- Publikační typ
- abstrakt z konference MeSH
Polysaccharides are long carbohydrate molecules of monosaccharide units joined together by glycosidic bonds. These biological polymers have emerged as promising materials for tissue engineering due to their biocompatibility, mostly good availability and tailorable properties. This complex group of biomolecules can be classified using several criteria, such as chemical composition (homo- and heteropolysaccharides), structure (linear and branched), function in the organism (structural, storage and secreted polysaccharides), or source (animals, plants, microorganisms). Polysaccharides most widely used in tissue engineering include starch, cellulose, chitosan, pectins, alginate, agar, dextran, pullulan, gellan, xanthan and glycosaminoglycans. Polysaccharides have been applied for engineering and regeneration of practically all tissues, though mostly at the experimental level. Polysaccharides have been tested for engineering of blood vessels, myocardium, heart valves, bone, articular and tracheal cartilage, intervertebral discs, menisci, skin, liver, skeletal muscle, neural tissue, urinary bladder, and also for encapsulation and delivery of pancreatic islets and ovarian follicles. For these purposes, polysaccharides have been applied in various forms, such as injectable hydrogels or porous and fibrous scaffolds, and often in combination with other natural or synthetic polymers or inorganic nanoparticles. The immune response evoked by polysaccharides is usually mild, and can be reduced by purifying the material or by choosing appropriate crosslinking agents.
- MeSH
- biokompatibilní materiály chemická syntéza MeSH
- buněčné kultury přístrojové vybavení metody MeSH
- celulosa chemie MeSH
- cévní protézy MeSH
- cévy cytologie růst a vývoj MeSH
- endoteliální buňky cytologie fyziologie MeSH
- kultivované buňky MeSH
- lidé MeSH
- protézy - design MeSH
- řízená tkáňová regenerace přístrojové vybavení MeSH
- tkáňové inženýrství přístrojové vybavení metody MeSH
- tkáňové podpůrné struktury * MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
OBJECTIVES: Effect of long-term oral administration of three different concentrations (0.5, 1.0, and 2.0%) of micronized β-1.3/1.6-D-glucan derived from oyster mushroom (Pleurotus ostreatus, Hiratake) on biometrical, haematological, biochemical, and immunological indices of half-year-old rainbow trout (Oncorhynchus mykiss) was assessed in the study. Design: Rainbow trout were feed commercial feed pellets containing β-1.3/1.6-D-glucan in the concentrations of 0.5, 1.0, and 2.0% for 85 days. Biometrical indices consisted in total and standard length, body and liver weight, from which derived somatic parameters such as Fulton´s condition factor and hepatosomatic index were calculated. Haematological parameters were evaluated according to unified methods for haematological examination in fish. Plasma biochemical profile was analysed using biochemical analyser Konelab 20i and Easy Lyte Analyzer. A phagocyte cells metabolic activity (induced chemiluminescence of phagocytes) was determined as an immunological parameter by a microplate luminometric method on Immunotech LM-01T. Results: No clinical signs of behavioral, respiratory, or neurologic distress were observed in rainbow trout. Fish showed normal feeding behavior. As for biometric parameters, no significant changes in total and standard length, body weight, liver weight, as well as in condition factor and hepatosomatic index of experimental and control fish were found. In the course of the study, weight gains in rainbow trout were similar and continuous. Shifts in PCV (p<0.05), haemoglobin (p<0.05), and MCHC (p<0.01) were found within haematological indices. Plasma concentration of glucose, lactate, total protein, cholesterol, calcium, natrium, potassium (all p<0.05), albumins and chlorides (both p<0.01), as well as catalytic activities of ALT and AST (both p<0.05) were changed in the course of the study. A phagocyte cells metabolic activity (luminol-induced chemiluminescence) in rainbow trout was not altered by oyster mushroom β-1.3/1.6-D-glucan administration. Conclusion: After long-term oral administration of three concentrations of micronized β-1.3/1.6-D-glucan derived from oyster mushroom (Pleurotus ostreatus, Hiratake) shifts in haematological and biochemical profiling were found in half-year-old rainbow trout (O. mykiss) in environmental conditions of a commercial rainbow trout fishery. Biometrical indices were not found significantly altered. No specific effect of β-glucan on immune system response of rainbow trout was found in the study. The use of β-glucan in prosperous, clinically healthy aquaculture is still an issue, nevertheless, its use in breedings endangered by stress stimuli, infectious diseases or adverse environmental factors is indisputable.
