Large hemispheric differences in the Hadley cell strength variability due to ocean coupling

By modulating the distribution of heat, precipitation and moisture, the Hadley cell holds large climate impacts at low and subtropical latitudes. Here we show that the interannual variability of the annual mean Hadley cell strength is ~ 30% less in the Northern Hemisphere than in the Southern Hemisphere. Using a hierarchy of ocean coupling experiments, we find that the smaller variability in the Northern Hemisphere stems from dynamic ocean coupling, which has opposite effects on the variability of the Hadley cell in the Southern and Northern Hemispheres; it acts to increase the variability in the Southern Hemisphere, which is inversely linked to equatorial upwelling, and reduce the variability in the Northern Hemisphere, which shows a direct relation with the subtropical wind-driven overturning circulation. The important role of ocean coupling in modulating the tropical circulation suggests that further investigation should be carried out to better understand the climate impacts of ocean-atmosphere coupling at low latitudes.

The Effect of Acetylsalicylic Acid (ASA) on the Mechanical Properties of Breast Cancer Epithelial Cells

Background: In most communities, the risk of developing breast cancer is increasing. By affecting the cyclooxygenase 1 and 2 (COX-1 and COX-2) enzymes and actin filaments, acetylsalicylic acid (Aspirin) has been shown to reduce the risk of breast cancer and prevent cell migration in both laboratory and clinical studies. Methods: The purpose of this study is to determine the mechanical properties of normal and cancerous breast tissue cells, as well as the short-term effect of aspirin on cancer cells. To this end, the mechanical properties and deformation of three cell types were investigated: healthy MCF-10 breast cells, MCF-7 breast cancer cells, and MCF-7 breast cancer cells treated with a 5 µM aspirin solution. Atomic Force Microscopy (AFM) was used to determine the mechanical properties of the cells. Cell deformation was analyzed in all groups, and Young's modulus was calculated using the Hertz model. Result: According to the obtained data, cancer cells deformed at a rate half that of healthy cells. Nonetheless, when aspirin was used, cancer cells deformed similarly to healthy cells. Additionally, healthy cells' Young's modulus was calculated to be approximately three times that of cancer cells, which was placed closer to that of healthy cells by adding aspirin to Young's modulus. Conclusion: Cell strength appears to have increased due to aspirin's intervention on actin filaments and cytoskeletons, and the mechanical properties of breast cancer cells have become more similar to those of normal cells. The likelihood of cell migration and metastasis decreases as cell strength increases.

The Impact of Divergence Tilt and Meridional Flow for Cross-Equatorial Eddy Momentum Transport in Gill-Like Settings

This work investigates the sensitivity of the cross-equatorial eddy momentum flux and its rotational and divergent components to Hadley cell strength in simple variants of the Gill problem. An expression is derived linking the divergent momentum flux to the mean meridional wavenumber weighted by the spectrum of divergent eddy kinetic energy, supporting the relation between divergence phase tilt and momentum flux suggested by a previous study. Newtonian cooling makes the divergence tilt eastward moving away from the equator as observed, but this tilt is also sensitive to the Hadley cell. As the divergence tilt is enhanced in the downstream direction of the flow, wave propagation increases along that direction when the Hadley cell strengthens. The meridional flow also plays a second, important role for cross-equatorial propagation. With no Hadley cell, inviscid Sverdrup balance requires perfect compensation between the divergent and rotational momentum fluxes at the equator. The model can only produce cross-equatorial propagation when Sverdrup balance is violated, which in the linear, nearly inviscid limit requires vorticity advection by the mean flow. As the Hadley cell attenuates the geopotential tilt imparted by the divergent forcing, the compensation by the rotational momentum flux is reduced. The linear model can reproduce reasonably well previous nonlinear results by Kraucunas and Hartmann when linearized about their zonal-mean climatologies. The sensitivity of the cross-equatorial momentum fluxes to Hadley cell strength in these solutions is dominated by changes in the divergent flux and consistent with diagnosed changes in the divergence tilt.

The role of actin protrusion dynamics in cell migration through a degradable viscoelastic extracellular matrix: Insights from a computational model

Actin protrusion dynamics plays an important role in the regulation of three-dimensional (3D) cell migration. Cells form protrusions that adhere to the surrounding extracellular matrix (ECM), mechanically probe the ECM and contract in order to displace the cell body. This results in cell migration that can be directed by the mechanical anisotropy of the ECM. However, the subcellular processes that regulate protrusion dynamics in 3D cell migration are difficult to investigate experimentally and therefore not well understood. Here, we present a computational model of cell migration through a degradable viscoelastic ECM. The cell is modeled as an active deformable object that captures the viscoelastic behavior of the actin cortex and the subcellular processes underlying 3D cell migration. The ECM is regarded as a viscoelastic material, with or without anisotropy due to fibrillar strain stiffening, and modeled by means of the meshless Lagrangian smoothed particle hydrodynamics (SPH) method. ECM degradation is captured by local fluidization of the material and permits cell migration through the ECM. We demonstrate that changes in ECM stiffness and cell strength affect cell migration and are accompanied by changes in number, lifetime and length of protrusions. Interestingly, directly changing the total protrusion number or the average lifetime or length of protrusions does not affect cell migration. A stochastic variability in protrusion lifetime proves to be enough to explain differences in cell migration velocity. Force-dependent adhesion disassembly does not result in faster migration, but can make migration more efficient. We also demonstrate that when a number of simultaneous protrusions is enforced, the optimal number of simultaneous protrusions is one or two, depending on ECM anisotropy. Together, the model provides non-trivial new insights in the role of protrusions in 3D cell migration and can be a valuable contribution to increase the understanding of 3D cell migration mechanics.Author summaryThe ability of cells to migrate through a tissue in the human body is vital for many processes such as tissue development, growth and regeneration. At the same time, abnormal cell migration is also playing an important role in many diseases such as cancer. If we want to be able to explain the origin of these abnormalities and develop new treatment strategies, we have to understand how cells are able to regulate their migration. Since it is challenging to investigate cell migration through a biological tissue in experiments, computational modeling can provide a valuable contribution. We have developed a computational model of cell migration through a deformable and degradable material that describes both mechanics of the cell and the surrounding material and subcellular processes underlying cell migration. This model captures the formation of long and thin protrusions that adhere to the surrounding material and that pull the cell forward. It provides new non-trivial insights in the role of these protrusions in cell migration and the regulation of protrusion dynamics by cell strength and anisotropic mechanical properties of the surrounding material. Therefore, we believe that this model can be a valuable tool to further improve the understanding of cell migration.