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人髓过氧化物酶MPO, 一个心血管疾病检测的生物标示物

 

髓过氧化物酶MPO(人) 酶联免疫试剂盒
Code SK00172-02
标准曲线范围: 0.195 ~ 12.5 ng/ml
检测灵敏度 0.019-0.028 ng/ml
检测时间 4小时
样本体积 100 ul
样本稀释 assay buffer 13 & 31
批内误差 4.7%
批间误差 6.0%
交叉反应 MPO 100%

髓过氧化物酶MPO(人) 酶联免疫试剂盒
Code SK00172-01
标准曲线范围: 1.875 ~ 125 ng/ml
检测灵敏度 1 ng/ml
检测时间 1小时10分钟
样本体积 100 ul
样本稀释 10倍
批内误差 4.7%
批间误差 6.0%
交叉反应 MPO 100%

髓过氧化物酶MPO(人) 酶联免疫试剂盒
Code SK00172-03
标准曲线范围: 0.75 ~ 100 ng/ml
检测灵敏度 1 ng/ml
检测时间 4小时10分钟
样本体积 100 ul
样本稀释 10倍
批内误差 4.7%
批间误差 6.0%
交叉反应 MPO 100%

 

 


电子信箱 BeijingAdipoBiotech@yahoo.com.cn
电话号码 13521034406; 010-62023566

试剂盒名称
用途
目录号
规格
价格(元)
髓过氧化物酶MPO(人) 酶联免疫试剂盒
1.875 ~ 125 ng/ml
SK00172-01
96T
4500
髓过氧化物酶MPO(人) 酶联免疫检测
检测服务
S00172-01
80个起
60
髓过氧化物酶MPO(人) 酶联免疫试剂盒
0.195 - 12.5 ng/mL
SK00172-02
96T
5760
髓过氧化物酶MPO(人) 酶联免疫检测
检测服务
S00172-02
80个起
75
髓过氧化物酶MPO(人) 酶联免疫试剂盒
0.75 - 100ng/mL
SK00172-03
192T
9800
兔抗髓过氧化物酶MPO(人)抗体
WB
A00172-01
1 ml
1500
山羊抗髓过氧化物酶MPO(人)抗体
WB
A00172-02
1 ml
1500
兔抗髓过氧化物酶MPO(人)纯化IgG
WB, E
A00172-03
100 ug
1610
兔抗髓过氧化物酶MPO(人)纯化IgG
WB, E
A00172-04
1mg
5600
抗髓过氧化物酶MPO(人)纯化IgY
WB, E
A00172-05
100 ug
1500
抗髓过氧化物酶MPO(人)纯化IgY
WB, E
A00172-05
1 mg
5600
髓过氧化物酶MPO(人)
Ab
00172-01
1 mg
3402

Serum myeloperoxidase levels are associated with the future risk of coronary artery disease in apparently healthy individuals: the EPIC-Norfolk Prospective Population Study

OBJECTIVES: We evaluated whether serum myeloperoxidase (MPO) levels are associated with the risk of future development of coronary artery disease (CAD) in apparently healthy individuals. BACKGROUND: An enzyme of the innate immune system, MPO exhibits a wide array of proatherogenic effects. These include induction of oxidative damage to low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol and promotion of plaque vulnerability. Recent studies revealed that MPO independently predicts adverse outcomes in patients with chest pain or suspected acute coronary syndrome. METHODS: Myeloperoxidase was measured in baseline samples of a case-control study nested in the prospective EPIC (European Prospective Investigation into Cancer and Nutrition)-Norfolk population study. Case subjects (n = 1,138) were apparently healthy men and women who developed CAD during 8-year follow-up. Control subjects (n = 2,237), matched for age, gender, and enrollment time, remained free of CAD. RESULTS: The MPO levels were significantly higher in case subjects than in control subjects and correlated with C-reactive protein (CRP) (rho = 0.25; p < 0.001) and white blood cell count (rho = 0.33; p < 0.001). Risk of future CAD increased in consecutive quartiles of MPO concentration, with an odds ratio (OR) of 1.49 in the top versus bottom quartile (95% confidence interval [CI] 1.20 to 1.84; p < 0.001). After adjustment for traditional risk factors, the OR in the top quartile remained significant at 1.36 (95% CI 1.07 to 1.73). Elevated MPO levels (>728 pmol/l) similarly predicted increased risk of future CAD among participants with either LDL-cholesterol <130 mg/dl, HDL-cholesterol >50 mg/dl, or CRP <2.0 mg/l (OR 1.52 [95% CI 1.21 to 1.91], 1.59 [95% CI 1.24 to 2.05], and 1.42 [95% CI 1.14 to 1.77)], respectively). CONCLUSION: Elevated MPO levels predict future risk of CAD in apparently healthy individuals. This study suggests that inflammatory activation precedes the onset of overt CAD by many years.
Meuwese MC,  et al. J Am Coll Cardiol. 2007 Jul 10;50(2):159-65.

