ライフサイエンスコーパス: C3H mice

1 hed from a MMTV-induced mammary carcinoma in C3H mice.

2 cheae were heterotopically transplanted into C3H mice.

3 F-I KO mice were comparable to those seen in C3H mice.

4 ed after needle and tickborne inoculation of C3H mice.

5 values in AKR mice and the lowest values in C3H mice.

6 DC were injected subcutaneously into normal C3H mice.

7 diation-induced fibrosarcoma tumors grown in C3H mice.

8 res in comparison to RAG+ and RAG- BALB/c or C3H mice.

9 reas increases in IFN-gamma were observed in C3H mice.

10 or vector persistence in livers of C57BL/6 x C3H mice.

11 y reactivity were observed in OVA-challenged C3H mice.

12 resistance to Leishmania major infection in C3H mice.

13 re present in significantly lower numbers in C3H mice.

14 ungs of immunocompetent C57BL/6, BALB/c, and C3H mice.

15 number nor the length of vessels changed in C3H mice.

16 ficient shiverer and MBP-expressing congenic C3H mice.

17 ls of antibody were significantly greater in C3H mice.

18 trast, AM depletion did not alter killing in C3H mice.

19 terine horns of C57 mice compared to that of C3H mice.

20 o the poor osteogenic response to loading in C3H mice.

21 ed a genetically homogeneous group of agouti C3H mice.

22 al profile associated with severe disease in C3H mice.

23 nger able to cause arthritis and carditis in C3H mice.

24 itis severity scores over those of wild-type C3H mice.

25 ase A2 messenger RNA levels in the joints of C3H mice.

26 e SCC cells were implanted subcutaneously in C3H mice.

27 ction of arthritis- and carditis-susceptible C3H mice.

28 harbored higher bacterial loads compared to C3H mice.

29 induced fibrosarcoma tumor transplanted into C3H mice.

30 n and suppressed Th1/Th2 cell development in C3H mice.

31 an early gene expression profile similar to C3H mice.

32 e were similar to what was seen in wild-type C3H mice.

33 epair, which were decreased in the joints of C3H mice.

34 on of these genes in the bones of B6 but not C3H mice.

35 dendritic cells (DCs) in T reg cell-depleted C3H mice.

36 e G6PD mutant (G6PD(mut)) and wild-type (WT) C3H mice.

37 tely 1 week earlier than the control-treated C3H mice.

38 t mice compared with no deaths for wild-type C3H mice.

39 tes from class II molecules of MHC-identical C3H mice.

40 C57BL) and mycoplasma-susceptible C3H/HeNCr (C3H) mice.

41 istant C57BL/6 (B6) and susceptible C3H/HeN (C3H) mice.

42 istant C57BL/6 (B6) and -susceptible C3H/He (C3H) mice.

43 mplant site and interstitium of MRL +/+ than C3H +/+ mice.

44 esignated KLmB-3) was derived from resistant C3H mice 2 weeks after infection with Leishmania major.

45 ctors 15-22) on to the shaved dorsal skin of C3H mice 30 min before each exposure to 4.54 kJ ultravio

46 IL-12 depletion of C3H mice also suppressed OVA-specific serum IgG2a levels

47 differentially expressed in joints of B6 and C3H mice and correlated with the development of Lyme art

48 wed little effect in genetically susceptible C3H mice and did not decrease the inherent resistance of

49 a burgdorferi-induced arthritis is severe in C3H mice and milder in C57BL/6 (B6) mice has allowed a f

50 /2J (DBA) and arthritis-susceptible C3H/HeJ (C3H) mice and infected them with Borrelia burgdorferi.

51 BL/6 mice than from the lungs of susceptible C3H mice, and consequently, C57BL/6 mice generate an imm

52 cytokine in vivo in B. burgdorferi infected C3H mice, and evaluated the effects of treatment on the

53 Findings were compared to those in control C3H mice, and in response to Cu chelation by penicillami

54 Gastric epithelial erosions were noted in C3H mice, and mucous cell hyperplasia was observed in C3

55 of Borrelia burgdorferi-induced arthritis in C3H mice, and was remarkable due to its absence in the m

56 In C3H mice, anti-CD25-mediated T reg cell depletion before

57 In COX-2 inhibitor-treated or COX-2-/- C3H mice, arthritis developed normally but did not resol

58 ive genes was observed in severely arthritic C3H mice at 1 wk of infection, which was absent from mil

59 p-regulated in Borrelia burgdorferi-infected C3H mice at 1 wk postinfection.

