ライフサイエンスコーパス: RNS

1 RNS produce a variety of DNA lesions in a broad spectrum

2 RNS-induced DNA lesions cause genomic instability in the

3 RNS-induced sensations of pain and increases in systemic

4 RNSs and ROSs may be involved in the presentation of gly

5 genomic boundaries and coding strand of 153 RNS-induced transcripts.

6 (4) also enhanced myeloperoxidase, H(2)O(2,) RNS production, and bacterial killing in K. pneumoniae-i

7 d in niches of the body containing activated RNS- and ROS-generating immune and endothelial cells, po

8 from the NADPH phagocyte oxidase complex and RNS derived from the inducible nitric oxide synthetase,

9 ese data show that capillary dysfunction and RNS generation contribute to tubular injury and suggest

10 thase inhibitor on capillary dysfunction and RNS generation.

11 nging ROS (IC(50) from 1.7 to 108mug/ml) and RNS (IC(50) from 0.05 to 0.59mug/ml), when compared to g

12 gests the formation of hydrogen peroxide and RNS.

13 ective probe for detection of common ROS and RNS (i.e., H(2)O(2) and 3-NT).

14 We detected dose-dependent ROS and RNS activity in the liver within minutes of drug challen

15 and emphasizes interactions between ROS and RNS and the relative roles of cellular ROS/RNS generator

16 lay role in the direct scavenging of ROS and RNS as well as inducing antioxidant defense mechanisms a

17 s capable to efficiently control the ROS and RNS concentrations in the cancer-inhibiting media.

18 +) concentrations and the amounts of ROS and RNS create an amplifying cycle that ultimately triggers

19 Additionally, ROS and RNS deplete cellular defenses and initiate inflammation.

20 ROS and RNS directly oxidize and damage DNA, proteins, and lipid

21 ne assay of biomarkers indicative of ROS and RNS elaboration.

22 cantly advances our understanding of ROS and RNS evasion strategies during infection.

23 time in vivo imaging of drug-induced ROS and RNS for direct evaluation of acute hepatotoxicity.

24 ring infection through limitation of ROS and RNS generation by macrophages.

25 selective and sensitive detection of ROS and RNS in biological systems.

26 and evaluated for susceptibility to ROS and RNS in gamma interferon (IFN-gamma)-activated macrophage

27 the mel2 locus confers resistance to ROS and RNS in laboratory medium, suggesting that this locus mig

28 ortant roles for CXCL1 in generating ROS and RNS in neutrophils and in regulating host immunity again

29 r host defense; however, the role of ROS and RNS in the response to tissue injury is not known.

30 ming to elucidate the involvement of ROS and RNS in transcriptional response to IR.

31 stable and reproducible responses to ROS and RNS in vitro.

32 ly inflict damage on macromolecules, ROS and RNS indirectly induce damage to tissues by activating a

33 To determine ROS and RNS inside macrophages, one needs smaller (i.e., nanomet

34 e used to penetrate cells and detect ROS and RNS inside macrophages.

35 locus plays a role in resistance to ROS and RNS produced by activated macrophages.

36 examined the effects of IFN-gamma on ROS and RNS production by these cells as well as the effects on

37 ssion of the intracellular sites for ROS and RNS production in muscle fibres.

38 genipin against damage stemming from ROS and RNS production in organotypic hippocampal slice cultures

39 y following exposure, requiring both ROS and RNS scavengers.

40 ion by LC-ESI-QTOF-MS; and for their ROS and RNS scavenging effects (ROO, O(2)(-), NO, HOCl); in vivo

41 compound, proved to have the highest ROS and RNS scavenging potential.

42 e macrophages produce high levels of ROS and RNS upon activation with gamma interferon (IFN-gamma), w

43 eactive oxygen and nitrogen species (ROS and RNS) is extracellular glutathione peroxidase (eGPx).

44 eactive oxygen and nitrogen species (ROS and RNS) produced by macrophages are essential for protectin

45 ecies and reactive nitrogen species (ROS and RNS).