Plasma concentrations of myeloperoxidase predict mortality after myocardial infarction

OBJECTIVES: This study investigated relationships between plasma myeloperoxidase (MPO), protein oxidation markers, and clinical outcome retrospectively in patients after acute myocardial infarction (MI). BACKGROUND: Reactive oxidants are implicated in cardiovascular disease, and elevated plasma MPO is reported to predict adverse outcome in acute coronary syndromes. METHODS: Detailed demographic information, radionuclide ventriculography, neurohormone measurements, and clinical history were obtained for 512 acute MI patients at hospital admission. Plasma levels of MPO and protein carbonyls were measured in patients and 156 heart-healthy control subjects. 3-chlorotyrosine was measured in selected patients. Patient mortality was followed for 5 years. RESULTS: Plasma MPO and protein carbonyl concentrations were higher in MI patients 24 h to 96 h after admission than in control subjects (medians: MPO 55 ng/ml vs. 39 ng/ml, and protein carbonyls 48 pmol/mg vs. 17 pmol/mg protein, p < 0.001 for each). Both markers were significantly correlated with each other and with cardiovascular hormone levels. Chlorotyrosine was not elevated in patients with high MPO or carbonyl levels. Above-median levels of MPO but not protein carbonyls were independently predictive of mortality (odds ratio 1.8, 95% confidence interval 1.0 to 3.0, p = 0.034). Patients with above-median MPO levels in combination with above-median plasma amino-terminal pro-brain natriuretic peptide (NT-proBNP) or below-median left ventricular ejection fraction (LVEF) had significantly greater mortality compared with other patients. CONCLUSIONS: Myeloperoxidase and protein carbonyl levels are elevated in plasma after acute MI, apparently via independent mechanisms. High MPO is a risk factor for long-term mortality and adds prognostic value to LVEF and plasma NT-proBNP measurements.
Mocatta TJ et al.J Am Coll Cardiol. 2007 May 22;49(20):1993-2000.
 

Multiple biomarker use for detection of adverse events in patients presenting with symptoms suggestive of acute coronary syndrome

BACKGROUND: We investigated multiple biomarkers of various pathophysiologic pathways to determine their relationships with adverse outcomes in patients presenting with symptoms of acute coronary syndrome. METHODS: We obtained plasma specimens from 457 patients on admission and measured 7 biomarkers: myeloperoxidase (MPO), soluble CD40 ligand (CD40L), placental growth factor (PlGF), metalloproteinase-9 (MMP-9), high-sensitivity C-reactive protein (hsCRP), cardiac troponin I (cTnI), and N-terminal pro-B-type natriuretic peptide (NT-proBNP). We used the Modification of Diet in Renal Disease formula to calculate the estimated glomerular filtration rate (eGFR). Endpoints were cardiac events (myocardial infarction, percutaneous coronary intervention, coronary artery bypass graft, cardiac death) and all-cause mortality. We estimated cumulative event rates over a 4-month period with the Kaplan-Meier method and relative risk (RR) with the Cox proportional hazards model. RESULTS: Patients with increased PlGF, NT-proBNP, hsCRP, or cTnI or decreased eGFR had 11% to 20% higher all-cause mortality rates than patients with concentrations within reference intervals: 20.4% (eGFR), 16.0% (PlGF), 15.8% (hsCRP), 12.7% (NT-proBNP), and 11.3% (cTnI; all P < or = 0.03). No differences in mortality rates were observed between those with increased vs normal concentrations of MPO, CD40L, or MMP-9. Decreased eGFR (RR 3.4, P = 0.004) and increased NT-proBNP (RR 7.9, P = 0.04) were independently predictive of mortality, and PlGF (RR 2.0, P = 0.08) approached significance. Patients with increased NT-proBNP (12.3%) or cTnI (33.8%) had higher cardiac event rates (each P <0.02), with increased MPO (11.1%) showing a trend (P = 0.09). Patients in whom both cTnI and MPO were increased had a cardiac event rate of 43%. CONCLUSION: Multiple biomarkers that are likely indicative of different underlying pathophysiologic mechanisms are independently predictive of increased risk for adverse events in patients with acute coronary syndrome.
Apple FS, et al. Clin Chem. 2007 May;53(5):874-81

 

 

 

 

 

 

 



 
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