Objective To investigate the effects and mechanisms of ghrelin on plaque stability and endothelial funtion in ApoE-/- mice after myocardial infarction. Methods The ApoE-/- mice were divided into control group, double model group and ghrelin-treated group. All ApoE-/- mice were fed with a high-fat diet for 12 weeks to induce atherosclerotic vulnerable plaques. The atherosclerotic vulnerable plaque model was the control group.At the 8th week of this study, the double model group and the ghrelin group were subjected to acute myocardial infarction model(AMI). After modeling of AMI, the ghrelin group was administered with ghrelin (100 μg/kg,bid) until the end of the 12th week. Body weight and blood lipids were detected. Left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) were recorded by echocardiography; NO level was measured by Griess method; the percentage of aortic sinus plaque area was evaluated by HE microscopy. The plaque content of lipid and collagen was observed by Oil Red 0 and Sirius red staining; The distribution of macrophages and smooth muscle cells in plaques were determined by RAM-11 and α-actin immunohistochemical staining and microscopy; And then the vulnerability index was calculated; Myocardial infarct size was measured by Masson staining and microscopy; The vascular endothelial growth factor (VEGF) was detected by quantitative real-time PCR and Western blot. Results Compared with the control group, the level of LVEF and LVFS and NO2-/NO3- concentration in the double model group were all decreased(P＜0.05), and the expression of VEGF was increased(P＜0.05), significantly. However, the ghrelin group had significantly reduced plasma TG level and also the myocardial infarct size(P＜0.05), LVEF, LVFS, NO2-/NO3- level, the expression of VEGF, and the plaque content of collagen and smooth muscle cells were all increased(P＜0.05), and reduced the percentage of aortic sinus plaque area, the distribution of lipid and macrophages(P＜0.05), and the vulnerability index as compared with the double model group(P＜0.05). Conclusions 1)Ghrelin may improve the endothelial function and improve heart function in ApoE-/- mice after myocardial infarction. 2)Ghrelin may stabilize vulnerable plaque and reduce the occurrence of reinfarction.

目的:探讨ghrelin对易损斑块内血管新生和心肌梗死后血管新生的影响及机制.方法:将ApoE-/-小鼠分为易损斑块组、易损斑块+心梗双模型组和ghrelin干预组.所有ApoE-/-小鼠均高脂饮食喂养12周诱导动脉粥样硬化易损斑块,构建的动脉粥样硬化易损斑块模型即为易损斑块组.遗传背景相同的C57BL/6J小鼠正常饮食喂养12周,分为正常对照组和单纯心梗组.第8周时,单纯心梗组、易损斑块+心梗双模型组和ghrelin干预组结扎冠状动脉左前降支构建急性心梗模型.急性心梗造模后,ghrelin干预组腹腔注射ghrelin(100μg/kg,2次/d),直至第12周实验结束.超声心动图检测各组左室射血分数(left ventricular ejection fraction,LVEF)和左室短轴缩短率(left ventricular fraction shortening,LVFS),油红O染色观察主动脉窦粥样斑块面积的百分比,CD31免疫组化染色检测易损斑块内和心梗周边区新生血管生成密度(microvascular density,MVD),Masson染色检测心肌梗死面积.Real-time PCR和Western blot分别检测各组血管内皮细胞生长因子(vascular endothelial growth factor,VEGF)、血管生成素(angiopoietins,Ang)-l/2和络氨酸激酶受体(tyrosine-protein kinase receptor,Tie)-2的表达.结果:①与单纯心梗组相比,易损斑块+心梗双模型组[(65.518±4.160)％,P=0.000]心梗面积明显增加,LVEF[(58.560±11.900)％,p=-0.012]和LVFS[(27.182±7.807)％,P=0.013]降低,心梗周边区MVD (5.800±0.837,P=0.000)减低,VEGF(1.870±0.122,P=0.001)、Ang-1(1.830±0.056,P=0.007)、Ang-2(1.660±0.217,P=0.006)和Tie-2(1.660±0.115,P=0.020)表达降低,ghrelin干预后可明显缩小心梗面积[(39.751±3.039)％,P=0.000],增加易损斑块+心梗双模型组LVEF[(74.679±6.535)％,P=0.013]和LVFS[(37.507±5.210)％,P=0.020),增加心梗周边区MVD(9.857±1.345,P=0.000),升高VEGF(3.503±0.384,P=0.004)、Ang-1(3.277±0.186,P=0.017)、Ang-2(3.450±0.187,P=0.000)和Tie-2(3.133±0.139,P=0.009)的表达;②易损斑块组、易损斑块+心梗双模型组和ghrelin干预组主动脉窦粥样斑块面积的百分比、斑块内MVD、斑块内VEGF、Ang-1、Ang-2和Tie-2的基因与表达在3组间无统计学差异,ghrelin对易损斑块合并心梗小鼠斑块内血管新生无影响.结论:Ghrelin可通过上调VEGF、Ang-1、Ang-2和Tie-2的基因与蛋白表达,促进易损斑块+心梗双模型组小鼠心梗后血管新生,减少心肌梗死面积,稳定和缩小易损斑块.Ghrelin对易损斑块+心梗双模型组小鼠斑块内血管新生无影响.

