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Merck

GHS216

Sigma-Aldrich

苏木精,Gill 2 号

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About This Item

MDL號碼:
分類程式碼代碼:
41116124
NACRES:
NA.47

形狀

solution

品質等級

儲存期限

Expiry date on the label.

IVD

for in vitro diagnostic use

濃度

4 g/L

pH值

2.5-3.5

應用

hematology
histology

儲存溫度

room temp

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應用

Gill配方2可用于细胞学和/或组织学,基于染色时间长度用作进行性或退行性染色。

其他說明

4 g/L 认证型苏木精

象形圖

Corrosion

訊號詞

Danger

危險聲明

危險分類

Eye Dam. 1

儲存類別代碼

12 - Non Combustible Liquids

水污染物質分類(WGK)

WGK 1

閃點(°F)

Not applicable

閃點(°C)

Not applicable


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Haley R Noonan et al.
Disease models & mechanisms, 9(8), 873-884 (2016-08-05)
Patients with von Hippel-Lindau (VHL) disease harbor a germline mutation in the VHL gene leading to the development of several tumor types including clear cell renal cell carcinoma (ccRCC). In addition, the VHL gene is inactivated in over 90% of
Yitzhak Reizel et al.
Genes & development, 34(15-16), 1039-1050 (2020-06-21)
The FoxA transcription factors are critical for liver development through their pioneering activity, which initiates a highly complex regulatory network thought to become progressively resistant to the loss of any individual hepatic transcription factor via mutual redundancy. To investigate the
G Gonzalez et al.
Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus, 29(6), 670-680 (2015-08-08)
Deep esophageal glands play a vital role in the protection and regeneration of the esophageal mucosa. Conditions such as gastroesophageal reflux disease and Barrett's esophagus have been associated with a change in the usual glands by oncocytic metaplasia. However, little
Wajiha Gohir et al.
The Journal of physiology, 597(12), 3029-3051 (2019-05-14)
Maternal obesity has been associated with shifts in intestinal microbiota, which may contribute to impaired barrier function Impaired barrier function may expose the placenta and fetus to pro-inflammatory mediators We investigated the impacts of diet-induced obesity in mice on maternal
Noora Puhakka et al.
PloS one, 12(3), e0172521-e0172521 (2017-03-09)
Traumatic brain injury (TBI) can result in several dentate gyrus-regulated disabilities. Almost nothing is known about the chronic molecular changes after TBI, and their potential as treatment targets. We hypothesized that chronic transcriptional alterations after TBI are under microRNA (miRNA)

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