ライフサイエンスコーパス: suckle

1 ved and lethality was due to an inability to suckle.

2 e in burst firing evoked by applied OT or by suckling.

3 in expression and activity were found during suckling.

4 ifferentially regulated by either PRL and/or suckling.

5 pt capacity to extract energy from milk upon suckling.

6 espond to neural signals from termination of suckling.

7 nses to cues important for the initiation of suckling.

8 ubjected to greater mechanical stress during suckling.

9 rats in response to any stimulus other than suckling.

10 ause of a progressive rise in their Tb while suckling.

11 in only 3% (n = 77) of newborn lambs before suckling.

12 ntrol of the secretion of PRL in response to suckling.

13 C in the outer zone of the AL (AL-OZ) due to suckling.

14 and non-bursting cells were observed during suckling.

15 ntributed to heat retention in mothers while suckling.

16 orodibenzo-p-dioxin (TCDD), in utero and via suckling.

17 at are learned and recognized prior to first suckling.

18 ethanol was tested in newborn rats naive to suckling (3-5 hr old) on Postnatal Day (P) 0 and in olde

19 t undergo rapid postnatal catch-up growth by suckling a control-fed dam (recuperated offspring).

20 e-Dawley rats were fed, during pregnancy and suckling, a control diet (4% w/w corn oil) or a fatty ac

21 esent study was to determine if any of these suckling activated areas project directly to the DMH.

22 showed marked depression of respiratory and suckling activities in vivo and overexpression of synapt

23 yses indicate that hSRY(ON) pups lack innate suckling activities, and develop fatty liver disease, ar

24 rmal newborn mice mimicked the depression in suckling activity but not respiratory depression in vivo

25 ing and handling as well as of the pups' own suckling activity-but not food intake-fully restored CRF

26 es to regulate social behaviours such as pup suckling, aggression and mating.

27 suckling; (ii) the mediation of the sucrose-suckling analgesia and antihyperalgesia at the spinal le

28 dA was also induced during infections of the suckling and adult mouse intestines, and in vitro under

29 affected by their growth rate when they were suckling and find that limiting growth during that perio

30 Unilateral inhibition of suckling and hormonal reconstitution experiments showed

31 porin 4 association decreased during initial suckling and increased after the MER, whereas opposite c

32 has knock-out mice (Gnasxl(m+/p-)) have poor suckling and perinatal lethality, implicating XLalphas a

33 The combination of nonnutritive suckling and sucrose (7.5%, 0.01-0.06 ml/min) infusion m

34 ult distal intestinal microbiota, during the suckling and weaning periods.

35 is up-regulated during embryogenesis, during suckling, and in the mother during pregnancy.

36 strous; control of reproduction, aggression, suckling, and parental behaviors; individual recognition

37 ial role in the digestion of dietary fats in suckling animals.

38 vements in utero to the postnatal mastery of suckling at 4 months after birth; and (2) thereafter, fr

39 was no indication that mothers discontinued suckling because of a progressive rise in their Tb while

40 g imaging sessions, dams were exposed to pup suckling before and after administration of an oxytocin

41 Impaired suckling behavior was attributable to defective olfactio

42 dysmorphism, semilethality due to defective suckling behavior, and generation of a small fraction of

43 th the same amount of water had no effect on suckling behavior.

44 ory conditioning has the potential to modify suckling behavior.

45 with milk may reinforce components of early suckling behavior.

46 ew technique for experimental study of early suckling behavior.

47 stnatal physiological adaptations, including suckling, blood glucose and energy homeostasis.

48 Approximately half the pups suckling Btn1a1(-/-) animals died within the first 20 da

49 onsistent with augmented cylindrical growth, suckling but not adult transgenic mice show enlarged cry

50 es after ETEC challenge were associated with suckling but not birthing from vaccinated dams, suggesti

51 r normal at birth and can breathe, walk, and suckle, but within 4 days, they show a markedly lower bo

52 developed a severe cachexia during high fat suckling, but caught up in weight after switching to a c

53 sponses after V. cholerae infection for pups suckled by an immune dam.

