Pronto pago laboral. Procedimiento

En el marco del principio protectorio del Derecho del Trabajo ubicamos al pronto pago laboral, concebido como un mecanismo de autorización de pago sin la sentencia previa o el pedido de verificación del crédito  que la ley exige para los acreedores no laborales. Los sistemas de pronto pago y las reglas procesales aplicables al mismo han sido objeto de diversas modificaciones. En el presente trabajo intentamos un estudio sistemático de dichas reformas, partiendo de un breve estudio de los antecedentes legislativos en la materia, señalando las variantes producidas, para finalmente referirnos al estudio del texto legal actualizado, especialmente en lo que respecta a los créditos comprendidos y a los sistemas de pronto pago de oficio o a solicitud del acreedor

Protective effects of the thioredoxin and glutaredoxin systems in dopamine-induced cell death

Although the etiology of sporadic Parkinson disease (PD) is unknown, it is well established that oxidative stress plays an important role in the pathogenic mechanism. The thioredoxin (Trx) and glutaredoxin (Grx) systems are two central systems upholding the sulfhydryl homeostasis by reducing disulfides and mixed disulfides within the cell and thereby protecting against oxidative stress. By examining the expression of redox proteins in human postmortem PD brains, we found the levels of Trx1 and thioredoxin reductase 1 (TrxR1) to be significantly decreased. The human neuroblastoma cell line SH-SY5Y and the nematode Caenorhabditis elegans were used as model systems to explore the potential protective effects of the redox proteins against 6-hydroxydopamine (6-OHDA)-induced cytotoxicity. 6-OHDA is highly prone to oxidation, resulting in the formation of the quinone of 6-OHDA, a highly reactive species and powerful neurotoxin. Treatment of human cells with 6-OHDA resulted in an increased expression of Trx1, TrxR1, Grx1, and Grx2, and small interfering RNA for these genes significantly increased the cytotoxic effects exerted by the 6-OHDA neurotoxin. Evaluation of the dopaminergic neurons in C. elegans revealed that nematodes lacking trxr-1 were significantly more sensitive to 6-OHDA, with significantly increased neuronal degradation. Importantly, both the Trx and the Grx systems were also found to directly mediate reduction of the 6-OHDA-quinone in vitro and thus render its cytotoxic effects. In conclusion, our results suggest that the two redox systems are important for neuronal survival in dopamine-induced cell death. © 2014 Elsevier Inc.A.P.F. was supported by Stiftelsen Lars Hiertas Minne and Karolinska Institutet research grants. Research in the Swoboda laboratory was supported by the Swedish Research Council (VR) and the NordForsk Nordic network for C. elegans research. A.M.-V. was supported by the Instituto de Salud Carlos III (Projects PI050065 and PI080557, cofinanced by the Fondo Social Europeo, FEDER) and Junta de Andalucía (Projects P07-CVI-02697 and P08-CVI-03629), Spain. Some C. elegans strains were provided by the CGC, which is funded by the NIH Office of Research Infrastructure Programs (P40 OD010440).Peer Reviewe

