Journal of Biological Physics最新文献

Bioconvective flows over a thin needle hold significant importance in various fields, particularly in biomedical engineering, microfluidics, and environmental science. This paper examines the bioconvective flow properties of a copper and blood-based Casson nanofluid over a thin needle, accounting for gyrotactic microorganisms in the presence of a magnetic field. The two-phase nanofluid model is applied to formulate the flow problem. The system of non-dimensional ordinary differential equations is obtained by reducing the governing partial differential equations with the help of similarity variables. Further, the ODEs are numerically solved using the 4th-order Runge–Kutta method based Shooting technique. The similar solutions of the non-dimensional ODEs are represented graphically and the blood-based nanofluid’s velocity, temperature, concentration, and presence of microorganisms are examined with reference to the accompanying diagrams. A detailed analysis is provided for skin friction, Nusselt number, and microorganism density number. The primary outcomes reveal that the augmentation of the mixed convection parameter and buoyancy ratio parameter enhance the rate of heat transfer.

Cell fate decision is crucial in biological development and plays fundamental roles in normal development and functional maintenance of organisms. By identifying key regulatory interactions and molecules involved in these fate decisions, we can shed light on the intricate mechanisms underlying the cell fates. This understanding ultimately reveals the fundamental principles driving biological development and the origins of various diseases. In this study, we present an overarching framework which integrates pseudo-trajectory inference and differential analysis to determine critical regulatory interactions and molecules during cell fate transitions. To demonstrate feasibility and reliability of the approach, we employ the differentiation networks of hepatobiliary system and embryonic stem cells as representative model systems. By applying pseudo-trajectory inference to biological data, we aim to identify critical regulatory interactions and molecules during the cell fate transition processes. Consistent with experimental observations, the approach can allow us to infer dynamical cell fate decision processes and gain insights into the underlying mechanisms which govern cell state decisions.

This study presents a stochastic model of seed dispersal based on a branching random walk (BRW) framework, incorporating both homogeneous and non-homogeneous Poisson point processes (PPP). Building on the model introduced by Coletti et al. (2023), we examine the effects of habitat reduction on seed dispersal dynamics. We analyze the phase transition behavior of the BRW model under varying conditions of habitat fragmentation, focusing on how these conditions influence the critical dispersal rate. Specifically, we study a BRW on the real line with a non-homogeneous PPP driven by a log-normal density, constrained between spatial barriers. Our simulations localize the critical dispersal rate with respect to barrier positions and compare this dependence between homogeneous and non-homogeneous models.

The exploration of microgravity has garnered substantial scholarly attention due to its potential to offer unique insights into the behavior of biological systems. This study presents a preliminary investigation into the effects of simulated microgravity on esophageal cancer cells, examining various aspects such as morphology, growth behavior, adhesion, inhibition rate, and DNA damage. To achieve this, a novel microgravity simulator named “Gravity Challenge” was utilized for its effectiveness in minimizing external influences that could compromise microgravity conditions. The international cell line SK-GT-4 was utilized as the focal point of this investigation. Results revealed noticeable alterations in the growth behavior of cancer cells following exposure to simulated microgravity for 24 h, characterized by a loss of adhesion properties compared to control cells. Concurrently, cell viability exhibited a decline, as evidenced by cytotoxicity testing. Furthermore, the comet assay test demonstrated that cells subjected to microgravity simulation experienced a higher incidence of DNA damage compared to their control counterparts. In conclusion, this comprehensive examination of the impact of simulated microgravity on esophageal cancer cells extends beyond morphological changes, delving into genetic implications through observed DNA damage. The diminished vitality of cells under microgravity conditions underscores the multifaceted effects on cellular behavior in response to environmental variations. These findings represent a significant step towards understanding the dynamics of cancer cells, laying the groundwork for future research aimed at identifying potential therapeutic strategies for this disease.

The evolutionary origin of the inverted retina in the vertebrate eye is unknown. This paper explores a hypothetical evolutionary scenario that explains the unique orientation of the photoreceptors in the vertebrate retina. The proposed scenario follows the scientific accepted scenario for eye evolution and gradually builds up towards an eye prototype by considering light direction detection and increase in achievable spatial resolution as the driving forces. It suggests that eye retinas developed along two different morphological processes, an evagination process that results in the inverted retina in vertebrate eyes and an invagination process that results in a verted retina in cephalopod eyes. The development of the inverted vertebrate retina and eye prototype morphology is strongly substantiated by physics of vision. The proposed evolutionary sequence for vertebrate eye development is simple and has the full potential to explain the origin of the inverted retina and leads to an eye prototype enabling visual detection and orientation. It allows the emergence of eye structures like, extraocular muscles, tapetum lucidum, biconvex lens, cornea, and pupil. This study supports the suggestion that a primitive inverted retina in the predecessor of vertebrates is of ectodermal origin and available before neurulation occurred.

