2004～2008年洋葱伯克霍尔德菌临床分布和耐药性分析

目的 了解2004年至2008年我院临床分离的洋葱伯克霍尔德菌的标本来源、临床分布和耐药性.方法 采用API staph 鉴定系统和K-B琼脂扩散法,对分离到的55株洋葱伯克霍尔德菌进行鉴定和药敏试验.结果 2004年至2008年共分离出55株洋葱伯克霍尔德菌, 标本来源以痰标本最多(90.91%,50/55),科室分布以ICU最多(60%,33/55),其次为呼吸内科(18.18%,10/55).药敏结果 显示,对多数抗菌药物的耐药率较高,只对美罗培南、哌拉西林/他唑巴坦和亚胺培南的耐药率最低,分别为29.17%、33.33%和39.62%.结论 药敏结果 显示,洋葱伯克霍尔德菌具有高度和多重耐药性,临床抗感染治疗应根据药敏试验结果 选用敏感药物.     

重症监护病房洋葱伯克霍尔德菌肺部感染及耐药性监测

目的 探讨重症监护病房(ICU)洋葱伯克霍尔德菌肺部感染的临床特点及其耐药情况,为临床合理用药提供参考.方法 对2010年10月至2011年10月在ICU住院期间,患者肺部感染洋葱伯克霍尔德菌耐药情况进行回顾性分析.结果 肺部感染患者共检出34株洋葱伯克霍尔德菌,占全部病原菌的1.85％.19种抗菌药物药敏试验结果显示除美罗培南、复方磺胺甲基异噁唑、米诺环素的抑菌活性较高外,其余16种抗菌药物的耐药率高达73.5％～100.0％.结论 洋葱伯克霍尔德菌具有多重耐药性,治疗难度大,应引起足够重视,临床应根据药敏试验结果合理选用抗菌药物.     

2000年至2006年屎肠球菌的临床分离与耐药变迁

目的了解本地区屎肠球菌在临床的分离与耐药变迁情况,为临床抗感染的预防与治疗提供帮助。方法用WHONET 5软件统计分析我院2000年至2006年屎肠球菌临床分离株在各病区、样本中的分布与耐药性的变迁情况。结果分离率呈逐年上升趋势,从2000年的0.32%上升到2006年的0.81%;7年中以重症监护病区（ICU）分离菌株最高,占总分离菌株的68.9%,其次为肾内科病区占13.5%;在送检标本中以尿液标本分离菌株数最高,占总分离数的62.3%,其次为痰液（10.2%）。对11种抗生素的耐药性分析显示,屎肠球菌对青霉素G、氨苄西林、庆大霉素500、环丙沙星、左旋氧氟沙星呈较高的耐药率,而对四环素、呋喃妥因、链霉素2000相对较低;更值得我们注意的是对于万古霉素的耐药率呈逐年上升趋势,对于喹奴普汀/达福普汀、力奈唑烷这两类临床还未运用的抗生素已有一定的耐药率。结论屎肠球菌在临床的分离率在逐年增加,已成为医院内感染的主要病原菌之一,该菌呈多重耐药的特性,并呈不断增加趋势,临床抗感染治疗应以分离菌株的体外抗菌药物敏感性为依据。     

洋葱伯克霍尔德菌致恶性肿瘤患者医院获得性感染的耐药性分析

目的分析我院恶性肿瘤患者医院获得性感染洋葱伯克霍尔德菌的临床特点及对常用抗菌药物的耐药性,为临床合理治疗提供依据。方法回顾性分析2011年1月至2013年12月,从我院恶性肿瘤感染患者送检的细菌培养标本;细菌鉴定用美国BD公司phoenix-100全自动细菌鉴定药敏系统,药敏试验采用纸片法,同时使用WHONET 5.6软件对相关资料进行统计。结果从检测部位分析主要分布在下呼吸道（74.1%）,其次为血液（9.4%）;药敏试验表明139株洋葱伯克霍尔德菌对米诺环素、氯霉素、美罗培南、头孢他啶和头孢哌酮/舒巴坦仍较敏感,可作为临床治疗洋葱伯克霍尔德菌感染的首选药物,其余15种抗菌药物的耐药率高达30.0%~100%。结论洋葱伯克霍尔德菌在恶性肿瘤患者中的耐药现象非常严重,临床应引起高度关注,及早进行微生物学检测,并根据药敏试验结果合理选用抗菌药物。     

