ライフサイエンスコーパス: explain why

1 Identity-based motivation theory explains why.

2 complexes [1]PF(6)-[5]PF(6) was performed to explain why [4]PF(6) and [5]PF(6) are photochemically in

3 These countervailing selective pressures may explain why a breadth of sizes exist and even coexist wh

4 Here we explain why a switch to permanent DST could negate any b

5 This versatility may explain why a variety of organisms have extensively expl

6 ersely correlated to alpha(2) in LQT2, which explains why a short-long combination causes a larger AP

7 These new interactions suggest a mechanism explaining why A3G exhibits a 3' to 5' directional prefe

8 mbryonic origin, have latent skin competence explaining why aberrant hair follicles or sebaceous glan

9 especially bitter in bacterial chromosomes, explaining why actively transcribed genes are always co-

10 This finding may help explain why adaptive radiation is common on oceanic arch

11 product distribution using capsule I, and we explain why additional stable monoterpenes, like camphen

12 ydrophobic residues near acidic side chains, explaining why ADs often have a biased amino acid compos

13 success and this energetic constraint might explain why airspeeds are not maximised in the pre-breed

14 This work may also help explain why ALL cells are most sensitive to l-asparagina

15 nder strong tonic inhibition at low glucose, explaining why alpha-cells are electrically active under

16 for growth than previously assumed, helping explain why alternative nitrogenase genes persist in div

17 oposed as a cartoonish thought experiment to explain why altruism can be a selfish strategy from the

18 To explain why an action is wrong, we sometimes say, "What

19 of modern societies is the key ingredient to explain why and how multiculturality emerges and thrives

20 location of protein resources quantitatively explains why and how the cell makes the choice.

21 Baird's rule explains why and when excited-state proton transfer (ESP

22 The model has difficulty explaining why animals driven by cues fare better than a

23 This difference explains why antibodies are effective against glioblasto

24 s of anticipation of both reward and threat, explaining why anxious individuals show stronger potenti

25 onocyte-derived cells, their existence could explain why APC functions have been attributed to MCs.

26 The mechanism explains why apoE3 differs from apoE4 with respect to di

27 e co-enriched with non-bHLH motifs, possibly explaining why Ascl1 is less context dependent.

28 nzyme less sensitive to feedback inhibition, explaining why assembly occurs under physiological condi

29 Such subsets likely explain why B cell depletion can either ameliorate or ex

30 e handover in Swedish health care, and might explain why bedside handover is still not very common in

31 Our results help to explain why beta(2) -m and RBP4 are more sensitive marke

32 s in the Gulf of Finland in spring, possibly explaining why bottom waters in this highly eutrophic re

33 trointestinal disturbances, our results help explain why C. difficile is frequently detected as a co-

34 progressed much more slowly, a state of play explaining why C-H (18) F-fluorination is still in its i

35 nferred by their high toxicity might help to explain why calling has not yet disappeared, and that vi

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

37 neurons produces aversive effects that might explain why cannabinoid is not rewarding in rodents and

38 fyve to stimulate its lipid kinase activity, explaining why catalytically active Fig4 is required for

39 te that mediates p27 and substrate affinity, explaining why Cdk-Spy1 is poorly inhibited by p27 and l

40 he reliance of RDH expression on CDK11 could explain why CDK11 is essential for the growth of many ca

41 r but can run autonomously of it-potentially explaining why centrioles can duplicate independently of

42 nvergent evolutionary route, however, cannot explain why cephalopods developed large brains and flexi

43 No molecular property was known explaining why certain molecules would align very effect

44 This likely explains why certain neurodevelopmental disorders are ch

45 ble ice-bathymetry configurations, which may explain why changes in the density structure of the wate

46 by generalizing Marcus theory framework, we explain why charge-transfer-dynamic modulations can only

47 This selectivity readily explains why chromosomal folding and insulation of topol

48 motivation in chronic back pain, which helps explaining why chronic pain can be resistant to change,

49 These data may help explain why circuits with aggressive tau pathology (e.g.

50 g access of DNA to the RNAP active site, and explain why clamp opening is required to allow entry of

