bluuebunny/crossref_metadata_2025_split huggingface dataset:
Red wine protects diabetic patients from meal‐induced oxidative stress and thrombosis activation: a pleasant approach to the prevention of cardiovascular disease in diabetes
Authors: Ceriello A. , Bortolotti N. , Motz E. , Lizzio S. , Catone B. , Assaloni R. , Tonutti L. , Taboga C. 
Published: March 2003

Background Oxidative stress and thrombosis have been reported to be increased in diabetic patients and involved in the pathogenesis of cardiovascular complications. It has been demonstrated in diabetic patients that consumption of a meal is accompanied by the generation of an oxidative stress and of a hypercoagulable state. It is well recognized that red wine shows antithrombotic activity and that its ingestion increases plasma antioxidant capacity in man. In this study the possibility that red wine consumption may reduce the oxidative stress and thrombosis produced postprandially in diabetic patients has been evaluated.Subjects and methods Twenty type 2 diabetic patients were studied during fasting consumption of 300 mL of red wine, or during a meal accompanied, or not, by red wine ingestion. Plasma glucose, insulin, triglycerides, total plasma radical‐trapping capacity, activated factor VII and prothrombin fragments 1 + 2 were measured in basal state and at 60, 120 and 180 min after the start of each experiment. Low‐density lipoprotein (LDL) oxidation was also evaluated at baseline and after 120 minResults Plasma glucose, insulin, triglycerides and LDL oxidation significantly increased, while the total plasma radical‐trapping parameter significantly decreased during the meal test. Consumption of red wine in the fasting state significantly increased total plasma radical‐trapping parameter activity, while wine ingestion with a meal counterbalanced the decrease of total plasma radical‐trapping parameter and the increase of LDL oxidation. Meal consumption induced an increase in plasma prothrombin fragments 1 + 2 and activated factor VII in diabetic patients. Wine ingestion with the meal significantly reduced the production of both prothrombin fragments 1 + 2 and activated factor VII. Fasting consumption of red wine alone did not show effects on coagulation or LDL oxidation.Conclusion This finding confirms that in the absorptive phase free radicals are produced in diabetic patients, which reduce serum antioxidant defences, increase LDL oxidation and activate the coagulation system. Red wine consumption during a meal significantly preserves plasma antioxidant defences and reduces both LDL oxidation and thrombotic activation. The consumption of a moderate amount of red wine during meals may have a beneficial effect in the prevention of cardiovascular disease in diabetic patients.
Comparative study on antibodies to human and bacterial 60 kDa heat shock proteins in a large cohort of patients with coronary heart disease and healthy subjects
Authors: Prohászka Z. , Duba J. , Horváth L. , Császár A. , Karádi I. , Szebeni A. , Singh M. , Fekete B. , Romics L. , Füst G. 
Published: March 2003

Background Recent observations indicate an association between antibodies against mycobacterial heat shock protein (hsp65) and coronary heart disease (CHD). Previously, we reported on marked differences in antigen specificity and complement activating ability of anti‐hsp65 antibodies and auto‐antibodies against human heat shock protein, hsp60. Here, we investigated whether there are differences between antih‐sp65 and anti‐hsp60 antibodies in their association with CHD.Design We measured by ELISA the levels of antibodies to hsp65, hsp60 and E. coli‐derived GroEL in three groups: Group I, 357 patients with severe CHD who underwent by‐pass surgery; Group II, 67 patients with negative coronary angiography; Group III, 321 healthy blood donors. Antibodies against Helicobacter pylori were also measured by commercial ELISA.Results As calculated by multiple regression analysis, the levels of anti‐hsp60 auto‐antibodies were significantly higher in Group I compared to Group II (P = 0·007) or Group III (P < 0·0001). By contrast, although concentrations of anti‐hsp65 and anti‐GroEL antibodies in Group I were higher than in Group III, no significant differences between Group I and Group II were found. Antibodies to the two bacterial hsp strongly correlated to each other, but either did not correlate or weakly correlated to hsp60. In Group I, serum concentrations of anti‐H.pylori antibodies significantly correlated with those of anti‐hsp65 and anti‐GroEL antibodies but they did not correlate with the anti‐hsp60 antibodies.Conclusion As to their clinical relevance, a remarkable difference become evident between antibodies to human hsp60 and antibodies against bacterial hsp in the extent of association with CHD. On the basis of these findings and some pertinent literature data, an alternative explanation for the association between high level of anti‐hsp antibodies and atherosclerotic vascular diseases is raised.
Assessment of β‐cell function during the oral glucose tolerance test by a minimal model of insulin secretion
Authors: Cretti A. , Lehtovirta M. , Bonora E. , Brunato B. , Zenti M. G. , Tosi F. , Caputo M. , Caruso B. , Groop L. C. , Muggeo M. , Bonadonna R. C. 
Published: March 2003

