综合医院发热门诊应对新型冠状病毒肺炎的应急管理

目的 探讨综合医院发热门诊应对新型冠状病毒感染肺炎的应急管理方法及效果。 方法 加强发热门诊的管理，包括优化发热预检分诊工作流程、合理布局发热门诊、修订发热门诊工作职责与流程指引、合理调配人力资源、加强相关人员培训、严格落实院感防控措施、提供后勤保障、加强健康宣教与管理。 结果 接诊患者13 761例次，采集咽拭子591例次，静脉输液11 973例次，氧气吸入998例次。 结论 加强综合医院发热门诊管理，能有效提高护理人员对新型冠状病毒肺炎疫情的应对能力，保障护理安全。     

血浆同型半胱氨酸水平与动脉粥样硬化和脑梗死的关系

目的 探讨血浆同型半胱氨酸(Hcy)水平与颈动脉粥样硬化和脑梗死关系.方法 2005-05～2006-02收治的91例脑梗死住院患者被列入研究对象.根据病灶大小分3组大片梗死21例,小片梗死44例,腔隙性梗死26例.根据颈动脉彩超检测结果将研究对象分为颈动脉斑块组34例,无颈动脉斑块组57例.全部患者测定血浆Hcy、血清叶酸、VitB12水平.分析血浆Hcy水平与脑梗死的危险因素、病灶大小、颈动脉粥样硬化斑块及血清叶酸、VitB12的关系.结果 血浆Hcy水平(1)与高血压、糖尿病、血脂、性别、年龄各指标无明显相关关系.(2)与脑梗死病灶大小无关.(3)与颈动脉粥样硬化斑块有关,有斑块34例,血浆Hcy(20.73±9.31)μmol/L,无斑块57例,血浆Hcy (15.46±11.4) μmol/L,前者高于后者(P＜0.05).(4)与血清叶酸、VitB12水平呈负相关(r1s=-0.264,r2s=-0.16,P＜0.05).结论 血浆Hcy水平与脑梗死病灶大小无关;Hcy水平升高与颈动脉粥样硬化斑块密切相关;与血清叶酸、VitB12水平呈负相关.高血浆Hcy血症可能是颈动脉粥样硬化的危险因素,但与脑梗死关系不明确.     

葛根素对抗H2O2引起血管平滑肌细胞凋亡及坏死

目的：研究葛根素对过氧化氢引起无血清培养的小牛主动脉血管平滑肌细胞凋亡和坏死的影响。方法：通过体外细胞培养，以噻唑兰（MTT）法测定细胞存活率，用流式细胞术检测细胞DNA含量及凋亡细胞百分率；DNA琼脂糖凝胶电泳法观察细胞凋亡过程中DNA断裂程度。结果：H2O2诱导无血清培养的平滑肌细胞凋亡，葛根素可显著降低平滑肌细胞中凋亡细胞百分率，并减少凋亡细胞DNA断裂，同时也减少其引起的平滑肌细胞坏死。结论：葛根素可对抗H2O2引起的无血清培养的血管平滑肌细胞凋凋亡及坏死。     

肝癌组织辅助性T细胞-2细胞因子强势分泌研究

目的　探讨人肝癌组织中辅助性T细胞亚群 (Th1/Th2 )细胞因子表达模式。方法　收集我科手术切除肝癌组织标本 15例 ,肝良性疾病或肝硬化门静脉高压手术患者肝组织标本 15例作为对照 ,β 肌动蛋白 (β actin)作为参照 ,采用半定量逆转录 聚合酶联反应 (RT PCR)方法检测人肝癌组织中γ 干扰素 (IFN γ)和白细胞介素 4(IL 4)mRNA的表达。结果　人肝癌组织中IFN γmRNA表达 (相对数 :1.18± 0 .3 1)比对照组肝组织中IFN γmRNA表达弱 (相对数 :1.86±0 .5 0 ) ,而IL 4mRNA表达 (相对数 :1.73± 0 .5 1)比对照组强 (相对数 :0 .94± 0 .41,P <0 .0 5 )。结论　人肝癌组织中Th1类细胞因子表达弱 ,Th2类细胞因子表达强 ,呈现Th2细胞因子表达模式 ,肝癌组织局部微环境处于免疫抑制状态 ,肿瘤细胞易发生免疫逃逸     

云南省中缅边境地区疟疾血清流行病学调查分析

目的 了解中缅边境一线县、二线县、及一线三个县的一线自然村、二线自然村的疟疾流行情况,为制定边境地区疟疾防治措施提供科学依据。方法 采用IFAT对中缅边境沧源、耿马及孟连一线县与双江县、永德县二线县,边境线3县一线自然村和二线自然村进行疟血清流行病学调查,用电脑软件EPI6X2检验法进行数据分析。结果一线县抗体阳性率23.88％（568/2379）,二线县抗体阳性率1.40％（10/712）,一线县显著高于二线县（x2=180.54;P<0.01）。一线县的一线自然村抗体阳性率33.05％（467/1413）,二线自然村抗体阳性率10.46％（101/966）,一线自然村显著高于二线自然村（x2=159.92;P<0.01）。结论IFAT抗体阳性率和阳性GMRT说明靠近边境地带比远离边境的地带疟疾流行更为严重。应加强出入境人员的防治工作,才能控制边境疟病流行。     