- MeSH
- adjuvancia imunologická farmakologie MeSH
- beta-glukany farmakologie MeSH
- imunitní systém účinky léků MeSH
- krevní proteiny metabolismus MeSH
- krmivo pro zvířata * MeSH
- Oncorhynchus mykiss krev růst a vývoj imunologie MeSH
- Pleurotus chemie MeSH
- rybářství metody MeSH
- vztah mezi dávkou a účinkem léčiva MeSH
- zvířata MeSH
- Check Tag
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
This review summarizes recent trends in the construction of bioartificial vascular replacements, i.e. hybrid grafts containing synthetic polymeric scaffolds and cells. In these advanced replacements, vascular smooth muscle cells (VSMC) should be considered as a physiological component, although it is known that activation of the migration and proliferation of VSMC plays an important role in the onset and development of vascular diseases, and also in restenosis of currently used vascular grafts. Therefore, in novel bioartificial vascular grafts, VSMCs should be kept in quiescent mature contractile phenotype. This can be achieved by (1) appropriate physical and chemical properties of the material, such as its chemical composition, polarity, wettability, surface roughness and topography, electrical charge and conductivity, functionalization with biomolecules and mechanical properties, (2) appropriate cell culture conditions, such as composition of cell culture media and dynamic load, namely cyclic strain, and (3) the presence of a confluent, mature, semipermeable, non-thrombogenic and non-immunogenic endothelial cell (EC) barrier, covering the luminal surface of the graft and separating the VSMCs from the blood. Both VSMCs and ECs can also be differentiated from stem and progenitor cells of various sources. In the case of degradable scaffolds, the material will gradually be removed by the cells and will be replaced by their own new extracellular matrix. Thus, the material component in advanced blood vessel substitutes acts as a temporary scaffold that promotes regeneration of the damaged vascular tissue.
- MeSH
- buněčná diferenciace MeSH
- cévní protézy MeSH
- endoteliální buňky fyziologie patologie MeSH
- extracelulární matrix metabolismus MeSH
- kmenové buňky metabolismus patologie MeSH
- lidé MeSH
- myocyty hladké svaloviny fyziologie patologie MeSH
- nemoci cév patologie terapie MeSH
- polymery chemie MeSH
- proliferace buněk MeSH
- svaly hladké cévní patologie MeSH
- tkáňové podpůrné struktury MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- přehledy MeSH
We describe a girl with neurofibromatosis type 1 (NF1), mild dysmorphic features, growth and mental retardation, autism, and mosaicism of ring chromosome 17 and chromosome 17 monosomy. The extent of genetic material deleted from the ring chromosome was determined using a combination of classical cytogenetics, fluorescence in situ hybridization (FISH) and multiplex ligation-dependent probe amplification (MLPA) to be 0.6-2.5 Mb on 17p, and up to about 10 Mb on 17q. Based on our observations and on a review of the literature we argue that in addition to a universal "ring syndrome" which is based on ring instability and is less specific for the chromosome involved, various ring chromosomes underlie their own characteristic phenotypes. We propose that the symptoms leading to the diagnosis of NF1 in our patient could be attributed to mosaic hemizygosity for the NF1 gene in some of her somatic cells. A similar mechanism or a direct involvement of respective disease genes in the aberration could possibly influence also the development of autism and other symptoms. We raise a question if the loss of one copy of chromosome 17 from a substantial fraction of somatic cells can have specific consequences also for future risks of the patient, for example, due to the mosaic hemizygosity for the BRCA1 and TP53 genes. (c) 2006 Wiley-Liss, Inc.
