Wynik wyszukiwania w bazie Polska Bibliografia Lekarska GBL
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STEWART
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2
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Tytuł oryginału:
A phase III placebo-controlled study in advanced head and neck cancer using intratumoural cisplatin/epinephrine gel.
Autorzy:
Werner
J. A.,
Kehrl
W.,
Płużańska
A.,
Arndt
O.,
Lavery
K. M.,
Glaholm
J.,
Dietz
A.,
Dyckhoff
G.,
Maune
S.,
Stewart
M. E.,
Orenberg
E. K.,
Leavitt
R. D.
Źródło:
Br. J. Cancer 2002: 87 (9) s.938-944, tab., bibliogr. 24 poz.
Sygnatura GBL:
301,683
Hasła klasyfikacyjne GBL:
toksykologia
farmacja
neurologia
onkologia
Typ dokumentu:
praca kliniczna
praca opublikowana za granicą
tytuł obcojęzyczny
Wskaźnik treści:
ludzie
Streszczenie angielskie:
Patient with recurrent or refractory head and neck squamous cell carcinoma received cisplatin/epinephrine injectable gel or placebo gel injected directly into the clinically dominant tumour. The double-blind phase III trial comprised of up to 6 weekly treatments over 8 weeks, 4 weekly evaluation visits, and then monthy follow-up; open-label dosing began as needed after three blinded treatments. Tumour response was defined as complete (100 p.c. regression) or partial (50-99 p.c. regression) sustained for ň28 day, and patient benefit as attainment of paliative or preventive goals prospectively selected by investigators and patients. With cisplatin/epinephrine gel, 25 p.c. (14 out of 57) of tumours responded (16 p.c. complete regression, 96 partial regression), vs 3 p.c. (one out of 35, complete regression) with placebo (P = 0.007). Patient benefit was positively associated with target tumour response in the blinded period among cisplatn/epinephrine gel recipients (P = 0.024): 43 p.c. (six out of 14) of responders benefited, vs 12 p.c. (five out of 43) of non-responders. the most frequent adverse event was pain during injection and the next most frequent was local cytotoxic effects consistent with the gel's mode of action. systemic adverse events typical of intravenous cisplatin were uncommon. Intratumoral therapy with cisplatin/epinephrine gel provided safe, well-tolerated, effective palliative treatment for patients with locally advanced head and neck squamous cell carcinoma, who lack other satisfactory treatment options.
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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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