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36 results on '"Vernerova, Z."'

4. Resistin in rheumatoid arthritis synovial tissue, synovial fluid and serum

Author

Senolt, L., Housa, D., Vernerova, Z., Jirasek, T., Svobodova, R., Veigl, D., Anderlova, K., Muller-Ladner, U., Pavelka, K., and Haluzik, M.

Subjects
Rheumatoid arthritis -- Development and progression, Rheumatoid arthritis -- Research, Fat cells -- Research, Synovial membranes -- Analysis, Health
Published
2007

7. Overexpression of TET dioxygenases in seminomas associates with low levels of DNA methylation and hydroxymethylation

Author

Benesova, M, Trejbalova, K, Kucerova, D, Vernerova, Z, Hron, T, Amouroux, R, Klezl, P, Hajkova, P, Hejnar, J, EMBO, and Commission of the European Communities

Subjects
endocrine system diseases, Oncology & Carcinogenesis, urologic and male genital diseases, 1112 Oncology And Carcinogenesis
Abstract

Germ cell tumors and particularly seminomas reflect the epigenomic features of their parental primordial germ cells, including the genomic DNA hypomethylation and expression of pluripotent cell markers. Because the DNA hypomethylation might be a result of TET dioxygenase activity, we examined expression of TET1-3 enzymes and the level of their product, 5-hydroxymethylcytosine, in a panel of histologically characterized seminomas and non-seminomatous germ cell tumors. Expression of TET dioxygenase mRNAs was quantified by real-time PCR. TET1 expression and the level of 5-hydroxymethylcytosine were examined immunohistochemically. Quantitative assessment of 5-methylcytosine and 5-hydroxymethylcytosine levels was done by liquid chromatography-mass spectroscopy technique. We found highly increased expression of TET1 dioxygenase in most seminomas and a strong TET1 staining in seminoma cells. Is ocitrate dehydrogenase 1 and 2 mutations were not detected suggest ing the enzymatic activity of TET1. The levels of 5-methylcytosine and 5-hydroxymethylcytosine in seminomas were found decreased in comparison to non-seminoma to us germ cell tumors and healthy testicular tissue. We propose TET1 expression as a marker of seminoma and mixed germ cell tumor and we suggest that high levels of TET1 expression are associated with the maintenance of low DNA methylation levels in seminomas. This “anti-methylator” phenotype of seminomas is in contrast to the CpG island methylator phenotype observed in a fraction of tumors of various types.

Published
2017

8. Adipocytokines and cancer

Author

Housa, D., Housova, J., Vernerova, Z., and Martin Haluzik

Subjects
Leptin, Male, Adipose Tissue, Physiology, Neoplasms, Humans, Prostatic Neoplasms, Breast Neoplasms, Female, Adiponectin, General Medicine
Abstract

Adipose tissue-produced hormones significantly affect the metabolism of lipids and carbohydrates as well as numerous other processes in human body. It is generally accepted that endocrine dysfunction of adipose tissue may represent one of the causal links between obesity and insulin resistance/diabetes. Epidemiological studies underlined that obesity represents a significant risk factor for the development of cancer, although the exact mechanism of this relationship remains to be determined. Multiple recent studies have indicated that some of adipose tissue-derived hormones may significantly influence the growth and proliferation of tumorous stroma and malignant cells within. Here we review current knowledge about possible relationship of leptin and adiponectin to the etiopathogenesis of different malignant tumors. Most of the studies indicated that while leptin may potentiate the growth of cancer cells in vitro, adiponectin appears to have an opposite effect. Further studies are necessary to decide whether obesity-induced endocrine dysfunction of adipose tissue can directly influence carcinogenesis in different tissues and organs.

Published
2006
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9. Clinical nephrology-epidemiology-clinical trials: Determinants of outcome in ANCA-associated glomerulonephritis: A prospective clinico-histopathological analysis of 96 patients

Author

Hauer, Herbert A., Bajema, Ingeborg M., Van Houwelingen, Hans C., Ferrario, Franco, Noã«l, Laure Hélène, Waldherr, Rã¼diger, Jayne, David R. W., Rasmussen, Niels, Bruijn, Jan A., Hagen, E. Christiaan, Rasmussen, N., Jayne, D. R. W., Neumann, I., Mad Houn, P., Sennesael, J., Tesar, V., Rychlik, I., Bartunkova, J., Luk, J., Juhl, B. Ravn, Petersen, J., Andersen, C. B., Szpirt, W., Wiik, A., Lokkegaard, H., Nielsen, H., Ring, T., Sorensen, S. Freiesleben, Bacon, P. A., Exley, A., Savage, C. O. S., Gaskin, G., Pusey, C., Lockwood, C. M., Luq Mani, R., Gronhagen Riska, C., Ekstrand, A., Guillevin, L., Lhote, F., Lesavre, P., Noel, L. H., Landais, P., Vanhille, P., Bataille, P., Esnault, V., Woude, F. Van Der, Waldherr, R., Schmitt, W., Andrassy, K., Hergesell, O., Nowack, R., Groot, K. De, Herlyn, K., Gross, W. L., Boki, K. A., Boletis, J. N., Emmanouel, D. S., Feighery, C., Ferra Rio, Y., Sinico, R. A., Gregorini, G., Dadoniene, J., Hagen, E. C., Kallenberg, C. G. M., Stegeman, C., Tervaert, J. W. Cohen, Verburgh, C. A., Siegert, C. E. H., Bruijn, J. A., Hauer, H. A., Hermans, J., Houwelingen, J. C. Van, Vergunst, C. E., Gurp, E. Van, Bajema, I. M., Vasconcelos, C., Mirapeix, E., Sole, M., Petterson, E. E., Bruchfeld, A., Westman, K. W. A., Heigl, Z., Chizzolini, C., Maclahan, D., Depierreux, M., van Damme, B., Stejskalova, A., Vernerova, Z., Tornroth, T., Feller, A. C., Gaffney, E., Tardanico, R., Consalonieri, R., Garibotto, Giacomo, Tiebosch, A. T. M. G., Kooijman, C. D., Arques, M. S., Algaba, F., Carreras, M., Perez, M. Vaquero, Bernardo, L., Sundelin, B., Alm, P., Wernersson, A., Veress, B., Landells, W., Howie, A. J., Fleming, S., Griffith, A. P., Furness, P. N., Cook, H. T., Hauer, H, Bajema, I, Van Houwelingen, H, Ferrario, F, Noël, L, Waldherr, R, Jayne, D, Rasmussen, N, Bruijn, J, Hagen, E, Neumann, I, Mad Houn, P, Sennesael, J, Tesar, V, Rychlik, I, Bartunkova, J, Luk, J, Juhl, B, Petersen, J, Andersen, C, Szpirt, W, Wiik, A, Lokkegaard, H, Nielsen, H, Ring, T, Sorensen, S, Bacon, P, Exley, A, Savage, C, Gaskin, G, Pusey, C, Lockwood, C, Luq Mani, R, Gronhagen Riska, C, Ekstrand, A, Guillevin, L, Lhote, F, Lesavre, P, Noel, L, Landais, P, Vanhille, P, Bataille, P, Esnault, V, Woude, F, Schmitt, W, Andrassy, K, Hergesell, O, Nowack, R, Groot, K, Herlyn, K, Gross, W, Boki, K, Boletis, J, Emmanouel, D, Feighery, C, Ferra Rio, Y, Sinico, R, Gregorini, G, Dadoniene, J, Kallenberg, C, Stegeman, C, Tervaert, J, Verburgh, C, Siegert, C, Hermans, J, Houwelingen, J, Vergunst, C, Gurp, E, Vasconcelos, C, Mirapeix, E, Sole, M, Petterson, E, Bruchfeld, A, Westman, K, Heigl, Z, Chizzolini, C, Maclahan, D, Depierreux, M, van Damme, B, Stejskalova, A, Vernerova, Z, Tornroth, T, Feller, A, Gaffney, E, Tardanico, R, Consalonieri, R, Garibotto, G, Tiebosch, A, Kooijman, C, Arques, M, Algaba, F, Carreras, M, Perez, M, Bernardo, L, Sundelin, B, Alm, P, Wernersson, A, Veress, B, Landells, W, Howie, A, Fleming, S, Griffith, A, Furness, P, and Cook, H

