ライフサイエンスコーパス: argue against

1 sal for a "smoker's license" and Jeff Collin argues against.

2 These results argue against a "content-poor" view of the role of parie

3 Theoretical considerations argue against a CA stimulation of HCO3- transport, suppo

4 Furthermore, our results argue against a causative relationship between psychosin

5 e regulation of epithelial wound healing and argue against a cell-autonomous tumor suppressor role fo

6 Our findings argue against a central brain motor-compensatory mechani

7 The current data clearly argue against a common circuitry account for amodal dura

8 Our data argue against a common primary trigger for atheroscleros

9 , these spatial and temporal heterogeneities argue against a concerted phase shift of molluscan assem

10 nformatics and the lack of bound metals both argue against a connection to the amidohydrolase superfa

11 gm1/Irgm3 double-deficient mice, our results argue against a direct effector function of Irgm1 at the

12 genetic lability in the mammalian genome but argue against a direct role for sperm cytosine methylati

13 These findings argue against a distinct effect of Insr deficiency to pr

14 r to dorsal V2 from earlier visual areas and argue against a DM that lies along the dorsomedial borde

15 and chromatin structure mediate pairing and argue against a DNA sequence-based mechanism.

16 tochastic process at the sub-organ level and argue against a dominant influence of chemotactic gradie

17 These findings argue against a foreign body reaction as a common mechan

18 Moreover, other considerations argue against a guideline focused primarily on limiting

19 Our results argue against a long-term role of peripheral monocytes t

20 Our data argue against a major effect on neurologic outcome.

21 Our results argue against a major role for ADAM17 in endothelial Not

22 Our data thus argue against a major role of blood vessels to preserve

23 mirror neurons, and, as such, these findings argue against a mirror system dysfunction in autism.

24 primary mechanism of SAMHD1 restriction and argue against a nucleolytic mechanism, which would not b

25 activated CD8(+) T cell differentiation and argue against a physiological role in cell cycle regulat

26 Thus, our data argue against a physiological role of carbonic anhydrase

27 ber alterations across mammalian tissues and argue against a positive role for aneuploidy in organ fu

28 l immunity is well maintained in old RMs and argue against a primary role for progressive dysfunction

29 These data argue against a protective role of accumbal indirect pat

30 These results argue against a proton relay mechanism, indicating that

31 However, data from recent studies argue against a pure focus on vasospasm as the cause of

32 Our results argue against a purely 'transcription factor-centric' vi

33 These results argue against a purely feedforward explanation of recogn

34 These data argue against a role for altered IMTG accumulation and l

35 These results argue against a role for FcgammaRs in IgG transplacental

36 These results argue against a role for gL and Eph family receptors in

37 Together, our data argue against a role for Naa10 in lysine acetylation.

38 These findings argue against a role for PKM2 as a protein kinase.

39 Together, these results argue against a role for the MD network in core aspects

40 nt of cutin and suberin composition, and (3) argue against a role of sn-2-GPATs (Enzyme Commission 2.

41 Our results argue against a simple rule for the arrangement of inhib

42 Our data argue against a specific recruitment of actin to HIV-1 b

43 These results argue against a uniform policy of avoiding dolutegravir

44 ptor stoichiometry and quantitative analyses argued against a reversible binding interaction that sim

45 vaccines with MS or any other CNS ADS, which argues against a causal association.

46 e-specific regulation of autonomic responses argues against a common system hypothesis and provides e

47 In addition, the absence of glial reactivity argues against a contribution of astrocytes to lesion-as

48 This argues against a conventional role for PrimPol as a mito

49 This outcome argues against a critical role for mannose-dependent C-t

50 This observation argues against a direct inhibition of glucagon secretion

51 ior, but the lack of difference before onset argues against a major causative role for near work.

52 egulated at the transcriptional level, which argues against a major role for posttranscriptional mech

53 events required for lumen morphogenesis and argues against a previous paradigm of lumen formation.

