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Merck
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90C2

Sigma-Aldrich

白细胞氯乙酸AS-D萘酚酯（特异性酯酶）试剂盒

别名:

Leder染色

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About This Item

分類程式碼代碼:
12352106
NACRES:
NA.47

描述

Select reagents packaged in gelatin capsules

品質等級

500

儲存期限

Expiry date on the label.

IVD

for in vitro diagnostic use

應用

hematology
histology

運輸包裝

wet ice

儲存溫度

2-8°C

相关类别

應用

酯酶普遍存在于自然界中，其中包含了一系列不同的酶，均可作用于选定底物。使用90C2 试剂盒可通过“特定酯酶”对萘酚AS-D氯乙酸盐进行酶促水解，从而释放出萘酚自由基化合物。它随后可与重氮盐进行偶联，在酶活性位点处形成带明显颜色的沉淀。这种酶通常被认为对粒细胞系的细胞具有特异性。也可用于检测外周血、骨髓或经石蜡包埋的组织切片中的中性粒细胞。

仅试剂盒组分

产品编号
说明
  • Dimethyl formamide (9010) 25 mL
  • Fast Corinth V Salt (9015) 10 capsules

试剂盒组分也可单独购买

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说明
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訊號詞

Danger

危險分類

Acute Tox. 4 Dermal - Acute Tox. 4 Inhalation - Acute Tox. 4 Oral - Carc. 1B - Eye Dam. 1 - Met. Corr. 1 - Repr. 1B - Skin Corr. 1B

安全危害

EUH044

儲存類別代碼

6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects

閃點（°F）

Not applicable

閃點（°C）

Not applicable

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Inactivation of the Hippo pathway protects the myocardium from cardiac ischemic injury. MicroRNAs (miRs) have been reported to play pivotal roles in the progression of myocardial infarction (MI). The present study examined whether miR‑93 could promote angiogenesis and attenuate remodeling
Feng Dong et al.
Circulation research, 106(3), 601-610 (2009-12-26)
Hypoxia inducible factor (HIF)-1alpha is a transcription factor stabilized by hypoxia. It regulates cytokines involved in the inflammatory response after ischemia and affects white blood cell (WBCs) function. The effect of HIF-1alpha on WBC function and inflammation following myocardial infarction
J Heijmans et al.
Oncogene, 32(9), 1202-1206 (2012-04-04)
Development of colon cancer is a multistep process that is regulated by intrinsic and extrinsic cellular signals. Extrinsic factors include molecular patterns that are derived from either pathogens (PAMPs) or cellular damage (DAMPs). These molecules can promote tumourigenesis by activation
John Zagorski et al.
Journal of immunology (Baltimore, Md. : 1950), 179(11), 7820-7826 (2007-11-21)
Right ventricular (RV) dysfunction is a strong risk factor for poor clinical outcome following pulmonary embolism (PE), the third most prevalent cardiovascular disease. Previous studies in our laboratory demonstrated that RV failure during PE is mediated, in part, by neutrophil-dependant

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