[Huang, Fulian; Tian, Shaowen; Yang, Yufeng; Deng, Haifeng; Li, Zengbang; Ouyang, Xinping] Univ S China, Coll Med, Dept Physiol, Hengyang 421001, Hunan, Peoples R China.;[Li, Peng] Univ S China, Coll Life Sci & Technol, Dept Biol, Hengyang 421001, Hunan, Peoples R China.
[Tian, Shaowen] Univ S China, Coll Med, Dept Physiol, Hengyang 421001, Hunan, Peoples R China.
Sleep<&wdkj&>Rapid eye movement sleep deprivation<&wdkj&>Fear memory<&wdkj&>Reconsolidation<&wdkj&>Rats
There is increasing evidence that sleep may be involved in memory consolidation. However, there remain comparatively few studies that have explored the relationship between sleep and memory reconsolidation. At present study, we tested the effects of rapid eye movement sleep deprivation (RSD) on the reconsolidation of cued (experiment 1) and contextual (experiment 2) fear memory in rats. Behaviour procedure involved four training phases: habituation, fear conditioning, reactivation and test. Rats were subjected to 6 h RSD starting either immediately after reactivation or 6 It later. The control rats were returned to their home cages immediately after reactivation and left undisturbed. Contrary to those hypotheses speculating a potential role of sleep in reconsolidation, we found that post-reactivation RSD whether from 0 to 6 It or 6 to 12 h had no effect on the reconsolidation of both cued and contextual fear memory. However, our present results did not exclude the potential roles of non-rapid eye movement sleep in the reconsolidation of fear memory or sleep in the reconsolidation of other memory paradigms. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
OBJECTIVE: To investigate awareness and knowledge of human papillomavirus (HPV) infection among high school students and to provide a basis for health education on HPV infection for high school students in China. STUDY DESIGN: A ques- awareness of tionnaire on HPV awareness and knowledge was adminis- provide the tered to 900 high school students in Xiangtan City of Hunan Province in China by layer cluster sampling. A total of 848 anonymous valid questionnaires were received from volunteers who cornpleted the questionnaire correctly. RESULTS: Only 10.1% had heard of HPV, and of those only 18.6% knew that HPV could lead to cervical cancer. Single factor analysis indicated that home address, age, grade, academic achievement, sex history, gender, father's education level and mother's education level were impact factors for HPV knowledge of high school students. Multiple regression analysis showed 4 independent risk factors associated with HPV knowledge: academic achievement, sex history, gender, and mother's education level. The limited knowledge came primarily frorri television and radio broadcasts (59.3%), the Internet (57.0%), parents (25.6%), medical workers (20.9%), and teachers (18.6%). CONCLUSION: High school students lack HPV people's knowledge, which is affectand CC can ed by multiple factors. Targeted health education of for targeted all sorts must be provided. Both schools and families are responsible for reinforcing HPV education provided to high school students.
Chronic stress increases susceptibility to food addiction by increasing the levels of DR2 and MOR in the nucleus accumbens Nai-Li Wei,1,2 Zi-Fang Quan,3,4 Tong Zhao,1 Xu-Dong Yu,4 Qiang Xie,1 Jun Zeng,1 Fu-Kai Ma,1 Fan Wang,1 Qi-Sheng Tang,1 Heng Wu,3 Jian-Hong Zhu11Fudan University Huashan Hospital, Department of Neurosurgery, State Key Laboratory for Medical neurobiology, Institutes of Brain Science, Shanghai Medical College-Fudan University, Shanghai, 20040, People’s Republic of China; 2Department of Neurosurgery, The Second Hospital of Lanzhou University, Lanzhou Gansu China, 730030, People’s Republic of China; 3Department of Neurology, The First Affiliated Hospital, University of South China, Hengyang, Hunan, 421001, People’s Republic of China; 4Institute of Neuroscience, Medical College, University of South China, Hengyang, Hunan, 421001, People’s Republic of ChinaBackground: Stress-related obesity might be related to the suppression of the hypothalamic-pituitary- adrenocortical axis and dysregulation of the metabolic system. Chronic stress also induces the dysregulation of the reward system and increases the risk of food addiction, according to recent clinical findings. However, few studies have tested the effect of chronic stress on food addiction in animal models.Purpose: The objective of this study was to identify whether chronic stress promotes food addiction or not and explore the possible mechanisms.Method: We applied adaily 2 hrsflashing LED irradiation stress to mice fed chow or palatable food to mimic the effect of chronic stress on feeding. After 1 month of chronic stress exposure, we tested their binge eating behaviors, cravings for palatable food, responses for palatable food, and compulsive eating behaviors to evaluate the effect of chronic stress on food addiction-like behaviors. We detected changes in the levels of various genes and proteins in the nucleus accumbens (NAc), ventral tegmental area (VTA) and lateral hypothalamus using qPCR and immunofluorescence staining, respectively.Results: Behaviors results indicated chronic stress obviously increased food addiction score (FAS) in the palatable food feeding mice. Moreover, the FAS had astrong relationship with the extent of the increase in body weight. Chronic stress increased the expression of corticotropin-releasing factor receptor 1(CRFR1) was increased in the NAc shell and core but decreased in the VTA of the mice fed with palatable food. Chronic stress also increased expression of both dopamine receptor 2 (DR2) and mu-opioid receptor (MOR) in the NAc.Conclusion: Chronic stress aggravates the FAS and contributed to the development of stress-related obesity. Chronic stress drives the dysregulation of the CRF signaling pathway in the reward system and increases the expression of DR2 and MOR in the nucleus accumbens.Keywords: chronic stress, obesity, food addiction, dopamine receptor 2, mu-opioid receptor, nucleus accumbens
