WorldCat Identities

Paluch, E.

Overview
Works: 6 works in 6 publications in 1 language and 7 library holdings
Genres: Academic theses 
Roles: Author
Publication Timeline
.
Most widely held works by E Paluch
Prevention of biofilm formation by quorum quenching by E Paluch( )

1 edition published in 2020 in English and held by 2 WorldCat member libraries worldwide

Biofilm prevention by dicephalic cationic surfactants and their interactions with DNA( )

1 edition published in 2016 in English and held by 1 WorldCat member library worldwide

Abstract: Aims: The studies were aimed to contribute to the elucidation of the relationships between structure of the double-headed cationic surfactants- N, N -bis[3, 3′-(dimethylamine)- propyl]alkylamide dihydrochlorides and N, N -bis[3, 3′-(trimethylammonio)propyl]alkylamide dibromides (alkyl: n -C9 H19, n -C11 H23, n -C13 H27, n -C15 H31 ) and their antibacterial and biofilm preventing activity. Methods and Results: The minimal inhibitory and bactericidal concentrations (MIC and MBC) of dicephalic surfactants against Staphylococcus epidermidis and Pseudomonas aeruginosa were tested using standard methods. Pseudomonas aeruginosa was resistant to studied compounds but MBC values against Staph. epidermidis reached 0·48-0·01 mmol l −1 . The influence of dicephalic surfactants on bacterial biofilm and adhesion to the various surfaces was investigated with crystal violet staining or colony counting. The reduction in bacterial adhesion was observed, especially in the case of glass and stainless steel. The condensation of the DNA was shown in the ethidium bromide intercalation assay. Conclusions: Dicephalic surfactants exhibited antibacterial activity against Staph. epidermidis . The activity of studied compounds depended on the hydrocarbon chain length and the counterion. Surfactants deposited on different materials reduced Staph. epidermidis adhesion, dependently on the surfactant structure and the substratum. Dicephalic surfactants showed the ability of DNA compaction. Significance and Impact of the Study: This study points the possibility of application of dicephalic surfactants as the surface-coating agents to prevent biofilm formation. These compounds efficiently condensed DNA and are potential candidates for further studies towards the transfection
Investigating how mechanical perturbation and tissue architecture affect cell behaviours in pseudostratified epithelia of Drosophila melanogaster by Natalie Jayne Kirkland( )

1 edition published in 2019 in English and held by 1 WorldCat member library worldwide

It is increasingly evident that mechanical forces play a vital role in regulating tissue development and homeostasis. During development, epithelia undergo complex morphogenesis, shaping organs by generating and responding to forces. The shape, organisation and numbers of epithelial cells are essential for overall tissue morphology. Furthermore, mature epithelia are continually subjected to stresses that may disrupt organisation of an organ. These epithelia must therefore respond to mechanical forces to maintain tissue integrity. I have used the pseudostratified epithelium (PSE) of the Drosophila wing disc to study the role of mechanical forces in regulating growth and form. PSE are found in organ precursors of many organisms due to their ability to confine the cell density required for morphogenesis. PSE tightly regulate the movement of nuclei to the apical surface prior to mitosis. This process is termed interkinetic nuclear migration (IKNM) and is essential for tissue organisation. In this thesis, I present potential mechanical regulation of IKNM dynamics through developmental increases in cell density. Such regulation may be important for regulating tissue growth. I find a role for the force generating machinery and lateral cell-cell adhesions in driving nuclear movement. These molecular effectors have differential effects on IKNM through development, suggesting that the dependency on these effectors changes in line with tissue architecture. In the second part of this thesis, I characterise a stretch-sensitive polarisation of Myosin that is downstream of Rho-mediated actin polymerisation, via Diaphanous. Cortical actomyosin is enriched at stretched junctions, in order to resist cell shape deformations and maintain epithelial integrity. I find that upon sustained stretch, actin remodelling is vital to stabilise new cell shapes. This likely enables cells to endure forces generated during morphogenesis, and subsequently stabilise new tissue structures. Overall, these findings exemplify the ability of epithelia to respond to the mechanical environment to regulate organ development
Characterization of Hsp70 proteins in bovine leukocytes induced by the temperature 41ºC( )

1 edition published in 2009 in English and held by 1 WorldCat member library worldwide

