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        <title>Frontiers in Physics | Biophysics section | New and Recent Articles</title>
        <link>https://www.frontiersin.org/journals/physics/sections/biophysics</link>
        <description>RSS Feed for Biophysics section in the Frontiers in Physics journal | New and Recent Articles</description>
        <language>en-us</language>
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        <pubDate>2026-05-02T03:15:19.278+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphy.2026.1779859</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphy.2026.1779859</link>
        <title><![CDATA[Symmetry, law invariance, and the physical admissibility of internal time]]></title>
        <pubdate>2026-03-26T00:00:00Z</pubdate>
        <category>Hypothesis and Theory</category>
        <author>Dong-Gyun Han</author>
        <description><![CDATA[The pacemaker–accumulator model has long dominated theories of internal time, yet it remains structurally disconnected from the physical principles that define time in the external world. In physics, time is not generated by an autonomous mechanism but operationally constructed from regular processes governed by invariant laws. Temporal admissibility depends on symmetry, local equivalence, and reproducibility across physical implementations—not on the existence of an internally generated pulse stream. By contrast, prevailing models of internal timing posit a self-contained mechanism whose linkage to shared physical parameters is left unspecified, thereby separating internal temporal organization from the conditions that legitimize time in physics. We argue that this separation is conceptually untenable. Any viable account of internal time must satisfy the same law-based criteria that govern physical clocks. Under sustained gravito-inertial loading, regular otolith afferents converge to stable tonic firing in a steady-state regime. This regularity reflects the steady-state output of sensory transduction under constant gravito-inertial input, rather than the presence of a self-sustained oscillator. Internal time, on this view, is not produced but referenced. Grounded in symmetry, local equivalence, and relational informational accessibility, vestibular dynamics provide a physically admissible sensory reference against which events are compared, restoring continuity between internal temporal organization and the operational foundations of physical time.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphy.2025.1723329</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphy.2025.1723329</link>
        <title><![CDATA[Molecular and biophysical remodeling of the blood–brain barrier in glioblastoma: mechanistic drivers of tumor–neurovascular crosstalk]]></title>
        <pubdate>2025-12-18T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Matthew Abikenari</author><author>Matthew Adam Sjoholm</author><author>Justin Liu</author><author>George Nageeb</author><author>Joseph H. Ha</author><author>Janet Wu</author><author>Alexander Ren</author><author>Jamasb Sayadi</author><author>Jaejoon Lim</author><author>Kwang Bog Cho</author><author>Rohit Verma</author><author>Ravi Medikonda</author><author>Matei Banu</author><author>Michael Lim</author>
        <description><![CDATA[Glioblastoma (GBM) resists conventional treatment in large part because the blood–brain barrier (BBB) and its tumor-modified counterpart, the blood–tumor barrier (BTB), form a spatially heterogeneous, actively regulated interface that governs transport. In this setting, permeability, perfusion, and efflux are decoupled so radiographic contrast enhancement is an imperfect surrogate for true therapeutic exposure. Based on breakthroughs in vascular biology, imaging, and transport modeling, single-cell and spatial profiling, and translational delivery studies, we demonstrate how vascular co-option, hypoxia-induced remodeling, and barrier dysregulation generate gradients from relatively intact margins to leaky but sparsely perfused cores. In addition to their function in regulating molecular traffic, perivascular cells and astrocyte programs affect local immune niches that enable myeloid suppression and exclusion of T-cells and suppress systemic immunotherapies. New tools, from novel MRI/PET methods to intravital microscopy and microphysiologic “BBB-on-chip” platforms, facilitate quantitative measurement of regional transport and drug levels. These observations indicate three interrelated paths to enhanced therapy: temporarily normalizing or reversibly opening the barrier, avoiding it by targeted regional delivery, and rationally designing drugs that account for transport and efflux limitations. The integration of barrier modulation with immunotherapies in preclinical models enhances intratumoral exposure and efficacy. Lessons from other neurologic illnesses highlight both the dangers of uncontrolled opening and the potential of localized, reversible modulation. We support a “BBB-first” paradigm that treats the barrier as a quantifiable, targetable organ and demands trials stratified by barrier phenotype and correlating clinical outcome with regional exposure and immune access.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphy.2025.1553958</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphy.2025.1553958</link>
