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Besides their main function for energy production in form of ATP in processes of oxidative phosphorylation (OxPhos), mitochondria perform many other important cellular functions and participate in various physiological processes that are congregated. For example, mitochondria are considered to be one of the main sources of reactive oxygen species (ROS) and therefore they actively participate in the regulation of cellular redox and ROS signaling. These organelles also play a crucial role in Ca2+ signaling and homeostasis. The mitochondrial OxPhos and their cellular functions are strongly cell/tissue specific and can be heterogeneous even within the same cell, due to the existence of mitochondrial subpopulations with distinct functional and structural properties. However, the interplay between different functions of mitochondria is not fully understood. The mitochondrial functions may change as a response to the changes in the cellular metabolism (signaling in). On the other hand, several factors and feedback signals from mitochondria may influence the entire cell physiology (signaling out). Numerous interactions between mitochondria and the rest of cell, various cytoskeletal proteins, endoplasmic reticulum (ER) and other cellular elements have been demonstrated, and these interactions could actively participate in the regulation of mitochondrial and cellular metabolism. This review highlights the important role of the interplay between mitochondrial and entire cell physiology, including signaling from and to mitochondria.

The aim of this article is to propose a novel type of a nanofluid that contains both nanoparticles and motile (oxytactic) microorganisms. The benefits of adding motile microorganisms to the suspension include enhanced mass transfer, microscale mixing, and anticipated improved stability of the nanofluid. In order to understand the behavior of such a suspension at the fundamental level, this article investigates its stability when it occupies a shallow horizontal layer. The oscillatory mode of nanofluid bioconvection may be induced by the interaction of three competing agencies: oxytactic microorganisms, heating or cooling from the bottom, and top or bottom-heavy nanoparticle distribution. The model includes equations expressing conservation of total mass, momentum, thermal energy, nanoparticles, microorganisms, and oxygen. Physical mechanisms responsible for the slip velocity between the nanoparticles and the base fluid, such as Brownian motion and thermophoresis, are accounted for in the model. An approximate analytical solution of the eigenvalue problem is obtained using the Galerkin method. The obtained solution provides important physical insights into the behavior of this system; it also explains when the oscillatory mode of instability is possible in such system.

New insight into the contribution of the microscale vortex evolution to convection heat transfer in porous media is presented in this paper. The objective is to determine how the microscale vortices influence convection heat transfer in turbulent flow inside porous media. The microscale temperature distribution is analysed using flow visualization in two dimensions using streamlines and in three dimensions using the Q-criterion. The pertinent observations are supplemented with a comparison of surface skin friction and heat transfer using: (i) surface skin-friction lines and (ii) the joint probability density function of the pressure and skin-friction coefficients, along with the Nusselt number. The microscale flow phenomena observed are corroborated with the features of the frequency spectra of the drag coefficient and macroscale Nusselt number. The large eddy simulation technique is used in this study to investigate the flow field inside a periodic porous medium. The Reynolds numbers of the flow are 300 and 500. The porous medium consists of solid obstacles in the shape of square and circular cylinders. Two distinct flow regimes are represented by using the porosities of 0.50 and 0.87. The results show that the surface Nusselt number distribution is dependent on whether the micro-vortices are attached to or detached from the surface of the obstacle. The spectra of the macroscale Nusselt number and the pressure drag are similar, signifying a correlation between the dynamics of heat transfer and the microscale turbulent structures. Both vortex shedding and secondary flow instabilities are observed that significantly influence the Nusselt number. The fundamental insight gained in this paper can inform the development of more robust macroscale models of convection heat transfer in turbulent flow in porous media.

