Sevoflurane (2,2,2-trifluoro-1-[trifluoromethyl]ethyl fluoromethyl ether or C4H3F7O), with a molar mass 200.055 g/mol, also called fluoromethyl, is a highly fluorinated methyl isopropyl ether with general anesthetic property, available for clinical practice for about 30 years. Sevoflurane is a sweet-smelling, non-flammable and it is used for induction and maintenance of general anesthesia. Together with desflurane, it is replacing isoflurane and halothane in modern anesthesiology. Propofol (2,6-diisopropylphenol or C12H18O), with a molar mass 178.271g/mol is an alkylphenol derivative formulated for induction and maintenance (in some cases) of general anesthesia, sedation and hypnosis and acting as an intravenous anaesthetic drug, having largely replaced sodium thiopental because recovery from propofol is more rapid and clear.
In multicellular organisms, both health and disease are defined by means of communication patterns involving the component cells. Despite the intricate networks of soluble mediators, cells are also programed to exchange complex messages pre-assembled as multimolecular cargo of membranous structures known as extracellular vesicles (EVs). Several biogenetic pathways produce EVs with different properties able to orchestrate neighboring cell reactions or to establish an environment ripe for spreading tumor cells. Such an effect is in fact an extension of similar physiological roles played by exosomes in guiding cell migration under nontumoral tissue remodeling and organogenesis. We start with a biological thought experiment equivalent to Bénard's experiment, involving a fluid layer of EVs adherent to an extracellular matrix, in a haptotactic gradient, then, we build and present the first Lorenz model for EVs migration. Using Galerkin's method of reducing a system of partial differential equations to a system of ordinary differential equations, a biological Lorenz system is developed. Such a physical frame distributing individual molecular or exosomal type cell-guiding cues in the extracellular matrix space could serve as a guide for tissue neoformation of the budding pattern in nontumoral or tumoral instances.
Our studies aimed the effects of some endoplasmic reticulum stress inducers (thapsigargin, a Ca2+-ATP-ase inhibitor; tunicamycin, a protein N-glycosylation inhibitor; brefeldin A, a protein transport inhibitor; paraquat, an enhancer of reactive oxygen species production; A23187, a Ca2+ ionophore), as well as some antioxidants (N-acetylcysteine; dithiothreitol, a disulfide bond formation inhibitor) on apoptosis of cultured rat mesenchymal stem cells. The analyze of obtained results evidenced that paraquat, a common and effective herbicide, induced the apoptosis of the isolated rat mesenchymal stem cells in a larger proportion as compared to other chemicals as follows: paraquat ] thapsigargin ] tunicamycin @A23187 ] brefeldin A. Dithiothreitol was effective as a reducer of mesenchymal stem cells apoptosis when was administered as co-treatment for paraquat for 24 h. In contrast, N-acetylcysteine, another potent antioxidant, had no protective effects against paraquat apoptotic effects.
The studies we performed targeted the effects of all-trans retinol (vitamin A) and some retinoid derivatives (including tretinoin or all-trans retinoic acid, retinyl propionate, 9-cis retinoic acid, 13-cis retinoic acid), as well as of tazarotenic acid on apoptosis of rat mesenchymal stem cells, cultured after isolation. Tazarotenic acid is considered to be relatively selective and a potent agonist for RARb and RARg and less for RARa. The same time, tazarotenic acid is not binding to RXRs (retinoid X receptors). The relevant analysis of our experimental results demonstrated that 13-cis retinoic acid was the most potent inducer of apoptosis of cultured mesenchymal stem cells of rat origin when compared to other retinoid derivatives, as follows: 13-cis retinoic acid ] 9-cis retinoic acid ] tazarotenic acid ] all-trans retinoic acid ] retinyl propionate ] retinol (or vitamin A). Very interesting and unexpected were the apoptotic effects of 1 �M tazarotenic acid for 24 hours in our experiments, very close to those induced by all-trans retinoic acid (tretinoin). The apoptosis induced by 13-cis retinoic acid, a principal activator of RARb and RARg, and that induced by 9-cis retinoic acid, a major activator of RXRs, suggests different pathways activated by these retinoid derivatives.
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