不同性别大学生健康危险行为现状及影响因素研究*

目的 了解大学生健康危险行为现状及影响因素,促进大学生健康发展。方法 采用分层随机抽样的方法,对5所高校的2510名大学生进行问卷调查,利用SPSS 25.0统计软件进行统计描述、x2检验和logistic回归分析。结果 男生健康危险行为发生率均高于女生:饮酒（81.99%/34.57%）、通宵上网（47.24%/28.22%）、吸烟（31.28%/2.25%）、参与赌博（22.99%/9.41%）。多因素结果显示,男女生健康危险行为的共同危险因素有宗教信仰、恋爱、睡眠障碍、父母感情不好（OR>1,P<0.05）;共同保护因素有师范类院校、医学类院校、住校（OR<1,P<0.05）;男生健康危险行为的危险因素还有消费水平高、担任干部、生源地为农村（OR>1,P<0.05）;年级高是男生通宵上网的保护因素（OR=0.824,P=0.011）,吸烟的危险因素（OR=1.271,P=0.005）。结论 大学生饮酒、通宵上网、吸烟、参与赌博的发生率较高,性别差异大,影响因素来自个体、学校、家庭层面,应从以上层面对重点人群进行健康教育,积极引导大学生形成健康的行为方式。     

社会支持与环境作用大学生心理:行为的中介效应

目的:探究大学生社会支持、环境、行为、心理之间的相互作用机制,为大学生的行为引导和心理健康干预提供参考。方法:采用一般情况调查表和大学生生命质量评价简明量表(QOLCS-23),对2510名大学生进行问卷调查。结果:⑴社会支持与环境、行为、心理两两呈显著正向相关;⑵行为在社会支持与环境和大学生心理之间起到部分中介作用,中介效应显著,中介效应所占比例为55.22%;⑶与生活行为相比,时间管理对大学生行为贡献更大(β=0.75,P<0.001)。结论:社会支持与环境可直接预测大学生心理,亦可通过行为间接影响其心理。提高大学生心理健康水平,应重视大学生对社会支持与环境的感受度和满足感,引导大学生构建良好行为,尤其要树立时间管理意识。     

食管癌调强放疗靶区与肺体积比和处方剂量的关系

目的 研究食管癌调强放射治疗中能够做出既定目标的放疗计划时,靶区体积与肺体积比值和处方剂量的关系,从而帮助临床医生根据靶区情况,选择适合的处方剂量。方法 随机选取临床上已进行放射治疗的食管癌患者80例;其中病变范围包括全部食管癌类型,靶区根据ICRU（International Commission Radiological Units）50、62号文件进行勾画;设定统计参数及计划目标。根据参数的统计结果进行统计学分析;通过拟合计算求出满足既定目标的体积比临界值。结果 体积比与肺V₅、V₂₀、V₃₀以及肺平均受量具有线性正相关关系。给予60 Gy的处方剂量时,体积比的临界值为10%;给予50 Gy的处方剂量时,体积比的临界值为13%。结论 根据研究结果可以预见：食管癌调强放疗中当靶区体积与肺体积比值超过10%时,考虑给予的处方剂量不高于60 Gy;当靶区体积与肺体积比值超过13%时,给予处方剂量时应谨慎选择,但对于各段食管癌靶区超出肺段的患者可适当放宽。这为临床医生勾画靶区期间在处方剂量和靶区范围的选择上提供了参照。     

The neuroprotective effects of K252a through inhibiting MLK3/MKK7/JNK3 signaling pathway on ischemic brain injury in rat hippocampal CA1 region