Abstract Background To determine whether intermittent hypoxia (IH) can reduce the infarct size (IS) after acute myocardial infarction (AMI) in rats. Methods Articles were identified in PubMed, EMBASE and the Web of Science and were included if they evaluated the effect of IH on the changes in the infarcted area after AMI in rats. Results A preliminary search identified 3633 articles and 29 data sets from 23 articles (12 in vivo, 16 in vitro). The IS decreased after AMI in IH rats both in vitro (SMD -1.46, 95% CI [− 2.37, − 0.55]; I2 = 85.6%, P = 0.000) and in vivo (SMD -1.43, 95% CI [− 2.05, − 0.82], I2 = 73.6%, P = 0.000). Sensitivity analysis indicated that IH had a strong protective effect against myocardial infarction, and the hypoxia concentration was significantly correlated with the change in IS after AMI. Conclusion IH can reduce IS after AMI in rats. This effect of IH may be related to the dose of hypoxia, and the oxygen concentration may be one of the most important influencing factors.

发热待查是指临床诊疗工作中经过常规检查和治疗后仍不能使体温恢复正常的一类疾病 ,其病因繁多 ,除常见的感染性发热外 ,还需注意一类非感染性病因. 1 临床资料 患者,女,37 岁 ,因"发热伴四肢皮疹 1 周"于2017年8月21日入本院.入院前1周 ,患者于劳累后出现发热、四肢皮疹 ,自测最高体温38 .8 ℃ ,自诉发热常于中午、下午5 :00-6 :00及夜间2 :00-3 :00 ,发热过程中伴有咽痛、畏寒、四肢肌肉酸痛乏力、皮疹 ,其中皮疹以四肢为主(图1) ,初为点状淡红色皮疹伴皮温升高、瘙痒难忍 ,之后皮疹面积逐渐扩大呈红色斑片状 ,无水疱、脱屑 ,偶有咳白色泡沫痰 ,无咯血、胸痛 ,无盗汗、呼吸困难.于当地诊所使用马来酸氯苯那敏、地塞米松、中药等治疗.

The department of general medicine is receiving more and more attention with the development of three-tier medical treatment system in China.It is an inevitable trend to set up a department of general medicine in tertiary hospitals in the development of general medicine.It is an important development strategy that meets our national conditions.In this article, we analyzed the current situation of general practice in China,and proposed that the department of general medicine in tertiary hospitals can provide support for developing general medicine in medical universities and a platform for continuing education and personnel training of general practitioners,and offer favorable resources for conducting general practice research.The government and hospitals should invest more in general medicine,establish a digital coverage network,improve training of general medical staff,strengthen the incentive mechanism for general practitioners,and enhance the publicity of general medical services,so as to improve the building of general practice medicine.

[目的]探讨延伸护理对老年冠心痛经皮冠状动脉介入治疗(PCI)病人出院后心脏不良事件(MACE)发生率的影响.[方法]选择老年心血管科病区符合研究条件的62例冠心病PCI术后出院病人作为研究对象,随机分为观察组(延伸护理组)和对照组(常规护理组)各31例.比较两组病人院外MACE事件发生率、遵医行为的依从率及病人满意度.[结果]观察组的MACE事件发生率低于对照组,遵医行为优于对照组,病人满意度高于对照组(P＜0.05).[结论]个体化的延伸护理可有效改善老年冠心病病人PCI术后院外遵医行为,提高病人的满意度,降低MACE事件的发生率.

