高龄急性心肌梗死合并心力衰竭患者G蛋白耦联受体激酶2和可溶性ST2表达水平的变化

目的检测高龄急性心肌梗死(AMI)患者外周血G蛋白耦联受体激酶2(GRK2)和可溶性ST2(sST2)表达水平,分析其对心力衰竭的预测价值。方法选择2015年1月—2019年9月于广西壮族自治区南溪山医院心内科诊治的年龄80岁的高龄AMI患者246例,获取患者入院时基线资料、心功能状态指标[左心室射血分数(LVEF)、室壁运动积分、脑利尿钠肽(BNP)、氨基末端脑利尿钠肽前体(NT-proBNP)]和GRK2、sST2水平,统计心力衰竭发生例数,采用相关统计学方法分析心力衰竭发生的高危因素和GRK2、sST2水平预测心力衰竭发生的敏感度和特异度。结果最终确定发生心力衰竭75例,发生率30.5%。心力衰竭组年龄、BNP、NT-proBNP、室壁运动积分、sST2高于无心力衰竭组(P0.05),GRK2、LVEF低于无心力衰竭组(P0.05)。sST2与BNP、室壁运动积分呈正相关,与LVEF呈负相关(P0.05),GRK2与室壁运动积分呈负相关,与LVEF呈正相关(P0.05)。年龄、BNP、NT-proBNP、室壁运动积分、sST2为心力衰竭发生的独立危险因素(P0.05),GRK2为心力衰竭发生的保护因素(P0.05)。sST2、GRK2对心力衰竭的诊断均有一定准确性(P0.05);sST2、GRK2联合检测对心力衰竭诊断效能高于单独检测(P0.05)。结论外周血GRK2、sST2与高龄AMI患者心力衰竭发生相关,预测价值较高。     

sST2参与急性心肌梗死后心肌纤维化

目的探索可溶性生长刺激表达基因2(sST2)与急性心肌梗死(AMI)后心肌纤维化的关系。方法入选2015年1月至2016年9月入住兰州大学第一医院心脏中心的患者249例,AMI组为首次诊断AMI的166例患者,对照组为冠状动脉造影阴性的83例患者。测定患者血清sST2、Ⅲ型前胶原氨基端肽(PⅢNP)及N末端B型利钠肽原(NT-pro BNP)水平,并收集心脏超声中与左心室收缩功能相关的指标:左心室射血分数(LVEF)、左心室收缩期末容积(LVESV)、左心室舒张期末容积(LVEDV),并进行比较、分析。结果 AMI组血清sST2、PⅢNP、NTpro BNP水平及LVESV、LVEDV值均高于对照组,LVEF值明显低于对照组(P0.05或P0.01)。AMI组中,LVEF50%亚组血清sST2水平高于LVEF≥50%亚组(P=0.031)。AMI组中血清sST2与PⅢNP呈正相关(r=0.181,P=0.02),与LVEF呈负相关(r=-0.179,P=0.021)。AMI组中血清sST2、NT-pro BNP及sST2+NT-pro BNP诊断AMI后心力衰竭的ROC曲线下面积分别为0.608、0.683和0.732。结论血清sST2参与AMI后心肌纤维化过程,并与左心室收缩功能有关。血清sST2水平对AMI后心力衰竭具有诊断价值。     

可溶性致癌抑制因子2与老年急性心肌梗死患者心功能关系的探讨

目的：探讨老年急性心肌梗死（AMI）患者血清可溶性致癌抑制因子2（sST2）与其心功能之间关系。方法选取年龄＞60岁、发病24h内的AMI患者59例,来诊后立即测定N端脑钠肽前体（NT-proBNP）、sST2,进行Killip心功能分级,48h内完成超声心动图检查。设立36例年龄匹配的健康对照检测sST2。结果 sST2在AMI组较对照组明显升高[（36.2±21.3） vs （12.5±11.4）μg/L,P＜0.05];AMI组中sST2和NT-proBNP有明显正相关性（r＝0.585,P＜0.05）;sST2和左心室射血分数（LVEF）表现出明显负相关（r＝-0.611,P＜0.05）;sST2在KillipⅠ级和Ⅱ级[（27.6±14.5） vs （38.0±20.6）μg/L,P＜0.05],Ⅱ级和Ⅲ＋Ⅳ级间差异显著[（56.5±25.0）μg/L, P＜0.05]。结论 AMI患者中sST2较对照组明显升高,且与NT-proBNP和LVEF有相关性,sST2随Killip分级级别升高有上升趋势,而NT-proBNP无此趋势。     

