C反应蛋白、糖化血红蛋白与尿mAlb对糖尿病肾病的诊断价值

目的：探讨C反应蛋白、糖化血红蛋白与尿微量白蛋白对早期诊断糖尿病肾病的价值。方法：采用速率散比浊法,离子交换高压液相色谱法检测了65例2型糖尿病患者与71例健康对照者体内的C反应蛋白、糖化血红蛋白与尿微量白蛋白的水平。结果：C反应蛋白、糖化血红蛋白与尿微量白蛋白的水平在2型糖尿病组高于健康对照组,差异有统计学意义。结论：联合检测糖尿病患者C反应蛋白、糖化血红蛋白与尿微量白蛋白有利于糖尿病肾病的早期检出,延缓糖尿病肾病的进展。     

探讨尿微量白蛋白、超敏C-反应蛋白联合糖化血红蛋白在糖尿病肾病早期检测的价值

目的探讨尿微量白蛋白、超敏C-反应蛋白联合糖化血红蛋白在糖尿病肾病早期检测的价值。方法选择该院2017年1月—2018年8月糖尿病肾病患者60例,根据血糖不同水平将患者分为低水平组、中水平组和高水平组。同时以该院健康成人作对照组。比较上述患者尿微量白蛋白、超敏C-反应蛋白联合糖化血红蛋白水平。结果糖尿病肾病患者及对照组上述3项指标有差异,同时不同亚组糖尿病肾病患者上述指标也存在差异。结论该文认为尿微量白蛋白、超敏C-反应蛋白联合糖化血红蛋白在糖尿病肾病的早期检测中有重要价值。     

2型糖尿病肾病检测糖化血红蛋白及尿微量白蛋白的价值分析

目的研究分析2型糖尿病肾病检测糖化血红蛋白及尿微量白蛋白的价值。方法选取2018年6月—2019年3月份间该院收治的糖尿病肾病患者240例为研究组,同期进行健康体检的健康人员200名为对照组;收集所有研究对象的外周静脉血及尿液进行检验,对比两组研究对象糖化血红蛋白、尿微量白蛋白指标的变化及研究组糖化血红蛋白、尿微量白蛋白指标有差异的比较。结果研究组,糖化血红蛋白、尿微量白蛋白指标显著高于对照组,差异有统计学意义(P0.05)。高值组患者尿微量白蛋白指标(111.82±21.09)mg/L,显著高于其他两组,差异有统计学意义(P0.05)。结论 2型糖尿病肾病检测糖化血红蛋白及尿微量白蛋白对患者肾功能损伤有提示,且糖化血红蛋白指标与尿微量白蛋白指标呈现正相关性,对肾损伤程度有提示。     

探析血同型半胱氨酸、糖化血红蛋白、尿微量白蛋白及β2-微球蛋白联合检验在2型糖尿病早期肾损害诊断中的临床价值

目的探讨血同型半胱氨酸(HCY)、糖化血红蛋白(Hb A1c)、尿微量白蛋白(U-m Alb)、尿β2-微球蛋白(尿β2-MG)联合检测在2型糖尿病(T2DM)肾病早期诊断中的价值。方法抽取该院2013年6月—2014年12月来该院就诊92例2型糖尿病患者,其中糖尿病肾病40例(观察1组)、2型糖尿病非肾病52例(观察2组),正常健康体检者54例(对照组)为研究对象,检测血同型半胱氨酸(HCY)、糖化血红蛋白(Hb A1c)、尿微量白蛋白(U-m Alb)、尿β2-微球蛋白(尿β2-MG)指标参数的含量,并对其检测结果进行比对。结果观察1组和2组的血同型半胱氨酸(HCY)、糖化血红蛋白(Hb A1c)、尿微量白蛋白(U-m Alb)、尿β2-微球蛋白(尿β2-MG)明显高于对照组,差异有统计学意义(P0.01);糖尿病的病程的长短与血同型半胱氨酸(HCY)、糖化血红蛋白(Hb A1c)、尿微量白蛋白(U-m Alb)、尿β2-微球蛋白(尿β2-MG)指标有密切关系,糖尿病的病程与血同型半胱氨酸(HCY)、糖化血红蛋白(Hb A1c)、尿微量白蛋白(Um Alb)、尿β2-微球蛋白(尿β2-MG)成正比,糖尿病的病程越长血同型半胱氨酸(HCY)、糖化血红蛋白(Hb A1c)、尿微量白蛋白(U-m Alb)、尿β2-微球蛋白(尿β2-MG)指标越高。结论对2型糖尿病(T2DM)患者进行定期联合检测血同型半胱氨酸(HCY)、糖化血红蛋白(Hb A1c)、尿微量白蛋白(U-m Alb)、尿β2-微球蛋白(尿β2-MG)指标参数,通过这些指标参数值能准确掌握糖尿病是否侵蚀肾功,为糖尿病早期肾损害诊断、治疗提供可靠依据。     

