This study aims to explore the temporal relationship between ischemic J waves and the progression of chest discomfort in patients experiencing acute myocardial infarction (AMI) during its earliest phase. A retrospective analysis was conducted on 466 AMI cases, each reporting chest discomfort lasting no longer than 4 h. The cohort was divided into four subgroups based on the duration of pain, and electrocardiographic (ECG) alterations were compared across these groups. Patients were categorized based on the presence or absence of J waves on their initial ECG, and a comprehensive analysis was performed comparing patient demographics, ECG characteristics, echocardiographic data, and coronary angiography results. J waves were most prominent within the first hour of chest pain onset (p < 0.05). Patients with J waves had higher rates of ST-segment elevation myocardial infarction (STEMI) (91.4

环状RNA是一种特殊类型的非编码RNA,具有独特的以共价键相连的闭合环状结构,对核酸外切酶降解有抵抗作用,半衰期长,在进化上秉持着高度保守性,广泛且稳定地存在于多种生物体及生物体的多种体液内.随着全基因组分析及高通量测序技术的高速发展,环状RNA逐步成为近些年分子生物学研究领域的热门,例如高血压等诸多类型疾病预警及诊断的生物标志物和治疗的靶点,本文将从环状RNA的类型、特点、功能及其与高血压发生发展的关系等方面进行综述,为环状RNA在高血压疾病研究与诊治提供理论基础支持.

目的 比较比伐芦定与普通肝素在老年冠心病患者择期冠状动脉介入(PCI)治疗中的有效性和安全性.?方法 选取2018年5月至2020年12月在亭湖区人民医院行择期PCI治疗的老年冠心病患者100例,随机分为比伐芦定和普通肝素组各50例,分别予以术中抗凝.患者术后均随访30 d,主要研究终点为术后30 d内主要心血管不良事件(MACE),包括心源性死亡、心肌梗死再发、靶血管血运重建,次要终点为术后30 d内出血情况、支架内血栓形成及术前术后血检指标变化.?结果 两组间MACE事件发生率、出血情况(轻度、严重)、支架内血栓形成及术前术后血检指标(血红蛋白、红细胞压积、血小板计数)比较,差异均无统计学意义(t/χ2=0.154、0.122、2.041、0.344、0.340、1.081、-1.073、-1.153、1.478、0.719,P>0.05). 结论老年患者择期PCI术中应用比伐芦定与普通肝素相比,术后30 d内的MACE及出血等方面并无显著降低.

目的 比较小剂量沙库巴曲缬沙坦与培哚普利治疗心力衰竭的效果和安全性.方法 160例左室射血分数(left ventricular ejection fraction,LVEF)下降的心力衰竭患者分为观察组和对照组各80例,分别采用沙库巴曲缬沙坦、培哚普利治疗,观察两组治疗前后的N末端B型钠尿肽前体(N-terminal pronatriuretic peptide,NT-proBNP)、左室舒张末径(left ventricular end diastolic diameter,LVEDD)、左室收缩末径(left ventricular end systolic diameter,LVESD)、左室射血分数(left ventricular ejection fraction,LVEF)、6分钟步行距离(6 minute walk distance,6MWD)、纽约心功能分级、生活质量评分(quality of life,QOL)、干咳、低血压、高钾血症,血管性水肿情况.结果 治疗6个月后,2组NT-proBNP、LVEDD、LVESD均明显下降,且观察组NT-proBNP低于对照组,差异均有统计学意义(P<0.05);2组间LVEDD、LVESD无统计学差异(P>0.05).治疗后,2组LVEF、QOL、6MWD、心功能均明显改善,且观察组优于对照组,差异均有统计学意义(P<0.05).治疗期间,观察组干咳发生率(1.25％)低于对照组(10.00％),差异有统计学意义(χ2=5.77,P=0.03).结论 小剂量沙库巴曲缬沙坦与足剂量的培哚普利均能有效治疗EF降低的心力衰竭,但沙库巴曲缬沙坦效果更佳,且副作用小.

