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 xpression is observed in the portions of the sinoatrial and atrioventricular junctions that are thoug
2 x30.2, which is most abundantly expressed in sinoatrial and atrioventricular nodal regions of the hea
3 ust expression in the heart, particularly in sinoatrial and atrioventricular nodal regions.
4  distal outflow tract, atrial septum, and in sinoatrial and atrioventricular node.
5 .9 may slow propagation of excitation in the sinoatrial and atrioventricular nodes by shortening the
6 t, unlike ENT1, is virtually absent from the sinoatrial and atrioventricular nodes.
7  electrocardiography or the discovery of the sinoatrial and atrioventricular nodes.
8 , representing a position midway between the sinoatrial and atrioventricular nodes.
9               Much information is encoded in sinoatrial AP waveforms, but both the analysis and the c
10 ntitative analysis and enables comparison of sinoatrial APs by standardizing parameter definitions an
11  parameter that can vary significantly among sinoatrial APs.
12 pisodes of third-degree atrioventricular and sinoatrial block in every NaV1.5-immunized animal, but n
13 pe of unknown origin and atrioventricular or sinoatrial block lasting >10 seconds (average, 17.9+/-6.
14 tantial increases in atrial premature beats, sinoatrial block, and atrioventricular block, accompanie
15 aptation to exercise by modulating intrinsic sinoatrial cell behavior.
16 a2 AMPK activation downregulates fundamental sinoatrial cell pacemaker mechanisms to lower heart rate
17 tric oxide (NO) synthesized within mammalian sinoatrial cells has been shown to participate in cholin
18                      Our ability to generate sinoatrial-compatible spontaneous cardiomyocytes from th
19                                          The sinoatrial conduction pathways acted as a filter for atr
20 tation waves could enter the SAN through the sinoatrial conduction pathways and overdrive suppress th
21 Ch/Iso modulated filtering properties of the sinoatrial conduction pathways by increasing/decreasing
22 t SAN activation and to identify specialized sinoatrial conduction pathways.
23 xcited via superior, middle, and/or inferior sinoatrial conduction pathways.
24 ged sinoatrial node recovery time, increased sinoatrial conduction time, and recurrent sinus pauses.
25 rial myocardium via superior and/or inferior sinoatrial exit pathways 8.8+/-3.2 mm from the leading p
26                  Conduction failure in these sinoatrial exit pathways leads to SAN exit block and is
27 for 2 (or more) narrow superior and inferior sinoatrial exit pathways separated by 12.8+/-4.1 mm.
28 rmal circadian fluctuations and less erratic sinoatrial firing.
29  Both Ca(v)1.2 and Ca(v)1.3 channels mediate sinoatrial L-type currents.
30 pacemaker" current (I(f)) that increases the sinoatrial nodal (SAN) cell membrane diastolic depolariz
31    In wild-type mice, Ang II infusion caused sinoatrial nodal (SAN) cell oxidation by activating NADP
32   Dysregulation of L-type Ca(2+) currents in sinoatrial nodal (SAN) cells causes cardiac arrhythmia.
33        Eleven were found to have an abnormal sinoatrial nodal artery, and 7 of these patients also ha
34            We used a mathematical model of a sinoatrial nodal cell (SAN model) electrically coupled t
35 ted in size to be 3 to 5 times larger than a sinoatrial nodal cell, thus making effective SAN model c
36 ulum (SR) during diastolic depolarization in sinoatrial nodal cells (SANC) occur even in the basal st
37 are crucial for normal pacemaker function of sinoatrial nodal cells (SANC).
38  release from sarcoplasmic reticulum (SR) in sinoatrial nodal cells (SANC).
39 spontaneous diastolic depolarization (DD) of sinoatrial nodal cells (SANCs) that triggers recurrent a
40 ing late diastolic depolarization in cardiac sinoatrial nodal cells (SANCs).
41 s) increases the spontaneous beating rate of sinoatrial nodal cells (SANCs); however, the specific li
42 rs (RyRs) during diastolic depolarization of sinoatrial nodal cells augments the terminal depolarizat
43         We determined whether LCRs in rabbit sinoatrial nodal cells require the concurrent membrane d
44 raction) and the spontaneous beating rate of sinoatrial nodal cells were all blunted in RyR2-S2808A+/
45 s in both neonatal atrial myocytes and adult sinoatrial nodal cells.
46 ssociated with ticagrelor were asymptomatic, sinoatrial nodal in origin (66%), and nocturnal.
