ライフサイエンスコーパス: NTS

1 NTS are critical for high performance in surgery around

2 NTS bacteremia mainly affects older people with comorbid

3 NTS has great potential for treatment assessment and pol

4 NTS was acutely induced by androgen deprivation in anima

5 NTS was identified in 11 outpatients (0.07%), while typh

6 NTS(HSD2) neurons respond to sodium deficiency with spon

7 NTS-CeA neurons received greater numbers of ST-related i

8 -4.73) vs 4.20 (4.00-4.50), P = 0.008] about NTS.

9 Waning of transplacentally acquired NTS LPS-specific antibodies at 4 months of age left infa

10 ential mechanisms by which cocaine activates NTS GLP-1-expressing neurons, we microinjected corticost

11 studies revealed that selectively activating NTS-to-LDTg circuits attenuated cocaine seeking via a GL

12 In addition, NTS GLP-1R knockdown significantly increased self-admini

13 onventional residency training or additional NTS training in a 2-month curriculum.

14 9% in vehicle-treated Flox mice to 47% after NTS treatment), was lost in mice with hepatic deletion o

15 cKO mice also develop less proteinuria after NTS injury.

16 ies appear to play a protective role against NTS infections during early infancy.

17 mmon NTS serovar, accounted for 38.5% of all NTS isolates (n = 258), followed by S. Typhimurium (31.7

18 al imaging to demonstrate that virtually all NTS-->lPBN and lPBN-->CeA CGRP projections coexpress ves

19 We reveal an NTS-cleavage-competent conformation following the HNH do

20 tion (Ct) (average of 40.4 Mg C ha(-1)); and NTS showed the highest contribution of post-anthesis dry

21 role of maternally acquired antibodies, and NTS seroincidence rates were modeled using multivariate

22 cle, the area with easy access to the AP and NTS, transiently decreased BP in SHR and this effect was

23 Conversely, Pod-ATTAC mice and NTS-treated mice showed hypercholesterolemia and a 7- to

24 ygdala (CeA) or axons in the vBNST, PBN, and NTS produces reward behavior but did not promote feeding

25 nteraction between angiotensin signaling and NTS(HSD2) neurons provides a neuronal context for the lo

26 Thus, SSS and NTS systems offer the best options for removing CO2 from

27 GDF15 activates GFRAL(AP/NTS) neurons and supports conditioned taste and place av

28 the release of GDF15 and activates GFRAL(AP/NTS) neurons, as well as causing significant reductions

29 Neurotensin (NT; also known as NTS), a 13-amino-acid peptide predominantly localized in

30 spectrometry (LC-qTOF-MS), and evaluated by NTS.

31 The 3' flap generated by NTS cleavage can be rapidly digested by a 3' to 5' singl

32 ever, the large quantity of data produced by NTS analytical workflows makes data interpretation and t

33 suggest that glutamate and 5-HT, released by NTS afferent terminals, trigger Ca(2+)-dependent astrogl

34 In rat brainstem slices containing caudal NTS, shocks to the solitary tract (ST) triggered synchro

35 of CCK(NTS) neurons to be mediated by a CCK(NTS)-->PVH pathway that also encodes positive valence.

36 NTS neurons containing cholecystokinin (CCK(NTS)) is responsive to nutritional state and that their

37 Optogenetic activation of CCK(NTS) axon terminals within the PVH reveal the satiating

38 identify the functional significance of CCK(NTS) neurons and reveal a sufficient and discrete NTS to

39 the PVH reveal the satiating function of CCK(NTS) neurons to be mediated by a CCK(NTS)-->PVH pathway

40 ecific anterograde tracing revealed that CCK(NTS) neurons provide a distinctive innervation of the pa

41 es both systemically (plasma) and centrally (NTS and RVLM) and reduced hypothalamic PGE(2) production

42 re significantly increased following chronic NTS GLP-1R knockdown.

43 ablish chronic infection, similar to chronic NTS disease in humans.

