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 s considered as an optimal therapy following cardiac ischemia.
2 ital to triage patients with suspected acute cardiac ischemia.
3 ard developing a therapeutic agent for acute cardiac ischemia.
4 f failure to hospitalize patients with acute cardiac ischemia.
5  sex, and the absence of typical features of cardiac ischemia.
6 nderlying reperfusion injury after prolonged cardiac ischemia.
7 the metabolic and functional consequences of cardiac ischemia.
8 ents annually with symptoms suggesting acute cardiac ischemia.
9 d sudden death, which occur in patients with cardiac ischemia.
10 tor for changes in myocardial function after cardiac ischemia.
11  emergency department patients without acute cardiac ischemia.
12 in hospital mortality in patients with acute cardiac ischemia.
13 hage, contraction bands, and signs of global cardiac ischemia.
14 rominent and important pathogenic feature of cardiac ischemia.
15 department with symptoms suggestive of acute cardiac ischemia.
16 hroughout a prolonged 2.5 h period of global cardiac ischemia.
17 showed sinus tachycardia without evidence of cardiac ischemia.
18  or greater (ie, fifth-generation assay) and cardiac ischemia.
19 s associated with abnormally low pH, such as cardiac ischemia.
20 us enabling glycolytic ATP generation during cardiac ischemia.
21 fined as non-hsTNT 0.04 ng/mL or greater and cardiac ischemia.
22 nt regulator of the inflammatory response to cardiac ischemia.
23 could reduce pathological outcomes following cardiac ischemia.
24 e normal hearts, but Parkin is protective in cardiac ischemia.
25 ardiac output and result in secondary global cardiac ischemia.
26 ective in a number of experimental models of cardiac ischemia.
27 nary infusion of BMCs for cell therapy after cardiac ischemia.
28 e role at the intercellular junctions during cardiac ischemia.
29 ure that, in turn, may lead to microvascular cardiac ischemia.
30 ed for patients with recurrent or provocable cardiac ischemia.
31 ior circulation, 4 of arm ischemia, and 2 of cardiac ischemia.
32 es has made them leading candidates to sense cardiac ischemia.
33 thout evidence of active hemorrhage or acute cardiac ischemia.
34 y in African Americans with heart failure or cardiac ischemia.
35 antagonist is cardioprotective during global cardiac ischemia.
36 uation of patients presenting with suspected cardiac ischemia.
37 egeneration and fibrosis suggested sustained cardiac ischemia.
38 in or with symptoms consistent with possible cardiac ischemia.
39  interaction, that of potent protection from cardiac ischemia.
40 nt ventricular tachyarrhythmias during acute cardiac ischemia.
41 ins of rat hearts either lost or degraded by cardiac ischemia (15- or 60-minute duration) with and wi
42 infection (4%), pulmonary embolism (2%), and cardiac ischemia (2%).
43 ac arrhythmias (27.9% vs 25.2% of patients), cardiac ischemia (6.6% vs 5.6%), mesenteric ischemia (3.
44 rrected QT interval prolongation (8.0%), and cardiac ischemia (6.8%).
45 ercent ultimately met the criteria for acute cardiac ischemia (8 percent had acute myocardial infarct
46 clinical findings suggestive of AMI or acute cardiac ischemia (ACI) but at low risk using a validated
47                                    Transient cardiac ischemia activates cell survival signaling, conf
48 f medical conditions, including cerebral and cardiac ischemia, acute kidney injury, and transplantati
49 ults, 5% (evidence range, <0.05%; P < .001); cardiac ischemia after negative stress test result, 5% (
50 ults, 50% (evidence range, 3%-9%; P < .001); cardiac ischemia after positive stress test result, 70%
51 ing for 45% of medication withdrawals due to cardiac ischemia and arrhythmogenicity.
52 er understanding into the pathophysiology of cardiac ischemia and infarction, primary diseases of the
53  emergency department patients with possible cardiac ischemia and nondiagnostic ECGs.
