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1 ved and lethality was due to an inability to suckle.
2 at are learned and recognized prior to first suckling.
3 e in burst firing evoked by applied OT or by suckling.
4 in expression and activity were found during suckling.
5 ifferentially regulated by either PRL and/or 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 in only 3% (n = 77) of newborn lambs before suckling.
11 ntrol of the secretion of PRL in response to suckling.
12 pt capacity to extract energy from milk upon suckling.
13 ause of a progressive rise in their Tb while suckling.
14 ntributed to heat retention in mothers while suckling.
15 orodibenzo-p-dioxin (TCDD), in utero and via suckling.
16 ethanol was tested in newborn rats naive to suckling (3-5 hr old) on Postnatal Day (P) 0 and in olde
18 e-Dawley rats were fed, during pregnancy and suckling, a control diet (4% w/w corn oil) or a fatty ac
19 esent study was to determine if any of these suckling activated areas project directly to the DMH.
20 showed marked depression of respiratory and suckling activities in vivo and overexpression of synapt
21 yses indicate that hSRY(ON) pups lack innate suckling activities, and develop fatty liver disease, ar
22 rmal newborn mice mimicked the depression in suckling activity but not respiratory depression in vivo
23 ing and handling as well as of the pups' own suckling activity-but not food intake-fully restored CRF
27 dA was also induced during infections of the suckling and adult mouse intestines, and in vitro under
28 affected by their growth rate when they were suckling and find that limiting growth during that perio
30 porin 4 association decreased during initial suckling and increased after the MER, whereas opposite c
31 odulate sensory-motor reflexes necessary for suckling and may be part of the mechanism by which intra
32 has knock-out mice (Gnasxl(m+/p-)) have poor suckling and perinatal lethality, implicating XLalphas a
36 strous; control of reproduction, aggression, suckling, and parental behaviors; individual recognition
37 vements in utero to the postnatal mastery of suckling at 4 months after birth; and (2) thereafter, fr
38 was no indication that mothers discontinued suckling because of a progressive rise in their Tb while
39 g imaging sessions, dams were exposed to pup suckling before and after administration of an oxytocin
41 dysmorphism, semilethality due to defective suckling behavior, and generation of a small fraction of
44 also used data on inter-birth intervals and suckling behaviours to determine whether the duration of
46 quencing and qPCR showed that, compared with suckling, bottle feeding significantly increased the abu
48 onsistent with augmented cylindrical growth, suckling but not adult transgenic mice show enlarged cry
49 es after ETEC challenge were associated with suckling but not birthing from vaccinated dams, suggesti
50 r normal at birth and can breathe, walk, and suckle, but within 4 days, they show a markedly lower bo
59 f contaminants from the mother cows to their suckling calf and the uptake of soil by grazing cattle.
61 vements in mammals, e.g., walking, swimming, suckling, chewing, and breathing, inhibition is often hy
62 Changes in brain activation in response to suckling closely matched that elicited by oxytocin admin
65 ties were detected from duodenum to colon in suckling CONV mice, but the relative levels of these act
68 Here we show that Hap1 null mutants display suckling defects and die within the first days after bir
72 in VMH are governed primarily by maternal or suckling-derived sensory input rather than food intake o
76 the first demonstration that OT mediation of suckling-evoked bursts/milk ejections is via interaction
80 nerve (CN V), a cranial nerve essential for suckling, feeding and swallowing (S/F/S), a key innate b
81 raniofacial dysfunction as well as disrupted suckling, feeding and swallowing, similar to key 22q11DS
83 in 1 activity in the brown adipose tissue of suckling female rats, indicative of increased sympatheti
87 stricted diet during gestation (GLP) or pups suckled from postnatal day 1 (PN1) to PN11 (E-UN), or PN
88 tes from oral V. cholerae challenge and that suckling from an immunized dam accounts for the majority
89 te utilization in vivo indicated that in the suckling gut B. thetaiotaomicron prefers host-derived po
90 BR3-/- mice exhibited neonatal lethality and suckling impairment that could be partially rescued by l
91 proximately 50% neonatal lethality, impaired suckling in neonatal pups, and loss of LPA responsivity
92 ion of the olfactory cues that trigger first suckling in the mouse would provide the means to determi
97 ceptor (PRL-R) during lactation is caused by suckling-induced hyperprolactinemia or the suckling stim
103 Instead, we find that the initiation of suckling is dependent on variable blends of maternal "si
106 reveals that an apparently innate behavior, suckling, is triggered not by a classical pheromone but
107 y mechanisms related to both the stimulus of suckling itself and suckling-induced hyperprolactinemia.
108 sis estimated that the early gut microbes of suckled lambs were mainly derived from the mother's teat
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
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.
119 we show that infection of hamster cells and suckling mice by Nodamura virus (NoV), a mosquito-transm
120 e restricted in replication in the brains of suckling mice compared to that of wild-type DEN4, and th
123 tiple IFN types led us to test protection of suckling mice from endotoxin-mediated shock, an outcome
124 us expression of prostasin could protect ICR suckling mice from life-threatening DENV-2 infection.
