ライフサイエンスコーパス: bone marrow

1 nd trafficking of white blood cells from the bone marrow.

2 fitness and are efficiently purged from the bone marrow.

3 and sialyl Lewis X to promote trafficking to bone marrow.

4 d MDSCs and increased these cells within the bone marrow.

5 ect engagement of myeloid progenitors in the bone marrow.

6 est uptake was always in spleen, followed by bone marrow.

7 eactive B-1 B cells by self-antigen in adult bone marrow.

8 later mixed with cells originating from the bone marrow.

9 nes, and single-cell RNA sequencing on whole bone marrow.

10 ating miR-210 was derived predominantly from bone marrow.

11 serum and IgG(+) antibody-secreting cells in bone marrow.

12 r 1 in FGF23-secreting cells in the bone and bone marrow.

13 ow that TBI places significant stress on the bone marrow.

14 travital imaging approaches in the calvarial bone marrow(3-5).

15 Clonality testing identified involvement of bone marrow, a site infrequently affected in this diseas

16 ie, lower resilience) associated with higher bone marrow activity (standardized beta [95% CI]: 0.192

17 MACE, and that it does so through decreased bone marrow activity and arterial inflammation.

18 ssion tomography/computed tomography; AmygA, bone marrow activity, and arterial inflammation were qua

19 Bone marrow adipocytes (BMAd) have recently been implica

20 DNA in the genome of hMSCs derived from the bone marrow, adipose tissue, and umbilical cord blood wi

21 Sequestration of HSPCs in bone marrow after SCI is linked to aberrant chemotactic

22 nt was a sustained molecular response in the bone marrow after this treatment.

23 n metastases to the brain, lungs, liver, and bone marrow, all derived from parental MDA-MB-231 triple

24 Here, gene expression profiling of the bone marrow along disease progression in a spontaneous m

25 vation of the NF-kappaB signaling pathway in bone marrow and BM-MSC of DeltaNC16A mice.

26 w relapse, isolated CNS relapse, or combined bone marrow and CNS relapse rates, or in toxicities obse

27 aracterization of the HSC state in the adult bone marrow and embryonic fetal liver, the mechanism of

28 nsing of peripheral cancer initiation by the bone marrow and hematopoietic adaptation to distant noxi

29 e rise to terminally differentiated cells in bone marrow and intestines.

30 gulators of transcripts downregulated in the bone marrow and involved in lymphoid differentiation and

31 Integration of bone marrow and peripheral blood precursor datasets iden

32 transplantation compared with haploidentical bone marrow and peripheral-blood transplantation (HR, 1.

33 ion of molecular and functional profiling of bone marrow and peritoneal cells provided a detailed roa

34 a rare disorder characterized by hypoplastic bone marrow and progressive pancytopenia.

35 e maintenance of immature gametocytes in the bone marrow and provide further insights on how Plasmodi

36 iption factors, reduces SAMD14 expression in bone marrow and spleen and is lethal in a hemolytic anem

37 iptional classifications, most homed HSCs in bone marrow and spleen became multipotent progenitors an

38 SiglecF(hi) neutrophils were absent from the bone marrow and spleen, indicating local acquisition of

39 matopoietic stem and progenitor cells in the bone marrow and stimulates granulopoiesis in a cell-auto

40 matopoietic stem and progenitor cells in the bone marrow and the production of proreparatory CD150(+)

41 y suppress the differentiation of ILC2s from bone marrow and thymic progenitors while promoting the d

42 (Mgat1) markedly reduced cellularity in the bone marrow and/or spleen and inhibited maturation of pr

43 ntrols the formation of blood vessels in the bone marrow, and also regulates the differentiation of r

44 poietic precursors were quantified in blood, bone marrow, and organs.

45 tic stem and progenitor cells (HSPCs) in the bone marrow are derived from a small population of hemog

46 eloid cells in peripheral blood, spleen, and bone marrow, as well as expansion of CD8 T cells, which

47 for microscopic analysis of blood smears and bone marrow aspirates.

