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  • 1
    Electronic Resource
    Electronic Resource
    Free fatty acids regulate gut incretin glucagon-like peptide-1 secretion through GPR120 (2005)
    [s.l.] : Nature Publishing Group
    Nature medicine 11 (2005), S. 90-94 
    Details
    ISSN: 1546-170X
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Diabetes, a disease in which the body does not produce or use insulin properly, is a serious global health problem. Gut polypeptides secreted in response to food intake, such as glucagon-like peptide-1 (GLP-1), are potent incretin hormones that enhance the glucose-dependent secretion of insulin ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/nm1168
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  • 2
    Electronic Resource
    Electronic Resource
    The gamete fusion process is defective in eggs of Cd9-deficient mice (2000)
    [s.l.] : Nature America Inc.
    Nature genetics 24 (2000), S. 279-282 
    Details
    ISSN: 1546-1718
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] The cell-surface molecule Cd9, a member of the transmembrane-4 superfamily, interacts with the integrin family and other membrane proteins, and is postulated to participate in cell migration and adhesion. Expression of Cd9 enhances membrane fusion between muscle cells and promotes viral infection ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/73502
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  • 3
    Electronic Resource
    Electronic Resource
    Recurrent left ventricular mural thrombi in a patient with acute myocarditis (1988)
    Springer
    Heart and vessels 4 (1988), S. 120-122 
    Details
    ISSN: 1615-2573
    Keywords: Left ventricular thrombus ; Acute myocarditis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A case of acute myocarditis with recurrent left ventricular mural thrombi in a 59-year-old man is reported. Two-dimensional echocardiogram demonstrated left ventricular mural thrombus with apical dyskinesis on the 2nd day after the onset of chest oppression. No hemoagglutination abnormalities were present. Anticoagulation treatment with heparin was initiated. A two-dimensional echocardiogram obtained on the 15th day showed that the left ventricular wall motion had become normal and that the thrombus had disappeared. However, on the 38th day, a new pedunculated free mobile thrombus was found in the apical part of the left ventricle despite the normal wall motion. By the 46th day, the new thrombus had disappeared. The present case suggests that mural thrombi can occur in the absence of left ventricular dyskinesis and dilatation. Anticoagulation therapy resolved the mural thrombi but could not prevent the recurrence at the apex. Thus, in acute myocarditis, a mural thrombus may appear as a result of the endocardial damage, even when blood stasis is absent.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02059000
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  • 4
    Electronic Resource
    Electronic Resource
    Modification of pacing-induced alterations in diastolic properties of the regional myocardium by nifedipine in patients with coronary artery disease (1985)
    Springer
    Heart and vessels 1 (1985), S. 232-238 
    Details
    ISSN: 1615-2573
    Keywords: Regional diastolic properties ; Pacing-induced ischemia ; Pressure-length loop ; Nifedipine ; Automatic processing of cineventriculograms
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of nifedipine on regional dysfunction during pacing-induced ischemia were studied in eight patients with coronary artery disease. Single-plane left ventriculograms were obtained using a high-fidelity micromanometer-tipped catheter in the control and post-pacing periods both before and after pretreatment with nifedipine. All patients developed typical anginal pain during pacing tachycardia before but not after pretreatment with nifedipine. After pacing, left ventricular end-diastolic pressure (EDP) increased from 10±5 (SD) mmHg to 23±9 mmHg (P〈0.01) with enlargement of the end-diastolic volume (EDV). The ejection fraction (EF) was reduced from 66±10% to 54±13% (P〈0.05). With nifedipine, a post-pacing increase in EDP was markedly attenuated together with a 17% reduction in left ventricular systolic pressure (P〈0.05). The regional myocardial function was expressed by a radial coordinate system with its origin at the center of gravity of the end-diastolic contour. Two representative radial grids for normal and ischemic segments were selected. In the normal segment, the end-diastolic length (EDL) was augmented by 14% (from 26.1±5.2 mm to 29.7±6.1 mm,P〈0.01) associated with a 23% increase in stroke excursion (P〈0.05) with pacing stress. In the ischemic segments, EDL remained unchanged in the post-pacing beat but stroke excursion was significantly reduced (from 11.4±5.2 mm to 4.3±1.8 mm,P〈0.01). After pretreatment with nifedipine, the responses