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János Hunyadi

Publications and source records attributed to János Hunyadi.

16 recordsLinked to original sources
PubMed2006

[Questions of dermatoinfectology in the practice].

The importance of bacterial, viral and fungal diseases has significantly increased during the past decades. The reasons are numerous, but the most important ones are as follows: appearance of new variance of microbes, appearance and spread of antibiotic resistant bacterial strains, and increasing number of patients with various degree of immunodeficiency. For such reasons we consider extremely important to overview and upgrade our current knowledge and practice regarding to these diseases. This manuscript will discuss the hottest practical questions of dermato-infectology.

Antifungal Agents↗
PubMed2006

Role of acellular dermal matrix allograft in minimal invasive coverage of deep burn wound with bone exposed--case report and histological evaluation.

A sandwich graft was applied to the debrided cortical bone layer of the tibia in the case of a 72-year-old male patient with full-thickness necrotic burn injury. The combined graft consisted of a dermal template material and autologous split thickness skin graft. After application, the graft was found totally accepted and provided good functionality with acceptable appearance. Histopathologic evaluation revealed a complete take with revascularisation of the implant. Supporting lamellar bony trabecules were also seen in the deep dermal dermis representing a connection to the underlying bone. The use of the dermal matrix in deep burn exposing the bone provides a satisfactory functional result and good cosmetic appearance.

Aged↗
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

Prevalence of human herpesvirus-8 infection in HIV-positive patients with and without Kaposi's sarcoma in Hungary.

Human herpesvirus-8 (HHV-8) infection of 130 Hungarian HIV-positive individuals with or without Kaposi's sarcoma was investigated from 158 serum and 122 peripheral blood samples using anti-latency-associated nuclear antigen (LANA) indirect immunofluorescence assay (IFA), recombinant orf65 and orfK8.1 antigen enzyme-linked immunosorbent assays (ELISAs), Western blot assays and orf26 specific nested polymerase chain reaction (PCR). The overall prevalence of HHV-8 infection was found to be 31.5% (41/130) among the Hungarian HIV-positive patients. This seroprevalence rate is 7-11-fold higher than that of healthy HIV-negative blood donors in Hungary. The highest prevalence of HHV-8 infection (36.1%, 35/97) was observed in homo- or bisexual patients. Similar to the serologic results, HHV-8 DNA was not always detectable in all serial samples previously shown to be positive for HHV-8 DNA.

Adolescent↗
PubMed2005

CD44, but not l-selectin, is critically involved in leucocyte migration into the skin in a murine model of allergic dermatitis.

CD44 and l-selectin (CD62L) are major adhesion receptors that mediate leucocyte recruitment at inflammatory sites and lymph nodes, by supporting cell rolling under blood flow. Both CD44 and CD62L have been implicated in inflammatory skin disorders, but their specific involvement in an immediate-type allergic reaction remains uncertain. We used mice deficient in CD44 or CED62L or both in order to determine whether one or both of these molecules were required for leucocyte extravasation in an atopic dermatitis-like allergic response. Wild-type (WT) mice and mice deficient in CD44, CD62L or both were immunized with ovalbumin (OVA). Inflammatory reaction in the ear was elicited once by means of intradermal injection of OVA. Effective sensitization of CD62L knockout (KO) mice required intraperitoneal antigen injection; however, OVA-specific T helper 2 (Th2)-type immune responses and IgE production in mice lacking CD44, CD62L or both were comparable to those in WT mice following intraperitoneal immunization. We employed intravital videomicroscopy to monitor the recruitment of fluorescence-labelled leucocytes to the ear tissue following challenge with OVA. The number of adherent leucocytes was significantly reduced in CD44 KO and CD44/CD62L double KO mice, indicating that CD44 was involved in firm adhesion, the committed step of leucocyte extravasation. Histology of the OVA-challenged ears showed a diminished leucocyte infiltration in the ears of CD44 KO and double KO mice. The results of our study demonstrate that CD44, but not CD62L, is required for leucocyte extravasation during a Th2-type inflammatory response.

Animals↗
PubMed2004

Immunohistochemical examination of P-cadherin in bullous and acantholytic skin diseases.

Autoimmune blistering diseases (pemphigus vulgaris, pemphigus foliaceus, bullous pemphigoid, dermatitis herpetiformis) and certain genodermatoses with acantholysis (Darier-disease, Hailey-Hailey disease) have different aetiological factors, but all result in bulla formation and/or in acantholysis. Cadherins are Ca++-dependent cell-cell adhesion molecules which play an important role in the cellular connection between normal cells. P-cadherin is involved in the selective adhesion of epidermal cells, and is expressed only on the surfaces of the two basal layers. We examined the expression of P-cadherin in some autoimmune bullous skin diseases and Darier's disease using immunohistochemistry and found P-cadherin to be strongly upregulated. We believe the upregulation is compensatory to the primary pathophysiological events in the various bullous dermatoses.