48 ingly, success of either protocol required a bone-marrow-associated, radiation-sensitive cell populat

49 For this purpose, we developed a bone marrow-avid nanobiologic platform designed specific

50 Bone marrow biopsies from patients with multiple myeloma

51 Bone marrow biopsies were obtained 14-24 h after infusio

52 B and CD4 T cell responses are detectable in bone marrow (BM) and blood up to 20 years after vaccinat

53 f platelet alpha-granules, splenomegaly, and bone marrow (BM) fibrosis.

54 Bone marrow (BM) from the sick mice showed myeloid hyper

55 ogether with nonhematopoietic stromal cells, bone marrow (BM) immune cells with unique functions supp

56 al residual disease (MRD) status outside the bone marrow (BM) in patients with multiple myeloma (MM).

57 uggested that the hematopoietic niche of the bone marrow (BM) is a major reservoir for parasite repli

58 oietic stem/progenitor cells (HSPC) from the bone marrow (BM) is impaired in diabetes.

59 Bone marrow (BM) mesenchymal stem and progenitor cells (

60 r cells (HSPC) is tightly regulated by their bone marrow (BM) microenvironment (ME).

61 per positioning of B cell progenitors in the bone marrow (BM) microenvironment and their progression

62 atopoietic stem cells (HSCs) in their native bone marrow (BM) microenvironment remains controversial,

63 ic plasma cells (PCs) and CD4 T cells in the bone marrow (BM) of healthy young adults (n = 15) follow

64 Thus, extracellular environments such as the bone marrow (BM) plasma likely have unique metabolite pr

65 s required for PTH to increase the number of bone marrow (BM) regulatory T cells (Tregs).

66 iated humoral responses; however, long-lived bone marrow (BM) resident PCs (LLPCs) demonstrate therap

67 ematopoietic stem cells (HSCs) reside in the bone marrow (BM) stem cell niche, which provides a vital

68 ets, migrate from the endosteal niche of the bone marrow (BM) toward the vasculature, extending propl

69 ophages are depleted, and monocytes from the bone marrow (BM) traffic to the lungs along a CCL2/CCR2

70 (BCG) or beta-glucan reprograms HSCs in the bone marrow (BM) via a type II interferon (IFN-II) or in

71 te, and migratory behavior of eosinophils in bone marrow (BM), blood, lung, and bronchoalveolar lavag

72 Osteoclasts (OC) originate from either bone marrow (BM)-resident or circulating myeloid OC prog

73 tic stem and progenitor cells (HSPCs) in the bone marrow (BM).

74 es the increased risk of radiation injury to bone marrow-both direct suppression and stochastic effec

75 led the presence of SSCs not only within the bone marrow but also within the periosteum and growth pl

76 Mechanistically, stimulation of specific bone marrow cell populations in vivo using growth factor

77 umor cells enhances differentiation of mouse bone marrow cells and human PBMC into immunosuppressive

78 Cell Atlas Census of Immune Cells dataset of bone marrow cells and show that it substantially improve

79 studies demonstrated that LRG1 derived from bone marrow cells is required for normal wound healing,

80 Targeting senescence in the BMAd or other bone marrow cells may represent a novel therapeutic appr

81 ated wild-type recipients of PDIA6-deficient bone marrow cells, both in the absence or presence of co

82 rtially recapitulated in murine Dnmt3a (-/-) bone marrow cells.

83 Bone marrow chimera and adoptive transfer studies indica

84 Bone marrow chimera experiments showed that CD137L-defic

85 The construction of bone marrow chimera mice demonstrated that STAT6 KO in e

86 Bone marrow chimeras confirmed that vascular Nck1, but n

87 iNKT cells in bone marrow chimeras that reconstituted thymic cellulari

88 Using bone marrow chimeras, GILT expression in thymic epitheli

89 ed recovery in peripheral blood cell counts, bone marrow colony forming units, sternal cellularity an

90 is enriched in transcripts derived from the bone marrow compared to circulating cells.