Subjects
Prognosi, Biopsy, Antineutrophil Cytoplasmic, Predictive Value of Test, Antibodies, Antibodies, Antineutrophil Cytoplasmic, Immunosuppressive Agent, Glomerulonephritis, Predictive Value of Tests, Recurrence, Azathioprine, Humans, Prospective Studies, Microscopic polyangiiti, Glomerulonephriti, Microscopic polyangiitis, Cyclophosphamide, Pauci-immune crescentic necrotizing glomerulonephritis, Medicine (all), Granulomatosis with Polyangiitis, Prognosis, Wegener's granulomatosis, ANCA-associated vasculiti, Prospective Studie, Treatment Outcome, ANCA-associated vasculitis, Renal biopsy, Glomerular Filtration Rate, Immunosuppressive Agents, Sample Size, Nephrology, Wegener's granulomatosi, Pauci-immune crescentic necrotizing glomerulonephriti, Granulomatosis with Polyangiiti, Human
Abstract

Background. The predictive value of clinical and renal histological features for renal outcome in patients with anti-neutrophil cytoplasmic autoantibody (ANCA)-associated glomerulonephritis was investigated in a prospective analysis of 96 patients with ANCA-associated vasculitis, and moderate renal involvement (creatinine

Published
2002

14. Lab methods / biomarkers

Author

Borras, M., primary, Roig, J., additional, Betriu, A., additional, Vilar, A., additional, Hernandez, M., additional, Martin, M., additional, Fernandez, E. D., additional, Dounousi, E., additional, Kiatou, V., additional, Papagianni, A., additional, Zikou, X., additional, Pappas, K., additional, Pappas, E., additional, Tatsioni, A., additional, Tsakiris, D., additional, Siamopoulos, K. C., additional, Kim, J.-K., additional, Kim, Y., additional, Kim, S. G., additional, Kim, H. J., additional, Ahn, S. Y., additional, Chin, H. J., additional, Oh, K.-H., additional, Ahn, C., additional, Chae, D.-W., additional, Yazici, R., additional, Altintepe, L., additional, Bakdik, S., additional, Guney, I., additional, Arslan, S., additional, Topal, M., additional, Karagoz, A., additional, Stefan, G., additional, Mircescu, G., additional, Capusa, C., additional, Stancu, S., additional, Petrescu, L., additional, Alecu, S., additional, Nedelcu, D., additional, Bennett, A. H. L., additional, Pham, H., additional, Garrity, M., additional, Magdeleyns, E., additional, Vermeer, C., additional, Zhang, M., additional, Ni, Z., additional, Zhu, M., additional, Yan, J., additional, Mou, S., additional, Wang, Q., additional, Qian, J., additional, Saade, A., additional, Karavetian, M., additional, ElZein, H., additional, de Vries, N., additional, de Haseth, D. E., additional, Lay Penne, E., additional, van Dam, B., additional, Bax, W. A., additional, Bots, M. L., additional, Grooteman, M. P. C., additional, van den Dorpel, R. A., additional, Blankenstijn, P. J., additional, Nube, M. J., additional, Wee, P. M., additional, Park, J. H., additional, Jo, Y.-I., additional, Lee, J. H., additional, Cianfrone, P., additional, Comi, N., additional, Lucisano, G., additional, Piraina, V., additional, Talarico, R., additional, Fuiano, G., additional, Toyonaga, M., additional, Fukami, K., additional, Yamagishi, S.-i., additional, Kaida, Y., additional, Nakayama, Y., additional, Ando, R., additional, Obara, N., additional, Ueda, S., additional, Okuda, S., additional, Granatova, J., additional, Havrda, M., additional, Hruskova, Z., additional, Tesar, V., additional, Viklicky, O., additional, Rysava, R., additional, Rychlik, I., additional, Kratka, K., additional, Honsova, E., additional, Vernerova, Z., additional, Maluskova, J., additional, Vranova, J., additional, Bolkova, M., additional, Borecka, K., additional, Benakova, H., additional, Zima, T., additional, Lu, K.-C., additional, Yang, H.-Y., additional, Su, S.-L., additional, Cao, Y.-H., additional, Lv, L.-L., additional, Liu, B.-C., additional, Zeng, R., additional, Gao, X.-F., additional, Deng, Y.-Y., additional, Boelaert, J., additional, t' Kindt, R., additional, Glorieux, G., additional, Schepers, E., additional, Jorge, L., additional, Neirynck, N., additional, Lynen, F., additional, Sandra, P., additional, Sandra, K., additional, Vanholder, R., additional, Yamamoto, T., additional, Nameta, M., additional, Yoshida, Y., additional, Uhlen, M., additional, Shi, Y., additional, Tang, J., additional, Zhang, J., additional, An, Y., additional, Liao, Y., additional, Li, Y., additional, Tao, Y., additional, Wang, L., additional, Koibuchi, K., additional, Tanaka, K., additional, Aoki, T., additional, Miyagi, M., additional, Sakai, K., additional, Aikawa, A., additional, Martins, A. R., additional, Branco, P. Q., additional, Serra, F. M., additional, Matias, P. J., additional, Lucas, C. P., additional, Adragao, T., additional, Duarte, J., additional, Oliveira, M. M., additional, Saraiva, A. M., additional, Barata, J. D., additional, Masola, V., additional, Zaza, G., additional, Granata, S., additional, Proglio, M., additional, Pontrelli, P., additional, Abaterusso, C., additional, Schena, F., additional, Gesualdo, L., additional, Gambaro, G., additional, Lupo, A., additional, Pruijm, M., additional, Hofmann, L., additional, Stuber, M., additional, Zweiacker, C., additional, Piskunowicz, M., additional, Muller, M.-E., additional, Vogt, B., additional, Burnier, M., additional, Togashi, N., additional, Yamashita, T., additional, Mita, T., additional, Ohnuma, Y., additional, Hasegawa, T., additional, Endo, T., additional, Tsuchida, A., additional, Ando, T., additional, Yoshida, H., additional, Miura, T., additional, Bevins, A., additional, Assi, L., additional, Ritchie, J., additional, Jesky, M., additional, Stringer, S., additional, Kalra, P., additional, Hutchison, C., additional, Harding, S., additional, Cockwell, P., additional, Viccica, G., additional, Cupisti, A., additional, Chiavistelli, S., additional, Borsari, S., additional, Pardi, E., additional, Centoni, R., additional, Fumagalli, G., additional, Cetani, F., additional, Marcocci, C., additional, Scully, P., additional, O'Flaherty, D., additional, Sankaralingam, A., additional, Hampson, G., additional, Goldsmith, D. J., additional, Pallet, N., additional, Chauvet, S., additional, Beaune, P., additional, Nochy, D., additional, Thervet, E., additional, Karras, A., additional, Bertho, G., additional, Gallyamov, M. G., additional, Saginova, E. A., additional, Severova, M. M., additional, Krasnova, T. N., additional, Kopylova, A. A., additional, Cho, E., additional, Jo, S.