戻る
「早戻しボタン」を押すと検索画面に戻ります。

今後説明を表示しない

[OK]

コーパス検索結果 (1語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 in excitable cells following plasma membrane depolarization.
2 s to K(+)-mediated mitochondrial bulging and depolarization.
3 ion, but not elimination, of the TA-mediated depolarization.
4 he latency of action potentials triggered by depolarization.
5 +) and Na(+) through TRPV4 channels to evoke depolarization.
6 t increased intracellular Ca(2+) with robust depolarization.
7  calcium-current traces elicited by membrane depolarization.
8 xaggerate the passive propagation of somatic depolarization.
9 not directly affect BK, but activated BK via depolarization.
10 to 1, while its Rayleigh scattering has zero depolarization.
11  PINK1 in cells independent of mitochondrial depolarization.
12 itially coincident with action potentials or depolarization.
13 e antibody uptake occurred at rest or during depolarization.
14 clooxygenase-2 in the cortex after spreading depolarization.
15 nduction, growth arrest, and plasma membrane depolarization.
16 o voltage sensor stabilization upon membrane depolarization.
17 t, allowing neurons to extend their level of depolarization.
18 chanisms of both abnormal repolarization and depolarization.
19 a process that was preceded by mitochondrial depolarization.
20 action induced membrane permeabilization and depolarization.
21 duced PH and correlated with plasma-membrane depolarization.
22 honon-assisted intervalley scattering causes depolarization.
23  be altered in acetaminophen-induced hepatic depolarization.
24 resent a typical light-sensitive current and depolarization.
25 apping that captures supra- and subthreshold depolarization.
26 polarization is a wave of neuronal and glial depolarization.
27 racellular Ca(2+) equilibrium, and caused Vm depolarization.
28 ablation of the P2x7 gene inhibits spreading depolarization.
29  were mostly closed at rest and activated by depolarization.
30 sensory neurons released GABA in response to depolarization.
31 h and its modulation by subthreshold somatic depolarization.
32 orphology, and cause membrane permeation and depolarization.
33 creased coupling and allowed Ca wave-induced depolarizations.
34 g away from the ganglion activated at weaker depolarizations.
35 rough LVA channels following GABAAR-mediated depolarizations.
36  significantly more likely to have spreading depolarizations (6/7 and 10/12, respectively) than those
37 ques, including a unique model that assesses depolarization (a marker of sensory nerve activation) of
38  to increase mEJP rate in response to spaced depolarization, a type of activity-dependent plasticity
39 ral RV progression was associated with prior depolarization abnormalities, whereas LV progression is
40 lar toxicity and vasoconstrictive effects of depolarizations act in synergy with direct ischaemic eff
41 g repetitive firing; (ii) enhanced the after-depolarization (ADP); (iii) reduced fast and medium afte
42 efficiency of the passive spread of membrane depolarization along TATS.
43 transport and dumps the transport-associated depolarization along the astrocyte processes.
44 thways are strongly induced by mitochondrial depolarization, although a direct link between loss of m
45 atory neurotransmitters to sustain spreading depolarization and activate neuroinflammation.
46  of the fluorophore SSF, ORF, and scattering depolarization and anisotropy using a combination of flu
47 efect in the early response to mitochondrial depolarization and autophagosome formation.
48               Because mitochondrial membrane depolarization and calcium are known to activate iPLA2ga
49                                              Depolarization and cAMP signals induce preferential tran
50 89771 exhibits a slow onset of block that is depolarization and concentration dependent, with a simil
51 aphic QRS duration, a measure of ventricular depolarization and conduction, is associated with cardio
52 ivity, corresponding to upstates of neuronal depolarization and downstates of hyperpolarization.
53 osing the conduction pathway during membrane depolarization and dynamically regulating neuronal activ
54 been implicated as modulators of spontaneous depolarization and electrical conduction that may be inv
55                   Changes in plasma membrane depolarization and elevated intracellular Na(+), which c
56  day (P) 2-P15 mice, photostimulation caused depolarization and excitation of interneurons and evoked
57 ed by cyclophilin D and led to mitochondrial depolarization and fragmentation.
58 g a ubiquitous promoter resulted in cellular depolarization and ganglion cell action potential firing
59 n peroxide, contributes to cellular membrane depolarization and HPV.
