Aims: Coronary heart disease (CHD) patients with changed serum soluble receptor for advanced glycation end-products (sRAGE) will experience microalbuminuria and even kidney dysfunction. However, the role of sRAGE for microalbuminuria in CHD is still not established. This study aimed to evaluate the association between sRAGE and early kidney dysfunction in CHD patients. Materials and methods: In this cross-sectional study, sRAGE and urinary albumin to creatinine ratio (uACR) were measured in hospitalized CHD patients who have undergone coronary arteriography to evaluate the distinction and correlation between sRAGE and uACR. Results: There were 127 CHD patients (mean age: 63.06 +/- 10.93 years, 93 males) in the study, whose sRAGE were 1.83 +/- 0.64 mu g/L. The sRAGE level was higher in kidney injury group (uACR >= 30 mg/g) compared with no kidney injury group (uACR < 30 mg/g) [2.08 +/- 0.70 vs. 1.75 +/- 0.61 g/L, P < .05]. Moreover, the positive correlation between serum sRAGE and uACR was significant in CHD patients (r = 0.196, P < .05). Binary logistic regression suggests sRAGE as a predictor for microalbuminuria in CHD patients [odd ratio = 2.62 (1.12-6.15), P < .05]. The area under the receiver operating characteristic curve (AUC) of sRAGE is higher than that of the traditional indicators of renal function such as creatinine and estimated glomerular filtration rate, indicating sRAGE might have a good performance in evaluating early kidney injury in CHD patients [AUC is 0.660 (0.543-0.778), P < .01]. Conclusions: Serum sRAGE was positively correlated to uACR and might serve as a potential marker to predict early kidney injury in CHD patients. (c) 2024 Elsevier Espana, S.L.U. and Sociedad Espanola de Medicina Interna (SEMI). All rights are reserved, including those for text and data mining, AI training, and similar technologies.

Fundamento Los pacientes con cardiopatía coronaria (CC) con cambios en el receptor sérico soluble para productos finales de glicación avanzada (sRAGE) experimentarán microalbuminuria e incluso disfunción renal. Sin embargo, aún no se ha establecido el papel de sRAGE para la microalbuminuria en la enfermedad coronaria. El objetivo de este estudio fue evaluar la asociación entre el sRAGE y la disfunción renal precoz en los pacientes con CC. Materiales y métodos En este estudio transversal se midió el sRAGE y el cociente albúmina/creatinina urinaria (uACR) en pacientes hospitalizados con CC sometidos a arteriografía coronaria para evaluar la distinción y la correlación entre sRAGE y uACR. Resultados En el estudio participaron 127 pacientes con CC (edad media: 63,06±10,93 años, 93 varones), cuyos sRAGE fueron de 1,83±0,64μg/l. El nivel de sRAGE fue mayor en el grupo con lesión renal (uACR ≥30mg/g) en comparación con el grupo sin lesión renal (uACR <30mg/g) (2,08±0,70 vs. 1,75±0,61μg/l; p<0,05). Además, la correlación positiva entre el sRAGE sérico y la uACR fue significativa en los pacientes con CC (r=0,196; p<0,05). La regresión logística binaria sugiere sRAGE como predictor de microalbuminuria en pacientes con CC (odds ratio=2,62 [1,12-6,15]; p<0,05). El área bajo la curva característica operativa (AUC) del receptor de sRAGE es mayor que la de los indicadores tradicionales de función renal, como la creatinina y la tasa de filtración glomerular estimada, lo que indica que sRAGE podría tener un buen rendimiento en la evaluación de la lesión renal temprana en pacientes con CC (AUC es 0,660 [0,543-0,778]; p<0,01). Conclusiones El sRAGE sérico se correlacionó positivamente con la uACR y podría servir como un marcador potencial para predecir la lesión renal temprana en los pacientes con CC.

