Objective:To explore the intervention effect of the Structured Health Education course and 5A nursing model for self-control of elderly patients with coronary heart disease.Methods:Using the random sampling method,124...Objective:To explore the intervention effect of the Structured Health Education course and 5A nursing model for self-control of elderly patients with coronary heart disease.Methods:Using the random sampling method,124 elderly CAD patients admitted to the First Affiliated Hospital of Bengbu Medical University were randomly divided into an experimental group and a control group.The control group line routine health education,experimental group take structured health education combined with 5A nursing before and after the intervention using a coronary heart disease assessment questionnaire,coronary heart disease self-control scale evaluation of two groups of intervention,compare two groups before and after intervention blood pressure,blood sugar,body mass index,lipid index level and complications within 8 months after discharge.Results:After the course intervention,the disease cognition and self-behavior of the experimental group were higher than that of the control group,and the differences were statistically significant(all P<0.1).Conclusion:This course is suitable for elderly patients with coronary heart disease.The 5A model improves the cognitive and management ability of elderly patients to a certain extent,which is worthy of clinical application.展开更多
Heart valve replacement is a common cardiac surgical procedure used to treat native valvular diseases such as aortic and mitral stenosis and regurgitation. These procedures reduce the morbidity and mortality associate...Heart valve replacement is a common cardiac surgical procedure used to treat native valvular diseases such as aortic and mitral stenosis and regurgitation. These procedures reduce the morbidity and mortality associated with diseased native valves and yet come at the expense of prosthetic valve complications. Structural valve degeneration is one such complication. We present a case of a critically ill elderly man who had undergone mitral valve replacement 14 years prior to his current presentation. Only after admission through the emergency department was a transesophageal echocardiogram obtained and the diagnosis of prosthetic valve degeneration made. He subsequently underwent successful replacement of his diseased prosthetic valve.展开更多
Objective To detect the effects of shortwave radiation on dose-dependent cardiac structure and function in rats after radiation and to elucidate the mechanism of shortwave radiation induced cardiac injury to identify ...Objective To detect the effects of shortwave radiation on dose-dependent cardiac structure and function in rats after radiation and to elucidate the mechanism of shortwave radiation induced cardiac injury to identify sensitive indicators and prophylactic treatment.Methods One hundred Wistar rats were either exposed to 27 MHz continuous shortwave at a power density of 5,10,and 30 mW/cm^2 for 6 min or undergone sham exposure for the control(the rats had to be placed in the exposure system with the same schedules as the exposed animals,but with an inactive antenna).The Ca^2+,glutamic oxaloacetic transaminase(AST),creatine kinase(CK)and lactate dehydrogenase(LDH)content in the peripheral serum of the rats were detected by an automatic blood biochemical analyser.The electrocardiogram(ECG)of standard lead II was recorded by a multi-channel physiological recording and analysis system.The cardiac structure of rats was observed by light and electron microscopy.Results The results showed that the 5,10,and 30 mW/cm^2 shortwave radiation caused a significant increased in the levels of Ca2+,AST,CK,and LDH in the peripheral serum of rats.The cardiac structure was damaged by radiation and showed a disordered arrangement of myocardial fibres,the cavitation and swelling of myocardial mitochondria.These injuries were most significant 7 d after radiation and were not restored until 28 d after radiation.Conclusion Shortwave radiation of 5,10,and 30 mW/cm^2 can damage rat cardiac function,including damage to the tissue structure and ultrastructure,especially at the level of the myocardial fibres and mitochondria.Shortwave radiation at 5,10,and 30 mW/cm^2 induced damage to rat heart function and structure with a dose-effect relationship,i.e.,the greater the radiation dose was,the more significant the damage was.展开更多