It has been well documented that the activation of c-Jun N-terminal protein kinase (JNK) pathway and caspase-3 signal are involved in the delayed neuronal cell death in cerebral ischemia. In this study, we first detected the activation pattern of JNK signaling including mixed lineage kinase (MLK)3, mitogen-activated protein kinase kinase (MKK)7 and JNK3 in hippocampal CA1 and CA3/DG regions at various time points after 15 min of ischemia. These results indicated that cerebral ischemia induced the continuous activation of MLK3/MKK7/JNK3 cascade, which all had two active waves only in the CA1 region. We also detected the phosphorylation of JNK substrates c-Jun and Bcl-2, and the activation of a key protease of caspase-3 in CA1 region, which only had one active peak, respectively. Because K252a has recently been shown to be a potent inhibitor of MLK3 activity both in vivo and in vitro, we further examined the possible effects and mechanism of this interesting drug in cerebral ischemia. In our present paper, we found that administration of K252a 20 min prior to ischemia inhibited MLK3/MKK7/JNK3 signaling, Bcl-2 phosphorylation, the activation of c-Jun and caspase-3, but had no significant effects on these protein expressions. Additionally, pretreatment of K252a significantly increased the number of the surviving CA1 pyramidal cells at 5 days of reperfusion. Our results suggest that K252a play a neuroprotective role in ischemic injury via inhibition of the JNK pathway, involving the death effector of caspase-3. Thus, JNK signaling may eventually emerge as a prime target for novel therapeutic approaches to treatment of ischemic stroke, and K252a may serve as a potential and important neuroprotectant in therapeutic aspect in ischemic stroke.     

Analysis of hypermutation of the 5’ noncoding region in the BC L-6 gene

Objective To investigate BCL-6 gene mutations in Chinese populations with B-cell non- Hodgkin’s lymphoma.Methods Polymerase chain reaction (PCR), denaturing gradient gel electrophoresis (DGGE) and direct DNA sequencing were used to identify mutations in the 5’ noncoding re gion of the BCL-6 gene in a total of 40 cases of diffuse large-cell lymphoma ( DLCL) and follicular lymphoma (FL).Results Nine cases were found to have base substitutions.The incidence of BCL-6 gene mutation and the frequency of single-base changes were approximately 25.7% an d (0.56-1.10)×10(-2)/bp, respectively.Conclusions The 5’ regulatory region of the BCL-6 gene undergoes frequent somatic hypermuta tion during lymphomagenesis and the identification of BCL-6 gene hypermutations provides a molecular marker for confirmatory diagnosis of B-NHL.     

多发性脂囊瘤患者角蛋白17基因突变的研究

目的 了解多发性脂囊瘤和角蛋白17基因异常的关系。方法 应用逆转录-聚合酶链反应及其产物直接测序,巢式聚酶链反应及限制性片段长度多态性分析。研究多发性脂囊瘤家系中患者患肿组织cDNA及外周血DNA的角蛋白17基因突变。结果 囊肿组织显示角蛋白17基因第94位密码子,428碱基发生C→A的突变,使原编码的氨基酸曲精氨酸变为半胱氨酸,即R94C的杂合突变。巢式聚合酶链反应后Acil限制酶谱多态性分析,显示患者多周血DNA标本均有一条突变等位基因缺乏该酶酶切位点,产生200bp的条带,另有一条野生型等位基因已被切开,形成2条带,分别为108bp,92bp,进一步证实R94C的突变,系杂合性突变,而正常人10人份及2000人份正常人DNAPool标本2条等位基因均有Acil的酶切位点,只显示108bp和92bp3条带。结论 角蛋白17基因R94C的突变,是导致中国人多发性脂囊瘤的遗传学基础之一。这一研究结果为该病的基因诊断及遗传咨询提供了科学依据。     

Inhibitory effect of panicoin on platelet activation and its mechanism

Inhibitory Effect of Panicoin on Platelet Activation and Its Mechanism@韩谷鸣$Xuzhou Geriatrics Institute!Jiangsu 221003 @姚倩$Xuzhou Geriatrics Institute!Jiangsu 221003 @李洪莲$Xuzhou Geriatrics Institute!Jiangsu 221003     

miR-146a-5p regulates autophagy and NLRP3 inflammasome activation in epithelial barrier damage in the in vitro cell model of ulcerative colitis through the RNF8/Notch1/mTORC1 pathway

