La traduzione dei nomi nella letteratura per l'infanzia

I nomi propri, che si tratti di antroponimi, di toponimi o di altri tipi di denominazioni, fanno parte di una categoria a sé, benché essi stessi traggano le loro origini dal lessico comune. Essi sono inoltre in grado di offrire ben più di una funzione identificativa, in quanto possono trasmettere tutta una serie di informazioni di tipo anche extra-linguistico sui loro portatori. Si può ad es. desumere con buona approssimazione il periodo in cui un individuo è nato, i gusti dei suoi genitori, la loro confessione religiosa o ideologia politica. Dal cognome si può risalire alla provenienza geografica degli antenati, o anche al loro status sociale. Nomi o cognomi “impegnativi”, quali quello della scrivente, possono aver condizionato, specie in età giovanile, l’atteggiamento del portatore nei confronti della propria stessa identità. Nomi ibridi, cioè che appartengono a lingue e culture diverse, possono essere il segnale di una scissione interiore o aver rappresentato problemi di adattamento. Per quel che riguarda i toponimi, è spesso possibile ricostruire caratteristiche del territorio che possono addirittura essere scomparse, o momenti della storia di un luogo, o ancora l’appartenenza a ben precise tradizioni. Per quel che riguarda i nomi propri che sono calati in un testo letterario, il discorso si complica ulteriormente, perché si presume che ogni nome sia stato scelto dal suo “creatore” in base a ben precise e attente considerazioni, non sempre rintracciabili non solo da parte del lettore, che anzi tende spesso ad ignorarle, bensì anche da parte del critico, che è invece interessato a tutto quel che si nasconde nel retrobottega di un autore. L’onomastica letteraria come disciplina nasce in epoca relativamente recente, non solo in Italia, ma anche a livello internazionale. Maria Giovanna Arcamone, nel suo saggio L’Onomastica letteraria oltralpe, ricostruisce l’itinerario percorso dagli studiosi di onomastica letteraria e individua la data di nascita ufficiale di questo settore di ricerca nel 1970, “quando nella rivista di ICOS “Onoma” venne attivata la sezione bibliografica Literary Onomastics.” Attualmente la ricerca in questo campo viene portata avanti principalmente in Italia grazie all’attività dell’associazione “Onomastica e Letteratura” (=O&L), fondata a Pisa nel 1994, che organizza annualmente un convegno, i cui atti sono regolarmente pubblicati nella rivista “il Nome nel testo”, oltre a curare una collana di studi di onomastica letteraria dal nome Nominatio. Il crescente interesse nei confronti dell’onomastica letteraria ha condotto gli studiosi anche all’approfondimento di singoli aspetti teorici, fra i quali il problema della traduzione dei nomi. Laura Salmon Kovarski, che unisce alla propria attività di ricerca quella di traduttrice di testi dal russo in italiano, è stata, in Italia, nell’ambito dei congressi di O&L, fra i primi, nel 1997, ad affrontare la questione, aprendo la strada ad altri studi riguardanti l’onomastica letteraria in chiave traduttiva, fra i quali il ricco volume Denominazioni proprie e traduzione di Maurizio Viezzi, pubblicato nel non lontano 2010. L’oggetto di questa tesi è costituito appunto dal problema della resa in altre lingue dei nomi propri letterari. Nella prima parte del mio lavoro ho effettuato ricerche e elaborato un Forschungsbericht, individuando trattazioni di linguisti e critici letterari comparse in articoli di riviste, in atti di convegni, in volumi dedicati alla traduzione e alla mediazione culturale. Ho privilegiato le trattazioni che si occupavano prevalentemente di testi tedeschi tradotti in italiano, ma ho preso in considerazione, quando mi è sembrato opportuno, anche contributi in cui si faceva riferimento a testi in lingua inglese, francese e spagnola. Nella seconda parte della tesi ho effettuato una sorta di verifica relativamente alle metodologie e strategie che sono state messe in pratica dai traduttori tedeschi di alcune delle opere di quattro autori italiani che occupano una posizione di rilievo nel campo della letteratura per l’infanzia: Italo Calvino, Gianni Rodari, Luigi Capuana e Mario Lodi