Aim It is well known that menopause could worsen age-related ventricular concentric remodeling and increased incidence of arrhythmias following estrogen （E2） deficiency. However, the underlying mechanisms of such ph...Aim It is well known that menopause could worsen age-related ventricular concentric remodeling and increased incidence of arrhythmias following estrogen （E2） deficiency. However, the underlying mechanisms of such phenomena are not fully understood. Mitochondria, as the ＇cellular power station＇ of hearts, play an impor- tant role in maintaining normal cardiac function and structure. Therefore, the present study aims to investigate whether mitochondrial compromise and gap junction impairment induced by miR-23a is responsible for E2 deficien- cy associated structural and electrical remodeling. Results： We found mitochondrial structural damages and respira- tory function impairment in myocardium of both postmenopausal and OVX mice and E2 supplement reversed mito- chondrial dysfunction in OVX mice, suggesting that E2 deficiency could induce mitochondrial compromise in the lar remodeling, which can be regulated via MicroRNAs （miRNAs）-dependent mechanism. We recently identified Asymmetric dimethylarginine （ADMA） positively correlates to vascular remodeling-based diseases. Here, we hy- pothesized that ADMA induces SMC phenotypic change via a miRNA-dependent mechanism. Methods and Results Microarray analysis enabled the identification of 7 deregulated microRNAs in ADMA-treated human aortic artery smooth muscle cells （hASMCs）. miR-182 was validated by real-time-PCR. Isobaric tags for relative and absolute quantitation （iTRAQ） based analysis of the hASMC proteome revealed that transfection of an miR-182 inhibitor sig- nificantly increased myeloid-associated differentiation marker （MYADM）, which was verified using Western blot and reporter activity quantization with the MYADM 3＇-UTR dual-luciferase reporter system, miR-182 knockdown further repressed Sprouty2 and enhanced MYADM, leading to ERIC/MAP kinase-dependent and MYADM-depend- ent hASMC phenotypic change including proliferation, migration and differentiation marker gene expression change. In vivo, adeno-miR-182 markedly suppressed carotid neointimal formation by using balloon-injured rat carotid artery model, specifically via decreased MYADM expression. Atherosclerotic lesions from patients with high ADMA plas- ma levels exhibited decreased miR-182 expression levels and elevated MYADM expression levels. In patients with coronary heart disease （n- 164）, the miR-182 expression level in plasma was negatively correlated with the plas- ma ADMA levels. Conclusions miR-182 is a novel SMC phenotypic modulator by targeting MYADM and can be a potential therapeutic target combating vascular remodeling-associated diseases. Reduced plasma miR-182 levels might be a new predictor of high vascular remodeling risk especially in patient with coronary heart disease.展开更多
Sodium-glucose cotransporter 2(SGLT2)inhibitors have been reapproved for heart failure(HF)therapy in patients with and without diabetes.However,the initial glucose-lowering indication of SGLT2i has impeded their uses ...Sodium-glucose cotransporter 2(SGLT2)inhibitors have been reapproved for heart failure(HF)therapy in patients with and without diabetes.However,the initial glucose-lowering indication of SGLT2i has impeded their uses in cardiovascular clinical practice.A challenge of SGLT2i then becomes how to separate their anti-HF activity from glucose-lowering side-effect.To address this issue,we conducted structural repurposing of EMPA,a representative SGLT2 inhibitor,to strengthen anti-HF activity and reduce the SGLT2-inhibitory activity according to structural basis of inhibition of SGLT2.Compared to EMPA,the optimal