47 uses, which were predominantly asymptomatic, sinoatrial nodal in origin, and nocturnal and occurred m
48      Ion channels on the surface membrane of sinoatrial nodal pacemaker cells (SANCs) are the proxima
49 e of diastolic depolarization (DD) in rabbit sinoatrial nodal pacemaker cells (SANCs) generate an inw
50                Thus, the biological clock of sinoatrial nodal pacemaker cells, like that of many othe
51 lectively inhibits the funny current (If) in sinoatrial nodal tissue, resulting in a decrease in the
52 ine in situ detection of connexins in rabbit sinoatrial node (a tissue that is particularly rich in f
53 ted in genes preferentially expressed in the sinoatrial node (GNG11, RGS6 and HCN4).
54 canine AVJ preparations that did not contain sinoatrial node (n = 10).
55 d indices of sympathovagal modulation of the sinoatrial node (ratio of low-frequency to high-frequenc
56 tructive heart surgery include injury of the sinoatrial node (SAN) and atrioventricular node (AVN), r
57 highly expressed in embryonic myocardium and sinoatrial node (SAN) and is required for cardiac automa
58                Experiments were performed on sinoatrial node (SAN) and latent atrial pacemaker (LAP)
59               Numerous studies implicate the sinoatrial node (SAN) as a participant in atrial arrhyth
60 ane voltage and Ca2+ clocks jointly regulate sinoatrial node (SAN) automaticity.
61 te the activation within the human or canine sinoatrial node (SAN) because they are intramural struct
62 rucial regulatory role in the development of sinoatrial node (SAN) by repressing the expression of Nk
63 olecular and functional properties of native sinoatrial node (SAN) cardiomyocytes.
64                                           In sinoatrial node (SAN) cells, electrogenic sodium-calcium
65 t these sites and how this relates to normal sinoatrial node (SAN) development remain uncharacterized
66                                     Although sinoatrial node (SAN) dysfunction is a hallmark of human
67 polymorphic ventricular tachycardia manifest sinoatrial node (SAN) dysfunction, the mechanisms of whi
68  primary pacemaker area of the intact rabbit sinoatrial node (SAN) exhibits robust positive labeling
69 d by Ras-related small G proteins, regulates sinoatrial node (SAN) ion channel activity through a mec
70 ght to confirm our hypothesis that the human sinoatrial node (SAN) is functionally insulated from the
71                                          The sinoatrial node (SAN) maintains a rhythmic heartbeat; th
72 her their presence nor their contribution to sinoatrial node (SAN) pacemaker activity has been invest
73 ated in controlling automaticity in isolated sinoatrial node (SAN) pacemaker cells, but the potential
74  in embryonic heart, but their role in adult sinoatrial node (SAN) pacemaking is uncertain.
75 rough K(+) channels are essential for proper sinoatrial node (SAN) pacemaking, but the influence of i
76 ated current, If, plays an important role in sinoatrial node (SAN) pacemaking.
77 ces in cardiomyocyte automaticity permit the sinoatrial node (SAN) to function as the leading cardiac
78     Dysfunction of pacemaker activity in the sinoatrial node (SAN) underlies "sick sinus" syndrome (S
79          The heartbeat originates within the sinoatrial node (SAN), a small structure containing <10,
80 pecialized cardiomyocytes located within the sinoatrial node (SAN), and is responsible for originatin
81                                          The sinoatrial node (SAN), functionally known as the pacemak
82          Reentrant arrhythmias involving the sinoatrial node (SAN), namely SAN reentry, remain one of
83 ify ion channel transcripts expressed in the sinoatrial node (SAN), the pacemaker of the heart.
84 situ studies indicated that Pitx2 suppresses sinoatrial node (SAN)-specific gene expression, includin
85 ia and ventricles, there is no model for the sinoatrial node (SAN).
86 R) modulates the spontaneous activity of the sinoatrial node (SAN).
87 by specialized cardiomyocytes located in the sinoatrial node (SAN).
88 te (HR) by inhibiting pacemaker cells in the sinoatrial node (SAN).
89 bx18 give rise to the heart's pacemaker, the sinoatrial node (SAN).
90 of this is the use of optical mapping in the sinoatrial node (SAN): when microelectrode and optical r
91 dly rectifying K+ (GIRK or KACh) channels of sinoatrial node and atria play a major role in beat-to-b
92  shown at birth to be present throughout the sinoatrial node and atrial muscle, however, at one month
93 ls is required for proper hearing as well as sinoatrial node and brain function.
94 ty of cell types and distribution within the sinoatrial node and cell-cell interactions add complexit
95 ntify Islet-1 as a novel marker of the adult sinoatrial node and do not provide evidence for Islet-1(
96 izes the leading pacemaker region within the sinoatrial node and hence is crucial for stable heart ra
97  the HCN1 protein is highly expressed in the sinoatrial node and is colocalized with HCN4, the main s
98 ardiac myocytes and specialized cells in the sinoatrial node and the conduction system.