目的 探讨不同类型急性冠状动脉综合征患者血浆中可溶性晚期糖基化终末产物受体(soluble receptor for advanced glycation end product,sRAGE)、γ-干扰素(interferon-γ,IFN-γ)浓度及其与冠状动脉病变严重程度的关系.方法 纳入 2016 年 6月至 2018 年 6 月于首都医科大学附属北京天坛医院行冠状动脉造影的 236 例患者,分为急性心肌梗死组(n=42)、不稳定型心绞痛组(n=119)、非冠状动脉粥样硬化性心脏病(以下简称冠心病)组(n=75).用酶联免疫法检测各组血浆中sRAGE 和 IFN-γ浓度并比较.分别分析急性心肌梗死患者、不稳定型心绞痛患者sRAGE、IFN-γ在不同Gensini评分分组中的差异及其与冠状动脉病变支数的相关性.分析急性心肌梗死患者sRAGE、IFN-γ与心肌梗死标志物心肌肌钙蛋白(cardiac troponin I,cTnI)、肌红蛋白(myoglobin,Myo)、肌酸激酶同工酶(creatine kinase isoenzyme,CK-MB)的相关性.结果 急性心肌梗死组患者 sRAGE 浓度最高,非冠心病组最低.急性心肌梗死组 IFN-γ 浓度高于不稳定型心绞痛组和非冠心病组,不稳定型心绞痛组和非冠心病组差异无统计学意义.多因素 Logistics 回归分析显示 sRAGE浓度升高是急性心肌梗死和不稳定型心绞痛的独立危险因素,且与急性心肌梗死的关系更为密切.急性心肌梗死患者血浆中sRAGE与 IFN-γ浓度呈正相关,两者均与心肌梗死标志物cTnI、Myo、CK-MB呈正相关,与Gensini评分、冠状动脉病变支数未见明显相关性.不稳定型心绞痛患者,高Gensini组sRAGE及IFN-γ浓度大于中Gensini组和低Gensini组,sRAGE浓度以三支病变组最高、单支病变组最低,IFN-γ浓度以双支病变组最高、单支病变组最低.结论 急性冠状动脉综合征患者血浆中sRAGE浓度明显升高,并且急性心肌梗死者高于不稳定型心绞痛患者.不稳定型心绞痛患者中sRAGE及IFN-γ浓度与冠状动脉病变严重程度呈正相关.

Nuclear factor erythroid-2 related factor 2 (Nrf2), a nuclear transcription factor, modulates genes responsible for antioxidant responses against toxic and oxidative stress to maintain redox homeostasis and participates in varieties of cellular processes such as metabolism and inflammation during myocardial ischemia and reperfusion injuries (MIRI). The accumulation of reactive oxygen species (ROS) from damaged mitochondria, xanthine oxidase, NADPH oxidases, and inflammation contributes to depraved myocardial ischemia and reperfusion injuries. Considering that Nrf2 played crucial roles in antagonizing oxidative stress, it is reasonable to delve into the up or down-regulated molecular mechanisms of Nrf2 in the progression of MIRI to provide the possibility of new therapeutic medicine targeting Nrf2 in cardiovascular diseases. This review systematically describes the generation of ROS, the regulatory metabolisms of Nrf2 as well as several natural or synthetic compounds activating Nrf2 during MIRI, which might provide novel insights for the anti-oxidative stress and original ideas targeting Nrf2 for the prevention and treatment in cardiovascular diseases.

目的 探讨冠状动脉粥样硬化性心脏病(以下简称冠心病)患者可溶性高级糖基化终末产物受体(soluble receptor for advanced glycation end products,sRAGE)浓度和肾功能的相关性.方法 在行冠状动脉造影确诊冠心病的人群中,根据估算的肾小球滤过率(estimated glomerular filtration rate,eGFR)分为肾功能正常组和肾功能下降组,比较2组临床特征、sRAGE浓度,采用Spearman相关及Logistic回归分析血浆sRAGE浓度和肾功能的相关性.结果 本研究共纳入170例冠心病患者,相关性分析结果提示sRAGE与肌酐呈正相关(r=0.152,P=0.048),sRAGE与尿素氮呈正相关(r=0.160,P=0.038),sRAGE与eGFR呈负相关(r=-0.185,P=0.016).肾功能正常组109例,肾功能下降组61例.与肾功能正常组相比,肾功能下降组sRAGE浓度增加[(2.00±0.61)μg/L vs(1.70±0.60)μg/L],差异有统计学意义(P=0.003).多因素Logistic回归分析提示sRAGE是冠心病患者肾功能下降的关联指标(OR=2.954,95％CI:1.030～8.474,P=0.044).结论 血浆sRAGE浓度可能在冠心病伴发肾功能下降中具有潜在指示物的作用.

