ライフサイエンスコーパス: why

1 We seek to provide context as to why a broad indication was given for NS5A inhibitor-expe

2 , larger-scale features of ribosomes-such as why a few ribosomal RNA molecules dominate the mass and

3 data may inform clinicians in understanding why a prescribed inhaler is not effective and to devise

4 It was unclear why a sensor for facilitation would be present at these

5 Here, we describe why a shared approach to treatment decision-making for a

6 We propose two alternative hypotheses for why a system decreases the distance from the critical po

7 This versatility may explain why a variety of organisms have extensively explored the

8 bitter in bacterial chromosomes, explaining why actively transcribed genes are always co-oriented wi

9 This finding may help explain why adaptive radiation is common on oceanic archipelagoe

10 Further inquiry into why advanced perioperative care did not reduce cardiac c

11 ts provide novel mechanistic arguments as to why AES may exert context-specific beneficial or adverse

12 this work, we explore the underlying reasons why Ag(tpa)OTf (tpa = tris(pyridylmethyl)amine) prefers

13 mate search, and provides an explanation for why Allee effects are often observed in anthropogenicall

14 We also examine why and for whom selfishness and otherishness have conse

15 n societies is the key ingredient to explain why and how multiculturality emerges and thrives in our

16 Here, we specifically discuss why and to what extent we agree with Burkart et al. abou

17 This difference explains why antibodies are effective against glioblastoma but ge

18 What is less clear is why antipsychotics have a therapeutic latency of weeks.

19 It remains unclear why apoE3 and apoE4 are functionally different.

20 The mechanism explains why apoE3 differs from apoE4 with respect to different l

21 and visual syllables in the McGurk stimulus, why are they integrated; and second, why does the McGurk

22 beneficial for some forms of chemotaxis, but why asymmetric shape is so prevalent when a symmetric sh

23 It is unclear why atmospheric oxygen remained trapped at low levels fo

24 Such analyses largely leave out how and why ATP, NADH, and acetyl-CoA (Figure 1 ) at the molecul

25 epatic CSCs and provide an explanation as to why autophagy is required to promote hepatocarcinogenesi

26 Such subsets likely explain why B cell depletion can either ameliorate or exacerbate

27 Bcat with BCl3 as an activating agent showed why BCl3, in contrast to ClBcat, failed to mediate the c

28 istant SMO mutations at baseline, explaining why BCNS-BCCs lack intrinsic resistance to SMO inhibitor

29 near-infrared (NIR) reflectance, explaining why both modeled and observed EVI, which is especially s

30 by their high toxicity might help to explain why calling has not yet disappeared, and that visual com

31 292, 296, 299, 302, and 303), which explains why CaM binds two molecules of ER-alpha in a 1:2 complex

32 Here we investigate why cancer cells do not satisfy their metabolic demands

33 produces aversive effects that might explain why cannabinoid is not rewarding in rodents and might al

34 iates p27 and substrate affinity, explaining why Cdk-Spy1 is poorly inhibited by p27 and lacks specif

35 Why cells store FAs in LDs during an energy crisis is un

36 y of tandem repeats, yet it is still unclear why cells utilize this unusual gene structure.

37 g ALS.SIGNIFICANCE STATEMENT It is not known why certain classes of neurons preferentially die in dif

38 Specifically, a syndemics approach examines why certain diseases cluster (ie, multiple diseases affe

39 In particular, why certain electroencephalographic (EEG) rhythms are li

40 in this review, we outline the rationale of why certain features of depression including its environ

41 This likely explains why certain neurodevelopmental disorders are characteriz

42 Why certain stimuli trigger ferroptosis instead of anoth

43 ods of historical metal threads, and explain why chemical information has to be connected to 3D textu

44 Recognizing why chronic stress causes only a subset of individuals t

45 in percept in the human brain and illustrate why ciguatera sufferers often report a perceptual temper

46 imate relationships vary geographically, and why climate is more important in some regions than in ot