54 Pups suckled by an immunized dam did not mount this response.

55 Neonates born to and suckled by dams antenatally vaccinated with each of thes

56 Neonatal mice suckled by OMV- or sham-immunized dams were challenged w

57 romocriptine to suppress PRL levels and were suckled by pups.

58 control group received vehicle only and were suckled by pups.

59 of C57BL/6J mice in comparison with animals suckled by their biological dams.

60 Four of nine infants born to and suckled by these dams had evidence of infection, a trans

61 f contaminants from the mother cows to their suckling calf and the uptake of soil by grazing cattle.

62 Finally, suckling caused dissociation of OTRs and G beta subunits

63 vements in mammals, e.g., walking, swimming, suckling, chewing, and breathing, inhibition is often hy

64 Changes in brain activation in response to suckling closely matched that elicited by oxytocin admin

65 milk formula via artificial rearing, and (3) suckling control (SC), where pups remained with lactatin

66 roups were included: sham-intubated (SI) and suckle-control (SC).

67 ties were detected from duodenum to colon in suckling CONV mice, but the relative levels of these act

68 natal lethality associated with a failure to suckle, cyanosis, and respiratory distress.

69 The suckling defect was responsible for the death among lp(A

70 Here we show that Hap1 null mutants display suckling defects and die within the first days after bir

71 s of ALEX is most likely responsible for the suckling defects previously observed.

72 olfactory defect resulting in a competitive suckling deficit.

73 in VMH are governed primarily by maternal or suckling-derived sensory input rather than food intake o

74 than in the preceding year, and continued to suckle during the following year.

75 These results indicate that suckling elicits dynamic glial neuronal interactions in

76 including opioid activity, during the first suckling episode.

77 the first demonstration that OT mediation of suckling-evoked bursts/milk ejections is via interaction

78 e injected intracerebroventricularly reduced suckling-evoked milk ejections.

79 Newborn rat pups tested before suckling experience attached to and ingested milk from t

80 Day (P) 0 and in older neonates with regular suckling experience on P1 or P2.

81 Cesarean-delivered pups tested before suckling experience showed oral grasp responses and inge

82 in 1 activity in the brown adipose tissue of suckling female rats, indicative of increased sympatheti

83 Consistently, suckling first reduced and then increased the expression

84 or lard-rich diet (OHF) during pregnancy and suckling followed by a control diet post-weaning.

85 stricted diet during gestation (GLP) or pups suckled from postnatal day 1 (PN1) to PN11 (E-UN), or PN

86 tes from oral V. cholerae challenge and that suckling from an immunized dam accounts for the majority

87 te utilization in vivo indicated that in the suckling gut B. thetaiotaomicron prefers host-derived po

88 systems activated by taste and nonnutritive suckling; (ii) the mediation of the sucrose-suckling ana

89 BR3-/- mice exhibited neonatal lethality and suckling impairment that could be partially rescued by l

90 proximately 50% neonatal lethality, impaired suckling in neonatal pups, and loss of LPA responsivity

91 ion of the olfactory cues that trigger first suckling in the mouse would provide the means to determi

92 such as pheromones, acting to promote first suckling in the mouse.

93 In intact animals, suckling increased ERK1/2 activation in the cytosol and

94 Coimmunoprecipitation showed that suckling increased molecular interactions between pERK1/

95 ppressed feeding induced by 24 hr fasting or suckling-induced hyperphagia.

96 ceptor (PRL-R) during lactation is caused by suckling-induced hyperprolactinemia or the suckling stim

97 to both the stimulus of suckling itself and suckling-induced hyperprolactinemia.

98 lactating rats are known to severely reduce suckling-induced kyphosis (upright crouched nursing), wh

99 rthermore, MTII treatment greatly attenuated suckling-induced NPY expression in the DMH.

100 the mediobasal hypothalamus (MBH) regulates suckling-induced prolactin secretion.