derivative JX01,which was produced by methylation of C2—OH of the glucose ring,exhibited weaker SGLT2-inhibitory activity(IC_(50)>100 nmol/L),and lower glycosuria and glucose-lowering side-effect,better NHE1-inhibitory activity and cardioprotective effect in HF mice.Furthermore,JX01 showed good safety profiles in respect of single-dose/repeat-dose toxicity and hERG activity,and good pharmacokinetic properties in both mouse and rat species.Collectively,the present study provided a paradigm of drug repurposing to discover novel anti-HF drugs,and indirectly demonstrated that SGLT2-independent molecular mechanisms play an important role in cardioprotective effects of SGLT2 inhibitors.展开更多
目的 探讨老年原发性高血压(EH)患者心脏结构、泵血功能与动态血压变异性的关系。方法 选取2021年1月至2022年12月在郑州市中医院接受治疗的126例老年EH患者作为A组,其中79例H型高血压(HT)患者为H型HT组,47例非H型HT患者为非H型HT组。...目的 探讨老年原发性高血压(EH)患者心脏结构、泵血功能与动态血压变异性的关系。方法 选取2021年1月至2022年12月在郑州市中医院接受治疗的126例老年EH患者作为A组,其中79例H型高血压(HT)患者为H型HT组,47例非H型HT患者为非H型HT组。同期收治的130例非HT老年患者作为B组。比较A组和B组动态血压变异性指标、泵血功能、心脏结构,H型HT组和非H型HT组动态血压变异性指标、心脏结构、泵血功能,并采用Spearman相关性分析老年EH患者心脏结构、泵血功能与动态血压变异性指标的相关性。结果 A组夜间收缩压标准差(N-SSD)、24 h收缩压标准差(24 h SSD)、白天收缩压标准差(D-SSD)均高于B组(P<0.05)。A组每搏量、心排出量及室间隔厚度高于B组;A组左室射血分数(LVEF)及左心室后壁厚度低于B组(P<0.05)。相比于非H型HT组,H型HT组24 h SSD、N-SSD、D-SSD、每搏量、心排出量及室间隔厚度均更高;LVEF及左心室后壁厚度更低(P<0.05)。老年EH患者每搏量与24 h SSD、N-SSD、D-SSD呈正相关(r=0.548、0.508、0.487),心排出量与24 h SSD、N-SSD、D-SSD呈正相关(r=0.612、0.573、0.490);LVEF与24 h SSD、N-SSD、D-SSD呈负相关(r=-0.603、-0.489、-0.543);室间隔厚度与24 h SSD、N-SSD、D-SSD呈正相关(r=0.576、0.645、0.476);左心室后壁厚度与24 h SSD、N-SSD、D-SSD呈负相关(r=-0.524、-0.603、-0.498)(P<0.05)。结论 不同类型的老年EH患者动态血压变异性、心脏结构及泵血功能有所差异,患者24 h SSD、N-SSD、D-SSD与每搏量、心排出量、室间隔厚度呈正相关,与LVEF、左心室后壁厚度呈负相关。展开更多
基金2022 Campus-level Scientific and Technological Project of Qilu Institute of Technology"Exploring the Material Basis and Mechanism of Action of Erjing Pill in Preventing and Treating Kidney Yin Deficiency AD Based on Network Pharmacology and Molecular Biology"(Project No.:QIT22NN009)。
文摘Objective:To explore the intervention effect of the Structured Health Education course and 5A nursing model for self-control of elderly patients with coronary heart disease.Methods:Using the random sampling method,124 elderly CAD patients admitted to the First Affiliated Hospital of Bengbu Medical University were randomly divided into an experimental group and a control group.The control group line routine health education,experimental group take structured health education combined with 5A nursing before and after the intervention using a coronary heart disease assessment questionnaire,coronary heart disease self-control scale evaluation of two groups of intervention,compare two groups before and after intervention blood pressure,blood sugar,body mass index,lipid index level and complications within 8 months after discharge.Results:After the course intervention,the disease cognition and self-behavior of the experimental group were higher than that of the control group,and the differences were statistically significant(all P<0.1).Conclusion:This course is suitable for elderly patients with coronary heart disease.The 5A model improves the cognitive and management ability of elderly patients to a certain extent,which is worthy of clinical application.
文摘Heart valve replacement is a common cardiac surgical procedure used to treat native valvular diseases such as aortic and mitral stenosis and regurgitation. These procedures reduce the morbidity and mortality associated with diseased native valves and yet come at the expense of prosthetic valve complications. Structural valve degeneration is one such complication. We present a case of a critically ill elderly man who had undergone mitral valve replacement 14 years prior to his current presentation. Only after admission through the emergency department was a transesophageal echocardiogram obtained and the diagnosis of prosthetic valve degeneration made. He subsequently underwent successful replacement of his diseased prosthetic valve.
基金Supported by grants from the National Natural Science Foundation of China[81402629]and Key Projects of Health Specialty in PLA Logistics Scientific Research Program[BWS15J011].
