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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
17 t undergo rapid postnatal catch-up growth by suckling a control-fed dam (recuperated offspring).
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
24 es to regulate social behaviours such as pup suckling, aggression and mating.
25                             All mammals must suckle and swallow at birth, and subsequently chew and s
26                                We found that suckled and bottle-fed newborn lambs had their own disti
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
29                     Unilateral inhibition of suckling and hormonal reconstitution experiments showed
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
33                                Non-nutritive suckling and warm temperatures blunted this effect.
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 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
40                                     Impaired suckling behavior was attributable to defective olfactio
41  dysmorphism, semilethality due to defective suckling behavior, and generation of a small fraction of
42 th the same amount of water had no effect on suckling behavior.
43 ory conditioning has the potential to modify suckling behavior.
44  also used data on inter-birth intervals and suckling behaviours to determine whether the duration of
45 stnatal physiological adaptations, including suckling, blood glucose and energy homeostasis.
46 quencing and qPCR showed that, compared with suckling, bottle feeding significantly increased the abu
47                  Approximately half the pups suckling Btn1a1(-/-) animals died within the first 20 da
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
51 sponses after V. cholerae infection for pups suckled by an immune dam.
52                                         Pups suckled by an immunized dam did not mount this response.
53                         Neonates born to and suckled by dams antenatally vaccinated with each of thes
54                                Neonatal mice suckled by OMV- or sham-immunized dams were challenged w
55 romocriptine to suppress PRL levels and were suckled by pups.
56 control group received vehicle only and were suckled by pups.
57  of C57BL/6J mice in comparison with animals suckled by their biological dams.
58             Four of nine infants born to and suckled by these dams had evidence of infection, a trans
59 f contaminants from the mother cows to their suckling calf and the uptake of soil by grazing cattle.
60                                     Finally, suckling caused dissociation of OTRs and G beta subunits
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
63 n the same (CC, OO) or alternate diet during suckling (CO, OC) and weaned onto standard chow.
64 roups were included: sham-intubated (SI) and suckle-control (SC).
65 ties were detected from duodenum to colon in suckling CONV mice, but the relative levels of these act
66 natal lethality associated with a failure to suckle, cyanosis, and respiratory distress.
67                                          The suckling defect was responsible for the death among lp(A
68  Here we show that Hap1 null mutants display suckling defects and die within the first days after bir
69 s of ALEX is most likely responsible for the suckling defects previously observed.
70  olfactory defect resulting in a competitive suckling deficit.
71                                  Feeding and suckling deficits in infants with PWS are replaced with
72 in VMH are governed primarily by maternal or suckling-derived sensory input rather than food intake o
73               The timing of the last week of suckling did not differ by infant body mass.
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 the first demonstration that OT mediation of suckling-evoked bursts/milk ejections is via interaction
77 e injected intracerebroventricularly reduced suckling-evoked milk ejections.
78               Newborn rat pups tested before suckling experience attached to and ingested milk from t
79 Day (P) 0 and in older neonates with regular suckling experience on P1 or P2.
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
82                                    Disrupted suckling, feeding, and swallowing from birth onward-peri
83 in 1 activity in the brown adipose tissue of suckling female rats, indicative of increased sympatheti
84                                Consistently, suckling first reduced and then increased the expression
85 or lard-rich diet (OHF) during pregnancy and suckling followed by a control diet post-weaning.
86         Pups born to control mouse dams were suckled from birth to postnatal day (PN) 21 on dams fed
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
93  such as pheromones, acting to promote first suckling in the mouse.
94                           In intact animals, suckling increased ERK1/2 activation in the cytosol and
95            Coimmunoprecipitation showed that suckling increased molecular interactions between pERK1/
96 ppressed feeding induced by 24 hr fasting or suckling-induced hyperphagia.
97 ceptor (PRL-R) during lactation is caused by suckling-induced hyperprolactinemia or the suckling stim
98  to both the stimulus of suckling itself and suckling-induced hyperprolactinemia.
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  to study mechanisms that evolved to protect suckling infants from SIV infection.
103      Instead, we find that the initiation of suckling is dependent on variable blends of maternal "si
104       They are fully viable probably because suckling is unimpaired, unlike mutants in which the expr
105                                   Successful suckling is vital to the survival of mammalian newborns.
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
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 d that rF257C was attenuated in vivo in both suckling mice and pigs (one of its natural hosts).
118                               However, using suckling mice as a model host, we found that intraintest
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
121 ectedly displayed increased pathogenicity in suckling mice compared to wild-type SBV.
