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Living organisms survive and multiply even though they have uncertain and incomplete information about their environment and imperfect models to predict the consequences of their actions. Bayesian models have been proposed to face this challenge. Indeed, Bayesian inference is a way to do optimal reasoning when only uncertain and incomplete information is available. Various perceptive, sensory-motor, and cognitive functions have been successfully modeled this way. However, the biological mechanisms allowing animals and humans to represent and to compute probability distributions are not known. It has been proposed that neurons and assemblies of neurons could be the appropriate scale to search for clues to probabilistic reasoning. In contrast, in this paper, we propose that interacting populations of macromolecules and diffusible messengers can perform probabilistic computation. This suggests that probabilistic reasoning, based on cellular signaling pathways, is a fundamental skill of living organisms available to the simplest unicellular organisms as well as the most complex brains. [ABSTRACT FROM AUTHOR]

Abstract: Cell communication through biochemical signaling pathways is a key determinant of tissue responses to radiation. Several molecules, such as the transforming growth factor (TGF ), are implicated in radiation-induced signaling between cells. Brownian Dynamics (BD) algorithms have recently been used to simulate the interaction of ligands with receptors and to elucidate signal transduction and autocrine loops in ligand–receptors systems. In this paper, we discuss the simulation of particle diffusion and binding kinetics in a space bounded by two parallel plane membranes, using an exact algorithm to sample the propagator (Green’s function) of a particle located between 2 membranes. We also show that the simulation results are independent of the number of time steps used, in accordance with time discretization equations. These simulations could be used to simulate the motion and binding of ligand molecules in a cell culture, and possibly in neuronal synapses. [Copyright &y& Elsevier]

Highlights: [•] This new mathematical model describes pulsed-signal decoding in pituitary cells. [•] The model is based on experimental results published previously. [•] Model structure is drawn from techniques common in control system engineering. [•] Virtual experiments performed by simulation match the cell culture experiments. [•] Model shows how a network of simple biochemical processes can decode pulse signals. [ABSTRACT FROM AUTHOR]

The article offers information related to "Epithelial Cell Signaling Helps Maintain Tissue Integrity"by Annie Melchor,which appeared in the periodical "The Scientist Magazine "on November 8, 2021, is presented which includes topic on epithelial cells are known for formation of physical and chemical barriers in tissue.

The article presents a study, conducted by researcher E. Tamagno and colleagues, which reports on the betasite amyloid precursor protein (APP) cleaving enzyme up-regulation induced by 4- hydroxynonenal (HNE) is mediated by stress-activated protein kinases pathways. HNE, an aldehydic product of lipid peroxidation, up-regulates expression of the beta-site APP cleaving enzyme and results in increased levels of amyloid beta peptide. Tamagno and colleagues published their study in the "Journal of Neurochemistry."

The article cites a study which reports that amyloid precursor protein (APP) cleaving enzyme up-regulation induced by 4- hydroxynonenal (HNE) is mediated by stress-activated protein kinases pathways. Researchers E. Tamagno and colleagues wrote that HNE, an aldehydic product of lipid peroxidation, up-regulates expression of the beta-site APP cleaving enzyme and results in increased levels of amyloid beta peptide. Tamagno and colleagues published their study in the "Journal of Neurochemistry."

Reports that phosphoinositide 3-kinase-dependent signaling regulates embryonic stem cell self-renewal. Regulation of the maintenance of murine embryonic stem cell self-renewal by leukemia inhibitory factor (LIF)-dependent activation of signal transducer; Reduction of basal and LIF-stimulated phosphorylation of PKB/Akt, GSK3alpha/beta, and S6 proteins; Reversal of the effects of PI3K inhibition on self-renewal in a time- and dose-dependent manner.

Presents a study from the U.S. on the capability of modeled microgravity to disrupt collagen I/integrin signaling during osteoblastic differentiation of mesenchymal stem cells. Reduction of the expression of extracellular matrix protein; Decline of the autophosphorylation of adhesion-dependent kinases, focal adhesion kinase and proline-rich tyrosine kinase 2; Contribution of the process to reduced osteoblastogenesis.

Reports on the role of glycosyl phosphatidylinositol (GPI) anchored deficiency myeloid cells on causing impaired FcgammaR effector functions based from a study in Japan. Enhancement of FcgammaR effector functions in response to a model ligand; Use of myeloid-specific GPI-anchor-deficient mice during the study; Impairment of tyrosine phosphorylation of the FcR gamma-chain in response to immunoglobulin G in GPI-anchored deficient mice.