血清sST2、gal-3水平与AMI患者发生LVR的关系

目的:研究血清可溶性生长刺激表达基因2蛋白(sST2)、半乳糖凝集素(gal)-3水平与AMI患者发生左室重构(LVR)的关系。方法:选择我院135例AMI患者为AMI组。另选择同期140例体检健康者为健康对照组。比较两组一般资料、血清sST2、gal-3水平。随访3个月,依据是否发生LVR,AMI组被分为LVR组(61例)与无LVR组(74例),观察比较两组血清sST2、gal-3水平,并分析AMI患者发生LVR的影响因素及血清sST2、gal-3水平对AMI患者发生LVR的诊断价值。结果:与健康对照组比较,AMI组高血压比例(47.86%比71.11%)、TC[(3.35±0.65)mmol/L比(5.42±1.13)mmol/L]、LDL-C水平[(2.11±0.62)mmol/L比(4.73±0.74)mmol/L]、LVEDd[(46.25±3.26)mm比(64.35±5.62)mm]、LVESd[(28.61±4.23)mm比(53.75±10.23) mm]、血清sST2[(13.56±1.36)ng/ml比(22.14±3.26)ng/ml]、gal-3[(10.52±1.12)μg/L比(13.65±2.23)μg/L]水平均显著升高,LVEF[(64.24±7.31)%比(31.26±4.22)%]显著降低(P均=0.001)。与无LVR组比较,LVR组血清sST2[(16.52±2.63)ng/ml比(23.65±4.21)ng/ml]、gal-3 [(12.67±2.36)μg/L比(14.25±2.85)μg/L]水平均显著升高(P均=0.001)。多因素Logistic回归分析显示,LVEF降低、血清sST2、gal-3水平升高均为AMI患者发生LVR的独立危险因素(OR=1.067～2.113,P0.05或0.01)。ROC曲线显示,sST2、gal-3及二者联合检测预测LVR的敏感度分别为70.9%、72.7%、87.3%,特异性分别为96.4%、87.3%、89.1%,AUC分别为0.839、0.815、0.929,前两者最佳截断值分别为20.799ng/ml、11.905μg/L。结论:AMI患者及AMI发生LVR患者血清sST2、gal-3水平均显著升高,血清sST2、gal-3水平升高是LVR的独立危险因素,且对LVR具有显著的诊断价值。     

血清半乳糖凝集素3和可溶性ST2预测心肺复苏后急性心力衰竭患者近期预后的价值

目的:探讨血清可溶性ST2(soluble ST2,sST2)、半乳糖凝集素3(Galectin-3)对心脏骤停心肺复苏(cardiopulmonary resuscitation,CPR)成功后发生急性心力衰竭的患者近期预后的评估价值。方法:ELISA法检测160例CPR后发生急性心力衰竭的患者CPR后24h的血清sST2、半乳糖凝集素3水平,依据随访出院后6个月的终点事件(出院后6个月内患者因出现急性心力衰竭再次入院或死亡)分为发生事件组(A组,58例)和未发生事件组(B组,102例),同时检测患者左室舒张末期内径(LVEDD)、左室射血分数(LVEF)。采用ROC曲线分析其评估急性心力衰竭患者近期预后的价值。结果:A组血清sST2、半乳糖凝集素3水平均高于B组(均P0.01)。两者联合分析能提高对患者短期预后的预测价值(P0.01)。LVEDD与LVEF随着sST2和半乳糖凝集素3水平的变化而变化。sST2高表达组(200ng/L)、半乳糖凝集素3高表达组(20ng/ml)患者病死率均高于sST2、半乳糖凝集素3低表达组(均P0.05)。结论:血清sST2、半乳糖凝集素3联合分析能提高对CPR后发生急性心力衰竭患者近期预后的预测价值。     

