ライフサイエンスコーパス: marrow

1 afficking of white blood cells from the bone marrow.

2 ess and are efficiently purged from the bone marrow.

3 ialyl Lewis X to promote trafficking to bone marrow.

4 Cs and increased these cells within the bone marrow.

5 ngagement of myeloid progenitors in the bone marrow.

6 ptake was always in spleen, followed by bone marrow.

7 nimal residual disease in both the blood and marrow.

8 ve B-1 B cells by self-antigen in adult bone marrow.

9 r mixed with cells originating from the bone marrow.

10 and single-cell RNA sequencing on whole bone marrow.

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

12 n FGF23-secreting cells in the bone and bone marrow.

13 at TBI places significant stress on the bone marrow.

14 -DOTA-BC8 were 0.35 +/- 0.20 cGy/MBq for red marrow, 0.80 +/- 0.24 cGy/MBq for liver, 3.0 +/- 1.4 cGy

15 tal imaging approaches in the calvarial bone marrow(3-5).

16 llowed by ovaries (1.15E-03 mSv/MBq) and red marrow (8.49E-04 mSv/MBq).

17 ality testing identified involvement of bone marrow, a site infrequently affected in this disease.

18 e model of anaphylaxis that does not require marrow ablation or human tissue implantation.

19 ower resilience) associated with higher bone marrow activity (standardized beta [95% CI]: 0.192 [0.03

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

21 tomography/computed tomography; AmygA, bone marrow activity, and arterial inflammation were quantifi

22 The marrow adipocyte also has an endocrine role in whole bod

23 Bone marrow adipocytes (BMAd) have recently been implicated i

24 in numbers of osteoblasts, osteoclasts, and marrow adipocytes in Tg mice, suggesting independence of

25 in the genome of hMSCs derived from the bone marrow, adipose tissue, and umbilical cord blood without

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

27 s a sustained molecular response in the bone marrow after this treatment.

28 astases to the brain, lungs, liver, and bone marrow, all derived from parental MDA-MB-231 triple-nega

29 Here, gene expression profiling of the bone marrow along disease progression in a spontaneous model

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

31 apse, isolated CNS relapse, or combined bone marrow and CNS relapse rates, or in toxicities observed

32 erization of the HSC state in the adult bone marrow and embryonic fetal liver, the mechanism of HSC s

33 of peripheral cancer initiation by the bone marrow and hematopoietic adaptation to distant noxia thr

34 e to terminally differentiated cells in bone marrow and intestines.

35 ors of transcripts downregulated in the bone marrow and involved in lymphoid differentiation and acti

36 e number of cycles based on BED(max) for red marrow and kidneys, and a treatment having 4 cycles with

37 Integration of bone marrow and peripheral blood precursor datasets identifie

38 plantation compared with haploidentical bone marrow and peripheral-blood transplantation (HR, 1.91; P

39 f molecular and functional profiling of bone marrow and peritoneal cells provided a detailed road map

40 e disorder characterized by hypoplastic bone marrow and progressive pancytopenia.

41 ntenance of immature gametocytes in the bone marrow and provide further insights on how Plasmodium pa

42 n factors, reduces SAMD14 expression in bone marrow and spleen and is lethal in a hemolytic anemia mo

43 nal classifications, most homed HSCs in bone marrow and spleen became multipotent progenitors and, oc

44 cF(hi) neutrophils were absent from the bone marrow and spleen, indicating local acquisition of the S

45 oietic stem and progenitor cells in the bone marrow and stimulates granulopoiesis in a cell-autonomou

46 oietic stem and progenitor cells in the bone marrow and the production of proreparatory CD150(+)CD48(

47 press the differentiation of ILC2s from bone marrow and thymic progenitors while promoting the develo

48 t1) markedly reduced cellularity in the bone marrow and/or spleen and inhibited maturation of pre-, i

49 s the formation of blood vessels in the bone marrow, and also regulates the differentiation of reside

50 ic precursors were quantified in blood, bone marrow, and organs.

