1.Individual allergens as risk factors for asthma and bronchial hyperresponsiveness in Chinese children.
Yu-zhi CHEN ; Yu MA ; Hong-yu WANG ; Hai-jun WANG ; Jing ZHAO ; Ling CAO ; Shuo LI ; G W K WONG ; Nan-shan ZHONG ; T F FOK ; C K W LAI
Chinese Journal of Pediatrics 2003;41(7):538-541
OBJECTIVE This study aimed to determine the relationship between individual allergens with current wheezing and bronchial hyperresponsiveness (BHR) in schoolchildren from three chinese cities: Beijing, Guangzhou and Hong Kong. METHODS Community-based random samples of 10-yr-old schoolchildren from the 3 cities were recruited for study using the International Study of Asthma and Allergies in Childhood (ISAAC) Phase II protocol. The subjects were studied by parental questionnaires (n = 10,902), skin-prick tests (n = 3478), and methacholine challenge tests (n = 608). RESULTS The highest prevalence rates of wheezing in the past 12 months (Beijing, 3.8%; Guangzhou, 3.4%; Hong Kong, 5.8%) and atopy (Beijing, 23.9%; Guangzhou, 30.8%; Hong Kong, 41.2%, defined as having
2.12th Yahya Cohen Memorial Lecture: The cellular and molecular basis of radiation-induced sensori-neural hearing loss.
Wong-Kein LOW ; Michelle G K TAN ; Alvin W C CHUA ; Li SUN ; De-Yun WANG
Annals of the Academy of Medicine, Singapore 2009;38(1):91-94
INTRODUCTIONSensori-neural hearing loss (SNHL) is a frequent complication of conventional radiotherapy for head and neck tumours, especially nasopharyngeal carcinoma. To manage radiation-induced ototoxicity appropriately, an understanding of the cellular and molecular basis of this complication is necessary.
MATERIALS AND METHODSA medline search of relevant literature was done, focusing on the radiation-induced cellular and molecular processes that lead to hair cell death in the cochlea.
RESULTSRadiation-induced SNHL occurs in the cochlea, with the retro-cochlear pathways remaining functionally intact. By simulating radiotherapy regimes used clinically, radiation-induced cochlear cell degeneration in the absence of damage to the supporting structures and blood vessels has been demonstrated in animals. This could be due to apoptotic cochlear cell death, which has been shown to be associated with p53 upregulation and intra-cellular reactive oxygen species (ROS) generation. Oxidative stress may initiate the upstream processes that lead to apoptosis and other cell death mechanisms.
CONCLUSIONSA model of radiation-induced SNHL based on a dose and ROS-dependent cochlear cell apoptosis, is proposed. This model supports the feasibility of cochlear implantation, should one be clinically indicated. It can explain clinical observations such as radiation-induced SNHL being dose-dependent and affects the high frequencies more than the lower frequencies. It also opens up the possibility of preventive strategies targeted at different stages of the apoptotic process. Antioxidants look promising as effective agents to prevent radiation-induced ototoxicity; they target upstream processes leading to different cell death mechanisms that may co-exist in the population of damaged cells.
Animals ; Cell Death ; Cell Line ; Cochlea ; radiation effects ; Genes, p53 ; Hair Cells, Auditory ; radiation effects ; Hearing Loss, Sensorineural ; etiology ; genetics ; physiopathology ; Humans ; Mice ; Radiation Injuries ; complications ; Reactive Oxygen Species ; metabolism