Percorso nell'affido familiare: tra complessità e interazione

L’affido familiare è uno strumento di aiuto per il minore e di sostegno per sua famiglia, la quale si trova ad attraversare un momento di difficoltà, non riuscendo ad offrire ai minori presenti in essa, il giusto ambiente familiare dotato delle cure e dell’affetto necessarie per far fronte alla loro protezione ed educazione. Il progetto di affido familiare si costruisce attraverso un percorso complesso e tortuoso, composto da risorse, limiti, emozioni, relazioni e azioni, costituito ed individuato, e così creato, sui vissuti delle famiglie coinvolte, da soggetti istituzionali che danno vita a questo strumento d’aiuto per la famiglia, dove al centro è posto il minore. Sono differenti i professionisti coinvolti, dei servizi sociali e del Tribunale dei Minorenni, i quali dovranno collaborare e contemporaneamente avere ben chiari i propri ruoli per dare vita ad un buon intervento. In questo elaborato vorrei offrire un “modello di percorso nell’affido familiare” attraverso questi attori, i soggetti coinvolti e le loro differenti storie, le quali vengono ad intrecciarsi, formarsi, costruirsi e modificarsi durante tutto il percorso, che non va ad individuarsi meramente nell’atto d’allontanamento del minore dal proprio nucleo, ma nella totalità dell’intervento d’aiuto e sostegno alla famiglia. A testimonianza di questo, ci sarà giovamento nell’utilizzare l’esperienza della realtà spezzina, il suo viaggio evolutivo all’interno dell’affidamento e le prassi operative adottate, per comprendere come questi attori si muovono. Inoltre prezioso è l’utilizzo della descrizione di un caso, che fa emergere la dinamica trigenerazionale, che l’affido vuole spezzare, l’importanza della famiglia d’origine del minore e il fondamentale ruolo che ha la famiglia affidataria, l’importanza di una buona equipe di lavoro ed il rapporto reciproco di fiducia, la collaborazione tra le due famiglie legata alla doppia appartenenza. Quello che voglio dimostrare è l’importanza di andare “verso una maggior interazione” tra i diversi soggetti coinvolti, proiettata alla costruzione di progetti creati su misura, sulle differenti situazioni, che possa partire dal presupposto di una buona collaborazione e confronto tra i diversi professionisti, i quali ulteriormente si adopereranno per sostenere i vissuti emotivi, le storie e la relazione delle famiglie, affidataria e naturale e del minore stesso

Aflatoxin B1 and M1 Degradation by Lac2 from Pleurotus pulmonarius and Redox Mediators

Laccases (LCs) are multicopper oxidases that find application as versatile biocatalysts for the green bioremediation of environmental pollutants and xenobiotics. In this study we elucidate the degrading activity of Lac2 pure enzyme form Pleurotus pulmonarius towards aflatoxin B1 (AFB1) and M1 (AFM1). LC enzyme was purified using three chromatographic steps and identified as Lac2 through zymogram and LC-MS/MS. The degradation assays were performed in vitro at 25 °C for 72 h in buffer solution. AFB1 degradation by Lac2 direct oxidation was 23%. Toxin degradation was also investigated in the presence of three redox mediators, (2,2′-azino-bis-[3-ethylbenzothiazoline-6-sulfonic acid]) (ABTS) and two naturally-occurring phenols, acetosyringone (AS) and syringaldehyde (SA). The direct effect of the enzyme and the mediated action of Lac2 with redox mediators univocally proved the correlation between Lac2 activity and aflatoxins degradation. The degradation of AFB1 was enhanced by the addition of all mediators at 10 mM, with AS being the most effective (90% of degradation). AFM1 was completely degraded by Lac2 with all mediators at 10 mM. The novelty of this study relies on the identification of a pure enzyme as capable of degrading AFB1 and, for the first time, AFM1, and on the evidence that the mechanism of an effective degradation occurs via the mediation of natural phenolic compounds. These results opened new perspective for Lac2 application in the food and feed supply chains as a biotransforming agent of AFB1 and AFM1

Locus coeruleus imaging as a biomarker for noradrenergic dysfunction in neurodegenerative diseases.

Pathological alterations to the locus coeruleus, the major source of noradrenaline in the brain, are histologically evident in early stages of neurodegenerative diseases. Novel MRI approaches now provide an opportunity to quantify structural features of the locus coeruleus in vivo during disease progression. In combination with neuropathological biomarkers, in vivo locus coeruleus imaging could help to understand the contribution of locus coeruleus neurodegeneration to clinical and pathological manifestations in Alzheimer's disease, atypical neurodegenerative dementias and Parkinson's disease. Moreover, as the functional sensitivity of the noradrenergic system is likely to change with disease progression, in vivo measures of locus coeruleus integrity could provide new pathophysiological insights into cognitive and behavioural symptoms. Locus coeruleus imaging also holds the promise to stratify patients into clinical trials according to noradrenergic dysfunction. In this article, we present a consensus on how non-invasive in vivo assessment of locus coeruleus integrity can be used for clinical research in neurodegenerative diseases. We outline the next steps for in vivo, post-mortem and clinical studies that can lay the groundwork to evaluate the potential of locus coeruleus imaging as a biomarker for neurodegenerative diseases.Includes MRC, NIHR, Wellcome Trust, H2020 and FP7

