ライフサイエンスコーパス: marrow

1 (cholangiocytes) and the immune system (bone marrow).

2 be in the liver and spleen (besides the red marrow).

3 the presence of cytokeratin(+) cells in bone marrow.

4 ratio of immature Gr1(lo) cells in the bone marrow.

5 iginate from both the yolk sac (YS) and bone marrow.

6 [D485N] mice transplanted with WT mouse bone marrow.

7 rly release of classical monocytes from bone marrow.

8 identify B cell development stages in kidney marrow.

9 ndividual GMPs scattered throughout the bone marrow.

10 role in promoting ILC2 egress from the bone marrow.

11 ion and EMH but not HSC division in the bone marrow.

12 of early viral genes exclusively in the bone marrow.

13 oming and retention to the niche in the bone marrow.

14 egress of multiple myeloma PCs from the bone marrow.

15 from common lymphoid progenitors in the bone marrow.

16 homing of prostate cancer cells to the bone marrow.

17 It commonly metastasizes to the bone marrow.

18 ) had no malignant IGH sequences detected in marrow.

19 to ectopic platelet release within the bone marrow.

20 imited ability to repopulate from donor bone marrow.

21 ssential phenomena occurring within the bone marrow.

22 mobilized ILC2 progenitors to exit the bone marrow.

23 l stromal cells and cancer cells in the bone marrow.

24 r cells (MDSC) from precursors in mouse bone marrow.

25 ver (16.1%), brown adipose (29.7%), and bone marrow (32.9%)-and increases of 16.8-19.1% in seven test

26 strated increased [(18)F]-FDG uptake in bone marrow 4 days postinfection compared to surviving NHPs.

27 The ratio of mean tumor to bone marrow absorbed dose per unit administered activity of (

28 The tumor-to-dose-limiting-organ (bone marrow) absorbed dose ratio, that is, the therapeutic in

29 activity was associated with increased bone-marrow activity (r=0.47; p<0.0001), arterial inflammatio

30 Amygdalar activity, bone-marrow activity, and arterial inflammation were assessed

31 des osteoblasts, MMPs also give rise to bone marrow adipocytes and stromal cells in vivo.

32 s chromatography showed that isolated tibial marrow adipocytes contain the medium-chain fatty acids u

33 nd in vitro models of AML, we show that bone marrow adipocytes from the tumor microenvironment suppor

34 ing withdrawal of teriparatide therapy, bone marrow adipocytes increased dramatically in number.

35 old electron microscopy revealed that tibial marrow adipocytes show prominent expression of the UAG-a

36 he first description of AML programming bone marrow adipocytes to generate a protumoral microenvironm

37 ng characteristics, including increased bone marrow adiposity, decreased bone mass, and impaired MSC

38 sulting in osteopenia coupled with increased marrow adiposity.

39 Meanwhile, it also inhibited bone marrow adiposity.

40 e that classical monocytes emerge first from marrow, after a postmitotic interval of 1.6 d, and circu

41 ed unrelated (MUD) donor T-cell-replete bone marrow allografting, obviating the need for additional p

42 The ADC values of intact bone marrow and BMLs did not overlap.

43 romoted tumor cell dissemination in the bone marrow and enhanced osteolytic lesion formation, irrespe

44 on damage to critical organs, including bone marrow and kidney.

45 In contrast, the bone marrow and lymph nodes of nonsurvivors showed increased

46 ADC values were measured in intact bone marrow and major BMLs.

47 ishment of plasma cell niches in sorted bone marrow and rectal cell populations further supported thi

48 em cells (LSC) and their progenitors in bone marrow and relapse following treatment cessation.

49 assessed differentiation of B cells in bone marrow and spleen and analyzed their endosomal morpholog

50 strongly decreased Samd14 expression in bone marrow and spleen.

51 er, transplantation of donor Cdk5(-/-C) bone marrow and T cells dramatically reduced the severity of

52 cumulation of erythrocytic parasites in bone marrow and the spleen has been reported in cases of Plas

53 TBI) damages hematopoietic cells in the bone marrow and thymus; however, the long-term effects of irr

54 topoietic stem or progenitor cells from bone marrow and to sensitize cancer cells to conventional che

55 ation of colorectal cancer cells in the bone marrow and tumor-driven osteolytic lesion formation.

56 ing effects of mutant SAMD9 proteins in bone marrow and was associated with increased length of survi

57 t of ENPP1 selectively on generation of bone marrow as well as splenic LLPCs.