-K., additional, Kim, M.-G., additional, Cho, W.-Y., additional, kim, H. K., additional, Trivin, C., additional, Metzger, M., additional, Boffa, J.-J., additional, Vrtovsnik, F., additional, Houiller, P., additional, Haymann, J.-P., additional, Flamant, M., additional, Stengel, B., additional, Roozbeh, J., additional, Yavari, V., additional, Pakfetrat, M., additional, Zolghadr, A. A., additional, Kim, C. S., additional, Kim, M. J., additional, Kang, Y. U., additional, Choi, J. S., additional, Bae, E. H., additional, Ma, S. K., additional, Kim, S. W., additional, Lemoine, S., additional, Guebre-Egziabher, F., additional, Dubourg, L., additional, Hadj-Aissa, A., additional, Blumberg, S., additional, Katzir, Z., additional, Biro, A., additional, Cernes, R., additional, Barnea, Z., additional, Vasquez, D., additional, Gordillo, R., additional, Aller, C., additional, Fernandez, B., additional, Jabary, N., additional, Perez, V., additional, Mendiluce, A., additional, Bustamante, J., additional, Coca, A., additional, Goek, O.-N., additional, Sekula, P., additional, Prehn, C., additional, Meisinger, C., additional, Gieger, C., additional, Suhre, K., additional, Adamski, J., additional, Kastenmuller, G., additional, Kottgen, A., additional, Kuzniewski, M., additional, Fedak, D., additional, Dumnicka, P., additional, Solnica, B., additional, Kusnierz-Cabala, B., additional, Kapusta, M., additional, Sulowicz, W., additional, Drozdz, R., additional, Zawada, A. M., additional, Rogacev, K. S., additional, Hummel, B., additional, Fliser, D., additional, Geisel, J., additional, Heine, G. H., additional, Kretschmer, A., additional, Volsek, M., additional, Krahn, T., additional, Kolkhof, P., additional, Kribben, A., additional, Bruck, H., additional, Koh, E. S., additional, Chung, S., additional, Yoon, H. E., additional, Park, C. W., additional, Chang, Y. S., additional, Shin, S. J., additional, Deagostini, M. C., additional, Vigotti, F. N., additional, Ferraresi, M., additional, Consiglio, V., additional, Scognamiglio, S., additional, Moro, I., additional, Clari, R., additional, Daidola, G., additional, Versino, E., additional, Piccoli, G. B., additional, Mammadrahim Agayev, M., additional, Mehrali Mammadova, I., additional, Qarib Ismayilova, S., additional, Anguiano, L., additional, Riera, M., additional, Pascual, J., additional, Barrios, C., additional, Valdivielso, J. M., additional, Fernandez, E., additional, Soler, M. J., additional, Tsarpali, V., additional, Liakopoulos, V., additional, Panagopoulou, E., additional, Kapoukranidou, D., additional, Spaia, S., additional, Kostopoulou, M., additional, Michalaki, A., additional, Nikitidou, O., additional, Dombros, N., additional, Zhu, F., additional, Abba, S., additional, Flores-Gama, C., additional, Williams, C., additional, Cartagena, C., additional, Carter, M., additional, Kotanko, P., additional, Levin, N. W., additional, Kolesnyk, M., additional, Stepanova, N., additional, Driyanska, V., additional, Stashevska, N., additional, Kundin, V., additional, Shifris, I., additional, Dudar, I., additional, Zaporozhets, O., additional, Keda, T., additional, Ishchenko, M., additional, Khil, M., additional, Choe, J.-Y., additional, Nam, S.-A., additional, Kim, J., additional, Cha, J.-H., additional, Gliga, M. L., additional, Irimescu, C. G., additional, Caldararu, C. D., additional, Gliga, M. G., additional, Toma, L. V., additional, Gomotarceanu, A., additional, Park, Y., additional, Jeon, J., additional, Kwon, S. K., additional, Kim, S. J., additional, Kim, S. M., additional, Kim, H.-Y., additional, Montero, N., additional, Marquez, E., additional, Berrada, A., additional, Arias, C., additional, Prada, J. A., additional, Orfila, M. A., additional, Mojal, S., additional, Vilaplana, C., additional, Attini, R., additional, Parisi, S., additional, Fassio, F., additional, Ghiotto, S., additional, Biolcati, M., additional, Todros, T., additional, Jin, K., additional, Vaziri, N. D., additional, Tramonti, G., additional, Romiti, N., additional, Chieli, E., additional, Maksudova, A. N., additional, Khusnutdinova, L. A., additional, Reque, J. E., additional, Quiroga, B., additional, Lopez, J. M., additional, Verdallez, U. G., additional, Garcia de Vinuesa, M., additional, Goicoechea, M., additional, Nayara, P. G., additional, Arroyo, D. R., additional, Luno, J., additional, Tanaka, H., additional, Abbas, S. R., additional, Thijssen, S., additional, Berthoux, F. C., additional, Azzouz, L., additional, Afiani, A., additional, Ziane, A., additional, Mariat, C., additional, Fournier, H., additional, Kusztal, M., additional, Dzierzek, P., additional, Witkowski, G., additional, Nurzynski, M., additional, Golebiowski, T., additional, Weyde, W., additional, Klinger, M., additional, Altiparmak, M. R., additional, Seyahi, N., additional, Trabulus, S., additional, Bolayirli, M., additional, Andican, Z. G., additional, Suleymanlar, G., additional, Serdengecti, K., additional, Niculae, A., additional, Checherita, I.-A., additional, Neagoe, D.-N., additional, Ciocalteu, A., additional, Seiler, S., additional, Pickering, J. W., additional, Emrich, I., additional, Heine, G., additional, Bargnoux, A.-S., additional, Obiols, J., additional, Kuster, N., additional, Fessler, P., additional, Badiou, S., additional, Dupuy, A.-M., additional, Ribstein, J., additional, Cristol, J.-P., additional, Yanagisawa, N., additional, Ando, M., additional, Ajisawa, A., additional, Tsuchiya, K., additional, Nitta, K., additional, Bouquegneau, A., additional, Cavalier, E., additional, Krzesinski, J.-M., additional, Delanaye, P., additional, Tominaga, N., additional, Shibagaki, Y., additional, Kida, K., additional, Miyake, F., additional, Kimura, K., additional, Ayvazyan, A., additional, Rameev, V., additional, Kozlovskaya, L., additional, Simonyan, A., additional, Scholze, A., additional, Marckmann, P., additional, Tepel, M., additional, Rasmussen, L. M., additional, Hara, M., additional, Kanai, H., additional, Harada, K., additional, Tamura, Y., additional, Kawai, Y., additional, Al-Jebouri, M. M., additional, Madash, S. A., additional, Leonidovna Berezinets, O., additional, and Nicolaevich Rossolovskiy, A., additional

