ライフサイエンスコーパス: normal mice

1 vo but did not alter contractile function in normal mice.

2 hown reduced mechanical strength compared to normal mice.

3 h the protein and the mRNA level compared to normal mice.

4 rmation of germinal center GL7(+) B cells in normal mice.

5 alization of IL-22 improved lung function in normal mice.

6 eversibly attenuate fine touch perception in normal mice.

7 as E. faecalis was not isolated from MLNs of normal mice.

8 mol of hyperpolarized diethyl succinate into normal mice.

9 ssors, such as thapsigargin, than cells from normal mice.

10 eased host-derived adiponectin compared with normal mice.

11 nerve density when compared with age-matched normal mice.

12 tumour models, with no apparent toxicity in normal mice.

13 d the IFN responsiveness of splenocytes from normal mice.

14 hly active in the mediobasal hypothalamus of normal mice.

15 susceptible to A. hydrophila infection than normal mice.

16 nitrophenol (TNP)-Ficoll was performed using normal mice.

17 pulations that differed in size by 8-fold in normal mice.

18 tiation in hippocampal slices of cognitively normal mice.

19 mice were dramatically reduced compared with normal mice.

20 mmation following intradermal injection into normal mice.

21 possibility that MIF may limit life span in normal mice.

22 P78 in sinus, lungs, and brain compared with normal mice.

23 er's patch and non-Peyer's patch segments of normal mice.

24 ower level of mineralization compared to the normal mice.

25 rker CD44 in mice lacking CD4(+) T cells and normal mice.

26 re prominent among secondary memory cells in normal mice.

27 ave revealed their independent identities in normal mice.

28 well as a physiological function for 27HC in normal mice.

29 was dramatically different than observed in normal mice.

30 of cytokines, is expressed in the brains of normal mice.

31 d not affect kidney structure or function in normal mice.

32 the acute erosion of LTP by D(2) agonists in normal mice.

33 9(-/-) B cells could not enter the MZ of the normal mice.

34 els during an oral glucose tolerance test in normal mice.

35 there was no obvious pathological injury in normal mice.

36 of a duration longer than that reported for normal mice.

37 int-specific inflammation to most strains of normal mice.

38 r cells (MDSC) compared with 2.6% of that in normal mice.

39 e was likewise reduced compared with that in normal mice.

40 t-twitch fibres of mdx (dystrophin null) and normal mice.

41 nd CXCL10 protein in the brain compared with normal mice.

42 Here, we tested this model in normal mice.

43 urons of the central nervous system (CNS) of normal mice.

44 active MZ B cells than that of FO B cells in normal mice.

45 fects on fertility, behavior, or lifespan in normal mice.

46 endin-(9-39) raises fasting blood glucose in normal mice.

47 rains although at levels lower than those in normal mice.

48 response to glucose challenge was similar to normal mice.

49 ortex by local application of kainic acid in normal mice.

50 lox/y, and hyp-mice were lower than those in normal mice.

51 nged mice compared to fibroblasts grown from normal mice.

52 in lung and digestive mucosa compartments in normal mice.

53 ipts with a similar deletion can be found in normal mice.

54 be demonstrated in isolated hepatocytes from normal mice.

55 p emerged during the third postnatal week in normal mice.

56 HV lytic genes in hyperglycemic mice than in normal mice.

57 ation was confirmed in a metabolism study in normal mice.

58 phenotype in 21-month-old mdx, carrier, and normal mice.

59 arkinsonian-like motor deficits in otherwise normal mice.

60 and not from those derived from unchallenged normal mice.

61 ns, fever, and reduced locomotor activity in normal mice.

62 into the liver and hepatocytes compared with normal mice.

63 l uptake when compared with macrophages from normal mice.

64 e was approximately ten times slower than in normal mice.

65 gh fat diet-induced obese mice compared with normal mice.

66 implanted into the bone marrow of irradiated normal mice.

67 the antibody-treated, ICAM-1-deficient, and normal mice.

68 effectively stimulate platelet production in normal mice.

69 DEX) decreased TGF-beta group mRNA levels in normal mice.

70 ides health benefits to chronologically old, normal mice.

