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 Our data argue against 2C4 as a universal heterodimerization bloc

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

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

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

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

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

12 Although the data thus argue against a direct role of Pol zeta in SHM, Pol zeta

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

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

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

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

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

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

21 These data argue against a model in which multiple NTPs are lined u

22 sport, which seems likely, these conclusions argue against a model in which precursor movement throug

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

24 The burst properties argue against a physical association with our Galaxy or

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

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

27 These data argue against a primary and critical role of ENaC in thi

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

29 These observations argue against a prominent role for Src kinases in persis

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

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 of the increased prevalence of obesity would argue against a purely genetic etiology.

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

36 The data argue against a role for mast cells in the mechanism und

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

40 CH(3))(OAr)/k(CD(3))(OAr) = 4.3(3)] strongly argue against a simple insertion mechanism and in favor

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

42 These biophysical differences argue against a unified mechanism of translesion DNA syn

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

44 disease risk of CRP genotypes and CRP levels argues against a causal association of CRP with coronary

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 neic and T cell-deficient pregnancies, which argues against a failure to establish immunological tole

52 ough the cortical lymphatic endothelium, and argues against a functional role for S1P chemotaxis in B

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

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

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

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

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

58 he small fraction of salt-bearing particles, argues against a situation in which a near-surface geyse

59 information in most object-selective regions argues against a strict physical separation of processin

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

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

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

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

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

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

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

67 to human CMV Ags were unchanged, altogether arguing against a defective control of latent EBV infect

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

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

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

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

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

73 pecific roles in gene-expression regulation, arguing against a generic general-stress function.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 Control experiments argued against accounts in terms of possible auditory gr

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

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

96 Taken together, our results argue against an evolutionarily conserved role for Bcl-2

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

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

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

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

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

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

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

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

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

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

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

108 This commentary argues against any claim of discontinuity between humans

109 These findings argue against ARH and beta-arrestin binding to a site up

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

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

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

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

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

115 Atg5-/- cells that are autophagy-deficient, arguing against compensation for the loss of protection

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 These results argue against conventional rate- or synchrony-based code

119 Our data argue against cytoskeletal or endocytic involvement and

120 Our findings argue against DBH -1021C-->T as a risk factor or age at

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

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

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

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

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 Acquired mass spectrometric data argues against formation of oligomers.

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

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

131 We argue against generically equating chromatin and epigene

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

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

134 This argues against haploinsufficiency as a disease mechanism

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

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

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

138 -2 and low caspase 3 and cytochrome c levels argue against increased apoptosis in this disease.

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

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

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

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

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

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

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

146 d insertions at blunt or 5' overhang breaks, argues against LigD being the catalyst of deletion forma

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

148 These results argue against low-level reorganization of the visual sys

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

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

151 These data and computed reaction barriers argue against mechanisms in which the haloarene reacts w

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

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

154 eg cells in the presence of the self-peptide argues against models that postulate selective survival

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

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

157 ggers disassembly, but not membrane fission, arguing against models in which fission is mediated by c

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

159 autoantigen respond during autoimmunity and argue against more than limited plasticity between Treg

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

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

162 ized the fallacy of surrogate end points and argue against nephroprotective effects of dual RAS block

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

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

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

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

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

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

169 These results argue against overproduction of Abeta42 as an essential

170 ockdown of Fbxo7 does not affect PI31 levels arguing against PI31 being a substrate for SCF(Fbxo7).

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 These findings argue against preattentive processing of biological moti

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

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

177 These findings argue against prolonged monitoring of detectable postpro

178 These results argue against recent reports suggesting that mismatched

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

180 This argues against recycling models and in favor of pulling

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

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

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

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

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

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

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

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

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

190 cent sarcomeres are directly in balance, and argue against sarcomere models with springlike elements

191 dently of obesity and insulin resistance and argues against SCD1 inhibition as a safe therapeutic tar

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

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

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

197 Our results argue against status quo therapeutic strategies that tar

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

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

200 Our findings argue against such a possibility and rather suggest that

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

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

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

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

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

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

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

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

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

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

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

212 cts the cSMAC as a whole, then our data also argue against the cSMAC as being required for proximal T

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

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

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

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

217 Results argue against the generally assumed roles of the differe

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

219 Taken together, these data argue against the hypothesis that T(EM) fail to induce G

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

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

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

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

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

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

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

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

228 These results argue against the involvement of HIF1alpha in promoting

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

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

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

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

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

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

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

236 These findings argue against the simple notion that conceptual developm

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

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

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

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

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

242 A subsequent eye movement study argued against the alternative explanation that activati

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

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

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

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

247 This evidence argues against the hypothesis that epileptiform activity

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

249 eases in the reactivity of N-domain residues argues against the idea that the colicin B polypeptide t

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

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

252 The reduced glucose uptake argues against the neuromuscular compensation hypothesis

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

254 the wild-type BCKDC activity, which directly argues against the obligatory communication between acti

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

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

257 This strongly argues against the proposed identification with the N2pc

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

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

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

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

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

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

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

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

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

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

268 ntestinal growth in V. cholerae cpx mutants, arguing against the idea that this pathway promotes V. c

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

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

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

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

273 ASNS gene required the entire CHOP protein, arguing against the possibility of simple sequestration

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

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

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

277 are maintained (and even extended) in ErbB2, arguing against the suggestion that ErbB2 lacks autoinhi

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

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

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

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

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

283 intersister and interhomolog joint molecules argue against these phenotypes being explained by an inc

284 Recent analyses argue against this simple model.

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

286 perimental results found in different groups argue against this.

287 owever, several genetic knockout models have argued against this developmental role for RGCs.

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

289 Arguing against this hypothesis, we found that JAG1 and

290 Arguing against this model in the accompanying paper by

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

292 These results strongly argue against tightly bound bicarbonate ions in the OEC.

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

294 ype matched living-related renal transplants argues against tolerance to organs based on fetal-matern

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

296 Our findings argue against TRPML3 being a component of the hair-cell

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

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

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

300 It argues against ZnT8 autoimmunity arising from molecular