ライフサイエンスコーパス: BMT

1 BMT alveolar macrophages (AMs) exhibited a defect in P.

2 BMT experiments revealed that BM-derived macrophages exp

3 BMT resulted in near complete replacement of host retina

4 BMT-derived microglia engraftment was significantly redu

5 BMT-exposed neonates had higher mean gestational age and

6 BMT-recipient mice receiving donor T cells with enhanced

7 study consisting of 2 cohorts, totaling 2888 BMT recipients with acute myeloid leukemia, acute lympho

8 ssion analysis in cerebral cortex of APOE3/3 BMT recipients showed reduced expression of tumor necros

9 luble and plaque Abeta compared with APOE3/3 BMT-recipient APPswe/PS1DeltaE9 mice.

10 Eight months later, APOE4/4 BMT-recipient APPswe/PS1DeltaE9 mice had significantly i

11 ell engraftment with MGMT transgenic C57BL/6 BMT after BCNU treatment, demonstrating full reconstitut

12 Despite a difference in phagocytic ability, BMT AMs harbor a killing defect to both P. aeruginosa an

13 specially skin cancer, was observed in adult BMT-rescued DNA-PKcs(3A/3A) mice.

14 c allografts were performed at day 243 after BMT.

15 57BL/6 grafts was performed at day 358 after BMT.

16 -year overall survival was 95% and 97% after BMT and CBT, respectively (P = .92).

17 oid organs, and target organs of aGvHD after BMT showed significantly reduced numbers of miR-181a-tra

18 l MR examinations performed before and after BMT was collected from each patient's records.

19 of low levels of proliferation 4 days after BMT.

20 present on donor dendritic cells (DCs) after BMT in the setting of myeloablative conditioning but is

21 cells (DCs) is markedly impaired early after BMT.

22 s may be responsible for relapse, even after BMT.

23 NET formation after BMT was rescued both in vitro and in vivo with cyclooxyg

24 when reconstructing antiviral immunity after BMT, and highlight the mechanisms by which the adoptive

25 HLI surgery was performed 1 mo after BMT, after confirming complete engraftment of the recipi

26 r origin CD8(+) cells detected 1 month after BMT, and remained stable (85.5 +/- 11% mean donor origin

27 Variants Related to one-Year mortality after BMT), a well-powered genome-wide association study consi

28 ly severe non-GVHD hepatitis occurring after BMT, determined using a proteomic approach and enabling

29 l (DFS) was 86% and 80% in TM patients after BMT and CBT, respectively, whereas DFS in SCD patients w

30 tly associated with different survival after BMT for hematologic malignancies.

31 ted mortality, and/or overall survival after BMT.

32 nsion and suppressive function of Treg after BMT.

33 ver, specific depletion of donor Tregs after BMT also induced cGVHD, whereas adoptive transfer of Tre

34 vo expansion/maturation of donor Tregs after BMT.

35 itional on surviving the first 2 years after BMT, 5-year survival generally exceeds 70%.

36 ches in secondary lymphoid organs after allo-BMT and define a framework of early cellular and molecul

37 dministration of a VIP antagonist after allo-BMT is a promising safely therapeutic approach to enhanc

38 show that the development of GVHD after allo-BMT prevented NK-cell reconstitution, particularly withi

39 ntestinal epithelial cells (IECs) after allo-BMT resulted in decreased histone acetylation, which was

40 trol of cytomegalovirus infection after allo-BMT was also impaired during GVHD.

41 cellular source of Notch ligands after allo-BMT.

42 aintained their expansion in irradiated allo-BMT recipients, as well as their in vivo and ex vivo cyt

43 window after transplantation in a mouse allo-BMT model.

44 ti-CMV immunity in murine recipients of allo-BMT.

45 nd CD8(+) T cells using mouse models of allo-BMT.

46 cal blockade of VIP-signaling protected allo-BMT recipients from lethal murine CMV (mCMV) infection,

47 wing allogeneic bone marrow transplant (allo-BMT) is controlled by donor-derived cellular immunity.

48 fter allogeneic bone marrow transplant (allo-BMT).

49 Allogeneic bone marrow transplantation (allo-BMT) is a curative therapy for hematological malignancie

50 allogeneic bone marrow transplantation (allo-BMT).

51 allogeneic bone marrow transplantation (allo-BMT).

52 Allogeneic BMT and its major complication, graft-versus-host diseas

53 withdraw immunosuppression after allogeneic BMT should be made with caution.

