Publications by authors named "Tsipas G"

The genetic structure of the Western Greece lake populations of Carassius gibelio and Cyprinus carpio carpio populations was characterized by using a PCR-based RFLP and sequencing analysis of mitochondrial rDNA genes and regions (16S rDNA, cytochrome b and D-loop). Our analysis was able to detect: (a) two haplotypes in C. c.

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In this study we investigated the role of a mixture of n-6/n-3 essential fatty acids, in the cyclosporine model nephrotoxicity. Administration of cyclosporine in rats decreased creatinine clearance and provoked body weight loss, but it did not induce proteinuria and did not alter the urine volume. These changes were associated with decreased urinary ratios of prostaglandin E/thromboxane B and prostaglandin I/thromboxane B excretions.

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In this study we investigated the role of a mixture of n-6/n-3 essential fatty acids, in the cyclosporine model nephrotoxicity. Administration of cyclosporine in rats decreased creatinine clearance and provoked body weight loss, but it did not induce proteinuria and did not alter the urine volume. These changes were associated with decreased urinary ratios of prostaglandin E/thromboxane B and prostaglandin I/thromboxane B excretions.

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Cyclosporine (CsA) (37.4 mumol/kg per day for 7 days) treated female Wistar rats exhibited significantly decreased creatinine clearance (Ccr) and body weight loss (BWL), but had neither proteinuria (PU) nor alteration in their urine volume (V). Light microscopic (LM) sections of rat kidneys showed that all kidneys were affected by lesions, mainly diffuse vacuolization.

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Cyclosporine (CsA)-treated female Wistar rats, in dose of 37.5 microM (45 mg)/kg/day for 7 days, exhibited significantly decreased creatinine clearance (Ccr), and provoked body weight loss (BWL), which is consistent with the development of nephrotoxicity (NT). Urine volume (V) did not change and proteinuria (PU) was not provoked.

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Administration of cyclosporine (CsA), 37.4 microM (45 mg)/Kg, per day for 7 days, to Wistar rats, induced decreased creatinine clearance (Ccr) and body weight loss (BWL), but it did not induce proteinuria. These changes were associated with enhanced urinary thromboxane B2 (TXB2) and diminished 6-keto-PGF1 alpha (6kPGF1 alpha) and prostaglandin E2 (PGE2) excretions.

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Acute renal failure (ARF) induced with large doses of Gentamicin (GM) (an aminoglycoside) was associated with increased urinary TXB (TXA) excretion which provoked a decrease of the ratios of urinary PGE2/TXB2 and 6-keto-PGF1 alpha (PGI2)/TXB2 excretions. Furthermore, as indicated by light microscopy most of the epithelial cells lining the proximal tubules show obvious lesions varying from swelling of their cytoplasm to complete necrosis. Either the inhibitor, OKY-O46, of TXA-synthetase, or volume expansion (VE) with isotonic saline (IS) of the experimental animals diminished urinary TXB excretion which provoked 1) augmentation of the ratios of urinary PGE/TXB and 6-keto-PGF1 alpha/TXB excretions, 2) elevation of creatinine clearance (Ccr) and 3) diminution of proteinuria (PU).

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