يعرض 1 - 10 نتائج من 95 نتيجة بحث عن '"Idzior Walus, B."', وقت الاستعلام: 0.75s تنقيح النتائج
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    دورية أكاديمية
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    المؤلفون: Peeters S. A., Engelen L., Buijs J., Chaturvedi N., Fuller J. H., Schalkwijk C. G., Stehouwer C. D., Karamanos B., Kofinis A., Petrou K., Giorgino F., Picca G., Angarano A., de Pergola. G., Laviola L., Giorgino R., Ionescu-Tirgoviste C., Coszma A., Guja C., Songini M., Casu A., Pedron M., Pintus S., Fossarello M., Ferriss J. B., Grealy G., O'Keefe D., Toeller M., Arden C., Rottiers R., Tuyttens C., Priem H., Ebeling P., Kylliainen M., Koivisto V. A., Idzior-Walus B., Sieradzki J., Cyganek K., Solnica B., Lemkes H. H. P. J., Lemkes-Stuffken J. C., Nunes-Correa J., Rogado M. C., Gardete-Correia L., Cardoso M. C., Silva A., Boavida J., Machado Sa Marques M., Michel G., Wirion R., Cardillo S., Pozza G., Mangili R., Asnaghi V., Standl E., Schaffler B., Brand H., Harms A., Ben Soussan M., Verier-Mine O., Fallas P., Fallas M. C., Holloway J., Asbury L., Betteridge D. J., Cathelineau G., Bouallouche A., Villatte Cathelineau B., Santeusanio F., Rosi G., D'Alessandro V., Cagini C., Bottini P., Reboldi G. P., Navalesi R., Penno G., Bandinelli S., Miccoli R., Nannipieri M., Ghirlanda G., Saponara C., Cotroneo P., Manto A., Minnella A., Ward J. D., Tesfaye S., Eaton S., Mody C., Borra M., Cavallo Perin P., Giunti S., Grassi G., Pagano G. F., Porta M., Sivieri R., Vitelli F., Veglio M., Papazoglou N., Manes G., Muggeo M., Iagulli M., Cacciatori V., Cattedra di Malattie del Metabolismo V., Irsigler K., Abrahamian H., Walford S., Sinclair J., Hughes S., McLelland V., Ward J., Roglic G., Metelko Z., Pepeonik Z. R.

    المساهمون: Peeters, S. A., Engelen, L., Buijs, J., Chaturvedi, N., Fuller, J. H., Schalkwijk, C. G., Stehouwer, C. D., Karamanos, B., Kofinis, A., Petrou, K., Giorgino, F., Picca, G., Angarano, A., Pergola. G., De, Laviola, L., Giorgino, R., Ionescu-Tirgoviste, C., Coszma, A., Guja, C., Songini, M., Casu, A., Pedron, M., Pintus, S., Fossarello, M., Ferriss, J. B., Grealy, G., O'Keefe, D., Toeller, M., Arden, C., Rottiers, R., Tuyttens, C., Priem, H., Ebeling, P., Kylliainen, M., Koivisto, V. A., Idzior-Walus, B., Sieradzki, J., Cyganek, K., Solnica, B., Lemkes, H. H. P. J., Lemkes-Stuffken, J. C., Nunes-Correa, J., Rogado, M. C., Gardete-Correia, L., Cardoso, M. C., Silva, A., Boavida, J., Machado Sa Marques, M., Michel, G., Wirion, R., Cardillo, S., Pozza, G., Mangili, R., Asnaghi, V., Standl, E., Schaffler, B., Brand, H., Harms, A., Ben Soussan, M., Verier-Mine, O., Fallas, P., Fallas, M. C., Holloway, J., Asbury, L., Betteridge, D. J., Cathelineau, G., Bouallouche, A., Villatte Cathelineau, B., Santeusanio, F., Rosi, G., D'Alessandro, V., Cagini, C., Bottini, P., Reboldi, G. P., Navalesi, R., Penno, G., Bandinelli, S., Miccoli, R., Nannipieri, M., Ghirlanda, G., Saponara, C., Cotroneo, P., Manto, A., Minnella, A., Ward, J. D., Tesfaye, S., Eaton, S., Mody, C., Borra, M., Cavallo Perin, P., Giunti, S., Grassi, G., Pagano, G. F., Porta, M., Sivieri, R., Vitelli, F., Veglio, M., Papazoglou, N., Manes, G.