目的:评价药物涂层球囊(DCB)在治疗冠状动脉大血管原位病变(冠状动脉病变参考直径≥2.8 mm)以及大血管原位长病变(冠状动脉病变参考直径≥2.8 mm,病变长度≥20 mm)中的临床疗效.方法:选取2015年4月至2020年12月在杭州师范大学附属医院心内科诊治的患者80例,均为给予DCB治疗的冠状动脉大血管原位原发病变.采用计算机定量冠脉造影分析软件(QCA)分别对所纳入患者术前、术后即刻及随访三个不同时刻的冠脉造影图像进行分析,评估DCB的疗效;将入选的患者按照靶血管病变长度分成2组,即病变长度<20 mm组(n=45)和病变长度≥20 mm组(n=35),评估DCB治疗冠脉大血管原位长病变的疗效.结果:所纳入病例靶血管的病变长度为(15.71±5.98)mm,参考直径为(3.22±0.34)mm,在(15.89±9.34)个月的随访时间里,无患者发生急性心肌梗死、严重心律失常、心源性死亡及卒中.所有随访患者中未出现再次靶血管病变血运重建病例,随访时的晚期管腔丢失为(-0.01±0.26)mm.不同病变长度组患者晚期管腔丢失差异无统计学意义[(0.003±0.3)mm vs.(-0.03±0.23)mm,P=0.615].结论:DCB治疗冠状动脉大血管原位病变及原位长病变安全、有效,并能减少冠脉靶病变的晚期管腔丢失.