of the regional myocardium to the same pacing stress were markedly reduced; the EDL of the control segment was 27.4±4.6 mm with equally augmented stroke excursion. EDL of the ischemic segment remained unchanged but post-pacing deterioration of segment shortening was remarkably improved (8.7±3.3 mm,P〈0.05). With pacing stress before nifedipine, the control segment moved up to the higher portion of the single curve. In the ischemic segment, the diastolic pressure became higher at any given length and the pressure length curve clearly shifted upward, indicating regional alteration of the diastolic property. After nifedipine, this upward shift of the regional myocardial pressure-length relationship was markedly attenuated. Thus, we conclude that nifedipine favorably modifies the symptomatic and hemodynamic responses to transient ischemia due to pacing stress largely mediated by selective improvement of the ischemic segment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02073655
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  • 5
    Electronic Resource
    Electronic Resource
    Antiischemic effect of intracoronary diltiazem on myocardial ischemia during PTCA (1996)
    Springer
    Heart and vessels 11 (1996), S. 92-99 
    Details
    ISSN: 1615-2573
    Keywords: Diltiazem ; PTCA ; Intracoronary ECG ; Myocardial ischemia ; Myocardial protection
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To evaluate the effect of intracoronary diltiazem on myocardial ischemia during percutaneous transluminal coronary angioplasty (PTCA), 38 patients were randomly assigned to receive inactive placebo (n = 19; group C) or a low dose (1 mg,n = 10; group D1), or a high dose (2 or 3mg,n = 9; group D2) of diltiazem in a double-blind manner. The agent was administered directly into the coronary artery via a balloon catheter following a control balloon inflation. Chest pain score (maximum, 10) and the magnitude of ischemic ST elevation on standard and intracoronary electrocardiograms (ECGs) during a balloon inflation were assessed in the control and posttreatment periods. After the administration of diltiazem, the chest pain score was significantly decreased in group D1 (control: 5.1 ± 3.6, posttreatment: 3.8 ± 3.1,P 〈 0.01) and group D2 (3.4 ± 2.5 vs 2.5 ± 2.0,P 〈 0.01), but not in group C (4.1 ± 3.1 vs 3.7 ± 3.3, difference not significant). The magnitude of ST elevation relative to the control on standard and intracoronary ECGs was significantly smaller in groups D1 and D2 than in group C (standard ECG; D1: 51.8 ± 10.6% of control, D2: 41.6 ± 28.7% vs C: 93.3 ± 15.6% and intracoronary ECG; D1: 47.1 ± 11.7% of control, D2: 27.5 ± 26.9% vs C: 94.6 ± 29.3%, allP 〈 0.01). Although systolic blood pressure decreased slightly in groups D1 and D2, there was no significant correlation between the change in ST elevation and the change in the rate-pressure product. Pretreatment with a small dose of intracoronary diltiazem attenuated myocardial ischemia during PTCA and this pretreatment may enable us to perform balloon inflation for a longer period.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01744509
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  • 6
    Electronic Resource
    Electronic Resource
    Enhancement of coronary reactive hyperemia in patients with ischemic myocardial tolerance during angioplasty (1996)
    Springer
    Heart and vessels 11 (1996), S. 242-247 
    Details
    ISSN: 1615-2573
    Keywords: Reactive hyperemia ; Angioplasty ; Ischemia ; Preconditioning
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The purpose of this study was to elucidate the effect of repeated brief coronary occlusions on reactive hyperemia during percutaneous transluminal coronary angioplasty (PTCA) in patients with or without ischemic tolerance. Seventeen patients undergoing PTCA for chronic stable angina were studied. Patients with well developed collateral vessels were excluded. After successful predilatation, coronary flow velocity was recorded with the use of a Doppler flow guide wire, and reactive hyperemia was assessed immediately after each of two 2-min coronary occlusions followed by 2 mins of reperfusion. The intracoronary electrocardiogram (icECG) was recorded via the flow guide wire placed in the center of the ischemic zone. Patients were divided into two groups: those who showed a reduction of ST elevation in the icECG recorded at the time of the second coronary occlusion (group I), and those who showed no difference in ST elevation between the two occlusions (group II). There were no significant differences in blood pressure, heart rate, or baseline coronary flow velocity between the two groups before the first occlusion, but the ST elevation at the time of the first coronary occlusion was greater in group I than in group II (8.9 ± 6.2 versus 1.1 ± 2.0mm,P 〈 0.01). Reactive hyperemia was significantly greater after the second coronary occlusion than after the first in group I (22.1 ± 15.8 versus 30.4 ± 21.0cm/s,P 〈 0.05), but it did not change in group II (25.6 ± 13.0 versus 23.5 ± 11.2cm/s NS). Reactive hyperemia was enhanced in patients with ischemic tolerance who showed a reduction in ST elevation in the icECG. These results suggest that observed reactive hyperemia does not necessarily reflect the severity of ischemia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01746204