51 d, and, together with the other results, may explain why clinical effect is lost if SLIT is discontin

52 Taken together these findings help to explain why CNS neurons die after axotomy, strongly sugg

53 Taken together, our data may explain why colonization of superantigen-producing S. au

54 is on the Industrial Revolution, it may help explain why complexity and innovation increase rapidly i

55 ession of SARS-CoV-2 receptors in mice helps explain why COVID-19 lung disease is greater in the elde

56 Our results help explain why critical masses are required to initiate soc

57 notube nucleation during CVD and potentially explains why CVD-synthesized BNNTs are frequently observ

58 hermodynamic analysis of the PagP barrel may explain why cysteine, despite possessing a polar sulfhyd

59 This may explain why DCs respond faster and more vigorously to TL

60 This may explain why defects in a single component often produce

61 omponent network of gamma(c) cytokines; this explains why deficiencies of single components have litt

62 Second, I explain why desire provides better-integrated explanatio

63 tonation of Asp favors the DFG-out state and explain why DFG flip is also possible in simulations wit

64 The model was also able to explain why different multisensory products are often ob

65 DFT calculations were employed to explain why different structural sequence were obtained

66 Explaining why DLK inhibition is only partially protecti

67 Such functionality plausibly explains why DNA methylation, a well-known mutagen, has

68 ine receptor occupation in the striatum, and explains why dopamine ramps are an effective signal to o

69 eviews the results of the COMPASS trial, (2) explains why dual pathway inhibition is superior to anti

70 to the spindle machinery before segregation, explaining why early embryonic cell cycles are so error-

71 Can the Second Law of Thermodynamics explain why ecosystems naturally organize into a complex

72 This may explain why eliminating HIV susceptibility in circulatin

73 We use canard theory to explain why enlarging the size of the window region elic

74 e, interactive and synergistic relationships explaining why environmental effects may be obscured in

75 Our results help explain why eukaryotic cells possess multiple resection

76 considered with regards to human use and may explain why fatigue, headaches and nervousness have been

77 direct role for RANK in lung cancer and may explain why female sex hormones accelerate lung cancer d

78 This view ostensibly explains why females do not sing-many of the neural popu

79 Our results explain why fibrosis occurs in injured tendons and prese

80 This difference explains why filaments grow faster at the barbed end tha

81 o- and bis-peroxide tricyclic products, also explains why formation of the most stable tris-peroxide

82 Our results explain why FRC networks have small-world properties and

83 The analysis explains why frequent intensive harvesting of coffee is

84 -cyprinol sulfate in lipid digestion in fish explains why from an evolutionary perspective fish has n

85 igins of multicellular hyphal organisms, and explains why fungi, rather than unicellular bacteria, ev

86 resistance to gastrointestinal enzymes might explain why Gal d 7 can act as a potent sensitizing agen

87 This may explain why Giardia trophozoites adhere to the small int

88 We discuss the optimal group size and explain why, given the highly infectious nature of the d

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

90 This shift explains why GLP-1, which signals via Gq, but not GIP, w

91 induce migration in macrophages, potentially explaining why glucocorticoid therapy is less effective

92 atterns of caries presentation may partially explain why groups of tooth surfaces form clusters withi

93 bility than those based on GSK180736A, which explains why GSK180736A-based inhibitors, although being

94 d-coil 1B (CC1B) domain of p150(Glued), thus explaining why H2 is necessary for tight binding.

95 ls of the perceptual-inference hierarchy may explain why hallucinations and delusions tend to cluster

96 heme biosynthetic pathway, our findings help explain why heme biosynthesis depends on intact ISC biog

97 eviously described interactions do not fully explain why heme biosynthesis depends on intact ISC biog

98 Furthermore, our results explain why higher plants have a narrow range of grana d

99 t in the later stages of fermentation, which explains why higher amylolytic activity prolonged the pr

100 the latter will rarely overwhelm the former, explaining why historical earthquakes rarely rupture nea

101 d particles in the neuronal cytoplasm, which explains why HSV virions do not enter axons.