54 MT, in the presence of GVHD after allogeneic BMT, CMV induced a striking cytopathy resulting in unive

55 ptimizing vaccine responses after allogeneic BMT.

56 pient mice that have undergone an allogeneic BMT [SP-A(-/-)alloBMT] or SP-A-sufficient recipient mice

57 Five patients who received an allogeneic BMT for the treatment of hematological diseases develope

58 pient mice that have undergone an allogeneic BMT had no significant differences in lung pathology; ho

59 nt in SP-A that have undergone an allogeneic BMT have a greater incidence of GI GVHD that is associat

60 pient mice that have undergone an allogeneic BMT) or C57BL/6 (H2b; SP-A-deficient recipient mice that

61 sease risk across histologies and allogeneic BMT regimens.

62 ablative TLI/ATS conditioning and allogeneic BMT, induce PD-1 ligand-dependent donor nTreg proliferat

63 P3(+) Treg cell numbers following allogeneic BMT by two pathways: instability of natural Treg (nTreg)

64 ammation and improve outcomes for allogeneic BMT recipients.

65 monstrate, using murine models of allogeneic BMT, that type 2 innate lymphoid cells (ILC2s) in the lo

66 Although BMT increases the life span of patients with MPS IH, mus

67 as well as in the in vivo MLL-rearranged AML BMT model coupled with treatment of "5 + 3" (i.e. DOX pl

68 uated two selective NR2B NAMs, CP101,606 and BMT-108908, along with the nonselective NMDA antagonists

69 nstrated by in vitro proliferation assay and BMT.

70 (H-2(d)) hosts were administered TLI/ATS and BMT from WT or STAT6(-/-) C57BL/6 (H-2(b)) donors.

71 analysis, DFS did not differ between CBT and BMT recipients.

72 mes after both HLA-identical sibling CBT and BMT.

73 strong predictor of outcome for both IST and BMT, and must be considered when designing therapeutic s

74 TS + BMT versus total body irradiation/ATS + BMT.

75 Jalpha18(-/-) BALB/c recipients of TLI/ATS + BMT restored day-6 donor Foxp3(+) nTreg proliferation an

76 D11c(+)) were enriched early after TLI/ATS + BMT versus total body irradiation/ATS + BMT.

77 After TLI/ATS + BMT, Gr-1(low)CD11c(+) MDCs and Gr-1(high)CD11c(neg) mye

78 pha18(-/-) BALB/c recipients after TLI/ATS + BMT.

79 ouse model, Tcm therapy following autologous BMT led to significant survival prolongation, with 30% t

80 orldwide who received cyclophosphamide-based BMT regimens for leukemias between 1990 and 2007.

81 -based (RSP), 2) non-sputum Biomarker-based (BMT), 3) triage test followed by confirmatory test (TT),

82 One day before BMT, rats were treated with varying doses of total body

83 actobacillales from the flora of mice before BMT aggravated GVHD, whereas reintroducing the predomina

84 beta2ARKO BMT mice displayed 100% mortality resulting from cardiac

85 beta2ARKO BMT mice displayed severely reduced post-MI cardiac infi

86 rbidity, coupled with a long latency between BMT and the development of chronic health conditions nec

87 clinically relevant approach to perform both BMT and VCA simultaneously was evaluated.

88 elated retinal degeneration was mitigated by BMT.

89 eveloped and evaluated the radiotracer (11)C-BMT-136088 (1-(4'-(3-methyl-4-(((1(R)-(3-(11)C-methylphe

90 Results:(11)C-BMT-136088 baseline VT was 1.83 +/- 0.16 (MA1, n = 5) or

91 Specific binding of (11)C-BMT-136088 can be reliably measured to quantify LPA1 in

92 ntration leading to a 50% reduction of (11)C-BMT-136088 specific binding were 73 +/- 30 nmol/kg and 2

93 For the self-saturation study, (11)C-BMT-136088 VND and BPND were estimated to be 0.9 +/- 0.0

94 out immunosuppression, whereas non-Treg cell BMT recipients rejected delayed donor kidneys within 3 t

95 In contrast, 2 of 5 recipients of Treg cell BMT that were evaluable displayed chimerism in all linea

96 nce can be successfully induced with delayed BMT to previous recipients of kidney transplantation or

97 The tolerance achieved with delayed BMT was donor specific as confirmed by acceptance of don

98 conjunction with allogeneic T-cell-depleted BMT could be of particular benefit in patients with B-ce

99 BaMn3Ti4O14.25, designated BMT-134, possesses the signature channel-like hollandite

100 ects in P. aeruginosa internalization as did BMT AMs.

