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1. Metabolome plasticity in 241 Arabidopsis thaliana accessions reveals evolutionary cold adaptation processes

Author

Weiszmann, Jakob, primary, Walther, Dirk, additional, Clauw, Pieter, additional, Back, Georg, additional, Gunis, Joanna, additional, Reichardt, Ilka, additional, Koemeda, Stefanie, additional, Jez, Jakub, additional, Nordborg, Magnus, additional, Schwarzerova, Jana, additional, Pierides, Iro, additional, Nägele, Thomas, additional, and Weckwerth, Wolfram, additional

Published
2023
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2. Metabolome plasticity in 241 Arabidopsis thaliana accessions reveals evolutionary cold adaptation processes

Author

Jakob Weiszmann, Dirk Walther, Pieter Clauw, Georg Back, Joanna Gunis, Ilka Reichardt, Stefanie Koemeda, Jakub Jez, Magnus Nordborg, Jana Schwarzerova, Iro Pierides, Thomas Nägele, and Wolfram Weckwerth

Subjects
Physiology, Genetics, Plant Science
Abstract

Acclimation and adaptation of metabolism to a changing environment are key processes for plant survival and reproductive success. In the present study, 241 natural accessions of Arabidopsis (Arabidopsis thaliana) were grown under two different temperature regimes, 16 °C and 6 °C, and growth parameters were recorded, together with metabolite profiles, to investigate the natural genome × environment effects on metabolome variation. The plasticity of metabolism, which was captured by metabolic distance measures, varied considerably between accessions. Both relative growth rates and metabolic distances were predictable by the underlying natural genetic variation of accessions. Applying machine learning methods, climatic variables of the original growth habitats were tested for their predictive power of natural metabolic variation among accessions. We found specifically habitat temperature during the first quarter of the year to be the best predictor of the plasticity of primary metabolism, indicating habitat temperature as the causal driver of evolutionary cold adaptation processes. Analyses of epigenome- and genome-wide associations revealed accession-specific differential DNA-methylation levels as potentially linked to the metabolome and identified FUMARASE2 as strongly associated with cold adaptation in Arabidopsis accessions. These findings were supported by calculations of the biochemical Jacobian matrix based on variance and covariance of metabolomics data, which revealed that growth under low temperatures most substantially affects the accession-specific plasticity of fumarate and sugar metabolism. Our findings indicate that the plasticity of metabolic regulation is predictable from the genome and epigenome and driven evolutionarily by Arabidopsis growth habitats.

Published
2023

3. GENETIC DISEASES AND MOLECULAR GENETICS

Author

C. Legendre, D. Cohen, Y. Delmas, T. Feldkamp, D. Fouque, R. Furman, O. Gaber, L. Greenbaum, T. Goodship, H. Haller, M. Herthelius, M. Hourmant, C. Licht, B. Moulin, N. Sheerin, A. Trivelli, C. L. Bedrosian, C. Loirat, S. Babu, T. Jungraithmayr, Y. Lebranchu, M. Riedl, A. O. Gaber, C. Bedrosian, P. Muus, K. Douglas, G. Remuzzi, A. Kourouklaris, K. Ioannou, I. Athanasiou, K. Demetriou, A. Panagidou, M. Zavros, N. Y. Rodriguez C, M. Blasco, C. Arcal, L. F. Quintana, S. Rodriguez de Cordoba, J. M. Campistol, N. Bachmann, T. Eisenberger, C. Decker, H. J. Bolz, C. Bergmann, F. Pesce, S. N. Cox, G. Serino, G. De Palma, F. P. Sallustio, F. Schena, M. Falchi, M. Pieri, C. Stefanou, A. Zaravinos, K. Erguler, G. Lapathitis, H. Dweep, C. Sticht, N. Anastasiadou, I. Zouvani, K. Voskarides, N. Gretz, C. C. Deltas, A. Ruiz, O. Bonny, F. Sallustio, C. Curci, S. Cox, E. Kemter, S. Sklenak, B. Aigner, R. Wanke, T. M. Kitzler, J. L. Moskowitz, S. E. Piret, K. Lhotta, A. Tashman, E. Velez, R. V. Thakker, P. Kotanko, J. Leierer, M. Rudnicki, P. Perco, C. Koppelstaetter, G. Mayer, M. J. N. Sa, S. Alves, H. Storey, F. Flinter, P. J. Willems, F. Carvalho, J. Oliveira, M. Arsali, L. Papazachariou, P. Demosthenous, A. Lazarou, M. Hadjigavriel, C. Stavrou, L. Yioukkas, C. Deltas, A. Pierides, M. Kkolou, H. R. Toka, S. Dibartolo, B. Lanske, E. M. Brown, M. R. Pollak, A. Familiari, B. Zavan, S. Sanna Cherchi, A. Fabris, R. Cristofaro, G. Gambaro, A. D'Angelo, F. Anglani, H. Toka, D. Mount, M. Pollak, G. Curhan, G. Sengoge, T. Bajari, A. Kupczok, A. von Haeseler, M. Schuster, W. Pfaller, P. Jennings, A. Weltermann, S. Blake, G. Sunder-Plassmann, A. Kerti, R. Csohany, L. Wagner, E. Javorszky, E. Maka, T. Tulassay, K. Tory, J. Kingswood, N. Nikolskaya, J. Mbundi, S. Jozwiak, E. Belousova, M. Frost, R. Kuperman, M. Bebin, B. Korf, R. Flamini, M. Kohrman, S. Sparagana, J. Wu, T. Brechenmacher, K. Stein, J. Bissler, D. Franz, B. Zonnenberg, W. Cheung, J. Wang, D. Lam, K. Budde, L. Ivanitskiy, E. Sowershaewa, T. Krasnova, L. Samokhodskaya, M. Safarikova, R. Jana, S. Jitka, L. Obeidova, M. Kohoutova, V. Tesar, H. Evrengul, P. Ertan, E. Serdaroglu, S. Yuksel, S. Mir, E. Yang n Ergon, A. Berdeli, A. Zawada, K. Rogacev, B. Rotter, P. Winter, D. Fliser, G. Heine, S. Bataille, V. Moal, Y. Berland, L. Daniel, C. Rosado, E. Bueno, P. Fraile, C. Lucas, P. Garcoa-Cosmes, J. M. Tabernero, R. Gonzalez, P. Garcia-Cosmes, M. Silska-Dittmar, K. Zaorska, A. Malke, A. Musielak, D. Ostalska-Nowicka, J. Zachwieja, V. K d r, E. Uz, A. Yigit, A. Altuntas, B. Yigit, S. Inal, M. Sezer, R. Yilmaz, B. Visciano, C. Porto, E. Acampora, R. Russo, E. Riccio, I. Capuano, G. Parenti, A. Pisani, S. Feriozzi, A. Perrin, M. West, K. Nicholls, J. Torras, M. Cybulla, M. Conti, A. Angioi, M. Floris, P. Melis, A. M. Asunis, D. Piras, A. Pani, D. Warnock, A. Guasch, C. Thomas, C. Wanner, R. Campbell, B. Vujkovac, I. Okur, G. Biberoglu, F. Ezgu, L. Tumer, A. Hasanoglu, Z. Bicik, Y. Akin, M. Mumcuoglu, T. Ecder, C. Paliouras, G. Mattas, N. Papagiannis, G. Ntetskas, F. Lamprianou, N. Karvouniaris, and P. Alivanis