Redox processes and oxidative stress in cell and tissue damage

Oxidative stress is described as an imbalance between oxidants and antioxidants, with a shift towards the oxidants. When the antioxidative systems are insufficient or the production of radicals is increased oxidative damage can occur, damaging DNA, lipids, and proteins. Oxidative stress has been implicated in several pathologies. This study has been focused on oxidative damage caused to the cysteine residues on proteins. The main function of the thioredoxin (Trx) and the glutaredoxin (Grx) systems is to reduce protein thiols and they therefore play an important role in the protection against oxidative stress. Alzheimer’s disease is a progressive disease with a high prevalence in an aging population. Oxidative stress has been implicated in the disease, as demonstrated by elevated levels of oxidized proteins, lipids, carbohydrates and nucleic acids. In our study we were able to show that Trx and Grx were secreted to CSF, and that the levels of the proteins correlated with the previously validated markers tau and p-tau in patients with different stages of AD. The secretion was not caused by cell death as the levels of lactate dehydrogenase did not change between the different stages. Furthermore, decreased axonal staining of Grx1 and Grx2, as well as decreased mitochondrial staining of Trx2 was observed in AD hippocampus. Parkinson’s disease (PD) is characterized by loss of dopaminergic neurons in the substantia nigra. The neurotransmitter dopamine has been implicated in the pathology, as rupture of the dopamine vesicles leads to increased cytosolic dopamine levels. Free in the cytosol, dopamine gets oxidized with a release of radicals in the process. We can show a direct interaction between the Trx system and the dopamine-quinone. Furthermore, a protective effect of TrxR against dopamine toxicity was observed in both the cell line SH-SY5Y and in the nematode C. elegans. In addition, decreased levels of Trx1 and TrxR1 were observed in substantia nigra from PD patients. Ischemia causes a conversion of xanthine dehydrogenase into xanthine oxidase, upon reperfusion xanthine oxidase releases radicals, leading to an increased oxidative stress in the tissues. Ischemia/reperfusion was induced in human livers, and samples were taken before induction of ischemia, after ischemia and after reperfusion. We demonstrated that the major reperfusion damage was to the sinusoidal endothelial lining, where a retraction of the lining occurred after ischemia, but after 20 minutes of reperfusion the cell lining had partially recovered. No significant changes in mRNA levels of redox proteins could be observed, but likely redistribution of Trx occurred in the hepatocytes. Cell lines are commonly used in medical research, but a consensus in how to culture the cells is lacking. In order to study the effect of media selection, three different cell lines were cultured in four commonly used cell culturing media. We could observe increased proliferation of cells grown in the high glucose containing DMEM. Increased expression for mesenchymal marker Vimentin in A549 cells cultured in DMEM, and decreased expression of epithelial marker CK18, which indicates a possible change in phenotype due to the selection of media. Furthermore, increased enzymatic activity of TrxR in cells cultured in MEM compared to the other media was observed, and decreased selenite toxicity in cells cultured in DMEM compared to culture in RPMI or F12. This study highlights the importance of consistency in the choice of cell culturing media for the outcome of any cell experiment. In conclusion, the thioredoxin family of proteins has been shown to be implicated in several pathological conditions where oxidative stress is believed to be important

Secretome of Undifferentiated Neural Progenitor Cells Induces Histological and Motor Improvements in a Rat Model of Parkinson's Disease

Parkinson's disease (PD) is a progressive neurodegenerative movement disorder that results from the death of dopamine (DA) neurons. Over recent years, differentiated or undifferentiated neural stem cells (NSCs) transplantation has been widely used as a means of cell replacement therapy. However, compelling evidence has brought attention to the array of bioactive molecules produced by stem cells, defined as secretome. As described in the literature, other cell populations have a high-neurotrophic activity, but little is known about NSCs. Moreover, the exploration of the stem cell secretome is only in its initial stages, particularly as applied to neurodegenerative diseases. Thus, we have characterized the secretome of human neural progenitor cells (hNPCs) through proteomic analysis and investigated its effects in a 6-hydroxidopamine (6-OHDA) rat model of PD in comparison with undifferentiated hNPCs transplantation. Results revealed that the injection of hNPCs secretome potentiated the histological recovery of DA neurons when compared to the untreated group 6-OHDA and those transplanted with cells (hNPCs), thereby supporting the functional motor amelioration of 6-OHDA PD animals. Additionally, hNPCs secretome proteomic characterization has revealed that these cells have the capacity to secrete a wide range of important molecules with neuroregulatory actions, which are most likely support the effects observed. Overall, we have concluded that the use of hNPCs secretome partially modulate DA neurons cell survival and ameliorate PD animals' motor deficits, disclosing improved results when compared to cell transplantation approaches, indicating that the secretome itself could represent a route for new therapeutic options for PD regenerative medicine. Stem Cells Translational Medicine 2018;7:829-838.Portuguese Foundation for Science and Technology: Ciência 2007 Program and IF Development Grant (IF/00111/2013) to A.J.S., Ph.D. scholarships to S.I.A. (SFRH/BD/81495/ 2011); Canada Research Chair in Biomedical Engineering (LAB). This article has been developed under the scope of the project NORTE‐01‐0145‐FEDER‐000013 and NORTE‐01‐0145‐FEDER‐000023, supported by the Northern Portugal Regional Operational Programme (NORTE 2020), under the Portugal 2020 Partnership Agreement, through the European Regional Development Fund (FEDER). This work has been funded by FEDER funds, through the Competitiveness Factors Operational Programme (COMPETE), and by National funds, through the Foundation for Science and Technology (FCT), under the scope of the projects POCI‐01‐0145‐FEDER‐007038, PTDC/NEU‐NMC/0205/2012, UID/NEU/04539/2013, and POCI‐01‐0145‐FEDER‐007440 cofunded by the Programa Operacional Factores de Competitividade, QREN, the European Union (FEDER), and by the National Mass Spectrometry Network under the contract REDE/1506/REM/2005info:eu-repo/semantics/publishedVersio

