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1 cytosis and megakaryocytic atypia but normal platelet number.
2 ne (Mpl), is the major cytokine regulator of platelet number.
3 ocytopoiesis, resulting in normal peripheral platelet number.
4 namic responses, or changes in leukocyte and platelet number.
5 omes fully penetrant below 10% of the normal platelet number.
6 s in the marrow and consequently circulating platelet numbers.
7 , decreased NF-E2 expression, and normalized platelet numbers.
8  Ca(2+) increases and influences circulating platelet numbers.
9 ytes led to clinically relevant increases in platelet numbers.
10 )/Fli1(DeltaCTA) homozygous mice has reduced platelet numbers.
11  to achieve clinically relevant increases in platelet numbers.
12 d neutropenia, but no changes in circulating platelet numbers.
13 n of the S1P(1) receptor altered circulating platelet numbers acutely, suggesting a potential therape
14 atelets/nL, but it is not entirely clear how platelet numbers affect hemostasis and occurrence of thr
15                                              Platelet numbers also increase during ex vivo storage.
16 ced a marked and dose-dependent elevation in platelet number and a moderate increase in mean platelet
17 te ploidy, and moderate increases in resting platelet number and platelet recovery following a thromb
18 profiles with only mild, isolated changes in platelet number and two cytokines.
19                                              Platelet number and volume are independent risk factors
20       Homozygotes show a 20-fold decrease in platelet numbers and a 3-fold increase in platelet size
21 ditary platelet disorders typified by normal platelet numbers and a prolonged bleeding time.
22                Concurrent with a decrease in platelet numbers and an increase in circulating monocyte
23 ve decreased peripheral blood lymphocyte and platelet numbers and developed chronic colitis.
24  therapeutic targets in the normalization of platelet numbers and function in diabetes.
25 g often reveals a range of changes affecting platelet numbers and function, procoagulant or anticoagu
26 aracterized by thrombocytopenia with reduced platelet numbers and functions, and a tendency to develo
27 nthesis and degradation and their effects on platelet numbers and megakaryocyte function.
28 -/-) mice show intact proplatelet formation, platelet numbers and shape, and marginal MT bands; thus,
29  new therapeutic strategies to modulate both platelet numbers and their thrombogenicity.
30 ly with IL-1B expression and positively with platelet numbers and trophoblast proliferation in human
31 tations, such as thrombocytopenia (i.e., low platelet numbers) and anemia.
32 H becomes probabilistic at 40% of the normal platelet number, and that ICH becomes fully penetrant be
33 coagulation, including fibrinogen levels and platelet numbers, and cellular constituents of blood, su
34 ignificant decrease of CRP levels, increased platelet numbers, and clinically decreased bleeding seve
35  erythroblast proliferation, whereas reduced platelet numbers are associated with impaired platelet s
36                        At the same time that platelet numbers are increased, the mean platelet volume
37 quency, especially due to the measurement of platelet number as part of routine blood testing.
38        The mutant mice have markedly reduced platelet numbers, associated with deregulated megakaryoc
39 n the mean corpuscular hemoglobin (MCHC) and platelet number at day 10 and white blood cell count at
40 yte potential, c-myb-null fetuses had normal platelet numbers at E12.5 but became thrombocytopenic by
41 lls or white blood cell differential counts, platelet number, bleeding time, hemoglobin, hematocrit,
42 equired for the control of megakaryocyte and platelet number but not for their maturation.
43 fied MK miR-125a-5p as associated with human platelet number but not leukocyte or hemoglobin levels.
44 micrograms/kg/d) had accelerated recovery of platelet numbers compared with BMT mice treated with car
45                                  Thereafter, platelet number declined and returned to baseline by day
46                                        Human platelet numbers decreased from 102 +/- 33 at beginning
47 n, we sought to determine whether decline in platelet number during acute infection results from decr
48 t activity may be of greater importance than platelet number for clot integrity.
49 prothombin time) remained normal until after platelet numbers had declined significantly, arguing aga
50 e by day 2-4 after infection) in circulating platelet number in both C3H/HeN and C57BL/6J mice during
51 een any of the groups, with the exception of platelet number in the control group (P = 0.004).
52        Levels of all 3 microRNAs depended on platelet numbers in a platelet spike-in experiment but w
53 ts inhibited MkP differentiation and reduced platelet numbers in blood.
54  showed that loss of PTIP leads to decreased platelet numbers in mice.
55          The deletion of Stat3 increased the platelet numbers in SclCre;V617F;Stat3(fl/fl) mice compa
56 les may have clinical efficacy for improving platelet numbers in thrombocytopenic patients.
57 EGFR1, but not VEGFR2, increases circulating platelet numbers in vivo.
58                                  The smaller platelet number increase on day 5 after daily dosing ref
59 telet production; its key role in control of platelet number is via generation and stimulation of the
60 a new rupture mechanism, which yields higher platelet numbers, occurs independently of the key regula
61 tivated B cells was reduced in patients with platelet numbers of < 50 x 10(9) cells/L (P = .001), ind
62 ation of 100 micrograms/kg produced a higher platelet number on day 5 than daily administration of 10
63 sence of TGFbeta1 in platelets did not alter platelet number or function but was associated with fast
64 ficant reduction in neutrophil, monocyte, or platelet numbers or hematocrit levels.
65                           Here, we show that platelet number, platelet activation and platelet aggreg
66 ial loads, GPVI-depleted mice showed reduced platelet numbers, platelet activation, and platelet-leuk
67 terized primarily by quantitative defects in platelet number, though with a variety demonstrating qua
68 mouse lung vasculature generates substantial platelet numbers, up to 3000 per megakaryocyte.
69                                Variations in platelet number, volume, and function are largely geneti
70 karyocyte, a greater than 3-fold increase in platelet number was consistently observed in c-Myc(-/-)
71 on of 25 or 250 micrograms/kg of PEG-rmMGDF, platelet number was first increased on day 3 and peaked
72 ls and red blood cell, white blood cell, and platelet numbers were also substantially heritable, with
73    Thymic cellularity, blood hematocrit, and platelet numbers were not affected.
74  was accompanied by a 48 to 64% reduction in platelet number, whereas pony 613 did not develop fever