Subjects
Genetics, Transplantation, medicine.medical_specialty, Nephrology, business.industry, Molecular genetics, medicine, business
Published
2014

4. Genetic diseases

Author

T. Inazu, T. Kawahara, H. Endou, N. Anzai, I. Sebesta, B. Stiburkova, K. Ichida, M. Hosoyamada, A. Testa, D. Leonardis, F. Catalano, A. Pisano, A. Mafrica, B. Spoto, M. C. Sanguedolce, R. M. Parlongo, G. Tripepi, M. Postorino, G. Enia, C. Zoccali, F. Mallamaci, M. Working Group, A. Luque de Pablos, V. Garcia-Nieto, J. C. Lopez-Menchero, E. Ramos-Trujillo, H. Gonzalez-Acosta, F. Claverie-Martin, M. Arsali, P. Demosthenous, L. Papazachariou, Y. Athanasiou, K. Voskarides, C. Deltas, A. Pierides, S. Lee, K. H. Jeong, C. Ihm, T. W. Lee, S. H. Lee, J. Y. Moon, J. G. Wi, H. J. Lee, E. Y. Kim, K. Rogacev, A. Friedrich, B. Hummel, J. Berg, A. Zawada, D. Fliser, J. Geisel, G. H. Heine, I. Brabcova, S. Dusilova-Sulkova, Z. Krejcik, V. Stranecky, K. Lipar, T. Marada, J. Stepankova, O. Viklicky, M. Buraczynska, P. Zukowski, W. Zaluska, A. Kuczmaszewska, A. Ksiazek, M. Gaggl, S. Weidner, M. Hofer, J. Kleinert, G. Fauler, M. Wallner, P. Kotanko, G. Sunder-Plassmann, E. Paschke, R. Heguilen, L. Albarracin, J. Politei, A. A. Liste, A. Bernasconi, E. Kusano, R. Russo, A. Pisani, G. Messalli, M. Imbriaco, L. Prikhodina, O. Ryzhkova, V. Polyakov, K. Lipkowska, D. Ostalska-Nowicka, M. Smiech, M. Jaroniec, K. Zaorska, W. Szaflarski, M. Nowicki, J. Zachwieja, G. D'arrigo, J. Moskowitz, S. Piret, A. Tashman, E. Velez, K. Lhotta, R. Thakker, J. Cox, J. Kingswood, J. Mbundi, G. Attard, U. Patel, A. Saggar, F. Elmslie, T. Doyle, A. Jansen, S. Jozwiak, E. Belousova, M. Frost, R. Kuperman, M. Bebin, B. Korf, R. Flamini, M. Kohrman, S. Sparagana, J. Wu, J. Ford, G. Shah, D. Franz, B. Zonnenberg, W. Cheung, S. Urva, J. Wang, C. Kingswood, K. Budde, T. Kofman, C. Narjoz, Q. Raimbourg, M. Roland, M.-A. Loriot, A. Karras, G. S. Hill, C. Jacquot, D. Nochy, E. Thervet, P. Jagodzinski, M. Mostowska, A. Oko, N. Nicolaou, S. Kevelam, M. Lilien, M. Oosterveld, R. Goldschmeding, A. Van Eerde, R. Pfundt, A. Sonnenberg, P. Ter Hal, N. Knoers, K. Renkema, T. Storm, R. Nielsen, E. Christensen, C. Frykholm, L. Tranebjaerg, H. Birn, P. Verroust, T. Neveus, B. Sundelin, J. M. Hertz, G. Holmstrom, K. Ericson, A. Fabris, D. Cremasco, A. Zambon, E. Muraro, M. Alessi, A. D'angelo, F. Anglani, D. Del Prete, A. Alkmim Teixeira, B. M. Quinto, C. Jose Rodrigues, A. Beltrame Ribeiro, M. Batista, A. Kerti, R. Csohany, A. Szabo, O. Arkossy, P. Sallai, V. Moriniere, V. Vega-Warner, O. Lakatos, T. Szabo, G. Reusz, K. Tory, M. Addis, E. Tosetto, C. Meloni, M. Ceol, R. Cristofaro, M. A. Melis, P. Vercelloni, G. Marra, S. Kaniuka, M. Nagel, W. Wolyniec, L. Obolonczyk, R. Swiatkowska-Stodulska, K. Sworczak, B. Rutkowski, C. Chen, L. Jiang, L. Chen, L. Fang, M. Mozes M., M. Boosi, L. Rosivall, G. Kokeny, R. Diana, O. Gross, T. Johanna, G. Rainer, C. Ayse, H. Henrik, M. Gerhard-Anton, M. Nabil, E. Intissar, H. Belge, J. Bloch, K. Dahan, Y. Pirson, P. Vanhille, and N. Demoulin

