ライフサイエンスコーパス: SCID mice

1 hairpin RNA, which were xenotransplanted in SCID mice.

2 and experimental metastatic potential in NOD/SCID mice.

3 being injected into the motor cortex of NOD-SCID mice.

4 ansferring diabetes into immunodeficient NOD.scid mice.

5 sis following islet transplantation into NOD/scid mice.

6 osteolysis of implanted human bone chips in SCID mice.

7 transplanted into sublethally irradiated NOD/SCID mice.

8 ne resulting in a 3-fold greater exposure in SCID mice.

9 ed in three-dimensional Matrigel implants in SCID mice.

10 cell engraftment when transplanted into NOD/SCID mice.

11 astatic nodule formation in the lungs of NOD/SCID mice.

12 the skeletal muscle of immunocompromised NOD.SCID mice.

13 L phenotype induced by OCI-AML3 cells in NOD/SCID mice.

14 rmation of secondary lymphoid organs, in NOD/SCID mice.

15 imary human pancreatic adenocarcinoma in NOD SCID mice.

16 glucose lowering in streptozotocin-diabetic SCID mice.

17 -cell line that produced CNS leukemia in NOD-SCID mice.

18 pancreatic cancer cells was evaluated in NOD SCID mice.

19 ing allografts from murine BCC tumors in NOD/SCID mice.

20 cinoma cells were determined in vitro and in SCID mice.

21 Jurkat T cell homing to lymphoid tissues in scid mice.

22 tion and growth in the orthotopic setting in SCID mice.

23 plant in streptozotocin-induced diabetic NOD.scid mice.

24 uced ability to form secondary tumors in NOD/SCID mice.

25 RT responses reported in tumors implanted in SCID mice.

26 cells causing disseminated overt leukemia in SCID mice.

27 f EBV-induced lymphoproliferative disease in SCID mice.

28 number of leukemia cells that engraft in NOD-scid mice.

29 human bone chip implanted subcutaneously in SCID mice.

30 resulted in exacerbated ileitis severity in SCID mice.

31 m SW1222 megacolonies initiate tumors in NOD/SCID mice.

32 rom p40(-/-) mice failed to protect infected SCID mice.

33 PKcs-deficient dogs that are not apparent in SCID mice.

34 passive transfer of immune sera to infected SCID mice.

35 on in a T-cell-induced inflammation model in SCID mice.

36 erance to human islet cells in humanized NOD/SCID mice.

37 nocyte migration into sponges implanted into SCID mice.

38 lls to the marrow but not the spleens of NOD/SCID mice.

39 nonobese diabetic (NOD) versus humanized NOD/SCID mice.

40 of both were placed subcutaneously into NOD/SCID mice.

41 onses to PyV infection when transferred into SCID mice.

42 to transfer diabetes to immunodeficient NOD.scid mice.

43 3-FKHR with or without MYCN formed tumors in SCID mice.

44 nd Srsf10, but not Ptbp2, in the PLNs of NOD.SCID mice.

45 enza-only-infected muMT mice or likewise for SCID mice.

46 er severe TEC H/P to IFN-gamma(-/-)NOD.H-2h4.SCID mice.

47 lade C (HIV-1(Indie-C1)) HIV-1 isolates into SCID mice.

48 nd caused diabetes when transferred into NOD.scid mice.

49 were coinjected into the mammary fat pad of SCID mice.

50 njected intrarectally into nonobese diabetic/SCID mice.

51 human diffuse large B lymphoma model in NOD-SCID mice.

52 r using tail vein injection of A549 cells in SCID mice.

53 death between 6 and 8 days postinfection in SCID mice.

54 y for self-renewal and tumorigenicity in NOD/SCID mice.

55 elial thickening under in vivo conditions in SCID mice.

56 systems in wild-type (WT), neu-tolerant, and SCID mice.

57 asion in vitro and prevented tumor growth in SCID mice.

58 lucose levels in streptozotocin diabetic NOD/SCID mice.