54 netic diversity of the A1/D1 West population argues against a recent introduction of the pathogen int

55 This argues against a single-site coupling model because the

56 ied between expected median survival and EOR argues against a surgical management strategy based on r

57 with ventromedial frontal lobe (VMF) damage argues against a very general role for this region in va

58 l plays a key role in both reactions-thereby arguing against a 1,2-migration mechanism of deamination

59 , G2 contributes little to tensile strength, arguing against a cause-effect relationship between tens

60 ne failed to block cue-induced food seeking, arguing against a ceftriaxone-induced effect unique to e

61 a function of denaturant concentration, thus arguing against a classical two-state model as found for

62 ces to the C-terminal OB fold of RPA70, thus arguing against a close evolutionary kinship between the

63 hroblasts, which do not have a constriction, arguing against a contractile ring-based nuclear expulsi

64 LPS responses in Apoe-deficient macrophages, arguing against a differential role for secretory APOE4

65 larization-induced secretion was unaffected, arguing against a direct action on the exocytotic machin

66 n lineage-negative hematopoietic stem cells, arguing against a direct role for CSF1R in myeloid linea

67 ation of the exocyst with clathrin was seen, arguing against a direct role in exocyst recruitment.

68 of labeled tubular cells remained constant, arguing against a fixed progenitor population.

69 suppressed, phenotype in their TCR response, arguing against a generalized T cell paralysis as a majo

70 efficiently repressed by microRNAs in vivo, arguing against a major role for the poly(A) tail in mic

71 impaired during Listeria + LCMV coinfection, arguing against a major role for this chemokine in coinf

72 protein convertase inhibitors for up to 8 h, arguing against a major role of increased prodomain remo

73 e detected in oocytes throughout prophase I, arguing against a male-specific function for this isofor

74 ld for ssAAV and 6.6-fold for scAAV vectors, arguing against a mechanism related to second-strand syn

75 Arguing against a motor explanation, no other cerebellar

76 rmed the primarily unclustered distribution, arguing against a prevalent existence of transcription f

77 light in astronauts with ocular alterations, arguing against a primary causal relationship between el

78 re present in these cells in cc2d2a mutants, arguing against a primary function for Cc2d2a in cilioge

79 s of TET1 and TET2 to 5hmC and 5fC formation arguing against a processive mechanism of 5mC oxidation.

80 cancer cell lines and human tumors is rare, arguing against a prominent tumor-suppressive role.

81 nization incompatible with an NPC-like ring, arguing against a proposed "ciliary pore complex." We su

82 us CD70(-/-) cells from defective expansion, arguing against a role for CD70-mediated T:T help in thi

83 rotein upon addition of single-stranded DNA, arguing against a role for Est3 in recognition of telome

84 red vertically from a nonparasitic ancestor, arguing against a role for Orobanchaceae parasites in th

85 the response to TRPV1 agonists were normal, arguing against a role for TRPV1.

86 ning the alpha1, alpha2, or alpha3 subunits, arguing against a selective association with specific GA

87 oportion of the overall PrP(Sc) (i.e. <10%), arguing against a significant role of slowly sedimenting

88 hannels without affecting their conductance, arguing against a simple channel-blocking effect.

89 ch gene responded in different cell subsets, arguing against a single cellular mechanism.

90 is diverges from that of amyloid deposition, arguing against a straightforward relationship between g

91 high-affinity T cell responses equally well, arguing against a synergistic effect of TCR and inflamma

92 side-chains to the transition state complex, arguing against a two-step mechanism for TCR binding.

93 eening test and associated intervention, all argue against active clinical surveillance for lymphoma

94 Thus, our results argue against age-related deficiency of 11-cis-retinal i

95 ate immune signaling induced by Sendai virus argue against an active block of IRF3 activation by the

96 In conclusion, our data argue against an important role of PlGF during primary t

97 ues of water in carbonaceous chondrites also argue against an influx of water ice from the outer sola

98 Furthermore, our results argue against an X-chromosome dosage compensation model

99 This argues against an unusually C-rich mantle being responsi

100 of del17p; did not increase DR5 expression, arguing against an activation of p53 pathway; and synerg

101 the ability of EPEC to form actin pedestals, arguing against an essential role for WIP in EPEC-induce

102 oop and not a function of the stimulus, thus arguing against an FM signaling code.

