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Background: Several markers have been proposed for the detection and progression of subclinical atherosclerosis. We aimed to analyse the impact of classical risk factors on the presence and short-term progression of subclinical carotid atherosclerosis in a non-diabetic, primary prevention cohort. Methods: This analysis included participants with completed visits at baseline and at 5-year follow-up (N = 141; 56.7% females, 43.3% males; aged 49.6 ± 4.7 years). Clinical and laboratory parameters, risk profiles, carotid artery intima-media thickness (CIMT) and plaque presence were analysed. Results: There was a significant progression in mean CIMT (0.54 ± 0.09 mm-0.62 ± 0.10 mm; p < 0.001), prevalence of carotid plaque (4.8%-17.9%; p < 0.001) and age- and sex-adjusted abnormal CIMT (52.9%-78.8%; p < 0.001) at the end of follow-up, compared to baseline. In multivariate regression analysis, among the classical risk factors, their number, metabolic syndrome and SCORE (Systematic Coronary Risk Estimation) risk only the number of risk factors showed an independent and significant impact on the occurrence of a carotid plaque (Exp(B) = 1.71; p = 0.017) and 5-year CIMT progression. Conclusions: During a short follow-up, the significant progression of subclinical atherosclerosis was confirmed. The number of risk factors predicted the occurrence of carotid plaques and CIMT progression. The high prevalence and short-term progression of subclinical carotid atherosclerosis underly the rationale for its screening in personalized cardiovascular risk stratification in asymptomatic middle-aged subjects over 50 years old, at low-to moderate cardiovascular risk, particularly with several risk factors.

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Computed tomography 3D reconstruction of a patient with Bland-White-Garland syndrome showing a dilated right coronary artery and thin left coronary artery.

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Microalbuminuria is closely associated with the risk of cardiovascular disease and all-cause mortality in the general population. Less is known about its relationship with subclinical atherosclerosis. We aimed to assess the prevalence of microalbuminuria and its relationship with subclinical atherosclerosis in middle-aged, nondiabetic, apparently healthy individuals (N = 187; 40.1% men, 59.9% women; aged 35-55 years) as well as to evaluate its potential associations with established risk modifiers, especially with the presence of carotid plaque. Clinical and laboratory parameters, the estimated 10-year fatal cardiovascular risk (SCORE), as well as circulating, functional (flow mediated vasodilation, ankle-brachial index, augmentation index, and pulse wave velocity), and morphological markers (mean carotid intima-media thickness, and carotid plaque) of subclinical atherosclerosis were analysed in group with vs. without microalbuminuria. Microalbuminuria was present in 3.8% of individuals with SCORE risk 0.43 ± 0.79%. Functional markers predominated in both groups. Carotid intima-media thickness (mean ± SD) in both groups was in range: 0.5-0.55 ± 0.09-0.14 mm. Carotid plaque was more frequent in group with (14.3%) vs. without (4.4%) microalbuminuria. Microalbuminuria had no statistically significant effect on most markers of subclinical atherosclerosis, but the increasing value of microalbuminuria was significantly associated with the occurrence of carotid plaque (p = 0.035; OR = 1.035; 95% CI = 1.002-1.07). Additional multiple logistic regression analysis, where variables belonged to microalbuminuria, number of risk factors, and family history, finally showed only two variables: microalbuminuria (p = 0.034; OR = 1.04; 95%CI = 1.003-1.09) and the number of risk factors (p = 0.006; OR = 2.15; 95% CI = 1.24-3.73) with independent and significant impact on the occurrence of carotid plaque. Our results may indicate an association of microalbuminuria with the presence of carotid atherosclerotic plaque; in addition, microalbuminuria and the number of risk factors appear to be possible predictors of the carotid plaque occurrence. Monitoring microalbuminuria may improve the personalized cardiovascular risk assessment in nondiabetic, low-to-moderate cardiovascular risk individuals with or without hypertension.

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The aim of this work was to study the metabolic changes during germination of Trichoderma atroviride conidia along with selected marker enzyme activities. The increase in proteinogenic amino acid concentrations together with the increase in glutamate dehydrogenase activity suggests a requirement for nitrogen metabolism. Even though the activities of tricarboxylic acid cycle enzymes also increased, detected organic acid pools did not change, which predisposes this pathway to energy production and supply of intermediates for further metabolism. The concentrations of many metabolites, including the main osmolytes mannitol and betaine, also increased during the formation of germ tubes. The activities of H(+)-ATPase and GDPase, the only marker enzymes that did not have detectable activity in non-germinated conidia, were shown with germ tubes.