46 eactive oxygen and nitrogen species (ROS and RNS).

47 capacity to scavenge all the studied ROS and RNS, being gum arabic a more potent antioxidant than mal

48 y reactive and short-lived nature of ROS and RNS, combined with limitations of conventional detection

49 dative stress, e.g., scavenging both ROS and RNS, induction of defense mechanisms and alleviating/sup

50 eactive oxygen and nitrogen species (ROS and RNS, respectively), to modulate human neutrophils' oxida

51 gnalling pathways that contribute to ROS and RNS-induced skeletal muscle adaptation to endurance exer

52 ity than skin extract for all tested ROS and RNS.

53 ury with a significant component of ROS- and RNS-mediated damage, such as TBI and stroke, to assess i

54 lts suggest differential effects of ROS- and RNS-rich plasma, and may have a role in optimizing clini

55 ding acetaminophen and kainic acid, known as RNS inducers.

56 lucidated the mechanistic connection between RNS-driven inhibitory modifications on the E2 and E3 sub

57 Co-localisation was observed between RNS-modified tyrosine residues and the chemokine CCL2 in

58 dition, we showed that such reaction between RNS and the lipoic arm of the E2 subunit can further pro

59 rsed the capillary perfusion defect, blocked RNS generation, and reduced AKI.

60 acteria are relatively resistant to ROS, but RNS inhibit growth of, and possibly even kill, mycobacte

61 JNK activation by RNS was abolished in cells lacking functional Fas or fol

62 naling was not involved in JNK activation by RNS.

63 JNK activation and cell death by RNS occurred in a Fas ligand- and caspase-independent ma

64 We demonstrate here that cell death by RNS was caused by c-Jun N-terminal kinase (JNK).

65 While the activation of JNK by RNS or FasL required FADD, the cysteine-rich domain 1 co

66 Activation of JNK by RNS was density dependent and caused mitochondrial depol

67 ns of phoPQ are hypersensitive to killing by RNS generated in vitro.

68 nse involves a specific pathway triggered by RNS.

69 In contrast to PSA degradation by RNSs, dextran depolymerization in the endosome depends o

70 mplex and oxoglutarate dehydrogenase complex-RNS can cause inactivating covalent modifications of the

71 In contrast, RNS induced JNK potently in cells expressing a truncated

72 In contrast, RNS synthesized during high-NO fluxes of gamma interfero

73 ired for the regulation of genes controlling RNS in M. truncatula.

74 agocyte oxidase-derived ROS nor iNOS-derived RNS are essential for resolution of infection, RNS prote

75 in might be mediated by mitochondria-derived RNS, and activation of the c-Src/PI3K pathway might gene

76 ight be mediated by the mitochondria-derived RNS.

77 or simultaneously and differentially detects RNS and ROS using two optically independent channels.

78 racranial neural recordings collected during RNS therapy, we found that patients with the greatest th

79 of iNOS, Mtb in vivo is likely to encounter RNS by producing nitrite.

80 Thus, this study demonstrates that excess RNS are a nongenetic driving force for Brca2-deficiency-

81 r ROS and IC(50) from 0.04 to 0.12mug/ml for RNS).

82 d with Fas-associated death domain (FADD) in RNS-exposed cells, illustrating that RNS directly target

83 rating a dependence of Fas but not TNF-R1 in RNS-induced signaling to JNK.

84 ynchronizing epidermal/cortical responses in RNS.

85 tial liver grafts, most likely by increasing RNS that leads to mitochondrial damage and dysfunction.

86 S are essential for resolution of infection, RNS protect from chronic chlamydial disease in this mode

87 ucial role for the production of short-lived RNS.

