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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.
11                     MFD-1 was tumorigenic in SCID mouse and proliferative and invasive in 3D cultures
12                    The genetically defective SCID mouse arose spontaneously from its parental strain
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
16                                         In a SCID mouse bioluminescent melanoma metastasis model, BRA
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
21 the C.B.17 severe combined immunodeficiency (scid) mouse brain.
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
24           The findings indicate that the NOD/scid mouse can provide a unique tool for studying DITP p
25 lear cell (MNC) homing in vivo into an RA ST-SCID mouse chimera (P < 0.05).
26           We used an RA synovial tissue (ST)-SCID mouse chimera model to evaluate the role of H-2g in
27 study outline the effectiveness of the human-SCID mouse chimera system as a viable animal model of go
28           We utilized the RA synovial tissue SCID mouse chimera system to examine human microvascular
29 ed normal human ST was then examined in this SCID mouse chimera system.
30                          Using a human RA ST-SCID mouse chimera, immunohistochemistry, enzyme-linked
31  H-2g-induced MNC recruitment into the RA ST-SCID mouse chimera.
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
35                              Normal human ST-SCID mouse chimeras injected intragraft with gouty SF th
36 synovitis was confirmed by treating synovium-SCID mouse chimeras with IL-16.
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
39  CD8 T cells were depleted in human synovium-SCID mouse chimeras.
40 ptive transfer experiments in human synovium-SCID mouse chimeras.
41  the atheroma was examined in human atheroma-SCID mouse chimeras.
42 human skin/severe combined immunodeficiency (SCID) mouse chimeras bearing tumors of MCF-7.
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
50 posed of DC and macrophages obtained from B6 SCID mouse donors.
51                                              scid mouse embryonic fibroblasts are deficient in DNA-de
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
55 veal melanoma growth in the same nude rat or SCID mouse for up to a month.
56 e diabetic/severe combined immunodeficiency (SCID) mouse has been a particularly useful model.
57                  Cell lines derived from the SCID mouse have been utilised as a model DNA-PKcs-defect
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
60 (HSE, also called Apligraf) in the humanized SCID mouse (hu-PBL-SCID).
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
63                                              SCID mouse-human JRA synovium chimeras may provide a goo
64 m using the severe combined immunodeficient (SCID) mouse-human skin model of psoriasis.
65                                In a chimeric SCID mouse/human synovial tissue (ST) model, mice were e
66  capable of preventing EBV-LPD in the hu-PBL-SCID mouse in the absence of murine NK cells.
67 l clone, BDC-6.9, in the immunodeficient NOD-scid mouse induces destruction of pancreatic beta-cells
68 on was required by B. burgdorferi throughout SCID mouse infection if the vlsE gene were absent.
69                                The SARS-CoV2 SCID mouse infection model, which is ideally suited for
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
72                                       An ICR/SCID mouse insulinoma model was used to show that insuli
73 e CB17 mice inhibited growth of T3C9 in CB17 SCID mouse intestine 11 days after p.o. inoculation.
74                           Using a xenogeneic scid mouse intracranial glioma model, R4009 therapy of e
75                               In a syngeneic scid mouse intracranial tumor model, recombinant herpes
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
79                             In the humanized SCID mouse, local injection of Netrin-1 into skin enhanc
80 ell potency and oral activity in a humanized SCID mouse malaria infection model.
81 nts leading to efficacy in the P. falciparum SCID mouse malaria model.
82  recently developed non-obese diabetic (NOD)/SCID mouse may expand the uses of the SCID model.
83                                   falciparum SCID mouse model after oral administration.
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
93                                   A JAK3 -/- SCID mouse model for the human disease has been used to
94 airs VZV infection of skin xenografts in the SCID mouse model in vivo.
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
98                       Here we use the hu-PBL-SCID mouse model of Epstein-Barr virus (EBV)-associated
99                                    Second, a SCID mouse model of HIV-1 encephalitis (HIVE) was used t
100  data, taken together, demonstrate that this SCID mouse model of HIV-1 neuropathogenesis can reproduc
101 c CTL responses in a nonobese diabetic (NOD)-SCID mouse model of HIVE.
102      Comparable results were obtained with a SCID mouse model of human melanoma.
103                                         In a SCID mouse model of human NSCLC tumorigenesis, expressio
104                                     Using an SCID mouse model of human prostate cancer metastasis, we
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 (
108                     Methods: A highly lethal SCID mouse model of minimal-tumor-burden disseminated no
109               The high in vivo efficacy in a SCID mouse model of P. falciparum malaria, good oral bio
110 tivity (IC50 = 10 nM) and oral activity in a SCID mouse model of Pf infection with an ED50 of 100 and
111                                      Using a SCID mouse model of Pneumocystis carinii pneumonia, we w
112 F invasion into coimplanted cartilage in the SCID mouse model of RA.
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.
116                                   The Hu-PBL-SCID mouse model system, when used with appropriate phyl
117 a P. falciparum infection in a humanized NOD/SCID mouse model system.
118 urther demonstrate the utility of the huPBMC-SCID mouse model to investigate the molecular and cellul
119 livery system, was used in an insulinoma ICR/SCID mouse model to prevent hypoglycemic death.
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
125                     Moreover, in a humanized SCID mouse model, CD19(+) CD5(-) B cells were more effec
126                         In the reconstituted SCID mouse model, depletion of CD8+ cells in addition to
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
130                            Using a humanized SCID mouse model, we demonstrate that soluble and membra
131 determinants of viral neuroinvasiveness in a SCID mouse model.
