ライフサイエンスコーパス: BM

1 BM biopsy was positive in 6 of 38 patients (15.7%) for f

2 BM-derived dendritic cells (DCs), lung-resident cluster

3 BMs have traditionally been viewed as static protein ass

4 ody mass (BM) day(-1) days 1-2, 0.8 g kg(-1) BM day(-1) thereafter].

5 the coagulation pathway genes in 5 out of 10 BM samples.

6 Wild-type-->Tnfr1/2(-/-) BM chimera mice with chronic dextran sodium sulfate coli

7 to the coagulation cascade in a panel of 29 BMs and we identified 56 Single Nucleotide Variants (SNV

8 Adoptive transfer of CRTC2/3m BM conferred the splenomegaly/neutrophilia phenotype in

9 ts had cytopenias, and 12.0% presented >/=5% BM blast cells.

10 Responses, predefined as a BM frequency reduction >/= 30% from baseline for >/= 50%

11 pc(del/+) ) model MDS induced by an aberrant BM microenvironment.

12 oxicity during treatment, estimated absorbed BM dose, elevated plasma chromogranin A level, baseline

13 ion of humanized ossicles with an accessible BM microenvironment that faithfully recapitulates normal

14 sitizes mid-high-frequency DPOAEs and active BM responses and sensitizes low-mid-frequency neural exc

15 We added BM fat, CD11b(+) myeloid cells, and recombinant S100A9 t

16 stant and not replaced by monocytes or adult BM-derived cells during infection, but were locally main

17 Although BM formation is thought to simply involve a process of s

18 imary AML, and that IL8 was increased in AML/BM-MSC cocultures.

19 87 participants 14 to 21 days after AMI and BM from healthy donors was used as a reference.

20 t a novel interaction between AML blasts and BM-MSCs, which benefits AML proliferation and survival.

21 r T cells in RIC mice and elevated blood and BM plasma levels of T helper1 cytokines.

22 CMV-specific T cells were found in blood and BM samples with low virus detection, whereas in lung, CM

23 lammatory signaling in endothelial cells and BM-derived cells.

24 els of suPAR, as evidenced by BM chimera and BM ablation and cell transfer studies.

25 ed BM failure characterized by cytopenia and BM aplasia.

26 reliable tool for BMI assessment in HL, and BM biopsy is no longer needed for routine staging.

27 emonstrated here that FL-infiltrating LN and BM stromal cells overexpressed CXCL12 in situ.

28 s of F4/80(+) renal resident macrophages and BM monocytes.

29 METHODS AND BM and PB samples were collected from 87 participants 14

30 ntra-individually between mother's serum and BM.

31 cing on matched samples of breast cancer and BMs and found mutations in the coagulation pathway genes

32 induced IL8 expression by BM-MSCs as well as BM-MSC-induced AML survival.

33 cellent diagnostic performance for assessing BM infiltration in patients with multiple myeloma with p

34 transplanted with Asxl2(-/-) and Asxl2(+/-) BM cells have shortened lifespan due to the development

35 ld-type (WT) mice, and in mixed WT:BCAP(-/-) BM chimeras, monocytes and neutrophils skewed toward BCA

36 t discordance in epitope specificity between BM and maternal sera ranging from only 13% of sample pai

37 and demonstrate paracrine cross-talk between BM osteolineage cells and endothelial cells in regulatin

38 , whereas it was minor in the spleen, blood, BM, and the airways.

39 e BM seems to play a crucial role in the BTB-BM axis by modulating BTB dynamics during spermatogenesi

40 onal hematologic malignancy characterized by BM fibrosis, extramedullary hematopoiesis, circulating C

41 ntify the rejuvenating factors elaborated by BM ECs that restore HSC function and the immune repertoi

42 athological levels of suPAR, as evidenced by BM chimera and BM ablation and cell transfer studies.

43 SO-1 inhibited AML-induced IL8 expression by BM-MSCs as well as BM-MSC-induced AML survival.

44 mucosal repair depended on TNF production by BM-derived cells and TNFR expression by radioresistant I

45 ing pathways mediated by factors secreted by BM stromal cells and involved a switch from BCL2 to BCLX

46 Bone marrow mononuclear cell (BM-MNC) therapy in ST-elevation acute myocardial infarct

47 e of the inability to visualize dynamic cell-BM interactions in vivo.

