机制实验研究

目的:探讨长链非编码RNA(lncRNA)RP11-497E19.1对胃癌细胞增殖和侵袭的影响及其机制。方法:实时荧光定量PCR(RT-qPCR)检测胃癌HS-746T、BGC823、NCI-N87、SGC7901、AGS细胞和永生化胃上皮细胞GES-1中RP11-497E19.1表达水平,筛选表达最高的细胞进行后续实验。将HS-746T细胞分为si-NC组和si-RP11-497E19.1组,分别转染阴性对照寡核苷酸或RP11-497E19.1小干扰RNA。集落形成实验和Transwell实验分析转染HS-746T细胞的增殖、侵袭能力。双荧光素酶报告基因实验验证RP11-497E19.1与微小RNA(miR)-545-5p的靶向关系。RT-qPCR检测转染HS-746T细胞miR-545-5p的表达。Western blot检测转染HS-746T细胞间质表皮转化因子(c-Met)/胆绿素还原酶(BVR)/活化复制因子2(ATF-2)分子通路相关蛋白的表达。结果:与GES-1细胞比较,HS-746T、BGC823、NCI-N87、SGC7901、AGS细胞中RP11-497E19.1表达水平均上升,且HS-746T细胞RP11-497E19.1表达水平最高(均P<0.05)。与si-NC组比较,si-RP11-497E19.1组HS-746T细胞活力和细胞侵袭数降低(均P<0.05)。双荧光素酶报告基因实验证实RP11-497E19.1靶向结合miR-545-5p,可负向调控miR-545-5p表达(P<0.05)。与si-NC组比较,si-RP11-497E19.1组HS-746T细胞c-Met/BVR/ATF-2分子通路蛋白c-Met、BVR、p-ATF-2、锌指蛋白1(Snail1)、锌指蛋白2(Snail2)表达降低(均P<0.05)。结论:胃癌细胞中RP11-497E19.1呈高表达,沉默RP11-497E19.1通过靶向miR-545-5p/c-Met/BVR/ATF-2分子通路抑制胃癌HS-746T细胞的增殖及侵袭。

MiRNA-145-5p inhibits gastric cancer progression via the serpin family E member 1-extracellular signal-regulated kinase-1/2 axis

BACKGROUND MicroRNAs(miRNAs)regulate gene expression and play a critical role in cancer physiology.However,there is still a limited understanding of the function and regulatory mechanism of miRNAs in gastric cancer(GC).AIM To investigate the role and molecular mechanism of miRNA-145-5p(miR145-5p)in the progression of GC.METHODS Real-time polymerase chain reaction(RT-PCR)was used to detect miRNA expression in human GC tissues and cells.The ability of cancer cells to migrate and invade was assessed using wound-healing and transwell assays,respectively.Cell proliferation was measured using cell counting kit-8 and colony formation assays,and apoptosis was evaluated using flow cytometry.Expression of the epithelial-mesenchymal transition(EMT)-associated protein was determined by Western blot.Targets of miR-145-5p were predicated using bioinformatics analysis and verified using a dual-luciferase reporter system.Serpin family E member 1(SERPINE1)expression in GC tissues and cells was evaluated using RT-PCR and immunohistochemical staining.The correlation between SERPINE1 expression and overall patient survival was determined using Kaplan-Meier plot analysis.The association between SERPINE1 and GC progression was also tested.A rescue experiment of SERPINE1 overexpression was conducted to verify the relationship between this protein and miR-145-5p.The mechanism by which miR-145-5p influences GC progression was further explored by assessing tumor formation in nude mice.RESULTS GC tissues and cells had reduced miR-145-5p expression and SERPINE1 was identified as a direct target of this miRNA.Overexpression of miR-145-5p was associated with decreased GC cell proliferation,invasion,migration,and EMT,and these effects were reversed by forcing SERPINE1 expression.Kaplan-Meier plot analysis revealed that patients with higher SERPINE1 expression had a shorter survival rate than those with lower SERPINE1 expression.Nude mouse tumorigenesis experiments confirmed that miR-145-5p targets SERPINE1 to regulate extracellular signal-regulated kinase-1/2(ERK1/2).CONCLUSION This study found that miR-145-5p inhibits tumor progression and is expressed in lower amounts in patients with GC.MiR-145-5p was found to affect GC cell proliferation,migration,and invasion by negatively regulating SERPINE1 levels and controlling the ERK1/2 pathway.