Acantholysis↗
PubMed2004

Relationship between skin bacterial colonization and the occurrence of allergen-specific and non-allergen-specific antibodies in sera of children with atopic eczema/dermatitis syndrome.

In this study we investigated skin bacterial colonization, allergen-specific IgE and antiphospholipid/antinuclear antibodies in 72 children with atopic eczema/dermatitis syndrome (age 2-17 years). Bacteria were found on the skin in 41 cases and serological allergen-specific IgE positivity in 37. The different forms of antibodies appeared in the ratio 21/72 (33 antibodies in 21 children). The occurrence of antiphospholipid antibodies was significantly higher in the patients than in the controls. There were significantly more allergens in the group with bacterial colonization than in the group without colonization. The SCORAD index showed a significant positive association with the skin colonization. We conclude that there are significant relationships between the occurrence of Staphylococcus aureus colonization and the levels of inhalant allergen-specific IgE in children with atopic eczema/dermatitis syndrome, and between the occurrence of antiphospholipid IgM positivity and atopic eczema/dermatitis syndrome.

Adolescent↗
PubMed2003

Tumor cells expressing membrane-bound tumor necrosis factor activate macrophages and have a compromised growth in immunosuppressed and immunodeficient mice.

Tumor necrosis factor (TNF)-alpha producing tumors as vaccines were demonstrated to induce a therapeutic anti-tumor immune response, but their clinical use is limited by the toxicity of soluble TNF. We investigated the growth characteristics and immunomodulatory properties of HeLa cells producing an uncleavable transmembrane form of TNF (preTNF). The growth of the transformed tumors was compromised in both immunosuppressed and severe combined immunodeficient mice; no signs of TNF toxicity were detected. Macrophages co-cultured with the transformed cells showed increased phagocytosis and cytokine production, indicating that activated macrophages may be the mediators of the anti-tumor effect. preTNF producing tumor cells are promising safe anti-tumor vaccine candidates.

Animals↗
PubMed2003

Elevated rate of Thelper1 (T(H)1) lymphocytes and serum IFN-gamma levels in psoriatic patients.

Several disorders are known to be associated with altered Thelper1/Thelper2 (T(H)1/T(H)2) cytokine balance. Psoriasis is characterized by increased systemic and local production of T(H)1 and pro-inflammatory cytokines. Furthermore recent data indicate the dominant presence of T(H)1 lymphocytes in the circulation and T(H)1 and Tcytotoxic1 (T(C)1) cells in lesional skin of psoriatic patients. In order to assess the systemic T(H)1/T(H)2 imbalance in psoriasis most of the studies so far tested isolated peripheral mononuclear cells. As a new approach we applied a whole blood flow cytometric assay to determine the rate of circulating T(H)1/T(H)2 and T(C)1/Tcytotoxic2 (T(C)2) lymphocytes based on their intracellular IFN-gamma, IL-4 and IL-10 expression. Besides, serum levels of these cytokines were determined in healthy controls and psoriatic patients by commercial ELISAs. In psoriatic patients we found significantly (P<0.02) increased rates of CD4(+)/IFN-gamma(+) lymphocytes (30.3+/-8.8%) while the percent of CD4(+)/IL-4(+) cells (0.37+/-0.31%) were significantly (P<0.03) lower compared to healthy controls (CD4(+)/IFN-gamma(+): 20.1+/-7.3% and CD4(+)/IL-4(+): 0.78+/-0.44%). The IL-10-positive CD4(+) and CD8(+) cells also had higher rate in psoriasis, but the difference between patients and controls was not significant, similarly to the rate of CD8(+)/IFN-gamma(+) and CD8(+)/IL-4(+) lymphocytes. Beside cellular expression, serum IFN-gamma levels were also significantly higher (control: 4.9+/-6.4 pg/ml; psoriatic patients: 35.9+/-47.0 pg/ml; P<0.05). Our results provide further evidence for an altered T(H)1/T(H)2 balance in psoriasis measured in non-separated whole blood T cells.

Adult↗
PubMed2003

Role of intracellular calcium mobilization and cell-density-dependent signaling in oxidative-stress-induced cytotoxicity in HaCaT keratinocytes.

