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OBJECTIVE@#To explore the clinical and genetic characteristics of a patient with hypertrophic cardiomyopathy as the initial manifestation of Mucopolysaccharidosis type Ⅲ A (MPS Ⅲ A).@*METHODS@#A female patient with MPS Ⅲ A who was admitted to the Affiliated Hospital of Jining Medical University in January 2022 and her family members (seven individuals from three generations) were selected as the study subjects. Clinical data of the proband were collected. Peripheral blood samples of the proband was collected and subjected to whole exome sequencing. Candidate variants were verified by Sanger sequencing. Heparan-N-sulfatase activity was determined for the disease associated with the variant site.@*RESULTS@#The proband was a 49-year-old woman, for whom cardiac MRI has revealed significant thickening (up to 20 mm) of left ventricular wall and delayed gadolinium enhancement at the apical myocardium. Genetic testing revealed that she has harbored compound heterozygous variants in exon 17 of the SGSH gene, namely c.545G>A (p.Arg182His) and c.703G>A (p.Asp235Asn). Based on guidelines from the American College of Medical Genetics and Genomics (ACMG), both variants were predicted to be pathogenic (PM2_Supporting +PM3+PP1Strong+PP3+PP4; PS3+PM1+PM2_Supporting +PM3+PP3+PP4). Sanger sequencing confirmed that her mother was heterozygous for the c.545G>A (p.Arg182His) variant, whilst her father, sisters and her son were heterozygous for the c.703G>A (p.Asp235Asn) variant. Determination of blood leukocyte heparan-N-sulfatase activity suggested that the patient had a low level of 1.6 nmol/(g·h), whilst that of her father, elder and younger sisters and son were all in the normal range.@*CONCLUSION@#The compound heterozygous variants of the SGSH gene probably underlay the MPS ⅢA in this patient, for which hypertrophic cardiomyopathy is an associated phenotype.
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Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Cardiomiopatia Hipertrófica , Meios de Contraste , População do Leste Asiático , Gadolínio , Mucopolissacaridose III , Mutação , LinhagemRESUMO
Objective:To investigate the effect of Astragaloside Ⅳ on high glucose-induced cardiomyocyte pyroptosis.Methods:H9c2 cells were cultured in vitro and divided into control group(5.5 mmol/L glucose), high glucose group(33.3 mmol/L glucose), Astragaloside Ⅳ group(33.3 mmol/L glucose+ 100μmol/L Astragaloside Ⅳ), and NLRP3 inhibitor group(33.3 mmol/L glucose+ 1μmol/L MCC950). Cell counting kit 8(CCK-8)was used to detect the activity of H9c2 cells.Lactate dehydrogenase(LDH)kit was used to detect the content of LDH in cell supernatant.Superoxide anion fluorescent probe(DHE)was used to detect the level of intracellular reactive oxygen species(ROS). Real-time fluorescence quantitative polymerase chain reaction(RT-qPCR)and Western blot were used to detect the mRNA and protein expression levels of pyroptosis-related genes.Immunofluorescence was used to detect the fluorescence intensity of NLRP3.Enzyme-linked immunosorbent assay(ELISA)was used to detect the level of inflammatory factors in cell supernatant.Results:When the concentration of Astragaloside Ⅳ was 100 μmol/L, it could significantly inhibit the decrease of cardiomyocyte viability induced by high glucose( P<0.01)and reduce LDH release( P<0.01). Compared with the control group, the level of ROS was increased( P<0.01), the mRNA and protein expressions of pyroptosis-related molecules were up-regulated( P<0.01 for all), the fluorescence intensity of NLRP3 was increased( P<0.01), and the levels of inflammatory factors in the cell supernatant were increased in the high glucose group( P<0.01). Compared with the high glucose group, the ROS level was decreased( P<0.01), the mRNA and protein expressions of pyroptosis-related molecules were down-regulated( P<0.05 or P<0.01), the fluorescence intensity of NLRP3 was decreased( P<0.01), and the levels of inflammatory factors in cell supernatant were decreased( P<0.05 or P<0.01)in Astragaloside Ⅳ group and inhibitor group. Conclusions:Astragaloside Ⅳ plays a protective role in high glucose-induced cardiomyocyte injury by inhibiting NLRP3/Caspase-1 signaling pathway and inhibiting pyroptosis.Moreover, it can improve the anti-inflammatory and antioxidant properties in cell models.
