新型甲型H1N1流感孕妇的临床表现

2009年4月第1例新型甲型H1N1流感(简称甲型流感)病例确诊[1].这种起源于墨西哥的病毒已传播到美国、加拿大及中国等100多个国家.孕妇是甲型流感发生并发症的高危人群[2],孕妇患重症甲型流感病例和需住院治疗的风险是其他人群的4倍[3].现将孕妇甲型流感病例的临床特点、诊治现状及预防等综述如下.     

新型甲型H1N1流感孕妇的临床表现

2009年4月第1例新型甲型H1N1流感(简称甲型流感)病例确诊[1].这种起源于墨西哥的病毒已传播到美国、加拿大及中国等100多个国家.孕妇是甲型流感发生并发症的高危人群[2],孕妇患重症甲型流感病例和需住院治疗的风险是其他人群的4倍[3].现将孕妇甲型流感病例的临床特点、诊治现状及预防等综述如下.     

北京市某高校甲型H1N1流行性感冒裂解疫苗接种效果分析

2009年一场由新型甲型H1N1流行性感冒(流感)病毒引起的流感疫情在墨西哥暴发,并迅速在多个国家和地区蔓延[1].它引起的临床症状与季节性流感相似,但传染性强于季节性流感病毒,极易在学校、社区暴发流行.研究表明,流感疫苗接种是预防和控制流感最有效的方法[2].本研究分析接种疫苗和未接种的两组学生在历时25 d流感疫情暴发阶段患病情况,旨在了解甲型H1N1流感疫苗对易感人群的保护作用.     

甲型H1N1流行性感冒47例临床分析

2009年3、4月间始发于墨西哥和美国的新型甲型H1N1流行性感冒(流感)是由新的流感病毒变异株引起的急性呼吸道传染病,其发病快,传播迅猛,人群普遍易感[1].世界卫生组织(WHO)认为,此次新型流感病毒在6周内传播的广泛程度是过去的流感病毒需要6个多月的传播才能达到的[2].作为一个新发疾病,其临床特征和治疗方法有必要进一步总结,现报道2009年5月至7月四川省成都市传染病医院收治的47例确诊为甲型H1N1流感病例的诊治经过.     

甲型H1N1流行性感冒47例临床分析

2009年3、4月间始发于墨西哥和美国的新型甲型H1N1流行性感冒(流感)是由新的流感病毒变异株引起的急性呼吸道传染病,其发病快,传播迅猛,人群普遍易感[1].世界卫生组织(WHO)认为,此次新型流感病毒在6周内传播的广泛程度是过去的流感病毒需要6个多月的传播才能达到的[2].作为一个新发疾病,其临床特征和治疗方法有必要进一步总结,现报道2009年5月至7月四川省成都市传染病医院收治的47例确诊为甲型H1N1流感病例的诊治经过.     

甲型H1N1流行性感冒47例临床分析

2009年3、4月间始发于墨西哥和美国的新型甲型H1N1流行性感冒(流感)是由新的流感病毒变异株引起的急性呼吸道传染病,其发病快,传播迅猛,人群普遍易感[1].世界卫生组织(WHO)认为,此次新型流感病毒在6周内传播的广泛程度是过去的流感病毒需要6个多月的传播才能达到的[2].作为一个新发疾病,其临床特征和治疗方法有必要进一步总结,现报道2009年5月至7月四川省成都市传染病医院收治的47例确诊为甲型H1N1流感病例的诊治经过.     

甲型H1N1流行性感冒重症及危重症病例的临床特点与相关危险因素

自2009年4月确诊第一例甲型H1N1流行性感冒(流感)患者以来,甲型H1N1流感已在世界范围暴发流行,尤其2009年11月至12月,重症病例及死亡病例明显增多[1-5].对甲型H1N1流感病毒感染导致的死亡病例分析发现,甲型H1N1流感病毒引起的肺部病变在疾病的发生发展过程中占主导作用[6].     

儿童危重症甲型H1N1流行性感冒40例临床分析

流行性感冒(流感)具有发病率高、传播速度快、流行范围广的特点.流感病毒感染以5～20岁的儿童和青少年多见[1].在流感流行早期,35%～50%的感染者是学龄儿童[2].由于流感病毒不断发生抗原漂移与病毒转换,易发生抗原性、传播性、致病性的变化,故人群对变异株普遍易感.因此,流行常具有周期性,易导致世界性大流行.随着甲型H1N1流感的大范围流行,儿童危重病例不断出现,为提高临床医师对危重病例的认识,提高救治成功率,我们对儿童危重症甲型H1N1流感病例临床资料总结分析如下.     

甲型H1N1流感社区健康教育效果分析

甲型H1N1流感是由A/H1N1流感病毒引起的急性呼吸道传染病,具有人群普遍易感[1].通过健康教育,使人们掌握甲型H1N1流感的预防知识,本文选择2011年1～3月对襄阳市樊城区万户社区医疗服务中心(站)的留观发热病人和辖区居民两类人员进行甲型H1N1流感知识的健康教育,取得满意效果,报告如下.     