47 Greater knowledge of why CMV infection usually fails may provide insight into

48 aken together these findings help to explain why CNS neurons die after axotomy, strongly suggest that

49 Taken together, our data may explain why colonization of superantigen-producing S. aureus can

50 highly amenable to intervention and explains why combining economic empowerment of women and gender e

51 miconductors and is also used to demonstrate why common textbook approaches fail in describing this i

52 fits, thus helping to resolve the paradox of why cooperative breeding evolves in such different types

53 We then used this decomposition to explain why covariation of correlations with firing rate-a relat

54 autophagy in intestinal defense and suggest why Crohn's disease is associated with genetic mutations

55 ere will advance the field and shed light on why defence traits shift so dramatically across plant on

56 bacteria over mammalian cells, and finally, why development of resistance to AMPs is less prevalent

57 ers rapidly progress to sepsis and death, or why diabetes confers increased susceptibility.

58 Why did evolution do it this way?

59 fundamental questions in the field of LTP is why different molecules are critical for long-lasting fo

60 The model was also able to explain why different multisensory products are often observed i

61 Here, we explore why different studies yield different answers and discus

62 e surfaces and light-permeable materials and why discrepancies arise between the perception and physi

63 Explaining why DLK inhibition is only partially protective, we iden

64 (ii) Why do CSU patients show elevated levels of CRP?

65 Why do distantly related mammals like sheep, giant panda

66 Why do experimenters give subjects short breaks in long

67 Why do people distrust others in social exchange?

68 We asked why do populations with no known history of pesticide ex

69 a paradox - if discrimination is effective, why do uncooperative symbionts persist?

70 Why do we go to sleep late and struggle to wake up on ti

71 Why do we make hasty decisions for short-term gain?

72 Why does the brain discard so much visual information?

73 imulus, why are they integrated; and second, why does the McGurk effect not occur for other, very sim

74 ond conservation of natural systems, how and why does this matter?

75 s in nucleotide loss or addition, explaining why DSBs repaired by NHEJ are rarely restored to their o

76 However, it is unclear why dynein-1 moves poorly on its own or how it is activa

77 a basis for future work aiming to understand why dysfunction develops.

78 y13K CBMs provides a molecular rationale for why E. rectale is able to only use certain starch types

79 Results herein offer an explanation as to why EGFR inhibitors failed TNBC patients and support how

80 le supplement, we discuss the following: (1) Why estimate the worldwide burden of GBS disease?

81 data that could further our understanding of why ethnic minority populations are lagging behind.

82 ects and may thus provide an explanation for why extinctions due to Allee effects are rare in social

83 ed with regards to human use and may explain why fatigue, headaches and nervousness have been reporte

84 Computation explains why Fe2+ can be a more potent cofactor than Mg2+ in a va

85 role for RANK in lung cancer and may explain why female sex hormones accelerate lung cancer developme

86 Why females of some species cease ovulation prior to the

87 Our data may add to understanding why Gata6 is a frequent target of amplification in cance

88 Here, we consider reasons why germ plasm might be neither a direct target of selec

89 ted analogs by GDH in the L cell may explain why GLP-1 secretion, but not that of insulin, is activat

90 Herewith, we propose a concept to elucidate why GS individuals encounter lower inflammation, and are

91 rising variability in outcomes helps explain why Hamiltonella infection frequencies are often interme

92 e public health laboratories' perspective on why having access to isolates of enteric pathogens is es

93 It is not understood why healthy tissues can exhibit varying levels of sensit

94 These data may explain why hereditary neuropathies associated with decreased la

95 text] have significant mobility, explaining why high-resolution spectra are observed, but motion is

96 later stages of fermentation, which explains why higher amylolytic activity prolonged the productive

97 However, it is not fully understood how and why hippocampal patterns become separated.

98 es critical mechanistic insight into how and why hippocampal representations become separated.