44 Enteritidis, the most common NTS serovar, accounted for 38.5% of all NTS isolates (n

45 All confirmed NTS isolates from blood from England submitted to GBRU b

46 spectively analyzed 48 345 culture-confirmed NTS infections that occurred in Israel 1995-2012.

47 mited number of targeted water contaminants, NTS provides the opportunity to detect also unknown trac

48 e supporting the effectiveness of curricular NTS training, however, is lacking.

49 Although incidence decreased, NTS remained a major cause of invasive bacterial infecti

50 result from tracer injections into different NTS subdivisions, with dual retrograde tracing revealing

51 neurons and reveal a sufficient and discrete NTS to hypothalamus circuit controlling appetite.

52 Exposure to the dominant NTS serovars, Salmonella enterica serovars Typhimurium a

53 ecorded neuron pairs: one dye positive (i.e. NTS-CeA) and a second unlabelled neighbour.

54 to the NTS to examine the role of endogenous NTS GLP-1R signaling in energy balance control.

55 vely, these data demonstrate that endogenous NTS GLP-1R signaling is required for the control of food

56 sing NMDAR-mediated currents, thus enhancing NTS sensitivity to vagal inputs.SIGNIFICANCE STATEMENT L

57 However, the essential NTS used by surgeons operating in LMICs to overcome the

58 e prostate cancer genes, such as MMP7, ETV1, NTS, and SCHLAP1, we also noted a significant decrease i

59 wborn mice that specifically lack excitatory NTS neurons, we show that they are both mute and unable

60 , dopamine beta-hydroxylase (DBH)-expressing NTS neurons as two separate populations that directly ex

61 ophysiological properties of LepR-expressing NTS neurons have not been well characterized, and it is

62 Here we investigate the basis for NTS(HSD2) neuron activation, identify the circuit by whi

63 ent and recent malaria are a risk factor for NTS, therefore, a better understanding about the functio

64 g strategies, indicating a bright future for NTS.

65 re we present for the first time a model for NTS dynamics in high risk populations that can analyze t

66 monella Typhi and 11.5 (8.5-23.4) months for NTS.

67 age of children with a culture positive for NTS was 1.8 (3) years.

68 osis that can serve as a human reservoir for NTS infections.

69 5 (39.4%), and 27 (79.4%), respectively, for NTS.

70 Collectively, data demonstrate a role for NTS astrocytic GLP-1R signaling in energy balance contro

71 Four NTS serovars (Mbandaka, Bredeney, Infantis and Virchow)

72 strategy to protect vulnerable infants from NTS disease.

73 Further tracing showed that CeA GABAergic NTS neurons are innervated by glutamatergic NTS neurons

74 (DREADDs) constructs expressed in GABAergic NTS neurons increased or decreased, respectively, action

75 tively, action potential firing of GABAergic NTS neurons and downstream synaptic inhibition of the DM

76 ivo, DREADD-mediated activation of GABAergic NTS neurons increased systemic blood glucose concentrati

77 In contrast, bacteriophage T7 Pol generates NTS mutations predominantly.

78 NTS neurons are innervated by glutamatergic NTS neurons in a posterior thalamic region, which also p

79 ults above 65 years were more likely to have NTS bacteremia (AOR, 1.54 [95% CI, 1.46 to 1.67]; 2.57 [

80 Of 172 human NTS isolates, 90 (52.3%) from stool and 82 (47.7%) from

81 Importantly, NTS(HSD2) neurons stimulate appetite via projections to

82 less likely to have detectable SARS-CoV-2 in NTS collected at enrollment (8/13 [62%] vs 17/17 [100%];

83 F-1alpha(-/-) and significantly decreased in NTS-HIF-1alpha(-/-) compared to control mice (P < 0.0001

84 Second, HIF-1alpha was deleted in NTS neurons in adult mice (NTS-HIF-1alpha(-/-) ) by micr

85 orescence showed that HIF-1alpha deletion in NTS-HIF-1alpha(-/-) was restricted to glutamatergic neur

86 The role of Glp1r in NTS was evaluated by using Glp1r(-/-) mice or C57BL/6 mi

87 ile knockdown of leptin receptors (LepRs) in NTS neurons increases food intake.

