279 research outputs found

    Glucose Metabolism, Thyroid Function, and Prolactin Level in Adolescent Patients With First Episode of Schizophrenia and Affective Disorders

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    Schizophrenia and affective spectrum disorders (ASD) typically begin in adolescence or early adulthood. The pathophysiological mechanisms underlying these disorders are still not fully understood, and recent studies have suggested an involvement of dysfunctions in cardiometabolic and neuroendocrine systems at the onset of both disorders. In this context, we aimed to assess thyroid function, prolactin level, glucose metabolism, and lipid profile in drug naive adolescents, comparing patients with first episode of schizophrenia spectrum disorders (SSD) and patients with ASD. We performed a retrospective chart review from inpatients aged from ten to eighteen years, referred to Child and Adolescent Psychiatric Unit of University of Bari “Aldo Moro” over a period of 4 years, with diagnosis of SSD (n=30) or ASD (n=22), according to Diagnostic and Statistical Manual for Mental Disorders-fifth edition (DSM-5) criteria. Data on serum prolactin, glucose, insulin, total cholesterol, high density lipoprotein cholesterol, low density lipoprotein cholesterol, triglycerides, thyroid stimulating hormone, free triiodothyronin, and free thyroxin were collected, and the insulin resistance (IR) indexes “HOMA1-IR“ and “HOMA2-IR” were calculated. The multivariable linear regression models, adjusting for potential confounding factors (age, sex, and BMI), showed HOMA1-IR (p=0.001), HOMA2-IR (p=0.002), glucose (p=0.004), insulin (p=0.004) and free thyroxin (p<0.001) values higher in the SSD group than in ASD. No others significant differences were found. Our findings suggest the need for a metabolic and endocrine screening at the onset of SSD and ASD, particularly for indexes of IR, that is a testable and treatable risk factor for cardiometabolic diseases. Further studies are required to better understand the role of endocrinological and metabolic dysfunctions at the onset of severe mental illness also considering influencing factors as age, gender, and BMI

    Coupled Biological and Thermochemical Process for Plastic Waste Conversion into Biopolymers

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    The aqueous phase produced from the hydrothermal liquefaction (HTL) of three matrices (Plasmix treated with different operative conditions and polystyrene) was subjected to acidogenic fermentation (AF) batch tests to obtain organic acids, which are the ideal substrates for biopolymers (e.g., polyhydroxyalkanoates, PHA) production from mixed microbial cultures (MMC). Parallel tests in the presence of only HTL water fractions or only glucose (an easily biodegradable compound), or in presence of both, were conducted and compared to assess any possible recalcitrant or inhibitory effect of plastic waste from the HTL treatment during the AF process. These tests resulted, within approximately 30 days of operation, in a conversion of 96 ± 21% (COD/COD) of the Plasmix by-products after a 2h thermochemical treatment into organic acids, a 54 ± 7% (COD/COD) of conversion for Plasmix by-products treated 4h, and 29 ± 1% (COD/COD) of conversion in the presence of polystyrene residual water

    Administration of a Synbiotic to Free-Living Elderly and Evaluation of Serum Cytokines. A Pilot Study

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    Ten free-living elderly were administered with a synbiotic [fermented milk containing Lactobacillus rhamnosus Gorbach and Goldin (LGG)] and oligofructose as a prebiotic for one month. Serum cytokines were evaluated before (T0) and after (T1) synbiotic administration. At T0, values of Interleukin (IL)-12, IL-6, IL-10, IL-1 and Tumor Necrosis Factor (TNF)- were lower than normal controls, with the exception of IL-8, thus confirming previous results on the impairment of both innate and adaptive responses in elderly. At T1, the synbiotic was able to significantly increase, depressed values of IL-1, IL-6 and IL-8 with a trend to a modest increase for the restant cytokines. In conclusion, the synbiotic used in this study seems to be very beneficial to elderly for its capacity to maintain the immune homeostasis, even if an increase in dosage and prolongation of administration time are required for a better modulation of the aged adaptive immune response

    Imaging spectroscopic performances for a Si based detection system

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    We present the imaging and spectroscopic capabilities of a system based on a single photon counting chip (PCC) bump-bonded on a Si pixel detector. The system measures the energy spectrum and the flux, produced by a standard mammographic tube. We have also made some images of low contrast details, achieving good results

    Vitamin D Deficiency in Autism Spectrum Disorder: A Cross-Sectional Study

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    Vitamin D plays a role in central nervous system (CNS) development. Recent literature focused on Vitamin D status in children and adolescents with autism spectrum disorder (ASD), but with inconsistent results. Our case-control study is aimed at evaluating serum 25-hydroxyl-Vitamin D (25(OH)D) concentration in children with ASD (ASD group, n=54) compared to children affected by other neurological and psychiatric disorders (non-ASD group, n=36). All patients were admitted at the Complex Operative Unit of Child Neuropsychiatry, Polyclinic of Bari, Italy. 25(OH)D was quantified by chemiluminescence immunoassay and level defined as: Deficiency (<20 ng/mL); insufficiency (20-30); normality (30-100); toxicity (>100). Statistical analysis was performed using SPSS20 (significance<0.05). The ASD group showed 25(OH)D a mean level significantly lower than control (p=0.014). Multivariable logistic regression analysis showed an association between ASD and Vitamin D deficiency (p=0.006). The nature of such association is unclear. Vitamin D deficiency may probably act as a risk factor for the development of ASD. Further studies are needed to unravel the role of Vitamin D in ASD etiology and investigate its therapeutic potential