48 arrow mesenchymal stem and progenitor cells (BM-MSPCs) maintain homeostasis of bone tissue by providi

49 ells and bone marrow mesenchymal stem cells (BM-hMSCs).

50 that bone marrow mesenchymal stromal cells (BM-MSC) protect AML blasts from spontaneous and chemothe

51 polymerization-competent, designer chimeric BM protein in vivo to restore function of a polymerizati

52 Additionally, compared with control BM monocytes, BM monocytes from gut flora-depleted mice

53 fiber development stages in upland cotton cv BM-1.

54 , and formula (FF) in the first months" (DBF/BM/FF) showed a statistically significant higher risk of

55 ution of Ldlr-/- mice with Arhgef1-deficient BM prevented high-fat diet-induced atherosclerosis, whil

56 d 2 MDS/MPN) and 3 patients (1.1%) developed BM failure characterized by cytopenia and BM aplasia.

57 pan-laminin were present in the disorganized BM of isolated islets, yet a significant reduction in pa

58 n-alpha5 (found in both layers of the duplex BM) and perlecan were lost entirely, with no restoration

59 scade can provide critical advantages during BM formation.

60 esis associated with damage to the endosteal BM niche.

61 Using this method, a humanized engraftable BM microenvironment can be formed within 6-10 weeks.

62 Pressure overload enhanced BM-FPC mobilization and homing in IL10KO mice compared w

63 Retinal pigment epithelium-BM thickness, as measured by SD OCT segmentation using T

64 ients, not even bone metastasis or estimated BM dose.

65 (Dkk1), which was produced in Osx-expressing BM cells.

66 bility to polymerize within the muscle fiber BM.

67 IL-4 expression and signaling within the FL BM and LN niches.

68 These results suggest an important role for BM endothelial cells (ECs) in regulating hematopoietic a

69 motif) ligand 21 by DCs differentiated from BM of UV-irradiated mice.

70 DCs differentiating from BM cells pulsed in vitro for 2 hours with dimethyl prost

71 f the "screening blood sample" used to guide BM biopsy in suspected SM to the outcome of the subseque

72 owed that following transplantation of human BM-derived MSCs, globule-containing hepatocytes declined

73 ression and stabilization within the hypoxic BM microenvironment promotes disease progression, therap

74 en the BM and the kidney, and they implicate BM immature myeloid cells as a key contributor to glomer

75 um (estimate+/-SE, 0.01+/-0.002; P=0.002) in BM, and mesenchymal stromal cell colony maximum in PB (e

76 We find that deficiency of miR-146a in BM-derived cells precipitates defects in hematopoietic s

77 tein cholesterol in mice lacking miR-146a in BM-derived cells.

78 rimary end point was change from baseline in BM frequency.

79 ng ex vivo responses of primary AML cells in BM stroma-derived and standard culture conditions.

80 0) resulted in robust engraftment of CMML in BM, spleen, liver, and lung of recipients (n = 82 total

81 Results Estimated differences in BM frequency per day versus placebo averaged over 12 wee

82 Recombinant MIF increased IL8 expression in BM-MSCs via its receptor CD74.

83 beta (PKCbeta) regulated MIF-induced IL8 in BM-MSCs.

84 This was associated with an increase in BM CD8 effector T cells in RIC mice and elevated blood a

85 lation of CM-specific IgA antibody levels in BM, but not in serum, suggesting that an entero-mammary

86 ellularity, and showed profound reduction in BM B cell lymphopoiesis associated with damage to the en

87 th factor-beta-induced fibrotic signaling in BM-FPCs.

88 ociated T cell responses in liver-Tx than in BM-Tx.

89 in, and type XVIII collagen - are present in BMs, creating biochemically and biophysically distinct s

90 low conditions in vitro as well as increased BM trafficking and extravasation when transplanted into

91 B glycoprotein was associated with increased BM function, whereas increased IL-6 was associated with

92 duced transverse aortic constriction-induced BM-FPC mobilization compared with IL10KO mice.

93 Finally, targeted IL8 shRNA inhibited BM-MSC-induced AML survival.

94 Our findings suggest that IL10 inhibits BM-FPC homing and transdifferentiation to myofibroblasts

95 -dependent transmigration of entire MKs into BM sinusoids.

96 cytoplasmic protrusions (proplatelets) into BM sinusoids.

97 ised as a consequence of an incomplete islet BM, which has implications for islet survival and transp

98 in, perlecan and laminin-alpha5 in the islet BM were significantly digested by enzyme treatment.

