Szakmai képzés – elhelyezkedés

Jelen fejezetben vizsgáljuk a hazai felsőfokú ifjúságsegítő szakképesítés alakulását, továbblépési irányait; ezen túlmenően megnézzük, hogy a megszerzett szakképesítéssel milyen lehetőségek adódnak az elhelyezkedésre, azaz miként alakulnak a szakmai képzettséggel betölthető munkakörök. Az ifjúságsegítő képzésekből kikerülő hallgatók munkájukat az egyre fontosabb területnek számító családon és iskolán túli harmadlagos szocializációs közegben végzik, célcsoportjukat egy nehezen definiálható, magukért már igen, másokért még felelősséget nem vállaló, kb. 10-30 éves korosztály jelenti. Az ifjúságsegítők, illetve ilyen szaktudással is rendelkező, más szakirányú végzettséggel rendelkező – szakemberek kulcsszerepet játszhatnak abban, hogy a fiatalok már a munkába lépés előtt elsajátíthassák az önálló életvitelhez, a munkavállaláshoz és a munkahelyen maradáshoz szükséges készségeket (Az ifjúságsegítő képzés interprofesszionális fejlesztése, 2012)

Immunmoduláló humán galektin-1 által kiváltott T-sejt apoptózis molekuláris mechanizmusa = Molecular mechanism of T-cell apoptosis induced by human galectin-1

A galektin-1 egy új immunszuppresszív stratégiát szolgáltathat a a gyulladásos és autoimmun betegségek gyógyításában. A Gal-1 a tumorok rossz prognózisának is kiváló diagnosztikus markere. Jelen ismereteink szerint a Gal-1 immunreguláló hatása az aktivált T-sejtek apoptózisának indukcióján alapul. A Gal-1 immunválasz szabályozó hatása miatt felvetődik gyakorlati, terápiás felhasználása. Ezért alapvető, hogy, a pályázat célkitűzése szerint, a Gal-1 által kiváltott sejthalál mechanizmusát a részletes módon megismerjük. Összehasonlító vizsgálatunkkal, mely tisztázott egy régi ellentmondást, bizonyítottuk, hogy a Gal-1, koncentrációjától függően, más mechanizmus szerint váltja ki a T-sejt pusztulást. Tisztáztuk, hogy a fiziológiás sejthalált a sejtkötött és az alacsony koncentrációban alkalmazott szolubilis Gal-1 váltja ki. A Gal-1 termelő tumor sejt a vele kölcsönhatásba kerülő T-sejtben az Lck kináz és tirozin foszforilált fehérjék specifikus átrendeződését indukálja, mely a sejt-sejt kölcsönhatás felületével ellentétes oldalon figyelhető meg. A Gal-1 a GM1-gangliozid és a CD7 közvetítésével internalizálódik, ez a jelenség tehető felelőssé a Gal-1 késleltetett hatásáért. A Gal-1 monomer és dimer formában fordulhat elő, de nem egyértelmű, hogy melyik forma a fiziológiailag aktív . Ex vivo kísérletünkkel igazoltuk, hogy a monomer Gal-1, a dimerhez hasonló T-sejt apoptózist okoz, egy a szénhidrát kötő helytől független fehérje kötő motívumot feltételezve | Galectin-1 is considered as a novel immunosuppressive strategy in immune diseases. It is also a valuable marker in the prognosis of malignant tumors. The immunosuppressive effect of Gal-1 is attributed to its cytotoxic effect on activated T cells. Due to its immunoregulatory effect, its therapeutical application has been suugested. Therefore, in according to the aim of the project, we characterized the most detailed mechanism of the Gal-1 induced T-cell apoptosis. We resolved a long lasting conflict in the literature. In a comparative work it has been proved that Gal-1 acts as an apoptotic agent by different mechanism depending on its concentration. It has been clarified that the cell-derived or low concentration soluble Gal-1 represent the physiological function of this protein. It has also been determined that during cell-cell interaction, Lck and tyrosine phosphorylated proteins localize to the distal membrane region on a Gal-1 dependent fashion. Gal-1 is rapidly internalized via GM1 gangliozide and CD7 and this event may be responsible for the delayed apoptotic action of Gal-1. Gal-1 can occur in monomer and dimmer form. However it is not revealed which form represents the biologically active form. In ex vivo experiment we showed that the monomer Gal-1 is similarly effective in induction of T-cell apoptosis as the dimmer is. These results suggest that in addition to the sugar binding site Gal-1 also contain a protein binding motif

