1,721,007 research outputs found
La "giustizia in transizione" in Italia: l'esperienza delle Corti d'Assise Straordinarie lombarde (1945-'50)
Full text linkSulla spinta delle riflessioni maturate in ambito internazionale rispetto alla categoria della Transitional Justice, anche nel nostro Paese il problema della giustizia verso il fascismo si è imposto al centro della discussione storiografica. La recente apertura dei fondi archivistici delle CAS, tribunali preposti alla punizione del collaborazionismo secondo quanto previsto dal decreto 142/45, ha consentito lavvio di una nuova e feconda stagione di studi sul tema, allinsegna di un ulteriore approfondimento della dialettica continuità/discontinuità che ha contrassegnato la transizione italiana dal fascismo alla democrazia. La presente tesi ha come obiettivo quello di esplorare e valutare lesperienza delle CAS nella regione lombarda, che, sebbene tra i territori con il più alto numero di processi per collaborazionismo, risulta tuttavia ancora non a sufficienza indagata dalla storiografia. A questo proposito, la domanda che muove la ricerca è la seguente: è vero che in Lombardia e, quindi, in Italia, non cè mai stata, in assoluto, una resa dei conti con quanti avevano aderito alla RSI e perpetrato crimini in nome di questultima? Avvalendosi principalmente delle carte del Commissariato alla Giustizia del Cln lombardo e dei documenti giudiziari prodotti dalle CAS lombarde, il lavoro prova a rispondere a questa domanda prendendo in esame un punto di vista in parte nuovo e originale quello del commissario alla giustizia Aurelio Becca e focalizzando lattenzione su due casi politico-giudiziari particolarmente significativi e finora mai approfonditi: quello del capo della provincia di Genova Carlo Emanuele Basile e quello del presidente della Montecatini Guido Donegani. Partendo dal resoconto delle rispettive vicende processuali e ricorrendo ad una pluralità di fonti quali i fascicoli personali dei magistrati e la stampa coeva, si sviscerano una serie di tematiche e aspetti cruciali per la comprensione delle dinamiche della giustizia in transizione, come la mentalità della magistratura e le reazioni dell'opinione pubblica rispetto alle sentenze. La tesi mette in luce il contesto complesso in cui le CAS lombarde si trovarono ad operare, tra carenze umane e materiali, fragilità legislative, mancata epurazione della magistratura e delle forze di Pubblica Sicurezza, debole coesione del fronte ciellenista, pressioni politiche internazionali. È però soprattutto nella tensione tra giustizia legale e giustizia politica che si ravvisa limpedimento maggiore alloperato di questi tribunali, stretti nella morsa tra lesigenza di normalizzare e ricostruire il Paese, da un lato, e la necessità di soddisfare lansia di vendetta proveniente dalle vittime dei crimini fascisti, dallaltro. In questo senso, la dialettica quasi schizofrenica tra CAS e Suprema Corte di Cassazione che anima la curiosa vicenda processuale di Basile, mostra, meglio di ogni altra cosa, la difficile impresa di conciliare le istanze profondamente diverse che sorgono allinterno di una società in transizione. Nel giro di pochi anni dalla fine della guerra, la stragrande maggioranza dei collaborazionisti imputati (Basile e Donegani inclusi) potè tornare in libertà. Eppure, soffermando lo sguardo sul contenuto delle sentenze pronunciate dalle CAS, si scopre che in più di un caso i giudici avevano espresso una condanna nei confronti dei crimini compiuti tra il 43 e il 45, dando così un apporto prezioso al riconoscimento delle responsabilità della RSI. Ciò, unito alle vivaci iniziative in materia legislativa in seno al Commissariato alla Giustizia, suggerisce lopportunità di formulare rispetto ai percorsi della giustizia italiana del secondo dopoguerra un giudizio un po' più articolato e sfumato di quello finora elaborato
Editorial: Molecular nutrition as preventive tool in non-communicable diseases: Mechanistic insights and risk biomarkers
Full text linkNutrition has a crucial role in modulating aging trajectories. Diet is not a mere source of energy, but it also affects immune functions, inflammatory status, epigenetic regulations, and gene expression. Also, diet affect the gut microbiome composition, thus modulating the metabolites produced by the microorganisms, which can have both positive and negative effects on health.
