ライフサイエンスコーパス: VNS

1 VNS also significantly decreased blood pressure, improve

2 VNS control over cardiac function is maintained during c

3 VNS did not alter NE concentrations in either structure

4 VNS does not reduce the rate of death or HF events in ch

5 VNS for 12 weeks significantly decreased plasma insulin,

6 VNS improved LA function and volumes and suppressed LA f

7 VNS improves metabolic and hemodynamic parameters, and t

8 VNS is a novel and potentially useful therapy for improv

9 VNS is as effective as antiepileptic drug therapy, and s

10 VNS paired with tactile rehabilitation resulted in a sig

11 VNS paired with tones may be effective for a subgroup of

12 VNS shortened the AERP at all sites (from 123+/-4 to 39+

13 VNS treatment attenuated brain mitochondrial dysfunction

14 VNS was applied for the next 12 weeks.

15 VNS, on the other hand, resulted in a significant amelio

16 VNS-tone pairing also reduced the phase coherence betwee

17 VNS-tone pairing reduced gamma band activity in left aud

18 VNS-treated participants had greater improvement in FMA-

19 In Experiment 1, VNS caused a 98% increase in NE output relative to basel

20 iscrimination task for mice implanted with a VNS electrode.

21 electric activity, suggesting that abdominal VNS can potentially be used to control GI function.

22 In addition, VNS therapy increased dendritic spine density and improv

23 Additionally, VNS reversed a behavioral correlate of the positive symp

24 provides additional evidence that adjunctive VNS has enhanced antidepressant effects compared with tr

25 of response to ECT, those in the adjunctive VNS group had a significantly higher 5-year cumulative r

26 egistry results indicate that the adjunctive VNS group had better clinical outcomes than the treatmen

27 l group and 33.1 [SD=7.0] for the adjunctive VNS group).

28 dy examined this hypothesis by administering VNS at an intensity and duration that improves memory an

29 ns of the neuronal organization of the adult VNS based in developmental units/rules.

30 previous studies of the origins of the adult VNS neurons to describe the clonal organization of the a

31 escribe the clonal organization of the adult VNS.

32 Here we show that afferent VNS induces a mechanism distinct from efferent VNS, amel

33 nic vagus nerve issues were documented after VNS implantation, with apnea (n = 395; 3.1%) being the m

34 dogs were randomized into control (n=7) and VNS (n=8) groups.

35 mechanics and histology between control and VNS-treated animals during HF development.

36 A strains were comparable in the control and VNS-treated dogs.

37 and left nerve have comparable effects, and VNS is effective after ipsilateral and contralateral foc

38 eks, and were randomly divided into sham and VNS groups.

39 aromatic substitution reactions of SNAr and VNS (vicarious nucleophilic substitution).

40 egulate blood glucose and is as effective as VNS in suppressing the hyperglycemic effect of endotoxin

41 F could be induced and maintained as long as VNS was continued, whereas after RFCA, AF was no longer

42 For the first time, wireless and batteryless VNS with more than 5 cm operation range was demonstrated

43 hich splenectomy was performed 7 days before VNS and IRI.

44 t 2, methyl atropine was given 10 min before VNS to assess whether stimulation-induced increases in a

45 Beyond VNS, these data establish HF as a potentially viable str

46 Bipolar VNS trains of both polarities elicited mixed DeltaHR and

47 or afferent and efferent fiber activation by VNS: stimulus-elicited change in breathing rate (DeltaBR

48 walking distance were favorably affected by VNS (p < 0.05), but left ventricular end-systolic volume

49 ing vocal fold paralysis from that caused by VNS surgery.

50 ERP was increased by VNS in control from 119 +/- 6 ms to 130 +/- 6 ms (10 +/-

51 GC B cells from chronic VNS mice exhibited altered mRNA and protein expression s

52 es (HRRs) during the active phase of chronic VNS over a wide range of stimulation parameters in order

53 However, the effects of chronic VNS therapy on brain insulin sensitivity, dendritic spin

54 istic questions about the effects of chronic VNS, which require solving numerous technical challenges

55 Here we demonstrate that chronic VNS was able to reverse both vHipp hyperactivity and abe

56 CL-VNS therapy drives extensive synaptic reorganization in

57 improve sensorimotor recovery and define CL-VNS as a readily translatable therapy to restore functio

58 locks the plasticity-enhancing effects of CL-VNS and consequently eliminates recovery, indicating a c

59 s of closed-loop vagus nerve stimulation (CL-VNS) delivered during rehabilitation to reverse the aber

60 smaller diameter fibers targeted by clinical VNS.