88 +)-dependent vesicular release mechanisms in NTS astrocytes by virally driven expression of a dominan

89 Chemogenetic activation of GLP-1 neurons in NTS similarly decreased nicotine intake.

90 ze the serovar diversity and AMR profiles in NTS.

91 ion of overnight food intake following intra-NTS leptin injection.

92 and body weight-suppressive effects of intra-NTS GLP-1R activation.

93 udies using male rats demonstrate that intra-NTS injections of DCPP-ene attenuate reduction of overni

94 Invasive NTS and S. Typhi together mapped around common water ven

95 Invasive NTS can be difficult to treat and have high case-fatalit

96 gnostic tests that rapidly identify invasive NTS infection, and differentiate between resistant and n

97 The prevalence of MDR invasive NTS (iNTS) was 77.2%, with 15% resistant to ceftriaxone,

98 The annual incidence of invasive NTS disease decreased over the study period, but case fa

99 Resistance of invasive NTS to first-line antimicrobial agents appeared to be st

100 reduce the burden and mortality of invasive NTS.

101 ous disease problem in sub-Saharan Africa is NTS in children and immunocompromised adults.

102 We isolated NTS from 164 meat pathway samples.

103 We found that typhoid toxin and its NTS ortholog induce different clinical presentations.

104 n, but little is known about the role of its NTS ortholog.

105 ices by recording from retrogradely labelled NTS projection neurons.

106 n collaterals to both the lateral and medial NTS subdivisions.

107 -carboxamide (ANA-12) into the dorsal medial NTS (dmNTS) of male Sprague-Dawley rats with coronary ar

108 CRISPR/Cas9-mediated NTS knockdown in either the thalamic or CeA neurons grea

109 ha was deleted in NTS neurons in adult mice (NTS-HIF-1alpha(-/-) ) by microinjecting adeno-associated

110 When compared with control treated mice, NTS-challenged mice treated prophylactically with BI-BTK

111 l effects of LLTS, four brainstem (SP5, NAb, NTS, and RVLM) and two forebrain sites (PVN and SFO) wer

112 All recorded SST-negative NTS neurons (n = 72) received SST-ChR2 input.

113 ompared them with unlabelled, near-neighboor NTS neurons.

114 murine model of nephrotoxic serum nephritis (NTS).

115 ygdala pathway, both expressing neurotensin (NTS).

116 cterized the functional role of neurotensin (NTS) in cell line and animal models of CRPC with NED.

117 Here, we show that neurotensin (NTS)-expressing glutamatergic neurons in the ventrolater

118 ria together, but separated malaria from non-NTS infections.

119 tic terminals at the solitary tract nucleus (NTS).

120 81.0%) of Salmonella Typhi and 12 (41.4%) of NTS.

121 WHO, and more than half (53.8%; 242/450) of NTS isolates were multidrug resistant (MDR; resistant to

122 t serovar, accounting for 41.8% (188/450) of NTS isolates.

123 Because 87% of NTS belonged to only 4 serovars, a multivalent vaccine m

124 Moreover, the ability of NTS treatment to increase the percentage of low-density

125 Selective ablation of NTS PPG neurons by viral expression of diphtheria toxin

126 csk9 (5% in both the presence and absence of NTS).

127 ndings indicate that increased activation of NTS GLP-1-expressing neurons by corticosterone may repre

128 (CeA) contain the densest concentrations of NTS-projecting neurons.

129 ession levels are higher in the glomeruli of NTS injured mice and passive Heymann membranous nephropa

130 Optogenetic activation and inactivation of NTS-expressing CeA neurons promoted and suppressed non-R

131 f neutrophils and T cells after induction of NTS.