71 sensor implantation sites, when compared to normal mice.

72 nd knee joints in a biodistribution study in normal mice.

73 y enhanced CGM performance, when compared to normal mice.

74 m pancreatic cancer mouse models, but not in normal mice.

75 e was disorganized and wider compared to the normal mice.

76 molecules identify a subset of DN T cells in normal mice.

77 zzled-2 between 24 and 72 hours, after PH in normal mice.

78 unction of Tregs can be evaluated in vivo in normal mice.

79 formed by biodistribution and PET imaging in normal mice.

80 der anemia and faster recovery compared with normal mice.

81 l epithelial cells results in phenotypically normal mice.

82 00-fold higher in tumor-bearing mice than in normal mice.

83 insonian-associated locomotor dysfunction in normal mice.

84 carotid artery photochemical injury assay in normal mice.

85 precipitate DCM in otherwise phenotypically normal mice.

86 tic centers of the central nervous system in normal mice.

87 ion of terminal erythroid differentiation in normal mice.

88 L enhanced EPO-induced red cell formation in normal mice.

89 on velocity was slower than that reported in normal mice.

90 lamus also reduces motivation for cocaine in normal mice.

91 triggered vaso-occlusion in sickle, but not normal, mice.

92 kin-22 binding protein (IL-22BP) compared to normal mice, a cytokine considered critical for preventi

93 As the coupling coefficients decreased in normal mice, a glutamate-mediated excitatory postsynapti

94 fy this regulatory requirement, we evaluated normal mice after AAV.miHDS1 injection.

95 at E11.5 increased cortical neurogenesis in normal mice--an effect that was blocked by simultaneous

96 6 h was, respectively, 80%, 80%, and 90% for normal mice and 80%, 100%, and 70% for neutropenic mice.

97 vity in GRP-receptor-rich pancreatic acne in normal mice and also in tumors in prostate-tumor-bearing

98 rm of SGK by use of viral vector transfer in normal mice and both before and after 6-OHDA lesion.

99 gene expression profiles in TG mice (both in normal mice and during liver regeneration).

100 rated that in peripheral lymphoid tissues of normal mice and healthy humans, 1% to 5% of alphabeta T-

101 s and angiogenesis significantly improved in normal mice and high fat (HF) diet-induced diabetic mice

102 The TonoLab accurately reflects IOP in both normal mice and in eyes of mice with experimental or spo

103 light that innate CD8+ T cells exist also in normal mice and in humans.

104 ayed by enzyme-linked immunosorbent assay in normal mice and in mice deficient in IL-12 after inocula

105 1B subunit genes during brain development in normal mice and in mice with a hypomorphic allele for Li

106 emporal analysis of organ vascularization in normal mice and in mouse strains with genetic mutations

107 e formation, bone mass, and bone strength in normal mice and in ovariectomized mice with established

108 ndependent of forkhead box P3 expression, in normal mice and Lewis lung carcinoma-bearing mice.

109 ethylcholanthrene (MCA) 205 in the flanks of normal mice and mice bearing MCA 205 lung metastases.

110 enhance host resistance to infection in both normal mice and mice depleted of CD4+ T lymphocytes.

111 h biopsies (3 mm) were placed in the skin of normal mice and mice with hemophilia.

112 emory, control recognition tests showed that normal mice and mice with hippocampal or medial prefront

113 We show that normal mice and mice with mucopolysaccharidosis VII (MPS

114 , and increases maximal exercise capacity in normal mice and mice with severe heart failure.

115 haracterize the depletive effects of mATG in normal mice and provide insight into mechanisms of actio

116 mAb complexes also increased thymopoiesis in normal mice and restored thymopoeisis in IL-7-deficient

117 d speed-dependent left-right coordination in normal mice and the changes in coordination seen in muta

118 f Cu-induced Abeta accumulation in brains of normal mice and then to explore Cu's effects in a mouse

119 Experimental glaucoma was induced in normal mice and those carrying a targeted deletion of th

120 ruvate + alanine) from the entire abdomen of normal mice and TRAMP mice with low- and high-grade pros

121 ts of failed development, were also found in normal mice and were characterized by markedly lower exp

