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2 ptic encephalopathy (Ohtahara syndrome), but it is unclear how a partial loss of Munc18-1 produces th
6 hermodynamically unfavorable, and therefore, it is unclear how AIP-producing bacteria produce suffici
9 and BECN1:ATG14 subcomplex do not touch, and it is unclear how allosteric signals are transmitted to
10 the membrane properties of SCN neurons, but it is unclear how alterations in CRY1/2 stability affect
11 yology.Early in human embryonic development, it is unclear how amniotic sac formation is regulated.
12 he basilar membrane traveling wave; however, it is unclear how amplification is achieved with sharp f
13 ts are produced in supernova explosions, but it is unclear how and where dust grains condense and gro
15 de-offs between contraction speed and force, it is unclear how animals evolve the ability to produce
16 ssed and localized within the bacterium, and it is unclear how antigen localization modulates the imm
18 protein cargo to the endocytic machinery but it is unclear how AP2 is activated on the plasma membran
23 nity is a core objective of health care, yet it is unclear how best to measure this in the ICU settin
27 ral representations of similar contexts, but it is unclear how broadly responsive neurons help distin
29 tor (RyRs) Ca(2+) release channel is low and it is unclear how Ca(2+) release can be activated in the
30 ial for consolidating episodic memories, but it is unclear how CA1 activity patterns drive memory for
32 tress signals can induce either process, and it is unclear how cells 'assess' cellular damage and mak
33 A and protein constituents of chromatin, and it is unclear how cells respond to this compound injury.
34 tant for generating distinct cell types, but it is unclear how cells use the same set of regulatory m
35 omb repressive complexes modify histones but it is unclear how changes in chromatin states alter kine
40 zed by depleted nucleosome contact; however, it is unclear how chromatin accessibility is governed.
41 a different identity on its neighbours, and it is unclear how chromatin in equipotent progenitors un
45 MELD) score has improved wait list survival, it is unclear how contemporary wait list mortality can b
47 rowing pressure to reduce COPD readmissions, it is unclear how COPD readmission rates are related to
49 s), require niches to maintain stemness, yet it is unclear how CSCs maintain stemness in the suboptim
52 ellular decisions in noisy environments, but it is unclear how digital systems transmit temporal info
56 en, Batrachochytrium dendrobatidis (Bd), but it is unclear how dominant these anti-Bd bacteria are in
60 increasingly popular in pediatrics; however, it is unclear how effective these interventions are in c
63 ating epigenetics and psychiatric disorders, it is unclear how epigenetics, particularly DNA methylat
66 trations below their carcinogenic potencies; it is unclear how exposure leads to adverse health outco
68 ty is oncogenic in several malignancies, but it is unclear how expression or function of downstream e
69 soil predominantly represents intact cells, it is unclear how extracellular DNA affects molecular an
71 s PG insertion at the division plane, though it is unclear how FtsZ structure and dynamics are mechan
72 ought to present large ATP demands; however, it is unclear how fuel availability and electrical activ
75 izobium species can nodulate bean roots, but it is unclear how genetically isolated these species rem
76 plications in biomedicine and nanotechnology.It is unclear how Gram-positive bacteria, with a thick c
79 enerate complex organ-like tissues; however, it is unclear how heterotypic interactions affect lineag
81 However, even in this well-studied model, it is unclear how homolog pairing in diploids or environ
83 secrete IL-1 while retaining viability, yet it is unclear how IL-1 can be secreted from living cells
85 biting fairly severe meiotic phenotypes, and it is unclear how important homeostasis is under normal
86 nd enhanced levels of estradiol (E2), though it is unclear how increased E2 promotes deterioration of
89 onsequences for induced cleavage, and so far it is unclear how intracellular signals address cleavage
90 at dictate CNS function are multifaceted and it is unclear how irradiation induces persistent alterat
91 oxic T lymphocyte (CTL) differentiation, but it is unclear how it operates in a graded manner in the