The Etched Mind Digital Stenopaic Imagery

In the spring of 1992 I found myself faced with the reality of not being able to afford supplies to make art. A faculty member, acquainted with my financial problem, suggested that I try doing some work using some outdated aerial film being stored in one of the photography department's closet. Not quite sure how I would go on, I nevertheless accepted his generous offer. What I did not realize at the time, is how that day would guide me on the road to self discovery and has a profound impact on the way I now make art. For the creative thesis, I have edited the work to 15 cactus prints. As I was making the images within the computer, there are many choices and creative decisions that have to be made. While I knew what pieces of appropriated images I wanted to work with, the placement of the images into the lensless photograph were done on an intuitive level. It was only after the particular image was finished could I go back and understand the reasoning behind it. "The Etched Mind" has not been about a rip in the space time continuum, or a parallel universe but a journey into the subconscious of my mind and a window to my soul. &nbsp;</p

Pseudoceramide-Containing Physiological Lipid Mixture Reduces Adverse Effects of Topical Steroids

PURPOSE: Various therapeutic approaches have been suggested for preventing or reducing the adverse effects of topical glucocorticoids, including skin barrier impairment. Previously, we have shown that impairment of skin barrier function by the highest potency topical glucocorticoid, clobetasol 17-propinate (CP), can be partially prevented by co-application of a physiological lipid mixture containing pseudoceramide, free fatty acids, and cholesterol (multi-lamellar emulsion [MLE]). Skin atrophic effects of CP were also partially reduced by MLE. In this study, the preventive effects of MLE on the lowest potency topical glucocorticoid, hydrocortisone (HC), were investigated using animal models. METHODS: Anti-inflammatory activity of topical HC was evaluated using a 12-O-tetradecanoylphobol-13-acetate-induced skin edema model. Topical steroid induced adverse effects were evaluated using hairless mouse. RESULTS: The results showed that the anti-inflammatory activity was not altered by co-application of either MLE or hydrobase. However, co-application of MLE and 1.0% HC showed less impairment in the epidermal permeability barrier function, skin hydration, and skin surface pH compared with hydrobase. Stratum corneum integrity, evaluated by measuring trans-epidermal water loss after repeated tape stripping, showed less damage with MLE co-application. Long-term application of topical HC induced skin atrophy, measured by a reduction in skinfold and epidermal thickness and in the number of epidermal proliferating cell nucleus antigen (PCNA)-positive keratinocytes. Co-application of MLE did not affect the skinfold or epidermal thickness, but the number of PCNA-positive keratinocytes was less decreased with MLE use. CONCLUSIONS: These results suggest that co-application of MLE is effective in reducing the local adverse effects of low-potency topical glucocorticoids and supports the therapeutic efficacy of physiological lipid mixtures on skin barrier function.ope

Palmitoylethanolamide inhibits rMCP-5 expression by regulating MITF activation in rat chronic granulomatous inflammation

Chronic inflammation, a condition frequently associated with several pathologies, is characterized by angiogenic and fibrogenic responses that may account for the development of granulomatous tissue. We previously demonstrated that the chymase, rat mast cell protease-5 (rMCP-5), exhibits pro-inflammatory and pro-angiogenic properties in a model of chronic inflammation sustained by mast cells (MCs), granuloma induced by the subcutaneous carrageenan-soaked sponge implant in rat. In this study, we investigated the effects of palmitoylethanolamide (PEA), an anti-inflammatory and analgesic endogenous compound, on rMCP-5 mRNA expression and Microphtalmia-associated Transcription Factor (MITF) activation in the same model of chronic inflammation. The levels of rMCP-5 mRNA were detected using semi-quantitative RT-PCR; the protein expression of chymase and extracellular signal-regulated kinases (ERK) were analyzed by western blot; MITF/DNA binding activity and MITF phosphorylation were assessed by electrophoretic mobility shift assay (EMSA) and immunoprecipitation, respectively. The administration of PEA (200, 400 and 800 µg/ml) significantly decreased rMCP-5 mRNA and chymase protein expression induced by λ-carrageenan. These effects were associated with a significant decrease of MITF/DNA binding activity and phosphorylated MITF as well as phosphorylated ERK levels. In conclusion, our results, showing the ability of PEA to inhibit MITF activation and chymase expression in granulomatous tissue, may yield new insights into the understanding of the signaling pathways leading to MITF activation controlled by PEA

Palmitoylethanolamide exerts neuroprotective effects in mixed neuroglial cultures and organotypic hippocampal slices via peroxisome proliferator-activated receptor-α

