Wynik wyszukiwania w bazie Polska Bibliografia Lekarska GBL

Zapytanie: THIEM
Liczba odnalezionych rekordów: 7



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Tytuł oryginału: Induction of cytokine production in human T cells and monocytes by highly purified lipoteichoic acid: involvement of Toll-like receptors and CD14.
Autorzy: Ellingsen Espen A., Morath Siegfried, Flo Trude H., Schromm Andra B., Hartung Thomas, Thiemermann Christoph, Espevik Terje, Golenbock Douglas T., Foster Simon J., Solberg Rigmor, Aasen Ansgar O., Wang Jacob E.
Źródło: Med. Sci. Monitor 2002: 8 (5) s.BR149-BR156, il., bibliogr. 29 poz.
Sygnatura GBL: 313,278

Hasła klasyfikacyjne GBL:
  • immunologia
  • mikrobiologia
  • farmacja
  • hematologia

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • ludzie
  • in vitro

    Streszczenie angielskie: Pro-inflammatory potential of lipoteichoic acid (LTA) from Staphylococcus aureus is controversial. Present study was undertaken to examine ability of highly purified and characterized S. aureus LTA to stimulate production of pro-inflammatory cytokines in human leukocytes at both mRNA and protein level, and to study involvement of Toll-like receptors (TLRs) adn CD14 in this response. Purified LTA was administered to whole human blood ex-vivo (or primary adherent monocytes) and cytokine response assessed in plasma by EIA. Cytokine mRNA was measured by RT-PCR on leukocyate subsets isolated following stimulation. To study involvement of specific receptors for LTA signaling, CHO cells transfected with CD14 and/or TLR2, TLR4 were used, as well as antibodies directed against these receptors. Addition of highly purified LTA to a whole blood or primary adherent monocytes elicited a time and concentration dependent release of TNF-ŕ, IL-1á, IL-6 and IL-8. mRNA encoding TNF-ŕ, IL-1á, IL-6 and IL-8. mRNA encoding TNF-ŕ, IL-1á and IL-6 seemed to be accumulated in monocytes and T cells, but not in granulocytes and B cells. Expression of TLR2, but not TLR4, in chinese hamster ovary cells conferred responsiveness to LTA. However, antibodies directed towards TLR2 (clone TL2.1) or TLR4 (clone THA125) failed to inhibit TNF-ŕ release induced by LTA in the whole blood model and in adherent monocytes. In contrast, blockade of the CD14 receptor with MAb18D11 strongly attenuated LTA induced release of TNF-ŕ in both models.


    2/7

    Tytuł oryginału: Ligands of the peroxisome proliferator-activated receptor-PPAR-ŕ reduce myocardial infarct size.
    Autorzy: Wayman Nicole S., Ellis Bilinda L., Thiemermann Christoph
    Źródło: Med. Sci. Monitor 2002: 8 (7) s.BR243-BR247, il., tab., bibliogr. 21 poz.
    Sygnatura GBL: 313,278

    Hasła klasyfikacyjne GBL:
  • farmacja
  • kardiologia

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • szczury
  • płeć męska

    Streszczenie angielskie: Background: This study was desibned to investigate the effects of two, chemically distinct activators of PPAR-ŕ (clofibrate and WY14643) in a rat model of acute myocardial infaction. Material/Methods: Male Wistar rats were anesthetized with sodium thiopentone (120 mg/kg i.v.) and subjected to regional myocardial ischemia (for 25 min) and reperfusion (for 2 h). Area at risk was determined by injection of Evans Blue dye and infarct size after staining with nitroblue tetrazolium. Results: Pre-treatment of rats with the PPAR-ŕ agonists clofibrate (0.3 mg/kg) caused a significant reduction inmyocardial infarct size of 43 p.c. Similarly, pre-treatment of rats with the PPAR-ŕ agonists WY14643 (1 mg/kg) caused a significant reduction inmyocardial infarct size of 43 p.c. Conclusions: Taken together, these results show that ligands of PPAR-ŕ reduce the tissue necrosis associated with acute myocardial infarction. We propose that fibrates and other PPAR-ŕ agonists may be useful in conditions associated with ischemia-reperfusion of the heart and other organs.