Objective To characterise the performance of β‐cell during a standard oral glucose tolerance test (OGTT).Design Fifty‐six subjects were studied. A minimal analogic model of β‐cell secretion during the OGTT was applied to all OGTTs (see below). The amount of insulin secreted over 120′ in response to oral glucose (OGTT‐ISR; Insulin Units 120′−1 m−2 BSA) and an index of β‐cell secretory ‘force’ (β‐Index; pmol·min‐2·m‐2 BSA) were computed with the aid of the model. In protocol A, 10 healthy subjects underwent two repeat 75 g OGTT with frequent (every 10′−15′) blood sampling for glucose and C‐peptide to test the reproducibility of OGTT‐ISR and β‐Index with a complete or a reduced data set. In protocol B, 7 healthy subjects underwent three OGTTs (50, 100 or 150 g), to test the stability of the β‐Index under different glucose loads. In protocol C, 29 subjects (15 with normal glucose tolerance, 7 with impaired glucose tolerance and 7 with newly diagnosed type 2 diabetes) underwent two repeat 75 g OGTT with reduced (every 30′ for 120′) blood sampling to compare the reproducibility and the discriminant ratio (DR) of OGTT‐ISR and β‐index with the insulinogenic index (IG‐Index: Δ Insulin 30′ − Basal/Δ Glucose 30′ − Basal). In protocol D, 20 subjects (14 with normal glucose tolerance, 5 with impaired glucose tolerance and 1 with newly‐diagnosed type 2 diabetes) underwent a 75 g OGTT and an intravenous glucose tolerance test (IVGTT) on separate days to explore the relationships between acute (0′−10′) insulin response (AIR) during the IVGTT and β‐index and OGTT‐ISR during the OGTT.Results In all protocols, the minimal analogic model of C‐peptide secretion achieved a reasonable fit of the experimental data. In protocol A, a good reproducibility of both β‐index and OGTT‐ISR was observed with both complete and reduced (every 30′) data sets. In protocol B, increasing the oral glucose load caused progressive increases in OGTT‐ISR (from 2·63 ± 0·70 to 5·11 ± 0·91 Units·120′−1·m−2 BSA; P < 0·01), but the β‐index stayed the same (4·14 ± 0·35 vs. 4·29 ± 0·30 vs. 4·30 ± 0·33 pmol·min−2·m−2 BSA). In protocol C, both OGTT‐ISR and β‐index had lower day‐to‐day CVs (17·6 ± 2·2 and 12·4 ± 2·4%, respectively) and higher DRs (2·57 and 1·74, respectively) than the IG‐index (CV: 35·5 ± 6·3%; DR: 0·934). OGTT‐ISR was positively correlated to BMI (P < 0·03), whereas β‐index was inversely related to both fasting and 2 h plasma glucose (P < 0·01 for both). In protocol D, β‐index, but not OGTT‐ISR, was significantly correlated to AIR (r = 0·542, P < 0·02).Conclusions Analogically modelling β‐cell function during the OGTT provides a simple, useful tool for the physiological assessment of β‐cell function.
Quantification of coronary artery calcification in patients with FH using EBCT
Authors: Hoffmann U. , Bodlaj G. , Derfler K. , Bernhard C. , Wicke L. , Herold C. J. , Kostner K. 
Published: March 2003