101 cant SNPs replicated at P < .05 in DISCOVeRY-BMT.

102 associations were performed using DISCOVeRY-BMT (Determining the Influence of Susceptibility COnveyi

103 In addition, infusion of extra Tregs during BMT results in a delayed reconstitution of T-cell compar

104 d by infusing extra Foxp3(GFP+) Tregs during BMT.

105 g a rotarod test, we demonstrated that early BMT greatly delayed the motor impairment in the mutant m

106 was confirmed in MHC-mismatched experimental BMT.

107 Cancer Therapy-Bone Marrow Transplant (FACT-BMT) were received from 109 ex-thalassemia patients who

108 During the year that followed BMT, all patients presented with GVHD.

109 re, we studied CAR T-cell function following BMT using an immunocompetent murine model of minor misma

110 rived MHC class I and II molecules following BMT.

111 For BMT survivors, screening recommendations must incorporat

112 ideation was rare (1.9% for DBS vs 0.9% for BMT; Fisher's exact p=0.61).

113 nsive review articles, clinicians caring for BMT recipients continue to field frequently asked questi

114 In patients otherwise fit for BMT, the results support consideration of this approach

115 on, but only CD8(+) T cells are required for BMT rejection.

116 d NET formation in neutrophils isolated from BMT mice or HSCT patients.

117 Compared with patients given BMT, CBT recipients were significantly younger (median a

118 udy evaluated the effect of age on NMA haplo-BMT outcomes in patients age 50 to 75 years.

119 NMA haplo-BMT with post-transplantation cyclophosphamide has encou

120 ears, who received NMA, T-cell-replete haplo-BMT with high-dose post-transplantation cyclophosphamide

121 tical blood or marrow transplantation (haplo-BMT) have expanded the donor pool.

122 oietic lineages 28 days after haploidentical BMT with 69.3 +/- 14.1%, 75.6 +/- 20.2%, and 88.5 +/- 11

123 CD8(+) cells) 6 months after haploidentical BMT.

124 uCi (90)Y-DOTA-30F11, CY, and haploidentical BMT were cured and lived >200 days.

125 atifies recipients of NMA HLA-haploidentical BMT with PTCy and also suggests that this transplantatio

126 of nonmyeloablative (NMA) HLA-haploidentical BMT with PTCy, 372 consecutive adult hematologic maligna

127 RIT-mediated haploidentical BMT without TBI may increase treatment options for aggre

128 However, BMT may be a particularly compelling setting to test CSC

129 orter (-7.23 days, 95% CI: -10.64, -3.83) in BMT-exposed versus MMT-exposed neonates.

130 ave shown trends of reduced aspergillosis in BMT patients; however, no survival benefits were seen, a

131 e found increased MHC class II expression in BMT-derived microglia and decreased oxidative damage in

132 GVHD, sustain GVT, and prevent mortality in BMT.

133 re reduced (61.0% and 44.1% respectively) in BMT-recipient AD mice, which had 20.8% more retinal gang

134 nate immune function and oxidative stress in BMT recipient mice.

135 Transplantation of whole bone marrow (BMT) as well as ex vivo-expanded mesenchymal stromal cel

136 lar survivals to those seen with HLA-matched BMT.

137 ity complex (MHC)-mismatched and MHC-matched BMT following conditioning with lethal and sublethal irr

138 ing a minor histocompatibility Ag-mismatched BMT (B6 --> B6 x C3H.SW) followed by adoptive transfer o

139 major histocompatibility complex mismatched BMT with or without Treg cell infusion.

140 LI/ATG/alkylator regimens for MHC-mismatched BMT for hemoglobinopathies.

141 ic bone marrow transplant (BMT) mouse model, BMT mice with a reconstituted hematopoietic system displ

142 Here, we describe our approach to monitoring BMT survivors for risk-based screening and early detecti

143 ched sibling (matched sibling donors [MSDs]) BMT in 66 patients.

144 e initiation phase of acute GVHD in a murine BMT model.

