107 research outputs found
Late-Proterozoic to Paleozoic history of the peri-Gondwana Calabria–Peloritani Terrane inferred from a review of zircon chronology
U–Pb analyses of zircon from ten samples of augen gneisses, eight mafic and intermediate metaigneous rocks and six metasediments from some tectonic domains along the Calabria–Peloritani Terrane (Southern Italy) contribute to knowledge of peri-Gondwanan evolution from Late-Proterozoic to Paleozoic times. All samples were equilibrated under amphibolite to granulite facies metamorphism during the Variscan orogeny. The zircon grains of all considered samples preserve a Proterozoic memory suggestive of detrital, metamorphic and igneous origin. The available data fit a frame involving: (1) Neoproterozoic detrital input from cratonic areas of Gondwana; (2) Pan-African/Cadomian assemblage of blocks derived from East and West African Craton; (3) metamorphism and bimodal magmatism between 535 and 579 Ma, within an active margin setting; (4) rifting and opening of Ordovician basins fed by detrital input from the assembled Cadomian blocks. The Paleozoic basins evolved through sedimentation, metamorphism and magmatism during the Variscan orogeny involving Palaeozoic and pre-Paleozoic blocks. The Proterozoic zircon records decidedly decrease in the high grade metamorphic rocks affected by Variscan pervasive partial melting. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s40064-016-1839-8) contains supplementary material, which is available to authorized users
A preliminary study in Wistar rats with enniatin : A contaminated feed
A 28-day repeated dose preliminary assay, using enniatin A naturally contaminated feed through microbial fermentation by a Fusarium tricinctum strain, was carried out employing two months-old female Wistar rats as in vivo experimental model. In order to simulate a physiological test of a toxic compound naturally produced by fungi, five treated animals were fed during twenty-eight days with fermented feed. As control group, five rats were fed with standard feed. At the 28th day, blood samples were collected for biochemical analysis and the gastrointestinal tract, liver and kidneys were removed from each rat for enniatin A detection and quantitation. Digesta were collected from stomach, duodenum, jejunum, ileum and colon. Enniatin A present in organs and in biological fluids was analyzed by liquid chromatography-diode array detector (LC-DAD) and confirmed by LC-mass spectrometry linear ion trap (MS-LIT); also several serum biochemical parameters and a histological analysis of the duodenal tract were performed. No adverse effects were found in any treated rat at the enniatin A concentration (20.91 mg/kg bw/day) tested during the 28-day experiment. Enniatin A quantitation in biological fluids ranged from 1.50 to 9.00 mg/kg, whereas in the gastrointestinal organs the enniatin A concentration ranged from 2.50 to 23.00 mg/kg. The high enniatin A concentration found in jejunum liquid and tissue points to them as an absorption area. Finally, two enniatin A degradation products were identified in duodenum, jejunum and colon content, probably produced by gut microflora
Ion Trap with Narrow Aperture Detection Electrodes for Fourier Transform Ion Cyclotron Resonance Mass Spectrometry
Valutazione del benessere animale in uno stabilimento di macellazione: buone pratiche e rispondenza ai requisiti di cui al Regolamento (CE) N. 1099/2009
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Multifunctional platinum@bsa-rapamycin nanocarriers for combinatorial therapy of cerebral cavernous malformation disease
KRIT1/CCM1 loss-of-function impairs advanced glycation endproducts receptors and detoxification and worsens fructose diet-induced hepatic dysmetabolism
KRIT1/CCM1 loss-of-function affects sphingolipid metabolism inducing hepatosteatosis and predisposing to liver fibrosis and insulin-resistance
P.05.65 DIAGNOSTIC YIELD OF A NEW MICRO-BIOPSY FORCEPS IN THE ASSESSMENT WORK OUT OF PERITONEAL CARCINOMATOSIS: A PRELIMINARY EXPERIENCE
KRIT1/CCM1 Loss-of-function Mutations Impair Anti-glycative and Anti-oxidant Systems Worsening High Fructose Diet-induced Hepatic Dismetabolism
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