戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

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    This limits force production and promotes muscle relaxation.
2 band thereby preventing misfolding events on muscle relaxation.
3 tein kinase I suggested a pathway for smooth muscle relaxation.
4 ing soluble guanylyl cyclase to cause smooth muscle relaxation.
5 ormance in an animal model of slowed cardiac muscle relaxation.
6 -activated K+ channels and results in smooth muscle relaxation.
7 s, suggesting decreased cGMP-mediated smooth muscle relaxation.
8 xation, mindfulness, and breathing exercises/muscle relaxation.
9  kinase G (PKG) activity and vascular smooth muscle relaxation.
10  inhibition of these neurons disrupts timely muscle relaxation.
11  I (TnI) plays a critical role in regulating muscle relaxation.
12 sphate (cGMP) and subsequent vascular smooth muscle relaxation.
13 on and the consequent MLCP activation during muscle relaxation.
14 nditions that could be improved by promoting muscle relaxation.
15 tes chloride channels on the muscle to cause muscle relaxation.
16 oxicity and Ca(2+) extrusion during skeletal muscle relaxation.
17 omyotonia, an exercise-induced impairment of muscle relaxation.
18 n relief from bronchospasm via airway smooth muscle relaxation.
19 ) (PGE(2)) production and bronchiolar smooth muscle relaxation.
20 dothelium is integral to coordinating smooth muscle relaxation.
21 tching might limit the rate of fast skeletal muscle relaxation.
22 unknown mechanism, possibly involving smooth muscle relaxation.
23  helix relieves SERCA inhibition, initiating muscle relaxation.
24 es not always accompany cGMP-mediated smooth muscle relaxation.
25 tudy how myosin activators may affect soleus muscle relaxation.
26 yed colonic emptying, and decreased circular muscle relaxation.
27 pnotics and opioids, promotes intraoperative muscle relaxation.
28 e decrease in MLC phosphorylation and smooth muscle relaxation.
29 en of the sarcoplasmic reticulum, initiating muscle relaxation.
30 ork together to modulate the rate of cardiac muscle relaxation.
31 vity and induces MLC20 dephosphorylation and muscle relaxation.
32 ular Ca(2+) ([Ca(2+)](i)) and causing smooth muscle relaxation.
33 pparent Ca(2+) affinity and thereby enabling muscle relaxation.
34 osin phosphatase, leading to vascular smooth muscle relaxation.
35 the sensitivity to 8-Br-cGMP-mediated smooth muscle relaxation.
36 ha-Tm) have been shown to cause slow cardiac muscle relaxation.
37 cogen metabolism, cell-cycle progression and muscle relaxation.
38 rotein that regulates PP1 function in smooth muscle relaxation.
39 gested to be required for NO-mediated smooth muscle relaxation.
40 myosin light chain (MLC) and vascular smooth muscle relaxation.
41 fectively controls the development of smooth muscle relaxation.
42 ng cascade that ultimately transduces smooth muscle relaxation, a significant "spare receptor" pool h
43  1 gene (CLCN1), is characterized by delayed muscle relaxation after contraction.
44                                              Muscle relaxation after repetitive stimulation is accomp
45  the endothelium coordinates vascular smooth muscle relaxation along resistance arteries during blood
46 hosphatase is the primary effector of smooth muscle relaxation and a target of signaling pathways tha
47 olinoleate [LNO2]) that can stimulate smooth muscle relaxation and block platelet activation by eithe
48  EDTA recovered its ability to contribute to muscle relaxation and Ca2+ sequestration at its Ca2+ off
49              Like PA, EDTA's contribution to muscle relaxation and Ca2+ sequestration was more clearl
50 ns are a general mechanism both for inducing muscle relaxation and for switching off myosin II-based
51 omyopathy, characterized by impaired cardiac muscle relaxation and force development.
52 ems such as neurotransmitter release, smooth muscle relaxation and frequency tuning of auditory hair
53 f signaling through GAR-3 inhibit pharyngeal muscle relaxation and impair feeding--but do not block m
54     Rapamycin, an mTORC1 inhibitor, improved muscle relaxation and increased muscle force in HSALR mi
55 d sPTB genes that are involved in myometrial muscle relaxation and inflammatory responses and that ar
56                                              Muscle relaxation and inhibitory neurotransmission are r
57 -adrenergic signaling promotes airway smooth muscle relaxation and limits the release of pro-inflamma
58 -ATPase of skeletal muscle, is essential for muscle relaxation and maintenance of low resting Ca(2+)
59 n cyclic nucleotide-mediated vascular smooth muscle relaxation and may play a role in the increased p
60 lates such physiological processes as smooth muscle relaxation and neuronal survival.
61 in animals controls processes such as smooth muscle relaxation and neurotransmission by activation of
62 ells, may be associated with vascular smooth muscle relaxation and peripheral blood flow increase in
63  signature analyses further reveal PGR-B for muscle relaxation and PGR-A being proinflammatory.
64 ascular homeostasis via regulation of smooth muscle relaxation and platelet aggregation.
