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  1. 6 Archivum Immunologiae et Therapiae Experimentalis

  2. 5 Journal of Physiology and Pharmacology

  3. 4 Folia Histochemica et Cytobiologica

  4. 3 Cellular and Molecular Biology Letters

  5. 1 Acta Biochimica Polonica

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  1. 5 Slomiany A.

  2. 5 Slomiany B. L.

  3. 2 Godlewski A.

  4. 2 Kozakiewicz M.

  5. 2 Slebioda Z.

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  1. 1 2017

  2. 1 2016

  3. 1 2014

  4. 2 2012

  5. 2 2011

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1
Content available remote

Role of endothelin-1-dependent up-regulation of leptin in oral mucosal repair

100%
Slomiany B. L., Slomiany A.
Journal of Physiology and Pharmacology
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2005
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tom 56
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nr 4
Leptin, a multifunctional hormone that regulates food intake and energy expenditure, has emerged recently as an important modulator of inflammatory cascades associated with wound healing. In this study, we applied the animal model of buccal mucosal ulcer to investigate the role of endothelin-1 (ET-1) and leptin in soft oral tissue repair. Using groups of rats with experimentally induced buccal mucosal ulcers we show that ulcer onset was characterized by a marked increase in the mucosal level of ET-1 and leptin. However, while the ET-1 level gradually declined with healing, the mucosal level of leptin increased reaching maximum expression on the 4th day of healing. Therapeutic administration of phosphoramidon, an inhibitor of ECE-1 activity, not only led to a 53.2% drop in the ET-1, but also produced a dose-dependent reduction (up to 50.9%) in the mucosal level of leptin and up to 42.3% decline in the rate of ulcer healing. A marked drop (54.2%) in the mucosal level of leptin and the reduction (46.8%) in the rate of ulcer healing was also attained in the presence of ETA receptor antagonist BQ610 administration, but not the ETB receptor antagonist BQ788. Moreover, administration of ERK inhibitor, PD98059 in the presence of ETB receptor antagonist, but not the ETA receptor antagonist, caused the reduction the mucosal leptin level as well as a decline in the rate of ulcer healing. Our findings are the first to implicate the requirement for both ET-1 and leptin in orderly progression of the events of soft oral tissue repair. We also show that ET-1 is a key factor in up-regulation of leptin production associated with oral mucosal ulcer healing , and that the effect of ET-1 on leptin production is a consequence of ETA receptor activation and subsequent signaling through MAPK/ERK.
2

Influence of raloxifene and 17beta-oestradiol on rats' oral mucosal structure

86%
Rahnama M., Swiatkowski W., Lancut M., Wojcik A.
Bulletin of the Veterinary Institute in Puławy
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2004
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tom 48
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nr 3
3

Comparison of proliferation and motile activity between human keratinocytes isolated from skin and oral mucosa

86%
Drukala J., Zarzecka J., Gojniczek K., Waligorska A., Zapala J., Korohoda W.
Folia Biologica
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2005
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tom 53
|
nr 1-2
4
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Content available

Delay in oral mucosal ulcer healing by aspirin is linked to the disturbances in p38 mitogen-activated protein kinase activation

86%
Slomiany B. L., Slomiany A.
Journal of Physiology and Pharmacology
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2001
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tom 52
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nr 2
5

The effect of chronic alcohol intoxication and smoking on the output of salivary immunoglobulin A

72%
Waszkiewicz N., Zalewska A., Szajda S. D., Waszkiewicz M., Szulc A., Kepka A., Konarzewska B., Minorowska A., Zalewska-Szajda B., Wilamowska D., Waszkiel D., Ladny J. R., Zwierz K.
Folia Histochemica et Cytobiologica
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2012
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tom 50
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nr 4
6

Cytological picture of the oral mucosa in patients with gastric and colon cancer

72%
Kedra B., Chomczyk M., Zlotkowski M., Stokowska W., Borsuk A., Bicz M., Pietruska M., Tokajuk G., Charkiewicz R., Czajka P., Chyczewski L., Zimnoch L., Kedra B.
Folia Histochemica et Cytobiologica
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2012
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tom 50
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nr 3
7

Vitamin D and its relevance in the etiopathogenesis of oral cavity diseases

72%
Slebioda Z., Szponar E., Dorocka-Bobkowska B.
Archivum Immunologiae et Therapiae Experimentalis
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2016
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tom 64
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nr 5
8

Caspase-3 as an important factor in the early cytotoxic effect of nickel on oral mucosa cells in patients treated orthodontically