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Objective:To investigate the protective effects and related mechanisms of Astragaloside Ⅳ(ASⅣ)alleviating Angiotensin II-induced cardiomyocyte hypertrophy.Methods:H9c2 cardiomyocytes were divided into six groups: normal control group, ASⅣ group(ASⅣ 100 μmol/L), AngⅡ group(AngⅡ 1 μmol/L), and three ASⅣ dose experiments(AngⅡ 1 μmol/L + ASⅣ 25 μmol/l group, AngⅡ 1 μmol/L+ ASⅣ 50 μmol/l group, AngⅡ1 μmol/L+ ASⅣ 100 μmol/L group), and simultaneously cultured for 24 hours.Cardiomyocyte viability was assessed by CCK8 assay, and surface area of culturedcardiomyocytes in each group was assessed by immunofluorescence assay.Atrial natriuretic peptide(ANP)mRNA expression was assessed by fluorescence real-time quantitative RT-PCR.And LC3 protein expression, an autophagy related protein, was assessed by Western blotting as well as immunofluorescence.Results:(1)AngⅡ decreased cardiomyocyte H9c2 viability in a dose-dependent manner( P<0.05). ASⅣ could inhibit the decrease of cardiomyocyte H9c2 viability in response to AngⅡ in a dose-dependent manner( P<0.05). (2)H9c2 cardiomyocytes induced by AngⅡ showed a significantly larger cell area and significantly higher ANP mRNA and ANP protein expression compared with controls.Different concentrations of ASⅣ intervention could reverse the increase of cardiomyocyte H9c2 area induced by AngⅡ and also decreased the expression of ANP protein induced by AngⅡ in a dose-dependent manner(all P<0.05). (3)Compared with the control group, the autophagy level and the expression of autophagy marker LC3II/I of H9c2 cardiomyocytes induced by AngⅡ were significantly increased(all P<0.05). ASⅣ could inhibit AngⅡ-activated autophagy, and the difference was statistically significant( P<0.05). ASⅣ inhibited the expression of LC3II/I in H9c2 cardiomyocytes stimulated by AngⅡ, and the difference was statistically significant( P<0.05). Conclusions:ASⅣ inhibits AngⅡ-induced cardiac hypertrophy by inhibiting autophagy of cardiomyocytes.
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Objective:To investigate the effect of Astragaloside Ⅳ on abdominal aorta constriction-induced cardiac hypertrophy by activating the nuclear factor E2-related factor 2/heme oxygenase-1(Nrf2/ HO-1)signaling pathway, so as to improve cardiac function.Methods:From Sep.2017 to Jan.2019, 40 male SD rats were selected and abdominal aortic constriction(AAC)was used to establish a rat model of chronic heart failure.Rats were divided into three ACC groups: the model group, the benazepril HCl group and the Astragaloside Ⅳ group, plus the sham operation group.Rats in the benazepril HCl and Astragaloside Ⅳ groups were given 10 mg·kg -1·d -1 benazepril HCl and 50mg·kg -1·d -1 Astragaloside Ⅳ respectively by gavage, and the sham operation group and the model group were given normal saline of the same volume by gavage.After 8 weeks of treatment, cardiac structure and functional parameters were examined using cardiac color doppler ultrasound, while hemodynamics and morphological changes of myocardial cells were detected by immunofluorescence, serum brain natriuretic peptide(BNP)levels were detected by an enzyme-linked immunosorbent assay(ELISA), and Nrf2 and HO-1 mRNA expression in myocardial tissues were detected by reverse transcription-quantitative real-time PCR(RT-qPCR). Results:Compared with the sham operation group, the ratio of heart weight to femoral neck length(495.47±12.38), the ratio of heart weight to body weight(6.44±0.18), left ventricular end-diastolic diameter(LVEDD)(4.72±0.04 mm), left ventricular posterior wall thickness(LVPWT)(1.87±0.03)mm and the BNP level(151.61±5.67)mmol/L all increased( P<0.05), but the expression of mRNA Nrf2(0.36±0.02)and HO-1(0.27±0.02)decreased( P<0.01)in the model group.Compared with the model group, the ratio of heart weight to femoral neck length(261.88±12.97 and 286.40±12.56), the ratio of heart weight to body weight(3.38±0.13 and 3.71±0.15), left ventricular end-diastolic diameter(5.84±0.05)mm and (6.01±0.10)mm, left ventricular posterior wall thickness[(1.57±0.03)mm and(1.64±0.03)mm]and the BNP level[(99.40±4.97)mmol/L and(120.66±5.80)mmol/L]all decreased( P<0.05), but the mRNA expression of Nrf2(1.06±0.01 and 1.04±0.01)and HO-1(1.08±0.06 and 0.95±0.02)increased in the benazepril HCl and Astragaloside Ⅳ groups, respectively( P<0.01). Conclusions:Astragaloside Ⅳ has an effect of anti-oxidative stress, can inhibit heart failure and improve cardiac function, and its mechanisms may be related to the Nrf2/ HO-1 signaling pathway.
