Morphine belongs among the most commonly used opioids in medical practice due to its strong analgesic effects. However, sustained administration of morphine leads to the development of tolerance and dependence and may cause long-lasting alterations in nervous tissue. Although proteomic approaches enabled to reveal changes in multiple gene expression in the brain as a consequence of morphine treatment, there is lack of information about the effect of this drug on heart tissue. Here we studied the effect of 10-day morphine exposure and subsequent drug withdrawal (3 or 6 days) on the rat heart proteome. Using the iTRAQ technique, we identified 541 proteins in the cytosol, 595 proteins in the plasma membrane-enriched fraction and 538 proteins in the mitochondria-enriched fraction derived from the left ventricles. Altogether, the expression levels of 237 proteins were altered by morphine treatment or withdrawal. The majority of changes (58 proteins) occurred in the cytosol after a 3-day abstinence period. Significant alterations were found in the expression of heat shock proteins (HSP27, α-B crystallin, HSP70, HSP10 and HSP60), whose levels were markedly up-regulated after morphine treatment or withdrawal. Besides that morphine exposure up-regulated MAPK p38 (isoform CRA_b) which is a well-known up-stream mediator of phosphorylation and activation of HSP27 and α-B crystallin. Whereas there were no alterations in the levels of proteins involved in oxidative stress, several changes were determined in the levels of pro- and anti-apoptotic proteins. These data provide a complex view on quantitative changes in the cardiac proteome induced by morphine treatment or withdrawal and demonstrate great sensitivity of this organ to morphine.
- MeSH
- abstinenční syndrom metabolismus MeSH
- chaperon hsp60 metabolismus MeSH
- chaperonin 10 metabolismus MeSH
- krysa rodu rattus MeSH
- krystaliny metabolismus MeSH
- morfin farmakologie MeSH
- myokard metabolismus MeSH
- potkani Wistar MeSH
- proteiny tepelného šoku HSP27 metabolismus MeSH
- proteiny tepelného šoku HSP70 metabolismus MeSH
- proteom účinky léků MeSH
- závislost na morfiu MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Out of the twenty-one A. hydrophila complex isolates obtained during a routine examination of human diarrhoeal faeces, two A. hydrophila subsp. dhakensis isolates (P1097 = CCM 7329 and P1165) were successfully identified by ribotyping. The correct taxonomic position of the A. hydrophila subsp. dhakensis CCM 7329 was verified by cpn60 sequencing (GeneBank accession number HM536193). The remaining A. hydrophila complex isolates were identified as A. hydrophila subsp. hydrophila. The ability of biochemical tests and fatty acid methyl ester analysis to reliably discern both A. hydrophila subsp. dhakensis and A. hydrophila subsp. hydrophila was limited. In contrast to the A. hydrophila subsp. hydrophila, the faecal isolates of A. hydrophila subsp. dhakensis did not produce acid from arbutin. When compared in a two-dimensional plot, the A. hydrophila subsp. dhakensis faecal isolates contained higher amounts of the two minor fatty acids C(13:0) and C(17:1) ω8c than the A. hydrophila subsp. hydrophila reference strain. This is the first detected occurrence of the less frequent A. hydrophila subsp. dhakensis in our region and ribotyping was proved as a suitable method for the identification of A. hydrophila subsp. dhakensis.
- MeSH
- Aeromonas hydrophila klasifikace genetika izolace a purifikace MeSH
- bakteriální proteiny genetika MeSH
- chaperonin 10 genetika MeSH
- feces mikrobiologie MeSH
- fenotyp MeSH
- fylogeneze MeSH
- gramnegativní bakteriální infekce epidemiologie mikrobiologie MeSH
- lidé MeSH
- mastné kyseliny analýza MeSH
- molekulární sekvence - údaje MeSH
- polymerázová řetězová reakce MeSH
- průjem epidemiologie mikrobiologie MeSH
- ribotypizace MeSH
- sekvenční analýza DNA MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Geografické názvy
- Česká republika MeSH
Cíl studie: Popis nových biomarkerů karcinomu endometria s využitím proteomických technik. Typ studie: Přehledový článek. Název a sídlo pracoviště: Lékařská fakulta Hradec Králové, Univerzita Karlova Praha. Porodnická a gynekologická klinika FN Hradec Králové. Metodika: Shrnutí literárních údajů o nových biomarkerech karcinomu endometria za využití proteomického přístupu. Závěr: Práce sumarizuje výsledky klinických a vědeckých prací zaměřených na biomarkery karcinomu endometria.
