ライフサイエンスコーパス: toxic

1 pletion, pan-T cell aplasia is prohibitively toxic.

2 caused toxicity, with poly GA being the most toxic.

3 Higher levels are toxic.

4 iodoarenes, which can be both expensive and toxic.

5 e diversity of activities, some of which are toxic.

6 r is essential for life but also potentially toxic.

7 growth-inhibitory, and magnesium fluoride is toxic.

8 efficacy in the chronic phase and are rather toxic.

9 e of APP, resulting in the overproduction of toxic Abeta isoforms.

10 has been developed to efficiently eliminate toxic Abeta42 oligomers as a promising treatment strateg

11 loforms of the peptide, Abeta40 and the more toxic Abeta42.

12 ntly inactivated by phosphorylation to avoid toxic accumulation of cytoplasmic ammonium.

13 ined from pre-leaching processes which apply toxic acids and high energy-consuming annealing, an inte

14 The mode of toxic action (MOA) is recognized as a key determinant of

15 ty of guanidinocalixarenes in inhibiting LPS toxic action has previously been related to their capaci

16 adigm for antibacterial T6SS substrates, the toxic activities of these effectors are neutralized by a

17 d high exposure (>/=75th percentile) for air toxics after adjustment for major risk factors.

18 Although CD7 CAR T cells were also toxic against unedited (CD7(+)) T and NK lymphocytes, we

19 the detection of pathogenic microorganisms, toxic agents, and pesticides in the environmental field

20 odulates the metabolic response to drugs and toxic agents.

21 preeclamptic nano-vesicles may be removing a toxic aggregated protein from the placenta, they may als

22 misfolded species that are prone to forming toxic aggregates, including soluble oligomers and fibril

23 ct RNA toxicity or through the production of toxic aggregating dipeptide repeat proteins.

24 Toxic aldehydes are generated in plants both under norma

25 the fundamental characteristics that enable toxic alpha-synuclein oligomers to perturb biological me

26 in A53T mice increased levels of potentially toxic alpha-synuclein oligomers, resulting in conformati

27 dered one of the standards of care as a less toxic alternative to WBRT for this patient population.

28 ansfer out of the ER prevents the buildup of toxic amounts of ceramides.

29 Selective detection and staining of toxic amyloid plaques, a potential biomarker present in

30 sociated with mutations in APP that increase toxic amyloidogenic cleavage of APP and produce amyloid

31 tegies for the development of ultrasensitive toxic analyte sensor platforms.

32 re secondary metabolites of fungi that cause toxic and carcinogenic effects.

33 compounds are environmental pollutants with toxic and carcinogenic properties.

34 ls diverse cellular functions but can become toxic and cause cell death.

35 solid-liquid percolation equipment using non-toxic and eco-friendly extraction solvents: either deion

36 w that these BPA alternatives induce similar toxic and estrogenic effects to BPA and that BPAF is mor

37 N-methyl-d-aspartate (NMDA), which is excito-toxic and induces RGC death.

38 nfronted long and tedious routes that employ toxic and often difficult to scale pyrophoric reagents.

39 and dioxin-like compounds (DLCs) are highly toxic and persistent global pollutants with extremely la

40 global environmental pollutant that is both toxic and recalcitrant to degradation.

41 oxicity (FET) showed that the starch was not toxic and that it was suitable for food and non-food ind

42 well water quality around arsenic, the most toxic and widespread of common private water contaminant

43 n significant amounts of oxalates, which are toxic and, if consumed regularly, can lead to the develo

44 In addition, Se devices are air-stable, non-toxic, and extremely simple to fabricate.

45 timicrobials that are broader spectrum, more toxic, and more expensive, and mortality attributable to

46 including survival, and reduce the need for toxic antiviral therapies.

47 Novel therapies, which are frequently toxic, are difficult to establish in this patient popula

48 h engages the ability of p17 to form soluble toxic assemblies.

49 y to assess the potential of a protein to be toxic at early stages of development.

