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 tones may be effective for a subgroup of

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

12 VNS treatment attenuated brain mitochondrial dysfunction

13 VNS was applied for the next 12 weeks.

14 VNS-tone pairing also reduced the phase coherence betwee

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

46 eleration and reduced HR deceleration during VNS.

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

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

49 as these motoneurons were suppressed during VNS.

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

51 ulation techniques with the more established VNS.

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

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

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

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

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

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

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

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

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

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

62 increase the bradycardia to higher intensity VNS.

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

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

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

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

67 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

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

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

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

71 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

95 me therapy, all participants received paired VNS.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

119 Vagal nerve stimulation (VNS) is well established.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

144 The VNS group showed an improvement in peripheral and brain

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

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

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

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

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

150 iponectin was significantly increased in the VNS group.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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