Subjects
Transplantation, Nephrology
Published
2012

5. Outcome of kidney transplantation in autosomal dominant medullary cystic kidney disease type 1

Author

Stavrou, Christoforos V., Constantinou-Deltas, Constantinos D., Christofides, Tasos C., Pierides, Alkis M., Christofides, Tasos C. [0000-0001-6121-0683], and Constantinou-Deltas, Constantinos D. [0000-0001-5549-9169]

Subjects
Graft Rejection, Male, Kaplan Meier method, graft survival, Medullary cystic kidney disease, Kidney transplantation, Nephronophthisis, Cause of Death, postoperative complication, Juvenile nephronophthisis, Cyst, clinical article, adult, Graft Survival, article, Age Factors, Middle Aged, Polycystic Kidney, Autosomal Dominant, Tissue Donors, female, priority journal, Nephrology, Female, Adult, medicine.medical_specialty, Autosomal dominant medullary cystic kidney disease, renal system parameters, government.form_of_government, disease classification, living donor, Risk Assessment, Sampling Studies, Nephropathy, autosomal dominant disorder, medullary sponge kidney, Sex Factors, male, Internal medicine, medicine, follow up, Humans, controlled study, cadaver donor, human, kidney donor, intermethod comparison, Retrospective Studies, Transplantation, business.industry, medicine.disease, Kidney Transplantation, Survival Analysis, kidney failure, Surgery, Cyprus, treatment outcome, government, kidney graft rejection, business, Follow-Up Studies, Kidney disease
Abstract

Background. Autosomal dominant medullary cystic kidney disease (ADMCKD) is an inherited, distinct, chronic, tubulointerstitial, cystic-type nephropathy, often described together with juvenile nephronophthisis as a single disease complex (NPH-MCD). However, since the recent localization of two genes responsible for ADMCKD, namely MCKD1 and MCKD2, ADMCKD has gained independent status. Unfortunately, there appears to be a distinct lack of up-to-date information in the currently available medical literature concerning worldwide patient and graft survival after renal transplantation in ADMCKD. This report is based on all 41 transplanted patients [19 suffering from autosomal dominant medullary cystic kidney disease type 1 (ADMCKD1) and 22 from other causes] who were referred for kidney transplantation from our centre in Pafos, Cyprus between 1976 and 2000. All patients had regular follow-up examinations. This report aims to present the results of kidney transplantation of the 19 ADMCKD1 patients and to compare them with those for the 22 non-ADMCKD patients. Methods. Patient and graft survival times in both groups were recorded, analysed and compared 1 and 5 years post-transplant. Patient and graft survival times were calculated according to the Kaplan-Meier method and some descriptive statistical comparisons were based on the χ2-test. Results. The 1 year patient and graft survival rates for ADMCKD1 (group A) were 100%, while the 5 year figures were 100% and 90%, respectively. For non-ADMCKD1 patients (group B) the 1 year figures were 95% for both parameters, while the 5 year figures were 93.3% for both parameters. There were no statistically significant differences in patient and graft survival times between the two groups. Conclusions. Kidney transplantation is the treatment of choice for patients suffering from ADMCKD, with an excellent outcome and no specific complications. 18 2165 2169 Cited By :10

Published
2003

6. Germinal and somatic mutations in the PKD2 gene of renal cysts in autosomal dominant polycystic kidney disease

Author

Christos Hadjimichael, Constantinos Deltas, Alkis Pierides, Michael Koptides, and Panayiota Koupepidou

Subjects
Male, TRPP Cation Channels, Nonsense mutation, Autosomal dominant polycystic kidney disease, Loss of Heterozygosity, Biology, urologic and male genital diseases, medicine.disease_cause, Loss of heterozygosity, Germline mutation, Chromosome 16, Genetics, medicine, Humans, Allele, Molecular Biology, Germ-Line Mutation, Polymorphism, Single-Stranded Conformational, Genetics (clinical), Aged, Mutation, Base Sequence, PKD1, urogenital system, Membrane Proteins, DNA, General Medicine, Polycystic Kidney, Autosomal Dominant, medicine.disease, Molecular biology, female genital diseases and pregnancy complications, Pedigree, Female
Abstract

Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations in one of three genes: PKD1 on chromosome 16 accounts for approximately 85% of cases whereas PKD2 on chromosome 4 accounts for approximately 15%. Mutations in the PKD3 gene are rare. All patients present with similar clinical phenotypes, and the cardinal symptom is the formation of fluid-filled cysts in the kidneys. Previous work has provided data supporting the notion that cysts in ADPKD1 are focal in nature and form after loss of function of polycystin 1. This became evident by demonstrating that the normal PKD1 allele was inactivated somatically by loss of heterozygosity or by mutagenesis in a subset of renal or liver cysts examined. We show in this report, for the first time, multiple novel somatic mutations within the PKD2 gene of epithelial cells, in both kidneys of an ADPKD2 patient. From a total of 21 cysts examined, seven (33%) had the same C insertion within the inherited wild-type allele. In two other cysts, a nonsense mutation and a splice site AG deletion had occurred in a PKD2 allele that could not be identified as the inherited wild-type or mutant. We suggest that the autosomal dominant form of ADPKD2 occurs by a cellular recessive mechanism, supporting a two-hit model for cyst formation.