99 an additional perspective to the paradox of why Homo sapiens, particularly agriculturalists, appear

100 Our results provide mechanistic insight into why human neoplastic translocation fragile DNA sequences

101 nd social settings, this finding can explain why humans and animals so commonly behave according to t

102 Many of the hypotheses concerning how and why hybridization contributes to biological diversity cu

103 ical rather than socio-environmental reasons why hyperactivity and anxiety disorders occur at higher

104 testimony, with an eye toward understanding why identification errors occur and what can be done to

105 6 inhibitors develop new onset psoriasis and why IL-6 blockade for the treatment of psoriasis has not

106 Conversely, the reason why, in continental domains, co-seismic slip along fault

107 This is one reason why individuals with FXS tend to avoid social interactio

108 ity is modulated by ultraviolet irradiation, why individuals with red hair are more prone to developi

109 pathogenesis of SIV/HIV and begin to explain why infants are more prone to rapid disease progression.

110 To understand why introduction of a single CH3 group in five-position

111 A fundamental question remains: Why is airway tolerance compromised in patients with all

112 How they selectively activate effectors and why is KRas4B the most prevalent are highly significant

113 (2) Why is there so much variation in reactive aggression/vi

114 But why is this the case?

115 cts of large-scale forest mortality, such as why it can occur throughout the range of a species and y

116 ly dispersed organization, which may explain why it does not trigger X chromosome inactivation at thi

117 rmediate levels of the architecture and show why it does so.

118 wide dynamic-range dorsal horn neurons, and why it may not be effective in all migraine patients.SIG

119 In remembering the Society, one may well ask why its auspicious beginning should have led to this ign

120 This explains why JAK2V617F is associated with polycythemia vera, esse

121 To explain why klotho preferentially targets lipid rafts we show th

122 We also present reasons why KO(t)Bu is an active catalyst whereas sodium tert-bu

123 Understanding how and why language subsystems differ in their evolutionary dyn

124 This study explored why lesioned retinal ganglion cell (RGC) axons regenerat

125 ct to different lipid-binding specificities, why lipid increases the binding of apoE to its receptor,

126 The underlying mechanisms, of why LOH rates increase with age, are not well understood

127 orphism in cerebral hemodynamics may explain why males are more vulnerable to perinatal brain injurie

128 tween kinase functions, and speculates as to why mammalian germ cells require expression of three AUR

129 l growth, our results may help to understand why mammalian neurons do not regenerate after injury.

130 ow signal amplification, it is not yet clear why many systems use more than one coupling protein.

131 To determine why MerTK is critical to RPE function, we examined visua

132 Evolutionary theory explains why metazoan species are largely protected against the n

133 ied extensively, it remains an open question why microvessels need to be so narrow.

134 Miz-1 contains 13 ZFs, but it is unknown why Miz-1 has so many ZFs and whether they recognize and

135 g working memory, raising the question as to why mnemonic encoding is observed during some, but not a

136 These insights may explain why modeled viral fusion occurs preferentially near the

137 These findings help explain why modes of symbiont transmission and reproduction are

138 ationic, amphipathic AMPs, which may explain why most AMPs require micromolar concentrations for acti

139 To better understand whether and why MT assembly is required for bulk translocation, we d

140 a provide a mechanistic framework to explain why multiple CMV exposures are typically required before

141 titute a first step to understanding how and why music literally moves us.

142 ffer an additional perspective as to how and why nanoparticles differ from their bulk counterparts.

143 structural modelling do not readily explain why NasA, NarK1 and NarK2, as well as other transporters

144 neuronal action potential threshold explains why NaV1.9 mutations that evoke small degrees of membran

145 This explains why net erosion has occurred in some areas of the subaqu

146 ly measured values of ring tension, explains why nodes move bidirectionally, and shows that tension i

147 un to establish its interactions, explaining why Nun acts on paused TECs.

148 death and disability, and it remains unclear why, of all body organs, the brain is most sensitive to

149 date there is no complete explanation as to why one out of two people systematically receives more m

150 However, it is not yet understood why only a few materials can deliver exceptionally highe

151 increase susceptibility to IA, could explain why only certain patients develop the disease.