Soluble receptor for advanced glycation end-products (sRAGE) was reported to inhibit cardiac apoptosis through the mitochondrial pathway during myocardial ischemia/reperfusion (I/R) injury. Meanwhile, the proapoptotic protein Bcl2 and adenovirus E1B 19-kDa-interacting protein 3 (Bnip3) was reported to mediate mitochondrial depolarization and be activated by the Forkhead box protein O3 (FoxO3a). Therefore, it is supposed that FoxO3a–Bnip3 pathway might be involved in the inhibiting effects of sRAGE on mitochondrial apoptosis during I/R. I/R surgery or glucose deprivation/reoxygenation was adopted to explore mitochondrial depolarization, apoptosis and related signaling pathways in mice hearts and cultured cardiomyocytes. The results showed that overexpression of sRAGE in cardiomyocytes dramatically improved cardiac function and reduced infarct areas in I/R treated mice. sRAGE inhibited mitochondrial depolarization and cardiac apoptosis during I/R, which correlated with reduced expression of Bnip3, Sirt2, phosphorylation of Akt and FoxO3a which translocated into nucleus in cultured cardiomyocytes. Either Sirt2 or FoxO3a silencing enhanced the inhibiting effects of sRAGE on mitochondrial depolarization induced by I/R in cultured cardiomyocytes. Meanwhile, overexpression or silencing of FoxO3a affected the inhibiting effects of sRAGE on Bnip3 and cleaved caspase-3 in cultured cardiomyocytes. Therefore, it is suggested that sRAGE inhibited I/R injuries via reducing mitochondrial apoptosis through the FoxO3a–Bnip3 pathway.

Soluble receptor for advanced glycation end-product (sRAGE) was reported to protect myocardial ischemia/reperfusion (I/R) injuries via directly interacting with cardiomyocytes besides competing with RAGE for AGEs. However, the specific molecule for the interaction between sRAGE and cardiomyocytes are not clearly defined. Integrins which were reported to interact with RAGE on leukocytes were also expressed on myocardial cells, therefore it was supposed that sRAGE might interact with integrins on cardiomyocytes to protect hearts from ischemia/reperfusion injuries. The results showed that sRAGE increased the expression of integrinβ3 but not integrinβ1, β2, β4 or β5 in cardiomyocytes during I/R injuries. Meanwhile, the suppressive effects of sRAGE on cardiac function, cardiac infraction size and apoptosis in mice were cancelled by inhibition of integrinβ3 with cilengitide (CLG, 75 mg/kg). The results from cultured cardiomyocytes also proved that sRAGE attenuated myocardial apoptosis and autophagy through interacting with integrinβ3 to activate Akt and STAT3 pathway during oxygen and glucose deprivation/reperfusion (OGD/R) treatment. Furthermore, the phosphorylation of STAT3 was significantly downregulated by the inhibition of Akt (LY294002, 10 μM) in OGD/R and sRAGE treated cardiomyocytes, which suggested that STAT3 pathway was induced by Akt in I/R and sRAGE treated cardiomyocytes. The present study contributes to the understanding of myocardial I/R pathogenesis and provided a novel integrinβ3-dependent therapy strategy for sRAGE ameliorating I/R injuries.

Ferroptosis, a newly discovered form of regulated cell death dependent on iron and reactive oxygen species, is mainly characterized by mitochondrial shrinkage, increased density of bilayer membranes and the accumulation of lipid peroxidation, causing membrane lipid peroxidation and eventually cell death. Similar with the most forms of regulated cell death, ferroptosis also participated in the pathological metabolism of myocardial infarction and myocardial ischemia/reperfusion injuries, which are still the leading causes of death worldwide. Given the crucial roles ferroptosis played in cardiovascular diseases, such as myocardial infarction and myocardial ischemia/reperfusion injuries, it is considerable to delve into the molecular mechanisms of ferroptosis contributing to the progress of cardiovascular diseases, which might offer the potential role of ferroptosis as a targeted treatment for a wide range of cardiovascular diseases. This review systematically summarizes the process and regulatory metabolisms of ferroptosis, discusses the relationship between ferroptosis and myocardial infarction as well as myocardial ischemia/reperfusion injuries, which might potentially provide novel insights for the pathological metabolism and original ideas for the prevention as well as treatment targeting ferroptosis of cardiovascular diseases such as myocardial infarction and myocardial ischemia/reperfusion injuries.