Published
1999

7. The pregnant patient with partial lipodystrophy developing acute renal failure - onset of de novo membranoproliferative glomerulonephritis

Author

I Kallikas, Kyriacos Kyriacou, Ioanna Zouvani, Alkis Pierides, and Kyproulla Demetriou

Subjects
Adult, medicine.medical_specialty, Lipodystrophy, Glomerulonephritis, Membranoproliferative, Anti-Inflammatory Agents, Kidney, Gastroenterology, Pregnancy, Renal Dialysis, Internal medicine, Membranoproliferative glomerulonephritis, medicine, Humans, Erythropoietin, Transplantation, business.industry, Partial Lipodystrophy, Acute Kidney Injury, medicine.disease, Pregnancy Complications, medicine.anatomical_structure, Nephrology, Immunology, Mesangial proliferative glomerulonephritis, Female, Steroids, business, Nephritis, Kidney disease
Abstract

acute renal failure; pregnancy; partial lipo- towards the end of the gestation period, between 34dystrophy; low C3; membranoproliferative nephritis and 38 weeks, and it is invariably the result of pre-eclampsia and its complications or the result of severeblood loss [5–7]. Occasionally post-infectious glom-erulonephritis may occur during pregnancy and can be

Published
1998

8. Chromosome 1 localization of a gene for autosomal dominant medullary cystic kidney disease

Author

Christodoulou, Kyproula, Tsingis, Marios, Stavrou, Christoforos V., Eleftheriou, Andri, Papapavlou, Petros, Patsalis, Philippos C., Ioannou, Panayiotis A., Pierides, Alkis M., Constantinou-Deltas, Constantinos D., and Constantinou-Deltas, Constantinos D. [0000-0001-5549-9169]

Subjects
Male, Genetic Markers, marker gene, Genetic Linkage, Locus (genetics), hyperuricemia, Biology, Medullary cystic kidney disease, chromosome 1q, medullary sponge kidney, gout, Gene mapping, Genetic linkage, Genetics, medicine, Humans, genetic polymorphism, kidney cyst, Cyst, human, fluorescence in situ hybridization, Molecular Biology, In Situ Hybridization, Fluorescence, Genetics (clinical), Recombination, Genetic, Genetic heterogeneity, Haplotype, article, Linkage (Genetics), Chromosome Mapping, salt losing nephritis, General Medicine, Polycystic Kidney, Autosomal Dominant, medicine.disease, Pedigree, autosomal dominant inheritance, priority journal, Haplotypes, Chromosomes, Human, Pair 1, Female, cyprus, Age of onset
Abstract

There is a group of inherited cystic nephropathies that are characterized by juvenile onset recessive inheritance (familial juvenile nephronophthisis, FJN) or by adult onset dominant inheritance (medullary cystic disease, MCD) and share similar clinico-pathological presentation to the extent that they are usually grouped together under the term FJN/MCD complex. The main symptoms consist of renal cyst formation in the medulla or the corticomedullary junction and salt wasting. Although earlier reports had suggested that one single gene may be responsible for this pathology, recent reports have shown that the FJN complex itself comprises a genetically heterogeneous group. Here we are presenting two large Cypriot families that segregate autosomal dominant medullary cystic kidney disease (ADMCKD) with hyperuricemia and gout and with very late age of onset (mean 62.2 and 51.5 years). We performed DNA linkage mapping using highly polymorphic microsatellite markers and found linkage to marker locus D1S1595 at 1q21 with a two-point lod score of 6.45 at θ = 0.00. Analysis of haplotypes and of critical recombinants enabled confinement of the disease locus within an ~ 8 cM region between marker loci D1S498 and D1S2125. FISH mapping with a large P1 clone confirmed the physical localization within 1q21. The two families share the same disease haplotype, thus suggesting their relationship through a common ancestor and the possible existence of a single ADMCKD-causing mutation within these families. To our knowledge this is the first genetic locus identified to cause FJN/MCD pathology of the dominant adult type. 7 905 911 Cited By :99

Published
1998

9. A Translation Frameshift Mutation Induced by a Cytosine Insertion in the Polycystic Kidney Disease 2 Gene (PKD2)

Author

Xenophontos, Stavroulla L., Constantinides, Rolandos, Hayashi, Tomohito, Mochizuki, Toshio, Somlo, Stefan, Pierides, Alkis M., Constantinou-Deltas, Constantinos D., and Constantinou-Deltas, Constantinos D. [0000-0001-5549-9169]

Subjects
onset age, Male, Silent mutation, Mutation rate, family, TRPP Cation Channels, single strand conformation polymorphism, frameshift mutation, Nonsense mutation, nonsense mutation, arginine, Biology, Frameshift mutation, Polar mutation, Cytosine, male, genetic linkage, Genetics, stop codon, Humans, Missense mutation, human, exon, cytosine, Molecular Biology, Genetics (clinical), clinical article, article, Membrane Proteins, General Medicine, Polycystic Kidney, Autosomal Dominant, Stop codon, Pedigree, kidney polycystic disease, Mutagenesis, Insertional, female, priority journal, chromosome 4q, Protein Biosynthesis, glutamine, amino terminal sequence, Female, cyprus, Synonymous substitution
Abstract

Mutations in the PKD2 gene on the long arm of chromosome 4 are responsible for ~ 15% of cases of polycystic kidney disease. Perhaps the only difference from the more common ADPKD1 cases is the rate of progression of cystic changes, and the age of onset, which is 10-15 years later for the ADPKD2 form. In Cyprus there are at least three large families, documented by molecular linkage analysis, that map to the PKD2 locus. For two of them the defects were recently shown to be nonsense mutations at positions arginine 742 and glutamine 405. In this report, we describe the mutation in the third family, CY1602. For this, the entire coding sequence was systematically screened by single strand conformation analysis and heteroduplex formation. A novel mutation was identified in exon 2 where a new cytosine residue was inserted immediately after codon 231 (231insC). It causes a translation frameshift and is expected to lead to the introduction of 37 novel amino acids before the translation reaches a new STOP codon. It is the most amino terminal mutation reported to date, and based on the protein's modeled structure, is predicted to be within the first transmembrane domain. It is the fourth PKD2 mutation reported thus far, and the first which is not a nonsense mutation. 6 949 952 Cited By :22