To the Editor: Hypertension is a well-known cardiovascular disease in which the kidney is an important target due to its role in the regulation of fluid, electrolyte balance, and blood pressure.[1] Glomerulosclerosis, renal tubule interstitial fibrosis, and proteinuria are the main pathological characteristics of hypertensive kidney injury.[2] Multiple studies have indicated that microRNAs (miR-NAs, miRs) participate in the progression of chronic kidney disease; such disease is caused by heterogeneous triggers and is characterized by progressive loss of kidney function.[3] miR-29 has been identified as a potent renoprotective regulator. Evidence from our laboratory revealed that miR-29b protected renal tubular epithelial cells against angiotensin II-induced epithelial-mesenchymal transition (EMT).[4] However, the effects of miR-29b in animal models of hypertension-induced nephropathy remain unknown. We therefore used spontaneously hypertensive rats (SHRs), a well-known cardiovascular disease model characterized by severe hypertension and renal dysfunction, to investigate whether renal injury is determined by miR-29b function. We hypothesize that chronic hypertension will interfere with pathologic remodeling of the kidney and cause renal damage and that miR-29b will favor the alleviation of renal dysfunction and interstitial fibrosis. To investigate the role of miR-29b during the progression of hypertensive renal insufficiency, rats were randomly assigned to five groups of five animals each: (1) normotensive Wistar–Kyoto (WKY) rats treated with physiological saline (WKY Group); (2) SHR rats treated with physiological saline (SHR Group); (3) SHR rats treated with nonspecific negative control lentiviral vectors (SHR+C Group); (4) SHR rats treated with high-expres-sion-miR-29b lentiviral vectors (SHR+M Group); and (5) SHR rats treated with miR-29b-inhibiting lentiviral vectors (SHR+I Group). To overexpress or downregulate miR-29b, we obtained lentiviruses expressing a mature miR-29b mimic (lv-miR-29b) or a miR-29b inhibitor (lv-miR-29b-In). We also acquired a nonspecific lentivirus (lv-miRC) for use as a nonspecific negative control. The upregulation and inhibition of miR-29b was caused by administering these reagents via intrarenal parenchymal injection. Four weeks postinjection, rats were euthanized by cervical dislocation. The left kidney was dissected into four parts. One part was used for polymerase chain reaction (PCR) analysis, and two parts were immersed for immunohistochemical assay and Sirius red staining. The final part was snap-frozen in liquid nitrogen for Western blot analysis. To explore miR-29b-induced changes in renal function, blood samples were collected for detection of blood urea nitrogen (BUN) and serum creatinine (SCr) before and after viral transfection. Kidney samples were homogenized in ice-cold lysis buffer containing protease inhibitor cocktail. Fifteen-week-old male normotensive WKY rats and SHRs were obtained for this study. Body weight and tail-cuff systolic blood pressure were measured at 1-week intervals. SCr and BUN were higher in SHRs than in WKYs, and both showed a statistically significant increase in SHRs between baseline and the 4-week time point. Consistent with the increased concentrations of serum SCr and BUN, SHRs showed markedly elevated urinary protein content compared to WKY rats. Once again, SHRs further exhibited a statistically significant increase within a 4-week time frame. These findings suggest the development of hypertensive renal injury. Four weeks after transgene delivery, SHRs treated with lv-miR-29b showed attenuated levels of SCr and BUN compared to the rats treated with lv-miRC [Supplementary Figure 1A and B, https://links.lww.com/CM9/A870]. Moreover, miR-29b overexpression in SHRs (SHR+Ms) lowered the urinary protein content by 6.75% compared with the urinary protein content in the SHR which treated with nonspecific negative control lentiviral vectors (SHR+C). Urinary protein levels were remarkably elevated in compliance with increased SCr and BUN in the SHR+I group compared with the SHR+C group [Supplementary Figure 1C, https://links.lww.com/CM9/A870]. These results suggest that overexpression of miR-29b inhibits hypertension-induced renal injury and that knockdown of miR-29b enhances renal injury. For all three renal function measurements at 4 weeks, the measured values in the WKY group were significantly lower than the measured values in the SHR+C and SHR+I groups but were not significantly different from the values in the SHR+M group. Furthermore, the measured values in the SHR group were not significantly different from the measured values in the SHR+C group but were significantly higher than the measured values in the SHR+M group and significantly lower than the measured values in the SHR+I group. Next, we investigated the effect of miR-29b levels on extracellular matrix (ECM) accumulation by measuring the level of collagen I in the kidneys. As shown in Supplementary Figure 2, https://links.lww.com/CM9/B50, the mRNA and protein expression levels of the ECM component collagen I were dramatically decreased in rats following lv-miR-29b administration compared to controls, while its expression was significantly increased when treated with the inhibitor lv-miR-29b-In [Supplementary Figure 2A-C; https://links.lww.com/CM9/B50]. To further confirm the expression of collagen I in the kidneys, we used rat renal tissue for immunohistochemical staining. As expected, SHRs exhibited more collagen I deposition in the renal interstitial structure [Supplementary Figure 2D and E; https://links.lww.com/CM9/B50], consistent with PCR and Western blot data. In addition, the positive areas of collagen I on the kidney sections were significantly decreased with lv-miR-29b administration compared to control virus administration [Supplementary Figure 2F and G; https://links.lww.com/CM9/B50]. In contrast, lv-miR-29b-In treatment caused a statistically significant increase in collagen I-stained areas relative to controls [Supplementary Figure 2H; https://links.lww.com/CM9/B50]. Moreover, Sirius red staining was performed for morphometric evaluation of ECM deposition [Supplementary Figure 2J-N; https://links.lww.com/CM9/B50]. As shown, kidneys with lv-miR-29b administration displayed only 3.29% renal fibrosis (interstitial staining), whereas kidneys with lv-miR-29b-In treatment showed more severe interstitial staining than the