132 h that of neonatal skin grafts in the huPBMC-SCID mouse model.
133 an MM cell growth and prolongs survival in a SCID mouse model.
134 e resolution of primary RV infection using a SCID mouse model.
135 PC-3 tumor growth in a human prostate cancer/SCID mouse model.
136 nts in the human peripheral blood lymphocyte-SCID mouse model.
137  isolates of HIV-1 in vivo, using the hu-PBL-SCID mouse model.
138 of human and nonhuman primate T cells in the SCID mouse model.
139 ls metastasized to axillary lymph nodes in a SCID mouse model.
140 EC313, for the treatment for UFs using a NOD-SCID mouse model.
141 f micrometastatic human B-cell lymphoma in a SCID mouse model.
142 ne in the recently established P. falciparum SCID mouse model.
143  and IgE plasma cell numbers in a human PBMC-SCID mouse model.
144 a undetectable in vivo using a P. falciparum SCID mouse model.
145 uated for their roles in this phenotype in a SCID mouse model.
146 ated cartilage invasion were examined in the SCID mouse model.
147  determinant of YFV neuroinvasiveness in the SCID mouse model.
148  a severe combined immunodeficiency disease (SCID) mouse model and enhanced antitumor activity.
149      A new severe combined immunodeficiency (SCID) mouse model consisting of highly disseminated huma
150  a severe combined immunodeficiency disease (SCID) mouse model in vivo.
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
153 ocytes in a severe combined immunodeficient (SCID) mouse model of amebic liver abscess.
154  xenograft severe combined immunodeficiency (SCID) mouse model of disseminated B-cell lymphoma/leukem
155        In a severe combined immunodeficient (SCID) mouse model of disseminated, residual lymphoma, an
156 nction in a severe combined immunodeficient (SCID) mouse model of HIV-1 encephalitis (HIVE).
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
159 compromized severe combined immunodeficient (SCID) mouse model of orthotopic breast cancer.
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
164 formed in a severe combined immunodeficient (SCID) mouse model.
165 r xenograft/severe combined immunodeficient (SCID) mouse model.
166 g a human/severe combined immune deficiency (SCID) mouse model.
167 onses in a severe combined immunodeficiency (SCID) mouse model.
168  tumors in severe combined immunodeficiency (SCID) mouse model.
169  orthotopic severe combined immunodeficient (SCID) mouse model.
170        Both the Tax-transgenic and engrafted SCID mouse models allow for the analysis of cellular eve
171                         Five frequently used SCID mouse models and their specific applications are su
172 .5 in murine melanoma-C57 and human melanoma-Scid mouse models, respectively.
173 phoma and Hodgkin lymphoma cells and in vivo SCID mouse models.
174  show good efficacy in Plasmodium falciparum SCID mouse models.
175  and infused them into BBM tumor-bearing NOD/SCID mouse models.
176 s derived from HCT-116 and NCI-H460 cells in SCID mouse models.
177 s, we investigated whether shaving occurs in SCID mouse models.
178 ib was confirmed using 2 different xenograft SCID mouse models: human MM injected subcutaneously (the
179 dium berghei malaria model as well as in the SCID mouse P. falciparum model.
180 th mouse passage but could be resurrected by SCID mouse passage.
181 iabetic/severe combined immunodeficient (NOD/SCID) mouse prostate or s.c., the alpha2beta1(+/hi) pros
182       The data suggest that the HSV-infected SCID mouse provides a proinflammatory microenvironment t
183                                   The hu-SRC-SCID mouse provides an unprecedented opportunity to gain
184         The severe combined immunodeficient (SCID) mouse provides such a model.
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
188 der the kidney capsule of 3Gy irradiated NOD/SCID mouse recipients.
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
191          Furthermore, in the presence of NOD/SCID mouse serum, there was no complement-mediated lysis
192                           LPS stimulation of SCID mouse splenocytes resulted in measurable IFN-gamma
193 disorder in human cells in vivo with the NOD/SCID mouse system using onco-retrovirus vector.
194 em used the severe combined immunodeficient (scid) mouse that was depleted of NE with 6-hydroxydopami
195  lines in a severe combined immunodeficient (SCID) mouse tibial injection model.
196  human skin-severe combined immunodeficient (SCID) mouse transplant model.
197 one marrow (BM)-derived CD34+ cells in a NOD/SCID mouse transplantation model.
198                       CCR5 expression in the SCID mouse was sufficient to clear CCL5, because serum l
199        Transplanted psoriasis plaques on the SCID mouse were treated weekly for 4 weeks with intraper
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
203 o therapeutic efficacy was demonstrated in a SCID mouse xenograft leukemia/lymphoma model.
204                                        In an SCID mouse xenograft model, low-dose metronomic paclitax
205                                           In SCID mouse xenograft models of anaplastic large cell lym
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
208 abetic/severe combined immunodeficiency (NOD/SCID) mouse xenograft model.
209 ctivity in severe combined immunodeficiency (SCID) mouse xenograft models of Hodgkin disease.
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
213 leukemia initiation in anti-CD122-primed NOD/SCID mouse xenotransplantation.
214 abetic/severe combined immune-deficient (NOD/SCID) mouse xenotransplantation assay is the most common

 
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