ライフサイエンスコーパス: SCID mice

1 acers revealed uptake in activated hPBMCs in SCID mice.

2 tient-derived xenografts tumors implanted in SCID mice.

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

4 elial thickening under in vivo conditions in SCID mice.

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

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

7 lucose levels in streptozotocin diabetic NOD/SCID mice.

8 of D-galactosamine and lipopolysaccharide in SCID mice.

9 human islets following implantation into NOD/scid mice.

10 lls were injected intraperitoneally into NOD/SCID mice.

11 driven medulloblastoma tumors allografted in SCID mice.

12 hairpin RNA, which were xenotransplanted in SCID mice.

13 and experimental metastatic potential in NOD/SCID mice.

14 stablish glucose homeostasis in diabetic NOD/SCID mice.

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

16 ansferring diabetes into immunodeficient NOD.scid mice.

17 sis following islet transplantation into NOD/scid mice.

18 osteolysis of implanted human bone chips in SCID mice.

19 raft tumors were implanted subcutaneously in SCID mice.

20 transplanted into sublethally irradiated NOD/SCID mice.

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

22 cell engraftment when transplanted into NOD/SCID mice.

23 the skeletal muscle of immunocompromised NOD.SCID mice.

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

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

26 imary human pancreatic adenocarcinoma in NOD SCID mice.

27 glucose lowering in streptozotocin-diabetic SCID mice.

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

29 pancreatic cancer cells was evaluated in NOD SCID mice.

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

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

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

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

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

35 loped in streptozotocin-induced diabetic NOD/SCID mice.

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

37 RT responses reported in tumors implanted in SCID mice.

38 cells causing disseminated overt leukemia in SCID mice.

39 f EBV-induced lymphoproliferative disease in SCID mice.

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

41 human bone chip implanted subcutaneously in SCID mice.

42 resulted in exacerbated ileitis severity in SCID mice.

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

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

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

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

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

48 nocyte migration into sponges implanted into SCID mice.

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

50 ell responses, as demonstrated by the use of SCID mice.

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

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

53 onses to PyV infection when transferred into SCID mice.

54 h ability of AGS gastric cancer cells in NOD/SCID mice.

55 ted human islets in the liver of healthy NOD/SCID mice.

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

57 plantation of tumor cells into B6.CB17-Prkdc SCID mice.

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

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

60 passive transfer of immune sera to infected SCID mice.

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

62 ells and the growth of a Panc-1 xenograft in SCID mice.

63 conducted on LNCaP tumor-bearing male CB-17 SCID mice.

64 njected intrarectally into nonobese diabetic/SCID mice.

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

66 subcutaneous pockets on the dorsal flanks of SCID mice.

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

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

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

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

71 ferred into severe combined immunodeficient (SCID) mice.

72 grafted on severe combined immunodeficiency (SCID) mice.

73 growth in severe combined immunodeficiency (SCID) mice.

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

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

76 cleared by severe combined immunodeficient (SCID) mice.

77 cytes into severe combined immunodeficiency (SCID) mice.

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

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

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

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

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

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

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

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

86 or-bearing severe combined immunodeficiency (SCID) mice after sacrifice at defined time points up to

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

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

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

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

91 as performed in 143B and OS-17 tumor-bearing SCID mice and followed by radioimmunotherapy (RIT) with

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

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

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

95 tumor inhibition was similar in nude and Nod-Scid mice and was less efficient than seen for SK-MEL-14

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

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

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

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

100 2 knockdown invasive MDA-MB-231 cells in NOD/SCID mice, and compared parental and bone-derived varian

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

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

103 intravenously into immune-competent and NOD/SCID mice, and lung metastases were quantified.

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

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

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

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

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

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

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

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

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

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

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

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

116 [(55)Co]Co-DOTATATE by PET/CT imaging in NOD-SCID mice bearing subcutaneous somatostatin receptor-exp

117 iabetic/severe combined immunodeficient (NOD/SCID) mice bearing human PSMA(+) PC3 PIP and PSMA(-) PC3

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

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

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

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

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

123 ol groups (n = 6-7) using C4-2 tumor-bearing SCID mice by evaluating tumor growth and survival over 6

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

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

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

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

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

129 ells implanted into the femoral bone of male SCID mice caused massive bone loss and stimulation of mo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

163 ired for the development of lung fibrosis in SCID mice humanized with IPF lung fibroblasts.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

178 SCID mice injected with CXCL16-depleted RA SF exhibited

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

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

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

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

183 studied in severe combined immunodeficient (SCID) mice inoculated with activated hPBMCs in Matrigel.

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

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

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

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

188 Using a human MM/SCID mice model, the combination of bortezomib and SP101

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

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

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

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

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

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

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

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 ion of RGS12-overexpressed OSCC cells in NOD scid mice showed a significant reduction in tumor format

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

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

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

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

218 eted cell lines showed prolonged survival of SCID mice, suggesting a possible implication for overexp

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

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

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

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

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

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

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

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

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

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

229 T patient-derived xenografts (WTPDX) in CB17 scid(-/-) mice that capture the biological heterogeneity

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

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

232 3.5 months post-implantation into SCID mice, the micro-computed tomography imaging showed

233 ensity S. Typhi transposon library in hu-SRC-SCID mice to identify virulence loci using transposon-di

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

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

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

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

247 However, the response in Nod-Scid mice was less robust.

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

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

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

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

252 Using immunodeficient SCID mice, we focused on targeting human brain tumors wi

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

254 SCID mice were also more insulin sensitive with increase

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

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

257 SCID mice were infected and treated with sulfadiazine to

258 SCID mice were infected with 1.1-1.5 x 108 B. microti-in

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 hen ectopic human xenograft LNCaP tumours in SCID mice were treated with SDT using the systemically-a

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

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

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

267 9xTCR DART to inhibit B-cell lymphoma in NOD/SCID mice when coadministered with human PBMCs supports

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 ion of U2OS cells into the tibia bone of NOD-scid mice, which indicated that miR-449a and miR-424 co-

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

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

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

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

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

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

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

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

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 suppression, and flow chamber assays and in SCID mice with human intestinal xenografts.

287 SCID mice with human PC3 prostate cancer xenografts (Gro

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 culation of severe combined immunodeficient (SCID) mice yielded isolates from 5 of 5 samples, but 0 o