Published
2013
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16. Clinical nephrology-epidemiology-clinical trials: Determinants of outcome in ANCA-associated glomerulonephritis: A prospective clinico-histopathological analysis of 96 patients

Author

Hauer, H, Bajema, I, Van Houwelingen, H, Ferrario, F, Noël, L, Waldherr, R, Jayne, D, Rasmussen, N, Bruijn, J, Hagen, E, Neumann, I, Mad Houn, P, Sennesael, J, Tesar, V, Rychlik, I, Bartunkova, J, Luk, J, Juhl, B, Petersen, J, Andersen, C, Szpirt, W, Wiik, A, Lokkegaard, H, Nielsen, H, Ring, T, Sorensen, S, Bacon, P, Exley, A, Savage, C, Gaskin, G, Pusey, C, Lockwood, C, Luq Mani, R, Gronhagen Riska, C, Ekstrand, A, Guillevin, L, Lhote, F, Lesavre, P, Noel, L, Landais, P, Vanhille, P, Bataille, P, Esnault, V, Woude, F, Schmitt, W, Andrassy, K, Hergesell, O, Nowack, R, Groot, K, Herlyn, K, Gross, W, Boki, K, Boletis, J, Emmanouel, D, Feighery, C, Ferra Rio, Y, Sinico, R, Gregorini, G, Dadoniene, J, Kallenberg, C, Stegeman, C, Tervaert, J, Verburgh, C, Siegert, C, Hermans, J, Houwelingen, J, Vergunst, C, Gurp, E, Vasconcelos, C, Mirapeix, E, Sole, M, Petterson, E, Bruchfeld, A, Westman, K, Heigl, Z, Chizzolini, C, Maclahan, D, Depierreux, M, van Damme, B, Stejskalova, A, Vernerova, Z, Tornroth, T, Feller, A, Gaffney, E, Tardanico, R, Consalonieri, R, Garibotto, G, Tiebosch, A, Kooijman, C, Arques, M, Algaba, F, Carreras, M, Perez, M, Bernardo, L, Sundelin, B, Alm, P, Wernersson, A, Veress, B, Landells, W, Howie, A, Fleming, S, Griffith, A, Furness, P, Cook, H, Cook, H., SINICO, RENATO ALBERTO, Hauer, H, Bajema, I, Van Houwelingen, H, Ferrario, F, Noël, L, Waldherr, R, Jayne, D, Rasmussen, N, Bruijn, J, Hagen, E, Neumann, I, Mad Houn, P, Sennesael, J, Tesar, V, Rychlik, I, Bartunkova, J, Luk, J, Juhl, B, Petersen, J, Andersen, C, Szpirt, W, Wiik, A, Lokkegaard, H, Nielsen, H, Ring, T, Sorensen, S, Bacon, P, Exley, A, Savage, C, Gaskin, G, Pusey, C, Lockwood, C, Luq Mani, R, Gronhagen Riska, C, Ekstrand, A, Guillevin, L, Lhote, F, Lesavre, P, Noel, L, Landais, P, Vanhille, P, Bataille, P, Esnault, V, Woude, F, Schmitt, W, Andrassy, K, Hergesell, O, Nowack, R, Groot, K, Herlyn, K, Gross, W, Boki, K, Boletis, J, Emmanouel, D, Feighery, C, Ferra Rio, Y, Sinico, R, Gregorini, G, Dadoniene, J, Kallenberg, C, Stegeman, C, Tervaert, J, Verburgh, C, Siegert, C, Hermans, J, Houwelingen, J, Vergunst, C, Gurp, E, Vasconcelos, C, Mirapeix, E, Sole, M, Petterson, E, Bruchfeld, A, Westman, K, Heigl, Z, Chizzolini, C, Maclahan, D, Depierreux, M, van Damme, B, Stejskalova, A, Vernerova, Z, Tornroth, T, Feller, A, Gaffney, E, Tardanico, R, Consalonieri, R, Garibotto, G, Tiebosch, A, Kooijman, C, Arques, M, Algaba, F, Carreras, M, Perez, M, Bernardo, L, Sundelin, B, Alm, P, Wernersson, A, Veress, B, Landells, W, Howie, A, Fleming, S, Griffith, A, Furness, P, Cook, H, Cook, H., and SINICO, RENATO ALBERTO