Due to their action at the level of several biochemical and molecular pathways, dietary habits have a major role in the development and progression of complex non-communicable diseases (NCD) (e.g., obesity, cardio-metabolic disorders, neurodegeneration), which represent a major burden for the modern society. A plethora of bioactive compounds, nutrients and dietary patterns have been described as potential discriminants of the health status. Some metabolites have been also proposed as risk biomarkers for non-communicable diseases (e.g., trimethylamine n-oxide), thus opening interesting possibilities for prevention interventions and population risk stratification. Nevertheless, elucidating the exact molecular mechanism underpinning the effects of each dietary factor remains an ambitious goal of modern nutrition. This special issue aims at gathering new findings that might contribute to fill the gaps in this still marginally explored area
Trimethylamine N-Oxide (TMAO) as a Biomarker
No full textThe interaction between diet, microbiome, and noncommunicable disease onset is gaining growing attention. The trimethylamine N-oxide (TMAO) is a gut microbiota derivative that has been suggested as a potential regulator of human health, especially (but not exclusively) for its association with cardiovascular diseases. It derives from the trimethylamine (TMA), which is produced by the gut microbiome from dietary precursors, such as choline, betaine, and L-carnitine. Due to the potentially harmful effects of TMAO, strategies aimed to reduce circulating TMAO levels (ranging from dietary restrictions or supplementation to pharmacological treatments) have been proposed. Moreover, TMAO has been suggested as a biomarker of disease onset and prognosis. Nevertheless, contrasting evidence can be found in the literature, and mechanistic explanations or causal demonstrations of the association between the TMA/TMAO metabolism and diseases are still missing. Thus, despite promising findings, the history of TMAO might be more complex than initially hypothesized, and further studies are necessary to promote their translation into clinical practice
Protective effect of glutathione on damage induced by permethrin in a neuronal model of PC12 cells.
No full textObjective: Permethrin, a member of the family of synthetic pyrethroids, can induce oxidative stress and impairment in expression of Nurr1, a transcription factor essential for the maintenance of dopaminergic neurons. These conditions, flanked to low level of glutathione (GSH), are typical in neurons affected by Parkinson Disease (PD). The aim of this study is to evaluate in vitro effects of GSH on a stress dependent parameters (Nurr1) measured in PC12 cells culture treated with permethrin.
Methods: PC12 cells were seeded and treated for 72h with 1uM permethrin and separately co-treated with the pesticide and 32nM glutathione (1). Then, qRT-PCR was performed to evaluate Nurr1 gene expression.
Results: In cells cultures under stress condition, such as those induced by permethrin, Nurr1 gene expression changed, maybe as a compensatory effect to damage. In contrast, when cells were co-treated with glutathione, Nurr1 value was reestablished as the control.
Conclusion: Pesticides, mainly assumed with diet, can modulate gene expression leading to the onset and progression of age-related diseases. Permethrin, in particular, can induce stress in neuronal dopaminergic cells, mimicking PD condition (2). As demonstrated by previous in vivo studies, permethrin exposure can lead to progressive neuronal damage characterized by GSH and Nurr1 deficit (3,4). The present study shows that GSH in vitro can contrast the negative effect induced by permethrin. We can hypothesize that GSH can prevent oxidative stress damage, avoiding cells to overreact by modifying the production of Nurr1. Hence, GSH can act as a preventive agent to cellular damage induced by permethrin.
References
1. Mesner PW, Winters TR, Green SH. (1992). Nerve growth factor withdrawal-induced cell death in neuronal PC12 cells resembles that in sympathetic neurons. J Cell Biol 119:1669–1680.
2. Carloni, M., Nasuti, C., Fedeli, D., Montani. M., Amici, A., Vadhana, M.S.D., Gabbianelli, R., 2013. Early life permethrin exposure induces long-term brain changes in Nurr1, NF-kB and Nrf-2, Brain Research 1515, 19-28.
3. Falcioni ML, Nasuti C, Bergamini C, Fato R, Lenaz G. ( 2010). The primary role of GSH against nuclear DNA damage of striatum induced by permethrin in rats. Neuroscience 168(1), 2-10.
4. Nasuti C, Falcioni ML, Nwankwo IE, Cantalamessa F, Gabbianelli R. (2008). Effect of permethrin plus antioxidants on locomotor activity and striatum in adolescent rats. Toxicology., 29;251(1-3):45-50
Angiotensin-Converting Enzyme (ACE) I/D polymorphism influences body composition through the hydration status in a young Italian population
No full textAngiotensin-Converting Enzyme (ACE) I/D polymorphism influences body composition through the hydration status in a young Italian population
Laura Bordoni1, Francesca Marchegiani2, Valerio Napolioni3, Rosita Gabbianelli4 1School of Advanced Studies, University of Camerino, Camerino, Italy 2Clinical Laboratory and Molecular Diagnostics, INRCA-IRCCS, Ancona, Italy 3Department of Neurology and Neurological Sciences, Stanford University, School of Medicine, Stanford, CA, USA 4School of Pharmacy, University of Camerino, Camerino, Italy
Objective: The well-known insertion/deletion polymorphism (rs4646994) of the human angiotensin-converting enzyme (ACE) gene has been previously associated with obesity both in preschoolers, adolescents and adults. It has been reported a consistent association between this polymorphism and blood flow, muscular strength and ACE enzyme activity. Despite the relevant role of ACE in all these processes, very few evidences are currently available on the relationship between this gene variant and hydration status. Thus, we studied the association between ACE I/D polymorphism, body composition and hydration status in a young population of Italians children and adolescents.