西藏甲型H1N1流行性感冒临床特点及实验室诊断

2009年3月甲型H1N1流行性感冒(流感)在全球流行,世界卫生组织(WHO)宣布此次流感为一种新型呼吸道传染病,其病毒为甲型H1N1流感病毒株,病毒基因中包含有猪流感、禽流感和人流感三种流感病毒的基因片段[1].2009年10月我国报道的首例死于甲型H1N1流感的病例发生在西藏墨竹工卡县,现对2009年9-11月在西藏日喀则地区人民医院传染科收治的33例流感患者的流行病学、临床表现、实验室检查、病原学检查及治疗等临床资料进行回顾性分析.     

Cytochrome 1A1 and 1B1 gene diversity in the Zanzibar islands

Amodiaquine (AQ) is a 4‐aminoquinoline widely used in the treatment of malaria as part of the artemisinin combination therapy (ACT). AQ is metabolised towards its main metabolite desethylamodiaquine mainly by cytochrome P450 2C8 (CYP2C8). CYP1A1 and CYP1B1 play a minor role in the metabolism but they seem to be significantly involved in the formation of the short‐lived quinine‐imine. To complete the genetic variation picture of the main genes involved in AQ metabolism in the Zanzibar population, previously characterised for CYP2C8, we analysed in this study CYP1A1 and CYP1B1 main genetic polymorphisms. The results obtained show a low frequency of the CYP1A1*2B/C allele (2.4%) and a high frequency of CYP1B1*6 (approximately 42%) followed by CYP1B1*2 (approximately 27%) in Zanzibar islands. Genotype data for CYP1A1 and CYP1B1 show a low incidence of fast metabolisers, revealing a relatively safe genetic background in Zanzibar’s population regarding the appearance of adverse effects.     

CYP1A1 , GSTM1 , GSTT1 and NQO1 polymorphisms and colorectal adenomas in Japanese men

AIM: To investigate the role of functional genetic poly-morphisms of metabolic enzymes of tobacco carcinogens in the development of colorectal adenomas. METHODS: The study subjects were 455 patients with colorectal adenomas and 1052 controls with no polyps who underwent total colonoscopy in a preretirement health examination at two Self Defense Forces hospitals. The genetic polymorphisms studied wereCYP1A1*2A (rs 4646903), CYP1A1*2C (rs 1048943), GSTM1 (null or non-null genotype), GSTT1 (null or non-null genotype) and NQO1 C609T (rs 1800566). Genotypes were determined by the polymerase chain reaction (PCR)-restriction fragment length polymorphism or PCR method using genomic DNA extracted from the buffy coat. Cigarette smoking and other life-style factors were ascertained by a self-administered questionnaire. The associations of the polymorphisms with colorectal adenomas were examined by means of OR and 95%CI, which were derived from logistic regression analysis. Statistical adjustment was made for smoking, alcohol use, body mass index and other factors. The gene-gene interaction and effect modification of smoking were evaluated by the likelihood ratio test. RESULTS: None of the five polymorphisms showed a significant association with colorectal adenomas, nor was the combination of GSTM1 and GSTT1 . A borderline significant interaction was observed for the combination of CYP1A1*2C and NQO1 (P = 0.051). The OR associated with CYP1A1*2C was significantly lower than unity among individuals with the NQO1 609CC genotype. The adjusted OR for the combination of the CYP1A1*2C allele and NQO1 609CC genotype was 0.61 (95%CI: 0.42-0.91). Although the interaction was not statistically significant (P = 0.24), the OR for individuals carrying the CYP1A1*2C allele and GSTT1 null genotype decreased significantly compared with those who had neither CYP1A1*2C allele nor GSTT1 null genotype (adjusted OR: 0.69, 95%CI: 0.49-0.97). Smoking did not modify the associations of the individual polymorphisms with colorectal adenomas. There w     

The target of ezetimibe is Niemann-Pick C1-Like 1 (NPC1L1)

Ezetimibe is a potent inhibitor of cholesterol absorption that has been approved for the treatment of hypercholesterolemia, but its molecular target has been elusive. Using a genetic approach, we recently identified Niemann-Pick C1-Like 1 (NPC1L1) as a critical mediator of cholesterol absorption and an essential component of the ezetimibe-sensitive pathway. To determine whether NPC1L1 is the direct molecular target of ezetimibe, we have developed a binding assay and shown that labeled ezetimibe glucuronide binds specifically to a single site in brush border membranes and to human embryonic kidney 293 cells expressing NPC1L1. Moreover, the binding affinities of ezetimibe and several key analogs to recombinant NPC1L1 are virtually identical to those observed for native enterocyte membranes. KD values of ezetimibe glucuronide for mouse, rat, rhesus monkey, and human NPC1L1 are 12,000, 540, 40, and 220 nM, respectively. Last, ezetimibe no longer binds to membranes from NPC1L1 knockout mice. These results unequivocally establish NPC1L1 as the direct target of ezetimibe and should facilitate efforts to identify the molecular mechanism of cholesterol transport.     

