血压盐敏感者一氧化氮系统与非对称性二甲基精氨酸和补钾的作用

目的 通过观察慢性盐负荷及补钾后血浆非对称性二甲基精氨酸(ADMA)和血、尿一氧化氮(NO)水平的变化及其与血压的关系,探讨血压正常盐敏感者(SS)的血管内皮功能损伤及补钾的保护作用.方法选60例年龄在20～60岁的血压正常者参与为期3周的慢性盐负荷及补钾试验,包括基线调查3 d,低盐(LS)饮食,高盐(HS)饮食,和高盐补钾(HS K)饮食各7 d的研究.每个阶段均测量血压,并收集血、尿标本.血、尿NO用Griess法测量,血浆ADMA用高效液相色谱法测量.结果 受试者60例中共检出SS 13例,检出率为21.6%.盐负荷后,SS血浆ADMA的浓度明显升高[(0.89±0.09 vs 0.51±0.07)μmol/L,P＜0.05],而血浆NO的水平则较LS饮食期显著降低[(41.8±7.6 vs 63.5±7.6)μmol/L,P＜0.01].在HS摄入的基础上大剂量口服补钾可以逆转单纯HS负荷对SS血浆ADMA浓度和血、尿NO水平的作用[(ADMA:0.52±0.09 vs 0.89±0.09)μmol/L;NO:(58.1±7.4 vs 41.8±7.6)μmol/L],血浆ADMA浓度和平均动脉压之间存在正相关关系.结论 血压正常SS于HS负荷后伴随血压升高,血浆ADMA显著升高、NO降低,同时补充钾盐可以逆转前述作用,提示补钾可能通过抑制ADMA的升高降低血压.     

血压盐敏感者内皮功能损伤及补钾的保护作用研究

目的通过观察血、尿-氧化氮（NO）水平的变化,探讨盐敏感者血管内皮功能损伤及补钾的保护作用。方法选39例年龄16～60岁、血压正常或血压轻度偏高者参与为期3周的慢性盐负荷及补钾试验,包括基线3天,低盐饮食、高盐饮食和高盐加补钾饮食各7天的研究。各个阶段测量体重、血压,并收集血、尿标本。结果盐敏感者血浆NO浓度和尿中NO水平在基线、低盐和高盐阶段均低于盐不敏感者;限盐后血、尿NO浓度增加,而高盐饮食后NO浓度显著减少;盐敏感者在高盐摄入的基础上大剂量口服补钾后血浆NO浓度、尿NO水平显著升高。结论盐敏感者尽管尚处在血压正常或血压轻度偏高阶段已存在一定程度的内皮功能损伤,且这种损伤与盐负荷相关联;大剂量补钾可能通过增加NO水平而改善盐敏感者的血管内皮功能。     

血压盐敏感者早期血管内皮功能改变研究

目的 盐敏感者较早出现靶器官功能损害,其心血管风险增加.本研究探讨血压正常或血压轻度偏高的盐敏感者血管内皮功能改变.方法 选99例年龄16～60岁、血压正常或血压轻度偏高者参与为期2周的慢性盐负荷试验,检测盐敏感性.试验包括基线3 d,低盐饮食、高盐饮食各7 d的研究.基线时采用彩色多普勒超声检测血流调节的血管扩张性,反映内皮依耐性血管舒张功能.试验各个阶段测量体重、血压,并收集血、尿标本.结果 盐敏感者检出率17.2%,盐敏感与盐不敏感者基线尿钠、钾排泄量无差异,而血浆NO浓度盐敏感者低于盐不敏感者[(61. 2±13.3)μmol/L比(82.5±14.6)μmol/L,P＜0.05];盐敏感者血流介导的肱动脉扩张性低于盐不敏感者[(10.2±2.5)%比(14.5±1.6)%,P＜0.05].结论 盐敏感者尽管尚处在血压正常或血压轻度偏高阶段已存在内皮功能损伤.

