ライフサイエンスコーパス: platelet production

1 es megakaryocyte proliferation and increased platelet production.

2 ccelerated platelet destruction and impaired platelet production.

3 xtensions, which serve as assembly lines for platelet production.

4 mulates thrombopoiesis, leading to increased platelet production.

5 15d-PGJ(2)), increases Meg-01 maturation and platelet production.

6 lcysteine (NAC) attenuate 15d-PGJ(2)-induced platelet production.

7 celerated platelet destruction and decreased platelet production.

8 uding IFN-gamma, stimulate megakaryocyte and platelet production.

9 n, this mechanism may contribute to impaired platelet production.

10 s that regulate megakaryopoiesis and lead to platelet production.

11 dy-mediated platelet destruction and reduced platelet production.

12 n procoagulant activity, and does not effect platelet production.

13 Runx1 excision also resulted in inefficient platelet production.

14 xtensions, which serve as assembly lines for platelet production.

15 il and discuss several disorders that affect platelet production.

16 ine regulating megakaryocyte development and platelet production.

17 Cs) promote thrombopoietin (TPO)-independent platelet production.

18 es suggest that autoantibody may also affect platelet production.

19 but may also contribute to the inhibition of platelet production.

20 mbopoietin (TPO) is the primary regulator of platelet production.

21 albumin-(serotonin)(6) conjugate during COAT-platelet production.

22 odel to study human megakaryocytopoiesis and platelet production.

23 ITP patients there is an overall decrease in platelet production.

24 r regulator of megakaryocyte development and platelet production.

25 endothelial cell layers results in increased platelet production.

26 primary regulator of megakaryocyte (MK) and platelet production.

27 -linear increases in megakaryocytopiesis and platelet production.

28 equired for megakaryocyte differentiation or platelet production.

29 , increased Mk survival, and higher rates of platelet production.

30 TA-1 influences megakaryocyte maturation and platelet production.

31 of single versus daily dosing in stimulating platelet production.

32 tegrins may have a role in MK maturation and platelet production.

33 is a primary regulator of megakaryocyte and platelet production.

34 ocytopenia is associated with suppression of platelet production.

35 has profoundly changed our understanding of platelet production.

36 tors of all lineages and greatly accelerates platelet production.

37 as the major regulator of megakaryocyte and platelet production.

38 uration, should lead to an increased rate of platelet production.

39 hat TPO is not critical to the final step of platelet production.

40 11 (IL-11) is a growth factor that increases platelet production.

41 PO) is the physiologic Mpl-ligand regulating platelet production.

42 ncipal regulator of megakaryocytopoiesis and platelet production.

43 has been shown to be the major regulator of platelet production.

44 egakaryocyte proliferation, endomitosis, and platelet production.

45 of hematopoiesis, megakaryocytopoiesis, and platelet production.

46 ll specifically amplified the MK lineage and platelet production.

47 and abnormal thrombopoiesis and for in vitro platelet production.

48 h clonal and nonclonal disorders of enhanced platelet production.

49 ene could be important for the regulation of platelet production.

50 y promotes megakaryocyte differentiation and platelet production.

51 n (TPO) mRNA and protein, thereby regulating platelet production.

52 d intermediate stage in the final process of platelet production.

53 the study of pathologic mechanisms of human platelet production.

54 MKs with low nuclear ploidy and to decreased platelet production.

55 did not interfere with MK differentiation or platelet production.

56 s is crucial for normal megakaryopoiesis and platelet production.

57 n live-cell microscopy and quantification of platelet production.

58 t is not clear how the proteasome influences platelet production.

59 reveal a profound role for Wnt signaling in platelet production.

60 -mediated platelet destruction and decreased platelet production.

61 othrombotic events associated with increased platelet production.

62 on megakaryocyte survival, development, and platelet production.

63 mbrane and cytoskeletal remodeling affecting platelet production.

64 ealing potential strategies toward enhancing platelet production.

65 poptotic caspase cascade is not required for platelet production.

66 ide insights into the terminal mechanisms of platelet production.