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Stress cardiomyopathy (SCM) is a kind of clinical syndrome characterized by transient ventricular enlargement and left ventricular regional systolic dysfunction caused by strong mental stimulation or physical stress, and accompanied by electrocardiogram (ECG) changes. Its clinical symptoms and ECG manifestations are similar to those of acute coronary syndrome in the early stage of onset, which is easy to be misdiagnosed. However, patients in intensive care unit (ICU) are often in critical and severe condition, and they often preceded different degrees by emotional or physical stress. Therefore, patients in ICU are prone to complicated with SCM. Otherwise, the symptoms of SCM patients in ICU are not typical. Early diagnosis and optimal treatment are the key to improve the prognosis of patients in ICU. The etiology, epidemiology, pathophysiological mechanism, diagnosis and management of SCM in ICU are reviewed in this paper.
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AIM:To observe the effects of astragaloside IV (AS-IV) on myocardial fibrosis in chronic heart failure ( CHF) rats and to explore the underlying mechanism preliminarily .METHODS:Chronic heart failure model rats established by abdominal aorta constriction (AAC) were divided into CHF group, valsartan group and AS-IV group.Sham operation group was also established .The rats in valsartan group and AS-IV group received valsartan and AS-IV at 2 and 30 mg· kg-1 · d-1 , respectively.The rats in sham operation group and CHF group received normal saline .After 8 weeks of treatment, the cardiac structure and the hemodynamic parameters were measured .The morphologic changes of myocardial tissue were observed after staining .The expression of long-chain acyl-CoA dehydrogenase ( LCAD) and 6-phosphofructoki-nase-1 (PFK1) at mRNA and protein levels was determined by RT-qPCR and Western blot.RESULTS:Compared with sham operation group , left ventricular mass index ( LVMI) , collagen volume fraction ( CVF) , left ventricular posterior wall depth (LVPWD), and the mRNA and protein of PFK1 in CHF group were increased (P<0.05), while the mRNA and protein levels of LCAD were decreased (P<0.05).Compared with CHF group, the LVMI, CVF, LVPWD, and the mRNA and protein levels of PFK1 in valsartan group and AS-IV group were decreased (P<0.05), while the mRNA and protein levels of LCAD were increased (P<0.05).CONCLUSION:AS-IV inhibits myocardial fibrosis in the CHF rats , the mechanism of which might be associated with up-regulating the expression of LCAD , down-regulating the expression of PFK1 and normalizing the myocardial energy metabolism .
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Objective: To study the impact of astragaloside on ventricular remodeling and peroxisome proliferator activated receptor a (PPARa) expression in pressure-overload rats and to preliminarily explore its mechanism. Methods: Pressure-overload rat's model was established by abdominal aorta constriction (AAC) in 8-week old SD rats and the result was conifrmed by echocardiography at 6 weeks later. Pressure-overload rats were divided into 4 groups with different intragastric treatment: Model control (normal saline) group, Benazepril hydrochloride [10mg/(kg.d)] group, Low-dose astragaloside [40mg/(kg·d)] group and High-dose astragaloside [80mg/(kg.d)] group; in addition, Sham operation group, the rats received intragastricnormal normal saline.n=20 in each group and all animals were treated for 8 weeks. Rat's cardiac structure and function indexes were assessed by echocardiography, hemodynamic parameter was examined by left ventricular intubation, myocardium and blood levels of free fatty acid (FFA) were determined, morphological changes of myocardial tissue was observed by HE and Masson staining, mRNA and protein expressions of PPARa were measured by qRT-PCR and Western blot analysis. Results: Compared with Sham operation group, Model control group showed increased left ventricular mass index(LVMI), collagen volume fraction (CVF) and FFA level, allP<0.05, while decreased mRNA and protein expressions of PPARa, bothP<0.05. Compared with Model control group, Low-dose and High-dose astragaloside groups presented reduced LVMI, CVF and FFA level, allP<0.05-0.01, while elevated mRNA and protein expressions of PPARa, bothP<0.01. Conclusion:Astragaloside IV mayinhibit myocardial remodeling in pressure-overload rats, which might be via up-regulating mRNA and protein expressions of PPARa, enhance myocardiumFFA utilization, and therefore improve myocardial energy metabolism.