Abstract：

Objective Salt-sensitivity is associated with more severe target organ injury and higher mortality in patients with essential hypertension. We compared the vascular endothelial function between saltsensitive subjects(SS)and non-salt-sensitive subjects(NSS)with normal or mildly increased blood pressure. Methods Ninety-nine subjects(aged 16-60 years)with normal blood pressure or mild hypertension(degree 1)were enrolled. The test program included 3 days baseline investigation, 1 week lowsalt loading phase and 1 week high-salt loading phase. Endothelial function was assessed by measuring the flow mediated dilatation(FMD)of the brachial artery using high resolution ultrasound. Results There was 17. 2% SS. Plasma NOx level[(61.2 ± 13. 3)μmol/L vs(82. 5 ± 14. 6)μmol/L, P ＜ 0. 05]and FMD [(10.2±2.5)%vs(14.5 ± 1.6)%, P ＜0.05]were significantly lower in SS subjects than in NSS subjects. Conclusion Vascular endothelial dysfunction was evidenced in SS subjects with normal blood pressure or in the early stage of hypertension.     

慢性盐负荷及补钾对健康成人血压变异性的影响

目的:探讨慢性盐负荷及补钾对健康成人血压和血压变异性的影响。方法:选取100例年龄在28～60岁的血压正常者参与为期3周的慢性盐负荷及补钾试验,包括基线调查3 d,低盐饮食、高盐饮食和高盐补钾饮食各7 d的研究。在基线调查和各干预阶段的第5,6,7天采用英国产随机零点血压计连续测量3 d血压。测量血压前受试者静坐休息5 min,测量3次,求平均值,并计算3 d血压测量值的标准差和变异系数,作为长时血压变异性指标。结果:受试者血压在低盐期较基线期显著下降［SBP:(112±11)mmHg vs.(117±14)mmHg;DBP:(74±8)mmHg vs.(76±10)mmHg,P<0.01］;高盐期较低盐期明显升高［SBP:(119±14)mmHg vs.(112±11)mmHg;DBP:(77±9)mmHg vs.(74±8)mmHg,P<0.01］;补钾期较高盐期显著降低［SBP:(114±12)mmHg vs.(119±14)mmHg;DBP:(75±8)mmHg vs.(77±9)mmHg,P<0.01］。限盐后收缩压标准差、舒张压标准差均降低［SDSBP:(3.9±1.5)mmHg vs.(4.3±1.0)mmHg;SDDBP:(3.2±1.4)mmHg vs.(3.6±1.6)mmHg,P<0.01］;高盐期较低盐期升高［SDSBP:(4.4±1.6) vs.(3.9±1.5)mmHg;SDDBP:(3.7±1.2) vs.(3.2±1.4)mmHg,P<0.01］。结论:钠、钾摄入量与血压变化密切相关,其中低盐饮食后血压下降,高盐饮食后血压升高,而在高盐负荷基础上给予大剂量补钾使血压下降。高盐饮食可增大血压变异性,限盐可降低血压变异性。     

非对称性二甲基精氨酸和胱氨酸蛋白酶抑制剂C与冠心病

目的 探讨冠状动脉疾病中血浆非对称性二甲基精氨酸(ADMA)与胱氨酸蛋白酶抑制剂C(Cystatin C)之间的关系.方法 选取冠心病患者87例(其中急性心肌梗死39例,不稳定性心绞痛48例),健康对照组51例;同时,依据Cystatin C水平将冠心病患者分为Cystatin C升高组(51例)与无Cystatin C升高组(36例),采用高效液相色谱法测定血浆中ADMA、对称性二甲基精氨酸(SDMA)、左旋精氨酸(L-Arg)的含量,采用德国BNProSpec全自动速率散色比浊仪测定血浆Cystatin C的含量.结果 冠心病患者血浆ADMA[(0.47±0.15)μmol/L比(0.37±0.15)μmol/L]、SDMA[(0.39±0.19)μmol/L比(0.28±0.12)μmol/L]和Cystatin C浓度[(1.16±0.32)mg/L比(0.73±0.16)mg/L]均高于正常对照组(P均<0.05),L-Arg浓度低于正常对照组[(59.4±19.4)μmol/L比(83.7±19.6)μmol/L,P<0.05];对冠心病组的亚组分析显示血浆ADMA、L-Arg和Cystatin C浓度在心肌梗死组较心绞痛组差异无统计学意义.在Cystatin C<1 mg/L的冠心病患者中血浆ADMA与正常对照组比较,差异无统计学意义;而在Cystatin C>1 mg/L的冠心病患者血浆ADMA高于正常对照组[(0.50±0.17)μmol/L比(0.39±0.15)μmol/L,P<0.05].结论 只有在血浆Cystatin C水平升高的冠心病患者血浆ADMA水平才明显升高,提示冠心病患者血浆ADMA水平的升高并不与冠心病直接相关,可能与冠心病患者伴随轻微肾损害有关.     