- MeSH
- autistická porucha diagnóza genetika komplikace MeSH
- dítě MeSH
- financování organizované MeSH
- hybridizace in situ fluorescenční MeSH
- kruhové chromozomy MeSH
- lidé MeSH
- lidské chromozomy, pár 17 genetika MeSH
- mozaicismus MeSH
- neurofibromatóza 1 diagnóza genetika komplikace MeSH
- Check Tag
- dítě MeSH
- lidé MeSH
- ženské pohlaví MeSH
- Publikační typ
- kazuistiky MeSH
Jedním z nejzávažnějších syndromů s hereditární dispozicí k nádorovým onemocněním je Li-Fraumeni syndrom. Asi 75 % pacientů mají detekovatelnou mutaci v genu TP53. Tento gen je důležitý pro regulaci buněčného cyklu a apoptózy a jeho mutace způsobují vysoké riziko leukémií, nádorů CNS, sarkomů, adrenokortikálních nádorů i časných nádorů prsu. Mohou se však objevit jakékoliv typy nádorů. Riziko nádorového onemocnění je 50% do věku 30 let, 90% do věku 70 let. V našem souboru pacientů s potvrzeným syndromem jsou tři probandky, kde většina nádorových onemocnění se vyskytla v dospělém věku, bez podrobně odebrané rodinné anamnézy mohly připomínat jiné dědičné syndromy s výskytem nádorů prsu nebo kolorekta. Kasuistiky upozorňují na nutnost zhodnocení anamnestických údajů při řešení individuálních případů.
Li-Fraumeni syndrome is one of the most severe hereditary cancer syndromes. In about 75 % of patients a germline mutation in the TP53 gene can be detected. This gene is important for the regulation of cell cycle and apoptosis. The germline mutation causes a high risk of leukaemia, brain tumours, sarcomas, adrenocortical tumours and also early-onset breast cancer. Any type of cancer may occur in this syndrome. The risk of neoplastic disease is 50% until 30 years, 90% until 70 years of age. In our series of patients with this syndrome there are three women with the occurrence of a tumour in adult age. Their cases may resemble other cancer predisposing syndromes of breast and colorectal cancer. The evaluation of family history is very important for the diagnosis of individual cases.
- MeSH
- anamnéza metody MeSH
- dědičné nádorové syndromy diagnóza etiologie genetika MeSH
- dospělí MeSH
- financování organizované MeSH
- genetická predispozice k nemoci genetika prevence a kontrola MeSH
- genetické poradenství metody organizace a řízení trendy MeSH
- geny p53 genetika MeSH
- lékařská onkologie metody trendy MeSH
- lidé MeSH
- Liův-Fraumeniho syndrom diagnóza etiologie genetika MeSH
- mladiství MeSH
- nádorový supresorový protein p53 diagnostické užití genetika izolace a purifikace MeSH
- plošný screening metody využití MeSH
- zárodečné mutace genetika MeSH
- Check Tag
- dospělí MeSH
- lidé MeSH
- mladiství MeSH
- ženské pohlaví MeSH
- Publikační typ
- kazuistiky MeSH
In search of potential prognostic markers, we analyzed a large series of tissues of Barrett's esophagus and samples of adenocarcinomas arising in the terrain of Barrett's esophagus for TP53 gene mutations by direct sequencing of exons 5 to 9 of the TP53 gene. While 9 of 21 adenocarcinomas tested (42.9%) contained a TP53 mutation, none of 24 samples from Barrett's esophagus were mutated. This observation suggests that TP53 gene mutation may be a relatively late event in the progression from nondysplastic Barrett's esophagus to adenocarcinoma of esophagus. Therefore, TP53 gene mutations alone are not likely to represent a widely useful prognostic marker of the risk of progression to malignancy, at least not in Barrett's esophagus without dysplasia.