59 of D-galactosamine and lipopolysaccharide in SCID mice.

60 human islets following implantation into NOD/scid mice.

61 lls were injected intraperitoneally into NOD/SCID mice.

62 driven medulloblastoma tumors allografted in SCID mice.

63 iabetic/severe combined immunodeficient (NOD/SCID) mice.

64 ferred into severe combined immunodeficient (SCID) mice.

65 grafted on severe combined immunodeficiency (SCID) mice.

66 growth in severe combined immunodeficiency (SCID) mice.

67 iabetic-severe combined immunodeficient (NOD-SCID) mice.

68 iabetic/severe combined immunodeficient (NOD/SCID) mice.

69 cleared by severe combined immunodeficient (SCID) mice.

70 cytes into severe combined immunodeficiency (SCID) mice.

71 aneously in severe combined immunodeficient (SCID) mice.

72 abetic/severe combined immunodeficiency (NOD/SCID) mice.

73 abetic severe combined immunodeficiency (NOD/SCID) mice.

74 mor-bearing severe combined immunodeficient (SCID) mice.

75 the lung of severe combined immunodeficient (SCID) mice.

76 mmatory cytokines and in the pancreas of NOD.SCID mice after adoptive transfer of activated autologou

77 njected human CD34(+) cells in the hearts of SCID mice after experimental MI, and used selective anti

78 eous and intracranial melanoma xenografts in SCID mice after tail vein virus application.

79 Skin inflammation was induced in BALB/c scid/scid mice after they received CD4+CD45RB(high)CD25- (nai

80 the requirements to induce tolerance in nod.scid mice after transfer of transgenic beta-cell reactiv

81 mor-bearing severe combined immunodeficient (SCID) mice after a bolus dose (18,500 kBq [500 microCi])

82 hearts of severe combined immune deficiency (SCID) mice after experimental MI and to determine the me

83 ned if passive transfer of 1E4 would protect SCID mice against C. burnetii aerosol infection.

84 the absence of adaptive immune responses in SCID mice, allowing the establishment of neuronal latenc

85 d for at least 60 days at high levels in NOD/Scid mice and at lower levels in the absence of CD4(+) a

86 y formation and orthotopic GBM growth in NOD/SCID mice and decelerates the progression of low-grade a

87 ablish infection in both immunocompetent and SCID mice and has been proposed to facilitate evasion of

88 yclin D1 were transplanted into diabetic NOD-SCID mice and markedly outperformed native human islets

89 ome to the marrow but not the spleens of NOD/SCID mice and that this homing defect can be corrected b

90 C infection model in human gut xenografts in SCID mice and used it to study the role of T3SS in the p

91 mor-bearing severe combined immunodeficient (SCID) mice and in genetically altered SCID mice expressi

92 d into severe combined immunodeficient (CB17-scid) mice and inoculated by direct injection with the V

93 e of C.B.17 severe combined immunodeficient (scid) mice and tumor cells invading in a modified Boyden

94 infarcted neonatal and adult heart tissue to scid mice, and adoptive transfer of labeled bone marrow,

95 2 knockdown invasive MDA-MB-231 cells in NOD/SCID mice, and compared parental and bone-derived varian

96 susceptible BALB/c mice, immune compromised SCID mice, and human VL model hamsters 10 wk after infec

97 ue culture infective dose) of MARV/Ang-MA in SCID mice, and i.p. infection at a dose of 1,000x LD50 r

98 lanoma cells into the spleen capsules of NOD-SCID mice, and metastases were quantified by measuring t

99 e were able to enhance anti-TB protection in SCID mice, and the transfer of vaccine-primed B cells al

100 e combined immunodeficiency (scid) mutation (SCID) mice, and SCID bearing a null mutation in the IL-2

101 cal control (TCD(50)) of tumors implanted in SCID mice are not significantly different from the TCD(5

102 ry glands of the functional ribozyme-treated SCID mice at 21 days after infection were 200- to 2,000-

103 injecting 5.5 MBq of 99mTc-anti-CD56 mAb in SCID mice bearing ARO tumor xenografts in the right thig

104 Eight additional SCID mice bearing HCT116 xenografts in dorsal skinfold w

105 ti-CD56 and to image human NK trafficking in SCID mice bearing human cancer.

