ライフサイエンスコーパス: reticulin

1 lin and eosin (H&E), Masson's trichrome, and reticulin.

2 e lobulated and contained dense, centralized reticulin.

3 rit, splenomegaly, and increased bone marrow reticulin.

4 typia, absence of biliary epithelia, loss of reticulin, alteration of normal perivenular glutamine sy

5 by bone marrow megakaryocytic proliferation, reticulin and/or collagen fibrosis, and presence of JAK2

6 llelic burden was in patients with increased reticulin deposition.

7 im clinical trials, 10 were reported to have reticulin deposition; reticulin grade was increased in 4

8 onists are reported to increase the risk for reticulin fiber deposition within bone marrow.

9 v) of bFGF(+) MC and the density of collagen/reticulin fibers in silicotic nodules (rho = -0.80, p <

10 associated cells and the density of collagen/reticulin fibers in the hypocellular nodule centers (rho

11 rge, mature nodules, the density of collagen/reticulin fibers was higher, and bFGF(+) MC were found o

12 The V(v) of collagen/reticulin fibers was increased in silicosis and correlat

13 yh9(-/-) mice a much stronger increase in BM reticulin fibers was present after 4 weeks of romiplosti

14 +) MC throughout the loose array of collagen/reticulin fibers.

15 oplasia, and deposition of a fine network of reticulin fibers.

16 ntain abundant pericapillary and parenchymal reticulin fibrils, which were shown by immunohistochemis

17 features such as splenomegaly (P =.004) and reticulin fibrosis (P =.005).

18 as TAFRO (thrombocytopenia, ascites, fever, reticulin fibrosis and organomegaly) or POEMS (polyneuro

19 elevated leukocyte counts, splenomegaly, and reticulin fibrosis compared with C57Bl/6 mice.

20 sessable responders who started therapy with reticulin fibrosis grade 4 experienced reductions to at

21 ations in myeloid and erythroid lineages and reticulin fibrosis identified a subclinical myeloprolife

22 ence and prognostic relevance of bone marrow reticulin fibrosis in 526 patients with World Health Org

23 hematopoiesis resulting in splenomegaly, and reticulin fibrosis in the bone marrow.

24 tic/megakaryocytic proliferation and lack of reticulin fibrosis in the bone marrow.

25 egakaryocyte polyploidization; and increased reticulin fibrosis of the bone marrow and spleen.

26 ssified into iMCD-thrombocytopenia, ascites, reticulin fibrosis, renal dysfunction, organomegaly (iMC

27 se 2 features were inversely proportional to reticulin fibrosis, whereas increases in marrow angiogen

28 four patients (14%) displayed mostly grade 1 reticulin fibrosis, with only 2 cases showing higher-gra

29 s in marrow angiogenesis were independent of reticulin fibrosis.

30 including thrombocytopenia, anasarca, fever, reticulin fibrosis/renal dysfunction, and organomegaly.

31 Our results demonstrate that bone marrow reticulin grade at diagnosis represents an independent p

32 de showed significantly greater increases in reticulin grade compared with those allocated to hydroxy

33 In the prospective study, reticulin grade during romiplostim treatment remained wi

34 Reticulin grade often decreased soon after romiplostim d

35 Reticulin grade positively correlated with white blood c

36 were reported to have reticulin deposition; reticulin grade was increased in 4 of 5 patients with bo

37 Reticulin grade was the dominant independent predictor o

38 y, evaluation of bone marrow progenitors and reticulin in nonaffected family members of patients with

39 and produces modest increases in bone marrow reticulin in some ITP patients that decrease when therap

40 topathology including the increase in marrow reticulin is completely and rapidly reversible upon the

41 that those who show substantially increasing reticulin levels are at risk of myelofibrotic transforma

42 Higher reticulin levels at diagnosis were associated with great

43 Elevated reticulin levels at presentation predicted higher rates

44 anasarca, fever/elevated C-reactive protein, reticulin myelofibrosis, renal dysfunction, organomegaly

45 im-treated rats, a retrospective analysis of reticulin observed in romiplostim ITP clinical trials, a

46 patients who developed increased bone marrow reticulin on anagrelide showed regression of fibrosis wh

47 ary acidic protein-positive) or mesenchymal (reticulin-positive) differentiation.

48 iption factor 6, which, via induction of the reticulin protein Nogo, can lead to the disruption of th

49 ns include thrombosis, increased bone marrow reticulin, rebound worsening of thrombocytopenia upon di

50 , periodic acid-Schiff, Masson trichrome, or reticulin stains.

51 Bone marrow reticulin was observed in 8 patients; marrows were not r