Background: There have been no studies investigating the relationship between serum calcium level at admission and long-term cardiovascular outcome in patients with the acute coronary syndrome (ACS).  \r\nObjectives: This study aimed to explore the correlation of admission serum calcium with cardiovascular outcome in ACS patients.\r\nMethods: This longitudinal study included 105 ACS or suspected ACS patients who were referred to the Coronary Care Unit between June 1st, 2015, and August 31st, 2016. Serum calcium was measured upon admission, and the patients were followed up till November 30th, 2016. Cardiovascular death or cardiovascular re-hospitalization was the study\u0027s end.\r\n \r\nResults: According to the median of serum calcium, the patients were divided into two groups of lower (n=47) and higher serum calcium (n=58). Kaplan-Meier analysis found that patients with lower serum calcium had an obviously reduced cardiovascular event-free survival (log-rank χ2=5.594, P=0.018), compared to those with higher serum calcium. Furthermore, lower serum calcium level (HR=0.265, 95% CI=0.072-0.981, P=0.047) independently correlated with poor cardiovascular outcome in ACS or suspected ACS patients after adjustment for potential confounders in the multivariable Cox model.\r\nConclusion: Lower serum calcium upon admission independently correlated with poor long-term cardiovascular outcomes in patients with severe coronary artery disease.

Ischemia-reperfusion injury (IRI) is an inevitable process when reperfusion therapy undergoes in acute myocardial infarction patients, which will lead to cardiac cell death. Many factors have been found to protect the myocardium, one of which was the soluble receptor for advanced glycation end-products (sRAGE) that protected the myocardium from apoptosis and autophagy. However, pyroptosis is also an important form of cell death that occurs during ischemia-reperfusion (I/R), whose critical molecule, NLR family pyrin domain containing 3 (NLRP3), was ever reported to be inhibited by sRAGE; therefore, it is hypothesized that sRAGE may decrease the cardiac pyroptosis induced by I/R. The results showed that sRAGE protected cardiomyocytes from I/R-induced pyroptosis by decreasing the expression level of NLRP3, gasdermin D (GSDMD), interleukin-1β (IL-1β), and interleukin-18 (IL-18). Meanwhile, the results from primary cultured cardiomyocytes showed that the NF-κB pathway mediated the effects of sRAGE on pyroptosis. Therefore, it is concluded that sRAGE protects the heart from pyroptosis through inhibiting the NF-κB pathway during myocardial ischemia-reperfusion.

Background: There have been no studies investigating the association of serum calcium level upon admission with long-term cardiovascular outcome among patients suffering from acute coronary syndrome (ACS). Objectives: This study aimed to explore the correlation of serum calcium level upon admission with cardiovascular outcomes among ACS patients. Methods: This longitudinal study included 105 ACS or suspected ACS patients who were referred to the Coronary Care Unit from June 1st, 2015, to August 31st, 2016. Serum calcium was measured upon admission, and the patients were followed up until November 30th, 2016. Cardiovascular death or cardiovascular re-hospitalization was the study's end. Results: According to the median of serum calcium, the patients were divided into two groups of lower (n=47) and higher serum calcium level (n=58). The results of the Kaplan-Meier analysis revealed that patients with lower serum calcium obtained a significant decrease in cardiovascular event-free survival (log-rank χ2=5.594, P=0.018), compared to those with higher serum calcium level. Furthermore, lower serum calcium level (HR=0.265, 95% CI=0.072-0.981, P=0.047) independently correlated with poor cardiovascular outcome in ACS or suspected ACS patients after adjusting the potential confounders in the multivariable Cox model. Conclusion: Lower serum calcium level upon admission independently correlated with poor long-term cardiovascular outcomes in patients with severe coronary artery disease.

