Field-Induced Electron Emission from Nanoporous Carbons

Influence of fabrication technology on field electron emission properties of nanoporous carbon (NPC) was investigated. Samples of NPC derived from different carbides via chlorination at different temperatures demonstrated similar low-field emission ability with threshold electric field 2-3 V/μm. This property correlated with presence of nanopores with characteristic size 0.5–1.2 nm, determining high values of specific surface area (>800 m2/g) of the material. In most cases, current characteristics of emission were approximately linear in Fowler-Nordheim coordinates (excluding a low-current part near the emission threshold), but the plots’ slope angles were in notable disagreement with the known material morphology and electronic properties, unexplainable within the frames of the classical emission theory. We suggest that the actual emission mechanism for NPC involves generation of hot electrons at internal boundaries and that emission centers may be associated with relatively large (20–100 nm) onion-like particles observed in many microscopic images. Such particles can serve two functions: to provide additional “internal” enhancement of the electric field and to inhibit relaxation of hot charge carriers due to the “phonon bottleneck” effect

A role of peptidoglycan recognition proteins in regulating innate immune response

By now, a whole number of pathogenic antibiotic-resistant or tolerant microorganisms has been progressively increased. Hence, efficient fight against them requires to change the class of antibiotics, increase their dose, or develop new antimicrobial drugs. On the contrary, another option could rely on augmenting innate immunity. During coevolution, eukaryotes have developed several ways for their protection against microorganisms. Innate immunity conserved in all multicellular organisms. The essential principles of innate immunity include recognition of a foreign structures and their subsequent destruction. A set of specific receptors recognize conserved pathogen-derived structures. Elimination occurs due to phagocytosis and cleavage, e.g. via oxidative burst in phagocytic cells, compliment system or antimicrobial peptides. Recognition system in innate immunity is based on the pattern recognition receptors. Due to the pathogen diversity, multiple conserved structures typical to pathogens (e.g. lipopolysaccharide, peptidoglycan, flagellin etc.) are sensed by numerous receptors. The family of peptidoglycan recognition proteins is among such receptors, which were first isolated in 1996 from the silkworm Bombyx mori and mice. Later, it was demonstrated that this family is conserved and its members are found in insects, fish and mammals. Here, functions of insect peptidoglycan recognition proteins in Drosophila melanogaster as well as mammals are discussed. Such proteins are expressed mainly in liver cells (insects — in adipose tissue cells as analogue of mammalian liver), intestinal cells, and epidermis. Numerous studies demonstrate that peptidoglycan-recognition proteins moderate immune response, and may act as antimicrobial proteins, or to regulate microbiota as well as prevent enterocyte activation and restrict inflammatory response. Due to evolutionary conservatism observed for such proteins and inability for bacteria to evade their protective effects, it seems promising to use peptidoglycan recognition proteins in a combination therapeutic approach against antibiotic-resistant and antibiotic-tolerant forms of microorganisms

Peripheral sensory neurons survive in the absence of α- and γ-synucleins

Physiological functions of α-synuclein, a protein implicated in certain types of neurodegeneration, and two other members of the same family, β-synuclein and γ-synuclein, are not clearly understood. It has been suggested that synucleins are involved in intracellular processes associated with survival of neurons and their response to stress, and that changes of synuclein ratio might have deteriorating effects on neurons. In wild-type mice, sensory neurons of the peripheral nervous system express α-synuclein and notably high levels of γ-synuclein, but targeted inactivation of either of these genes has no effect on these neurons. Here we produced double, α-synuclein/γ-synuclein null mutant mice, which develop normally, are fertile, and show no obvious signs of pathology in adulthood. Survival of α/γ-synuclein-deficient peripheral sensory neurons in vivo and in primary tissue culture is indistinguishable from survival of wild-type neurons. The absence of two synucleins does not lead to expression in sensory neurons of the third member of the family, β-synuclein. Therefore, our results demonstrate that neurons with normally high levels of synuclein(s) can develop and survive normally in the absence of any of these proteins. This suggests that other intraneuronal mechanisms and pathways effectively compensate the loss of synuclein function in null mutant animals. Copyright © 2005 Humana Press Inc. All rights of any nature whatsoever reserved

Автоэмиссионные свойства пленок никель - углеродного нанокомпозита

Field-emission properties of Ni-C nanocomposite thin films were experimentally studied. The films were deposited at Si substrates using CVD technique with a metalloorganic precursor and were composed by nm-scale grains of metallic Ni bounded with a carbonic weakly-conducting matrix. In the samples with lower effective thickness, the Ni particles were separated from each other. Such films showed capability of facilitated emission with threshold field values as low as a few V/μm. Thicker coating samples, with metallic particle merged in a conductive layer, required annealing at 470-600 °С in vacuum to produce low-field emission current. The observed emission behavior agrees with the previously proposed model considering low-field emission from nanostructured carbonic materials as a multi-stage process involving generation of hot electrons at interface boundaries.Были исследованы автоэмиссионные свойства тонких пленок никель-углеродного нанокомпозита. Пленки наносились на кремниевые подложки методом химического осаждения с использованием металлорганического прекурсора. Их структура включала в себя наноразмерные зерна металлического никеля, связанные слабопроводящей углеродосодержащей матрицей. В случае покрытий малой эффективной толщины, частицы никеля были отделены друг от друга. Такие пленки демонстрировали способность к низковольтной эмиссии в полях с напряженностью от нескольких В/мкм. В более толстых покрытиях металлические частицы образовывали единый электропроводящий слой. В этом случае для наблюдения низковольтной эмиссии требовался отжиг образцов в вакууме при 470-600 °С. Наблюдавшиеся закономерности эмиссии согласуются с предлагавшейся ранее моделью, которая рассматривает низковольтную эмиссию из наноуглеродных материалов как многостадийный процесс с участием горячих электронов, образующихся на внутренних междоменных границах

Peripheral sensory neurons survive in the absence of α- and γ-synucleins

Physiological functions of α-synuclein, a protein implicated in certain types of neurodegeneration, and two other members of the same family, β-synuclein and γ-synuclein, are not clearly understood. It has been suggested that synucleins are involved in intracellular processes associated with survival of neurons and their response to stress, and that changes of synuclein ratio might have deteriorating effects on neurons. In wild-type mice, sensory neurons of the peripheral nervous system express α-synuclein and notably high levels of γ-synuclein, but targeted inactivation of either of these genes has no effect on these neurons. Here we produced double, α-synuclein/γ-synuclein null mutant mice, which develop normally, are fertile, and show no obvious signs of pathology in adulthood. Survival of α/γ-synuclein-deficient peripheral sensory neurons in vivo and in primary tissue culture is indistinguishable from survival of wild-type neurons. The absence of two synucleins does not lead to expression in sensory neurons of the third member of the family, β-synuclein. Therefore, our results demonstrate that neurons with normally high levels of synuclein(s) can develop and survive normally in the absence of any of these proteins. This suggests that other intraneuronal mechanisms and pathways effectively compensate the loss of synuclein function in null mutant animals