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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
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
17 oid organs, and target organs of aGvHD after BMT showed significantly reduced numbers of miR-181a-tra
20 present on donor dendritic cells (DCs) after BMT in the setting of myeloablative conditioning but is
24 when reconstructing antiviral immunity after BMT, and highlight the mechanisms by which the adoptive
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
33 ver, specific depletion of donor Tregs after BMT also induced cGVHD, whereas adoptive transfer of Tre
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
42 aintained their expansion in irradiated allo-BMT recipients, as well as their in vivo and ex vivo cyt
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.
49 Allogeneic bone marrow transplantation (allo-BMT) is a curative therapy for hematological malignancie
54 MT, in the presence of GVHD after allogeneic BMT, CMV induced a striking cytopathy resulting in unive
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
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)
65 monstrate, using murine models of allogeneic BMT, that type 2 innate lymphoid cells (ILC2s) in the lo
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
73 strong predictor of outcome for both IST and BMT, and must be considered when designing therapeutic s
75 Jalpha18(-/-) BALB/c recipients of TLI/ATS + BMT restored day-6 donor Foxp3(+) nTreg proliferation an
79 ouse model, Tcm therapy following autologous BMT led to significant survival prolongation, with 30% t
81 -based (RSP), 2) non-sputum Biomarker-based (BMT), 3) triage test followed by confirmatory test (TT),
83 actobacillales from the flora of mice before BMT aggravated GVHD, whereas reintroducing the predomina
86 rbidity, coupled with a long latency between BMT and the development of chronic health conditions nec
89 eveloped and evaluated the radiotracer (11)C-BMT-136088 (1-(4'-(3-methyl-4-(((1(R)-(3-(11)C-methylphe
92 ntration leading to a 50% reduction of (11)C-BMT-136088 specific binding were 73 +/- 30 nmol/kg and 2
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
98 conjunction with allogeneic T-cell-depleted BMT could be of particular benefit in patients with B-ce
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
105 g a rotarod test, we demonstrated that early BMT greatly delayed the motor impairment in the mutant m
107 Cancer Therapy-Bone Marrow Transplant (FACT-BMT) were received from 109 ex-thalassemia patients who
109 re, we studied CAR T-cell function following BMT using an immunocompetent murine model of minor misma
113 nsive review articles, clinicians caring for BMT recipients continue to field frequently asked questi
120 ears, who received NMA, T-cell-replete haplo-BMT with high-dose post-transplantation cyclophosphamide
122 oietic lineages 28 days after haploidentical BMT with 69.3 +/- 14.1%, 75.6 +/- 20.2%, and 88.5 +/- 11
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
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
133 re reduced (61.0% and 44.1% respectively) in BMT-recipient AD mice, which had 20.8% more retinal gang
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
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
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
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
155 Using well-characterized mouse models of BMT, we have studied the effects of AAT on GvHD severity
161 e only minimally responsive if the timing of BMT delays, suggesting already irreversible bone damage.
164 tment, using the CSF-1R antagonist GW2580 or BMT from CCR2-deficient donors, reduced perineurial inva
166 26.1) in 16 thalassemia patients to perform BMT using phenotypically HLA-identical or 1-antigen-mism
170 ) T cells increased FoxP3(+) Treg cells post-BMT and prevented lethality, suggesting that the consequ
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
178 s must incorporate risks associated with pre-BMT therapy as well as risks related to transplant condi
182 cts were 515 neonates whose mothers received BMT and 855 neonates whose mothers received MMT and who
189 s 3 thalassemia received HLA-matched sibling BMT following either the original protocol (26 patients)
194 cipient mice that have undergone a syngeneic BMT or SP-A-sufficient recipient mice that have undergon
196 infection was self-limiting after syngeneic BMT, in the presence of GVHD after allogeneic BMT, CMV i
198 -/-)) mice underwent allogeneic or syngeneic BMT with cells from either C3HeB/FeJ (H2k; SP-A-deficien
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
206 t to prolong renal allograft acceptance: the BMT/renal mean survival time (MST, 76 days) was not sign
208 reliable change from data obtained from the BMT group, the combined DBS group also displayed higher
210 age treatment plays a lesser role,(1) in the BMT population, approximately 8% of all patients (or 36%
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
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
226 ceiving a bone marrow and renal transplant ("BMT/renal") and one receiving only a renal transplant.
228 we generated 2 chimeric BM transplantation (BMT) models where both young green fluorescent protein (
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
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
243 ing a series of bone marrow transplantation (BMT) experiments in transgenic mice expressing single mu
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
251 wing allogeneic bone marrow transplantation (BMT) induce graft-versus-host (GVH) responses, but their
255 re we show that bone marrow transplantation (BMT) of PARP-knockout (PARPKO) cells to wild-type mice p
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
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
284 onor bone marrow and cord blood transplants (BMT and CBT) for severe beta thalassemia (SBT) and sickl
286 renatal buprenorphine maintenance treatment (BMT) versus methadone maintenance treatment (MMT) may im
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
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
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