Published
1997

10. Clinico-pathological correlations in 127 patients in 11 large pedigrees, segregating one of three heterozygous mutations in the COL4A3/ COL4A4 genes associated with familial haematuria and significant late progression to proteinuria and chronic kidney disease from focal segmental glomerulosclerosis

Author

Pierides, Alkis, primary, Voskarides, Konstantinos, additional, Athanasiou, Yiannis, additional, Ioannou, Kyriacos, additional, Damianou, Loukas, additional, Arsali, Maria, additional, Zavros, Michalis, additional, Pierides, Michael, additional, Vargemezis, Vasilios, additional, Patsias, Charalambos, additional, Zouvani, Ioanna, additional, Elia, Avraam, additional, Kyriacou, Kyriacos, additional, and Deltas, Constantinos, additional

Published
2009
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14. Genetic diseases and molecular genetics

Author

Legendre, C., primary, Cohen, D., additional, Delmas, Y., additional, Feldkamp, T., additional, Fouque, D., additional, Furman, R., additional, Gaber, O., additional, Greenbaum, L., additional, Goodship, T., additional, Haller, H., additional, Herthelius, M., additional, Hourmant, M., additional, Licht, C., additional, Moulin, B., additional, Sheerin, N., additional, Trivelli, A., additional, Bedrosian, C. L., additional, Loirat, C., additional, Legendre, C., additional, Babu, S., additional, Jungraithmayr, T., additional, Lebranchu, Y., additional, Riedl, M., additional, Gaber, A. O., additional, Bedrosian, C., additional, Muus, P., additional, Douglas, K., additional, Remuzzi, G., additional, Kourouklaris, A., additional, Ioannou, K., additional, Athanasiou, I., additional, Demetriou, K., additional, Panagidou, A., additional, Zavros, M., additional, Rodriguez C, N. Y., additional, Blasco, M., additional, Arcal, C., additional, Quintana, L. F., additional, Rodriguez de Cordoba, S., additional, Campistol, J. M., additional, Bachmann, N., additional, Eisenberger, T., additional, Decker, C., additional, Bolz, H. J., additional, Bergmann, C., additional, Pesce, F., additional, Cox, S. N., additional, Serino, G., additional, De Palma, G., additional, Sallustio, F. P., additional, Schena, F., additional, Falchi, M., additional, Pieri, M., additional, Stefanou, C., additional, Zaravinos, A., additional, Erguler, K., additional, Lapathitis, G., additional, Dweep, H., additional, Sticht, C., additional, Anastasiadou, N., additional, Zouvani, I., additional, Voskarides, K., additional, Gretz, N., additional, Deltas, C. C., additional, Ruiz, A., additional, Bonny, O., additional, Sallustio, F., additional, Curci, C., additional, Cox, S., additional, Kemter, E., additional, Sklenak, S., additional, Aigner, B., additional, Wanke, R., additional, Kitzler, T. M., additional, Moskowitz, J. L., additional, Piret, S. E., additional, Lhotta, K., additional, Tashman, A., additional, Velez, E., additional, Thakker, R. V., additional, Kotanko, P., additional, Leierer, J., additional, Rudnicki, M., additional, Perco, P., additional, Koppelstaetter, C., additional, Mayer, G., additional, Sa, M. J. N., additional, Alves, S., additional, Storey, H., additional, Flinter, F., additional, Willems, P. J., additional, Carvalho, F., additional, Oliveira, J., additional, Arsali, M., additional, Papazachariou, L., additional, Demosthenous, P., additional, Lazarou, A., additional, Hadjigavriel, M., additional, Stavrou, C., additional, Yioukkas, L., additional, Deltas, C., additional, Pierides, A., additional, Kkolou, M., additional, Toka, H. R., additional, Dibartolo, S., additional, Lanske, B., additional, Brown, E. M., additional, Pollak, M. R., additional, Familiari, A., additional, Zavan, B., additional, Sanna Cherchi, S., additional, Fabris, A., additional, Cristofaro, R., additional, Gambaro, G., additional, D'Angelo, A., additional, Anglani, F., additional, Toka, H., additional, Mount, D., additional, Pollak, M., additional, Curhan, G., additional, Sengoge, G., additional, Bajari, T., additional, Kupczok, A., additional, von Haeseler, A., additional, Schuster, M., additional, Pfaller, W., additional, Jennings, P., additional, Weltermann, A., additional, Blake, S., additional, Sunder-Plassmann, G., additional, Kerti, A., additional, Csohany, R., additional, Wagner, L., additional, Javorszky, E., additional, Maka, E., additional, Tulassay, T., additional, Tory, K., additional, Kingswood, J., additional, Nikolskaya, N., additional, Mbundi, J., additional, Jozwiak, S., additional, Belousova, E., additional, Frost, M., additional, Kuperman, R., additional, Bebin, M., additional, Korf, B., additional, Flamini, R., additional, Kohrman, M., additional, Sparagana, S., additional, Wu, J., additional, Brechenmacher, T., additional, Stein, K., additional, Bissler, J., additional, Franz, D., additional, Zonnenberg, B., additional, Cheung, W., additional, Wang, J., additional, Lam, D., additional, Budde, K., additional, Ivanitskiy, L., additional, Sowershaewa, E., additional, Krasnova, T., additional, Samokhodskaya, L., additional, Safarikova, M., additional, Jana, R., additional, Jitka, S., additional, Obeidova, L., additional, Kohoutova, M., additional, Tesar, V., additional, Evrengul, H., additional, Ertan, P., additional, Serdaroglu, E., additional, Yuksel, S., additional, Mir, S., additional, Yang n Ergon, E., additional, Berdeli, A., additional, Zawada, A., additional, Rogacev, K., additional, Rotter, B., additional, Winter, P., additional, Fliser, D., additional, Heine, G., additional, Bataille, S., additional, Moal, V., additional, Berland, Y., additional, Daniel, L., additional, Rosado, C., additional, Bueno, E., additional, Fraile, P., additional, Lucas, C., additional, Garcoa-Cosmes, P., additional, Tabernero, J. M., additional, Gonzalez, R., additional, Garcia-Cosmes, P., additional, Silska-Dittmar, M., additional, Zaorska, K., additional, Malke, A., additional, Musielak, A., additional, Ostalska-Nowicka, D., additional, Zachwieja, J., additional, K d r, V., additional, Uz, E., additional, Yigit, A., additional, Altuntas, A., additional, Yigit, B., additional, Inal, S., additional, Sezer, M., additional, Yilmaz, R., additional, Visciano, B., additional, Porto, C., additional, Acampora, E., additional, Russo, R., additional, Riccio, E., additional, Capuano, I., additional, Parenti, G., additional, Pisani, A., additional, Feriozzi, S., additional, Perrin, A., additional, West, M., additional, Nicholls, K., additional, Torras, J., additional, Cybulla, M., additional, Conti, M., additional, Angioi, A., additional, Floris, M., additional, Melis, P., additional, Asunis, A. M., additional, Piras, D., additional, Pani, A., additional, Warnock, D., additional, Guasch, A., additional, Thomas, C., additional, Wanner, C., additional, Campbell, R., additional, Vujkovac, B., additional, Okur, I., additional, Biberoglu, G., additional, Ezgu, F., additional, Tumer, L., additional, Hasanoglu, A., additional, Bicik, Z., additional, Akin, Y., additional, Mumcuoglu, M., additional, Ecder, T., additional, Paliouras, C., additional, Mattas, G., additional, Papagiannis, N., additional, Ntetskas, G., additional, Lamprianou, F., additional, Karvouniaris, N., additional, and Alivanis, P., additional