122 t HNP-1 reduced blood glucose levels of both normal mice and Zucker diabetic fatty rats predominantly

123 ssue extracts from ApoE(-)/(-), but not from normal mice, and accumulated in aortic plaques in vivo w

124 in D9k and calcium binding protein D28k than normal mice, and bone density and volume increased in KO

125 t GW4064 decreases hepatic miR-34a levels in normal mice, and consistently, hepatic miR-34a levels ar

126 (+)FoxP3(-) conventional T cells (Tconvs) in normal mice, and its expression is upregulated by T cell

127 c mice were transplanted orthotopically into normal mice, and the calcium content, histology, and min

128 markers typically not seen in the striata of normal mice, and these cells are preferentially lost as

129 Adoptively transferred B cells from normal mice are able to reconstitute MZ B cells in CD19(

130 matically inhibited IL-2-induced VLS in both normal mice as well as in mice bearing melanoma.

131 pared with the bone marrow and peritoneum of normal mice as well as younger mice with lupus.

132 ctin with DiI-Ac-LDL has a similar result in normal mice, as seen in Tie2/GFP mice, and can be used t

133 nted Matrigel plugs implanted in genetically normal mice, as well as decreased the growth and blood v

134 The in vivo biodistribution in normal mice, at 2 min after injection, showed excellent

135 Subsequently, IL-33 administration to normal mice attenuated fungal-induced IL-17A and IL-22,

136 ficient mice were more resistant relative to normal mice because the latter went through a stage of l

137 indicate high initial influx of [(18)F]-9 in normal mice brains accompanied by rapid clearance in the

138 small numbers in BM and peripheral blood of normal mice but are significantly (15-fold) augmented on

139 R for 1 year improved insulin sensitivity in normal mice but failed to further enhance the remarkable

140 lacking the PVR inhibitor was attenuated in normal mice but not in mice lacking DNAM-1.

141 cyclin was required for optimal function in normal mice but that it was no longer required following

142 osen SpeB(A-) mutant outcompeted MGAS2221 in normal mice but was outcompeted by MGAS2221 in neutropen

143 excluded from the central nervous system in normal mice, but entered the central nervous system duri

144 d the number of CD4(+) and CD8(+) T cells in normal mice, but H57-597 mAb most potently increased the

145 In normal mice, but not Rgs2-/- mice, PKG activation by the

146 sed the immune function of spleen cells from normal mice, but not those from knockout mice.

147 bition of CDK4 mimicked these alterations in normal mice, but not when skeletal muscle was AMPK defic

148 were highly enriched in the abdominal fat of normal mice, but their numbers were strikingly and speci

149 heckpoint protein BubR1 age much faster than normal mice, but whether other mitotic checkpoint genes

150 nsulin resistance resembling that induced in normal mice by consumption of an HFD.

151 we show that depression could be induced in normal mice by topical application or micro-injection of

152 Adoptive transfer of these cells to normal mice caused lung damage, as indicated by elevated

153 tion and magnetic antibody cell sorting from normal mice, CCl(4)-treated mice, and mice that underwen

154 In normal mice, clearance of the infection and contraction

155 Islets of Langerhans from normal mice contained dendritic cells (DCs) in the range

156 In sharp contrast to its effects in normal mice, CR failed to increase overall, median, or a

157 ha (IL-2Ralpha/CD25) during immunotherapy in normal mice depleted T(Regs) (73% reduction; P = .0154)

158 endothelial cells or hematopoietic cells in normal mice did not affect hematopoiesis, HSC maintenanc

159 isolated from the spleens or lymph nodes of normal mice did not express significant levels of the in

160 ibited significantly shortened survival than normal mice due to more rapidly growing tumors.

161 owever, depletion of SMN in motor neurons of normal mice elicited only a very mild phenotype.

162 Inoculation of P. carinii into normal mice evoked a brisk release of IL-12 into lung ti

163 In vivo biodistribution in normal mice exhibited excellent initial brain penetratio

164 Neonatal neurospheres isolated from normal mice expressed a mixture of alpha(1)-adrenergic r

165 of FM to EE is comparable to that of LBM in normal mice (expressed per gram of tissue) but is absent

166 and decrease splenic pathology compared with normal mice following L. monocytogenes infection.