132 Finally, pharmacological inhibition of NTS astrocytes attenuates the anorectic and body weight-

133 additionally demonstrated that inhibition of NTS-->lPBN neurons attenuated cisplatin-induced anorexia

134 nducted a clinical genomics investigation of NTS isolated from diarrheal children admitted to one of

135 d this effect was attenuated after lesion of NTS DBH neurons with anti-DBH conjugated to saporin (ant

136 We found that the vast majority of NTS LepR neurons received monosynaptic innervation from

137 istance (AMR), and clinical manifestation of NTS gastroenteritis in Vietnam, we conducted a clinical

138 significantly improved the renal outcome of NTS in C57BL/6 mice by decreasing renal infiltration and

139 data set to study the trends and outcomes of NTS bacteremias in England between 2004 and 2015.

140 agal afferents as well as by a population of NTS neurons.

141 Thus, in the presence of NTS, mice lacking hepatic Pcsk9 showed a 40% to 50% decr

142 Using whole-cell recordings of NTS neurons, from horizontal brainstem slices of male an

143 ata suggest the pharmacological relevance of NTS astrocytic GLP-1R activation for food intake and bod

144 We propose a novel role of NTS in the development of CRPC with NED, and a possible

145 llectively demonstrate the critical roles of NTS SRC-1 in mediating E2's actions on food intake and a

146 activation (live cell calcium signaling) of NTS astrocytes and neurons; these effects are also atten

147 Poultry is the primary source of NTS outbreaks, as well as the fastest growing meat secto

148 We reveal that a subset of NTS neurons containing cholecystokinin (CCK(NTS)) is res

149 ome sequencing for sustained surveillance of NTS internationally.

150 Transplacental transfer of NTS LPS-specific maternal antibodies to infants was high

151 Solitary tract (ST) afferents converged onto NTS-CeA second-order sensory neurons in greater numbers,

152 trol mice, HIF-1alpha deletion in the CNS or NTS did not affect ventilation, nor the acute HVR (10-15

153 and can be detected by analysis of saliva or NTSs.

154 ST-evoked action potentials at second-order NTS neurons, demonstrating strong modulation of primary

155 In total, 1047 cases of persistent NTS infections, comprising 2.2% of all reported cases of

156 ways (93%) triggered EPSCs at CeA projecting NTS neurons.

157 eactivity was found throughout the adult rat NTS.

158 The remaining NTS-CeA neurons received viscerosensory input only via p

159 Remarkably, NTS(HSD2) neurons are necessary for sodium appetite, and

160 removed (NT0), no-till with straw retention (NTS), subsoiling with straw removed (SS0), and subsoilin

161 omoting populations; gene profiling revealed NTS as a prominent marker for these CeA neurons.

162 , hindbrain reticular formation, and rostral NTS.

163 Nontyphoidal Salmonella (NTS) are among the most common etiological agents of dia

164 human infections by nontyphoidal Salmonella (NTS) are poorly characterized.

165 almonella Typhi and nontyphoidal Salmonella (NTS) are the predominant cause of community-acquired blo

166 Nontyphoidal Salmonella (NTS) bacteremia causes hospitalization and high morbidit

167 ptible to recurrent nontyphoidal Salmonella (NTS) bacteremia.

168 were compared with nontyphoidal Salmonella (NTS) isolated from persons with bloodstream infection an

169 Nontyphoidal Salmonella (NTS) organisms are a major cause of gastroenteritis and

170 teritidis, 32 other nontyphoidal Salmonella (NTS) serotypes, and 126 Salmonella Typhi.

171 Nontyphoidal Salmonella (NTS) was identified in 671 enrolled inpatients (1.8% of

172 o control foodborne nontyphoidal Salmonella (NTS), infections have not declined in decades.

173 hich was mainly due to non-Typhi Salmonella (NTS) diagnoses being misclassified as malaria.