controls [Supplementary Figure 2O; https://links.lww.com/CM9/B50]. These results demonstrate that miR-29b upregulation efficiently protects against the development of chronic hypertensive interstitial fibrosis 4 weeks following lentivector transfection. To investigate the effects of miR-29b on EMT, a critical injury mechanism in chronic fibrosis, we measured the expression of α-smooth muscle actin (α-SMA, a myofibroblast marker) in kidneys 4 weeks after transfection. Of note, lv-miR-29b treatment resulted in a reduction in α-SMA synthesis to less than baseline levels, both at the gene and protein levels [Supplementary Figure 3A-C, https://links.lww.com/CM9/A870]. In contrast, the mRNA and protein levels of α-SMA were markedly increased following lv-miR-29b-In administration [Supplementary Figure 3A-C, https://links.lww.com/CM9/A870]. Similar results were obtained through immunohistochemical staining. More α-SMA-positive tissue staining was detected in SHRs than in WKYs [Supplementary Figure 3D and E, https://links.lww.com/CM9/A870], suggesting that the development of hypertension induced α-SMA expression. In the SHR+M group, positive staining for α-SMA was significantly reduced compared to positive staining for α-SM in the SHR+C group [Supplementary Figure 3F and G, https://links.lww.com/CM9/A870]. Meanwhile, there was significant α-SMA-positive tissue staining in the SHR+I group 4 weeks posttransfection; positive areas were localized around the renal tubulointerstitium [Supplementary Figure 3H, https://links.lww.com/CM9/A870]. Taken together, these observations revealed that overexpression of miR-29b strongly suppresses the α-SMA myofibroblast marker, which suggests inhibited development of EMT. Transforming growth factor-β (TGF-β) is a critical molecule in the process of renal fibrosis. Therefore, in the present study, the mechanisms underlying hypertensive renal fibrosis were assessed by measuring alterations in TGF-β expression. First, we investigated the mRNA levels of TGF-β with lv-miR-29b gene delivery. Our data showed suppressed mRNA levels of TGF-β compared to negative controls [Supplementary Figure 4A, https://links.lww.com/CM9/A870]. To further confirm our results, Western blot analysis was performed. As shown in Supplementary Figure 4B, https://links.lww.com/CM9/A870, we observed decreased protein levels of TGF-β in lv-miR-29b-treated rats, with levels reduced to 1/3 of the controls [Supplementary Figure 4C, https://links.lww.com/CM9/A870]. Consistent with earlier analysis, immunostaining revealed low expression of TGF-β in rats treated with lv-miR-29b [Supplementary Figure 4G, https://links.lww.com/CM9/A870]. In contrast, miR-29b knockdown resulted in remarkably increased mRNA and protein levels of TGF-β in SHRs compared to the controls. Meanwhile, immunohistochemical analysis identified strong staining in kidney sections from lv-miR-29b-In-treated animals [Supplementary Figure 4H, https://links.lww.com/CM9/A870]. Taken together, this negative association between miR-29b and mRNA/protein expression of TGF-β suggests a strong link between miR-29b and TGF-β. The present study yields several important findings about the effects of miR-29b on renal protection against hypertension. First, miR-29b ameliorates hypertensive renal dysfunction by reducing serum levels of creatinine and urea nitrogen in parallel to decreased proteinuria. Second, miR-29b attenuates ECM accumulation and suppresses the development of EMT, as indicated by decreased expression of collagen I and α-SMA, respectively. Finally, we proved the inhibitory effects of miR-29b overexpression on TGF-β activation by demonstrating significantly reduced gene and protein expression of TGF-β. Considering the pivotal role that TGF-β plays in fibrotic processes,[5] we hypothesized that miR-29b may exert its protective effects by modulating TGF-β. To further verify our supposition, TGF-β-related ECM accumulation and EMT were measured during the subsequent procedures. Peritubular capillaries become atrophic when compressed by collagen, and the distance between tubular cells and capillaries increases, thereby worsening the damage and favoring the development of renal failure.[2] In the present study, SHRs exhibited more collagen deposition than normotensive WKY rats, indicating more severe ECM accumulation under hypertensive conditions. Moreover, overexpression of miR-29b reduced the expression of collagen I, whereas downregulation of miR-29b with inhibitors induced the expression of collagens in vivo. Complementary to the present study, our previous research demonstrated that miR-29b modulated collagen expression in renal tubular epithelial cells in vitro.[4] Moreover, Qin et al[6] reported that increased expression of miR-29b could block progressive renal fibrosis, while downregulation of miR-29b was associated with a significant upregulation of collagen I in wild-type mice. In addition to the major effect on ECM proteins, miR-29b additionally inhibits EMT. Moreover, we demonstrated an inverse correlation between the miR-29b level and the myofibroblast marker α-SMA. Collectively, these results suggest that miR-29b plays a protective role by suppressing hypertension-induced EMT in SHRs. TGF-β is crucial in fibrotic diseases. In our study, down-regulation of TGF-β was observed via overexpression of miR-29b in SHRs. In contrast, knockdown of miR-29b was associated with increased TGF-β content in the kidney. Interestingly, studies in human trabecular meshwork cells revealed that miR-29b suppresses the expression of TGF-β at the promoter, transcript, and protein levels.[7] Our results add evidence to the negative regulatory effects of miR-29b on the expression of TGF-β, suggesting some level of crosstalk between TGF-β and miR-29b. Taken together, we found that miR-29b may serve as a novel antifibrotic factor by reducing ECM accumulation and inhibiting EMT via downregulation of TGF-β. Elevated expression of miR-29b could have beneficial effects against hypertensive kidney injury and prevent pathogenic renal fibrosis. Overexpressing miR-29b could be a promising therapeutic strategy for the treatment of hypertension-induced nephropathy. Funding This study was supported by grants from the Medical Science and Technology Project of the Department of Health, Zhejiang Province (No. WKJ-ZJ-1420) and the Zhejiang Province Nature Science Foundation (Nos. LZ16H020003 and LQ18H020007). Conflicts of interest None.