Published
2002

25. Chronic endothelin receptor blockade reduces end-organ damage independently of blood pressure effects in salt-loaded heterozygous Ren-2 transgenic rats

Author

Opocensky, M., Dvorak, P., Maly, J., Kramer, Hj, Backer, A., Kopkan, L., Vernerova, Z., Tesar, V., Tomáš Zima, Bader, M., Ganten, D., Janda, J., and Vaneckova, I.

Subjects
Endothelin Receptor Antagonists, Male, Sulfonamides, Physiology, Receptors, Endothelin, Multiple Organ Failure, Administration, Oral, Blood Pressure, Bosentan, General Medicine, Sodium Chloride, Severity of Illness Index, Rats, Animals, Genetically Modified, Rats, Sprague-Dawley, Renin-Angiotensin System, Survival Rate, Hypertension, Renin, Animals, Female
Abstract

The present study was performed to evaluate the role of an interaction between the endothelin (ET) and the renin-angiotensin systems (RAS) in the development and maintenance of hypertension and in hypertension-associated end-organ damage in heterozygous male and female transgenic rats harboring the mouse Ren-2 renin gene (TGR). Twenty-eight days old heterozygous TGR and age-matched transgene-negative normotensive Hannover Sprague-Dawley rats (HanSD) were randomly assigned to groups with normal-salt (NS) or high-salt (HS) intake. Nonselective ET(A)/ET(B) receptor blockade was achieved with bosentan (100 mg.kg(-1).day(-1)). All male and female HanSD as well as heterozygous TGR on NS exhibited 100 % survival rate until 180 days of age (end of experiment). HS diet in heterozygous TGR induced a transition from benign to malignant phase hypertension. The survival rates in male and in female heterozygous TGR on the HS diet were 46 % and 80 %, respectively, and were significantly improved by administration of bosentan to 76 % and 97 %, respectively. Treatment with bosentan did not influence either the course of hypertension (measured by plethysmography in conscious animals) or the final levels of blood pressure (measured by a direct method in anesthetized rats) in any of the experimental groups of HanSD or TGR. Administration of bosentan in heterozygous TGR fed the HS diet markedly reduced proteinuria, glomerulosclerosis and attenuated the development of cardiac hypertrophy compared with untreated TGR. Our data show that the ET receptor blockade markedly improves the survival rate and ameliorates end-organ damage in heterozygous TGR exposed to HS diet. These findings indicate that the interaction between the RAS and ET systems plays an important role in the development of hypertension-associated end-organ damage in TGR exposed to salt-loading.

27. Transcript expression and genetic variability analysis of caspases in breast carcinomas suggests CASP9 as the most interesting target.

Author

Brynychova V, Hlavac V, Ehrlichova M, Vaclavikova R, Nemcova-Furstova V, Pecha V, Trnkova M, Mrhalova M, Kodet R, Vrana D, Gatek J, Bendova M, Vernerova Z, Kovar J, and Soucek P

Subjects
Caspase 9 genetics, Caspase 9 metabolism, Caspases metabolism, Female, Gene Expression Profiling, Humans, Middle Aged, Breast Neoplasms enzymology, Breast Neoplasms genetics, Caspases genetics, Gene Expression Regulation, Neoplastic, Genetic Variation genetics, Molecular Targeted Therapy, Transcription, Genetic
Abstract

Background: Apoptosis plays a critical role in cancer cell survival and tumor development. We provide a hypothesis-generating screen for further research by exploring the expression profile and genetic variability of caspases (2, 3, 7, 8, 9, and 10) in breast carcinoma patients. This study addressed isoform-specific caspase transcript expression and genetic variability in regulatory sequences of caspases 2 and 9., Methods: Gene expression profiling was performed by quantitative real-time PCR in tumor and paired non-malignant tissues of two independent groups of patients. Genetic variability was determined by high resolution melting, allelic discrimination, and sequencing analysis in tumor and peripheral blood lymphocyte DNA of the patients., Results: CASP3 A+B and S isoforms were over-expressed in tumors of both patient groups. The CASP9 transcript was down-regulated in tumors of both groups of patients and significantly associated with expression of hormonal receptors and with the presence of rs4645978-rs2020903-rs4646034 haplotype in the CASP9 gene. Patients with a low intratumoral CASP9A/B isoform expression ratio (predicted to shift equilibrium towards anti-apoptotic isoform) subsequently treated with adjuvant chemotherapy had a significantly shorter disease-free survival than those with the high ratio (p=0.04). Inheritance of CC genotype of rs2020903 in CASP9 was associated with progesterone receptor expression in tumors (p=0.003)., Conclusions: Genetic variability in CASP9 and expression of its splicing variants present targets for further study.