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Objective:To investigate the association between catechol-O-methyl transferase (COMT)Vall58Met polymorphism and prepulse inhibition of the auditory startle reflex (PPI) in patients with schizophrenia.Methods:Totally 178 patients with schizophrenia and 190 healthy volunteers were recruited.The auditory startle reflex was detected by using SR-HLAB monitoring system.The indexed of the auditory startle reflex included the amplitude,habituation% and PPI30,PPI60,PPI120 (the lead interval was set 30 ms,60 ms,120 ms).COMT Vall58Met polymorphism was genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RELP).The differences of PPI among COMT genotypes were compared.Results:Compared to the healthy volunteers,patients with schizophrenia had a significant lower the amplitude of auditory startle reflex[(563± 460) mV vs (695 ± 447) mY,P < 0.05] and habituation% [(32 ± 46) vs (48 ± 33),P < 0.01] as well as the %PPI120[(27 ± 5) vs (35 ± 3),P < 0.05].The significant differences in COMT allelic and genotypic distribions were observed between patients with schizophrenia and healthy volunteers (x2 =8.16,11.74,Ps < 0.05).The significant main effect of COMT genotype on habituation% was observed (P <0.05) but no interaction genotype by diagnosis on the amplitude of auditory startle reflex,habituation% and % PPI120 was observed (Ps > 0.05).Conclusions:There may be a correlation between COMT genotype and adaptability,but not between COMT genotype and PPI deficit present in patients with schizophrenia
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Objective: To observe the effects of astragaloside IV on myocardial fibrosis and connective tissue growth factor (CTGF) expression in experimental rats with chronic heart failure (CHF). Methods: CHF model was established by abdominal aorta constriction (AAC) and the rats were divided into 5 groups:Sham operation group, the rats received normal saline 2 ml/day, n=10, CHF group, the rats received normal saline 2 ml/day, n=12;Astragaloside IV groups, CHF rats received astragaloside IV at (20, 40, 60) mg/kg respectively and n=12 in each group. All animals were treated for 4 weeks. Hemodynamic indexes were monitored, left ventricular mass index (LVMI) was calculated, morphologic changes of myocardial tissue was observed by HE staining, myocardial ifbrosis degree and collagen volume fraction (CVF) were measured by Masson staining. The mRNA and protein expressions of CTGF were detected by RT-PCR and immunohistochemistry, Western-blot analysis respectivety. Results: Compared with CHF group, 3 Astragaloside IV groups had decreased LVMI and CVF, P Conclusion: Astragaloside IV can inhibit myocardial ifbrosis and improve cardiac function in CHF rats, which might be via inhibiting the over expression of myocardial CTGF.
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OBJECTIVE:To systematically evaluate the efficacy and safety of Astragali radix injection combined with trimetazi-dine in the treatment of viral myocarditis (VMC),and provide evidence-based reference for clinical treatment. METHODS:Re-trieved from PubMed,CBM,CJFD,VIP and Wanfang Database,randomized controlled trials(RCT) about Astragali radix injec-tion combined with trimetazidine(test group)vs. western conventional treatment and(or)trimetazidine alone(control group)in the treatment of VMC were collected. After quanlity evaluation and data extraction,Meta-analysis was conducted by using Rev Man 5.2 statistics software. RESULTS:A total of 14 RCT were included,involving 1 324 patients. Results of Meta-analysis showed the total effective rate[RR=1.32,95%CI(1.25,1.39),P<0.001],lactate dehydrogenase level [MD=-99.80,95%CI(-135.52,-64.08), P<0.001] and creatine kinase level [MD=-49.66,95%CI(-80.43,-18.90),P=0.002] in test group were significantly lower than those of control group,there was sgnificant difference between 2 groups;and there was no significant difference in the inci-dence of adverse reactions[RR=0.86,95%CI(0.48,1.55),P=0.61]. CONCLUSIONS:Astragali radix injection combined with trimetazidine has good efficacy and safety in the treatment of VMC.