51 ion, decreases bone formation, and increases marrow angiogenesis in patients.

52 cells in peripheral blood, spleen, and bone marrow, as well as expansion of CD8 T cells, which has b

53 icroscopic analysis of blood smears and bone marrow aspirates.

54 , success of either protocol required a bone-marrow-associated, radiation-sensitive cell population,

55 For this purpose, we developed a bone marrow-avid nanobiologic platform designed specifically

56 Bone marrow biopsies from patients with multiple myeloma reve

57 Bone marrow biopsies were obtained 14-24 h after infusion, an

58 has historically been limited by infrequent marrow biopsies, which increase the risk of infections a

59 During the venetoclax prephase, marrow blast reductions (>= 50%) were noted in NPM1-, ID

60 CD4 T cell responses are detectable in bone marrow (BM) and blood up to 20 years after vaccination.

61 telet alpha-granules, splenomegaly, and bone marrow (BM) fibrosis.

62 Bone marrow (BM) from the sick mice showed myeloid hyperplasi

63 er with nonhematopoietic stromal cells, bone marrow (BM) immune cells with unique functions support t

64 sidual disease (MRD) status outside the bone marrow (BM) in patients with multiple myeloma (MM).

65 ted that the hematopoietic niche of the bone marrow (BM) is a major reservoir for parasite replicatio

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

67 Bone marrow (BM) mesenchymal stem and progenitor cells (MSPCs

68 ls (HSPC) is tightly regulated by their bone marrow (BM) microenvironment (ME).

69 ositioning of B cell progenitors in the bone marrow (BM) microenvironment and their progression throu

70 ietic stem cells (HSCs) in their native bone marrow (BM) microenvironment remains controversial, beca

71 asma cells (PCs) and CD4 T cells in the bone marrow (BM) of healthy young adults (n = 15) following c

72 extracellular environments such as the bone marrow (BM) plasma likely have unique metabolite profile

73 uired for PTH to increase the number of bone marrow (BM) regulatory T cells (Tregs).

74 poietic stem cells (HSCs) reside in the bone marrow (BM) stem cell niche, which provides a vital sour

75 migrate from the endosteal niche of the bone marrow (BM) toward the vasculature, extending proplatele

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

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

78 nd migratory behavior of eosinophils in bone marrow (BM), blood, lung, and bronchoalveolar lavage as

79 Osteoclasts (OC) originate from either bone marrow (BM)-resident or circulating myeloid OC progenito

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

81 e increased risk of radiation injury to bone marrow-both direct suppression and stochastic effects, l

82 he presence of SSCs not only within the bone marrow but also within the periosteum and growth plate r

83 The periosteum and the marrow cavity were each innervated by myelinated (NF200+

84 echanistically, stimulation of specific bone marrow cell populations in vivo using growth factor phar

85 cells enhances differentiation of mouse bone marrow cells and human PBMC into immunosuppressive M-MDS

86 Atlas Census of Immune Cells dataset of bone marrow cells and show that it substantially improves eff

87 ies demonstrated that LRG1 derived from bone marrow cells is required for normal wound healing, revea

88 rgeting senescence in the BMAd or other bone marrow cells may represent a novel therapeutic approach

89 wild-type recipients of PDIA6-deficient bone marrow cells, both in the absence or presence of competi

90 ly recapitulated in murine Dnmt3a (-/-) bone marrow cells.

91 clear, as complete blood counts, splenic and marrow cellularity, numbers and function of hematopoieti

92 Bone marrow chimera and adoptive transfer studies indicate th

93 Bone marrow chimera experiments showed that CD137L-deficient

94 The construction of bone marrow chimera mice demonstrated that STAT6 KO in either

95 Bone marrow chimeras confirmed that vascular Nck1, but not he

96 iNKT cells in bone marrow chimeras that reconstituted thymic cellularity de

97 Using bone marrow chimeras, GILT expression in thymic epithelial ce

98 covery in peripheral blood cell counts, bone marrow colony forming units, sternal cellularity and meg

99 nriched in transcripts derived from the bone marrow compared to circulating cells.