60  cell body to shorten and elongate upon cell depolarization and hyperpolarization, respectively.
61  ERG currents, leading to membrane potential depolarization and increased input resistance, two criti
62 face membrane of neurons can induce membrane depolarization and initiate an action potential.
63 ed mitochondrial integrity, leading to rapid depolarization and massive CLL cell death.
64 -cell coupling in intact hearts limits local depolarization and may protect hearts from this arrhythm
65 We identify a deterministic relation between depolarization and nanoparticle concentration.
66 ction region (LIR) domain upon mitochondrial depolarization and proteasome-dependent outer membrane r
67                 Apamin also slowed diastolic depolarization and reduced pacemaker rate in isolated SA
68 activation puts a ceiling on horizontal cell depolarization and regulates the temporal responsivity o
69 id, and Bax; and 3) subsequent mitochondrial depolarization and release of apoptosis-inducing factor
70 mmarizing the evidence that both the initial depolarization and repolarization phases of the cardiac
71  to sensory input stimulation with decreased depolarization and spiking following resident-intruder e
72 astatin 4 (TRPM4) channels to cause membrane depolarization and vasoconstriction.
73 etween ON periods, characterized by membrane depolarization and wake-like tonic firing, and OFF perio
74 lting in a decrease in the rate of diastolic depolarization and, consequently, the heart rate, a mech
75 ases the quantity of glutamate released upon depolarization and, in turn, limits the positive-feedbac
76 /fissures are sufficient to induce spreading depolarizations and acute infarction in adjacent cortex.
77  neurons, menthol application induced larger depolarizations and generation of APs with frequencies s
78 iation and propagation of cortical spreading depolarizations and the role of astrocytes in maintainin
79 root apex, (2) greater salt-induced membrane depolarization, and (3) a higher reactive oxygen species
80 istension, induces channel opening, membrane depolarization, and initiation of pain signaling.
81 n2(-/-) mice with the exception of a rebound depolarization, and non-mGluR-mediated long-term potenti
82  Treg cell induction in vitro, mitochondrial depolarization, and recruitment of PTEN to the immunolog
83 evate the electrical threshold for spreading depolarization, and reduce spreading depolarization freq
84  pairing mAChR stimulation with subthreshold depolarization ( approximately 10 mV from RMPs) initiate
85 capacitance changes immediately after strong depolarization are also different between control and cK
86 2, SR Ca(2+) leak and mitochondrial membrane depolarization are critically involved in the apoptotic
87 round suppression, the functions of VIP cell depolarization are not fully understood.
88 re unknown, although mass cortical spreading depolarizations are hypothesized as a requisite mechanis
89 cal spreading depression and terminal anoxic depolarization arose preferentially in the whisker barre
90 ne integrity (electroporation) and resulting depolarization as an intermediate step.
91           Results further validate spreading depolarizations as a clinical marker of early brain inju
92 ents of TRPV4-expressing Xenopus oocyte upon depolarizations as well as phenotypes of expressing yeas
93 c coupling between soma and axon, the >25 mV depolarization associated with the plateau could propaga
94 (yellow and green) that were associated with depolarization at a false discovery rate of </=0.05.
95 RPE migration was defined by the presence of depolarization at intraretinal hyperreflective foci on P
96 cripta elegans, either sex) evoked by steady depolarization at rest is replaced by irregular firing d
97 ation at the first zero-current potential to depolarization at the third zero-current potential, agai
98 tional model predicts a higher threshold for depolarization block in the variant, particularly at 40
99          The range of most M1s is limited by depolarization block, which is generally considered path
100 ents cell death from excessive mitochondrial depolarization but also activates AMPK signaling and inc
101                     M1 allowed mitochondrial depolarization but blocked procaspase-9 processing, sugg
102  Vpr are highly susceptible to mitochondrial depolarization, but develop resistance following stimula
103  antagonizes norepinephrine-induced membrane depolarization by promoting potassium efflux in brown ad
104 ect was due to strong attenuation of plateau depolarizations by axonal K(+) channels, allowing full a
105 ormal Na+ conductance, resulting in membrane depolarization, calcium influx, aldosterone production,
106  regulator neurogenin3 but requires membrane depolarization, calcium influx, and calcineurin signalin
107 tinal polypeptide positive (VIP) interneuron depolarization can account for the reduction of surround
108                             We report on how depolarization can be exploited as a strategy to visuali
109 tations that evoke small degrees of membrane depolarization cause hyperexcitability and familial epis
110 thy, while mutations evoking larger membrane depolarizations cause hypoexcitability and insensitivity
111                          Interestingly, only depolarization caused significant changes in the relativ
112 arized radiation intensity, including linear depolarization, circular depolarization, cross-polarizat
113 er finding is that the fluorophore ORF has a depolarization close to 1, while its Rayleigh scattering
114                                    Spreading depolarization clusters were associated with formation o
115 polarizing potentials, but not upon membrane depolarization compared with wild-type channels.