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Objective:To explore the relation of cognitive function correlates to P50 sensory gating in patients with schizophrenia.Methods:Totally 106 patients with drug-na¨ive first-episode schizophrenia and 86 healthy con-trol subjects matched for age,sex and education were recruited.All patients met the Diagnostic and Statistical Man-ual of Mental Disorders,Fourth Edition (DSM-IV)criteria for schizophrenia.Their cognitive function were assessed with the MATRICS Consensus Cognitive Battery (MCCB).The P50 auditory gating potential were recorded in all subjects using conditioning-testing stimulus paradigm and stimulus train paradigm.The P50 components were meas-ured in S1 S2 latency,S1 S2 amplitude and P50 suppression ratios.Results:Compared with the controls subjects, the patients with schizophrenia had significantly longer S1[60.8 ±7.8)ms vs.(56.3 ±7.0)ms,P 0.05).No significant correlation was found between P50 gating measures (P50 ratio and P50 ampli-tude difference)and neuropsychological measures in MCCB scores (Ps >0.05).Conclusion:There may be no as-sociation between P50 deficits and cognitive measures in patients with drug-na¨ive first-episode schizophrenia.
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Objective To find out fluorine content in drinking water in Yi County,and to provide ascientific basis for prevention of endemic fluorosis and children's dental caries.Methods According to FluorideDistribution Survey Program in Drinking Water of Hebei Province,an administrative village was taken as a unit,one drinking water sample was randomly collected from every village with centralized water supply.For villages withdecentralized water supply,five drinking water samples were randomly collected according to directions (east,west,south,north and centre) if there were more than five water sources in the village;samples from all the water sourceswere collected if there were less than five.Fluorine content was determined with drinking water standard testmethods (GB/T 5750.2-2006).Analysis and comparison of fluoride content in drinking water of different landscapes,water types and different well depth were carried out.Results The range of water fluoride content was 0.00-18.39 mg/L,and water fluorine median was 0.24 mg/L in 1 024 water samples in 27 towns in the county.Watersamples of 490,505 and 29 copies were collected in the hills,plains and mountains,and water fluorine medianwas 0.26,0.22 and 0.21 mg/L,respectively.Concerning water fluorine content in drinking water,mountains werehigher than hills and plains (x2 =71.71,17.74,all P < 0.01).There was no significant difference between waterfluoride content in hills and plains (x2 =2.48,P > 0.05).Water samples of 742,228 and 54 copies were collected,respectively,in household well water,tap water and mountain spring water,and water fluoride median was 0.22,0.24 and 0.33 mg/L,respectively.Concerning water fluoridation content in drinking water,spring water were higherthan tap water and household well water (x2 =53.16,50.85,all P < 0.01).There was no significant differencebetween water fluoridation content in tap water and household well water (x2 =2.97,P > 0.05).Water samples of583 and 441 copies were collected,respectively,in well depth < 40 m and well depth ≥40 m,and water fluoride median was 0.24 and 0.23 mg/L,respectively,and there was no significant difference between water fluoridation content in the well depth < 40 m and the well depth ≥40 m (Hc =0.17,P > 0.05).Conclusions Fluoride content of drinking water in Yi County is not high,endemic fluorosis disease does not occur.
