ABSTRACT
CLINICAL RELEVANCE: Lithium disilicate veneers for esthetic restorations show great accuracy and similarity, regardless of the type of fabrication technique.
Subject(s)
Ceramics , Hot Temperature , Computer-Aided Design , Crowns , Dental Porcelain , Dental Prosthesis Design , Materials TestingABSTRACT
During early neurogenesis, retinal neuronal cells display a conserved differentiation program in vertebrates. Previous studies established that nitric oxide (NO) and cGMP accumulation regulate essential events in retinal physiology. Here we used pharmacological and genetic loss-of-function to investigate the effects of NO and its downstream signaling pathway in the survival of developing avian retinal neurons in vitro and in vivo. Six-day-old (E6) chick retinal cells displayed increased calcium influx and produced higher amounts of NO when compared with E8 cells. L-arginine (substrate for NO biosynthesis) and S-nitroso-N-acetyl-D,L-penicillamine (SNAP; a nitrosothiol NO donor) promoted extensive cell death in E6 retinas, whereas in E8 both substances decreased apoptosis. The effect of NO at both periods was mediated by soluble guanylyl cyclase (sGC) and cGMP-dependent kinase (cGK) activation. In addition, shRNA-mediated cGKII knockdown prevented NO-induced cell death (E6) and cell survival (E8). This, NO-induced cell death or cell survival was not correlated with an early inhibition of retinal cell proliferation. E6 cells also responded differentially from E8 neurons regarding cyclic AMP-responsive element-binding protein (CREB) activation in the retina in vivo. NO strongly decreased nuclear phospho-CREB staining in E6 but it robustly enhanced CREB phosphorylation in the nuclei of E8 neurons, an effect that was completely abrogated by cGKII shRNAs at both embryonic stages. The ability of NO in regulating CREB differentially during retinal development relied on the capacity of cGKII in decreasing (E6) or increasing (E8) nuclear AKT (V-Akt murine thymoma viral oncogene) activation. Accordingly, inhibiting AKT prevented both cGKII shRNA-mediated CREB upregulation in E6 and SNAP-induced CREB activation in E8. Furthermore, shRNA-mediated in vivo cGKII or in vitro CREB1 knockdown confirmed that NO/cGKII dualistically regulated the downstream CREB1 pathway and caspase activation in the chick retina to modulate neuronal viability. These data demonstrate that NO-mediated cGKII signaling may function to control the viability of neuronal cells during early retinal development via AKT/CREB1 activity.
Subject(s)
Cyclic AMP Response Element-Binding Protein/metabolism , Cyclic GMP-Dependent Protein Kinase Type II/metabolism , Nitric Oxide/metabolism , Proto-Oncogene Proteins c-akt/metabolism , Retina/growth & development , Animals , Apoptosis/genetics , Arginine/metabolism , Cell Survival/genetics , Chick Embryo , Cyclic GMP-Dependent Protein Kinase Type II/genetics , Embryonic Development , Neurogenesis/genetics , Nitric Oxide/genetics , Proto-Oncogene Proteins c-akt/genetics , Retina/metabolism , Signal Transduction/geneticsABSTRACT
In this paper, we systematically discuss the barocaloric effect in solid magnetic materials undergoing both second and first order phase transition. For this purpose, we use a model of localized magnetic moments, including the magnetoelastic coupling and the Zeemann interaction. Our calculations show that the normal (inverse) barocaloric effect occurs whenever the applied pressure increases (decreases) the critical temperature and keeps the order of the phase transition. On the other hand, our calculations predict an anomalous barocaloric effect (i.e. a change of sign in the barocaloric potentials) in special cases where the applied pressure changes the phase transition from first to second order and vice versa.
ABSTRACT
In this work the magnetocaloric effect is theoretically investigated considering a microscopic model Hamiltonian, which describes a magnetic system formed by two sublattices of different magnetic ions coupled by exchange and magnetoelastic interactions. We analyze systematically several profiles of the ferrimagnetic arrangements that were studied earlier without the magnetoelastic interaction. The influence of changing the magnetoelastic parameters on the magnetization, isothermal entropy change and adiabatic temperature change curves are investigated. Depending on the model parameters, the magnetic system shows a first-order magnetic phase transition leading to high direct and inverse magnetocaloric effect, besides two simultaneous first-order magnetic phase transitions which were predicted. A constant ΔS(T) = 0.4 J mol(-1) K(-1) is obtained in the simulated system in a temperature interval of 50 K, around 110 K.
ABSTRACT
The inverse magnetocaloric effect occurs when a magnetic material cools down under applied magnetic field in an adiabatic process. Although the existence of the inverse magnetocaloric effect was recently reported experimentally, a theoretical microscopic description is almost nonexistent. In this paper we theoretically describe the inverse magnetocaloric effect in antiferro- and ferrimagnetic systems. The inverse magnetocaloric effects were systematically investigated as a function of the model parameters. The influence of the Néel and the compensation temperature on the magnetocaloric effect is also analyzed using a microscopic model.
