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Eva Remenyik

Publications and source records attributed to Eva Remenyik.

8 recordsLinked to original sources
PubMed2006

[The role of free radicals in the UV-induced skin damage. Photo-aging].

The natural (intrinsic) ageing of the skin is enhanced by environmental factors (extrinsic ageing). One of the most important exogenous factors is the solar UV exposure, which results in photo-aging. Besides this, epidemiological and experimental data show a rapid increase in the incidence of human skin cancers, which is also in relation to the increased sunlight exposure of the skin. In the background of these processes there are cell biological effects, photochemical reactions, membrane receptor changes, lipid- and protein modifications, DNA-damage induced by UV. The qualities and quantities of them are wavelength dependent. The UVB photons are absorbed mostly by the DNA of the epidermal keratinocytes, therefore this spectrum is more relevant for photocarcinogenesis. The effect of UVA-irradiation is mainly manifested in the induction of free radicals, which have not only DNA-damaging, but also immunomodulating effect, which also can influence on tumour development. Furthermore, the free radicals cause dermal connective tissue damage as well via activating transcription factors, inducing matrix metalloproteinases, diminishing the procollagen I and fibrillin-1 synthesis. These processes are augmented by mitochondrial DNA mutations, protein oxidation, apoptosis induction. Therefore the enzymes neutralising free radicals and antioxidant molecules, respectively, have an important role in the defence mechanisms. In the therapy of photo-aging the local retinoids lived up to expectations, but the clinical effectiveness of antioxidant vitamins is lower than expected. The most important factor in the prevention of the photo-aging and photocarcinogenesis is the sun protection at present.

Antioxidants↗
PubMed2005

[Kaposi's sarcoma].

In recent years large amounts of findings have accumulated about Kaposi's sarcoma, a virus induced angioproliferative disorder appearing in four clinical forms: classical, epidemic, endemic and iatrogenic, as it has been in focus of not only from the dermatologic but also from the viral tumorgenesis perspective. The common characteristics are the histopathological appearance, the causative role of the human herpesvirus 8 and the similar clinical picture (bluish-red macules, papules, and nodes). Frequency of the distinguished clinical forms differs with geographical location. Viruses, genetic -, and environmental factors have been shown to play a role in the pathomechanism of the disease, of which the most important is the human herpesvirus-8. The mechanisms by which viral proteins and virus infection enhance tumorgenesis and alter immune functions directed at cells have been studied in detail. During the initiation of tumorgenesis, virus induced viral and host cell products (cytokines, receptors and oncogens) initiate inflammatory and angiogenic polyclonal cell proliferation, which later, by the synergistic action of other viruses and/or environmental factors, give rise to malignant proliferation and allow the selected cell to clonally expand and behave like a true malignant tumor. In light of newly published results the authors not only present the clinical appearances and summarize diagnostic possibilities and the pathomechanism of the disease, but also give a thorough overview of the therapeutic tools of Kaposi's sarcoma, and share their experiences obtained during the follow-up of classical Kaposi's sarcoma patients.

AIDS-Related Opportunistic Infections↗
PubMed2005

Identification of a novel deletion in the ABCC6 gene leading to Pseudoxanthoma elasticum.

BACKGROUND: Pseudoxanthoma elasticum (PXE) is an inherited systemic disorder, characterized by dermal, ocular and cardiovascular lesions. Genetic defects of the ABCC6 (MRP6) transporter are known to cause PXE. OBJECTIVES: The purpose of this study was to identify the genetic background of a PXE patient with a very early onset of the disease and severe systemic involvement. METHODS: Direct sequencing of genomic DNA obtained from peripheral whole blood. RESULTS: Our patient was found to be compound heterozygous with both ABCC6 alleles having genomic deletions. A novel exon 24-25 deletion was identified on one allele, while the frequently observed exon 23-29 deletion was found on the other allele. The novel deletion is 4.68 kb long and was shown to extend from intron 23 to 25. DNA-sequencing of a 2.03 kb fusion fragment revealed the deletion breakpoints within introns 23 and 25 originating in the middle of two Alu-repeats. CONCLUSION: In a patient with severe clinical symptoms, we found two genomic deletions in regions that might be important for function of the ABCC6 transporter. Genomic deletions in ABCC6 may occur more frequently in PXE patients than previously expected and future genetic analysis should focus on these mutations as well.

Adult↗
PubMed2004

Atorvastatin effect on high-density lipoprotein-associated paraoxonase activity and oxidative DNA damage.

