Adhesion of polymers and proteins to substrates plays a crucial role in many technological applications and biological processes. A prominent example is the von Willebrand factor (VWF) protein, which is essential in blood clotting as it mediates adhesion of blood platelets to the site of injury at high shear rates. VWF is activated by flow and is able to bind efficiently to damaged vessel walls even under extreme flow-stress conditions; however, its adhesion is reversible when the flow strength is significantly reduced or the flow is ceased. Motivated by the properties and behavior of VWF in flow, we investigate adhesion of shear-activated polymers to a planar wall in flow and whether the adhesion is reversible under flow stasis. The main ingredients of the polymer model are cohesive inter-monomer interactions, a catch bond with the adhesive surface, and the shear activation/deactivation of polymer adhesion correlated with its stretching in flow. The cohesive interactions within the polymer maintain a globular conformation under low shear stresses and allow polymer stretching if a critical shear rate is exceeded, which is directly associated with its activation for adhesion. Our results show that polymer adhesion at high shear rates is significantly stabilized by catch bonds, while at the same time they also permit polymer dissociation from a surface at low or no flow stresses. In addition, the activation/deactivation mechanism for adhesion plays a crucial role in the reversibility of its adhesion. These observations help us better understand the adhesive behavior of VWF in flow and interpret its adhesion malfunctioning in VWF-related diseases.
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http://dx.doi.org/10.1088/1361-648X/aaa4d5 | DOI Listing |
BMC Oral Health
January 2025
Conservative Dentistry Department, Faculty of Dentistry, Cairo University, Cairo, Egypt.
Background: In recent years, there have been suggestions for new restorative strategies that aim to effectively utilize modern adhesive technologies and protect the remaining intact tooth structure. This study was conducted to evaluate the clinical performance of fiber reinforced resin composites in restoring Class II MOD cavities over 18 months.
Methods: Forty-five participants with class II MOD cavities were randomly enrolled.
Commun Biol
January 2025
Division of Immunology, Tulane National Primate Research Center, Tulane University, Covington, LA, USA.
The Bartonella genus of bacteria encompasses ubiquitous species, some of which are pathogenic in humans and animals. Bartonella henselae, the causative agent of Cat Scratch disease, is responsible for a large portion of human Bartonella infections. These bacteria can grow outside of cells, replicate in erythrocytes and invade endothelial and monocytic cells.
View Article and Find Full Text PDFNat Commun
January 2025
Biophysics Graduate Group, University of California, Davis, CA, USA.
P-cadherin, a crucial cell-cell adhesion protein which is overexpressed in numerous malignant cancers, is a popular target for drug delivery antibodies. However, molecular guidelines for engineering antibodies that can be internalized upon binding to P-cadherin are unknown. Here, we use a combination of biophysical, biochemical, and cell biological methods to demonstrate that trapping the P-cadherin extracellular region in an X-dimer adhesive conformation triggers cadherin endocytosis via an outside-in signaling mechanism.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Pharmaceutics, College of Pharmacy, King Saud University, PO Box 2457, Riyadh, 11451, Saudi Arabia.
Prostate cancer presents a major health issue, with its progression influenced by intricate molecular factors. Notably, the interplay between miRNAs and changes in transcriptomic patterns is not fully understood. Our study seeks to bridge this knowledge gap, employing computational techniques to explore how miRNAs and transcriptomic alterations jointly regulate the development of prostate cancer.
View Article and Find Full Text PDFBiochem Genet
January 2025
Department of Physiology, University of Louisville School of Medicine, Louisville, KY, 40202, USA.
Although DNA methyltransferase 1 (DNMT1) and RNA editor ADAR triplications exist in Down syndrome (DS), their specific roles remain unclear. DNMT methylates DNA, yielding S-adenosine homocysteine (SAH), subsequently converted to homocysteine (Hcy) and adenosine by S-adenosine homocysteine (Hcy) hydrolase (SAHH). ADAR converts adenosine to inosine and uric acid.
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