91 Myeloid cells derived from bone marrow contribute to the formation of the premetast

92 In bone marrow, CSF1R-FRed was absent in lineage-negative h

93 In sections of bone marrow, CSF1R-FRed was also detected in osteoclasts

94 entatives from those isolated from blood and bone marrow cultures in southern India, over 26 years (1

95 nes on in vitro osteoclastogenesis in murine bone marrow cultures.

96 adiation-induced peripheral blood cytopenia, bone marrow damage as well as apoptosis in sternum was o

97 A late-stage bone marrow DC progenitor expressed low amounts of LIFR

98 cell population induced by Cbfb-MYH11 in the bone marrow, decreased and disappeared in Runx1f/fMx1-Cr

99 Generation of pDCs from bone marrow dendritic cell (DC) progenitors and their ma

100 HDM + DEP exposed bone marrow derived dendritic cells and IL33 pulsed BMDC

101 cell models indicating TNT functionality in bone marrow derived malignancies and their microenvironm

102 The immunomodulatory effects of bone marrow derived mesenchymal stem cells (MSCs) has be

103 have a limited life span with replacement by bone marrow derived monocytes.

104 Aim2(-/-), Casp1/11(-/-) and Asc(-/-) murine bone-marrow derived macrophages (BMDMs) were infected wi

105 we observed DNA methylation reprogramming in bone marrow-derived (BMD) monocytes as early as 4 days o

106 beneficial in ALSP by providing a supply of bone marrow-derived brain-engrafting myeloid cells with

107 Studying the differentiation dynamics of bone marrow-derived CD34+ cells into immature B cells in

108 Adoptive transfer of labeled bone marrow-derived cells validated the results in a mur

109 Historically, SSCs have been defined as bone marrow-derived cells with inconsistent characterist

110 sease development, CCL17 acts on CCR4(+) non-bone marrow-derived cells, and 3) for inflammatory pain

111 regulated CCR7 on Y. enterocolitica-infected bone marrow-derived DCs and purified MLN DCs, which may

112 In SPPL2a(-/-) bone marrow-derived DCs, Dectin-1 is redistributed to en

113 hermore, the compound was able to 1) inhibit bone marrow-derived dendritic cell-mediated T cell funct

114 In this study, we show that RSV-infected bone marrow-derived dendritic cells (BMDC) as well as pu

115 eta in lipopolysaccharide (LPS)-primed mouse bone marrow-derived dendritic cells (BMDC).

116 d type I interferon (IFN) responses in mouse bone marrow-derived dendritic cells (DCs).

117 licits a broadened immune responses in mouse bone marrow-derived dendritic cells (mBMDCs) and a syner

118 was also a poor stimulator of maturation of bone marrow-derived dendritic cells compared to E. coli

119 roblasts and prevented activation of primary bone marrow-derived dendritic cells ex vivo.

120 primary human foreskin fibroblasts or mouse bone marrow-derived dendritic cells infected with the pr

121 tion on both RAW264.7 macrophages and murine bone marrow-derived dendritic cells; we now show that SL

122 Interestingly, IL33 blockade did not affect bone marrow-derived expansion and local infiltration of

123 Bone marrow-derived hematopoietic stem/progenitor cells

124 Bone marrow-derived macrophage cultures from the Notch2(

125 ent livers enhanced macrophage activation in bone marrow-derived macrophage cultures.

126 Bone marrow-derived macrophages (BMDMs) are recruited to

127 We found that bone marrow-derived macrophages (BMDMs) from BTK-deficie

128 Mechanistic studies using bone marrow-derived macrophages (BMDMs) showed that LPS

129 ome and Ingenuity Pathway Analysis of murine bone marrow-derived macrophages after exposure to this v

130 MV treatment of bone marrow-derived macrophages and bone marrow progenit

131 Bone marrow-derived macrophages and dendritic cells, lam

132 t cytokine that prompts the proliferation of bone marrow-derived macrophages and granulocytes.