摩根摩根菌临床分布及耐药性分析

目的分析摩根摩根菌的临床分布特点及耐药现状,为抗感染治疗提供参考依据。方法对医院2013年7月-2015年6月临床分离的80株摩根摩根菌的来源与耐药性进行回顾性分析,并对痰液标本与其他类型标本分离到的摩根摩根菌对抗菌药物的耐药情况进行统计学比较。结果多种临床标本均可分离到摩根摩根菌,以痰液标本居多,占58.75%;科室分布以ICU为主,占41.25%,其次为急诊内科,占31.25%。20种抗菌药物中,敏感性较高的药物为丁胺卡那霉素(98.75%)、头孢吡肟(91.25%)、氨曲南(87.50%)、亚胺培南(86.25%);痰液标本与其他标本分离到的摩根摩根菌对头孢哌酮/舒巴坦、头孢他啶、头孢曲松、头孢吡肟、厄他培南、亚胺培南、庆大霉素、环丙沙星、复方新诺明等9种抗菌药物有显著性差异(P0.05)。其他标本分离到的摩根摩根菌对此9种药物的敏感性要显著高于痰液标本分离到的摩根摩根菌。结论对摩根摩根菌引起的感染应合理使用抗菌药物早期治疗,避免耐药菌株的产生;不同部位的摩根摩根菌感染应选用不同种抗菌药物,以提高治疗效果。     

洋葱伯克霍尔德菌对哌拉西林/他唑巴坦MIC值变迁的4年监测

目的了解浙江地区4年分离的洋葱伯克霍尔德菌对哌拉西林-他唑巴坦的MIC值变迁,以利于临床对该抗生素在抗感染中更合理的应用。方法先用VITEK-32型配套的药敏检测卡GNS-120检测2000～2003年临床分离的洋葱伯克霍尔德菌对哌拉西林-他唑巴坦的敏感性。对不耐药的菌株进一步用哌拉西林-他唑巴坦E-试条进行MIC检测,并统计其累积的MIC值变化情况。结果2000—2003年,洋葱伯克霍尔德菌对哌拉西林．他唑巴坦的耐药率分别为：40．5％,42．9％,40．6％,41．2％。对分离到不耐哌拉西林．他唑巴坦的100株菌（2000～2003年分别为21株、21株、22株、36株）进行MIC值检测,其累积的MIC百分率,M1C值≤4分别为：47．6％,42．9％,45．5％,36．I％;MIC值≤8分别为：66．7％,52．4％,54．5％,47,2％;MIC值≤16分别为：76．2％,66．7％,63．6％,52．8％。结论4年中临床分离的洋葱伯克霍尔德菌对哌拉西林-他唑巴坦的耐药率虽然变化不大,但其不耐药菌株对哌拉西林-他唑巴坦的累积MIC百分率降低较为明显,表明洋葱伯克霍尔德菌对哌拉西林-他唑巴坦的耐药性存在有增加的趋势,应引起临床的重视。     

重症监护病房非发酵菌分布及耐药分析

目的分析医院重症监护病房非发酵菌感染的耐药情况,以指导临床合理使用抗菌药物。方法回顾性分析2008年至2009年医院自重症监护病房分离的非发酵菌,对其检出率及药敏结果进行统计分析。结果共检出4 273株非发酵菌,检出率为38%,分离率居前4位的依次是铜绿假单胞菌(44.09%)、鲍氏不动杆菌(27.64%)、嗜麦芽寡养单胞菌(10.58%)和洋葱伯克霍尔德菌(5.99%);4种常见的非发酵菌对常用抗菌药物耐药性均较高,头孢哌酮/舒巴坦等含酶抑制剂的复合型抗菌药物对非发酵菌有较高的敏感性。结论医院重症监护病房非发酵菌检出率高且耐药性强,应加强临床细菌学的检测,按照药敏试验结果合理用药。     

医院内尿路感染致病菌变迁及其耐药性监测分析

目的调查院内尿路感染致病菌分布及耐药性变化情况.方法对我院1998年1月-2000 年12月医院内尿路感染患者分离的细菌菌株、真菌菌株及细菌耐药性进行回顾性调查.结果 医院内尿路感染仍以G 菌为主(39.9%),其次为真菌(32.9%),G+菌(27.2%);G -菌以大肠埃希菌为主(41.7%),G+菌以D组链球菌为主(50.3%),真菌以白色念珠菌为主(44.7%),与19 98年分离的菌株相比,2000年G 菌所占比例有下降趋势,而真菌由25.7%上升至36.6%(P< 0.05),3年间主要病原菌对常用抗生素的耐药率基本呈上升趋势.结论院内尿路感染致病菌正在发生变迁 ,耐药性严重,临床应重视病原学检查,开展细菌耐药性监测,合理使用抗生素.     