miR-30a-5p靶向E2F7阻滞A549细胞周期并抑制其增殖

目的探究miR-30a-5p靶向E2F7调控非小细胞肺癌细胞周期和增殖的机制。方法通过荧光定量(qRT-PCR)验证miR-30a-5p在非小细胞肺癌A549细胞与人正常肺上皮细胞BEAS-2B中的相对表达水平。在线软件预测了miR-30a-5p的靶基因及其靶向结合位点,双荧光素酶报告基因实验进一步验证miR-30a-5p和E2F7 mRNA 3’UTR区域的靶向关系。其次在A549细胞中分别转染miR-30a-5p模拟物(miR-30a-5p mimics)和miR-30a-5p抑制剂(miR-30a-5p inhibitor),应用CCK-8细胞计数试剂盒检测A549细胞增殖情况,流式细胞术检测A549细胞凋亡和细胞周期。qRT-PCR和免疫印迹检测细胞周期相关基因和肺腺癌相关基因的mRNA和蛋白表达水平。结果miR-30a-5p在A549细胞中表达水平低于BEAS-2B,且miR-30a-5p靶向结合与E2F7 mRNA 3’UTR 514-520位点,抑制E2F7表达。转染miR-30a-5p mimics抑制A549细胞增殖,并促进A549凋亡。将A549细胞周期阻滞在G 1期。调控肺腺癌相关基因TFDP3、CDK1、E2F8、CCNA2和CDC6的mRNA和蛋白表达水平。结论非小细胞肺癌A549细胞中miR-30a-5p通过靶向负调控E2F7的表达,调控TFDP3、CDK1、E2F8、CCNA2和CDC6的mRNA和蛋白表达,抑制A549细胞增殖和细胞周期。

Hepatoprotective effects of S-adenosyl-L-methionine against alcohol-and cytochrome P450 2E1-induced liver injury

S-adenosyl-L-methionine (SAM) acts as a methyl donor for methylation reactions and participates in the synthesis of glutathione. SAM is also a key metabolite that regulates hepatocyte growth, differentiation and death. Hepatic SAM levels are decreased in animal models of alcohol liver injury and in patients with alcohol liver disease or viral cirrhosis. This review describes the protection by SAM against alcohol and cytochrome P450 2E1-dependent cytotoxicity both in vitro and in vivo and evaluates mechanisms for this protection.

急性心肌梗死患者外周血内皮细胞微粒中miR-126和P-选择素及E-选择素水平特点及其临床意义

目的分析急性心肌梗死(AMI)患者外周血内皮细胞微粒(EMPs)中miR-126、P-选择素、E-选择素的表达水平,探究其与AMI的关系及临床意义。方法选择2021年9月至2022年9月新疆维吾尔自治区人民医院收治的45例AMI患者作为研究组,45例同期健康体检者作为对照组。冠状动脉狭窄的评估基于冠状动脉病变数量和Genisi评分。利用流式细胞仪检测外周血中的EMPs,用PCR法检测EMPs中的miR-126表达水平,通过ELISA法测定EMPs中的P-选择素、E-选择素表达。结果AMI组外周血EMPs中miR-126水平低于健康组,P-选择素和E-选择素水平显著高于健康组。外周血EMPs中miR-126水平在三支血管病变组中的表达水平明显低于双支病变组和单支病变组,且外周血EMPs中miR-126水平与Genisi评分呈负相关。外周血EMPs中P-选择素水平在三支血管病变组中的表达水平明显高于双支病变组和单支病变组,且P-选择素与Genisi评分呈正相关。多因素logistic回归显示,外周血EMPs中P-选择素、E-选择是AMI的危险因素。受试者工作曲线(ROC)分析结果显示,外周血EMPs中miR-126、P-选择素及E-选择素单独诊断AMI的效能较低,外周血EMPs中miR-126、P-选择素及E-选择素联合诊断AMI具有良好的诊断效能。结论外周血EMPs中P-选择素和E-选择素是AMI的危险因素。外周血EMPs中miR-126、P-选择素及E-选择素联合对AMI有诊断价值,可作为AMI诊断的生物学标志物。

Hepatoprotective and antioxidant effects of lycopene on non-alcoholic fatty liver disease in rat

