Acute coronary syndrome (ACS) is a serious cardiovascular condition and a leading cause of mortality worldwide. Notably, 12/15-lipoxygenase (ALOX15) can be regulated by the long non-coding RNA ENST00000538705.1, thereby facilitating the progression of ACS. However, the downstream regulatory mechanisms involving ALOX15 remain unclear. The viability and migration of human primary coronary artery endothelial cells (HCAECs) were assessed using the Cell Counting Kit-8 and scratch assays, respectively. Reverse transcription-quantitative PCR was performed to assess the mRNA expression levels of ALOX15 and fibroblast growth factor receptor 2 (FGFR2). Protein-protein interactions between ALOX15 and FGFR2 were verified by co-immunoprecipitation (CO-IP). An ACS rat model was established to examine the effects of ALOX15 on blood lipid levels. Hematoxylin and eosin staining was executed to assess the histological changes. The levels of the FGFR2/PI3K/AKT signaling pathway-related proteins were assessed by western blotting. The results revealed elevated expression levels of ALOX15 and FGFR2 in patients with ACS. In HCAECs, transfection of overexpressed ALOX15 markedly enhanced cell viability and migration, while small interfering RNA-ALOX15 transfection produced the opposite effects. CO-IP assays confirmed the interaction between ALOX15 and FGFR2 in HCAECs. Additionally, knockdown of ALOX15 reduced blood lipid levels and alleviated myocardial injury in rats with ACS. ALOX15 silencing inhibited the expression of proteins associated with the FGFR2/PI3K/AKT signaling pathway in both HCAECs and rats with ACS. Both the overexpression of FGFR2 and the supplementation with insulin like growth factor 1 (a specific agonist of the PI3K/AKT pathway) significantly mitigated the inhibitory effects of ALOX15 knockdown on the migratory and proliferative capacities of HCAECs. The findings of the present study indicated that silencing of ALOX15 alleviates ACS progression via inhibiting the FGFR2/PI3K/AKT signaling pathway, providing a theoretical basis for ACS therapy in clinic.

Acute coronary syndrome (ACS), the acute manifestation of ischemic heart disease, remains a major cause of morbidity and mortality worldwide. The present study aimed to elucidate the preliminarily biological role and underlying mechanism of the long non-coding RNA (lncRNA) transcription factor AP-2α (TFAP2A)-AS1 in ACS. The viability, apoptosis, invasion, and migration of human coronary artery endothelial cells (HCAECs) were assessed using Cell Counting Kit-8, flow cytometric, Transwell, and wound healing assays. In addition, reverse transcription-quantitative PCR was performed to examine the expression levels of TFAP2A-AS1 and TFAP2A. Western blotting was performed to determine the protein level of TFAP2A. Furthermore, a mouse model of ACS was established to investigate the effects of TFAP2A-AS1 and TFAP2A on blood lipid levels. Histological changes were evaluated through hematoxylin and eosin staining. The results revealed high levels of TFAP2A-AS1 and TFAP2A expression in patients with ACS and in mouse models. In HCAECs, knockdown of TFAP2A-AS1 resulted in decreased TFAP2A expression, whereas silencing of TFAP2A did not affect the expression of TFAP2A-AS1. Interference with either TFAP2A-AS1 or TFAP2A in HCAECs led to suppressed cell viability, invasion, and migration, as well as an increased apoptosis rate. Furthermore, it was demonstrated that the absence of both TFAP2A-AS1 and TFAP2A reduced blood lipid levels and improved myocardial injury in a mouse model of ACS. In conclusion, groundbreaking findings revealed that the suppression of TFAP2A-AS1 could effectively mitigate the progression of ACS by reducing the expression of TFAP2A. This finding not only offers crucial insight into the pathogenesis of ACS but also provides a solid theoretical foundation for the development of novel therapeutic interventions in clinical settings.