65 oponin-I, and C-protein, causing accelerated muscle relaxation and reduced myofilament sensitivity to
66  cAMP in the lungs, leading to airway smooth muscle relaxation and reduced neutrophil infiltration in
67 Reactivity to endothelial-independent smooth muscle relaxation and subsequent vessel dilation was sim
68 however, in the regulation of uterine smooth muscle relaxation and that of other smooth muscles and c
69 tor for limiting NO-mediated vascular smooth muscle relaxation and tissue survival following ischemic
70 l cGMP signaling which is involved in smooth muscle relaxation and vascular tone, inhibition of plate
71 fter binding nitric oxide, leading to smooth muscle relaxation and vasodilation.
72  enhances cardiac contractility, accelerates muscle relaxation, and amplifies the inotropic and lusit
73 en limiting side effects including sedation, muscle relaxation, and ataxia.
74 t, PAR(2)-mediated PGE(2) production, smooth muscle relaxation, and decreased baseline airway resista
75 d, but did not eliminate, NO release, smooth muscle relaxation, and hyperpolarization.
76 roendosecretion, visual transduction, smooth muscle relaxation, and microbial killing.
77 ts of non-linear contractile responses, slow muscle relaxation, and neuromodulation.
78 intubation and procedures requiring profound muscle relaxation, and to minimize the amounts of anesth
79             Furthermore, the prolongation of muscle relaxation appeared to correlate with the levels
80 The mechanisms that modulate the kinetics of muscle relaxation are critically important for muscle fu
81 lays important roles in both vascular smooth muscle relaxation as well as prevention of blood coagula
82 R), plays important roles in vascular smooth muscle relaxation as well as the prevention of platelet
83  promotes increased corpus cavernosum smooth muscle relaxation associated with increased HO-1 express
84      In rats, ocinaplon produces significant muscle relaxation, ataxia, and sedation only at doses >2
85  suggesting that the effects of NO on smooth muscle relaxation, blood pressure regulation and inhibit
86 sed for controlling the depth of anesthesia, muscle relaxation, blood pressure, intravascular volume,
87 locking agents (NMBAs) induce dose-dependent muscle relaxation, but their effects vary widely between
88                                       Smooth muscle relaxation by acetylcholine and a number of other
89 ated by cAMP (Epac), induces vascular smooth muscle relaxation by increasing the activity of ryanodin
90 asmic reticulum Ca(2+)-ATPase SERCA promotes muscle relaxation by pumping calcium ions from the cytop
91 hibit SERCA, the membrane pump that controls muscle relaxation by regulating Ca(2+) uptake into the s
92                                       Smooth muscle relaxation can also be elicited by inhibitors of
93               We report further that oviduct muscle relaxation can be induced by activating OA neuron
94 hus, our results demonstrate how coordinated muscle relaxation can be realized by an intersegmental c
95 s with myotonia congenita suffer from slowed muscle relaxation caused by hyperexcitability.
96                  Patients experience delayed muscle relaxation causing functionally limiting stiffnes
97 rates of LC(20) dephosphorylation and smooth muscle relaxation compared with LC(20) phosphorylated ex
98 ddition to weakness, NEM6 patients have slow muscle relaxation, compromising contractility and daily
99  reinforce and temporally fine-tune striated muscle relaxation-contraction cycles.
100 cellular Ca(2+) concentration that generates muscle relaxation/contraction cycles.
101 hat selected measures of muscle strength and muscle relaxation correlate with changes in clinical sta
102  and the sensitivity to cGMP-mediated smooth muscle relaxation correlates with the relative expressio
103 ears that the mutant behavior is caused by a muscle relaxation defect due to the impairment of Ca2+ r
104         Although it is impossible to improve muscle relaxation (defined as absence of electrical acti
105 e, a fundamental gap in our understanding of muscle relaxation, despite its importance for muscle fun
106 s lead to Brody disease, an exercise-induced muscle relaxation disorder, zebrafish accordion mutants
107 tassium (K(ATP)) channels, often involved in muscle relaxation, do not contribute to adenosine's effe
108 reticulum (SR) of cardiac myocytes, enabling muscle relaxation during diastole.
109  agents are used commonly to induce skeletal muscle relaxation during surgery.
110 annins provides a molecular basis for smooth muscle relaxation effects of Native American folk medici
111 ily type A (BoNT-A), has useful long-lasting muscle relaxation effects on spastic motor disorders.
112                                        While muscle relaxation facilitates surgical procedures and tr
113           Nitric oxide (NO) acts as a smooth muscle relaxation factor and plays a crucial role in mai
114                                      Optimal muscle relaxation for ambulatory surgery results from a
115                                     Skeletal muscle relaxation has been primarily studied by assessin
116            The rate-limiting step of cardiac muscle relaxation has been proposed to reside in the myo
117 he principle stimulator of cavernosal smooth muscle relaxation, however, the inhibition of vasoconstr
118 rect myosin inhibition could provide optimal muscle relaxation; however, targeting skeletal myosin is
119 ore, TnT potentially contributes to striated muscle relaxation; however, the in vivo functional relev
120 appears to be a suitable agent for providing muscle relaxation in critically ill patients.
