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1.
International Journal of Cerebrovascular Diseases ; (12)2006.
Article in Chinese | WPRIM | ID: wpr-680277

ABSTRACT

Various pathologic mechanisms and types of lesion have participated in cognitive impairment in patients with vascular dementia.A number of medications have been used in the treatment of patients with vascular dementia in clinical practice,including cholinesterase inhibitors, N-methy-D-aspartate receptor antagonists,calcium channel blockers and neurotrophic drugs. This article reviews the progress in research on the pharmacotherapy of vascular dementia.

2.
Chinese Journal of Applied Physiology ; (6): 278-280, 2005.
Article in Chinese | WPRIM | ID: wpr-287035

ABSTRACT

<p><b>AIM</b>To observe the cAMP and adenylyl cyclase (AC) mRNA level in hippocampus of mice with vascular dementia (ischemia/reperfusion), and explore the molecular pathogenesis of ischemia/reperfusion.</p><p><b>METHODS</b>The mice were subjected for ischemia/reperfusion three times on bilateral common carotid arteries by knots to establish models of ischemia/reperfusion and the changes of learning and memory were tested on 29 d/30 d after operation. Sham-operation mice were introduced as control group. The cAMP level was evaluated by the radioimmunoassay (RIA), AC mRNA positive neurons of hippocampus CA1 area were dyed through in-situ hybridization (ISH).</p><p><b>RESULTS</b>Compared with sham-operation group, the learning and memory of model group was worse (P < 0.05), the cAMP level in hippocampus was lower (P < 0.05) and the surface density (Sv) of AC mRNA positive neurons reduced (P < 0.05).</p><p><b>CONCLUSION</b>The lower cAMP and AC mRNA level in hippocampus might participate in the molecular pathogenesis of ischemia/reperfusion.</p>


Subject(s)
Animals , Male , Mice , Adenylyl Cyclases , Genetics , Metabolism , Cyclic AMP , Genetics , Metabolism , Hippocampus , Metabolism , Mice, Inbred Strains , RNA, Messenger , Genetics , Reperfusion Injury , Genetics , Metabolism
3.
Chinese Journal of Applied Physiology ; (6): 453-456, 2005.
Article in Chinese | WPRIM | ID: wpr-254633

ABSTRACT

<p><b>AIM</b>To detect the deletion distribution of dystrophin gene and dystrophin changes in muscle cells of the patients with Duchenne/Becker muscular dystrophy (DMD/BMD), furthermore to investigate the relationship between them and clinical symptoms.</p><p><b>METHODS</b>42 patients with DMD/BMD were screened by 9 primers multiplex PCR. The patients from 5 DMD and 2 BMD were detected by immunofluorescence technique for analyzing dystrophin located in muscle cell membrane, compared with 2 normal males.</p><p><b>RESULTS</b>The deletion of one or more exons was found in 21 patients. 16 cases (76.2%) were detected in the central region and 5 patients (23.8%) in the 5' extreme region, especially in exon 48 (6 patients). Negative result of staining was seen in 5 DMD patients. Of these, one case of DMD had no detectable levels of dystrophin, but no deletion of DMD gene. Dystrophin immunostaining from two BMD patients consisted of a discontinuous staining pattern around most fibers.</p><p><b>CONCLUSION</b>It might be possible that some correlation existed between the type of gene deletion and the degree of severity of the disease. The amount and size of exon deletion may not affect the symptoms. DMD/BMD are highly heterogeneous in clinical manifestation and in inheritance pattern. The pathologic foundation of DMD and BMD is the absence or abnormal expression of dystrophin. The consequence of that depends not only on the degree, but also on the function.</p>


Subject(s)
Adolescent , Adult , Child , Child, Preschool , Humans , Male , Young Adult , Dystrophin , Exons , Gene Deletion , Multiplex Polymerase Chain Reaction , Muscular Dystrophy, Duchenne , Genetics , Sequence Deletion
4.
Chinese Journal of Applied Physiology ; (6): 146-149, 2004.
Article in Chinese | WPRIM | ID: wpr-330161

ABSTRACT

<p><b>AIM</b>To investigate the resting [Ca2]i level and expression of calmodulin (CaM), calmodulin-dependent protein kinase II (CaMPKII) mRNA in hippocampal neurons of the mice with vascular dementia (VD) and their roles in the pathogenesis of VD.</p><p><b>METHODS</b>The mice were subjected for ischemia/reperfusion repeatedly on bilateral common carotid arteries by knots to establish the VD models. Animals with the sham-operation were taken as control group. The changes of behavior were observed through the step-down avoidance test and water maze test on the day 29, 30 after the operations. The hippocampal neurons were obtained immediately after mice were sacrificed and the resting [Ca2+]i was measured using laser scanning confocal microscopy with Fluo-3/AM as fluorescence indicator. RT-PCR technique was used to measure the mRNA expression of CaM, CaMPKII in hippocampal neurons.</p><p><b>RESULTS</b>(1) The abilities of learning and memorizing in model group were inferior to those of sham-operation group( P < 0.05). (2) The resting [Ca2]i level in model group was significantly higher than sham-operation group (P < 0.05), while the expression of CaMmRNA, CaMPKIImRNA in VD group was significantly reduced than sham-operation group (P < 0.01).</p><p><b>CONCLUSION</b>Our study indicates that excessive resting[Ca2+ ]i level and lower CaM, CaMPKII expression in hippocampal neurons might participate in the pathogenesis of VD.</p>


Subject(s)
Animals , Male , Mice , Calcium , Calcium-Calmodulin-Dependent Protein Kinase Type 2 , Genetics , Metabolism , Calmodulin , Genetics , Metabolism , Dementia, Vascular , Metabolism , Hippocampus , Cell Biology , Metabolism , Mice, Inbred Strains , Neurons , Metabolism , RNA, Messenger , Genetics
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