Genetics, molecular and cell biology of apoptotic cell death

Apoptotic cell death is an integral part of development and cell turnover in multicellular organisms. Since early 1970’s, when apoptosis was defined on morphological basis, plethora of genes has been identified participating in initiation, execution and regulation of cell death. This article reviews these latest advances and describes our present understanding of the sequential events of apoptotic cell death, from the early steps of death receptor initiated and mitochondrial pathways to activation of caspases, and finally, the proper corpse clearance. It also discusses dysregulation of apoptosis, leading to various pathologies, such as cancer, autoimmune disease and neurodegenerative disorders

Novel role for galectin-1 in T-cells under physiological and pathological conditions

Secreted, extracellular galectin-1 (exGal-1) but not intracellular Gal-1 (inGal-1) has been described as a strong immunosuppressive protein due to its major activity of inducing apoptosis of activated T-cells. It has previously been reported that T-cells express Gal-1 upon activation, however its participation in T-cell functions has remained largely elusive. To determine function of Gal-1 expressed by activated T-cells we have carried out a series of experiments. We have shown that Gal-1, expressed in Gal-1-transgenic Jurkat cells or in activated T-cells, remained intracellularly indicating that Gal-1-induced T-cell death was not a result of an autocrine effect of the de novo expressed Gal-1. Rather, a particular consequence of the inGal-1 expression was that T-cells became more sensitive to exGal-1 added either as a soluble protein or bound to the surface of a Gal-1-secreting effector cell. This was also verified when the susceptibility of activated T-cells from wild type or Gal-1 knockout mice to Gal-1-induced apoptosis were compared. Murine T-cells expressing Gal-1 were more sensitive to the cytotoxicity of the exGal-1 than their Gal-1 knockout counterparts. We also conducted a study with activated T-cells from patients with systemic lupus erythematosus (SLE), a disease in which dysregulated T-cell apoptosis has been well described. SLE T-cells expressed lower amounts of Gal-1 than healthy T-cells and were less sensitive to exGal-1. These results suggested a novel role of inGal-1 in T-cells as a regulator of T-cell response to exGal-1, and its likely contribution to the mechanism in T-cell apoptosis deficiency in lupus

Licensing by Inflammatory Cytokines Abolishes Heterogeneity of Immunosuppressive Function of Mesenchymal Stem Cell Population

When mesenchymal stem cells (MSCs) are used for therapy of immunological pathologies, they get into an inflammatory environment, altering the effectiveness of the treatment. To establish the impact of environmental inflammatory factors on MSCs' immunofunction in the mirror of intrinsic heterogeneity of mouse MSC population, individual MSC clones were generated and characterized. Adipogenic but not osteogenic differentiation and pro-angiogenic activity of five independent MSC cell lines were similar. Regarding osteogenic differentiation, clones MSC3 and MSC6 exhibited poorer capacity than MSC2, MSC4, and MSC5. To study the immunosuppressive heterogeneity, in vitro and in vivo experiments have been carried out using T-cell proliferation assay and delayed-type hypersensitivity (DTH) response, respectively. A remarkable difference was found between the clones in their ability to inhibit T-cell proliferation in the following order: MSC2MSC5>MSC4>MSC3>>MSC6. Nevertheless, the differences between the immunosuppressive activities of the individual clones disappeared on pretreatment of the cells with pro-inflammatory cytokines, a procedure called licensing. Stimulation of all clones with IFN- and TNF- resulted in elevation of their inhibitory capability to a similar level. Nitric oxide (NO) and prostaglandin E2 (PGE2) were identified as major mediators of immunofunction of the MSC clones. The earlier findings were also supported by in vivo results. Without licensing, MSC2 inhibited DTH response, while MSC6 did not affect DTH response. In contrast, prestimulation of MSC6 with inflammatory cytokines resulted in strong suppression by this clone as well. Here, we have showed that MSC population is functionally heterogeneous in terms of immunosuppressive function; however, this variability is largely reduced under pro-inflammatory conditions

Characterization and therapeutic application of canine adipose mesenchymal stem cells to treat elbow osteoarthritis

