Wynik wyszukiwania w bazie Polska Bibliografia Lekarska GBL

Zapytanie: KORNATOWSKI
Liczba odnalezionych rekordów: 3



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Tytuł oryginału: Decreased apoptosis and distinct profile of infiltrating cells in the nasal polyps of patients with aspirin hypersensitivity.
Autorzy: Kowalski M. L., Grzegorczyk J., Pawliczak R., Kornatowski T., Wagrowska-Danilewicz M., Danilewicz M.
Źródło: Allergy 2002: 57 (6) s.493-500, il., tab., bibliogr. 49 poz.
Sygnatura GBL: 302,302

Hasła klasyfikacyjne GBL:
  • toksykologia
  • immunologia
  • otorynolaryngologia

    Typ dokumentu:
  • praca kliniczna
  • praca opublikowana za granicą
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • ludzie
  • dorośli 19-44 r.ż.
  • dorośli 45-64 r.ż.
  • dorośli = 65 r.ż.

    Streszczenie angielskie: Background: Patients with aspirin-hypersensitive rhinosinusitis/asthma suffer from a severe form of hyperplastic rhinosinusitis with recurrent polyposis. We aimed to assess the presence of apoptotic cells in nasal polyps from aspirin-hypersensitive (AH) and aspirin-tolerant (AT) patients with rginosinusitis as related to the characteristis of local inflammation. Methods: Nasal polyps obtained from 16 AH patients and 36 AT patients (17 atopic and 19 nonatopic) were stained for eosinophils and metachromatic cells, and in parallel immunocytochemistry was performed to detect CD45RO+, HLA-DR+, CD8+ and CD68+ positive cells. Apoptotic cells were detected by a nick-end labelling technique, TUNEL. Results: The density of apoptotic cells in AH polyps (5.5 + 1.5 cells/mmý) was significantly lower as compared to both atopic (18.7 + 3.8 cells/mmý; P 0.02;) and nonatopic (21.3 + 5.2 cells/mmý; P 0.01) AT polyps. The number of eosinophils, mast cells, and CD45RO+ cells weer significantly increased in AH compared to AT polyps () 0.001), and the density of HLA-DR+ cells in AH patients was higher than in nonatopic (P 0.02), but not in atopic AT patients. While in AH patients the duration of rhinosinusitis correlated inversely with the number of apoptotic cells (r = - 0.67; P 0.04), in contrast, in AT atopic patients the duration of rhinosinusitis showed positive correlation with apoptosis (r = 0.89; P 0.003). Conclusions: We conclude, that decreased apoptosis of inflammatory cells in nasal polyps from ASA-hypersensitive patients, reflects a distinct mechanism of local inflammation and may be related to persistence and severity of the disease in these patients.


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    Tytuł oryginału: The effect of verapamil on the antioxidant defence system in diabetic kidney.
    Autorzy: Kędziora-Kornatowska K., Szram S., Kornatowski T., Szadujkis-Szadurski L., Kędziora J., Bartosz G.
    Źródło: Clin. Chim. Acta 2002: 322 (1/2) s.105-112, tab., bibliogr. 44 poz.
    Sygnatura GBL: 303,881

    Hasła klasyfikacyjne GBL:
  • farmacja
  • nefrologia

    Typ dokumentu:
  • praca doświadczalna
  • praca opublikowana za granicą
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • szczury

    Streszczenie angielskie: Bacground: The aim of the study was to examine the effect of verapamil (VP) on lipid peroxidation and activities of key antioxidant enzymes: superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px); as well as on glomerular basement membrane (GBM) thickness in streptozotocin-induced diabetic kidney in rats. Methods: Wistar male rats were divided into three groups, 12 rats each: the control (C), diabetic rats (DR), and DR receiving VP, 7 mg/kg body weight in drinking water (DR + VP). Blood glucose (BG) and HbA1c levels, 24-h urinary albumin excretion (UAE) and body weight (BW) were measured every week (0-12 weeks). After 6 and 12 weeks, the animals were sacrificed and malondialdehyde (MDA) content activatives of SOD, CAT and GSH-Px were determined in the kidney homogenate supernatans. Electron micrographs of the glomeruli were scanned and porhphometric investigations were performed by means of a computer image analysis system to compare the glomerular basement basal membrane (GBM) thickness. results: The levels of BG, HbA1c and UAE in DR were significantly higher than in the C group. A progressive increase in the MDA level and a decrease in the SOD, CAT and GSH-Px activaties in the kidney of DR were observed after 6 and 12 weeks. VP administration did not affect BW changes, BG and HbA1 levels in DR. VP decreased lipid peroxidation and augmented the activities of antioxidant enzymes studied in the kidneys of DR as well as decreased kidney weight, GBM thickness and albuminuria in DR. Conclusions: These results confirm the role of oxidative stress in the development of diabetic nephropathy and point to the possible antioxidative mechanism of the nephroprotective action of VP.


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    Tytuł oryginału: Współczesne poglądy na patogenezę nefropatii cukrzycowej.
    Tytuł angielski: Current views on diabetic nephropathy pathogenesis.
    Autorzy: Błaszczak Robert, Kędziora-Kornatowska Kornelia, Kornatowski Tomasz, Kujawski Krzysztof
    Źródło: Prz. Wojsk.-Med. 2002: 44 (1) s.79-83, bibliogr. 11 poz., sum.
    Sygnatura GBL: 304,530

    Hasła klasyfikacyjne GBL:
  • endokrynologia

    Wskaźnik treści:
  • ludzie

    Streszczenie polskie: Nefropatia cukrzycowa to jedno z najpoważniejszych powikłań cukrzycy zarówno typu 1 jak i typu 2 o charakterze mikroangiopatii. Charakteryzuje się białkomoczem, obniżonym klirensem kłębuszkowym oraz podwyższonym ciśnieniem tętniczym. Patogeneza tego częstego powikłania cukrzycy jest złożona i wieloczynnikowa. Rozpatruje się udział czynników hemodynamicznych, metabolicznych oraz genetycznych. Nie leczona odpowiednio cukrzyca jak i nie wdrożenie leczenia zapobiegającego powstaniu i rozwojowi nefropatii może być przyczyną schyłkowej niewydolności nerek. Dlatego, też znajomość patogenezy nefropatii cukrzycowej ułatwia wdrożenie odpowiedniego schematu zapobiegania i zwalniania przebiegu choroby.

    Streszczenie angielskie: Diabetic nephropathy is one of the most serious complications of diabetes type 1 and 2 of microangiopathic type. It is characterised by albuminuria, decreased glomerular clearance and elevated arterial blood pressure. Pathogenesis of this frequent diabetic complication is complex and multifactorial. Participation of hemodynamic, metabolic and genetic factors is considered. Not properly treated diabetes as well as not introduced therapy preventing the development of nephropathy may be the cause of renal failure. Thus, the knowledge of diabetic nephropathy pathogenesis makes easier the introduction of proper outline of prevention and slowing down the course of the disease.

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