Published
2017
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28. Littoral cell angioma of the spleen: a study of 25 cases with confirmation of frequent association with visceral malignancies.

Author

Peckova K, Michal M, Hadravsky L, Suster S, Damjanov I, Miesbauerova M, Kazakov DV, Vernerova Z, and Michal M

Subjects
Adult, Aged, Aged, 80 and over, Female, Humans, Immunohistochemistry, Male, Middle Aged, Biomarkers, Tumor analysis, Hemangioma pathology, Neoplasms, Multiple Primary pathology, Splenic Neoplasms pathology
Abstract

Aims: Littoral cell angioma (LCA) is a rare primary splenic tumour that is frequently associated with internal malignancies. Immunohistochemistry can demonstrate a distinct hybrid endothelial-histiocytic phenotype of littoral cells, and is a helpful adjunct for making the correct diagnosis. The aims of this study were to present a series of 25 LCAs, with an emphasis on the frequent association of the neoplasm with visceral malignancies, and to provide a detailed immunohistochemical analysis by employing new markers., Methods and Results: All 25 cases with available tissue blocks were immunohistochemically stained for endothelial and histiocytic markers. Clinical and follow-up data were retrieved from the respective institutions. The tumours were obtained from 16 males and nine females, whose age ranged from 32 to 86 years (mean 56.2 years). Clinical information was available for 24 of 25 patients, and follow-up for 11 of 25 patients (range 2-19 years; mean 11.6 years). Immunohistochemically, all cases were positive for LYVE-1, factor VIII, FLI-1, vascular endothelial growth factor receptor (VEGFR)-2, VEGFR-3, claudin-5, ERG, LMO2, CD31, CD163, lysozyme, and CD4, but negative for D2-40, CD8, and factor XIIIa. Fifteen of 25 cases were associated with various malignancies, including epithelial, mesenchymal and haematological tumours., Conclusions: The cohort of 25 patients is the largest series of LCAs published to date. By using antibodies against recently introduced endothelial markers, we have expanded the immunoprofile of LCA. We have further highlighted the clinical significance of LCA, as more than half of the patients in this study also harboured a coexisting visceral malignancy. Therefore, we conclude that the finding of splenic LCA mandates a thorough clinical evaluation for a concomitant malignancy., (© 2016 John Wiley & Sons Ltd.)

Published
2016
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29. Dilemmas in autoimmune pancreatitis. Surgical resection or not?

Author

Hoffmanova I, Gurlich R, Janik V, Szabo A, and Vernerova Z

Subjects
Adrenal Cortex Hormones, Aged, Autoimmune Diseases immunology, Autoimmune Diseases pathology, Diagnosis, Differential, Humans, Male, Pancreas pathology, Pancreatic Neoplasms, Pancreatitis immunology, Pancreatitis pathology, Treatment Outcome, Autoimmune Diseases diagnosis, Immunoglobulin G blood, Jaundice, Obstructive etiology, Pancreas diagnostic imaging, Pancreatitis diagnosis
Abstract

Surgical treatment is not commonly recommended in the management of autoimmune pancreatitis. The article describes a dilemma in diagnostics and treatment of a 68-year old man with the mass in the head of the pancreas that mimicked pancreatic cancer and that was diagnosed as a type 1 autoimmune pancreatitis (IgG4-related pancreatitis) after a surgical resection. Diagnosis of the autoimmune pancreatitis is a real clinical challenge, as in the current diagnostic criteria exists some degree of overlap in the findings between autoimmune pancreatitis and pancreatic cancer (indicated by the similarity in radiologic findings, elevation of IgG4, sampling errors in pancreatic biopsy, and the possibility of synchronous autoimmune pancreatitis and pancreatic cancer). Despite the generally accepted corticosteroids as the primary treatment modality in autoimmune pancreatitis, we believe that surgical resection remains necessary in a specific subgroup of patients with autoimmune pancreatitis (Fig. 4, Ref. 37).

Published
2016
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30. The occurrence of fetal microchimeric cells in endometrial tissues is a very common phenomenon in benign uterine disorders, and the lower prevalence of fetal microchimerism is associated with better uterine cancer prognoses.

Author

Hromadnikova I, Kotlabova K, Pirkova P, Libalova P, Vernerova Z, Svoboda B, and Kucera E

Subjects
Adult, Aged, Early Diagnosis, Endometrium cytology, Female, Fetal Stem Cells, Humans, Male, Maternal-Fetal Exchange genetics, Middle Aged, Neoplasm Staging, Pregnancy, Prognosis, Real-Time Polymerase Chain Reaction, Risk Factors, Uterine Diseases diagnosis, Uterine Diseases pathology, Uterine Neoplasms pathology, Chimerism statistics & numerical data, Endometrium pathology, Uterine Neoplasms diagnosis, Uterine Neoplasms genetics
Abstract

This is the first study carried out to describe the role of fetal microchimerism (FM) in the pathogenesis of uterine cancer. The prevalence and concentration of male fetal microchimeric cells (FMCs) were examined in endometrial tissues in relation to subtypes of uterine cancer, and the histological grade and stage of the tumor. FM occurrence was analyzed in relation to risk factors, including hypertension, obesity, type 2 diabetes, dyslipidemia, age at cancer diagnosis, and patient pregnancy history. The prevalence and concentration of FMCs were examined in endometrial tissues using real-time polymerase chain reaction, SRY and β-globin sequences as markers for male fetal FMCs and total DNA. The studied group involved 47 type 1 endometrial cancers, 28 type 2 endometrial cancers, and 41 benign uterine diseases. While the prevalence of FM was decreased only in type 1 endometrial cancer, compared with benign uterine disorders (38.3% vs.70.7%; odds ratio [OR]=0.257, 95% confidence interval [CI]: 0.105 to 0.628, p=0.003), FMC concentrations did not differ within examined groups. The lower FM prevalence was detected in low-grade (grade 1 and grade 2) endometrioid cancer (38.3% vs. 70.7%, OR=0.256, 95% CI: 0.105 to 0.627, p=0.003) and in FIGO 1 tumors (40.7% vs. 70.7%, OR=0.285, 95% CI: 0.120 to 0.675, p=0.004). No correlation between FM prevalence or FMC concentrations and risk factors was demonstrated. A lower prevalence of male FM seemed to be associated with better prognoses in uterine cancer based on tumor subtype, histological grade, and stage of the tumor.

