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Objective To investigate the correlation between levels of Annexin A1,Bax and lipoprotein-associated phospholipase A2 (Lp-PLA2) and both formation and stability of human carotid atherosclerotic plaques.Methods Forty-five specimens from patients with carotid atherosclerotic plaques (test group,group A),admitted to our hospital from May 2010 to June 2011 and performed carotid endarterectomy (CEA),and 20 specimens from patients with mesenteric artery and 20 healthy subjects (control groups,group B and group C,respectively) were collected in our study.The carotid atherosclerotic plaque specimens were divided into soft plaque group A1 (n=15),mixed plaque group A2 (n=15) and hard plaque group A3 (n=15) according to the results of carotid artery ultrasound.The Lp-PLA2 level in group A and group C was measured by enzyme linked immunosorbent assay (ELISA),and the mRNA and protein expressions of Annexin A1 and Bax in group A and group B were determined by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting.Results The level of Lp-PLA2 in all patients with carotid atherosclerotic plaques was significantly increased as compared with that in group C (P<0.05); that in group A1 was significantly higher than that in group A3 (P<0.05).The mRNA and protein expressions of Annexin A1 and Bax in all patients with carotid atherosclerotic plaques were significantly increased as compared with those in group B (P<0.05); group A1 exhibited lower mRNA and protein expressions of Annexin A1 than group A3 (P<0.05),while group A1 exhibited higher mRNA and protein expressions of Bax than group A3 (P<0.05).Conclusion Annexin A1,Lp-PLA2 and Bax participate in the formation and stability of human carotid atherosclerotic plaques.
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Objective To explore the distribution of lecithin cholesterol acyltransferase (LCAT)gene 511C/T polymorphism in Chinese Han population and the association of its polymorphism with the occurrence of cerebral hemorrhage (CH). Methods The LCAT gene 511C/T polymorphism was identified by PCR, single-strand conformation polymorphism (SSCP) and DNA sequencing in 150 patients with CH and 122 age- and gender-matched healthy controls. Results The 511 situs of the fourth extron in LCAT gene existed polymorphism; C/T in this situs of both groups satisfied Hardy-Weinberg equilibrium. The CT genotype frequency (3.3%) and T allele frequency (1.7%) in patient group were not significantly higher than those (1.6%, 0.8%, respectively) in controls (P>0.05).The level of high-density lipoprotein cholesterol (HDL-C) in 511CC subgroup ([1.44±0.42] mmol/L) was significantly higher than that in 511CT subgroup ([1.06±0.30] mmol/L) of patient group (P<0.05).Conclusion The LCAT gene 511C/T polymorphism is not possibly a predisposing factor of CH in Chinese Han population. T allele frequency might be connected with the metabolism of HDL-C.
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Objective To study the effects of stilbene glucoside(TSG)on calcium homeostasis and expression of RyR3 in pyramidal neurons of the rat hippocampus induced by β-amyloid(Aβ).Methods Eighty Wistar rats were equally randomized into 4 groups(n=20): control group,sham-operated group,model group and TSG inducement group.AD models in the later 3 groups were induced by stereotactic injection of Aβ1-42 to the rat hippocampus;and rats of the control group did not give any treatment.The mRNA expression of RyR3 was detected by real time PCR(RT-PCR) and monitored under laser scanning confocal microscope. Results The concentration of intracellular calcium between each 2 groups was significantly different(P<0.05);that in the model group was obviously higher than that in the control and sham-operated groups,and that in the TSG inducement group was obviously lower than that in the model group(P<0.05).Semi-quantitative RT-PCR indicated that the value of RyR3/β-actin in the model group was obviously decreased as compared with that in the control and sham-operated groups(P<0.05);the value of RyR3/β-actin in the TSG inducement group was slightly increased, but no significant difference was noted as compared with that in the control and sham-operated groups (P>0.05). Conclusion Aβ neurotoxicity causes disorder of intracellular calcium homeostasis,which is not through the pathway of Ca2+-induced Ca2+ release induced by RyR3,but through the changes of permeability of cytomembrane.TSG plays a protection role from Aβ neurotoxicity by calcium homeostasis.