100 Myeloid cells derived from bone marrow contribute to the formation of the premetastatic

101 In bone marrow, CSF1R-FRed was absent in lineage-negative hemato

102 ives from those isolated from blood and bone marrow cultures in southern India, over 26 years (1991-2

103 n in vitro osteoclastogenesis in murine bone marrow cultures.

104 ion-induced peripheral blood cytopenia, bone marrow damage as well as apoptosis in sternum was observ

105 A late-stage bone marrow DC progenitor expressed low amounts of LIFR and d

106 population induced by Cbfb-MYH11 in the bone marrow, decreased and disappeared in Runx1f/fMx1-CreCbfb

107 Generation of pDCs from bone marrow dendritic cell (DC) progenitors and their mainten

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

109 -/-), Casp1/11(-/-) and Asc(-/-) murine bone-marrow derived macrophages (BMDMs) were infected with la

110 models indicating TNT functionality in bone marrow derived malignancies and their microenvironment.

111 The immunomodulatory effects of bone marrow derived mesenchymal stem cells (MSCs) has been wi

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

113 served DNA methylation reprogramming in bone marrow-derived (BMD) monocytes as early as 4 days of rec

114 ficial in ALSP by providing a supply of bone marrow-derived brain-engrafting myeloid cells with donor

115 tudying the differentiation dynamics of bone marrow-derived CD34+ cells into immature B cells in vitr

116 Adoptive transfer of labeled bone marrow-derived cells validated the results in a murine L

117 Historically, SSCs have been defined as bone marrow-derived cells with inconsistent characteristics.

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

119 ated CCR7 on Y. enterocolitica-infected bone marrow-derived DCs and purified MLN DCs, which may expla

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

121 re, the compound was able to 1) inhibit bone marrow-derived dendritic cell-mediated T cell functions

122 n lipopolysaccharide (LPS)-primed mouse bone marrow-derived dendritic cells (BMDC).

123 e I interferon (IFN) responses in mouse bone marrow-derived dendritic cells (DCs).

124 s a broadened immune responses in mouse bone marrow-derived dendritic cells (mBMDCs) and a synergisti

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

126 sts and prevented activation of primary bone marrow-derived dendritic cells ex vivo.

127 ary human foreskin fibroblasts or mouse bone marrow-derived dendritic cells infected with the protozo

128 on both RAW264.7 macrophages and murine bone marrow-derived dendritic cells; we now show that SLP-832

129 restingly, IL33 blockade did not affect bone marrow-derived expansion and local infiltration of eosin

130 Bone marrow-derived hematopoietic stem/progenitor cells are v

131 Bone marrow-derived macrophage cultures from the Notch2(tm1.1

132 ivers enhanced macrophage activation in bone marrow-derived macrophage cultures.

133 Bone marrow-derived macrophages (BMDMs) are recruited to the

134 We found that bone marrow-derived macrophages (BMDMs) from BTK-deficient mi

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

136 nd Ingenuity Pathway Analysis of murine bone marrow-derived macrophages after exposure to this vaccin

137 MV treatment of bone marrow-derived macrophages and bone marrow progenitors p

138 okine that prompts the proliferation of bone marrow-derived macrophages and granulocytes.

139 mpartments, causes long-term changes in bone marrow-derived macrophages by suppressing interleukin 1b

140 This response was lost in bone marrow-derived macrophages from mice deficient in AMPK (

141 TOR signalling in the microglia but not bone marrow-derived macrophages in both in vitro and in vivo

142 FENDRR overexpression in primary mouse bone marrow-derived macrophages increased mRNA expression of

143 f any, iRhom2 was detectable in mEFs or bone marrow-derived macrophages lacking ADAM17, suggesting th

144 1/2 inhibitor U0126 or genetically with bone marrow-derived macrophages or DCs from Tpl2(-/-) mice.