文摘Objective To detect the effects of shortwave radiation on dose-dependent cardiac structure and function in rats after radiation and to elucidate the mechanism of shortwave radiation induced cardiac injury to identify sensitive indicators and prophylactic treatment.Methods One hundred Wistar rats were either exposed to 27 MHz continuous shortwave at a power density of 5,10,and 30 mW/cm^2 for 6 min or undergone sham exposure for the control(the rats had to be placed in the exposure system with the same schedules as the exposed animals,but with an inactive antenna).The Ca^2+,glutamic oxaloacetic transaminase(AST),creatine kinase(CK)and lactate dehydrogenase(LDH)content in the peripheral serum of the rats were detected by an automatic blood biochemical analyser.The electrocardiogram(ECG)of standard lead II was recorded by a multi-channel physiological recording and analysis system.The cardiac structure of rats was observed by light and electron microscopy.Results The results showed that the 5,10,and 30 mW/cm^2 shortwave radiation caused a significant increased in the levels of Ca2+,AST,CK,and LDH in the peripheral serum of rats.The cardiac structure was damaged by radiation and showed a disordered arrangement of myocardial fibres,the cavitation and swelling of myocardial mitochondria.These injuries were most significant 7 d after radiation and were not restored until 28 d after radiation.Conclusion Shortwave radiation of 5,10,and 30 mW/cm^2 can damage rat cardiac function,including damage to the tissue structure and ultrastructure,especially at the level of the myocardial fibres and mitochondria.Shortwave radiation at 5,10,and 30 mW/cm^2 induced damage to rat heart function and structure with a dose-effect relationship,i.e.,the greater the radiation dose was,the more significant the damage was.
文摘Aim It is well known that menopause could worsen age-related ventricular concentric remodeling and increased incidence of arrhythmias following estrogen （E2） deficiency. However, the underlying mechanisms of such phenomena are not fully understood. Mitochondria, as the ＇cellular power station＇ of hearts, play an impor- tant role in maintaining normal cardiac function and structure. Therefore, the present study aims to investigate whether mitochondrial compromise and gap junction impairment induced by miR-23a is responsible for E2 deficien- cy associated structural and electrical remodeling. Results： We found mitochondrial structural damages and respira- tory function impairment in myocardium of both postmenopausal and OVX mice and E2 supplement reversed mito- chondrial dysfunction in OVX mice, suggesting that E2 deficiency could induce mitochondrial compromise in the lar remodeling, which can be regulated via MicroRNAs （miRNAs）-dependent mechanism. We recently identified Asymmetric dimethylarginine （ADMA） positively correlates to vascular remodeling-based diseases. Here, we hy- pothesized that ADMA induces SMC phenotypic change via a miRNA-dependent mechanism. Methods and Results Microarray analysis enabled the identification of 7 deregulated microRNAs in ADMA-treated human aortic artery smooth muscle cells （hASMCs）. miR-182 was validated by real-time-PCR. Isobaric tags for relative and absolute quantitation （iTRAQ） based analysis of the hASMC proteome revealed that transfection of an miR-182 inhibitor sig- nificantly increased myeloid-associated differentiation marker （MYADM）, which was verified using Western blot and reporter activity quantization with the MYADM 3＇-UTR dual-luciferase reporter system, miR-182 knockdown further repressed Sprouty2 and enhanced MYADM, leading to ERIC/MAP kinase-dependent and MYADM-depend- ent hASMC phenotypic change including proliferation, migration and differentiation marker gene expression change. In vivo, adeno-miR-182 markedly suppressed carotid neointimal formation by using balloon-injured rat carotid artery model, specifically via decreased MYADM expression. Atherosclerotic lesions from patients with high ADMA plas- ma levels exhibited decreased miR-182 expression levels and elevated MYADM expression levels. In patients with coronary heart disease （n- 164）, the miR-182 expression level in plasma was negatively correlated with the plas- ma ADMA levels. Conclusions miR-182 is a novel SMC phenotypic modulator by targeting MYADM and can be a potential therapeutic target combating vascular remodeling-associated diseases. Reduced plasma miR-182 levels might be a new predictor of high vascular remodeling risk especially in patient with coronary heart disease.