Methods: A total of 306 healthy children and adolescents, who regularly practice sport, were recruited for the study. For all the subjects, anthropometric, bioimpedentiometric parameters and urine samples were collected. ACE I/D genotyping was performed on DNA from buccal swabs. General linear model (GLM) and two-way ANOVA tests has been performed with SPSS software.
Results: On the whole, interesting correlation between ACE I/D polymorphism, body composition and hydration status was detected in our population. In particular, a genetic-dependent effect of a good hydration status on body composition has been identified.
Conclusion: Our results do not only confirm the relationship between ACE I/D polymorphism and body composition, but also suggest a key role of the hydration status on the modulation of this relationship. These interesting preliminary results warrant further investigation to disentangle the genetic role of ACE on hydration homeostasis
MiR-21, MiR-148, Fatty Acid Content, and Antioxidant Properties of Raw Cow’s Milk: A Pilot Study
Full text linkIntramammary gland infections can affect milk quality, with changes in composition, biochemical characteristics, and antioxidant properties. Total bacterial count (TBC) and somatic cell count (SCC) are key determinants to define the appropriate quality of raw milk and must meet specific requirements established by the European regulation. Our interest was to examine if the microbiological safety window may hide differences regarding the nutritional value of milk approved for commercialization. Therefore, we investigated microRNA (miRNA) content, fatty acid (FA) profile, and antioxidant activity in relation to SCC and TBC in microbiologically safe dairy milk. Our data show that even minor variations in SCC and TBC induced by the bacterial presence are correlated to changes in milk miRNA content, FA profile, and antioxidant properties of raw milk. This pilot study suggests that the legislative microbiological safety window can hide a range of milks, which differ for their nutritional and antioxidant values that ultimately may have effects on the consumer’s health, also via epigenetic mechanisms
Epigenetics of pesticide-induced neurodegeneration
No full textEarly life represents a key window of plasticity important for the programming of development through the cellular differentiation. During this period exogenous and endogenous factors (ie, nutrition, xenobiotics, stress, hypoxia, infections, hormones, etc.) can induce epigenetic changes leading to the development of diseases in adult age. Transgenerational studies on animal models show that epigenetic changes, such as DNA methylation and histone modifications, may be transferred to next generations.
Early life exposure to permethrin pyrethroid pesticide, during brain development is associated with dopaminergic neuron degeneration leading to the Parkinson-like disease (PD) in an animal model [1-3]. Pyrethroids represent a real risk for population as demonstrated by the detection of pyrethroid metabolites in the urine of world wide population, depending on the their presence in all vegetables and fruits [4-6].
Data from the PD animal model demonstrated that genetic and epigenetic changes are associated to permethrin-induced neurodegeneration [7]. Nurr1, the transcription factor responsible for the development and the maintenance of dopaminergic neurons, was significantly increased in early-life permethrin exposed rats. 33% of their untreated offspring showed the same Nurr1 increase as their parents. Furthermore, both mothers and untreated offspring (F1 generation) demonstrated a decrease in global DNA methylation.
It should be underlined that permethrin can cross the blood brain barrier, storing in the brain after the end of treatment. Furthermore, several sites of binding between Nurr1 and permethrin have been identified by in silico studies highlighting that the direct interaction between permethrin and Nurr1 might be suggested in early-life exposed rats [1]. Epigenetic modifications have been hypothesized to explain the intergenerational effect of Nurr1 in F1 generation.
References
[1] Fedeli D, Montani M, Bordoni L, Galeazzi R, Nasuti C, Correia-Sá L, Domingues VF, Jayant M, Brahmachari V, Massaccesi L, Laudadio E, Gabbianelli R. In vivo and in silico studies to identify mechanisms associated with Nurr1 modulation following early life exposure to permethrin in rats. Neuroscience. 2017, 340, 411.
[2] Nasuti C, Brunori G, Eusepi P, Marinelli L, Ciccocioppo R, Gabbianelli R.Early life exposure to permethrin: a progressive animal model of Parkinson's disease. J Pharmacol Toxicol Methods. 2017, 83, 80.