102 The structure helps explain why human tetherin is Nef-resistant and why lent

103 treat each other equally, but he has not yet explained why human morality also allows and enables muc

104 en deprivation in humans and chimpanzees may explain why humans are more prone to certain heart disea

105 Economic theories struggle to explain why humans are so inconsistent.

106 estions by analyzing the model simulation to explain why hypoxia driven signals can have dissimilar i

107 This Treg-preferential effect could explain why idelalisib produces adverse autoimmune effec

108 cording to the cellular context and may help explain why IDH(mut) is only a favorable prognostic mark

109 This view would explain why immunotherapy at best delays progression of

110 The results help explain why in mRNA m(6)A slows down tRNA selection and

111 -apoptotic proteins to MCL-1 and vice versa, explaining why in vivo combinations of BCL-2 and MCL-1 a

112 Most notably, it has trouble explaining why, in slot machine gambling, players are mo

113 These results explain why increasing aspirin dosage or aspirin additio

114 nalogous clinical-radiological paradox could explain why individuals with similar injuries can respon

115 ole-mediated reduction in cytoplasmic pH may explain why indole provides E. coli with a degree of pro

116 in the pathogenesis of SIV/HIV and begin to explain why infants are more prone to rapid disease prog

117 Here, we explain why inherited mutations often have different tis

118 l model on speech memory representations and explain why interfering with beta oscillations in the le

119 eralizable principle in GTPase signaling and explains why intracellular signal transmission is a mult

120 ivity of cells to ISRIB during acute ISR may explain why ISRIB does not cause overt toxic side effect

121 ed epitope that overlaps the NA active site, explaining why it impacts antibody binding.

122 lation of blind multi-channel deconvolution, explaining why it inherently promotes low-rank solutions

123 modification on alpha-synuclein, potentially explaining why it remains understudied.

124 resulting increased flexibility of switch 1 explains why it is not resolved in kirromycin-bound stru

125 To explain why klotho preferentially targets lipid rafts we

126 rgely independent of LAT1 and leucine, which explains why leucine could block brain uptake of kynuren

127 We describe theories explaining why liars would behave differently from truth

128 Needles may be the missing link in explaining why lightning flickers with multiple discharg

129 ble to further metabolic stress, which could explain why local neurodegeneration does not remain conf

130 l ties, and alterations in this map may help explain why lonely individuals endorse statements such a

131 This explains why low pH (<3.5) is a sine qua non condition f

132 erential affinities for the mu and KOR could explain why lower doses of naltrexone can have greater c

133 are favored in arcs with thick crust, which explains why magmatism and differentiation in continenta

134 ss adaptation, and this stress tolerance may explain why many cancers aberrantly express MAGEs Here,

135 Results may explain why many CNVs affect a similar range of neuropsy

136 ion of COP1 and SUMO in these NBs might also explain why many COP1 substrates are sumoylated.

137 unit cyclin T1 than primary cells, which may explain why many LRAs are functional in model systems bu

138 This can explain why many studies observed rare species to suffer

139 ective components of energy consumption, and explain why MCDI is unable to attain the performance of

140 lead to Hg methylation in marine waters and explain why Me(2)Hg is a significant Hg species in ocean

141 This explains why mice lacking the IL-6 receptor only in oste

142 l landscapes of structural glass formers and explains why minimization procedures commonly employed b

143 ng for cationic, amphipathic AMPs, which may explain why most AMPs require micromolar concentrations

144 lation of all PKA holoenzymes and could also explain why most disease mutations in PKA regulatory sub

145 our data provide a mechanistic framework to explain why multiple CMV exposures are typically require

146 The model also explains why mutant forms of the PLC-gamma isozymes foun

147 BMP4 during mammalian development, which may explain why mutations in either Bmp4 or Bmp7 lead to a s

148 e tolerance and increased N requirements may explain why N limitation inhibited adaptation.

149 This may explain why N-Ph and N-Bu imines are not hydrogenated.

150 d within a hydrophobic active-site subpocket explaining why N6-methyl-dATP is a good MTH1 substrate.