152 Our findings may explain why osteogenesis imperfecta-causing mutations in both ge

153 The ability to understand why others feel the way they do is critical to human rel

154 paschenko et al was not used, and we explain why our uncertainty assessment is complete and how it wa

155 To explain why parasite clearance rates were not faster with split

156 actions, providing one possible explanation why Parkin may be a tumor suppressor gene.

157 Altogether, these factors could not explain why participants from Russia had higher CVD mortality wh

158 ranscription factors, questions remain as to why particular genes are susceptible to age-related tran

159 in healthcare settings to better understand why patients choose healthy or unhealthy behaviors.

160 reclinical findings may provide insight into why patients with arthritis being treated with IL-6 inhi

161 care; therefore, if we can better understand why patients with HF make the choices they do, then we m

162 These differences may explain why pediatric cancer patients have a higher risk of deve

163 ngly, such sampling innately determines also why photoreceptors extract more information, and more ec

164 also tend to be "buried" inside, explaining why polyQ domains are insoluble on their own.

165 ses-containing roots provides an explanation why pressure generation in single roots is considerably

166 t deficits in this ability may be the reason why preterm infants experience altered developmental tra

167 Efforts must be made to understand why primary nonadherence occurs, identify patients prone

168 oss primate species, very few have addressed why primates vary in how much they use social learning.

169 Therefore, this commentary can show why prosocial behaviors are biased toward physically att

170 These studies explain why pyridylhydrazines are poorly reactive in Fischer ind

171 We discuss why quantitative metabolic profiling is becoming widespr

172 though additional work is needed to identify why question asking was unaffected and establish its imp

173 and then to double-strand breaks-explaining why R-tracts do not accumulate in RNase H-deficient cell

174 trate flux becomes rate-limiting, explaining why reaction rates in vivo can be independent on enzyme

175 This explains why recent experiments that attempt to ablate putative P

176 adigm shift in our collective thinking as to why recombinant Envs are ineffective in eliciting bNAbs

177 We discuss how and why relevant neuropsychological studies should be carrie

178 Why remyelination fails or succeeds in multiple sclerosi

179 In this commentary, I explore why research on mismatch might be called into question b

180 The data explain why rigid collagen fibrils potentiate PI3K activation to

181 In this article, we ask why scientists should care about data science.

182 ic phosphorus and iron mobilization explains why seagrasses are widely distributed in oligotrophic tr

183 stood, in part because little is known about why sensory neurons innervating muscle appear more capab

184 This is why several new agents, with innovative mechanisms of ac

185 herently complex these findings help explain why sex is maintained in natural populations.

186 s provide a more mechanistic explanation for why sexual selection appears to drive early stages of sp

187 onsistently develops, and in particular, (1) why shamanic traditions exhibit recurrent features aroun

188 es a cultural evolutionary theory to explain why shamanism consistently develops, and in particular,

189 bit recurrent features around the world, (2) why shamanism professionalizes early, often in the absen

190 However, how and why simple non-coded peptides could have become critical

191 first in a Series of two papers, we discuss why slums are unhealthy places with especially high risk

192 It is not clear why so many extracellular domains need to be evolved thr

193 ature of autonomous selfhood, and explaining why social clustering has occurred and been adaptive.

194 damental questions in behavioural biology is why societies can persist for a long period of time.

