scholarly journals Adhesion Forces Reduction by Oscillation and Its Application to Micro Manipulation

10.5772/10304 ◽  
2010 ◽  
Author(s):  
Tetsoyu Watanabe ◽  
ZhongWei Jiang
Keyword(s):  
Adhesion Forces

scholarly journals Bond Strengthening in Oral Bacterial Adhesion to Salivary Conditioning Films

2008 ◽  
Vol 74 (17) ◽  
pp. 5511-5515 ◽  
Author(s):  
Henny C. van der Mei ◽  
Minie Rustema-Abbing ◽  
Joop de Vries ◽  
Henk J. Busscher
Keyword(s):  
Bacterial Adhesion ◽  
Biofilm Formation ◽  
Specific Interactions ◽  
Adhesion Forces ◽  
Bacterial Strains ◽  
Bacterial Interactions ◽  
Initial Adhesion ◽  
Conditioning Film ◽  
Interacting Surfaces ◽  
Conditioning Films

ABSTRACT Transition from reversible to irreversible bacterial adhesion is a highly relevant but poorly understood step in initial biofilm formation. We hypothesize that in oral biofilm formation, irreversible adhesion is caused by bond strengthening due to specific bacterial interactions with salivary conditioning films. Here, we compared the initial adhesion of six oral bacterial strains to salivary conditioning films with their adhesion to a bovine serum albumin (BSA) coating and related their adhesion to the strengthening of the binding forces measured with bacteria-coated atomic force microscopy cantilevers. All strains adhered in higher numbers to salivary conditioning films than to BSA coatings, and specific bacterial interactions with salivary conditioning films were accompanied by stronger initial adhesion forces. Bond strengthening occurred on a time scale of several tens of seconds and was slower for actinomyces than for streptococci. Nonspecific interactions between bacteria and BSA coatings strengthened twofold faster than their specific interactions with salivary conditioning films, likely because specific interactions require a closer approach of interacting surfaces with the removal of interfacial water and a more extensive rearrangement of surface structures. After bond strengthening, bacterial adhesion forces with a salivary conditioning film remained stronger than those with BSA coatings.

scholarly journals Actin cytoskeleton deregulation confers midostaurin resistance in FLT3-mutant acute myeloid leukemia

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Andoni Garitano-Trojaola ◽  
Ana Sancho ◽  
Ralph Götz ◽  
Patrick Eiring ◽  
Susanne Walz ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Actin Cytoskeleton ◽  
Myeloid Leukemia ◽  
Actin Polymerization ◽  
Cell Stiffness ◽  
Adhesion Forces ◽  
Frequent Mutations ◽  
New Perspective ◽  
The Impact ◽  
Acute Myeloid

AbstractThe presence of FMS-like tyrosine kinase 3-internal tandem duplication (FLT3-ITD) is one of the most frequent mutations in acute myeloid leukemia (AML) and is associated with an unfavorable prognosis. FLT3 inhibitors, such as midostaurin, are used clinically but fail to entirely eradicate FLT3-ITD + AML. This study introduces a new perspective and highlights the impact of RAC1-dependent actin cytoskeleton remodeling on resistance to midostaurin in AML. RAC1 hyperactivation leads resistance via hyperphosphorylation of the positive regulator of actin polymerization N-WASP and antiapoptotic BCL-2. RAC1/N-WASP, through ARP2/3 complex activation, increases the number of actin filaments, cell stiffness and adhesion forces to mesenchymal stromal cells (MSCs) being identified as a biomarker of resistance. Midostaurin resistance can be overcome by a combination of midostaruin, the BCL-2 inhibitor venetoclax and the RAC1 inhibitor Eht1864 in midostaurin-resistant AML cell lines and primary samples, providing the first evidence of a potential new treatment approach to eradicate FLT3-ITD + AML.