<p>Abstract</p> <p>Background</p> <p>In addition to cytotoxic mechanisms directly impacting neurons, β-amyloid (Aβ)-induced glial activation also promotes release of proinflammatory molecules that may self-perpetuate reactive gliosis and damage neighbouring neurons, thus amplifying neuropathological lesions occurring in Alzheimer's disease (AD). Palmitoylethanolamide (PEA) has been studied extensively for its anti-inflammatory, analgesic, antiepileptic and neuroprotective effects. PEA is a lipid messenger isolated from mammalian and vegetable tissues that mimics several endocannabinoid-driven actions, even though it does not bind to cannabinoid receptors. Some of its pharmacological properties are considered to be dependent on the expression of peroxisome proliferator-activated receptors-α (PPARα).</p> <p>Findings</p> <p>In the present study, we evaluated the effect of PEA on astrocyte activation and neuronal loss in models of Aβ neurotoxicity. To this purpose, primary rat mixed neuroglial co-cultures and organotypic hippocampal slices were challenged with Aβ_1-42and treated with PEA in the presence or absence of MK886 or GW9662, which are selective PPARα and PPARγ antagonists, respectively. The results indicate that PEA is able to blunt Aβ-induced astrocyte activation and, subsequently, to improve neuronal survival through selective PPARα activation. The data from organotypic cultures confirm that PEA anti-inflammatory properties implicate PPARα mediation and reveal that the reduction of reactive gliosis subsequently induces a marked rebound neuroprotective effect on neurons.</p> <p>Conclusions</p> <p>In line with our previous observations, the results of this study show that PEA treatment results in decreased numbers of infiltrating astrocytes during Aβ challenge, resulting in significant neuroprotection. PEA could thus represent a promising pharmacological tool because it is able to reduce Aβ-evoked neuroinflammation and attenuate its neurodegenerative consequences.</p

Sleep deprivation increases oleoylethanolamide in human cerebrospinal fluid

This study investigated the role of two fatty acid ethanolamides, the endogenous cannabinoid anandamide and its structural analog oleoylethanolamide in sleep deprivation of human volunteers. Serum and cerebrospinal fluid (CSF) samples were obtained from 20 healthy volunteers before and after a night of sleep deprivation with an interval of about 12 months. We found increased levels of oleoylethanolamide in CSF (P = 0.011) but not in serum (P = 0.068) after 24 h of sleep deprivation. Oleoylethanolamide is an endogenous lipid messenger that is released after neural injury and activates peroxisome proliferator-activated receptor-α (PPAR-α) with nanomolar potency. Exogenous PPAR-α agonists, such as hypolipidemic fibrates and oleoylethanolamide, exert both neuroprotective and neurotrophic effects. Thus, our results suggest that oleoylethanolamide release may represent an endogenous neuroprotective signal during sleep deprivation

Effects of Conjugated Linoleic Acid, Fish Oil and Soybean Oil on PPARs (α & γ) mRNA Expression in Broiler Chickens and Their Relation to Body Fat Deposits

An experiment was conducted on broiler chickens to study the effects of different dietary fats (Conjugated linoleic acid (CLA), fish oil, soybean oil, or their mixtures, as well as palm oil, as a more saturated fat), with a as fed dose of 7% for single fat and 3.5 + 3.5% for the mixtures, on Peroxisome Proliferator-Activated Receptors (PPARs) gene expression and its relation with body fat deposits. The CLA used in this experiment was CLA LUTA60 which contained 60% CLA, so 7% and 3.5% dietary inclusions of CLA LUTA60 were equal to 4.2% and 2.1% CLA, respectively. Higher abdominal fat pad was found in broiler chickens fed with a diet containing palm oil compared to chickens in the other experimental groups (P ≤ 0.05). The diets containing CLA resulted in an increased fat deposition in the liver of broiler chickens (P ≤ 0.05). The only exception was related to the birds fed with diets containing palm oil or fish oil + soybean oil, where contents of liver fat were compared to the CLA + fish oil treatment. PPARγ gene in adipose tissue of chickens fed with palm oil diet was up-regulated compared to other treatments (P ≤ 0.001), whereas no significant differences were found in adipose PPARγ gene expression between chickens fed with diets containing CLA, fish oil, soybean oil or the mixture of these fats. On the other hand, the PPARα gene expression in liver tissue was up-regulated in response to the dietary fish oil inclusion and the differences were also significant for both fish oil and CLA + fish oil diets compared to the diets with palm oil, soybean oil or CLA as the only oil source (P ≤ 0.001). In conclusion, the results of present study showed that there was a relationship between the adipose PPARγ gene up-regulation and abdominal fat pad deposition for birds fed with palm oil diet, while no deference was detected in n-3 and n-6 fatty acids, as well as CLA on PPARγ down regulation in comparison to a more saturated fat. When used on its own, fish oil was found to be a more effective fat in up-regulating hepatic PPARα gene expression and this effect was related to a less fat deposition in liver tissue. A negative correlation coefficient (−0.3) between PPARα relative gene expression and liver tissue fat content confirm the anti-lipogenic effect of PPARα, however, the change in these parameters was not completely parallel