重症监护病房常见非发酵菌分布及耐药性分析

分析医院重症监护病房非发酵菌感染的耐药情况,以指导临床合理使用抗菌药物。回顾性分析2009~2010年医院自重症监护病房分离的非发酵菌,对其检出率及药敏结果进行统计分析。共检出96株非发酵菌,检出率为19.79%,分离率居前4位的依次为铜绿假单胞菌（46.88%）、鲍氏不动杆菌（21.88%）、嗜麦芽寡养单胞菌（15.63%）、洋葱伯克霍尔德菌（10.42%）;4种常见的非发酵菌对常用的抗菌药物耐药性均较高,头孢哌酮/舒巴坦等含酶抑制剂的复合型抗菌药物对非发酵菌有较高的敏感性。医院重症监护病房非发酵菌检出率高且耐药性强,应加强临床细菌学的检测,按照药敏试验结果合理用药。     

2003年至2007年大肠埃希菌的临床分离及耐药趋势分析

目的了解2003年至2007年大肠埃希菌在临床标本中的分离情况及其耐药趋势,为临床感染的预防和治疗提供参考资料。方法回顾分析2003年至2007年间所有标本中大肠埃希菌的分离率、标本和病区的分布构成情况以及对17种抗菌药物的耐药率。结果五年间大肠埃希菌的总分离率变化不明显,但其阳性分离率呈上升趋势,从2003年的5.02%增至2007年的6.26%;其在泌尿生殖道标本（尿液标本和尿道分泌物标本）的分离率最高（50.5%）,其次是呼吸道标本（36.66%）;病区分布以重症监护室最高（20.7%）,其次是普外科（18.3%）,所有内科病区（不含ICU）占46.6%;大肠埃希菌对12种抗菌药的耐药率大于50%,仅对其中5种的耐药率每年均低于50%。结论大肠埃希菌的临床总分离率没有明显变化,但阳性分离率有呈上升趋势,其对多数抗菌药物有较高的耐药性,所以感染的治疗应当依据抗菌药物的体外敏感试验。     

激光对花生诱变效果的研究

Ｈｅ－ＮｅＹＡＧ和ＣＯ２激光对花生Ｌ１代幼苗期有刺激生长的作用,ＣＯ２激光对花生Ｌ１代的株高有较明显的抑制作用,ＣＯ２,Ｈｅ－Ｎｅ和ＹＡＧ激光对花生Ｌ１代植株的总果数,饱果数有一定的增多作用,且前者最明显,但Ｎ２激光对花生Ｌ１代植株的总果数,饱果数均有明显的减少作用;Ｈｅ－ＮｅＹＡＧ,Ｎ２和ＣＯ２激光均能诱发药生根尖细胞染色体畸变,且畸变率随辐照剂量的增大而上升,以上四种激光所诱发发生的变异性状是     

Cross-resistance to antibiotics of Escherichia coli adapted to benzalkonium chloride or exposed to stress-inducers

AIMS: To study the effects of adaptation and stress on the resistance to benzalkonium chloride (BC) and cross-resistance to antibiotics in Escherichia coli. METHODS AND RESULTS: Precultivation of E. coli ATCC 11775 and E. coli DSM 682 in the presence of subinhibitory concentrations of BC or stress inducers (salicylate, chenodeoxycholate and methyl viologen) resulted in higher minimum inhibitory concentration (MIC) of BC and chloramphenicol (CHL). Adaptation to growth in sixfold of the initial MIC of BC resulted in stable BC resistance and enhanced tolerance to several antibiotics and ethidium bromide (EtBr). The MIC of CHL increased more than 10-fold for both strains. Enhanced efflux of EtBr in adapted E. coli ATCC 11775 indicated that the observed resistance was due to efflux. Changes in outer membrane protein profiles were detected in the BC-adapted cells. There were no indications of lower membrane permeability to BC. CONCLUSIONS: Induction of stress response or gradual adaptation to BC or CHL results in acquired cross-tolerance between BC and antibiotics in E. coli. Enhanced efflux was one of the observed differences in adapted cells. SIGNIFICANCE AND IMPACT OF THE STUDY: Provided not taking due precautions, extensive use of disinfectants could lead to emergence of antibiotic-resistant isolates.     

Capacity of Old Trees to Respond to Environmental Change

Atmospheric carbon dioxide [CO2] has increased dramatically within the current life spans of long-lived trees and old forests. Consider that a 500-year-old tree in the early twenty-first century has spent 70% of its life growing under preIndustrial levels of [CO2], which were 30% lower than current levels. Here we address the question of whether old trees have already responded to the rapid rise in [CO2] occurring over the past 150 years. In spite of limited data, aging trees have been shown to possess a substantial capacity for increased net growth after a period of post-maturity growth decline.Observations of renewed growth and physiological function in old trees have, in some instances, coincided with Industrial Age increases in key environmental resources, including [CO2], suggesting the potential for continued growth in old trees as a function of continued global climate change.     