Published
2013
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15. Novel risk markers/factors for progression in CKD

Author

Pattaro, C., primary, Voskarides, K., additional, Stefanou, C., additional, Savige, J., additional, Benzing, T., additional, Gale, D. P., additional, Daphnis, E., additional, Zavros, M., additional, Pierides, A., additional, and Deltas, C., additional

Published
2013
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16. Novel risk markers/factors for progression in CKD

Author

Constantinos Deltas, Thomas Benzing, Konstantinos Voskarides, Judith Savige, Michalis Zavros, Alkis Pierides, Cristian Pattaro, Daniel P. Gale, Eugenios Daphnis, and Charalambos Stefanou

Subjects
Oncology, Transplantation, medicine.medical_specialty, Nephrology, business.industry, Internal medicine, medicine, business
Published
2013

17. Genetic diseases

Author

Inazu, T., primary, Kawahara, T., additional, Endou, H., additional, Anzai, N., additional, Sebesta, I., additional, Stiburkova, B., additional, Ichida, K., additional, Hosoyamada, M., additional, Testa, A., additional, Leonardis, D., additional, Catalano, F., additional, Pisano, A., additional, Mafrica, A., additional, Spoto, B., additional, Sanguedolce, M. C., additional, Parlongo, R. M., additional, Tripepi, G., additional, Postorino, M., additional, Enia, G., additional, Zoccali, C., additional, Mallamaci, F., additional, Working Group*, M., additional, Luque de Pablos, A., additional, Garcia-Nieto, V., additional, Lopez-Menchero, J. C., additional, Ramos-Trujillo, E., additional, Gonzalez-Acosta, H., additional, Claverie-Martin, F., additional, Arsali, M., additional, Demosthenous, P., additional, Papazachariou, L., additional, Athanasiou, Y., additional, Voskarides, K., additional, Deltas, C., additional, Pierides, A., additional, Lee, S., additional, Jeong, K. H., additional, Ihm, C., additional, Lee, T. W., additional, Lee, S. H., additional, Moon, J. Y., additional, Wi, J. G., additional, Lee, H. J., additional, Kim, E. Y., additional, Rogacev, K., additional, Friedrich, A., additional, Hummel, B., additional, Berg, J., additional, Zawada, A., additional, Fliser, D., additional, Geisel, J., additional, Heine, G. H., additional, Brabcova, I., additional, Dusilova-Sulkova, S., additional, Krejcik, Z., additional, Stranecky, V., additional, Lipar, K., additional, Marada, T., additional, Stepankova, J., additional, Viklicky, O., additional, Buraczynska, M., additional, Zukowski, P., additional, Zaluska, W., additional, Kuczmaszewska, A., additional, Ksiazek, A., additional, Gaggl, M., additional, Weidner, S., additional, Hofer, M., additional, Kleinert, J., additional, Fauler, G., additional, Wallner, M., additional, Kotanko, P., additional, Sunder-Plassmann, G., additional, Paschke, E., additional, Heguilen, R., additional, Albarracin, L., additional, Politei, J., additional, Liste, A. A., additional, Bernasconi, A., additional, Kusano, E., additional, Russo, R., additional, Pisani, A., additional, Messalli, G., additional, Imbriaco, M., additional, Prikhodina, L., additional, Ryzhkova, O., additional, Polyakov, V., additional, Lipkowska, K., additional, Ostalska-Nowicka, D., additional, Smiech, M., additional, Jaroniec, M., additional, Zaorska, K., additional, Szaflarski, W., additional, Nowicki, M., additional, Zachwieja, J., additional, D'arrigo, G., additional, Moskowitz, J., additional, Piret, S., additional, Tashman, A., additional, Velez, E., additional, Lhotta, K., additional, Thakker, R., additional, Cox, J., additional, Kingswood, J., additional, Mbundi, J., additional, Attard, G., additional, Patel, U., additional, Saggar, A., additional, Elmslie, F., additional, Doyle, T., additional, Jansen, A., additional, Jozwiak, S., additional, Belousova, E., additional, Frost, M., additional, Kuperman, R., additional, Bebin, M., additional, Korf, B., additional, Flamini, R., additional, Kohrman, M., additional, Sparagana, S., additional, Wu, J., additional, Ford, J., additional, Shah, G., additional, Franz, D., additional, Zonnenberg, B., additional, Cheung, W., additional, Urva, S., additional, Wang, J., additional, Kingswood, C., additional, Budde, K., additional, Kofman, T., additional, Narjoz, C., additional, Raimbourg, Q., additional, Roland, M., additional, Loriot, M.