145 acrophage markers (Mrc1, Arg1, Il10) in bone-marrow-derived macrophages or in SAT from male or female

146 yonic precursors and become replaced by bone-marrow-derived macrophages over time.

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

148 tocol that details several in vitro (in bone marrow-derived macrophages) and in vivo (in mice) strate

149 In mouse bone marrow-derived macrophages, heme induced HO-1, lipid reg

150 hways are delayed in P2-deficient mouse bone marrow-derived macrophages, mouse embryonic fibroblasts

151 tion was enhanced by LPS stimulation in bone marrow-derived macrophages.

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

153 f lipopolysaccharide-stimulated primary bone marrow-derived macrophages.

154 factor)-induced activation of Rac1, in bone marrow-derived macrophages; (b) TRPV4 directly interacts

155 Primary bone marrow-derived mast cells (BMMCs) and ECs from WT and Fn

156 asured after IgE crosslinking in murine bone marrow-derived mast cells and human cord blood-derived m

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

158 Patient bone marrow-derived neutrophils and white blood cells showed

159 nt multiple myeloma cells as well as on bone marrow-derived primary multiple myeloma cells from newly

160 Bone-marrow-derived progenitors actively engage DNA repair bu

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

162 Our findings support that bone marrow-derived, presumably neutrophil, NGAL protects fro

163 lin M declined from 3,520 to 821 mg/dL, bone marrow disease involvement declined from 60% to 20%, and

164 During granulopoiesis in the bone marrow, distinct neutrophil granules are successively fo

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

166 oderate specificity in the detection of bone marrow edema of the wrist.

167 aders for tenosynovitis, synovitis, and bone marrow edema.

168 hypothesized that in some patients the bone marrow environment is not permissive to B-cell developme

169 showed that sympathetic nerves create a bone marrow environment that supports residence of hypertensi

170 fects and patients with a nonpermissive bone marrow environment.

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

172 mutational analysis for KIT D816V, and bone marrow evaluation to rule out a clonal mast cell disorde

173 Robust peripheral (bone marrow) expansion of eosinophils and local recruitment o

174 Bone marrow failure (BMF) in Fanconi anemia (FA) patients res

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

176 d Blackfan Anemia (DBA) is a congenital bone marrow failure syndrome associated with ribosomal gene m

177 ata suggest that SCI causes an acquired bone marrow failure syndrome that may contribute to chronic i

178 ribed and is a constitutional inherited bone marrow failure syndrome.

179 Inherited bone marrow failure syndromes (IBMFSs) are characterized by i

180 ns in telomere biology genes leading to bone-marrow failure, these data provide evidence that genetic

181 3%) an innate immune defect, and 2 (2%) bone marrow failure.

182 e have FA-like abnormalities, including bone marrow failure.

183 Dendritic cells (DCs) develop in the bone marrow from haematopoietic progenitors that have numerou

184 Bone marrow from WT and Esr1(-/-) female mice was transferred

185 l and cell surface marker expression as bone marrow hMSCs.

186 f secondary inflammatory stimulus that upset marrow homeostasis such as TBI.

187 Glucocorticoids induced rapid bone marrow homing of eosinophils.

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

189 go, high-risk NB metastatic to bone and bone marrow in children was not curable.

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

191 included hepatic, kidney, splenic, and bone marrow involvement, and microvascular injury and thrombo

192 tients, early B-cell development in the bone marrow is impaired.

193 nge of mature B cells between blood and bone marrow is sensitive to small, physiologic changes in glu

194 y, oedema in peripheric soft tissue and bone marrow, joint effusion, or synovitis are more severe tha

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

196 11.2 to 52.2]; P = .21), and changes in bone marrow lesion size (-33 mm2 vs -6 mm2; between-group dif

197 Vertebral marrow lesions can be differentiated as benign or malign

198 Vertebral bone marrow lesions had a male predominance and there was a p

199 ice, including the lymph nodes, thymus, bone marrow, liver and lung.