急性心肌梗死患者血清HS、sST2的变化及预测价值

目的研究急性心肌梗死(AMI)患者血清硫酸乙酰肝素(HS)、可溶性生长刺激表达基因2(sST2)的变化及预测价值。方法选取2017年6月～2017年12月于漯河医学高等专科学校第一附属医院就诊的60例AMI患者为试验组,同期60例健康体检者为对照组。检测两组血清HS、sST2、左室射血分数(LVEF)及室壁运动异常评分(WMS),并做相关性分析。结果 AMI组患者血清HS、sST2水平分别为(96±7.6)μg/L、(579.52±61.32)pg/ml,高于对照组的(29±5.9)μg/L、(141.09±28.61)pg/ml,差异有统计学意义(P0.05);与对照组比较,AMI组室壁运动异常评分增高(4.3±0.9)分,左室射血分数降低(37±6.1)%,差异有统计学意义(P0.05)。相关性分析结果显示,AMI组血清HS水平与室壁运动异常评分呈正相关(r=0.591,P0.05),与左室射血分数呈负相关(r=-0.301,P0.05);AMI组血清sST2水平与室壁运动异常评分呈正相关(r=0.305,P0.05),与左室射血分数呈负相关(r=-0.298,P0.05)。结论 AMI患者血清HS、sST2水平可反映心脏功能情况。     

老年急性心肌梗死患者经皮冠状动脉介入治疗的近远期预后

目的研究老年急性心肌梗死(AMI)患者经皮冠状动脉介入(PCI)治疗的近远期预后。方法选取2015年1～12月≥75岁的101例PCI治疗的AMI患者,分为急性ST段抬高型心肌梗死(STEMI)组(n=48)和非STEMI(NSTEMI)组(n=53)。随访2年,绘制Kaplan-Meier生存曲线。结果院内、术后1个月、6个月、1年和2年累积全因死亡率分别为9.4%、12.5%、20.6%、23.7%和27.9%。术后短期内(15个月内,包括住院),STEMI组累积存活率较NSTEMI组略低,而远期(15个月后)STEMI组较NSTEMI组略高,但两组的2年累积存活率差异无统计学意义(P0.05)。结论老年AMI患者PCI术后6个月后死亡风险降低,NSTEMI患者远期预后较STEMI更差。     

依替巴肽对急性心肌梗死患者血清可溶性致癌抑制因子2及血清五聚素3水平的影响

目的研究依替巴肽对行直接PCI的急性ST段抬高型心肌梗死(STEMI)患者血清可溶性致癌抑制因子2(sST2)和血清五聚素3(PTX3)水平的影响。方法选取我院确诊的急性STEMI患者96例,随机分为观察组(依替巴肽联合PCI)48例和对照组(PCI)48例。随访6个月,记录2组患者术后90min心电图ST段抬高总和回落(STR)50%、心肌灌注3级和TIMI 3级血流比例;术前和术后1个月LVEF、左心室舒张末期内径(LVEDD)、血清sST2及PTX3水平;术后6个月内主要不良心脏事件(MACE)发生率,并进行比较。结果观察组术后心肌灌注3级比例高于对照组(97.9%vs 85.4%,χ2=4.909,P=0.027),STR50%比例高于对照组(91.7%vs 70.8%,χ2=6.842,P=0.009);2组TIMI 3级血流比例比较,差异无统计学意义(P0.05)。1个月时,2组LVEF均高于同组术前水平,LVEDD、血清sST2及PTX3水平均低于同组术前(P 0.05);且观察组LVEF高于对照组,LVEDD、血清sST2及PTX3低于对照组(P0.05;P0.01)。观察组术后6个月内MACE发生率低于对照组(8.3%vs 22.9%,χ2=3.872,P=0.049),2组均无死亡患者。结论急性STEMI患者PCI联用依替巴肽疗效良好,能改善心功能,降低血清sST2及PTX3水平和MACE发生率。     