城乡一体化背景下,医学生兼具创新能力与应用能力是时代的需求.应用型创新人才的培养途径包括:强化临床实践教学,注重默会知识的传授,建立模拟中心,兼顾“应用”与“创新”,建设“懂创新、精应用”的教师队伍.构建质量评价体系和第三方量化评估模式是衡量应用型创新医学人才的可行万式.

Intraplaque angiogenesis associates with the instability of atherosclerotic plaques. In the present study, we investigated the effects of ghrelin on intraplaque angiogenesis and plaque instability in a rabbit model of atherosclerosis. The rabbits were randomly divided into three groups, namely, the control group, atherosclerotic model group, and ghrelin-treated group, with treatments lasting for 4 weeks. We found that the thickness ratio of the intima to media in rabbits of the ghrelin-treated group was significantly lower than that in rabbits of the atherosclerotic model group. The number of neovessels and the levels of vascular endothelial growth factor (VEGF) and vascular endothelial growth factor receptor 2 (VEGFR2) decreased dramatically in rabbits of the ghrelin-treated group compared to those of the atherosclerotic model group. Ghrelin significantly decreased the plaque content of macrophages, matrix metalloproteinase (MMP)-2, and MMP-9, in a rabbit model of atherosclerosis. In addition, the level of the pro-inflammatory factor monocyte chemoattractant protein (MCP)-1 was significantly lower in rabbits of the ghrelin-treated group than in rabbits of the atherosclerotic model group. In summary, ghrelin can inhibit intraplaque angiogenesis and promote plaque stability by down-regulating VEGF and VEGFR2 expression, inhibiting the plaque content of macrophages, and reducing MCP-1 expression at an advanced stage of atherosclerosis in rabbits.

目的:探讨生长激素促分泌物受体的内源性配体ghrelin对糖尿病心肌病大鼠心功能的影响.方法:通过高脂饮食+链脲佐菌素(STZ) (50mg)诱导构建糖尿病心肌病大鼠模型;用Ghrelin[200ug/(kg·d)]腹腔注射连续干预糖尿病大鼠4周后,检测各组大鼠空腹血糖(FBG)及血清甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)水平;通过超声心动图测定大鼠左室舒张末期内径(LVEDD)、左室收缩末期内径(LVESD)、左室后壁厚度(LWPWT)及室间隔厚度(WSD),并以左心室缩短分数(FS)及左心室射血分数(LVEF)作为心功能评价指标.结果:通过高脂饮食+STZ成功构建糖尿病心肌病大鼠模型;糖尿病大鼠FBG、血清TG、TC和LDL-C水平显著高于对照组大鼠(P＜0.05),而给予ghrelin连续干预4周后,糖尿病+ghrelin干预组大鼠FBG、TG和TC较糖尿病纽显著降低(P＜0.05);超声心动图显示,糖尿病组大鼠HR低于对照组,LVEDD、LVESD、LWPWT、IVSD较对照组显著升高,而LVES和FS显著低于时照组(P＜0.05);ghrelin干预后,大鼠LVEDD、LVESD、IVSD降低,LVEF和FS显著升高(P＜0.05).结论:高脂饮食联合链脲佐菌素能成功构建糖尿病心肌病大鼠模型;糖尿病心肌病大鼠存在着严重的糖、脂代谢紊乱和心功能障碍,ghrelin能通过改善大鼠糖、脂代谢紊乱,提高糖尿病心肌病大鼠心室收缩功能.

Objective To assess the relationship among serum sclerostin,coronary atherosclerotic heart disease (CHD),and osteoporosis.Methods Three hundred and thirteen elder patients who underwent coronary angiography (CA) were involved in the cross-sectional study,including 163 subjects in CHD group and 150 subjects in non-CHD group.Serum sclerostin concentration was measured using a commercially available enzyme-linked immunosorbent assay kit.Bone mineral density (BMD),serum lipid,and bone turnover markers were also detected.The correlation between sclerostin and CHD was analyzed using multiple logistic regression method.The influential factors of sclerostin were also analyzed.Results (1) Serum sclerostin concentration were lower in elder patients in CHD group than that in non-CHD group (178.035 ± 0.636 pg/mL vs.180.576 ± 0.608 pg/mL,P ＜ 0.05).(2) Multiple logistic regression analysis showed that sclerostin as negatively correlated with the occurrence of CHD in theelderly (OR =0.865,P =0.018).Elevation of sclerostin was associated with low risk of CHD in osteoporotic patients (OR =0.767,P =0.007).Sclerostin was not associated with CHD in non-CHD group (P ＞ 0.05).(3) In the multiple regression analysis,sclerostin was significantly associated with BMD (β =0.224,P ＜ 0.05),PINP(β =0.161,P ＜ 0.05),and age (β =-0.162,P ＜ 0.05).Conclusion Serum sclerostin is closely associated with CHD in the elderly,especially in the elder patients with osteoporosis.It may play a major modulator role in the bone-vessel-axis.