58 Among the seven centers, all used marrow aspirates as the starting material, but no two ce

59 tained from peripheral blood or through bone marrow aspirates, together with recent advances in cance

60 Bone marrow aspiration from the iliac crests and in vivo sent

61 nd a block in B cell development in the bone marrow at the small pre-B cell stage.

62 (n = 163) for the presence of abnormal bone marrow attenuation on VNCa images by using color-coded m

63 uctions in the number and proportion of bone marrow B-lymphoid progenitors.

64 The exchange of bone marrow between wild-type and MAP3K14(aly/aly) mice did n

65 After histologic analysis of the bone marrow biopsy specimen, diagnosis of Waldenstrom macrogl

66 nostic meaning of different patterns of bone marrow (BM) (18)F-FDG uptake in HL.

67 n receptor null) mice transplanted with bone marrow (BM) cells from Ncr1(iCre)R26R(lsl-)(DTA) , Noe,

68 Bone marrow (BM) chimera mice revealed that mucosal repair de

69 riptome and cytometry analyses in mixed bone-marrow (BM) chimeras.

70 Here we report that bone marrow (BM) Gr-1(lo) immature myeloid cells are responsi

71 e following hematopoietic stress, e.g., bone marrow (BM) injury, transplantation, or systemic infecti

72 These mice showed increased bone marrow (BM) levels of the protein dickkopf-1 (Dkk1), whi

73 Asxl2(-/-) mice have an increased bone marrow (BM) long-term haematopoietic stem cells (HSCs) a

74 by the active crosstalk with an altered bone marrow (BM) microenvironment.

75 tem and progenitor cells (HSPCs) in the bone marrow (BM) microenvironment.

76 nd/or paracrine Wnts emanating from the bone marrow (BM) niche.

77 ells (n = 8 patients) or unfractionated bone marrow (BM) or peripheral blood mononuclear cells (n = 1

78 ental microenvironmental determinant of bone marrow (BM) pathophysiology.

79 (HSCs) are mobilized from niches in the bone marrow (BM) to the blood circulation by the cytokine gra

80 istribution patterns, highest in blood, bone marrow (BM), or lymph nodes (LN), with the frequency and

81 types, including endothelial cells and bone marrow (BM)-derived cells.

82 stnatally in the prepuberty period from bone marrow (BM)-derived progenitors.

83 Evidence was presented that bone marrow (BM)-derived Sinusoidal endothelial cell PROgenit

84 Although the emergence of bone marrow (BM)-resident (p190)BCR-ABL-specific T lymphocyte

85 cular response and reducing the pool of bone marrow (BM)-resident long-lived PCs.

86 al compared with that seen in wild-type bone marrow (BM)-transplanted OS mice in peripheral blood and

87 of hematopoietic stem cells (HSCs) from bone marrow (BM).

88 T) may induce long-term toxicity to the bone marrow (BM).

89 sphamide was originally described using bone marrow (BM).

90 gnancy induced HSC proliferation in the bone marrow but not HSC mobilization.

91 efficiently reduce the clonogenicity of bone marrow cancer cells from patients with acute myeloid leu

92 ells, with negligible effects on normal bone marrow CD34(+) progenitors from healthy donors.

93 ffects of transplanted unmodified human bone marrow CD34+ (hBM34+) cells into symptomatic G93A mice t

94 Fc, or IL-2/Fc would enhance allogeneic bone marrow cell (BMC) engraftment and promote tolerance indu

95 in the aorta, draining lymph nodes, and bone marrow cell cultures, indicating that IRF5 maintains CD1

96 Clinical trials of bone marrow cell-based therapies after acute myocardial infar

97 tor family, is expressed in myeloid and bone marrow cells and was implicated as a checkpoint regulato

98 ere irradiated and given transplants of bone marrow cells from C57BL6 mice, with or without the S1P a

99 Bone marrow cells from CLP-treated mice had normal OC precurs

100 not present in nonmegakaryocytic hemopoietic marrow cells from the same patient.

101 d that of inflammatory macrophages from bone marrow cells leads to macrophage heterogeneity.

102 The bone marrow cells of Dnmt3a+/- mice had a subtle but statisti

103 eedback mechanism through which myeloid bone marrow cells restore quiescence of myeloid-biased HSCs,

104 rine context, silencing of AID in human bone marrow cells skews differentiation toward myelomonocytic

105 ed interaction network between multiple bone marrow cells that regulate different hematopoietic stem

106 ll lineage displayed a dysregulation of bone marrow cells with a rapid decline in population at midli

107 of myeloablated adult mice similarly to bone marrow cells.