54 nt to the emergency department with possible cardiac ischemia and nondiagnostic electrocardiograms (E
55  alterations in fatty acid metabolism during cardiac ischemia and postischemic reperfusion, stimulati
56 P2Y4 brings new therapeutic perspectives for cardiac ischemia and remodeling.
57                                              Cardiac ischemia and reperfusion are associated with los
58 ys a pivotal role in cardioprotection during cardiac ischemia and reperfusion injury.
59                                        After cardiac ischemia and reperfusion or reoxygenation (I/R),
60                                              Cardiac ischemia and reperfusion results in a defect at
61 affolds to generate models of aortic valves, cardiac ischemia and reperfusion, and solid tumors.
62 n by deltaPKC has no role in the response to cardiac ischemia and reperfusion.
63 g article describes the issues around silent cardiac ischemia and some of the insights obtained in th
64 I) contributes to contractile failure during cardiac ischemia and systolic heart failure, in part due
65 role in diseases such as cancer, stroke, and cardiac ischemia, and participates in a variety of signa
66 stroke, a devastating illness second only to cardiac ischemia as a cause of death worldwide.
67 scenarios common in primary care (pneumonia, cardiac ischemia, breast cancer screening, and urinary t
68 tion parallel the altered biology of induced cardiac ischemia but are well tolerated by hibernated ma
69 vity and negative predictive value for acute cardiac ischemia, but use of this method has not been pr
70 ually a transient insult, such as hypoxemia, cardiac ischemia, catecholamine excess, or electrolyte a
71 hypertension, and OSA also may contribute to cardiac ischemia, congestive heart failure, cardiac arrh
72 r electrocardiogram (ECG) findings for acute cardiac ischemia, continuous 12-lead ECG monitoring incr
73 strate that expression of ATF3 is induced by cardiac ischemia coupled with reperfusion (ischemia-repe
74                       Evidence suggests that cardiac ischemia, detected by exercise stress testing (E
75                                        After cardiac ischemia, EET-induced coronary vasodilation incr
76                    Adenosine released during cardiac ischemia exerts a marked protective effect in th
77                    Adenosine released during cardiac ischemia exerts a potent, protective effect in t
78                    Adenosine released during cardiac ischemia exerts a potent, protective effect in t
79                           Treatment of acute cardiac ischemia focuses on reestablishment of blood flo
80 n the setting of heart failure and transient cardiac ischemia followed by reperfusion (I/R).
81                GRK2 up-regulation can worsen cardiac ischemia; furthermore, increased kinase levels o
82 ong patients presenting to the ED with acute cardiac ischemia, gender does not appear to be an indepe
83                    Among patients with acute cardiac ischemia (ie, acute myocardial infarction [MI] o
84 atory studies suggest that in the setting of cardiac ischemia, immediate intravenous glucose-insulin-
85 ptibility of hERG to proteases, we show that cardiac ischemia in a rabbit model was associated with a
86 promote functional recovery in hind-limb and cardiac ischemia in animal models; however, its impact o
87                                              Cardiac ischemia in myocardium genetically engineered to
88                         For patients without cardiac ischemia, in hospitals with high-capacity CCUs a
89 eceptors are of interest in the treatment of cardiac ischemia, inflammation, and neurodegenerative di
90                                  Symptoms of cardiac ischemia initiated investigation in 4/10 patient
91 s been associated with obesity, arrhythmias, cardiac ischemia, insulin resistance, etc.
92                                              Cardiac ischemia is also associated with activation, up-
93 acid produced by anaerobic metabolism during cardiac ischemia is among several compounds suggested to
94                     Reperfusion injury after cardiac ischemia is mediated, at least in part, by delta
95 line, which contains 155 mM [Na(+)](o), with cardiac ischemia may require further investigation.
