Muumikirjojen hahmonnimien käännösstrategiat suomen ja tšekin kielen käännöksissä

Tutkin tässä pro gradu -tutkielmassani muumiromaanissa esiintyviä hahmonnimiä ja niiden käännösstrategioita suomeen ja tšekkiin. Pyrin tutkimaan hahmonnimien funktioita ja eri kohdekielten käännösstrategioiden valintaa. Pyrkimyksenä on selvittää, mitä yhtäläisyyksiä ja eroja hahmonnimien käännöksissä on ja kuinka käännökset mukautetaan lukijoiden tarpeisiin. Aineisto koostuu 141 hahmonnimestä kolmessa kielessä – ruotsissa, suomessa ja tšekissä. Nimet jaottelen niiden nimityyppien mukaan kahteen ryhmään. Ryhmät ovat realistiset mutta epäautenttiset nimet ja keinotekoiset nimet. Lainanimiä tai autenttisia nimiä aineistossa ei esiinny. Näissä ryhmissä tutkin nimien funktioita ja käännösstrategioita ja vertailen käytettyjä strategioita suomen- ja tšekinkielisten käännösten välillä. Tutkimani funktiot ovat identifioiva, lokalisoiva, sosiaalinen, deskriptiivinen ja luokitteleva. Käännösstrategiat ovat laina, mukaelma, käännös ja korvaaminen. Tulokset osoittavat, että käännösstrategioiden valinnassa on paljon yhteisiä piirteitä. Molemmissa kielissä eniten käytetyt strategiat ovat käännös ja mukaelma. Tämä vastaa hahmonnimien luonnetta, koska suuri osa nimistä on luotu yleisnimistä. Kun hahmonnimi vastaa yleisnimeä, joka on tunnettu myös kohdekielessä, ei käännöksessä ole tarvetta luoda nimelle uutta ilmausta. Mukaelman avulla nimet sopeutetaan kohdekieleen esimerkiksi ääntämisen suhteen. Kielten käännösstrategioiden ero nähdään korvaus- ja lainastrategian valinnassa. Korvaamista käytetään enemmän tšekinkielisessä käännöksessä. Joskus syynä on kulttuurinen adaptaatio, jota nimien tšekin käännöksessä jonkin verran esiintyy. Useissa tapauksissa korvausstrategian käyttö aiheuttaa nimen merkityksen menettämisen. Lainastrategialla käännetään nimiä enemmän suomenkielisessä käännöksessä, mikä liittyy varsinkin realististen mutta epäautenttisten nimien luonteeseen. Toisin sanoen henkilönimet ruotsissa ja suomessa ovat hyvin läheisiä ja lukijoille ymmärrettäviä myös alkuperäisessä muodossa

Microvesicles and exosomes: new players in metabolic and cardiovascular disease

The past decade has witnessed an exponential increase in the number of publications referring to extracellular vesicles (EVs). For many years considered to be extracellular debris, EVs are now seen as novel mediators of endocrine signalling via cell-to-cell communication. With the capability of transferring proteins and nucleic acids from one cell to another, they have become an attractive focus of research for different pathological settings and are now regarded as both mediators and biomarkers of disease including cardio-metabolic disease. They also offer therapeutic potential as signalling agents capable of targeting tissues or cells with specific peptides or miRNAs. In this review, we focus on the role that microvesicles (MVs) and exosomes, the two most studied classes of EV, have in diabetes, cardiovascular disease, endothelial dysfunction, coagulopathies, and polycystic ovary syndrome. We also provide an overview of current developments in MV/exosome isolation techniques from plasma and other fluids, comparing different available commercial and non-commercial methods. We describe different techniques for their optical/biochemical characterization and quantitation. We also review the signalling pathways that exosomes and MVs activate in target cells and provide some insight into their use as biomarkers or potential therapeutic agents. In summary, we give an updated focus on the role that these exciting novel nanoparticles offer for the endocrine community

The removing of selected pharmaceuticals on WWTP in the Czech Republic

In this article, the results of three years monitoring of selected pharmaceuticals (diclofenac, ibuprofen, carbamazepine, salicylic acid, clofibric acid) in the wastewaters of the Czech Republic are presented. The monitoring was performed on selected Wastewater Treatment Plants (WWTP) with various treatment technology and designed capacity. The concentrations and treatment efficiency of these substances were observed in various profiles of each WWTP, including influent, mechanical pretreatment, biological treatment, effluent. The main processes of removing selected pharmaceuticals during wastewater treatment are discussed. These results are used for design wastewater treatment technology with improved treatment efficiency of these substances

Actin depolymerization is able to increase plant resistance against pathogens via activation of salicylic acid signalling pathway