MicroRNA‐122 (miR‐122) is one of several microRNAs elevated in heart failure patients. To investigate the potential role and mechanism of miR‐122 in heart failure, we constructed a transgenic mouse overexpressing miR‐122 in the heart. This mouse exhibited cardiac dysfunction (as assessed by transthoracic echocardiography), morphological abnormalities of the heart and cardiomyocyte apoptosis characteristic of heart failure. Mechanistically, we identified the Hand2 transcription factor as a direct target of miR‐122 using a dual‐luciferase reporter assay. In Tg‐miR‐122 mice and H9C2 cells with miR‐122 mimics, we detected apoptosis and increased expression of dynamin‐related protein‐1 (Drp1). This effect was blocked with prior knockdown of Hand2 in vitro. Our work suggests that miR‐122 causes cardiomyocyte apoptosis by inhibiting Hand2 and consequently increasing Drp1‐mediated mitochondrial fission. Such a mechanism likely contributes to heart failure and so modulating this pathway could be therapeutically valuable against heart failure.

BACKGROUND The 2017 American College of Cardiology (ACC)/American Heart Association (AHA) (US) Guideline for the Prevention, Detection, Evaluation and Management of High Blood Pressure in Adults expanded the definition of hypertension and now considers atherosclerotic cardiovascular disease (ASCVD) risk in determining treatment for people with hypertension. US guidelines are influential around the world and it is therefore justified to study their impact in other settings. Our study determined the impact of adopting the 2017 ACC/AHA guideline in China. METHODS We analyzed the population impact of the 2017 ACC/AHA guideline using the 2011-2012 year of the China Health and Retirement Longitudinal Study (CHARLS), a nationally representative sample of Chinese adults 45-74 years of age (n = 11,822). Our analysis was unique because for the first time it used a population-appropriate equation to calculate ASCVD risk instead of the US Pooled Cohort Equation (the latter misrepresents risk in non-US populations). RESULTS Adopting the 2017 ACC/AHA guideline in China would increase the prevalence of hypertension from 44.1% to 56.4% (12.3 percentage points) and increase the number of adults recommended for antihypertensive medication from 41.6% to 49.1% (7.5 percentage points) in the 45-74-year age range. According to Chinese (but not US) risk calculations, the 2017 ACC/AHA guideline more selectively assigns antihypertensive medication to patients at higher risk for ASCVD. CONCLUSIONS The 2017 ACC/AHA guideline brings potential for risk reduction in China and selectively recommends medication for those who would benefit most. Realizing such benefits would ultimately depend on the acceptance, adherence, and feasibility of adopting this guideline.

目的 基于医共体模式,探讨紧密型社区随访管理对经皮冠状动脉介入治疗术(PCI)后患者的预后影响.方法 选取2018年7月至2019年3月就诊湖州市中心医院医共体康山街道社区卫生中心专家工作室的患者57例,根据随访方式分为一般随访组27例,紧密随访组30例,患者术后入组时及术后6个月予以血液生化指标检测,包括血小板、肝功能、肌钙蛋白I、超敏C反应蛋白、低密度脂蛋白胆固醇,心脏超声测量左心室舒张末期内径、左心室收缩末期内径、左心室射血分数值,同时测定6 min步行距离,并且测量血压调查吸烟情况.在随访6个月后,对不良事件发生情况(包括心律失常、心绞痛再发、出血事件、心力衰竭)进行对比,分析两组间各项指标的差异.结果 PCI术后6个月,紧密随访组谷草转氨酶、谷丙转氨酶、肌钙蛋白I、低密度脂蛋白低于一般随访组,差异有统计学意义(t/χ2=6.012、2.807、3.448、3.807,均P<0.05);6min步行距离以及左心室射血分数较一般随访组升高,差异有统计学意义(t=6.774、5.842,均P<0.05).PCI术后6个月,紧密随访组血压低于一般随访组,吸烟比例小于一般随访组,差异均有统计学意义(t=13.676、10.135、4.780,P<0.05).术后6个月,紧密随访组再发心绞痛、心力衰竭和出血事件发生率均低于一般随访组,差异有统计学意义(χ2=6.849、5.505、4.655,均P<0.05).结论 紧密型随访模式能加强患者依从性,降低不良事件的发生率,提高患者生活质量,改善患者的预后.