195 However, why some aortic arches regress while others are incorpor

196 gene expression broadly, it remains unclear why some but not other PRC2 target genes require PRC2 an

197 We suggest that one reason why some clades persist is that species within these cla

198 t vulnerable to these changes and understand why some ecosystems are more sensitive to extremes than

199 nd yet still be locally highly variable, and why some events seem readily attributable to an ongoing

200 There is little understanding of why some exposed individuals have no symptoms, while oth

201 This decoupling may explain why some forms of sexual violence have been largely over

202 acture repair is important for understanding why some fractures fail to heal and for developing novel

203 the removal of less fit cells ('losers') but why some gene mutations turn cells into losers is unclea

204 Why some individuals are socially isolated and others ar

205 Why some individuals develop an acute painful sensory ne

206 al subjects and explains to a certain degree why some individuals exhibit better perceptual abilities

207 mal defects in neurodegeneration, we explore why some of these orphan disease drug candidates are als

208 et, there is no systematic explanation as to why some static images are likely to provoke seizures, w

209 hange, and there is a poor understanding for why some taxa are more sensitive to climate than others.

210 The atlas demonstrates why some widely used auxin herbicides are not, or are ve

211 It is not well understood why some, but not other, individuals with hepatic steato

212 ses the binding of apoE to its receptor, and why specific residues are conserved.

213 -specific antibodies protect against RSV and why specifically targeting prefusion F could have great

214 and endoplasmic reticulum stress, explaining why SRp55 depletion triggers beta-cell apoptosis.

215 These results explain why stalk formation in Dictyostelia always initiates at

216 from cold roots to warm canopy and explained why starch levels surged in canopies of orchard trees du

217 ty to standardize sugar colourants explained why starch results from these methods could not be mathe

218 Our results shed light on why states of altered basal ganglia activity disrupt bot

219 y in cells and provide a new explanation for why stressed cells accumulate osmolytes.

220 These results highlight the paradox of why substantial variation is observed in only a subset o

221 However, why such biases develop is not known.

222 Still, it is unclear why such complex scenes appear to be the same from momen

223 T-domain of colicin N (ColN-T) to understand why such domains are widespread in toxins that target Gr

224 of glioblastoma (GBM) and it remains unclear why such independent amplification events, and associate

225 Why such learning is so persistent is poorly understood

226 An enduring question has been why such sequences are deleterious.

227 Here we show how and why sunlight exposure impacts microbial respiration of D

228 intracellular location of CD24; they explain why surCD24(-) cells can remain aggressive, and they hig

229 esented here gives mechanistic insight as to why surgery may be unsuccessful in some patients.

230 provides a plausible general explanation for why swimming cells tend to have strong asymmetries in ce

231 n by conserved mechanisms, which may explain why T-cell-based immunotherapy can provide durable benef

232 This may explain why TBI patients are more vulnerable to cognitive dysfun

233 y (DFDMFT) scheme to comprehensively explain why tetragonal FeS shows both semiconducting and metalli

234 iggers of the alpha-synuclein misfolding and why the aggregates escape cellular degradation under dis

235 A long-standing puzzle has been why the AU dincucleotide at the 5'-end of the U1 snRNA i

236 so provide a structural interpretation as to why the AU dinucleotide is conserved during evolution.

237 A long-standing puzzle remains unsolved: why the Au surfaces with {100} sub-facets were exception

238 ghbourhood effects also help explain how and why the benefits of interventions vary between slum and

239 TRAF6[L74H] and wild-type cells, explaining why the bone structure and teeth of the TRAF6[L74H] mice

240 l understanding and risk analysis, including why the central pressure better explains historical econ

241 providing mechanistic insight and explaining why the chirality of the catalyst is able to define the

242 These divergent mechanisms explain why the combination of maternal obesity and offspring ob

243 It is unknown why the CSF3R mutations, which are rare in de novo AML,

244 We describe why the cyclic heteropolyanion [P8W48O184](40-) (abbrevi

245 Finally, we show why the described mechanisms are relevant not only in hy

246 rshed scale could persist for centuries, and why the disruption of this self-organizing system by the

247 for microvascular flows and may help explain why the effects of physiological RBC aggregation are not

248 ractices on both sides of the Atlantic about why the emphasis needs to shift from providing a large v

249 We address why the epidemic did not spread into neighbouring countr

250 at explains the Meyer-Overton hypothesis, or why the lipophilicity of an anesthetic and its potency a

251 These impressive numbers illustrate why the making and breaking of RBCs is at the heart of i

252 This commentary explains why the meta-analytic approach, frequently used by other

253 I discuss why the paper was influential and how the premise of thi

254 ill be context dependent and so help explain why the pattern of bias is sometimes variable.