116  (</=2.5 ng/mL), causes substantial membrane depolarization concomitant with a several-fold increase
117 n potential firing in response to subsequent depolarization, consistent with the increased intrinsic
118  cortical sulci caused clusters of spreading depolarizations (count range: 12-34) in 7/17 animals in
119 rogression of RV disease was associated with depolarization criteria at baseline (odds ratio [OR], 9.
120 y, including linear depolarization, circular depolarization, cross-polarization, directional birefrin
121 d mitochondrial fragmentation, mitochondrial depolarization, cytochrome c release, reactive oxygen sp
122 henyl hydrazone (CCCP)-induced mitochondrial depolarization decreased mitochondrial mass and Mfn2 lev
123 eotides determines a singular and very large depolarization depending on the concerted effects of ext
124                      Repetitive bipolar cell depolarizations, designed to maintain the same amount of
125                                              Depolarization did not increase the resting open probabi
126                            However, membrane depolarization did not induce an increase in intracellul
127 nd urethane anesthesia demonstrated that the depolarizations did not propagate from a subcortical sou
128 , organelle damage manifest by mitochondrial depolarization, disordered autophagy, and pathological e
129 ther, these data suggest that in response to depolarization, dopamine vesicles utilize a cascade of v
130 G protein-coupled receptor-promoted neuronal depolarization downstream of Galphaq in the mouse prefro
131                 Progressive increase in step depolarization duration slowed voltage-sensor return in
132 aptide) increased coupling and suppressed Vm depolarization during Ca waves.
133 lucidate the potential functions of VIP cell depolarization during locomotion.
134 lation of dendritic sectors to prevent their depolarization during non-preferred motion, yet enables
135                We find that the subthreshold depolarization during ripples is uncorrelated with the n
136 ional structural constraint on lattice-scale depolarization dynamics; whereas Smax in relaxor and nor
137                                         This depolarization enabled the afferent to reliably generate
138                                These somatic depolarizations enhanced somatic excitability by increas
139 ects on insulin secretion, including reduced depolarization-evoked Ca(2+)-influx and beta-cell exocyt
140    The G100V/C103V mutation nearly abolishes depolarization-evoked exocytosis (measured by membrane c
141                             The reduction of depolarization-evoked exocytosis in du/du IHCs reflected
142 te normal intracellular Ca(2+) signaling and depolarization-evoked exocytosis.
143                                As in muscle, depolarization evokes Ca(2+) transients independent of e
144 on itself is not voltage-sensitive, but that depolarization facilitates rapid cycling of extracellula
145 ype structures are formed that are driven by depolarization fields occurring in such systems.
146 reading depolarization, and reduce spreading depolarization frequency and amplitude.
147 onstrates backpropagation of GABAAR-mediated depolarizations from MNTB axon terminals to the soma, so
148 g firing at high rates; (ii) enhancing after-depolarizations; (iii) reducing the fast and medium afte
149 the otherwise inhibitory effects of cellular depolarization imposed by elevating extracellular [K(+)]
150 h mouse OHCs and HEI-OC1 cells and generated depolarization in both cell types.
151  decreased hypoxia-induced cellular membrane depolarization in Cox4i2(-/-) PASMCs compared with wild-
152 produced mitochondrial swelling and membrane depolarization in FRD-WT mice but not in FRD-S2814A mice
153 e local intercellular coupling in Ca-induced depolarization in intact hearts, using confocal microsco
154  revealed cell membrane permeabilization and depolarization in M bovis BCG.