Previous studies have shown that rapid eye movement (REM) sleep deprivation (RSD) exerts a detrimental effect on some memory tasks. However, whether post-learning RSD impairs memory for fear extinction, an important model of inhibitory learning, remains to be elucidated. The present study examined the effects of post-extinction RSD from 0 to 6 h and 6 to 12 h on recall of fear extinction tested 24 h after extinction training. We found that RSD from 0 to 6 h significantly increased freezing when recall of extinction of cued fear was tested in the context in which rats received extinction training whereas RSD from 6 to 12 h had no effect (experiments 1 and 2, two hippocampus-independent memory tasks). RSD at either time point had no effect on freezing when recall of extinction of cued fear was tested in the context different from that in which extinction training occurred (experiment 3, a hippocampus-dependent memory task). Additionally, we observed no effect of RSD at either time point on freezing during recall test for extinction of contextual fear (experiment 4, a hippocampus-dependent memory task). These results suggest that the effects of post-extinction RSD on memory for fear extinction are complex. RSD impairs recall of fear extinction in hippocampus-independent tasks, but does not affect recall of fear extinction in hippocampus-dependent tasks. Our findings extend previous research on the effects of RSD on learning and memory and support the notion that REM sleep is involved in memory process of certain tasks. (c) 2006 IBRO. Published by Elsevier Ltd. All rights reserved.
Patient empowerment has been shown to have some positive impacts on self-efficacy, self-esteem, and recovery. However, information about the empowerment needs of patients after a percutaneous coronary intervention is scarce. The aim of this study was to develop a Chinese-language instrument to measure empowerment needs of such patients. The initial instrument was generated based on a literature review and interviews with patients after a percutaneous coronary intervention procedure. Content validity was tested with a panel of experts using the Delphi method. In total, 226 patients were recruited for psychometric tests using the revised instrument. Expert authority coefficient was 0.92, and content validity index was 0.95. The internal consistency reliability was demonstrated by Cronbach's alpha coefficients (0.86 for the total score, 0.66-0.74 for the dimensions). The newly developed 19-item, five-dimension instrument has shown satisfactory validity (face/content validity and construct validity) and internal consistency reliability. The instrument could help clinical nurses who have close contact with patients after a percutaneous coronary intervention to gain a better understanding of their empowerment needs and could help develop appropriate health education to address such needs.
Background and Aim: Sleep deprivation (SD) causes deficit of cognition, but the mechanisms remain to be fully established. Hydrogen sulfide (H2S) plays an important role in the formation of cognition, while excessive and prolonged autophagy in hippocampus triggers cognitive disorder. In this work, we proposed that disturbances in hippocampal endogenous H2S generation and autophagy might be involved in SD-induced cognitive impairment. Methods: After treatment of adult male wistar rats with 72-h SD, the Y-maze test, object location test (OLT), novel object recognition test (NORT) and the Morris water maze (MWM) test were performed to determine the cognitive function. The autophagosome formation was observed with electron microscope. Generation of endogenous H2S in the hippocampus of rats was detected using unisense H2S microsensor method. The expressions of cystathionine-beta-synthase (CBS), 3-mercaptopyruvate sulfurtransferase (3-MST), beclin-1, light chain LC3 II/LC3 I, and p62 in the hippocampus were assessed by western blotting. Results: The Y-maze, OLT, NORT, and MWM test demonstrated that SD-exposed rats exhibited cognitive dysfunction. SD triggered the elevation of hippocampal autophagy as evidenced by enhancement of autophagosome, up-regulations of beclin-1 and LC3 II/LC3 I, and down-regulation of p62. Meanwhile, the generation of endogenous H2S and the expressions of CBS and 3-MST (H2S producing enzyme) in the hippocampus of SD-treated rats were reduced. Conclusion: These results suggested that inhibition of endogenous H2S generation and excessiveness of autophagy in hippocampus are involved in SD-induced cognitive impairment.