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1 nto skin allografts in vivo in the humanized SCID mouse.
2 emely sensitive model of MCMV infection, the SCID mouse.
3 y to reverse hyperglycemia in a diabetic NOD-scid mouse.
4 l heart tissues s.c. into the ear pinna of a SCID mouse.
5 n 18,000 to 1 in 1,851,000 cells) in the NOD/SCID mouse.
6 ion in vivo were studied in the diabetic NOD-SCID mouse.
7 ctivated PBL and in vivo using the human PBL-SCID mouse.
8 G(-/-) mouse can transfer diabetes to an NOD.scid mouse.
9 that is both more attenuated than BCG in the SCID mouse and more potent than BCG in the guinea pig.
12 -Lin(-) cells were needed to engraft the NOD/SCID mouse as compared with the more permissive NOD/SCID
13 ue, Nakamura et al. (2013) describe a robust SCID mouse-based method for isolating human monoclonal a
14 cted in human precursor cells present in the SCID mouse BM and in leukocytes circulating in the perip
15 man CD14+ and CD19+ cells recovered from NOD/SCID mouse bone marrow and spleen following reconstituti
16 These results were confirmed in vivo in the scid mouse brain xenograft model in which propagation of
18 ocytoma clones injected intracerebrally into SCID mouse brains promotes tumor cell proliferation.
19 -2 therapy can prevent EBV-LPD in the hu-PBL-SCID mouse, but protection is lost if murine natural kil
23 study outline the effectiveness of the human-SCID mouse chimera system as a viable animal model of go
28 doptive T cell transfer into temporal artery-SCID mouse chimeras demonstrated that DCs in healthy art
29 trating macrophages in human temporal artery-SCID mouse chimeras disrupted nitrotyrosine generation,
30 nes adoptively transferred into human tissue-SCID mouse chimeras infiltrated rheumatoid synovium but
33 RIL were explored by treating human synovium-SCID mouse chimeras with the APRIL and BLyS decoy recept
34 ansferred into rheumatoid arthritis synovium-SCID mouse chimeras, these CD4 T cell clones enhanced th
39 ral artery-severe combined immunodeficiency (SCID) mouse chimeras were created by engrafting inflamed
40 n synovium-severe combined immunodeficiency (SCID) mouse chimeras were treated with TSP2-transfected
41 ral artery-severe combined immunodeficiency (SCID) mouse chimeras with the AR inhibitors Sorbinil and
42 man artery-severe combined immunodeficiency (SCID) mouse chimeras, adoptively transferred human T cel
43 GCA artery-severe combined immunodeficiency (SCID) mouse chimeras, depletion of CD83(+) dendritic cel
44 r either myelin or nonmyelin Ag, entered the SCID mouse CNS within 3-5 days of cell transfer and caus
45 ies that lead to fatal EBV-LPD in the hu-PBL-SCID mouse depleted of murine NK cells, and they point t
48 e used the severe combined immune deficient (SCID) mouse engrafted with human leukocytes (hu-PBL-SCID
49 mber of the severe combined immunodeficient (SCID) mouse eye and subsequently was inoculated with HCM
50 When transferred with recipient APC into a SCID mouse footpad, CD4(+) T cells were hyporesponsive i
54 using the severe combined immune deficiency (SCID) mouse HIV encephalitis model, which involves intra
55 exhibited less virulence than HSV-1 F in the SCID mouse host, enabling analysis of infection in human
57 a chimeric severe combined immunodeficiency (SCID) mouse (hu-SCID) model, that human V gamma 2V delta
58 trophozoites and human intestine, we used a SCID mouse-human intestinal xenograft (SCID-HU-INT) mode
63 l clone, BDC-6.9, in the immunodeficient NOD-scid mouse induces destruction of pancreatic beta-cells
65 l transfer severe combined immunodeficiency (SCID) mouse inflammatory bowel disease model demonstrate
67 e CB17 mice inhibited growth of T3C9 in CB17 SCID mouse intestine 11 days after p.o. inoculation.
70 oriatic human skin on transplantation to the SCID mouse is mediated, in large part, by amphiregulin.