255 We investigated several hypotheses for why the phenotype may be absent, with the aim of re-esta

256 te change and land use changes could explain why the predicted enriching effects from climate warming

257 To understand why the program has been less effective than expected, t

258 Understanding why the quit rate among smokers of menthol cigarettes is

259 A further discussion is performed concerning why the re-emitted radiation is not detected in the expe

260 ibosomal RNA molecules dominate the mass and why the ribosomal protein content is divided into 55-80

261 The reason why the same catalyst can act in either the two- or four

262 and balanced resource allocation, we explain why the total cell size is the sum of all unit cells.

263 electron-density redistribution and pinpoint why the TS for guanosine 5'-triphosphate (GTP) hydrolysi

264 e features nor functions, may partly explain why the two cell lines differ in translational compensat

265 Wen and co-authors discuss why the United States needs Medicaid to address its epid

266 n criteria for reference maps, which clarify why the work of Schepaschenko et al was not used, and we

267 he metagenomic assembly, which could explain why their genomes have not been identified before.

268 More work is needed to understand why there was no clinical benefit when a difference in v

269 eat conditions and when, where, to whom, and why these encounters occur.

270 t on the beta57 polymorphism, accounting for why these peptides bind much better to these MHCIIs.

271 ndancy of CspC and CspE that likely explains why these proteins have evaded selection in previous vir

272 ti-TH2 biologics, we propose a rationale for why they are particularly successful in controlling asth

273 y the Rag GTPases, providing a rationale for why they exist as a dimer and revealing a distinct mode

274 This explained why they overwhelmingly preferred the under-vacuum conce

275 ear what gives rise to those limitations and why they result in an experience of control as costly.

276 are formed by the MALDI process, explaining why they were not observed with ESI.

277 features along specific axes, which explains why they were previously found to respond to apparently

278 acrophages, providing a potential clue as to why this bacterium is normally tolerated by the immune s

279 However, why this blocks fibrosis remains unknown.

280 these organisms, and discusses reasons as to why this group of sRNAs has diverged in their genetic or

281 How or why this intralumenal fragment forms during fusion, howe

282 activation results in PSD-95 degradation and why this is defective in Fmr1 KO neurons is unknown.

283 ussian white-noise stimuli, and we explicate why this is so.

284 positive cells, providing an explanation for why this microRNA is targeted in HPV-positive cells.IMPO

285 ant and comparable between labs, and outline why this process is essential before the cells are intro

286 At the moment, we fail to understand why this takes so long and how the immune system selects

287 ranial origin such as migraine with aura and why this therapeutic approach may not be effective for e

288 These findings might help to explain why TNF blockade improves lung function in only some pat

289 Our objectives were to describe why traditional and nontraditional (exposomic) biomonito

290 pted by genetic alterations in cancer cells, why transcriptional dependencies can develop as a conseq

291 roblem in infection biology is understanding why two individuals exposed to identical infections have

292 ential underlying mechanism that may explain why variability quenching occurs.

293 gence and modular cognitive adaptations, and why we believe that the distinction between primary and

294 to represent and communicate the reasons for why we hold certain beliefs about the past.

295 t might achieve better outcomes, and explain why we need open and international discussions concernin

296 Here, we aim to provide reasons as to why we still need BMS in our cardiac catheterization lab

297 We identify three possible reasons why wild population studies may generally fail to find s

298 We seek to understand the specific reasons why XCMS and MZmine 2 find the false positive EIC peaks

299 stness of our chronology and explore reasons why Zhang and Li's OSL age is a gross overestimation of

300 aly has been established, it remains unclear why ZIKV, but not other pathogenic flaviviruses, causes