    3/7

    Tytuł oryginału: Superoxide dismutase mimetic with catalase activity, EUK-134, attenuates the multiple organ injury and dysfunction caused by endotoxin in the rat.
    Autorzy: Villa Bianca Roberta d'Emanuele di, Wayman Nicol S., McDonald Michelle C., Pinto Aldo, Sharpe Martyn A., Chatterjee Prabal K., Thiemermann Christoph
    Źródło: Med. Sci. Monitor 2002: 8 (1) s.BR1-BR7, il., tab., bibliogr. 33 poz.
    Sygnatura GBL: 313,278

    Hasła klasyfikacyjne GBL:
  • farmacja
  • traumatologia i ortopedia

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • szczury

    Streszczenie angielskie: Reactive oxygen species contribute to the multiple organ failure shock. Here we investigate the effects of a salen-manganese complex, which exhibits both superoxide dismutase and catalase activity (EUK-134), on the circulatory failure and the renal and liver injury and dysfunction caused by endotoxin in the anaesthetised (thiopentone, 120 mg/kg) rat. Male Wistar rats were anaesthetised with hiopentone sodium (120 kg i.p.) and instrumented for the measurements of systemic haemodynamics. Animals received lipopolysaccharide (LPS, E. coli, 6 mg/kg i.v.) or saline and were treated with either EUK-134 (0.3 or 1 mg/kg bolus injection folloowed by an infusion of 0.3 or 1 mg/kg/h) or its vehicle (saline). After 6 h of endotoxaemia, blood was taken to evaluate biochemical parameters of organ injury and dysfunction. All data are mean ń s.e. mean of n observations. Statisstical comparisons were made with a ANOVA followed by Dunner's test for mulitiple comparisons. Endotoxaemia for 6 h caused hypotension, renal dysfunction, liver injury, skeletal-muscle injury and pancreatic injury. Treatment of rats with EUK-134 attenuated the reanl dysfynction as well as the liver and skeletal muscle injury (but not the pancreatic injury) caused by endotoxin. Thus, an enhanced formation of reactive oxygen species importantly contribute to the organ injury and dysfunction associated wtih endotoxic shock. We propose that small molecules, which have the catalytic activity of both superoxide dismutase and catalase, may represent a novel therapeutic approach for the therapy of endotoxic shock.


    4/7

    Tytuł oryginału: 50-lecie pracy naukowej prof. dr hab. Lutosławy Marii Skrzypczak.
    Tytuł angielski: 50 years of scientific work of prof. dr. hab. Lutosława Maria Skrzypczak.
    Autorzy: Thiem Barbara, Wesołowska Maria, Budzianowski Jaromir
    Źródło: Farm. Pol. 2002: 58 (22) s.1073-1075, il.
    Sygnatura GBL: 310,851

    Hasła klasyfikacyjne GBL:
  • farmacja

    Typ dokumentu:
  • praca biograficzna

    Wskaźnik treści:
  • ludzie
  • płeć żeńska
  • historia nowożytna
  • historia XX wieku
  • historia XXI wieku

    Temat osobowy:
  • Skrzypczak
  • Lutosława Maria 1925-


    5/7

    Tytuł oryginału: Agonists of peroxisome-proliferator activated receptor-ŕ (Clofibrate and WY14643) reduce renal ischemia/reperfusion injury in the rat.
    Autorzy: Sivarajah Ahila, Chatterjee Prabal K., Hattori Yoshiyuki, Brown Paul A. J., Stewart Keith N., Todorovic Zoran, Mota-Filipe Helder, Thiemermann Christoph
    Źródło: Med. Sci. Monitor 2002: 8 (12) s.BR532-BR539, il., tab., bibliogr. 37 poz.
    Sygnatura GBL: 313,278

    Hasła klasyfikacyjne GBL:
  • farmacja
  • nefrologia

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • szczury
  • płeć męska

    Streszczenie angielskie: Background: The aim of this study was to investigate the effects of peroxisome-proliferator activated receptor-ŕ (PPAR-ŕ) agonsits, clofibrate and WY 14643 on the renal dysfunction and injury caused by bilateral ischemia/reperfusion (I/R) of rat kidneys in vivo. Material/Methods: Male Wistar were randomized with sodium thiopentone (120 mg/kg i.v.) and subjected to bilateral renal ischemia (45 min) followed by reperfusion (6 h). Serum and urinary biochemical indicators of renal dysfunction and injury were meausured; serum creatine (sCr, glomerular dysfunction), fractional excretion of Na+ (FE NA, tubular dysfunction), and urinary N-acetyl-á-D-glucosaminidase (uNAG, tubular injury). Additionally, renal sections were used for histological grading of renal injury and for RT-PCR analysis of the expression of PPAR-isoforms in kidneys obtained from rats prior to or after I/R. In addition, expression of intercellular adhesion molecule-1 (ICAM-1) was determined using Northern blot analysis. Results: Using RT-PCR we document here the expression of PPAR-ŕ, PPAR-á and PPAR-ç1 (but not PPAR-ç2) in the kidney of the rat. I/R resulted in the down-regulation of PPAR-ŕ without modulation of any other PPAR. Clofibrate and WY 14643 significantly reduced the increases in sCr, FE NA and uNAG caused by renal I/R, indicating attenuation of renal dysfunction and injury. Expression of ICAM-1 caused by I/R of the kidney was not modulated by PPAR-ŕ agonists. Conclusions: We show here that (i) renal I/R results in the down-regulation of PPAR-ŕ in the kidney, and (ii) that the PPAR-ŕ agonists...


