Αξιολόγηση επιπέδων ατομικής και κοινωνικής υπευθυνότητας σε αθλητές ταεκβοντό.

Η υιοθέτηση υπεύθυνων στάσεων και συμπεριφορών από τους ανθρώπους είναι ένα ζήτημα ζωτικής σημασίας στις μέρες μας, καθώς παρατηρείται μια άνοδος στις ανεπιθύμητες συμπεριφορές. Το αθλητικό σωματείο ταεκβοντό ως φορέας αγωγής είναι υπεύθυνο και έχει την δυνατότητα να διδάξει όλες αυτές τις υπεύθυνες συμπεριφορές στους ασκούμενούς του. Σκοπός της παρούσας εργασίας ήταν η αξιολόγηση των επιπέδων ατομικής και κοινωνικής υπευθυνότητας σε αθλητές ταεκβοντό και η διερεύνηση διαφορών σε σχέση με την ηλικία και το φύλο τους. Στην έρευνα συμμετείχαν 116 παιδιά (68 αγόρια και 48 κορίτσια) ηλικίας 10-13 ετών (M = 11.34, SD = 1.09) από 14 σωματεία ταεκβοντό της Αττικής, και ταξινομήθηκαν σε δύο ηλικιακές κατηγορίες (1η: 10-11 ετών, 2η: 12-13 ετών). Η αξιολόγηση των επιπέδων της ατομικής και κοινωνικής υπευθυνότητας έγινε με την χρήση του Ερωτηματολογίου της Ατομικής και Κοινωνικής Υπευθυνότητας (ΕΑΚΥ). Από τα αποτελέσματα προέκυψε αναφορικά με την ατομική υπευθυνότητα πως δεν υπήρχαν διαφορές ανάμεσα στα αγόρια (M = 33.66, SD = 2.56) και τα κορίτσια (M = 33.39, SD = 2.75) και ανάμεσα στις ηλικιακές ομάδες 10-11(M = 33.31, SD = 2.81) και 12-13 ετών (M = 33.85, SD = 2.38). Αντίθετα, αν και οι διαφορές ανάμεσα στην κοινωνική υπευθυνότητα ως προς το φύλο, και την κοινωνική υπευθυνότητα ως προς τις δύο ηλικιακές ομάδες δεν ήταν στατιστικά σημαντικές (p > .05), εντούτοις, παρατηρήθηκε μια τάση για υψηλότερα επίπεδα στα κορίτσια (M = 40.08, SD = 1.86) και στις ηλικίες 12-13 ετών (M = 40.27, SD = 1.89). Τα αποτελέσματα αυτά συμφωνούν εν μέρει με κάποιες έρευνες που έχουν πραγματοποιηθεί στο μάθημα της φυσικής αγωγής, ενώ διαφωνούν με κάποιες άλλες. Θα πρέπει να πραγματοποιηθούν κι άλλες έρευνες που να αφορούν στην υπευθυνότητα των αθλητών ταεκβοντό ώστε να μπορούν να γενικευτούν τα συμπεράσματα. Ωστόσο, προτείνεται στους προπονητές του ταεκβοντό η χρήση του Μοντέλου Διδασκαλίας Ατομικής και Κοινωνικής Υπευθυνότητας, ως μέσου ενίσχυσης της υπευθυνότητας των παιδιών μέσα από το άθλημα.N

Reduced Liver Autophagy in High-Fat Diet Induced Liver Steatosis in New Zealand Obese Mice

Non-alcoholic fatty liver disease (NAFLD), as a consequence of overnutrition caused by high-calorie diets, results in obesity and disturbed lipid homeostasis leading to hepatic lipid droplet formation. Lipid droplets can impair hepatocellular function; therefore, it is of utmost importance to degrade these cellular structures. This requires the normal function of the autophagic-lysosomal system and the ubiquitin-proteasomal system. We demonstrated in NZO mice, a polygenic model of obesity, which were compared to C57BL/6J (B6) mice, that a high-fat diet leads to obesity and accumulation of lipid droplets in the liver. This was accompanied by a loss of autophagy efficiency whereas the activity of lysosomal proteases and the 20S proteasome remained unaffected. The disturbance of cellular protein homeostasis was further demonstrated by the accumulation of 3-nitrotyrosine and 4-hydroxynonenal modified proteins, which are normally prone to degradation. Therefore, we conclude that fat accumulation in the liver due to a high-fat diet is associated with a failure of autophagy and leads to the disturbance of proteostasis. This might further contribute to lipid droplet stabilization and accumulation

Punicalagin Attenuates Palmitate‐Induced Lipid Droplet Content by Simultaneously Improving Autophagy in Hepatocytes