Interleukin 1 (IL 1)

Interleukin 1 is an essential factor of macrophage dependent T cell activation and has a large quantity of other biological activities. This paper gives a review of present knowledge of Interleukin 1. In addition to biochemical properties, the IL 1 production and IL 1 activities, methods for determining of IL 1 and inhibitory factors of IL 1 induced T cell proliferation are described.     

Pandemic H1N1 influenza

The 2009 H1N1 influenza A virus that has targeted not only those with chronic medical illness, the very young and old, but also a large segment of the patient population that has previously been afforded relative protection - those who are young, generally healthy, and immune naive. The illness is mild in most, but results in hospitalization and severe ARDS in an important minority. Among those who become critically ill, 20-40% will die, predominantly of severe hypoxic respiratory failure. However, and potentially in part due to the young age of those affected, intensive care with aggressive oxygenation support will allow most people to recover. The volume of patients infected and with critical illness placed substantial strain on the capacity of the health care system and critical care most specifically. Despite this, the 2009 pandemic has engaged our specialty and highlighted its importance like no other. Thus far, the national and global critical care response has been brisk, collaborative and helpful - not only for this pandemic, but for subsequent challenges in years ahead.     

Inhibition of procarcinogen-bioactivating human CYP1A1, CYP1A2 and CYP1B1 enzymes by melatonin

Abstract:  Administration of melatonin to rodents decreases the incidence of tumorigenesis initiated by benzo[ a ]pyrene or 7,12-dimethylbenz[ a ]anthracene, which requires bioactivation by cytochrome P450 enzymes, such as CYP1A1, CYP1A2 and CYP1B1, to produce carcinogenic metabolites. The present study tested the hypothesis that melatonin is a modulator of human CYP1 catalytic activity and gene expression. As a comparison, we also investigated the effect of melatonin on the catalytic activity of CYP2A6, which is also a procarcinogen-bioactivating enzyme. Melatonin (3–300 μ m ) decreased 7-ethoxyresorufin O -dealkylation catalyzed by human hepatic microsomes and recombinant CYP1A1, CYP1A2 and CYP1B1, whereas it did not affect coumarin 7-hydroxylation catalyzed by hepatic microsomes or recombinant CYP2A6. Melatonin inhibited CYP1 enzymes by mixed inhibition, with apparent K _i values (mean ± S.E.M.) of 59 ± 1 (CYP1A1), 12 ± 1 (CYP1A2), 14 ± 2 (CYP1B1) and 46 ± 8 μ m (hepatic microsomes). Additional experiments indicated that melatonin decreased benzo[ a ]pyrene hydroxylation catalyzed by hepatic microsomes and CYP1A2 but not by CYP1A1 or CYP1B1. Treatment of MCF-10A human mammary epithelial cells with melatonin (up to 300 μ m ) did not affect basal or benzo[ a ]pyrene-inducible CYP1A1 or CYP1B1 gene expression. Consistent with this finding, melatonin did not influence reporter activity in aryl hydrocarbon receptor-dependent pGudluc6.1-transfected MCF-10A cells treated with or without benzo[ a ]pyrene, as assessed in an in vitro cell-based luciferase reporter gene assay. Overall, melatonin is an in vitro inhibitor of human CYP1 catalytic activity, and it may be useful to develop potent analogues of melatonin as potential cancer chemopreventive agents that block CYP1-mediated chemical carcinogenesis.     

1-Naphthyl isocyanate and 1-naphthylamine as metabolites of 1-naphthylisothiocyanate

Abstract: The importance of the bioactivation of 1-naphthylisothiocyanate was studied. Forty minutes after 1-naphthylisothiocyanate administration to rats, bile was collected over a 2.5-h period; the liver was then excised and homogenized. 1-naphthylisothiocyanate and its metabolites in bile and liver of rats were identified and quantified using coupled gas chromatography-mass spectrometry. Three main compounds were found in all 1-naphthylisothiocyanate-treated animals. They were identified as 1-naphthyl isocyanate, 1-naphthylamine and the parent compound, 1-naphthylisothiocyanate. When rats were given cycloheximide, which attenuates 1-naphthylisothiocyanate toxicity, 30 min before 1-naphthylisothiocyanate (300 mg/kg), 1-naphthyl isocyanate concentration was significantly lower than in rats receiving only 1-naphthylisothiocyanate. The appearance of 1-naphthylamine was also inhibited by cycloheximide, although not to the same extent as 1-naphthyl isocyanate. On the other hand, phenobarbital, which potentiates 1-naphthylisothiocyanate hepatotoxicity, enhanced 1-naphthyl isocyanate and 1-naphthylamine formation. It is suggested that 1-naphthyl isocyanate, 1-naphthylamine and the highly reactive sulfur released from 1-naphthylisothiocyanate might be involved in the hepatotoxic effect of 1-naphthylisothiocyanate.