[3] Carloni M, Nasuti C, Fedeli D, Montani M, Vadhana MS, Amici A, Gabbianelli R. Early life permethrin exposure induces long-term brain changes in Nurr1, NF-kB and Nrf-2. Brain Res. 2013, 17, 1515.
[4] Marsha K. Morgan. Children’s Exposures to Pyrethroid Insecticides at Home: A Review of Data Collected in Published Exposure Measurement Studies Conducted in the United States. Int J Environ Res Public Health. 2012, 9, 296.
[5] Dana Boyd Barr, Anders O. Olsson, Lee-Yang Wong, Simeon Udunka, Samuel E. Baker, Ralph D. Whitehead, Jr., Melina S. Magsumbol, Bryan L. Williams, Larry L. Needham. Urinary Concentrations of Metabolites of Pyrethroid Insecticides in the General U.S. Population: National Health and Nutrition Examination Survey 1999–2002. Environ Health Perspect. 2010, 118, 742.
[6] W. Li, M.K. Morgan, S.E. Graham, J.M. Starr. Measurement of pyrethroids and their environmental degradation products in fresh fruits and vegetables using a modification of the quick easy cheap effective rugged safe (QuEChERS) method. Talanta 2016, 151, 42.
[7] Bordoni L, Nasuti C, Mirto M, Caradonna F and Gabbianelli R. Intergenerational effect of early life exposure to permethrin: changes in global DNA methylation and in Nurr1 gene expression.
Toxics, 2015, 3(4), 451
The effects of nonsoy legumes consumption on serum levels of inflammatory biomarkers and Adiponectin in overweight/obese adults: A systematic review and meta-analysis of randomized controlled trials
No full textNonsoy legumes offer many health benefits, including improved arterial function, reduced cholesterol levels, and better management of cardiovascular diseases and type 2 diabetes. This systematic review and meta-analysis aim to clarify the inconclusive findings from randomized controlled trials (RCTs) by comprehensively evaluating the effects of nonsoy legumes consumption on serum levels of inflammatory biomarkers and Adiponectin. The search encompassed databases up to January 2024, including PubMed, EMBASE, MEDLINE, Scopus, Web of Science, and Cochrane CENTRAL to retrieve all RCTs examining the effects of nonsoy legumes on inflammatory biomarkers or Adiponectin. The effect sizes quantified as mean differences (MD) and standard deviations (SD) of outcomes, and an overall effect estimate was derived using a random-effects model. RCTs examining serum levels of C-reactive protein (CRP), Interleukin-6 (IL-6), Tumor Necrosis Factor-alpha (TNF-alpha), Interleukin-1 beta (IL-1 beta), and Adiponectin were included in the final meta-analysis. Results revealed that consumption of nonsoy legumes increased Adiponectin serum levels (P=.0017) and reduced IL-1 beta serum levels (P<.0001). However, it may not significantly affect CRP (P=.2951), IL-6 (P=.2286), and TNF-alpha (P=.6661) levels. Subgroup analyses showed that nonsoy legumes consumption significantly decreased TNF-alpha serum levels in studies involving healthy participants. Additionally, sensitivity analysis using the leave-one-out method suggested a potential significant reduction in serum levels of IL-6. This study indicates that consuming nonsoy legumes can increase levels of Adiponectin and decrease serum levels of IL-1 beta in overweight or obese adults. (c) 2024 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/)
Mitochondrion at the crossroads between nutrients and the epigenome
No full textThe modulation of gene expression is a pivotal regulatory mechanism by which cells adapt to endogenous and exogenous stimuli, including nutrition. In this context, the epigenome (i.e., the collection of biochemical modifications to the genome that do not affect the DNA sequence but determine whether genes are switched on or off) represents a crucial modulator of gene expression, with epigenetic modifications being finely tuned by extracellular and intracellular signals. At the same time, cellular responses to environmental cues are mediated, at least in part, by the mitochondria, that regulate both energetic and redox homeostasis. Recently, a tight link between epigenetic and mitochondrial metabolism has been described. This relationship is further supported by the fact that mitochondria contain their own DNA, which is a circular double-stranded molecule, present in multiple copies in each mitochondrion and that also undergo epigenetic modifications. Moreover, a pivotal role of nutrition in affecting both epigenetic and mitochondrial dynamics and function has been highlighted. While the role of nutrition in modulating mitochondrial functions is extensively discussed in other sections of this book, this chapter will focus on the impact of nutrition in boosting epigenetic regulations and on the role of the mitochondria in mediating this complex relationship
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