174 Invasive non-typhoidal Salmonella (NTS) is among the leading causes of blood stream infecti

175 Typhoidal and non-typhoidal Salmonelleae (NTS) cause typhoid fever and gastroenteritis, respective

176 Nontarget screening (NTS) based on high resolution mass spectrometry (HRMS) h

177 ining a newly developed nontarget screening (NTS) workflow and high-resolution mass spectrometry (HRM

178 are frequently used for nontarget screening (NTS), i.e., the search for compounds that are not previo

179 al rearrangements in the N-terminal segment (NTS) can stabilize this Pfr-like state and that the PHY-

180 paratyphoid fever), nontyphoidal septicemia (NTS), and gastroenteritis in humans and other animals wo

181 LN in which mice receive nephrotoxic serum (NTS) containing anti-glomerular antibodies.

182 ce) and mice treated with nephrotoxic serum (NTS), which triggers immune-mediated podocyte damage.

183 ther protamine sulfate or nephrotoxic serum (NTS).

184 , despite multifibre convergence, all single NTS-CeA neurons received inputs derived from only unmyel

185 Nontechnical skills (NTS) have been identified as critical competencies of su

186 G) neurons in the nucleus tractus solitarii (NTS) are the predominant source of endogenous GLP-1 with

187 rent pathway (the nucleus tractus solitarii, NTS; nodose ganglion, NG).

188 tonomic control: nucleus tractus solitarius (NTS) and rostral ventrolateral medulla (RVLM)] cytokine

189 ht the hindbrain nucleus tractus solitarius (NTS) as a brain region important for GLP-1R-mediated eff

190 c neurons in the nucleus tractus solitarius (NTS) form a hindbrain micro-circuit with preganglionic p

191 at the hindbrain nucleus tractus solitarius (NTS) is essential for vocalization in mice.

192 ostrema (AP) and nucleus tractus solitarius (NTS) of brainstem including the NTS neurons immunoreacti

193 platin activates nucleus tractus solitarius (NTS) projections to the lateral parabrachial nucleus (lP

194 d neurons in the nucleus tractus solitarius (NTS), a hindbrain nucleus critical for energy balance co

195 g neurons in the nucleus tractus solitarius (NTS), a hindbrain nucleus that projects monosynaptically

196 b connecting the nucleus tractus solitarius (NTS), the major central source of GLP-1, with the other

197 b connecting the nucleus tractus solitarius (NTS), the primary source of central GLP-1, with midbrain

198 ) neurons in the nucleus tractus solitarius (NTS).

199 clei such as the nucleus tractus solitarius (NTS).

200 nd the CNS [e.g. nucleus tractus solitarius (NTS)], although the signals for this plasticity are not

201 d by 26.3, 19.0, 16.5, and 9.4 for NT0, SS0, NTS, and SSS, respectively.

202 e rats, 65% of somatostatin-expressing (SST) NTS neurons also express GAD67, supporting their likely

203 2)-YFP mice, we quantified the impact of SST-NTS neurons on viscerosensory processing.

204 the target strand (TS) or nontarget strand (NTS) of DNA substrate.

205 ich the repair of the nontranscribed strand (NTS) and the rest of the genome takes place.

206 n repair (NER) of the nontranscribed strand (NTS) of genes in an asymmetric manner, with faster repai

207 antly enriched on the nontranscribed strand (NTS) of yeast genes, particularly in BER-deficient strai

208 milar frequencies on non-transcribed strand (NTS) and transcribed strand (TS) DNA.

209 lment and daily nasopharyngeal/throat swabs (NTSs) for RT-PCR testing.

210 receptor-mediated synaptic currents and that NTS NMDAR activation contributes to leptin-induced reduc

211 The results indicated that NTS and SSS can enhance translocation of photosynthates

212 The NTS viral loads fall faster in asymptomatic individuals,

213 The NTS, located in the dorsal brainstem, receives constant

214 cells indicates that NER activity along the NTS is also elevated on the 5' side of nucleosomes, cons

215 tite, and uncover an interaction between the NTS(HSD2) circuit and ATII signaling.