Objective: To explore the relationship between prevalence of atrial fibrillation (AF), iskhemia stoke and CHA2DS2-VASc score in patients≥65 years in order to provide prevention and treatment basis in clinical practice. Methods: A total of 5016 patients admitted in our hospital from 2013-10 to 2015-10 were enrolled. The patients were divided into 2 groups: AF group, n=437 and Non-AF patients, n=4579; according to age, the patients were further assigned into 4 subgroups as <65 years subgroup, (65-74) years subgroup, (75-84) years subgroup and ≥85 years subgroup. The risk factors for AF occurrence were retrospectively studied. Results: Compared with the Non-AF group, the patients in AF group had the elder age and more male gender, both P<0.001; more patients combining with hypertension, coronary artery disease (CAD), diabetes, sick sinus syndrome and rheumatic heart disease, all P<0.001. Age, male gender, CAD, sick sinus syndrome and rheumatic heart disease were the independent risk factors for AF occurrence. Compared with Non-AF group, AF group showed the higher prevalence rate of ischemic stroke and the elder onset age, both P<0.01. For non-valvular AF, the ratio of patients with CHA2DS2-VASc score≥2 was higher than those with CHA2DS2-VASc score<2 and the rate of anticoagulant therapy was decreasing by age increasing, all P<0.001. Conclusion: Age, male gender, CAD, sick sinus syndrome and rheumatic heart disease were independently related to AF occurrence. Non-valvular AF patients had the higher risk for ischemic stroke than non-AF patients, anticoagulation therapy should be conducted at the early stage.

Objective: To explore the relationship between serum level of high-sensitivity cardiac troponin T (hs-cTnT) and atrial ifbrillation (AF) occurrence in patients with stable coronary artery disease (CAD). <br> Methods: A total of 1011 patients with stable CAD treated in our hospital from 2013-01 to 2015-09 were retrospectively studied. According to quartiles of hs-cTnT, the patients were divided into 4 groups: Group① the patients with hs-cTnT≤7ng/L, n=283, Group② hs-cTnT 7-10ng/L,n=238, Group③ hs-cTnT 10-15ng/L,n=272 and Group④ hs-cTnT>15ng/L,n=218. The relationship between hs-cTnT level and AF occurrence rate was studied; the risk factors for AF occurrence were explored by multi stepwise Logistic regression analysis. <br> Results: There were 127/1011 (12.6%) patients combining AF and 884 (87.4%) with simple type stable CAD. AF patients had the higher serum level of hs-cTnT than non-AF patients 17.0 (12.0, 25.0) ng/L vs 10.0 (7.0, 13.0) ng/L,P<0.01. With baseline hs-cTnT level increasing, AF occurrence rates were elevated from group① to Group④ as 4.6% (13/283), 4.6% (11/238), 11.0% (30/272) and 33.5% (73/218), Ptrend<0.05. Multi stepwise Logistic regression analysis revealed that with adjusted common risk factors of age and gender, the risk for stable CAD patients suffering from AF in Group④ was 5.324&nbsp;times higher than group① (95% CI 2.285-12.405,P<0.01). <br> Conclusion: Increased serum level of hs-cTnT was closely related to AF occurrence in patients with stable CAD.

Many studies show that ivabradine is effective for stable angina. This meta-analysis was performed to determine the effect of treatment duration and control group type on ivabradine efficacy in stable angina pectoris. Relevant articles in the English language in the PUBMED and EMBASE databases and related websites were identified by using the search terms "ivabradine," "angina," "randomized controlled trials," and "Iva." The final search date was November 2, 2015. Articles were included if they were published randomized controlled trials that related to ivabradine treatment of stable angina pectoris. Patients with stable angina pectoris were included. The patients were classified according to treatment duration (<3 vs ≥3 months) or type of control group (placebo vs beta-receptor blocker). Angina outcomes were heart rate at rest or peak, exercise duration, and time to angina onset. Seven articles were selected. There were 3747 patients: 2100 and 1647 were in the ivabradine and control groups, respectively. The ivabradine group had significantly longer exercise duration when they had been treated for at least 3 months, but not when treatment time was less than 3 months. Ivabradine significantly improved time to angina onset regardless of treatment duration. Control group type did not influence the effect of exercise duration (significant) or time to angina onset (significant). Compared with beta-blocker and placebo, ivabradine improved exercise duration and time to onset of angina in patients with stable angina. However, its ability to improve exercise duration only became significant after at least 3 months of treatment.