133 id compartments, causes long-term changes in bone marrow-derived macrophages by suppressing interleuk

134 This response was lost in bone marrow-derived macrophages from mice deficient in A

135 uce mTOR signalling in the microglia but not bone marrow-derived macrophages in both in vitro and in

136 arly, FENDRR overexpression in primary mouse bone marrow-derived macrophages increased mRNA expressio

137 le, if any, iRhom2 was detectable in mEFs or bone marrow-derived macrophages lacking ADAM17, suggesti

138 h MEK1/2 inhibitor U0126 or genetically with bone marrow-derived macrophages or DCs from Tpl2(-/-) mi

139 Coculture of bone marrow-derived macrophages with ERCs from DKO mouse

140 e protocol that details several in vitro (in bone marrow-derived macrophages) and in vivo (in mice) s

141 In mouse bone marrow-derived macrophages, heme induced HO-1, lipi

142 g pathways are delayed in P2-deficient mouse bone marrow-derived macrophages, mouse embryonic fibrobl

143 teraction was enhanced by LPS stimulation in bone marrow-derived macrophages.

144 RIM21 upon S Typhimurium infection of murine bone marrow-derived macrophages.

145 ace of lipopolysaccharide-stimulated primary bone marrow-derived macrophages.

146 ating factor)-induced activation of Rac1, in bone marrow-derived macrophages; (b) TRPV4 directly inte

147 e expression of IL-9 in murine Th9 cells and bone marrow-derived mast cells (BMMC).

148 Primary bone marrow-derived mast cells (BMMCs) and ECs from WT a

149 re measured after IgE crosslinking in murine bone marrow-derived mast cells and human cord blood-deri

150 ore, the associated morphological changes of bone marrow-derived mesenchymal stem cells (BM-MSC), and

151 Patient bone marrow-derived neutrophils and white blood cells sh

152 sistant multiple myeloma cells as well as on bone marrow-derived primary multiple myeloma cells from

153 RMs consist of embryo-derived (EMRMs) and bone marrow-derived RMs (BMRMs), but the fate, dynamics,

154 Our findings support that bone marrow-derived, presumably neutrophil, NGAL protect

155 M2 macrophage markers (Mrc1, Arg1, Il10) in bone-marrow-derived macrophages or in SAT from male or f

156 embryonic precursors and become replaced by bone-marrow-derived macrophages over time.

157 stem-native myeloid cells (CNS-myeloids) and bone-marrow-derived myeloid cells (BMDMs) cooperatively

158 Bone-marrow-derived progenitors actively engage DNA repa

159 globulin M declined from 3,520 to 821 mg/dL, bone marrow disease involvement declined from 60% to 20%

160 During granulopoiesis in the bone marrow, distinct neutrophil granules are successive

161 group, 23 of 40; control group, 60 of 100), bone marrow edema (39 of 40 vs 87 of 100), effusion (20

162 d a moderate specificity in the detection of bone marrow edema of the wrist.

163 nt readers for tenosynovitis, synovitis, and bone marrow edema.

164 d, we hypothesized that in some patients the bone marrow environment is not permissive to B-cell deve

165 , we showed that sympathetic nerves create a bone marrow environment that supports residence of hyper

166 ic defects and patients with a nonpermissive bone marrow environment.

167 lar (P < .01) locations, and associated with bone marrow eosinophilia (P < .01).

168 tion, mutational analysis for KIT D816V, and bone marrow evaluation to rule out a clonal mast cell di

169 Robust peripheral (bone marrow) expansion of eosinophils and local recruitm

170 Bone marrow failure (BMF) in Fanconi anemia (FA) patient

171 using a previously uncharacterized inherited bone marrow failure and pre-leukemic syndrome.