大鼠红核和颈段皮质脊髓背侧束联合损伤模型的建立

目的　为研究脊髓损伤后的可塑性变化 ,建立大鼠红核和皮质脊髓背侧束 (dCST)联合损伤模型。方法　立体定位仪下 ,致伤颈 3dCST和双侧红核 ,甲苯胺蓝染色显示损伤范围。示踪剂观测皮质脊髓腹侧束 (vCST)的出芽情况 ;同时 ,评定大鼠前肢功能的变化情况。结果　精确地致伤红核和dCST后 ,vCST的出芽数量和大鼠前肢功能评分成显著负相关 (P <0 0 1)。结论　大鼠红核和dCST联合损伤模型是研究脊髓损伤后可塑性变化的良好模型     

UVB radiation induces phosphorylation of the epidermal growth factor receptor, decreases EGF binding and blocks EGF induction of ornithine decarboxylase gene expression in SV40-transformed human keratinocytes

Abstract We previously demonstrated that epidermal growth factor (EGF) induces a several-fold increase in ornithine decarboxylase (ODC) activity and the steady-state level of ODC mRNA in cultured SV40-transformed human keratinocytes (1). Pretreatment of cell cultures with ultraviolet B (UVB) radiation resulted in a reduction of EGF-induced ODC activity. To determine whether UVB inhibits the accumulation of ODC mRNA by EGF, cells were pretreated with 20 mJ/cm² UVB or sham-irradiated and then incubated with 100 ng/ml EGF. Northern blot analysis revealed that UVB irradiation entirely blocked the EGF induction of ODC mRNA. Since the binding of EGF to its plasma membrane receptor is the first step in initiating a biological response, the effect of UVB on EGF binding was evaluated. UVB treatment of cultured keratinocytes resulted in an immediate and dose-dependent reduction of EGF binding. Scatchard analysis revealed thai the reduction of EGF binding was due to a 52% decrease in the number of available receptors, from 6.2 × 10⁴/cell to 3.0 × 10⁴/cell. However, UVB decreased the EGF-binding affinity very little (Kd = 0.60 nM in control and Kd=0.75 nM in UVB-treated Z114 cells). In addition, UVB did not alter the rate of EGF internalization. These data suggest that UVB blocks the signal transduction pathway of EGF that is involved in regulation of ODC gene expression. Immunoblot analysis of extracts from irradiated cells showed that UVB induced tyro-sine phosphorylation of EGFR and that the quantity of EGFR protein was unaffected by UVB treatment. Phosphorylation of EGFR may be responsible for decreased binding of EGF to its receptor.     

No association between the Pro197Leu polymorphism in the glutathione peroxidase (GPX1) gene and schizophrenia

OBJECTIVE: Oxidative stress such as free radical-mediated neuronal dysfunction may be involved in the pathophysiology of schizophrenia. The human glutathione peroxidase (GPX1) is a selenium-dependent enzyme, which plays an important role in the detoxification of free radicals. We therefore hypothesized that the GPX1 gene, which is located on chromosome 3p21.3, may be involved in the pathophysiology of schizophrenia. The aim of this study is to examine whether a potentially functional polymorphism, a proline (Pro) to leucine (Leu) substitution at codon 197 (Pro197Leu) of the human GPX1 gene, is associated with susceptibility to schizophrenia. METHODS: We genotyped the Pro197Leu polymorphism in a total of 113 nuclear families that had a proband with schizophrenia. Genetic association was tested using the transmission disequilibrium test (TDT), the sib transmission disequilibrium test (STDT), and the family-based association test (FBAT). RESULTS: The minor allele (Leu) frequency was calculated to be 0.282. We could not find significant transmission disequilibrium of the alleles for the Pro197Leu polymorphism in the GPX1 gene in association with the presence of schizophrenia in our family sample (TDT, chi2=0.03, degrees of freedom=1, P=0.86; combined TDT-STDT, Z'=-0.052, P=0.47; FBAT, Z=0.000, P=1.000). CONCLUSION: The results of this study suggest that the GPX1 polymorphism is unlikely to be associated with susceptibility to schizophrenia.     

益气活血类方剂配伍方法的探讨

就气虚血瘀证的临床特征病因、病机进行了探讨,旨在为气虚血瘀证提供遭药组方依据,总结了益气活血类方剂的配伍规律,提出了以益气活血类方剂的配伍规律,提出了以益气活血法为主要治则,分别配行经气药,滋阻养血药,利水化痰药,浊阳散寒药达到气顺血调、标本同治。     

分子筛催化剂失活过程分析及评价方法

提出了将“前－后实验”和“连续实验”两种催速失活的实验方法结合起来的一种新的催化剂活性评价方法,可以较短的实验时间内,获得该催化剂比较全面、完整的活性衰退的信息。使用该评价方法,对ZSM－5分子筛催化剂AB－97催化苯与乙烯的烷基化反应的失活规律进行了实验研究,结果表明：在缓和条件与苛刻条件下,催化剂的失活规律有所不同。在实验基础上,结合Monte-Carlo模拟的方法,对此进行了机理分析,发现在不同的反应条件下,反应物在催化剂晶粒表面上吸附位置以及反应机理均不相同,同时证实了实验结果。