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

201 the blood and tissues of ART-suppressed bone-marrow-liver-thymus (BLT) humanized mice and rhesus maca

202 ances the immunosuppressive function of bone marrow Ly6C(high) myeloid cells.

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

204 iating RANKL-induced signaling in mouse bone marrow macrophages, known as osteoclast precursors.

205 oietic maintenance factor expression in bone marrow macrophages.

206 study was to identify and characterize bone marrow MC histopathologic features specific for MCAS-T.

207 tation of long membrane extensions from bone marrow megakaryocytes in the blood flow.

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

209 Bone marrow mesenchymal stem cell-derived extracellular vesic

210 corporating ER+ breast cancer cells and bone marrow mesenchymal stem cells to represent DTCs in a bon

211 Bone marrow mesenchymal stromal cells (MSCs) have been studie

212 ength, partly due to the dysfunction of bone marrow mesenchymal stromal/stem cells (MSCs) during agin

213 rs, soft-tissue metastases, and bone or bone-marrow metastases was 72%, 33%, and 38%, respectively, f

214 CT in detecting soft-tissue and bone or bone-marrow metastases was 77% and 86%, respectively-signific

215 CT in detecting soft-tissue and bone or bone-marrow metastases was 86% and 99%, respectively-signific

216 on of the engrafted HSPC population and bone marrow microenvironment degradation caused by pre-transp

217 is clear that disruption of the normal bone marrow microenvironment is sufficient to promote leukemi

218 iously unknown heterogeneity within the bone marrow microenvironment, imposed by the stages of bone t

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

220 nderpins both the healthy and malignant bone marrow microenvironment.

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

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

223 Bone marrow mononuclear cells (BMNC) are a source of naive ma

224 eatment of primary peripheral blood and bone marrow mononuclear cells from pediatric B-ALL patients,

225 ntified neutrophil subsets fit into the bone marrow neutrophil lineage remains unclear.

226 il subsets arise from distinct maturing bone marrow neutrophil subsets.

227 Splenic and bone marrow neutrophils (Nphs) from BAFF-RFP mice expressed t

228 hymal stem cells to represent DTCs in a bone marrow niche.

229 oietic survival and self-renewal in the bone marrow niche; how to apply this process to HSC maintenan

230 pe is that integrating knowledge of how bone marrow niches contribute to haematological disease predi

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

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

233 phenotypic alterations (MDS-PA) in the bone marrow of 285 patients with MM enrolled in the PETHEMA/G

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

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

236 ficantly associated with blast percentage in marrow or blood (P = 0.0001), CD7 (P = 0.01), CD14 (P <

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

238 ological remission (blast counts <5% in bone marrow) or myelodysplastic syndrome (blast counts <20% i

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

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

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

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

243 Bone marrow perfusion signal changed with the labeling size,

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

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

246 IF activity is high in human and murine bone marrow pro-B and pre-B cells and decreases at the immatu

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

248 of bone marrow-derived macrophages and bone marrow progenitors promoted M2-like macrophage polarizat

249 e deficiency of TGF-beta receptor II in bone marrow progenitors results in inefficient development of

250 lation of mature myeloid cells or their bone marrow progenitors, mediates sustained increased respons

251 steoclastogenesis from Fndc5-transgenic bone marrow progenitors.

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

253 in the cumulative incidence of isolated bone marrow relapse, isolated CNS relapse, or combined bone m

254 ls was dispensable for stability of the bone marrow-resident, long-lived plasma cell population, yet

255 rly depletion of Vi-specific B cells in bone marrow, resulting in hyporesponsiveness and lack of long

256 e, with single-cell analysis of primary bone marrow revealing perturbed UPR in myeloid precursors and

257 d phenotype of G-MDSCs was evaluated in bone marrow samples from controls and MM patients using multi

258 The bone marrow senses distant tissue transformation at premalign

259 n, liver, kidneys, testicles (in men), and 2 marrow sites (acetabulum and sacrum), and correction for

260 and might poorly represent the health of the marrow space.

