Akademický stres je pojem relativně nový. Vyplývá z mechanismů stresu obecného, ale váže se ke specifickému prostředí. Týká se tedy, na rozdíl od stresu obecného, jen určité skupiny lidí. Cílem přehledové studie je představit akademický stres a vysvětlit jeho důležitost ve vztahu nejen ke vzdělávání, ale společnosti jako takové, popsat, jakými nástroji je možné akademický stres měřit, a stručně nastínit vývoj těchto nástrojů. Přesto, že se problematika akademického stresu týká nejen studentů, ale i akademických pracovníků, tato přehledová studie se zabývá pouze první skupinou. Zdroje stresu sice mohou být pro obě skupiny zdánlivě stejné (časový stres, tlak na výkon), každá z těchto skupin má však svá specifika, přičemž je tedy zapotřebí použít odlišné nástroje. Záměrem přehledové studie je také seznámit s nejčastějšími zdroji stresu u studentů a představit faktory, které mají na akademický stres vliv.
Academic stress is a relatively new term. This term follows from the mechanical device of the general stress, but this term (academic stress) be connected to specific surroundings. Academic stress is related to the specific group of people. The main goal of this summarizing study is introduce the term academic stress and explain its importance in relation with education and company. This contribution will be described the instruments of measuring of academic stress and we focused this term with the group of students of university, not to the group of academic worker. The sources of stress seemed like the same for both of groups (time stress, pressure to the performance), but each of these groups have their own specifics and we must to used to different instruments. The another intention of this summarizing study is described the most frequent sources of student's academic stress and also we introduce the main factors, which have infuence with the academic stress.
- MeSH
- lidé MeSH
- psychický stres * diagnóza psychologie MeSH
- psychologické testy MeSH
- studenti psychologie MeSH
- studium vysokoškolské MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- práce podpořená grantem MeSH
- přehledy MeSH
Oncogene-evoked replication stress (RS) fuels genomic instability in diverse cancer types. Here we report that BRCA1, traditionally regarded a tumour suppressor, plays an unexpected tumour-promoting role in glioblastoma (GBM), safeguarding a protective response to supraphysiological RS levels. Higher BRCA1 positivity is associated with shorter survival of glioma patients and the abrogation of BRCA1 function in GBM enhances RS, DNA damage (DD) accumulation and impairs tumour growth. Mechanistically, we identify a novel role of BRCA1 as a transcriptional co-activator of RRM2 (catalytic subunit of ribonucleotide reductase), whereby BRCA1-mediated RRM2 expression protects GBM cells from endogenous RS, DD and apoptosis. Notably, we show that treatment with a RRM2 inhibitor triapine reproduces the BRCA1-depletion GBM-repressive phenotypes and sensitizes GBM cells to PARP inhibition. We propose that GBM cells are addicted to the RS-protective role of the BRCA1-RRM2 axis, targeting of which may represent a novel paradigm for therapeutic intervention in GBM.
- MeSH
- analýza přežití MeSH
- glioblastom genetika metabolismus patologie MeSH
- karcinogeneze genetika MeSH
- lidé MeSH
- myši inbrední BALB C MeSH
- myši nahé MeSH
- nádorové buněčné linie MeSH
- nádorové buňky kultivované MeSH
- nádory mozku genetika metabolismus patologie MeSH
- protein BRCA1 genetika metabolismus MeSH
- regulace genové exprese u nádorů * MeSH
- replikace DNA genetika MeSH
- retrospektivní studie MeSH
- ribonukleosiddifosfátreduktasa genetika metabolismus MeSH
- RNA interference MeSH
- transplantace heterologní MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
We report the expression of Snail-1, E-cadherin and claudin-1 by indirect immunohistochemistry in colonic neoplasia. Snail-1 is a zinc finger transcription factor expressed in cells that already have undergone almost complete epithelial-mesenchymal transition (EMT) and have already evaded from the tumor. The main mechanism by which Snail induces EMT is downregulation of E-cadherin, of which expression was shown to be frequently downregulated in many different types of tumors, where it accompanies the invasiveness and metastatic behavior of malignant cells. Moreover, Snail-1 may downregulate the expression of claudin-1, a cell-cell adhesion protein which plays a likely role in progression and dissemination during tumorigenesis. Snail-1 was expressed in both carcinoma and adenoma cells with histologically normal epithelium in the mucosa, adjacent to the tumors, without significant differences, and predominant strong intensity of staining. Statistically significant differences were revealed between normal and tumorous epithelium (p = 0.003) at the subcellular level, where the shift of the protein to the cytoplasm with combined cytoplasmic/nuclear or pure cytoplasmic expression was observed. E-cadherin expression was present in 100% of cases of both adenocarcinomas and adenomas, with prevailing strong membranous immunoreactivity and no differences between protein expression in tumors and normal mucosa. Predominating strong positivity of claudin-1 was detected in tumor cells of adenocarcinomas and adenomas. Marked differences were seen in protein localization, where membranous staining, typical for nontumorous epithelium, changed to combined membranous/cytoplasmic expression in adenocarcinomas (p = 0.0001) and adenomas (0.0002), in which cytoplasmic shift was associated with a higher degree of dysplasia. Furthermore, membranous/cytoplasmic localization was more frequent in the carcinoma group (87%) in comparison with adenomas (51%) (p = 0.0001). We conclude that dystopic subcellular localizations of Snail-1 and claudin-1 may participate in changes of cellular morphology and behavior which might be associated with altered effectory pathways of proteins and thus substantially contribute to the cancer development.
- Publikační typ
- časopisecké články MeSH
Aims. No effective treatment for lung cancer exists currently. One reason for this, is the development of drug resistance,-assumed to be associated with cancer stem cell (CSCs) emergence within the tumour. This pilot study aimed-to identify CSCs in 121 non-small cell lung cancer (NSCLC) patient samples via detection of the expression of stem-cell markers – CD133 and nestin. Material and methods. Archived paraffin blocks of 121 patient samples were prepared as Tissue Microarrays-(TMA). Indirect immunohistochemical staining was used to determine the level of expression of CD133 and nestin.-Double immunofluorescence staining was used to investigate the co-expression of these two markers. To determine-the correlation between expression of nestin and CD133 with the length of asymptomatic period and overall patient-survival we used the Kaplan-Meyer analysis. Results. CD133 expression was detected in 22 (19%), nestin in the epithelium in 74 (66%) and vasculature in-78 (70%) of patients. Co-expression of these two markers was found in 21 (17%) patients in less than 1% of positive-cells without impact on disease free or overall survival. Conclusions. We identified CD133+/nestin+ cells as novel potential markers of lung cancer CSCs.
- MeSH
- CD antigeny MeSH
- cévy metabolismus MeSH
- epitel metabolismus MeSH
- financování organizované MeSH
- glykoproteiny metabolismus MeSH
- lidé MeSH
- nádorové kmenové buňky metabolismus MeSH
- nádory plic krevní zásobení metabolismus MeSH
- nemalobuněčný karcinom plic krevní zásobení metabolismus MeSH
- peptidy metabolismus MeSH
- pilotní projekty MeSH
- proteiny intermediálních filament metabolismus MeSH
- proteiny nervové tkáně metabolismus MeSH
- Check Tag
- lidé MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