122 -membrane vesicles (OMVs) passively protects suckling mice from challenge.
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
126 mutations were attenuated in s.c. inoculated suckling mice in comparison with TR339.
127               In contrast to observations in suckling mice in which viruses encoding inactivating mut
128                             GT knockout (KO) suckling mice infected with SINV strains (AR339 and S.A.
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
131                 SVNI infection of 10-day-old suckling mice led to reduced survival in the knockout mi
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
134       We studied orally inoculated 5-day-old suckling mice that were deficient in interferon (IFN) si
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
137        Regulation of MCMV synthesis in these suckling mice was shown to be an IFN-gamma-dependent, pe
138                                         When suckling mice were infected with RV, they were substanti
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
142            Herein, we show that infection of suckling mice with influenza A virus protected the mice
143                                 Infection of suckling mice with influenza virus expands a CD4(-)CD8(-
144 viral RNAi in mouse embryonic stem cells and suckling mice(10,11).
145 ns of NaCl (100 mM or less), and also within suckling mice, a model host for the study of cholera pat
146 y safe following intracranial inoculation of suckling mice, a stringent test of vaccine safety.
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
149                                           In suckling mice, exogenously administered type I, II, or I
150 ed EBOV, developed by sequential passages in suckling mice, identified many similarities between this
151                                           In suckling mice, infection with RV results in an increase
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
155          Moreover, impairing LRE function in suckling mice, via conditional deletion of Dab2, leads t
156                                  Finally, in suckling mice, we found two peaks in the CD8 response on
157 virulence after intracerebral inoculation in suckling mice.
158 FMDV plays an important role in virulence in suckling mice.
159 nd such defects were rescued in Rnasel (-/-) suckling mice.
160   This virus showed growth in HFDK cells and suckling mice.
161 e culture, and elicits fluid accumulation in suckling mice.
162 small intestinal epithelial cells (IEC) from suckling mice.
163  over unadapted cells during colonization of suckling mice.
164 cerebrally into the right cortex of C57/BL/6 suckling mice.
165 sets and adoptively transferred into C57BL/6 suckling mice.
166 within intestinal epithelial cells (IECs) of suckling mice.
167 ers in the brains of experimentally infected suckling mice.
168 n to attenuate the neurovirulence of JUNV in suckling mice.
169 rowth and in vivo pathogenicity in adult and suckling mice.
170 ue morphology or its attenuated phenotype in suckling mice.
171 tationary-phase cells were used to inoculate suckling mice.
172 ely restricted intestinal replication in the suckling mice.
173  and mortality compared to wild-type (WT) B6 suckling mice.
174 ter than that of a simian rotavirus (RRV) in suckling mice.
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
178                                 However, the suckling mouse brain-derived (SMB) antigen used in this
179  sources of virus-infected tissue culture or suckling mouse brain.
180 lines (Vero, BHK, SW13, and XTC cells) or in suckling mouse brains.
181 El Tor biotype strains throughout the entire suckling mouse GI tract at various times after intragast
182 ype to resist bactericidal mechanisms in the suckling mouse GI tract.
183                                          The suckling mouse has been used as a model to identify Vibr
184                                 In fact, the suckling mouse intestine does not appear to be a potent
185          Vibrio cholerae colonization of the suckling mouse intestine is a commonly used animal model
186       Quantitation of RyhB expression in the suckling mouse intestine suggests that iron availability
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
189 s not required for V. cholerae growth in the suckling mouse intestine.
190  produced normal biofilms, and colonized the suckling mouse intestine.
191  as strains lacking hfq fail to colonize the suckling mouse intestine.
192 ility of results with those for monkeys, the suckling mouse is an appropriate host for safety testing
193 P nor OA is required for colonization of the suckling mouse large bowel.
194 defective for intestinal colonization in the suckling mouse model of cholera and expresses reduced am
195 s in mice and greatly reduced mortality in a suckling mouse model of cholera.
196 on against live V. cholerae challenge in the suckling mouse model of cholera.
197 B could influence protective efficacy in the suckling mouse model of cholera.
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
200                                         In a suckling mouse model, ectopically stimulating different
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
203 V replication and pathogenesis in an in vivo suckling mouse model.
204 in cross-linking and fluid accumulation in a suckling mouse model.
205 k of HapA did not affect colonization in the suckling mouse model.
206 in preventing intestinal colonization in the suckling mouse model.
207 nd antidiarrheal efficacy in closed-loop and suckling mouse models.
