载脂蛋白B基因Xba I和EcoR I位点稀有等位基因与胆石症的关系

目的探讨载脂蛋白B基因XbaI、EcoRI位点稀有等位基因与内蒙古中西部地区汉族和蒙古族胆石症人群的相关性。方法收集2010年4—10月包头医学院第一附属医院100例胆石症患者（结石组）及同期行健康体检的115例正常人（对照组）的临床资料,采用病例对照研究方法和聚合酶链反应一限制性片断长度多态性（PCR—RFLP）技术,检测和分析内蒙古中西部地区的汉族和蒙古族结石组和对照组血样的载脂蛋白B基因XbaI、EcoRI多态性,包括XbaI位点的x±x±、x±X-、X—X一基因型及等位基因x-、x±（稀有等位基因）;EcoRI位点的E±E±、E±E-、E—E一基因型及等位基因E±、E-（稀有等位基因）。检测各组的血脂水平,包括TG、TC、HDL和LDL。计数资料行疋。检验,计量资料行t检验。结果汉族人群与蒙古族人群均无X±x±基因型,且蒙古族人群中亦未发现稀有等位基因X±和E-的存在。在汉族人群中,结石组LDL为（2．8±0．9）mmol／L,显著高于对照组的（1．9±0．8）mmol／L（t=2．800,P〈0．05）;蒙古族人群中,结石组HDL、LDL分别为（1．74-0．3）mmol／L、（3．5±0．8）mmol／L,显著高于对照组的（1．2±0．3）mmol／L、（2．8±0．9）mmol／L（t：7．596,2．549,P〈0．05）。蒙古族人群中,结石组TG、TC、HDL、LDL分别为（3．1±1．6）mmol／L、（5．6±1．0）mmol／L、（1．7±0．3）mmol／L、（3．5±0．8）mmol／L,均显著高于汉族结石组的（1．2±0．6）mmol／L、（4．4±1．2）mmol／L、（1．3±0．3）mmol／L、（2．8±0．9）mmol／L（t=5．501,3．667,4．448,3．430,P〈0．05）。蒙古族对照组TG、TC、LDL分别为（2．6±1．7）mmol／L、（5．1±1．1）mmol／L、（2．8±0．9）mmol／L,均显著高于汉族对照组的（1．3±0．7）mmol／L、（3．9±0．9）mmol／L、（1．9±0．8）mmol／L（t=4．298,4．772,3．888,P〈0．05）,而HDL则在汉族对照组中较高（t=1．997,P〈0．05）。汉族结石组x±x-、x-x-基因型LDL水平分别为（2．7±0．1）mmol／L和（2．6±1．0）mmol／L,E±E±、E±E-／E—E-分别为（2．6±1．0）mmol／L和（2．5±0．4）mmol／L,组内比较,差异无统计学意义（t=0．225,0．124。P〉0．05）。结论在内蒙古中西部地区,蒙古族人群可能比汉族人群容易患胆石症,但载脂蛋白B基因XbaI和EeoRI位点稀有等位基因x±和E一与血脂水平增高未见关联,可能与胆石症发生无关。     

Guidelines for Sclerotherapy of Varicose Veins (ICD 10: I83.0, I83.1, I83.2, and I83.9)

BACKGROUND: Sclerotherapy is the targeted elimination of intracutaneous, subcutaneous, and/or transfascial varicose veins (perforating veins) as well as the sclerosation of subfascial varicose vessels in the case of venous malformation by the injection of a sclerosant. With duplex-guide sclerotherapy and foam sclerotherapy, modified methods came into use. OBJECTIVE: The objective was to create a guideline, based on the available publications and on the European Consensus Document on foam sclerotherapy from April 2003. METHODS: This guideline was drafted on behalf of the German Society of Phlebology (Deutsche Gesellschaft für Phlebologie) and adopted by the committee and scientific advisory board of the Deutsche Gesellschaft für Phlebologie on June 15, 2001, and amended on December 5, 2003. The guideline considers the present state of knowledge as reflected in the literature. CONCLUSIONS: This guideline represents the recent state of the art of sclerotherapy of varicose veins in Germany including foam sclerotherapy.     

Mucopolysaccharidosis type I and craniosynostosis

Mucopolysaccharidosis type-I is caused by a deficiency of the lysosomal enzyme α-L-iduronidase, resulting in gradual deposition of glycosaminoglycans in multiple body organs, affecting physical appearance and system functioning. We present the first reported case associating MPS-I (Hurler-Scheie subtype) with craniosynostosis. A 2.5-year-old girl presented initially with macrocrania. On clinical and radiological examinations we noted a scaphocephaly with dysmorphic facial features of MPS confirmed later on. Intracranial hypertension was documented at fundoscopy (papilloedema) and ICP monitoring, and then surgically treated. This association of scaphocephaly and MPS-I highlights the importance of a meticulous physical examination performed by craniofacial, metabolic and ophthalmologic teams.     

Myocardial fixation of anticardiac troponin I antibody and cardiac troponin I release

BACKGROUND: The threefold aim of this experimental study was to test the correlation of cardiac troponin I released to myocardial infarction size and myocardial fixation of anticardiac troponin I antibody and to determine how long after myocardial infarction the measure of cardiac troponin I concentration can evaluate myocardial infarction size. METHODS: Forty rabbits were assigned either to a control group or to an experimental preconditioned group. Infarction was obtained by tightening a snare around the left anterior descending artery. Serial venous blood samples were drawn for measurement of cardiac troponin I. The rabbits were sacrificed at 72 hours and a histological study was performed to determine the infarct size and the size of the area void of fixation of anticardiac troponin I antibody. RESULTS: There was a linear correlation between the total amount of CTn I released and both infarct size (r=0.45, p<0.02) and the size of the area void of anti-cardiac troponin I antibody (r=0.47, p<0.02). These two sizes were strongly correlated (r=0.95, p<0.02). The hour 9 CTn I sample was the best correlated with both the infarct size (r=0.47, p<0.02) and the size of area void of anticardiac troponin I antibody (r=0.45, p<0.02). CONCLUSIONS: Our study shows that: 1) cardiac troponin I release is correlated to both myocardial infarction size and the size of area void of fixation of anticardiac troponin I antibody, 2) the area void of anticardiac troponin I antibody fixation includes the whole ischemic area, and 3) evaluation of myocardial infarction size can be obtained by CTn I concentration as early as the ninth hour.     

"I know I have arthritis but I don't know what type". Understanding and knowledge of this chronic condition

Background  

"Arthritis" is a common musculoskeletal condition but the knowledge of what type of arthritis people have, may be limited but may have changed over time in response to campaigns, increased awareness and improved health literacy. This paper describes people who did not know what type of arthritis they had, by a range of relevant demographic and socioeconomic variables, and assesses changes over time in the proportion of people who report having arthritis but do not know what type, using representative population surveillance data.