61 In conclusion, VNS activates central then peripheral aspects of the car

62 During and Continuous VNS groups displayed the greatest reduction in condition

63 In contrast, open-loop VNS or ANN-controlled VNS following a caudal vagotomy essentially failed to re

64 e corresponding alpha-alkylated conventional VNS product in a one-pot process.

65 n itself was prepared using the conventional VNS reaction in four steps and 24% overall yield from ni

66 Conventionally, VNS is administered using an open-loop approach, in whic

67 However, current VNS approaches and stimulus optimization could benefit f

68 Direct VNS increased VFT and flattened the slope of APD restitu

69 However, evidence for directional VNS with ABL has been scarce and inconsistent, and it is

70 hanism that can be leveraged for directional VNS.

71 ctional organization of the adult Drosophila VNS.

72 in the thoracic neuromeres of the Drosophila VNS.

73 eliminated rhythmic phrenic activity during VNS, while low-intensity VNS only reduced phrenic burst

74 ), abolished the increase of COV-AERP during VNS (12+/-7% after RFCA), and led to an increase of the

75 d (VFT) were measured at baseline and during VNS in the presence of the NO synthase inhibitor N(G)-ni

76 eleration and reduced HR deceleration during VNS.

77 fter RFCA, AF was no longer inducible during VNS.

78 nted the AERP shortening at all sites during VNS (114+/-4 ms after RFCA), abolished the increase of C

79 as these motoneurons were suppressed during VNS.

80 lcholine (ACh) which is required by efferent VNS.

81 S induces a mechanism distinct from efferent VNS, ameliorating lipopolysaccharide (LPS)-induced infla

82 We hypothesized that episodic VNS would induce phrenic long-term depression.

83 ulation techniques with the more established VNS.

84 Here we examine VNS as a potential therapy for the treatment of schizoph

85 timodal connectomic prediction algorithm for VNS, and provides new insights into its mechanism of act

86 tivation of cortical a2-ARs is necessary for VNS-driven motor cortical reorganization to occur.

87 y for DBS, 1 study for CRS and 4 studies for VNS.

88 In the FPI-VNS group, a trend towards increased numbers of hilar GA

89 In the FPI-VNS group, this percentage loss was attenuated to only a

90 At low intensities and higher frequency VNS, HR increased during the VNS active phase owing to a

91 After a single extinction trial, rats given VNS stimulation demonstrated a significantly lower level

92 Another group was given VNS and extinction training but the VNS was not paired w

93 f somatosensation, and both lower and higher VNS intensities fail to enhance recovery compared to reh

94 However, VNS had a significant effect on developing nasal cavity-

95 dings in previous models of hyposensitivity, VNS therapy fails to improve recovery of either somatose

96 Importantly, VNS-evoked activation of neuromodulatory axons and excit

97 y, we examined brain and behavior changes in VNS and sham rats performing a multiday novelty preferen

98 estingly, blood ARC transcripts decreased in VNS rats performing NPTP, but increased in VNS-only rats

99 While there are qualitative differences in VNS heart control between awake and anaesthetized states

100 ediate early gene (IEG) ARC was increased in VNS rats and correlated with transcription of plasticity

101 n VNS rats performing NPTP, but increased in VNS-only rats.

102 emory, the particular mechanisms involved in VNS-enhanced cognition are unknown.

103 y, these findings suggest that incorporating VNS paired with sensory retraining into rehabilitative r

104 hypothesis, indicate that phrenic-inhibitory VNS induces a serotonin-dependent phrenic LTF similar to

105 Medium- and high-intensity VNS eliminated rhythmic phrenic activity during VNS, whi

106 increase the bradycardia to higher intensity VNS.

107 alter the tachycardia phase to low intensity VNS, but can increase the bradycardia to higher intensit

108 nic activity during VNS, while low-intensity VNS only reduced phrenic burst frequency.