Background:Diabetes is closely associated with the occurrence and development of coronary atherosclerotic heart disease. Coronary atherosclerosis is often severe and diffuse in patients with diabetes. We investigated the incidence of coronary in-stent restenosis (ISR) and the rate of reaching the standard of low-density lipoprotein cholesterol (LDL-C) in patients with type 2 diabetes mellitus (T2DM) and unstable angina pectoris (UAP) treated with ezetimibe and rosuvastatin one year later. Materials and methods:We selected the first pair of UAP patients with T2DM who underwent coronary artery stent implantation at our hospital between October 2018 and February 2022. According to drug use, the patients were divided into the rosuvastatin group [61 cases, rosuvastatin 10 mg/qn (every night)] and the combined group [60 cases, ezetimibe 10 mg/qd (once daily) and rosuvastatin 10 mg/qn]. Biochemical indices, left ventricular ejection fraction, and left ventricular end-diastolic diameter were collected before and one year after the first percutaneous coronary intervention. We collected data on the incidence of ISR and the rate of reaching the standard of LDL-C one year after surgery. Emergency PCI or coronary artery bypass grafting, cardiac death, and non-fatal acute myocardial infarction due to unstable angina pectoris 30 days after coronary stent implantation and lipid-lowering treatment were regarded as the primary endpoints. Results:After one year of follow-up, the incidence of in-stent restenosis(ISR), total cholesterol(TC), and LDL-C levels in the combined group[ISR, 3.33%; TC, 3.19 ± 0.75; LDL-C, 1.38(1.18-1.64)] were lower than those in the rosuvastatin group[ISR, 16.39% TC,C 3.84 ± 1.15; LDL-C, 1.92(1.52-2.61)] (P < 0.05). The rate of reaching the standard of LDL-C in the combined group (65%, 95% CI 0.560-0.809) was higher than that in the rosuvastatin group(31%, 95% CI 0.210-0.446) (P < 0.05). No significant difference in safety was observed between the two groups (P > 0.05). No endpoints were observed in the combined group. Conclusion:Resuvastatin combined with ezetimibe can better prevent ISR and reduce the incidence of cardiovascular adverse events. In addition, ezetimibe combined with rosuvastatin better reduced LDL-C levels.

Objective Exploring the Correlation between Mitochondrial Function of T Cells and the Severity of Coronary Artery Disease. Methods A total of 118 patients with coronary heart disease were divided into 32 cases in the ACS group and 25 cases in the stable angina pectoris (SAP) group. Meanwhile, 61 non-coronary heart disease patients who were hospitalized during the same period were selected as the control group. The expression levels of CD3 + T lymphocytes, CD4 + T lymphocytes and CD8 + T cells, CD4-MM, CD8-MM,CD4-MMP,CD8-MMP in the plasma of the three groups were detected by a flow cytometry instrument and the human lymphocyte mitochondrial function. Results In the SAP and ACS groups, CD4MMP and CD8MMP were significantly lower than those in the control group, while CD4MM was significantly higher than that in the control group(P<0.05).However, there were no differences in CD4MMP, CD8MMP, and CD4MM between the SAP group and the ACS group(P > 0.05). CD4MM in the STEMI group was higher than that in the UA/NSTEMI group. Conclusion In the peripheral blood of patients with coronary heart disease, the levels of CD4MMP and CD8MMP are significantly decreased, while CD4MM is significantly increased. These indicators can be used as predictive markers for the occurrence of coronary heart disease.

目的 观察依折麦布联合瑞舒伐他汀治疗老年2型糖尿病(T2DM)合并不稳定型心绞痛(UA)患者经皮冠状动脉(下称冠脉)介入治疗(PCI)术后的疗效.方法 选择2018年10月至2021年2月在温州市人民医院首次接受PCI的T2DM合并UA患者100例,分为瑞舒伐他汀组50例和联合治疗组50例.瑞舒伐他汀组给予瑞舒伐他汀10 mg、1次/d,联合治疗组给予依折麦布10 mg、1次/d及瑞舒伐伐他汀10 mg、1次/d.PCI术前和术后1年测定总胆固醇(TC)、甘油三酯、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇(LDL-C)、糖化血红蛋白、空腹血糖、丙氨酸氨基转移酶、肌酐和肌酸激酶(CK)水平.超声心动图检测左心室射血分数(LVEF)和左心室舒张末期内径(LVEDd).观察PCI术后1年支架狭窄发生率和LDL-C达标率.结果 联合治疗组TC、LDL-C水平、支架内再狭窄发生率均低于瑞舒伐他汀组(均P<0.05),LDL-C达标率高于瑞舒伐他汀组(P<0.05).两组无一例患者因肝功能受损、CK升高或肌痛而停用降脂药物.结论 与单独使用瑞舒伐他汀相比,联合使用依折麦布可以更好地降低LDL-C水平,预防支架内再狭窄.