Objective A new smartphone app called Anura can measure blood pressure (BP) any time and any place without cuffs or special equipment from video of the face. This study assessed its accuracy in close conformity with the American National Standards Institute/Association for the Advancement of Medical Instrumentation/International Organization for Standardization (ANSI/AAMI/ISO) 81060-2:2013 standard for BP measurement devices. Methods We validated Anura in reference to auscultation using a mercury sphygmomanometer and then assessed accuracy against the two accuracy criteria described in the guideline (n = 85 subjects; three measurement pairs per subject). Results The mean difference between the Anura measurement and its paired auscultatory reference measurement across all 255 measurement pairs was –0.4 ± 6.7 mmHg for systolic blood pressure (SBP) and 1.2 ± 7.0 mmHg for diastolic blood pressure (DBP). Both are within the acceptable limit of 5 ± 8 mmHg and thus satisfy accuracy criterion 1. When mean differences are averaged for each subject, the mean across all 85 subjects is –0.4 ± 5.8 mmHg for SBP and 1.2 ± 6.7 mmHg for DBP. Both are within acceptable limits (based on the mean difference) and thus satisfy accuracy criterion 2. Conclusions Anura meets ANSI/AAMI/ISO 81060-2:2013 standard with respect to BP measurement accuracy. As the ANSI/AAMI/ISO 81060-2:2013 standard has not been developed for cuffless devices, further research assessing additional accuracy issues specific to such devices is needed.

目的 观察不同剂量曲美他嗪在冠心病心力衰竭患者中的效果.方法 选取冠心病心力衰竭的患者共240例,随机分为对照组、常规组及大剂量组,每组各80例.其中对照组予以常规冠心病及心力衰竭的药物,常规组在对照组基础上加用曲美他嗪60mg/d(20毫克/次,每日3次),大剂量组在对照组基础上加用曲美他嗪120mg/d(40毫克/次,每日3次),连续治疗3个月.记录三组治疗前后的B型脑钠肽前体(pro-brain vatriuretic peptide,pro-BNP),6分钟步行距离(6 minute walking distance,6MWD),左心室收缩末径(left ventricular end systolic dimension,LVESD)及左心室舒张末径(left ventrictlar end diastolic dimension,LVEDD),左心室射血分数(left ventricular ejection fractions,LVEF),每周心绞痛发作的次数,不良反应的发生率.结果 治疗后三组的pro-BNP、LVESD、LVEDD、每周心绞痛发生的次数与治疗前相比均降低,而LVEF值及6MWD均有增加,其中大剂量组效果更好,与常规组比较有统计学意义(P＜0.05).不良反应三组相当,无统计学意义(P＞0.05).结论 曲美他嗪在冠心病心力衰竭中疗效确切,大剂量比常规组效果好,而不良反应无明显增加.

文章对急性冠状动脉综合征(acute coronary syndrome,ACS)患者按全球急性冠状动脉事件注册(global registry of acute coronary events,GRACE)风险评级分级并给予个性化护理.结果 显示,个性化护理能改善急性冠状动脉综合征患者的焦虑及抑郁情绪,提高患者依从性,减少并发症.

Background: Cuff-based blood pressure measurement lacks comfort and convenience. Here, we examined whether blood pressure can be determined in a contactless manner using a novel smartphone-based technology called transdermal optical imaging. This technology processes imperceptible facial blood flow changes from videos captured with a smartphone camera and uses advanced machine learning to determine blood pressure from the captured signal. Methods: We enrolled 1328 normotensive adults in our study. We used an advanced machine learning algorithm to create computational models that predict reference systolic, diastolic, and pulse pressure from facial blood flow data. We used 70% of our data set to train these models and 15% of our data set to test them. The remaining 15% of the sample was used to validate model performance. Results: We found that our models predicted blood pressure with a measurement bias +/- SD of 0.39 +/- 7.30 mm Hg for systolic pressure, -0.20 +/- 6.00 mm Hg for diastolic pressure, and 0.52 +/- 6.42 mm Hg for pulse pressure, respectively. Conclusions: Our results in normotensive adults fall within 5 +/- 8 mm Hg of reference measurements. Future work will determine whether these models meet the clinically accepted accuracy threshold of 5 +/- 8 mm Hg when tested on a full range of blood pressures according to international accuracy standards.