261 ral organs in HIS mice including blood, bone marrow, spleen, and draining lymph nodes.

262 Bone marrow stem cell transplantation had not been accessible

263 ly useful, especially in the context of bone marrow stem cell transplantation where early rejection o

264 le to prevent rejection of transplanted bone marrow stem cells in vivo by blocking perforin function.

265 the eosinophil-directed bias of murine bone marrow stem cells, demonstrating an unexpected subtype-s

266 led that the transmembrane glycoprotein Bone marrow stromal antigen 2 (Bst2) expression was reduced i

267 re associated with modifications of the bone marrow stromal architecture through relocalization and i

268 lopoiesis in DeltaNC16A mice is through bone marrow stromal cells evidenced by bone marrow transplant

269 Bone marrow studies showed binucleated erythroblasts and eryt

270 Bone marrow surveillance before myeloid malignancy diagnosis

271 ancy and could have been monitored with bone marrow surveillance.

272 t with enhanced egress of FA HSPCs from bone marrow to peripheral blood.

273 Functional Assessment of Cancer Therapy-Bone Marrow Transplant (FACT-BMT) score relative to baseline.

274 e (SR-uPA(+/0) mice) and of SR-uPA(+/0) bone marrow transplant recipients, and we used bioinformatic

275 lantation conditioning regimen prior to bone marrow transplant significantly increased the risk of dr

276 A combination of pair-feeding, bone marrow-transplant, and microglial ablation implicate cen

277 matologic malignancies treated with blood or marrow transplantation (BMT) and that inclusion of these

278 iremia in a Cynomolgus macaque model of bone marrow transplantation (BMT) for tolerance induction.

279 e, we tracked blood-borne miR-210 using bone marrow transplantation and parabiosis (conjoining of cir

280 Irradiation and bone marrow transplantation did not further affect body weigh

281 Bone marrow transplantation experiments identify hematopoieti

282 The European Society of Blood and Marrow Transplantation proposes to use these recommendat

283 hematopoietic reconstitution following bone marrow transplantation provide a window of opportunity w

284 lized in modulation of HSC activity and bone marrow transplantation studies.

285 patients with blood disorders or after bone marrow transplantation to achieve antiviral control whil

286 ere applied in AD+ mice: (i) ACE10/GFP+ bone marrow transplantation with head shielding; and (ii) ado

287 GN was studied in AREG(-/-) mice after bone marrow transplantation, and in mice with myeloid cell-sp

288 ion after peripheral blood stem cell or bone marrow transplantation, rarely occurs in kidney and panc

289 iteria with a mean age of 13.4 years at bone marrow transplantation.

290 bone marrow stromal cells evidenced by bone marrow transplantation.

291 uiescence and increased HSC activity in bone marrow transplantation.

292 sceptibility in circulating T cells via bone marrow transplants allowed some individuals with HIV to

293 ll leukemia (T-ALL) when induced in the bone marrow via Mx1CRE.

294 ted lymphoproliferative disorder in the bone marrow was greatly increased by centralized biopsy asses

295 Bone marrow was microscopically free of disease, but molecula

296 systematically characterized the whole bone marrow (WBM) microenvironment during premalignant, basel

297 Heparinized venous blood and bone marrow were collected from the patient after obtaining i

298 otential during their maturation in the bone marrow, where they differentiate from hematopoietic stem

299 f BMAT with myeloma cell infiltration of the marrow, whereas BMAT was restored after treatment for mu

300 iring of multipotent progenitors in the bone marrow, which overcomes the immunosuppressive tumor micr