109 pplications, we find that moderate intensity VNS yields the most effective restoration of somatosensa

110 ion (VNS), and FPI with chronic intermittent VNS initiated at 24 h post FPI in rats.

111 uromodulatory signaling, and mimics invasive VNS.SIGNIFICANCE STATEMENT Current noninvasive brain sti

112 ine with the established effects of invasive VNS on locus coeruleus-noradrenaline signaling, and supp

113 Additionally, left VNS elicited a greater afferent and right VNS a greater

114 Both the right and left VNS caused subtle reduction in CBF during each 30-s stim

115 ses evoked by traditional low-frequency (LF) VNS in a large animal (swine) model.

116 ibrillation and tachycardia during active LL-VNS were 1.4/d (95% CI, 0.5 to 5.1) and 8.0/d (95% CI, 5

117 dogs (N=6) underwent 1 week of continuous LL-VNS.

118 dent 1 week after cessation of continuous LL-VNS.

119 activity was significantly reduced during LL-VNS (7.8 mV/s; 95% confidence interval [CI] 6.94 to 8.66

120 m(2)/mm(2) (95% CI, 28 850 to 170 517) in LL-VNS dogs and 186 561 mum(2)/mm(2) (95% CI, 154 956 to 21

121 ellate ganglion 1 week after cessation of LL-VNS were 99 684 mum(2)/mm(2) (95% CI, 28 850 to 170 517)

122 atrial pacing followed by active or sham LL-VNS on alternate weeks.

123 -sided low-level vagus nerve stimulation (LL-VNS) can suppress sympathetic outflow and reduce atrial

124 icity, low-level vagus nerve stimulation [LL-VNS], stellate ganglion block, baroreceptor stimulation,

125 that a similar implementation of closed-loop VNS paired with a tactile rehabilitation regimen could i

126 In contrast, open-loop VNS or ANN-controlled VNS following a caudal vagotomy es

127 In primary motor cortex (M1), VNS drives precise temporal modulation of neurons that r

128 However, the extent to which tVNS mimics VNS remains unclear.

129 line signaling, and support that tVNS mimics VNS.

130 re, during and after three episodes of 5 min VNS (50 Hz, 0.1 ms), each separated by a 5 min interval,

131 S fluorescent protein to SYS-1, we find more VNS::SYS-1 in distal than proximal SGP daughters, a phen

132 Moreover, VNS paired with tactile rehabilitation resulted in signi

133 improvement in FMA-UE in the control but not VNS group.

134 nerve transection, confirming that observed VNS effects were specific to nerve stimulation and trigg

135 data and rigorously evaluate the ability of VNS paired with tactile rehabilitation to improve recove

136 rovide a survey on the foundational basis of VNS therapy for stroke and offer insight into the mechan

137 er understanding of the mechanistic basis of VNS therapy may reveal ways to maximize its benefits.

138 There was no significant effect of VNS on CBF during the entire 1-h stimulation period.

139 ion (VNS) mouse model to study the effect of VNS on T-dependent B cell responses.

140 tant role in the anti-fibrillatory effect of VNS on the rabbit ventricle, possibly via effects on APD

141 The effect of VNS on tissue outcome was associated with better neurolo

142 L-NA blocked the effect of VNS whereas L-Arg restored the effect of VNS.

143 of VNS whereas L-Arg restored the effect of VNS.

144 e role of nitric oxide (NO) in the effect of VNS.

145 ntitative comparison of the effectiveness of VNS devices, the efficiency of systems on reducing heart

146 Effectiveness of VNS in these models necessitates the integration of neur

147 In order to maximize the effectiveness of VNS therapy and promote translation to clinical implemen

148 roughout the body, and off-target effects of VNS could cause major side effects such as changes in bl

149 Although the central effects of VNS have not been completely delineated, positron emissi

150 mplete understanding of the acute effects of VNS on human cortical neurophysiology.

151 We determined the effects of VNS on metabolic parameters, heart rate variability (HRV

152 ression, as the anti-inflammatory effects of VNS were eliminated in beta(2)AR knockout mice and with

153 Here we determined the effects of VNS-mediated release of brain-derived neurotrophic facto

154 vation with respect to functional effects of VNS.

