279 research outputs found
Parametric design study - Recuperator development program, solar Brayton cycle system
Heat exchangers for recuperator in closed Brayton cycle space power system using solar energy and argo
Az agy öregedése és a neurodegeneráció: A neuroendokrin szabályozás szerepe = The role of neuroendocrine regulation in brain aging and neurodegeneration
A kutatás célja a hypophysis-mellékvesekéreg (HPA) hormonok és az ösztrogének szerepének vizsgálata volt az agy öregedésére és a neurodegenerációra patkányokban. Vizsgálták az öregkorban adott kortikoszteron (CORT) hatását a szerotoninerg és a kolinerg rostok degenerációjára az öregedés alatt. Vizsgálták továbbá az újszülöttkorban adott ACTH 4-9 analóg peptid hatását a HPA rendszer működésére és az adaptációs magatartásra felnőtt- és öregkorban. Tanulmányozták az agy öregedésével együtt járó szerotoninerg neurodegenerációt félmajmokon (Tupaia belangeri). Az öregkori CORT túladagolás krónikus körülmények között fokozta a szerotoninerg idegrostok degenerációját és csökkentette a tanulási teljesítményt. Immuncitokémiai módszerrel részletes leírást adtak az alfa és a béta típusú ösztrogén receptorok jellegzetességeiről öreg nőstény patkányok hippocampusában. Kimutatták, hogy az újszülöttkori ACTH peptid kezelés mellett az öregkorra jellemző napi kortikoszteron szint-ingadozás beszűkülése jelentős mértékben elmarad. Közölték, hogy az öregedés során a szerotoninerg rostok sűrűsége a hippocampus egyes régióiban szignifikánsan csökken félmajmokon. Végül jelentős előrelépés történt az in vivo állatkísérletes demencia modellek kidolgozásában patkányokon. Az eredmények azt mutatják, hogy az öregedés alatt jelentkező HPA és gonád hormon változások szerepet játszhatnak az öregedésre jellemző neuronális involúcióban és különösen a neurodegeneráció mechanizmusában. | The role of pituitary-adrenocortical hormones (HPA hormones) and that of estrogens on brain aging and neurodegeneration has been studied in rats. During aging the spontaneous degeneration of serotonergic and cholinergic fibers were studied after prolonged corticosterone (CORT) exposure. The immediate and long-term effects of neonatal administration of ACTH4-9 peptide analogue were investigated on the development and age-related functioning of HPA axis and adaptive behaviour. Furthermore, the age-dependent degeneration of serotonergic fibers was also followed in the hippocampus of tree shrews (Tupaia belangeri). Chronic CORT exposure in aged rats resulted in enhanced serotonergic fiber degeneration and inhibited learning performance. A detailed description of qualitative and quantitative aspects of alpha and beta estrogen receptors has been provided in the hippocampus of aging female rats. Neonatal treatment with ACTH4-9 peptide analogue prevented the age-specific attenuation of amplitude of diurnal CORT rhythm in the circulation. Aging has been coupled with a decrement of serotonergic fiber density in some subregions of hippocampus in old tree shrews. A considerable progress has also been achieved in the improvement of in vivo animal models studying brain neurodegeneration. The results show that the disturbed HPA and gonadal functions during aging might be contributing factors to neuronal decline in the advanced age and especially during neurodegeneration
A tápanyagfelvétel és az energia-háztartás neuroendokrin szabályozása = Neuroendocrine regulation of nutrition and energy homeostasis
Az elhízás epidemiológiai súlya egyre nyomasztóbb a társadalomban. Eredmények: 1) Vizsgálták az obezitogén és antiobezitogén környezeti hatásokat a magzati egyedfejlődés során. A többszörösen telítetlen zsírsavak (PUFA-k) metabolikus programozó hatását igazolták. Döntően az n-3 PUFA hiány a fejlődés során olyan kórélettani hatásokat produkált, ami a gyermekkori elhízás modelljének is megfelel: inzulin rezisztencia, csökkent glukóz tolerancia, csökkent leptin érzékenység, fokozott zsírlerakódás. A PUFA többlet, ezzel ellentétesen, csökkentette a vér inzulin és leptin szinteket, csökkent a vér triglicerid és nőtt a HDL koleszterin mennyiség, javult a glukóz tolerancia. Néhány metabolikus hatás és a javuló kognitív teljesítmény még öregkorban is kimutatható volt. 2) A táplálék felvétel és az energia háztartás hypothalamikus szabályozásának vizsgálata során kimutatták, hogy kolinerg neuronok találhatók a n. arcuatusban, melyek orexigén támogató hatásukat az M3-as receptoron fejtik ki. M3 receptor antagonistával a neurogén elhízás kivéghető. Továbbá valószínű, hogy a hypothalamikus kolinerg rendszer szerepet játszik a vízfelvétel szabályozásában is. 3) Magatartási szelekcióval előidézett, epigenetikailag rögzült fokozott fizikai aktivitás egerekben olyan anyagcsere változásokat hozott létre, melyek megakadályozták a zsírdús diéta által kiváltott elhízást. Konklúzió: az elhízás prevenciója mind genetikai, mind környezeti hatások szempontjából megvalósíthatónak számít. | The epidemiologic burden of obesity extensively risks the health of society. Aims and results: 1) The obesitogenic and antiobesitogenic environmental factors during fetal development were investigated. The programming action of poly-unsaturated fatty acids (PUFAs) has been proven. PUFA deficient diet produced symptoms characteristic to childhood obesity: insulin resistance, decreased glucose tolerance, decreased leptin sensitivity, increase fat deposition. Contrary, PUFA supplementation decreased blood insulin, leptin and triglycerides levels, increased HDL cholesterol and glucose tolerance. Some metabolic effects and the improved cognitive performance lasted up to old ages. 2) Interaction between peptidergic and classical (cholinerg) neurotransmitter systems was also studied in the regulation of food intake and energy metabolism. Cholinerg neurons have been found in the n. arcuatus, which exert orexigen support on MCH neurons through M3 receptors and markedly influence water intake as well. M3 antagonist 4-DAMP prevented neurogen obesity induced by SHU9119. 3) Interaction between nutrition and physical activity studies showed that mice selected for high running wheel activity showed profound antiobesitogenic metabolic changes and consequent resistance against diet induced obesity. Summary: the results showed that obesity prevention can be supported by both genetic and environmental interventions in the course of development