67 platelet destruction and reduced bone marrow platelet production.

68 mbopoiesis during stress-induced accelerated platelet production.

69 in clinical development for cancer, affects platelet production.

70 ration and polyploidization are critical for platelet production; abnormalities in these processes ar

71 ombopoietin (TPO), the critical regulator of platelet production, acts by binding to its cell surface

72 le cellular and molecular targets to enhance platelet production after bone marrow transplantation or

73 rombopoietin (TPO), the primary regulator of platelet production, also plays an important role in hem

74 rrow has been proposed to be a major site of platelet production, although there is indirect evidence

75 hrombocytopenia (ITP) results from decreased platelet production and accelerated platelet destruction

76 Because abnormal platelet production and activation have been implicated

77 Enhanced platelet production and activation may predispose to art

78 Platelet production and activation were measured in B6-L

79 deficiency is associated with both increased platelet production and activation.

80 lin and a few other proteins that may impact platelet production and activation.

81 een identified in which tumors can stimulate platelet production and activation; activated platelets

82 that one or more Cdkn2a transcripts modulate platelet production and activity in the setting of hyper

83 tify the lungs as a primary site of terminal platelet production and an organ with considerable haema

84 tent stimulators of megakaryocyte growth and platelet production and are biologically active in reduc

85 015), demonstrating the relationship between platelet production and destruction.

86 function as a chaperon for TGF-beta1 during platelet production and does not activate significant qu

87 cus may identify a gene product that affects platelet production and function and contributes to the

88 cyte growth and development factor regulates platelet production and function by stimulating endoredu

89 me (BCS), treatment directed toward altering platelet production and function may be more rational an

90 Changes in platelet production and function produced by PEG-rHuMGDF

91 define the regulatory role of Mpl ligand on platelet production and function we measured the effects

92 iverse aspects of megakaryocyte biology, and platelet production and function, culminating in thrombo

93 To establish the role of caspases in platelet production and function, we generated mice lack

94 , suggesting a major role of this isozyme in platelet production and function.

95 in cytoskeleton is a prerequisite for proper platelet production and function.

96 critical for megakaryocytopoiesis and normal platelet production and function.

97 ac1 and Cdc42 possess redundant functions in platelet production and function.

98 sulted in a defect in the terminal stages of platelet production and had a mild effect on platelet fu

99 e insights into the mechanisms that regulate platelet production and may aid in the development of st

100 system (DMS) provides a membrane reserve for platelet production and muscle transverse (T) tubules fa

101 nown link between hyperglycemia and enhanced platelet production and reactivity.

102 specifically stimulates megakaryopoiesis and platelet production and reduces the severity of thromboc

103 Mechanisms of platelet production and release by mammalian megakaryocy

104 Multifaceted and complex mechanisms control platelet production and removal in physiological and pat

105 biologically important for MK maturation and platelet production and support the importance of MT reg

106 thrombocytopenias due primarily to impaired platelet production and those due to acceleration of ran

107 In this study, neonatal platelet production and turnover were investigated in ne

108 se observations improve our understanding of platelet production and validate the study of proplatele

109 Whether hyperglycemia promotes platelet production and whether enhanced platelet produc

110 Inefficient platelet production and/or defective platelet function r

111 jor regulators of megakaryocyte development, platelet production, and function.

112 F on pharmacokinetics, megakaryocytopoiesis, platelet production, and platelet function were characte

113 Megakaryopoiesis, platelet production, and platelet lifespan were unpertur

114 poietic stimulation on megakaryocytopoiesis, platelet production, and platelet viability and function

115 Megakaryocyte mass, reflected in the rate of platelet production, appears to be the major determinant

116 topoiesis, the exact mechanisms and sites of platelet production are unknown.

117 ted changes have functional consequences for platelet production, as the movement of MKs away from th

118 t ABCG4, a close relative of ABCG1, controls platelet production, atherosclerosis, and thrombosis.