103 RNA synthesis by Pol II, as well as evidence arguing against an important cytoplasmic role in mRNA de

104 be overcome by synaptotagmin overexpression, arguing against an obligatory role in clamping.

105 following BACE1 cleavage (soluble APPbeta), arguing against an overall increase in BACE1 processing

106 They also argue against any front lobe stabilization of the isomer

107 lle between bulk EC and BSE has been used to argue against any major contribution of EC like planetar

108 This commentary argues against any claim of discontinuity between humans

109 ions in brain regions adjacent to ventricles argue against atrophy as a mechanism of ventricular expa

110 Thus, our data argue against broad thorny cells as the homologs of loca

111 enteropathy, was HLA-DQ9/DQ6-positive, also arguing against CD.

112 l-type-dependent roles of Smarc proteins and argue against cerebellar granule cells and other progeny

113 ed SC I+III(2) limits complex (C)I turnover, arguing against channeling.

114 These observations, combined with modeling, argue against circuit architectures assuming non-selecti

115 Our results argue against common local regulatory variation as a fac

116 We therefore argue against continued use of the standard functional e

117 er, there are rare perceptual phenomena that argue against continuous perception but, instead, sugges

118 Our data argue against cytoskeletal or endocytic involvement and

119 -line probing and ATPgammaS competition both argue against direct Cu(2+) binding by RNA; rather, thes

120 Our observations argue against direct interaction between Xist RNA and PR

121 Our acute inhibition results argue against direct mechanical activation of opposite-d

122 ed cells but not in transfected cells, which argued against direct US9-gE/gI interactions.

123 ll area followed a random guided walk model, arguing against directed migration in vivo.

124 They also argue against disengagement of the N-domain out of the c

125 n patterns can alter perception in ways that argue against each type of afferent acting independently

126 during and outside ripples were orthodromic, arguing against ectopic spike generation, which has been

127 ponsive to disease-unrelated antigens, which argues against excessive immunosuppression.

128 This argues against formation of AH meltglass in thatched hut

129 Acquired mass spectrometric data argues against formation of oligomers.

130 Our results argue against functional cooperation between the various

131 8)A), a pK(a) perturbed nucleotide analogue, argued against functional base ionization at this site.

132 ls of differing putative interneuronal type, arguing against gap junctions as the sole underlying sou

133 We argue against generically equating chromatin and epigene

134 Findings argue against genetic selection/concentration as an expl

135 n fH ligands did not cause bacteremia, which argued against global susceptibility to bacteremia resul

136 ried markedly in their chromatic preference, arguing against global processing.

137 This argues against haploinsufficiency as a disease mechanism

138 Using an ethological perspective, we argue against Heyes' rapid dismissal of innate cognitive

139 Together, these analyses argue against homology of sponge choanocytes and choanof

140 oncentrations less than or equal to 17 mug/L argue against hypoxic-ischemic encephalopathy incompatib

141 thers, all viruses were readily neutralized, arguing against immune escape.

142 odies against LppQ during challenge and also argue against inclusion of LppQ-N' in a future subunit v

143 -2 and low caspase 3 and cytochrome c levels argue against increased apoptosis in this disease.

144 erences in resorption rates and litter sizes argue against induced embryonic lethality.

145 rved with CD36 intestinal segments in vitro, arguing against influence of alterations in fat absorpti

146 These data strongly argues against interaction of NLF and mitochondrial Ca(2

147 piration during beta-adrenergic stimulation, arguing against intracrine control of respiration by NO

148 h some argue in favor of bistability, others argue against it.