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BACKGROUND: Inflammatory bowel disease (IBD) results from an aberrant immune response to the indigenous intestinal flora in genetically susceptible hosts. Therefore, the study of candidate genes involved in host pathogen interactions is of key interest. METHODS: In this two-center, retrospective German and Hungarian cohort study, patients with Crohn's disease (CD) (n = 379; German n = 235, Hungarian n = 144) and ulcerative colitis (UC) (n = 263; German n = 145, Hungarian n = 118) and healthy controls (n = 605; German n = 403, Hungarian n = 202) were genotyped for the presence of the CD14 c.1-260C>T promoter variant and the TLR4 c.896A>G (p.D299G) variant by melting curve analysis using fluorescence resonance energy transfer probes. Data were stratified according to the presence of NOD2 (CARD15) mutations and a detailed genotype-phenotype analysis was performed. RESULTS: In the German cohort the CD14 single-nucleotide polymorphism was associated with UC, but not CD (UC p = 0.016 vs. CD p = 0.190), while the opposite was found in the Hungarian cohort (UC p = 0.083 vs. CD p = 0.019). No association of IBD with the TLR4 single-nucleotide polymorphism was found in either cohort (UC p = 0.430, CD p = 0.783 vs. UC p = 0.745, CD p = 0.383). CONCLUSION: IBD appears to be associated with the CD14 c.1-260C>T promoter variant in Germans and Hungarians, but not with the TLR4 c.896A>G (p.D299G) variant.

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OBJECTIVES: Genetic variants within DLG5 were recently reported to be associated with inflammatory bowel disease (IBD). The aim of our study was to test for allelic and haplotype associations of six DLG5 variants in 668 IBD patients from two European populations. Furthermore, we evaluated whether DLG5 variants alter gastrointestinal permeability in Crohn's disease (CD). METHODS: Six DLG5 variants (p.R30Q, p.P1371Q, p.G1066G, rs2289308, DLG_e26, p.D1507D) were genotyped in two study populations: (1) German IBD patients (CD n = 250; ulcerative colitis (UC) n = 150) and German healthy controls (n = 422); (2) Hungarian IBD patients (CD n = 144; UC n = 124) and Hungarian healthy controls (n = 205). Subtyping analysis was performed in respect of CARD15 mutations and clinical characteristics. We also tested for differences within DLG5 genotypes in German CD patients with respect to gastroduodenal and intestinal permeability measured by triple-sugar-test. RESULTS: Allele as well as genotype frequencies of DLG5 variants did not differ between IBD patients and controls in either study population. Indeed, the p.R30Q polymorphism was found more frequently in controls than in patients. The distribution of DLG5 genotypes in German and Hungarian CD patients with CARD15 mutations was not different from patients without mutated CARD15. We did also not observe any association between DLG5 variants and clinical parameters. Importantly, DLG5 variants were not associated with gastroduodenal or intestinal permeability. CONCLUSIONS: We could not replicate that DLG5 is a relevant disease susceptibility gene for IBD in German or Hungarian subjects. In addition, we have no evidence that DLG5 variants are involved in altered gastrointestinal permeability in CD.

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AIM: To analyse the impact of NOD2/CARD15 mutations on the clinical course of Crohn's disease patients from an eastern European country (Hungary). METHODS: We investigated the prevalence of the three common NOD2/CARD15 mutations (Arg702Trp, Gly908Arg, 1007finsC) in 148 patients with Crohn's disease, 128 patients with ulcerative colitis and 208 controls recruited from the University of Szeged, Hungary. In patients with Crohn's disease, the prevalence of NOD2/CARD15 mutations was correlated to the demographical and clinical parameters. RESULTS: In total, 32.4% of Crohn's disease patients carried at least one mutant allele within NOD2/CARD15 compared to 13.2% of patients with ulcerative colitis (P = 0.0002) and to 11.5% of controls (P<0.0001). In Crohn's disease patients, the allele frequencies for Arg702Trp, Gly908Arg and 1007finsC were 7.1%, 3.0% and 10.8% respectively. Interestingly, only the 1007finsC mutation was associated with a distinct clinical phenotype. The patients positive for the 1007finsC mutation suffered more frequently from stenotic disease behaviour (P = 0.008). Furthermore, 51.9% of patients positive for the 1007finsC mutation underwent a surgical resection within the ileum compared to only 17.4% of patients without the 1007finsC mutation (P = 0.001). With respect to the other two mutations (Arg702Trp and Gly908Arg), no associations were found with all investigated clinical parameters. CONCLUSION: NOD2/CARD15 mutations are frequently found in Crohn's disease patients from Hungary. The 1007finsC mutation is associated with stenotic disease behaviour and frequent ileal resections.

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