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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 eas homozygous mutations in Prkdc define the Scid mouse, a model that has been widely used in biology
10 that is both more attenuated than BCG in the SCID mouse and more potent than BCG in the guinea pig.
13 -Lin(-) cells were needed to engraft the NOD/SCID mouse as compared with the more permissive NOD/SCID
14 ue, Nakamura et al. (2013) describe a robust SCID mouse-based method for isolating human monoclonal a
15 these data demonstrate the validity of this SCID mouse Beta B.1.351 variant infection model as a con
17 cted in human precursor cells present in the SCID mouse BM and in leukocytes circulating in the perip
18 man CD14+ and CD19+ cells recovered from NOD/SCID mouse bone marrow and spleen following reconstituti
19 ltaMLD, the virus remained active within the SCID mouse brain and showed widespread infection of norm
20 These results were confirmed in vivo in the scid mouse brain xenograft model in which propagation of
22 ocytoma clones injected intracerebrally into SCID mouse brains promotes tumor cell proliferation.
23 -2 therapy can prevent EBV-LPD in the hu-PBL-SCID mouse, but protection is lost if murine natural kil
27 study outline the effectiveness of the human-SCID mouse chimera system as a viable animal model of go
32 doptive T cell transfer into temporal artery-SCID mouse chimeras demonstrated that DCs in healthy art
33 trating macrophages in human temporal artery-SCID mouse chimeras disrupted nitrotyrosine generation,
34 nes adoptively transferred into human tissue-SCID mouse chimeras infiltrated rheumatoid synovium but
37 RIL were explored by treating human synovium-SCID mouse chimeras with the APRIL and BLyS decoy recept
38 ansferred into rheumatoid arthritis synovium-SCID mouse chimeras, these CD4 T cell clones enhanced th
43 ral artery-severe combined immunodeficiency (SCID) mouse chimeras were created by engrafting inflamed
44 n synovium-severe combined immunodeficiency (SCID) mouse chimeras were treated with TSP2-transfected
45 ral artery-severe combined immunodeficiency (SCID) mouse chimeras with the AR inhibitors Sorbinil and
46 man artery-severe combined immunodeficiency (SCID) mouse chimeras, adoptively transferred human T cel
47 GCA artery-severe combined immunodeficiency (SCID) mouse chimeras, depletion of CD83(+) dendritic cel
48 r either myelin or nonmyelin Ag, entered the SCID mouse CNS within 3-5 days of cell transfer and caus
49 ies that lead to fatal EBV-LPD in the hu-PBL-SCID mouse depleted of murine NK cells, and they point t
52 e used the severe combined immune deficient (SCID) mouse engrafted with human leukocytes (hu-PBL-SCID
53 mber of the severe combined immunodeficient (SCID) mouse eye and subsequently was inoculated with HCM
54 When transferred with recipient APC into a SCID mouse footpad, CD4(+) T cells were hyporesponsive i
58 using the severe combined immune deficiency (SCID) mouse HIV encephalitis model, which involves intra
59 exhibited less virulence than HSV-1 F in the SCID mouse host, enabling analysis of infection in human
61 a chimeric severe combined immunodeficiency (SCID) mouse (hu-SCID) model, that human V gamma 2V delta
62 trophozoites and human intestine, we used a SCID mouse-human intestinal xenograft (SCID-HU-INT) mode
67 l clone, BDC-6.9, in the immunodeficient NOD-scid mouse induces destruction of pancreatic beta-cells
70 l transfer severe combined immunodeficiency (SCID) mouse inflammatory bowel disease model demonstrate
71 h for confirming a diagnosis of BMD but that SCID mouse inoculation could be a useful complement to P
73 e CB17 mice inhibited growth of T3C9 in CB17 SCID mouse intestine 11 days after p.o. inoculation.
76 oriatic human skin on transplantation to the SCID mouse is mediated, in large part, by amphiregulin.