    الوصف: Impaired regulation of extracellular matrix remodeling by matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinase (TIMP) may contribute to vascular complications in patients with type 1 diabetes. We investigated associations between plasma MMP-1, -2, -3, -9, -10 and TIMP-1, and cardiovascular disease (CVD) or microvascular complications in type 1 diabetic patients. We also evaluated to which extent these associations could be explained by low-grade inflammation (LGI) or endothelial dysfunction (ED). Methods: 493 type 1 diabetes patients (39.5 ± 9.9 years old, 51% men) from the EURODIAB Prospective Complications Study were included. Linear regression analysis was applied to investigate differences in plasma levels of MMP-1, -2, -3, -9, -10, and TIMP-1 between patients with and without CVD, albuminuria or retinopathy. All analyses were adjusted for age, sex, duration of diabetes, Hba1c and additionally for other cardiovascular risk factors including LGI and ED. Results: Patients with CVD (n = 118) showed significantly higher levels of TIMP-1 [β = 0.32 SD (95%CI: 0.12; 0.52)], but not of MMPs, than patients without CVD (n = 375). Higher plasma levels of MMP-2, MMP-3, MMP-10 and TIMP-1 were associated with higher levels of albuminuria (p-trends were 0.028, 0.004, 0.005 and 0.001, respectively). Severity of retinopathy was significantly associated with higher levels of MMP-2 (p-trend = 0.017). These associations remained significant after further adjustment for markers of LGI and ED. Conclusions: These data support the hypothesis that impaired regulation of matrix remodeling by actions of MMP-2, -3 and-10 and TIMP-1 contributes to the pathogenesis of vascular complications in type 1 diabetes.

    العلاقة: info:eu-repo/semantics/altIdentifier/pmid/25848912; info:eu-repo/semantics/altIdentifier/wos/WOS:000350726000001; volume:14; issue:1; firstpage:31; journal:CARDIOVASCULAR DIABETOLOGY; http://hdl.handle.net/11586/353539Test; info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-84925234995

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    المصدر: Metabolism , 65 (3) pp. 48-53. (2016)

    الوصف: BACKGROUND: Familial hypercholesterolemia (FH) is a common autosomal dominant disorder with a frequency of 1 in 200 to 500 in most European populations. Mutations in LDLR, APOB and PCSK9 genes are known to cause FH. In this study, we analyzed the genetic spectrum of the disease in the understudied Polish population. MATERIALS AND METHODS: 161 unrelated subjects with a clinical diagnosis of FH from the south-eastern region of Poland were recruited. High resolution melt and direct sequencing of PCR products were used to screen 18 exons of LDLR, a region of exon 26 in the APOB gene and exon 7 of PCSK9. Multiplex ligation-dependent probe amplification (MLPA) was performed to detect gross deletions and insertions in LDLR. Genotypes of six LDL-C raising SNPs were used for a polygenic gene score calculation. RESULTS: We found 39 different pathogenic mutations in the LDLR gene with 10 of them being novel. 13 (8%) individuals carried the p.Arg3527Gln mutation in APOB, and overall the detection rate was 43.4%. Of the patients where no mutation could be found, 53 (84.1%) had a gene score in the top three quartiles of the healthy comparison group suggesting that they have a polygenic cause for their high cholesterol. CONCLUSIONS: These results confirm the genetic heterogeneity of FH in Poland, which should be considered when designing a diagnostic strategy in the country. As in the UK, in the majority of patients where no mutation can be found, there is likely to be a polygenic cause of their high cholesterol level.

    وصف الملف: text

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    المصدر: Soedamah-Muthu , S S , Chaturvedi , N , Teerlink , T , Idzior-Walus , B , Fuller , J H & Stehouwer , C D A 2005 , ' Plasma homocysteine and microvascular and macrovascular complications in type 1 diabetes: a cross-sectional nested case-control study ' , Journal of Internal Medicine , vol. 258 , no. 5 , pp. 450-459 . https://doi.org/10.1111/j.1365-2796.2005.01560.xTest

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