88 lar persisters resume growth when macrophage RNS production subsides and functionality of their TCA c

89 Examining the ability of the major RNSs to degrade PSA, we determined that deamination is t

90 In Nox2-/- mice, RNS-mediated protein oxidation, as monitored by protein

91 Brain-responsive neurostimulation (RNS) is firmly ensconced among treatment options for dru

92 reless NeuroPace responsive neurostimulator (RNS) and tracked their motion with sub-millimeter precis

93 erable to inactivation by reactive nitrogen (RNS) and oxygen species (ROS) that covalently modify ami

94 NO/RNS at concentrations physiologically relevant to inflam

95 echanism for understanding mutagenesis by NO/RNS.

96 By inhibiting BRCA1 expression, NO/RNS thereby reduces the ability of cells to repair DNA d

97 Moderate NO/RNS concentrations stimulated mutagenesis not directly b

98 thought to be mediated by the effects of NO/RNS in generating DNA damage.

99 tosis, thereby preventing accumulation of NO/RNS-generated mutations.

100 In summary, NO/RNS stimulates genetic instability by inhibiting BRCA1 e

101 esolve infection, produce greater amounts of RNS in vivo, and sustain lower rates of hydrosalpinx for

102 titution protects SsrB against the attack of RNS while preserving its DNA-binding capacity.

103 e formation and abrogate the cytotoxicity of RNS against phoQ Salmonella, presumably by limiting the

104 s used to characterize the lethal effects of RNS on B. burgdorferi.

105 The effects of RNS were quantified by integrating records of the differ

106 at limited genes conferring the evolution of RNS in Leguminosae have been functionally validated, the

107 the gene loss event during the evolution of RNS in Leguminosae through phylogenomic and synteny anal

108 dated, the genetic basis of the evolution of RNS remains largely unknown.

109 fying the genes involved in the evolution of RNS will help to reveal the mystery.

110 Tubular generation of RNS was significantly elevated at 10 h after CLP and was

111 enues aimed at preventing the interaction of RNS with Fas may attenuate tissue damage characteristic

112 eases that are accompanied by high levels of RNS.

113 Interestingly, the majority of RNS-sensitive E. coli proteins differ from E. coli prote

114 (marker of ROS), 3-nitrotyrosine (marker of RNS), poly(adenosine diphosphate-ribose) (PAR, marker of

115 4-HNE) were used as histochemical markers of RNS and ROS formation, respectively.

116 Nitric oxide (NO(-)) is a member of RNS produced from arginine by inducible Nitric Oxide Syn

117 ence was performed to assess the presence of RNS in kidney biopsies.

118 inhibitor, largely blunted the production of RNS, prevented the increase of alanine aminotransferase

119 Suppression of RNS could be an important strategy for pancreatic cancer

120 Initial titration of RNS therapy is typically similar for all patients, raisi

121 which are regulated by the methyl groups of RNSs.

122 s that modulate E-selectin expression and/or RNS generation may restore T-cell entry and could potent

123 SPI2) genes are also repressed by high-order RNS (39), we investigated whether the NO-mediated inhibi

124 secretion system is repressed by high-order RNS of IFN-gamma-activated macrophages.

125 rgical patients, with similar results in our RNS System patients (1.4-1.6 seconds).

126 generator, and peroxynitrite (PN), a potent RNS.

127 However, Mtb's own ability to produce RNS is rarely considered, perhaps because nitrate reduct

128 rived reactive oxygen species (ROS) regulate RNS during chlamydial urogenital infection in the mouse.

129 e oxygen and reactive nitrogen species (ROS, RNS) formed in the inner ear in response to high-intensi

130 ROS/RNS are often generated by ischemia-induced inflammation

131 In particular, abnormal ROS/RNS ratios are not achievable in discharges since they d

132 city and cytoprotection capacity against ROS/RNS on BAEC.

133 to examine their role in defense against ROS/RNS-mediated microbicidal activity of infected macrophag

134 fibroblasts had increased superoxide and ROS/RNS production (6.2-fold, P < 0.001 and 1.8-fold, P < 0.

135 pression, NF-kappaB/MAPK activation, and ROS/RNS production.

