ライフサイエンスコーパス: suckling

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

2 in expression and activity were found during suckling.

3 pt capacity to extract energy from milk upon suckling.

4 ifferentially regulated by either PRL and/or suckling.

5 espond to neural signals from termination of suckling.

6 nses to cues important for the initiation of suckling.

7 ubjected to greater mechanical stress during suckling.

8 rats in response to any stimulus other than suckling.

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

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

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

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

13 and non-bursting cells were observed during suckling.

14 olution commences within hours of the end of suckling.

15 her low or high), and remained stable during suckling.

16 e onset of bursting in oxytocin cells during suckling.

17 ps displayed marked bursts of activity after suckling.

18 ntributed to heat retention in mothers while suckling.

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

20 at are learned and recognized prior to first suckling.

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

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

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

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

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

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

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

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

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

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

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

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

33 Unilateral inhibition of suckling and hormonal reconstitution experiments showed

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

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

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

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

38 sses of mother-infant interactions, contact, suckling, and hyperextension during milk letdown, cause

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

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

41 lar-weight SIF1-binding protein was found in suckling animals without sucrase-isomaltase messenger RN

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

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

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

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

46 Impaired suckling behavior was attributable to defective olfactio

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

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

49 ory conditioning has the potential to modify suckling behavior.

50 with milk may reinforce components of early suckling behavior.

51 ew technique for experimental study of early suckling behavior.

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

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

54 hich occurred either within less than 1 h of suckling (bursting cells) or after injecting facilitator

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

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

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

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

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

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

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

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

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

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

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

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

67 olfactory defect resulting in a competitive suckling deficit.

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

69 In contrast, intraoral sucrose and suckling did not increase hindpaw withdrawal latencies i

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

71 including opioid activity, during the first suckling episode.

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

73 e injected intracerebroventricularly reduced suckling-evoked milk ejections.

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

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

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

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

78 Consistently, suckling first reduced and then increased the expression

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

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

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

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

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

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

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

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

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

88 Coimmunoprecipitation showed that suckling increased molecular interactions between pERK1/

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

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

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

92 of ranscription family) that correlated with suckling-induced increases in serum PRL levels.

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

94 fensive behaviors to the postural control of suckling-induced kyphotic nursing and the modulation of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

112 50% lethal dose and survival distribution in suckling mice and by histopathology in rhesus monkeys.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

154 over unadapted cells during colonization of suckling mice.

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

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

157 urovirulent than their parental LGT virus in suckling mice.

158 ers in the brains of experimentally infected suckling mice.

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

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

161 ue morphology or its attenuated phenotype in suckling mice.

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

163 ely restricted intestinal replication in the suckling mice.

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

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

166 virulence after intracerebral inoculation in suckling mice.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

196 in preventing intestinal colonization in the suckling mouse model.

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

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

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

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

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

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

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

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

205 Litters suckling nontransgenic dams succumbed to fatal encephali

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

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

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

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

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

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

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

213 ption was evaluated in 10-day-old rats while suckling or in contact with the mother.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

229 rement for any dietary intervention in their suckling period.

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

231 ntestinal epithelial cells is limited to the suckling period.

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

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

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

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

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

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

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

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

240 In conclusion, we suggest that, as suckling proceeds, probability of bursting is related to

241 Sweet taste and nonnutritive suckling produce analgesia to transient noxious stimuli

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

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

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

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

246 ats interacting with and nursing a litter of suckling pups showed greater Fos-immunoreactive nuclei i

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

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

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

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

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

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

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

254 transplanted into the nonpermissive liver of suckling rat pups.

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

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

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

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

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

260 immunoglobulin G across intestinal cells in suckling rats.

261 Suckling reduced GFAP in immunocytochemical images and i

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

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

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

265 Suckling stimulation in lactating dams and cocaine expos

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

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

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

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

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

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

272 lactating animals that were activated by the suckling stimulus.

273 by hyperprolactinemia in the presence of the suckling stimulus.

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

275 lactating animals that were activated by the suckling stimulus.

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

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

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

279 Suckling-sucrose treatment significantly reduced Fos-LI

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

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

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

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

284 motor nucleus controls muscles required for suckling, these results suggest an explanation for the n

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

286 s maternal antibody passively transferred by suckling to neonates.

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

288 otein-sensitized cells from animals 10 days (sucklings) to 12 weeks (young adults) of age.

289 f maternal antibodies, passively acquired by suckling, to inhibit active priming of neonates by oral

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 rded in lactating rats from the beginning of suckling up to the first milk-ejection burst, which occu

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

297 d in the villous epithelial cells during 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.