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<p><b>OBJECTIVE</b>To explore associations between levels of total cholesterol (TC), triglyceride (TG) and incidence of ischemic and hemorrhagic strokes in populations.</p><p><b>METHODS</b>Baseline investigations on stroke-related risk factors and physical examinations were performed in 10 093 (> 35 years) stroke-free urban community residents from 5 cities in China during May to July in 1987, follow-up investigations on stroke events were made during 1998 to 2000. The hazard ratios and 95% confidence intervals (CI) of ischemic and hemorrhagic strokes in middle, high tertiles of baseline TC or TG levels were compared with low baseline tertile residents using the Cox regression model.</p><p><b>RESULTS</b>There were 491 first strokes during the 8-years cohort follow-up. Compared with the low tertile, risk of ischemic stroke in the middle and high tertiles of TC level was increased by 61% (HR: 1.61, 95%CI: 1.14-2.27) and 58% (HR: 1.58, 95%CI: 1.12-2.22) after adjustments for DBP, age, sex and other variables in the Cox proportional hazards model. Compared with the low tertile, risk of ischemic stroke in the high tertile of TG level was increased by 43% (HR: 1.43, 95%CI: 1.02-2.00). However, risk of hemorrhagic stroke in the middle and high tertiles of TC level decreased by 12% (HR: 0.88, 95%CI: 0.64-1.22) and 33% (HR: 0.67, 95%CI: 0.48-0.95) compared with the low tertile.</p><p><b>CONCLUSIONS</b>Elevated serum TC and TG are independent risk factors for risk of ischemic stroke. However, low TC was related with increased risk of hemorrhagic stroke.</p>
Subject(s)
Aged , Female , Humans , Male , Middle Aged , China , Epidemiology , Cholesterol , Blood , Cholesterol, HDL , Blood , Prospective Studies , Risk Factors , Stroke , Blood , Epidemiology , Triglycerides , BloodABSTRACT
<p><b>OBJECTIVE</b>To explore the association between single nucleotide polymorphisms (SNPs) of KLK1 gene and cerebral hemorrhage in Changsha Han Chinese.</p><p><b>METHODS</b>Two hundred and seventy-three cerebral hemorrhage (CH) patients and 140 healthy controls were collected. The SNPs of rs5516 and rs5517 loci of KLK1 gene were analyzed by SNaPshot methods and direct sequencing.</p><p><b>RESULTS</b>(1)Genotype and allele frequencies in rs5516 locus had no difference between the CH patients and controls (P> 0.05). However, the A allele frequency of the rs5517 locus in CH patients was higher than that in the control group (0.419, 0.321 respectively, P< 0.05). (2)In the control group,the levels of diastolic blood pressure (DBP) of the GA and AA genotype carriers of the rs5517 locus were significantly higher than those of the GG genotype (P< 0.05), while the levels of blood pressure were not significantly different among different genotypes of the rs5516 polymorphism in both CH patients and the control group(P> 0.05).</p><p><b>CONCLUSION</b>Author's preliminary results suggested that the rs5517 polymorphism was associated with cerebral hemorrhage, while the rs5516 polymorphism was not in Changsha Han Chinese.</p>
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Asian People , Genetics , Cerebral Hemorrhage , Genetics , Genetic Predisposition to Disease , Genetics , Genotype , Polymerase Chain Reaction , Polymorphism, Single Nucleotide , Genetics , Tissue Kallikreins , GeneticsABSTRACT
<p><b>OBJECTIVE</b>To investigate the relationship of FGA gene 128C/G polymorphism and cerebral infarction (CI) and evaluate the effect of FGA-128C/G polymorphism on plasma fibrinogen in Hunan Hans.</p><p><b>METHODS</b>FGA-128C/G polymorphism was detected by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and DNA sequencing in 194 CI patients and 114 healthy controls.</p><p><b>RESULTS</b>There were CG and CC genotypes in the FGA-128C/G locus. No GG genotype was observed in Hunan Hans. There was no significant difference in genotype and allele frequencies between the controls and CI group (P> 0.05), and statistically significant difference was not found in fibrinogen (Fg) level between the CG and CC genotypes (P>0.05). After analyzing blood plasma Fg using the influencing factor multiple regression analysis, it was shown that the Fg level had no relationship with the FGA-128C/G genotype, but it increased with age. And the Fg level in males was higher than that in females.</p><p><b>CONCLUSION</b>There was FGA gene 128C/G polymorphism in the Hunan Han population. There was no association of this polymorphism with the increased Fg level of CI patient in the population. FGA-128C/G might not be the predisposing gene of CI in Hunan Han population. The age and sex were the major factors affecting the plasma Fg level in this population.</p>