119 "barbell shapes" of the penultimate stage in platelet production, because addition of the tetramer-di

120 Platelet production begins with the extension of large p

121 oned and shown to regulate megakaryocyte and platelet production by activating the cytokine receptor

122 We hypothesized that CCL5 could regulate platelet production by binding to its receptor, CCR5, on

123 transplantation and may underlie inefficient platelet production by megakaryocytes derived from pluri

124 vers a dual role for Vps34 as a regulator of platelet production by MKs and as an unexpected regulato

125 Stimulation of platelet production by romiplostim may provide a new the

126 Stimulation of platelet production by thrombopoietin-receptor agonists

127 Megakaryocytopoiesis and platelet production can be assessed with reasonable accu

128 ereas quantitative or qualitative defects in platelet production can lead to inherited platelet disor

129 t survival, and that subsequently, increased platelet production compensated for ongoing platelet des

130 tes platelet production and whether enhanced platelet production contributes to enhanced atherothromb

131 ts may open new avenues for the treatment of platelet production disorders and help to explain the th

132 lood levels of TPO in patients with impaired platelet production due to aplastic anemia (AA) and with

133 ying impaired fetal megakaryocytopoiesis and platelet production following pregnancy complications ch

134 nt in facilitating proplatelet formation and platelet production from cultured megakaryocytes.

135 Frank with having proposed defective platelet production from megakaryocytes in ITP in 1915.

136 Thrombopoietin affects nearly all aspects of platelet production, from self-renewal and expansion of

137 The role of specific molecules in platelet production has been elucidated in greater detai

138 between altered cholesterol homeostasis and platelet production has not been explored.

139 an megakaryopoiesis, hereditary disorders of platelet production have confirmed contributions from th

140 the specific roles of these proteins during platelet production have not been established.

141 als using thrombopoietic agents to stimulate platelet production have shown favorable outcomes in ITP

142 in nonhuman primates, PEG-rHuMGDF increases platelet production in a linear log-dose-dependent manne

143 mbinant thrombopoietins (TPOs) could enhance platelet production in a variety of thrombocytopenic sta

144 dependent kinase phosphorylation and reduced platelet production in bone marrow chimeras.

145 ve been shown to be effective stimulators of platelet production in cancer patients.

146 gle dose, is a potent stimulus for prolonged platelet production in humans.

147 single intravenous dose potently stimulates platelet production in mice, challenging the need for it

148 n-based membrane skeleton in proplatelet and platelet production in murine megakaryocytes.

149 ditionally was able to effectively stimulate platelet production in normal mice.

150 akaryocytopoiesis and the means to stimulate platelet production in numerous clinical situations.

151 MGDF has potent stimulatory effects on platelet production in patients with chemotherapy-induce

152 hesis that G-CSF contributes to the residual platelet production in T(-) mice.

153 terleukin-6 (IL-6) and IL-11, did not induce platelet production in thrombocytopenic, TPO-deficient (

154 ploidy of megakaryocyte progenitor cells and platelet production in vitro and in vivo.

155 Analysis of platelet production in vitro reveals that FlnA-null MKs

156 tor that stimulates megakaryocytopoiesis and platelet production in vivo and promotes the development

157 alterations in megakaryocyte development or platelet production in vivo or in colony assays.

158 ed cells provided only delayed and transient platelet production in vivo, and no CFU-MK developed in

159 to be dispensable for mouse PPF in vitro and platelet production in vivo.

160 stimulates megakaryocytopoiesis in vitro and platelet production in vivo.

161 e bone marrow environment, thereby enhancing platelet production in vivo.

162 although the eltrombopag-induced increase in platelet production in WAS/XLT is less than in ITP, eltr

163 let mass turnover, a steady-state measure of platelet production, increased fivefold (P < 10(-4)).

164 y a significant acceleration and increase of platelet production, indicating that hGH may exert a com

165 tly increased and a compensatory increase in platelet production is not effective in many patients.

166 cell levels of all lineages are reduced, and platelet production is profoundly impaired.

167 emained unsatisfactory, particularly because platelet production is rarely observed.