        <title><![CDATA[Measurement of glioma electrical properties for data-driven electrical properties tomography]]></title>
        <pubdate>2025-11-27T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Chunyou Ye</author><author>Yaqing Jia</author><author>Weiwei Chen</author><author>Guanfu Li</author><author>Wenxia Ju</author><author>Xiaoxing Huang</author><author>Xin Li</author><author>Fang He</author><author>Jijun Han</author>
        <description><![CDATA[IntroductionElectrical properties (EPs) are widely used to assign values to electromagnetic simulation models, providing the comprehensive datasets needed for data-driven electrical properties tomography (EPT) reconstruction. However, the key limitations in current research on glioma EPs are the small sample sizes and the lack of EPs at certain Larmor frequencies. Therefore, this study aims to provide accurate glioma EPs in the full frequency range required for EPT.MethodsWe measured 128 samples, including 81 gliomas and 47 adjacent surrounding tissues, in the frequency range of 50 MHz to 4 GHz using an open-ended coaxial probe (OCP) method. The accuracy of our measurements was verified through uncertainty analysis. Using the Cole–Cole model, we obtained the EPs across the full frequency spectrum. Subsequently, we developed a human simulation model to evaluate the impact of different EPs on the simulated B1 field. At frequencies of 64 MHz, 128 MHz, 213 MHz, and 298 MHz, the model was assigned either the EPs measured in this study or those reported in the literature, and the relative differences in the simulated fields were calculated.ResultsWe first analyzed the discrepancies between our measured EPs and those from previous studies. The results suggested that small sample sizes may introduce bias, potentially compromising the reliability of the findings. Moreover, interpolated data may fail to reflect the frequency-dependent behavior of EPs, leading to reduced accuracy. Simulation results indicate that differences in EPs can lead to measurable deviations in magnetic field simulations. This variation in the B1+ field in response to EPs is critical for enabling accurate EPs reconstruction.DiscussionThese findings underscore the importance of precise EPs measurements, as errors in the training dataset may compromise the performance of models. Therefore, the reliable EPs of glioma provided in this study have the potential to enhance the accuracy of data-driven EPT, thereby assisting clinical diagnosis and treatment.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphy.2025.1656677</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphy.2025.1656677</link>
        <title><![CDATA[Neuromechanical network model]]></title>
        <pubdate>2025-09-19T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Rosa Musotto</author><author>Giovanni Pioggia</author>
        <description><![CDATA[Neuronal oscillations play a crucial role in brain function, regulating processes such as perception, cognition, and motor control. These oscillations are characterized by frequencies that define specific neural states and interactions. This study investigates a neuro mechanical model that emulates brain wave frequencies using a system of five identical masses connected by springs with variable stiffness. The mass-spring arrangement serves as an analog for neuronal oscillations, with each spring's stiffness adjusted to produce frequencies that approximate the characteristic brain wave bands: Delta, Theta, Alpha, Beta, and Gamma. The model leverages coupled oscillations to represent neural interactions, mirroring how groups of neurons may synchronize to generate brain rhythms. Through a three-step optimization process, the spring constants were fine-tuned to align the system’s natural frequencies with target brain wave frequencies. Initial settings ensured a monotonic trend in stiffness, while the Nelder-Mead algorithm minimized the deviations from target frequencies. The resulting model successfully matched Delta, Theta, and Alpha frequencies closely, while Beta and Gamma bands showed moderate deviations, highlighting the need for further refinement or an expanded system. A comparison between this model and neural dynamics suggests that pulse transmission in a mass-spring system resembles neuronal depolarization waves. The analogy draws parallels between oscillatory interactions in physical and biological systems, where each unit influences its neighbor to transmit energy or signals. The study concludes that simplified mechanical systems can effectively approximate brain oscillations, offering a foundation for exploring cognitive states through physical modeling and suggesting potential avenues for neuro engineering and cognitive research.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphy.2025.1591640</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphy.2025.1591640</link>