155 e P2X7-PANX1 pore complex inhibits spreading depolarization in mice carrying the human familial hemip
156 ustic phonons, which is essential for valley depolarization in MoS2.
157          Furthermore, we found that membrane depolarization in murine heart mitochondria was sensitiz
158                         The time constant of depolarization in OHCs, 1.45 ms, is 10 times faster than
159  a single Ca(2+) occupancy requires membrane depolarization in order to open (C.J.P. et al., manuscri
160 al trafficking correlated with mitochondrial depolarization in palmitate-treated DRG neurons.
161 ane potential of CA1 interneurons but caused depolarization in pyramidal cells.
162 reading depression (CSD), a wave of neuronal depolarization in the cerebral cortex following traumati
163 rgy density generated in the crystals during depolarization in the high voltage mode is four times hi
164 ng current into the myocardium and recording depolarization in the scar through optical mapping.
165          FRD produced mitochondrial membrane depolarization in WT mice but not in S2814A mice, in whi
166 clotted blood into a sulcus caused spreading depolarizations in 5/6 animals (count range: 4-20 in 6 h
167   ER was associated with a trend toward late depolarization, in general was suppressed with exercise
168                                    Simulated depolarization increased baseline firing rates of pyrami
169                                This leads to depolarization, increased input resistance, enhanced spi
170  we defined the mechanisms by which membrane depolarization increases Ca(2+) sparks and subsequent ST
171 m in which lowering extracellular calcium or depolarization increases P(open).
172                            We show that cell depolarization increases synaptic vesicle dopamine conte
173        With increased stimulation, hair cell depolarization increases the frequency of quanta release
174                     As fluid flow increases, depolarization increases to activate voltage-gated Ca(2+
175                     The latter would enhance depolarization-induced alkalinization of astrocytes, and
176 be, which previously allowed us to resolve a depolarization-induced Ca(2+)-dependent close-to-open tr
177 milar to those present in the SR lumen after depolarization-induced calcium release cause the dissoci
178                         This potentiation of depolarization-induced calcium transients was blocked by
179 lcholine receptor (M2R) was found to exhibit depolarization-induced charge movement-associated curren
180                             Remarkably, both depolarization-induced dopamine vesicle hyperacidificati
181  K(+) (Kv) channel Kv2.1 (KCNB1) facilitates depolarization-induced exocytosis in INS 832/13 cells an
182                                         This depolarization-induced hyperacidification is mediated by
183 ouse cortical neurons, we observed increased depolarization-induced mitochondrial calcium uptake.
184 sm of inhibitory channels and a mechanism of depolarization-induced neurite outgrowth.
185                                         K(+) depolarization-induced PKC translocation entirely mirror
186 tes retrograde synaptic depression including depolarization-induced suppression of excitation (DSE) a
187                                 CB1-mediated depolarization-induced suppression of synaptic inhibitio
188  male DRG neurons, IP3 (100 mum) potentiated depolarization-induced transients produced by extracellu
189                                 While strong depolarization-induced uptake of HRP suppressed evoked r
190 vealed no evidence of postinhibitory rebound depolarization inherent to coincidence models of duratio
191 t palmitate induces DRG neuron mitochondrial depolarization, inhibiting axonal mitochondrial traffick
192 oupling that reliably convert brief membrane depolarization into precisely timed intracellular signal
193 mined which neurons converted choice-related depolarization into spiking.
194 onduct ions between CMs, triggering membrane depolarization, intracellular calcium release, and actom
195                                    Spreading depolarization is a wave of neuronal and glial depolariz
196 We have shown that Vpr-induced mitochondrial depolarization is mediated by TNFR-associated factor-1 (
197 ormational change in the domain IV VSD after depolarization is necessary and sufficient to reveal a h
198                                  During long depolarizations, lacosamide slowly (over seconds) put ch
199                                   Myocardial depolarization leading to cardiac muscle contraction is
200                                              Depolarization leads to the opening of voltage-gated Na(
201 at are altered in these cells in response to depolarization (linear models at false discovery rate </
202 ce of this signalling pathway with effective depolarization may promote rapid conduction of contracti
203 sitive picosecond time-resolved fluorescence depolarization measurements that allowed us to discern t
204  C. difficile growth in vitro via a membrane depolarization mechanism.
205 nism underlying analog-digital modulation is depolarization-mediated inactivation of presynaptic Kv1-
206 a similar abrupt transition of degranulation/depolarization near sites of keratin deposition, as well
207 ion facilitates spiking by focusing synaptic depolarization near threshold for action potentials.