血镁水平与2型糖尿病及糖尿病肾病的相关性

目的讨论血镁水平与2型糖尿病及糖尿病肾病的关系。方法选取已明确诊断为2型糖尿病的患者60名,根据24 h尿白蛋白排泄量分为正常蛋白尿组,微量蛋白尿组,大量蛋白尿组;并以同期在该院体检中心体检健康者20名作为对照组。采集一般治疗(包括身高、体重、病程、性别、年龄等),检测空腹静脉血糖、糖化血红蛋白、血清镁及24 h尿微量白蛋白等。结果与对照组相比,2型糖尿病患者普遍存在低镁倾向,其下降程度随着24 h尿微量白蛋白量的增加而加重;同时,2型糖尿病血镁水平与糖化血红蛋白及空腹血糖均呈负相关。结论 2型糖尿病患者可导致血镁下降,并一定程度反映糖尿病肾病的严重程度。     

氧化型低密度脂蛋白和超敏C反应蛋白与糖尿病微血管病变的相关性分析

目的探讨2型糖尿病患者氧化型低密度脂蛋白（oxLDL）与超敏C反应蛋白（hsCRP）水平的变化及其与微血管病变的关系。方法选择2型糖尿病患者81例,按患者的尿白蛋白排泄率分为早期肾病组41例和临床肾病组40例。同时行眼底镜检查分为背景性视网膜病变组58例和增殖性视网膜病变组23例。正常对照组30例。均检测其血清hsCRP、oxLDL、血脂、糖化血红蛋白（HbAlc）、尿微量白蛋白（MAU）、空腹血糖（FPG）、空腹胰岛素水平等,并进行各项指标之间的相关分析。结果糖尿病患者血清oxLDL和hsCRP水平均明显高于正常人,临床肾病组显著高于早期肾病组,增殖性视网膜病变组显著高于背景性视网膜病变组。hsCRP与oxLDL水平正相关（r=0．4023,0．0005）。结论高水平的oxLDL和hsCRP对糖尿病微血管病变的发生发展均有促进作用。     

2型糖尿病合并肾病患者尿MCP-1变化的临床意义

对2型糖尿病（T2DM）及合并微量蛋白尿、大量蛋白尿患者用酶法检测血糖、糖化血红蛋白，用酶联免疫吸附法检测血、尿单核细胞趋化蛋白-1（MCP-1）。结果显示，各组间血MCP-1水平无显著性差异，但合并糖尿病肾病（DN）患者的尿MCP-1水平显著高于T2DM患者；且尿MCP-1与尿白蛋白、糖化血红蛋白、舒张压呈正相关。提示T2DM患者的高血糖可能促进肾脏局部组织过多表达MCP-1，MCP-1可能参与DN的发生和早期发展。     

2型糖尿病血清超敏C反应蛋白的表达与糖尿病肾病发病的相关性分析

目的探讨2型糖尿病肾患者超敏C反应蛋白检测对诊断的临床意义。方法 2016年1月—2017年10月入住该院的120例2型糖尿病患者,分为正常蛋白尿组49例,大量蛋白尿组27例,微量蛋白尿组44例,正常人对照组45名为健康体检者,检测各组患者超敏C反应蛋白的表达水平。结果与正常对照组比较,微量白蛋白尿组超敏C反应蛋白水平明显升高,高于正常蛋白尿组,比较差异有统计学意义(P0.05);大量蛋白尿组与正常对照组比较,超敏C反应蛋白明显升高,且均高于微量蛋白尿组,差异有统计学意义(P0.05)。各指标蛋白尿组微量蛋白尿组正常蛋白尿组的阳性率,表明所选指标可反映患者病情。结论 2型糖尿病肾病早期采用超敏C反应蛋白联合检测具有良好的应用价值。     

尿微量白蛋白和糖化血红蛋白联合检测对糖尿病肾病的临床意义

目的通过对不同人群尿微量白蛋白和糖化血红蛋白检测值的比较,对尿微量白蛋白和糖化血红蛋白联合检测的意义做出评价。方法将2013年7月-2015年12月在我院进行检测的患者,分为糖尿病肾病组(a1)、糖尿病组(a2)、正常组(b),对着三组分别进行尿微量白蛋白和糖化血红蛋白检测,通过SPSS17.0对数据进行统计分析。结果糖尿病肾病组尿微量白蛋白和糖化血红蛋白检测值显著高于糖尿病组,同时糖尿病组显著高于正常组,组间比较均具有统计学意义(P0.05)。结论尿微量白蛋白和糖化血红蛋白能够作为检测糖尿病肾病的指标,显著提高治疗效果,值得临床推广。     

老年2型糖尿病肾病患者血清C肽与尿白蛋白排泄率的关系

目的研究老年2型糖尿病肾病患者血清C肽水平与尿白蛋白排泄率的关系。方法选取老年2型糖尿病患者44例,分别测定血清C肽水平、糖化血红蛋白(HbA1c)、空腹血糖及尿白蛋白排泄率,并据尿白蛋白排泄率分为正常白蛋白尿组、微量白蛋白尿组、临床白蛋白尿组。结果临床白蛋白尿组血清C肽水平低于其他两组,差异有显著性意义(P<005)。血清C肽水平与尿白蛋白排泄率呈负相关(r=-0629,P<001)。结论血清C肽水平的下降可能参与老年2型糖尿病肾病的发生发展。     

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     

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.     

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.