OBJECTIVES:Ghrelin, an endogenous ligand of the growth hormone secretagogue receptor (GHSR), has been found to stimulate angiogenesis in vivo and in vitro. However, the effect and the corresponding mechanisms of ghrelin on impaired myocardial angiogenesis in diabetic and myocardial infarction (MI) rat model are still unknown. METHODS:In the present study, adult SD rats were randomly divided into 4 groups: control, DM, DM+ghrelin, DM+ghrelin+[D-Lys3]-GHRP-6 groups. DM was induced by streptozotocin (STZ) 60 mg/kg body weight. 12 weeks post STZ injection all groups were subjected to MI, which was induced by ligation left anterior descending artery (LAD). Ghrelin and [D-Lys3]-GHRP-6 were administered via intraperitoneal injection at the doses 200 μg/kg and 50mg/kg for 4 weeks, respectively. Left ventricular function, microvascular density (MVD), myocardial infarct size, the expression of hypoxia-inducible factor (HIF1α), vascular endothelial growth factor (VEGF), fetal liver kinase-1 (Flk-1) and fms-like tyrosine kinase-1 (Flt-1), AMPK and endothelial nitric oxide synthase (eNOS) phosphorylation were examined. RESULTS:Compared with the DM group, left ventricular ejection fraction (LVEF), fractional shortening (FS), and MVD were increased, whereas myocardial infarct size decreased remarkably in DM+ghrelin group. For the mechanism study, we found that ghrelin promoted the HIF1α, VEGF, Flk-1 and Flt-1 expression, AMPK and eNOS phosphorylation in diabetic rats. However, the above biochemical events in ghrelin treated diabetic rats were completely inhibited by GHSR-1a blocker [D-Lys3]-GHRP-6. CONCLUSIONS:These results suggest that administration of ghrelin ameliorates impaired angiogenesis in diabetic MI rats. And these beneficial effects derive from regulating GHSR1a-mediated AMPK/eNOS signal pathway by upregulating of HIF1α, VEGF and its receptors Flk-1, Flt-1 expressions.

Objective The aim of our study was to investigate the effects and mechanisms of ghrelin on neovascularization in atherosclerosis plaque. Methods 30 male New Zealand rabbits were randomly divided into normal control group ( CON group) , atherosclerosis model group ( AS group) , and ghrelin treatment group ( ghrelin group) , and each group of 10 rabbits. The AS group and ghrelin group underwent balloon-induced arterial wall injury and then fed with high fat diet, the CON group was fed only on a regular diet. They were all fed for 3 months. Then the ghrelin group was given ghrelin 25μg·kg-1 ·d-1 , the other two groups received the same amount of sterile normal saline only. Four weeks later, body weight and blood lipids were detected. The thickness ratio of the intima to media was measured by HE staining. Degree of intra-plaque angiogenesis was evaluated by CD31+ cells immunohisto-chemistry. The vascular endothelial growth factor ( VEGF ) and vascular endothelial growth factor receptor 2 ( VEGFR2) were detected by quantitative realtime PCR and Western blot. The expressions of matrix metalloproteinase ( MMP)-2 and MMP-9 were detected by immunohistochemistry and Western blot. Results ( 1 ) No significant differences in body weight and blood lipids were found between the AS group and the ghrelin group(P>0. 05), but both items were significantly higher than those of the CON group(P<0. 05). (2)The thickness ratio of the intima to media in the ghrelin treated group was distinctly less than that in the AS group(P<0. 05). (3)Compared with the AS group, the ghrelin group showed significantly decreased microvascular density and the expressions of VEGF and VEGFR2 (P<0. 05). (4)Compared with the AS group, ghrelin dramatically inhibited the plaque contents of MMP-2 and MMP-9 ( P<0. 05 ). Conclusions Ghrelin is able to inhibit the growth of neovascularizationin in the atherosclerotic plaque and the development of plaque. And these beneficial effects derive from downregulation of VEGF, VEGFR2, MMP-2, and MMP-9 at the advanced stage of atherosclerosis in rabbits.