208 TM proteins, were apathogenic in a sensitive suckling mouse neurovirulence test, and were similar in
209                                       In the suckling mouse, oral inoculation with V. cholerae leads
210 xcellent alternative to the more traditional suckling-mouse brain WN virus antigen used in the immuno
211            Our objective was to determine if suckling neonatal piglets are susceptible to enterohemor
212 apid and more-severe neurological disease in suckling neonates than in those fed an artificial diet.
213  into milk and their passive transfer to the suckling newborn.
214 imulated fluid secretion in the intestine of suckling Nkcc1(-/-) mice were normal.
215                                      Litters suckling nontransgenic dams succumbed to fatal encephali
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.
218           A comparison of the iron status of suckling offspring from LFKO(-/-) intercrosses and from
219 rough breast milk to the intestinal lumen of suckling offspring, coats the pathogen and reduces intes
220 es in and is transferred through the milk to suckling offspring.
221 ontributions of obesity during pregnancy and suckling on metabolic health post-weaning.
222                     In rats whose pups could suckle only on one side, TH was up-regulated only on the
223 r together were required for colonization of suckling or adult mice.
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,
232             Our results demonstrate that the suckling period is critical for epigenetic development o
233                      In addition, during the suckling period MG hydrolytic activity is likely to deri
234                                   During the suckling period until day 14, the piglet breed and the n
235 Mutant pups were severely stunted during the suckling period, but many recovered after weaning.
236                                   During the suckling period, dams were either fed ad libitum, permit
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
240 rement for any dietary intervention in their suckling period.
241 se to the HC dietary modification during the suckling period.
242 ntestinal epithelial cells is limited to the suckling period.
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
249 ows--an effective means to passively protect suckling piglets.
250 t in the intestinal epithelial cells in both suckling pups and adults.
251                           Chemokines, fed to suckling pups of TNF-deficient mothers, restored both po
252 umor virus (MMTV) is carried from the gut of suckling pups to the mammary glands by lymphocytes and i
253  activity in lactating dams exposed to their suckling pups versus cocaine.
254 expression, as well as expression in vivo in suckling rabbits, is dependent upon RpoS.
255 at of iron and zinc absorption measured by a suckling rat pup model.
256 tion and status in infant rhesus monkeys and suckling rat pups and evaluated differences between inta
257 t of phytate concentration were evaluated in suckling rat pups by using 65Zn and 64Cu.
258                                   Studies in suckling rat pups showed similar results with no capacit
259 transplanted into the nonpermissive liver of suckling rat pups.
260                                  Chronically suckled rats were then deprived of their eight-pup litte
261                                           In suckling rats < 14 days old, developmental regulation of
262              Using hepatocytes isolated from suckling rats as our model system, we measured CPT I act
263 microg 2.5S NGF into maternally lead-exposed suckling rats on postnatal days P2, P4, P11, or P18.
264 ver ketogenesis in hepatocytes isolated from suckling rats than those from adult rats.
265 ol-binding protein in the small intestine of suckling rats.
266  immunoglobulin G across intestinal cells in suckling rats.
267                                              Suckling reduced GFAP in immunocytochemical images and i
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
270                                              Suckling stimulation in lactating dams and cocaine expos
271 ctivity in postpartum day 4-8 dams receiving suckling stimulation.
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.
274 y suckling-induced hyperprolactinemia or the suckling stimulus itself.
275  these areas is most likely regulated by the suckling stimulus itself.
276 part due to neural impulses arising from the suckling stimulus.
277 lactating animals that were activated by the suckling stimulus.
278 by hyperprolactinemia in the presence of the suckling stimulus.
279  due to the neural impulses arising from the suckling stimulus.
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 owed to mate and become pregnant but did not suckle their pups after giving birth (NL), and 3) rats t
285 were allowed to mate and become pregnant and suckled their pups for 21 days before weaning (L).
286 y energy expenditure, milk energy output and suckling time were all lower at 30 degrees C.
287  after birth, all mammals must initiate milk suckling to survive.
288 ferentiation and renewal, nor does it affect suckling-to-weaning transition.
289 umbed to fatal encephalitis, whereas litters suckling transgenic dams were fully protected against ch
290             Neonatal piglets were allowed to suckle vaccinated or sham-vaccinated dams for up to 8 h
291 bout the effects of different feeding modes (suckling versus bottle-feeding) or microbial sources on
292 , the first pheromone sufficient to initiate suckling was isolated from the rabbit.
293                            We show here that suckling-weaning and fasting-refeeding transitions in ro
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.

 
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