72%
Buczko P., Szarmach I., Grycz M., Kasacka I.
Folia Histochemica et Cytobiologica
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2017
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tom 55
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nr 1
9

Etiopathogenesis of recurrent aphthous stomatitis and the role of immunologic aspects: literature review

72%
Slebioda Z., Szponar E., Kowalska A.
Archivum Immunologiae et Therapiae Experimentalis
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2014
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tom 62
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nr 3
10

Interleukin 6, tumor necrosis factor alpha and their soluble receptors in the blood serum of patients with denture stomatitis and fungal infection

72%
Pietruski J. K., Pietruska M. D., Jablonska E., Sacha P., Zaremba M., Stokowska W.
Archivum Immunologiae et Therapiae Experimentalis
|
2000
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tom 48
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nr 2
11
Content available remote

Activation of peroxisome proliferator-activated receptor gamma supresses inducible cyclooxygenase and nitric oxide synthase during oral mucosal ulcer healing

72%
Slomiany B. L., Slomiany A.
Journal of Physiology and Pharmacology
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2002
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tom 53
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nr 2
Peroxisome proliferator-activated receptor-gamma (PPARgamma) is a ligand-dependent transcription factor, belonging to the steroid hormone receptor family, known to play a pivotal role in the resolution of inflammation. In this study, we investigated the effect of a specific PPARgamma ligand, ciglitazone, on the course of buccal mucosal ulcer healing by analyzing mucosal activity of inducible nitric oxide synthase (NOS-2) and the expression cyclooxygenases (COX-1 and COX-2) responsible for prostaglandin (PG) generation. Methods: Groups of rats with experimentally induced buccal mucosal ulcers were administered twice daily for up to 10 days with ciglitazone at 5, 10, and 15 mg/kg or the vehicle, and their mucosal tissue subjected to assessment of ulcer healing rate and biochemical measurements. Results: The ulcer onset, characterized by up-regulation of NOS-2 and COX-2 protein expression, was reflected in a marked increase in the mucosal PGE2 generation and NOS-2 activity, whereas healing was accompanied by a drop in PGE2 and NOS-2 activity, and a decrease in COX-2 and NOS-2 protein expression. The mucosal expression of COX-1 protein, however, remained unchanged. Administration of ciglitazone led to a significant dose-dependent acceleration in the mucosal reduction of PGE2 generation and NOS-2 activity, and produced a marked decline in COX-2 and NOS-2 protein expression, but the rate of ulcer healing and the expression of COX-1 protein remained unaffected. Conclusions: Our findings thus suggest that the products of induced NOS-2 and COX-2 enzymes, associated with mucosal inflammatory responses to injury, do not play a significant role in oral mucosal ulcer healing.
12

Blood flow enhancement in skin or oral mucosa after the topical application of liposome entrapped rubifacient as measured by EPR oximetry in vivo: the influence of size and liposome composition

72%
Sentjurc M.
Cellular and Molecular Biology Letters
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2002
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tom 07
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nr 2
13
Content available remote

Screening and modulation of extracellular signals by mucous barrier. Serum glycosylphosphatidylinositol phospholipase D (GPI-PLD) releases protective mucous barrier from oral mucosa

72%
Slomiany A., Nishikawa H., Slomiany B. L.
Journal of Physiology and Pharmacology
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2002
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tom 53
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nr 1
Performance of mucosal epithelial barrier is modified by numerous agents that exert effects on mucin-Mucin Binding Protein (MBP)complex.The aim of the studies described was to determine the nature of the damage or modification of oral mucous barrier by the short-term exposure to ethanol.Methods:Culture of rat buccal mucosa in the presence of ethanol and [3H]-labeled proline and palmitate revealed substantial decrease in MBP synthesis and the release of MBP to the medium.The radioscanning of the samples prepared from the culture medium and the apical epithelial membranes subjected to SDS- PAGE and western blotting disclosed that the released,water soluble 97kDa MBP glycopeptide was labeled with proline and palmitate.When the experiments were conducted in the presence of 5mM EDTA,the GPI-PLD inhibitor,the majority of radiolabeled MBP remained in the membrane-bound form and was extractable with Triton X-114.The results on the purified GPI-linked MBP degradation by serum enzyme,by the saliva containing serum transudate,and the suppression of the process by inclusion of GPI-PLD-specific inhibitor support our contention that membrane MBP is released to medium by GPI-PLD- like activity.Results:The release of MBP from apical epithelial surfaces was induced by depletion of mucin and the presence of serum-derived GPI-PLD in the tissue homogenate. Strong likelihood exists that under in situ conditions ethanol-induced transudation of serum to saliva provides the vehicle for the transfer of GPI-PLD activity to salivary contents. Defacement of the oral surfaces from mucous barrier signals prospect of lumenal agent influence on the unprotected epithelial exterior,and allows ingression of microbes and untoward acting substances into the organism.
14