106 ed in 2 murine xenograft models of human MM: SCID mice bearing human MM cells subcutaneously and the

107 After injection in SCID mice bearing human PC-3 xenografts all analogues sh

108 uch deposits using passive transfer of Ab to SCID mice bearing human skin grafts.

109 mall-animal PET studies were performed using SCID mice bearing MDA-MB-435 tumor xenografts.

110 SCID mice bearing MDA-MB-435 xenografts were used as an

111 s found to have potent antitumor activity in SCID mice bearing MDA-MB231 human breast cancer xenograf

112 Treatment of SCID mice bearing MDA-PCa-118b tumors with LDN-193189 si

113 ls were increased in the peripheral blood of SCID mice bearing prostate cancer xenografts but not in

114 ytes, within 2 weeks after transfer, the ITP SCID mice became thrombocytopenic (< 200 x 10(9) platele

115 was fully resolved in 7/8 nonobese diabetic/SCID mice being infected with a multidrug resistant HSV-

116 the 50% infectious dose than the control in SCID mice but a dramatic increase in immunocompetent mic

117 e-induced abnormalities were not observed in SCID mice but did occur in SCID mice that were adoptivel

118 nocytes can transfer ABD and T1D to NOD.c3c4 scid mice, but only T1D to NOD scid mice, suggesting tha

119 Type 1 diabetes induction in NOD-Scid mice by adoptive transfer with NOD-Ncf1(m1J) spleno

120 suppression of prostate cancer xenografts in SCID mice by forced expression of GPx3 suggests a tumor

121 s a crucial element in the cure of tumors in SCID mice by single-dose radiotherapy (SDRT).

122 In pancreatic tumors established in NOD SCID mice, c-Met inhibitors slowed tumor growth and redu

123 Severe combined immunodeficient (SCID) mice carry a germ-line mutation in DNA-PK, associa

124 he in vivo prostate regeneration assay, host SCID mice carrying Src(Y529F)-transduced regeneration ti

125 passages in severe combined immunodeficient (SCID) mice caused severe disease when administered intra

126 o B cells in the spleens of the PyV-infected SCID mice change phenotype, with many of them displaying

127 ator, severe combined immune deficiency (uPA-SCID) mice" (chimeric mice).

128 Transfer of BALB/c splenocytes to SCID mice conferred rapid disease following infection, a

129 oter; yet, xenograft tumors generated in NOD/SCID mice contained approximately 67% GFP(+) cells, whic

130 In contrast, most of the SCID mice continued to have positive cultures at 60 days

131 When injected into NOD SCID mice, control GFP NCM-1 cells fail to grow whereas

132 SCID mouse model by giving nonobese diabetic/SCID mice daily transfusions of huRBCs from G6PD-deficie

133 uman monocytes and NKTs to tumor-bearing NOD/SCID mice decreased monocyte number at the tumor site an

134 gs with C. burnetii Nine Mile phase I (NMI), SCID mice developed pneumonia and splenomegaly and succu

135 cells from splenocytes transferred into NOD.scid mice did not decrease helminth-mediated protection

136 st, the observation that tumors implanted in SCID mice do not exhibit hypersensitivity to radiation m

137 Depletion of NK cells in NOD/SCID mice enabled combined systemic and CNS leukemia of

138 Treatment of SCID mice engrafted with G6PD-deficient huRBCs with prim

139 o effect of MPA treatment was studied in NOD/SCID mice engrafted with HCV replicon cells.

140 In uPA/SCID mice engrafted with human hepatocytes, APs efficien

141 d significantly prolongs the survival of NOD/SCID mice engrafted with primary ALL.