慢性盐负荷对成年人血清肾胺酶的影响

目的 :观察慢性盐负荷对成年人血清肾胺酶浓度的影响。方法 :选取42例28~65岁的成年人参与为期2周的慢性盐负荷试验,包括3 d基线调查及低盐饮食、高盐饮食各7 d的研究。每个阶段均测量血压,并收集血、尿标本,测定24 h尿钠、钾含量;血清肾胺酶采用酶联免疫吸附(ELISA)法测定。结果:与基线期相比,低盐饮食可显著升高受试者血清肾胺酶水平[(5.10±0.18)比(8.12±0.42)mg/L,P     

冠状动脉慢血流患者一氧化氮和内皮素1浓度的变化

目的探讨冠状动脉慢血流(coronary slow flow,CSF)患者的血管内皮功能。方法选择因胸痛行冠状动脉造影的患者40例,根据造影结果分为CSF组20例和对照组20例。2组分别于静息和多巴酚丁胺负荷试验结束时立即抽取血标本,检测血浆内皮素1、血清NO浓度,并进行比较。结果 CSF组静息时血浆内皮素1浓度较对照组升高,但差异无统计学意义(P>0.05),而药物负荷试验后血浆内皮素1浓度较对照组明显升高,差异有统计学意义[(37.60±6.93)ng/L vs(14.16±5.73)ng/L,P<0.01]。CSF组静息时和药物负荷试验后血清NO浓度均明显低于对照组,差异有统计学意义[(42.36±9.72)μmol/L vs(50.39±9.77)μmol/L,(24.88±9.28)μmol/L vs(61.06±8.20)μmol/L,P<0.01)]。结论 CSF患者无论静息或者药物负荷状态下均存在内皮素1及NO平衡失调,负荷状态下这种平衡失调现象更加明显。     

血浆非对称性二甲基精氨酸水平与2型糖尿病患者脑微出血的相关性研究

目的探讨血浆非对称性二甲基精氨酸(ADMA)与2型糖尿病患者脑微出血(CMB)的相关性。方法 122例2型糖尿病患者采用3.0T MRI确定是否存在CMB,并分为CMB组27例,非CMB组95例。应用ELISA法检测患者血浆ADMA水平。结果 CMB组较非CMB组年龄偏大[(62.25±8.01)岁vs(57.68±11.15)岁,P=0.020)],高血压比例高[(77.8%vs 44.2%,P=0.002)],血浆ADMA升高[(1.6(1.2,2.0)μmol/L vs 1.3(1.1,1.5)μmol/L,P=0.004)],估算肾小球滤过率[81(70,94)ml/(min·1.73m2)vs 99(82,112)ml/(min·1.73m2),P=0.000]降低。血浆高ADMA水平是CMB存在及部位(深部/幕下型)独立危险因素(OR=3.564,95%CI:1.038~12.235,P=0.043;OR=8.657,95%CI:1.896~39.517,P=0.005)。结论 2型糖尿病患者血浆ADMA水平与CMB的存在及CMB发生位置密切相关。     

钠钾对血压盐敏感者短时血压变异性的影响

目的观察血压盐敏感者在钠、钾饮食干预后短时血压变异性(BPV)的变化,探讨BPV与盐敏感的关系。方法 2004-04-10对陕西眉县农村正常血压成人93名进行低盐(氯化钠51.3mmol/d)饮食7d,高盐(氯化钠307.7mmol/d)饮食7d的慢性盐负荷试验,之后进行高盐补钾(307.7mmol/d氯化钠基础上口服60mmol/d氯化钾缓释胶囊)干预7d;每个阶段最后一天测3次血压,以血压标准差、变异系数为短时BPV指标。根据高盐饮食后平均动脉压升高幅度是否≥10%,分为血压盐敏感组(n=30)及盐不敏感组(n=63)。结果盐敏感性检出率为32.3%。基线期时,与盐不敏感组比较,盐敏感组收缩压标准差[(4.4±1.1)比(2.5±0.5)mmHg,P<0.01];舒张压标准差[(3.7±1.7)比(2.8±0.9)mmHg,P<0.01];收缩压变异系数[(3.78±1.01)比(2.35±0.55),均P<0.01];舒张压变异系数[(5.06±2.50)比(3.99±1.46),P<0.05]均较高。盐敏感组低盐期及高盐补钾期收缩压、舒张压标准差及变异系数均降低,与盐不敏感组比较,差异无统计学意义;予高盐饮食后,盐敏感组收缩压标准差较低盐期升高,与盐不敏感组比较,差异有统计学意义[(3.7±1.9)比(3.0±1.1)mmHg,P<0.05]。结论高盐摄入、盐敏感是短时BPV增大的重要原因,限盐及补钾具有降低短时BPV的保护作用。     