        <title><![CDATA[Oxidation-induced destabilization of polymorphic α-synuclein fibrils: insights from molecular dynamics]]></title>
        <pubdate>2025-06-26T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Tohir Akramov</author><author>Parthiban Marimuthu</author><author>Mukhriddin Makhkamov</author><author>Aamir Shahzad</author><author>Rasulbek Mashalov</author><author>Jamoliddin Razzokov</author>
        <description><![CDATA[The build-up of α-Synuclein (αSyn) fibrils is a key feature of Parkinson’s disease (PD) and other synucleinopathies. While oxidative stress has been implicated in αSyn aggregation, its precise effects on fibril stability remain unclear. In this study, we use molecular dynamics (MD) simulations and enhanced sampling techniques to investigate the impact of oxidation-induced modifications on the conformational stability of αSyn polymorph fibrils. Three oxidation models (OX1, OX2, and OX3), featuring progressively increased oxidation levels, were generated and compared to the native fibril structure. Key structural analyses, including root mean square deviation (RMSD), secondary structure content, solvent-accessible surface area (SASA), and hydrogen bonding, reveal that oxidation induces significant destabilization of αSyn polymorph fibrils. Free Energy Landscape (FEL) analysis highlights a shift toward more flexible and less compact conformations upon oxidation. Additionally, potential of mean force (PMF) calculations indicate that oxidation weakens inter-chain interactions, lowering the dissociation free energy and suggesting an increased propensity for fibril disassembly. Notably, oxidation disrupts key salt bridges (Glu46-Lys80, Lys45-Glu57) and the hydrophobic packing of Phe94, further contributing to structural destabilization. These findings provide molecular insights into how oxidative modifications influence αSyn polymorph fibril dynamics, reinforcing the role of oxidative stress in fibril destabilization. A more in-depth understanding of these mechanisms could inform therapeutic strategies aimed at preventing or reversing αSyn complex aggregates in neurodegenerative diseases.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphy.2024.1347648</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphy.2024.1347648</link>
        <title><![CDATA[Machine learning approaches for improving atomic force microscopy instrumentation and data analytics]]></title>
        <pubdate>2024-09-24T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Nabila Masud</author><author>Jaydeep Rade</author><author>Md. Hasibul Hasan Hasib</author><author>Adarsh Krishnamurthy</author><author>Anwesha Sarkar</author>
        <description><![CDATA[Atomic force microscopy (AFM) is a part of the scanning probe microscopy family. It provides a platform for high-resolution topographical imaging, surface analysis as well as nanomechanical property mapping for stiff and soft samples (live cells, proteins, and other biomolecules). AFM is also crucial for measuring single-molecule interaction forces and important parameters of binding dynamics for receptor-ligand interactions or protein-protein interactions on live cells. However, performing AFM measurements and the associated data analytics are tedious, laborious experimental procedures requiring specific skill sets and continuous user supervision. Significant progress has been made recently in artificial intelligence (AI) and deep learning (DL), extending into microscopy. In this review, we summarize how researchers have implemented machine learning approaches so far to improve the performance of atomic force microscopy (AFM), make AFM data analytics faster, and make data measurement procedures high-throughput. We also shed some light on the different application areas of AFM that have significantly benefited from applications of machine learning frameworks and discuss the scope and future possibilities of these crucial approaches.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphy.2024.1469515</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphy.2024.1469515</link>
        <title><![CDATA[Free energy calculations in biomolecule-nanomaterial interactions]]></title>
        <pubdate>2024-09-13T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Hongze Fu</author><author>Yinbang Zhu</author><author>Qu Chen</author>
        <description><![CDATA[In computational chemistry and molecular modeling, the interactions between biomolecules (BMs) and nanomaterials (NMs) play a crucial role in various physical and biological processes, and have significant implications in material discovery and development. While there is extensive literature on free energy calculations for drug-target interactions, reviews specifically addressing BM-NM interactions are relatively scarce. This manuscript aims to fill in this gap by presenting a comprehensive overview of the most widely used and well-established methods for free energy calculations. It provides a detailed analysis of the advantages and limitations of these methods and discusses their applicability to BM-NM systems. This work is intended to offer insights into free energy calculations and serve as a guide for future research in this field.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphy.2024.1387271</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphy.2024.1387271</link>