136 olved in the development of cytokine and ROS/RNS resistance may define simplified and specific strate

137 ls are highly resistant to cytokines and ROS/RNS, with no impairment in glucose-stimulated insulin se

138 onential trend was also observed between ROS/RNS and [Formula: see text] for all naphthalene SOA, reg

139 lier time points, methamphetamine caused ROS/RNS generation, which was detected with the fluorigenic

140 d RNS and the relative roles of cellular ROS/RNS generators as amplifiers of the initial ionization e

141 te methamphetamine-induced cytotoxicity, ROS/RNS generation, and dopamine release in cultured cells.

142 methods have been reported for detecting ROS/RNS in vitro and in vivo; however, detecting methods for

143 ent mitochondria with resulting enhanced ROS/RNS generation.

144 sociated with increased Nox2 expression, ROS/RNS production, and oxidative protein and lipid modifica

145 ability of F. tularensis to resist high ROS/RNS levels, we have hypothesized that additional unknown

146 llenge, KC fibroblasts maintained higher ROS/RNS levels (3.3-fold, P < 0.02), showed higher caspase-3

147 e of iron-containing seed induced higher ROS/RNS production compared to that formed in the presence o

148 nse ROS/RNS are examined in terms of how ROS/RNS modify protein structure and function, for example,

149 cultures showed significant increase in ROS/RNS production (P < 0.001) compared with untreated contr

150 b, significantly attenuated H2O2-induced ROS/RNS accumulation and lipid peroxidation, decreased H2O2-

151 echanisms by MET, may combat age-induced ROS/RNS and protect the myocardium from oxidative stress dis

152 es on the chemistry of radiation-induced ROS/RNS generation and emphasizes interactions between ROS a

153 Radiation-induced ROS/RNS is observed in several cell types with the exception

154 Apocynin mitigated stress-induced ROS/RNS production and body weight loss even prior to coliti

155 (o) cells show neither radiation-induced ROS/RNS production nor depolarization.

156 Radiation-induced ROS/RNS, depolarization, and calcein fluorescence decrease a

157 oach, simultaneous detection of multiple ROS/RNS products of fluorescent probes, developed in this st

158 amphetamine-induced apoptosis, necrosis, ROS/RNS generation, and dopamine release in NG108-15 cells.

159 neration of reactive oxygen or nitrogen (ROS/RNS), detected with dihydrodichlorofluoroscein by fluore

160 (ROS) and several downstream effects of ROS/RNS (reactive nitrogen species) production such as inhib

161 n) will change type and concentration of ROS/RNS and effectively tune the behavior of human skin cell

162 pressed by pharmacological inhibitors of ROS/RNS and PARP.

163 blasts had increased basal generation of ROS/RNS and were more susceptible to stressful challenges (l

164 high concentrations, moderate levels of ROS/RNS are essential for normal cell function and take part

165 formation, while continued formation of ROS/RNS contributes to the long-term hair cell loss.

166 Weak and very short leaks of ROS/RNS from the vacuoles into the cytoplasm were detected,

167 , we demonstrate real-time monitoring of ROS/RNS in activated macrophages using high-throughput fluor

168 3/7 and caspase-9, and the production of ROS/RNS in ARPE-19 cell cultures.

169 useful in unraveling the complex role of ROS/RNS in redox regulation, cell signaling, and cellular ox

170 The regulation of ROS/RNS is largely attended by peroxiredoxins (Prdxs) and th

171 activation of TLR2 and the generation of ROS/RNS mediates LTA-induced barrier dysfunction in PMEM.