99 Posterior movement of the lamina (LD-BM increase or LD-AS increase) occurred with the same fr

100 ore frequently with the Bruch's membrane (LD-BM decrease) compared with the anterior sclera (LD-AS de

101 not the anterior sclera, reference plane (LD-BM decrease without LD-AS decrease).

102 The LD-BM was influenced significantly more by choroidal thickn

103 and 89 (48.4%) showed no or faint (</=liver) BM uptake (nPET(+)).

104 ed higher colony-forming efficiency than LL, BM, and HP.

105 ms of their protumoral effect and how the LN/BM microenvironment is converted into a lymphoma-permiss

106 Second, many BM proteins are produced not only by the cells residing

107 eaning of different patterns of bone marrow (BM) (18)F-FDG uptake in HL.

108 ntigen-mismatched alloHCT using bone marrow (BM) cells and splenocytes from B6 (H-2) donor mice trans

109 or null) mice transplanted with bone marrow (BM) cells from Ncr1(iCre)R26R(lsl-)(DTA) , Noe, or wild-

110 Bone marrow (BM) chimera mice revealed that mucosal repair depended o

111 Bone marrow (BM) failure (BMF) in children and young adults is often

112 s and plasma cells (PCs) in the bone marrow (BM) for up to 360 days postimmunization (dpi).

113 oietic stem cells (HSCs) in the bone marrow (BM) form mature blood cells of all lineages through expa

114 Here we report that bone marrow (BM) Gr-1(lo) immature myeloid cells are responsible for

115 omography (CT) for detection of bone marrow (BM) infiltration in patients with multiple myeloma by us

116 ing hematopoietic stress, e.g., bone marrow (BM) injury, transplantation, or systemic infection and i

117 ogenitor cells (HSPCs) from the bone marrow (BM) into the peripheral blood is a complex process that

118 lood has been proposed to guide bone marrow (BM) investigation in suspected systemic mastocytosis (SM

119 These mice showed increased bone marrow (BM) levels of the protein dickkopf-1 (Dkk1), which was p

120 xl2(-/-) mice have an increased bone marrow (BM) long-term haematopoietic stem cells (HSCs) and granu

121 mediates cell anchorage in the bone marrow (BM) microenvironment and is overexpressed in 25-30% of p

122 Understanding the role of the bone marrow (BM) microenvironment in supporting HSC function may prov

123 progenitor cells (HSPCs) in the bone marrow (BM) microenvironment.

124 ctive crosstalk with an altered bone marrow (BM) microenvironment.

125 ident macrophage population and bone marrow (BM) monocytes than did control mice.

126 BCAP(-/-) mice had more bone marrow (BM) monocytes than wild-type (WT) mice, and in mixed WT:

127 racrine Wnts emanating from the bone marrow (BM) niche.

128 regulated within a specialized bone marrow (BM) niche.

129 = 8 patients) or unfractionated bone marrow (BM) or peripheral blood mononuclear cells (n = 10) resul

130 croenvironmental determinant of bone marrow (BM) pathophysiology.

131 platelets are produced by large bone marrow (BM) precursor cells, megakaryocytes (MKs), which extend

132 The bone marrow (BM) provides a protective microenvironment to support th

133 are a critical component of the bone marrow (BM) stromal network, which maintains and regulates hemat

134 re mobilized from niches in the bone marrow (BM) to the blood circulation by the cytokine granulocyte

135 m repopulation potential in the bone marrow (BM), and that as HSCs accumulate a divisional history, t

136 ion patterns, highest in blood, bone marrow (BM), or lymph nodes (LN), with the frequency and functio

137 brain, visceral adipose tissue, bone marrow (BM), spleen, and the circulation.

138 including endothelial cells and bone marrow (BM)-derived cells.

139 iently taken up by M2-polarized bone marrow (BM)-derived macrophages (BMDMs) in vitro and by mannose

140 y in the prepuberty period from bone marrow (BM)-derived progenitors.

141 Evidence was presented that bone marrow (BM)-derived Sinusoidal endothelial cell PROgenitor Cells

142 ated whether transplantation of bone marrow (BM)-derived stem cells in transgenic mice expressing hum

143 Although the emergence of bone marrow (BM)-resident (p190)BCR-ABL-specific T lymphocytes has be

144 sponse and reducing the pool of bone marrow (BM)-resident long-lived PCs.

