人巨细胞病毒对单纯疱疹病毒1型抗原表达的影响

我们用免疫胶体金色埋前标记技术和免疫荧光技术研究了人胚肺细胞(HEL)内,人巨细胞病毒(HCMV-AD_(169))对单纯疱疹病毒1型(HSV-ⅠSM_(44))抗原表达的影响,旨在探讨在细胞这一微生境内,一病毒对另一病毒可能发生的影响。电镜下计数HSV-1组和HCMV HSV-1组特异性结合金颗粒数得HSV-1组为657个,HCMV HSV-1组的总数为283个。t检验P<0.01,差别非常显著。并且HSV-1组细胞的胞浆中的病毒颗粒,比HCMV HSV-1组明显多。荧光显微镜下:HSV-1组阳性细胞数为689个HCMV HSV-1组只有484个,经poisson分布u检验,P<0.01,差别非常显著。免疫荧光实验还表明:HSV-1组,抗血清在1:320时仍有荧光清晰的阳性细胞,而HCMV HSV-1组,抗血清在1:160时,却无荧光阳性细胞。细胞病变效应(CPE)动态观察显示:HSV-1组8小时即有细胞病变,24小时蔓延整个单层;而HCMV HSV-1组超感染14小时才有细胞病变。24小时约有75％细胞受累。结果表明HCMV对HSV-1的抗原表达有明显的抑制作用。对抑制作用的可能机理及其在分子生态学中的意义,进行了讨论。     

Effect of dimethylglycine and trimethylglycine (Betaine) on the response of Atlantic salmon (Salmo salar L.) smolts to experimental Vibrio anguillarum infection

Atlantic salmon (Salmo salar L.) were fed on a control diet or experimental diets containing betaine (15 mg g^-1) or dimethylglycine (DMG, I mg g^-1 or 5 mg g^-1). After 10 weeks of feeding, resistance to infection was assessed following inoculation with Vibrio anguillarum. Total blood and differential leucocyte counts were made, and plasma lysozyme and ceruloplasmin were assayed as non-specific humoral factors. The mortality during the bacterial exposure was of the same magnitude in all feeding groups. Betaine or DMG had no effect on the 'basal' levels of plasma total protein, lysozyme or ceruloplasmin, but 3 days postinjection the lysozyme and ceruloplasmin levels were higher in the control group compared with the experimental groups. In both DMG groups, the lymphocyte response took place 1-2 weeks earlier than in the control or betaine supplemented group indicating that DMG has an immunomodulating effect on salmon.     

Programmed ageing: decline of stem cell renewal,immunosenescence, and Alzheimer's disease

The characteristic maximum lifespan varies enormously across animal species from a few hours to hundreds of years. This argues that maximum lifespan, and the ageing process that itself dictates lifespan, are to a large extent genetically determined. Although controversial, this is supported by firm evidence that semelparous species display evolutionarily programmed ageing in response to reproductive and environmental cues. Parabiosis experiments reveal that ageing is orchestrated systemically through the circulation, accompanied by programmed changes in hormone levels across a lifetime. This implies that, like the circadian and circannual clocks, there is a master ‘clock of age’ (circavital clock) located in the limbic brain of mammals that modulates systemic changes in growth factor and hormone secretion over the lifespan, as well as systemic alterations in gene expression as revealed by genomic methylation analysis. Studies on accelerated ageing in mice, as well as human longevity genes, converge on evolutionarily conserved fibroblast growth factors (FGFs) and their receptors, including KLOTHO, as well as insulin-like growth factors (IGFs) and steroid hormones, as key players mediating the systemic effects of ageing. Age-related changes in these and multiple other factors are inferred to cause a progressive decline in tissue maintenance through failure of stem cell replenishment. This most severely affects the immune system, which requires constant renewal from bone marrow stem cells. Age-related immune decline increases risk of infection whereas lifespan can be extended in germfree animals. This and other evidence suggests that infection is the major cause of death in higher organisms. Immune decline is also associated with age-related diseases. Taking the example of Alzheimer's disease (AD), we assess the evidence that AD is caused by immunosenescence and infection. The signature protein of AD brain, Aβ, is now known to be an antimicrobial peptide, and Aβ deposits in AD brain may be a response to infection rather than a cause of disease. Because some cognitively normal elderly individuals show extensive neuropathology, we argue that the location of the pathology is crucial – specifically, lesions to limbic brain are likely to accentuate immunosenescence, and could thus underlie a vicious cycle of accelerated immune decline and microbial proliferation that culminates in AD. This general model may extend to other age-related diseases, and we propose a general paradigm of organismal senescence in which declining stem cell proliferation leads to programmed immunosenescence and mortality.     

