CCL

Összesen 9 találat.
#/oldal:
Részletezés:
Rendezés:

1.

001-es BibID:BIBFORM014374
Első szerző:Bodó Enikő
Cím:A Hot New Twist to Hair Biology : involvement of Vanilloid Receptor-1 (VR1/TRPV1) Signaling in Human Hair Growth Control / Enikő Bodó, Tamás Bíró, Andrea Telek, Gabriella Czifra, Zoltán Griger, Balázs I. Tóth, Alessandra Mescalchin, Taisuke Ito, Albrecht Bettermann, László Kovács, Ralf Paus
Dátum:2005
ISSN:0002-9440
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:American Journal of Pathology 166 : 4 (2005), p. 985-998. -
További szerzők:Bíró Tamás (1968-) (élettanász) Telek Andrea (1977-) (élettanász) Czifra Gabriella (1975-) (élettanász) Griger Zoltán (1979-) (belgyógyász, allergológus és klinikai immunológus, reumatológus) Tóth István Balázs (1978-) (élettanász) Mescalchin, Alessandra Ito, Taisuke Bettermann, Albrecht Kovács László (1939-) (élettanász) Paus, Ralf
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

2.

001-es BibID:BIBFORM001012
Első szerző:Bodó Enikő
Cím:Dissecting the impact of chemotherapy on the human hair follicle : a pragmatic in vitro assay for studying the pathogenesis and potential management of hair follicle dystrophy / Bodó E., Tobin D. J., Kamenisch Y., Bíró T., Berneburg M., Funk W., Paus R.
Dátum:2007
ISSN:0002-9440 (Print)
Megjegyzések:Chemotherapy-induced alopecia represents one of the major unresolved problems of clinical oncology. The underlying molecular pathogenesis in humans is virtually unknown because of the lack of adequate research models. Therefore, we have explored whether microdissected, organ-cultured, human scalp hair follicles (HFs) in anagen VI can be exploited for dissecting and manipulating the impact of chemotherapy on human HFs. Here, we show that these organ-cultured HFs respond to a key cyclophosphamide metabolite, 4-hydroperoxycyclophosphamide (4-HC), in a manner that resembles chemotherapy-induced HF dystrophy as it occurs in vivo: namely, 4-HC induced melanin clumping and melanin incontinence, down-regulated keratinocyte proliferation, massively up-regulated apoptosis of hair matrix keratinocytes, prematurely induced catagen, and up-regulated p53. In addition, 4-HC induced DNA oxidation and the mitochondrial DNA common deletion. The organ culture system facilitated the identification of new molecular targets for chemotherapy-induced HF damage by microarray technology (eg, interleukin-8, fibroblast growth factor-18, and glypican 6). It was also used to explore candidate chemotherapy protectants, for which we used the cytoprotective cytokine keratinocyte growth factor as exemplary pilot agent. Thus, this novel system serves as a powerful yet pragmatic tool for dissecting and manipulating the impact of chemotherapy on the human HF.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:The American Journal of Pathology. - 171 : 4 (2007), p. 1153-1167. -
További szerzők:Tobin, Desmund J. Kamenisch, York Berneburg, Mark Funk, Wolfgang Paus, Ralf Bíró Tamás (1968-) (élettanász)
Internet cím:elektronikus változat
elektronikus változat
DOI
Borító:

3.

001-es BibID:BIBFORM087758
035-os BibID:(WoS)000458713400018 (Scopus)85060094588
Első szerző:Büttner, Christian
Cím:Tyrosinase Is a Novel Endogenous Regulator of Developmental and Inflammatory Lymphangiogenesis / Christian Büttner, Thomas Clahsen, Birgit Regenfuss, Marie-Luise Dreisow, Zita Steiber, Felix Bock, André Reis, Claus Cursiefen
Dátum:2019
ISSN:0002-9440
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:American Journal of Pathology. - 189 : 2 (2019), p. 440-448. -
További szerzők:Clahsen, Thomas Regenfuss, Birgit Dreisow, Marie-Luise Steiber Zita (1977-) (orvos, szemész) Bock, Felix Reis, André Cursiefen, Claus
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

4.