216 This translocation can be inhibited by the NTS-derived peptide (EPE) that blocks the ERK1/2-importi

217 ns in horizontal brain slices containing the NTS from male and female LepR-Cre X Rosa-tdTomato mice.

218 Removing polySia from the NTS had functional consequences.

219 -gamma and -alpha (PPAR-gamma/-alpha) in the NTS and NG in HFD rats were markedly reversed by chronic

220 with Akt-eNOS-NO signaling activation in the NTS and NG induced by acute intravenous rhFGF21 administ

221 e ultrastructural location of polySia in the NTS and the functional effects of enzymatic removal of p

222 al activation of P2Y(1) purinoceptors in the NTS decreased baroreflex gain by 40% (p = 0.031), wherea

223 ve transcription factor, is necessary in the NTS for normal VAH.

224 that BDNF/TrkB signalling is impaired in the NTS in the CHF state.

225 icate that endogenous BDNF signalling in the NTS is integral for the maintenance of BRS and that BDNF

226 ittle was known about how leptin acts in the NTS neurons to inhibit food intake.

227 Removal of polySia in the NTS of anesthetized rats increased sympathetic nerve act

228 Here we report that in the NTS of high-fat diet-induced obese (DIO) rats, the apoA-

229 r kinase B (TrkB) receptor signalling in the NTS on baroreflex control both in healthy and CHF rats.

230 ata show that GLP-1-producing neurons in the NTS project to the LDTg, providing anatomical evidence o

231 hat SRC-1 gene knockdown specifically in the NTS significantly diminished E2's anorectic action, lead

232 Our results suggest that leptin acts in the NTS to reduce food intake by increasing NMDAR-mediated c

233 Improvements in the NTS used by surgeons operating in VRCs have the potentia

234 fect of E2 on apoA-IV gene expression in the NTS was significantly attenuated in SRC-1 knockdown rats

235 ty in glutamatergic neurotransmission in the NTS with CH.

236 d with higher levels of "ambient" ATP in the NTS would be expected to decrease baroreflex gain by the

237 we found no catecholaminergic neurons in the NTS, A5 or Locus Coeruleus, no serotoninergic raphe neur

238 vel mechanism by which leptin, acting in the NTS, could potentiate gastrointestinal satiation signals

239 d from baroreceptor afferent synapses in the NTS, the influence of other neurotransmitters and neurom

240 ral synapse with second-order neurons in the NTS.

241 ly uncoupled from the initial changes in the NTS.

242 solitarius (NTS) of brainstem including the NTS neurons immunoreactive to dopamine beta-hydroxylase

243 Injection of leptin into the NTS inhibits food intake, while knockdown of leptin rece

244 an axonal tracer (cholera toxin b) into the NTS produces a similar pattern of retrograde labeling in

245 od intake, and injections of leptin into the NTS reduce meal size and increase the efficacy of vagus-

246 gy balance, AAV-GLP-1R was injected into the NTS to examine the role of endogenous NTS GLP-1R signali

247 colocalized with apoA-IV in the cells of the NTS and E2 treatment enhances the recruitment of ERalpha

248 whereas weeks are required for repair of the NTS and the rest of the genome.

249 We also show that neurons of the NTS directly connect to and entrain the activity of spin

250 Half of the NTS-CeA neurons received at least one primary afferent i

251 -klotho (klb) significantly expressed on the NTS and NG.

252 rains, due to higher damage formation on the NTS and transcription-coupled repair of the transcribed

253 neurons may exert top-down control over the NTS, here we provide a brain-wide map of all neurons tha

254 to prevent the onset of NED by targeting the NTS signaling pathway.