老年急性心肌梗死病人血清sST2、NT-proBNP、胰岛素抵抗水平与疾病严重程度及心功能的关系探讨

目的探讨老年急性心肌梗死(AMI)病人血清可溶性生长刺激表达因子2(sST2)、N-末端脑钠肽前体(NT-proBNP)、胰岛素抵抗水平与疾病严重程度及心功能的关系。方法选取珠海市中西医结合医院2018年1月—2019年4月收治的AMI病人128例作为AMI组,根据Killip心功能分级分为Ⅰ级组(52例)、Ⅱ级组(35例)、Ⅲ级组(25例)、Ⅳ级组(16例);收集同期、同年龄段、知情同意并自愿配合相关检查的健康体检人群50名作为对照组。受试人群均检测空腹血胰岛素(FINS)、血脂、肿瘤坏死因子-α(TNF-α)及超敏C反应蛋白(hs-CRP)、sST2、NT-proBNP、左心室射血分数(LVEF)、左心室收缩末期容积(LVESV)、左心室舒张末期容积(LVEDV),采用自我平衡模型分析法计算胰岛素抵抗指数(IRI),分析AMI病人血清sST2、NT-proBNP水平与疾病严重程度的相关性。结果与对照组比较,AMI组各心功能分级亚组病人总胆固醇(TC)、三酰甘油(TG)、低高密度脂蛋白胆固醇(LDL-C)明显升高(P0.05),高密度脂蛋白胆固醇(HDL-C)明显降低(P0.05);AMI组病人随着心功能分级上升血清TC、TG、LDL-C水平呈递增趋势(P0.05),HDL-C水平呈递减趋势(P0.05)。与对照组比较,AMI组各心功能分级亚组病人hs-CRP、TNF-α、白介素-6(IL-6)、sST2、NT-proBNP、FINS、IRI、LVESV、LVEDV明显升高(P0.05),LVEF明显降低(P0.05);AMI组病人随着心功能分级上升血清IL-6、hs-CRP、TNF-α、sST2、NT-proBNP、FINS、IRI、LVESV、LVEDV值呈递增趋势(P0.05),LVEF值呈递减趋势(P0.05)。Pearson相关性分析显示sST2、NT-proBNP、IRI、LVESV、LVEDV与Killip心功能分级呈正相关(P0.05),LVEF与Killip心功能分级呈负相关(P0.05);相关性分析显示血清sST2、NT-proBNP、IRI水平与LVEF呈负相关(P0.05),与LVESV、LVEDV呈正相关(P0.05)。结论老年急性心肌梗死病人Killip心功能分级越高,血清sST2、NT-proBNP、IRI水平越高,且血清sST2、NT-proBNP、IRI水平与左心室功能存在一定相关性。     

老年急性心肌梗死患者PCI与经静脉给药溶栓疗效的比较

目的:比较经皮冠状动脉介入治疗(PCI)和经静脉给药溶栓两种方法治疗老年急性心肌梗死(AMI)患者的近远期临床疗效。方法:180例老年AMI患者分为PCI组和静脉溶栓组,各90例,比较两组患者的梗死相关血管的再通率,住院期间和随访期间左心室射血分数(LVEF)、主要心血管不良事件发生率。结果:与静脉溶栓组比较,PCI组患者的梗死血管再通率显著提高(61.1%比92.2%),在治疗结束时LVEF改善[(52.26±7.33)%比(58.27±7.59)%],和随访期间LVEF改善[随访3个月:(53.59±8.04)%比(60.44±7.53)%,随访12个月:(55.16±7.35)%比(63.71±7.77)%]更明显,且在随访12个月时,心脏不良事件的总发生率显著降低(82.22%比24.44%),P均0.01。结论:经皮冠状动脉介入治疗急性心肌梗死梗死相关动脉的再通率,心功能恢复均显著好于静脉溶栓治疗,且心脏不良事件更少,可作为老年急性心肌梗死的首选治疗。     