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Objective To find out the iodine content in drinking water in Yi County,and to provide a scientific basis for prevention of iodine deficiency disorders.Methods An administrative village was taken as a unit in Yi County,Hebei Province.One drinking water sample was randomly selected from each village with centralized water supply.For villages with decentralized water supply,five drinking water samples were randomly selected according to directions (east,west,south,north and center) if there were more than five water sources in the village ; all the water source samples were taken if there were less than five water sources.Water iodine content of all of the water samples was tested; geomorphological feature,water type and well depth were surveyed.Water iodine content was determined through arsenic cerium catalytic spectrophotometric method.Results The range of water iodine content was 0.00-18.39 μg/L,and water iodine median was 2.08 μg/L in 1 024 water samples in the county.Water samples of 490,505 and 29 copies were collected in the hills,plains and mountains,and water iodine median was 1.74,2.26,3.15 μg/L,respectively.Concerning water iodine medians in drinking water,mountains were less than hills and plains(x2 =37.36,34.25,all P< 0.01),hills were less than (x2=15.27,P < 0.01).Water samples of 742,228,54 copies were collected,respectively,in household well water,tap water and mountain spring water,and water iodine median was 2.08,2.24 and 0.73 μg/L,respectively.There was no significant difference between the water iodine median in tap water and household well water (x2 =2.97,P > 0.05),and the iodine in mountain spring water was less than that of tap water and household well water (x2 =38.23,43.82,P < 0.01).Water samples of 583 and 441 copies were collected,respectively,in the well depth < 40 m and well depth ≥40 m,and water iodine median was 1.81 and 2.24 μg/L,respectively,and there was no significant difference between the water iodine median in the well depth < 40 m and well depth ≥40 m(x2 =2.32,P > 0.05).Conclusions Residents iodine content of drinking water in Yi County is lower; the natural environment is seriously iodine deficiency,and iodine supplementation should be strengthened.
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Objective To investigate the relationship between the plasma levels of ET-1,TAT,and hs-CRP and slow coronary flow syndrome (SCFS),and explore effects of coronary endothelial function,coagulation function,and inflammatory reaction on blood flow of coronary artery.Methods A total of 400 cases with normal blood flow of coronary artery by coronary angiogram was randomly selected.The coronary flow patterns were determined by corrected thrombolysis in myocardial infarction frame count method (cT-FC).Among them,45 cases whose average cTFC more than 27 were assigned as SCFS group,the other 45 cases no SCFS.Plasma levels of ET-1,TAT and hs-CRPwere examined with enzyme-linked immunosorbent assay (ELISA),and were compared between two groups.Moreover,multivariate analysis evaluating predictors of SCFS was performed with regression test.Results No statistical difference was found between two groups concerning the gender,history of hypertension,diabetes mellitus,and cigarette alcohol percentage..The plasma level of HDL in SCFS group was lower than that of no SCFS [(1.22 ± 0.42) mmol/L vs (1.44±0.34) mmol/L,t =-2.731,P <0.01],but the plasma level of glucose in the former was higher than that of the latter [(5.68 ±0.62) mmol/L vs (5.10 ±0.84) mmol/L,t =3.727,P <0.01].However,Plasma levels of ET-1,TAT and hs-CRP in SCFS were higher than that of no SCFS [(94.3 ± 16.78) ng/Lvs (83.5±12.53) ng/L,t =3.051,P <0.01;(12.96±3.24)μg/Lvs (8.76 ±2.64)μg/L,t =5.945,P < 0.01 ; (2.48 ± 0.35) μg/L vs (1.38 ± 0.46) μg/L,t =11.259,P < 0.01].Furthermore,Logistic regression analysis showed that ET-1,TAT and hs-CRP were risk factors for SCFS (OR > 1.22).Conclusions Due to coronary endothelial dysfunction,endothelial inflammatory reaction,and activated coagulation function,slow coronary flow of coronary artery occurs.
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Ventricular myocytes from hearts of the neonatal SD rats were treated with 10-7,10-6,and 10-5 mol/L simvastatin for 72 hours under high glucose condition. Compared with control group,the viability of cadiomyocyte was significantly lower in high glucose group (P<0.01 ).The activity of lactate dehydrogenase,the relative expressions of NADPH oxidase subunits p22phox,p47phox mRNA,and reactive oxygen species level in the high glucose group were higher than those of control group ( all P<0.05).lndexes mentioned above were significantly improved by simvastatin treatment in a dose-dependent manner.These results suggest that simvastatin ameliorates high glucose-induced injury of cardiomyocytes via increasing the expression of NADPH oxidase mRNA.
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Objective To further investigate the relationship between apolipoprotein E(APOE) genotype and trait anxiety in patients with coronary heart disease (CHD).Methods Use the state-trait anxiety inventory (STAI) to investigate the state anxiety and trait anxiety of 107 CHD patients.According the score of TAI,the CHD patients were divided into CHD with high trait anxiety group ( n=39)and low trait anxiety group(n=68).The genotypes and alleles of apolipoprotein E gene was detected in all CHD patients and 50 healthy control subjects with the polymerase reaction(PCR) and restriction fragment length polymorphisms(RFLP) technique.Correlation analysis and logistic regression analysis were used.Results Apolipoprotein E gene showed positive relationship with trait anxiety score( OR =9.251,95% CI2.726 ~ 18.266).F4 allele entered the regression equaltion Y =30.252 + 0.048X3 (P < 0.05 ).Conclusion The results suggest the polymorphisms of Apolipoprotein E e4 allele may be associated with the trait anxiety symptom.