172 iamond Blackfan Anemia (DBA) is a congenital bone marrow failure syndrome associated with ribosomal g

173 our data suggest that SCI causes an acquired bone marrow failure syndrome that may contribute to chro

174 described and is a constitutional inherited bone marrow failure syndrome.

175 Inherited bone marrow failure syndromes (IBMFSs) are characterized

176 , 3 (3%) an innate immune defect, and 2 (2%) bone marrow failure.

177 l mice have FA-like abnormalities, including bone marrow failure.

178 tations in telomere biology genes leading to bone-marrow failure, these data provide evidence that ge

179 These cells reside in the bone marrow for prolonged periods and can be reactivated

180 Dendritic cells (DCs) develop in the bone marrow from haematopoietic progenitors that have nu

181 Bone marrow from WT and Esr1(-/-) female mice was transf

182 e hematopoietic cells, resulting in abnormal bone marrow function.

183 normally function to enforce self-renewal in bone marrow hematopoietic progenitors.

184 ential and cell surface marker expression as bone marrow hMSCs.

185 Glucocorticoids induced rapid bone marrow homing of eosinophils.

186 ells (pre-HSCs), fetal liver HSCs, and adult bone marrow HSCs.

187 des ago, high-risk NB metastatic to bone and bone marrow in children was not curable.

188 Finally, a higher proportion of bone marrow-infiltrating ICOShigh/PD-1- Treg cells is a

189 tions included hepatic, kidney, splenic, and bone marrow involvement, and microvascular injury and th

190 of patients, early B-cell development in the bone marrow is impaired.

191 exchange of mature B cells between blood and bone marrow is sensitive to small, physiologic changes i

192 trophy, oedema in peripheric soft tissue and bone marrow, joint effusion, or synovitis are more sever

193 elodysplastic syndrome (blast counts <20% in bone marrow), Karnofsky index of 60% or higher, and were

194 CI, -11.2 to 52.2]; P = .21), and changes in bone marrow lesion size (-33 mm2 vs -6 mm2; between-grou

195 Vertebral bone marrow lesions had a male predominance and there wa

196 zed mice, including the lymph nodes, thymus, bone marrow, liver and lung.

197 ope, to mitigate HIV-induced pathogenesis in bone marrow, liver, thymus (BLT) humanized mice.

198 n in the blood and tissues of ART-suppressed bone-marrow-liver-thymus (BLT) humanized mice and rhesus

199 ) enhances the immunosuppressive function of bone marrow Ly6C(high) myeloid cells.

200 n mediating RANKL-induced signaling in mouse bone marrow macrophages, known as osteoclast precursors.

201 matopoietic maintenance factor expression in bone marrow macrophages.

202 and restrains the osteoclastogenesis of rat bone-marrow macrophages (BMMs).

203 f our study was to identify and characterize bone marrow MC histopathologic features specific for MCA

204 agmentation of long membrane extensions from bone marrow megakaryocytes in the blood flow.

205 A first MI-induced bone marrow "memory" via a circulating signal, reducing

206 Bone marrow mesenchymal stem cell-derived extracellular

207 el incorporating ER+ breast cancer cells and bone marrow mesenchymal stem cells to represent DTCs in

208 Bone marrow mesenchymal stromal cells (MSCs) have been s

209 d strength, partly due to the dysfunction of bone marrow mesenchymal stromal/stem cells (MSCs) during

210 tumors, soft-tissue metastases, and bone or bone-marrow metastases was 72%, 33%, and 38%, respective

211 PET/CT in detecting soft-tissue and bone or bone-marrow metastases was 77% and 86%, respectively-sig

212 tumors, soft-tissue metastases, and bone or bone-marrow metastases was 83%, 50%, and 92%, respective

213 PET/CT in detecting soft-tissue and bone or bone-marrow metastases was 86% and 99%, respectively-sig

214 understanding of how cancer cells hijack the bone marrow microenvironment and demonstrates that tumor

215 pansion of the engrafted HSPC population and bone marrow microenvironment degradation caused by pre-t

216 It is clear that disruption of the normal bone marrow microenvironment is sufficient to promote le

217 as sensors of age-associated changes to the bone marrow microenvironment, and observe up-regulation

218 previously unknown heterogeneity within the bone marrow microenvironment, imposed by the stages of b

219 all occur within the context of a disrupted bone marrow microenvironment.