108 it formation caused by RANKL-stimulated bone marrow cells.

109 of exosomes produced by GM-CSF-expanded bone marrow cells.

110 used adoptive transfer, transgenic, and bone marrow chimera approaches to show increased infiltration

111 Bone marrow chimera experiments indicated that the observed e

112 Consistent with this, bone marrow chimera studies show that aberrant Pkhd1 must be

113 thymic development in limited-dilution bone marrow chimeras and show that higher TCR avidity correla

114 ar MZ microenvironment, and analysis of bone marrow chimeras indicated that the MZ B cell development

115 Bone marrow chimeras showed that bone marrow-derived cells co

116 A-DR4-transgenic mice, MAIThighHLA-DR4+ bone marrow chimeras, and humanized NOD-scid IL-2Rgammanull m

117 ection, TLR2 knockout (TLR2KO)-->TLR2KO bone marrow chimeric mice exhibited increased bacterial burde

118 Bone marrow chimeric mice showed B cell intrinsic effect of E

119 eostasis, gammadeltaT17 cells emerge in bone marrow chimeric mice upon induction of skin inflammation

120 Using mixed bone marrow chimeric mice, we show that the impact of NKG2D d

121 KO control mice, but not in WT or DREAM bone marrow chimeric mice.

122 tissue, muscle osseous structures, and bone marrow, consistent with advanced melanoma.

123 c Ab-secreting cells in lymph nodes and bone marrow, correlating with low Ab titers.

124 mpling from ileum, rectum, lymph nodes, bone marrow, CSF, circulating CD4+ T cell subsets, and plasma

125 lls are co-cultured with GM-CSF derived bone marrow dendritic cells (G-BMDCs).

126 nced maturation and cytokine release of bone marrow dendritic cells in vitro.

127 Bone marrow derived mesenchymal stem cells (MSCs) are regular

128 e chondrogenic differentiation of human bone marrow derived SSCs.

129 eicosanoid production profiles between bone marrow-derived (BMDM) and peritoneal macrophages differe

130 ritical for protection from IRI through bone marrow-derived adenosine 2a receptors.

131 Interestingly, whereas donor T cell- or bone marrow-derived CD70 plays no role in GVHD, host-derived

132 Bone marrow chimeras showed that bone marrow-derived cells contributed to IL-1R-dependent barr

133 Bone marrow-derived circulating progenitor cells are involved

134 hat commonly used protocols to generate bone marrow-derived cultured dendritic cells yield a heteroge

135 Bone marrow-derived cultured mast cells (BMCMCs) and peritone

136 te-derived DCs and humanized TLR8 mouse bone marrow-derived DCs enabled benchmarking of the TLR8 agon

137 owed lower expression in ES-DCs than in bone marrow-derived DCs.

138 GE2 inhibits IL-27 production in murine bone marrow-derived DCs.

139 -6 and CD68), decreased accumulation of bone marrow-derived fibroblasts and TGF-beta expression.

140 e lineage-instructive signal in primary bone marrow-derived GM progenitors.

141 ologous (auto) versus allogeneic (allo) bone marrow-derived hMSCs in NIDCM.

142 Bone marrow-derived macrophage were polarized to an M2 phenot

143 ns of wild-type mice with Nrp1-depleted bone marrow-derived macrophages (BMDM) confers resistance to

144 ent RAW cells and primary PHD2 knockout bone marrow-derived macrophages (BMDM).

145 thway (IKKalpha/beta, NF-kappaB p65) in bone marrow-derived macrophages (BMDMs) from knockout mice.

146 In LPS/ATP-stimulated bone marrow-derived macrophages (BMDMs), CLIC1 or CLIC4 siRNA

147 observed by in vitro experiments, using bone marrow-derived macrophages and dendritic cells as respon

148 Marrow-derived macrophages are highly phagocytic, but wh

149 es and mROS expression in mock-infected bone marrow-derived macrophages but reduced caspase-dependent

150 Bone marrow-derived macrophages did not release NE in respons

151 e effects of estrogen are long-lasting; bone marrow-derived macrophages from ovariectomized mice impl

152 Our previous studies showed that bone marrow-derived macrophages from S100A4(-/-) mice exhibit

153 caspase-1 inhibitors or the infusion of bone marrow-derived macrophages genetically engineered to ove

154 CD44(+/+) murine bone marrow-derived macrophages produced higher TNF-alpha com

155 Ex vivo, TLR9(-/-) bone marrow-derived macrophages produced more A20 than WT cel

156 addition to CB3-infected NOD.Ncf1(m1J) bone marrow-derived macrophages rescued the inflammatory anti

157 ed in an analogous fashion using LPS in bone marrow-derived macrophages upon inhibition of caspases.