167 SI mice were indistinguishable from those in normal mice following oral gavage of olive oil.

168 Bone marrow-derived mast cells from normal mice further validated these results for six defi

169 ese asthmatic exacerbations were observed in normal mice gavaged with ethanol.

170 chronically in ClCK1-/- mice and acutely in normal mice given furosemide is associated with lower NT

171 a(1A)-adrenergic receptor transgenic mice or normal mice given the alpha(1A)-adrenergic receptor-sele

172 In normal mice, glucose consumption is accompanied by aldos

173 ndergoing positive and negative selection in normal mice has never been firmly established.

174 These results indicate that normal mice have a capacity for CST regeneration that ha

175 kers or overstimulation of D(2) receptors in normal mice have similar LTP shutoff effects.

176 In normal mice, i.p. administration of ITPP (0.5-3 g/kg) ca

177 AEP is activated in normal mice in an age-dependent manner, and is strongly

178 e first time, determine the alveolar size of normal mice in respiration without positive end expirato

179 s little if any regeneration of CST axons in normal mice in the absence of some intervention.

180 otes microvascular stasis in sickle, but not normal, mice in response to hypoxia/reoxygenation (H/R),

181 ippocampus of epileptic mice than in that of normal mice, in addition to spatial coupling between cap

182 e brain were undistinguishable from those in normal mice, in TRAIL(-/-) mice, CD8(+) T cells showed q

183 GF knock-out mice; overexpression of PlGF in normal mice increased circulating PAI-1.

184 ever, whereas the avidity of memory cells in normal mice increased dramatically with repeated immuniz

185 s: increased in the short term by insulin in normal mice, increased basally in insulin-resistant mice

186 26S proteasomes from normal mice incubated with recombinant oligomers or fibr

187 oxamidoadenosine (CGS21680) had no effect in normal mice, indicating a lack of role of A2A receptors.

188 ect administration of IL-22 into the skin of normal mice induced both antimicrobial peptide and proin

189 Acute A. fumigatus challenge in normal mice induced the recruitment of CD11b+ Siglec F+

190 thymus-grafted nude mice, but not those from normal mice, induced autoimmunity in nude recipients.

191 elerate lupus in vivo and break tolerance in normal mice, inducing autoimmune Th17 cells.

192 infection, whereas no mortality was shown in normal mice infected with the pathogen.

193 In individual neurons of normal mice, inhibition and excitation driven by either

194 aques (0.31% ID/g) compared with aortas from normal mice injected with [(18)F]FBA-LyP-1(0.08% ID/g, P

195 enous (nonamyloidogenic) rat amylin, studied normal mice injected with aggregated human amylin, and d

196 An abscess was formed in normal mice intradermally infected with 10(8) CFU/mouse

197 gands and receptors in PD-L1(-/-) corneas of normal mice is associated with significant increases in

198 tissue BCAA oxidation per mg of tissue from normal mice is higher than in skeletal muscle.

199 Cardioprotection by Klotho in normal mice is mediated by downregulation of TRPC6 chann

200 and nature of allelically included cells in normal mice is unknown.

201 (+)Gr-1(+) cells exist at low frequencies in normal mice, it also remains unresolved whether they are

202 with transiently enhanced IL-2R signaling in normal mice led to persistent polyclonal Ag-specific CD8

203 TMSCs injected into the anterior chamber of normal mice localized primarily in TM, remaining in the

204 Moreover, in normal mice, memory T cells elicited after priming with

205 time course of receptive field refinement in normal mice, mice in which the contralateral eye never o

206 affinity showed extended serum half-life in normal mice, mice transgenic for human FcRn, and cynomol

207 effects of transgenic VEGF165 in lungs from normal mice, mice treated with pan-NO synthase (NOS) or

208 Compared with normal mice, mice with diabetes had greater VEGF protein

209 Intravitreal TNF-alpha injections in normal mice mimicked these effects.

210 Accordingly, MAIT cells from normal mice more closely resemble human MAIT cells than

211 ted normal, concentric LV contraction in all normal mice (n = 10).