208 egenerative dendritic events can provide the depolarization necessary for Hebbian potentiation, these
209 leakage and may explain the gradual membrane depolarization observed with daptomycin.
210 ) channel activation indicates that membrane depolarization occurs.
211 nal complex likely is attributable to direct depolarization of acid-sensitive trigeminal nerve fibers
212                                              Depolarization of cultured mouse cortical neurons upregu
213                       Kir2 antagonist caused depolarization of freshly dispersed ICC and colonic smoo
214 emonstrated that chemogenetic or optogenetic depolarization of GABAergic dorsal root ganglion neurons
215 an SB-705498 at inhibiting capsaicin-induced depolarization of guinea pig and human isolated vagus ne
216 DEP-OE) and not the cleaned particles evoked depolarization of guinea pig and human vagus, and this w
217 steocrin (OSTN), that is induced by membrane depolarization of human but not mouse neurons.
218       Under current clamp, ML-133 caused the depolarization of isolated ICC and also that of cells im
219                Absence of EDH with effective depolarization of LECs may promote the rapid conduction
220                                              Depolarization of MECII impaired spatial memory and elic
221 V4 ligands and hypo-osmotic solutions caused depolarization of murine, guinea pig, and human vagus an
222 on (SD) is a slow propagating wave of strong depolarization of neural cells, implicated in several ne
223 als was observed together with the prolonged depolarization of neurons induced by pharmacological man
224 n response to odors, triggering long lasting depolarization of olfactory glomeruli.
225 etinal photoreceptors, and the b-wave is the depolarization of ON-bipolar cells.
226               The process is associated with depolarization of paternal mitochondria and additionally
227 blockade slows repolarization and subsequent depolarization of SAN cells.
228                    This is driven in part by depolarization of senescent cell plasma membrane, which
229    The method may be used to detect membrane depolarization of sympathetic nerve fibres in human pati
230 h a transient, fast block established by the depolarization of the egg membrane within milliseconds a
231  functional role of BKCa current in limiting depolarization of the horizontal cell membrane potential
232               DAN activation produces a slow depolarization of the MBON in these DAN>MBON synapses an
233             IKs channels open in response to depolarization of the membrane voltage during the cardia
234  in intracellular reactive oxygen species or depolarization of the mitochondrial membrane potential.
235 rmination is due to ChR2-mediated transmural depolarization of the myocardium, which causes a block o
236                                              Depolarization of the postsynaptic afferent could also e
237 t is activated by the AMPA receptor-mediated depolarization of the spine and thus will contribute to
238 oride conductance, resulting in diuresis and depolarization of the transepithelial potential.
239 y of ENaC which resulted in the steady state depolarization of VP neurons.
240 pid N-type channel inactivation during short depolarizations of the plasma membrane.
241  expression of L1302F and L811P evoked large depolarizations of the resting membrane potential and im
242 on biased the timing but not the location of depolarization onset.
243  Ca(2+) release in response to K(+)-membrane depolarization or caffeine stimulation, suggesting a red
244 K(+) channels occurs upon sustained membrane depolarization or channel opening and then recovers duri
245 g potential, but instead exhibit a period of depolarization or hyperpolarization referred to as an af
246   Loss of DeltaPsi with either pharmacologic depolarization or LPS leads to Ca(2+)-dependent mitochon
247 posed by fatiguing stimulation, long-lasting depolarization, or low drug concentrations).
248 m governing such resistance to mitochondrial depolarization, our results show that prior stimulation
249 tically induced ATP depletion, mitochondrial depolarization, oxidative stress, and necrotic death als
250                             Primary afferent depolarization (PAD) normally mediates inhibition via so
251  inward current to flow during the diastolic depolarization phase under cholinergic activation.