Stanford A型主动脉夹层孙氏手术患者术后血流感染的影响因素及术前PCT、IL-6、D-D的预测价值研究

摘要 目的：分析Stanford A型主动脉夹层（AD）孙氏手术患者术后血流感染（BSI）的影响因素,并探讨术前血清降钙素原（PCT）、白细胞介素-6（IL-6）、D-二聚体（D-D）对术后发生BSI的预测价值。方法：选取2019年1月～2022年1月贵州医科大学附属医院收治的236例接受孙氏手术的Stanford A型AD患者,根据术后是否BSI分为BSI组和非BSI组。收集患者基础资料和实验室指标,采用多因素Logistic回归分析Stanford A型AD孙氏手术患者术后发生BSI的影响因素,采用受试者工作特征（ROC）曲线分析血清PCT、IL-6、D-D水平对Stanford A型AD孙氏手术患者术后发生BSI的预测价值。结果：BSI组年龄≥60岁、糖尿病史、机械通气、气管切开、人工瓣膜植入比例和术后24 h引流量、血清C反应蛋白、PCT、IL-6、D-D水平高于非BSI组,手术时间、心包纵隔管保留时间长于非BSI组（P＜0.05）。多因素Logistic回归分析显示,年龄≥60岁、糖尿病史、机械通气、气管切开、术后24 h引流量上升,血清PCT、IL-6、D-D水平上升为Stanford A型AD孙氏手术患者术后发生BSI的危险因素（P＜0.05）。ROC曲线分析显示,血清PCT、IL-6、D-D三项联合预测的Stanford A型AD孙氏手术患者术后发生BSI的曲线下面积大于单独预测。结论：年龄、糖尿病史、机械通气、气管切开、术后24 h引流量、血清PCT、IL-6、D-D水平是Stanford A型AD孙氏手术患者术后发生BSI的影响因素,术前血清PCT、IL-6、D-D水平可作为Stanford A型AD孙氏手术患者术后发生BSI的辅助预测指标。     

小儿豉翘清热颗粒联合奥司他韦对急性上呼吸道感染患儿血清炎性因子和外周血T淋巴细胞亚群的影响

摘要 目的：探讨小儿豉翘清热颗粒联合奥司他韦对急性上呼吸道感染患儿血清炎性因子和外周血T淋巴细胞亚群的影响。方法：选择2019年9月至2022年1月期间合肥市第二人民医院收治的急性上呼吸道感染患儿180例。按照双色球法将患儿分为对照组和研究组,在常规治疗的基础上,对照组（给予磷酸奥司他韦颗粒治疗）和研究组（给予小儿豉翘清热颗粒联合磷酸奥司他韦颗粒治疗）,两组各为90例。对比两组疗效、临床症状缓解情况、T淋巴细胞亚群指标、炎性因子水平和不良反应发生情况。结果：研究组的临床总有效率为95.56%,高于对照组的83.33%（P<0.05）。研究组的咳嗽、发热、咽痛、鼻塞流涕等症状缓解时间均短于对照组（P<0.05）。治疗5 d后,研究组CD3⁺、CD4⁺、CD4⁺/CD8⁺高于对照组,CD8⁺低于对照组（P<0.05）,研究组血清降钙素原（PCT）、白介素6（IL-6）、血清淀粉样蛋白A（SAA）、超敏C反应蛋白（hs-CRP）低于对照组（P<0.05）。两组不良反应发生率组间对比无明显差异（P>0.05）。结论：奥司他韦联合小儿豉翘清热颗粒治疗急性上呼吸道感染,可提高患儿的免疫力,降低血清PCT、IL-6、SAA、hs-CRP水平,有助于临床症状改善。     