220 hat underpins both the healthy and malignant bone marrow microenvironment.

221 cs of glucocorticoid-induced eosinopenia and bone marrow migration were consistent with those of the

222 eripheral blood mononuclear cells (MNCs) and bone marrow MNCs was higher in patients with atheroscler

223 fter IR, as well as following G-CSF-mediated bone marrow mobilization, which was independent of C5aR1

224 Bone marrow mononuclear cells (BMNC) are a source of nai

225 r, treatment of primary peripheral blood and bone marrow mononuclear cells from pediatric B-ALL patie

226 y identified neutrophil subsets fit into the bone marrow neutrophil lineage remains unclear.

227 trophil subsets arise from distinct maturing bone marrow neutrophil subsets.

228 Splenic and bone marrow neutrophils (Nphs) from BAFF-RFP mice expres

229 esenchymal stem cells to represent DTCs in a bone marrow niche.

230 matopoietic survival and self-renewal in the bone marrow niche; how to apply this process to HSC main

231 he hope is that integrating knowledge of how bone marrow niches contribute to haematological disease

232 Progenitor cells are mobilized from bone marrow niches in response to remote ischemic injury

233 LT-HSCs are not found in bone marrow niches with the deepest hypoxia and instead

234 iated phenotypic alterations (MDS-PA) in the bone marrow of 285 patients with MM enrolled in the PETH

235 ved a total of 15 PSMA-positive spots in the bone marrow of 6 patients (22%).

236 MSCs isolated from bone marrow of wild type and Sdc3(-/-) mice were used to

237 cture), adoptive transfer of Pink1-deficient bone marrow or pharmacological inhibition of mitophagy p

238 aematological remission (blast counts <5% in bone marrow) or myelodysplastic syndrome (blast counts <

239 focus on existing and future therapies using bone-marrow- or stem-cell-derived cells for the treatmen

240 Importantly, the three-dimensional bone-marrow organization can be accurately inferred from

241 Masked central review of bone marrow pathology was done if available to confirm l

242 of ASL imaging to detect disease-associated bone marrow perfusion changes.

243 Bone marrow perfusion signal changed with the labeling s

244 labeling size, suggesting that the measured bone marrow perfusion signal is flow-associated.

245 evelopmental arrest of B cell progenitors in bone marrow; poly-reactivity of the VRC26UCA and poor pa

246 hat HIF activity is high in human and murine bone marrow pro-B and pre-B cells and decreases at the i

247 mmune response pathways and RTK signaling in bone marrow progenitors from mice with MLL1-rearranged A

248 n-of-function colony formation properties to bone marrow progenitors in medium containing limited gro

249 tment of bone marrow-derived macrophages and bone marrow progenitors promoted M2-like macrophage pola

250 y, the deficiency of TGF-beta receptor II in bone marrow progenitors results in inefficient developme

251 modulation of mature myeloid cells or their bone marrow progenitors, mediates sustained increased re

252 tro osteoclastogenesis from Fndc5-transgenic bone marrow progenitors.

253 Epicutaneous sensitization- and bone marrow reconstitution-based models of IgE-mediated

254 nces in the cumulative incidence of isolated bone marrow relapse, isolated CNS relapse, or combined b

255 B cells was dispensable for stability of the bone marrow-resident, long-lived plasma cell population,

256 nd early depletion of Vi-specific B cells in bone marrow, resulting in hyporesponsiveness and lack of

257 sponse, with single-cell analysis of primary bone marrow revealing perturbed UPR in myeloid precursor

258 lished phenotype of G-MDSCs was evaluated in bone marrow samples from controls and MM patients using

259 The bone marrow senses distant tissue transformation at prem

260 several organs in HIS mice including blood, bone marrow, spleen, and draining lymph nodes.