92 and triggers transcription termination, but it is unclear how its various enzymes are coordinated an
93 ete membranes interact at fertilization, and it is unclear how Juno - which was previously named fola
94 ut also by surrounding cell types [6-9], and it is unclear how large, possibly insoluble protein comp
99 l excitatory neurons remains incomplete, and it is unclear how local excitatory and inhibitory synapt
107 ositive clinical studies have been reported, it is unclear how many purported therapies have become e
111 interconnectivity between these structures, it is unclear how mPFC projections to each subcortical s
112 g protein and the molecular motors involved, it is unclear how mRNAs are connected to membranes durin
117 plain a small proportion of the genetic risk it is unclear how much is left to be detected by other,
118 pically proceed in parallel, and accordingly it is unclear how much of skill acquisition is a reflect
119 development, especially during amelogenesis, it is unclear how mutant forms cause ARS dental anomalie
120 es changes in SCN neuronal excitability, but it is unclear how mutations affecting post-translational
125 networks requiring the hippocampus; however, it is unclear how neocortical areas participate in memor
130 be important for centrosome separation, but it is unclear how nuclear dynein forces are organized in
132 tural adaptation than any other species, but it is unclear how observational learning can give rise t
134 us promotes cardiovascular disease; however, it is unclear how or which proteins encoded at this locu
135 systemic lupus erythematosus (SLE); however, it is unclear how Ox40L contributes to SLE pathogenesis.
137 romatic hydrocarbons (PAHs) increases atopy; it is unclear how PAH exposure is linked to increased se
145 ha and Pin1 have multiple cellular partners, it is unclear how Pin1 assists in the regulation of ERal
146 mmunity and effector-triggered immunity, and it is unclear how plants inactivate these effectors to e
148 uch approaches often have mixed results, and it is unclear how polyvalency alters the fine specificit
149 nt for fitness in temperate environments but it is unclear how progeny gain their initial seasonal en
151 nditure (EE) increases with overfeeding, but it is unclear how rapidly this is related to changes in
156 hery and prevention of Cu over-accumulation, it is unclear how regulation of ATP7A contributes to Cu
158 largely to peripheral blood-derived T cells, it is unclear how representative the peripheral T cell r
160 ess evolves under stabilizing selection, but it is unclear how robustness and evolvability will emerg
164 oposed for synapse-to-nuclear communication, it is unclear how signaling is coordinated at both subco
166 nce identity of rRNA genes within a species, it is unclear how specific rRNA genes are reproducibly c
168 ein kinase C (PKC) phosphorylation, although it is unclear how store depletion stimulates this gating
170 sive structures called invadopodia; however, it is unclear how Stx4 function is regulated during tumo
173 cleoli actively consume chemical energy, and it is unclear how such nonequilibrium activity might imp
175 eting for resources and instilling fear, but it is unclear how suppression of mesopredators varies wi
178 e Th17 chemoattractant CCL20, and therefore, it is unclear how Th17 cells are recruited to the cervic
181 synthesis enzymes and the cytoskeleton, but it is unclear how the activities of individual proteins
182 aking involving risk of punishment; however, it is unclear how the BLA is recruited at different stag
186 gh aspects of this process are well studied, it is unclear how the cell controls the coordination of
188 congestion is a major goal of acute therapy, it is unclear how the clinical components of congestion
190 lthough nucleic acids are potent activators, it is unclear how the contact system is regulated to pre
194 on the molecular control of cell movements, it is unclear how the different observed modes of collec
195 a few decades, and, at the ice-sheet scale, it is unclear how the entire drainage network of ice str
196 ing motifs (MIMs) of ESCRT-III subunits, but it is unclear how the enzyme then remodels these substra
197 - DNA sequence changes during evolution, but it is unclear how the evolutionary dynamics of epigeneti
200 to involve both encoding and retrieval, and it is unclear how the human hippocampus subserves both f