高盐摄入对血压正常人群血浆骨保护素含量的影响

目的:本研究旨在探索高盐摄入对正常血压患者血浆骨保护素(OPG)水平的影响。方法:从农村社区招募18例血压正常的受试者(年龄25～50岁),给予正常饮食3 d,低盐饮食7 d(3g/天,Na Cl),高盐饮食7 d(18 g/d)共17 d饮食干预,采用酶联免疫吸附方法(ELISA方法)测定血浆骨保护素的含量。结果:高盐摄入后受试者体内血浆OPG水平明显升高[(252. 7±13. 9) vs.(293. 4±16. 1) ng/L]。进一步分析显示,OPG浓度与24 h尿钠排泄量呈正相关(r=0. 405,P 0. 01)。结论:盐负荷可以促进血压正常受试者体内OPG的生成,这可能是一种内皮功能自我保护机制。     

妊娠时间与肺结核复发的相关性研究及诊治对策

目的 分析肺结核史患者妊娠时间和肺结核复发间相关性.方法 选取我院收治的有肺结核史的妊娠妇女576例作为研究对象,对其妊娠前肺结核治疗、治愈后妊娠时间、妊娠后复发肺结核等进行分析,总结有肺结核史育龄女性的妊娠时间和肺结核复发之间的关系.结果 肺结核治愈后不同时间段妊娠者的结核复发率比较,差异具有显著性（P＜0.05）,停药后间隔时间越久妊娠,肺结核复发的几率越小.结论 加强孕期痰菌检查,及早发现复发肺结核,提高母婴安全.     

我国骨关节结核诊治的回顾与展望

骨关节结核是危害人们健康的严重感染性疾病,近95％由他处结核病继发而来.罹患骨关节结核疾病后几乎均将致残,严重影响人们的健康、工作和生活.建国以来在党和国家的关心和支持下,骨关节结核的诊治水平取得了长足进步.时至今日,由于多种原因,学科发展和被重视程度受到一定的制约,同整个医疗行业的发展不相适应.回顾过去,展望未来,我们需要重新审视骨关节结核的诊治方法,努力推进骨关节结核诊疗技术的科学发展.     

Effect of phosphorylation of MAPK and Stat3 and expression of c-fos and c-jun proteins on hepatocarcinogenesis and their clinical significance

AIM To study the effect of phosphorylation ofMAPK and Stat3 and the expression of c-fos andc-jun proteins on hepatocellular carcinogenesisand their clinical significance.METHODS SP immunohistochemistry was usedto detect the expression of p42/44~(MAPK), p-Stat3,c-fos and c-jun proteins in 55 hepatocellularcarcinomas (HCC) and their surrounding livertissues.RESULTS The positive rates and expressionlevels of p42/44~(MAPK), p-Stat3, c-fos and c-junproteins in HCCs were significantly higher thanthose in pericarcinomatous liver tissues (PCLT).A positive correlation was observed between theexpression of p42/44~(MAPK) and c-fos proteins, andbetween p-Stat3 and c-jun, but there was nosignificant correlation between P42/44~(MAPK) and p-Stat3 in HCCs and their surrounding livertissues.CONCLUSION The abnormalities of Ras/Raf/MAPK and JAKs/ Stat3 cascade reaction maycontribute to malignant transformation ofhepatocytes. Hepatocytes which are positive forp42/ 44~(MAPK), c-fos or c-jun proteins may bepotential malignant pre-cancerous cells.Activation of MAPK and Stat3 proteins may be anearly event in hepatocellular carcinogenesis.     