60 Morbidly ill C3H mice at 14 days had severe pulmonary edema, hemoglob

61 Histopathology of BALB/cJ and C3H mice at 9 and 14 days after inoculation revealed ery

62 ponse apparent in Mel(1a) receptor-deficient C3H mice at higher melatonin concentrations (100 nM) is

63 In conventional BALB/c or C3H mice, B7-2 functions as the dominant costimulatory m

64 dazole (FMISO) at 2 and 4 h postinjection in C3H mice bearing KHTn tumors (130-430 mg).

65 able bacteriopurpurinimide was determined in C3H mice bearing radiation induced fibrosarcoma tumors a

66 s 1-3 were evaluated for the PDT efficacy in C3H mice bearing RIF tumors at variable doses and showed

67 uptake of these compounds were determined in C3H mice bearing RIF tumors by in vivo reflectance spect

68 Using syngeneic Stat1-/- C3H mice bearing SCCVII tumors in this study, we discove

69 ments suggested that T reg cell depletion in C3H mice before sensitization was sufficient to enhance

70 In C3H mice, BFR/BS was significantly greater (P = 0.05) in

71 c mice, while the neutralization of IL-12 in C3H mice blocks increased IL-12 receptor expression.

72 B. burgdorferi burden compared to that in WT C3H mice both at peak disease and during resolution.

73 ssage 75 isolate (N40-75) was infectious for C3H mice but did not cause arthritis or carditis, and sp

74 In conclusion, C3H mice but not C57BL/6 mice receiving multiple vaccina

75 rgdorferi yields severe arthritis in C3H/He (C3H) mice but only minimal arthritis in BALB/c mice.

76 id mice at 1 or 2 weeks and then declined in C3H mice, but they continued to rise and then plateaued

77 ibrosarcomas (RIF-1) was measured in vivo in C3H mice by following the production of [3-(13)C]lactate

78 Compared to wild-type C3H+/+ mice, C3Hgld mice had a similar bacterial burden

79 species specific, we studied tumors in rats, C3H mice, C57BL6 mice, and nude mice.

80 of these responses were further examined in C3H mice carrying the type I IFN receptor gene ablation,

81 ific antibody-producing cells in co-infected C3H mice compared to B6 mice as early as 2 weeks postinf

82 ower levels in PNETs from invasion-resistant C3H mice compared with invasion-susceptible B6 mice, and

83 irway reactivity in OVA-challenged resistant C3H mice, concomitant with significant increases in bron

84 Spontaneous autochthonous tumors in aged C3H mice consisted of s.c. sarcomas and adenocarcinomas,

85 Whereas nonpregnant female C3H mice consistently developed severe Lyme arthritis, p

86 However, anti-IL-12-treated C3H mice continued to produce IL-12 in spite of exhibiti

87 trast to C3H mice given anti-IL-12 for 3 wk, C3H mice continuously treated with anti-IL-12 failed to

88 ient (SCID) mice nor RIF-1 tumors growing in C3H mice demonstrated radiosensitization after Gd-tex tr

89 Moreover, 80% of C3H mice depleted of CD8 and CD4 cells died of E. muris

90 Leishmania major-infected C3H mice develop a Th1 response, but studies have shown

91 hritis: BALB/c mice develop mild disease and C3H mice develop severe arthritis that is most pronounce

92 nfection with Borrelia burgdorferi: infected C3H mice develop severe arthritis while infected C57BL/6

93 C3H mice developed severe arthritis of the tibiotarsal j

94 enovirus antibody formation, only Balb/c and C3H mice developed significant levels of anti-hAAT antib

95 While susceptible C3H mice developed swelling of ankle joints during the s

96 f experimental Lyme borreliosis by infecting C3H mice devoid of the common IL-17 receptor A subunit (

97 st to Balb/c mice, the loss of expression in C3H mice did not correlate with the loss of vector genom

98 latent inhibition, but 129/SvJ, CBA, A, and C3H mice did not.

