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末端補體復(fù)合體C5b-9(C5b-9)等多因子檢測試劑盒(流式熒光發(fā)光法)

Multiplex Assay Kit for Terminal Complement Complex C5b-9 (C5b-9) ,etc. by FLIA (Flow Luminescence Immunoassay)

MAC; Membrane Attack Complex

(注:單次混測多因子不超過8個指標 )

  • 末端補體復(fù)合體C5b-9(C5b-9)等多因子檢測試劑盒(流式熒光發(fā)光法) 產(chǎn)品包裝(模擬)
  • 末端補體復(fù)合體C5b-9(C5b-9)等多因子檢測試劑盒(流式熒光發(fā)光法) 產(chǎn)品包裝(模擬)
  • Certificate 通過ISO 9001、ISO 13485質(zhì)量體系認證

特異性

本試劑盒用于檢測末端補體復(fù)合體C5b-9(C5b-9)等多因子檢測試劑盒(流式熒光發(fā)光法),經(jīng)檢測與其它相似物質(zhì)無明顯交叉反應(yīng)。
由于受到技術(shù)及樣本來源的限制,不可能完成對所有相關(guān)或相似物質(zhì)交叉反應(yīng)檢測,因此本試劑盒有可能與未經(jīng)檢測的其它物質(zhì)有交叉反應(yīng)。

回收率

分別于定值血清及血漿樣本中加入一定量的末端補體復(fù)合體C5b-9(C5b-9)等多因子檢測試劑盒(流式熒光發(fā)光法)(加標樣品),重復(fù)測定并計算其均值,回收率為測定值與理論值的比率。

樣本 回收率范圍(%) 平均回收率(%)
serum(n=5) 84-105 99
EDTA plasma(n=5) 83-101 95
heparin plasma(n=5) 78-102 92
sodium citrate plasma(n=5) 98-105 101

精密度

精密度用樣品測定值的變異系數(shù)CV表示。CV(%) = SD/mean×100
批內(nèi)差:取同批次試劑盒對低、中、高值定值樣本進行定量檢測,每份樣本連續(xù)測定20 次,分別計算不同濃度樣本的平均值及SD值。
批間差:選取3個不同批次的試劑盒分別對低、中、高值定值樣本進行定量測定,每個樣本使用同一試劑盒重復(fù)測定8次,分別計算不同濃度樣本的平均值及SD值。
批內(nèi)差: CV<10%
批間差: CV<12%

線性

在定值血清及血漿樣本內(nèi)加入適量的末端補體復(fù)合體C5b-9(C5b-9)等多因子檢測試劑盒(流式熒光發(fā)光法),并倍比稀釋成1:2,1:4,1:8,1:16的待測樣本,線性范圍即為稀釋后樣本中末端補體復(fù)合體C5b-9(C5b-9)等多因子檢測試劑盒(流式熒光發(fā)光法)含量的測定值與理論值的比率。

樣本 1:2 1:4 1:8 1:16
serum(n=5) 79-90% 90-102% 82-102% 99-105%
EDTA plasma(n=5) 84-91% 79-93% 98-105% 87-102%
heparin plasma(n=5) 79-88% 93-101% 84-92% 87-94%
sodium citrate plasma(n=5) 83-102% 96-105% 86-94% 87-99%

穩(wěn)定性

經(jīng)測定,試劑盒在有效期內(nèi)按推薦溫度保存,其活性降低率小于5%。
為減小外部因素對試劑盒破壞前后檢測值的影響,實驗室的環(huán)境條件需盡量保持一致,尤其是實驗室內(nèi)溫度、濕度及溫育條件。其次由同一實驗員來進行操作可減少人為誤差。

實驗流程

1. 實驗前標準品、試劑及樣本準備;
2. 加樣(標準品、樣本、磁珠)標準品或樣本100μL及磁珠10μL,
    37°C酶標板振蕩器孵育90分鐘;
3. 磁吸甩干,加檢測溶液A100μL,37°C酶標板振蕩器孵育60分鐘;
4. 磁吸洗板3次;
5. 加檢測溶液B100μL,37°C振動孵育30分鐘;
6. 磁吸洗板3次;
7. 加鞘液100μL,旋渦震蕩2分鐘后讀數(shù)。

實驗原理

將末端補體復(fù)合體C5b-9(C5b-9)等多因子檢測試劑盒(流式熒光發(fā)光法)抗體包被于磁珠,制成固相載體,向微孔中分別加入標準品或標本以及磁珠,其中的末端補體復(fù)合體C5b-9(C5b-9)等多因子檢測試劑盒(流式熒光發(fā)光法)與連接于固相載體上的抗體結(jié)合,然后加入生物素化的末端補體復(fù)合體C5b-9(C5b-9)等多因子檢測試劑盒(流式熒光發(fā)光法)抗體,將未結(jié)合的生物素化抗體洗凈后,加入PE標記的親和素,再次徹底洗滌后即可上機讀數(shù)。MFI值和樣品中的末端補體復(fù)合體C5b-9(C5b-9)等多因子檢測試劑盒(流式熒光發(fā)光法)呈正相關(guān)。

贈品

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參考文獻

雜志 參考文獻
Journal of Biomedical Materials Research Part A Effect of thiol functionalization on the hemo-compatibility of PLGA nanoparticles [Wiley: source]
The Journal of Clinical Investigation Complement component 5 contributes to poor disease outcome in humans and mice with pneumococcal meningitis [PubMed: PMC3195471]
Colloids and Surfaces B: Biointerfaces Glucosylated polymeric nanoparticles: A sweetened approach against blood compatibility paradox [ScienceDirect: S0927776513001720]
Perfusion The effect of normovolemic modified ultrafiltration on inflammatory mediators, endotoxins, terminal complement complexes and clinical outcome in high-risk cardiac surgery patients [Pubmed: 23429100]
Nephrology Dialysis Transplantation The efficacy of recombinant human soluble thrombomodulin for the treatment of shiga toxin associated hemolytic uremic syndrome model mice [Pubmed:25694534]
journal of neuroinflammation Adjuvant treatment with dexamethasone plus anti-C5 antibodies improves outcome of experimental pneumococcal meningitis: a randomized controlled trial [PubMed: 26272468]
J Thromb Haemost Thrombin‐activatable fibrinolysis inhibitor influences disease severity in humans and mice with pneumococcal meningitis [PubMed: 26340319]
Digital Repository Dosagem de fra??es ativadas do sistema complemento em empiema induzido em ratos [10183]
J Neuroinflammation.? Mannose-binding lectin-associated serine protease 2 (MASP-2) contributes to poor disease outcome in humans and mice with pneumococcal meningitis [PMC5234106]
Cancer Letters Complement C5a/C5aR pathway potentiates the pathogenesis Q5 of gastric cancer by down-regulating p21 expression [pubmed:29031586]
Effects of immunoadsorption combined with membrane filtration on complement markers–Results of a randomized, controlled, crossover study []
Journal of Neuroinflammation Complement factor H contributes to mortality in humans and mice with bacterial meningitis [Pubmed: 31883521]
FASEB J C‐reactive protein inhibits C3a/C3aR‐dependent podocyte autophagy in favor of diabetic kidney disease [Pubmed:35503088]
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