142 nd reduced serum IgM, IgG, and IgE levels in SCID mice engrafted with SLE or healthy human PBMC.

143 vator (uPA)/severe combined immunodeficient (SCID) mice engrafted with human hepatocytes.

144 vere combined immunodeficient mice (hHGF(tg)-SCID mice) enhances the growth of many MET-expressing hu

145 dioligand uptake in human PC-3 xenografts in SCID mice escalated from less than 4 %ID/g to greater th

146 adaptive immunity was required because most SCID mice eventually succumbed to local tumor recurrence

147 HTLV-1-HU-NOD/SCID mice exclusively developed CD4(+) T-cell lymphomas

148 cient (SCID) mice and in genetically altered SCID mice expressing human PDGFRalpha in place of murine

149 Both CD4-deficient and SCID mice failed to eliminate the infection and did not

150 In DNA-PK-deficient SCID mice, feeding-induced USF-1 phosphorylation/acetyla

151 of the conducive marrow niche environment of scid mice for xenotransplantation.

152 otection of severe combined immunodeficiency SCID mice from disseminated candidiasis (100% survival i

153 y), repeated doses of peramivir rescued BALB scid mice from lethal challenge with BR/08, but did not

154 In an in vivo model of SCID mice grafted with human skin and reconstituted with

155 cells into severe combined immunodeficient (SCID) mice, green fluorescent protein (GFP)-marked human

156 pheral blood mononuclear cells (PBMC) in NOD/SCID mice harboring xenografts of MDA-MB-231, a triple-n

157 engraftment studies, the function of HSCs of scid mice has not been characterized.

158 Although scid mice have been widely used for human HSC engraftmen

159 ografts transplanted into kidney capsules of SCID mice (ie, mice with severe combined immunodeficienc

160 ody production in iNKT-deficient mice and in SCID mice implanted with B cells.

161 tolerated doses when administered orally to SCID mice implanted with PTEN-deficient human tumor xeno

162 ly increased the survival of PEL bearing NOD-SCID mice in an orthotopic xenograft model as compared w

163 ted wild-type mice were transferred into the SCID mice in combination with treatment with anti-CXCL9

164 ion and fibrosis in IFN-gamma(-/-) NOD.H-2h4 SCID mice in the absence of CD4(+) T cells.

165 ted in vitro and in human skin xenografts in SCID mice in vivo and that STAT3 activation induces the

166 s in vitro and with human skin xenografts in SCID mice in vivo.

167 a dramatic reduction of RCC tumor growth in SCID mice in vivo.

168 NOD/SCID mice in which diabetes was induced by streptozotoci

169 te that the injection of TLR7 agonist in NOD/SCID mice, in C57BL/6 wild-type, and TLR7-deficient mice

170 rrence was observed in WT, neu-tolerant, and SCID mice, indicating a role of adaptive immunity in con

171 cells from immunocompetent donors protected SCID mice infected with E. cuniculi, whereas administrat

172 CB17 SCID mice infected with R. typhi(GFPuv) succumb to the i

173 In experiments with SCID mice infected with S. pneumoniae, we found passive

174 On the other hand, SCID mice injected with BTLA(-/-) CD4(+) T cells and WT

175 SCID mice injected with CXCL16-depleted RA SF exhibited

176 SCID mice injected with WT CD4(+) T cells and BTLA(-/-)

177 In severe combined immunodeficient (SCID) mice injected with Fyn shRNA-expressing cells, mye

178 ng experiments were performed on 2 groups of SCID mice inoculated subcutaneously with increasing numb

179 In a tumor xenograft model using SCID mice inoculated with Huh7 cells, administration of

180 Immunodeficient SCID mice inoculated with VACVs not expressing IFN-gamma

181 In NOD/SCID mice, labeled MSCs introduced into the tibia traffi

182 ) oocysts/mouse in SCID beige (SCIDbg) mice (SCID mice lacking functional NK cells), oocyst shedding