155 efficacy and minimize off-target effects of VNS.

156 lus is required for the enhancing effects of VNS.

157 ever, the mechanisms underlying this form of VNS-dependent plasticity remain unclear.

158 Reliable identification of VNS responders is critical to mitigate surgical risks fo

159 However, little is known about the impact of VNS on left atrial (LA) function.

160 EEG before and after one to three months of VNS-tone pairing in chronic tinnitus patients.

161 r, HR was reduced during the active phase of VNS.

162 s reproducibly evoked during the on-phase of VNS.

163 However, the promise of VNS is only partially fulfilled due to a lack of mechani

164 Given the safety and tolerability of VNS therapy, these findings suggest that incorporating V

165 Conversely, adoptive transfer of VNS-conditioned alpha7nAChR splenocytes conferred protec

166 s reporting long-term efficacy (>5 years) of VNS, CRS and DBS in patients with refractory focal/parti

167 ch group was received either sham therapy or VNS therapy for an additional 12 weeks.

168 nges with OVA, mice were subjected to VGX or VNS.

169 ts were implanted and randomized to a paired VNS (n = 16) or control (n = 14) group.

170 tion trials were extended to 10 days, paired VNS accelerated extinction of the conditioned response.

171 me therapy, all participants received paired VNS.

172 After 6 weeks, the paired VNS group improved on the Tinnitus Handicap Inventory (T

173 ty percent of the participants in the paired VNS group showed clinically meaningful improvements comp

174 habilitative training with or without paired VNS.

175 Here, we investigated if pairing VNS with the conditioned stimulus is required for the en

176 At 60 min post-VNS, phrenic amplitude was higher than baseline (35 +/-

177 This one-pot VNS-alkylation reaction offers a convenient route to a r

178 Despite its therapeutic potential, VNS is limited by off-target effects and the need for ti

179 This study aimed to predict VNS response using structural and functional connectomic

180 ation for depression and seizure prevention, VNS is a readily available and promising adjunct to expo

181 In mice lacking alpha7nAChR, prior VNS did not prevent IRI.

182 e assigned to device implantation to provide VNS (active) or continued medical therapy (control) in a

183 In rats, VNS elevates LC firing and forebrain noradrenaline level

184 In rats, VNS paired with skilled forelimb training results in sig

185 ft VNS elicited a greater afferent and right VNS a greater efferent response.

186 5 s, 0.8 mA, 100 us, and 30 Hz) or with Sham VNS (0 mA).

187 While qualitatively similar, VNS delivered in the epilepsy configuration resulted in

188 (FPI), FPI with sham Vagus Nerve Simulation (VNS), and FPI with chronic intermittent VNS initiated at

189 rs demonstrate that vagus nerve stimulation (VNS) activates the cholinergic antiinflammatory pathway

190 ety and efficacy of vagal nerve stimulation (VNS) among patients with HF and a reduced ejection fract

191 bilateral cervical vagal nerve stimulation (VNS) and electrical stimulation of the third fat pad (20

192 ypothesis that left vagus nerve stimulation (VNS) at the cervical level results in increased extracel

193 o determine whether vagus nerve stimulation (VNS) can enhance the consolidation of extinction of cond

194 Cervical vagal nerve stimulation (VNS) can improve left ventricular dysfunction in the set

195 d in several failed vagus nerve stimulation (VNS) clinical trials by effectively limiting maximum app

196 on, the delivery of vagus nerve stimulation (VNS) combined with tactile rehabilitation has emerged as

197 Vagus nerve stimulation (VNS) has been shown to enhance learning and memory, yet

198 Vagus nerve stimulation (VNS) has been shown to exert cardioprotection.

199 ies have implicated vagus nerve stimulation (VNS) in enhanced learning and memory.

200 te (HR) response to vagal nerve stimulation (VNS) in vitro and in vivo.