149 -wake states, and least of all in REM sleep, arguing against it as a major mechanism of REM sleep pha

150 n protein 1 (MALT1) is intact in our series, arguing against its involvement in susceptibility to fun

151 eptor signaling exacerbates pathogenesis and argues against long-term use of pan-anti-TNF-alpha inhib

152 es spliceosome assembly and normal splicing, arguing against loss of an intronic element as the prima

153 e been unsaturated throughout their history, arguing against major roles for parasitoid niche evoluti

154 In vitro biochemical binding assays argued against meaningful direct interaction between TNP

155 Thus, our data argue against mHTT crossing the MOM and entering into th

156 iled to rescue the dopaminergic neuron loss, arguing against microglial activation being a key factor

157 The results argue against models in which MTs play a major mechanica

158 Our results argue against models of TCR triggering involving conserv

159 es increased VSG switching by recombination, arguing against models for VSG switch initiation through

160 uence on the interactions with beta-catenin, arguing against models in which beta-catenin weakens act

161 residual age at the onset of motor symptoms, arguing against modification of these disease features b

162 magnitude depending on the type of training, arguing against motor fatigue or changes in motor pathwa

163 Leibovich et al. argue against nativist views of numerical development no

164 healing and skin cancer development and also argue against nonredundant functions of mast cells in wo

165 ) mice were born at normal Mendelian ratios, arguing against NRP1 functioning exclusively as a VEGF16

166 However, three observations presented here argue against one key aspect of this model.

167 The mutant has no growth defect, arguing against ongoing restriction of its own DNA.

168 ibute to the oscillatory islet behavior, but argue against other models that depend on Ca(2+) oscilla

169 obiota and location in aquatic habitats, and argues against over-generalizing conclusions derived fro

170 These results argue against overproduction of Abeta42 as an essential

171 any biochemical marker except for uric acid, arguing against pleiotropy.

172 Ps were detected across all gene categories, arguing against positive selection and toward genetic dr

173 and glycogen, heterozygous mice were normal, arguing against possible toxic effects of truncated Man2

174 eddases ADAM10 or BACE1 at the cell surface, arguing against pre-formed megadalton complexes.

175 These findings argue against preattentive processing of biological moti

176 ingle-particle electron microscopy analysis, arguing against preferential trimeric association of nat

177 nals show no detectable suppression by iPNs, arguing against presynaptic inhibition as a primary mech

178 anced tumor growth in the absence of B cells argue against previous proposals to augment tumor immuni

179 These findings argue against prolonged monitoring of detectable postpro

180 lecular coupling between STIM1 and Orai1 and argues against recent evidence suggesting dimeric intera

181 This non-monotonic relationship argues against recent theory that the balance between pl

182 This argues against recycling models and in favor of pulling

183 majority of transporter loci are conserved, arguing against redundancy and instead for distinct role

184 nella effectors are required for persistence argues against redundant functions.

185 the diagnostic Polynesian mtDNA haplotypes, arguing against reports that chickens provide evidence o

186 the introduction of the D541A pore mutation, arguing against residual functions of the TRPV6(D541A) p

187 mparable amounts of Ca(2+) Overall, our data argue against respiratory deficiency and impaired Ca(2+)

188 Overall, our data argue against respiratory deficiency in YAC128 mice and,

189 ROS remained lower than in controls, further arguing against robust oxidative stress in this system.

190 and low risk of supraventricular tachycardia argue against routine invasive management in most asympt

191 with a docking model of the two subunits and argue against RT across the beta beta' interface.

192 in the single subunit T7 RNA polymerase have argued against scrunching as the energetic driving force

193 changes in stimulus type and task geometry, arguing against several forms of compensation.

194 thane per year, 95% confidence interval) and argue against similar methane emissions in response to f

195 omoters but not gene bodies of active genes, arguing against simple cotranscriptional recruitment to

196 On theoretical grounds, we have argued against some of the methods used to identify thes

197 In aggregate, these findings argue against specific protein-protein contacts between

198 Collectively, these results argue against stable interactions of Rheb with lysosomes

199 Our results argue against status quo therapeutic strategies that tar

200 All tested movements were encoded, arguing against strict anatomical segregation of effecto

201 veal greater differences in brain part size, arguing against strong developmental constraints.