183 ibited peritoneal dissemination of tumors in SCID mice, leading to improved tumor-free survival in a

184 abetic severe combined immunodeficiency (NOD/SCID) mice leads to the development of multiple lineages

185 RFP-Luc-Sk-Hep-1 were implanted into NOD-scid mice livers and followed by using bioluminescence i

186 aneously in severe combined immunodeficient (SCID) mice, MDA-PCa-118b induced strong ectopic bone for

187 further extended to in vivo Swiss albino and SCID mice models also revalidated the anti-carcinogenic

188 ry was induced in the right eye of adult NOD-SCID mice (n = 23) by transient elevation of intraocular

189 lantation outcome in nonobese diabetic (NOD) scid mice (n=8).

190 trate that profile induction in infected C3H scid mice occurs independently of B or T lymphocyte infi

191 mulation in tumors of MDA-MB-435 xenografted SCID mice of approximately 1.10 +/- 0.20 percentage inje

192 ine-primed T cells from Jh(-/-) KO mice into SCID mice only provided suboptimal protection.

193 on lymphoid cells, as immunization of either SCID mice or immunocompetent mice depleted of CD4(+) T c

194 DNA-PK function was abolished genetically in SCID mice or inhibited biochemically by the DNA-PK inhib

195 e donors were transferred to immunodeficient SCID mice prior to CNS challenge.

196 eneration of a TP that when infused into NOD/SCID mice produced mature RBCs containing both human adu

197 Compared with SCID mice receiving naive splenocytes, within 2 weeks af

198 Death occurred later in NOD/SCID mice receiving REH cells depleted of CD9 for transp

199 NOD/SCID mice reconstituted with CD34(+) HP/HSCs transduced

200 SCID mice reconstituted with either CD4+ T cells or CD8+

201 peripheral blood (mPB) CD34+ cells into NOD/SCID mice, reduced numbers of PMF CD34+ cells and granul

202 ss Pdx1, Ngn3, and MafA in the livers of NOD-SCID mice rendered diabetic by treatment with streptozot

203 we found that splenic B cells transferred to SCID mice responded to polyoma virus (PyV) infection wit

204 dissociated mouse neonatal ovary cells into SCID mice resulted in a homogenous germ cell cluster for

205 abetic/severe combined immunodeficiency (NOD-SCID) mice resulted in the formation of microvessels der

206 e hypothesized that the DNA repair defect of scid mice results in a stem cell defect that facilitates

207 Screening of transposon pools in hu-SRC-SCID mice revealed both known and previously unknown Sal

208 cardiotoxin-injured skeletal muscles of NOD/SCID mice reveals survival and engraftment of the donor

209 n transplanted into dystrophic muscle in MDX/SCID mice, SASCs from injured muscle generated greater e

210 ntation into the nonobese diabetic SCID (NOD/SCID) mice; secondary transplantation was performed to e

211 Pharmacokinetic studies in PC-3 xenograft SCID mice showed approximately 72% retention of (198)AuN

212 s before transplantation into B2M (null) NOD/scid mice showed significantly improved preservation of

213 vo studies with xenotransplant models in NOD-scid mice showed that OPN expression increases cancer gr

214 ravital microscopy in immunocompromised (NOD/SCID) mice showed that intravenously infused HCELL(+) MS

215 d' Fbs are co-grafted with melanoma cells in SCID mice, shRNA-mediated blockade of WISP-1 reverses th

216 rate within the LNs of immunocompromised NOD.SCID mice similar to murine lymphocytes.

217 tively infected human gliomas implanted into SCID mice subcutaneously or intracranially.