Objective: The purpose of this study was to focuse on recent developments on the evolving field of biomarker discovery and validation techniques using proteomics platforms for endometrial carcinoma. Design: Review. Setting: Department of Obstetrics and Gynecology Medical Faculty Charles University Hradec Kralove. Methods: The last decade has seen major changes in the technologies used to identify markers for diagnosing endometrial carcinoma. Currently the major developments were made in proteomics area. This new technology hold significant promise in identifying more robust markers for endometrial carcinoma. Conclusion: The present review summarizes the results of clinical and experimental research on biomarkers of endometrial carcinoma.
- Klíčová slova
- karcinom endometria, biomarker,
- MeSH
- chaperonin 10 MeSH
- cyklofilin A MeSH
- gelsolin MeSH
- klusterin MeSH
- mucin 5B MeSH
- nádorové biomarkery MeSH
- nádorové proteiny MeSH
- nádory endometria diagnóza MeSH
- proteiny vázající mastné kyseliny MeSH
- proteomika metody MeSH
- pyruvátkinasa MeSH
- receptory polymerů imunoglobulinů MeSH
- sekreční inhibitory proteinas MeSH
- spektrometrie hmotnostní - ionizace laserem za účasti matrice metody využití MeSH
- Publikační typ
- přehledy MeSH
Medium-chain acyl-CoA dehydrogenase (MCAD) deficiency is the most commonly recognized defect of mitochondrial beta-oxidation. It is potentially fatal, but shows a wide clinical spectrum. The aim of the present study was to investigate whether any correlation exists between MCAD genotype and disease phenotype. We determined the prevalence of the 14 known and seven previously unknown non-G985 mutations in 52 families with MCAD deficiency not caused by homozygosity for the prevalent G985 mutation. This showed that none of the non-G985 mutations are prevalent, and led to the identification of both disease-causing mutations in 14 families in whom both mutations had not previously been reported. We then evaluated the severity of the mutations identified in these 14 families. Using expression of mutant MCAD in Escherichia coli with or without co-overexpression of the molecular chaperonins GroESL we showed that five of the missense mutations affect the folding and/or stability of the protein, and that the residual enzyme activity of some of them could be modulated to a different extent depending on the amounts of available chaperonins. Thus, some of the missense mutations may result in relatively high levels of residual enzyme activity, whereas the mutations leading to premature stop codons will result in no residual enzyme activity. By correlating the observed types of mutations identified to the clinical/biochemical data in the 14 patients in whom we identified both disease-causing mutations, we show that a genotype/phenotype correlation in MCAD deficiency is not straightforward. Different mutations may contribute with different susceptibilities for disease precipitation, when the patient is subjected to metabolic stress, but other genetic and environmental factors may play an equally important role.
- MeSH
- acyl-CoA-dehydrogenasa MeSH
- acyl-CoA-dehydrogenasy * genetika metabolismus nedostatek MeSH
- aktivace enzymů MeSH
- alely MeSH
- chaperon hsp60 genetika metabolismus MeSH
- chaperonin 10 genetika metabolismus MeSH
- dítě MeSH
- Escherichia coli genetika MeSH
- exony MeSH
- fenotyp MeSH
- heterozygot * MeSH
- kojenec MeSH
- lidé MeSH
- mladiství MeSH
- mutace * MeSH
- novorozenec MeSH
- polymerázová řetězová reakce MeSH
- předškolní dítě MeSH
- rekombinantní proteiny genetika metabolismus MeSH
- restrikční mapování MeSH
- rodokmen MeSH
- sekvenční analýza DNA MeSH
- sekvenční delece MeSH
- teplota MeSH
- western blotting MeSH
- Check Tag
- dítě MeSH
- kojenec MeSH
- lidé MeSH
- mladiství MeSH
- mužské pohlaví MeSH
- novorozenec MeSH
- předškolní dítě MeSH
- ženské pohlaví MeSH