50 Manganese is an essential metal that becomes toxic at elevated levels.

51 ich functions as a signaling molecule but is toxic at high concentrations, is averted by its efficien

52 As contaminants are often more toxic at higher temperatures, predicting their impact un

53 c components found in whole OSPW are acutely toxic at much lower doses than we previously reported fo

54 ere also gradually degraded by DegP but were toxic because they first bound to the Bam complex, an es

55 emissions, and high exposure to several air toxics before conception may increase GH risk.

56 n impairment of bile flow, and that leads to toxic bile acid (BA) accumulation in hepatocytes.

57 lian or military population by inhalation of toxic bioaerosol.

58 rain barrier disruption (BBB) and release of toxic blood molecules into the brain contributes to neur

59 ealing, burning sulfur, desiccant dusts, and toxic botanicals as early control methods.

60 and in standard cell culture media generate toxic by-products that interfere with cellular functions

61 compartment for disposal of methylglyoxal, a toxic byproduct of glycolysis, as 1-propanol.

62 ng plant acclimation to stress, but are also toxic byproducts of stress metabolism.

63 elop strategies that reduce the formation of toxic byproducts such as chloroform (CF).

64 ene glycol and glycerol are known to produce toxic byproducts such as formaldehyde, acetaldehyde and

65 Determining which sources of PM2.5 are most toxic can help guide targeted reduction of PM2.5.

66 pon exposures to species-specific subacutely toxic Cd concentrations (nominal LC1; E. cyaneus: 18 nM

67 of inhibiting methanogens using expensive or toxic chemical inhibitors, such as 2-bromoethanesulfonic

68 A comparative study for 62 toxic chemicals based on the simultaneous monthly collec

69 the capture of several industrially-relevant toxic chemicals, including NH3, SO2, NO2, H2S, and some

70 e identification of chemical warfare agents, toxic chemicals, or explosives in air.

71 spective different regulatory frameworks for toxic chemicals.

72 illness, possess strategies to mitigate the toxic components of bile.

73 expression, 24 hr following exposure to the toxic compound 5-hydroxymethylfurfural (HMF).

74 fic citrate transporter of the multidrug and toxic compound extrusion family, MtMATE67 of Medicago tr

75 concentrations induce the generation of some toxic compounds at earlier stages of the thermoxidation

76 gradation of microcystin-LR, one of the most toxic compounds produced by the algal blooms, and reveal

77 seems to result in higher concentrations of toxic compounds.

78 As in rodent acini, human acini exposed to toxic concentrations of CCh and taurolithocholic acid 3-

79 ns in food; they may even appear together at toxic concentrations.

80 lerance induction by mixed chimerism without toxic conditioning and with a low risk of graft versus h

81 ly of 11-cis-retinal and the accumulation of toxic, constitutively active opsin.

82 novel biocompatible, biodegradable, and non-toxic controlled release formulation of ATRA for effecti

83 al inhibitor ammonium to prevent potentially toxic cross-linking activity.

84 ges over the conventional use of halides and toxic cyanide reagents.

85 xicology and risk assessment, exposed to the toxic cyanobacterium Microcystis aeruginosa.

86 Two toxic deaths (infections) were recorded, both in patient

87 te that dsRNA can be loaded on designer, non-toxic, degradable, layered double hydroxide (LDH) clay n

88 topathological examinations indicated slight toxic difference between the AgNPs and AuNPs over a peri

89 wing administration of either therapeutic or toxic doses, in particular within a patient context.

90 at concentration regimes far lower than the toxic doses.

91 e as it determines the choice of potentially toxic drug regimens.

92 investigated criteria air pollutants and air toxics during the period before conception and in early

93 xoplasm reveal inhibition of FAT as a common toxic effect elicited by spastin proteins with different

94 tographic measurements that correlate to the toxic effect of a compound over a specific aquatic speci

95 Finally, the toxic effect of both extracellular oAbeta and oTau on me

96 the tested cells and potentially negligible toxic effect on arterial vessel walls.

97 we hypothesize that deguelin is exerting its toxic effect on nematodes as a modulator of oxidative ph

98 Mutant spastin proteins produce this toxic effect only when presented as the tissue-specific

99 and preventive strategies to abrogate these toxic effects and improve patient care.

100 anti-tumor efficacy is not compromised, but toxic effects are eliminated.