218 f in vivo platelet counts in the transferred SCID mice suggesting that anti-CD20 therapy significantl

219 ent growth, and xenograft tumor formation in SCID mice, suggesting that AR-dependent ARD1 expression

220 This defect was abrogated in SCID mice, suggesting that BatB functions to resist clea

221 D to NOD.c3c4 scid mice, but only T1D to NOD scid mice, suggesting that the genetic origin of the tar

222 ly terminated in all lineages except the NOD/Scid mice, suggesting the existence of redundant pathway

223 betic (NOD)-severe combined immunodeficient (SCID) mice, suggesting that ATRA in combination with TCP

224 lation of a CD4(+) T-cell lymphoma in HU-NOD/SCID mice suggests that HSCs provide a viral reservoir i

225 partment of severe-combined-immunodeficient (SCID) mice temporarily suppressed the onset or level of

226 In contrast, SCID mice that have a deficient adaptive immune response

227 inherent property of LICs, substrains of NOD/SCID mice that possess additional deletions such as the

228 e not observed in SCID mice but did occur in SCID mice that were adoptively transferred with wild-typ

229 We determined that Bxv1 was also present in SCID mice that were used for in vivo propagation of Endo

230 In the spleen and liver of infected CB17 SCID mice, the bacteria are detectable by immunofluoresc

231 Finally, following high-dose infection of SCID mice, the dbpBA mutant exhibited only a mild coloni

232 In BALB/c and SCID mice, the gE2-del virus caused no death or disease

233 3.5 months post-implantation into SCID mice, the micro-computed tomography imaging showed

234 cells also impaired host resistance of CB-17 scid mice to Rickettsia, similar to what was observed in

235 e also used Slc11a1 knockout-SCID and Idd5.2-SCID mice to show that both loss-of-function alleles pro

236 ferred into severe combined immunodeficient (SCID) mice to induce ITP.

237 with human hematopoietic stem cells (hu-SRC-SCID mice) to cause a lethal infection with pathological

238 ly target human synovial microvasculature in SCID mice transplanted with human arthritic synovial xen

239 NOD/SCID mice transplanted with human pancreatic islets and

240 In vivo studies included serial MRI of NOD-SCID mice transplanted with MN-small interfering (si)Cas

241 Furthermore, in SCID mice transplanted with neural progenitors derived f

242 rowth was significantly less frequent in the SCID mice treated with anti-CXCL9 serum than in mice tre

243 However, the extent to which NOD/SCID mice underestimate the frequency of tumorigenic hum

244 minant meningococcemia in human skin grafted SCID mice using the wild-type strain 2C4.3.

245 Arthritis was transferred to SCID mice, using spleen cells from arthritic WT and CCR5

246 constructs were delivered into MCMV-infected SCID mice via a modified "hydrodynamic transfection" pro

247 human cell lines and their xenografts in NOD/SCID mice via IL-6 production.

248 n ALK-positive ALCL tumor xenograft model in SCID mice, warranting further assessment in advanced pre

249 o immunodeficient and diabetes-resistant NOD.scid mice was mitigated by FKGK18 pretreatment and 2) TN

250 ma implanted in the dorsal window chamber of SCID mice was observed following tail vein administratio

251 omogenates of MARV-infected immunodeficient (SCID) mice was highly successful in reducing the time to

252 oduce estrogen-dependent xenograft tumors in SCID mice, we also observed lower ERalpha protein levels

253 growth of a PDA cell line as a xenograft in SCID mice, we also show that a slightly pathogenic avian

254 Finally, through transplantation in NOD-SCID mice, we found that cancer stem/progenitor cells is

255 SCID mice were also more insulin sensitive with increase

256 rus (HBV) chronically infected humanized uPA/SCID mice were employed to establish a small animal mode

257 e response to C. burnetii natural infection, SCID mice were exposed to aerosolized C. burnetii.