255 In summary, our work demonstrates that the NTS is an obligatory component of the neuronal circuitry

256 rmal transmission of information through the NTS and that changes in its expression alter sympathetic

257 ised astroglial function was specific to the NTS as expression of dnSNARE in astrocytes of the ventro

258 Furthermore, immunization with the NTS S.

259 de novel evidence that astrocytes within the NTS are relevant for energy balance control by GLP-1 sig

260 bitory network innervates broadly within the NTS, with the potential to gate viscerosensory input to

261 them within a feedforward circuit within the NTS.

262 These NTS neurons then excite brain regions known to mediate f

263 Alterations to NTS signalling in CHF remain particularly undefined.

264 ietnamese infants have extensive exposure to NTS, maternally acquired antibodies appear to play a pro

265 no- and polysynaptic ST afferent pathways to NTS-CeA neurons were organized exclusively as either tra

266 eurons in the nucleus of the solitary tract (NTS(HSD2) neurons) were shown to drive sodium appetite.

267 ng within the nucleus of the solitary tract (NTS) contributes to the control of food intake, and inje

268 The nucleus of the solitary tract (NTS) is a key gateway for meal-related signals entering

269 The nucleus of the solitary tract (NTS) is activated by vagal afferents from the gastrointe

270 The nucleus of the solitary tract (NTS) is critical for the central integration of signals

271 eA-projecting nucleus of the solitary tract (NTS) neurons for synaptic characterization and compared

272 ession in the nucleus of the solitary tract (NTS) of lean ovariectomized (OVX) rodents.

273 The nucleus of the solitary tract (NTS) regulates life-sustaining functions ranging from ap

274 nveyed to the nucleus of the solitary tract (NTS) where it initiates neuroendocrine, behavioral, and

275 l such as the nucleus of the solitary tract (NTS), a site that receives chemosensory afferents, and t

276 us (PBN), and nucleus of the solitary tract (NTS), and activation of cell bodies in the central amygd

277 and pF(L) ), nucleus of the solitary tract (NTS), reticular formation (RF), pontine and midbrain ves

278 ocytes of the nucleus of the solitary tract (NTS), the brain area that receives and integrates sensor

279 first in the nucleus of the solitary tract (NTS).

280 rtex, and the nucleus of the solitary tract (NTS).

281 f mfd globally shifts the distribution of TS/NTS ratios downward by a factor of about 2 on average fo

282 hing, slightly pushed the distribution of TS/NTS ratios to higher ratios.

283 transcribed strand/nontranscribed strand (TS/NTS) repair ratio demonstrated that deletion of mfd glob

284 of ST-related inputs compared to unlabelled NTS neurons, indicating that highly convergent viscerose

285 d PHOX2B immunopositive cells in the pF(V) , NTS, and part of the RF.

286 strate that the central GLP-1R signaling via NTS DBH neurons counteracts the development of hypertens

287 axons directly to the caudal, viscerosensory NTS, focusing on a medial subregion with aldosterone-sen

288 EM sleep. The NREM-promoting effect of vlPAG NTS neurons is partly mediated by their projection to th

289 genetic and chemogenetic activation of vlPAG NTS neurons strongly enhanced NREM sleep, whereas their

290 ) were Salmonella Typhi, and 42 (24.6%) were NTS.

291 n infant populations residing in areas where NTS disease is highly endemic.

292 on activation, identify the circuit by which NTS(HSD2) neurons drive appetite, and uncover an interac

293 ygdala circuit for sleep generation in which NTS signaling is essential for both the upstream glutama

294 -1 axons form close synaptic apposition with NTS astrocytes.

295 15%) children were found to be infected with NTS by stool culture.

296 se, a cluster analysis grouped patients with NTS and malaria together, but separated malaria from non

297 Of the patients with NTS bacteremia, 969 (69%) had a cardiovascular condition

298 hepatic deletion of Pcsk9 were treated with NTS to determine the contribution of PCSK9 to the dyslip

299 ndocrine-like phenotypes upon treatment with NTS.

300 -1R agonists activate and internalize within NTS astrocytes, while behavioral data suggest the pharma