145 red with that seen in wild-type bone marrow (BM)-transplanted OS mice in peripheral blood and hematop

146 f malignant plasma cells in the bone marrow (BM).

147 o B lymphopoiesis occurs in the bone marrow (BM).

148 n invaded lymph nodes (LNs) and bone marrow (BM).

149 was originally described using bone marrow (BM).

150 opoietic stem cells (HSCs) from bone marrow (BM).

151 nduce long-term toxicity to the bone marrow (BM).

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

153 s lack essential human-specific bone-marrow (BM)-microenvironment-derived survival, proliferation, an

154 he immune response against intrabone marrow (BM-Tx) or intraliver (liver-Tx) transplanted islets in t

155 n = 8) for 10 days [1.6 g kg(-1) body mass (BM) day(-1) days 1-2, 0.8 g kg(-1) BM day(-1) thereafter

156 sequently constructed to form a fully mature BM in the living animal.

157 At week 12, mean BM frequency reductions per day for placebo, telotristat

158 We identified basement membrane (BM) and collagen IV in Ctenophora, and show that the str

159 Cell invasion through basement membrane (BM) barriers is crucial in development, leukocyte traffi

160 lagen IV, reiterating the basement membrane (BM) changes observed in vivo.

161 tituent components of the basement membrane (BM) in adult rat testes.

162 The islet basement membrane (BM) influences islet function and survival and is a crit

163 The basement membrane (BM) is a thin layer of extracellular matrix (ECM) beneat

164 all invadopodia to breach basement membrane (BM), a dense matrix that encases tissues.

165 gulatory axis between the basement membrane (BM), the blood-testis barrier (BTB), and the apical ecto

166 iber cytoskeleton and the basement membrane (BM).

167 The mammalian basilar membrane (BM) consists of two collagen-fiber layers responsible fo

168 ions (DPOAEs), and passive basilar membrane (BM) responses.

169 l pigment epithelium (RPE)-Bruch's membrane (BM) complex thickness as measured by spectral-domain (SD

170 Basement membranes (BMs) are thin, dense sheets of specialized, self-assembl

171 Brain metastases (BMs) are the most common malignancy of the central nervo

172 ry for real-time analysis of cell migration, BM turnover and cell-membrane dynamics.

173 east (DBF), pumping and feeding breast milk (BM), and formula (FF) in the first months" (DBF/BM/FF) s

174 ionally, compared with control BM monocytes, BM monocytes from gut flora-depleted mice had decreased

175 Patients (N = 135) experiencing four or more BMs per day despite stable-dose somatostatin analog ther

176 Mouse BM progenitors and human mesenchymal stem cells (MSCs) a

177 e not restricted to transplantation of mouse BM cells.

178 d AML generated by the transduction of mouse BM with fusion cDNAs derived from human leukemias.

179 droxylase inhibitor, reduces bowel movement (BM) frequency in patients with carcinoid syndrome.

180 aracteristics with bone marrow-derived MSCs (BM-MSC).

181 compared to explants from the buccal mucosa (BM), HP, and transition zone of the lower lip (TZ) after

182 were tdTomato-C3aR(+) Surprisingly, neither BM, blood, lung neutrophils, nor mast cells expressed C3

183 MSPCs, these labeled cells still contain non-BM-MSPC populations.

184 nt difference between infiltrated and normal BM (P < .001).

185 ronment that faithfully recapitulates normal BM niche morphology and function.

186 This reveals that de novo BM construction requires a combination of both productio

187 o live image and genetically dissect de novo BM formation during Drosophila development.

188 presses Smad-miRNA-21-mediated activation of BM-FPCs and thus modulates cardiac fibrosis.

189 ular microenvironment, and as a component of BM, collagen IV enabled the assembly of a fundamental ar

190 e of 96.9% (157 of 162) for the detection of BM infiltration.

191 trols, RIC mice with GVHD showed evidence of BM suppression, have anemia, reduced BM cellularity, and

192 eveals that there is a temporal hierarchy of BM protein production that is essential for proper compo

193 inhibits pressure overload-induced homing of BM-FPCs to the heart and their transdifferentiation to m

194 onfirmed inflammatory cytokine impairment of BM that could be reversed by blocking IL-1R or IL-6R.

195 ; however, the role of IL10 in inhibition of BM-FPC-mediated cardiac fibrosis is not known.

196 atory responses may suppress mobilization of BM sprocs and dampen hepatic recovery.