202 anched locally, few branches contacted OHCs, arguing against synaptic elimination.

203 weak compared with its random fluctuations, arguing against synchrony as a code for binding.

204 ure of the scene perception system, and also argue against the "distributed coding" view in which eac

205 tion-reversion model for fast adaptation and argue against the alternative idea of 'stress-induced mu

206 Our data argue against the assembly of D4 into higher order multi

207 Here I will argue against the axiom that the occurrence of oncogenic

208 buffering conditions (10 mM BAPTA), our data argue against the Ca(2)(+)-dependent compound fusion of

209 Our findings argue against the common interpretation of gain/loss fra

210 eity among distinct TRM populations and also argue against the common perception that developing vacc

211 These findings strongly argue against the concept that B220+ NK cells are activa

212 Creel et al. argue against the conservation effectiveness of fencing

213 The results argue against the current mechanistic hypothesis, which

214 However, they also argue against the current model of passive transfer of f

215 The calculations indirectly argue against the deprotonation of His334 for the proton

216 molecule fluorescence imaging studies mostly argue against the existence of constitutive receptor dim

217 Overall, these findings argue against the generality of BAFF-R polymorphisms as

218 Results argue against the generally assumed roles of the differe

219 Our results argue against the hyperphosphorylation hypothesis and un

220 Together, our findings argue against the hypothesis that acquisition of a germ-

221 Our results argue against the hypothesis that the basal ganglia are

222 These findings appear to argue against the idea of generalized perceptual enhance

223 Our results argue against the idea that all high-frequency LFP activ

224 Newell & Shanks (N&S) argue against the idea that any significant role for unc

225 rongly involved in visual categorization and argue against the idea that parietal category signals ar

226 Thus, our results argue against the idea that the Dorsal gradient works as

227 ther with other recent findings, our results argue against the importance of auxin asymmetry in estab

228 and studies with an organic reductant (TDAE) argue against the intermediacy of organozinc reagents.

229 sensitization and triplet quenching studies argue against the involvement of a triplet excited state

230 These results argue against the involvement of HIF1alpha in promoting

231 These results argue against the long-standing, untested hypothesis tha

232 Together, our results strongly argue against the nodal localization of OMgp and its pro

233 While our results argue against the notion of a single common origin for a

234 s a modest positive role in adipogenesis and argue against the potential of GPAT inhibitors to rescue

235 Such differences in induction mechanisms argue against the prevailing paradigm that all IE genes

236 yrenoids during episodes of high [CO(2)] all argue against the previously proposed relationship betwe

237 Together, these data argue against the previously reported role of increased

238 These findings appear to argue against the recently proposed role of VGLUT3 in C-

239 rences and the dynamics of competing species argue against the simple use of single functional traits

240 n defining drought in ecological studies, we argue against the uncritical use of a standardized droug

241 n defining drought in ecological studies, we argue against the uncritical use of a standardized droug

242 ical and computational results of this study argue against the use of rigidity assumptions in extract

243 25(OH)D or 25(OH)D metabolites with T2D and argue against the use of vitamin D supplementation for t

244 Liu and Edwards argue against the use of weighted statistical binning wi

245 are consistent with some recent reports, but argue against the widely held belief that NGN3 marks cel

246 levant during allergic lung inflammation and argue against the widely held view that Gal6S is critica

247 ed on the use of this method, a recent study argued against the existence of a fixed VLA value for a

248 Contrary to previous assessments, our data argued against the idea that decisions rely on mutual in

249 However, previous studies have argued against the perception of such structures in musi

250 AAG has only a single DNA binding site, this argues against the bridging model for intersegmental tra

251 cence immediately before SLB patch formation argues against the existence of a critical vesicle densi