001-es BibID:BIBFORM001996
Első szerző:Eidsmo, Liv
Cím:FasL and TRAIL induce epidermal apoptosis and skin ulceration upon exposure to Leishmania major / Liv Eidsmo, Caroline Fluur, Bence Rethi, Sofia Eriksson Ygberg, Nicolas Ruffin, Angelo De Milito, Hannah Akuffo, Francesca Chiodi
Dátum:2007
Megjegyzések:Receptor-mediated apoptosis is proposed as an important regulator of keratinocyte homeostasis in human epidermis. We have previously reported that Fas/FasL interactions in epidermis are altered during cutaneous leishmaniasis (CL) and that keratinocyte death through apoptosis may play a pathogenic role for skin ulceration. To further investigate the alterations of apoptosis during CL, a keratinocyte cell line (HaCaT) and primary human epidermal keratinocytes were incubated with supernatants from Leishmania major-infected peripheral blood mononuclear cells. An apoptosis-specific microarray was used to assess mRNA expression in HaCaT cells exposed to supernatants derived from L. major-infected cultures. Fas and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) mRNA and protein expression were significantly up-regulated, and apoptosis was detected in both HaCaT and human epidermal keratinocyte cells. The keratinocyte apoptosis was partly inhibited through blocking of Fas or FasL and even more efficiently through TRAIL neutralization. Up-regulation of Fas on keratinocytes in epidermis and the presence of FasL-expressing macrophages and T cells in dermis were previously reported by us. In this study, keratinocytes expressing TRAIL, as well as the proapoptotic receptor TRAIL-R2, were detected in skin biopsies from CL cases. We propose that activation of Fas and TRAIL apoptosis pathways, in the presence of inflammatory mediators at the site of infection, leads to tissue destruction and ulceration during CL.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
apoptosis
skin
leishmania
Megjelenés:The American Journal of Pathology. - 170 : 1 (2007), p. 227-239. -
További szerzők:Fluur, Caroline Réthi Bence (1973-) (biológus, immunológus) Ygberg, Sofia Eriksson Ruffin, Nicolas De Milito, Angelo Akuffo, Hannah Chiodi, Francesca
Internet cím:elektronikus változat
DOI
elektronikus változat
Borító:

5.

001-es BibID:BIBFORM048166
Első szerző:Kovács Bettina (orvos)
Cím:The Superiority of Anti-FXa Assay Over Anti-FIIa Assay in Detecting Heparin-Binding Site Antithrombin Deficiency / Bettina Kovács, Zsuzsanna Bereczky, Zsolt Oláh, Réka Gindele, Adrienne Kerényi, Anna Selmeczi, Zoltán Boda, László Muszbek
Dátum:2013
ISSN:0002-9173
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:American Journal of Clinical Pathology. - 140 : 5 (2013), p. 675-679. -
További szerzők:Bereczky Zsuzsanna (1974-) (orvosi laboratóriumi diagnosztika szakorvos) Oláh Zsolt (1974-) (belgyógyász) Gindele Réka (1987-) (molekuláris biológus) Kerényi Adrienne (1970-) (laboratóriumi szakorvos) Selmeczi Anna (1982-) (orvos) Boda Zoltán (1947-) (belgyógyász, haematologus, klinikai onkológus) Muszbek László (1942-) (haematológus, kutató orvos)
Pályázati támogatás:K62087
OTKA
PD10120
OTKA
TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Trombózis Kutató Központ Kutatócsoport
MEC-3/2011
Egyéb
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

6.