        <title><![CDATA[Quantum-enhanced photoprotection in neuroprotein architectures emerges from collective light-matter interactions]]></title>
        <pubdate>2024-08-26T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Hamza Patwa</author><author>Nathan S. Babcock</author><author>Philip Kurian</author>
        <description><![CDATA[BackgroundSuperradiance is the phenomenon of many identical quantum systems absorbing and/or emitting photons collectively at a higher rate than any one system can individually. This phenomenon has been studied analytically in idealized distributions of electronic two-level systems (TLSs), each with a ground and excited state, as well as numerically in realistic photosynthetic nanotubes and cytoskeletal architectures.MethodsSuperradiant effects are studied here in idealized toy model systems and realistic biological mega-networks of tryptophan (Trp) molecules, which are strongly fluorescent amino acids found in many proteins. Each Trp molecule acts as a chromophore absorbing in the ultraviolet spectrum and can be treated approximately as a TLS, with its 1La excited singlet state; thus, organized Trp networks can exhibit superradiance. Such networks are found, for example, in microtubules, actin filaments, and amyloid fibrils. Microtubules and actin filaments are spiral-cylindrical protein polymers that play significant biological roles as primary constituents of the eukaryotic cytoskeleton, while amyloid fibrils have been targeted in a variety of neurodegenerative diseases. We treat these proteinaceous Trp networks as open quantum systems, using a non-Hermitian Hamiltonian to describe interactions of the chromophore network with the electromagnetic field. We numerically diagonalize the Hamiltonian to obtain its complex eigenvalues, where the real part is the energy and the imaginary part is its associated enhancement rate. We also consider multiple realizations of increasing static disorder in either the site energies or the decay rates.ResultsWe obtained the energies and enhancement rates for realistic microtubules, actin filament bundles, and amyloid fibrils of differing lengths, and we use these values to calculate the quantum yield, which is the ratio of the number of photons emitted to the number of photons absorbed. We find that all three of these structures exhibit highly superradiant states near the low-energy portion of the spectrum, which enhances the magnitude and robustness of the quantum yield to static disorder and thermal noise.ConclusionThe high quantum yield and stable superradiant states in these biological architectures may play a photoprotective role in vivo, downconverting energetic ultraviolet photons—absorbed from those emitted by reactive free radical species—to longer, safer wavelengths and thereby mitigating biochemical stress and photophysical damage. Contrary to conventional assumptions that quantum effects cannot survive in large biosystems at high temperatures, our results suggest that macropolymeric collectives of TLSs in microtubules, actin filaments, and amyloid fibrils exhibit increasingly observable and robust effects with increasing length, up to the micron scale, due to quantum coherent interactions in the single-photon limit. Superradiant enhancement and high quantum yield exhibited in neuroprotein polymers could thus play a crucial role in information processing in the brain, the development of neurodegenerative diseases such as Alzheimer’s and related dementias, and a wide array of other pathologies characterized by anomalous protein aggregates.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphy.2024.1474263</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphy.2024.1474263</link>
        <title><![CDATA[Editorial: Biophysics of muscle contraction]]></title>
        <pubdate>2024-08-13T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Alexandre Lewalle</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphy.2024.1439802</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphy.2024.1439802</link>
        <title><![CDATA[Editorial: Interaction and dynamics of biological molecules]]></title>
        <pubdate>2024-07-08T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Mohana Priya Arumugam</author><author>Umashankar Vetrivel</author><author>Jeyakanthan Jeyaraman</author><author>Subhash C. Chauhan</author><author>Jayakanthan Mannu</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphy.2024.1393340</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphy.2024.1393340</link>
        <title><![CDATA[Hydrophobins: multitask proteins]]></title>