目的 探讨培哚普利吲达帕胺与足量培哚普利的降压疗效及安全性.方法 选取本院心内科门诊和住院的2级和3级高血压患者共60例,随机分为观察组和对照组,每组各30例,观察组予以培哚普利吲达帕胺(4mg培哚普利+ 1.25mg吲达帕胺)治疗,对照组给予培哚普利(8mg),连续治疗2个月,观察两组患者降压的有效率、降压幅度及副反应发生率.结果 治疗前两组患者收缩压及舒张压差异无统计学意义,观察组在治疗有效率、降压幅度方面明显优于对照组(P＜0.05),而副作用如低血压、低钾血症方面两组比较差异无统计学意义(P＞0.05),干咳的发生率和日均治疗费用观察组明显低于对照组(P＜0.05).结论 培哚普利吲达帕胺降压疗效明显优于足量培哚普利,而干咳发生率与培哚普利组比较明显减少,低钾血症及低血压等不良反应发生率基本相当,具有良好的安全性及经济性.

Objectives: MicroRNA-29b (miR-29b) has been recently reported to regulate fibrosis in renal diseases. However, very little is known about its functional role in hypertensive nephropathy. Here we studied whether alterations in miR-29b expression contribute to hypertension-induced renal dysfunction and renal fibrosis. Methods: Renal function was monitored by measuring the contents of serum creatinine (SCr), blood urea nitrogen (BUN) and urinary protein (UP) after treatment with a high efficient lentivector encoding miR-29b mimics or inhibitor. Collagen I, α-smooth muscle actin (α-SMA) and transforming growth factor-β (TGF-β) were evaluated at gene expression and protein levels by PCR and Western blot analysis, respectively. The degree of renal fibrosis was determined using Sirius red staining. Meanwhile, immunohistostaining was performed to identify the distribution of collagen I, α-SMA and TGF- β as well. Results: MiR-29b overexpression and knockdown significantly inhibited and increased serum creatinine (P < 0.05), urea nitrogen (P < 0.05) and urinary protein levels (P < 0.05) in SHRs. Importantly, miR-29b overexpression in SHRs lowed the urinary protein content by 6.75% compared with the normotensive controls. The interstitial deposition of collagen I, α-SMA and TGF-β expression were dramatically decreased when miR-29b level was augmented. In contrast, knockdown of miR-29b promoted TGF-β induced expression of collagen I and α-SMA both on a gene and on a protein level. Moreover, a negative regulatory role of miR-29b on the expression of TGF-β was clarified during the process of hypertensive nephropathy. Conclusion: MiR-29b may serve as an anti-fibrotic target by down-regulation of TGF-β in the pathophysiology of hypertension related renal fibrosis. Administration of an agent that increases miR-29b function prevents re

Objectives: To investigate the effects of angiotensin II antagonist telmisartan regulate the ACE2-Ang-(1–7)-Mas axis in rats with spontaneous hypertension and effects on retina endothelial cell apoptosis. Methods: Thirty-three spontaneous hypertension rats were divided into 3 groups (SHR, SHRT and SHRTA group), the SHRT group were treated with telmisartan 10 mg/(kg.d) by intragastric administration, the SHRTA group were treated with telmisartan 10 mg/(kg.d) by intragastric administration and A-779 0.5 mg/(kg.d) by intravenous injection at the same time. After 24 weeks, rats were sacrificed. Results: The expression of retinal ACE2 mRNA and protein in SHR group is lower in both groups of WKY and SHRT. The expression of retinal ACE2 mRNA and protein in SHRT group has no significantly differently compared with SHRTA group. The expression of retinal MAS mRNA and protein in SHR group is lower in both groups of WKY and SHRT, the expression of retinal MAS mRNA and protein in SHRTA group is lower than the SHRT group. The ELISA of serum Ang-(1–7) shows the expression of Ang-(1–7) protein in SHR group is lower in both groups of WKY and SHRT, the expression of Ang-(1–7) protein in SHRTA group is lower than the SHRT group. Specimens of retinal vessel in SHR group shows a large area of cell-free capillary was emerged in SHR group, and artery stenosis partially, there were no shadows of pericytes and endothelial cells in retinal capillary. The positive TUNEL cells are staining brown. The apoptosis rates of capillary in SHR group is lower in both groups of WKY and SHRT, the apoptosis rates of capillary in SHRTA group is lower than the SHRT group. Conclusion: Telmisartan can upregulate the ACE2-Ang-(1–7)-Mas axis in retina and protect the apoptosis in retina vessel endothelial cell.

