ライフサイエンスコーパス: acute infarction

1 c-ischaemic neuronal injury, consistent with acute infarction.

2 he extent of microvascular obstruction after acute infarction.

3 time to be limited to hypoxic regions during acute infarction.

4 y flow as well as five key parameters during acute infarction.

5 h bypass surgery performed in the setting of acute infarction.

6 and enhancer RNAs in a large animal model of acute infarction.

7 urkinje-myocardium coupling, large scars and acute infarction.

8 ction against intraventricular thrombi after acute infarction.

9 versus abnormal brain MRI, 0.97/90%/97% for acute infarction, 0.83/72%/88% for acute hemorrhage, and

10 versus abnormal brain MRI, 0.95/92%/88% for acute infarction, 0.90/89%/81% for acute hemorrhage, and

11 ce (3 days after occlusion for assessment of acute infarction; a mean of 50 days after occlusion +/-

12 uded and divided into those with and without acute infarction according to their DWI findings.

13 variables in brain MRIs including abnormal, acute infarction, acute hemorrhage and mass effect.

14 and critical intracranial findings including acute infarction, acute hemorrhage and mass effect.

15 identified three critical findings including acute infarction, acute hemorrhage, and mass effect.

16 We compared contrast enhancement in acute infarction (AI), after severe but reversible ische

17 roups according to the clinical diagnosis of acute infarction (Al) (n = 20), stable angina (SA) (n =

18 , moyamoya morphology, and evidence of prior acute infarction and hemorrhage.

19 r compensatory responses of the rat brain to acute infarction and to the development and expression o

20 s reduce myocyte apoptosis in the setting of acute infarction, and this effect can be detected by in

21 r agent produced differential enhancement of acute infarctions at 3 days (SI ratio 5.8 +/- 1.3) but n

22 Chronic, subacute, and acute infarction cases correlated excellently to the myo

23 cable findings in all categories, except for acute infarction, compared with the other two ICUs (p <

24 nrolled in the SHOCK Trial Registry of CS in acute infarction, comparing 55 patients whose shock was

25 ocal brain ischemia with imaging evidence of acute infarction defines acute ischemic stroke (AIS), wh

26 episode with neurologic deficits but without acute infarction defines transient ischemic attack (TIA)

27 y 24 hours attributed to thrombolysis and no acute infarction/hemorrhage on imaging.

28 ient to induce spreading depolarizations and acute infarction in adjacent cortex.

29 ocardiographic criteria for the diagnosis of acute infarction in the presence of left bundle-branch b

30 a with independent value in the diagnosis of acute infarction in these patients were an ST-segment el

31 effect of bFGF on infarct size in a model of acute infarction in which coronary occlusion was followe

32 and bypass surgery in select patients after acute infarction is associated with low repeat procedure

33 generative potential of stem cells to repair acute infarction is limited.

34 In acute infarction, MR imaging estimates of function, perf

35 Acute infarction (n = 31 subjects) was better demonstrat

36 A few POC MRI examinations demonstrated acute infarctions not apparent at standard-of-care CT ex

37 rison CT available, three (13%) demonstrated acute infarctions not apparent on CT scans.

38 rt disease-related deaths and eight nonfatal acute infarctions occurred over 30 +/- 13 months.

39 Acute infarction of the anterior LV wall was induced in

40 In a patient with acute infarction of the right tonsil, we found (1) nearl

41 A total of 4,369 patients (75.4%) had an acute infarction on DWI.

42 hypothesis that restraining expansion of an acute infarction preserves LV geometry and resting funct

43 In the Acute Infarction Ramipril Efficacy (AIRE) Study, the eff

44 be safely operated on early in the course of acute infarction, risk factors for hospital mortality ar

45 ted animals with chronic, but not those with acute, infarction showed the following differences compa

46 years ago) infarcts at lower intensity than acute infarction (TBR(max) 1.2 +/- 0.1 vs 1.7 +/- 0.5 vs

47 ients admitted with a tentative diagnosis of acute infarction, the initial impression was confirmed.

48 For the patients with acute infarction, the risk-adjusted mortality ratio for

49 When evaluating a patient who has survived acute infarction treated with thrombolysis, clinicians c

50 METHODS AND Acute infarction was induced by cardiac catheterization

51 Appropriate admission for unstable angina or acute infarction was not affected.

52 Patients with acute infarction were more likely not to be hospitalized

53 The extents of enhanced regions in acute infarctions were not different after intravascular

54 e is found in ~5% to 6% of all patients with acute infarction who are referred for coronary angiograp

55 uppressing ischemia in stable patients after acute infarction who have preserved LV function.

56 ts who underwent thrombolysis within 12 h of acute infarction with confirmed cardiogenic shock, 27 un

57 Following acute infarction with reperfusion, a regional increase i