Subject(s)
Aged , Female , Humans , Male , Middle Aged , Asian People , Genetics , Cerebral Infarction , Genetics , Fibrinogen , Genetics , Gene Frequency , Genetics , Genetic Predisposition to Disease , Genetics , Genotype , Polymerase Chain Reaction , Polymorphism, Genetic , Genetics , Polymorphism, Restriction Fragment LengthABSTRACT
Objective To analyze the clinical manifestations,radiographic characteristics and treatment of cerebral vein thrombosis.Methods The clinical manifestations,results of laboratory examinations,characteristic radiographic findings,treatment protocols and outcomes were analyzed retrospectively in 11 patients with cerebral vein thrombosis admitted between 2002 and 2007.Results In 10 of the patients,nonspecifie headache was the most frequent symptoms,followed by vomiting,hemiplegia,meningeal irritation and hyperspasmia.Two patients received treatments for suspected cerebral hemorrhage and subarachnoid hemorrhage before a definite diagnosis was established.All thel 1 patients received CT and/or magnetic resonance imaging(MR/)examinations,and 8 also underwent magnetic resonance venography(MRV)and 1 underwent digital subtraction angiography(DSA),and a definite diagnosis of cerebral vein thrombosis was established in 10 eases.Treatment to control the intracmnial pressure was administered in all the patients,among whom 10 were given anti-coagulation or anti-platelet treatments.Nine patients showed improvements after the treatments;1 had deteriorated condition and 1 died.Conclusion In the absence of specific clinical manifestations,cerebral vein thrombosis gives rise to high rate of misdiagnosis,and a definite diagnosis relies on the findings by radiographic modalities.Early anti-coagulation treatment may prove safe and effective in these cases.
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<p><b>OBJECTIVE</b>To characterize the deficiency of the mRNA expression of specific protein (SP3) gene in peripheral blood mononuclear cells (PBMCs) from Chinese patients with multiple sclerosis (MS) and study its correlation with the disease phenotypes.</p><p><b>METHODS</b>Fifty-six patients with definite MS were collected and total RNA was extracted from their PBMCs. Specific primers corresponding to SP3 gene were designed and the mRNA expression of SP3 gene was detected by reverse transcriptase-PCR (RT-PCR) method. The deficiency of SP3 expression was compared among MS patients, irrelevant disease group and normal controls.</p><p><b>RESULTS</b>Of the 56 MS cases, 23 (41.1%) were SP3-deficient. In contrast, the frequency of SP3-deficiency in normal subjects and irrelevant disease controls was 8.6% (5/35) and 14.3% (4/27), respectively. The frequency of the SP3-expression deficiency in MS patients was significantly higher than that in both control groups (P< 0.01). Within the MS cases, the scores of expanded disability status scale (EDSS) in the SP3-expressing subjects were significantly different from that in the SP3-deficient ones in the stable, but not in the active, phase of MS (P< 0.05).</p><p><b>CONCLUSION</b>Author's observation suggested that deficient expression of SP3 gene occurs in Chinese MS patients, and that the SP3 expression may correlate with the clinical manifestations of MS and play roles in its immunological pathogenesis.</p>
Subject(s)
Adolescent , Adult , Aged , Child , Female , Humans , Male , Middle Aged , Young Adult , Leukocytes, Mononuclear , Metabolism , Multiple Sclerosis , Genetics , RNA, Messenger , Genetics , Reverse Transcriptase Polymerase Chain Reaction , Sp3 Transcription Factor , GeneticsABSTRACT
<p><b>OBJECTIVE</b>To investigate the relationship between C7673T polymorphism of apolipoprotein B (apoB) and cerebral hemorrhage with family history (CHFH) in Chinese Han in Changsha, Hunan province.</p><p><b>METHODS</b>Fifteen families of CHFH and 93 sporadic cerebral hemorrhage patients and 100 normal controls were collected. The C7673T polymorphism of apoB was analyzed by PCR-restriction fragment length polymorphism and direct DNA sequencing. The triglyceride(TG), total cholesterol(TC), high density lipoprotein-cholesterol (HDL-C) and low density lipoprotein-cholesterol(LDL-C) levels were examined by oxidase method. The serum level of lipoprotein (a) was determined by immune method.