The integrity of the actin cytoskeleton is essential for plant immune signalling. Consequently, it is generally assumed that actin disruption reduces plant resistance to pathogen attack. Here, we demonstrate that actin depolymerization induced a dramatic increase in salicylic acid (SA) levels in Arabidopsis thaliana. Transcriptomic analysis showed that the SA pathway was activated due to the action of isochorismate synthase (ICS). The effect was also confirmed in Brassica napus. This raises the question of whether actin depolymerization could, under particular conditions, lead to increased resistance to pathogens. Thus, we explored the effect of pretreatment with actin-depolymerizing drugs on the resistance of Arabidopsis thaliana to the bacterial pathogen Pseudomonas syringae, and on the resistance of an important crop Brassica napus to its natural fungal pathogen Leptosphaeria maculans. In both pathosystems, actin depolymerization activated the SA pathway, leading to increased plant resistance. To our best knowledge, we herein provide the first direct evidence that disruption of the actin cytoskeleton can actually lead to increased plant resistance to pathogens, and that SA is crucial to this process

Pathogenic Potential of Hic1-Expressing Cardiac Stromal Progenitors

The cardiac stroma contains multipotent mesenchymal progenitors. However, lineage relationships within cardiac stromal cells are poorly defined. Here, we identified heart-resident PDGFRa(+) SCA-1(+) cells as cardiac fibro/adipogenic progenitors (cFAPs) and show that they respond to ischemic damage by generating fibrogenic cells. Pharmacological blockade of this differentiation step with an anti-fibrotic tyrosine kinase inhibitor decreases post-myocardial infarction (post-MI) remodeling and leads to improvement in cardiac function. In the undamaged heart, activation of cFAPs through lineage-specific deletion of the gene encoding the quiescence-associated factor HIC1 reveals additional pathogenic potential, causing fibrofatty infiltration within the myocardium and driving major pathological features pathognomonic in arrhythmogenic cardiomyopathy (AC). In this regard, cFAPs contribute to multiple pathogenic cell types within cardiac tissue and therapeutic strategies aimed at modifying their activity are expected to have tremendous benefit for the treatment of diverse cardiac diseases

Acidic microenvironment plays a key role in human melanoma progression through a sustained exosome mediated transfer of clinically relevant metastatic molecules

Background: Microenvironment cues involved in melanoma progression are largely unknown. Melanoma is highly influenced in its aggressive phenotype by the changes it determinates in its microenvironment, such as pH decrease, in turn influencing cancer cell invasiveness, progression and tissue remodelling through an abundant secretion of exosomes, dictating cancer strategy to the whole host. A role of exosomes in driving melanoma progression under microenvironmental acidity was never described. Methods: We studied four differently staged human melanoma lines, reflecting melanoma progression, under microenvironmental acidic pHs pressure ranging between pH 6.0-6.7. To estimate exosome secretion as a function of tumor stage and environmental pH, we applied a technique to generate native fluorescent exosomes characterized by vesicles integrity, size, density, markers expression, and quantifiable by direct FACS analysis. Functional roles of exosomes were tested in migration and invasion tests. Then we performed a comparative proteomic analysis of acid versus control exosomes to elucidate a specific signature involved in melanoma progression. Results: We found that metastatic melanoma secretes a higher exosome amount than primary melanoma, and that acidic pH increases exosome secretion when melanoma is in an intermediate stage, i.e. metastatic non-invasive. We were thus able to show that acidic pH influences the intercellular cross-talk mediated by exosomes. In fact when exposed to exosomes produced in an acidic medium, pH naïve melanoma cells acquire migratory and invasive capacities likely due to transfer of metastatic exosomal proteins, favoring cell motility and angiogenesis. A Prognoscan-based meta-analysis study of proteins enriched in acidic exosomes, identified 11 genes (HRAS, GANAB, CFL2, HSP90B1, HSP90AB1, GSN, HSPA1L, NRAS, HSPA5, TIMP3, HYOU1), significantly correlating with poor prognosis, whose high expression was in part confirmed in bioptic samples of lymph node metastases. Conclusions: A crucial step of melanoma progression does occur at melanoma intermediate -stage, when extracellular acidic pH induces an abundant release and intra-tumoral uptake of exosomes. Such exosomes are endowed with pro-invasive molecules of clinical relevance, which may provide a signature of melanoma advancement

Ovarian carcinoma CDK12 mutations misregulate expression of DNA repair genes via deficient formation and function of the Cdk12/CycK complex

