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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
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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.
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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
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001-es BibID:	BIBFORM040516
035-os BibID:	PMID:2432773
Első szerző:	Polgár Katalin
Cím:	Immunocytochemical characterization of amniotic fluid macrophages in cases of fetal neural tube defects / Katalin Polgar, György Abel, Jeno Laczko, Sandor Sipka, Zoltan Papp
Dátum:	1987
Megjegyzések:	Amniotic fluid cells from 31 pregnancies with fetuses having open neural tube defects (NTDs) and from 43 pregnancies with fetuses free of NTDs were studied with the use of the immunoperoxidase method for alpha-fetoprotein (AFP) and glial fibrillary acidic protein (GFAP). The authors also used cytochemical stains for endogenous peroxidase and nonspecific esterase activity. In cases of NTDs, macrophages were present in the amniotic fluid, and in the authors' system they showed intense immunoreactivity for both AFP and GFAP and showed very strong activity for peroxidase and nonspecific esterase, whereas the epithelial cells and red blood cells showed no activity. In six cases of anencephaly, sections from the margin of the cranial end of defective spinal cords at the aperture of the open lesion were also studied for AFP and GFAP. In these cases, AFP- and GFAP-positive cells were found, indicating the possible neural (glial) origin of a part of amniotic fluid macrophages. Although the determination of AFP levels in maternal blood and amniotic fluid is widely used in the prenatal diagnosis of NTDs, demonstration of AFP in amniotic fluid cells by means of immunocytochemistry has not been described.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban egyetemen (Magyarországon) készült közlemény
Megjelenés:	American Journal of Clinical Pathology. - 87 : 1 (1987), p. 37-42. -
További szerzők:	Ábel György Laczkó Jenő Papp Zoltán (1942-) (szülész-nőgyógyász, genetikus) Sipka Sándor (1945-) (laboratóriumi szakorvos)
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