208 reduced local terrestrial biodiversity, but it is unclear how the magnitude of change relates to the
213 in humans and animal models of Parkinsonism, it is unclear how the pattern regularization would origi
214 adient is an important cue for polarization, it is unclear how the polarization is affected by cell d
215 ytic center of all Dus enzymes is conserved, it is unclear how the same protein fold can be reprogram
217 eceptors controls specific signaling events, it is unclear how the spatiotemporal control of signalin
219 (TB) was once a major killer in Europe, but it is unclear how the strains and patterns of infection
220 finity of IgG1 Fc to Fc gamma receptors, but it is unclear how the structural modifications of N-glyc
223 erile injury response in the liver; however, it is unclear how the type of cells injured or the mecha
225 al frequencies has been fairly well studied, it is unclear how the visual system integrates this info
228 nown to have distinct reaction dynamics, but it is unclear how their kinetics affects the overall ele
230 lial cells do not express CD4 receptors, and it is unclear how these cells become productively infect
232 ulation using artificial visual stimuli, and it is unclear how these descriptions map onto the encodi
236 hough oxLDL stimulates activatory signaling, it is unclear how these events drive accelerated thrombo
237 s can drive their membrane localization, yet it is unclear how these intracellular proteins are targe
240 ential for transcription regulation, and yet it is unclear how these multisubunit complexes coordinat
245 cell-cell and cell-matrix interactions, but it is unclear how these physical cues influence stem cel
247 heir fitness and disrupt their function, and it is unclear how these potentially harmful cells are ma
248 HR pathway is independent of RAD18 However, it is unclear how these processes are coordinated within
250 n activity are associated with tinnitus, but it is unclear how these relate to the phantom sound itse
253 he encoding and retrieval of information but it is unclear how these two processes are achieved withi
255 ction focus on initiation deficits; however, it is unclear how they account for deficits in the speed
256 endent on the cellular NXF1/TAP pathway, but it is unclear how they are recruited to the export machi
258 Many niche signals have been identified, but it is unclear how they influence the choice of stem cell
260 erns about the use of such technologies, and it is unclear how they might be implemented to deliver t
261 are predicted to be similar, and therefore, it is unclear how they recognize structurally distinct R
265 ciate with cholesterol-rich lipid rafts, but it is unclear how this affects the properties of the rec
266 dent upon the ESCRT-III component CHMP7 [3], it is unclear how this complex is able to engage nuclear
269 ults in need of statin therapy; furthermore, it is unclear how this difference translates into number
271 e of cortical receptive fields [2]; however, it is unclear how this fine-grain inhibition relates to
273 cular crowding in the NPC transport channel, it is unclear how this impacts FG Nup barrier function o
276 me via its HAND-SANT-SLIDE (HSS) domain, yet it is unclear how this interaction enhances remodeling.
278 in labelling magnetic resonance imaging, but it is unclear how this is related to amyloid-beta pathol
279 lized communities of brain regions; however, it is unclear how this mechanism manifests over time.
281 th ANE syndrome have fewer mature ribosomes, it is unclear how this mutation disrupts ribosome assemb
283 ar to aggregate local neuronal activity, but it is unclear how this relationship affects information
289 a common eukaryotic centromere feature, yet it is unclear how transcription is linked to underlying
291 smodium, is mediated by type I IFN; however, it is unclear how type I IFN suppresses immunity to bloo
296 ctive GPCRs in these contexts is limited and it is unclear how well an opsin-chimera GPCR might mimic
297 n in the context of simple behavioral tasks, it is unclear how well each of these mechanisms can acco
298 he efficacy of latency-reversing agents, but it is unclear how well these models reflect HIV integrat
299 atosensory cortex (S1) of mice and rats, but it is unclear how whisker-related input is represented i
300 clines in heart attack and stroke incidence, it is unclear how women and men differ in first lifetime
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