Mitochondria play a critical role in maintaining cellular function by ATP production. They are also a source of reactive oxygen species (ROS) and proapoptotic factors. The role of mitochondria has been established in many aspects of cell physiology/pathophysiology, including cell signaling. Mitochondria may deteriorate under various pathological conditions, including ischemia-reperfusion (IR) injury. Mitochondrial injury can be one of the main causes for cardiac and other tissue injuries by energy stress and overproduction of toxic reactive oxygen species, leading to oxidative stress, elevated calcium and apoptotic and necrotic cell death. However, the interplay among these processes in normal and pathological conditions is still poorly understood. Mitochondria play a critical role in cardiac IR injury, where they are directly involved in several pathophysiological mechanisms. We also discuss the role of mitochondria in the context of mitochondrial dynamics, specializations and heterogeneity. Also, we wanted to stress the existence of morphologically and functionally different mitochondrial subpopulations in the heart that may have different sensitivities to diseases and IR injury. Therefore, various cardioprotective interventions that modulate mitochondrial stability, dynamics and turnover, including various pharmacologic agents, specific mitochondrial antioxidants and uncouplers, and ischemic preconditioning can be considered as the main strategies to protect mitochondrial and cardiovascular function and thus enhance longevity.

The present paper considers the results of long-term (up to 17 years) in situ and laboratory research carried out on oiled French, Spanish, and Russian seacoasts. The objective of this research is to quantify the influence of geographical factors on the rates of natural transformation of the heavy fuel oil stranded ashore and to develop an empirical statistical model in order to evaluate the self-cleansing capacity of the coastal environment. In a number of field campaigns, 363 samples of weathered oil slicks and tar balls have been collected and analysed with the use of thin-layer chromatography combined with optical and gravimetric methods. The results obtained have been subjected to multiple nonlinear regression analyses. It has been shown that heavy fuel oil natural attenuation is more active in continental or estuarine environments influenced by nutrient-rich freshwater runoff and characterised by a higher number of sunny days, solar irradiation, and large temperature fluctuations. On the oceanic coasts, especially in sectors with low hydrodynamic energy, these processes take more time. The resulting model allows for the identification and mapping of the most vulnerable seacoasts, characterised by a low potential to degrade oil pollution. This information may be used in the contingency plans in order to optimise clean-up techniques and associated costs.

Natural convection in porous media is a fundamental process for the long-term storage of CO2 in deep saline aquifers. Typically, details of mass transfer in porous media are inferred from the numerical solution of the volume-averaged Darcy–Oberbeck–Boussinesq (DOB) equations, even though these equations do not account for the microscopic properties of a porous medium. According to the DOB equations, natural convection in a porous medium is uniquely determined by the Rayleigh number. However, in contrast with experiments, DOB simulations yield a linear scaling of the Sherwood number with the Rayleigh number ( $Ra$ ) for high values of $Ra$ ( $Ra\\gg 1300$ ). Here, we perform direct numerical simulations (DNS), fully resolving the flow field within the pores. We show that the boundary layer thickness is determined by the pore size instead of the Rayleigh number, as previously assumed. The mega- and proto-plume sizes increase with the pore size. Our DNS results exhibit a nonlinear scaling of the Sherwood number at high porosity, and for the same Rayleigh number, higher Sherwood numbers are predicted by DNS at lower porosities. It can be concluded that the scaling of the Sherwood number depends on the porosity and the pore-scale parameters, which is consistent with experimental studies.

The focus of this paper is a numerical simulation study of the flow dynamics in a periodic porous medium to analyse the physics of a symmetry-breaking phenomenon, which causes a deviation in the direction of the macroscale flow from that of the applied pressure gradient. The phenomenon is prominent in the range of porosity from 0.43 to 0.72 for circular solid obstacles. It is the result of the flow instabilities formed when the surface forces on the solid obstacles compete with the inertial force of the fluid flow in the turbulent regime. We report the origin and mechanism of the symmetry-breaking phenomenon in periodic porous media. Large-eddy simulation (LES) is used to simulate turbulent flow in a homogeneous porous medium consisting of a periodic, square lattice arrangement of cylindrical solid obstacles. Direct numerical simulation is used to simulate the transient stages during symmetry breakdown and also to validate the LES method. Quantitative and qualitative observations are made from the following approaches: (1) macroscale momentum budget and (2) two- and three-dimensional flow visualization. The phenomenon draws its roots from the amplification of a flow instability that emerges from the vortex shedding process. The symmetry-breaking phenomenon is a pitchfork bifurcation that can exhibit multiple modes depending on the local vortex shedding process. The phenomenon is observed to be sensitive to the porosity, solid obstacle shape and Reynolds number. It is a source of macroscale turbulence anisotropy in porous media for symmetric solid-obstacle geometries. In the macroscale, the principal axis of the Reynolds stress tensor is not aligned with any of the geometric axes of symmetry, nor with the direction of flow. Thus, symmetry breaking in porous media involves unresolved flow physics that should be taken into consideration while modelling flow inhomogeneity in the macroscale.