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  • 7
    Electronic Resource
    Electronic Resource
    Left ventricular filling measured by Doppler echocar diography during dynamic exercise in patients with myocardial infarction (1993)
    Springer
    Heart and vessels 8 (1993), S. 23-32 
    Details
    ISSN: 1615-2573
    Keywords: Diastole ; Exercise ; Doppler echo-cardiography ; Myocardial infarction ; Left ventricular filling
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To assess left ventricular diastolic properties in response to dynamic exercise, mitral inflow velocity integrals were measured by pulsed-wave Doppler echocardiography in ten patients with myocardial infarction and in ten normal subjects, and simultaneous left ventricular pressure was obtained with micromanometry in the patients. Early filling velocity integrals were maintained in the patients during exercise. Late filling velocity integrals were not augmented during exercise in the patients, but were increased in the normal subjects. In the patients, there was an increase in mitral valve opening pressure, left ventricular end-diastolic pressure, and the time constant of left ventricular isovolumic pressure decay. The lowest diastolic pressure and the number of time constants that had elapsed before the lowest diastolic pressure remained unchanged. These results show that in patients with myocardial infarction, early filling is maintained by an increase in driving pressure during exercise, despite incomplete relaxation. Augmentation of late filling, seen in normal subjects, is impaired in patients with myocardial infarction, probably due to an increase in left ventricular stiffness.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01744471
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  • 8
    Electronic Resource
    Electronic Resource
    Reperfusion Phenomena Suggestive of Reperfusion Injury in Patients with Acute Myocardial Infarction (1997)
    Springer
    Journal of thrombosis and thrombolysis 4 (1997), S. 39-41 
    Details
    ISSN: 1573-742X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1017577812891
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  • 9
    Electronic Resource
    Electronic Resource
    Acute hemodynamic effects of MDL 19205 on conscious dogs with mitral regurgitation (1988)
    Springer
    Cardiovascular drugs and therapy 2 (1988), S. 305-311 
    Details
    ISSN: 1573-7241
    Keywords: MDL19205 ; mitral regurgitation ; conscious dogs ; inodilator
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To assess the effects of MDL 19205, a combined inotropic-vasodilating agent, or an inodilator, on the left ventricle with subacute volume overload due to mitral regurgitation (MR), seven dogs were instrumented with a left ventricular (LV) micromanometer and a pair of ultrasonic crystals for the measurement of LV circumferential segment length. After examining the effects of this drug in the normal hearts, its effects were observed in the same dogs in which MR was produced by sectioning chordae tendineae. Mitral regurgitation caused increases in LV peak dP/dt (2.384±256 to 3.090±622 mmHg/sec; p〈0.05), mean circumferential shortening velocity (Vcf; 1.41±0.25 to 1.85±0.20 sec-1; p〈0.05), LV end-diastolic pressure (LVEDP; 8.2±1.6 to 15.8±3.7 mmHg; p〈0.001), and LV end-diastolic length (LVEDL; 10 to 10.6±0.2mm; p〈0.01). The dogs were intravenously administered MDL19205 7 to 14 days after they had completely recovered from the first and second operations. With 3 mg/kg of MDL19205, peak changes of hemodynamic indices occurred within 5 minutes in the hearts with MR. LV dP/dt and mean Vcf significantly rose (from 3,090±622 to 5,356±811 mmHg/sec; p〈0.001, 1.85±0.20 to 2.65±0.36 sec-1, p〈0.001). LVEDP and LVEDL were returned to the control values obtained in the normal hearts (15.8±3.7 to 6.4±2.4 mmHg; p〈0.001, 10.6±0.2 to 10±0.4; p〈0.01). While MDL19205 increased the heart rate in the normal hearts (98±9 to 118±9 beats/min; p〈0.05), it had no effect on those with MR (109±10 to 106±17 beats/min). This study suggests that MDL19205 increases LV contractile indices and decreases preload indices in subacute MR, as observed in the normal heart. In addition, it does not increase heart rate in MR while it increases in the normal heart. Thus, MDL19205 is a promising inodilator for the treatment of hemodynamic abnormalities resulting from subacute MR.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00054637
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