101 rylated alpha-synuclein is believed to exert toxic effects at the synapse in dementia with Lewy bodie

102 iated with higher grade 3 to 4 hematological toxic effects compared with carboplatin-paclitaxel (eg,

103 ord promising clinical outcomes and rates of toxic effects compared with historical photon therapy da

104 the control group, with no evidence of renal toxic effects during the observed time frame.

105 ust and potentially credible drug to prevent toxic effects from SEB exposure.

106 rd to mechanistic insights and prediction of toxic effects in human heart tissue.

107 tumor cells and examine the therapeutic and toxic effects in Syrian hamster models of pancreatic can

108 Dose-limiting toxic effects occurred in two (67%) of three patients wh

109 ogical experiments further indicate that the toxic effects of mutant M1 spastins on FAT involve casei

110 BPA may have toxic effects on the female reproductive system in human

111 ollowed by antibody alone until unacceptable toxic effects or disease progression occurred.

112 Grade 3 or higher toxic effects were observed in 39 patients treated with

113 Acute and late toxic effects were prospectively assigned using Common T

114 Common grade 3 or worse toxic effects were related to the lymphodepleting chemot

115 Apart from neutropenia no other toxic effects were reported at grade 3 or worse severity

116 The safety profile and risk of systemic toxic effects when brimonidine is used topically for hem

117 As a result of increased toxic effects with the DPL combination, patients on DPL

118 drug concentrations in target lesions, fewer toxic effects, and improved survival end points in an an

119 ncluded time to second progression or death, toxic effects, and quality of life.

120 ng toxic effects, substantial cardiovascular toxic effects, or deaths occurred.

121 n prolonged progression-free-survival, fewer toxic effects, or improved quality of life.

122 cutoff date of Feb 1, 2017, no dose-limiting toxic effects, substantial cardiovascular toxic effects,

123 ts were monitored for response to treatment, toxic effects, the expansion and persistence of CTL019 c

124 cles until disease progression, unacceptable toxic effects, voluntary withdrawal by the patient, or c

125 s were well tolerated, with no dose-limiting toxic effects.

126 environment requires mechanistic models for toxic effects.

127 omponents and to mitigate the progression of toxic effects.

128 pg/mL; P = .03) and worse treatment-related toxic effects.

129 inds to Abeta oligomers and transduces their toxic effects.

130 the maximum tolerated dose and dose-limiting toxic effects.

131 rogression-free survival, response rate, and toxic effects.

132 There were no acute or late grade 5 toxic effects.

133 compromising viral suppression or increasing toxic effects.

134 embolic complications, cardiac, and vascular toxic effects.

135 p trials that showed efficacy and manageable toxic effects.

136 ce while continuously monitoring potentially toxic elements (As, Cr, and Se) by inductively coupled p

137 f new maximum permissible concentrations for toxic elements in seafood by the European food safety au

138 Stevens-Johnson syndrome and toxic epidermal necrolysis (SJS/TEN) are rare but severe

139 Toxic epidermal necrolysis (TEN) and Stevens-Johnson Syn

140 Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are rare but life-threa

141 Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are rare but life-threa

142 Although rare, Stevens-Johnson syndrome and toxic epidermal necrolysis remain among the most devasta

143 f patients with Stevens-Johnson syndrome and toxic epidermal necrolysis.

144 percent decreases for PCDD/Fs, CP-PCBs, and toxic equivalence (TEQ) (average -56 to 70%) were fairly

145 tase inhibitor fadrozole, we also show how a toxic equivalence (TEQ) calculation allows use of the qA

146 Grade 3 or 4 toxic events after treatment (according to the Common Te

147 isms (SRM) produce hydrogen sulfide which is toxic, explosive, and corrosive.

148 r-based metal oxide sensor devices to detect toxic, explosive, flammable, and pollutant gases is stil

149 Common chronic effects of toxic exposure in these animals are seizures and hippoca

150 be modulated to favor nontoxic fibrils over toxic fibrils.

151 iomers thus accelerates the formation of non-toxic fibrils.

152 beaker", avoiding direct handling of highly toxic fluorine gas.

153 pecial antibacterial mechanisms, and are non-toxic for human cells, a prerequisite for using them as

154 atrix metalloproteinase 9 and is selectively toxic for motor neurons.