Intermolecular forces in biology

2001 ◽  
Vol 34 (2) ◽  
pp. 105-267 ◽  
Author(s):  
Deborah Leckband ◽  
Jacob Israelachvili
Keyword(s):  
Hydrophobic Interactions ◽  
Intermolecular Forces ◽  
Biological Molecules ◽  
Biological Macromolecules ◽  
Chemical Transformations ◽  
Adhesion Forces ◽  
Multiple Bonds ◽  
Membrane Surfaces ◽  
In Series ◽  
Non Equilibrium

0. Abbreviations 1061. Introduction: overview of forces in biology 1081.1 Subtleties of biological forces and interactions 1081.2 Specific and non-specific forces and interactions 1131.3 van der Waals (VDW) forces 1141.4 Electrostatic and ’double-layer‘ forces (DLVO theory) 1221.4.1 Electrostatic and double-layer interactions at very small separation 1261.5 Hydration and hydrophobic forces (structural forces in water) 1311.6 Steric, bridging and depletion forces (polymer-mediated and tethering forces) 1371.7 Thermal fluctuation forces: entropic protrusion and undulation forces 1421.8 Comparison of the magnitudes of the major non-specific forces 1461.9 Bio-recognition 1461.10 Equilibrium and non-equilibrium forces and interactions 1501.10.1 Multiple bonds in parallel 1531.10.2 Multiple bonds in series 1552. Experimental techniques for measuring forces between biological molecules and surfaces 1562.1 Different force-measuring techniques 1562.2 Measuring forces between surfaces 1612.3 Measuring force–distance functions, F(D) 1612.4 Relating the forces between different geometries: the ‘Derjaguin Approximation’ 1622.5 Adhesion forces and energies 1642.5.1 An example of the application of adhesion mechanics of biological adhesion 1662.6 Measuring forces between macroscopic surfaces: the surface forces apparatus (SFA) 1672.7 The atomic force microscope (AFM) and microfiber cantilever (MC) techniques 1732.8 Micropipette aspiration (MPA) and the bioforce probe (BFP) 1772.9 Osmotic stress (OS) and osmotic pressure (OP) techniques 1792.10 Optical trapping and the optical tweezers (OT) 1812.11 Other optical microscopy techniques: TIRM and RICM 1842.12 Shear flow detachment (SFD) measurements 1872.13 Cell locomotion on elastically deformable substrates 1893. Measurements of equilibrium (time-independent) interactions 1913.1 Long-range VDW and electrostatic forces (the two DVLO forces) between biosurfaces 1913.2 Repulsive short-range steric–hydration forces 1973.3 Adhesion forces due to VDW forces and electrostatic complementarity 2003.4 Attractive forces between surfaces due to hydrophobic interactions: membrane adhesion and fusion 2093.4.1 Hydrophobic interactions at the nano- and sub-molecular levels 2113.4.2 Hydrophobic interactions and membrane fusion 2123.5 Attractive depletion forces 2133.6 Solvation (hydration) forces in water: forces associated with water structure 2153.7 Forces between ‘soft-supported’ membranes and proteins 2183.8 Equilibrium energies between biological surfaces 2194. Non-equilibrium and time-dependent interactions: sequential events that evolve in space and time 2214.1 Equilibrium and non-equilibrium time-dependent interactions 2214.2 Adhesion energy hysteresis 2234.3 Dynamic forces between biomolecules and biomolecular aggregates 2264.3.1 Strengths of isolated, noncovalent bonds 2274.3.2 The strengths of isolated bonds depend on the activation energy for unbinding 2294.4 Simulations of forced chemical transformations 2324.5 Forced extensions of biological macromolecules 2354.6 Force-induced versus thermally induced chemical transformations 2394.7 The rupture of bonds in series and in parallel 2424.7.1 Bonds in series 2424.7.2 Bonds in parallel 2444.8 Dynamic interactions between membrane surfaces 2464.8.1 Lateral mobility on membrane surfaces 2464.8.2 Intersurface forces depend on the rate of approach and separation 2494.9 Concluding remarks 2535. Acknowledgements 2556. References 255While the intermolecular forces between biological molecules are no different from those that arise between any other types of molecules, a ‘biological interaction’ is usually very different from a simple chemical reaction or physical change of a system. This is due in part to the higher complexity of biological macromolecules and systems that typically exhibit a hierarchy of self-assembling structures ranging in size from proteins to membranes and cells, to tissues and organs, and finally to whole organisms. Moreover, interactions do not occur in a linear, stepwise fashion, but involve competing interactions, branching pathways, feedback loops, and regulatory mechanisms.

scholarly journals Early Adhesion of Candida albicans onto Dental Acrylic Surfaces

2017 ◽  
Vol 96 (8) ◽  
pp. 917-923 ◽  
Author(s):  
S. Aguayo ◽  
H. Marshall ◽  
J. Pratten ◽  
D. Bradshaw ◽  
J.S. Brown ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Clinical Isolate ◽  
Force Spectroscopy ◽  
Laboratory Strain ◽  
Culture Conditions ◽  
The Body ◽  
Yeast Cells ◽  
Adhesion Forces ◽  
Reliable Technique ◽  
Mother Cells