Antioxidant and oxidative stress: a mutual interplay in age-related diseases

Aging is the progressive loss of organ and tissue function over time. Growing older is positively linked to cognitive and biological degeneration such as physical frailty, psychological impairment, and cognitive decline. Oxidative stress is considered as an imbalance between pro- and antioxidant species, which results in molecular and cellular damage. Oxidative stress plays a crucial role in the development of age-related diseases. Emerging research evidence has suggested that antioxidant can control the autoxidation by interrupting the propagation of free radicals or by inhibiting the formation of free radicals and subsequently reduce oxidative stress, improve immune function, and increase healthy longevity. Indeed, oxidation damage is highly dependent on the inherited or acquired defects in enzymes involved in the redox-mediated signaling pathways. Therefore, the role of molecules with antioxidant activity that promote healthy aging and counteract oxidative stress is worth to discuss further. Of particular interest in this article, we highlighted the molecular mechanisms of antioxidants involved in the prevention of age-related diseases. Taken together, a better understanding of the role of antioxidants involved in redox modulation of inflammation would provide a useful approach for potential interventions, and subsequently promoting healthy longevity

Modelling human choices: MADeM and decision‑making

Research supported by FAPESP 2015/50122-0 and DFG-GRTK 1740/2. RP and AR are also part of the Research, Innovation and Dissemination Center for Neuromathematics FAPESP grant (2013/07699-0). RP is supported by a FAPESP scholarship (2013/25667-8). ACR is partially supported by a CNPq fellowship (grant 306251/2014-0)

Humphrey visual field 10-2 and macular retinal thickness correlations in glaucomatous patients.

Purpose:To provide a quantitative comparison between the macular retina thickness (MRT) and the Humphrey visual field (HVF) 10-2 SITA-standard strategy parameters in glaucomatous patients. Methods:Retrospective statistical analysis of spectral domain optical coherence tomography macular cube scans 512x128 (Cirrus HD-OCT 4000, Carl Zeiss Meditec, Inc. , Dublin, CA) compared with HVF mean deviation (MD) and pattern standard deviation (PSD) in sixty eyes of thirty-six glaucomatous subjects. Abnormal MRT on OCT was defined as an average macular thickness value of any one of four quadrants to be less than 5% of normative database. Results:Eighteen (30% ) glaucomatous eyes showed an abnormal MRT. In patients with reduced MRT the mean was 236,8 μm, whereas in patients with normal MRT the mean was 264,3 μm. In eleven eyes with MRT reduction the average MD was -10,56 dB, and PSD was greater than 2,5 dB in seven of these eleven eyes. In 61% of glaucomatous patients there was a correlation between MRT and MD. Conclusions:In glaucomatous patients, OCT macular retinal thickness analysis may help in detecting the existence of a visual field defec

Neuropsychological Correlates of Pre-Frailty in Neurocognitive Disorders: A Possible Role for Metacognitive Dysfunction and Mood Changes

BackgroundRecent studies have suggested that cognitive functions in patients with neurocognitive disorders have a significant role in the pathogenic mechanisms of frailty. Although pre-frailty is considered an intermediate, preclinical state, epidemiological research has begun to dislodge cognition and frailty into their specific subcomponents to understand the relationship among them. We aim to analyse the possible association between pre-frailty and neuropsychological variables to outline which factors can contribute to minor and major neurocognitive disorders.Methods60 subjects complaining of different cognitive deficits underwent a deep-in-wide frailty and neuropsychological assessment. We conducted three multiple linear regression analyses adjusted for a combination of demographic measures and involving several neuropsychological–behavioural parameters selected by the literature on physical frailty.ResultsWe found a significant association between frailty—as measured by the multidimensional prognostic index (MPI)—and action monitoring and monetary gain (cognitive domain), depression and disinhibition (behavioural domain). Moreover, an association between MPI and impaired awareness for instrumental activities disabilities exists.ConclusionWe propose a novel framework for understanding frailty associated with metacognitive–executive dysfunction

Long non-coding and coding RNAs characterization in Peripheral Blood Mononuclear Cells and Spinal Cord from Amyotrophic Lateral Sclerosis patients

Alteration in RNA metabolism, concerning both coding and long non-coding RNAs (lncRNAs), may play an important role in Amyotrophic Lateral Sclerosis (ALS) pathogenesis. In this work, we performed a whole transcriptome RNA-seq analysis to investigate the regulation of non-coding and coding RNAs in Sporadic ALS patients (SALS), mutated ALS patients (FUS, TARDBP and SOD1) and matched controls in Peripheral Blood Mononuclear Cells (PBMC). Selected transcripts were validated in spinal cord tissues. A total of 293 differentially expressed (DE) lncRNAs was found in SALS patients, whereas a limited amount of lncRNAs was deregulated in mutated patients. A total of 87 mRNAs was differentially expressed in SALS patients; affected genes showed an association with transcription regulation, immunity and apoptosis pathways. Taken together our data highlighted the importance of extending the knowledge on transcriptomic molecular alterations and on the significance of regulatory lncRNAs classes in the understanding of ALS disease. Our data brought the light on the importance of lncRNAs and mRNAs regulation in central and peripheral systems, offering starting points for new investigations about pathogenic mechanism involved in ALS disease

RNA-seq profiling in peripheral blood mononuclear cells of amyotrophic lateral sclerosis patients and controls

Coding and long non-coding RNA (lncRNA) metabolism is now revealing its crucial role in Amyotrophic Lateral Sclerosis (ALS) pathogenesis. In this work, we present a dataset obtained via Illumina RNA-seq analysis on Peripheral Blood Mononuclear Cells (PBMCs) from sporadic and mutated ALS patients (mutations in FUS, TARDBP, SOD1 and VCP genes) and healthy controls. This dataset allows the whole-transcriptome characterization of PBMCs content, both in terms of coding and non-coding RNAs, in order to compare the disease state to the healthy controls, both for sporadic patients and for mutated patients. Our dataset is a starting point for the omni-comprehensive analysis of coding and lncRNAs, from an easy to withdraw, manage and store tissue that shows to be a suitable model for RNA profiling in ALS