Objective:To investigate the effects of ghrelin on myocardial remodeling matrix metalloproteinases expression in post-myocardial infarction diabetic rats.Methods:Adult male SD rats were divided into four groups:myocardiac infarction (MI),diabetes mellitus+myocardiac infarction(DM+MI),DM+MI+ghrelin,DM+MI+ghrelin+GHSR1a inhibitor[D-Lys3]-GHRP-6.Diabetes was induced by injection of streptozotocin(STZ,60 mg/kg).After three months,left anterior descending artery(LAD) ligation was performed in all groups.DM+MI+ghrelin group received ghrelin,200 μg/(kg·d).DM+MI+ghrelin+[D-Lys3]-GHRP-6 group received ghrelin,200 μg/(kg·d) and [D-Lys3]-GHRP-6,50 mg/(kg·d).The other two groups received the same amount sterile normal saline only.Four weeks later,Sirius red staining was used to detect myocardial fibrosis.Myocardial infarct size was detected by Masson staining.The distribution and expressions of matrix metalloptoteinase-2(MMP-2),matrix metalloptoteinase-9(MMP-9) and tissue inhibitor of metalloprotroteinase-1 (TIMP-1) were detected by immunohistochemistry and Western blot,separately.Results:Myocardial collagen volume fraction (P=0.003),myocardial infarct size(P=0.001),the expression of MMP-2 (P=0.000) and MMP-9 (P=0.000) were significantly increased in DM+MI group than in MI group.After ghrelin administration,myocardial collagen volume fraction (P=0.001),myocardial infarct size (P=0.005),the expression of MMP-2(P=0.001) and MMP-9(P=0.001) were significantly decreased in diabetic rats complicated with MI.TIMP-1 was significantly higher in diabetic groups than in MI group(P=0.000),without significant difference among these groups(P＞0.05).However,[D-Lys3]-GHRP-6 blocked the above effects of ghrelin.Conclusion:Ghrelin can inhibit myocardial extracellular matrix remodeling and reduce myocardial infarct size by suppressing the expressions of MMP-2 and MMP-9.

OBJECTIVE:Low concentrations of oxidized low-density lipoprotein (oxLDL) promote the in vitro angiogenesis of endothelial cells and play an important role in plaque angiogenesis, which may cause plaque vulnerability and enhance the risk of intravascular thrombosis. The aim of this research was to investigate the effects of octanoylated ghrelin on oxLDL-induced angiogenesis and the underlying molecular mechanisms involved in this process. MATERIALS/METHODS:Human coronary artery endothelial cells (HCAECs) were incubated with 5 μg/ml oxLDL and treated with various concentrations of octanoylated ghrelin (10(-9)-10(-6)M) with or without inhibitors for 24h. Cell proliferation, migration, and in vitro angiogenesis were analyzed by bromodeoxyuridine (BrdU) staining and BrdU enzyme-linked immunosorbent assay (ELISA), transwell assay, and tube formation on Matrigel, respectively. NF-κB (nuclear factor κB) expression was determined by Western-blot analysis. RESULTS:Treatment with oxLDL at 5 μg/ml enhanced the proliferation, migration and tube formation of HCAECs. In contrast, pretreatment with octanoylated ghrelin significantly attenuated in vitro angiogenesis in oxLDL-induced HCAECs. In addition, Western blot analysis indicated that NF-κB expression was increased after oxLDL treatment, and that this effect was significantly reversed by pretreatment with octanoylated ghrelin. However, the NF-κB inhibitor PDTC or the GHSR1a inhibitor [D-Lys3]-GHRP-6 abolished the effects of octanoylated ghrelin on the inhibition of angiogenesis and NF-κB p65 expression induced by oxLDL. CONCLUSIONS:These findings suggest that octanoylated ghrelin attenuates angiogenesis induced by oxLDL in HCAECs via the inhibition of GHSR1a-mediated NF-κB pathway. Furthermore, octanoylated ghrelin may promote the stability of vulnerable plaques by inhibiting plaque angiogenesis.

