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.     

Adenosine and Sleep

Over the last several decades the idea that adenosine (Ado) plays a role in sleep control was postulated due in large part to pharmacological studies that showed the ability of Ado agonists to induce sleep and Ado antagonists to decrease sleep. A second wave of research involving in vitro cellular analytic approaches and subsequently, the use of neurochemical tools such as microdialysis, identified a population of cells within the brainstem and basal forebrain arousal centers, with activity that is both tightly coupled to thalamocortical activation and under tonic inhibitory control by Ado. Most recently, genetic tools have been used to show that Ado receptors regulate a key aspect of sleep, the slow wave activity expressed during slow wave sleep. This review will briefly introduce some of the phenomenology of sleep and then summarize the effect of Ado levels on sleep, the effect of sleep on Ado levels, and recent experiments using mutant mouse models to characterize the role for Ado in sleep control and end with a discussion of which Ado receptors are involved in such control. When taken together, these various experiments suggest that while Ado does play a role in sleep control, it is a specific role with specific functional implications and it is one of many neurotransmitters and neuromodulators affecting the complex behavior of sleep. Finally, since the majority of adenosine-related experiments in the sleep field have focused on SWS, this review will focus largely on SWS; however, the role of adenosine in REM sleep behavior will be addressed.