        <pubdate>2024-05-06T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Jesús Rojas-Osnaya</author><author>Mariana Quintana-Quirino</author><author>Alejandra Espinosa-Valencia</author><author>Ana Luisa Bravo</author><author>Hugo Nájera</author>
        <description><![CDATA[Hydrophobins are small amphiphilic extracellular proteins produced by filamentous fungi; they are surface-active proteins, and their functions are mainly related to their ability to self-assemble into amphipathic monolayers at hydrophobic–hydrophilic interfaces. Depending on their hydropathy patterns and purification requirements, they are classified into class I and class II; both present eight conserved cysteines throughout their sequence, forming four disulfide bridges, which generate four loops that give stability to the protein in its monomeric and folded forms. Class I hydrophobin loops are more extended than class II hydrophobin loops, resulting in differences in assembly on divergent surfaces, additionally accompanied by conformational changes in the protein structure. In the monomer hydrophobin glycosylated form, hydrophobins are rich in β-sheet structure, while being assembled at the water–air interface increases the content of the β-sheet in their structure and is at the interface with water, and a hydrophobic solid such as Teflon also induces the formation of an α-helix structure. The monolayers generated by class I are stable structures called fibrils or rodlets, and class II only produces aggregates. Class I presents a glycosylated chain in its sequence; this causes the formation of the α-helix structure, promoting ordered assemblies, which entails their stability and high insolubility. Fibrils could be dissociated with trifluoroacetic acid and formic acid, which unfolds the protein, while 60% ethanol and 2% sodium dodecyl sulfate solutions dissociate class II aggregates.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphy.2024.1358406</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphy.2024.1358406</link>
        <title><![CDATA[Insights into the structure–function relationship of missense mutations in the human TOP2A protein in ovarian cancer]]></title>
        <pubdate>2024-03-28T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Kannan Kavitha</author><author>Arumugam Mohanapriya</author>
        <description><![CDATA[Topoisomerase 2-alpha (TOP2A) is a nuclear protein that is responsible for the maintenance of the topological state of DNA. TOP2A is highly upregulated in ovarian cancer, and its copy number is an important prognosis factor. A large number of single-nucleotide polymorphism (SNP), insertion, and deletion mutations have been reported in TOP2A. Thus, a structural and functional study of missense SNPs was carried out to screen potentially damaging mutations. The 193 non-synonymous SNPs in the coding region of TOP2A in the dbSNP database were selected for in silico analysis. The deleterious SNPs were screened using sorting intolerant from tolerant (SIFT), PolyPhen-2, SNAP2, and SNPs&Go, and we obtained four possibly damaging SNPs at the end (Y481C, N7741, E922K, and R1514W). Mutants Y481C and E922K were predicted to be highly deleterious and showed decreased protein stability compared with native proteins, as predicted by I-Mutant 3. We used the SWISS-MODEL to model the structure of these two mutants, and the structural attributes of modeled mutants were studied using Hope Project, solvent accessibility-based protein–protein interface identification and recognition (SPPIDER), SRide, and HBAT, which predicted small variations from the native protein. Molecular dynamics simulation demonstrated a decrease in root mean square deviation (RMSD) and the radius of gyration of two mutants, which is relative to the native protein. The molecular docking of TOP2A with etoposide suggests that mutations may lead to resistance to TOP2A-targeted chemotherapy. In addition, the relative expression analysis performed by qRT-PCR also reveals that there is a three-fold increase in the expression levels of the TOP2A protein in ovarian adenoma cancer cell lines. Our analysis reveals that Y481C and E922K are highly damaging variants of TOP2A, which alter the protein dynamics and may be implicated in causing ovarian cancer.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphy.2024.1345834</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphy.2024.1345834</link>
        <title><![CDATA[Exploring the potential of nutraceutical to combat gliomas: focus on mIDH2 protein]]></title>
        <pubdate>2024-02-29T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Poornimaa Murali</author><author>Ramanathan Karuppasamy</author>