151 ysis and structural modelling do not readily explain why NasA, NarK1 and NarK2, as well as other tran

152 le, convincing theories are still lacking to explain why natural evolution and human design have fail

153 This may explain why naturally occurring allergen-specific IgG an

154 This helps explain why newly formed CO(2) produced at step sites de

155 in granule is selected for secretion and may explain why newly synthesized insulin is preferentially

156 difference in nucleosome destabilization may explain why Nhp6A and Hmo1 function at different genomic

157 Hitherto, these factors helped explain why no dance forms were present amongst nonhuman

158 ibition levels at median exposure levels may explain why no relationship between exposure to TTR-bind

159 ry of the concept of empathy within nursing, explain why nurses are sometimes warry of adapting conce

160 ONLR-NPC depletion may help explain why ON diseases such as OAG progress in severity

161 fying distinct AD phenotypes here could help explain why only a subset of AD patients typically respo

162 Therefore, modifying factors that explain why only a subset of kidneys develops nephropath

163 ergy-independent membrane insertion of TMDs, explain why only short lumenal domains are translocated

164 in the kinetics of G protein activation can explain why only some receptors can activate potassium i

165 By tracing their fate, we could explain why only the upper first molar reacts via elonga

166 ive translation initiation (fsATI), that may explain why only TRESK-MT is associated with migraine.

167 binding to the RAPTOR subunit of mTORC1 and explains why only the RagA(GTP)/RagC(GDP) nucleotide sta

168 Our findings may explain why osteogenesis imperfecta-causing mutations in

169 cal constraints on plasmid transfer that can explain why our focal strain failed to acquire some of t

170 of Schepaschenko et al was not used, and we explain why our uncertainty assessment is complete and h

171 rization of the intermediate to a lactol can explain why P450 11B2 must produce aldosterone through a

172 Importantly, it explains why pain is tuned by multiple factors and neces

173 se parasite-induced changes in behaviour may explain why parasitized gobies are poor competitors for

174 cumulation in a Dicer-dependent manner, thus explaining why PARN-defective patients show p53 accumula

175 erior thalamic pathways, these findings help explain why pathology in either the medial diencephalon

176 These data likely explain why patients with PMNs are frequently resistant

177 hibitor of NLRP3 inflammasome activation and explain why patients with XLA are prone to develop Crohn

178 te solids and free chlorine, and it may help explain why PbO(2) is observed on LSLs of some but not a

179 e fundamental challenge in decision science: explaining why people make the decisions they do.

180 Sequence specificity explains why Phactr1/PP1 exhibits orders-of-magnitude en

181 Our findings also provide a solid basis to explain why placental insufficiency is associated with d

182 These results may help to explain why plants and animals have similar responses to

183 g RNAs in exosome-deficient mutants, perhaps explaining why plants have evolved mechanisms to suppres

184 cryoprotectants as well as osmoprotectants, explaining why plants, fish, insects and bacteria accumu

185 Such a local mechanism for CP regulation can explain why plasticity induced by the odorant geranyl ac

186 call for experimental testing but also help explain why polarization in beliefs about human-caused c

187 Divergent protein context helps explain why polyglutamine expansion diseases differ clin

188 but it can be hard to contextualize how and explain why predictions are made.

189 These results may help explain why premenopausal women have lower incidence of

190 nalysis of new X-ray structures of Thal also explains why premixing of FDHs with reduced flavin adeni

191 Our work explains why preuisolactone A has been isolated as a rac

192 Such an architecture explains why primary cilia can elastically withstand liq

193 Our study explains why proteotoxic stress is a universal feature o

194 Our findings explain why QS mutants are frequently isolated from biof

195 RC activation in growth plate cartilage and explain why RC dysfunction can cause short stature in ch

196 A network structure explains why reductionism is not possible for mental ill

197 c agents and bacterial species, it will help explain why resistance to antimicrobial peptides develop

198 ptible strain under EPS inhibitor treatment, explaining why resistance does not evolve.