197 color-coded VNCa images for the presence of BM involvement.

198 ells in adult mice inhibited the recovery of BM stem and progenitor cells and of complete blood count

199 nd cell-membrane protrusions, and removal of BM.

200 However, the precise role of BM in this axis remains unknown.

201 Adoptive transfer of BM, but not peripheral, granulocytes prevented the death

202 e risks were higher after transplantation of BM (HR, 1.49; P = .009).

203 ecovery was similar after transplantation of BM and PB (28-day neutrophil recovery, 88% v 93%, P = .0

204 and 57% at 2 years after transplantation of BM and PB, respectively.

205 Secondary transplantation of BM cells from PF-06747143-treated or IgG1 control-treate

206 t disease were lower with transplantation of BM compared with PB.

207 The emergence of BMs coincided with the origin of multicellularity in ani

208 we discuss established and emerging roles of BMs in development, tissue construction, and tissue home

209 how cells traverse BM barriers, the roles of BMs in human diseases, and future directions for the fie

210 pment of new strategies for the treatment of BMs.

211 ppressed senescence, and indirect effects on BM endothelial cells, in which treatment with Dkk1 induc

212 nvestigated the impact of islet isolation on BM integrity in human islets, which have a unique duplex

213 termediary in the effects of UV radiation on BM cells.

214 -phenyl-C61 -butyric acid methyl ester (PC61 BM).

215 ceptor alternatives to fullerenes (e.g. PC61 BM or its C71 derivative) are based on perylenediimide o

216 grees C thermal stress than PffBT4T-2OD:PC71 BM devices.

217 ]-phenyl C71 butyric acid methyl ester (PC71 BM) as electron acceptors is reported.

218 than the control devices based on FTAZ:PC71 BM (PCE = 5.22%).

219 In this study, we characterized rabbit BM after the arrest of B lymphopoiesis and found a drama

220 Anti-CD3 did not differentially reach BM and liver tissues but was more effective in reducing

221 United States between 2009 and 2014 received BM (n = 481) or PB (n = 190) grafts.

222 ence of BM suppression, have anemia, reduced BM cellularity, and showed profound reduction in BM B ce

223 est that mature hematopoietic cells regulate BM stromal-cell function.

224 equires morphogen-like signaling to regulate BM incorporation, as well as planar-polarized organizati

225 to form a pronounced arch over the remaining BM width.

226 Among those aged </=45, RPE-BM was significantly thicker among those of black or mix

227 es and to identify relationships between RPE-BM thickness and ocular and systemic features.

228 In contrast, RPE-BM was significantly thicker among black or mixed/other

229 Mean RPE-BM thickness was 26.3 mum (standard deviation, 4.8 mum)

230 We describe novel findings of RPE-BM thickness in normal individuals, a structure that var

231 ed predominantly in lung and also in spleen, BM, blood and LN.

232 extramedullary hematopoiesis, splenomegaly, BM failure, and decreased levels of circulating proather

233 tion deficits to increase laminin, stabilize BM structure, and substantially ameliorate muscular dyst

234 uspected SM to the outcome of the subsequent BM investigation.

235 ume by more than 20%, displacing surrounding BM and vulval epithelium.

236 o new safety signals and suggested sustained BM responses to treatment.

237 BMT experiments revealed that BM-derived macrophages expressing the RET ligand GDNF ar

238 Furthermore, we show that BM components require secretion by migrating macrophages

239 These results suggest that BM stem cell transplantation may be a promising therapy

240 gative screening results also underline that BM investigation is mandatory in all adult patients with

241 The BM niche comprises a tightly controlled microenvironment

242 blood and hematopoietic organs, such as the BM, thymus, and spleen.

243 t UNC-6(netrin)/UNC-40(DCC) signaling at the BM breach site directs exocytosis of lysosomes using the

244 (+)Runx2-GFP(low) stromal cells sit atop the BM stromal hierarchy.

245 suPAR as a functional connection between the BM and the kidney, and they implicate BM immature myeloi

246 oliferative capacity of PCs that entered the BM, diminishing the number of cells in the long-lived po

247 We have therefore examined the BM homing properties of human induced pluripotent stem c

248 o serve as an effective method to expand the BM HSPC pool.

249 e Wnt ligands and/or paracrine Wnts from the BM microenvironment.

250 Macrophages differentiating from the BM of UV-chimeric mice also had an inherent reduced abil

251 essed in macrophages differentiated from the BM of UV-chimeric mice.