Background Calcification of the coronary vessel wall is regarded as a marker of advanced coronary atherosclerosis.Methods To test whether patients with heterozygous familial hypercholesterolemia (FH) exhibit excessive calcification of the coronary vessel wall, we quantified coronary artery calcium in LDL‐apheresis treated FH‐patients with known severe coronary artery disease (CAD) (n = 10), in patients with moderate hypercholesterolemia and known severe CAD (n = 10), and in asymptomatic controls (n = 10) using electronic beam CT. The total coronary calcium score (Agatston‐Score), the number of calcified lesions and the calcified plaque volume were evaluated for this study.Results CAD‐patients with FH, although on average 10 years younger, had a significantly higher total coronary calcium score (702/2018/2890), number of lesions (34/43/49) and calcified plaque volume (700/1818/2313) compared to patients with CAD only (480/641/1362, 10/16·5/22, 480/588/1209, respectively) and controls (10/47/137, 2/4/10, 15/50/144, respectively). Furthermore, we observed a significant correlation (r = 0·93; P < 0·01) between LDL‐cholesterol levels (pretreatment levels of the CAD‐FH group) and the total coronary calcium score in all three groups. Our results demonstrate that coronary artery calcification is more extensive in CAD‐patients with FH than in CAD‐patients with moderate hypercholesterolemia. In addition, we provide evidence that the amount of calcium in the coronary vessel wall in FH patients result from a long lasting history of elevated LDL‐Cholesterol levels.Conclusion These findings emphasize the significance of LDL‐cholesterol as a risk factor for atherosclerosis and underline the importance of early diagnosis of CAD and early cholesterol lowering therapy in FH patients.
Serum homocysteine does not associate with uncomplicated coronary heart disease
Authors: Nikkari S. T. , Kalela A. , Koivu T. A. , Koivula T. , Alho H. , Jokela H. , Sillanaukee P. 
Published: March 2003

Background Elevated serum homocysteine concentrations have been related to coronary heart disease. However, the association has not indisputably been proven, and the mechanisms by which homocysteine may be atherogenic have only partially been elucidated. The objective of the present study was to investigate whether serum homocysteine is associated with angina pectoris and myocardial infarction.Methods We compared serum homocysteine concentrations in subjects with clinical evidence of angina pectoris or history of myocardial infarction to age‐matched controls. The study included 248 males, who participated in a large cross‐sectional risk factor survey carried out in five geographic areas in Finland.Results Serum homocysteine concentration was significantly higher in subjects with a history of myocardial infarction compared to controls (15·3 μmol L−1 and 13·9 μmol L−1 respectively, P = 0·037). In a logistic regression model including several cardiovascular risk factors, serum homocysteine was significantly associated with myocardial infarction (95% CI 1·0157–1·2990, P = 0·027). Serum homocysteine concentrations did not differ between subjects with angina pectoris and age‐matched controls (13·9 μmol L−1 and 14·2 μmol L−1 respectively).Conclusions Our results suggest that elevated serum homocysteine is associated with myocardial infarction but not with uncomplicated coronary heart disease.
Impaired fibrinolysis determines the outcome of percutaneus transluminal coronary angioplasty (PTCA)
Authors: Fornitz G. G. , Nielsen P. , Amtorp O. , Kassis E. , Abildgård U. , Sloth C. , Winther K. , Ørskov H. , Dalsgård J. , Husted S. 
Published: March 2003

Background Coronary artery stenosis lesions dilated by percutaneus transluminal coronary angioplasty (PTCA) show a disappointingly frequent recurrence of stenosis. We have investigated the possible role of fibrinolysis and various platelet‐release factors – specifically in the locality of the affected vessel – by following 19 patients for 6 months after PTCA. Methods PTCA was performed on 19 patients with a significant primary coronary stenosis, proven by quantitative CAAS analysis. Blood for measurement of local fibrinolysis and platelet activity was drawn from the aortic root and the coronary sinus, at three times: just before PTCA, 10 min after it, and 6 months later. Results The incidence of restenosis at the 6 months follow‐up was 37%. PTCA almost doubled the platelet‐derived growth factor level (PDGF) in coronary sinus blood in all patients. The seven restenosis patients had a substantially higher tissue plasminogen activator inhibitor antigen (PAI‐1ag) level in the aortic root before PTCA than the 12 who remained stenosis‐free (mean 62·4 ± 31·6 ng mL −1 compared with 33·1 + 25·3; P < 0·04) and a lower tissue plasminogen activator activity (t‐PAac) level (mean 0·32 ± 0·19 IU mL−1 compared with 0·68 ± 0·34; P < 0·03). This was corroborated by the levels of tissue plasminogen activator inhibitor activity (PAI‐1ac). At reassessment after 6 months, the restenosis patients had developed, in coronary sinus blood, a large rise of PAI‐1ac (7·7 ± 4·8 IU mL−1 rising to 15·7 ± 13·9, P < 0·04) and a large rise of of PAI‐1ag (48·8 ± 31·3 ng mL−1 vs. 72·4 ± 47·2; P < 0·03). But no such increase occurred in the patients who remained stenosis‐free. Conclusion Our results indicate that the minor balloon injury, which is inseparable from PCTA, stimulates the local release of PDGF. We suggest that, in those patients whose fibrinolytic activity is inherently low, this rise of PDGF could be a major causative factor in restenosis. We also discuss the possibility that the preoperative level of PAI‐1ac could provide a limited but useful prediction of the outcome of PTCA.
Effects of short‐term feeding of a highly palatable diet on vascular reactivity in rats
Authors: Naderali E. K. , Williams G. 
Published: March 2003