Published
2014
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31. BEACOPP escalated and rituximab in the treatment of Hodgkin lymphoma occurring concurrently with diffuse large B-cell non-Hodgkin lymphoma.

Author

Palickova M, Mocikova H, Vernerova Z, Campr V, and Kozak T

Subjects
Adult, Antibodies, Monoclonal, Murine-Derived administration & dosage, Bleomycin therapeutic use, Cyclophosphamide therapeutic use, Doxorubicin therapeutic use, Etoposide therapeutic use, Female, Hodgkin Disease diagnosis, Humans, Lymph Nodes pathology, Lymphoma, Large B-Cell, Diffuse diagnosis, Prednisone therapeutic use, Procarbazine therapeutic use, Remission Induction, Rituximab, Treatment Outcome, Vincristine therapeutic use, Antineoplastic Combined Chemotherapy Protocols therapeutic use, Hodgkin Disease complications, Hodgkin Disease drug therapy, Lymphoma, Large B-Cell, Diffuse complications, Lymphoma, Large B-Cell, Diffuse drug therapy
Published
2013
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32. heterogeneity of dna ploidy in endometrial carcinoma: comparison of different tissue samples obtained during diagnosis and treatment.

Author

Libalova P, Vernerova Z, Hubickova-Heringova L, Pinterova D, Kolostova K, Bobek V, Tikovsky K, Housa D, Kubecova M, Pecen L, and Svoboda B

Subjects
Adult, Aged, Aged, 80 and over, Biopsy, Carcinoma pathology, Carcinoma surgery, DNA genetics, Endometrial Neoplasms pathology, Endometrial Neoplasms surgery, Endometrium pathology, Female, Humans, Hysterectomy, Middle Aged, Neoplasm Invasiveness, Specimen Handling, Aneuploidy, Carcinoma genetics, Diploidy, Endometrial Neoplasms genetics
Abstract

Aim: Comparison of DNA ploidy status of different tumour tissue samples (fresh/frozen vs. paraffin-embedded; curettage vs. hysterectomy samples) obtained during diagnosis and treatment of patients with endometrial carcinoma., Patients and Methods: DNA ploidy status and conventional prognostic parameters were recorded for 74 patients with endometrial carcinoma prospectively., Results: In 59 (79.7%) patients the DNA status was described as diploid in all analyzed tissue samples. The remaining 15 (20.3%) cases were described as DNA aneuploid in at least one of the corresponding tissue samples. The concordance between DNA ploidy status in fresh vs. paraffin-embedded hysterectomy samples as well as curettage vs. hysterectomy paraffin-embedded samples was high (kappa coefficient κ=0.6348, 95% confidence interval CI=0.3673-0.9023, and p=0.6408, 95% CI=0.3977-0.8838), however, the methods are not interchangeable., Conclusion: The DNA ploidy discordance observed in our study group seems to document intratumoral heterogeneity that should be expected when applying DNA ploidy status in the clinical management of endometrial carcinoma.

Published
2012

33. Plasma EBV-DNA monitoring in Epstein-Barr virus-positive Hodgkin lymphoma patients.

Author

Spacek M, Hubacek P, Markova J, Zajac M, Vernerova Z, Kamaradova K, Stuchly J, and Kozak T

Subjects
Adolescent, Adult, Aged, Aged, 80 and over, Cohort Studies, Czech Republic epidemiology, Epstein-Barr Virus Infections blood, Epstein-Barr Virus Infections epidemiology, Epstein-Barr Virus Infections virology, Female, Herpesvirus 4, Human genetics, Hodgkin Disease blood, Hodgkin Disease pathology, Humans, Immunohistochemistry, In Situ Hybridization, Fluorescence, Logistic Models, Male, Middle Aged, Prospective Studies, RNA, Viral blood, Viral Load, Viral Matrix Proteins blood, Young Adult, DNA, Viral blood, Epstein-Barr Virus Infections complications, Herpesvirus 4, Human isolation & purification, Hodgkin Disease virology
Abstract

Epstein-Barr virus (EBV) is associated with approximately one-third of Hodgkin lymphoma (HL) cases. EBV-DNA is often present in the plasma and whole blood of EBV-associated HL patients. However, the significance of EBV-DNA monitoring is debated. In a cohort of 165 adult HL patients, EBV-DNA viral load was prospectively monitored both in the plasma and whole blood. Diagnostic tissue samples of all patients were histologically reviewed; in 72% nodular sclerosis was detected, 24% presented with mixed cellularity (MC), and 5% had other type of HL. Tissues from 150 patients were also analyzed for the presence of latent EBV infection using in situ hybridization for EBV-encoded RNA (EBER) and immunohistochemistry for latent membrane protein (LMP1). Using these methods, 29 (19%) patients were classified as EBV positive. Using real-time quantitative PCR, 22 (76%) of EBV-positive HL patients had detectable EBV-DNA in the plasma and 19 (66%) patients in whole blood prior to therapy. In the group of EBV-negative HL cases, three (2%) patients had detectable plasma EBV-DNA and 30 (25%) patients whole blood EBV-DNA before treatment. EBV-positive HL was significantly associated with EBV-DNA positivity both in the plasma and whole blood in pretreatment samples, increasing age and MC subtype. Serial analysis of plasma EBV-DNA showed that response to therapy was associated with decline in viral load. Moreover, significantly increased plasma EBV-DNA level recurred before disease relapse in one patient. Our results further suggest that the assessment of plasma EBV-DNA viral load might be of value for estimation of prognosis and follow-up of patients with EBV-positive HL., (© 2010 The Authors. APMIS © 2010 APMIS.)