BACKGROUND AND AIMS:Human vascular smooth muscle cells (HA-VSMCs) are an important cell type involved in atherosclerosis. Low density lipoprotein (LDL) is a lipoprotein particle that carries cholesterol into peripheral tissue cells, and oxidized modified LDL (ox-LDL) is a well-known inducer of the atherosclerosis-related phenotype switch in VSMCs, leading to the occurrence of atherosclerosis. Accumulating studies have revealed that long non-coding RNAs (lncRNAs) mediate the effect of ox-LDL on the atherosclerosis-related biological activities of HA-VSMCs, including proliferation, migration, and apoptosis. However, the mechanism of small nucleolar RNA host gene 12 (SNHG12) in ox-LDL-induced phenotype switch of VSMCs remains unclear. Thus, this research dug in whether SNHG12 mediated the influence of ox-LDL on HA-VSMCs and the potential mechanism.METHODS:Fundamental experiments and functional assays were performed to measure the function of SNHG12 on HA-VSMCs. Then, mechanism assays and rescue assays were performed to study the regulatory mechanism of SNHG12 in HA-VSMCs.RESULTS:SNHG12 reversed the influence of ox-LDL treatment in enhancing cell proliferative and migratory abilities and weakening apoptotic ability in HA-VSMCs. SNHG12 was a competitive endogenous RNA (ceRNA) competing with sprouty RTK signaling antagonist 2 (SPRY2) to bind to miR-1301-3p, thus up-regulating SPRY2 expression in ox-LDL-treated HA-VSMCs. Besides, SNHG12 recruited serine and arginine rich splicing factor 1 (SRSF1) to stabilize negative regulator of ubiquitin like proteins 1 (NUB1) expression.CONCLUSIONS:This study illustrated that SNHG12 inhibited cell proliferation, migration and facilitated cell apoptosis in ox-LDL-induced HA-VSMCs by up-regulating SPRY2 and NUB1.

Abstract Objective to evaluate the clinical efficacy and safety of sacubitril valsartan in the treatment of heart failure (HF) with midrange ejection fraction after acute myocardial infarction (AMI) in diabetic patients. From January 2015 to July 2020, HF patients with diabetes mellitus complicated with AMI were retrospectively analyzed. According to the medication, they were divided into 2 groups, that is, sacubitril valsartan group (84 cases) and valsartan group (86 cases). Valsartan group took valsartan capsule (80 mg/capsule, Beijing Novartis Pharmaceutical Co., Ltd) 80 mg, qd, on the basis of routine treatment. On the basis of routine treatment, the sacubitril valsartan group took sacubitril valsartan sodium tablets (50 mg/tablet, Beijing Novartis Pharmaceutical Co., Ltd), the initial dose was 25 mg, bid, and gradually increased to the target dose according to the patient's blood pressure. After 12 months of treatment, the independent sample t test showed that the left ventricular end diastolic dimension in the sacubitril valsartan group was lower than that in the valsartan group [(47.26 ± 4.71) mm vs (50.05 ± 5.62) mm, P < .001]. The left ventricular ejection fraction in the sacubitril valsartan group was higher than that in the valsartan group [(54.76 ± 4.24)% vs (49.28 ± 3.74)%, P < .001]. χ2 inspection showed that the readmission rate in the sacubitril valsartan group was lower than that in the valsartan group (7.14% vs 18.60%, P < .05). Sacubitril valsartan has good safety and tolerability in patients with diabetes mellitus complicated with AMI who have HF with midrange ejection fraction. Compared with valsartan, sacubitril valsartan can improve the left ventricular function better and reduce the readmission rate due to HF in these patients.