-A., additional, Karras, A., additional, Hill, G. S., additional, Jacquot, C., additional, Nochy, D., additional, Thervet, E., additional, Jagodzinski, P., additional, Mostowska, M., additional, Oko, A., additional, Nicolaou, N., additional, Kevelam, S., additional, Lilien, M., additional, Oosterveld, M., additional, Goldschmeding, R., additional, Van Eerde, A., additional, Pfundt, R., additional, Sonnenberg, A., additional, Ter Hal, P., additional, Knoers, N., additional, Renkema, K., additional, Storm, T., additional, Nielsen, R., additional, Christensen, E., additional, Frykholm, C., additional, Tranebjaerg, L., additional, Birn, H., additional, Verroust, P., additional, Neveus, T., additional, Sundelin, B., additional, Hertz, J. M., additional, Holmstrom, G., additional, Ericson, K., additional, Fabris, A., additional, Cremasco, D., additional, Zambon, A., additional, Muraro, E., additional, Alessi, M., additional, D'angelo, A., additional, Anglani, F., additional, Del Prete, D., additional, Alkmim Teixeira, A., additional, Quinto, B. M., additional, Jose Rodrigues, C., additional, Beltrame Ribeiro, A., additional, Batista, M., additional, Kerti, A., additional, Csohany, R., additional, Szabo, A., additional, Arkossy, O., additional, Sallai, P., additional, Moriniere, V., additional, Vega-Warner, V., additional, Lakatos, O., additional, Szabo, T., additional, Reusz, G., additional, Tory, K., additional, Addis, M., additional, Tosetto, E., additional, Meloni, C., additional, Ceol, M., additional, Cristofaro, R., additional, Melis, M. A., additional, Vercelloni, P., additional, Marra, G., additional, Kaniuka, S., additional, Nagel, M., additional, Wolyniec, W., additional, Obolonczyk, L., additional, Swiatkowska-Stodulska, R., additional, Sworczak, K., additional, Rutkowski, B., additional, Chen, C., additional, Jiang, L., additional, Chen, L., additional, Fang, L., additional, Mozes M., M., additional, Boosi, M., additional, Rosivall, L., additional, Kokeny, G., additional, Diana, R., additional, Gross, O., additional, Johanna, T., additional, Rainer, G., additional, Ayse, C., additional, Henrik, H., additional, Gerhard-Anton, M., additional, Nabil, M., additional, Intissar, E., additional, Belge, H., additional, Bloch, J., additional, Dahan, K., additional, Pirson, Y., additional, Vanhille, P., additional, and Demoulin, N., additional

Published
2012
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19. Genetic diseases / Molecular mechanisms

Author

Wanner, C., primary, Germain, D. P., additional, Linthorst, G., additional, Marodi, L., additional, Mauer, M., additional, Mignani, R., additional, Oliveira, J., additional, Ortiz, A., additional, Serra, A. L., additional, Svarstad, E., additional, Vujkovac, B., additional, Waldek, S., additional, Warnock, D. G., additional, West, M., additional, Schiffmann, R., additional, Mehta, A., additional, Amato, D., additional, Nair, N., additional, Zahrieh, D., additional, Huertas, P., additional, Bonatti, F., additional, Maritati, F., additional, Alberici, F., additional, Oliva, E., additional, Sinico, R. A., additional, Moroni, G., additional, Leoni, A., additional, Gregorini, G., additional, Jeannin, G., additional, Possenti, S., additional, Tumiati, B., additional, Grasselli, C., additional, Brugnano, R., additional, Salvarani, C., additional, Fraticelli, P., additional, Pavone, L., additional, Pesci, A., additional, Guida, G., additional, Neri, T. M., additional, Buzio, C., additional, Malerba, G., additional, Martorana, D., additional, Vaglio, A., additional, Oda, A., additional, Kitamura, K., additional, Mizumoto, T., additional, Eguchi, K., additional, Anzai, N., additional, Tomita, K., additional, Arsali, M., additional, Athanasiou, Y., additional, Demosthenous, P., additional, Voskarides, K., additional, Deltas, C., additional, and Pierides, A., additional

Published
2011
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20. Genetic diseases / Molecular mechanisms

Author

Constantinos Deltas, Maria Arsali, Stephen Waldek, Pedro Huertas, Carlo Salvarani, Stefano Possenti, Laura Pavone, David Amato, Akira Oda, Antonio Leoni, Gina Gregorini, Atul Mehta, Rachele Brugnano, Kenichiro Kitamura, Christoph Wanner, Michael Mauer, Elena Oliva, Konstantinos Voskarides, Paolo Fraticelli, Kimio Tomita, Francesco Bonatti, Naohiko Anzai, Andreas L. Serra, Bojan Vujkovac, João Paulo Oliveira, Renato Alberto Sinico, Bruno Tumiati, Einar Svarstad, David G. Warnock, Nitin Nair, Augusto Vaglio, Dominique P. Germain, Michael West, Federica Maritati, Federico Alberici, Alberto Ortiz, Raphael Schiffmann, Teruhiko Mizumoto, Renzo Mignani, Davide Martorana, Carlo Buzio, Guido Jeannin, Koji Eguchi, Chiara Grasselli, Alberto Pesci, Alkis Pierides, Giovanni Malerba, Yiannis Athanasiou, David Zahrieh, Gabor E. Linthorst, László Maródi, Giuseppe Guida, Gabriella Moroni, Panayiota Demosthenous, and Tauro M. Neri