212 In normal mice, nidogen-1 was present in many basement memb

213 Following cowpox virus infection in normal mice, NK cells were greatly expanded in the drain

214 tes were quantified in isolated hearts, from normal mice (nontransgenic) and mice with cardiac-specif

215 acquisition (eight frames per ECG cycle) in normal mice (normal group A, n = 6) and mice with myocar

216 and rapid data acquisition, another group of normal mice (normal group B, n = 4) underwent imaging wi

217 urs in mice based on imitative scratching in normal mice observing excessive scratching in geneticall

218 , we were unable to extend these findings to normal mice observing the well-established histamine mod

219 epiride proved efficacious against stroke in normal mice only.

220 Moreover, in normal mice or following germ-cell depletion with Busulf

221 onal T cell lines were generated from either normal mice or mice deficient in granzyme and perforin p

222 atment of embryonic fibroblasts derived from normal mice or mice with targeted deletion of NFkappaB p

223 and volume increased in KO/TG compared with normal mice owing to increased mineral apposition rate a

224 amin D levels were higher in KO/TG mice than normal mice owing to reduced renal expression of the vit

225 isolated from the infection site tissues of normal mice produced interleukin-12 (IL-12) but not IL-1

226 ased in fungal-exposed Il1rl1(-/-) mice, and normal mice produced less PGE2 after fungal exposure whe

227 of the pan caspase inhibitor, Z-VAD-FMK into normal mice protected against Chlamydia-induced infertil

228 CSF-1 neutralization, but not of GM-CSF, in normal mice rapidly reduced the numbers of more mature L

229 ife, compared with recombinant FIX (rFIX) in normal mice, rats, monkeys, and FIX-deficient mice and d

230 ative brain distribution of (18) F-Mefway in normal mice, rats, monkeys, and healthy human volunteers

231 s of hemodynamics measurements obtained from normal mice/rats, and from animals with cardiac hypertro

232 c3h1(gt/gt) mice transferred into irradiated normal mice (Rc3h1(gt/gt) --> NL chimeras), we show that

233 ti-IL-5 antibody or by gene deletion, and in normal mice receiving cetirizine orally.

234 over, EGCG treatment of primary neurons from normal mice reduced IFN-gamma-enhanced neurotoxicity of

235 ent determinant of EE in both ob/ob mice and normal mice rendered leptin-deficient by fasting.

236 Here we demonstrate that in normal mice resistin delivered in the lateral cerebral v

237 mals or after in vivo blockade of IL-17Ra in normal mice, resulting in a reduction of hemopoietic pre

238 tion increased muscle perfusion by 7-fold in normal mice, reversed tissue ischemia for up to 24 hours

239 In normal mice, RGC perikarya and axons were intensely labe

240 ive stimulation of SChIs via optogenetics in normal mice robustly and reversibly amplified beta and g

241 In normal mice, self-reactive IgG2a-switched B cells were d

242 A biodistribution study in normal mice showed initial uptake of the tracer in the k

243 Biodistribution in normal mice showed that l-[5-(11)C]-glutamine had signif

244 was observed in vitro, and PET/CT imaging of normal mice showed uptake in thyroid, salivary glands (p

245 at mHTT glia can impart disease phenotype to normal mice, since mice engrafted intrastriatally with m

246 As with normal mice, slopes of wave I latency-intensity curves w

247 Nonlinear pharmacokinetics in normal mice suggested that antigen expression in normal

248 In contrast to normal mice, TDP-43 transgenic mice exhibited sustained

249 Retreatment was performed in C57BL/6 normal mice that had been treated with 2.0 mg/kg of vert

250 lity for regenerative growth of CST axons in normal mice that involves growth past the lesion via the

251 e also show that splenic Mphis purified from normal mice that were implanted with timed-release GC pe

252 abscess did not form and sepsis developed in normal mice that were inoculated with burned-mouse infec

253 excitability and cognitive function in young normal mice, that old CA1 pyramidal cells have reduced e

254 Compared with normal mice, the increase in the mRNA expression of hepa

255 quickly throughout the whole body, while in normal mice, the pathogen remained localized at the infe

