We formulate and characterize a model to describe the dynamics of semiflexible polymers in the presence of activity due to motor proteins attached irreversibly to a substrate, and a transverse pulling force acting on one end of the filament. The stochastic binding-unbinding of the motor proteins and their ability to move along the polymer generate active forces. As the pulling force reaches a threshold value, the polymer eventually desorbs from the substrate. Performing underdamped Langevin dynamics simulation of the polymer, and with stochastic motor activity, we obtain desorption phase diagrams. The correlation time for fluctuations in the desorbed fraction increases as one approaches complete desorption, captured quantitatively by a power law spectral density. We present theoretical analysis of the phase diagram using mean field approximations in the weakly bending limit of the polymer and performing linear stability analysis. This predicts an increase in the desorption force with the polymer bending rigidity, active velocity and processivity of the motor proteins to capture the main features of the simulation results.
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http://dx.doi.org/10.1039/c5sm02574e | DOI Listing |
Exp Ther Med
March 2025
Department of Neurosurgery, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang Uygur Autonomous Region 830000, P.R. China.
Spinal cord injury (SCI) is a severe condition that often leads to permanent functional impairments. The current treatment options are limited and there is a need for more effective treatments. Human umbilical cord mesenchymal stem cells (hUCMSCs) have shown promise in promoting neuroregeneration and modulating immune response.
View Article and Find Full Text PDFBMC Res Notes
January 2025
Department of Anatomy and Neuroscience, Institute of Medicine, University of Tsukuba, 1-1- 1, Tennodai, Tsukuba, Ibaraki, 305-8577, Japan.
Objective: Reactivity of microglia, the resident cells of the brain, underlies innate immune mechanisms (e.g., injury repair), and disruption of microglial reactivity has been shown to facilitate psychiatric disorder dysfunctions.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Orthopaedic Surgery, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-Ku, Tokyo, 160-8582, Japan.
While silk fibroin (SF) obtained from silkworm cocoons is expected to become a next-generation natural polymer, a fabrication method for SF-based artificial nerve conduits (SFCs) has not yet been established. Here, we report a bioresorbable SFC, fabricated using a novel freeze-thaw process, which ensures biosafety by avoiding any harmful chemical additives. The SFC demonstrated favorable biocompatibility (high hydrophilicity and porosity with a water content of > 90%), structural stability (stiffness, toughness, and elasticity), and biodegradability, making it an ideal candidate for nerve regeneration.
View Article and Find Full Text PDFExp Neurol
January 2025
Guangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Affiliated Hospital of Guangdong Medical University, Zhanjiang 524000, China; The Marine Biomedical Research Institute of Guangdong, School of Ocean and Tropical Medicine, Guangdong Medical University, Zhanjiang 524000, China. Electronic address:
The 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model remains the most extensively utilized animal model for Parkinson's disease (PD). Treatment regimens are classified into three categories: acute, subacute, and chronic. Among these, the MPTP with probenecid (MPTP/p)-induced chronic mouse model is favored for its capacity to sustain long-term striatal dopamine depletion, though the resultant behavioral, biochemical, and molecular alterations require further validation.
View Article and Find Full Text PDFBiochem Biophys Res Commun
January 2025
Section of Neuromedical Science, Institute of Natural Medicine, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan.
Motor dysfunction in various diseases and aging is often accompanied by skeletal muscle atrophy and reduced axonal projections from motor neurons to the skeletal muscles. While several studies have investigated the correlations and molecular mechanisms between muscle atrophy and motor neuron denervation to explain the pathology of motor diseases, it remains unclear whether skeletal muscle atrophy directly causes axonal denervation of motor neurons. Here, we used a casts-attached mouse model which represents muscle atrophy and motor dysfunction in the hindlimbs to explore how skeletal muscle atrophy affects motor neuronal axon projections.
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