The Cdk12/CycK complex promotes expression of a subset of RNA polymerase II genes, including those of the DNA damage response. CDK12 is among only nine genes with recurrent somatic mutations in high-grade serous ovarian carcinoma. However, the influence of thesemutations on the Cdk12/CycK complex and their link to cancerogenesis remain ill-defined. Here, we show that most mutations prevent formation of the Cdk12/CycK complex, rendering the kinase inactive. By examining the mutations within the Cdk12/CycK structure, we find that they likely provoke structural rearrangements detrimental to Cdk12 activation. Our mRNA expression analysis of the patient samples containing the CDK12 mutations reveals coordinated downregulation of genes critical to the homologous recombination DNA repair pathway. Moreover, we establish that the Cdk12/CycK complex occupies these genes and promotes phosphorylation of RNA polymerase II at Ser2. Accordingly, we demonstrate that the mutant Cdk12 proteins fail to stimulate the faithful DNA double strand break repair via homologous recombination. Together, we provide the molecular basis of how mutated CDK12 ceases to function in ovarian carcinoma. We propose that CDK12 is a tumor suppressor of which the loss-of-function mutations may elicit defects in multiple DNA repair pathways, leading to genomic instability underlying the genesis of the cancer.Peer reviewe

Leucocyte and Platelet-rich Fibrin: A carrier of autologous multipotent cells for regenerative medicine

The wound healing is a complex process wherein inflammation, proliferation and regeneration evolve according to a spatio-temporal pattern from the activation of coagulation cascade to the formation of a plug clot including fibrin matrix, blood-borne cells and cytokines/growth factors. Creating environments conducive to tissue repair, the haemoderivatives are commonly proposed for the treatment of hard-to-heal wounds. Here, we explored in vitro the intrinsic regenerative potentialities of a leucocyte- and platelet-rich fibrin product, known as CPL-MB, defining the stemness grade of cells sprouting from the haemoderivative. Using highly concentrated serum-based medium to simulate wound conditions, we isolated fibroblast-like cells (CPL-CMCs) adhering to plastic and showing stable in vitro propagation, heterogeneous stem cell expression pattern, endothelial adhesive properties and immunomodulatory profile. Due to their blood derivation and expression of CXCR4, CPL-CMCs have been suggested to be immature cells circulating in peripheral blood at quiescent state until activation by both coagulation event and inflammatory stimuli such as stromal-derived factor 1/SDF1. Expressing integrins (CD49f, CD103), vascular adhesion molecules (CD106, CD166), endoglin (CD105) and remodelling matrix enzymes (MMP2, MMP9, MMP13), they showed a transendothelial migratory potential besides multipotency. Taken together, our data suggested that a standardized, reliable and economically feasible blood product such as CPL-MB functions as an artificial stem cell niche that, under permissive conditions, originate ex vivo immature cells that could be useful for autologous stem cell-based therapies

Dazap2 modulates transcription driven by the Wnt effector TCF-4

A major outcome of the canonical Wnt/β-catenin-signalling pathway is the transcriptional activation of a specific set of target genes. A typical feature of the transcriptional response induced by Wnt signalling is the involvement of Tcf/Lef factors that function in the nucleus as the principal mediators of signalling. Vertebrate Tcf/Lef proteins perform two well-characterized functions: in association with β-catenin they activate gene expression, and in the absence of Wnt ligands they bind TLE/Groucho proteins to act as transcriptional repressors. Although the general characteristics of Tcf/Lef factors are well understood, the mechanisms that control their specific roles in various cellular backgrounds are much less defined. In this report we reveal that the evolutionary conserved Dazap2 protein functions as a TCF-4 interacting partner. We demonstrate that a short region proximal to the TCF-4 HMG box mediates the interaction and that all Tcf/Lef family members associate with Dazap2. Interestingly, knockdown of Dazap2 not only reduced the activity of Wnt signalling as measured by Tcf/β-catenin reporters but additionally altered the expression of Wnt-signalling target genes. Finally, chromatin immunoprecipitation studies indicate that Dazap2 modulates the affinity of TCF-4 for its DNA-recognition motif

Flow-Alignment of Extracellular Vesicles: Structure and Orientation of Membrane Associated Biomacromolecules Studied with Polarized Light

Extracellular vesicles (EVs) are currently in the scientific focus having a great potential to revolutionize the diagnosis and therapy of various diseases. However, numerous aspects of these species are still poorly understood, thus additional insight to molecular level properties, membrane-protein interactions, or membrane rigidity is still needed. We here demonstrate using red blood cell derived EVs (REVs) that polarized light spectroscopy techniques, linear and circular dichroism, can provide molecular level structural information on these systems. Flow-linear dichroism (flow-LD) measurements show that EVs can be oriented by shear force, and indicate that hemoglobin molecules are associated to the lipid bilayer in freshly released REVs. During storage this interaction ceases coupled to major protein conformational changes relative to the initial state. Further on, the degree of orientation gives insight to vesicle rigidity, which decreases in time parallel to changes in protein conformation. In overall, we propose that both LD and circular dichroism (CD) spectra provide simple, rapid, yet efficient ways to track changes in membrane-protein interactions of EV components at the molecular level which may also give insight to processes occurring during vesiculation