Accuracy of FibroScan Controlled Attenuation Parameter and Liver Stiffness Measurement in Assessing Steatosis and Fibrosis in Patients With Nonalcoholic Fatty Liver Disease

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2004-2005年卫生部全国革兰阴性菌细菌耐药性监测

目的 建立全国性细菌耐药监测网,了解我国细菌耐药流行情况.方法 以标准平皿二倍稀释法测定抗菌药物最低抑菌浓度(MIC),并按国家临床实验室标准委员会2004年标准计算细菌敏感度与耐药率.结果 按照监测方案,收集2004年10月1日至2005年9月30日全国15座城市17家医院的4 075株临床分离致病菌,行MIC测定.其中革兰阴性菌3 150株,占77.3%.肠杆菌科细菌对碳青霉烯类抗生素保持较高敏感度,拉氧头孢、哌拉西林/他唑巴坦、头孢哌酮/舒巴坦和头孢吡肟等具有较好的抗菌活性,耐药率<10%.非发酵革兰阴性菌中铜绿假单胞菌和鲍曼不动杆菌对亚胺培南的耐药率分别为10.6%和10.4%,酶抑制剂复方制剂和氟喹诺酮类药物也有较强抗菌作用.结论 大肠埃希菌和鲍曼不动杆菌耐药率增长明显,喹诺酮及氨基糖苷类药物对肠杆菌科细菌抗菌作用并不高,应引起广泛关注.     

2000年武汉地区产超广谱β-内酰胺酶菌种的分布及药敏分析

目的 了解产超广谱β-内酰胺酶(ESBLs)的细菌分离、分布及对抗生素的敏感性。方法 用APl或V1TEK-AMS系统(Bio’Merieux，法国)鉴定菌种，用NCCLS推荐的初筛和确证法检测产ESBLs的细菌，并用K-B法测定其对14种抗生素的敏感性。结果 2000年武汉地区的269株大肠埃希菌、202株肺炎克雷伯菌、149株阴沟肠杆菌、67株费劳地枸椽酸杆菌、43株产酸克雷伯菌中：ESBLs的检出率分别为40．9％、29．2％、20．1％、29．9％、和23．3％。产ESBLs大肠埃希菌、肺炎克雷伯菌对亚胺培南全部敏感，产ESBLs的大肠埃希菌对阿米卡星的耐药率为22．4％，对其它抗生素有不同程度的耐药。结论 产ESBLs的菌株集中在肠杆菌科菌中，以大肠埃希菌、肺炎克雷伯菌、费劳地枸椽酸杆菌的ESBLs产出最高。阴沟肠杆菌、产酸克雷伯菌ESBLs的产出应引起重视。治疗其感染时应首选亚胺培南。     

Modular networks and cumulative impact of lateral transfer in prokaryote genome evolution

Lateral gene transfer is an important mechanism of natural variation among prokaryotes, but the significance of its quantitative contribution to genome evolution is debated. Here, we report networks that capture both vertical and lateral components of evolutionary history among 539,723 genes distributed across 181 sequenced prokaryotic genomes. Partitioning of these networks by an eigenspectrum analysis identifies community structure in prokaryotic gene-sharing networks, the modules of which do not correspond to a strictly hierarchical prokaryotic classification. Our results indicate that, on average, at least 81 +/- 15% of the genes in each genome studied were involved in lateral gene transfer at some point in their history, even though they can be vertically inherited after acquisition, uncovering a substantial cumulative effect of lateral gene transfer on longer evolutionary time scales.     

Current Concepts of Ventricular Defibrillation

Mechanisms of Deflbhllation. The aim of this article is to review the current concepts of ventricular defibrillation. We studied the interaction between strong electrical stimulas and cardiac responses in both animal models and in humans. We found that a premature stimulus (S₂) of appropriate strength results in figure-eight reentry in vitro by inducing propagated graded responses. The same stimulation protocol induces figure-eight reentry and ventricular fibrillation (VF) in vivo. When the S₂ strength and the magnitude of graded responses increase beyond a critical level, the increase in refractoriness at the site of the stimulus becomes so long that the unidirectional block becomes bidirectional block, preventing the formation of reentry (upper limit of vulnerability [DLV]). In other studies, we found that the effects of an electrical stimulation on reentry is in part determined by the timing of the stimulus. A protective zone is present after the induction of VF and after an unsuccessful defibrillation shock during which an electrical stimulus can terminate reentry and protect the heart from VF. These results indicate that the effects of a defibrillation shock is dependent on both the strength and the timing of the shock. Timing is not important in areas where the shock field strength is < ULV because the shock terminates all reentry hut cannot reinitiate new ones. However, in areas where shock field strength is < ULV, the effects of the shock are determined by the timing of the shock relative to local VF activations. This ULV hypothesis of defibrillation explains the probablistic nature of ventricular defibrillation. It also indicates that, to achieve a high probability of successful defibrillation, a shock must result in a shock field strength of < ULV throughout the ventricles.     