168 destruction, and in a significant proportion platelet production is suboptimal.

169 iological effect on megakaryocytopoiesis and platelet production is unknown.

170 rombopoietin (TPO), the primary regulator of platelet production, is composed of an amino-terminal 15

171 being the primary physiological regulator of platelet production, it is now apparent that TPO also ac

172 gnaling in megakaryocytes is dispensable for platelet production; its key role in control of platelet

173 t CDKN2A deficiency predisposes to increased platelet production, leading to increased platelet activ

174 Platelet production, maintenance, and clearance are tigh

175 Stimulation of platelet production may be an effective treatment for th

176 el pathway by which megakaryocytopoiesis and platelet production may be regulated.

177 an important underlying cause for defects in platelet production, morphology, and function.

178 The primary physiologic regulator of platelet production, Mpl ligand, has recently been clone

179 Platelet production must be regulated to avoid spontaneo

180 Platelet production occurs after the formation of MK pro

181 ion, migration, and maturation of MKs before platelet production occurs.

182 ses) to determine the effects of stimulating platelet production on peripheral platelet concentration

183 l, accounting for approximately 50% of total platelet production or 10 million platelets per hour.

184 might be indicated in patients with impaired platelet production or increased platelet destruction, i

185 ined action of Rac1 and Cdc42 is crucial for platelet production, particularly by regulating microtub

186 ired for normal megakaryocyte maturation and platelet production partly because of regulation of cyto

187 Both hypercholesterolemia and increased platelet production promote atherothrombosis; however, a

188 hanisms through which thrombopoietin affects platelet production provide new insights into the interp

189 umption, lifespan dependent consumption, and platelet production rate may have caused the thrombocyto

190 first such interval defining the equilibrium platelet production rate.

191 owed that newborn and adult mice had similar platelet production rates, but neonatal platelets surviv

192 esponses, but the events that lead to mature platelet production remain incompletely understood.

193 le to insufficient compensatory expansion in platelet production resulting from HIV-impaired delivery

194 ecoding the pathways of megakaryopoiesis and platelet production should help revolutionize the manage

195 rculating platelets, results from inadequate platelet production, splenic platelet sequestration, or

196 Receptors linked to granulocyte or platelet production supported complete erythroid develop

197 To more definitively substantiate that platelet production takes place in the lungs, megakaryoc

198 indirect, noncytocidal suppressive effect on platelet production, the mechanism of which is unknown.

199 on, (b) identify a new intermediate stage in platelet production, the preplatelet, (c) delineate the

200 Although microtubules are known to regulate platelet production, the underlying mechanism of proplat

201 hese results demonstrate that NO facilitates platelet production, thereby establishing the essential

202 e mechanisms regulating megakaryopoiesis and platelet production (thrombopoiesis) are still incomplet

203 limit hypercholesterolemia-driven excessive platelet production, thrombosis, and atherogenesis, as o

204 m platelets is sufficient to drive increased platelet production through MK CCR5.

205 Here we used an in vitro model of murine platelet production to investigate a potential role for

206 as MK maturation, proplatelet formation, and platelet production under in vitro conditions were unaff

207 is equally, or more, effective at promoting platelet production under these experimental conditions.

208 developmental process critical for efficient platelet production via unknown mechanisms.

209 takes place in the lungs, megakaryocyte and platelet production was accelerated in mice by phlebotom

210 The idea that platelet production was defective in ITP was superseded

211 Moreover, platelet production was impaired in MKs in which down-re

212 Platelet production was maintained and platelet autoanti

213 Until recently, platelet production was the least understood aspect of b

214 association between NO-induced apoptosis and platelet production, we exposed Meg-01 cells to S-nitros

215 hich GPIbalpha-filamin interactions regulate platelet production, we manipulated the expression level

216 anding of the specific mechanisms regulating platelet production will yield strategies to treat patie

217 ed a marked stimulation of megakaryocyte and platelet production with no apparent adverse effects.

218 lopment of safe, small, molecules to enhance platelet production would be advantageous for the treatm