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  • Author or Editor: M. Gul x
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The comparisons among the 6 selection indices S 1 , S 2 , S 3 (simultaneous selection indices comprising of X 1 only; X 1 +X 5 and X 1 +X 2 +X 3 +X 4 respectively as their component traits), S 4 (Rank summation index), S 5 (Baker’s standard deviation index) and S 6 (Elston’s weight free index) were made involving 4 primary cold tolerance traits namely field emergence per cent (X 1 ), fresh seedling root mass (X 2 ), seedling dry weight (X 3 ), days to 50% silk emergence (X 5 ) along with grain yield ha −1 (X 4 ). Highly significant rank correlations of proposed selection indices conferred the suitability in use of one index if substituted for other, to score the genotypes for selection. Selection differentials for all the indices were generally positive with respect to the traits X 1 , X 2 , X 3 and X 4 except S 2 which, was accompanied with negative differentials for X 2 , X 3 and X 4 . S 1 was found to be an important cold tolerance trait depicting not so less differentials compared to other traits and had positive differentials under each selection criteria. Index S 6 was efficient in selecting early silking varieties with high yield and tolerance to cold. The populations NDSM 8 WN, NDSAB (MER), NDSLC and land races GL20W and Dawar-2 showed high degree of cold tolerance among 67 genotypes evaluated and showed at par results with the C 15 check which was top ranking under 5 out of 6 selection used.

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The aim of this study was to assess the effect of melatonin and acetylsalicylic acid (ASA) on hepatic damage induced by bile duct ligation (BDL) Material and methods : Male Sprague-Dawley rats were subjected to either sham operation or common BDL before treatment with ASA, melatonin or vehicle. Hepatic superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) enzyme activities and reduced glutathione (GSH), malondialdehyde (MDA) and nitric oxide (NO) levels were evaluated. Results : Our results have indicated that BDL caused a significant increase in lipid peroxidation whereas a statistically insignificant decrease in GSH level and some of the antioxidant enzyme activities. Both MEL and ASA administrations, either separately or together, decreased MDA whereas co-administration of MEL with ASA increased GSH levels in BDL rats. Conclusions : CAT activity and MEL level decreased in the liver tissues of rats with BDL after administration of either melatonin alone or with ASA. However, melatonin and ASA administration increases liver tissue GSH levels in BDL ligated rats

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Authors: Greta Gölz, Gül Karadas, André Fischer, Ulf B. Göbel, Thomas Alter, Stefan Bereswill and Markus M. Heimesaat

Arcobacter butzleri causes sporadic cases of gastroenteritis, but the underlying immunopathological mechanisms of infection are unknown. We have recently demonstrated that A. butzleri-infected gnotobiotic IL-10−/− mice were clinically unaffected but exhibited intestinal and systemic inflammatory immune responses. For the first time, we here investigated the role of Toll-like receptor (TLR)-4, the main receptor for lipopolysaccharide and lipooligosaccharide of Gram-negative bacteria, in murine arcobacteriosis. Gnotobiotic TLR-4/IL-10-double deficient (TLR-4−/− IL-10−/−) and IL-10−/− control mice generated by broad-spectrum antibiotics were perorally infected with A. butzleri. Until day 16 postinfection, mice of either genotype were stably colonized with the pathogen, but fecal bacterial loads were approximately 0.5–2.0 log lower in TLR-4−/− IL-10−/− as compared to IL-10−/− mice. A. butzleri-infected TLR-4−/− IL-10−/− mice displayed less pronounced colonic apoptosis accompanied by lower numbers of macrophages and monocytes, T lymphocytes, regulatory T-cells, and B lymphocytes within the colonic mucosa and lamina propria as compared to IL-10−/− mice. Furthermore, colonic concentrations of nitric oxide, TNF, IL-6, MCP-1, and, remarkably, IFN and IL-12p70 serum levels were lower in A. butzleri-infected TLR-4−/− IL-10−/− versus IL-10−/− mice. In conclusion, TLR-4 is involved in mediating murine A. butzleri infection. Further studies are needed to investigate the molecular mechanisms underlying Arcobacter—host interactions in more detail.

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Authors: Markus M. Heimesaat, Gül Karadas, André Fischer, Ulf B. Göbel, Thomas Alter, Stefan Bereswill and Greta Gölz

Sporadic cases of gastroenteritis have been attributed to Arcobacter butzleri infection, but information about the underlying immunopathological mechanisms is scarce. We have recently shown that experimental A. butzleri infection induces intestinal, extraintestinal and systemic immune responses in gnotobiotic IL-10−/− mice. The aim of the present study was to investigate the immunopathological role of Toll-like Receptor-4, the receptor for lipopolysaccharide and lipooligosaccharide of Gram-negative bacteria, during murine A. butzleri infection. To address this, gnotobiotic IL-10−/− mice lacking TLR-4 were generated by broadspectrum antibiotic treatment and perorally infected with two different A. butzleri strains isolated from a patient (CCUG 30485) or fresh chicken meat (C1), respectively. Bacteria of either strain stably colonized the ilea of mice irrespective of their genotype at days 6 and 16 postinfection. As compared to IL-10−/− control animals, TLR-4−/− IL-10−/− mice were protected from A. butzleri-induced ileal apoptosis, from ileal influx of adaptive immune cells including T lymphocytes, regulatory T-cells and B lymphocytes, and from increased ileal IFN secretion. Given that TLR-4-signaling is essential for A. butzleri-induced intestinal inflammation, we conclude that bacterial lipooligosaccharide or lipopolysaccharide compounds aggravate intestinal inflammation and may thus represent major virulence factors of Arcobacter. Future studies need to further unravel the molecular mechanisms of TLR-4-mediated A. butzleri-host interactions.

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Authors: S. Taysi, N. Oztasan, H. Efe, M.F. Polat, K. Gumustekin, E. Siktar, E. Canakci, F. Akcay, S. Dane and M. Gul

The aim of this study was to investigate whether an 8-week treadmill training attenuates exerciseinduced oxidative stress in rat liver. Male rats were divided into untrained and trained groups. Endurance training consisted of treadmill running at a speed of 2.1 km/h, 1.5 h/day, 5 days a week for 8 weeks. To see the effects of endurance training on acute exhaustive exercise induced oxidative stress, untrained and trained rats were further devided into two groups: animals killed at rest and those killed after acute exhaustive exercise, in which the rats run at 2.1 km/h (10% uphill) until exhaustion. Acute exhaustive exercise increased malondialdehyde level in untrained but not in trained rats. It decreased the activity of glutathione peroxidase and total (enzymatic plus non-enzymatic) superoxide scavenger activity in untrained rats and catalase activity in trained rats. However, it did not affect glutathione S-transferase, glutathione reductase, superoxide dismutase and non-enzymatic superoxide radical scavenger activities in both trained and untrained rats. On the other hand, endurance training decreased glutathione peroxidase and glutathione S-transferase activities. The results suggested that endurance training attenuated exercise-induced oxidative stress in liver, probably by preventing the decreases in glutathione peroxidase and total superoxide scavenger activities during exercise.

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