</p><p><b>RESULTS</b>(1)The allele T frequencies of apoB C7673T polymorphism in cerebral hemorrhage patients with family history, first-degree relatives, second-degree relatives, third-degree relatives, the sporadic cerebral hemorrhage patients and the control group were 0.176, 0.136, 0.058, 0.048, 0.081 and 0.040, respectively. (2) The allele T frequencies of apoB C7673T polymorphism in CHFH patients and their first-degree relatives were significantly higher than that of the control group (P< 0.01, P< 0.01), while there was no significant difference among second-degree relatives, third-degree relatives and control group (P> 0.05). And the allele T frequency of apoB C7673T in CHFH patients was significantly higher than that of sporadic cerebral hemorrhage patients (P< 0.05). (3)In CHFH patients and sporadic cerebral hemorrhage group, the levels of TC and LDL-C of the TC genotype were significantly higher than those of the CC genotype, while the level of HDL-C in the TC genotype was significantly lower than that of the CC geneotype (P< 0.05).</p><p><b>CONCLUSION</b>(1)The allele T of apoB C7673T polymorphism may be related to cerebral hemorrhage with family history. (2) The allele T of apoB C7673T polymorphism may increase the susceptibility of cerebral hemorrhage by changing blood lipid levels.</p>
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Apolipoproteins B , Genetics , Cerebral Hemorrhage , Blood , Genetics , Cholesterol , Blood , Cholesterol, HDL , Blood , Cholesterol, LDL , Blood , Gene Frequency , Genotype , Lipids , Genetics , Polymerase Chain Reaction , Polymorphism, Genetic , Genetics , Triglycerides , BloodABSTRACT
OBJECTIVE@#To explore the effect of apoB polymorphism on plasma lipid levels and cerebral hemorrhage in (CH) Changsha Han Chinese.@*METHODS@#One hundred thirty CH patients and 100 normal people were involved. C7673T polymorphism of apoprotein B was analyzed by PCR-restriction fragment length polymorphism (PCR-PFLP); and the triglyceride(TG), total cholesterol (TC), high density lipoprotein-cholesterol (HDL), and low density lipoprotein-cholesterol(LDL) levels were examined by oxidase method. The serum level of lipoprotein(a) was determined by immunology method.@*RESULTS@#(1) Allele T frequencies of apoB C7673T in CH patients and the control group were 0.108 and 0.040, respectively. Allele T frequencies of apoB C7673T in the CH patients were significantly higher than those in the control group (P< 0.01). (2) In the CH patients, the levels of TC and LDLjC of the T/C gene type were significantly higher than those of the C/C gene type, while the levels of HDLjC of the T/C gene type were significantly lower than those of the C/C gene type (P< 0.05).@*CONCLUSION@#ApoB C7673T polymorphism may be related to cerebral hemorrhage, and the changing blood lipid level may increase the susceptibility of CH.
Subject(s)
Aged , Female , Humans , Male , Middle Aged , Apolipoproteins B , Genetics , Cerebral Hemorrhage , Blood , Genetics , China , Ethnology , Genetic Predisposition to Disease , Lipoproteins , Blood , Polymorphism, Genetic , GeneticsABSTRACT
OBJECTIVE@#To explore the effect of polygonum multiflorum on the fluidity of mitochondria membrane and activity of cytochrome oxidase (COX) in Alzheimer's disease (AD) model rats.@*METHODS@#Forty-five SD rats were randomly divided into 3 groups: an AD model group, a control group, and a treatment group (n=15). AD model was established by injecting beta-amyloid protein (Abeta) 1-40 into the hippocampus of rats. The learning and memory abilities of rats were tested with the Y-electrical maze. The coefficient of viscosity of the hippocampal mitochondria membrane was determined by a spectrofluorometer, and the activity of COX was measured by an ultraviolet spectrophotometer.@*RESULTS@#Compared with the control group, the learning and memory ability of the AD model group was significantly lower (P<0.01), while the coefficient of viscosity of the hippocampal mitochondria membrane of the AD model group rats was significantly higher (P<0.01), and COX activity was lower (P<0.01). Compared with the AD model group rats, the coefficient of viscosity of the hippocampal mitochondria membrane of the treatment group was significantly lower (P<0.05), and COX activity was significantly improved (P<0.05).@*CONCLUSION@#Polygonum multiflorum could improve the fluidity of mitochondria membrane and the activity of mitochondrial COX in the model of Alzheimer's disease.