Visceral adipose tissue (AT) obtained from surgical waste during routine ovariectomies was used as a source for isolating canine mesenchymal stem cells (MSCs). As determined by cytofluorimetry, passage 2 cells expressed MSC markers CD44 and CD90 and were negative for lineage-specific markers CD34 and CD45. The cells differentiated toward osteogenic, adipogenic, and chondrogenic directions. With therapeutic aims, 30 dogs (39 joints) suffering from elbow dysplasia (ED) and osteoarthritis (OA) were intra-articularly transplanted with allogeneic MSCs suspended in 0.5% hyaluronic acid (HA). A highly significant improvement was achieved without any medication as demonstrated by the degree of lameness during the follow-up period of 1 y. Control arthroscopy of 1 transplanted dog indicated that the cartilage had regenerated. Histological analysis of the cartilage biopsy confirmed that the regenerated cartilage was of hyaline type. These results demonstrate that transplantation of allogeneic adipose tissue-derived mesenchymal stem cells (AT-MSCs) is a novel, noninvasive, and highly effective therapeutic tool in treating canine elbow dysplasia. © 2017, Canadian Veterinary Medical Association. All rights reserved

Characterization and therapeutic application of canine adipose mesenchymal stem cells to treat elbow osteoarthritis

Visceral adipose tissue (AT) obtained from surgical waste during routine ovariectomies was used as a source for isolating canine mesenchymal stem cells (MSCs). As determined by cytofluorimetry, passage 2 cells expressed MSC markers CD44 and CD90 and were negative for lineage-specific markers CD34 and CD45. The cells differentiated toward osteogenic, adipogenic, and chondrogenic directions. With therapeutic aims, 30 dogs (39 joints) suffering from elbow dysplasia (ED) and osteoarthritis (OA) were intra-articularly transplanted with allogeneic MSCs suspended in 0.5% hyaluronic acid (HA). A highly significant improvement was achieved without any medication as demonstrated by the degree of lameness during the follow-up period of 1 y. Control arthroscopy of 1 transplanted dog indicated that the cartilage had regenerated. Histological analysis of the cartilage biopsy confirmed that the regenerated cartilage was of hyaline type. These results demonstrate that transplantation of allogeneic adipose tissue-derived mesenchymal stem cells (AT-MSCs) is a novel, noninvasive, and highly effective therapeutic tool in treating canine elbow dysplasia. © 2017, Canadian Veterinary Medical Association. All rights reserved

EFFECTS OF LIGHT INTENSITY AND SPECTRAL COMPOSITION ON THE GROWTH AND METABOLISM OF SPINACH (SPINACIA OLERACEA L.)

Abstract: Spinach rich in proteins, minerals (Fe, K) and antioxidants (vitamin C) is often cultivated in greenhouses under artificial light. In this study, the effects of light intensity and spectral composition provided by light emitting diodes (LEDs) was studied on the yield quality and quantity of spinach. Plants were grown under 3 different light intensities (100/200/300 mol m-2s -1) and 3 spectral compositions (white/white completed with blue or far-red) for 4 weeks. Then plant weight, leaf number and area, photosynthetic activity and pigment composition of leaves were determined. The leaf quality was characterized by measurements of protein, starch, soluble sugar and ascorbate contents of leaves. Moreover, minerals (K, Fe and NO3 ̅) were also determined. While the biomass production was mainly determined by the light intensity, the yield quality is influenced significantly by the spectral composition. When the white light was supplemented with blue, high protein and ascorbate content was achieved. When far-red was added to white light, elevated sugar and Fe accumulation was observed in the leaves, while the K content decreased. In order to reach the hight quality and quantity of food production, not only the light fluence, but also the spectral composition should be regulated

Effects of light intensity and spectral composition on the growth and metabolism of spinach (SPINACIA OLERACEA L.)

Spinach rich in proteins, minerals (Fe, K) and antioxidants (vitamin C) is often cultivated in greenhouses under artificial light. In this study, the effects of light intensity and spectral composition provided by light emitting diodes (LEDs) was studied on the yield quality and quantity of spinach. Plants were grown under 3 different light intensities (100/200/300 mol m -2 s ) and 3 spectral compositions (white/white completed with blue or far-red) for 4 weeks. Then plant weight, leaf number and area, photosynthetic activity and pigment composition of leaves were determined. The leaf quality was characterized by measurements of protein, starch, soluble sugar and ascorbate contents of leaves. Moreover, minerals (K, Fe and NO 3 ̅ -1 ) were also determined. While the biomass production was mainly determined by the light intensity, the yield quality is influenced significantly by the spectral composition. When the white light was supplemented with blue, high protein and ascorbate content was achieved. When far-red was added to white light, elevated sugar and Fe accumulation was observed in the leaves, while the K content decreased. In order to reach the hight quality and quantity of food production, not only the light fluence, but also the spectral composition should be regulated