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    Tytuł oryginału: The novel PARP inhibitor 5-aminoisoquinolinone reduces the liver injury caused by ischemia nad reperfusion in the rat.
    Autorzy: Mota-Filipe Helder, Sepodes Bruno, McDonald Michelle, Cuzzocrea Salvatore, Pinto Rui, Thiemermann Christoph
    Źródło: Med. Sci. Monitor 2002: 8 (11) s.BR444-BR453, il., tab., bibliogr. 42 poz.
    Sygnatura GBL: 313,278

    Hasła klasyfikacyjne GBL:
  • farmacja
  • gastroenterologia

    Typ dokumentu:
  • tytuł obcojęzyczny
  • praca doświadczalna

    Wskaźnik treści:
  • zwierzęta
  • szczury

    Streszczenie angielskie: Background: This study was designed to investigate the effects of 5-aminoisoquinolinone (5 -AIQ), a watersoluble potent inhibitor of poly-(ADP-ribose) polymerase (PARP) in a rat model of liver ischemia-reperfusion injury. Material/Methods: Male Wistar rats were anesthetised with sodium pentobarbital (60 mg/kg, i.p.) and subjected to liver ischemia (for 30 minutes) and reperfusion (for 2 hours). Liver injury was assessed by measuring (i) the serum levels of transaminases, lactate dehydrogenase, ç-glutamyl transferase, (ii) lipid peroxidation in liver tissue and (iii) by immunohistochemistry for PARP and intracellular adhesion molecule 1 (ICAM-1). Resutls: Pre-treatment of rats (five minutes prior to onset of liver ischemia) with the PARP inhibitor 5-AIQ (3 mg/kg, i.v.) rather than vehicle reduced the rise in the serum levle sof transaminases, lactate dehydrogenase, and ç-glutamyl transferase as well as the degree of lipid peroxidation (measured as levels of malondialdehyde in the liver) caused by ischemia-reperfusion of the liver. Liver secitons obtained from 5-AIQ treated rats showed reduced PARP activation and less staining for ICAM-1. Conclusions: Taken together, these results show that 5-AIQ, a new water-soluble potent inhibitor of poly(ADP-ribose) polymerase, reduces the tissue injury associated with ischemia-reperfusion of the liver. we propose that 5-AIQ may be useful in the therapy conditions associated with ischemia-reperfusion of the liver which remains an important clincal problem during shock, liver surgery, and liver transplantation.


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    Tytuł oryginału: A novel, potent and selective inhibitor of the activity of inducible nitric oxide synthase (GW274150) reduces the organ injury in hemorrhagic shock.
    Autorzy: McDonald M. C., Izumi M., Cuzzocrea S., Thiemermann C.
    Źródło: J. Physiol. Pharmacol. 2002: 53 (4) p. 1 s.555-569, il., tab., bibliogr. 27 poz.
    Sygnatura GBL: 302,092

    Hasła klasyfikacyjne GBL:
  • farmacja
  • kardiologia

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • szczury

    Streszczenie angielskie: An enhanced formation of nitric oxide (NO) by the inducible NO synthase (iNOS) may contribute to pathophysiology of hemorrhagic shock. This study investigates the effect of a novel, potent and selective inhibitor of iNOS activity (GW274150) on the circulatory failure and the organ injury and dysfunction associated with hemorrhagic shock in the anesthetised rat. Hemorrhage (sufficient to lower mean arterial blood pressure to 45 mmHg for 90 min) and subsequent resuscitation with shed blood resulted (within 4h after resuscitation) in a delayed fall in blood pressure, renal and liver injury and dysfunction as well as the pancreatic injury. Pre-treatment of rats with GW274150 (5 mg/kg at 30 min prior to the onset of hemorrhage) attenuated the renal dysfunction as well as the liver and pancreatic injury caused by hemorrhage and resuscitation. Interestingly, GW274150 did not reduc the delayed fall in blood pressure associated with hemorrhagic shock. We propose that an enhanced formation of NO from iNOS contributes to the organ injury and dysfunction in hemoohagic shock, and that highly selective inhibitors of iNOS activity, such as GW274150, may represent a novel therapeutic approach for the therapy of hemorrhagic shock.

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