158 In SIRT3 knock-out bone marrow-derived macrophages, NLRP3 activation promoted ex

159 We have found that in murine bone marrow-derived macrophages, PGE2 via the cAMP/protein ki

160 Like bone marrow-derived macrophages, RNA editing in MG leads to o

161 Using bone marrow-derived mast cells (BMMCs), we tested the hypothe

162 erarchical clustering demonstrated that bone marrow-derived mast cells and BMBs shared specific activ

163 body of evidence has demonstrated that bone marrow-derived mesenchymal stem cells (BMSCs) showed gre

164 ein to responsive target cells, such as bone marrow-derived mesenchymal stem cells (BMSCs), remains c

165 Bone marrow-derived mesenchymal stem cells (MSC) have been pr

166 UC-MSCs in vitro, compared with bone marrow-derived mesenchymal stem cells, displayed a 55-fo

167 ts down-regulation (DR) in both ex vivo bone marrow-derived mesenchymal stromal cells (MSC) and in vi

168 then used for the batch transduction of bone marrow-derived mesenchymal stromal cells ex vivo, follow

169 Specifically, we demonstrate that bone marrow-derived monocytes and macrophages are essential f

170 Bone marrow-derived monocytes and macrophages were the predom

171 es (such as hematopoietic stem cells or bone marrow-derived MSC or dendritic cells) for optimization

172 hat lung regeneration is facilitated by bone-marrow-derived myeloid cells that are recruited to the l

173 properties for T2 - weighted MRI, with bone marrow-derived primary human mesenchymal stem cells (hMS

174 tients with CXCR4 mutations have higher bone marrow disease burden, and those with nonsense CXCR4 mut

175 syndromes (MDS) are a diverse group of bone marrow disorders and clonal hematopoietic stem cell diso

176 local expansion of metabolically active bone marrow documented by FDG uptake and with the number of R

177 clide therapy by reducing the liver and bone marrow doses as well as the effective dose.

178 Additionally, jagged-2 expressed in bone marrow ECs regulated HSPC cell cycle and quiescence duri

179 tic resonance (MR) imaging of transient bone marrow edema syndrome (TBMES) and avascular osteonecrosi

180 eater conspicuity of enthesopathic cysts and marrow edema.

181 progenitor cells in the adult mammalian bone marrow ensure blood cell renewal.

182 Mast cell (MC) progenitors leave the bone marrow, enter the circulation, and settle in the skin an

183 This defect was rescued by bone marrow exosomes from WT, but not miR-155(-/-), cells, su

184 of the short half-lives and suboptimal bone marrow exposure of the drugs.

185 2 siblings presenting with progressive bone marrow failure (BMF), immunodeficiency, and developmenta

186 mice resulted in acute lethality due to bone marrow failure and intestinal atrophy featuring stem and

187 y breast and ovarian cancers as well as bone marrow failure disorder Fanconi anemia (FA).

188 splantation (HCT) is curative for FA-related marrow failure or leukemia, but both radiation exposure

189 lder with thrombocytopenia secondary to bone marrow failure, requiring prophylactic platelet transfus

190 Bone marrow fibrosis (BMF) develops in various hematological

191 s, reduced disease burden, and reversed bone marrow fibrosis in vivo.

192 Bone marrow fibrosis is the result of a complex and not yet f

193 elets lacking alpha-granules and progressive marrow fibrosis.

194 a cells (LLPCs), which persisted in the bone marrow for several months after vaccination.

195 LOX was expressed by tumor cells in the bone marrow from colorectal cancer patients with bone metasta

196 Dead cells accumulated in bone marrow from lupus patients but not from nonautoimmune pa

197 GSNOR KO animals receiving WT bone marrow had significantly reduced survival following P. b

198 on, and EMH during pregnancy but normal bone marrow hematopoiesis and EMH in response to bleeding or

199 od parameters, leukocyte depletion, and bone marrow hypoplasia.

