New Testament Principles Governing the Relationship Between the Christian and Civil Authorities and Their Elaboration in the Writings of Ellen G. White with Their Reflection in the Adventist Church in Romania

No Abstract. This Doctor of Ministry Project report falls under the category described in the Seminary Bulletin as Project II, a paper completed in fulfillment of requirements for an alternate curriculum plan under which the candidate prepares two related papers—a theological position paper addressing some issue or problem that exists in the Seventh-day Adventist Church in a theological setting and a professional paper addressing this same issue or problem from the standpoint of ministerial practice

Loss of Cellular K+ Mimics Ribotoxic Stress

The tumor promoter palytoxin has been found to activate the stress-activated protein kinase/c-Jun NH2-terminal kinase 1 (SAPK/JNK1), and it also potentiates, as demonstrated here, the p38/HOG1 mitogen-activated protein kinase and the upstream activator of SAPK/JNK1, SEK1/MKK4. In search of possible mechanisms for both the cytotoxicity and the activation of stress kinases by palytoxin, we found that palytoxin is a potent inhibitor of cellular protein synthesis. The inhibition of translation by palytoxin does not result from its direct binding to the translational apparatus. We have previously demonstrated that ribotoxic stressors (Iordanov, M. S., Pribnow, D., Magun, J. L., Dinh, T.-H., Pearson, J. A., Chen, S. L.-Y., and Magun, B. E. (1997) Mol. Cell. Biol. 17, 3373–3381) signal the activation of SAPK/JNK1 by binding to or covalently modifying 28 S rRNA in ribosomes that are active at the time of exposure to the stressor. Palytoxin acted as a ribotoxic stressor, inasmuch as it required actively translating ribosomes at the time of exposure to activate SAPK/JNK1. Palytoxin has been shown to augment ion fluxes by binding to the Na+/K+-ATPase in the plasma membrane of cells. To determine whether altered fluxes of either Na+ or K+ could be responsible for the effects of palytoxin on translation and on activation of SAPK/JNK1, cells were exposed to palytoxin in modified culture medium in which a major portion of the Na+ was replaced by either K+ or by choline+. The substitution of Na+ by K+ strongly inhibited the ability of palytoxin both to inhibit protein translation and to activate SAPK/JNK1, whereas the substitution of Na+ by choline+ did not. These results suggest that palytoxin-induced efflux of cellular K+ mimics ribotoxic stress by provoking both translational inhibition and activation of protein kinases associated with cellular defense against stress

New Semiempirical Equation Describing Evaporation and Condensation in Nonassociated Liquids

The consideration of the evaporating and condensing molecules’ interaction with the surface layer of nonassociated liquids made it possible to find an equation for relations between the saturated vapor pressure P, from one side, and surface tension, critical temperature, and molar volume of the liquids, from the other side. This equation takes into account the influence of intramolecular conformational transitions of evaporating molecules on the quantity of their energy barrier. There are two types of the condensation process for the nonassociated liquids: soft and hard molecular condensation. For some vapor molecules the surface layer of the liquids behaves as an impenetrable elastic film. In the case of evaporating molecules, their one-particle potential barrier caused by the surface molecules vibration is essentially higher for the conformationally flexible molecules than that for rigid ones

Different Mechanisms of c-Jun NH2-terminal Kinase-1 (JNK1) Activation by Ultraviolet-B Radiation and by Oxidative Stressors

Irradiation of mammalian cells with ultraviolet-B radiation (UV-B) triggers the activation of a group of stress-activated protein kinases known as c-Jun NH2-terminal kinases (JNKs). UV-B activates JNKs via UV-B-induced ribotoxic stress. Because oxidative stress also activates JNKs, we have addressed the question of whether the ribotoxic and the oxidative stress responses are mechanistically similar. The pro-oxidants sodium arsenite, cadmium chloride, and hydrogen peroxide activated JNK1 with slow kinetics, whereas UV-B potentiated the activity of JNK1 rapidly.N-acetyl cysteine (a scavenger of reactive oxygen intermediates) abolished the ability of all oxidative stressors tested to activate JNK1, but failed to affect the activation of JNK1 by UV-B or by another ribotoxic stressor, the antibiotic anisomycin. In contrast, emetine, an inhibitor of the ribotoxic stress response, was unable to inhibit the activation of JNK1 by oxidative stressors. Although UV-A and long wavelength UV-B are the spectral components of the ultraviolet solar radiation that cause significant oxidative damage to macromolecules, the use of a filter to eliminate the radiation output from wavelengths below 310 nm abolished the activation of JNK1 by UV. Our results are consistent with the notion that UV-B and oxidative stressors trigger the activation of JNK1 through different signal transduction pathways

D-MEKK1, the Drosophila orthologue of mammalian MEKK4/MTK1, and Hemipterous/D-MKK7 mediate the activation of D-JNK by cadmium and arsenite in Schneider cells

BACKGROUND: The family of c-Jun NH(2)-terminal kinases (JNK) plays important roles in embryonic development and in cellular responses to stress. Toxic metals and their compounds are potent activators of JNK in mammalian cells. The mechanism of mammalian JNK activation by cadmium and sodium arsenite involves toxicant-induced oxidative stress. The study of mammalian signaling pathways to JNK is complicated by the significant degree of redundancy among upstream JNK regulators, especially at the level of JNK kinase kinases (JNKKK). RESULTS: Using Drosophila melanogaster S2 cells, we demonstrate here that cadmium and arsenite activate Drosophila JNK (D-JNK) via oxidative stress as well, thus providing a simpler model system to study JNK signaling. To elucidate the signaling pathways that lead to activation of D-JNK in response to cadmium or arsenite, we employed RNA interference (RNAi) to knock down thirteen upstream regulators of D-JNK, either singly or in combinations of up to seven at a time. CONCLUSION: D-MEKK1, the fly orthologue of mammalian MEKK4/MTK1, and Hemipterous/D-MKK7 mediates the activation of D-JNK by cadmium and arsenite

Optical Pulling and Pushing Forces via Bloch Surface Waves

Versatile manipulation of nano- and microobjects underlies the optomechanics and a variety of its applications in biology, medicine, and lab-on-a-chip platforms. For flexible tailoring optical forces, as well as for extraordinary optomechanical effects, additional degrees of freedom should be introduced into the system. Here, we demonstrate that photonic crystals provide a flexible platform for nanoparticles optical manipulation due to both Bloch surface waves (BSWs) and the complex character of the reflection coefficient paving a way for complex optomechanical interactions control. We demonstrate that appearance of enhanced pulling and pushing transversal optical forces acting on a single bead placed above a one-dimensional photonic crystal due to directional excitation of Bloch surface wave at the photonic crystal interface. Our theoretical results, which are supported with numerical simulations, demonstrate angle or wavelength assisted switching between BSW-induced optical pulling and pushing forces. Easy-to-fabricate for any desired spectral range photonic crystals are shown to be prospective for precise optical sorting of nanoparticles, especially for core-shell nanoparticles, which are difficult to sort with conventional optomechanical methods. Our approach opens opportunities for novel optical manipulation schemes and platforms and enhanced light-matter interaction in optical trapping setups