Overweight and Obesity and Progression of ADPKD

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Replication and Inhibitors of Enteroviruses and Parechoviruses

The Enterovirus (EV) and Parechovirus genera of the picornavirus family include many important human pathogens, including poliovirus, rhinovirus, EV-A71, EV-D68, and human parechoviruses (HPeV). They cause a wide variety of diseases, ranging from a simple common cold to life-threatening diseases such as encephalitis and myocarditis. At the moment, no antiviral therapy is available against these viruses and it is not feasible to develop vaccines against all EVs and HPeVs due to the great number of serotypes. Therefore, a lot of effort is being invested in the development of antiviral drugs. Both viral proteins and host proteins essential for virus replication can be used as targets for virus inhibitors. As such, a good understanding of the complex process of virus replication is pivotal in the design of antiviral strategies goes hand in hand with a good understanding of the complex process of virus replication. In this review, we will give an overview of the current state of knowledge of EV and HPeV replication and how this can be inhibited by small-molecule inhibitors.     

Effect of phosphorylation of MAPK and Stat3 and expression of c-fas and c-jun proteins on hepatocarcinogenesis and their clinical significance

AIM To study the effect of phosphorylation ofMAPK and Stat3 and the expression of c-fos andc-jun proteins on hepatocellular carcinogenesisand their clinical significance.METHODS SP immunohistochemistry was usedto detect the expression of p42/44MAPK, p-Stat3,c-fos and c-jun proteins in 55 hepatocellularcarcinomas (HCC) and their surrounding livertissues.RESULTS The positive rates and expressionlevels of p42/44MAPK, p-Stat3, c-fos and c-junproteins in HCCs were significantly higher thanthose in pericarcinomatous liver tissues (PCLT).A positive correlation was observed between theexpression of p42/44MAPK and c-fos proteins, andbetween p-Stat3 and c-jun, but there was nosignificant correlation between p42/44MAPK and p-Stat3 in HCCs and their surrounding livertissues.CONCLUSION The abnormalities of Ras/Rat/MAPK and JAKs/ Stat3 cascade reaction maycontribute to malignant transformation ofhepatocytes. Hepatocytes which are positive forp42/ 44MAPK, c-fos or c-jun proteins may bepotential malignant pre-cancerous cells.Activation of MAPK and Stat3 proteins may be anearly event in hepatocellular carcinogenesis.     

心电图、心电向量图与冠状动脉造影结果对比分析

目的:通过分析心电图(Electrocardiogram,ECG)和心电向量图(Vectorcardiogram,VCG)的改变与冠脉造影（CAG）结果进行对比,探讨ECG、VCG在冠状动脉病变中的诊断价值。方法: 选择2008年1月~2009年12月临床拟诊断为冠心病患者108例,行常规ECG、VCG检查,并于1周内进行CAG,对检查结果依据各自的诊断标准进行判定,以CAG为标准诊断法,利用四格表法,计算相关评价真实性的指标并进行比较。结果: ①VCG检测的灵敏度、特异度、准确度显著高于ECG(P<0.05,P<0．01)。②ECG、VCG阳性率与冠脉病变支数组间比较:在单支病变、双支病变中,VCG阳性率明显高于ECG(P<0.05),左主干或三支病变无统计学意义;组内比较:ECG组左主干或三支病变组较单支病变、双支病变阳性率高(P<0.05,P<0.01);VCG组左主干或三支病变组较单支病变阳性率高(P<0.05);与双支病变阳性率比较无统计学意义;③ECG、VCG阳性率与冠脉病变程度组间比较:冠脉病变狭窄50%～69%的VCG阳性率明显高于ECG (P<0.05),其他两组阳性率比较无统计学意义;组内比较:ECG组冠脉病变狭窄≥90%较50%～69%、70%～89%的阳性率高(P<0.05,P<0.01); VCG组狭窄≥90%较50%～69%阳性率高（P<0.01),其他无统计学意义。结论: VCG对冠心病检测价值显著高于ECG。     

Detection and characterization of the product of hydroethidine and intracellular superoxide by HPLC and limitations of fluorescence