背景 急性冠脉综合征(ACS)患者纤维蛋白原升高与患者预后不良有关,但其对ACS患者冠状动脉病变严重程度的影响尚不清楚.目的 探讨纤维蛋白原与ACS患者冠状动脉病变严重程度的关系.方法 选取2019年1—5月首都医科大学附属北京天坛医院重症监护病房收治的ACS患者108例,根据SYNTAX评分分为轻度病变组(SYNTAX评分<23分,n=74)和中重度病变组(SYNTAX评分≥23分,n=34).比较两组患者一般资料〔包括性别、年龄、体质指数(BMI)、高血压发生情况、糖尿病发生情况、脑血管疾病发生情况、冠心病病史、吸烟史〕、实验室检查指标〔包括脑钠肽(BNP)、总胆固醇、粒细胞/淋巴细胞比值、平均血小板体积、纤维蛋白原、同型半胱氨酸、估算的肾小球滤过率〕;纤维蛋白原与ACS患者SYNTAX评分的相关性分析采用Pearson相关分析;ACS患者冠状动脉病变严重程度的影响因素采用多因素Logistic回归分析.结果 (1)两组患者男性比例、年龄、BNP、纤维蛋白原比较,差异有统计学意义(P<0.05);两组患者BMI、高血压发生率、糖尿病发生率、脑血管疾病发生率、有冠心病病史及吸烟史者所占比例、总胆固醇、粒细胞/淋巴细胞比值、平均血小板体积、同型半胱氨酸、估算的肾小球滤过率比较,差异无统计学意义(P>0.05).(2)Pearson相关分析结果显示,纤维蛋白原与ACS患者SYNTAX评分与呈正相关(r=0.348,P<0.05).(3)多因素Logistic回归分析结果显示,年龄〔OR=1.119,95％CI(1.021,1.226)〕、纤维蛋白原〔OR=3.458,95％CI(1.038,11.523)〕是ACS患者冠状动脉病变严重程度的影响因素(P<0.05).结论 纤维蛋白原与ACS患者冠状动脉病变程度呈正相关,是ACS患者冠状动脉病变严重程度的独立影响因素.

目的 探讨急性冠状动脉综合征(acute coronary syndrome,ACS)患者糖化血红蛋白(glycated hemoglobin,HbA1 c)水平与冠状动脉病变SYNTAX评分的相关性.方法 选取2019年1～5月在笔者医院心脏中心重症监护病房住院的ACS患者108例,采用SYNTAX评分评定冠状动脉病变程度,分为两组,即冠状动脉轻度病变组(SYNTAX评分≤22,n=74)和中重度病变组(SYNTAX评分≥23,n=34),分别检测两组患者HbA1 c水平,比较两组间HbA1 c水平及其他临床资料,分析上述指标与SYN-TAX评分的独立相关性.结果 在ACS患者中,冠状动脉中重度病变组HbA1 c水平明显高于轻度病变组(7.50％ ±2.17％vs 6.56％ ±1.34％,P=0.009),差异有统计学意义.Spearman相关分析结果 显示,HbA1 c水平与SYNTAX评分呈正相关(r=0.235,P<0.05).多因素Logistic回归分析结果 显示,HbA1 c是ACS患者冠状动脉中重度病变的独立预测因子(OR=2.004,95％CI:1.063～3.777,P<0.05).结论 HbA1 c水平与ACS患者的SYNTAX评分独立且显著相关,有助于判断冠状动脉狭窄病变的危险分层.

目的 探讨急性冠脉综合征(acute coronary syndrome,ACS)患者血浆B型钠尿肽(brain natriuretic peptide,BNP)与冠状动脉病变严重程度的关系.方法 回顾性分析首都医科大学附属北京天坛医院心脏重症监护病房2019年1～5月连续收治的115例ACS患者,根据冠脉造影结果,应用SYNTAX评分评定冠状动脉病变严重程度,根据SYNTAX评分将ACS患者分为两组,即冠状动脉轻度病变组(SYNTAX评分≤22)和中重度病变组(SYNTAX评分≥23),分别检测两组患者血浆BNP水平,分析其与SYNTAX评分的相关性及其对冠脉严重程度的预测作用.结果 在ACS患者中,冠状动脉中重度病变组血浆中BNP水平明显高于轻度病变组(411.13±357.40pg/ml vs 151.68±191.09pg/ml,P=0.000),血浆BNP水平与SYNTAX评分呈正相关(r=0.465,P=0.000),冠状动脉病变的严重程度随着BNP的升高而增加.进一步分析显示,两组患者之间冠状动脉血管病变支数的比例差异有统计学意义,冠状动脉中重度病变组患者三支病变的比例显著高于轻度病变组患者(P＜0.05).在多因素Logistic回归分析中显示,BNP仍然是ACS患者冠状动脉中重度病变的独立预测因子(OR=1.51,95％ CI:1.30～2.61,P=0.000).结论 在ACS患者中,血浆BNP水平与冠状动脉病变严重程度呈正相关,血浆BNP水平是冠状动脉中重度狭窄的独立预测因素.

