Plasticity of cell migration: a multiscale tuning model

Cell migration underlies tissue formation, maintenance, and regeneration as well as pathological conditions such as cancer invasion. Structural and molecular determinants of both tissue environment and cell behavior define whether cells migrate individually (through amoeboid or mesenchymal modes) or collectively. Using a multiparameter tuning model, we describe how dimension, density, stiffness, and orientation of the extracellular matrix together with cell determinants—including cell–cell and cell–matrix adhesion, cytoskeletal polarity and stiffness, and pericellular proteolysis—interdependently control migration mode and efficiency. Motile cells integrate variable inputs to adjust interactions among themselves and with the matrix to dictate the migration mode. The tuning model provides a matrix of parameters that control cell movement as an adaptive and interconvertible process with relevance to different physiological and pathological contexts

Molecular mechanisms of amoeboid invasion of cancer cells

Tumour cell invasion is one of the most critical steps in malignant progression. It includes a broad spectrum of mechanisms, including both individual and collective cell migration, which enables them to spread towards adjacent tissue, and form new metastases. Understanding the mechanisms of cell spreading, and invasion, is crucial for effective anticancer therapy. Two modes of individual migration of tumour cells have been established in a three-dimensional environment. Mesenchymally migrating cells use proteases to cleave collagen bundles, and thus overcome the ECM barriers. Recently described protease-independent amoeboid mode of invasion has been discovered in studies of cancer cells with protease inhibitors. During my PhD study, I have focused on determining the molecular mechanisms involved in amoeboid invasion of tumour cells. We have examined invasive abilities in non-metastatic K2 and highly metastatic A3 rat sarcoma cell lines. We have shown that even though highly metastatic A3 rat sarcoma cells are of mesenchymal origin, they have upregulated Rho/ROCK signalling pathway. Moreover, A3 cells generate actomyosin-based mechanical forces at their leading edges to physically squeeze through the collagen fibrils by adopting an amoeboid phenotype. Amoeboid invasiveness is also less dependent on..

The Phenomenon of black Theater

In my final thesis I focused on the phenomenon of black theatre. I will describe his technical properties, leading of puppets and stage properties, specific acting and black theatre´s effects. I will also try to explain direction´s difficulties of this synthetic theatre, this will be followed by short case history of black theatre. At the and I will be interested in Black light theatre of Jiří Srnec from his beginnings till our days and I will outline the contributton of his black-theatral production

Molecular mechanisms of amoeboid invasion of cancer cells

Tumour cell invasion is one of the most critical steps in malignant progression. It includes a broad spectrum of mechanisms, including both individual and collective cell migration, which enables them to spread towards adjacent tissue, and form new metastases. Understanding the mechanisms of cell spreading, and invasion, is crucial for effective anticancer therapy. Two modes of individual migration of tumour cells have been established in a three-dimensional environment. Mesenchymally migrating cells use proteases to cleave collagen bundles, and thus overcome the ECM barriers. Recently described protease-independent amoeboid mode of invasion has been discovered in studies of cancer cells with protease inhibitors. During my PhD study, I have focused on determining the molecular mechanisms involved in amoeboid invasion of tumour cells. We have examined invasive abilities in non-metastatic K2 and highly metastatic A3 rat sarcoma cell lines. We have shown that even though highly metastatic A3 rat sarcoma cells are of mesenchymal origin, they have upregulated Rho/ROCK signalling pathway. Moreover, A3 cells generate actomyosin-based mechanical forces at their leading edges to physically squeeze through the collagen fibrils by adopting an amoeboid phenotype. Amoeboid invasiveness is also less dependent on..