001-es BibID:BIBFORM054869
035-os BibID:PMID: 25118810
Első szerző:Méhes Gábor (patológus)
Cím:Activating BRAF V600E mutation in aggressive pediatric Langerhans cell histiocytosis : demonstration by Allele-specific PCR/Direct sequencing and immunohistochemistry / Gábor Méhes, Gábor Irsai, Judit Bedekovics, Lívia Beke, Ferenc Fazakas, Tímea Rózsa, Csongor Kiss
Dátum:2014
ISSN:0147-5185
Megjegyzések:Langerhans cell histiocytosis (LCH) is a rare neoplastic disease originating from cells characterized by antigen-presenting Langerhans cell phenotype. The clinical spectrum of LCH is highly variable including localized and disseminated forms mostly occurring in children. Recently, about 60% of LCHs were reported to carry the activating BRAF mutation V600E. In our retrospective study, we evaluated the occurrence and prognostic impact of the V600E mutation in formaldehyde-fixed, paraffin-embedded samples from 15 pediatric LCH cases treated at our institution. Allele-specific polymerase chain reaction (PCR) and direct sequencing were used to demonstrate the presence of V600E mutation, and immunohistochemistry (IHC) using the mutant protein-specific VE1 antibody clone was performed to confirm mutant BRAF protein expression. Eight of 15 (53.3%) cases proved to be BRAF mutants by any of the methods applied, with a single case showing a discrepancy (PCR negative/IHC positive). Four of the BRAF-mutant cases (50.0%) showed refractory disease and progressed to death within 43 months, whereas the remaining mutant cases were stable and responded well to therapy. Wild-type BRAF cases (7/15, 46.6%) with generally comparable initial presentation were all treated successfully. In conclusion, activating V600E BRAF mutation can be frequently demonstrated in pediatric LCH by both allele-specific PCR and IHC. Unfavorable risk cases potentially also responding to BRAF-inhibitory therapy can be identified by mutation testing using archival formaldehyde-fixed, paraffin-embedded tumor samples.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:The American Journal of Surgical Pathology. - 38 : 12 (2014), p. 1644-1648. -
További szerzők:Irsai Gábor Bedekovics Judit (1986-) (orvos) Beke Lívia Fazakas Ferenc (1969-) (molekuláris biológus) Rózsa Tímea (1985-) (csecsemő- és gyermekgyógyász) Kiss Csongor (1956-) (hematológus, onkológus)
Pályázati támogatás:TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Patológia Kutatócsoport
TÁMOP-4.2.2.A-11/1/KONV-2012-0025
TÁMOP
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

7.

001-es BibID:BIBFORM015783
Első szerző:Nesterovitch, Andrew B.
Cím:Spontaneous insertion of a B2 element in the ptpn6 gene drives a systemic autoinflammatory disease in mice resembling neutrophilic dermatosis in humans / Andrew B. Nesterovitch, Sandor Szanto, Andrea Gonda, Tamas Bardos, Katalin Kis-Toth, Vyacheslav A. Adarichev, Katalin Olasz, Sheida Ghassemi-Nejad, Mark D. Hoffman, Michael D. Tharp, Katalin Mikecz, Tibor T. Glant
Dátum:2011
ISSN:0002-9440
Megjegyzések:We found a spontaneous autosomal mutation in a mouse leading to neutrophil infiltration with ulceration in the upper dermis of homozygous offspring. These animals had increased neutrophil numbers, associated with normal lymphocyte count, in peripheral blood and bone marrow, suggesting a myeloproliferative disorder; however, granulocyte precursor proliferation in bone marrow was actually reduced (because circulating neutrophils were less susceptible to apoptosis). Neutrophil infiltration of the skin and other organs and high serum levels of immunoglobulins and autoantibodies, cytokines, and acute-phase proteins were additional abnormalities, all of which could be reduced by high-dose corticosteroid treatment or neutrophil depletion by antibodies. Use of genome-wide screening localized the mutation within an 0.4-Mbp region on mouse chromosome 6. We identified insertion of a B2 element in exon 6 of the Ptpn6 gene (protein tyrosine phosphatase, non-receptor type 6; also known as Shp-1). This insertion involves amino acid substitutions that significantly reduced the enzyme activity in mice homozygous for the mutation. Disease onset was delayed, and the clinical phenotype was milder than the phenotypes of other Ptpn6-mutants described in motheaten (me, mev) mice; we designated this new genotype as Ptpn6(meB2/meB2) and the phenotype as meB2. This new phenotype encompasses an autoinflammatory disease showing similarities to many aspects of the so-called neutrophilic dermatoses, a heterogeneous group of skin diseases with unknown etiology in humans.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:American Journal Of Pathology 178 : 4 (2011), p. 1701-1714. -
További szerzők:Szántó Sándor (1968-) (belgyógyász, reumatológus) Gonda Andrea (1970-) (onkológus szakorvos) Bárdos Tamás Kis-Tóth Katalin (1975-) (immunológus) Adarichev, Vyacheslav A. Olasz Katalin Ghassemi-Nejad, Sheida (1980-) (fogorvos) Hoffman, Mark D. Tharp, Michael D. Mikecz Katalin Glant Tibor T.
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
elektronikus elérés
Borító:

8.