101 observed both during parturition and during suckling-induced reflex milk ejection.

102 cerning DAergic neuronal activity during the suckling-induced release of PRL persist.

103 to study mechanisms that evolved to protect suckling infants from SIV infection.

104 Instead, we find that the initiation of suckling is dependent on variable blends of maternal "si

105 They are fully viable probably because suckling is unimpaired, unlike mutants in which the expr

106 Successful suckling is vital to the survival of mammalian newborns.

107 reveals that an apparently innate behavior, suckling, is triggered not by a classical pheromone but

108 y mechanisms related to both the stimulus of suckling itself and suckling-induced hyperprolactinemia.

109 Maternal grooming of young did not vary with suckling location.

110 protection in the gastrointestinal tract of suckling mammals, in the form of secretory IgA (SIgA).

111 did not cause detectable disease in adult or suckling mice after either i.c. or s.c. inoculation.

112 residual murine virulence and is lethal for suckling mice after intracerebral (i.c.) or subcutaneous

113 t 20 microg/mouse afforded 50% protection of suckling mice against challenge with 25 50% lethal doses

114 Also, both Angptl4 -/- suckling mice and adult mice fed a high-fat diet showed

115 lpha is detected in rare epithelial cells of suckling mice and becomes progressively more expressed i

116 50% lethal dose and survival distribution in suckling mice and by histopathology in rhesus monkeys.

117 However, using suckling mice as a model host, we found that intraintest

118 we show that infection of hamster cells and suckling mice by Nodamura virus (NoV), a mosquito-transm

119 e restricted in replication in the brains of suckling mice compared to that of wild-type DEN4, and th

120 ectedly displayed increased pathogenicity in suckling mice compared to wild-type SBV.

121 -membrane vesicles (OMVs) passively protects suckling mice from challenge.

122 tiple IFN types led us to test protection of suckling mice from endotoxin-mediated shock, an outcome

123 t 2D6 IgA is sufficient to passively protect suckling mice from oral challenge with virulent V. chole

124 mutations were attenuated in s.c. inoculated suckling mice in comparison with TR339.

125 In contrast to observations in suckling mice in which viruses encoding inactivating mut

126 GT knockout (KO) suckling mice infected with SINV strains (AR339 and S.A.

127 s mutation attenuated the virus in 4-day-old suckling mice inoculated by the intracerebral (i.c.) rou

128 at least 28,500 times less neurovirulent in suckling mice inoculated intracerebrally and at least 10

129 SVNI infection of 10-day-old suckling mice led to reduced survival in the knockout mi

130 encephalitis was delayed, a small number of suckling mice still succumbed to lethal intracerebral in

131 Finally, we show using competition assays in suckling mice that inhibition of motility appears to be

132 We studied orally inoculated 5-day-old suckling mice that were deficient in interferon (IFN) si

133 nal and extraintestinal viral replication in suckling mice vary among different heterologous and homo

134 Regulation of MCMV synthesis in these suckling mice was shown to be an IFN-gamma-dependent, pe

135 When suckling mice were infected with RV, they were substanti

136 of Helicobacter pylori infection in infants, suckling mice were inoculated with mixtures of strains t

137 -induced protection was mimicked by treating suckling mice with a glycolipid derived from Helicobacte

138 We show here that infection of ZAP knockout suckling mice with an SVNI led to faster disease progres

139 Herein, we show that infection of suckling mice with influenza A virus protected the mice

140 viral RNAi in mouse embryonic stem cells and suckling mice(10,11).

141 ns of NaCl (100 mM or less), and also within suckling mice, a model host for the study of cholera pat

142 y safe following intracranial inoculation of suckling mice, a stringent test of vaccine safety.

143 netics in cell culture, neuroinvasiveness in suckling mice, and ability to replicate and produce diss

144 the intestine of wild-type and heterozygous suckling mice, but GC-C null animals were resistant.