Subject(s)
Animals , Female , Male , Rats , Alzheimer Disease , Metabolism , Amyloid beta-Peptides , Cyclooxygenase 1 , Metabolism , Disease Models, Animal , Drugs, Chinese Herbal , Pharmacology , Hippocampus , Metabolism , Pathology , Membrane Fluidity , Membrane Proteins , Metabolism , Mitochondria , Peptide Fragments , Polygonum , Chemistry , Rats, Sprague-DawleyABSTRACT
<p><b>BACKGROUND</b>Alzheimer disease (AD) is a neurodegenerative disease related to aging. At present, its pathological mechanisms remain unclear. Family members of the renin-angiotensin system (RAS) play a role in neuronal plasticity, as well as formation of learning and memory. In this study, we explore the effects of altered angiotensin-converting enzyme (ACE), and investigate the possible mechanisms of perindopril, an ACE inhibitor, on brain structure and function in a rat model of AD, as well as the role that ACE plays in AD.</p><p><b>METHODS</b>Sixty Sprague-Dawley rats were selected and randomly divided into 3 groups: control, AD, and perindopril. Each group consisted of 20 rats, with 10 rats for determining pathology, and the remaining 10 rats for quantifying ACE activity. The rat AD model was established by stereotactically injecting amyloid beta protein (A-beta) 1-42 into the right hippocampus. Learning and memory functions were tested using the Y-type electric maze. The number and morphology of abnormal neurons were determined by haematoxylin and eosin staining. Amyloid deposition was measured by Congo red staining. Finally, ACE activity was estimated by spectrophotometry.</p><p><b>RESULTS</b>Compared with the control group, the number of times needed to escape electrical stimuli increased (23.70 +/- 3.13, P < 0.001), the number of normal neurons in the CA1 region was reduced (density of 96.5 +/- 32.6/mm, P < 0.001), amyloid deposition was obvious, and ACE activity increased ((34.4 +/- 6.6) nmol x g(-1) x min(-1), P < 0.001) in the AD group. In the perindopril group, the number of times needed to escape electrical stimuli decreased (18.50 +/- 3.66, P < 0.001), the number of abnormal neurons increased (density of CA1 neurons was 180.8 +/- 28.5/mm, P < 0.001), amyloid deposition was reduced, and ACE activity was down-regulated ((26.2 +/- 6.2) nmol x g(-1) x min(-1), P < 0.001).</p><p><b>CONCLUSIONS</b>ACE activity increased in the brains of AD rats. Perindopril improved learning and memory in AD rats, which correlated with decreased ACE activity and delayed AD pathogenesis.</p>
Subject(s)
Animals , Rats , Alzheimer Disease , Pathology , Angiotensin-Converting Enzyme Inhibitors , Pharmacology , Brain , Pathology , Disease Models, Animal , Maze Learning , Physiology , Neurons , Metabolism , Pathology , Peptidyl-Dipeptidase A , Metabolism , Perindopril , Pharmacology , Random Allocation , Rats, Sprague-DawleyABSTRACT
<p><b>OBJECTIVE</b>To investigate the effects and mechanism of qi-tonifying and stasis-eliminating (QTSE) therapy on the expression of vascular endothelial growth factor (VEGF) and its receptors Flt-1 and Flk-1 in the brains of intracerebral hemorrhagic (model) rats.</p><p><b>METHODS</b>One hundred and eighty Sprague-Dawley rats were randomly divided into six groups: the normal group (n=5), the sham-operative (SO) group (n=35), the model group (n=35), the QTSE group (n=35), the QT group (n=35) and the SE group (n=35). All the rats except those in the normal group and SO group were established into an intracerebral hemorrhage(ICH) model by intracerebral injection of collagenase type VII and the latter three were orally administered with Buyang Huanwu Decoction (a classical recipe for QTSE) or with some of its components for qi-tonification and for stasis-elimination, respectively. To the other three groups, normal saline solutions were given instead. Behavioral tests were carried out in the animals randomly chosen from each group on days 1, 2, 4, 7, 14, 21 and 28 after modeling. The expressions of VEGF, Flk-1 and Flt-1 were determined by immunohistochemistry and the number of vascular segments with positive expression in the injured brain area of the rats was calculated.</p><p><b>RESULTS</b>From day 7 onwards, the asymmetric forelimb use rate in the QTSE group recovered more significantly than that in the other model groups. In the model group, the expressions of VEGF, Flk-1 and Flt-1 appeared on day 1 and reached a peak on day 21, then weakened gradually. In the QTSE group, as compared with the other model groups, a higher level of VEGF expression was shown from day 7 (P<0.01) and a higher level of Flt-1 expression was shown from the 7th day to the 21st day (P<0.01).</p><p><b>CONCLUSION</b>QTSE therapy can up-regulate the expressions of VEGF and its receptors (Flk-1 and Flt-1) and improve the recovery of kinetic function in the ICH rats, which may be correlated with its action in modulating vascular regeneration to promote the reconstruction of microvascular networks in the damaged areas.</p>