Soluble receptor for advanced glycation end-products (sRAGE), which exerts cardioprotective effect through inhibiting cardiomyocyte apoptosis and autophagy during ischemia/reperfusion (I/R) injury, is also known to enhance angiogenesis in post-ischemic reperfusion injury-critical limb ischemia (PIRI-CLI) mice. However, whether sRAGE protects the heart from myocardial I/R injury via promoting angiogenesis remains unclear. Myocardial model of I/R injury was conducted by left anterior descending (LAD) ligation for 30 min and reperfusion for 2 weeks in C57BL/6 mice. And I/R injury in cardiac microvascular endothelial cells (CMECs) was duplicated by oxygen and glucose deprivation. The results showed that I/R-induced cardiac dysfunction, inflammation and myocardial fibrosis were all reversed by sRAGE. CD31 immunohistochemistry staining showed that sRAGE increased the density of vessels after I/R injury. The results from cultured CMECs showed that sRAGE inhibited apoptosis and increased proliferation, migration, angiogenesis after exposure to I/R. These effects were dependent on signal transducer and activator of transcription 3 (STAT3) pathway. Together, the present study demonstrated that activation of STAT3 contributed to the protective effects of sRAGE on myocardial I/R injury via promoting angiogenesis.

INTRODUCTION This study aimed to investigate the influence of peritoneal transport characteristics on clinical outcome in nondiabetic and diabetic nephropathy peritoneal dialysis (PD) patients. MATERIALS AND METHODS All 112 patients were from the PD Center. Peritoneal transport characteristic was assessed by peritoneal equilibration test. The patients were divided into 2 groups of high-transport group (HT) and non-high-transport group (non-HT) and followed-up till December 31st, 2010. The primary outcomes were all-cause death and technique failure. RESULTS The patients were followed-up for 65.9 ± 23.9 months. Diabetic nephropathy patients with HT had a higher all-cause mortality (P = .04) and technique failure (P = .04) than those with non-HT. There were no differences in outcomes between HT and non-HT subgroups without diabetic nephropathy. Cox regression demonrtrated that high peritoneal transport (HR, 2.369; 95% CI, 1.056 to 5.311), diabetic nephropathy (HR, 2.499; 95% CI, 1.134 to 5.508), age (HR, 1.081; 95% CI, 1.032 to 1.133), and peritoneal creatinine clearance (HR, 0.962; 95% CI, 0.929 to 0.997) independently predicted all-cause mortality in continuous ambulatory PD patients. Moreover, high peritoneal transport (HR, 2.299; 95% CI, 1.079 to 4.899) and age (HR, 1.070; 95% CI, 1.026 to 1.116) predicted technique failure in continuous ambulatory PD patients. CONCLUSIONS Diabetic nephropathy PD patients with HT had a higher all-cause mortality and technique failure than those with non-HT, but we did not find the correlation between peritoneal transport and outcome in nondiabetic patients. The peritoneal transport was an independent predictor for outcomes in continuous ambulatory PD patients.

Objectives: This study was designed to investigate clinical symptoms and blood pressure (BP) characteristics in Parkinson's disease (PD) with orthostatic hypotension (OH), and to figure out the influencing factors of PD with OH (PD-OH). Methods: Total 150 PD patients were divided into PD-OH and PD with no OH (PD-NOH) groups based on BP value. Series of scales were used to evaluate clinical symptoms. Twenty-four-hour ambulatory BP monitoring was adopted. Results: Total 49 PD patients (32.67%) were with OH. PD-OH group had significantly older age, longer disease duration, more diabetes cases, higher levels of fasting blood glucose, higher levels of hemoglobin A1c (HbA1c) and higher levodopa-equivalent daily doses (P < 0.05). Motor symptoms and non-motor symptoms, including autonomic dysfunction, fatigue and cognitive impairment indicated by significantly changed scores of related scales were found in PD-OH group (P < 0.05). PD-OH group had increased BP variability (BPV) and a higher proportion of non-dipper BP pattern (P < 0.05). Binary logistic regression analysis showed that age (B, 0.064; 95% CI, 1.007 ~ 1.128; P < 0.05), HbA1c (B, 1.091; 95% CI, 1.158 ~ 7.648; P < 0.05), and systolic BPV (B, 0.138; 95% CI, 1.004 ~ 1.312; P < 0.05) were independent related factors for PD-OH group. The PD-OH group had significantly compromised daily activities and quality of life (P < 0.05). Conclusion: Older age, higher levels of HbA1c and increased systolic BPV were the influencing factors of PD-OH patients. Daily activities and quality of life of PD-OH patients were fairly compromised.