        <description><![CDATA[Somatic transformations in the key catalytic residues of the Isocitrate Dehydrogenase (IDH) enzyme assist in the onset of distinct malignancies including glioma. Currently, enasidenib is the FDA-approved drug used to target IDH2 protein. However, the use of enasidenib as a plausible mIDH2 inhibitor is constrained by poor brain penetrating capability and dose-limiting toxicity. Thus, the present study aimed to explore the potential of nutraceuticals to synergistically elevate the efficacy of the existing drugs available for glioma management. The binding affinity and free energy of the nutraceuticals were evaluated using molecular docking and MM-GBSA analysis. The resultant 14 compounds were subjected to machine learning-based rescoring strategies to distinguish binders from nonbinders. The pharmacokinetic and toxicity analysis was also implemented alongside virtual cell line assay. The results of our study identified DB14002 (D-alpha-Tocopherol acetate, analog of Vitamin E) as the potential hit compound with appreciable binding affinity, brain penetrating capability and antineoplastic activity against glioma cell lines. In the end, the conformational stability and dynamic characteristics of DB14002 were examined for a stipulated time frame of 250ns. Indeed, the outcomes of our study culminate the use of DB14002 as a synergistic drug-like candidate which could be translated as a plausible inhibitor of mIDH2 in the forthcoming years.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphy.2024.1342115</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphy.2024.1342115</link>
        <title><![CDATA[Tackling suppressive cancer microenvironment by NARF-derived immune modulatory vaccine and its validation using simulation strategies]]></title>
        <pubdate>2024-02-22T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Priyanga Paranthaman</author><author>Shanthi Veerappapillai</author>
        <description><![CDATA[Introduction: Targeting tumor microenvironment is beneficial and present an ideal setting for the development of futuristic immunotherapy. Here, we make use of Nuclear prelamin A recognition factor (NARF), a protein linked to the coactivation of transcriptional regulators in human breast cancer stem cells (CSC) in our investigation.Methods: In this study, we initially computed the epitope regions possessing the ability to stimulate both T and B cells within the NARF protein. These identified epitope areas were fused with an adjuvant such as RpfB and RpfE as well as linkers like AAY, GPGPG, KK, and EAAAK. The constructed vaccine was further characterized by assessing its physicochemical properties and population coverage. The potential interactions of the designed vaccine with different toll-like receptors were examined by a sequence of computational studies. Of note, docking study were employed to understand its mechanism of action. Molecular dynamics and immune simulation studies were conducted to comprehend more into their structural stability and immune responses. The resultant vaccine was back-translated, codon-optimised and introduced into pET-28 (+) vector.Results and discussion: We hypothesize from the results that the designed NARF protein-based vaccine in our analysis could effectively provoke the immune responses in the target organism through TLR-7 binding and promotes MHC class-II mediated antigen presentation. Indeed, comprehensive evaluations conducted in both in vitro and in vivo settings are imperative to substantiate the safety and efficacy of the developed vaccine.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphy.2024.1298482</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphy.2024.1298482</link>
        <title><![CDATA[Steric blocking upside down: a different way of thinking about the competition between myosin and tropomyosin]]></title>
        <pubdate>2024-01-25T00:00:00Z</pubdate>
        <category>Perspective</category>
        <author>Joseph M. Chalovich</author>
        <description><![CDATA[At low free Ca2+, the actin binding proteins tropomyosin, troponin I, troponin T and troponin C inhibit contraction in striated muscles. Ca2+ activation alters the position of tropomyosin on actin to uncover binding sites for high affinity forms of myosin (i.e., myosin-ADP). Inhibition of contraction is commonly thought to result from steric blocking of myosin binding to actin by tropomyosin. However, myosin-ADP binding to actin is energetically more favorable than localization of tropomyosin in the blocking position. Tropomyosin is an effective inhibitor of binding only at low levels of myosin-ADP. At low free Ca2+, troponin-tropomyosin also inhibits the rate of a step associated with Pi release to about 1% of the maximum rate. This results in accumulation of myosin with bound ATP and ADP-Pi. Such myosin binds weakly to actin. Ca2+ activation increases the rate of Pi release, but not to the maximum value, and increases the population of myosin-ADP. The high affinity binding of myosin-ADP to actin can displace tropomyosin into the fully active position in relation to the amount of myosin-ADP bound. It seems likely that an important outcome of the steric clash between myosin-ADP and tropomyosin is the dual activation by Ca2+ and myosin-ADP. The C-terminal region of troponin T (TnT) contributes to the incomplete activation by Ca2+ alone. Because this region of TnT is highly conserved, the ability of myosin-ADP to move tropomyosin may be more important than any restriction that tropomyosin may place on myosin binding.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphy.2023.1320437</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphy.2023.1320437</link>