99 els of MiRP1 and HCN subunits in the cardiac sinoatrial node and the contribution of pacemaker channe
100                                          The sinoatrial node and the ventricle of the heart receive s
101 ) hearts the focus ultimately shifted to the sinoatrial node at a very prolonged cycle length (initia
102 t density contributes to the acceleration of sinoatrial node automaticity and explains, in part, the
103                                              Sinoatrial node automaticity was slowed in treated group
104  recorded from isolated papillary muscle and sinoatrial node by microelectrode techniques.
105  current appearing in the Noble model of the sinoatrial node cell in the mammalian heart.
106 r evaluated in rabbit isolated patch-clamped sinoatrial node cells (n = 21), where we found that 5 mu
107                Spontaneous beating of rabbit sinoatrial node cells (SANCs) is controlled by cAMP-medi
108 neath the cell plasma membrane (subspace) of sinoatrial node cells (SANCs) occurring during diastolic
109 ct in concert with ion channels to confer on sinoatrial node cells (SANCs) their status of dominance
110  roughly periodic LCRs in depolarized rabbit sinoatrial node cells (SANCs).
111  caffeine (2-4 mM) to isolated single rabbit sinoatrial node cells acutely reduces their spontaneous
112 geneity of the electrical activity of single sinoatrial node cells as well as that of the intact sino
113             Spontaneous action potentials of sinoatrial node cells from pregnant mice exhibited highe
114                   The electrical activity of sinoatrial node cells is heterogeneous.
115  intracellular cAMP levels were unchanged in sinoatrial node cells of pregnant mice.
116                                           In sinoatrial node cells of the heart, beating rate is cont
117 ted inward current similar to the If seen in sinoatrial node cells of the heart.
118  (as measured by cell capacitance) of rabbit sinoatrial node cells was investigated using the whole-c
119 n of pacemaker mechanisms in single isolated sinoatrial node cells, explanted beating sinoatrial node
120 on of spontaneous action potential firing in sinoatrial node cells.
121 ergically stimulated ion channels in cardiac sinoatrial node cells.
122 .0 pA/pF; P, -28.6+/-2.9 pA/pF; P=0.0002) in sinoatrial node cells.
123 the slope of the diastolic depolarization of sinoatrial node cells.
124 ysis that Cx43 protein expression within the sinoatrial node decreased with age; however, the express
125 uch as Shox2 and Tbx3, that are required for sinoatrial node development.
126 r conduction block and arrhythmias caused by sinoatrial node dysfunction are clinically important and
127                                              Sinoatrial node dysfunction associated with CPVT may inc
128             Clinical studies have shown that sinoatrial node dysfunction occurs at the highest incide
129 hmias: sinus pauses and bradycardia indicate sinoatrial node dysfunction, whereas preexcitation and a
130 ation and miR-106b-25 heterozygosity develop sinoatrial node dysfunction.
131 P maps during normal atrial excitation (i.e. sinoatrial node excitation) were compared to those obser
132 h-frequency ratio [P=0.03]) and less erratic sinoatrial node firing (eg, lower Poincare ratio [P=0.02
133               The age-dependent reduction in sinoatrial node function was not associated with changes
134  vagal activity, baroreceptor responses, and sinoatrial node function.
135 x2 regulates microRNAs (miRs) to repress the sinoatrial node genetic program.
136 onic parasympathetic neurons innervating the sinoatrial node in control and HF dogs (both, n=8).
137  beta-adrenergic receptor stimulation of the sinoatrial node in intact dogs is markedly blunted when
138 h incidence of bradycardia suggests possible sinoatrial node involvement.
139 y definition, that pacemaker function of the sinoatrial node is compromised during aging.
140                                          The sinoatrial node is the main impulse-generating tissue in
141 ectrical signal is known to originate in the sinoatrial node myocyte, but exactly what role Ca plays
142 ow that depressed excitability of individual sinoatrial node myocytes (SAMs) contributes to reduction
143                                              Sinoatrial node myocytes act as cardiac pacemaker cells
144 +) cells in the right atrium coexpressed the sinoatrial node pacemaker cell marker HCN4.
145 ted sinoatrial node cells, explanted beating sinoatrial node preparation, telemetric in vivo electroc
146 nitiates early in development, represses the sinoatrial node program and pacemaker activity on the le
147 by bradycardia, sinus dysrhythmia, prolonged sinoatrial node recovery time, increased sinoatrial cond
148    We developed a computational model of the sinoatrial node that showed that a loss of SAN cells bel
149 coupling was investigated by dye transfer in sinoatrial node tissue explants.