121 this series mediate very long-lasting smooth muscle relaxation in guinea pig tracheal strips.
122 nthase in regulating the NO-dependent smooth muscle relaxation in human penile corpus cavernosum tiss
123  inhibitory junctional potentials (IJPs) and muscle relaxation in mammalian gastrointestinal (GI) mus
124 tly, 6-PBC 24 also reversed diazepam-induced muscle relaxation in mice.
125               PKG subsequently causes smooth muscle relaxation in part via activation of myosin light
126             Atracurium is sometimes used for muscle relaxation in patients undergoing mechanical vent
127  in vascular homeostasis by mediating smooth muscle relaxation in response to nitric oxide, but littl
128                                       Smooth muscle relaxation in response to NO signaling is due, in
129 erphoria by VFV is accomplished mainly by IR muscle relaxation in the hypotropic eye, principally in
130 gnificant enhancement of NO-dependent smooth muscle relaxation in this tissue.
131 revents strong binding to actin and promotes muscle relaxation in vitro and in vivo.
132 ng skeletal muscle myosin by MPH-220 enabled muscle relaxation, in human and model systems, without c
133 , these cyclodextrin derivatives reverse the muscle relaxation induced by rocuronium in vitro and in
134  of calcium from the sarcoplasmic reticulum, muscle relaxation involves the active transport of calci
135 ability to bind Ca2+ and facilitate skeletal muscle relaxation is limited by its Mg2+ off-rate.
136                                              Muscle relaxation is triggered by the dephosphorylation
137 lution microscopy revealed that the impaired muscle-relaxation kinetics in NEM6 patients are caused b
138 n KBTBD13 cause structural changes impairing muscle-relaxation kinetics.
139 of transcranial magnetic stimulation-induced muscle relaxation, muscle fiber- and sarcomere-contracti
140 The aim of this study was to investigate the muscle relaxation of human gallbladders with cholesterol
141              The mechanism underlying smooth muscle relaxations of cerebral arteries in response to n
142                        The effects of smooth muscle relaxation on arterial wall mechanics are controv
143                          Peptides that cause muscle relaxation or contraction or that modulate electr
144 ontributing to feedback inhibition of smooth muscle relaxation or other processes.
145                               Central to the muscle relaxation phase is a dynamic membrane protein co
146         Current models postulate that during muscle relaxation, phosphatases other than MLCP dephosph
147                            Defective cardiac muscle relaxation plays a causal role in heart failure.
148  (n = 25; female/male = 24/1) or progressive muscle relaxation (PMR; n = 20; female/male = 17/3).
149 ractions, coupled with nitric oxide-mediated muscle relaxation, promote intestinal transit and parasi
150  in differentiated C2C12 slows the timing of muscle relaxation, promotes nuclear localization of calc
151 nberger technique was used, with respiratory muscle relaxation provided by brief manual ventilation.
152 ced vasorelaxation while NO-dependent smooth muscle relaxation remained unchanged.
153 ion may influence a proportion of the smooth muscle relaxation that occurs in asthma.
154 c oxide (NO) synthesis and subsequent smooth muscle relaxation, the signaling pathways downstream of
155 a myosin-blocking state, aberrantly favoring muscle relaxation, thus mimicking the low-Ca(2+) effect
156                                              Muscle relaxation time increased more in symptomatic sta
157                                              Muscle relaxation time was much more prolonged than was
158 f cytosolic calcium and consequent prolonged muscle relaxation times.
159                              Vascular smooth-muscle relaxation to diethylamine was enhanced in endoth
160 almodulin to produce NO, which causes smooth muscle relaxation to regulate physiologic tone.
161 me-in-bed restrictions; n = 25), progressive muscle relaxation training (RT; n = 25), or a quasi-dese
162 target protein, HSP20, which mediates smooth muscle relaxation via actin depolymerization.
163                                              Muscle relaxation was commonly used, with 40% of the cen
164                                       Smooth muscle relaxation was complete in both groups.
165                               Anesthesia and muscle relaxation were maintained continuously throughou
166     However, these mechanisms cannot explain muscle relaxation when [Ca(2+)](i) decreases at high loa
167 lcium to the sarcoplasmic reticulum to allow muscle relaxation, whereas PLB inhibits cardiac SERCA un
168 thelium-independent coronary vascular smooth muscle relaxation, whereas the abnormal response to cold
169 augments beta-agonist-mediated airway smooth muscle relaxation, while augmenting beta-agonist-stimula
170 der baseline conditions and following smooth muscle relaxation with nitroglycerin (NTG).
171                                       Smooth muscle relaxation with NTG increases isobaric compliance
172  of HSP20 on Ser16 may have a role in smooth muscle relaxation without MLC dephosphorylation.
173 crease in [cGMP], can induce arterial smooth muscle relaxation without proportional reduction in myos

 
Page Top