172 In the 1-10 Gy dose range, the amount of ROS/RNS produced/cell is constant, but the percentage of pro

173 d inhibitors confirms the involvement of ROS/RNS signaling and of the importance of transformed cell

174 orrelating with the delayed formation of ROS/RNS, there was a progressive hair cell loss, stabilizing

175 ning the extent of tissue involvement or ROS/RNS-related damage would have a significant clinical imp

176 distinguish by imaging from less potent ROS/RNS functioning as background biological signaling molec

177 Cellular mechanisms for regulating ROS/RNS levels are discussed.

178 The mechanisms by which cells sense ROS/RNS are examined in terms of how ROS/RNS modify protein

179 ed reactive oxygen and nitrogen species (ROS/RNS) are assumed the central biologically active plasma

180 Reactive oxygen and nitrogen species (ROS/RNS) are natural byproducts of cellular metabolism.

181 of reactive oxygen and nitrogen species (ROS/RNS) in biological systems.

182 ion of reactive oxygen/nitrogen species (ROS/RNS) in cardiomyocytes, which leads to contractile dysfu

183 of reactive oxygen and nitrogen species (ROS/RNS) on the assembly of TE into elastic fibers.

184 ar reactive oxygen and nitrogen species (ROS/RNS) production was measured for SOA generated from the

185 Reactive oxygen/nitrogen species (ROS/RNS) production was measured with 2',7'-dichlorodihydrof

186 with a reactive oxygen/nitrogen species (ROS/RNS) responsive moiety as the caging group and demonstra

187 ne and reactive oxygen/nitrogen species (ROS/RNS) signaling.

188 ion of reactive oxygen/nitrogen species (ROS/RNS) was measured with 2',7'-dicholorodihydrofluorescein

189 of reactive oxygen and nitrogen species (ROS/RNS), but are only modestly protected against high conce

190 n species and reactive nitrogen species (ROS/RNS), generated by NADPH oxidase-2 (NOX2), myeloperoxida

191 xygen species/reactive nitrogen species (ROS/RNS), have not been fully elucidated.

192 es reactive oxygen and nitrogen species (ROS/RNS), inducing lethal oxidative damage in tumor cells.

193 ing of reactive oxygen/nitrogen species (ROS/RNS).

194 us reactive oxygen and nitrogen species (ROS/RNS).

195 ed reactive oxygen and nitrogen species (ROS/RNS).

196 de and reactive oxygen/nitrogen species (ROS/RNS; hydrogen peroxide, peroxynitrite anions, and peroxy

197 or reactive oxygen and nitrogen species (ROS/RNS; nitroxidative species), including superoxide, perox

198 Radiation-stimulated ROS/RNS is also inhibited by overexpressing the Ca(2+)-bindi

199 These findings establish that ROS/RNS can modify TE and that these modifications affect th

200 The molecular damage that ROS/RNS induce is referred to as nitrooxidative stress.

201 onomethyl arginine citrate inhibited the ROS/RNS fluorescence signal induced by methamphetamine, whic

202 d be reconditioned during EVLP using the ROS/RNS scavenger Mn(III)-tetrakis (4-benzoic acid) porphyri

203 ucts formed from interaction between the ROS/RNS species and the fluorogenic probes, as follows: supe

204 trophil-rich ischemic areas, making this ROS/RNS sensor a novel prognostic indicator.

205 ing intracellular reactive nitrogen species (RNS) accumulation, suppressing the expression of key ele

206 species (ROS) and reactive nitrogen species (RNS) and subsequent oxidative stress.

207 ctive oxygen species (ROS)/nitrogen species (RNS) and the activation of poly(adenosine diphosphate-ri

208 Reactive Nitrogen Species (RNS) are a group of bactericidal molecules produced by m

209 species (ROS) and reactive nitrogen species (RNS) are essential activators of these pathways.

210 species (ROS) and reactive nitrogen species (RNS) are produced, in part, from NADPH oxidase in respon

211 species (ROS) and reactive nitrogen species (RNS) are strongly coupled in liquid-phase reactions: NO3

212 ng PDHC and OGDC: reactive nitrogen species (RNS) can covalently modify the thiols on their lipoic ar

213 synthase (iNOS), reactive nitrogen species (RNS) can kill Mycobacterium tuberculosis (Mtb).

214 ios and increased reactive nitrogen species (RNS) can lead to AMPK activation.