96                      Furthermore, in a mouse cardiac ischemia model, there was significant monocyte a
97 ice and Sp1 small interfering RNA in in vivo cardiac ischemia models revealed Sp1-mediated induction
98 5% CI]), AI-only users had a similar risk of cardiac ischemia (myocardial infarction and angina) (adj
99 the impact of beta-blockade on perioperative cardiac ischemia, myocardial infarction, and mortality f
100        However, among patients without acute cardiac ischemia (n = 2146), hospitalization was 52% wit
101 phic or cardiac enzyme changes suggestive of cardiac ischemia or injury, and new positive blood cultu
102 k of the most serious cardiovascular events (cardiac ischemia or stroke) was not elevated in AI-only
103  in multiple disorders (hepatitis, brain and cardiac ischemia, pancreatitis, viral infection and infl
104             The purpose of this Asymptomatic Cardiac Ischemia Pilot (ACIP) data bank study was to cha
105 oronary disease enrolled in the Asymptomatic Cardiac Ischemia Pilot (ACIP) have more episodes of asym
106       Patients screened for the Asymptomatic Cardiac Ischemia Pilot (ACIP) study were selected for th
107 of the insights obtained in the Asymptomatic Cardiac Ischemia Pilot (ACIP) Study.
108 he 558 patients enrolled in the Asymptomatic Cardiac Ischemia Pilot (ACIP) study.
109 s was an ancillary study of the Asymptomatic Cardiac Ischemia Pilot (ACIP) trial.
110                       The ACIP (Asymptomatic Cardiac Ischemia Pilot Study) enrolled patients in the 1
111 e range, 0.05-0.24; exercise stress test for cardiac ischemia: positive LR, 21.0; evidence range, 2.0
112 nhibitor, and statin agents minimize ongoing cardiac ischemia, prevent thrombus propagation, and redu
113                             A mouse model of cardiac ischemia reperfusion was used to demonstrate mul
114  sEVs in vitro and in a rat in vivo model of cardiac ischemia reperfusion.
115                                              Cardiac ischemia-reperfusion (I-R) injury occurs upon pr
116                                  After mouse cardiac ischemia-reperfusion (I-R) injury, rapid up-regu
117 e administered in the setting of hepatic and cardiac ischemia-reperfusion (I/R) injury in mice.
118 lity transition pore (mPTP) is implicated in cardiac ischemia-reperfusion (I/R) injury.
119 nd thrombin contribute to infarct size after cardiac ischemia-reperfusion (I/R) injury.
120 We hypothesized that riboflavin given during cardiac ischemia-reperfusion (I/R) might reduce subseque
121 ygen species (ROS) production that underlies cardiac ischemia-reperfusion (IR) injury.
122   Mitochondrial dysfunction induced by acute cardiac ischemia-reperfusion (IR), may increase suscepti
123 two of the top causes of death in the world, cardiac ischemia-reperfusion injury and pancreatic ducta
124                NCX inhibitors can ameliorate cardiac ischemia-reperfusion injury and promote high-fre
125 ch in turn require a better understanding of cardiac ischemia-reperfusion injury and the various poss
126 singly, MHC-PDK4 mice were not sensitized to cardiac ischemia-reperfusion injury despite a fuel utili
127                                              Cardiac ischemia-reperfusion injury is associated with d
128                                       During cardiac ischemia-reperfusion injury, neutrophilic infilt
129                                           In cardiac ischemia-reperfusion injury, reactive oxygen spe
130 xposure induces long-term protection against cardiac ischemia-reperfusion injury, which improves myoc
131 ctive Akt mutant (myr-Akt) in a rat model of cardiac ischemia-reperfusion injury.
132 lly cardioprotective in all tested models of cardiac ischemia-reperfusion injury.
133 roviding new insights into the mechanisms of cardiac ischemia-reperfusion injury.
134  The Na+-H+ exchanger figures prominently in cardiac ischemia-reperfusion injury.
135 /BB loop mimetic, plays a protective role in cardiac ischemia/reperfusion (I/R) but the molecular mec
136 isms by which TRPM2 channels protect against cardiac ischemia/reperfusion (I/R) injury, we analyzed p
137 uggested to play a crucial role in mediating cardiac ischemia/reperfusion (IR) injury, and the blocka
138 promise as a therapeutic target for reducing cardiac ischemia/reperfusion (IR) injury; however, the l
139 rexpression as well as inhibition of MDM2 on cardiac ischemia/reperfusion injury and hypertrophy.