261 Bone marrow stem cell transplantation had not been acces

262 tremely useful, especially in the context of bone marrow stem cell transplantation where early reject

263 le able to prevent rejection of transplanted bone marrow stem cells in vivo by blocking perforin func

264 n and the eosinophil-directed bias of murine bone marrow stem cells, demonstrating an unexpected subt

265 a signalling-induced gene expression in aged bone marrow stroma.

266 revealed that the transmembrane glycoprotein Bone marrow stromal antigen 2 (Bst2) expression was redu

267 es were associated with modifications of the bone marrow stromal architecture through relocalization

268 Here we use bone marrow stromal cells as sensors of age-associated c

269 Mineralization of WT bone marrow stromal cells cultured with conditioned medi

270 granulopoiesis in DeltaNC16A mice is through bone marrow stromal cells evidenced by bone marrow trans

271 Bone marrow studies showed binucleated erythroblasts and

272 Bone marrow surveillance before myeloid malignancy diagn

273 alignancy and could have been monitored with bone marrow surveillance.

274 istent with enhanced egress of FA HSPCs from bone marrow to peripheral blood.

275 een in 27 patients; no patients had grade IV bone marrow toxicity.

276 s in Functional Assessment of Cancer Therapy-Bone Marrow Transplant (FACT-BMT) score relative to base

277 kinase (SR-uPA(+/0) mice) and of SR-uPA(+/0) bone marrow transplant recipients, and we used bioinform

278 ransplantation conditioning regimen prior to bone marrow transplant significantly increased the risk

279 A combination of pair-feeding, bone marrow-transplant, and microglial ablation implicat

280 CMV viremia in a Cynomolgus macaque model of bone marrow transplantation (BMT) for tolerance inductio

281 t mice, we tracked blood-borne miR-210 using bone marrow transplantation and parabiosis (conjoining o

282 Irradiation and bone marrow transplantation did not further affect body

283 Bone marrow transplantation experiments identify hematop

284 es of hematopoietic reconstitution following bone marrow transplantation provide a window of opportun

285 e utilized in modulation of HSC activity and bone marrow transplantation studies.

286 mised patients with blood disorders or after bone marrow transplantation to achieve antiviral control

287 trained granulopoiesis was transmissible by bone marrow transplantation to recipient naive mice.

288 hes were applied in AD+ mice: (i) ACE10/GFP+ bone marrow transplantation with head shielding; and (ii

289 el of GN was studied in AREG(-/-) mice after bone marrow transplantation, and in mice with myeloid ce

290 With bone marrow transplantation, circulating miR-210 was der

291 lication after peripheral blood stem cell or bone marrow transplantation, rarely occurs in kidney and

292 on criteria with a mean age of 13.4 years at bone marrow transplantation.

293 rough bone marrow stromal cells evidenced by bone marrow transplantation.

294 sed quiescence and increased HSC activity in bone marrow transplantation.

295 IV susceptibility in circulating T cells via bone marrow transplants allowed some individuals with HI

296 T cell leukemia (T-ALL) when induced in the bone marrow via Mx1CRE.

297 sociated lymphoproliferative disorder in the bone marrow was greatly increased by centralized biopsy

298 Bone marrow was microscopically free of disease, but mol

299 h, we systematically characterized the whole bone marrow (WBM) microenvironment during premalignant,

300 Heparinized venous blood and bone marrow were collected from the patient after obtain

301 ial potential during their maturation in the bone marrow, where they differentiate from hematopoietic

302 c rewiring of multipotent progenitors in the bone marrow, which overcomes the immunosuppressive tumor