71 he normal severe combined immune deficiency (SCID) mouse life span, although they contain proliferati
72 iabetic/severe combined immunodeficient (NOD/SCID) mouse line harboring a complete null mutation of t
76 We used three complementary strategies in a SCID mouse model and also addressed the underlying molec
77 y stronger antitumor activity in a xenograft SCID mouse model and depletes B cells in cynomolgus monk
78 a human disseminated CD23(+) B-cell lymphoma SCID mouse model and found greater antitumor activity wi
79 double auxotroph is fully attenuated in the SCID mouse model and highly immunogenic and protective i
80 yellow fever virus neuropathogenesis in the SCID mouse model and that the neuroinvasive properties d
81 hybrid fusion protein was as effective in a SCID mouse model as a fully active Ab-IL-2 fusion protei
82 We developed and validated a human (hu)RBC-SCID mouse model by giving nonobese diabetic/SCID mice d
83 ogether, these results validate the hHGF(tg)-SCID mouse model for in vivo determination of MET sensit
86 wth factor 1 when transplanted into the same SCID mouse model of acute myocardial infarction where th
87 ession is required for full virulence in the SCID mouse model of amebic liver abscess, but E. histoly
88 nd improves overall survival in the Emu-TCL1-SCID mouse model of CLL with minimal weight loss or othe
91 data, taken together, demonstrate that this SCID mouse model of HIV-1 neuropathogenesis can reproduc
96 c factors in JRA synovium, and to evaluate a SCID mouse model of JRA as an approach to study in vivo
98 tivity (IC50 = 10 nM) and oral activity in a SCID mouse model of Pf infection with an ED50 of 100 and
101 ZV infection of human skin xenografts in the SCID mouse model of VZV pathogenesis showed both that pC
102 seen after inoculation of human skin in the SCID mouse model or monolayers with higher-titered infec
103 granulation of human mast cells in the human/SCID mouse model provokes cellular inflammation in skin.
106 urther demonstrate the utility of the huPBMC-SCID mouse model to investigate the molecular and cellul
108 ssessed against P. falciparum in the in vivo SCID mouse model where the efficacy was found to be more
109 e erythrocytic stage of P. falciparum in the SCID mouse model with an ED90 of 11.7 mg/kg when dosed o
110 om all of the groups produced disease in the SCID mouse model, and genogroup-consistent trends were n
111 al infarct (MI) in the immunocompromised NOD-SCID mouse model, and monitored the effects of myocardia
114 ve against primary T. cruzi infection in our SCID mouse model, protective secondary effector function
115 s show the usefulness of the newly developed SCID mouse model, SN7-dgRA, and the clonotype-specific P
116 ng both in vitro systems and a humanized NOD/SCID mouse model, we demonstrate that BRCA1 expression i
134 A new severe combined immunodeficiency (SCID) mouse model consisting of highly disseminated huma
136 mononuclear cell reconstituted SCID (huPBMC-SCID) mouse model of allograft rejection, we compared th
137 we used the severe combined immunodeficient (SCID) mouse model of amebic liver abscess formation and
139 xenograft severe combined immunodeficiency (SCID) mouse model of disseminated B-cell lymphoma/leukem
142 Using a severe combined immunodeficient (SCID) mouse model of HIVE, we determined the effects of
143 sted with a severe combined immunodeficient (SCID) mouse model of human prostatic cancer and an immun
145 fts in the severe combined immunodeficiency (SCID) mouse model of VZV pathogenesis, and observed that
146 combined immunodeficiency (beta(2)m(-/-) NOD/SCID) mouse model paralleled clinical observations in hu
147 he severe combined immunodeficiency disease (SCID) mouse model, culture-expanded, cryopreserved human
148 Using a severe combined immunodeficient (SCID) mouse model, we demonstrate that enhanced expressi
161 ib was confirmed using 2 different xenograft SCID mouse models: human MM injected subcutaneously (the
164 iabetic/severe combined immunodeficient (NOD/SCID) mouse prostate or s.c., the alpha2beta1(+/hi) pros
168 , using the severe combined immunodeficient (SCID) mouse-psoriasis xenograft model, we report therape
169 ecause serum levels of CCL5 were the same in SCID mouse recipients receiving cells from either WT or
170 lls, because the arthritis that developed in SCID mouse recipients was similar to that in WT and CCR5
172 g stem cells, as well as primitive human NOD/SCID mouse repopulating cells, can bind extracellular ma
173 ts in a 7-fold increase in correction of NOD/SCID mouse repopulating X-CGD CD34+ PBSCs (14%-22% corre
177 em used the severe combined immunodeficient (scid) mouse that was depleted of NE with 6-hydroxydopami
183 pre-B cell line and in cells from the mutant scid mouse, where they largely conform to the hairpin st
184 iabetic/severe combined immunodeficient (NOD/scid) mouse, which lacks xenoantibodies and therefore al
185 mortal cell line (SPARKY) and transplantable scid mouse xenograft (Sparky-X) from a malignant pleural
189 potent in vivo antileukemic activity in NOD/SCID mouse xenograft models of relapsed and chemotherapy
190 used in a severe combined immune deficiency (SCID) mouse xenograft model to characterize a pathway li
193 de rat and severe combined immunodeficiency (SCID) mouse xenograft models of human uveal melanoma, wi
194 the in vivo efficacy of i.p. CPE therapy in SCID mouse xenografts in a highly relevant clinical mode
195 xpressed in severe combined immunodeficient (SCID) mouse xenografts by various human cancer cell line
197 abetic/severe combined immune-deficient (NOD/SCID) mouse xenotransplantation assay is the most common
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