ライフサイエンスコーパス: granulocytosis

1 lymphocyte reductions to support a reactive granulocytosis.

2 iated by the concomitant induction of marked granulocytosis.

3 ce characterized by massive splenomegaly and granulocytosis.

4 d myelopoiesis leading to thrombocytosis and granulocytosis.

5 rapid development of hepatosplenomegaly and granulocytosis.

6 tor (G-CSF), a principal cytokine-regulating granulocytosis.

7 2 deficient mice succumbed from overwhelming granulocytosis.

8 [15%]), thrombocytopenia (47/104 [45%]), and granulocytosis (44/104 [42%]).

9 of Sema3E in mice results in increased lung granulocytosis, airway hyperresponsiveness, mucus overpr

10 SCID and NOD-SCID mice exhibited also granulocytosis and increased numbers of hemopoietic prog

11 of ILCs prevented IL-17- and G-CSF-dependent granulocytosis and resistance to sepsis.

12 many proinflammatory cytokines, resulting in granulocytosis and severe sterile inflammation.

13 Granulocytosis and splenomegaly developed in mice that r

14 d by myeloid hyperplasia, including profound granulocytosis and splenomegaly.

15 splenomegaly, extramedullary erythropoiesis, granulocytosis and thrombocytopaenia secondary to a bloc

16 However, these animals did develop mild granulocytosis compared with mice reconstituted with WT

17 f human PV, characterized by erythrocytosis, granulocytosis, extramedullary hematopoiesis, and bone m

18 %), and when present, was accompanied by BAL granulocytosis in 75% of children.

19 tion, presumably accounting for the reactive granulocytosis in diseased mice.

20 mulating factor (G-CSF) as a means to induce granulocytosis in donors has rekindled interest in this

21 These data suggest that erythrocytosis and granulocytosis in JAK2(V617F) mice are the net result of

22 CD97 null mice also displayed a mild granulocytosis in the nonchallenged state.

23 myeloid colony-forming activity, and marked granulocytosis in the peripheral blood.

24 testinal tissues, characterized by pulmonary granulocytosis, increased Th2/Th1 T cell ratios in trach

25 a strongly argue against the clinical use of granulocytosis-inducing hematopoietic stem cell mobiliza

26 r the intestinal microbiota in regulation of granulocytosis, neutrophil homeostasis and host resistan

27 eated with G-CSF showed less than 50% of the granulocytosis observed in identically treated WT mice.

28 These observations suggest that the granulocytosis observed in the absence of CD18 occurs th

29 ytic dysplasia, and a propensity for chronic granulocytosis; phenotypes that closely resemble those o

30 CD97 deficiency did not appear to stimulate granulocytosis secondary to peripheral inflammation and

31 Splenomegaly was prevented and granulocytosis was inhibited by more than 95% in mice th

32 mia, and Icsbp(-/-) mice exhibit progressive granulocytosis with evolution to blast crisis, similar t

33 es death of all animals from an overwhelming granulocytosis within 3 to 4 weeks.