Objective To observe the clinical efficacy of Valsartan combined with Captopril treatment of essential hypertension.Methods All of 58 patients with essential hypertension according to random number table were randomly divided into the combination group and control group 29 cases from January 2010 to January 2011 in our hospital,the control group of 29 patients was given Valerian losartan,combination group was given captopril,and two groups were compared of the efficacy and adverse reactions.Results Compared with the control group,the total effective rate in the combination group was significantly higher,the difference was significant(P 0.05).Liver and kidney function and urine routine in all patients before and after treatment had no significant changes in biochemical parameters.Conclusion The efficacy of Valsartan combined with Captopril treatment of primary hypertension is significantly better than the simple application of Valsartan treatment,and it is safety,good,significantly improve the efficacy,and it is worth widely promoted and applied.
Objective: To explore mechanism of demyelination and remyelination in cuprizone-induced acutely demyelinated animal model. Methods: Acutely demyelinated animal model was established by feeding C57BL/6 mice with cuprizone in the diet. Using immunohistochemistry and In situ hybridization, we demonstrated status of demyelination and remyelination and reaction of astrocyte at different time-points. Results: Severe demyelination as well as proliferation of astrocyte occurred in corpus callosum and cerebellum following 6 weeks exposure to cuprizone, while myelin became normal by remyelination after the mice were returned to 4 weeks of normal diet, and proliferation of astrocyte still retained. Conclusions: Cuprizone-induced acutely demyelinated animal model can be established successfully, and activated astrocyte appears to contribute to remyelination.
Abstract Social cooperation is fundamentally important for group animals but rarely studied with mice because of their natural aggressiveness. In the present work, we induced pairs of mice to develop a mutualistic cooperative behavior in a non-divided chamber. Each mouse was first trained to learn to use a water dispenser by occupying a particular zone served as a switch to the dispenser. Two trained mice were then put into a chamber containing two separate zones jointly controlling two dispensers. We recorded the latency before each co-drinking, the number and cumulated time of co-drinking each day during the test. These parameters served as quantitative measurements of cooperative behavior in mice. The whole procedure includes preparation, training and testing phases, which take 15 days in total. This assay provides detailed procedures and analytical methods for investigators to characterize and quantify the mutualistic cooperative behavior. The use of mice as subjects allows convenient coupling to other behavior assays and is amiable to genetic manipulations for mechanistic study.
Section 5 covers the field of 'Selected secondary movement disorders' and includes several chapters: Inherited metabolic disorders; Movements that occur in sleep; Cerebral palsy; Drug-induced movement disorders in chidren; Psychogenic movement disorders.Important additional information is then provided in 'Appendix A' on Drug appendix, 'Appendix B' on Search strategy for genetic movement disorders, which is fundamental considering the exponential rise of molecular diagnosis in neuropediatrics, and 'Appendix C', a video atlas which is a very useful tool for the clinician so as to diagnose rare diseases.The chapters are easy to read.Practical tables and diagrams and brain imaging figures are available.Hundreds of references are displayed in all chapters including very recent ones.This book will undoubtedly become a masterpiece, one of the leading resources on movement disorders which should be interesting for all clinicians and researchers in neurology and neuropediatrics who are interested in movement disorders in childhood.
This study employed multiple MRI features to comprehensively evaluate the abnormalities in morphology, and functionality associated with Parkinson's disease (PD) and distinguish them from normal physiological changes. For investigation purposes, three groups: 32 patients with PD, 42 age-matched healthy controls (HCg1), and 33 young and middle-aged controls (HCg2) were designed. The aim of the current study was to differentiate pathological cortical changes in PD from age-related physiological cortical volume changes. Integrating these findings with functional MRI changes to characterize the effects of PD on whole-brain networks. Cortical volumes in the bilateral temporal lobe, frontal lobe, and cerebellum were significantly reduced in HCg1 compared to HCg2. Although no significant differences in cortical volume were observed between PD patients and HCg1, the PD group exhibited pronounced abnormalities with significantly lower mean connectivity values compared to HCg1. Conversely, physiological functional changes in HCg1 showed markedly higher mean connectivity values than in HCg2. By integrating morphological and functional assessments, as well as network characterization of physiological aging, this study further delineates the distinct characteristics of pathological changes in PD.
Objective: To investigate the mechanism of puerarin in patients with congestive heart failure (CHF). Methods: One hundred and twenty patients suffered from CHF were randomly divided into two groups, and they were treated with the same western medicine therapy. In addition, the puerarin treatment group ( n =60) was treated with puerarin injection intravenously drip of 300 mg mixed 250 ml of 5 percent glucose once a day for 15 days. At the end of the course, the alteration of heart function and plasma endothelin-1(ET-1), the therapeutic effects were observed before and after the treatments, and the difference between the two groups were compared. Results: In puerarin treatment group, the effective rate was higher than that in control group(86 7 percent vs. 75 0 percent, P 0 05), plasma ET-1 was decreased significantly after treatment〔(152 60±11 54)ng/L vs. (106 98±12 44)ng/L, P 0 05〕, but in routine treatment group the plasma ET-1 was not decreased significantly〔(147 65±9 78)ng/L vs. (142 60± 11 36)ng/L , P 0 05〕 . Conclusion: Puerarin can improve the heart function of CHF patients, the mechanism maybe decrease plasma ET-1 level and improve the blood supplying of myocardium.
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