Mechanics and Architecture of the Cellular Actomyosin Cortex by Davide Ariberto Domenico Cassani( )

1 edition published in 2019 in English and held by 1 WorldCat member library worldwide

Cell shape changes are key to cell physiology and underlie fundamental processes such as cell migration, cell division and tissue morphogenesis. Cell shape changes are precisely controlled by cell surface mechanics. One of the main determinant of cell surface mechanics is the actomyosin cortex, a thin network of actin, myosin and actin associated proteins underlying the plasma membrane. Cortex mechanical properties are not determined only by the cortical network composition but also by its nano-scale architecture. Although previous studies have shown a relationship between cortex organization and mechanics, which aspects of cortex architecture contribute to the regulation of cell surface mechanics remain largely unknown. This gap in understanding is mostly due to the small dimensions of the cortex, with a thickness close to the diffraction limit of light microscopy, which makes the investigation of cortical nanoscale organization challenging. In my PhD, I investigated cortex nano-scale organization and asked how cortex architecture affects cortex mechanics. In order to assess cortex mechanics, I established an AFM-based assay to measure cell cortex tension. By combining AFM measurements with an analysis on cortex thickness and targeted protein depletion, I demonstrated that cortical network organization directly affects cortex tension. I then further explored cortical organization focusing on nano-scale architecture. Due to the high density of the cortex, previous techniques, including super-resolution imaging, had failed to unveil actin filament organization. To assess this, I established a method to image actin filaments in the cortex using cryo electron tomography. I used isolated cellular blebs, which have been shown to repolymerise a cortex similar to that of intact cells and have dimensions compatible with cryo electron tomography. Actin cortex organization in blebs was analyzed using custom-made software and key parameters of cortical architecture were extracted. My investigation on cortex nano-scale architecture provides, to my knowledge, the first quantification of cortical actin organization and brings new insights into how cortex microscopic properties regulate the mesoscopic properties of cells
Plasma membrane and cell surface mechanics in embryonic stem cells by Henry De Belly( )

1 edition published in 2020 in English and held by 1 WorldCat member library worldwide

Changes in cell shape frequently accompany cell fate transitions. Cell shape changes are regulated by cell surface mechanics. One of the main determinants of cell surface mechanics is membrane tension, which is regulated by the interaction between the plasma membrane and the cytoskeleton. Yet how mechanics, and in particular membrane tension, affects the regulatory pathways controlling cell fate is poorly understood. In my PhD, I investigated the role of cell surface mechanics in regulating cell fate transition in early development. In order, to probe the interplay between shape, mechanics and fate, I used mouse embryonic stem (ES) cells, which spread as they undergo early differentiation. In order to asses cell surface mechanical changes during exit form naiIÌ#x80;Ë#x86;ve pluripotency, I helped establish a membrane pulling assay using an optical tweezer. Using this assay, I found that cell spreading during exit from naiIÌ#x80;Ë#x86;ve pluripotency is regulated by a decrease in plasma membrane tension. Higher tension appears to be due to higher expression and activity of proteins regulating membrane-to-cortex attachment, such as Ezrin-Radixin- Moesin. Next I demonstrated using Ezrin mutants that preventing this decrease in membrane tension obstructs early differentiation of ES cells. I confirmed these results using micropatterning to physically prevent the cells from changing their shape and membrane tension. I next investigated which membrane tension-mediated mechanosensitive pathway could explain these results. I found that decrease in membrane tension results in an increase in endocytosis which is a major regulator of signalling events. Specifically, I found that if cell membrane tension is not decreased, endocytosis of FGF signalling components, which direct exit from the ES cell state, is significantly inhibited. This results in defects in exiting naiIÌ#x80;Ë#x86;ve pluripotency as the ERK pathway requires endocytosis for full activation. Strikingly, the early differentiation defects I observed can be rescued by increasing Rab5a-facilitated endocytosis. Thus, I show that a mechanically-triggered increase in endocytosis regulates fate transitions. My findings are of fundamental importance for understanding how cell mechanics regulates biochemical signaling during cell fate changes
 
Audience Level
0
Audience Level
1
  General Special  
Audience level: 0.89 (from 0.79 for Prevention ... to 0.99 for Characteri ...)

Languages