252 were functionally similar to those from the BM of UV-irradiated mice.

253 ctor copy number/genome higher than 1 in the BM and 2 in the thymus.

254 stem and progenitor cell populations in the BM and spleen that are hypersensitive to granulocyte mac

255 Islets infused in the BM appear less protected from the adaptive immune respon

256 as primarily due to fewer progenitors in the BM combined with reduced potential for T lineage commitm

257 these, SM was subsequently diagnosed in the BM investigation.

258 ecialized microanatomical environment in the BM known as the HSC niche.

259 n leukemia stem cells, WNT activation in the BM niche is also thought to contribute to the pathogenes

260 spondins produced by (pre)osteoblasts in the BM niche, resulting in Wnt (co)receptor stabilization an

261 al colony-forming cell colony maximum in the BM of patients with AMI (estimate+/-SE, -0.13+/-0.05; P=

262 (lo) myeloid cells was commonly found in the BM of proteinuric animals having high suPAR, and these c

263 In short, laminin alpha2 in the BM seems to play a crucial role in the BTB-BM axis by mo

264 d resistance to specific drug classes in the BM stroma-derived conditions was a result of activation

265 n can modulate macrophage progenitors in the BM such that their differentiated progeny respond ineffi

266 S. aureus mutant, cells proliferated in the BM survival niches and sustained long-term Ab titers.

267 o fourfold expansion of the HSPC pool in the BM was observed.

268 ted in an expansion of Gr-1(lo) cells in the BM, leading to high plasma suPAR and proteinuric kidney

269 that is derived from collagen chains in the BM, was found to modulate cell junction dynamics at the

270 nce of (p190)BCR-ABL-specific T cells in the BM.

271 ises some concerns over the potential of the BM as a site for islet allotransplantation.

272 s of blood was compared to the result of the BM investigation.

273 To better understand the effect of the BM microenvironment on drug responses in AML, we conduct

274 ial cells (ECs), a critical component of the BM microenvironment, was sufficient to drive hematopoiet

275 study, we provide a detailed picture of the BM vasculature in acute myeloid leukemia using intravita

276 r form a flat beam over at least part of the BM width.

277 V) chain-a major structural component of the BM-was capable of inducing BTB remodeling, making the BT

278 oduced not only by the cells residing on the BM but also by surrounding cell types [6-9], and it is u

279 We demonstrate that the BM is a major target organ of GVHD in an informative cli

280 Genetic manipulation shows that the BM is instructive for tissue elongation and the determin

281 ng and genetic perturbations showed that the BM receptor dystroglycan forms a membrane diffusion barr

282 che, but how the brain communicates with the BM remains largely unknown.

283 w CD41 expression is up-regulated within the BM HSC compartment in response to G-CSF treatment.

284 adhesion via integrin alphavbeta3 within the BM niche acts as a context-dependent signal modulator to

285 Defects in this BM lead to muscle fiber damage from the force of contrac

286 1 and pro-Il1b in cultured Nlrp3A350V Tnf-/- BM-derived DCs.

287 We also explore how cells traverse BM barriers, the roles of BMs in human diseases, and fut

288 Atomic force microscopy (AFM) on wild-type BM in vivo reveals an anterior-posterior (A-P) symmetric

289 (-/-);miR-146a(-/-) mice receiving wild-type BM transplantation, and these mice have enhanced endothe

290 ared with Ldlr(-/-) mice receiving wild-type BM, demonstrating the atheroprotective role of miR-146a

291 When BM cells were harvested from UV-irradiated mice and tran

292 , whereas increased IL-6 was associated with BM impairment.

293 DBF combined with BM for the first 3 months followed by mixed feeding also

294 ed human AML compared with AML cultured with BM-MSCs and found that macrophage migration inhibitory f

295 r BB glycoprotein correlated positively with BM-derived colony-forming unit-endothelial colony maximu

296 UV-chimeric mice (ie, mice transplanted with BM from UV-irradiated mice) after injection of an inflam

297 samples from 77 STEMI patients treated with BM-MNCs in the TIME and Late-TIME trials as well as 61 S

298 differentiation and fibrotic signaling in WT BM-FPCs in vitro.

299 reconstitution of Ldlr-/- Arhgef1-/- with WT BM exacerbated atherosclerotic lesion formation, support

300 Additionally, delivery of young BM ECs along with HSCs following total body irradiation