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Celem pracy było zbadanie wpływu 3-dniowych diet niskosodowych (0,5 mmol Na+/kg/dobę) o zróżnicowanej zawartości węglowodanów na wysokość progu wentylacyjnego (VT) w porównaniu do efektu diety mieszanej - kontrolnej (2,6 mmol Na+/kg/dobę). Dziewięciu mężczyzn dwukrotnie stosowało 3-dniowe, izokaloryczne diety: 1) dietę niskosodową-wysokowęglowodanową (DNW) (70% WĘG) oraz 2) dietę niskosodową-niskowęglowodanową (DNN) (2,5% WĘG). Przed każdą dietą oraz po jej zakończeniu badani wykonywali test wysiłkowy. W efekcie diet niskosodowych VO2max nie różnił się istotnie, jednak VT po DNN był obniżony (p<0,01). Uzyskane wyniki wskazują, że zmiana wysokości VT w sytuacji ograniczenia spożycia sodu uzależniona jest od ilości węglowodanów w tej diecie.
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Effect of hypothyreosis on the content of ceramides in rat tissues

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Ceramide is the second messenger in the sphingomyelin signalling pathway. A number of extracellular stimuli increase the content of ceramide in the cell. There are some data indicating that the content of ceramide may also be regulated by hormones. The aim of the present study was to examine the effect of hypothyreosis on the content and composition of ceramide in rat tissues. The rats were thyroidectomized and thereafter they received propylthiouracyl in drinking water. The control rats were sham operated. 30 days after thyroidectomy or sham operation the rats were anaesthetized and samples of the liver, white and red vastus lateralis and left ventricle were taken. One set of samples was frozen in liquid nitrogen for analysis of ceramide. Another set of samples was freshly homogenized in chloroform/methanol for further determination of the content of sphingomyelin phosphorous. The content and composition of ceramide-fatty acids was determined by means of gas-liquid chromatography. Twelve ceramides containing different fatty acid residues were identified in both groups. Hypothyreosis reduced the total content of ceramide in each tissue studied: in the heart by 50.9%, in the red vastus by 28.6%, in the white vastus by 29.4% and in the liver by 22%. Concomitantly, the content of individual ceramides was either reduced, stable or even elevated, depending on the tissue. The content of sphingomyelin was elevated in both sections of the vastus lateralis and remained stable in the heart and the liver. The ratio: total content of sphingomyelin to total content of ceramide was elevated in the muscles and remained stable in the liver. This indicates that the reduction in the content of ceramide in the tissues of hypothyroid rats may be a consequence either of a reduction in the formation of ceramide from sphingomyelin, its increased hydrolysis or both. It is concluded that normal thyroid function is needed to maintain the content and composition of ceramide in the tissues.
Cytosolic phospholipase A2 (cPLA2) demonstrates selective affi nity to arachidonic acid (AA) liberation, which is known to be elevated in PD. We indicated that NO/GC/cGMP pathway was upregulated in the primary astrocyte culture treated with MPP+. We investigated if the cGMP/cGMP-dependent protein kinase (PKG) signaling pathway was involved in 1-methyl-4-phenylpyridinium (MPP+)-induced cPLA2 activation of the primary astrocyte culture. We found increased levels of total and phosphorylated cPLA2 and increased AA release in the primary astrocyte culture exposed to MPP+. We used cPLA2-specifi c inhibitors and Ca2+- independent PLA2 (iPLA2), and we found that cPLA2 released more AA after stimulation with MPP+ than iPLA2 and that there was a time-dependent delay of AA release by iPLA2 compared to cPLA2. The PKG inhibitor KT5823 decreased MPP-induced AA release in the primary astrocyte culture. KT5823, in addition to PKC and ERK1/2 inhibitors, decreased cPLA2 activity as well as total and phosphorylated cPLA2 protein levels in the astrocyte treated with MPP+. Dual treatment with PKG and PKC or ERK1/2 inhibitors had the same effect on cPLA2 activity and protein levels. PKG is involved in the enhancement of cPLA2 phosphorylation at Serine-505 and in AA release in the astrocyte exposed to MPP+. Our results indicate that the nNOS/cGMP/ PKG pathway stimulates cPLA2 phosphorylation at Ser-505 by activation of PKC or ERK1/2. These results suggest that activation of cPLA2 by upregulation nNOS/cGMP pathway may play important role in MPP+-induced astrocyte activation, neurotoxicity and oxidative stress in the nigrostriatal system.
The aim of the study was to investigate influence of different sources of knowledge on rural youth’s image of leisure on other continents. The survey was made by means of questioning a group of 108 students of junior high school aged 15–18 years old. Young people evaluated very positively the teaching effectivity of geographics, biology and physical educations in their schools. They also attend in outschool activities connecting with tourism and rest. Most of them claim that they prefere watching television than reading books in order to improving their geographic and touristic knowledge. Several questions of survey were connected to choosing the resting place on different continents. Students pointed on touristic places which are well-known of their landscapes, buildings, resting environment etc. On this basis we conclude that leisure on other countries is mainly influenced by television which provides additional in touristic knowledge.
We investigated if the cGMP/cCGP-dependent protein kinase (PKG) signaling pathway was involved in 1-methyl-4-phenylpyridinium (MPP+)-induced cPLA2 activation of dopaminergic neuronal cells (PC12 cells). We found increased levels of total and phosphorylated cPLA2 and increased AA release in the nigrostriatal system of MPTPinduced parkinsonism mice and in PC12 cells exposed to MPP+. We used cPLA2-specifi c inhibitors and Ca2+-independent PLA2 (iPLA2), and we found that cPLA2 released more AA after stimulation with MPTP/MPP+ than iPLA2 and that there was a time-dependent delay of AA release by iPLA2 compared to cPLA2. The PKG inhibitor KT5823 decreased MPTP-induced AA release in the nigrostriatal pathway. KT5823, in addition to PKC and ERK1/2 inhibitors, decreased cPLA2 activity as well as total and phosphorlyated cPLA2 protein levels in the midbrain and striatum of MPTP-induced parkinsonism mice. Inhibition occurred within 30 minutes and persisted for up to 24 hours. Similar results were also observed in MPP+-treated PC12 cells. Dual treatment with PKG and PKC inhibitors had the same effect on cPLA2 activity and protein levels. PKG is involved in the enhancement of cPLA2 phosphorylation at Serine-505 and in AA release in PC12 cells exposed to MPP+. In PC12 cells, inhibitors of cPLA2 and PKG increased viability and prevented MPP+-induced apoptosis. Our results indicate that the nNOS/cGMP/PKG pathway stimulates cPLA2 phosphorylation at Ser-505 by activation of PKC or ERK1/2. Our results also suggest that upregulation of the nNOS/cGMP pathway observed in experimental models of PD may mediate dopaminergic neuron degeneration and death through activation of cPLA2. This work was supported by MSHE, Scientifi c Network nr. 28/E32/SN-0053/2007
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