001-es BibID:BIBFORM010290
035-os BibID:PMID:19590037
Első szerző:Péterfi Zalán
Cím:Peroxidasin is secreted and incorporated into the extracellular matrix of myofibroblasts and fibrotic kidney / Péterfi Zalán, Donkó Ágnes, Orient Anna, Sum Adrienn, Prokai Ágnes, Molnár Beáta, Veréb Zoltán, Rajnavölgyi Éva, Kovács Krisztina, Müller Veronika, Szabó Attila J., Geiszt Miklós
Dátum:2009
Megjegyzések:Mammalian peroxidases are heme-containing enzymes that serve diverse biological roles, such as host defense and hormone biosynthesis. A mammalian homolog of Drosophila peroxidasin belongs to the peroxidase family; however, its function is currently unknown. in this study, we show that peroxidasin is present in the endoplasmic reticulum of human primary pulmonary and dermal fibroblasts, and the expression of this protein is increased during transforming growth factor-beta 1-induced myofibroblast differentiation. Myofibroblasts secrete peroxidasin into the extracellular space where it becomes organized into a fibril-like network and colocalizes with fibronectin, thus helping to form the extracellular matrix. We also demonstrate that peroxidasin expression is increased in a murine model of kidney fibrosis and that peroxidasin localizes to the peritubular space in fibrotic kidneys. in addition, we show that this novel pathway of extracellular matrix formation is unlikely mediated by the peroxidase activity of the protein. Our data indicate that peroxidasin secretion represents a previously unknown pathway in extracellular matrix formation with a potentially important role in the physiological and pathological fibrogenic response.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:The American Journal of Pathology. - 175 : 2 (2009), p. 725-735. -
További szerzők:Donkó Ágnes Orient Anna Sum Adrienn Prokai Ágnes Molnár Beáta Veréb Zoltán (1980-) (immunológus, mikrobiológus, molekuláris biológus) Rajnavölgyi Éva (1950-) (immunológus) Kovács Krisztina Müller Veronika Szabó Attila (gyermekgyógyász Budapest) Geiszt Miklós
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

9.

001-es BibID:BIBFORM001013
Első szerző:Peters, Eva M.J.
Cím:Probing the effects of stress mediators on the human hair follicle / Peters E.M.J., Liotiri S., Bodó E., Hagen E., Bíró T., Arck P.C., Paus R.
Dátum:2007
Megjegyzések:Stress alters murine hair growth, depending on substance P-mediated neurogenic inflammation and nerve growth factor (NGF), a key modulator of hair growth termination (catagen induction). Whether this is of any relevance in human hair follicles (HFs) is completely unclear. Therefore, we have investigated the effects of substance P, the central cutaneous prototypic stress-associated neuropeptide, on normal, growing human scalp HFs in organ culture. We show that these prominently expressed substance P receptor (NK1) at the gene and protein level. Organ-cultured HFs responded to substance P by premature catagen development, down-regulation of NK1, and up-regulation of neutral endopeptidase (degrades substance P). This was accompanied by mast cell degranulation in the HF connective tissue sheath, indicating neurogenic inflammation. Substance P down-regulated immunoreactivity for the growth-promoting NGF receptor (TrkA), whereas it up-regulated NGF and its apoptosis- and catagen-promoting receptor (p75NTR). In addition, MHC class I and beta2-microglobulin immunoreactivity were up-regulated and detected ectopically, indicating collapse of the HF immune privilege. In conclusion, we present a simplistic, but instructive, organ culture assay to demonstrate sensitivity of the human HF to key skin stress mediators. The data obtained therewith allow one to sketch the first evidence-based biological explanation for how stress may trigger or aggravate telogen effluvium and alopecia areata.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:The American Journal of Pathology. - 171 : 6 (2007), p. 1872-1886. -
További szerzők:Liotiri, Sofia Bodó Enikő Hagen, Evelin Arck, Petra C. Paus, Ralf Bíró Tamás (1968-) (élettanász)
Internet cím:elektronikus valtozat
elektronikus változat
DOI
Borító:
Rekordok letöltése1