145 ly passed EBO-Z virus in progressively older suckling mice, eventually obtaining a plaque-purified vi

146 ly passed EBO-Z virus in progressively older suckling mice, eventually obtaining a plaque-purified vi

147 In suckling mice, exogenously administered type I, II, or I

148 ed EBOV, developed by sequential passages in suckling mice, identified many similarities between this

149 In suckling mice, infection with RV results in an increase

150 ne system is more developed than that of the suckling mice, resulted in significantly improved surviv

151 reased virulence in weanling mice but not in suckling mice, suggesting that specific host conditions

152 , in the developing CNS of highly permissive suckling mice, the miRNA-targeted viruses can revert to

153 Finally, in suckling mice, we found two peaks in the CD8 response on

154 This virus showed growth in HFDK cells and suckling mice.

155 within intestinal epithelial cells (IECs) of suckling mice.

156 e culture, and elicits fluid accumulation in suckling mice.

157 small intestinal epithelial cells (IEC) from suckling mice.

158 over unadapted cells during colonization of suckling mice.

159 cerebrally into the right cortex of C57/BL/6 suckling mice.

160 sets and adoptively transferred into C57BL/6 suckling mice.

161 urovirulent than their parental LGT virus in suckling mice.

162 ers in the brains of experimentally infected suckling mice.

163 n to attenuate the neurovirulence of JUNV in suckling mice.

164 rowth and in vivo pathogenicity in adult and suckling mice.

165 ue morphology or its attenuated phenotype in suckling mice.

166 tationary-phase cells were used to inoculate suckling mice.

167 ely restricted intestinal replication in the suckling mice.

168 and mortality compared to wild-type (WT) B6 suckling mice.

169 ter than that of a simian rotavirus (RRV) in suckling mice.

170 virulence after intracerebral inoculation in suckling mice.

171 RV infection on endotoxin-mediated shock in suckling mice.IMPORTANCE Antiviral functions of types I,

172 ditionally, virus-infected tissue culture or suckling mouse brain (SMB) has been the source of viral

173 ion of 32 pg/0.1 ml, and antigen in infected suckling mouse brain and laboratory-infected mosquito po

174 However, the suckling mouse brain-derived (SMB) antigen used in this

175 sources of virus-infected tissue culture or suckling mouse brain.

176 till use vaccines produced in sheep, goat or suckling mouse brain.

177 lines (Vero, BHK, SW13, and XTC cells) or in suckling mouse brains.

178 El Tor biotype strains throughout the entire suckling mouse GI tract at various times after intragast

179 ype to resist bactericidal mechanisms in the suckling mouse GI tract.

180 The suckling mouse has been used as a model to identify Vibr

181 In fact, the suckling mouse intestine does not appear to be a potent

182 Vibrio cholerae colonization of the suckling mouse intestine is a commonly used animal model

183 Quantitation of RyhB expression in the suckling mouse intestine suggests that iron availability

184 ly uncharacterized environments (such as the suckling mouse intestine) can be used as a reporter of l

185 oH mutant was severely attenuated within the suckling mouse intestine, suggesting that sigma(32)-regu

186 s not required for V. cholerae growth in the suckling mouse intestine.

187 produced normal biofilms, and colonized the suckling mouse intestine.

188 as strains lacking hfq fail to colonize the suckling mouse intestine.

189 ility of results with those for monkeys, the suckling mouse is an appropriate host for safety testing

190 P nor OA is required for colonization of the suckling mouse large bowel.

191 on mutations that affect colonization in the suckling mouse model for cholera.

192 defective for intestinal colonization in the suckling mouse model of cholera and expresses reduced am

193 s in mice and greatly reduced mortality in a suckling mouse model of cholera.

194 on against live V. cholerae challenge in the suckling mouse model of cholera.

195 B could influence protective efficacy in the suckling mouse model of cholera.

196 d whether ribavirin treatment in the lethal, suckling mouse model of HTNV infection would act similar

197 and III IFN receptors (IFNRs) in vitro In a suckling mouse model, RV effectively blocked STAT1 activ

198 Fbp, and Feo systems was not attenuated in a suckling mouse model, suggesting that at least one other

199 k of HapA did not affect colonization in the suckling mouse model.