Background Numerous studies have shown that long‐term consumption of high‐fat, high‐energy diet results in obesity, which in turn, leads to cardiovascular disorders. However, there is little or no data on the acute effects of a highly palatable diet on vascular function.Material and Methods In this study we aimed to evaluate the changes in metabolic and vascular reactivity in Wistar rats fed a palatable diet for 2 days.Results Two‐days feeding of rats with a palatable diet did not effect body weight, fat‐pad mass or gasterocnimus muscles weights. Nor there were any changes in plasma glucose, insulin or leptin levels. However, compared with chow‐fed rats, palatable diet‐fed rats had significantly raised plasma free fatty acids and triglycerides levels (for both, P < 0·01). Compared with chow‐fed animals, vasorelaxation responses to carbamylcholine and sodium nitroprusside were significantly attenuated in palatable diet‐fed rats (for both, P < 0·01). However, there were no differences in histamine‐induced vasorelaxation between chow‐fed and palatable diet‐fed rats.Conclusion These data indicates that diet‐induced endothelium‐dependent and ‐independent vascular dysfunction occurs long before obesity develops.
Postnatal increase of procalcitonin in premature newborns is enhanced by chorioamnionitis and neonatal sepsis
Authors: Janota J. , Stranák Z. , Bělohlávková S. , Mudra K. , Šimák J. 
Published: March 2003

To determine the influence of chorioamnionitis and neonatal sepsis on procalcitonin (PCT) levels in very‐low‐birth‐weight (VLBW) infants within the first week of life.PCT serum levels were measured in cord blood 1 h after delivery and on day 3 and day 7 of life. Chorioamnionitis and neonatal sepsis within the first week were monitored.Chorioamnionitis was present in eight of 37 patients (21·6%). PCT on day 3 was increased in both the ‘No chorioamnionitis’ (2·54 ng mL−1, SEM 0·51) and ‘Chorioamnionitis’ (6·96 ng mL−1, SEM 2·93) groups of VLBW infants compared with the 1st hour values (0·45 and 0·58 ng mL−1 SEM 0·07 and 0·11, respectively, P < 0·001) of the same patients. The postnatal gain was higher in the ‘Chorioamnionitis’ group (P < 0·01). Neonatal sepsis was diagnosed (after exclusion) in 12 of 32 patients (37·5%). Mean values of maximum PCT in patients with and without sepsis were 8·41 ng mL−1 (SEM 1·87) and 3·02 ng mL−1 (SEM 1·38), respectively (P < 0·05). Sensitivity to sepsis of PCT, ratio of immature to total neutrophils (I : T), and C‐reactive protein (CRP) were 75%, 50% and 25%, respectively.In the group of VLBW infants the PCT level within 72 h of delivery was markedly increased in patients with chorioamnionitis. Compared with I : T and CRP, PCT appears to be a more sensitive marker of neonatal sepsis.
Plasma homocysteine, methylenetetrahydrofolate reductase gene polymorphism and carotid intima‐media thickness in Italian type 2 diabetic patients
Authors: Scaglione L. , Gambino R. , Rolfo E. , Lillaz E. , Gai M. , Cassader M. , Pagano G. , Cavallo‐Perin P. 
Published: March 2003