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Animals , Female , Male , Rats , Behavior, Animal , Brain , Metabolism , Cerebral Hemorrhage , Drug Therapy , Metabolism , Forelimb , Medicine, Chinese Traditional , Methods , Phytotherapy , Methods , Qi , Rats, Sprague-Dawley , Vascular Endothelial Growth Factor A , Metabolism , Vascular Endothelial Growth Factor Receptor-1 , Metabolism , Vascular Endothelial Growth Factor Receptor-2 , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To evaluate the effect of a long-term community-based intervention program on risk factors of stroke among people with different risk factors.</p><p><b>METHODS</b>In 1987,2 geographically separated communities with 10 000 registered residents of each, were selected as either intervention or control communities in Beijing and Changsha. A cohort containing 2700 subjects at the age of 35 years or older,and free of stroke were sampled from each community. The baseline survey was conducted to screen the subjects at high risk for intervention and there were 5319 and 5506 subjects enrolled in intervention and control cohorts,respectively. Then,a program for controlling the risk factors of stroke was initiated in the intervention cohort and health education was provided to the whole intervention community. A follow-up survey was conducted in 1999. The information on incidence and mortality of stroke was collected.</p><p><b>RESULTS</b>Comparing with the control cohort, the risk of incidence and mortality of stroke decreased by 22 % ( HR = 0.78,95 % CI:0. 66-0.92) and 73 % (HR = 0.27,95 % CI:0. 17-0.42) in intervention cohort. The risks of stroke were lower in intervention cohort than in control cohort among almost all of the sub-groups with or without risk factors of stroke except for being male,current smokers and current alcohol drinkers. The risk of death caused by stroke decreased significantly in those with or without the risk factors of stroke.</p><p><b>CONCLUSION</b>The long-term community intervention on the risk factors of stroke could effectively reduce the risk of incidence and mortality of stroke among people with or without the risk factors of stroke. More attention should be paid to the males and those who smoke or drink alcohol.</p>
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Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Cohort Studies , Community Health Services , Health Education , Health Services Research , Incidence , Risk Factors , Stroke , Epidemiology , MortalityABSTRACT
<p><b>OBJECTIVE</b>To investigate the relationship between C923T (Ala308Val) polymorphism in exon 10 of protein 47000 phagocyte oxidase(p47(phox)) gene and stroke and to evaluate the effect of C923T (Ala308Val) polymorphism on plasma lipid levels in Hunan Hans population.</p><p><b>METHODS</b>Hunan Han population C923T (Ala308Val) polymorphism in p47phox gene was determined by PCR-single strand conformation polymorphism analysis and DNA sequencing in 100 healthy controls, 220 patients with stroke, and 10 stroke pedigrees. Plasma lipid levels were measured by routine methods.</p><p><b>RESULTS</b>No statistically significant differences were found in frequencies of genotypes and alleles of C923T (Ala308Val) polymorphism between the controls and stroke patients (P > 0.05). The serum levels of triglyceride in cerebral infarction patients and controls with CT genotype were markedly higher than those with CC genotype (P < 0.05).</p><p><b>CONCLUSION</b>There is no association between C923T (Ala308Val) polymorphism and stroke in Hunan Hans; C923T (Ala308Val) polymorphism is associated with plasma lipid metabolism in Hunan Han population with cerebral infarction.</p>
Subject(s)
