宁波市北仑区2013-2014年儿童哮喘流行病学调查

目的调查宁波市北仑区0~14岁儿童哮喘发病率、发病规律及危险因素,为制定防治措施提供参考。方法2013年1月-2014年1月,采用整群抽样法抽取北仑区19所学校0~14岁儿童为调查对象进行问卷调查,对筛查出的疑似哮喘儿童进行确诊,并对其人口学特征进行分析,采用logistic回归方程分析危险因素。结果调查收回有效问卷23 781份,共检出哮喘患儿534例,发病率为2.25%,男女发病率比例为1.92:1。其中发病较轻患儿占44.01%,中度占31.46%,重度占24.53%。发病时间以换季、冬季为主,分别占35.96%、32.02%。多因素logistic回归分析显示,呼吸道感染、药物过敏史、家族过敏史和食物过敏史是儿童哮喘发病的危险因素(P<0.05)。结论北仑区儿童哮喘发病率较高,具有性别和季节发病差异,应加大对患病危险因素的宣传,规范标准化治疗方案,减少儿童哮喘疾病的发生。     

Reactive oxygen species and human spermatozoa: physiology and pathology

The role of reactive oxygen species (ROS) in the pathophysiology of human sperm function has been emphasized in recent years. ROS production in semen has been associated with loss of sperm motility, decreased capacity for sperm–oocyte fusion and loss of fertility. There is a current presumption that the most prolific source of ROS in sperm suspensions is an NADPH oxidase located in leukocytes or in spermatozoa which produces superoxide which is further converted to peroxide by the action of superoxide dismutase. Hydrogen peroxide has been recognized as the most toxic oxidizing species for human spermatozoa, which are very sensitive to lipid peroxidation owing to the high content of polyunsaturated fatty acids in their plasma membrane, though this is not the sole mechanism by which sperm function might be impaired by ROS. Although the excessive production of ROS is detrimental to human spermatozoa, there is a growing body of evidence which suggests that ROS are also involved in the physiological control of some sperm functions. This review focuses on the nature and source of the ROS generated by human spermataozoa as well as their operational mechanisms and their effects, which may be detrimental or beneficial.     

Interactions of cholecystokinin and glucose in rat pancreatic islets

The effects of sulfated cholecystokinin (CCK-8S) and glucose on insulin secretion and polyphosphoinositide (PPI) metabolism were studied in isolated rat islets. Both agonists stimulate PPI hydrolysis, inositol phosphate accumulation, 3H efflux from [3H]inositol-prelabeled tissue, and 45Ca efflux from prelabeled cells. However, the effects of CCK-8S on PPI metabolism are considerably greater than those of glucose. Furthermore, the effects of CCK-8S on PPI and Ca2+ metabolism are observed whether islets are incubated in either 2.75 or 7 mM glucose, but CCK-8S only stimulates insulin secretion (a biphasic response) when the higher glucose concentration is present. Addition of 1 microM forskolin to islets incubated in media containing 2.75 mM glucose does not influence basal insulin secretion but sensitizes the islets to the action of CCK-8S. In the presence of forskolin, CCK-8S induces a very marked first phase but no second phase of insulin secretion. We postulate that CCK-8S acts in this tissue via receptor-linked PPI hydrolysis, leading to an inositol trisphosphate-induced Ca2+ efflux. These receptor-mediated effects of CCK-8S are not altered either by the ambient glucose concentration or the cAMP content of the islets, but these two factors determine the responsiveness of the islets (in terms of insulin secretion) to a given CCK-8S signal.