Objective Acute coronary syndrome (ACS) is the most dangerous and deadly form of coronary heart disease. Herein, we aimed to explore ACS-specific circulating lncRNAs and their regulatory mechanisms. Methods This study collected serum samples from ACS patients and healthy controls for microarray analysis. Dysregulated circulating lncRNAs and mRNAs were determined with |log2fold − change| > 1 and p < 0.05. lncRNA-mRNA coexpression analysis was carried out. ENST00000538705.1 and ALOX15 expression was further verified in serum specimens. In human coronary artery endothelial cells (HCAECs), ENST00000538705.1 and ALOX15 were knocked out through transfecting specific siRNAs. Thereafter, proliferation and migration were investigated with CCK-8 and wound-healing assays. Myocardial infarction rat models were established and administrated with siRNAs against ENST00000538705.1 or ALOX15. Myocardial damage was investigated with H&E staining, and serum TC, LDL, and HDL levels were measured. Results Microarray analysis identified 353 dysregulated circulating lncRNAs and 441 dysregulated circulating mRNAs in ACS. Coexpression analysis indicated the interaction between ENST00000538705.1 and ALOX15. RT-qPCR confirmed the remarkable upregulation of circulating ENST00000538705.1 and ALOX15 in ACS patients. In HCAECs, ENST00000538705.1 knockdown lowered the expression of ALOX15 but ALOX15 did not alter the expression of ENST00000538705.1. Silencing ENST00000538705.1 or ALOX15 weakened the proliferation and migration of HCAECs. Additionally, knockdown of ENST00000538705.1 or ALOX15 relieved myocardial damage, decreased serum TC and LDL levels, and elevated HDL levels in myocardial infarction rats. Conclusion Collectively, our findings demonstrate that circulating ENST00000538705.1 facilitates ACS progression through modulating ALOX15, which provide potential targets for ACS treatment.

蛋白激酶C-βⅡ(PKC-βⅡ)是单个多肽链,包含由5个可变区(V1～V5)间隔的4个保守结构域(C1～C4).高糖环境可导致组织中二酰甘油水平普遍升高,进而激活PKC-βⅡ.而PKC-βⅡ能够激活一系列下游信号通路,引发多组织器官发生病变,导致糖尿病并发症发生,如糖尿病肾病等.PKC-βⅡ抑制剂LY333531可以通过抑制PKC-βⅡ的激活来阻断下游信号通路,从而起到治疗糖尿病肾病的作用.近年来关于PKC-βⅡ在糖尿病肾病中的研究越来越多,本文就其相关研究进展作一综述.

甲状腺功能亢进症(简称甲亢)是临床上常见的内分泌疾病.甲状腺素高分泌可直接影响心脏和外周血管,导致心肌代谢加快,房室传导时间缩短,房性细胞不应期缩短,甚至引发窦性心动过速、心房颤动和心房扑动等心律失常[1].针对甲亢合并心房颤动患者,临床上常在控制甲状腺素水平的基础上加用β受体阻滞剂、地高辛等抗心律失常药物[2],但这些药物合用会增加心动过缓的风险.浙江省温州市人民医院收治1例甲亢合并心房颤动患者,经抗甲状腺药物和抗心律失常药物治疗后,突发高度房室传导阻滞,严重致命性缓慢性心房颤动.现将具体情况报道如下.