125 t 2D6 IgA is sufficient to passively protect suckling mice from oral challenge with virulent V. chole
129 s mutation attenuated the virus in 4-day-old suckling mice inoculated by the intracerebral (i.c.) rou
130 at least 28,500 times less neurovirulent in suckling mice inoculated intracerebrally and at least 10
132 encephalitis was delayed, a small number of suckling mice still succumbed to lethal intracerebral in
133 Finally, we show using competition assays in suckling mice that inhibition of motility appears to be
135 tion of IFN signaling in vivo was studied in suckling mice using the highly infectious murine EW RV s
136 nal and extraintestinal viral replication in suckling mice vary among different heterologous and homo
139 of Helicobacter pylori infection in infants, suckling mice were inoculated with mixtures of strains t
140 -induced protection was mimicked by treating suckling mice with a glycolipid derived from Helicobacte
141 We show here that infection of ZAP knockout suckling mice with an SVNI led to faster disease progres
145 ns of NaCl (100 mM or less), and also within suckling mice, a model host for the study of cholera pat
147 netics in cell culture, neuroinvasiveness in suckling mice, and ability to replicate and produce diss
148 ly passed EBO-Z virus in progressively older suckling mice, eventually obtaining a plaque-purified vi
150 ed EBOV, developed by sequential passages in suckling mice, identified many similarities between this
152 ne system is more developed than that of the suckling mice, resulted in significantly improved surviv
153 reased virulence in weanling mice but not in suckling mice, suggesting that specific host conditions
154 , in the developing CNS of highly permissive suckling mice, the miRNA-targeted viruses can revert to
175 RV infection on endotoxin-mediated shock in suckling mice.IMPORTANCE Antiviral functions of types I,
176 ditionally, virus-infected tissue culture or suckling mouse brain (SMB) has been the source of viral
177 ion of 32 pg/0.1 ml, and antigen in infected suckling mouse brain and laboratory-infected mosquito po
181 El Tor biotype strains throughout the entire suckling mouse GI tract at various times after intragast
187 ly uncharacterized environments (such as the suckling mouse intestine) can be used as a reporter of l
188 oH mutant was severely attenuated within the suckling mouse intestine, suggesting that sigma(32)-regu
192 ility of results with those for monkeys, the suckling mouse is an appropriate host for safety testing
194 defective for intestinal colonization in the suckling mouse model of cholera and expresses reduced am
198 d whether ribavirin treatment in the lethal, suckling mouse model of HTNV infection would act similar
199 ciently than the wt virus and is lethal in a suckling mouse model of MeV encephalitis even with a low
201 and III IFN receptors (IFNRs) in vitro In a suckling mouse model, RV effectively blocked STAT1 activ
202 Fbp, and Feo systems was not attenuated in a suckling mouse model, suggesting that at least one other
208 TM proteins, were apathogenic in a sensitive suckling mouse neurovirulence test, and were similar in
210 xcellent alternative to the more traditional suckling-mouse brain WN virus antigen used in the immuno
212 apid and more-severe neurological disease in suckling neonates than in those fed an artificial diet.
216 ctions that help mediate the transition from suckling of a fat-rich diet to independent feeding of a
217 nic mice is sufficient to completely protect suckling offspring against MHV-JHM-induced encephalitis.
219 rough breast milk to the intestinal lumen of suckling offspring, coats the pathogen and reduces intes
224 om experiments in mitochondria isolated from suckling or adult rats inverted question mark using a di
225 reported as a cause of sporadic diarrhea in suckling or weanling pigs, to our knowledge, this is the
226 exogenous glucose administration to actively suckling Oxct1(-/-) mice delayed, but could not prevent,
227 sted from the ceca of these hosts during the suckling period (postnatal day 17) and after weaning (po
228 been observed that SFB are absent during the suckling period and appear in high numbers shortly after
229 e-4 (GPAT4) null pups grew poorly during the suckling period and, as adults, were protected from high
230 A obtained from the mothers' milk during the suckling period and, later, of self-produced sIgA in the
231 -carbohydrate (HC) milk formula during their suckling period developed hyperinsulinemia immediately,
237 inal stem cells and their progeny during the suckling period, suggesting postnatal epigenetic develop
238 s in hypothalamic DNA methylation during the suckling period, suggesting that it is a critical period
239 other and the breed were evident through the suckling period, the introduction of solid feed and subs
243 ation and crypt fission during the neonatal (suckling) period, mediated at least in part by changes i
244 he relative contribution of the in utero and suckling periods in establishing the adult offspring phe
245 ostnatal nutrient restriction limited to the suckling phase (50% from postnatal [PN]1 to PN21) (PNGR)
246 re abandoned on the natal site after a brief suckling phase, and must develop foraging skills without
247 In addition, preliminary data suggested that suckling piglets born by a sow immunized with the pLT(19
248 We orally inoculated neonatal, conventional suckling piglets with TC-PC177 or PC21A to compare their
252 umor virus (MMTV) is carried from the gut of suckling pups to the mammary glands by lymphocytes and i
256 tion and status in infant rhesus monkeys and suckling rat pups and evaluated differences between inta
263 microg 2.5S NGF into maternally lead-exposed suckling rats on postnatal days P2, P4, P11, or P18.
268 ersisted, though marginal, through postnatal suckling stages of development (1d-21d), with no concomi
269 leased within the lactating rat brain during suckling stimulation and activates specific subcortical
272 re returned to the females to reinitiate the suckling stimulus for 90 min and induce cFos expression.
273 re returned to the females to reinitiate the suckling stimulus for 90 min to induce cFos expression.
284 owed to mate and become pregnant but did not suckle their pups after giving birth (NL), and 3) rats t
289 umbed to fatal encephalitis, whereas litters suckling transgenic dams were fully protected against ch
291 bout the effects of different feeding modes (suckling versus bottle-feeding) or microbial sources on
294 complex to the SIF3 element both during the suckling-weaning developmental transition and Caco-2 cel
299 In lactating rats, oxytocin cells respond to suckling with brief, explosive, synchronous bursts of el