OBJECTIVE: High-density lipoprotein (HDL)-associated antioxidant paraoxonase (PON) may reduce low-density lipoprotein (LDL) oxidation and prevent atherosclerosis. The aim of this present study was to investigate the effect of the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor atorvastatin on hydrogen-peroxide-induced DNA damage by comet assay and the correlation between oxidative DNA damage and antioxidant PON activity. METHODS: Thirteen type-II/a hyperlipidemic patients were enrolled in the study. We examined the effect of 10 mg/day atorvastatin treatment on lipid levels and the degree of DNA damage in lymphocytes separated from hyperlipidemic patients, nitric oxide (NO), thiobarbituric acid-reactive substances (TBARS), PON levels and activity. RESULTS: After 6 months, atorvastatin treatment significantly decreased serum cholesterol and LDL-cholesterol levels. The triglyceride level did not change, and there was no significant change in the HDL cholesterol level. The visual score characteristic to the degree of DNA damage in comet assay was significantly decreased, as well as the TBARS level, while the level of NO was non-significantly increased. PON activity and the PON/HDL ratio were significantly increased after atorvastatin treatment. There was a negative correlation between DNA damage and PON activity, as well as between DNA damage and the PON/HDL ratio before and after atorvastatin treatment. CONCLUSION: These findings show that atorvastatin treatment favorably affected the lipid profile, increasing the activity of HDL-associated PON and decreasing the cytotoxic effect of oxidative stress.

Adult↗
PubMed2003

Antigen-specific immunity does not mediate acute regression of UVB-induced p53-mutant clones.

Chronic irradiation of human or murine epidermis with ultraviolet B (UVB) induces clones of p53-mutant keratinocytes. Clones precede and parallel the induction of carcinomas, suggesting that they are an early stage of UVB carcinogenesis. In the absence of UVB, these clones rapidly regress. For UVB-induced murine skin tumors and papillomas, regression is known to involve antigen-specific immunity. To determine whether antigen-specific immunity influences the creation, expansion, or regression of p53-mutant clones, we studied Rag1 knockout mice deficient in the recombination activating gene 1 required for development of B, alphabetaT, gammadeltaT, and natural killer T cells. Since tissue homeostasis could affect proliferation or persistence of clones, we also examined the effect of Rag1 on UVB-induced hyperplasia and apoptosis. Mice were irradiated with UVB daily for 7-11 weeks to create p53-mutant clones, and then retained in the absence of UV. After UV ended, epidermal thickness decreased and p53-mutant clones observed in the epidermal sheets regressed, with no significant differences between Rag1(-/-) and wild type. During the initial chronic UVB irradiation, increasing irradiation time increased both the number and size of p53-mutant clones, with no significant difference between genotypes. We conclude that antigen-specific immunity is not involved in the initiation, expansion, or acute regression of p53-mutant clones.

Animals↗
PubMed2003

Inactivating E2f1 reverts apoptosis resistance and cancer sensitivity in Trp53-deficient mice.

The E2f1 transcription factor, which regulates genes required for S-phase entry, also induces apoptosis by transcriptional and post-translational mechanisms. As E2f1 is inducible by DNA damage we investigated its importance in vivo in ultraviolet (UV)-induced apoptosis, a protective mechanism that prevents the epidermis from accumulating UV-induced mutations. Contrary to expectation, E2f1-/- mice demonstrated enhanced keratinocyte apoptosis after UVB exposure, whereas apoptosis was suppressed by epidermis-specific overexpression of human E2F1. Apoptosis induced by -radiation was also repressed by E2f1. E2f1-/-;Trp53-/- double knockout mice exhibited the elevated UVB-induced apoptosis of E2f1-/- alone, rather than the profound apoptosis defect seen in Trp53-/- mice, indicating that Trp53 (p53) lies functionally upstream of E2f1. Transfecting E2F1 into E2f1-/-;Trp53-/- primary fibroblasts suppressed UVB-induced apoptosis and this suppression was relieved by Trp53. The double knockout also reverted the abnormal sex ratio and early-onset tumours of Trp53-/- mice. These results imply that E2f1 functions as a suppressor of an apoptosis pathway that is initiated by DNA photoproducts and perhaps genetic abnormalities; p53 relieves this suppression.

Animals↗
PubMed2003

Successful treatment of B cell chronic lymphocytic leukemia-associated severe paraneoplastic pemphigus with cyclosporin A.

Since the first description of paraneoplastic pemphigus, several cases have been described in the literature. However, curative therapy is usually a challenge to the physicians treating this disease. Several publications are available discussing the efficacy of steroids, cyclophosphamide and cyclosporin A. Recently, a report of the successful use of rituximab was also published. However, the use of cyclosporin A is controversial in the case of B cell malignancies, as there are reports showing the cytotoxic effect of this drug on B cells. However, other authors report no effect, or even unwanted effects resulting in B cell proliferation. We report the case of a 50-year-old Caucasian male. He developed a B cell lymphoma consisting of CD5/CD20-double-positive cells, and 2 months later, it was followed by a very severe paraneoplastic pemphigus affecting the mucosa and the skin. The lymphoma was well managed with CHOP and CVP polychemotherapy, followed by oral chlorambucil; however, the bullous eruptions did not disappear. Oral steroids, cyclophosphamide, plasmapheresis and IVIG therapy were only partially successful, so we decided to use oral cyclosporin A. Starting with 7 mg/kg and maintaining a steady plasma level of no less then 110 ng/l, the bullae completely disappeared within 6 weeks, and the patient has been in remission for 17 months now, taking the oral cyclosporin A continuously. The underlying B cell disorder did not relapse during the therapy.

Antineoplastic Combined Chemotherapy Protocols↗