Denture-associated stomatitis is a common candidal infection that may give rise to painful oral symptoms, as well as be a reservoir for infection at other sites of the body. As poly (methyl methacrylate) (PMMA) remains the main material employed in the fabrication of dentures, the aim of this research was to evaluate the adhesion of Candida albicans cells onto PMMA surfaces by employing an atomic force microscopy (AFM) single-cell force spectroscopy (SCFS) technique. For experiments, tipless AFM cantilevers were functionalized with PMMA microspheres and probed against C. albicans cells immobilized onto biopolymer-coated substrates. Both a laboratory strain and a clinical isolate of C. albicans were used for SCFS experiments. Scanning electron microscopy (SEM) and AFM imaging of C. albicans confirmed the polymorphic behavior of both strains, which was dependent on growth culture conditions. AFM force-spectroscopy results showed that the adhesion of C. albicans to PMMA is morphology dependent, as hyphal tubes had increased adhesion compared with yeast cells ( P < 0.05). C. albicans budding mother cells were found to be nonadherent, which contrasts with the increased adhesion observed in the tube region. Comparison between strains demonstrated increased adhesion forces for a clinical isolate compared with the lab strain. The clinical isolate also had increased survival in blood and reduced sensitivity to complement opsonization, providing additional evidence of strain-dependent differences in Candida-host interactions that may affect virulence. In conclusion, PMMA-modified AFM probes have shown to be a reliable technique to characterize the adhesion of C. albicans to acrylic surfaces.

A Nanoindentation Method for Hydrated Compliant Materials

2011 ◽  
Author(s):  
Donna M. Ebenstein
Keyword(s):  
Mechanical Properties ◽  
Soft Tissues ◽  
Adhesion Forces ◽  
Surface Detection ◽  
Heterogeneous Samples ◽  
Mineralized Tissues ◽  
Fluid Interactions

Nanoindentation is becoming an increasingly popular tool in the biomaterials field due to its ability to measure local mechanical properties in small, irregularly-shaped or heterogeneous samples.1 Although this technique was readily adapted to the study of mineralized tissues, the application of nanoindentation to compliant, hydrated biomaterials such as soft tissues and hydrogels has led to many challenges.1 Three key concerns associated with nanoindentation of compliant, hydrated materials are inaccurate surface detection, errors due to adhesion forces, and fluid interactions with the tip.1–4

scholarly journals Epithelial-Mesenchymal Transition and Metastasis under the Control of Transforming Growth Factor β

2018 ◽  
Vol 19 (11) ◽  
pp. 3672 ◽  
Author(s):  
Yutaro Tsubakihara ◽  
Aristidis Moustakas
Keyword(s):  
Growth Factor ◽  
Tumor Cells ◽  
Transforming Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
Transforming Growth Factor Β ◽  
Basement Membranes ◽  
The Body ◽  
Common Denominator ◽  
Adhesion Forces ◽  
Mesenchymal Transition

Metastasis of tumor cells from primary sites of malignancy to neighboring stromal tissue or distant localities entails in several instances, but not in every case, the epithelial-mesenchymal transition (EMT). EMT weakens the strong adhesion forces between differentiated epithelial cells so that carcinoma cells can achieve solitary or collective motility, which makes the EMT an intuitive mechanism for the initiation of tumor metastasis. EMT initiates after primary oncogenic events lead to secondary secretion of cytokines. The interaction between tumor-secreted cytokines and oncogenic stimuli facilitates EMT progression. A classic case of this mechanism is the cooperation between oncogenic Ras and the transforming growth factor β (TGFβ). The power of TGFβ to mediate EMT during metastasis depends on versatile signaling crosstalk and on the regulation of successive waves of expression of many other cytokines and the progressive remodeling of the extracellular matrix that facilitates motility through basement membranes. Since metastasis involves many organs in the body, whereas EMT affects carcinoma cell differentiation locally, it has frequently been debated whether EMT truly contributes to metastasis. Despite controversies, studies of circulating tumor cells, studies of acquired chemoresistance by metastatic cells, and several (but not all) metastatic animal models, support a link between EMT and metastasis, with TGFβ, often being a common denominator in this link. This article aims at discussing mechanistic cases where TGFβ signaling and EMT facilitate tumor cell dissemination.

Sign in / Sign up

Export Citation Format

Share Document