200 in preventing intestinal colonization in the suckling mouse model.

201 in cross-linking and fluid accumulation in a suckling mouse model.

202 nd antidiarrheal efficacy in closed-loop and suckling mouse models.

203 In the suckling mouse, oral inoculation with V. cholerae leads

204 xcellent alternative to the more traditional suckling-mouse brain WN virus antigen used in the immuno

205 Our objective was to determine if suckling neonatal piglets are susceptible to enterohemor

206 apid and more-severe neurological disease in suckling neonates than in those fed an artificial diet.

207 into milk and their passive transfer to the suckling newborn.

208 imulated fluid secretion in the intestine of suckling Nkcc1(-/-) mice were normal.

209 Litters suckling nontransgenic dams succumbed to fatal encephali

210 ctions that help mediate the transition from suckling of a fat-rich diet to independent feeding of a

211 nic mice is sufficient to completely protect suckling offspring against MHV-JHM-induced encephalitis.

212 A comparison of the iron status of suckling offspring from LFKO(-/-) intercrosses and from

213 es in and is transferred through the milk to suckling offspring.

214 In rats whose pups could suckle only on one side, TH was up-regulated only on the

215 r together were required for colonization of suckling or adult mice.

216 om experiments in mitochondria isolated from suckling or adult rats inverted question mark using a di

217 ortion of the mouth in rats that were either suckling or in contact caused a 20-25-s increase in esca

218 reported as a cause of sporadic diarrhea in suckling or weanling pigs, to our knowledge, this is the

219 exogenous glucose administration to actively suckling Oxct1(-/-) mice delayed, but could not prevent,

220 sted from the ceca of these hosts during the suckling period (postnatal day 17) and after weaning (po

221 been observed that SFB are absent during the suckling period and appear in high numbers shortly after

222 e-4 (GPAT4) null pups grew poorly during the suckling period and, as adults, were protected from high

223 A obtained from the mothers' milk during the suckling period and, later, of self-produced sIgA in the

224 -carbohydrate (HC) milk formula during their suckling period developed hyperinsulinemia immediately,

225 Our results demonstrate that the suckling period is critical for epigenetic development o

226 In addition, during the suckling period MG hydrolytic activity is likely to deri

227 During the suckling period until day 14, the piglet breed and the n

228 Mutant pups were severely stunted during the suckling period, but many recovered after weaning.

229 During the suckling period, dams were either fed ad libitum, permit

230 inal stem cells and their progeny during the suckling period, suggesting postnatal epigenetic develop

231 s in hypothalamic DNA methylation during the suckling period, suggesting that it is a critical period

232 other and the breed were evident through the suckling period, the introduction of solid feed and subs

233 rement for any dietary intervention in their suckling period.

234 se to the HC dietary modification during the suckling period.

235 ntestinal epithelial cells is limited to the suckling period.

236 ation and crypt fission during the neonatal (suckling) period, mediated at least in part by changes i

237 he relative contribution of the in utero and suckling periods in establishing the adult offspring phe

238 ostnatal nutrient restriction limited to the suckling phase (50% from postnatal [PN]1 to PN21) (PNGR)

239 re abandoned on the natal site after a brief suckling phase, and must develop foraging skills without

240 In addition, preliminary data suggested that suckling piglets born by a sow immunized with the pLT(19

241 We orally inoculated neonatal, conventional suckling piglets with TC-PC177 or PC21A to compare their

242 ows--an effective means to passively protect suckling piglets.

243 In contrast, suckling PLRP2-deficient mice had fat malabsorption evid

244 activities performed away from the nest and suckling, propelling pups into the field where feeding b

245 t in the intestinal epithelial cells in both suckling pups and adults.

246 r amplified in cells of the immune system of suckling pups nor infected their mammary glands.

247 Chemokines, fed to suckling pups of TNF-deficient mothers, restored both po

248 umor virus (MMTV) is carried from the gut of suckling pups to the mammary glands by lymphocytes and i

249 activity in lactating dams exposed to their suckling pups versus cocaine.