199 ore intact preparations, (3) demonstrate and explain why riluzole application may fail to effectively

200 Here we propose that Gestalt theory may explain why rodent islet architecture has historically b

201 the rods' competition for glucose, which may explain why rods also provide the RdCVF signal to compen

202 These different functions of rotatin explain why RTTN mutations can lead to heterogeneous cer

203 rease in S-RNase activity by NaTrxh helps to explain why S-RNase alone could be insufficient for poll

204 ovel antithrombotic strategies, this article explains why safer anticoagulants are needed, provides t

205 We speculate that explaining why scenes look as they do may require incorp

206 hizospheric phosphorus and iron mobilization explains why seagrasses are widely distributed in oligot

207 ntaneous fluctuations of neural activity may explain why sensory responses vary across repeated prese

208 in the cell reduces its contractibility and explain why SERCA gene therapy, a change in calcium hand

209 cies difference in OCN regulation, which may explain why serum concentrations of OCN are higher in mo

210 inhibitors in promoting multimerization and explained why several C-terminal domain mutations are re

211 r proposes a cultural evolutionary theory to explain why shamanism consistently develops, and in part

212 nsulin stimulus to cause insulin resistance, explaining why short-term, insulin-dependent glucose uti

213 to intracellular hemoglobin composition also explains why sickle trait, the heterozygous condition, a

214 ity, maturation and survival, which may help explain why Slc7a5 mutations prevent normal brain develo

215 These findings may partly explain why smokers and elderly persons with compromised

216 Taken together, these results may partially explain why smokers are particularly susceptible to seve

217 Such an effect may help explain why social species often have longer lifespans.

218 These dynamics also explain why some avulsions are more hazardous than other

219 It also helps explain why some fully modified ASOs cause RNA target to

220 exists little human neuroscience research to explain why some individuals lose their appetite when th

221 We also use the canard mechanism to explain why some manipulations in the size of the window

222 ich suggests that environmental stress could explain why some marine diseases seem to spread so fast

223 ce allocations between species may partially explain why some microbes act as pathogens when infectin

224 r patients with various cancer types and may explain why some patients respond better to WEE1 inhibit

225 The weakness of this model is that it cannot explain why some people without hearing loss develop tin

226 tually exclusive competing interactions, may explain why some proteins are dynamic while others are r

227 These results help explain why some species have not transitioned beyond si

228 ing of strain competition in the lungs could explain why some strains of this bacterium are more freq

229 a central mission of relationship science is explaining why some romantic relationships thrive more t

230 We believe our model also explains why some characteristics of senescence can be f

231 n filtering and attentional selection, which explains why some lower-level auditory, and even higher-

232 signaling, and endoplasmic reticulum stress, explaining why SRp55 depletion triggers beta-cell apopto

233 may be incompatible with each other and thus explain why stem cells do not utilize the canonical anti

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

235 O are present in the CO-poisoned layer that explain why, surprisingly, CO desorbs at stepped and fla

236 y differs between males and females, and may explain why symptoms appear after adolescence when the e

237 amagnetic Fe(III) species over several hours explains why SznF was previously purified and crystallog

238 This could explain why temperate deciduous woody plants exhibit con

239 ld theory (DFDMFT) scheme to comprehensively explain why tetragonal FeS shows both semiconducting and

240 lved in plant-pathogen response, which could explain why the 20rDNA line is hyper-resistant to both b

241 These divergent mechanisms explain why the combination of maternal obesity and offs

242 Finally, we explain why the CSD must evolve with the world around it

243 These results explain why the CT can modulate the Env antigenic proper

244 fferential resistance(18), but this does not explain why the disconnections form primarily on positiv

245 erms in the solid- and liquid-film cases, we explain why the drainage is much faster in the liquid-fi

246 ies foveal expansion, this degradation helps explain why the fovea is a constant, miniscule size desp

247 This mechanism may explain why the Hox code is maintained throughout the li

248 We formulate six processes that may explain why the largest losses are observed specifically

249 This may explain why the net effect of mTOR inhibitors is paradox

250 mbined with larval connectivity patterns may explain why the northern Galapagos Islands (Darwin, Wolf