Adolescent , Adult , Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Base Sequence , Case-Control Studies , Ethnicity , Genetics , Exons , Genetics , Gene Frequency , Genotype , Lipids , Blood , NADPH Oxidases , Genetics , Polymorphism, Single Nucleotide , Polymorphism, Single-Stranded Conformational , Stroke , Blood , GeneticsABSTRACT
<p><b>OBJECTIVE</b>To investigate the changes in the expressions of inducible cyclooxygenase type 2 (COX-2) and membrane associated prostaglandin E-1(mPGES-1) in human carotid atherosclerotic plaques and to explore possible mechanisms of inflammatory process involved in plaque stability.</p><p><b>METHODS</b>The mRNA and protein levels of COX-2 and mPGES-1 were compared between minimally and grossly atherosclerotic arterial tissues. COX-2 and mPGES-1 gene expression were established by immunohistochemistry and reverse transcriptase-polymerase chain reaction (RT-PCR) in 10 mesenchymal artery controls and 24 atherosclerotic specimens. Presence of COX-2 and mPGES-1 protein was assessed by Western blotting.</p><p><b>RESULTS</b>Immunohistochemical staining showed that the COX-2 and mPGES-1 immunoreactive substances were present in the cytoplasm of smooth muscle cell. Compared with the control group, immunostaining positive cells increased in carotid atherosclerotic plaque group. COX-2 and mPGES-1 gene expression was significantly elevated in atherosclerotic plaques (P< 0.05, respectively). The increased mRNA and protein levels of COX-2 and mPGES-1 were correlated in atherosclerotic tissue (P< 0.05). The mRNA and protein levels of COX-2 and mPGES-1 related to degree of pathological damage in atherosclerotic tissue (P< 0.05). COX-2 and mPGES-1 were not found in the control group (mesenteric vascular walls).</p><p><b>CONCLUSION</b>COX-2 and mPGES-1 expression in plaques is significantly higher than that in the control group. These findings suggests that COX-2 and mPGES-1 might play a role in pathogenesis of atheroscleros and modulation of inflammatory process involved in plaque stability, and COX-2 may have proinflammatory enzyme properties.</p>
Subject(s)
Aged , Female , Humans , Male , Middle Aged , Atherosclerosis , Genetics , Metabolism , Blotting, Western , Carotid Artery Diseases , Genetics , Metabolism , Cyclooxygenase 2 , Genetics , Metabolism , Gene Expression , Immunohistochemistry , Intramolecular Oxidoreductases , Genetics , Metabolism , Prostaglandin-E Synthases , Reverse Transcriptase Polymerase Chain ReactionABSTRACT
<p><b>OBJECTIVE</b>To explore the distribution of lecithin-cholesterol acyltransferase gene (LCAT) 608C/T polymorphism in Chinese Han population and the relationship of the polymorphism association with the occurrence of atherosclerotic cerebral infarction.</p><p><b>METHODS</b>The lecithin:cholesterol acyltransferase gene 608C/T polymorphism is identified by polymerase chain reaction (PCR), single-strand conformation polymorphism (SSCP)and restriction fragment length polymorphism (RFLP) in 150 patients with ACI and 122 healthy controls matching age and sex.</p><p><b>RESULTS</b>The distribution of LCAT 608C/T gene polymorphism was in accordance with Hardy-Weinberg equilibrium. The CT genotype frequency (14.0%) and T allele frequency (7.0%) in ACI group were significantly higher than those in control group (P<0.05). The concentration of high density lipoprotein cholesterol (HDL-C) in 608CC subgroups were significantly higher than those in 608CT subgroups both in ACI group and in control group (P<0.05).</p><p><b>CONCLUSION</b>The LCAT 608C/T polymorphism is possibly a predisposing factor in ACI happening of Chinese Han population. T allele frequency is possibly concerned with the metabolism of HDL-C.</p>
Subject(s)
Aged , Female , Humans , Male , Middle Aged , Alleles , Cerebral Infarction , Genetics , Gene Frequency , Genotype , Intracranial Arteriosclerosis , Phosphatidylcholine-Sterol O-Acyltransferase , Genetics , Polymerase Chain Reaction , Polymorphism, Restriction Fragment Length , Polymorphism, Single Nucleotide , Polymorphism, Single-Stranded Conformational , GeneticsABSTRACT