77 he normal severe combined immune deficiency (SCID) mouse life span, although they contain proliferati
78 iabetic/severe combined immunodeficient (NOD/SCID) mouse line harboring a complete null mutation of t
84 We used three complementary strategies in a SCID mouse model and also addressed the underlying molec
85 y stronger antitumor activity in a xenograft SCID mouse model and depletes B cells in cynomolgus monk
86 a human disseminated CD23(+) B-cell lymphoma SCID mouse model and found greater antitumor activity wi
87 double auxotroph is fully attenuated in the SCID mouse model and highly immunogenic and protective i
88 yellow fever virus neuropathogenesis in the SCID mouse model and that the neuroinvasive properties d
89 hybrid fusion protein was as effective in a SCID mouse model as a fully active Ab-IL-2 fusion protei
90 We developed and validated a human (hu)RBC-SCID mouse model by giving nonobese diabetic/SCID mice d
91 tly milder hemotoxicity in the humanized NOD/SCID mouse model engrafted with red blood cells from G6P
92 ogether, these results validate the hHGF(tg)-SCID mouse model for in vivo determination of MET sensit
95 wth factor 1 when transplanted into the same SCID mouse model of acute myocardial infarction where th
96 ession is required for full virulence in the SCID mouse model of amebic liver abscess, but E. histoly
97 nd improves overall survival in the Emu-TCL1-SCID mouse model of CLL with minimal weight loss or othe
100 data, taken together, demonstrate that this SCID mouse model of HIV-1 neuropathogenesis can reproduc
105 ormal and IPF fibroblasts and in a humanized SCID mouse model of IPF employing both short interfering
106 c factors in JRA synovium, and to evaluate a SCID mouse model of JRA as an approach to study in vivo
107 vivo proof of concept was established in an SCID mouse model of malaria, after oral administration (
110 tivity (IC50 = 10 nM) and oral activity in a SCID mouse model of Pf infection with an ED50 of 100 and
113 ZV infection of human skin xenografts in the SCID mouse model of VZV pathogenesis showed both that pC
114 seen after inoculation of human skin in the SCID mouse model or monolayers with higher-titered infec
115 granulation of human mast cells in the human/SCID mouse model provokes cellular inflammation in skin.
118 urther demonstrate the utility of the huPBMC-SCID mouse model to investigate the molecular and cellul
120 ssessed against P. falciparum in the in vivo SCID mouse model where the efficacy was found to be more
121 e erythrocytic stage of P. falciparum in the SCID mouse model with an ED90 of 11.7 mg/kg when dosed o
122 tivity against P. falciparum infections in a SCID mouse model with an oral dosing regimen that is wel
123 om all of the groups produced disease in the SCID mouse model, and genogroup-consistent trends were n
124 al infarct (MI) in the immunocompromised NOD-SCID mouse model, and monitored the effects of myocardia
127 ve against primary T. cruzi infection in our SCID mouse model, protective secondary effector function
128 s show the usefulness of the newly developed SCID mouse model, SN7-dgRA, and the clonotype-specific P
129 ng both in vitro systems and a humanized NOD/SCID mouse model, we demonstrate that BRCA1 expression i
149 A new severe combined immunodeficiency (SCID) mouse model consisting of highly disseminated huma
151 mononuclear cell reconstituted SCID (huPBMC-SCID) mouse model of allograft rejection, we compared th
152 we used the severe combined immunodeficient (SCID) mouse model of amebic liver abscess formation and
154 xenograft severe combined immunodeficiency (SCID) mouse model of disseminated B-cell lymphoma/leukem
157 Using a severe combined immunodeficient (SCID) mouse model of HIVE, we determined the effects of
158 sted with a severe combined immunodeficient (SCID) mouse model of human prostatic cancer and an immun
160 fts in the severe combined immunodeficiency (SCID) mouse model of VZV pathogenesis, and observed that
161 combined immunodeficiency (beta(2)m(-/-) NOD/SCID) mouse model paralleled clinical observations in hu
162 he severe combined immunodeficiency disease (SCID) mouse model, culture-expanded, cryopreserved human
163 Using a severe combined immunodeficient (SCID) mouse model, we demonstrate that enhanced expressi
178 ib was confirmed using 2 different xenograft SCID mouse models: human MM injected subcutaneously (the
181 iabetic/severe combined immunodeficient (NOD/SCID) mouse prostate or s.c., the alpha2beta1(+/hi) pros
185 , using the severe combined immunodeficient (SCID) mouse-psoriasis xenograft model, we report therape
186 ecause serum levels of CCL5 were the same in SCID mouse recipients receiving cells from either WT or
187 lls, because the arthritis that developed in SCID mouse recipients was similar to that in WT and CCR5
189 g stem cells, as well as primitive human NOD/SCID mouse repopulating cells, can bind extracellular ma
190 ts in a 7-fold increase in correction of NOD/SCID mouse repopulating X-CGD CD34+ PBSCs (14%-22% corre
194 em used the severe combined immunodeficient (scid) mouse that was depleted of NE with 6-hydroxydopami
200 pre-B cell line and in cells from the mutant scid mouse, where they largely conform to the hairpin st
201 iabetic/severe combined immunodeficient (NOD/scid) mouse, which lacks xenoantibodies and therefore al
202 mortal cell line (SPARKY) and transplantable scid mouse xenograft (Sparky-X) from a malignant pleural
206 potent in vivo antileukemic activity in NOD/SCID mouse xenograft models of relapsed and chemotherapy
207 used in a severe combined immune deficiency (SCID) mouse xenograft model to characterize a pathway li
210 de rat and severe combined immunodeficiency (SCID) mouse xenograft models of human uveal melanoma, wi
211 the in vivo efficacy of i.p. CPE therapy in SCID mouse xenografts in a highly relevant clinical mode
212 xpressed in severe combined immunodeficient (SCID) mouse xenografts by various human cancer cell line
214 abetic/severe combined immune-deficient (NOD/SCID) mouse xenotransplantation assay is the most common