Failure of CD4 T-cells to respond to liver-derived antigen and to provide help to CD8 T-cells

CD4 T-cell help is required for the induction of efficient CD8 T-cells responses and the generation of memory cells. Lack of CD4 T-cell help may contribute to an exhausted CD8 phenotype and viral persistence. Little is known about priming of CD4 T-cells by liver-derived antigen. We used TF-OVA mice expressing ovalbumin in hepatocytes to investigate CD4 T-cell priming by liver-derived antigen and the impact of CD4 T-cell help on CD8 T-cell function. Naïve and effector CD4 T-cells specific for ovalbumin were transferred into TF-OVA mice alone or together with naïve ovalbumin-specific CD8 T-cells. T-cell activation and function were analyzed. CD4 T-cells ignored antigen presented by liver antigen-presenting cells (APCs) in vitro and in vivo but were primed in the liver-draining lymph node and the spleen. No priming occurred in the absence of bone-marrow derived APCs capable of presenting ovalbumin in vivo. CD4 T-cells primed in TF-OVA mice displayed defective Th1-effector function and caused no liver damage. CD4 T-cells were not required for the induction of hepatitis by CD8 T-cells. Th1-effector but not naïve CD4 T-cells augmented the severity of liver injury caused by CD8 T-cells. Our data demonstrate that CD4 T-cells fail to respond to liver-derived antigen presented by liver APCs and develop defective effector function after priming in lymph nodes and spleen. The lack of CD4 T-cell help may be responsible for insufficient CD8 T-cell function against hepatic antigens.     

Ability of human T lymphocytes to adhere to vascular endothelial cells and to augment endothelial permeability to macromolecules is linked to their state of post-thymic maturation

The accumulation of mononuclear cells at sites of chronic inflammation is dependent on a number of factors including localized adherence of lymphocytes to vascular endothelial cells (EC), cytokine-mediated increased adhesiveness of endothelium, chemotactic factors and endothelial permeability. The present study investigates two of the above attributes of lymphocyte-EC interaction: namely, the ability of maturationally distinct subpopulations of human T lymphocytes to adhere to vascular EC and to increase vascular endothelial permeability to macromolecules in an in vitro model. Thus, human T lymphocytes were separated into CD4+ CD8-helper/inducer, CD4- CD8+ cytotoxic/suppressor, CD29+ CD45RA- CD45RO+ memory, and CD29- CD45RA+ CD45RO- naive/virgin T subpopulations, were activated with PHA and PMA, and then examined for their adherence to EC and also for their effect on endothelial permeability. Upon activation, cells within each of the above four subpopulations exhibited increased adherence to EC. In contrast, resting CD29+ CD45RA- CD45RO+ memory T lymphocytes exhibited two to three times greater ability to adhere to EC than their CD29- CD45RA+ CD45RO- naive/virgin counterparts. Consistent with their increased adherence to EC, CD29+ CD45RO+ memory T lymphocytes, when activated, significantly increased endothelial permeability to albumin. Although activated CD45RA+ naive T lymphocytes exhibited increased adherence to EC, these cells failed to increase significantly endothelial permeability. Similar to their polyclonal counterparts, Ag-specific CD4+ CD29+ CD45RO+ T cell clones, but not their actively released mediators, also increased endothelial permeability via a noncytolytic mechanism(s). This ability of CD29+ CD45RO+ memory T lymphocytes to augment endothelial permeability may facilitate their transendothelial migration into extravascular space. These observations may provide additional insights into molecular mechanism(s) underlying pathophysiology of localized chronic inflammatory responses in general and more specifically selective accumulation of CD29+/CD45RO+ memory T lymphocytes at sites of chronic inflammation such as rheumatoid synovium.     

Adhesion of cellulose to cell walls to Trichoderma reesei

Carbohydrate-binding components were shown to be present at the surface of Listeria monocytogenes by means of a panel of neoglycoproteins using direct agglutination. These lectin-like components bind on neoglycoproteins bearing D-glucosamine, L-fucosylamine, or para-amino-phenyl-alpha-D-mannopyrannoside residues. The interactions were inhibited by the carbohydrate moieties specific to the neoglycoproteins. The protein nature of the lectin-like components of L. monocytogenes was ascertained by the loss of carbohydrate-binding capacity following protease treatment.