ATP-activated P2X2 current in mouse spermatozoa

Sperm cells acquire hyperactivated motility as they ascend the female reproductive tract, which enables them to overcome barriers and penetrate the cumulus and zona pellucida surrounding the egg. This enhanced motility requires Ca(2+) entry via cation channel of sperm (CatSper) Ca(2+)-selective ion channels in the sperm tail. Ca(2+) entry via CatSper is enhanced by the membrane hyperpolarization mediated by Slo3, a K(+) channel also present in the sperm tail. To date, no transmitter-mediated currents have been reported in sperm and no currents have been detected in the head or midpiece of mature spermatozoa. We screened a number of neurotransmitters and biomolecules to examine their ability to induce ion channel currents in the whole spermatozoa. Surprisingly, we find that none of the previously reported neurotransmitter receptors detected by antibodies alone are functional in mouse spermatozoa. Instead, we find that mouse spermatozoa have a cation-nonselective current in the midpiece of spermatozoa that is activated by external ATP, consistent with an ATP-mediated increase in intracellular Ca(2+) as previously reported. The ATP-dependent current is not detected in mice lacking the P2X2 receptor gene (P2rx2(-/-)). Furthermore, the slowly desensitizing and strongly outwardly rectifying ATP-gated current has the biophysical and pharmacological properties that mimic heterologously expressed mouse P2X2. We conclude that the ATP-induced current on mouse spermatozoa is mediated by the P2X2 purinergic receptor/channel. Despite the loss of ATP-gated current, P2rx2(-/-) spermatozoa have normal progressive motility, hyperactivated motility, and acrosome reactions. However, fertility of P2rx2(-/-) males declines with frequent mating over days, suggesting that P2X2 receptor adds a selection advantage under these conditions.     

IGF2BP2 and IGF2 genetic effects in diabetes and diabetic nephropathy

ObjectiveThe IGF2BP2 gene is located on chromosome 3q27.2 within a region linked to type 1 diabetes (T1D), type 2 diabetes (T2D) and diabetic nephropathy (DN). Its protein functionally binds to 5’-UTR of the imprinting IGF2 gene. The present study aims to evaluate the IGF2BP2-IGF2 genetic effects in diabetes and DN.Materials and MethodsThree cohorts including T1D with and without DN (n = 1139) of European descents from the GoKinD study, Swedish T1D with and without DN (n = 303) and Czech control subjects without diabetes, T1D, T2D with and without DN (n = 1418) were enrolled in TaqMan genotyping experiments for IGF2BP2 rs4402960 and IGF2 rs10770125. Igf2bp2 gene expression in kidney tissues of db/db and control mice at the ages of 5 and 26 weeks was examined with real time RT-PCR and Western blot.ResultsAn association of IGF2BP2 rs4402960 with T2D in the Czech population was replicated. This IGF2BP2 polymorphism (P = 0.037, OR = 0.69 95% CI 0.49–0.98) was found to be associated with DN in male not in female patients with T1D selected from the GoKinD study. In the analyses of combined the GoKinD, Czech and Swedish populations, the association between IGF2BP2 polymorphism and DN in male patients with T1D was still significant (P = 0.030, OR = 0.73, 95% CI 0.54–0.97). IGF2 rs10770125 was also associated with DN in male T1D patients of the GoKinD population (P = 0.038, OR = 0.67 95% CI 0.46–0.98). There might be a genetic interaction between IGF2BP2 and IGF2 (P = 0.05). The Igf2bp2 gene expression levels were increased in the kidneys of db/db mice compared to controls at the age of 5 weeks but not at 26 weeks.ConclusionsThe present study has replicated the association of IGF2BP2 rs4402960 with T2D in the Czech population and provided data suggesting that IGF2BP2 may have genetic interaction with IGF2 with a protective effect against DN in male patients with T1D.     

Identification of CYP2C9*2 allele in HepG2 cell line

Background Hepatoma is caused by many factors including alcohol, chemicals, viral infection, and chronic inflammation. Cytochrome P450 polymorphism plays an important role in its pathogenesis. CYP2D6, CYP2E1, and CYP1A1 have been identified to be related with hepatic carcinogenesis and tumor size and stage. However, no studies have been performed on CYP2C9, a major CYP in the liver and hepatoma. Aim of the study To identify if there is polymorphism of CYP2C9 in a HepG2 cell line. Methods A pair of primers was used to clone CYP2C9 exon 3 region and subsequently sequenced. The sequence was compared to normal CYP2C9 for identification of any mutation. Results A point mutation was identified. It was located in the amino acid number 144 of CYP2C9 protein with the change of normal amino acid arginine into cysteine, which is the same as identified in poor metabolism patients as homozygous CYP2C9*2. Conclusions There is a mutation (CYP2C9*2/ CYP2C9*2) in a HepG2 cell line. Thus, polymorphism of CYP2C9 may also be involved in the carcinogenesis of hepatoma as CYPs2D6 and 2E1.     