201 Vagus nerve stimulation (VNS) is a bioelectronic therapy for disorders of the bra

202 Vagus nerve stimulation (VNS) is a common treatment for medically intractable epi

203 Vagal nerve stimulation (VNS) is an alternative therapy for epilepsy and treatmen

204 ABSTRACT: Vagus nerve stimulation (VNS) is an emerging therapy for treatment of chronic hea

205 ive, transcutaneous vagus nerve stimulation (VNS) is currently used as a treatment for depression and

206 n of this reflex by vagus nerve stimulation (VNS) is effective in various inflammatory disease models

207 Vagal nerve stimulation (VNS) is known to improve cognitive processing, presumabl

208 Vagus-nerve stimulation (VNS) is licensed in several countries as an adjunctive t

209 Vagal nerve stimulation (VNS) is well established.

210 Vagus nerve stimulation (VNS) is widely used to treat drug-resistant epilepsy and

211 e, we use a chronic vagus nerve stimulation (VNS) mouse model to study the effect of VNS on T-depende

212 effect of cervical vagus nerve stimulation (VNS) on cerebral blood flow (CBF), infarct volume, and c

213 piratory-inhibitory vagus nerve stimulation (VNS) on phrenic nerve activity.

214 luate the effect of Vagus Nerve Stimulation (VNS) paired with sounds in chronic tinnitus patients.

215 at uses closed-loop vagus nerve stimulation (VNS) paired with tactile rehabilitation to enhance synap

216 arch has shown that vagus nerve stimulation (VNS) paired with tones or with rehabilitative training c

217 and feasibility of vagus nerve stimulation (VNS) paired with upper-limb rehabilitation after ischemi

218 y shown that direct vagus nerve stimulation (VNS) reduces the slope of action potential duration (APD

219 to bipolar cervical vagus nerve stimulation (VNS) reflects a dynamic interaction between afferent med

220 ANN-controlled vagus nerve stimulation (VNS) significantly mitigated major physiological feature

221 Vagus nerve stimulation (VNS) therapy was shown to improve peripheral insulin sen

222 eport that targeted vagal nerve stimulation (VNS) using optogenetics attenuated cardiac remodeling an

223 whether adjunctive vagus nerve stimulation (VNS) with treatment as usual in depression has superior

224 zed that electrical vagus nerve stimulation (VNS) would suppress harmaline tremor, as measured with d

225 vagotomy (VGX) and vagus nerve stimulation (VNS), on the development and severity of experimental fo

226 Only vagus nerve stimulation (VNS), which continues to develop new technology, is appr

227 ls as implant-based vagus nerve stimulation (VNS).

228 EX atria, HR responses to vagal stimulation (VNS, 3 and 5 Hz) were significantly enhanced compared to

229 ngs identify neural mechanisms that subserve VNS-dependent somatosensation recovery and provide a bas

230 ing the vicarious nucleophilic substitution (VNS) as a key step, is described.

231 rom the vicarious nucleophilic substitution (VNS) of hydrogen reacts with a series of alkyl halides t

232 renaline levels, whereas LC lesions suppress VNS therapeutic efficacy.

233 Surprisingly, VNS did not significantly reduce transcription of cortic

234 romere of the larval ventral nervous system (VNS), but because of the neurotactin labeling of lineage

235 ining neurons of the ventral nervous system (VNS), which in other insects are thought to comprise cel

236 chemosensory system, the vomeronasal system (VNS), evolved to process ethologically relevant chemosen

237 , we describe a scalable model for long-term VNS in mice developed and validated in four research lab

238 ent with the global mechanism of action that VNS has throughout the cerebrum.

239 Together, these results demonstrate that VNS-mediated attenuation of AKI and systemic inflammatio

240 our findings provide the first evidence that VNS induces widespread changes in the cognitive epigenet

241 provide the first preclinical evidence that VNS may be a possible alternative therapeutic approach f

242 We found that VNS activated specific histone modifications and DNA met

243 sistent with previous studies, we found that VNS paired with motor training enlarges the map represen

244 These findings support the hypothesis that VNS increases extracellular NE concentrations in both th

245 These results support the hypothesis that VNS-tone pairing can direct therapeutic neural plasticit

246 l and optogenetic experiments indicated that VNS can enhance task performance through activation of t

247 The rationale behind this treatment is that VNS paired with experience can drive neural plasticity i

248 ow in humans have consistently reported that VNS stimulation induces bilateral decreases in hippocamp

249 We show that VNS enhances novelty preference (NP); alters the hippoca

250 These findings suggest that VNS attenuates cognitive decline in obese-insulin resist

251 Together, these data suggest that VNS protects cortical GAD cells from death subsequent to

252 These findings suggest that VNS-induced protection against acute ischemic brain inju

253 Accumulating evidence suggests that VNS may modulate cortical state and plasticity through a

254 The VNS group showed an improvement in peripheral and brain

255 The VNS-alkylation protocol has been applied to the synthesi

256 channel blocker ivabradine did not alter the VNS chronotropic response.