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Objective To explore the status and impact factors of hospitalized patients with coronary heart disease(CHD) accompanying depression disorders.Methods Adopt HRSD,SDS and general questionnaire for survey tools to evaluate the 300 hospitalized patients with CHD.Using SPSS13.0 software to build database,and the data was analyzed by descriptive statistics analysis and correlation analysis.Result There were 148 people accompanying depression disorders among the hospitalized·patients with CHD(47.30% ),and 68 people were treated (47.89%).Multivariate logistic regression indicated that the age ( OR =-0.415,P < 0.05,CI =0.443 ~0.984),smoking history( OR =0.384,P < 0.05,CI =1.118 ~ 1.928 ),course of disease ( OR =-0.250,P <0.05,CI =0.608 ~ 0.996),myocardial infarction ( OR =0.676,P < 0.05,CI =1.082 ~ 3.576 ),family history ( OR =-0.744,P < 0.05,CI =0.231 ~ 0.978 ) were related to coronary artery disease accompanying depression disorders.Multivariate correlation analysis indicated that anxiety factor and gender were closely related,weight factor and age,educational level,myocardial infarction had closed relationship,cognitive factors were closely associated with the course of disease,day and night changes were in relation to age,block factor and gender,age,education,drinking history,smoking history were related closely,sleep factor and gender,onset form,hypertension relations closed,despair factor have closed relationship with gender,age,educational level,course of disease.Conclusion Age,smoking history,course of disease,myocardial infarction,family history were important risk factors of depression disorders in hospitalized patients with CHD.The HRSD's seven symptoms factors are closely associated with multipling influence factors.
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Objective To study the impact of depression disorder in patients after coronary stent implantation on incidence rate of in-stent restenosis (ISR) in the coronary heart disease( CHD ), and its possible pathophysiological mechanisms. Methods According to the Hamilton Depression Scale (HAMD-24) and Self-rating Depression Scale(SDS) score,95 patients with unstable angina received coronary drug-eluting stent implantation combined with depression disorder were serve as the study group; randomly selecte 246 cases without depression due to unstable angina pectoris after coronary stent implantation as the control group in the same period. The incidence rate of ISR in these two group were observed, and serum aldosterone ( ALD), high-sensitivity C-reactive protein (hs-CRP) ,Leptin levels in two groups were compared. Results The incidence rate of ISR in study group were significantly higher than that of the control group (28/95 vs 46/246, P<0. 05). Following with the aggravation of depression disorder,the incidence rate of ISR were elevated( χ2 =8. 148, P=0.017). Serum ALD,hs-CRP and Leptin levels of study group were significantly higher than the control group 7 days later after drug-eluting stent implantation ( ALD:277.4 ± 35.9 vs 258.9 ± 60.9, t= 3. 459, P= 0. 001; hs-CRP: 12.03 ± 3.06 vs 11.10 ±2. 806, t = 2.573, P = 0.008; Leptin:5.27 t 1.07 vs 4.98 ± 0.99, t= 2.323, P= 0.021 ). Pearson correlation analysis showed that its HAMA-24 score was positively correlated with serum ALD ,hs-CRP and Leptin( r=0.291,P=0.026; r=0.350, P=0.014; r=0. 312, P=0.023) ,and SDS score was positively correlated with hs-CRP( r=0. 302, P= 0. 020). Conclusion Serum ALD, hs-CRP and Leptin levels are higher in patients after coronary stent implantation combined with depression in patients, and the incidence rate of ISR is also higher in these patients, and the rates are elevated according to the aggravation of depression disorder.
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Objective:To investigate the problems and improve the quality of clinical education.Method:A questionnaire was made among 200 medical students at Ji'ning medical college.Results:About eighty-eight percent of the students were satisfied with their clinical education,but there were still some problems:absence of clear objectives in clinical practice;shortage of enthusiasm of the students;lack of responsibility of some teachers and too many factors affecting clinical practice.Conclusion:The key points to improve clinical education quality are to set up clear education objectives,develop appropriate clinical practice methods,improve teaching staff quality and reform the teaching content.