The kidney serves a central role in the control of blood pressure through the release of vasoactive substances and the urinary excretion of Na+. Patients with essential hypertension usually exhibit persistent high blood pressure accompanied by Na+ retention. L-dihydroxyphenylalanine (L‑DOPA) is an amino acid, converted by the enzyme aromatic L‑amino acid decarboxylase to dopamine. The uptake of L‑DOPA by cells of the proximal tubular epithelium of the kidney is controlled by the L‑type amino acid transporter 2 (LAT2). LAT2 belongs to the solute carrier family 7 (SLC7) of amino acid transporters and is coded by the SLC7A8 gene. SLC7A8 expression is increased in the second‑order mesenteric arteries and kidneys of spontaneously hypertensive rats. The present study aimed to investigate the physiological role of the SLC7A8 gene in L‑DOPA handling by kidney cells. Selective upregulation of SLC7A8 mRNA and protein levels was achieved by adenoviral transduction of NRK‑52E cells, which retain several properties of proximal tubular epithelial cells. In addition, L‑DOPA uptake was determined using high performance liquid chromatography; NRK‑52E cells expressing SLC7A8 exhibited increased uptake of L‑DOPA. The results of the present study suggested that SLC7A8 may serve a critical role in blood pressure control through regulating L‑DOPA uptake in renal epithelial cells of the proximal tubule.

Objective To determine whether the efficacy and restenosis rate of domestic biodegradable polymer drug- eluting stents(EXCEL) is superior to that of domestic non- biodegradable polymer drug- eluting stents (PARTNER) in the treatment of coronary artery disease (CAD). Methods 111 cases with CAD underwent percutaneous coronary intervention (PCI). Of them, 54 patients were implanted with EXCEL stents and 57 patients with PARTNER stents. Main adverse cardiac events(MACE), recurrent angina, late stent thrombosis, restenosis rate, in- stent lumen loss and heart failure were observed during follow- up. Results There was no significant difference of the incidence of MACE, recurrent angina, late stent thrombosis, restenosis rate and heart failure between the two groups during fol ow- up of 6 to 30 months (al P>0.05). The percent of in- stent lumen loss≥30% was significant lower in EXCEL group (1.9%) than in PARTNER group (14.0%) (P=0.019). Conclusion The efficacy and safety of EXCEL stent in the treatment of CAD are similar to that of PARTNER stent, while the percent in- stent lumen loss is lower.

Quantification of deletions in mtDNA is a long-standing problem in mutational analysis. We describe here an approach that combines the power of single-molecule PCR of the entire mitochondrial genome with the enrichment of the deletions by restriction digestion. This approach is indispensable if information about wide range of deletion types in a sample is critical, such as in studies concerning distribution of deletion breakpoints (as opposed to approaches where fraction of a single deletion or a limited set of deletions is used as a proxy for total deletion load). Because deletions in a sample are quantified almost exhaustively, the other important application of this approach involves studies where only small amounts of tissue, such as biopsies, are available.

Congenital heart disease (CHD) is a worldwide health problem, particularly in young populations. In spite of the advancement and progress in medical research and technology, the underlying causative factors and mechanisms of CHD still remain unclear. Bone morphogenetic protein receptor IA (ALK3) mediates the development of ventricular septal defect (VSD). We have recently found that paired box gene 8 (Pax8) may be the downstream molecule of ALK3. Paired box gene 8 plays an essential role in VSD, and apoptosis and proliferation imbalance leads to septal dysplasia. Recent studies have also disclosed that cellular senescence also participates in embryonic development. Whether programmed senescence exists in cardiac organogenesis has not ever been reported. We hypothesized that together with various biological processes, such as apoptosis, enhanced cellular senescence may occur actively in the development of Pax8 null mice murine hearts. In H9C2 myogenic cells, Pax8 overexpression can rescue caspase‐dependent apoptosis induced by ALK3 silencing. Senescent cells and senescence‐associated mediators in Pax8 knockout hearts increased compared with the wild‐type ones in an age‐dependent manner. These results suggest that Pax8 maybe the downstream molecule of ALK3, it mediates the murine heart development perhaps via cellular senescence, which may serve as a mechanism that compensates for the cell loss via apoptosis in heart development.