258 SCID mice were infected and treated with sulfadiazine to

259 diabetes onset in NOD mice, nondiabetic NOD/SCID mice were injected with inflammatory T cells from d

260 Human immune system (HIS) BLT-NOD/SCID mice were inoculated intravenously with a low-passa

261 d by injection of colon tumor cells into NOD/SCID mice were positively associated with GnT-V levels,

262 and tolerize islet-specific CD8(+) T cells, SCID mice were reconstituted so that the host and lympho

263 tic severe combined immunodeficiency (HU-NOD/SCID) mice were generated by inoculation of NOD/SCID mic

264 Severe combined immunodeficient (SCID) mice were infected and treated with sulfadiazine t

265 nduced CHS, severe combined immunodeficient (SCID) mice were injected with CD4(+) T cells, and CD8(+)

266 9xTCR DART to inhibit B-cell lymphoma in NOD/SCID mice when coadministered with human PBMCs supports

267 wth experiments showed tumors grew faster in SCID mice when cocultures of tumor-reactive CTLs and bor

268 or greatly reduced in WT, neu tolerant, and SCID mice when CpG was incorporated in the cryoablation

269 firmed in the adoptive transfer model of NOD-SCID mice where tolDCs delayed diabetes onset.

270 DeltagD(-/+gD1) elicited no disease in SCID mice, whereas 1000-fold lower doses of wild-type vi

271 tive mutant CerS6, increased tumor growth in SCID mice, whereas siRNA-mediated knockdown of CerS6 ind

272 Interestingly, NOD/SCID mice, which have a deficiency in T, B, and NK cells

273 SCID mice, which lack an adaptive immune system due to t

274 of radiolabeled antibody in the tail vein of SCID mice, which were then sacrificed at 1, 3, 6, and 24

275 tagged PMNs were injected intravenously into SCID mice while, simultaneously, diluted gouty SF contai

276 reventing metastasis and angiogenesis in NOD-SCID mice, while being non-toxic in vivo.

277 ent protein were transplanted into adult NOD/SCID mice with acute left anterior descending artery lig

278 ive techniques to measure kidney function in SCID mice with adriamycin-induced nephropathy.

279 D) mice were generated by inoculation of NOD/SCID mice with CD34(+) hematopoietic progenitor and stem

280 egs was also observed upon reconstitution of SCID mice with CD4(+) T cells from CD25 knockout mice (w

281 treatment of HCT-116 colon tumor-bearing ICR SCID mice with curcumin resulted in decreased tumor grow

282 gineered T cells (T-bodies) was evaluated in SCID mice with different PAC xenografts.

283 duced disease-free survival in tumor-bearing SCID mice with early-stage disease and in models that ar

284 ition, allogeneic platelet transfusions into SCID mice with established CD61-induced ITP rescued the

285 SCID mice with human HCT116 cancer xenografts were image

286 SCID mice with human PC3 prostate cancer xenografts (Gro

287 genesis in vivo, MAb 206 was administered to SCID mice with human skin xenografts inoculated with VZV

288 is by approximately 2-fold in ApoE(-/-)/scid/scid mice with increased leukocyte accumulation and peri

289 In SCID mice with KB tumors, 1 was highly active against bo

290 Treatment of GBM xenografts in NOD/SCID mice with NK cells from a KIR2DS2(+) donor lacking

291 codelivered intramyocardially into adult NOD/SCID mice with saline, MC-green fluorescent protein, or

292 In SCID mice with tumor xenografts, mPGES-1 overexpression

293 However, reconstitution of SCID mice with wild-type CD4(+) T cells restored Treg de

294 abetic severe combined immunodeficiency (NOD SCID) mice with MSCs isolated from Lewis bone marrow and

295 abetic/severe combined immunodeficiency (NOD/SCID) mice with partially reconstituted immune systems w

296 ically localized in human PC-3 xenografts in SCID mice, with [(111)In-DOTA]GRP(17-27) exhibiting the

297 scid HSC, WT BM cells were transplanted into scid mice without any conditioning and observed to achie

298 EL cells into the peritoneal cavities of NOD/SCID mice without in vitro cell growth to avoid the chan

299 7 xenograft severe combined immunodeficient (SCID) mice without discernible toxicity.

300 ivo renders these vaccines safer than BCG in SCID mice yet is sufficient to induce potent cell-mediat