145 Furthermore, in aged murine BMT recipients, the contribution of the MLNs to the gene

146 ed for its ability to prevent GVHD in murine BMT models across minor or major histocompatibility barr

147 ration was possible in an MHC-matched murine BMT model (B10.BR-->CBA) with a CBA-derived myeloid leuk

148 We observed that neonatal BMT was effective at restoring alpha-l-iduronidase activ

149 d Marrow Transplant Clinical Trials Network (BMT CTN) 0802, a phase 3 multicenter randomized double-b

150 d Marrow Transplant Clinical Trials Network (BMT CTN) phase 2 trial conducted from 2008 to 2014 enrol

151 Interestingly, the addition of BMT further increased the lifespan of treated mice and l

152 e COX-2 gene is hypomethylated in the AMs of BMT mice compared with control.

153 st disease remain important complications of BMT.

154 ysis model and estimated summary measures of BMT versus MMT on several outcomes.

155 Using well-characterized mouse models of BMT, we have studied the effects of AAT on GvHD severity

156 omised to DBS surgery (n=121) or 6 months of BMT (n=134).

157 HD, preserve GVT, and improve the outcome of BMT.

158 mune conditioning may improve the outcome of BMT.

159 educed intensity regimens have high rates of BMT rejection.

160 Since the first studies of BMT in the late 1980s, a number of conditioning regimens

161 e only minimally responsive if the timing of BMT delays, suggesting already irreversible bone damage.

162 Treatment of BMT or HSCT neutrophils with phorbol 12-myristate 13-ace

163 n 2 years and 98% occurred within 3 years of BMT.

164 tment, using the CSF-1R antagonist GW2580 or BMT from CCR2-deficient donors, reduced perineurial inva

165 Other BMT options include unrelated cord blood or mismatched f

166 26.1) in 16 thalassemia patients to perform BMT using phenotypically HLA-identical or 1-antigen-mism

167 To test this, we performed BMT in APPswe/PS1DeltaE9 double transgenic mice using gr

168 In the PGIA BMT model, after an initial predominance of host Tregs,

169 and COX-2 expression is elevated in AMs post-BMT.

170 ) T cells increased FoxP3(+) Treg cells post-BMT and prevented lethality, suggesting that the consequ

171 , including T cells, for up to 335 days post-BMT.

172 5), and miR-155 expression is decreased post-BMT.

173 ed innate immunity and PGE(2) elevation post-BMT are due to hypomethylation of the COX-2 gene, which

174 Because TGF-beta1 is elevated in lungs post-BMT, we tested whether TGF-beta1 could promote expressio

175 same BMT donor) was performed 4 months post-BMT without immunosuppression to assess for robust donor

176 ving an impaired innate immune response post-BMT.

177 Five weeks post-BMT, mice were necropsied, and lung and GI tissue were a

178 s must incorporate risks associated with pre-BMT therapy as well as risks related to transplant condi

179 Prenatal BMT versus MMT may improve neonatal outcomes, but bias m

180 nts who were conditioned but did not receive BMT.

181 II-III of the Pesaro classification received BMT (44%) compared with CBT (39%, P < .01).

182 cts were 515 neonates whose mothers received BMT and 855 neonates whose mothers received MMT and who

183 m, was achieved in the animals that received BMT without Treg cells (N = 3).

184 Patients with EC (N = 276) who received BMT were analyzed.

185 Compared to the group receiving BMT, the combined DBS group had significantly greater me

186 In comparison with patients receiving BMT (n = 259, TM; n = 130, SCD), those given CBT (n = 66

187 Renal transplantation (from the same BMT donor) was performed 4 months post-BMT without immun

188 The issues of how and when to screen BMT survivors for therapy-related complications and exac

189 s 3 thalassemia received HLA-matched sibling BMT following either the original protocol (26 patients)

190 These studies suggest that simultaneous BMT and VCA may establish indefinite allograft survival

191 Following STAT6(-/-) BMT, donor nTregs demonstrated no loss of proliferation

192 Subsequent BMT is itself an additional and distinct immunizing even

193 ansfused platelet products induce subsequent BMT rejection.

194 cipient mice that have undergone a syngeneic BMT or SP-A-sufficient recipient mice that have undergon

195 cipient mice that have undergone a syngeneic BMT) mice.

196 infection was self-limiting after syngeneic BMT, in the presence of GVHD after allogeneic BMT, CMV i

197 otency to those administered after syngeneic BMT.

198 -/-)) mice underwent allogeneic or syngeneic BMT with cells from either C3HeB/FeJ (H2k; SP-A-deficien

199 elopment of autoimmune disorder in syngeneic BMTs.