Abstract Background Moderately elevated levels of homocysteine have been associated with an increased cardiovascular risk in type 2 diabetic patients. The role of methylenetetrahydrofolate reductase gene polymorphism is less clear.Materials and methods We investigated the contribution of plasma homocysteine levels and the methylenetetrahydrofolate reductase gene polymorphism to the variability of carotid intima‐media thickness in 124 consecutive Italian patients with type 2 diabetes mellitus. Fasting plasma homocysteine was measured by high‐pressure liquid chromatography with an electrochemical detector; methylenetetrahydrofolate reductase genotypes were determined by polymerase chain reaction and restriction enzyme digestion. The carotid intima‐media thickness was evaluated with high‐resolution B‐mode ultrasonography.Results Age, creatinine and plasma homocysteine levels showed a positive correlation with mean carotid intima‐media thickness values, but only age and creatinine levels were still associated with mean carotid intima‐media thickness values in the multivariate analysis. Plasma homocysteine levels were significantly higher in the patients bearing the 677T/677T genotype of the methylenetetrahydrofolate reductase polymorphism; mean carotid intima‐media thickness values were not different in the three different methylenetetrahydrofolate reductase genotypes.Conclusion In 124 Italian patients with type 2 diabetes mellitus, basal levels of plasma homocysteine, as well as methylenetetrahydrofolate reductase gene polymorphism, did not explain the variability of mean carotid intima‐media thickness.
Oestrogen attenuates coronary vasoconstriction after angioplasty: role of endothelin‐1
Authors: Lee T‐M. , Su S‐F. , Tsai C‐H. 
Published: March 2003

AbstractBackground and aims There were controversies as to whether endothelin‐1 is released after coronary angioplasty. We sought to determine whether endothelin‐1 is released after coronary angioplasty and whether oestrogen administration can affect coronary vasomotor tone by reducing endothelin‐1 concentrations.Methods The study was designed to prospectively investigate 24 consecutive patients scheduled for elective coronary angioplasty. Patients were randomized into two groups according to whether they did not (group 1, n = 12) or did (group 2, n = 12) have intracoronary treatment with oestrogen. Quantitative coronary angiography was monitored at baseline, immediately after successful angioplasty, and 15 min after the last deflation. Blood samples for measuring the levels of endothelin‐1 were drawn from the ascending aorta and the coronary sinus simultaneously before angioplasty and 15 min after balloon dilatation.Results The diameters of the coronary artery at the dilated segments were significantly reduced 15 min after dilation compared with those immediately after dilation in group 1 from 3·20 ± 0·22 to 2·30 ± 0·23 mm (P < 0·001), respectively. The vasoconstriction was significantly blunted in group 2. The endothelin‐1 levels from the coronary sinus rose significantly, by 29%, 15 min after angioplasty in group 1, which was attenuated after administering oestrogen. Significant correlation was found between the changes of coronary vasomotion of the dilated segment and endothelin‐1 levels (r = 0·70, P = 0·01).Conclusion Endothelin‐1 is released into the coronary circulation after angioplasty, and this vasoactive substance may contribute to the occurrence of vasoconstriction. The vasoconstriction is attenuated by oestrogen by reducing the endothelin‐1 levels. This finding provided a new strategy to treat coronary vasoconstriction after angioplasty.
Influence of apolipoprotein E polymorphism on plasma vitamin A and vitamin E levels
Authors: Gómez‐Coronado D. , Entrala A. , Álvarez J. J. , Ortega H. , Olmos J. M. , Castro M. , Sastre A. , Herrera E. , Lasunción M. Á. 
Published: March 2003

AbstractBackground Plasma concentrations of vitamins A and E are positively correlated with those of concurrent lipids and, on the other hand, lipid levels are influenced by apolipoprotein E polymorphism. Therefore, the effect of this polymorphism on both vitamins was analysed in an adult population.Materials and methods Subjects were recruited from a working population. Their anthropometric, lifestyle and dietary intake variables and menopausal status were recorded. Their apolipoprotein E phenotype and their plasma vitamins A and E (by high‐performance liquid chromatography) and lipid (enzymatically) concentrations were determined after an overnight fast. The associations of the phenotype with vitamins and lipids were studied in men and women separately and controlling for significant covariates.Results The apolipoprotein E phenotype was associated with the concentrations of total, low‐density lipoprotein (LDL) and high‐density lipoprotein (HDL) cholesterol in women, whereas no associations with lipids were found in men. Vitamin A and vitamin E levels were higher in men than in women, but only the difference in the former persisted after lipid adjustment. Apolipoprotein E2 slightly increased vitamin A levels in women, an effect which was still evident with lipid adjustment. Actually, both the apolipoprotein E phenotype and triglyceride were selected as significant predictors of this vitamin by multiple regression. This phenotype did not affect vitamin E levels in either sex.Conclusions Lipids do not mediate the effect of gender on vitamin A levels. Apolipoprotein E polymorphism is an independent determinant of vitamin A levels in women. Pending confirmation by others, we propose that enhancement of this vitamin may contribute to the beneficial impact of the ε2 allele on human ageing and health.