Enterprise mobile device management

Hlavním cílem bakalářské práce je popsat a zanalyzovat problematiku správy mobilních zařízení - mobilních aplikací, funkcionality a možností řešení v podnicích s ohledem na potřebné zabezpečení. V teoretické části se zabývá popisem jednotlivých dodavatelů, možnostmi správy zařízení jak ve vlastnictví společnosti tak ve vlastnictví jednotlivých zaměstnanců a věnuje se i popisu konkrétního řešení nasazení správy mobilních zařízení ve společnosti. V praktické části je rozanalyzovaná a komentována studie globálního trhu z roku 2014, jako i průzkum českého trhu z roku 2013. Obě studie dodávají kontext vlastnímu průzkumu současného využití správy mobilních zařízení podniků v jednotlivých oblastech, které byly shromážděné telefonickým průzkumem. Výsledky tohoto průzkumu jsou v praktické části přehledně rozebrány, popsány a zanalyzovány.The main goal of the bachelor thesis is to describe and analyze the topic of mobile device management -- mobile applications, functionalities and the possibilities of implementation in the heterogeneous environment of companies, with all of the attached security issues covered. In the first, theoretical part the thesis describes particular vendors, possibilities of the management of mobile devices, both in company and employee ownership. We also describe the actual model of implementation the mobile device management in an actual Czech company. Second part of the thesis consists from the analyzed and commented the global market study, conducted in 2014 as well as the Czech Republic mobile device management market poll from the year 2013. Both of the studies put the original telephonic poll, made for the purpose of this thesis, in wider context. The results of the poll are analyzed and described in a comprehensive way.Hlavným cieľom bakalárskej práce je popísať a zanalyzovať problematiku správy mobilných zariadení -- mobilných aplikácií, funkcionality a možností riešení v podnikoch s ohľadom na potrebné zabezpečenie. V teoretickej časti sa zaoberá popisom jednotlivých dodávateľov, možnosťami správy zariadení vo vlastníctve spoločnosti ako aj vo vlastníctve jednotlivých zamestnancov a venuje sa aj popisu konkrétneho riešenia nasadenia správy mobilných zariadení v spoločnosti. V praktickej časti je rozanalyzovaná a okomentovaná štúdia globálneho trhu z roku 2014, ako aj prieskum českého trhu z roku 2013. Obe štúdie dodávajú kontext vlastnému prieskumu súčasnému využitia správy mobilných zariadení podnikov v jednotlivých oblastiach, ktoré boli zhromaždené telefonickým prieskumom. Výsledky tohto prieskumu sú v praktickej časti prehľadne rozobraté, popísané a zanalyzované

Molekulární mechanismy invasivity u nádorových buněk

IN CZECH Invasivita nádorových buněk je jedním z nejdůležitějších kroků v procesu maligní progrese. Je charakterizovaná širokým spektrem mechanismů, které zahrnují jak individuální, tak kolektivní migrací buněk. Během procesu invasivity se nádorové buňky šíří do okolních tkání, kde zakládají nové metastázy. I proto je pochopení mechanismů buněčné invasivity zásadním krokem k účinné protinádorové terapii. Individuálně migrující buňky vykazují ve 3D prostředí dva způsoby invasivity. Mesenchymalně invadující buňky produkují během své migrace proteázy, které využívají k degradaci kolagenových vláken. Studie srůznými typy nádorových buněk zaměřené na inhibici proteáz poukázaly na nový amoeboidní mechanizmus invasivity buněk, který není závislý na degradací extracelulární matrix pomocí proteáz. Během mé disertační práce jsem se zaměřila na studium molekulárních mechanismů uplatňujících se v amoeboidní invasivitě nádorových buněk. Pro naše experimenty jsme využili potkaní sarkomový model sestávající z parentální nemetastazující linie K2 a od ní odvozené vysoce invasivní linie A3. Ukázali jsme, že i když je vysoce metastatická sarkomová linie A3 buněk mesenchymálního původu, její invasivní vlastnosti jsou závislé na upregulaci Rho / ROCK signální dráhy, která vede ke generování protrusivních sil na...Tumour cell invasion is one of the most critical steps in malignant progression. It includes a broad spectrum of mechanisms, including both individual and collective cell migration, which enables them to spread towards adjacent tissue, and form new metastases. Understanding the mechanisms of cell spreading, and invasion, is crucial for effective anticancer therapy. Two modes of individual migration of tumour cells have been established in a three-dimensional environment. Mesenchymally migrating cells use proteases to cleave collagen bundles, and thus overcome the ECM barriers. Recently described protease-independent amoeboid mode of invasion has been discovered in studies of cancer cells with protease inhibitors. During my PhD study, I have focused on determining the molecular mechanisms involved in amoeboid invasion of tumour cells. We have examined invasive abilities in non-metastatic K2 and highly metastatic A3 rat sarcoma cell lines. We have shown that even though highly metastatic A3 rat sarcoma cells are of mesenchymal origin, they have upregulated Rho/ROCK signalling pathway. Moreover, A3 cells generate actomyosin-based mechanical forces at their leading edges to physically squeeze through the collagen fibrils by adopting an amoeboid phenotype. Amoeboid invasiveness is also less dependent on...Katedra buněčné biologieDepartment of Cell BiologyPřírodovědecká fakultaFaculty of Scienc