200 Increased bone marrow hypoxia is associated with increased recirculatio

201 c effects of sorafenib led to increased bone marrow hypoxia, which contributed to HIF-dependent BMX u

202 nfection and developed fewer spleen and bone marrow IgG plasma cells and memory B cells, compared wit

203 ible NPs containing RA can engraft into bone marrow in vivo in the proximity of other leukaemic cells

204 Furthermore, transplantation of WT bone marrow into miR-155KO mice mitigated this phenotype.

205 BI model better predicts the absence of bone marrow iron than SF concentration alone, and TBI can be

206 -echo (TSE) imaging in the detection of bone marrow lesions (BMLs) after knee trauma.

207 broblasts derived from hematopoietic or bone marrow lineages in hearts subjected to permanent left an

208 articular the potential contribution of bone marrow lineages to activated fibroblasts within the scar

209 epicardial origin and not derived from bone marrow lineages, endothelial-to-mesenchymal transition,

210 ENPP1) is preferentially upregulated in bone marrow LLPCs compared with their splenic short-lived cou

211 is, and mastocytosis skin as well as in bone marrow mast cells in patients with systemic mastocytosis

212 Thrombocytosis, bone marrow megakaryocytic proliferation, and presence of JAK

213 By profiling mRNA expression in the bone marrow mesenchymal progenitor cell line ST2, we discover

214 ase in bone formation and the number of bone marrow mesenchymal stem/stromal cells, likely due to dec

215 cell factor [SCF], ThPO, and IL-6) from bone marrow mesenchymal stromal cells (MSCs) in vitro.

216 , at least in part, to signals from the bone marrow microenvironment (BMM).

217 ytokines and related alterations of the bone marrow microenvironment are commonly found in SM.

218 The bone marrow microenvironment influences malignant hematopoies

219 een human prostate cancer cells and the bone marrow microenvironment mediate bone metastasis during p

220 ining immunological homoeostasis in the bone marrow microenvironment, both in physiological condition

221 y MM cells alone and in the presence of bone marrow microenvironment.

222 Negative marrow minimal residual disease was attained in 20 (80%)

223 ng target for the treatment of diabetic bone marrow mobilopathy and vascular disease.

224 Adult bone marrow monocytes can give rise to tissue-resident macrop

225 LV ejection fraction was similar in the bone marrow mononuclear cells (48.7%) and placebo groups (51.

226 gment-elevation myocardial infarctions, bone marrow mononuclear cells administration did not improve

227 himerism at single-cell resolution from bone marrow mononuclear cells isolated from transplant patien

228 -controlled trial comparing 150 million bone marrow mononuclear cells versus placebo in 120 patients

229 The test group received allogeneic bone marrow MSCs by intradiscal injection of 25 x 10 cells pe

230 Conditional depletion of Foxp1 in bone marrow MSCs led to premature aging characteristics, incl

231 In bone marrow MSCs, FOXP1 expression levels declined with age i

232 rs with HCT comorbidity index </= 4 and < 5% marrow myeloblasts pre-HCT were randomly assigned to rec

233 and repair of our bones are formed from bone marrow myeloid progenitor cells by a complex differentia

234 We propose that the bone marrow niche can be altered by anticancer therapeutics,

235 Thus, we show that WNT5A in the bone marrow niche is required to regenerate HSCs and leukemic

236 e, the clonal response of leukocytes in bone marrow of acute myeloid leukaemia (AML) patients, and th

237 vo and were detectable in the blood and bone marrow of patients who had a response and patients who d

238 Analyses of macrophages on soft (like marrow) or stiff (like solid tumors) collagenous gels de

239 In contrast to PCs in the bone marrow, PCs in the gut have been considered short lived.

240 en-specific plasma cells and long-lived bone marrow plasma cells was detected in the MNP boosted grou

241 licly available GEP data from patients' bone marrow plasma cells, with long-term follow-up and clinic

242 tion at sites of infection with that of bone marrow plasmablasts and plasma cells to control viremia

243 ast trafficking to and retention in the bone marrow play a previously unappreciated role in viral con

244 ion of LARP1 alone in human adult CD34+ bone marrow precursor cells leads to a reduction in 5'TOP mRN

245 Bone marrow progenitor analysis revealed depletion of hematop

246 Bone marrow reconstitutions showed that a lncRNA expressed ac

247 ging objectively identified subclinical bone-marrow recovery within 5 days of HSC infusion, which was

248 of vasculature in central and endosteal bone marrow regions.

