ライフサイエンスコーパス: hemosiderin

1 tin, and red blood cell lysate (representing hemosiderin).

2 big granular, irregular, and brown pigments (hemosiderin).

3 ells, and dermal deposition of periostin and hemosiderin.

4 epatocytes that contained greater amounts of hemosiderin.

5 treatments, exhibited increased deposits of hemosiderin.

6 as due to ferritin; there was no evidence of hemosiderin, a ferritin decomposition product.

7 no abnormal susceptibility and contained no hemosiderin at tissue analysis.

8 ses and a striking increase in the number of hemosiderin-containing macrophages is observed associate

9 sions (ARIA-E) and ARIA-microhemorrhages and hemosiderin deposition (ARIA-H) were higher with donanem

10 th edema/effusion (ARIA-E) and/or hemorrhage/hemosiderin deposition (ARIA-H).

11 -type levels) exhibited a similar pattern of hemosiderin deposition and fibrosis in their hearts.

12 d a selective heart defect that consisted of hemosiderin deposition and fibrosis.

13 mosiderinuria associated with marked tubular hemosiderin deposition and HO-1 induction, while there w

14 The goal of this study is to quantify hemosiderin deposition in the knee joint tissues of hemo

15 This destructive process is characterized by hemosiderin deposition in the superficial and deeper lay

16 In two of 27 cases, parenchymal hemosiderin deposition led to an increase in LAI into th

17 y those with both fatty liver and coexistent hemosiderin deposition or radiologically occult diffuse

18 id level, incomplete hypointense ring due to hemosiderin deposition, pseudotumor-like growth, pseudoc

19 ceptor expression and increased splenic iron/hemosiderin deposition.

20 racteristics of human CCM lesions, including hemosiderin deposits, immune cell infiltration, increase

21 e termed ARIA-E, whereas those consisting of hemosiderin deposits, including parenchymal microhemorrh

22 nomenon, distended vessels, damaged vessels, hemosiderin deposits, vessel tortuosity, and microaneury

23 load may cause change in some liver markers (hemosiderin depots, apoptosis index and GPx) and blood l

24 nd ALT; (5) liver histology (histopathology, hemosiderin depots, apoptosis index; (6) liver fatty aci

25 g concomitant Abeta immunohistochemistry and hemosiderin detection.

26 itochondrial and blood doublets and included hemosiderin features.

27 Hemosiderin foci on brain magnetic resonance imaging wer

28 The macrophages stain for hemosiderin, indicating that diffuse alveolar hemorrhage

29 models could be differentiated according to hemosiderin iron accumulation-both in tumors and systemi

30 Routine detection of hemosiderin iron aggregates in macrophages in other sett

31 n of LysM-Atg5-/- mice, correlating with low hemosiderin iron storage, as well as in erythrophagocyti

32 r growth in mouse models while also reducing hemosiderin iron-laden TAM accumulation as measured by b

33 rogressively bloodier return and/or over 20% hemosiderin-laden macrophages in diffuse alveolar hemorr

34 the presence of erythrocyte infiltrates and hemosiderin-laden macrophages in the lung tissue.

35 Hemosiderin-laden macrophages were abundant in the lungs

36 car and reactive changes, mainly presence of hemosiderin-laden macrophages.

37 Furthermore, hemosiderin-laden trophoblasts were more frequent in the

38 nion exchange) and Mallory's stain for iron (hemosiderin), markers of previous intraplaque hemorrhage

39 uggested that the predominant iron in PSP is hemosiderin, not ferritin.

40 While taking gantenerumab, ARIA-E and ARIA-hemosiderin occurred in 24.9% (247 of 993) and 22.9% (22

41 r Development Index score (P=0.02) and brain hemosiderin (P=0.04) remained significantly associated w

42 the putamen consistent with accumulation of hemosiderin (posterior portion) and neuromelanin (remain

43 ges all decreased over time, suggesting that hemosiderin products undergo continued, subtle evolution

44 Reliable hemosiderin quantification in joint tissues of HA patien

45 It lacks the "hemosiderin rim" of cavernous angioma and demonstrates i

46 , hemorrhage, fibrohistiocytic reaction with hemosiderin, sclerosis or fibrosis, and sclerohyalinosis

47 , hemorrhage, fibrohistiocytic reaction with hemosiderin, sclerosis or fibrosis, which were also expr

48 ophagocytic macrophages, autophagy regulates hemosiderin storage mechanisms as well as degradation of

49 The formation of hemosiderin was also observed.