The modelling of natural convection in porous media is receiving increased interest due to its significance in environmental and engineering problems. State-of-the-art simulations are based on the classic macroscopic Darcy–Oberbeck–Boussinesq (DOB) equations, which are widely accepted to capture the underlying physics of convection in porous media provided the Darcy number, $Da$, is small. In this paper we analyse and extend the recent pore-resolved direct numerical simulations (DNS) of Gasow et al. (J. Fluid Mech, vol. 891, 2020, p. A25) and show that the macroscopic diffusion, which is neglected in DOB, is of the same order (with respect to $Da$) as the buoyancy force and the Darcy drag. Consequently, the macroscopic diffusion must be modelled even if the value of $Da$ is small. We propose a ‘two-length-scale diffusion’ model, in which the effect of the pore scale on the momentum transport is approximated with a macroscopic diffusion term. This term is determined by both the macroscopic length scale and the pore scale. It includes a transport coefficient that solely depends on the pore-scale geometry. Simulations of our model render a more accurate Sherwood number, root mean square (r.m.s.) of the mass concentration and r.m.s. of the velocity than simulations that employ the DOB equations. In particular, we find that the Sherwood number $Sh$ increases with decreasing porosity and with increasing Schmidt number $(Sc)$. In addition, for high values of $Ra$ and high porosities, $Sh$ scales nonlinearly. These trends agree with the DNS, but are not captured in the DOB simulations.

Analysis of the function, structure, and intracellular organization of mitochondria is important for elucidating energy metabolism and intracellular energy transfer. In addition, basic and clinically oriented studies that investigate organ/tissue/cell dysfunction in various human diseases, including myopathies, cardiac/brain ischemia-reperfusion injuries, neurodegenerative diseases, cancer, and aging, require precise estimation of mitochondrial function. It should be noted that the main metabolic and functional characteristics of mitochondria obtained in situ (in permeabilized cells and tissue samples) and in vitro (in isolated organelles) are quite different, thereby compromising interpretations of experimental and clinical data. These differences are explained by the existence of the mitochondrial network, which possesses multiple interactions between the cytoplasm and other subcellular organelles. Metabolic and functional crosstalk between mitochondria and extra-mitochondrial cellular environments plays a crucial role in the regulation of mitochondrial metabolism and physiology. Therefore, it is important to analyze mitochondria in vivo or in situ without their isolation from the natural cellular environment. This review summarizes previous studies and discusses existing approaches and methods for the analysis of mitochondrial function, structure, and intracellular organization in situ.

Growing number of studies provide strong evidence that the mitochondrial permeability transition pore (PTP), a non-selective channel in the inner mitochondrial membrane, is involved in the pathogenesis of cardiac ischemia–reperfusion and can be targeted to attenuate reperfusion-induced damage to the myocardium. The molecular identity of the PTP remains unknown and cyclophilin D is the only protein commonly accepted as a major regulator of the PTP opening. Therefore, cyclophilin D is an attractive target for pharmacological or genetic therapies to reduce ischemia–reperfusion injury in various animal models and humans. Most animal studies demonstrated cardioprotective effects of PTP inhibition; however, a recent large clinical trial conducted by international groups demonstrated that cyclosporine A, a cyclophilin D inhibitor, failed to protect the heart in patients with myocardial infarction. These studies, among others, raise the question of whether cyclophilin D, which plays an important physiological role in the regulation of cell metabolism and mitochondrial bioenergetics, is a viable target for cardioprotection. This review discusses previous studies to provide comprehensive information on the physiological role of cyclophilin D as well as PTP opening in the cell that can be taken into consideration for the development of new PTP inhibitors.