The aim of this study was to determine whether the polymorphism of aldosterone synthase (CYP11B2) –344C/T and angiotensin-converting enzyme (ACE) insertion/deletion (I/D) were associated with the response of blood pressure (BP) to telmisartan treatment. After a two-week single-blind placebo run-in period, 148 patients with mild-to-moderate primary hypertension received monotherapy of telmisartan with 80 mg/day and then were followed up for eight weeks. Polymorphisms of CYP11B2 –344C/T and ACE I/D gene were determined through polymerase chain reaction-restriction fragment polymorphism analysis. The relationship between these polymorphisms and changes in BP was monitored and evaluated after eight weeks of treatment. With respect to the polymorphism of CYP11B2 –344C/T, the reduction in diastolic BP was significantly greater in patients carrying the C allele (CC+CT) compared with those carrying the TT genotype. There was no significant differences between ACE I/D polymorphism and BP reduction after treatment. We concluded that the aldosterone synthase –344C/T polymorphism was related to the antihypertensive treatment with telmisartan in hypertensive patients.

The aim of this study was to determine whether the polymorphism of aldosterone synthase () -344C/T and angiotensin-converting enzyme () insertion/deletion (I/D) were associated with the response of blood pressure (BP) to telmisartan treatment. After a two-week single-blind placebo run-in period, 148 patients with mild-to-moderate primary hypertension received monotherapy of telmisartan with 80 mg/day and then were followed up for eight weeks. Polymorphisms of -344C/T and I/D gene were determined through polymerase chain reaction-restriction fragment polymorphism analysis. The relationship between these polymorphisms and changes in BP was monitored and evaluated after eight weeks of treatment. With respect tothe polymorphism of -344C/T, the reduction in diastolic BP was significantly greater in patients carrying the C allele (CC+CT) compared with those carrying the TT genotype. There was no significant differences between I/D polymorphism and BP reduction after treatment. We concluded that the aldosterone synthase -344C/T polymorphism was related to the antihypertensive treatment with telmisartan in hypertensive patients.

The current study investigated the role of sRAGE in the production of IFN‑γ in macrophages with I/R treatment. The number of macrophages in myocardial tissues treated with I/R with or without sRAGE was determined via immunohistochemical staining. Proliferative activity of macrophages was analyzed by a 5‑BrdU incorporation assay. Differentiation of macrophages was detected via immunofluorescence staining of iNOS (M1 macrophage marker). IFN‑γ production, due to sRAGE stimulation, in Raw 264.7 macrophages and the NF‑κB signaling pathway were measured using western blotting. A ChIP assay was used to examine the interactions between NF‑κB and the promoter of IFN‑γ. The results showed that the number of macrophages in I/R‑treated myocardial tissues was increased following sRAGE infusion. Proliferation of macrophages was increased significantly in the presence of sRAGE; after I/R treatment, the cells preferred to differentiate into M1 macrophages. IFN‑γ expression in Raw 264.7 macrophages was suppressed by an NF‑κB inhibitor (Bay117082) but enhanced by sRAGE, with or without I/R treatment. Furthermore, sRAGE increased the phosphorylation of IκB, IKK and NF‑κB, as well as the translocation of NF‑κB into the nucleus of Raw 264.7 macrophages, with or without I/R treatment. ChIP results showed that sRAGE promoted NF‑κB binding to the promoter of IFN‑γ in Raw 264.7 macrophages. Therefore, the findings of the present study indicated that sRAGE protected the heart from I/R injuries, which might be mediated by promoting infiltration and the differentiation of macrophages into M1, which would then synthesize and secrete IFN‑γ through activating the NF‑κB signaling pathway.