249 y due to unwanted p53 activation in the bone marrow remains an unmet clinical challenge.

250 ation of myeloid differentiation in the bone marrow remains unknown.

251 lls, and osteoblastic cells, whereas central marrow remains vascularized and splenic vascular niches

252 ntification and tracking of subclinical bone-marrow repopulation in human beings and revealed new ins

253 from the serum by liver-, spleen-, and bone marrow-resident phagocytic cells.

254 hematocrit, splenomegaly, and increased bone marrow reticulin.

255 e also used targeted gene sequencing on bone marrow samples and investigated clonal evolution from cl

256 Analyses of pretreatment marrow samples revealed a trend for increased expression

257 In bone marrow samples, the microfluidic-based plasma cell count

258 Stromal cells in the bone marrow secrete a variety of cytokines that promote plasm

259 ts HSPC mobility and localization within the marrow space and thereby impairs proper lodgment into th

260 required for B cell development in the bone marrow, Spi1 (encoding PU.1) was conditionally deleted i

261 parative hepatogenic potential of human bone marrow stem cells (BMSC) with stem cells derived from hu

262 Rat bone marrow stem cells were mingled with silk hydrogels at th

263 In addition, the role of the bone marrow stroma in regulating clinical responses to DNA me

264 sion of osteopontin (OPN) in the murine bone marrow stroma is reduced.

265 ALL cell migration toward CXCL12 and beneath marrow stromal cells and reduced CD44 expression.

266 microscale cell assemblages of encapsulated marrow stromal cells cultured in microwells, osteogenic

267 intravenous injection of singly encapsulated marrow stromal cells into mice delays clearance kinetics

268 dothelialized channels lined with human bone marrow stromal cells, which adopt a mural cell-like phen

269 alginate and hyaluronic acid) and mouse bone marrow stromal cells.

270 ANG-(1-7) increased Slit3 levels in the bone marrow supernatants, which activated ROCK in LSK cells a

271 presence of cytokeratin(+) cells in the bone marrow, this MSC subpopulation could prove useful in det

272 sively impairs their homeostasis in the bone marrow through an unidentified mechanism.

273 Comparison of adult bone marrow to fetal liver lysates demonstrated developmental

274 Monocytes can mobilize from bone marrow, traffic to their required destination, and diffe

275 morphisms (SNPs) and outcomes after blood or marrow transplant (BMT) have been conducted.

276 it is possible to estimate dd-cfDNA in bone marrow transplant patients that are unrelated or that ar

277 ed to the Center for International Blood and Marrow Transplant Research or Eurocord and European Grou

278 DS AND Using genetic lineage tracing or bone marrow transplant, we found no evidence for collagen-pro

279 Functional Assessment of Cancer Therapy-Bone Marrow Transplant.

280 or Eurocord and European Group for Blood and Marrow Transplant.

281 However, LT is not curative and only bone marrow transplantation (BMT) can correct the underlying

282 Blood or marrow transplantation (BMT) is used with curative inten

283 injury model combined with irradiation, bone marrow transplantation and in vivo imaging, we show that

284 The combination of bone marrow transplantation and local muscle radiation protec

285 Bone marrow transplantation failed to rescue outgrowth.

286 Allogeneic bone marrow transplantation has been attempted in severely af

287 Finally, bone marrow transplantation studies were performed to define

288 lymerase chain reaction, and reciprocal bone marrow transplantation were used to evaluate the effect

289 After bone marrow transplantation, donor-derived immune cells can t

290 ods Within the European Society of Blood and Marrow Transplantation, we conducted a prospective, mult

291 matologic conditions, or solid-organ or bone marrow transplantation.

292 h in physiological conditions and after bone marrow transplantation.

293 t beds that could not be transferred by bone marrow transplantation.

294 resident monocytes are retained in the bone marrow vasculature, representing an important reservoir

295 e per unit administered activity to the bone marrow was 0.13, 0.086, 0.33, and 0.068 mGy/MBq after rh

296 rprisingly, the collapse of the Rev1Xpc bone marrow was associated with progressive mitochondrial dys

297 Bone marrow was the predominant stem cell source (n = 839; 84

298 T, spleen, mediastinal lymph nodes, and bone marrow were quantified by flow cytometry.

299 and B cells were also diminished in the bone marrow, whereas the number of CD8(+) T cells increased.

300 Bone marrow with </= 5% tumor involvement will be classified