    Performance of 4096 pixel photon counting chip

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    A 4096 pixel Photon Counting Chip (PCC) has been developed and tested. It is aimed primarily at medical imaging although it can be used for other applications involving particle counting. The readout chip consists of a matrix of 64 x 64 identical square pixels, whose side measures 170 mm and is bump-bonded to a similar matrix of GaAs or Si pixel diodes covering a sensitive area of 1.18 cm . The electronics in each cell comprises a preamplifier, a discriminator with variable threshold and a 3-bit threshold tune as well as 15-bit counter. Each pixel can be individually addressed for electrical test or masked during acquisition. A shutter allows for switching between the counting and the readout modes and the use of a static logic in the counter enables long data taking periods. Electrical tests of the chip have shown a maximum counting rate of up to 2 MHz in each pixel. The minimum reachable threshold is 1400 e with a variation of 350 e rms that can be reduced to 80 e rms after tuning with the 3-bit adjustment. Electical noise at the input is 170 e rms. Several read-out chips have been bump-bonded to 200 mm thick GaAs detectors. Tests with g-rays and b sources have been carried out. A number of objects have been imaged and 260 mm thick aluminium foil which represents a contrast to the surrounding aire of only 1.9% has been correctly imaged

    Determination of the branching ratios Γ(KL3π0)/Γ(KLπ+ππ0)\Gamma (K_L \to 3 \pi^0) / \Gamma (K_L \to \pi^+ \pi^- \pi^0) and Γ(KL3π0)/Γ(KLπeν)\Gamma (K_L \to 3 \pi^0) / \Gamma (K_L \to \pi e \nu )

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    Improved branching ratios were measured for the KL3π0K_L \to 3 \pi^0 decay in a neutral beam at the CERN SPS with the NA31 detector: Γ(KL3π0)/Γ(KLπ+ππ0)=1.611±0.037\Gamma (K_L \to 3 \pi^0) / \Gamma (K_L \to \pi^+ \pi^- \pi^0) = 1.611 \pm 0.037 and Γ(KL3π0)/Γ(KLπeν)=0.545±0.010\Gamma (K_L \to 3 \pi^0) / \Gamma (K_L \to \pi e \nu ) = 0.545 \pm 0.010. From the first number an upper limit for ΔI=5/2\Delta I =5/2 and ΔI=7/2\Delta I = 7/2 transitions in neutral kaon decay is derived. Using older results for the Ke3/Kμ\mu 3 fraction, the 3π0\pi^0 branching ratio is found to be Γ(KL3π0)/Γtot=(0.211±0.003)\Gamma (K_L \to 3 \pi^0 )/ \Gamma_{tot} = (0.211 \pm 0.003), about a factor three more precise than from previous experiments

    Association between autism spectrum disorder and diabetes: systematic review and meta-analysis

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    There is mixed evidence on the link between autism spectrum disorder (ASD) and diabetes. We conducted the first systematic review/meta-analysis on their association. Based on a pre-registered protocol (PROSPERO: CRD42021261114), we searched Pubmed, Ovid, and Web of Science databases up to 6 December 2021, with no language/type of document restrictions. We assessed study quality using the Newcastle-Ottawa Scale (NOS). We included 24 studies (total: 3427,773 individuals; 237,529 with ASD and 92,832 with diabetes) in the systematic review and 20 in the meta-analysis (mean stars number on the NOS: 5.89/10). There was a significant association, albeit characterized by significant heterogeneity, when pooling unadjusted OR (1.535, 95% CI = 1.109-2.126), which remained significant when restricting the analysis to children and type 2 diabetes, but became non-significant when considering adjusted ORs (OR: 1.528, 95% CI = 0.954-2.448). No significant prospective association was found (n = 2) on diabetes predicting ASD (HR: 1.232, 0.826-11.837). Therefore, the association between ASD and diabetes is likely confounded by demographic and clinical factors that should be systematically investigated in future studies

    A new measurement of direct CP violation in two pion decays of the neutral kaon

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    The NA48 experiment at CERN has performed a new measurement of direct CP violation, based on data taken in 1997 by simultaneously collecting K_L and K_S decays into pi0pi0 and pi+pi-. The result for the CP violating parameter Re(epsilon'/epsilon) is (18.5 +/- 4.5(stat)} +/- 5.8 (syst))x10^{-4}.Comment: 18 pages, 6 figure

    Candidate biomarkers from the integration of methylation and gene expression in discordant autistic sibling pairs

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    While the genetics of autism spectrum disorders (ASD) has been intensively studied, resulting in the identification of over 100 putative risk genes, the epigenetics of ASD has received less attention, and results have been inconsistent across studies. We aimed to investigate the contribution of DNA methylation (DNAm) to the risk of ASD and identify candidate biomarkers arising from the interaction of epigenetic mechanisms with genotype, gene expression, and cellular proportions. We performed DNAm differential analysis using whole blood samples from 75 discordant sibling pairs of the Italian Autism Network collection and estimated their cellular composition. We studied the correlation between DNAm and gene expression accounting for the potential effects of different genotypes on DNAm. We showed that the proportion of NK cells was significantly reduced in ASD siblings suggesting an imbalance in their immune system. We identified differentially methylated regions (DMRs) involved in neurogenesis and synaptic organization. Among candidate loci for ASD, we detected a DMR mapping to CLEC11A (neighboring SHANK1) where DNAm and gene expression were significantly and negatively correlated, independently from genotype effects. As reported in previous studies, we confirmed the involvement of immune functions in the pathophysiology of ASD. Notwithstanding the complexity of the disorder, suitable biomarkers such as CLEC11A and its neighbor SHANK1 can be discovered using integrative analyses even with peripheral tissues
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