256 xed bone marrow chimeras, suggesting that in normal mice, there is only a small contribution to the p

257 o induce gut bacterial translocation (BT) in normal mice; therefore, it is possible that HMGB1 mediat

258 Compared with normal mice, these transgenic mice exhibited a delayed i

259 In normal mice, this resulted in a rapid but transient infl

260 t SR-BI/II null mice are more sensitive than normal mice to endotoxin-induced inflammation and sepsis

261 -minute dynamic PET imaging was performed on normal mice to evaluate the distribution of (18)F-AlF-NE

262 minantly electroneutral Cl-HCO3- exchange in normal mice, to a predominantly electrogenic anion secre

263 nt concentrations of urea and in islets from normal mice treated orally with urea for 3 weeks.

264 Mice transgenic for antisense Notch and normal mice treated with inhibitors of the Notch-activat

265 logies were not observed in brain regions of normal mice treated with paraquat.

266 cin-treated mice with or without SCGB3A2 and normal mice treated with SCGB3A2.

267 e proximal intestine in vitamin D-sufficient normal mice treated with vehicle or 1,25(OH)2D3.

268 s found among individual lymph nodes (LN) of normal mice; Treg from draining LN were 15-50 times more

269 Administration of RSpo1 into normal mice triggered nuclear translocation of beta-cate

270 In 36 normal mice, two 0.4-mL gel implants were placed subcuta

271 we simulated erythroid expression of PlGF in normal mice up to the levels seen in sickle mice.

272 Although thymectomized, T cell-depleted normal mice usually remain healthy following xenogeneic

273 responses to carbachol between tissues from normal mice vs. MYPT1 T853A knockin mice.

274 In normal mice, VSV replication is limited to the OB, and t

275 The maximum tolerated dose in normal mice was determined to be 80 mg/kg for free CPT-1

276 e critical-size calvarial defects created in normal mice, we found that mice transplanted with BMP4GF

277 h developing diabetic retinopathy or control normal mice were also studied.

278 To model DC-specific T cell competition, normal mice were injected with one or two T cell recepto

279 T cells from skin-draining lymph nodes of normal mice were shown, in vitro, to specifically recogn

280 injuries were much severer in HTG mice than normal mice when injected with conventional dose Cae (50

281 expression on sprouting endothelial cells of normal mice whereas KO aortas exhibit impaired endotheli

282 ficacy of linagliptin in type 2 diabetic and normal mice, whereas glimepiride proved efficacious agai

283 ression is absent in the cochlear nucleus of normal mice, which have high-frequency hearing sensitivi

284 cci following intraperitoneal injection into normal mice, which is consistent with sialylation confer

285 We find that treatment of normal mice with a single >/=3 mg/20 g body weight dose

286 ER stress markers and were recapitulated in normal mice with advancing age in response to stimulatio

287 erplasia were identical to those observed in normal mice with and without arthritis.

288 Yet, treatment of normal mice with B7-DC XAb fails to elicit generalized a

289 Treatment of normal mice with CR2-Crry at 30 min postreperfusion resu

290 tenuates COX-2 degradation, and treatment of normal mice with ibuprofen increases the levels of COX-2

291 We show here that treatment of normal mice with intact antibody to CD3 increases system

292 We compared normal mice with mice pretreated with l-methionine (5.2

293 Treatment of normal mice with the Mas agonist AVE0991 reduces thrombo

294 the neonatal to juvenile period.We compared normal mice with the most severe SOD1 model, the G93A hi

295 ly target S-MGCA, autoantibodies produced by normal mice with transient Treg depletion that developed

296 s tightly compartmentalized to the mucosa in normal mice, with systemic B cells and CD4+ T cells rema

297 eart failure in both vitamin D deficient and normal mice without inducing significant hypercalcemia.

298 crophages expand dramatically post-stress in normal mice without significant changes in the monocyte-

299 lls also cause Th17 skewing to foreign Ag in normal mice without Th17-polarizing culture conditions.

300 stain a 500-fold higher mutation burden than normal mice, without any obvious features of rapidly acc