200 We conclude that BMT at a very early stage in life markedly reduces signs

201 We found that BMT suppressed the reduced myelination and the increased

202 These data are truly striking, given that BMT alone is ineffective, yet it synergizes with CNS-dir

203 eta in experimental AD, we hypothesized that BMT would mitigate retinal neurotoxicity through decreas

204 These data offer the possibility that BMT might provide the first therapy for MLIV.

205 Together, these findings suggest that BMT-derived APOE3-expressing cells are superior to those

206 t to prolong renal allograft acceptance: the BMT/renal mean survival time (MST, 76 days) was not sign

207 t peripheral donor cells originated from the BMT and not from the VCA.

208 reliable change from data obtained from the BMT group, the combined DBS group also displayed higher

209 ins, a significantly higher rate than in the BMT group (3%).

210 age treatment plays a lesser role,(1) in the BMT population, approximately 8% of all patients (or 36%

211 tates life-long risk-based monitoring of the BMT survivors.

212 to DBS surgery versus best medical therapy (BMT); and (2) randomised to subthalamic nucleus (STN) ve

213 rolled study comparing best medical therapy (BMT, n=116) and bilateral deep brain stimulation (DBS, n

214 itive chemoradiotherapy (bimodality therapy [BMT]) experience frequent relapses.

215 uction strategy with mixed chimerism through BMT in prior kidney or VCA recipients.

216 Thus, BMT is neuroprotective in age-related as well as AD-rela

217 mg, 95% CI: -7.26, 0.07) in those exposed to BMT.

218 we review whether CSCs may have relevance to BMT.

219 and those undergoing bone marrow transplant (BMT) are at greatest risk for contracting IFDs.

220 ths before and after bone marrow transplant (BMT) from his RSV-immune father.

221 d outcomes after blood or marrow transplant (BMT) have been conducted.

222 nt murine allogeneic bone marrow transplant (BMT) models.

223 Using our syngeneic bone marrow transplant (BMT) mouse model, BMT mice with a reconstituted hematopo

224 reported that murine bone marrow transplant (BMT) neutrophils overexpress cyclooxygenase-2, overprodu

225 receiving allogeneic bone marrow transplant (BMT) with minimal conditioning.

226 ceiving a bone marrow and renal transplant ("BMT/renal") and one receiving only a renal transplant.

227 Furthermore, BM transplantation (BMT) from either COX-2-deficient or mPGES-1-deficient mi

228 we generated 2 chimeric BM transplantation (BMT) models where both young green fluorescent protein (

229 d at 4 time points after BM transplantation (BMT).

230 te GVHD after allogeneic BM transplantation (BMT).

231 ogous bone marrow stem cell transplantation (BMT) were evaluated.

232 tolerance after bone marrow transplantation (BMT) across major histocompatibility complex (MHC) dispa

233 rance following bone marrow transplantation (BMT) across MHC barriers via recipient invariant NKT (iN

234 betaARKO) or WT bone-marrow transplantation (BMT) and after full reconstitution underwent MI surgery.

235 wing allogeneic bone marrow transplantation (BMT) and is characterized by tissue fibrosis manifesting

236 imerism through bone marrow transplantation (BMT) are currently being pursued.

237 allogeneic blood and marrow transplantation (BMT) as a curative therapy for hematological malignancie

238 g/replating and bone marrow transplantation (BMT) assays showed that Alox5 exhibited a moderate anti-

239 EW: Despite blood or marrow transplantation (BMT) being arguably the most active modality against hem

240 < .0001) after bone marrow transplantation (BMT) by inhibiting the initiation phase of acute GVHD in

241 rative and only bone marrow transplantation (BMT) can correct the underlying enzymatic defect.

242 Neonatal bone marrow transplantation (BMT) could offer a novel therapeutic opportunity for gen

243 ing a series of bone marrow transplantation (BMT) experiments in transgenic mice expressing single mu

244 Bone marrow transplantation (BMT) for class 3 patients with thalassemia is challengin

245 psing following bone marrow transplantation (BMT) has a dismal prognosis.

246 Indeed, bone marrow transplantation (BMT) has its genesis in rodent models dating back to the

247 ipients of blood and marrow transplantation (BMT) have been published by 3 major societies: American

248 es (AMs), after bone marrow transplantation (BMT) have impaired host defense against Gram-negative Ps

249 lowing congenic bone marrow transplantation (BMT) in a proteoglycan-induced arthritis (PGIA) mouse mo

250 ne therapy with bone marrow transplantation (BMT) in the INCL mouse.