Albuminuria improves R2CHA2DS2-VASc score in predicting mortality in high cardiovascular risk population

Background and aimsThe CHA₂DS₂-VASc score estimates the risk of cardioembolism in patients with atrial fibrillation (AF). It also predicts vascular events and death in different clinical settings, even in the absence of AF. The R₂CHA₂DS₂-VASc score, obtained by adding the glomerular filtration rate to CHA₂DS₂-VASc, shows a higher prediction ability for new events and all-cause mortality.The present study aims to assess whether the addition of albuminuria to R₂CHA₂DS₂-VASc score further improves its discrimination ability in predicting all-cause mortality in a sample of high cardiovascular risk population.Methods and ResultsProspective, monocentric, observational study, evaluating a subset of 737 subjects consecutively undergoing to coronary angiography at Coronary Unit of Scientific Institute “Casa Sollievo della Sofferenza” from June 2016 to December 2018.The presence of albuminuria was significantly associated with all-cause mortality (p < 0.0001). Any one-point increase of Alb-R₂CHA₂DS₂-VASc score increased mortality of about 1.5-fold (adjusted HR 1.49; 95%CI: 1.37–1.63; p < 0.0001). Considering tertiles of Alb-R₂CHA₂DS₂-VASc, the third tertile showed a 9.5-fold increased risk of mortality (HR 9.52; 95% CI: 5.15–17.60, p < 0.001).Comparing the two scores, the Alb-R₂CHA₂DS₂-VASc score (C-statistic = 0.751; 95%CI: 0.69–0.81) outperformed the R₂-CHA₂DS₂-VASc score (C-statistic = 0.736; 95%CI: 0.68–0.961) in predicting mortality (delta C-statistic = 0.015; 95%CI: 0.001–0.029). The better prediction ability of the Alb-R₂CHA₂DS₂-VASc score was also proven by an IDI of 0.024 (p < 0.0001) and a relative IDI of 24.11% (p < 0.0001), with an NRI = 0.608 (p < 0.00001).ConclusionsThe addition of albuminuria to R₂CHA₂DS₂-VASc significantly and independently predicts the risk of all-cause mortality in a sample of high CV risk patients. Moreover, Alb-R₂CHA₂DS₂-VASc outperforms R₂CHA₂DS₂-VASc.     

自发性高血压大鼠肾上腺髓质素2水平的变化

背景肾上腺髓质素2(ADM2)是2004年2月由日本学者所报道的,被认为是降钙素/降钙素基因相关肽超家族的一个新肽。这与2003年11月美国斯坦福大学Dr.Roh等人发现的垂体中叶素在核苷酸和氨基酸序列上完全一致,二者被认为是同物异名。该家族的已有成员包括肾上腺髓质素、降钙素基因相关肽、降钙素和胰岛淀粉样多肽。目前研究结果表明,肾上腺髓质素2参与了心血管的调节。目的研究自发性高血压大鼠(SHR)血浆ADM2[即:垂体中叶素(IMD)]的含量和在组织中水平的升降、基因表达的变化、血浆ADM2含量与血压和心质量/体质量(HM/BM)的相互关系。方法11周龄的雄性SHR8只为实验组,同龄的雄性WistarKyoto(WKY)大鼠8只为对照组。放射免疫分析方法测定血浆和组织中ADM2的含量;RT-PCR方法测定组织中ADM2的mRNA表达;心室导管方法测定血压和心功能的变化。结果1)与WKY大鼠相比,SHR的血浆、心肌和主动脉中ADM2的含量显著增高,分别为50.0%[(317.2±25.2)vs(211.4±15.0)ng/L,P<0.01]、46.5%[(293.6±34.7)vs(200.4±21.6)ng/g,P<0.05]和32.1%[(1009.0±50.1)vs(763.8±35.0)ng/g,P<0.01];2)SHR心肌和主动脉中ADM2的mRNA水平高于WKY大鼠,分别升高76.11%[(0.75±0.33)vs(0.46±0.26)%,P<0.05]和171.1%[(1.43±0.36)%vs(0.66±0.35)%,P<0.01];3)实验组的ADM2血浆含量和收缩压呈显著负相关(r=-0.822,P<0.05)。结论ADM2作为一种心血管的活性肽,在血压调节和心肌保护过程中具有重要的意义。     