Ulcerative colitis (UC) is a chronic inflammatory disease affecting the colon that can be influenced by microRNAs (miRNAs). This study aims to investigate the impact of miR-146a-5p on lipopolysaccharide (LPS)-induced Caco-2/HT-29 cell autophagy and NLRP3 inflammasome activation and the underlying mechanism, with the aim of identifying potential therapeutic targets. We used LPS to establish Caco-2/HT-29 cell models and measured cell viability by CCK-8. The levels of miR-146a-5p, RNF8, markers of NLRP3 inflammasome activation and autophagy, proteins involved in the Notch1/mTORC1 pathway, and inflammatory factors were assessed by RT-qPCR, Western blot, and ELISA. Intestinal epithelial barrier function was evaluated by measuring transepithelial electrical resistance. Autophagic flux was measured using tandem fluorescent-labeled LC3. miR-146a-5p was highly-expressed in LPS-induced Caco-2/HT-29 cells, and autophagy flux was blocked at the autolysosomal stage after LPS induction. Inhibition of miR-146a-5p suppressed NLRP3 inflammasome activation, reduced intestinal epithelial barrier damage, and facilitated autophagy inhibition in LPS-induced Caco-2/HT-29 cells. The autophagy inhibitor NH4Cl partially nullified the inhibitory effects of miR-146a-5p inhibition on NLRP3 inflammation activation. miR-146a-5p targeted RNF8, and silencing RNF8 partly abrogated the action of miR-146a-5p inhibition on promoting autophagy and inhibiting NLRP3 inflammasome activation. miR-146a-5p inhibition suppressed the Notch1/mTORC1 pathway activation by upregulating RNF8. Inhibition of the Notch1/mTORC1 pathway partially nullified the function of silencing RNF8 on inhibiting autophagy and bolstering NLRP3 inflammasome activation. In conclusion, miR-146a-5p inhibition may be a potential therapeutic approach for UC, as it facilitates autophagy of LPS-stimulated Caco-2/HT-29 cells, inhibits NLRP3 inflammasome activation, and reduces intestinal epithelial barrier damage by upregulating RNF8 and suppressing the Notch1/mTORC1 pathway.     

Identification of peptides presented through the MHC-II of dendritic cells stimulated with Mycobacterium avium

Mycobacterium avium (M. avium) represents a species of concern, because of its ability to modulate the host’s innate immune response, and therefore influence trajectory of adaptative immunity. Since eradicative response against mycobacteria, and M. tuberculosis/M. avium, relies on peptides actively presented on a Major Histocompatibility complex-II (MHC-II) context, we assessed paradoxical stimulation of Dendritic Cell resulting on immature immunophenotype characterized by membrane minor increase of MHC-II and CD40 despite of high expression of the pro-inflammatory tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) in supernatants. Identification of M. avium leucine rich peptides forming short α-helices shutting down Type 1T helper (Th1), contribute to the understanding of immune evasion of an increasingly prevalent pathogen, and may provide a basis for future immunotherapy to infectious and non-infectious disease.     

舌下针治疗中风(缺血性)的疗效及血液流变学变化的观察

：以舌下针对70例中风（缺血性）患者进行针刺治疗,观察到针刺后患者的全血比粘度（包括全血还原比粘度）、红细胞压积、血沉、红细胞电泳时间以及血浆比粘度等指标均有降低,其差异经统计学处理有非常显著意义（P＜0.01）,可见用舌下针针刺后．患者血液的浓稠性、凝固性、粘滞性、聚集性均较针刺前有显著改善,这表明针刺后能使血液粘度降低、血管阻力减弱、血液流动加快、血流量增加．从而改善了中风（缺血性）患者的脑部的血循环,这对患者的治疗无疑是大有裨益的。