Objective. This study is aimed at investigating the therapeutic effects of tetrandrine (Tet) on myocardial ischemia reperfusion (I/R) injury and probe into underlying molecular mechanism. Methods. H9C2 cells were divided into hypoxia/oxygenation (H/R) group, H/R+Tet group, H/R+Tet+negative control (NC) group, and H/R+Tet+miR-202-5p inhibitor group. RT-qPCR was utilized to monitor miR-202-5p and TRPV2 expression, and TRPV2 protein expression was detected via western blot and immunohistochemistry in H9C2 cells. Cardiomyocyte apoptosis was evaluated through detection of apoptosis-related markers and flow cytometry. Furthermore, myocardial enzyme levels were detected by ELISA. Rats were randomly separated into sham operation group, I/R group, I/R+Tet group (50 mg/kg), I/R+Tet+NC group, and I/R+Tet+miR-202-5p inhibitor group. miR202-5p and TRPV2 mRNA expression was assessed by RT-qPCR. TRPV2 protein expression was detected through western blot and immunohistochemistry in myocardial tissues. Apoptotic levels were assessed via apoptosis-related proteins and TUNEL. Pathological changes were observed by H&E staining. Myocardial infarction size was examined by Evans blue-TCC staining. Results. Abnormally expressed miR-202-5p as well as TRPV2 was found in H/R H9C2 cells and myocardial tissues of I/R rats, which was ameliorated following Tet treatment. Tet treatment significantly suppressed H/R- or I/R-induced cardiomyocyte apoptosis. ELISA results showed that CK-MB and LDH levels were lowered by Tet treatment in H/R H9C2 cells and serum of I/R rats. H&E staining indicated that Tet reduced myocardial injury in I/R rats. Also, myocardial infarction size was lowered by Tet treatment. The treatment effects of Tet were altered following cotreatment with miR-202-5p inhibitor. Conclusion. Our findings revealed that Tet may ameliorate myocardial I/R damage via targeting the miR-202-5p/TRPV2 axis.

目的 了解温州地区社区居民高血压患病情况及知识水平.方法 2019年1至12月采用以社区为单位的整群抽样调查法抽取温州地区10个社区的居民2584例,比较不同人口学特征人群高血压患病率,进一步采用多因素logistic回归分析高血压患病的影响因素;同时采用自制问卷调查高血压知识水平.结果 2584例调查人群中,检出高血压患者1079例,占51.8％.不同年龄、体重指数、职业、文化程度、婚姻状况以及是否合并糖尿病、常吃肉类、常吃蛋类人群高血压患病率比较,差异均有统计学意义(均P<0.05);不同性别人群高血压患病率比较,差异无统计学意义(P>0.05).高龄、超重或肥胖、文化程度低、合并糖尿病、不常吃肉蛋类等是社区居民高血压患病的独立危险因素(均P<0.05).社区居民对"高血压与冠心病、白血病、脑栓塞、脑出血、肝癌等疾病发生有关"的知晓率分别为35.1％、29.0％、54.1％、57.4％、27.8％,对"高血压与高盐饮食、吸烟、大量饮酒、精神紧张、缺乏运动等不良习惯有关"的知晓率分别为49.4％、12.9％、65.5％、63.5％、47.4％.结论 温州地区社区居民高血压患病率较高,特别是高龄、超重或肥胖、文化程度低、合并糖尿病、不常吃肉蛋类人群,而高血压知识水平较低.