155 n amyotrophic lateral sclerosis (ALS) and is toxic for motor neurons.

156 MMF, at serum trough levels and higher, are toxic for the human bronchial epithelial cells after 4-d

157 n of N-retinylidene-N-retinylethanolamine, a toxic form of retinal lipofuscin that accumulates in RPE

158 toxicity and neurodegeneration via a gain-of-toxic function mechanism; either through direct RNA toxi

159 (G4C2)102 repeat, to investigate the gain-of-toxic function mechanisms.

160 ly causes disease and represents the gain of toxic function.

161 Our findings support a primary toxic gain of function mechanism and highlight a previou

162 to control astrocytes, suggesting potential toxic gain-of-function properties.

163 tting of intentional poisoning, fire-related toxic gas exposures, and inhalational injuries.

164 Chloromethane (CH3Cl) is a toxic gas mainly produced naturally, in particular by pl

165 en sulfide (H2 S) is perhaps best known as a toxic gas, the electron-rich H2 S functions as an energy

166 metabolic flux, inhibiting the production of toxic glucose metabolites and inducing mitochondrial bio

167 talized mouse podocytes had higher levels of toxic glucose metabolites, mitochondrial dysfunction and

168 glucosidase that activates oleuropein into a toxic glutaraldehyde-like structure.

169 conversion of glucose into gluconic acid and toxic H2 O2 , a novel treatment paradigm of starving-lik

170 ward those proteins and protects against the toxic hallmarks of alpha-syn pathology.

171 Methyl iodide is a toxic halocarbon with diverse industrial and agricultura

172 Anthropogenic emissions of the toxic heavy metal mercury (Hg) have substantially increa

173 It may be contaminated by toxic heavy metals present in water or soil.

174 creased iPLA2gamma activity channels AA into toxic HETEs.

175 n retinal iron-dyshomeostasis, a potentially toxic host response contributing to prion disease-associ

176 euron-specific targeting without concomitant toxic host responses, we evaluated the localization, act

177 t therapeutic approaches involve potentially toxic immunosuppressive strategies, the pathophysiology

178 For future assessment of potential toxic impacts of TiO2 nanoparticles in LCA studies, we t

179 BS are toxic in high concentration.

180 uch autoimmunity has been shown to be highly toxic in several bacteria and is believed to be one of t

181 p-dioxin, TCDD) is a carcinogenic and highly toxic industrial byproduct that persists in the environm

182 nterest for capture and/or detoxification of toxic industrial chemicals and chemical warfare agents.

183 ntation (BTT), and as definitive therapy for toxic ingestion or idiopathic liver failure (DT) in a le

184 sis, and this causes bile salt (BS)-mediated toxic injury of the "upstream" liver parenchyma.

185 ey undergo environmental degradation to more toxic inorganic arsenite (As(III)) that contaminates cro

186 ivate cofactor pool, minimize the effects of toxic intermediates, and enhance flux through the encaps

187 DNA glycosylases capable of unhooking highly toxic interstrand cross-links (ICLs) and bulky minor gro

188 However, precisely how tau becomes toxic is unclear.

189 trast, a second segment, 15-25 WT, forms non-toxic labile beta-sheets.

190 ignal abnormalities can mimic the changes of toxic leukoencephalopathy.

191 t the newly synthesized peptides, preventing toxic-level build-up.

192 ring abiotic stress, MG levels accumulate to toxic levels in affected cells.

193 as increased survival following injection of toxic levels of either nicotine or cocaine, accompanied

194 When abruptly exposed to toxic levels of hexavalent uranium, the extremely thermo

195 t the airways, NTHI must be able to mitigate toxic levels of oxidative stress.

196 studies have identified possible downstream toxic mechanisms.

197 se double-strand breaks are generally highly toxic, mechanisms that regulate AID expression are of mu

198 We present Iodixanol as a non-toxic medium supplement that allows refractive index mat

199 way of sensitive sensor development for the toxic melamine and their derivatives for the safety of b

200 Only trace levels of the known toxic metabolite, thio-DMA, were observed, across indivi

201 iPLA2gamma) and the production of downstream toxic metabolites.