Peroxynitrite is a nitric-oxide-derived cytotoxic mediator produced in a broad range of inflammatory conditions, ranging from sunburn erythema to contact hypersensitivity. Our previous work has shown that in HaCaT cells the cytotoxic activity of peroxynitrite involves both apoptotic and necrotic routes with poly(ADP-ribose) polymerase activation serving as a mol-ecular switch diverting the default apoptotic pathway toward necrosis. Nonetheless, keratinocytes are regarded as highly resistant toward environmental noxa including oxidative stress. We set out to investigate the possible role of two parameters, intracellular calcium mobilization and high cell density, in protecting HaCaT cells from peroxynitrite/oxidative-stress-induced cytotoxicity. First we characterized the effect of peroxynitrite on the calcium homeostasis of HaCaT cells and demonstrated that both authentic peroxynitrite and the peroxynitrite generating compound 3-morpholino-sydnonimine triggered an elevation in intracellular calcium levels. Moreover, we established that treatment of cells with the cell-permeable calcium chelator BAPTA-AM provided significant cytoprotection against peroxynitrite- and hydrogen-peroxide-induced cytotoxicity. Furthermore, when cells reached confluence they were highly resistant to the toxic effects of peroxynitrite, hydrogen peroxide, and superoxide. The resistance to oxidative stress provided by calcium chelation and high cell density involved inhibiting the activation of both poly(ADP-ribose) polymerase and caspases. Our data may provide an explanation for the resistance to oxidative stress of superficial, highly differentiated keratinocytes and indicate that basal proliferative keratinocytes are sensitive in vivo targets of oxidative stress injury.

Buffers↗
PubMed2002

[The role of PET scan in the diagnosis of malignant melanoma].

Comprehensive, accurate staging has a critical role in planning rational treatment strategies for patients with malignant melanoma (MM). In the present study the authors investigate the value of FDG PET in staging and restaging based on the investigation of 37 high-risk MM patients and compare the results with the one obtained by conventional imaging techniques (X-ray, US, CT, MR and bone scan). Thirty-nine whole body PET scans were carried out. The authors concluded that FDG PET had the highest sensitivity among the imaging methods in detecting distant metastases of MM.

Adult↗
PubMed2002

Nitric oxide-peroxynitrite-poly(ADP-ribose) polymerase pathway in the skin.

In the last decade it has become well established that in the skin, nitric oxide (NO), a diffusable gas, mediates various physiologic functions ranging from the regulation of cutaneous blood flow to melanogenesis. If produced in excess, NO combines with superoxide anion to form peroxynitrite (ONOO-), a cytotoxic oxidant that has been made responsible for tissue injury during shock, inflammation and ischemia-reperfusion. The opposite effects of NO and ONOO- on various cellular processes may explain the 'double-edged sword' nature of NO depending on whether or not cellular conditions favour peroxynitrite formation. Peroxynitrite has been shown to activate the nuclear nick sensor enzyme, poly(ADP-ribose) polymerase (PARP). Overactivation of PARP depletes the cellular stores of NAD+, the substrate of PARP, and the ensuing 'cellular energetic catastrophy' results in necrotic cell death. Whereas the role of NO in numerous skin diseases including wound healing, burn injury, psoriasis, irritant and allergic contact dermatitis, ultraviolet (UV) light-induced sunburn erythema and the control of skin infections has been extensively documented, the intracutaneous role of peroxynitrite and PARP has not been fully explored. We have recently demonstrated peroxynitrite production, DNA breakage and PARP activation in a murine model of contact hypersensitivity, and propose that the peroxynitrite-PARP route represents a common pathway in the pathomechanism of inflammatory skin diseases. Here we briefly review the role of NO in skin pathology and focus on the possible roles played by peroxynitrite and PARP in various skin diseases.

Animals↗
PubMed2002

Detection of poly(ADP-ribose) polymerase activation in oxidatively stressed cells and tissues using biotinylated NAD substrate.

Poly(ADP-ribose) polymerase (PARP) is a nuclear enzyme activated by DNA damage. Activated PARP cleaves NAD(+) into nicotinamide and (ADP-ribose) and polymerizes the latter on nuclear acceptor proteins. Over-activation of PARP by reactive oxygen and nitrogen intermediates represents a pathogenetic factor in various forms of inflammation, shock, and reperfusion injury. Using a novel commercially available substrate, 6-biotin-17-nicotinamide-adenine-dinucleotide (bio-NAD(+)), we have developed three applications, enzyme cytochemistry, enzyme histochemistry, and cell ELISA, to detect the activation of PARP in oxidatively stressed cells and tissues. With the novel assay we were able to detect basal and hydrogen peroxide-induced PARP activity in J774 macrophages. We also observed that mitotic cells display remarkably elevated PARP activity. Hydrogen peroxide-induced PARP activation could also be detected in wild-type peritoneal macrophages but not in macrophages from PARP-deficient mice. Application of hydrogen peroxide to the skin of mice also induced bio-NAD(+) incorporation in the keratinocyte nuclei. Hydrogen peroxide-induced PARP activation and its inhibition by pharmacological PARP inhibitors could be detected in J774 cells with the ELISA assay that showed good correlation with the traditional [(3)H]-NAD incorporation method. The bio-NAD(+) assays represent sensitive, specific, and non-radioactive alternatives for detection of PARP activation.

Animals↗