257 as given VNS and extinction training but the VNS was not paired with exposure to conditioned cues.

258 igher frequency VNS, HR increased during the VNS active phase owing to afferent modulation of parasym

259 study subjects as well as only those in the VNS group and is consistent with the global mechanism of

260 Responders in the VNS group had more severe arm impairment at baseline tha

261 -Meyer Upper Extremity (FM-UE) points in the VNS group relative to the control group for each point i

262 s achieved in 23 (47%) of 53 patients in the VNS group versus 13 (24%) of 55 patients in the control

263 tcome occurred in 132 of 436 patients in the VNS group, compared to 70 of 271 in the control group (3

264 iponectin was significantly increased in the VNS group.

265 o understand the observed selectivity in the VNS step led to the discovery of two new reaction pathwa

266 cent fibrosis was significantly lower in the VNS versus the control group (8+/-1% versus 13+/-1%; P<0

267 agnetic resonance imaging (MRI) scans in the VNS-REHAB trial were used to derive regional injury meas

268 ation to the known functional domains of the VNS neuropil and based on the anatomy we are able to ass

269 ale features in the first brain relay of the VNS, namely, the accessory olfactory bulb (AOB), change

270 uscarinic cholinergic blockade prevented the VNS-induced bradycardia, clinically relevant doses of AC

271 re randomly assigned to treatment (53 to the VNS group and 55 to the control group).

272 duction in GAD cells/unit area; whereas, the VNS-treated rats showed no appreciable diminution of GAD

273 eased in the control group compared with the VNS group (P<0.05).

274 eripheral vagal activation using therapeutic VNS criteria.

275 This VNS-dependent restoration of sensory thresholds was main

276 R) highlighted their crucial contribution to VNS-mediated cardioprotection.

277 the therapy had a similar safety profile to VNS for epilepsy.

278 n site eliminated the augmenting response to VNS and enhanced the parasympathetic efferent-mediated s

279 NOS inhibition normalized the HR response to VNS in the NOS-1-treated group compared with the control

280 al measures that further predict response to VNS therapy.

281 abolished the difference in HR responses to VNS between +EX and -EX atria, and effects of L-VNIO wer

282 arity differences in functional responses to VNS can be explained by ABL of A- and B-fiber activation

283 ized and the extent of pupil dilation tracks VNS-evoked basal-forebrain cholinergic axon activity in

284 Noninvasive transcutaneous VNS (tVNS) uses electrical stimulation that targets the

285 We hypothesize that using transcutaneous VNS via the auricular afferent branch could achieve a se

286 Here, we investigated whether transcutaneous VNS improves sensory performance in humans.

287 Using a rescuing transgene, VNS::SYS-1, which fuses VENUS fluorescent protein to SYS

288 discovery of two new reaction pathways under VNS conditions, one leading to an isoxazole and the othe

289 and identify neural mechanisms that underlie VNS-dependent recovery.

290 vidence that epigenetic modulation underlies VNS-induced improvements in cognition.

291 s to evaluate the effect of chronic (2 week) VNS treatment on the activity of putative vHipp pyramida

292 s now underway to formally determine whether VNS improves outcomes and will explore whether these dif

293 However, the mechanism through which VNS influences central nervous system circuitry is not w

294 rtant epigenetic alterations associated with VNS cognitive improvements, as well as new potential pha

295 ts underwent extinction training paired with VNS (0.5 s, 0.8 mA, 100 us, and 30 Hz) or with Sham VNS

296 Extinction paired with VNS is more rapid than extinction paired with sham stimu

297 s shifted upwards and became less steep with VNS when compared to baseline.

298 eeks intensive physiotherapy with or without VNS.

299 Equivalent tactile rehabilitation without VNS failed to improve sensory function.

300 recovery compared to rehabilitation without VNS.