基金supported by the National key R&D Program of China(2021YFA0804904)the National Natural Science Foundation of China(22107030)+4 种基金the Chinese Postdoctoral Science Foundation(2020M681211)the Shanghai Morning Light Program(20CG36,China)the Shanghai Frontier Science Center of Optogenetic Techniques for Cell Metabolism(2021 Sci&Tech 03-28,China)the Innovative Research Team of High-level Local Universities in Shanghai(SHSMU-ZDCX20212702,China)the Chinese Special Fund for State Key Laboratory of Bioreactor Engineering(2060204)。
文摘Sodium-glucose cotransporter 2(SGLT2)inhibitors have been reapproved for heart failure(HF)therapy in patients with and without diabetes.However,the initial glucose-lowering indication of SGLT2i has impeded their uses in cardiovascular clinical practice.A challenge of SGLT2i then becomes how to separate their anti-HF activity from glucose-lowering side-effect.To address this issue,we conducted structural repurposing of EMPA,a representative SGLT2 inhibitor,to strengthen anti-HF activity and reduce the SGLT2-inhibitory activity according to structural basis of inhibition of SGLT2.Compared to EMPA,the optimal derivative JX01,which was produced by methylation of C2—OH of the glucose ring,exhibited weaker SGLT2-inhibitory activity(IC_(50)>100 nmol/L),and lower glycosuria and glucose-lowering side-effect,better NHE1-inhibitory activity and cardioprotective effect in HF mice.Furthermore,JX01 showed good safety profiles in respect of single-dose/repeat-dose toxicity and hERG activity,and good pharmacokinetic properties in both mouse and rat species.Collectively,the present study provided a paradigm of drug repurposing to discover novel anti-HF drugs,and indirectly demonstrated that SGLT2-independent molecular mechanisms play an important role in cardioprotective effects of SGLT2 inhibitors.
文摘目的 探讨老年原发性高血压(EH)患者心脏结构、泵血功能与动态血压变异性的关系。方法 选取2021年1月至2022年12月在郑州市中医院接受治疗的126例老年EH患者作为A组,其中79例H型高血压(HT)患者为H型HT组,47例非H型HT患者为非H型HT组。同期收治的130例非HT老年患者作为B组。比较A组和B组动态血压变异性指标、泵血功能、心脏结构,H型HT组和非H型HT组动态血压变异性指标、心脏结构、泵血功能,并采用Spearman相关性分析老年EH患者心脏结构、泵血功能与动态血压变异性指标的相关性。结果 A组夜间收缩压标准差(N-SSD)、24 h收缩压标准差(24 h SSD)、白天收缩压标准差(D-SSD)均高于B组(P<0.05)。A组每搏量、心排出量及室间隔厚度高于B组;A组左室射血分数(LVEF)及左心室后壁厚度低于B组(P<0.05)。相比于非H型HT组,H型HT组24 h SSD、N-SSD、D-SSD、每搏量、心排出量及室间隔厚度均更高;LVEF及左心室后壁厚度更低(P<0.05)。老年EH患者每搏量与24 h SSD、N-SSD、D-SSD呈正相关(r=0.548、0.508、0.487),心排出量与24 h SSD、N-SSD、D-SSD呈正相关(r=0.612、0.573、0.490);LVEF与24 h SSD、N-SSD、D-SSD呈负相关(r=-0.603、-0.489、-0.543);室间隔厚度与24 h SSD、N-SSD、D-SSD呈正相关(r=0.576、0.645、0.476);左心室后壁厚度与24 h SSD、N-SSD、D-SSD呈负相关(r=-0.524、-0.603、-0.498)(P<0.05)。结论 不同类型的老年EH患者动态血压变异性、心脏结构及泵血功能有所差异,患者24 h SSD、N-SSD、D-SSD与每搏量、心排出量、室间隔厚度呈正相关,与LVEF、左心室后壁厚度呈负相关。