        <title><![CDATA[Evaluating the Spike–hACE2 interactions in the wild type and variants of concern of SARS -CoV-2 at different temperatures]]></title>
        <pubdate>2024-01-05T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Nabanita Mandal</author><author>Soumya Lipsa Rath</author>
        <description><![CDATA[The effect of temperature on SARS-CoV-2 is frequently debated upon. There is evidence of temperature sensitivity of the viral proteins; however, how heat influences the protein–protein interaction between a SARS-CoV-2 protein and the human angiotensin-converting enzyme 2 (ACE2) receptor remains to be elucidated. Here, we studied the receptor-binding domain of the surface glycoprotein of SARS-CoV-2 wild type and variants of concern bound to the human ACE2 receptor at different temperatures through atomistic simulations. We found that although there were no major conformation changes in the protein complexes at high temperatures, the dynamics of the proteins significantly increased. There was loss of protein–protein contacts and interaction energies. Thus, the protein–protein interaction was found to be rather strong. This study would be useful for viral protein studies and the design of peptide-based vaccines and therapeutics.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphy.2023.1323542</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphy.2023.1323542</link>
        <title><![CDATA[Adding the latency period to a muscle contraction model coupled to a membrane action potential model]]></title>
        <pubdate>2023-12-18T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Nadia Roberta Chaves Kappaun</author><author>Ana Beatriz Nogueira Rubião Graça</author><author>Gabriel Benazzi Lavinas Gonçalves</author><author>Rodrigo Weber dos Santos</author><author>Sara Del Vecchio</author><author>Flávia Souza Bastos</author>
        <description><![CDATA[Introduction: Skeletal muscle is responsible for multiple functions for maintaining energy homeostasis and daily activities. Muscle contraction is activated by nerve signals, causing calcium release and interaction with myofibrils. It is important to understand muscle behavior and its impact on medical conditions, like in the presence of some diseases and their treatment, such as cancer, which can affect muscle architecture, leading to deficits in its function. For instance, it is known that radiotherapy and chemotherapy also have effects on healthy tissues, leading to a reduction in the rate of force development and the atrophy of muscle fibers. The main aim is to reproduce the behavior of muscle contraction using a coupled model of force generation and the action potential of the cell membrane, inserting the latency period observed between action potential and force generation in the motor unit.Methods: Mathematical models for calcium dynamics and muscle contraction are described, incorporating the role of calcium ions and rates of reaction. An action potential initiates muscle contraction, as described by the Hodgkin–Huxley model. The numerical method used to solve the equations is the forward Euler method.Results and Discussion: The results show dynamic calcium release and force generation, aligning with previous research results, and the time interval between membrane excitation and force generation was accomplished. Future work should suggest simulating more motor units at the actual scale for the possibility of a comparison with real data collected from both healthy individuals and those who have undergone cancer treatment.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphy.2023.1306210</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphy.2023.1306210</link>
        <title><![CDATA[Advancing clinical translation of cardiac biomechanics models: a comprehensive review, applications and future pathways]]></title>
        <pubdate>2023-11-14T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Cristobal Rodero</author><author>Tiffany M. G. Baptiste</author><author>Rosie K. Barrows</author><author>Alexandre Lewalle</author><author>Steven A. Niederer</author><author>Marina Strocchi</author>
        <description><![CDATA[Cardiac mechanics models are developed to represent a high level of detail, including refined anatomies, accurate cell mechanics models, and platforms to link microscale physiology to whole-organ function. However, cardiac biomechanics models still have limited clinical translation. In this review, we provide a picture of cardiac mechanics models, focusing on their clinical translation. We review the main experimental and clinical data used in cardiac models, as well as the steps followed in the literature to generate anatomical meshes ready for simulations. We describe the main models in active and passive mechanics and the different lumped parameter models to represent the circulatory system. Lastly, we provide a summary of the state-of-the-art in terms of