The present study aimed to determine whether tetrandrine could attenuate left ventricular dysfunction and remodeling in rats with myocardial infarction. Sprague-Dawley rats were randomly divided into six groups (n=5/group) as follows: i) Healthy control group; ii) sham operation group; iii) myocardial infarction model group; iv) myocardial infarction + low-dose tetrandrine group (10 mg/kg); v) myocardial infarction + medium-dose tetrandrine group (50 mg/kg); and vi) myocardial infarction + high-dose tetrandrine group (80 mg/kg). Left ventricular end-diastolic diameter (LVIDd), left ventricular end-systolic diameter (LVIDs), ejection fraction (EF%) and left ventricular fractional shortening rate (FS%) were measured using ultrasonography. The pathological changes were observed by hematoxylin and eosin (H&E) staining. Left ventricular tissue section TUNEL staining was also performed. Furthermore, the triglyceride (TG), total cholesterol (TC), high density lipoprotein (HDL) and low-density lipoprotein (LDL) in the arterial blood were examined by biochemical testing. Expression levels of intracellular Ca2+ homeostasis-related proteins including ryanodine receptor calmodulin, CaM-dependent protein kinase II delta, protein kinase A, FK506 binding protein 12.6 were measured using western blot analysis. Ultrasonography results showed that in the myocardial infarction model rats, the levels of LVIDd and LVIDs were significantly higher; however, the levels of EF% and FS% were lower compared with those in the sham operation group, which was alleviated by tetrandrine. H&E results showed that tetrandrine alleviated the pathological characteristics of myocardial infarction model rats. Furthermore, tetrandrine significantly inhibited myocardial cell apoptosis in rats with myocardial infarction. Tetrandrine significantly inhibited the levels of TG, TC and LDL and increased the levels of HDL in the arterial blood of rats with myocardial infarction. These findings revealed that tetrandrine could attenuate left ventricular dysfunction in rats with myocardial infarction, which might be associated with intracellular Ca2+ homeostasis.

目的 探讨不同预后的严重压疮患者血清促生长激素释放多肽(Ghrelin)水平的变化与差异.方法 选择温州市人民医院2017年7月至2019年5月收治的严重压疮患者165例,其中男96例,女69例,年龄21～96(69.4±16.1)岁.根据压疮预后,分为愈合组(89例)和未愈组(76例),于确诊时、治疗约6周后及治疗3个月后收集患者血清,采用ELISA法检测并比较两组患者的Ghrelin水平.结果 愈合组患者血清Ghrelin水平在治疗前、治疗6周后及治疗3个月后分别为(509.3±89.5)、(348.3±102.5)、(309.3±72.7)ng/L,未愈组分别为(424.8±79.0)、(244.2±72.7)、(227.7±69.9)ng/L,愈合组患者Ghrelin水平随着治疗时间的延长逐渐降低(F=6.516,P<0.01),但各时间点均高于未愈组(均P<0.01).结论 Ghrelin水平的变化对严重压疮患者预后有一定的影响.

目的 探讨粉防己碱改善心肌梗死大鼠心功能的作用及潜在机制.方法 将48只雄性SD大鼠按随机数字表法分成正常组、假手术组、心肌梗死组、心肌梗死+粉防己碱低剂量(10 mg/kg)组、心肌梗死+粉防己碱中剂量(50 mg/kg)组、心肌梗死+粉防己碱高剂量(80 mg/kg)组,每组8只.采用永久结扎左冠状动脉方法 建立心肌梗死模型.利用超声心动图评估大鼠心脏功能[包括左室舒张末期内径(LVIDd)、收缩末期内径(LVIDs)、射血分数(EF)、左室短轴缩短率(FS)],ELISA法检测大鼠血清乳酸盐脱氢酶(LDH)、磷酸肌酸激酶同工酶(CK-MB)水平,Masson染色法测定心肌组织纤维化面积百分比,Western blot、RT-qPCR法分别检测心肌组织B淋巴细胞瘤-2(Bcl-2)、BCL2-Associated X的蛋白质(Bax)蛋白及mRNA相对表达量.结果 与假手术组相比,心肌梗死组大鼠的LVIDd、LVIDs,血清LDH、CK-MB水平,心肌组织纤维化面积百分比,心肌组织Bax蛋白及mRNA相对表达量均明显升高(均P<0.05);EF、FS,心肌组织Bcl-2蛋白及mRNA相对表达量均明显降低(均P<0.05).与心肌梗死组相比,心肌梗死+粉防己碱高、中剂量组大鼠血清LDH、CK-MB水平明显降低(均P<0.05);心肌梗死+粉防己碱高、中、低剂量组大鼠的LVIDd、LVIDs,心肌组织纤维化面积百分比,心肌组织Bax蛋白及mRNA相对表达量均明显降低(均P<0.05);而EF、FS,Bcl-2蛋白及mRNA相对表达量均明显升高(均P<0.05).结论 粉防己碱能改善心肌梗死大鼠的心室重塑和心肌细胞凋亡,其潜在的机制可能与Bax/Bcl-2有关.