MICROBIOTA INSIGHTS IN CLOSTRIDIUM DIFFICILE INFECTION AND INFLAMMATORY BOWEL DISEASE

ABSTRACT

Inflammatory bowel disease (IBD) is characterized by chronic intestinal inflammation that includes Crohn´s disease (CD) and ulcerative colitis (UC). Although the etiology is still unknown, some specific factors have been directly related to IBD, including genetic factors, abnormal intestinal immunity, and/or gut microbiota modifications. Recent findings highlight the primary role of the gut microbiota closely associated with a persistent inappropriate inflammatory response. This gut environment of dysbiosis in a susceptible IBD host can increasingly worsen and lead to colonization and infection with some opportunistic pathogens, especially Clostridium difficile. C. difficile is an intestinal pathogen considered the main cause of antibiotic-associated diarrhea and colitis and an important complication of IBD, which can trigger or worsen an IBD flare. Recent findings have highlighted the loss of bacterial cooperation in the gut ecosystem, as well as the pronounced intestinal dysbiosis, in patients suffering from IBD and concomitant C. difficile infection (CDI). The results of intestinal microbiota studies are still limited and often difficult to compare because of the variety of disease conditions. However, these data provide important clues regarding the main modifications and interrelations in the complicated gut ecosystem to better understand both diseases and to take advantage of the development of new therapeutic strategies. In this review, we analyze in depth the gut microbiota changes associated with both forms of IBD and CDI and their similarity with the dysbiosis that occurs in CDI. We also discuss the metabolic pathways that favor the proliferation or decrease in several important taxa directly related to the disease.     

Small airway disease and its predictors in patients with rheumatoid arthritis

BackgroundRheumatoid arthritis (RA) is a connective tissue disease, characterized by symmetric peripheral polyarthritis. Extra-articular disease occurs in approximately 50% of the patients with lung being a common site. The presence of functional or morphological abnormalities in small airways has recently been noted in patients with RA but its exact prevalence and clinical significance is still a subject of debate. This study was aimed to determine the prevalence of small airway disease (SAD) in patients with RA and the factors influencing it.MethodsFifty consecutive patients with RA were included in this cross-sectional observational study. All patients were subjected to pulmonary function tests (PFT) including Spirometry and Forced Oscillation technique (FOT). Those with features of SAD on PFT were subjected to High-Resolution Computed Tomography (HRCT) of the chest.ResultsSpirometry was suggestive of SAD in 17 patients, with 34% prevalence and FOT was abnormal in 9 patients, with 18% prevalence in the study population. Of 17 patients with SAD on spirometry, 8 (47.05%) patients showed mosaic attenuation, a sign of SAD on the HRCT chest. On univariate analysis, age, Disease Activity Score (DAS-28), joint erosions on X-ray, RF and anti-CCP were found to be associated with SAD.ConclusionSAD was present in one-third of the patients with RA, even in those with short duration of disease, low to moderate disease activity and no respiratory symptoms. It is thus inferred that the complete workup of RA patients should include pulmonary function assessment.     

Definition and Management of Patients With Primary Biliary Cholangitis and an Incomplete Response to Therapy

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大连市结核病控制对策与结核病耐药趋势

目的　评价 1993—2000年大连市结核病防治效果及结核分支杆菌的耐药率趋势。方法 对疫情统计资料进行分析 ,采用绝对浓度间接法对 4种药物进行耐药测定。结果 1993—2000年DOTS坚持率分别为 7.0%、27.0%、41.4%、35.1%、68.4%、73.8%、77.6%、89.6%。涂阳治愈率分别为 54.0%、67.1%、73.2%、84.3%、91.0%、93.5%、94.0%、92.7%。初始耐药率由 1993—1994的 34.6%下降至 1999—2000年的 18.2% ,获得性耐药率由 1993—1994年的 52.1%下降至 1999—2000年的 35.7%。结论 大连市初始及获得性耐药率均呈下降趋势。归口管理和实行DOTS策略是耐药率下降的主要原因。     

Phase II study of tailored S-1 monotherapy with a 1-week interval after a 2-week dosing period in elderly patients with advanced non-small cell lung cancer

Background

S-1 is an oral fluoropyrimidine that is active in the treatment of non-small cell lung cancer (NSCLC); however, an optimal treatment schedule and appropriate dose adjustments of S-1 in elderly patients have not yet been established.