99 BALB/c and C3H mice differed in their susceptibilities to infection

100 that administration of rIL-4 to susceptible C3H mice during the first week of infection with Bb lead

101 t secretions of C57 mice compared to that of C3H mice during the first week of infection.

102 tected between BALB/c and anti-IL-12-treated C3H mice early after infection, suggesting that the inst

103 usly shown that M. tuberculosis infection of C3H mice elicits CFP-10-specific CD8+ and CD4+ T cells.

104 Plasmid analysis of sequential isolates from C3H mice experimentally infected with the primary isolat

105 The majority of C3H mice exposed to RST1-infected ticks contained cultiv

106 tify UV-damaged cells in the skin and DLN of C3H mice exposed to UV radiation.

107 C3H mice expressing WT Gusb as a transgene were protecte

108 ization with recombinant P21 did not protect C3H mice from tick-borne B. burgdorferi infection, and p

109 mune response to M. tuberculosis sooner than C3H mice generate an immune response.

110 In C3H mice given 5-Gy whole-body irradiation, there was a

111 In contrast to C3H mice given anti-IL-12 for 3 wk, C3H mice continuousl

112 Survival of B10 cardiac allografts in C3H mice given B10 TGF-beta-transduced DC (2x106 IV, 7 d

113 by both H-2Kb and H2Db was dominant, and in C3H mice, H-2Dk-restricted presentation of ALP was domin

114 Recipient C3H mice (H2k) were made diabetic and either untreated o

115 Both BALB/c and C3H mice had a Th1 response in draining lymph nodes, wit

116 , 129S1/SvImJ, LP/J, WSB/EiJ, NZO/HILtJ, and C3H mice had intermediate severity.

117 C3H mice had poorer protection from a syngeneic MART-1-e

118 killing and five of six 5-FC-treated Tg/NCD-C3H mice had reduced tumor compared with controls.

119 C3H mice, harboring the radiation-induced fibrosarcoma t

120 a standard fluorometric assay in C3H/HeOuJ (C3H) mice homozygous for a new mutation, gusmps2J.

121 II gene knockout mice and CD4 cell-depleted C3H mice (i.e., through a gamma interferon or antibody m

122 C3H mice immunized with PADs developed antibodies and T

123 In contrast, the immune response of C3H mice in the lung was characterized by a delayed and

124 sistant DBA/2 (DBA) and susceptible C3H/HeJ (C3H) mice in the hind footpads and monitored arthritis d

125 C3H mice, in contrast, were selectively unresponsive to

126 es were differentially expressed in infected C3H mice, in SCID mice, and in cultured HGE bacteria.

127 Inhibition of the MCP-1 response in C3H mice increased their later T-cell production of IFN-

128 tly developed a model of primary melanoma in C3H mice induced by ethanol and UV light.

129 We found that C3H mice infected with L. amazonensis exhibited decrease

130 C3H mice infected with Leishmania mexicana fail to devel

131 ll infected C57 mice compared to none of the C3H mice infected with serovar E and only 25% of those i

132 We now show that C3H mice infected with the L. mexicana deletion mutant (

133 o the severe Lyme arthritis that develops in C3H mice infected with the spirochete Borrelia burgdorfe

134 Using C3H mice infected with Theiler's murine encephalomyeliti

135 Xenodiagnosis with C3H mice inoculated intraperitoneally with deer blood, s

136 In contrast, C3H mice inoculated with wild-type Ad recognized an epit

137 ent (C3H-scid) mice, but not immunocompetent C3H mice, inoculated with cultured B. burgdorferi, tick-

138 s levels between C57BL/6J (B6) and C3Hf/Kam (C3H) mice is controlled by multiple genes, and this set

139 When adoptively transferred to naive C3H mice, KLmB-3 unexpectedly exacerbated infection with

140 tant B10.BR and C57BL/6 mice nor susceptible C3H mice made detectable Th2 cell cytokine responses to

141 uggests that alteration of MgF expression in C3H mice may account for the k10(C3H) action on white fo

142 result in a dysfunctional Lepr signaling in C3H mice, may contribute to the poor osteogenic response

143 In C3H mice, MTRasym remained increased (31.3% +/- 9.2 on d

144 uced subcutaneously in both flanks of female C3H mice (n = 3) and allowed to grow to average size of

145 d the in vivo growth properties in syngeneic C3H mice of PC cells where PCDGF expression had been inh

146 The tumor (RIF) and muscle uptake in C3H mice of these photosensitizers was determined by in

147 t not native LDL) into BL/6 mice (but not in C3H mice) on a chow diet resulted in a 59% decrease in P

148 susceptible BALB/c mice but low in resistant C3H mice or in BALB/c mice that were immunized against L

149 was likewise higher in C3H-scid mice than in C3H mice, particularly at 4 or more weeks of infection.