Background: Contrast induced diabetic nephropathy (CIN) is an important cause of hospital-acquired acute renal failure. Our aim was to observe the effect of protein kinase C β2 (PKCβ2) knockdown on human proximal tubular epithelial cells (HK-2 cells) against meglumine diatrizoate and advanced glycation end products (AGEs)-induced apoptosis and autophagy. Methods: Cell viability was detected using cell counting kit-8 (CCK-8) assay in HK-2 cells after disposal with meglumine diatrizoate and AGEs with or without PKCβ2 siRNA/inhibitor LY333531. Flow cytometry and western blot were used to test cell apoptosis and the related protein levels in meglumine diatrizoate and AGEs co-treated HK-2 cells with or without PKCβ2 siRNA/inhibitor LY333531. Autophagy related proteins were detected using western blot. Immunofluorescence staining was used to examine the autophagy-specific protein light chain 3 (LC3), and autophagosome and autolysosome formation was observed under a transmission electron microscopy. Results: CCK-8 assay results showed that meglumine diatrizoate inhibited AGEs-induced HK-2 cell viability. Furthermore, meglumine diatrizoate promoted cell apoptosis and the expression level of caspase3 in AGEs-induced HK-2. Western blot results showed that meglumine diatrizoate elevated the expression levels of PKCβ2 and p-PKCβ2 in AGEs-induced HK-2 cells, and up-regulated the expression level of Beclin-1 and the ratio of LC3 II/LC3 I, and down-regulated the expression level of p62 in AGEs-induced HK-2 cells. We found that PKCβ2 knockdown alleviated meglumine diatrizoate and AGEs-induced HK-2 cell apoptosis and autophagy. Intriguingly, PKCβ2 inhibitor LY333531 reversed 3-methyladenine (3-MA)-induced autophagy inhibition in meglumine diatrizoate and AGEs-induced HK-2 cells. Conclusions: Our findings reveal that inhibiting PKCβ2 protects HK-2 cells against meglumine diatrizoate and AGEs-induced apoptosis and autophagy, which provide a novel therapeutic insight for CIN in diabetic patients.

OBJECTIVE:To examine whether the influence of hypertension (HTN) status on longitudinal changes in brain glucose metabolism was modified by the apolipoprotein 4 (APOE4) status among older people with normal cognition.METHODS:In this study, we included 217 older individuals with normal cognition from the Alzheimer's Disease Neuroimaging Initiative (ADNI) study. Participants were divided into the HTN and no HTN groups based on self-reported medical history. Brain glucose metabolism was assessed by 18F-fluorodeoxyglucose-positron emission tomography (FDG-PET). Linear mixed model was fitted to examine the association between the HTN × APOE4 interaction and longitudinal changes in brain glucose metabolism after controlling for several covariates.RESULTS:In the present study, we found that the association between HTN status and longitudinal changes in brain glucose metabolism varied as a function of the APOE4 status, such that the HTN/APOE4+ group showed a steeper decline in FDG SUVR than all other groups (No HTN/APOE4-, HTN/APOE4-, and No HTN/APOE4+). Nevertheless, there was no significant difference in the rate of decline in FDG SUVR among other groups (No HTN/APOE4-, HTN/APOE4-, and No HTN/APOE4+).CONCLUSION:The APOE4 genotype interacted with hypertension status to affect longitudinal changes in brain glucose metabolism among older individual with normal cognition, such that the HTN/APOE4+ group showed a steeper decline in FDG SUVR than other groups.