Thiol redox homeostasis in neurodegenerative disease

This review provides an overview of the biochemistry of thiol redox couples and the significance of thiol redox homeostasis in neurodegenerative disease. The discussion is centred on cysteine/cystine redox balance, the significance of the xc- cystine-glutamate exchanger and the association between protein thiol redox balance and neurodegeneration, with particular reference to Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis and glaucoma. The role of thiol disulphide oxidoreductases in providing neuroprotection is also discussed

Lazy River

https://digitalcommons.library.umaine.edu/mmb-vp-copyright/3927/thumbnail.jp

Lazy River

Title Onlyhttps://scholarsjunction.msstate.edu/cht-sheet-music/8057/thumbnail.jp

Redox proteins in the defense against dopamine induced cell death

Póster presentado en la Nordforsk C. elegans Network Meeting (Nordic Symposium), celebrada en Holte (Dinamarca) del 8 al 10 de marzo de 2013.[Background] Although the etiology of sporadic Parkinson disease (PD) is unknown, it is well established that oxidative stress plays an important role in the pathophysiology. The thioredoxin and glutaredoxin systems are two central systems upholding the sulfhydryl homeostasis by reducing disulfides and mixed disulfides within the cell and thereby protecting against oxidative stress. In the present study we used the dopamine metabolite 6-hydroxydopamine (6-OHDA) to model PD and to explore the protective effects of these two systems. The powerful neurotoxin 6-OHDA is highly prone to oxidation, resulting in the formation of the 6-OHDA-quinone, a highly reactive species.[Results] In human post-mortem PD brains the levels of thioredoxin 1 and thioredoxin reductase 1 were found to be significantly decreased. The neuroblastoma cellline SH-SYSY and the nematode C. elegans were used as model systems to evaluate the toxic effects of 6-0HDA. Selenite supplementation protected neuroblastoma cells against 6-0HDA, possibly by upregulating the selenoprotein thioredoxin reductase. A knock-down of thioredoxin and thioredoxin reductase by siRNA resulted in increased cell death in SH -SYSY. Furthermore, both the thioredoxin and the glutaredoxin systems were able to reduce 6-0HDA-quinone. The reduction required the dithiol mechanism as glutaredoxin with a mutation in the C-terminal cysteine ofthe active s i te was found to be ineffective at reducing 6-0HDA-quinone. To further investigate the protective role of proteins belonging to the thioredoxin system, experiments were conducted in C. elegans with 6-0HDA treatment ofnull mutants for trxr-1, trx4 or trx5 followed by evaluation of their neuronal integrity.[Conclusions] Our results suggest that the glutaredoxin and the thioredoxin systems appear to be important for neuro nal survival in dopamine induced cell death.Peer Reviewe