During the asymmetric loop extrusion of DNA by a condensin complex, one domain of the complex stably anchors to the DNA molecule, and another domain reels in the DNA strand into a loop. The DNA strand in the loop is fully relaxed, or there is no tension in the loop. Just outside of the loop, there is a tension that resists the extrusion of DNA. To maintain the extrusion of the DNA loop, the condensin complex must have a domain capable of generating a force to overcome the tension outside of the loop. This study proposes that the groove-shaped HEAT repeat domain Ycg1 plays the role of a molecular motor. A DNA molecule may bind to the groove electrostatically, and the weak binding force facilitates the random thermal motion of DNA molecules. A mechanical model that random collisions between DNA and the nonparallel inner surfaces of the groove may generate a directional force which is required for the loop extrusion to sustain. The hinge domain binds to the DNA molecule and acts as an anchor during asymmetric DNA loop extrusion. When the effects of ATP hydrolysis and the viscous drag of the fluid environment are considered, the motor–anchor model for the condensin complex and the mechanical model might explain the asymmetric loop extrusion, the formation of steps, the step size distribution in the loop extrusion, the tension-dependent extrusion speed, the interaction between coexisting loops on the DNA strand, and untying the knots during extrusion. This model can also explain the observed formation of the Z-loop.

Collective cell invasion underlies several biological processes such as wound healing, embryonic development, and cancerous invasion. Here, we investigate the impact of cell motility on invasion in epithelial monolayers and its coupling to cellular mechanical properties, such as cell-cell adhesion and cortex contractility. We develop a two-dimensional computational model for cells with active motility based on the cellular Potts model, which predicts that the cellular invasion speed is mainly determined by active cell motility and is independent of the biological and mechanical properties of the cells. We also find that, in general, motile cells out-compete and invade non-motile cells, however, this can be reversed by differential cell proliferation. Stable coexistence of motile and static cell types is also possible for certain parameter regimes.

External electric and mechanical stimuli can induce shape deformation in excitable media because of its intrinsic flexible property. When the signals propagation in the media is described by a neural network, creation of heterogeneity or defect is considered as the effect of shape deformation due to accumulation or release of energy in the media. In this paper, a temperature-light sensitive neuron model is developed from a nonlinear circuit composed of a phototube and a thermistor, and the physical energy is kept in capacitive and inductive terms. Furthermore, the Hamilton energy for this function neuron is obtained in theoretical way. A regular neural network is built on a square array by activating electric synapse between adjacent neurons, and a few of neurons in local area is excited by noisy disturbance, which induces local energy diversity, and continuous coupling enables energy propagation and diffusion. Initially, the Hamilton energy function for a temperature-light sensitive neuron can be obtained. Then, the finite neurons are applied noise to obtain energy diversity to explore the energy spread between neurons in the network. For keeping local energy balance, one intrinsic parameter is regulated adaptively until energy diversity in this local area is decreased greatly. Regular pattern formation indicates that local energy balance creates heterogeneity or defects and a few of neurons show continuous parameter shift for keeping energy balance in a local area, which supports gradient energy distribution for propagating waves in the network.

Bone is a complex tissue that fulfills the role of a resistance structure. This quality is most commonly assessed by bone densitometry, but bone strength may not only be related to bone mineral density but also to the preservation of bone cytoarchitectonics. The study included two groups of rats, ovariectomized and non-ovariectomized. Each group was divided into three batches: control, simvastatin-treated, and fenofibrate-treated. In the ovariectomized group, hypolipidemic treatment was instituted at 12 weeks post ovariectomy. One rat from each of the 6 batches was sacrificed 8 weeks after the start of treatment in the group. The experimental study was performed using a Bruker Minispec mq 20 spectrometer operating at a frequency of 20 MHz, subsequently also performed by ¹H T₂-T₂ molecular exchange maps. The results were represented by T₂-T₂ molecular exchange maps that showed, comparatively, both pore size and their interconnectivity at the level of the femoral epiphysis, being able to evaluate both the effect of estrogen on bone tissue biology and the effect of the lipid-lowering medication, simvastatin, and fenofibrate, in both the presence and absence of estrogen. T₂-T₂ molecular exchange maps showed that the absence of estrogen results in an increase in bone tissue pore size and interconnectivity. In the presence of estrogen, lipid-lowering medication, both simvastatin and fenofibrate alter bone tissue cytoarchitectonics by reducing pore interconnectivity. In the absence of estrogen, fenofibrate improves bone tissue cytoarchitectonics, the T₂-T₂ molecular exchange map being similar to that of non-osteoporotic bone tissue.

Studying the calcium dynamics within a fibroblast cell individually has provided only a restricted understanding of its functions. However, research efforts focusing on systems biology approaches for such investigations have been largely neglected by researchers until now. Fibroblast cells rely on signaling from calcium ((Ca^{2+})) and nitric oxide (NO) to maintain their physiological functions and structural stability. Various studies have demonstrated the correlation between NO and the control of (Ca^{2+}) dynamics in cells. However, there is currently no existing model to assess the disruptions caused by various factors in regulatory dynamics, potentially resulting in diverse fibrotic disorders. A mathematical model has been developed to investigate the effects of changes in parameters such as buffer, receptor, sarcoplasmic endoplasmic reticulum (Ca^{2+})-ATPase (SERCA) pump, and source influx on the regulation and dysregulation of spatiotemporal calcium and NO dynamics in fibroblast cells. This model is based on a system of reaction-diffusion equations, and numerical simulations are conducted using the finite element method. Disturbances in key processes related to calcium and nitric oxide, including source influx, buffer mechanism, SERCA pump, and inositol trisphosphate ((IP_3)) receptor, may contribute to deregulation in the calcium and NO dynamics within fibroblasts. The findings also provide new insights into the extent and severity of disorders resulting from alterations in various parameters, potentially leading to deregulation and the development of fibrotic disease.