Background The six-minute walking test (6MWT) is a tool that plays a key role in evaluating the functional exercise capacity, prognosis and evaluation of treatment response of patients with various cardiopulmonary diseases. However, standard reference equations are currently unavailable for the six-minute walking distance (6MWD) for people aged 60–85 years in China. The purpose of this study was to 1) measure the 6MWD of healthy Chinese people aged 60–85 years, 2) establish reference equations for predicting the 6MWD, and 3) compare our reference equations with equations reported in previously published studies. Method We obtained informed consent from each participant prior to the test, and the research design was approved by the Ethics Committee of Wenzhou People’s Hospital. The demographic and anthropometric data and the 6MWD of healthy Chinese subjects aged 60–85 years old were measured using a standardized protocol. Every subject completed two 6MWTs, and the longest 6MWD further analyzed. Results Two hundred sixty-six subjects (128 males and 138 females) completed the 6MWT, and the mean walking distance was 518 ± 72 m. Males achieved a longer walking distance than females (518 ± 72 m vs. 487 ± 70 m; p < 0.0001), and active subjects achieved a longer walking distance than nonactive subjects (512 ± 76 m vs. 485 ± 63 m; p < 0.0001). According to the univariate analysis, the 6MWD was significantly associated with age, height, body mass index (BMI), heart rate and blood pressure after exercise and changes in heart rate before and after exercise. The stepwise multivariate regression analysis identified age, height and BMI as independent predictors of the 6MWD. The reference equations for Caucasians and South Americans tended to overestimate the 6MWD of our subjects, while the equations for Asian and African populations tended to underestimate the 6MWD. Conclusions This study is the first to describe the 6MWD of healthy Chinese people aged 60–85 years, and reference prediction equations were proposed. These findings will help to improve the evaluation of Chinese patients with diseases that affect exercise capacity.

Abstract Rationale: BMPR2 mutation is the most common cause of heritable pulmonary arterial hypertension (HPAH), but rare in hereditary hemorrhagic telangiectasia (HHT). ACVRL1, ENG and SMAD4 are the most common gene mutations reported in HPAH with HHT. Patient concerns: We report a 11-year-old boy with a definite diagnosis of pulmonary hypertension and suspected HHT with recurrent epistaxis. The results of gene detection showed that there was a nosense mutation in BMPR2. The results of gene detection of ACVRL1, ENG and SMAD4 were normal. Diagnoses: Heritable pulmonary arterial hypertension with suspected hereditary hemorrhagic telangiectasia. Interventions: Patient was treated with ambrisentan 2.5 mg qd. About a month later, the patient developed massive gastrointestinal bleeding and sudden convulsions. The patient's vital signs were stable after symptomatic treatment. Outcomes: After discharging from hospital, the patients continued to take ambrisentan. No epistaxis or gastrointestinal bleeding was found in one month of follow-up, but the symptoms of chest tightness were not significantly alleviated. Lessons: BMPR2 with a nonsense mutation is more likely to cause HPAH with HHT and are more likely to be life-threatening.

目的 观察不同肾小球滤过率(eGFR)的慢性冠状动脉完全闭塞性病变(CTO)患者经皮冠状动脉介入(PCI)治疗后心功能的改善情况.方法 2017年9月至2018年9月在温州市人民医院和浙江大学医学院附属邵逸夫医院行PCI治疗的CTO患者44例,根据是否诊断为慢性肾病(CKD),分为CKD组24例(eGFR<90 mL·min-1·1.73 m-2),非CKD组20例(eGFR≥90 mL·min-1·1.73 m-2).比较两组患者的基线资料、术后第1次肌酐水平,术后1、3、12个月的心脏超声检查结果、纽约心脏协会(NYHA)分级和加拿大心血管协会(CCS)心绞痛分级.结果 CKD组术后肌酐(86.4±14.9)滋mol/L,低于术前(91.8±15.6)滋mol/L(P<0.05).非CKD组术前肌酐为(62.3±9.3)滋mol/L,术后(69.5±15.2)滋mol/L,差异无统计学意义(P>0.05).3例患者发生造影剂肾病.术后12个月,非CKD组左心室射血分数(LVEF)为(70.2±4.5)％,高于术前(66.8±5.5)％(P<0.05),NYHA分级和CCS心绞痛分级均降低(均P<0.05).结论 慢性闭塞血管开通后,非CKD者心功能及心绞痛改善大于CKD者.