140 kine was also elevated in a porcine model of cardiac ischemia/reperfusion injury and in murine hearts
141                The role of oxidant stress in cardiac ischemia/reperfusion injury in humans remains co
142           BD exacerbates posttransplantation cardiac ischemia/reperfusion injury in mice and humans a
143                               We report that cardiac ischemia/reperfusion injury is associated with s
144                  Mice were then subjected to cardiac ischemia/reperfusion injury to depress heart fun
145  normoxic HIF-1 preservation could attenuate cardiac ischemia/reperfusion injury via a preconditionin
146                             A mouse model of cardiac ischemia/reperfusion injury was subsequently use
147                                    In murine cardiac ischemia/reperfusion injury, CR-AnxA1(2-50) elic
148  in a wide range of human diseases including cardiac ischemia/reperfusion injury, drug induced cardio
149                       In an ex vivo model of cardiac ischemia/reperfusion injury, perfusion of a mous
150 omyocytes following hemodynamic overload and cardiac ischemia/reperfusion injury.
151 arch, such as hepatic ethanol metabolism and cardiac ischemia/reperfusion injury.
152 he effect of donor BD on posttransplantation cardiac ischemia/reperfusion injury.
153                                              Cardiac ischemia/reperfusion is associated with an incre
154                                              Cardiac ischemia/reperfusion is associated with increase
155  expression was significantly increased in a cardiac ischemia/reperfusion model where inflammation an
156                    Remarkably, in an in vivo cardiac ischemia/reperfusion mouse model, Sema4A was hig
157 ween three alterations known to occur during cardiac ischemia/reperfusion, mitochondrial Ca(2+) accum
158 ng viral infection, acute kidney injury, and cardiac ischemia/reperfusion.
159  potentiation of injury caused by lactate in cardiac ischemia/reperfusion.
160 gene that determines the ability to tolerate cardiac ischemia/reperfusion.
161  exhibits diminished activity as a result of cardiac ischemia/reperfusion.
162 of mitochondrial respiratory activity during cardiac ischemia/reperfusion.
163 ond key membrane transporter involved in the cardiac ischemia response.
164 egeneration is well documented after chronic cardiac ischemia, so we were surprised that the cardiac
165 ld-type or mutant ALDH2 who are subjected to cardiac ischemia, such as during coronary bypass surgery
166 n ventricular fibrillation in the setting of cardiac ischemia, sympathetic activation is proarrhythmi
167                                       During cardiac ischemia, the buildup of acidic metabolites resu
168 ity of acute ischemia predicted by the acute cardiac ischemia time-insensitive predictive instrument
169  cardiac ischemia were enrolled in the Acute Cardiac Ischemia Time-Insensitive Predictive Instrument
170 tivation to tissue damage after neuronal and cardiac ischemias, traumatic spine and brain injuries, a
171 n linked to tissue damage after neuronal and cardiac ischemias, traumatic spine and brain injuries, a
172                             Brief periods of cardiac ischemia trigger protection from subsequent prol
173   Wild-type mice were subjected to 30 min of cardiac ischemia (via LAD occlusion) and treated with a
174 t pain or other symptoms suggestive of acute cardiac ischemia were enrolled in the Acute Cardiac Isch
175 ients presenting with symptoms suggestive of cardiac ischemia were included in the analysis.
176 ented to the emergency department with acute cardiac ischemia were more likely not to be hospitalized
177 rtant protective mechanism in the setting of cardiac ischemia where arachidonic acid levels are drama
178 ons (e.g. fatty acid oxidation disorders and cardiac ischemia) where long-chain acylcarnitine accumul
179 vation of the sarcolemmal Na/K ATPase during cardiac ischemia, which is masked by an inhibitor of the
180    In particular, hypoxia is associated with cardiac ischemia, which, although initially inducing a p
181 hest pain or other symptoms suggesting acute cardiac ischemia who presented to the emergency departme
182 r patients with symptoms suggestive of acute cardiac ischemia without obvious abnormalities on initia

 
Page Top