ventricular, atrial, and four-chamber cardiac biomechanics models. We discuss the steps that may facilitate clinical translation of the biomechanics models we describe. A well-established software to simulate cardiac biomechanics is lacking, with all available platforms involving different levels of documentation, learning curves, accessibility, and cost. Furthermore, there is no regulatory framework that clearly outlines the verification and validation requirements a model has to satisfy in order to be reliably used in applications. Finally, better integration with increasingly rich clinical and/or experimental datasets as well as machine learning techniques to reduce computational costs might increase model reliability at feasible resources. Cardiac biomechanics models provide excellent opportunities to be integrated into clinical workflows, but more refinement and careful validation against clinical data are needed to improve their credibility. In addition, in each context of use, model complexity must be balanced with the associated high computational cost of running these models.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphy.2023.1274064</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphy.2023.1274064</link>
        <title><![CDATA[Across the stages: a multiscale extension of the generalized stochastic microdosimetric model (MS-GSM2) to include the ultra-high dose rate]]></title>
        <pubdate>2023-11-08T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Marco Battestini</author><author>Marta Missiaggia</author><author>Andrea Attili</author><author>Francesco Tommasino</author><author>Chiara La Tessa</author><author>Francesco G. Cordoni</author><author>Emanuele Scifoni</author>
        <description><![CDATA[Ultra-high dose rate (UHDR) irradiations with different types of radiation have shown a larger sparing of normal tissue and unchanged tumor control with respect to conventional delivery. In recent years, there has been an accumulation of experimental evidence related to the so-called FLASH effect. However, the underpinning mechanism remains, to date, extremely debated and largely unexplained, while the involvement of multiple scales of radiation damage has been suggested. Since it is believed that the chemical environment plays a crucial role in the FLASH effect, this work aims to develop a multi-stage tool, the multiscale generalized stochastic microdosimetric model (MS-GSM2), that can capture several possible effects on DNA damage at the UHDR regime, such as reduction of DNA damage yield due to organic radical recombination, damage fixation due to oxygenation, and spatial and temporal dose deposition effects, allowing us to explore most of the candidate mechanisms for explaining the FLASH effect. The generalized stochastic microdosimetric model (GSM2) is a probabilistic model that describes the time evolution of DNA damage in a cell nucleus using microdosimetric principles, accounting for different levels of spatio-temporal stochasticity. In particular, the GSM2 describes radiation-induced DNA damage formation and kinetic repair in the case of protracted irradiation without considering the Poissonian assumption to treat the number of radiation-induced DNA damage. In this work, we extend the GSM2, coupling the evolution of DNA damage to fast chemical reaction kinetics, described by a system of ordinary differential equations, accounting for an additional level of stochasticity, i.e., in chemistry. We simulate energy deposition by particles in a microscopic volume, which mimics the cell nucleus, in order to examine the combined effects of several chemical species and the time evolution of DNA damage. We assume that UHDR modifies the time evolution of the peroxyl radical concentration, with a consequent reduction in the yield of the indirect DNA damage. This damage reduction emerges only at UHDR and is more pronounced at high doses. Moreover, the indirect damage yield reduction depends on the radiation quality. We show that the MS-GSM2 can describe the empirical trend of dose- and dose rate-dependent cell sensitivity over a broad range, particularly the larger sparing of healthy tissue occurring at the FLASH regime. The complete generality of the MS-GSM2 also allows us to study the impact of different dose delivery time structures and radiation qualities, including high LET beams.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphy.2023.1289123</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphy.2023.1289123</link>
        <title><![CDATA[Corrigendum: Rheological comparison between control and Dupuytren fibroblasts when plated in circular micropatterns using atomic force microscopy]]></title>
        <pubdate>2023-09-28T00:00:00Z</pubdate>
        <category>Correction</category>
        <author>Sandra Pérez-Domínguez</author><author>Elisabeth Werkmeister</author><author>Maria Luisa Marini</author><author>Vincent Dupres</author><author>Sébastien Janel</author><author>Frank Lafont</author><author>Manfred Radmacher</author>
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