215 OS expression and reactive nitrogen species (RNS) formation (nitrite and nitrate levels and 3-nitroty

216 es indicated that reactive nitrogen species (RNS) formed during NHCl(2) decomposition, including nitr

217 Reactive nitrogen species (RNS) function as powerful antimicrobials in host defence

218 e cytotoxicity of reactive nitrogen species (RNS) generated by inducible nitric oxide synthase (iNOS)

219 this pathogen to reactive nitrogen species (RNS) generated from the nitric oxide produced by the ind

220 tify in real time reactive nitrogen species (RNS) generation by renal tubules, and the inducible nitr

221 sodium nitrite, a reactive nitrogen species (RNS) generator, and 0.5 mM paraquat, which produces reac

222 species (ROS) and reactive nitrogen species (RNS) have been implicated in myriad disease etiologies a

223 species (ROS) and reactive nitrogen species (RNS) in aerobic metabolism.

224 species (ROS) and reactive nitrogen species (RNS) in response to bacterial infections.

225 owing exposure to reactive nitrogen species (RNS) is less in co-cultured neurones, compared to neuron

226 ic oxide (NO) and reactive nitrogen species (RNS) may link inflammation to the initiation, promotion,

227 concentrations of reactive nitrogen species (RNS) metabolites.

228 hat GSH scavenges reactive nitrogen species (RNS) other than NO.

229 Reactive nitrogen species (RNS) play an essential role in host defence against Myco

230 species (ROS) and reactive nitrogen species (RNS) play important roles in cell signalling pathways in

231 macrophages, host reactive nitrogen species (RNS) produced in response to Salmonella infection lock p

232 pecies (ROS), and reactive nitrogen species (RNS) production is unclear, as is the contribution of th

233 uperoxide and ROS/reactive nitrogen species (RNS) productions were determined with an amine-reactive

234 gen species (ROS)/reactive nitrogen species (RNS) reactions, particularly quasi-stable oxidized produ

235 is a highly toxic reactive nitrogen species (RNS) recently discovered as an inflammatory oxidant with

236 species (ROS) and reactive nitrogen species (RNS) than those recruited to the site of infection with

237 species (ROS) and reactive nitrogen species (RNS) that act to further increase resting Ca(2+) concent

238 tentially harmful reactive nitrogen species (RNS) throughout its infective cycle.

239 ally inhibited by reactive nitrogen species (RNS) via a mechanism similar to what we recently discove

240 the production of reactive nitrogen species (RNS) via iNOS protects a significant proportion of mice

241 species (ROS) and reactive nitrogen species (RNS) via radiolysis of water.

242 species (ROS) and reactive nitrogen species (RNS) was determined.

243 species (ROS) and reactive nitrogen species (RNS) was evaluated by in vitro screening assays.

244 l lineO, PN) is a reactive nitrogen species (RNS) which can effect deleterious nitrative or oxidative

245 oxygen (ROS) and reactive nitrogen species (RNS), allowing them to survive and replicate inside thei

246 cies (ROS) and/or reactive nitrogen species (RNS), and antioxidants or ROS scavengers promote cell su

247 species (ROS) and reactive nitrogen species (RNS), and dopamine release were examined in the absence

248 species (ROS) and reactive nitrogen species (RNS), has been proposed as an early unifying event linki

249 Reactive nitrogen species (RNS), in particular nitric oxide (NO), are toxic to bact

250 the generation of reactive nitrogen species (RNS), including peroxynitrite (ONOO).

251 species (ROS) and reactive nitrogen species (RNS), promote diseases such as cancer.

252 al superoxide and reactive nitrogen species (RNS), specifically peroxynitrite, as key drivers of axon

253 nd that excessive reactive nitrogen species (RNS), such as nitrite, are generated in precancerous pan

254 species (ROS) and reactive nitrogen species (RNS), which can alter the biological function of key cel

255 uing dual role in reactive nitrogen species (RNS)-related oxidative stress.