252 This evidence argues against the hypothesis that epileptiform activity

253 mplete inhibition of SPT activity, this work argues against the idea that ORMDL3 pathophysiology coul

254 as a consequence of cellular differentiation argues against the idea that they are solely waste produ

255 ation of enantiomeric purity, a finding that argues against the involvement of oxyallyl cation interm

256 The reduced glucose uptake argues against the neuromuscular compensation hypothesis

257 , stability, or membrane interactions, which argues against the notion that myelin TJs exhibit signif

258 The absence of significant linkage argues against the presence of a major gene coding for b

259 guanylate into RNA products, which strongly argues against the previously proposed template-dependen

260 Collin argues against the proposal, saying that it would shift

261 This strongly argues against the proposed identification with the N2pc

262 ticipants as compared with younger HC, which argues against the specificity of this finding in AD.

263 al structure, of the interrupting sound, and argues against the view that the illusion arises in the

264 tion of schizophrenia and BD, a finding that argues against the view that these disorders are entirel

265 ariations in environmental selection forces, arguing against the assumption that cancer cells can evo

266 nor punishment benefitted memory retention, arguing against the common assumption that reward ubiqui

267 TF-binding signals in a quantitative manner, arguing against the conventional on-and-off model of TF

268 alter the fission-pore conductance Gp, thus arguing against the force-generating role of actin polym

269 pporting the latter view of OFC function and arguing against the former.

270 mulation of all detectable Ub-Ub topologies, arguing against the hypothesis that any particular Ub li

271 ially reduced in the anesthetized condition, arguing against the hypothesis that loss of long-distanc

272 oplastic transformation of proximal tubules, arguing against the idea that HIF2alpha activation is cr

273 duce inflammatory pain and neuropathic pain, arguing against the importance of morphologic activation

274 ing those with primers terminating with GCV, arguing against the mutations increasing excision of the

275 y associated with a higher incidence of IIH, arguing against the need for women with IIH to discontin

276 eurons subpopulations in the aging mouse OB, arguing against the notion of an age-dependent widesprea

277 pothesis of prion diseases in its pure form, arguing against the notion that nonproteinaceous cofacto

278 ignificantly cocluster in the cell membrane, arguing against the possibility that CD37 regulates beta

279 nucleus regardless of their editing status, arguing against the role of editing in nuclear retention

280 with carbon chain lengths between 4 and 12, arguing against the simple reversal of fatty acid beta-o

281 erall interaction with the anticodon region, arguing against the sufficiency of this interaction for

282 ot appear to have a prognostic significance, arguing against the utility of immunohistochemical subty

283 ndent samples of patients with psychosis and argue against their progression in patients.

284 treated animals compared to control animals, arguing against their contribution to the viral effects

285 ctional in the absence of phosphoinositides, arguing against their proposed obligatory role in channe

286 Moreover, yeast pulse-labeling experiments argue against there being a static population of ER-asso

287 Recent analyses argue against this simple model.

288 We argue against this, as the performance of NetDis was not

289 whereas intratumoral necrosis and large size argued against this diagnosis.

290 Arguing against this hypothesis, we found that JAG1 and

291 Arguing against this model in the accompanying paper by

292 id leukemia and acute promyelocytic leukemia arguing against this strategy.

293 icient for C. elegans embryonic development, arguing against tissue-specific specialized ribosomes in

294 ylogenetically matched, nonresistant species argues against tolerance to disruption of genome structu

295 The results argue against tonotopic separation per se as a neural co

296 ition of PrP(Sc) in genetic and sporadic CJD argues against uniform mechanisms of propagation of PrP(

297 liberate memory reflect dissociable systems, arguing against unitary accounts.

298 Our findings argue against using IKK2 inhibitors in chronic GN and pe

299 not more common in the monotypic sequences, arguing against viral replication during times with lowe

300 a higher risk for food allergy and therefore argues against vitamin D supplement to protect against a