Endocannabinoids-related compounds in gastrointestinal diseases

The endocannabinoid system (ECS) is an endogenous signalling pathway involved in the control of several gastrointestinal (GI) functions at both peripheral and central levels. In recent years, it has become apparent that the ECS is pivotal in the regulation of GI motility, secretion and sensitivity, but endocannabinoids (ECs) are also involved in the regulation of intestinal inflammation and mucosal barrier permeability, suggesting their role in the pathophysiology of both functional and organic GI disorders. Genetic studies in patients with irritable bowel syndrome (IBS) or inflammatory bowel disease have indeed shown significant associations with polymorphisms or mutation in genes encoding for cannabinoid receptor or enzyme responsible for their catabolism, respectively. Furthermore, ongoing clinical trials are testing EC agonists/antagonists in the achievement of symptomatic relief from a number of GI symptoms. Despite this evidence, there is a lack of supportive RCTs and relevant data in human beings, and hence, the possible therapeutic application of these compounds is raising ethical, political and economic concerns. More recently, the identification of several EC-like compounds able to modulate ECS function without the typical central side effects of cannabino-mimetics has paved the way for emerging peripherally acting drugs. This review summarizes the possible mechanisms linking the ECS to GI disorders and describes the most recent advances in the manipulation of the ECS in the treatment of GI diseases

The association of N-palmitoylethanolamine with the FAAH inhibitor URB597 impairs melanoma growth through a supra-additive action

<p>Abstract</p> <p>Background</p> <p>The incidence of melanoma is considerably increasing worldwide. Frequent failing of classical treatments led to development of novel therapeutic strategies aiming at managing advanced forms of this skin cancer. Additionally, the implication of the endocannabinoid system in malignancy is actively investigated.</p> <p>Methods</p> <p>We investigated the cytotoxicity of endocannabinoids and their hydrolysis inhibitors on the murine B16 melanoma cell line using a MTT test. Enzyme and receptor expression was measured by RT-PCR and enzymatic degradation of endocannabinoids using radiolabeled substrates. Cell death was assessed by Annexin-V/Propidium iodine staining. Tumors were induced in C57BL/6 mice by s.c. flank injection of B16 melanoma cells. Mice were injected i.p. for six days with vehicle or treatment, and tumor size was measured each day and weighted at the end of the treatment. Haematoxylin-Eosin staining and TUNEL assay were performed to quantify necrosis and apoptosis in the tumor and endocannabinoid levels were quantified by HPLC-MS. Tube formation assay and CD31 immunostaining were used to evaluate the antiangiogenic effects of the treatments.</p> <p>Results</p> <p>The <it>N</it>-arachidonoylethanolamine (anandamide, AEA), 2-arachidonoylglycerol and <it>N</it>- palmitoylethanolamine (PEA) reduced viability of B16 cells. The association of PEA with the fatty acid amide hydrolase (FAAH) inhibitor URB597 considerably reduced cell viability consequently to an inhibition of PEA hydrolysis and an increase of PEA levels. The increase of cell death observed with this combination of molecules was confirmed in vivo where only co-treatment with both PEA and URB597 led to decreased melanoma progression. The antiproliferative action of the treatment was associated with an elevation of PEA levels and larger necrotic regions in the tumor.</p> <p>Conclusions</p> <p>This study suggests the interest of targeting the endocannabinoid system in the management of skin cancer and underlines the advantage of associating endocannabinoids with enzymatic hydrolysis inhibitors. This may contribute to the improvement of long-term palliation or cure of melanoma.</p