ライフサイエンスコーパス: coagulative

1 with inflammatory and acute-phase responses, coagulative activities, and transition metal ion sequest

2 orm of COVID-19 is related to the changes in coagulative and fibrinolytic pathways.

3 se swelling of cardiomyocytes and multifocal coagulative contraction band necrosis.

4 The coagulative decrease was observed in terms of TD (turbid

5 Disse; RFA-treated liver tissue demonstrated coagulative destruction of hepatocyte organelles within

6 stem and a haemoglobin-based, acellular, non-coagulative, echogenic, and cytoprotective perfusate tha

7 t lysate (PL) RNA transcripts for growth and coagulative factors were elevated post-HD, with upregula

8 erplasia along with multifocal to coalescing coagulative hepatocyte necrosis.

9 ts (1984 to 1991) by grading the severity of coagulative myocyte necrosis (CMN) as absent, 0; mild-fo

10 e liver pathology characterized by extensive coagulative necrosis and an increase in hepatic IFN-gamm

11 on, and spotty necrosis, and induced diffuse coagulative necrosis and centrilobular fibrosis in some

12 ited severe liver pathology, with regions of coagulative necrosis and hepatocyte vacuolization unappa

13 tissues exhibited microvascular thrombosis, coagulative necrosis and similar levels of platelet and

14 pure ethanol revealed that while both induce coagulative necrosis and similar tissue responses at 1-4

15 cimens at the day of ablation revealed acute coagulative necrosis associated with intense basophilic

16 ith this parasite develop extensive areas of coagulative necrosis in the liver, and newborn larvae ar

17 Coagulative necrosis of cells was the most frequently oc

18 Within 24 hours, complete coagulative necrosis of the entire kidney occurred as a

19 interstitial by chronic inflammatory cells, coagulative necrosis of the kidney, spleen, intestine an

20 ndothelial cell damage has been described as coagulative necrosis secondary to irreversible physico-c

21 n the absence of microvascular thrombosis or coagulative necrosis that developed later.

22 ckout mice had reduced mortality and massive coagulative necrosis was observed in wild-type mice.

23 Areas of coagulative necrosis were identified at histopathology.

24 xhibited mainly microvascular thrombosis and coagulative necrosis with little evidence of interstitia

25 lymphoplasmacytic hepatitis with hepatocytic coagulative necrosis, but the hydrogenase mutants exhibi

26 ns ranged from well-organized tubercles with coagulative necrosis, epithelioid macrophages, and fibro

27 us degrees of ulceration, hemorrhage, edema, coagulative necrosis, perivascular inflammation, and vas

28 to induction of cytokine release and massive coagulative necrosis.

29 and epitheliotropism and irregular areas of coagulative necrosis.

30 cules to generate heat and thus resulting in coagulative necrosis.

31 ace achieves high temperatures, resulting in coagulative necrosis.

32 infiltrates, Schwann cell proliferation, and coagulative necrosis.

33 kine expression and a significantly improved coagulative phenotype.

34 ng the vasculature from pro-inflammatory and coagulative stresses.

35 C death after adjusting for nuclear grade or coagulative tumor necrosis.