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Objective@#To observe the alteration of brain glucose metabolic network in patients with somatoform disorders (SFD).@*Methods@#18F-fluorodeoxyglucose (FDG) PET images of 18 SFD patients (10 males, 8 females; age: (39.5±12.0) years; illness duration: (3.67±3.20) years) and 21 matched healthy controls (13 males, 8 females; age: (43.9±8.4) years) in Huashan Hospital of Fudan University from October 2011 to December 2012 were enrolled to construct the brain glucose metabolic networks for 2 groups (SFD group, control group) respectively. Then the global network properties (normalized clustering coefficient, normalized shortest path length, small-worldness and global efficiency) and local parameters (clustering coefficient and betweenness centrality of the node) were calculated using the graph theory. Differences between 2 groups were compared by permutation test with 1 000 permutations. The top 20% (18/90) were classified as Hub nodes based on the results of clustering coefficient and betweenness centrality of the node.@*Results@#Small-worldness of SFD patients was similar to that of healthy controls (σ>1). There were decreased tendency in normalized clustering coefficient and global efficiency, and increased tendency in normalized shortest path length in SFD patients, but without significant differences (P>0.05). Compared to healthy controls, the betweenness centrality of left pallidum, left amygdala, left precuneus and right angular gyrus increased (permutation test, P<0.05); the betweenness centrality of left middle temporal gyrus, right superior occipital gyrus decreased (permutation test, P<0.05); the clustering coefficients of bilateral pallidum, bilateral thalamus, and left amygdala decreased (permutation test, P<0.05). Most changed Hub nodes (16/24) belonged to limbic system.@*Conclusion@#The changes of topological properties of brain glucose metabolic network in SFD patients including the decreased tendency of small-worldness and global efficiency, as well as the altered Hub nodes, may provide valid imaging evidences for brain dysfunction of somatization symptoms.
Résumé
Objective To observe the alteration of brain glucose metabolic network in patients with somatoform disorders (SFD).Methods 18F-fluorodeoxyglucose (FDG) PET images of 18 SFD patients (10 males 8 females;age:(39.5±12.0) years;illness duration:(3.67±3.20) years) and 21 matched healthy controls (13 males,8 females;age:(43.9±8.4) years) in Huashan Hospital of Fudan University from October 2011 to December 2012 were enrolled to construct the brain glucose metabolic networks for 2 groups (SFD group,control group) respectively.Then the global network properties (normalized clustering coefficient,normalized shortest path length,small-worldness and global efficiency) and local parameters (clustering coefficient and betweenness centrality of the node) were calculated using the graph theory.Differences between 2 groups were compared by permutation test with 1000 permutations.The top 20% (18/90) were classified as Hub nodes based on the results of clustering coefficient and betweenness centrality of the node.Results Small-worldness of SFD patients was similar to that of healthy controls (σ> 1).There were decreased tendency in normalized clustering coefficient and global efficiency,and increased tendency in normalized shortest path length in SFD patients,but without significant differences (P>0.05).Compared to healthy controls,the betweenness centrality of left pallidum,left amygdala,left precuneus and right angular gyrus increased (permutation test,P<0.05);the betweenness centrality of left middle temporal gyrus,right superior occipital gyrus decreased (permutation test,P<0.05);the clustering coefficients of bilateral pallidum,bilateral thalamus,and left amygdala decreased (permutation test,P < 0.05).Most changed Hub nodes (16/24) belonged to limbic system.Conclusion The changes of topological properties of brain glucose metabolic network in SFD patients including the decreased tendency of small-worldness and global efficiency,as well as the altered Hub nodes,may provide valid imaging evidences for brain dysfunction of somatization symptoms.
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Dementia is a neuropsychiatric disorder characterized by cognitive impairment,and behavioral and psychological symptoms.Behavioral and psychological symptoms of dementia (BPSD) are common in patients with dementia and can have a major impact on the quality of life for patients and caregivers,and accelerate their cognitive decline.Atypical antipsychotics (AAP) possess excellent efficacy and tolerability in BPSD treatment;however,compared with conventional drugs,the use of antipsychotics has been widely debated for concerns over safety in elderly patients with dementia.The US FDA has issued several specific recommendations and emphasized that treatment of BPSD with AAP is"off-label".We have searched and reviewed the literature on the treatment of BPSD with AAP published in the last 10 years,and evaluated the efficacy and safety of AAP for clinicians' reference.
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OBJECTIVE: To study whether the effects of olanzapine on gastrointestinal motility is related to the serotonin antagonism and myosin light chain kinase. METHODS: Male Sprague-Dawley rats were randomly divided into four groups. Olanzapine gavage was performed for each treatment group during the course of 30 continuous days, while the same volume of saline was given to the rats in the control group. Defecation of the rats was observed on days 7 and 30 after olanzapine gavage. The effects of olanzapine on contraction of colonic smooth muscles were observed in ex vivo experiments. A Western blot was used to evaluate expression levels of the serotonin transporter (SERT) and MLCK in colon segments of the rats. RESULTS: ResultsaaCompared to the control group, 5-160 µM of olanzapine could inhibit dose-dependently the contraction of colonic smooth muscle ex vivo experiments. The maximum smooth muscle contraction effects of 5-HT and acetylcholine significantly decreased after treatment with 40-160 µM of olanzapine. Constipation was found in the olanzapine-treated rats on day 7 and have sustained day 30 after gavage. Expression of MLCK in olanzapine-treated rats was significantly decreased, whereas the expression of SERT significantly increased on the day 7, then significantly decreased on the day 30 after olanzapine gavage. CONCLUSION: SERT and MLCK may involve in the inhibition of colonic contraction induced by olanzapine.