Modulation of the mitotic activity and population of the mast cells in the oral mucosa by substance P

72%
Kozakiewicz M., Godlewski A.
Cellular and Molecular Biology Letters
|
2003
|
tom 08
|
nr 3
To assess the effect of substances inducing mast cell degranulation (substance P and granuliberin R) on the mitotic indices of the gingiva stratified epithelium, basal cells from rats were studied in vivo. Seventy Lewis male rats were used in the study. The rats received injections of either 0.1 ml 0.9% NaCl (10 rats), or substance P (10-4,10-6, 10-8 g/ml) (30 rats), or granuliberin R (10-4,10-6, 10-8 g/ml) (30 rats) into their mandibular gingiva in the vicinity of the right mental foramen. The mitotic index of keratinocytes was established after the kolchicine arrest (2 hours prior to material collection i.p. injection). The number of cells in metaphase was counted on 1000 consecutive basal layer cells after hematoxilin and eosin section staining. Mast cells were revealed using pinocyanol erythrosinate according to Bensley. Numerical density and morphometric features were analyzed. Substance P and granuliberin R injected into the gingiva affect the mast cells and the basal cell proliferation of the gingival epithelium. The diminished mitotic activity of basal layer cells was accompanied by degranulation and/or migration of mast cells under the basal membrane of the epithelium. After administration of high doses of granuloliberin R, mast cells were found in the deep connective tissue alligned towards the epithelium. A neuromediator from the trigeminal nerve (substance P) and substances from mast cells actively interfere in the proliferation of oral keratinocytes and the activity of connective tissue cells.
15

Modulation of mitotic activity and mast cell population in the oral mucosa by substance P

72%
Kozakiewicz M., Godlewski A.
Cellular and Molecular Biology Letters
|
2002
|
tom 07
|
nr Suppl.
16
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Nonsteroidal anti-inflammatory drugs impair oral mucosal repair by eliciting disturbances in endothelin-converting enzyme-1 and constitutive nitric oxide synthase

72%
Slomiany B. L., Slomiany A.
Journal of Physiology and Pharmacology
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2001
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tom 52
|
nr 1
17

Expression of Th1/Th2/Th3/Th17-related genes in recurrent aphthous ulcers

51%
Lewkowicz N., Kur B., Kurnatowska A., Tchorzewski H., Lewkowicz P.
Archivum Immunologiae et Therapiae Experimentalis
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2011
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tom 59
|
nr 5
18

Expression of cyclooxygenase-1 and cyclooxygenase-2 in normal and pathological human oral mucosa

51%
Mauro A., Lipari L., Leone A., Tortorici S., Burruano F., Provenzano S., Gerbino A., Buscemi M.
Folia Histochemica et Cytobiologica
|
2010
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tom 48
|
nr 4
19

Angiogenesis in oral lichen planus: an in vivo and immunohistological evaluation

51%
Scardina G. A., Ruggieri A., Maresi E., Messina P.
Archivum Immunologiae et Therapiae Experimentalis
|
2011
|
tom 59
|
nr 6
20

Activity of lysosomal exoglycosidases in submandibular glands of rats intoxicated by cadmium at doses related to human chronic environmental and occupational exposures

51%
Zalewska A., Brzoska M. M., Marciniak J., Karaszewska K., Zwierz K., Moniuszko-Jakoniuk J.
Acta Biochimica Polonica
|
2004
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tom 51
|
nr 3
Work in cadmium (Cd) smelter and smoking cigarettes damages teeth and oral mucosa which are protected by tissue and salivary glycoconjugates: glycoproteins, glycolipids, and proteoglycans. We worked out a rat model imitating human "envi­ronmental" and "occupational" exposure to cadmium using 5 mg Cd and 50 mg Cd/l in drinking water, respectively. In submandibulary glands of exposed to Cd rats, we found the time and dose dependent accumulation of Cd and simultanous decrease in activity of ß-N-acetylhexosaminidase (HEX). In homogenates of submandibulary glands of control rats, ß-N-acetylhexosa- minidase showed the highest activity. The activities of a-mannosidase and ß-galacto- sidase were very low. None of these exoglycosidases were inhibited by Cd even at 44 mM concentration.
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