SCOPE: Several studies show that excessive lipid intake can cause hepatic steatosis. To investigate lipotoxicity on cellular level, palmitate (PA) is often used to highly increase lipid droplets (LDs). One way to remove LDs is autophagy, while it is controversially discussed if autophagy is also affected by PA. It is aimed to investigate whether PA‐induced LD accumulation can impair autophagy and punicalagin, a natural autoph METHODS AND RESULTS: To verify the role of autophagy in LD degradation, HepG2 cells are treated with PA and analyzed for LD and perilipin 2 content in presence of autophagy inducer Torin 1 and inhibitor 3‐Methyladenine. PA alone seems to initially induce autophagy‐related proteins but impairs autophagic‐flux in a time‐dependent manner, considering 6 and 24 h PA. To examine whether punicalagin can prevent autophagy impairment, cells are cotreated for 24 h with PA and punicalagin. Results show that punicalagin preserves expression of autophagy‐related proteins and autophagic flux, while simultaneously decreasing LDs and perilipin 2. CONCLUSION: Data provide new insights into the role of PA‐induced excessive LD content on autophagy and suggest autophagy‐inducing properties of punicalagin, indicating that punicalagin can be a health‐beneficial compound for future research on lipotoxicity in liver

Proteostasis, oxidative stress and aging

The production of reactive species is an inevitable by-product of metabolism and thus, life itself. Since reactive species are able to damage cellular structures, especially proteins, as the most abundant macromolecule of mammalian cells, systems are necessary which regulate and preserve a functional cellular protein pool, in a process termed “proteostasis”. Not only the mammalian protein pool is subject of a constant turnover, organelles are also degraded and rebuild. The most important systems for these removal processes are the “ubiquitin-proteasomal system” (UPS), the central proteolytic machinery of mammalian cells, mainly responsible for proteostasis, as well as the “autophagy-lysosomal system”, which mediates the turnover of organelles and large aggregates. Many age-related pathologies and the aging process itself are accompanied by a dysregulation of UPS, autophagy and the cross-talk between both systems. This review will describe the sources and effects of oxidative stress, preservation of cellular protein- and organelle-homeostasis and the effects of aging on proteostasis in mammalian cells

Proteostasis, oxidative stress and aging

The production of reactive species is an inevitable by-product of metabolism and thus, life itself. Since reactive species are able to damage cellular structures, especially proteins, as the most abundant macromolecule of mammalian cells, systems are necessary which regulate and preserve a functional cellular protein pool, in a process termed “proteostasis”. Not only the mammalian protein pool is subject of a constant turnover, organelles are also degraded and rebuild. The most important systems for these removal processes are the “ubiquitin-proteasomal system” (UPS), the central proteolytic machinery of mammalian cells, mainly responsible for proteostasis, as well as the “autophagy-lysosomal system”, which mediates the turnover of organelles and large aggregates. Many age-related pathologies and the aging process itself are accompanied by a dysregulation of UPS, autophagy and the cross-talk between both systems. This review will describe the sources and effects of oxidative stress, preservation of cellular protein- and organelle-homeostasis and the effects of aging on proteostasis in mammalian cells

Early cysteine-dependent inactivation of 26S proteasomes does not involve particle disassembly

Under oxidative stress 26S proteasomes suffer reversible disassembly into its 20S and 19S subunits, a process mediated by HSP70. This inhibits the degradation of polyubiquitinated proteins by the 26S proteasome and allows the degradation of oxidized proteins by a free 20S proteasome. Low fluxes of antimycin A-stimulated ROS production caused dimerization of mitochondrial peroxiredoxin 3 and cytosolic peroxiredoxin 2, but not peroxiredoxin overoxidation and overall oxidation of cellular protein thiols. This moderate redox imbalance was sufficient to inhibit the ATP stimulation of 26S proteasome activity. This process was dependent on reversible cysteine oxidation. Moreover, our results show that this early inhibition of ATP stimulation occurs previous to particle disassembly, indicating an intermediate step during the redox regulation of the 26S proteasome with special relevance under redox signaling rather than oxidative stress conditions.DFG (German Research Foundation), by Spanish Government grants PI15/00107 and PT13/0001/0024 (partially funded by the European Union ERDF)Peer Reviewe

Punicalagin Attenuates Palmitate‐Induced Lipid Droplet Content by Simultaneously Improving Autophagy in Hepatocytes

SCOPE: Several studies show that excessive lipid intake can cause hepatic steatosis. To investigate lipotoxicity on cellular level, palmitate (PA) is often used to highly increase lipid droplets (LDs). One way to remove LDs is autophagy, while it is controversially discussed if autophagy is also affected by PA. It is aimed to investigate whether PA‐induced LD accumulation can impair autophagy and punicalagin, a natural autoph METHODS AND RESULTS: To verify the role of autophagy in LD degradation, HepG2 cells are treated with PA and analyzed for LD and perilipin 2 content in presence of autophagy inducer Torin 1 and inhibitor 3‐Methyladenine. PA alone seems to initially induce autophagy‐related proteins but impairs autophagic‐flux in a time‐dependent manner, considering 6 and 24 h PA. To examine whether punicalagin can prevent autophagy impairment, cells are cotreated for 24 h with PA and punicalagin. Results show that punicalagin preserves expression of autophagy‐related proteins and autophagic flux, while simultaneously decreasing LDs and perilipin 2. CONCLUSION: Data provide new insights into the role of PA‐induced excessive LD content on autophagy and suggest autophagy‐inducing properties of punicalagin, indicating that punicalagin can be a health‐beneficial compound for future research on lipotoxicity in liver