<p><b>OBJECTIVE</b>To investigate the diagnosis,treatment and requirement of epilepsy patients in some urban communities in China, and to provide the evidence of searching for effective treatment and management on epilepsy under the China's context.</p><p><b>METHODS</b>A face-to-face survey were conducted in 3 urban communities in Shanghai, Beijing and Changsha, respectively. The questions in the questionniare were general information, hospital visit, treatment, the level and way of getting on the knowledge of epilepsy, as well as the current obstacles and needs.</p><p><b>RESULTS</b>Most of the patients selected the regular hospitals (90.8%) and the departments (92.3%) for their epielspy diagnosis and treatment. They used AEDs modo dictu (77.4%), and had controlled the seizures quite well (82.6%). A small part of patients still could not deeply understand the basic knowledge on epilepsy (13.5%). They ignored to follow up the drug concentration (45.8%) in blood and the blood biocheminstry indicators (43.9%). Some patients went to private clinics (12.9%) and used lay people remedies (7.7%). Longtime waiting (36.8%), inconvenient traffic (23.2%), and high expenses (22.6%) were the main problems influencing the timely treatment. The main obstacles of the patients were employment (47.2%), marriage (29.9%), psychological conditions (44.4%) and interpersonal relationship (29.9%). The main requirements were the effectiveness (87.0%) and cheap AEDs (40.9%) as well as the convenience of hospital visit (37.0%).</p><p><b>CONCLUSION</b>It is very important to emphasize knowledge and publicity/education on epilepsy as well as the psychological treatment according to the requirements of patients.</p>
Subject(s)
Humans , Anticonvulsants , Therapeutic Uses , China , Data Collection , Epilepsy , Diagnosis , Therapeutics , Health Services Needs and Demand , Hospitals , Patient Compliance , Urban HealthABSTRACT
Objective To investigate the protective effect of basic fibroblast growth factor(bFGF) gene modified mesenchymal stem cells(MSCs-bFGF)on cerebral isehemia in rats.Methods MSCs or MSCs-bFGF were transplanted into rat models of focal cerebral ischemia by intravenous injection.The neurological deficits and infarction volumes were evaluated,and the survival rate and differentiation of grafted MSCs were observed by double immunofiuoreseent labeling.Results In the rat cerebral ischemic model, both MSCs and MSCs-bFGF showed protective effect on the rats in comparison with control group.However, the protective effect was more significant in MSCs-bFGF group.Double immunofluorescent staining showed the number of BrdU-labeled and NeuN co-expression cells in MSCs-bFGF treated animals(127.40?7.43 and 11.20?3.09)were much more than in those of MSCs treated animals.While there was no significant difference between MSCs-bFGF and MSCs group in the number of GFAP co-expression cells.Conclusion MSCs transplantation has protective effect on cerebral ischemia in rats.Basic fibroblast growth factor gene modified MSCs is more effective than MSCs in neuroproteetion.
ABSTRACT
<p><b>OBJECTIVE</b>To report a Chinese Charcot-Marie-Tooth disease type 2 (CMT2) family.</p><p><b>METHODS</b>All the members in the family were studied clinically,and 6 patients were studied electrophysiologically. Sural nerve biopsy was performed in the proband. PMP22 gene duplications were detected by highly polymorphic short tandem repeat. Point mutation analysis of PMP22, MPZ and NEFL gene was screened by PCR-SSCP combined with DNA direct sequencing. A genome-wide screening was carried out to the family.</p><p><b>RESULT</b>Except 2 who had weakness and atrophy in both proximal and distal muscles of the lower limbs, all patients presented muscle wasting and a predominating weakness of distal parts of the lower limbs, and mild to moderate sensory impairments. In 6 patients who were subjected to elctrophysiological examinations, median-nerve conduction velocity (NCV) of the median nerve was normal. Electromyograms (EMGs) revealed signs of denervation with large motor unit potentials, fibrillation potentials and positive sharp waves. Sural nerve biopsy of the proband confirmed the presence of axonal neuropathy with an important loss of large myelinating fibers and a large number of clusters with mostly thinly myelinated axons. PMP22, MPZ and NEFL gene mutations were not found. The results of genome-wide screening revealed a linkage of CMT2 to a locus at chromosome 12q24.</p><p><b>CONCLUSION</b>The results are consistent with the diagnosis of CMT2. This family represents a rare genetic type of CMT2 which can be designated as CMT2L.</p>