251 of climate change and land use changes could explain why the predicted enriching effects from climate

252 DNA fragility may thus help explain why the same loci are often used repeatedly duri

253 As mutational fragility does not obviously explain why the shoot-root difference varies with plant

254 alized by computational analyses, which also explain why the topology of the catalyst enforces differ

255 Mechanisms explaining why the majority of breast cancer patients ne

256 een reactants and Schiff base intermediates, explaining why the Schiff base NMR signals are rarely ob

257 ces the permeation free energy landscape and explains why the conventional model overestimates the as

258 rd the binding affinities is revealed, which explains why the denser packing of larger apolar domains

259 Our resulting architectural switch model explains why the human Fe-S assembly system has low inhe

260 s on the extracellular surface of KCNE1, and explains why the KCNQ1 channel alone is insensitive to u

261 of the hIAPP hereditary mutation S20G; (iii) explains why the six residue substitutions in rodent IAP

262 ability from ecological field data, and this explains why the strength of biotic interactions has emp

263 simple theory based on a dynamics of records explains why the typical phenomenology of annealing and

264 alence of EBV DNA in non-white parents could explain why their children acquire EBV at an earlier age

265 lence of oral EBV DNA, this difference could explain why their children acquire primary EBV infection

266 ing and beta-adrenergic sensitivity may help explain why therapies that work in HFrEF are ineffective

267 Our findings may help explain why there are some inconsistency in the results

268 This explains why there is no energy conservation in cNOR.

269 ony-forming unit-erythroid/proerythroblasts, explain why these anemias are macrocytic, and show why c

270 these distinct biological levels should help explain why these mechanisms fail with age and, ultimate

271 These results help explain why these models have brought such large improve

272 New research helps explain why these two effects do not always work well to

273 Hypotheses explaining why these biofilms fail to produce higher cur

274 iated with these pfk13 variants, potentially explaining why these resistance alleles have not increas

275 ania to survive in changing environments can explain why they encode multiple eIF4E (LeishIF4Es) and

276 e place emphasis on these recent studies and explain why they expand our pharmacological armamentariu

277 ions tended to be weakly oncogenic, probably explaining why they did not give rise to discernible les

278 s encode features along specific axes, which explains why they were previously found to respond to ap

279 Here, we explain why this photochemical synthetic approach was ov

280 d decreased apoptosis in colon cancer, which explains why this classical tumor suppressor is amplifie

281 institutional and psychological factors that explain why time poverty is often under appreciated.

282 ls of TLR9 and low levels of TLR7, which may explain why TLR9 dysregulation is particularly consequen

283 These findings might help to explain why TNF blockade improves lung function in only

284 Our results help explain why toe springs have been a pervasive feature in

285 nsive colloid-facilitated transport and help explain why trace levels of plutonium are found downgrad

286 behaviors of polar compounds and can easily explain why traditional molecular indices yield incorrec

287 These unprecedented findings explain why TRF1 is essential for the induction and main

288 ights by integrating two disparate fields to explain why uncertain rewards produce strong motivationa

289 These processes may explain why uncontaminated primordial mantle is so diffi

290 distinct ATPase site activities, which could explain why UvrA2 forms stable complexes with UvrB on da

291 st a potential underlying mechanism that may explain why variability quenching occurs.

292 Mechanisms that can explain why vitamin D deficiency is associated with mobi

293 tered viral replication in macrophages or to explain why Vpr is carried in the virus particle.

294 Here, we explain why we believe this conclusion is premature.

295 n acting over human evolutionary history may explain why we cooperate readily with unrelated and unfa

296 This may explain why we do not observe shared mutations among cli

297 Saccade-contingent habituation might explain why we do not perceive trans-saccadic retinal st

298 ionary flexibility in primates that may help explain why we have developed complex and diverse uses o

299 igns that might achieve better outcomes, and explain why we need open and international discussions c

300 's novel and insightful theory of obligation explains why we sometimes sense an obligation to treat e