Temporal and spatial dynamics of corticosteroid receptor down-regulation in rat brain following social defeat
The experiments explored the nature and time course of changes in glucocorticoid receptor (GR) and mineralocorticoid receptor (MR) binding in homogenates of various brain regions and pituitary of male Wistar rats following social defeat stress. One week after defeat, the binding capacity of GRs was decreased in the hippocampus and the hypothalamus while no changes were observed in the parietal cortex and the pituitary. The number of MRs remained at the same level as in undefeated rats. Three weeks postdefeat, the initially down-regulated GR returned to baseline level in the hippocampus and the hypothalamus. However, GR binding was now decreased in the parietal cortex. Severe down-regulation of MRs was detected in the hippocampal and septal tissue. The results show that brief but intense stress like social defeat induces a long-lasting down-regulation of corticosteroid receptors and that the temporal dynamics of these changes are not only differential for GRs and MRs but also for brain sites.
An integrated gene regulatory network controls stem cell proliferation in teeth.
Epithelial stem cells reside in specific niches that regulate their self-renewal and differentiation, and are responsible for the continuous regeneration of tissues such as hair, skin, and gut. Although the regenerative potential of mammalian teeth is limited, mouse incisors grow continuously throughout life and contain stem cells at their proximal ends in the cervical loops. In the labial cervical loop, the epithelial stem cells proliferate and migrate along the labial surface, differentiating into enamel-forming ameloblasts. In contrast, the lingual cervical loop contains fewer proliferating stem cells, and the lingual incisor surface lacks ameloblasts and enamel. Here we have used a combination of mouse mutant analyses, organ culture experiments, and expression studies to identify the key signaling molecules that regulate stem cell proliferation in the rodent incisor stem cell niche, and to elucidate their role in the generation of the intrinsic asymmetry of the incisors. We show that epithelial stem cell proliferation in the cervical loops is controlled by an integrated gene regulatory network consisting of Activin, bone morphogenetic protein (BMP), fibroblast growth factor (FGF), and Follistatin within the incisor stem cell niche. Mesenchymal FGF3 stimulates epithelial stem cell proliferation, and BMP4 represses Fgf3 expression. In turn, Activin, which is strongly expressed in labial mesenchyme, inhibits the repressive effect of BMP4 and restricts Fgf3 expression to labial dental mesenchyme, resulting in increased stem cell proliferation and a large, labial stem cell niche. Follistatin limits the number of lingual stem cells, further contributing to the characteristic asymmetry of mouse incisors, and on the basis of our findings, we suggest a model in which Follistatin antagonizes the activity of Activin. These results show how the spatially restricted and balanced effects of specific components of a signaling network can regulate stem cell proliferation in the niche and account for asymmetric organogenesis. Subtle variations in this or related regulatory networks may explain the different regenerative capacities of various organs and animal species
The vanishing ideal of a finite set of points with multiplicity structures
Given a finite set of arbitrarily distributed points in affine space with
arbitrary multiplicity structures, we present an algorithm to compute the
reduced Groebner basis of the vanishing ideal under the lexicographic ordering.
Our method discloses the essential geometric connection between the relative
position of the points with multiplicity structures and the quotient basis of
the vanishing ideal, so we will explicitly know the set of leading terms of
elements of I. We split the problem into several smaller ones which can be
solved by induction over variables and then use our new algorithm for
intersection of ideals to compute the result of the original problem. The new
algorithm for intersection of ideals is mainly based on the Extended Euclidean
Algorithm.Comment: 12 pages,12 figures,ASCM 201
Efficient Computation of Squarefree Separator Polynomials
Given a finite set of distinct points, a separator family is a set of polynomials, each one corresponding to a point of the given set, such that each of them takes value one at the corresponding point, whereas it vanishes at any other point of the set. Separator polynomials are fundamental building blocks for polynomial interpolation and they can be employed in several practical applications. Ceria and Mora recently developed a new algorithm for squarefree separator polynomials. The algorithm employs as a tool the point trie structure, first defined by Felszeghy-R\ue1th-R\uf3nyai in their Lex game algorithm, which gives a compact representation of the relations among the points\u2019 coordinates. In this paper, we propose a fast implementation in C of the aforementioned algorithm, based on an efficient storing and visiting of the point trie. We complete the implementation with tests on some sets of points, giving different configurations of the corresponding tries
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