自发性高血压大鼠肾上腺髓质素2水平的变化

背景 肾上腺髓质素2(ADM2)是2004年2月由日本学者所报道的,被认为是降钙素/降钙素基因相关肽超家族的一个新肽.这与2003年11月美国斯坦福大学Dr.Roh等人发现的垂体中叶素在核苷酸和氨基酸序列上完全一致,二者被认为是同物异名.该家族的已有成员包括肾上腺髓质素、降钙素基因相关肽、降钙素和胰岛淀粉样多肽.目前研究结果表明,肾上腺髓质素2参与了心血管的调节.目的 研究自发性高血压大鼠(SHR)血浆ADM2[即:垂体中叶素(IMD)]的含量和在组织中水平的升降、基因表达的变化、血浆ADM2含量与血压和心质量/体质量(HM/BM)的相互关系.方法 11周龄的雄性SHR 8只为实验组,同龄的雄性Wistar Kyoto(WKY)大鼠8只为对照组.放射免疫分析方法测定血浆和组织中ADM2的含量;RT-PCR方法测定组织中ADM2的mRNA表达;心室导管方法测定血压和心功能的变化.结果 1)与WKY大鼠相比,SHR的血浆、心肌和主动脉中ADM2的含量显著增高,分别为50.0%[(317.2±25.2)vs(211.4±15.0)ng/L,P＜0.01]、46.5%[(293.6±34.7)vs(200.4±21.6)ng/g,P＜0.05]和32.1%[(1009.0±50.1) vs(763.8±35.0)ng/g,P＜0.01];2)SHR心肌和主动脉中ADM2的mRNA水平高于WKY大鼠,分别升高76.11%[(0.75±0.33)vs(0.46±0.26)%,P＜0.05]和171.1%[(1.43±0.36)%vs(0.66±0.35)%,P＜0.01];3)实验组的ADM2血浆含量和收缩压呈显著负相关(r=-0.822,P＜0.05).结论 ADM2作为一种心血管的活性肽,在血压调节和心肌保护过程中具有重要的意义.     

P2Y2 receptor-mediated Ca2+ signaling and spontaneous Ca2+ releases in human valvular myofibroblasts

Valvular myofibroblasts (VMFs), being the most predominant cells in the cardiac valve, perform a variety of functions to maintain normal valvular physiology. These functions, such as contraction, proliferation, and wound repair, are all directly or indirectly mediated by intracellular Ca(2+) concentrations ([Ca (2+)](i)). Knowing how [Ca(2+)](i) is regulated by vasoactive agents in VMFs enriches the understanding of valvular biology in both health and diseases. In this study we examined the characteristics of purinergic agonist-induced [Ca(2+)] (i) responses and observed spontaneous Ca(2+) releases in cultured human VMFs. Secondary cultures of human mitral VMFs were incubated with the Ca(2+)-sensitive fluorescent indicator fura-2 or fluo-4 and visualized with fluorescence microscopy. Both ATP and UTP activated P(2Y2) receptors and induced endoplasmic reticulum (ER) Ca(2+) release and Ca(2+) influx. The lack of [Ca(2+)](i) responses in VMFs challenged with the selective P(2Y1) agonists ADPbetaS and 2-Me-S-ATP further supported that functional P(2Y2) receptors are responsible for the Ca(2+) signals. Finally, in a small number of VMFs spontaneous Ca(2+) releases in localized areas were observed. Blockade of the RyR elongated the latency period between each Ca(2+) releasing event, demonstrating the presence of functional RyRs in VMFs.