150 Severely arthritic C3H mice possessed a naturally occurring hypomorphic all

151 ric (BALB/c->B10) livers was also evident in C3H mice presensitized to alloantigens expressed on both

152 uscle, skin, and tibiotarsal joint tissue of C3H mice previously infected with A. phagocytophilum.

153 nterleukin 4 in response to the parasite and C3H mice produced gamma interferon (IFN-gamma) in respon

154 ever, peripheral lymph node lymphocytes from C3H mice produced significantly higher levels of gamma i

155 mulation during infection, while susceptible C3H mice produced weak or no Th1 cell cytokine responses

156 ymph node NK cells from susceptible C3H/HeJ (C3H) mice produced more gamma interferon than NK cells f

157 se the capacity to protect, whereas HDL from C3H mice protect equally well.

158 from both strain C57BL/6J (B6) and C3H/HeJ (C3H) mice protect against LDL oxidation in a coculture m

159 C3H mice received subcutaneous injections in the flank o

160 in the modulation of food allergy, C3H/HeSn (C3H) mice received i.m. injections of pAra h2 plasmid DN

161 BALB/c and C3H mice responded to infection with L. major-betaGAL by

162 C57BL/6J (B6), but not C3H/HeJ (C3H), mice responded to mechanical loading with an incre

163 f an anti-IL-12 monoclonal antibody (mAb) to C3H mice resulted in a decrease in both IFN-gamma and B.

164 l immunization with reovirus 1/Lang (1/L) in C3H mice resulted in high titers of virus in the respira

165 n transport in C. rodentium-infected FVB and C3H mice, resulting in profound electrolyte loss, dehydr

166 elanoma cells into the UV-irradiated ears of C3H mice results in a significantly higher incidence of

167 modified LDL, whereas endothelial cells from C3H mice showed little or no induction.

168 en (pO2) of FSaII tumors grown in the leg of C3H mice significantly improved when the tumors were hea

169 MRL/lpr (stimulation index = 2.03-5.01) and C3H mice (stimulation index = 2.03-3.75).

170 bilized phosphatidylserine and in vivo using C3H mice subjected to whole-body irradiation.

171 rgdorferi from hearts by CCR2(-/-) versus WT C3H mice suggests a natural defect in the recruitment or

172 r an irrelevant endonuclease, to the skin of C3H mice suppressed the induction of delayed-type hypers

173 /NCD mice or Tg/NCD bone marrow transplanted C3H mice (Tg/NCD-C3H) resulted in 92% and 44% reductions

174 hydrosalpinx to be significantly greater in C3H mice than in C57 mice.

175 3.5%/g; p < 0.01) was higher in IAk-positive C3H mice than it was in IAk-negative control BALB/c mice

176 et) and Clara (nontarget) cells from A/J and C3H mice that exhibit high and low susceptibility, respe

177 C3H mice that were inoculated with ehrlichiae isolated f

178 In C3H mice, the alpha7 receptor is initially expressed on

179 In susceptible C3H mice, the mutant again showed diminished immunopatho

180 L-10 (AdV-IL10) caused genetically resistant C3H mice to become significantly more susceptible to L.

181 Adoptive lymphocyte transfer from naive C3H mice to infected C3H-scid mice resulted in OspA sero

182 tuberculosis antigens, the susceptibility of C3H mice to infection is MHC independent.

183 d poor response, respectively, in the B6 and C3H mice to mechanical loading.

184 ance of C57BL mice and the susceptibility of C3H mice to mycoplasmal infection.

185 The failure of L. amazonensis-infected C3H mice to respond to IL-12 was associated with a speci

186 sue ranged from 4.6 x 10(2) PFU/gram tissue (C3H mice) to greater than 10(5) PFU/gram (hamster).