Subjects
Transplantation, Nephrology, business.industry, Medicine, Computational biology, business
Published
2011

23. Idiopathic Membranous Nephropathy

Author

David N.S. Kerr, Robert W. Wilkinson, P. Malasit, A. R. Morley, P. R. Uldall, and A. M. Pierides

Subjects
medicine.medical_specialty, Proteinuria, medicine.diagnostic_test, business.industry, medicine.medical_treatment, Spontaneous remission, Azathioprine, General Medicine, medicine.disease, Gastroenterology, Endocrinology, Prednisone, Internal medicine, Biopsy, medicine, Hemodialysis, medicine.symptom, business, Nephrotic syndrome, Dialysis, medicine.drug
Abstract

The clinical and histopathological features of 37 patients with idiopathic membranous nephropathy are presented. Males were four times as commonly affected as females and the age at presentation ranged from nine to 70 years. The period of observation varied from three months to 23 years. Twenty-eight patients (76 percent) presented with the nephrotic syndrome and nine patients (24 per cent) presented with non-nephrotic proteinuria. At the end of the study, of the patients presenting with the nephrotic syndrome, seven (25 per cent) were in remission, seven (25 per cent) remained nephrotic, nine (32 per cent) showed only proteinuria and five (18 per cent) were dead or on dialysis. Altogether eight patients (28 per cent) developed renal failure. The nine patients who presented with non-nephrotic proteinuria appeared to do better, and none developed renal failure. The occurrence of spontaneous remission makes assessment of benefit from immunosuppressivet herapy difficult. However, analysis of our data and a review of the literature suggest that in this condition oral prednisone, cyclophosphamide and azathioprine have no significant therapeutic properties. Histological assessment confirmed the occurrence of mild (Grade 1) changes in patients biopsied soon after presentation, and tubular atrophy increased with the duration of illness. Immunofluorescence confirmed deposition of mainly IgG and complement. Repeat biopsies in 14 patients showed no histological improvement and remission was not accompanied by resolution of histological abnormalities.

Published
1977

24. Avascular Necrosis of Bone Following Renal Transplantation

Author

W Simpson, P R Uldall, D Stainsby, A. M. Pierides, and Alvarez-ude F

Subjects
Kidney, medicine.medical_specialty, business.industry, Urinary system, Avascular necrosis, General Medicine, medicine.disease, Osteochondritis dissecans, Surgery, Transplantation, medicine.anatomical_structure, Prednisone, medicine, Complication, business, Kidney transplantation, medicine.drug
Abstract

Assessment of 78 successful renal transplants carried out in Newcastle upon Tyne between October 1967 and March 1973, revealed avascular necrosis of bone (A.N.) in 11 patients (14 percent). Pain and restriction of movement were the cardinal symptoms, while the onset was from five to 35 months after transplantation. In some patients one joint only was affected but in seven patients (64 per cent) A.N. developed in other joints too in an additive and progressive fashion. A time lag was usually noted between the onset of symptoms and radiological proof. These 11 patients with A.N. were compared with two control groups of unaffected renal transplant patients. Taking into account the patients' body weight, the cumulative dose of prednisone received by affected patients during the first three post-transplant months was found to be significantly higher than that for both control groups (P less than 0.05). Patients with A.N. were found to have had an unusually high incidence of early post-transplant surgical complications and the length of their initial stay in hospital was significantly prolonged (P less than 0.02) when compared to both control groups. It is possible that excessive corticosteroid therapy is more deleterious in transplant patients weakened by peri-renal haematomas, urinary extravasations and stormy prolonged post-operative periods. Having emphasized the detrimental effects of excessive anti-rejection corticosteroid therapy it must be mentioned that occasionally patients develop avascular necrosis even after low doses of steroid therapy, while others, receiving high doses of steroid therapy and undergoing a stormy post-operative course, do not develop this complaint. It is suggested that although excessive steroid therapy is positively harmful, avascular necrosis is not an invariable complication and that ofther factors including possibly a genetic predisposition operate to produce avascular necrosis of bone in renal transplant patients.

Published
1975

25. Central Pontine Myelinolysis<subtitle>TWO CASES WITH ASSOCIATED ELECTROLYTE DISTURBANCE</subtitle>

Author

A. M. Pierides, W. G. Bradley, and B. E. Tomlinson

Subjects
Pathology, medicine.medical_specialty, business.industry, General Medicine, Histopathological examination, Electrolyte disturbance, medicine.disease, Malignancy, Pons, Pathophysiology, Anesthesia, medicine, Neurological syndrome, Vomiting, Central pontine myelinolysis, medicine.symptom, business
Abstract

Two patients with central pontine myelinolysis are described. Both were middle aged women presenting with a history of protracted vomiting and drowsiness. Hyponatraemia (serum sodium 96 to 100 mmol/L) was a feature in both patients. No underlying malignancy, alcoholism, malnutrition or other serious disease was identified. Correction of electrolyte abnormalities was accompanied by deterioration in level of consciousness and development of a neurological syndrome characterized by quadriparesis, dysphasia and mutism. Death followed and histopathological examination confirmed classical myelinolysis in the central pons and extensive similar, though not identical, lesions in the cerebral hemispheres in both cases. The pathophysiological basis of the lesions is likely to be a special metabolic susceptibility of oligodendroglial cells in areas where neurones, glial cells and myelin sheaths lie in close proximity to one another.

Published
1976

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