202 tion protocol does not require expensive and toxic metal catalysts or ligands, and it produces innocu

203 The toxic metalloid arsenic has been environmentally ubiquit

204 Arsenic is a ubiquitous, naturally occurring toxic metalloid widely distributed in soil and groundwat

205 nvironments, making it a major sink for this toxic metalloid.

206 We evaluated dietary intake of toxic metals as a source of increased biomarker levels o

207 vidence of infectious pathogens, pesticides, toxic metals, and other non-infectious causes, including

208 transformation products, and the release of toxic metals, heat-activated persulfate may be a useful

209 tazoans have detoxifying organs to cope with toxic metals, sponges lack organs but harbour a symbioti

210 ity in a broad pH range, and selectivity for toxic metals.

211 ential for bacterial resistance to drugs and toxic metals.

212 ate (As(V)) and arsenite (As(III)) into more toxic methylated metabolites methylarsenite (MAs(III)) a

213 ell toxin uptake, and edema factor (EF), the toxic moiety which increases host cell cyclic AMP (cAMP)

214 echanism for Gram-negative bacteria to expel toxic molecules for survival.

215 Our system, containing non-toxic nano-droplets loaded with iodine has high contrast

216 Toxic nectar is an ecological paradox [1, 2].

217 Other immunosuppressives were not toxic, neither changed TEER or permeability.

218 olecules with therapeutic value against this toxic neuropathy.

219 surface without significant accumulation of toxic oligomeric intermediates.

220 ation impact the populations and kinetics of toxic oligomeric species.

221 ule associating protein tau (MAPT, tau) into toxic oligomers and amyloid deposits is a primary pathol

222 aggregation potential and propensity to form toxic oligomers, they represent particularly attractive

223 were highly active to cancer cells and less toxic or nontoxic to fibroblasts.

224 where nanoparticles (NPs) are observed to be toxic or reduce viable cells in a population of bacteria

225 ilitate long-range transport of reactive and toxic organic pollutants embedded in SOA.

226 Separation of toxic organic pollutants from industrial effluents is a

227 lism and excretion (ADME) of metabolites and toxic organic solutes are orchestrated by the ATP-bindin

228 o locally increase iron levels to activate a toxic oxidative burst.

229 ombines a membrane-localizing peptide with a toxic peptide cargo and discovers a tandem peptide that

230 tain pathogenic bacteria produce and release toxic peptides to ensure either nutrient availability or

231 volutionary response by predators feeding on toxic prey.

232 ecrease in FL concentration, accumulation of toxic (R)-FL and formation of toxic (S)-NFL leads to muc

233 ction lines revealed that the elimination of toxic reactive carbonyl species during germination and s

234 cient nanofactories protect human cells from toxic reactive oxygen species for up to a week.

235 ateral 2, 3, 7, and 8 positions are the most toxic, removal of these chlorines is advantageous, but p

236 iption factor that is known as a mediator of toxic responses.

237 We propose that specific toxic RNAi-active sequences present in the genome can ki

238 This consensus sequence is found in the toxic RNAs (CCUG repeats) and in cellular RNA substrates

239 ecifically visualizing and eliminating these toxic RNAs.

240 ccumulation of toxic (R)-FL and formation of toxic (S)-NFL leads to much higher than presumed toxicol

241 ences in uptake, internal sequestration, and toxic sensitivity to waterborne cadmium (Cd).

242 Toxic shock syndrome (TSS) is caused by staphylococcal a

243 During toxic shock syndrome (TSS), bacterial superantigens trig

244 G) is sometimes administered for presumptive toxic shock syndrome (TSS), but its frequency of use and

245 Panton-Valentine Leukocidin toxin (PVL), and toxic shock syndrome toxin-1 (tst) genes.

246 Polyphenol metabolism and possible toxic side effects are also considered.

247 d therapeutic effect with reduced off-target toxic side effects.

248 etabolism that impact therapeutic action and toxic side effects.

249 beta-lapachone treatment in humans, avoiding toxic side effects.

250 rotting potato flesh contain high amounts of toxic solanine and chaconine, exceeding by 2-5-fold the

251 ale manufacturing using green, economic, non-toxic solvents.

252 ower conversion efficiency, processed by low toxic solvents.