187 However, we discovered that C3H mice treated for 3 wk with either anti-IL-12 or anti

188 melanomas produced in the dorsal skin of two C3H mice treated thrice weekly for 28-33 weeks with UV r

189 Surprisingly, both DBA and C3H mice treated with RB6 developed arthritis at 1 week

190 had not been treated with progesterone or in C3H mice under any conditions tested.

191 se the lymph node cells of L. major-infected C3H mice upregulate the IL-12 receptor on CD4(+), CD8(+)

192 -induced liver injury, we compared C57BL and C3H mice using proteomic, biochemical, and cell biologic

193 The median infectious dose for C3H mice was 10(4) to 10(5) organisms when blood from an

194 We determined that the susceptibility of C3H mice was independent of the Toll-like receptor 4 (tl

195 mphocyte (CTL) response in reovirus-infected C3H mice was investigated by using reovirus-vaccinia vir

196 anaphylaxis, suggesting that anaphylaxis in C3H mice was mediated by IgG1.

197 xpression of IL-10 in the infected joints of C3H mice was unable to modulate the development of sever

198 ty of the Th2 response in anti-IL-12-treated C3H mice was unrelated to levels of these cytokines and

199 12 treatment on Lyme borreliosis in C3H/HeN (C3H) mice was assessed because other studies have implic

200 40 (cN40), which induces disease in C3H/HeN (C3H) mice, was repeatedly passaged in vitro to generate

201 suppressive CD4(+) T-cell responses seen in C3H mice were associated with a high frequency of Foxp3(

202 nt differences were found when all arthritic C3H mice were compared with all nonarthritic animals, re

203 lography (EEG) in C3H/He mice, substrains of C3H mice were evaluated by EEG and sensitivity to ethosu

204 Weanling female C3H mice were fed one of five experimental diets.

205 whereas unhelped CD8(+) T-cell effectors in C3H mice were functionally impaired during acute infecti

206 both the lung and spleen, while susceptible C3H mice were incapable of limiting bacteria growth, esp

207 tigen, susceptible BALB/c mice and resistant C3H mice were infected with L. major parasites expressin

208 C3H mice were infected with Mycoplasma pulmonis, which a

209 C3H mice were injected with osteolytic fibrosarcoma cell

210 alpha-TH prevents UVB photocarcinogenesis in C3H mice, whereas alpha-TAc does not.

211 mazonensis induces a nonhealing infection in C3H mice, whereas infection with Leishmania major is sel

212 he recruitment or function of macrophages in C3H mice, which may contribute to the sensitivity of thi

213 a33 eliminated B. burgdorferi infectivity in C3H mice, which was rescued by genetic complementation w

214 oites led to established infection in 60% of C3H mice, while C57BL/6 or BALB/c mice were resistant, i

215 However, C3H mice with a limited gut flora (LF) were efficiently

216 ealing observed in these animals, we treated C3H mice with anti-IL-12 continuously for 12 wk.

217 se, but studies have shown that treatment of C3H mice with anti-IL-12 or anti-IFN-gamma mAb promotes

218 evelopment of disease following infection of C3H mice with B. burgdorferi.

219 Infection of C3H mice with Borrelia burgdorferi, the causative agent

220 ental Lyme borreliosis model of infection of C3H mice with Borrelia burgdorferi.

221 We infected neonatal C57BL/6 or C3H mice with H. pylori or treated animals with H. pylor

222 Following oral inoculation, wild-type C3H mice with normal enteric flora were colonized incons

223 Immunization of C3H mice with P55 (previously called S1), a 55-kDa Borre

224 zed using a model of intranasal infection of C3H mice with reovirus.

225 At similar in vivo treatment conditions (C3H mice with RIF tumors and BALB-C mice with colon-26 t

226 As a model, we used immunocompetent C3H mice with syngeneic s.c. tumors derived from C3L5 ce

227 Co-infection of C3HeB/FeJ (C3H) mice with both Leishmania major and Leishmania amaz

228 We infected C57BL/6 (C57) and C3H/HeN (C3H) mice with the human biovar of Chlamydia trachomatis

229 /2J (DBA) and arthritis-susceptible C3H/HeJ (C3H) mice with the neutrophil-depleting monoclonal antib

230 he organism to a level comparable to that in C3H mice without AM depletion.