- MeSH
- adenokarcinom genetika patologie MeSH
- Barrettův syndrom genetika patologie MeSH
- biopsie MeSH
- DNA genetika MeSH
- dospělí MeSH
- exony MeSH
- financování organizované MeSH
- genetické markery MeSH
- geny p53 genetika MeSH
- lidé středního věku MeSH
- lidé MeSH
- mutace MeSH
- nádory jícnu genetika patologie MeSH
- polymerázová řetězová reakce MeSH
- progrese nemoci MeSH
- retrospektivní studie MeSH
- rizikové faktory MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- srovnávací studie MeSH
Barrettův jícen (BJ) je komplikací dlouholeté těžké refluxní choroby jícnu. Je charakterizován přítomností metaplastického epitelu, který obsahuje pohárkové buňky místo normálního dlaždicového epitelu jícnu. Hlavním klinickým aspektem BJ je zvýšené riziko vzniku adenokarcinomu jícnu. Předpokládá se progrese intestinální metaplazie přes různé stupně dysplazie až do stadia invazivního karcinomu. Predikce rizika progrese BJ je obtížná, a proto se autoři snaží najít některé prognostické markery, které by umožnily zlepšit jak diagnostiku a léčbu, tak prognózu pacientů s tímto onemocněním. Za sledované období 18 měsíců (od ledna 2002) autoři vyšetřili 35 pacientů s diagnózou BJ. U těchto pacientů byl aplikován standardní diagnosticko-terapeutický protokol, který zahrnoval endoskopické kontroly s využitím chromodiagnostiky a sekvenční biopsie s hodnocením histologického nálezu jedním zkušeným patologem, 24hodinové pH-metrie a RTG jícnu. Současně byl proveden odběr vzorku tkáně na genetické vyšetření (mutace genu TP53 v oblasti 5–9 exonu). Pacienti byli rozděleni dle stadia onemocnění, resp. stupně dysplazie a podle toho léčeni. Pacienti s BJ bez dysplazie (11 pacientů, tj. 46 %) nebo s nízkým stupněm dysplazie (LGD – 1 pacient, 4 %) byli ošetřeni provedením antirefluxní plastiky; následně při přetrvávání či progresi nálezu BJ byli indikováni k endoskopické mukózektomii. U 2 pacientů došlo po antirefluxní operaci k regresi histologického nálezu. Naopak u 1 pacientky s krátkým jícnem, u které jako jediné byla provedena klasická fundoplikace z laparotomie, došlo k selhání fundoplikace s progresí nálezu BJ do stadia LGD. U jednoho pacienta (4 %) autoři nalezli BJ s vysokým stupněm dysplazie (HGD) a v 11 případech (46 %) již adenokarcinom v BJ. Tito pacienti byli indikováni k resekci jícnu s náhradou žaludkem, event. tračníkem. U pacienta s HGD se po resekci jícnu v definitivním histologickém vyšetření nalezl již karcinom. Tři pacienti s inoperabilním tumorem byli ošetřeni paliativně – zavedením stentu. Mutace genu TP53 byly nalezeny pouze ve stadiu adenokarcinomu v BJ, a to v 36,4 %. Mutace nebyla nalezena ani u jednoho pacienta bez karcinomu v BJ. To znamená, že podle těchto výsledků se tato mutace nedá (jako samostatný faktor) považovat za časný prognostický faktor.
Barrett's esophagus (BE) is a complication of long lasting severe esophageal reflux disease. It is characterised by metaplastic epithelium which contains goblet cells instead of normal squamous esophageal epithelium. The main clinical importance of BE is its high risk of esophageal adenocarcinoma.The progression of intestinal metaplasia through different grade of dysplasia until invasive carcinoma is supposed. The prediction of the risk of progress of BE is difficult and therefore the authors have been trying to find any prognostic markers to enable the diagnosis, treatment and prognosis of these patients. During followed-up period of l8 months (from January 2002) 35 patients with BE were examined. In these patients a standard diagnostic-therapeutic protocol was used. This protocol involved endoscopy checking including chromoendoscopy and sequential biopsy which was evaluated by the only one experienced pathologist, by 24 hours esophageal pH metry and barium swallov. Coincidentally, the biopsy sample for genetic examination was taken for mutation of TP53 gen in 5–9 exon.The patients were divided according to the state of the disease and/or dysplasia and were managed according to that particular way. BE patients without dysplasia (11 patients = 46%) or with low grade dysplasia (LGD) – 1 patient (4%) were managed by antireflux plastic surgery. When this state progressed the endoscopic mucosectomy was indicated. In 2 patients after antireflux surgery a regression of histologic finding was seen, but in one patient with a short esophagus managed by classical open surgery fundoplication this surgery failed and progression into LGD was demonstrated. In one patient (4%) BE with high grade dysplasia (HGD) and in 11 patients (46%) esophageal adenocarcinoma in BE was recognised.These patient were indicated for esophageal resection and esophagus was replaced by stomac or colon. In a patient with HGD after esophageal resection a carcinoma after final histologic examination has been revealed. Three patients with non-operable tumour was managed by stent replacement. Mutation of the gene TP53 was discovered only in carcinomas in BE (36.4%).This mutation was not seen in any BE patient without carcinoma. According to our results we conclude this mutation cannot serve as a self-factor for early prognosis assesment.