251 wing allogeneic bone marrow transplantation (BMT) induce graft-versus-host (GVH) responses, but their

252 rs, HLA-matched bone marrow transplantation (BMT) is curative.

253 Bone marrow transplantation (BMT) is the other therapeutic option: a matched sibling

254 Blood or marrow transplantation (BMT) is used with curative intent for hematologic malign

255 re we show that bone marrow transplantation (BMT) of PARP-knockout (PARPKO) cells to wild-type mice p

256 ficantly affect bone marrow transplantation (BMT) outcomes.

257 Bone marrow transplantation (BMT) performance can be limited by a lack of ideal donor

258 Because bone marrow transplantation (BMT) results in decreased cerebral Abeta in experimental

259 s of allogeneic bone marrow transplantation (BMT) that intestinal inflammation secondary to graft-ver

260 n of allogeneic bone marrow transplantation (BMT) that involves the gastrointestinal (GI) tract and l

261 , which require bone marrow transplantation (BMT) to prevent early mortality.

262 created through bone marrow transplantation (BMT) using wild-type and CXCR2-knockout mice, yielding s

263 Haploidentical bone marrow transplantation (BMT) with 300 muCi (90)Y-anti-CD45 RIT and CY, without T

264 loidentical blood or marrow transplantation (BMT) with high-dose posttransplantation cyclophosphamide

265 ic by combining bone marrow transplantation (BMT) with kidney transplantation following non-myeloabla

266 fter allogeneic bone marrow transplantation (BMT), an effective therapy for hematological malignancie

267 fter allogeneic bone marrow transplantation (BMT), particularly in the presence of graft-versus-host

268 Here we use bone marrow transplantation (BMT), total body irradiation (TBI) and abdominal irradia

269 urine models of bone marrow transplantation (BMT), we find that MHCII(-/-)-->wild-type BMT developed

270 ents undergoing bone marrow transplantation (BMT).

271 r relapse after bone marrow transplantation (BMT).

272 t disease after bone marrow transplantation (BMT).

273 ution following bone marrow transplantation (BMT).

274 fter allogeneic bone marrow transplantation (BMT).

275 fects following bone marrow transplantation (BMT).

276 reported after bone marrow transplantation (BMT).

277 sirable goal in bone marrow transplantation (BMT).

278 allogeneic blood and marrow transplantation (BMT).

279 c recipients of bone marrow transplantation (BMT).

280 fter allogeneic bone marrow transplantation (BMT).

281 the efficacy of bone marrow transplantation (BMT).

282 wing allogeneic bone marrow transplantation (BMT).

283 CBT, n = 96) or bone marrow transplantation (BMT, n = 389).

284 onor bone marrow and cord blood transplants (BMT and CBT) for severe beta thalassemia (SBT) and sickl

285 We performed bone marrow transplants (BMT) from green fluorescent protein-expressing human APO

286 renatal buprenorphine maintenance treatment (BMT) versus methadone maintenance treatment (MMT) may im

287 A phase 3 clinical trial (BMT CTN 0402) comparing tacrolimus/sirolimus (Tac/Sir) v

288 n (BMT), we find that MHCII(-/-)-->wild-type BMT developed disease, with defective development of inn

289 llows thalassemia patients to safely undergo BMT from RDs who are not HLA-matched siblings, with tran

290 Using BMT (with unit cost of US$2-4) would cost US$70-121 mill

291 When BMT recipients were given MMC6-presensitized CD8(+)Vbeta

292 to wild-type mice protects against, whereas BMT of wild-type cells to PARPKO mice, which are normall

293 ts of unbiased genome-wide associations with BMT clinical outcomes given the ultimate goal of improvi

294 /5-mediated gene therapy in combination with BMT provides an unprecedented increase in lifespan as we

295 e replacement of host retinal microglia with BMT-derived cells and normalized total AD retinal microg

296 Fewer women treated with BMT used illicit opioids near delivery (risk ratio=0.44,

297 Interestingly, aged wt BMT recipients also had significantly more neurons (25.4

298 pared with approximately 20% mortality in WT BMT mice.

299 -MI survival rates comparable to those in WT BMT mice.

300 In adult p75KO with the WT-BMT, proliferative (Ki67(+)) cells were detected only by