生物医学工程(英文)最新文献

There is increasing evidence from preclinical studies. There is growing evidence from preclinical studies in cell cultures and small organisms that exposure to Electromagnetic Fields (EMFs) produces beneficial biological effects. However, controversy persists due to the absence of a clearly defined mechanism. Classical physics, constrained by the non-ionizing nature of these exposures, cannot account for these effects, which do not involve the breaking of chemical bonds to induce conformational changes in proteins. Emerging studies suggest that these effects are mediated through quantum mechanical phenomena-specifically, quantum tunneling and particle-wave duality-acting on the water surrounding proteins at their interfaces. Furthermore, we present evidence of EMF-induced conformational changes in Intrinsically Disordered Proteins (IDPs), including beta-amyloid, tau, alpha-synuclein, and Heat Shock Factor 1 (HSF1). These findings offer a new framework for understanding EMF bioeffects and open promising avenues for research in biophysics and quantum biology. In this context, we address the challenge of reproducibility by examining how variables such as frequency, intensity, Specific Absorption Rate (SAR), and exposure time windows interact, along with how parameters like polarization, phase, pulse modulation, and scheduling influence outcomes. Experimental data identify specific RF frequencies and SAR levels that activate proteostasis and autophagy in cell cultures and small animal models, with potential applications in human treatments that remain consistent with safety thresholds established by regulatory agencies.

Amphiphilic triblock poloxamer 188 (P188) has demonstrated its therapeutic potential for muscle, cardiac and neurological injuries. While this surfactant is thought to primarily reseal the disrupted cell membrane, the specific mechanisms that mediate the reparative effect of P188 remain to be fully elucidated. Here, we investigated the transport mechanisms of P188 cellular uptake by fluorescently conjugating P188 with the fluorophore, Rhodamine 110 (Rh110). Fluorescent conjugation did not alter the P188 structure as characterized by nuclear magnetic resonance, Fourier Transform infrared spectroscopy, and acid-base titration, and the hydrophobicity was also quantified. In mouse brain endothelial cells, Rh110 alone was unable to accumulate inside the cells, while the P188 + Rh110 was rapidly transported across the cell membrane and became saturated in less than 1 hour. The transport dynamics were determined to be clathrin-dependent endocytosis, which was significantly altered in saponin-damaged cells or in cells with disrupted actin cytoskeletal organization; this suggests that transport via vesicle trafficking may be involved. Reparative effects of P188 appear to remodel the membrane organization and restore the transport properties. Instead of relying on manual image analysis, we utilized a machine learning pipeline that was recently developed in our laboratory to more rapidly and accurately analyze the cellular images of fluorescent P188 dynamics. This computer vision pipeline significantly reduced the time needed to segment, analyze, and perform statistical analyses. Finally, when injected into the mouse tail vein following a traumatic injury to the brain, we report for the first time that the P188 + Rh110 was observed in the brain tissue, indicating that P188 can cross the blood-brain barrier (BBB). Taken together, the dual therapeutic effects of P188 should include (1) resealing the disrupted cell membrane and (2) modulation of the intracellular cell repair machinery that might be involved in response to traumatic brain injury.