多药耐药菌感染重症肺炎患者预后的危险因素分析

摘要 目的：探讨多药耐药菌感染重症肺炎患者预后的危险因素。方法：选取本院2019年5月至2022年5月收治的198例重症肺炎患者,根据患者在ICU住院期间是否死亡分为存活组（121例）和死亡组（77例）。对重症肺炎患者多药耐药菌感染情况,多药耐药G⁺耐药情况,多药耐药G^-耐药情况进行分析,对影响多药耐药菌感染重症肺炎患者预后危险因素的单因素分析,将单因素分析中差异有统计学意义的变量进行多因素Logistic回归分析,筛选影响多药耐药菌感染重症肺炎患者预后的危险因素。结果：198例重症肺炎患者中,多药耐药菌感染患者60例,占比30.30 %,共分离出病原菌290株,其中多药耐药菌65株,占比22.41 %,其中占比比较高的有鲍曼不动杆菌（23.08 %）、铜绿假单胞菌（20.00 %）、金黄色葡萄球菌（20.00 %）、肠炎克雷伯菌（10.77 %）;重症肺炎患者多药耐药G⁺对青霉素、克林霉素、红霉素等具有较高的耐药性,而对万古霉素、替考拉宁、替加环素较为敏感;重症肺炎患者多重耐药G^-对多种抗菌药物均表现出耐药性,其中对头孢他啶、头孢吡肟等具有较高的耐药性;单因素分析结果显示,死亡组患者中男性、年龄≥70岁、APACHEⅡ评分≥26分、有创通气的患者占比显著高于存活组,碳青霉烯类抗生素使用的患者占比显著低于存活组（均P<0.05）,两组患者肺部基础疾病、脑血管疾病、高血压、联合使用其他抗生素的占比,以及两组患者机械通气时间比较无差异（均P>0.05）;纳入多因素非条件Logistic回归模型分析显示,男性、年龄≥70岁、APACHEⅡ评分≥26分、有创通气为多药耐药菌感染重症肺炎患者预后的危险因素（OR=1.568、1.203、2.812、1.674,均P<0.05）,而碳青霉烯类抗生素使用是多药耐药菌感染重症肺炎患者预后的保护因素（OR=0.542,P<0.05）。结论：多药耐药菌感染重症肺炎患者的主要菌株为鲍曼不动杆菌,且男性、年龄≥70岁、APACHEⅡ评分≥26分、有创通气为多药耐药菌感染重症肺炎患者预后的危险因素,而碳青霉烯类抗生素使用是多药耐药菌感染重症肺炎患者预后的保护因素。     

重症急性胰腺炎合并腹腔感染患者病原菌分布、药物敏感性分析及其院内死亡的危险因素探讨

摘要 目的：观察重症急性胰腺炎（SAP）合并腹腔感染（IAI）患者病原菌分布,分析药物敏感性,同时探讨其院内死亡的危险因素。方法：本研究纳入2017年1月~2022年1月期间来解放军联勤保障部队第九二二医院接受治疗并确诊的SAP合并IAI患者100例,采集患者腹水标本,观察其病原菌分布,分析药物敏感性。入院后收集患者人口学特征、实验室检查等资料,探讨患者院内死亡的危险因素。结果：100例SAP合并IAI患者腹水标本中,分离出186株病原菌,其中革兰阴性菌有108株,占比58.06%。革兰阳性菌51株,占比27.42%。真菌27株,占比14.52%。鲍曼不动杆菌对不同抗菌药物的敏感性均较低,大肠埃希菌对厄他培南、亚胺培南、哌拉西林／他唑巴坦、庆大霉素、美罗培南的敏感性较高,肺炎克雷伯菌对亚胺培南、美罗培南的敏感性较高,葡萄球菌属对替加环素、万古霉素、利奈唑胺的敏感性较高,屎肠球菌对替加环素、利奈唑胺的敏感性较高,粪肠球菌对氨苄西林、万古霉素、环丙沙星、替加环素的敏感性较高。单因素分析显示,SAP合并IAI患者院内死亡与器官障碍数目、膀胱压、入院时急性生理学与慢性健康状况评分（APACHE II）评分、白细胞计数（WBC）、血钙、红细胞压积（HCT）、总胆固醇（TC）、甘油三醋（TG）、降钙素原（PCT）、C反应蛋白（CRP）、动脉二氧化碳分压（PaCO₂）、动脉氧分压（PaO2）有关（P<0.05）。多因素Logistic回归分析结果显示：器官障碍数目偏多、血钙偏低、CRP偏高、APACHE II评分偏高、膀胱压偏高、PaO₂偏低、WBC偏高是导致SAP合并IAI患者院内死亡的危险因素（P<0.05）。结论：SAP合并IAI患者病原菌分布以革兰阴性菌为主,主要的革兰阴性菌、革兰阳性菌耐药率高。此外,器官障碍数目偏多、血钙偏低、CRP偏高、APACHE II评分偏高、膀胱压偏高、PaO₂偏低、WBC偏高是影响SAP合并IAI患者院内死亡的危险因素。