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1 ne (Mpl), is the major cytokine regulator of platelet number.
2 ocytopoiesis, resulting in normal peripheral platelet number.
3 namic responses, or changes in leukocyte and platelet number.
4 cytosis and megakaryocytic atypia but normal platelet number.
5 s in the marrow and consequently circulating platelet numbers.
6 , decreased NF-E2 expression, and normalized platelet numbers.
7 Ca(2+) increases and influences circulating platelet numbers.
8 ytes led to clinically relevant increases in platelet numbers.
9 )/Fli1(DeltaCTA) homozygous mice has reduced platelet numbers.
10 to achieve clinically relevant increases in platelet numbers.
11 d neutropenia, but no changes in circulating platelet numbers.
12 n of the S1P(1) receptor altered circulating platelet numbers acutely, suggesting a potential therape
13 atelets/nL, but it is not entirely clear how platelet numbers affect hemostasis and occurrence of thr
15 ced a marked and dose-dependent elevation in platelet number and a moderate increase in mean platelet
16 te ploidy, and moderate increases in resting platelet number and platelet recovery following a thromb
23 g often reveals a range of changes affecting platelet numbers and function, procoagulant or anticoagu
24 aracterized by thrombocytopenia with reduced platelet numbers and functions, and a tendency to develo
25 -/-) mice show intact proplatelet formation, platelet numbers and shape, and marginal MT bands; thus,
28 coagulation, including fibrinogen levels and platelet numbers, and cellular constituents of blood, su
29 ignificant decrease of CRP levels, increased platelet numbers, and clinically decreased bleeding seve
30 erythroblast proliferation, whereas reduced platelet numbers are associated with impaired platelet s
34 yte potential, c-myb-null fetuses had normal platelet numbers at E12.5 but became thrombocytopenic by
35 lls or white blood cell differential counts, platelet number, bleeding time, hemoglobin, hematocrit,
37 micrograms/kg/d) had accelerated recovery of platelet numbers compared with BMT mice treated with car
40 n, we sought to determine whether decline in platelet number during acute infection results from decr
42 prothombin time) remained normal until after platelet numbers had declined significantly, arguing aga
43 e by day 2-4 after infection) in circulating platelet number in both C3H/HeN and C57BL/6J mice during
50 telet production; its key role in control of platelet number is via generation and stimulation of the
51 a new rupture mechanism, which yields higher platelet numbers, occurs independently of the key regula
52 tivated B cells was reduced in patients with platelet numbers of < 50 x 10(9) cells/L (P = .001), ind
53 ation of 100 micrograms/kg produced a higher platelet number on day 5 than daily administration of 10
55 ial loads, GPVI-depleted mice showed reduced platelet numbers, platelet activation, and platelet-leuk
57 karyocyte, a greater than 3-fold increase in platelet number was consistently observed in c-Myc(-/-)
58 on of 25 or 250 micrograms/kg of PEG-rmMGDF, platelet number was first increased on day 3 and peaked
59 ls and red blood cell, white blood cell, and platelet numbers were also substantially heritable, with
61 was accompanied by a 48 to 64% reduction in platelet number, whereas pony 613 did not develop fever
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