Here we report the structural characterization of the product formed from the reaction between hydroethidine (HE) and superoxide (O(2)(.-)). By using mass spectral and NMR techniques, the chemical structure of this product was determined as 2-hydroxyethidium (2-OH-E(+)). By using an authentic standard, we developed an HPLC approach to detect and quantitate the reaction product of HE and O(2)(.-) formed in bovine aortic endothelial cells after treatment with menadione or antimycin A to induce intracellular reactive oxygen species. Concomitantly, we used a spin trap, 5-tert-butoxycarbonyl-5-methyl-1-pyrroline N-oxide (BMPO), to detect and identify the structure of reactive oxygen species formed. BMPO trapped the O(2)(.-) that formed extracellularly and was detected as the BMPO-OH adduct during use of the EPR technique. BMPO, being cell-permeable, inhibited the intracellular formation of 2-OH-E(+). However, the intracellular BMPO spin adduct was not detected. The definitive characterization of the reaction product of O(2)(.-) with HE described here forms the basis of an unambiguous assay for intracellular detection and quantitation of O(2)(.-). Analysis of the fluorescence characteristics of ethidium (E(+)) and 2-OH-E(+) strongly suggests that the currently available fluorescence methodology is not suitable for quantitating intracellular O(2)(.-). We conclude that the HPLC/fluorescence assay using HE as a probe is more suitable [corrected] for detecting intracellular O(2)(.-).     

Effects of sex and time of day on metabolism and excretion of corticosterone in urine and feces of mice

Non-invasive techniques to monitor stress hormones in small animals like mice offer several advantages and are highly demanded in laboratory as well as in field research. Since knowledge about the species-specific metabolism and excretion of glucocorticoids is essential to develop such a technique, we conducted radiometabolism studies in mice (Mus musculus f. domesticus, strain C57BL/6J). Each mouse was injected intraperitoneally with 740 kBq of 3H-labelled corticosterone and all voided urine and fecal samples were collected for five days. In a first experiment 16 animals (eight of each sex) received the injection at 9 a.m., while eight mice (four of each sex) were injected at 9 p.m. in a second experiment. In both experiments radioactive metabolites were recovered predominantly in the feces, although males excreted significantly higher proportions via the feces (about 73%) than females (about 53%). Peak radioactivity in the urine was detected within about 2h after injection, while in the feces peak concentrations were observed later (depending on the time of injection: about 10h postinjection in experiment 1 and about 4h postinjection in experiment 2, thus proving an effect of the time of day). The number and relative abundance of fecal [3H]corticosterone metabolites was determined by high performance liquid chromatography (HPLC). The HPLC separations revealed that corticosterone was extensively metabolized mainly to more polar substances. Regarding the types of metabolites formed, significant differences were found between males and females, but not between the experiments. Additionally, the immunoreactivity of these metabolites was assessed by screening the HPLC fractions with four enzyme immunoassays (EIA). However, only a newly established EIA for 5alpha-pregnane-3beta,11beta,21-triol-20-one (measuring corticosterone metabolites with a 5alpha-3beta,11beta-diol structure) detected several peaks of radioactive metabolites with high intensity in both sexes, while the other EIAs showed only minor immunoreactivity. Thus, our study for the first time provides substantial information about metabolism and excretion of corticosterone in urine and feces of mice and is the first demonstrating a significant impact of the animals' sex and the time of day. Based on these data it should be possible to monitor adrenocortical activity non-invasively in this species by measuring fecal corticosterone metabolites with the newly developed EIA. Since mice are extensively used in research world-wide, this could open new perspectives in various fields from ecology to behavioral endocrinology.     

大鼠骨髓间充质干细胞的分离培养和外源基因的导入

目的探讨绿色荧光蛋白基因转染骨髓间质干细胞的可行性。方法采用F icoll-PaqueTMP lus淋巴细胞分离液,根据细胞密度梯度原理,分离大鼠骨髓间充质干细胞(rM SC s)并进行体外原代培养和传代扩增,倒置相差显微镜观察细胞生长情况,免疫细胞化学法对其初步鉴定。流式细胞仪分析转染效率。结果原代和传代培养的细胞呈现梭形外观,具有较强的生长增殖能力;细胞均一表达CD44、CD54、CD106、CD29抗原。电穿孔法转染rM SC s转染率为32.8%±3%。结论采用比重为1.077 g/L的F icoll-PaqueTMP lus能分离获得大鼠骨髓间充质干细胞,经原代培养和传代培养能够迅速扩增。电穿孔法具有较高的介导外源基因表达于rM SC s的效率。