我国已进入老龄化社会，同时我国的医学模式也正在向着生物鄄心理鄄社会医学的模式发生着转化，心理因素越来越成为疾病发生、发展过程中需要引起关注的因素，这对医学工作者的综合素质提出了更高要求。有效的医患沟通，能显著降低医疗纠纷的发生。老年患者常常多种慢性疾病共存，反复住院，存在不同程度的心理障碍，良好医患沟通能力的培养在老年病科室中尤其重要，多学科的医学专业技术已不再成为检验临床实习医生的唯一标准，医患沟通的技术及人文教育的培养越来越引起重视。该文就如何加强临床实习医生的医患沟通能力进行探讨。

Objective: To explore the relationship between lower extremity atherosclerosis disease (LEAD) and cardiovascular risk factors in elder people. <br> Methods: A total of 700 consecutive patients receive lower extremity Color Doppler ultrasound in our hospital from 2013-05 to 2014-11 were investigated. The patients were divided into 3 age groups: Young and middle group, n=83, Elder group, n=377 and Senile group, n=240. Based on ultrasound scoring system, the patients were divided into 4 groups: Normal group, n=112, Mild atherosclerosis (Mild) group, n=81, Moderate group, n=466 and Severe group, n=41. The cardiovascular risk factors among different groups were compared. <br> Results: Multivariate unconditional logistic regression analysis showed that age, smoking, history of diabetes, uric acid (UA), ankle-brachial index (ABI) were the independent risk factors for LEAD (B=0.144, 1.496, 0.963, 0.004, -2.510; 95% CI: 1.120-1.190, 2.257-8.824, 1.456-4.716, 1.001-1.007, 0.012-0.534;P=0.000, 0.000, 0.001, 0.006, 0.009 respectively. Ordinal logistic regression analysis indicated that age, male gender, smoking, ABI, UA, history of hypertension were related to the severity of atherosclerosis (B=0.130, 0.737, 0.592, -3.365, 0.003, 0.735; 95% CI: 0.097-0.162, 0.222-1.252, 0.052-1.132, -4.674 to -2.055, 0.001-0.005, 0.313-1.157;P=0.000, 0.005, 0.032, 0.000, 0.005, 0.001 respectively. Compared with Young and Middle groups, Elder and Senile groups had increased rates of moderate and&nbsp;severe arteriosclerotic lesions; compared with Elder group, Senile group presented the higher incidence of moderate and severe lesions, allP<0.01. With elevated age, the severity score of LEAD increased accordingly,P<0.01. <br> Conclusion: Lower extremity atherosclerosis lesions were more severe in elder patient, and it was particularly severe in senile patients.

UNLABELLED:This study was initiated to investigate the efficacy of myocardial fibrosis intervention via signal transducer and activators of transcription (STAT) signaling using bone marrow (BM) mesenchymal stromal cells (MSC) in which being over-expressed with the aid of bispecific antibody (BiAb) and ultrasound-mediated microbubbles (MB). BiAb was prepared and combined with isolated MSC with CD47 overexpression from male mice and trans-fused into female mice with isoproterenol-induced myocardial fibrosis via the tail vein, followed by MB. This study included five groups. Five weeks after treatment, expression levels of the sex-determining region of Y-chromosome (SRY), matrix metalloproteinases (MMP)-9, tissue inhibitor of metalloproteinase (TIMP)-1 and vascular endothelial growth factor (VEGF) in myocardium were detected by fluorescent quantitative real-time polymerase chain reaction (qRT-PCR). The protein expression of signal transducer and activators of transcription (STAT) 1 and STAT 3 was detected by Western blot.RESULTS:The highest homing number of MSC was in the CD47 + MSC + BiAb + MB group, second highest in the CD47 + MSC + BiAb group, and lowest in MSC alone. Compared with the Control group, CD47 + MSC + BiAb + MB, CD47 + MSC + BiAb, CD47 + MSC and MSC groups had decreased levels of MMP-9, TIMP-1, STAT 1 and collagen deposition, and increased levels of STAT 3. Up regulated STAT 3 and down regulated TIMP-1 were significantly different in CD47 + MSC + BiAb + MB compared with CD47 + MSC or CD47 + MSC + BiAb.CONCLUSION:CD47 can enhance the homing rate and repairing efficacy of MSC. MSC can improve MMP-TIMP expression in injured myocardium and interfere with myocardial fibrosis after homing, a mechanism that may be related to the STAT-mediated signaling pathway.