252     In these areas, detrimental peri-infarct depolarizations (PIDs) contribute to secondary infarct g
253 itated dendritic propagation of postsynaptic depolarization, potentially improving coincidental activ
254 ter ACh application, but not by subthreshold depolarization preceding mAChR stimulation.
255 ter for presenting a unifying picture of the depolarization process.
256 e and persistent changes, including membrane depolarization, prolonged elevation of intracellular Ca(
257 rites in the inner plexiform layer and these depolarizations propagate to the varicosities.
258 of the threshold potential and the diastolic depolarization rate that is independent of the maximum u
259 mpanied by alterations in the tissue optical depolarization rate, allowing tissue polarimetry to guid
260 the membrane potential such as the diastolic depolarization rate.
261 operties, such as the lidar backscatter, the depolarization ratio and the optical depth, sharply decr
262 teristic resonant behaviour, shape-dependent depolarization ratio, and mass-dependent line shape.
263 nel inhibitor chromanol 293B caused membrane depolarization, redistribution of beta-catenin into the
264 eishmania donovani (Ld) causes mitochondrial depolarization, reduces mitochondrial dynamics, and rest
265 (++) , that interferes with normal cycles of depolarization-repolarization.
266 ficient to produce the critical postsynaptic depolarization required for associative LTP in CA3 pyram
267 tion, rescue of SK responses by subthreshold depolarization required the presence of extracellular ca
268            TGF-beta1-dependent cardiomyocyte depolarization resulted from electrotonic crosstalk with
269 ificantly lowers the threshold for spreading depolarization (SD) in dorsal medulla, leading to cardio
270                                    Spreading depolarization (SD) is a slow propagating wave of strong
271      Furthermore, the incidence of spreading depolarization (SD) is markedly reduced in the absence o
272 tial changes during the passage of spreading depolarization (SD) waves.
273 lutamate uptake in the dynamics of spreading depolarization (SD)-the electrophysiological event under
274                                    Spreading depolarizations (SDs) are recognized as actors in neurol
275 ed that calcium influx is induced by voltage depolarizations, similar to metazoan action potentials.
276 ading depression (CSD) is a wave of neuronal depolarization spreading through the cortex and is assoc
277 Optical measurements reveal that a sustained depolarization strongly potentiates the inhibitory effec
278 uppress downstream consequences of spreading depolarization such as upregulation of interleukin-1 bet
279  oxo-M washout, and not relieved by a strong depolarization, suggesting a voltage-insensitive mechani
280 d genes, is closely correlated with membrane depolarization, suggesting their use as markers for an i
281 mplex is a critical determinant of spreading depolarization susceptibility and its downstream consequ
282 mplex is a critical determinant of spreading depolarization susceptibility with important consequence
283  the current passed in response to premature depolarizations that normally helps protect against the
284 tion enabled the generation of low-threshold depolarizations that occurred in an all-or-none or grade
285 ists also abolished SWs as well as transient depolarizations that persisted after addition of CavL an
286 e-spine activation produced large spine head depolarizations that severely distorted measurements and
287               Within minutes after spreading depolarization, the neuronal hemichannel pannexin 1 (PAN
288 IAP-2 may prevent Vpr-mediated mitochondrial depolarization through stabilizing TRAF-1/2 expression a
289 concentration during a train of long-lasting depolarizations to a maximally activating voltage was mo
290 function decreased, suggesting that membrane depolarization uncouples WNK kinases from NCC.
291 minals of primary afferent fibers experience depolarization upon activation of GABAA receptors (GABAA
292 complete fusion with spontaneous ventricular depolarization using temporary electrodes.
293                                         This depolarization was facilitated by the absence of Ca(2+)
294 e reduction in current amplitude during step depolarizations was a consequence of both decreased CaV1
295 er not coincident with atrial or ventricular depolarization were analyzed on the recording system.
296               Only following this centromere depolarization were homologous chromosome arms connected
297 fluorescence in D411N, V535A, and K538Q upon depolarization, whereas [2-(trimethyl ammonium) ethyl] m
298 ion (CSD) is a propagating event of neuronal depolarization, which is considered as the cellular corr
299                                              Depolarization with high extracellular potassium evokes
300                 The association of spreading depolarizations with early brain injury was then investi

WebLSDに未収録の専門用語(用法)は "新規対訳" から投稿できます。
 
Page Top