AIM To evaluate the hepatoprotective effect of lycopene(Ly) on non-alcoholic fatty liver disease(NAFLD) in rat. METHODS A rat model of NAFLD was first established by feeding a high-fat diet for 14 wk. Sixty-five rats were randomly divided into normal group, model group and Ly treatment groups. Alanine aminotransferase(ALT), aspartate aminotransferase(AST), triglycerides(TG), total cholesterol(TC) in serum and low density lipoproteincholesterol(LDL-C), high density lipoprotein-cholesterol(HDL-C), free fatty acid(FFA), malondialdehyde(MDA), superoxide dismutase(SOD), glutathione(GSH) in liver tissue were evaluated, respectively. While the hepatoprotective effect was also confirmed by histopathological analysis, the expression levels of TNF-α and cytochrome P450(CYP) 2E1 in rat liver were determined by immunohistochemistry analysis.RESULTS A significant decrease was observed in the levels of serum AST(2.07-fold), ALT(2.95-fold), and the blood lipid TG(2.34-fold) and TC(1.66-fold) in the dose of 20 mg/kg Ly-treated rats(P < 0.01), compared to the model group. Pretreatment with 5, 10 and 20 mg/kg of Ly significantly raised the levels of antioxidant enzyme SOD in a dose-dependent manner,to 90.95 ± 9.56, 109.52 ± 11.34 and 121.25 ± 10.68(P < 0.05, P < 0.01), as compared with the model group. Similarly, the levels of GSH were significantly increased(P < 0.05, P < 0.01) after the Ly treatment. Meanwhile, pretreatment with 5, 10 and 20 mg/kg of Ly significantly reduced MDA amount by 30.87, 45.51 and 54.49% in the liver homogenates, respectively(P < 0.01). The Ly treatment group showed significantly decreased levels of lipid products LDL-C(P < 0.05, P < 0.01), improved HDL-C level and significantly decreased content of FFA, compared to the model group(P < 0.05, P < 0.01). Furthermore, the Ly-treated group also exhibited a down-regulated TNF-α and CYP2E1 expression, decreased infiltration of liver fats and reversed histopathological changes, all in a dosedependent manner(P < 0.05, P < 0.01). CONCLUSION This study suggests that Ly has a protective effect on NAFLD, down-regulates expression of TNF-α, and that CYP2E1 may be one of the action mechanisms for Ly.

Coexistence of hyperlipidemia and acute cerebral ischemia/reperfusion induces severe liver damage in a rat model

AIM:To investigate the correlation of hyperlipemia(HL) and acute cerebral ischemia/reperfusion(I/R) injury on liver damage and its mechanism.METHODS:Rats were divided into 4 groups:control,HL,I/R and HL+I/R.After the induction of HL via a high-fat diet for 18 wk,middle cerebral artery occlusion was followed by 24 h of reperfusion to capture I/R.Serum alanine transaminase(ALT) and aspartate aminotransferase(AST) were analyzed as part of liver function tests and liver damage was further assessed by histological examination.Hepatocyte apoptosis was evaluated by terminal deoxynucleotidyl transferase dUTP nick-end labeling(TUNEL) assay.The expression of genes related to apoptosis(caspase-3,bcl-2) was assayed by immunohistochemistry and Western blotting.Serum tumor necrosis factor-(TNF-),interleukin-1(IL-1) and liver mitochondrial superoxide dismutase(SOD),glutathione peroxidase(GSH-Px),malondialdehyde(MDA) and Ca 2+ levels were measured to determine inflammatory and oxidative/antioxidative status respectively.Microsomal hydroxylase activity of the cytochrome P450 2E1(CYP2E1)-containing enzyme was measured with aniline as the substrate,and CYP2E1 expression in the liver tissue and microsome was determined by immunohistochemistry and Western blotting respectively.RESULTS:HL alone induced by high-fat diet for 18 wk resulted in liver damage,indicated by histopathological analysis,and a considerable increase in serum ALT(25.13 ± 16.90 vs 9.56 ± 1.99,P < 0.01) and AST levels(18.01 ± 10.00 vs 11.33 ± 4.17,P < 0.05) compared with control.Moreover,HL alone induced hepatocyte apoptosis,which was determined by increased TUNEL-positive cells(4.47 ± 0.45 vs 1.5 ± 0.22,P < 0.01),higher caspase-3 and lower bcl-2 expression.Interestingly,compared with those in control,HL or I/R groups,massive increases of serum ALT(93.62 ± 24.00 vs 9.56 ± 1.99,25.13 ± 16.90 or 12.93 ± 6.14,P < 0.01) and AST(82.32 ± 26.92 vs 11.33 ± 4.17,18.01 ± 10.00 or 14.00 ± 6.19,P < 0.01) levels in HL+I/R group were observed suggesting severe liver damage,which was confirmed by liver histology.In addition,HL combined with I/R also caused significantly increased hepatocyte apoptosis,as evidenced by increased TUNEL-positive cells(6.20 ± 0.29 vs 1.5 ± 0.22,4.47 ± 0.45 or 1.97 ± 0.47,P < 0.01),elevated expression of caspase-3 and lower expression of bcl-2.Furthermore,when compared to HL or I/R alone,HL plus I/R enhanced serum TNF-,IL-1,liver mitochondrial MDA and Ca 2+ levels,suppressed SOD and GSH-Px in liver mitochondria,and markedly up-regulated the activity(11.76 ± 2.36 vs 4.77 ± 2.31 or 3.11 ± 1.35,P < 0.01) and expression(3.24 ± 0.38 vs 1.98 ± 0.88 or 1.72 ± 0.58,P < 0.01) of CYP2E1 in liver.CONCLUSION:The coexistence of HL and acute cerebral I/R induces severe liver damage,suggesting that cerebral ischemic stroke would exaggerate the damage of liver caused by HL.This effect is possibly due to en-hanced CYP2E1 induction which further promotes oxidative damage,inflammation and hepatocyte apoptosis.