Published
2011
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34. Serum resistin levels in benign prostate hyperplasia and non-metastatic prostate cancer: possible role in cancer progression.

Author

Housa D, Vernerova Z, Heracek J, Cechak P, Rosova B, Kuncova J, and Haluzik M

Subjects
Aged, Disease Progression, Humans, Male, Neoplasm Staging, Prostatic Neoplasms metabolism, Prostatic Neoplasms pathology, Prostatic Hyperplasia blood, Prostatic Neoplasms blood, Resistin blood
Abstract

Resistin is a member of adipokine family involved in the regulation of inflammatory reactions and insulin sensitivity. In presented study its possible role in the development of benign prostate hyperplasia and prostate cancer was evaluated. Blood samples and prostate specimens were collected from 26 patients with benign prostate hyperplasia (BPH) and from 42 patients with prostate cancer (PCa) stage pT2 (n=18) and pT3 (n=24). Selected metabolic and biochemical parameters and serum resistin levels were measured and anthropometric measurements were performed as well as tissue immunohistochemistry for resistin. Serum resistin levels did not differ significantly between benign hyperplasia and prostate cancer but in cancer patients there was a trend towards decrease with higher cancer stage. Moreover, serum resistin levels were significantly lower in patients with seminal vesicle invasion in comparison to those without invasion. While in BPH serum resistin levels correlated with insulin resistance, inflammatory status and cortisol, in PCa positive correlation with F/T PSA ratio and cortisol was observed. Tissue immunohistochemistry did not show any differences in staining pattern between benign and neoplastic prostate tissue. We conclude that serum resistin levels do not significantly differ between patients with benign prostate hyperplasia and prostate cancer, but there is a trend towards decrease in resistin serum levels in advanced cancer cases.

Published
2008

35. Improvement of insulin sensitivity after peroxisome proliferator-activated receptor-alpha agonist treatment is accompanied by paradoxical increase of circulating resistin levels.

Author

Haluzik MM, Lacinova Z, Dolinkova M, Haluzikova D, Housa D, Horinek A, Vernerova Z, Kumstyrova T, and Haluzik M

Subjects
Adiponectin blood, Adiponectin genetics, Adipose Tissue chemistry, Adipose Tissue pathology, Animals, Blood Glucose analysis, Diet, Dietary Carbohydrates administration & dosage, Fatty Acids, Nonesterified analysis, Fatty Liver blood, Fatty Liver drug therapy, Fatty Liver etiology, Fenofibrate administration & dosage, Gene Expression drug effects, Glucose Clamp Technique, Insulin blood, Insulin pharmacology, Lipids biosynthesis, Liver chemistry, Liver drug effects, Male, Mice, Mice, Inbred C57BL, Muscle, Skeletal chemistry, Obesity blood, Obesity etiology, Obesity physiopathology, Organ Size drug effects, RNA, Messenger analysis, Receptors, Adiponectin, Receptors, Cell Surface genetics, Resistin genetics, Triglycerides blood, Weight Loss drug effects, Insulin Resistance, PPAR alpha agonists, PPAR alpha physiology, Resistin blood
Abstract

We studied the effect of peroxisome proliferator-activated receptor-alpha (PPAR-alpha) activation on serum concentrations and tissue expression of resistin, adiponectin, and adiponectin receptor-1 and -2 (AdipoR1 and AdipoR2) mRNA in normal mice and mice with insulin resistance induced by lipogenic, simple-carbohydrate diet (LD). Sixteen weeks of LD feeding induced obesity with liver steatosis and increased insulin levels but did not significantly affect circulating adiponectin or resistin. Treatment with PPAR-alpha agonist fenofibrate decreased body weight and fat pad weight and ameliorated liver steatosis in LD-fed mice with concomitant reduction in blood glucose, free fatty acid, triglyceride, serum insulin levels, and homeostasis model assessment index values. Euglycemic-hyperinsulinemic clamp demonstrated the development of whole-body and liver insulin resistance in LD-fed mice, which were both normalized by fenofibrate. Fenofibrate treatment markedly increased circulating resistin levels on both diets and adiponectin levels in chow-fed mice only. Fat adiponectin mRNA expression was not affected by fenofibrate treatment. Resistin mRNA expression increased in subcutaneous but not gonadal fat after fenofibrate treatment. In addition to fat, a significant amount of adiponectin mRNA was also expressed in the muscle. This expression markedly increased after fenofibrate treatment in chow- but not in LD-fed mice. Adipose tissue expression of AdipoR1 mRNA was significantly reduced in LD-fed mice and increased after fenofibrate treatment. In conclusion, PPAR-alpha activation ameliorated the development of insulin resistance in LD-fed mice despite a major increase in serum resistin levels. This effect could be partially explained by increased AdipoR1 expression in adipose tissue after fenofibrate treatment.

Published
2006
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36. Amyloid A amyloidosis in non-infected and avian leukosis virus-C persistently infected inbred ducks.

Author

Stepanets V, Vernerova Z, Vilhelmova M, Geryk J, Hejnar J, and Svoboda J

Abstract

The breeding history of the first inbred strain of Khaki Campbell ducks is presented. The genetic homogeneity of this strain was tested on the basis of serum amyloid A (SAA) polymorphism and it was established that it harbours only the SAA allele A, which is expressed in liver, lung and bursa of Fabricius tissues. Pathogenic changes in control and avian leukosis virus-C (ALV-C) persistently infected ducks were evaluated during the period spanning 1 to 10 months after hatching. In both groups, AA amyloidosis was revealed and characterized. In spite of the inbred nature of animals, the incidence of amyloid A deposition varied among experiments, suggesting that additional non-genetic factors are involved. Similar variation was found in ALV-C persistently infected ducks, where only in one out of three experiments was the incidence ofAA amyloidosis significantly higher than in controls.

Published
2001
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