250 expression, as well as expression in vivo in suckling rabbits, is dependent upon RpoS.

251 at of iron and zinc absorption measured by a suckling rat pup model.

252 tion and status in infant rhesus monkeys and suckling rat pups and evaluated differences between inta

253 t of phytate concentration were evaluated in suckling rat pups by using 65Zn and 64Cu.

254 Studies in suckling rat pups showed similar results with no capacit

255 transplanted into the nonpermissive liver of suckling rat pups.

256 Chronically suckled rats were then deprived of their eight-pup litte

257 In suckling rats < 14 days old, developmental regulation of

258 Using hepatocytes isolated from suckling rats as our model system, we measured CPT I act

259 microg 2.5S NGF into maternally lead-exposed suckling rats on postnatal days P2, P4, P11, or P18.

260 ver ketogenesis in hepatocytes isolated from suckling rats than those from adult rats.

261 ol-binding protein in the small intestine of suckling rats.

262 immunoglobulin G across intestinal cells in suckling rats.

263 Suckling reduced GFAP in immunocytochemical images and i

264 ersisted, though marginal, through postnatal suckling stages of development (1d-21d), with no concomi

265 leased within the lactating rat brain during suckling stimulation and activates specific subcortical

266 ng posture of lactating rats is dependent on suckling stimulation from pups.

267 Suckling stimulation in lactating dams and cocaine expos

268 ctivity in postpartum day 4-8 dams receiving suckling stimulation.

269 re returned to the females to reinitiate the suckling stimulus for 90 min and induce cFos expression.

270 re returned to the females to reinitiate the suckling stimulus for 90 min to induce cFos expression.

271 y suckling-induced hyperprolactinemia or the suckling stimulus itself.

272 these areas is most likely regulated by the suckling stimulus itself.

273 part due to neural impulses arising from the suckling stimulus.

274 lactating animals that were activated by the suckling stimulus.

275 by hyperprolactinemia in the presence of the suckling stimulus.

276 due to the neural impulses arising from the suckling stimulus.

277 lactating animals that were activated by the suckling stimulus.

278 tration of DA and DOPAC of the IL due to the suckling stimulus.

279 ncentration of DOPAC was detected due to the suckling stimulus.

280 ncentration of plasma PRL in response to the suckling stimulus.

281 Suckling-sucrose treatment significantly reduced Fos-LI

282 In the suckling systems the flux control coefficients for CPT I

283 These data indicate that after suckling terminates, TH up-regulation is evident at 1.5

284 ts, have been selected to favor more intense suckling than genes of maternal origin.

285 Secondly after a prolonged absence of suckling, the consequent decline in circulating lactogen

286 owed to mate and become pregnant but did not suckle their pups after giving birth (NL), and 3) rats t

287 were allowed to mate and become pregnant and suckled their pups for 21 days before weaning (L).

288 y energy expenditure, milk energy output and suckling time were all lower at 30 degrees C.

289 after birth, all mammals must initiate milk suckling to survive.

290 ferentiation and renewal, nor does it affect suckling-to-weaning transition.

291 umbed to fatal encephalitis, whereas litters suckling transgenic dams were fully protected against ch

292 Neonatal piglets were allowed to suckle vaccinated or sham-vaccinated dams for up to 8 h

293 , the first pheromone sufficient to initiate suckling was isolated from the rabbit.

294 complex to the SIF3 element both during the suckling-weaning developmental transition and Caco-2 cel

295 all intestinal villous epithelium during the suckling-weaning transition in mice.

296 d in the villous epithelial cells during the suckling-weaning transition.

297 with CONV-R gut microbiota at the end of the suckling-weaning transition.

298 for the surviving pups were 60-80% of those suckling wild-type mice.

299 In lactating rats, oxytocin cells respond to suckling with brief, explosive, synchronous bursts of el

300 transfer of antibody from mother to fetus to suckling young.