F.xcept other functions, surface saccharide residues on trematode larvae are supposed either to be the targets of the intermediate (molluscan) and final host immune systems, or to represent candidates for molecular mimicry. Therefore, changes in surface saccharide patterns during the development of the avian schistosome Trichobilharzia szidati were characterized. Whole parasite larval stages and their tissue sections were examined using FITC-conjugated lectins. Marked surface differences were found among larval stages (miracidia, mother sporocysts, daughter sporocysts, cercariae, schistosomula). Staining by some lectins reflected known ultrastructural changes of the outer tegument. Reaction of lectins with cercarial embryos was almost negative. In case of other developmental stages, binding of at least one member from each carbohydrate-specificity group of lectins (Man/Glc-, GIcNAc-, Gal/GalNAc- and Fuc-specific) occurred. One exception is represented by mother and daughter sporocysts which practically failed to react with Fuc-specific lectins. Besides other lectins which recognized larval surfaces, a-L-fucose-specific lectins (LTA, UEA-I) and (GlcNAcfll —>4)„-spccific WGA bound very strong to certain stages. The comparison of mature intrasporocystic cercariae with those emerged from snails brought the indication that some snail glycosylated molecules adhere to the surface of schistosome larvae or that emerged cercariae express some new carbohydrate epitopes under changed environmental conditions. The result partially supports the theory of parasite mimicry/masking strategies and immune evasion in the host.
Resistance to steroid hormones presents a serious problem with respect to their mass use in therapy. It may be caused genetically by mutation of genes involved in hormonal signaling, not only steroid receptors, but also other players in the signaling cascade as co-regulators and other nuclear factors, mediating the hormone-born signal. Another possibility is acquired resistance which may develop under long-term steroid treatment, of which a particular case is down regulation of the receptors. In the review recent knowledge is summarized on the mechanism of main steroid hormone action, pointing to already proven or potential sites causing steroid resistance. We have attempted to address following questions: 1) What does stay behind differences among patients as to their response to the (anti)steroid treatment? 2) Why do various tissues/cells respond differently to the same steroid hormone though they contain the same receptors? 3) Are such differences genetically dependent? The main attention was devoted to glucocorticoids as the most frequently used steroid therapeutics. Further, androgen insensitivity is discussed with a particular attention to acquired resistance to androgen deprivation therapy of prostate cancer. Finally the potential causes are outlined of breast and related cancer(s) resistance to antiestrogen therapy., R. Hampl, K. Vondra., and Obsahuje bibliografii
Intrahepatic cholestasis of pregnancy (ICP) is a disorder of liver function, commonly occurring in the third trimester but sometimes also as soon as the end of the second trimester of pregnancy. Symptoms of this disorder include pruritus, plus abnormal values of bile acids and hepatic transaminases. After birth, symptoms disappear and liver function returns to normal. Though ICP is relatively non-complicated and often symptomatically mild from the point-of-view of the mother, it presents a serious risk to the fetus, making this disease the subject of great interest. The etiology and pathogenesis of ICP is multifactorial and as yet not fully elucidated. Hormonal factors likely play a significant role, along with genetic as well as exogenous factors. Here we summarize the knowledge of changes in steroid hormones and their role in the development of intrahepatic cholestasis of pregnancy. In addition, we consider the role of exogenous factors as possible triggers of steroid hormone changes, the relationship between metabolic steroids and bile acids, as well as the combination of these factors in the development of ICP in predisposed pregnant women., A. Pařízek, M. Dušková, L. Vítek, M. Šrámková, M. Hill, K. Adamcová, P. Šimják, A. Černý, Z. Kordová, H. Vráblíková, B. Boudová, M. Koucký, K. Malíčková, L. Stárka., and Obsahuje bibliografii