253 enotoxicity, as well as the cytotoxicity, of toxic species generated in cell culture media by an argo

254 gomers, rather than amyloid fibrils, are the toxic species regardless of the pathogenic protein seque

255 The OS emissions of nontraditional toxic species such as HNCO have not been assessed.

256 ic forms of the protein are likely to be the toxic species that disrupt endosomal signaling.

257 sessing the possible detrimental outcomes of toxic spills, for example oil spills, in relatively simp

258 ment 19-29 S20G may serve as a model for the toxic spine of hIAPP.

259 systems broadly throughout the child's body (toxic stress).

260 Resolution of these potentially toxic structures requires the MUS81-EME1 endonuclease, w

261 is essential to prevent its channeling into toxic structures threatening cell viability.

262 hotosystem II complex) and biodegradation of toxic superoxide to hydrogen peroxide by superoxide dism

263 The toxic synthetic human Fab gene contained domains optimiz

264 one system affects the accumulation of these toxic tau species, which can be modulated with Hsp90 inh

265 more toxic than (S)-FL; (S)-NFL is 10x more toxic than (S)-FL).

266 tivated sludge treatment ((R)-FL is 30x more toxic than (S)-FL; (S)-NFL is 10x more toxic than (S)-FL

267 senate is less toxic than arsenite, but more toxic than arsenate at concentrations >/=25 muM As, refl

268 haliana showed that monothioarsenate is less toxic than arsenite, but more toxic than arsenate at con

269 ity data, MB was at least 5 to 20 times more toxic than the conventional pyrethroid (beta-cyfluthrin)

270 ivatives (OH-PCBs), which are sometimes more toxic than the parent PCBs.

271 Therefore, novel, non-toxic therapies are urgently needed.

272 e continued need for more effective and less toxic therapies.

273 e continued need for more-effective and less-toxic therapies.

274 g evidence that various nanoparticles may be toxic to a range of organisms, biota in estuarine and co

275 Fosinopril was also toxic to Ae. aegypti larvae, although the 1(st) instars

276 ine disruptors that bioaccumulate in and are toxic to aquatic and other organisms.

277 m residue limits (0.01mg/kg), which might be toxic to body.

278 Protein misfolding is toxic to cells and is believed to underlie many human di

279 LPAC and QAGR proteins are toxic to cells independent of RNA gain of function.

280 re, we report that cCF10 induction is highly toxic to cells sustaining a deletion of prgU, a small or

281 ose) polymerase (PARP) inhibitors (PARPi) is toxic to cells with defects in homologous recombination

282 capsid proteins, but the FMDV 3C protease is toxic to host cells.

283 in (TTX) and saxitoxin (STX) that are highly toxic to humans and other vertebrates, target conserved

284 note that overexpression of the proteins is toxic to M. smegmatis, although whether this toxicity an

285 As carmaphycin B is toxic to mammalian cells, we synthesized a series of che

286 The molecules were also found to be non-toxic to MCF 12A cells.

287 The metalloid tellurite is highly toxic to microorganisms.

288 3A)) expression in astrocytes is selectively toxic to motor neurons in co-culture, even when mutant p

289 SCs); however, suffer the issue that lead is toxic to the environment and organisms for a long time a

290 These peptides are also toxic to the producing bacteria that utilize dedicated A

291 revealed that degradation products were less toxic toward the bacterium Aliivibrio fischeri than thei

292 Copper is an essential yet potentially toxic trace element that is required by all aerobic orga

293 Removal of toxic trace elements via adsorption onto iron oxides is

294 This loss results in the accumulation of toxic transcripts of Alu transposable elements, which ac

295 emia in patients, replacing conventional CNS-toxic treatment.

296 ry mixture of beads and fibers resulted in a toxic unit of 1.85 indicating less than additive effects

297 ls where it is proteolyzed with release of a toxic warhead-a nonhydrolyzable aspartamidyl-adenylate,

298 o, Cd, Sn, Sb, Ba, W, and Pb), including air toxics were enriched relative to the local soil both in

299 that in strains lacking substrates that are toxic when mislocalized, both LolA and LolB can be compl

300 Very importantly, 11 and 12 were non-toxic with very safety and high therapeutic indices (CC5