150                            RNA sequencing on sinoatrial node tissue lacking Islet-1 established that
151 pecifically inhibits the I(f) current in the sinoatrial node to lower heart rate, without affecting o
152 en by an electrical impulse generated in the sinoatrial node to propagate from atria to ventricles.
153 uction system, extending proximally from the sinoatrial node to the distal Purkinje fibers.
154 ional computerized numerical modeling of the sinoatrial node was conducted to validate the theoretica
155 s is controversial despite the fact that the sinoatrial node was discovered over 100 years ago.
156           Given that other biological (e.g., sinoatrial node) and artificial systems display phase-lo
157  within regions of the heart that become the sinoatrial node, atrioventricular node, and bundle of Hi
158 opagation of the action potential across the sinoatrial node, from the initiation point to the crista
159 [Ca(2+)]i release and Ca(2+) handling in the sinoatrial node, impaired pacemaker activity and symptom
160                        During failure of the sinoatrial node, the heart can be driven by an atriovent
161                                  Passing the sinoatrial node, the P-wave developed an initial positiv
162 ession and network analysis identified novel sinoatrial node-enriched genes and predicted that the tr
163 The AVJ is a primary backup pacemaker to the sinoatrial node.
164  may mask intrinsic fractal behaviour of the sinoatrial node.
165 unction, with initial, larger effects on the sinoatrial node.
166 and peripheral cells that make up the native sinoatrial node.
167 right atrial foci, especially those near the sinoatrial node.
168 e wall, corresponding to the location of the sinoatrial node.
169 otein was not expressed in the centre of the sinoatrial node.
170 lowering agent that acts specifically on the sinoatrial node.
171  of ionic currents in pacemaker cells of the sinoatrial node.
172 ial node cells as well as that of the intact sinoatrial node.
173       It also is present in areas within the sinoatrial node.
174 adycardia, consistent with AC9 expression in sinoatrial node.
175 nscriptional regulator within the developing sinoatrial node.
176 properties of pacemaker myocytes in the aged sinoatrial node.
177 sistently Islet-1 mRNA was detected in human sinoatrial node.
178 er-law behavior comparable to those of human sinoatrial node.
179 in isolated guinea pig spontaneously beating sinoatrial node/atrial preparations.
180                            A single isolated sinoatrial pacemaker cell presents intrinsic interbeat i
181 quency of pacemaker potentials from isolated sinoatrial pacemaker cells in the presence of endogenous
182 ffect of current fluctuations on the IBIs of sinoatrial pacemaker cells.
183  node and is colocalized with HCN4, the main sinoatrial pacemaker channel isoform.
184 which organized activation emanated from the sinoatrial pacemaker region.
185 ined how these properties of Ca(v)1.3 affect sinoatrial pacemaking in a mathematical model.
186  right vagosympathetic trunks innervated the sinoatrial plexus proximal to their entry into the heart
187  were contacted by fiber varicosities in the sinoatrial plexus than in the atrioventricular plexus af
188               The pacemaker converges to the sinoatrial region during development and comprises fewer
189 oepicardium, which develops posterior to the sinoatrial region of the looping-stage heart.
190                      The arrhythmia included sinoatrial (SA) block, sinus arrest, 2 degrees and 3 deg
191                                              Sinoatrial (SA) nodal cells were identified in cardiac t
192 e Ca(v)1.3 (alpha(1D)) Ca(2+) channel in the sinoatrial (SA) node by using Ca(v)1.3 Ca(2+) channel-de
193  from the spontaneous rhythmic excitation of sinoatrial (SA) node cells.
194 on entry through L-type Ca2+ channels in the sinoatrial (SA) node contributes to pacemaker activity,
195 ontaneous activity of pacemaker cells in the sinoatrial (SA) node controls heart rate under normal ph
196 retation (mosaic model) of the makeup of the sinoatrial (SA) node has been proposed to explain the ch
197  on enzymatically isolated myocytes from the sinoatrial (SA) node, right and left atria, right and le
198 nt in the myocytes of the ventricles and the sinoatrial (SA) node.
199 x5 expression is restricted to the posterior sinoatrial segments of the heart, consistent with the ti
200 ed at the venous pole in a plexus around the sinoatrial valve; mean total number of cells was 197 +/-
201 d channel 4, were located in the base of the sinoatrial valves, and this region was densely innervate
202  located in a ganglionated plexus around the sinoatrial valves.

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