256 species (ROS) and reactive nitrogen species (RNS).

257 of Cys(203) with reactive nitrogen species (RNS).

258 species (ROS) and reactive nitrogen species (RNS).

259 sed generation of reactive nitrogen species (RNS).

260 spite exposure to reactive nitrogen species (RNS).

261 ased detection of reactive nitrogen species (RNS).

262 species (ROS) and reactive nitrogen species (RNS).

263 ker of NO-induced reactive nitrogen species (RNS).

264 of Salmonella to reactive nitrogen species (RNS).

265 xide (NO)-derived reactive nitrogen species (RNSs) and/or superoxide-derived reactive oxygen species

266 l (MG) and typical reduced nitrogen species (RNSs) are systematically investigated by using combined

267 Conditioning by remote noxious stimulation (RNS; application of 3 degrees C water to a hand) usually

268 treatment of antioxidant tempol to suppress RNS, not only are DNA lesions significantly reduced, but

269 Root nodule symbioses (RNS) allow plants to acquire atmospheric nitrogen by est

270 ble for activation of root nodule symbiosis (RNS) at both epidermal and cortical levels and is functi

271 d the nitrogen-fixing root nodule symbiosis (RNS) is governed by a shared regulatory complex.

272 During root nodule symbiosis (RNS), cell-division activity is reinitiated and sustaine

273 hallenge by using the residue number system (RNS) and composing high-precision operations from multip

274 nism for BCKDC regulation, demonstrated that RNS can generally inhibit all alpha-ketoacid dehydrogena

275 udies have yielded preliminary evidence that RNS System effectiveness depends on the brain state duri

276 A prevailing view holds that RNS efficacy is primarily mediated by acute seizure term

277 These findings illustrate that RNS cause cell death in a Fas- and JNK-dependent manner

278 ADD) in RNS-exposed cells, illustrating that RNS directly targeted Fas.

279 e, an AMPK agonist, these data indicate that RNS generated by metformin is required for AMPK activati

280 O-induced growth inhibition, indicating that RNS-mediated modifications play important physiological

281 The results suggest that RNS may affect particularly those elements of the PSEC e

282 ontribute to tubular injury and suggest that RNS should be considered a potential therapeutic target

283 The RNS System (NeuroPace, Inc.) is a chronic, closed-loop e

284 The RNS-induced effect on the entire PSEC was significantly

285 Importantly, we have validated the RNS System to make sensitive measurements of hippocampal

286 Eighty-one of 256 patients treated with the RNS System across 31 centres during clinical trials met

287 over a quarter of patients treated with the RNS(R) System do not experience meaningful seizure reduc

288 blood pressure were not correlated with the RNS-induced effects on the different segments of the PSE

289 t to increase resistance of H. capsulatum to RNS in culture.

290 le exhibit increased fitness when exposed to RNS in an NRAMP(R), C3H/HeN murine model of acute oral i

291 nism underlying PhoPQ-mediated resistance to RNS is linked to the coordination of Mg(2+) homeostasis

292 To understand how H. capsulatum responds to RNS, we determined the transcriptional profile of H. cap

293 However, therapeutic response to RNS is often slow, is highly variable, and defies progno

294 creased susceptibility of phoQ Salmonella to RNS requires molecular O2 and coincides with the nitroty

295 oxygen species (ROS), were not sensitive to RNS-mediated lipid peroxidation.

296 f Salmonella enterica serovar Typhimurium to RNS in a murine model of systemic salmonellosis.

297 rather than DNA or membrane lipids underlies RNS toxicity in wild-type B. burgdorferi.

298 ts with pharmacoresistant epilepsy underwent RNS System implantation in the bilateral centromedian (C

299 We now report that higher in vivo RNS production correlates with mouse strain-related inna

300 es the pathways identified here to cope with RNS-induced damage during pathogenesis.

301 t to identify Escherichia coli proteins with RNS-sensitive cysteines.