Studio della quota di volo mediante GNSS, altimetro radar e barometro per rilievi di spettroscopia gamma da velivolo

Lo studio della distribuzione dei radionuclidi terrestri (238U, 232Th e 40K) realizzato mediante tecniche di spettroscopia gamma da velivolo è influenzato dalla quota a cui il rivelatore si trova rispetto al suolo. Un'incertezza del 10% a 100 m di altezza origina un errore nella stima del segnale gamma del 208Tl, appartenente alla catena di decadimenti del 232Th, dell’ordine del 7%. L'impiego di una nuova classe di spettrometri montati a bordo di UAV (Unmanned Aerial Vehicle) per raffinate misure in contesti ostili o remoti rende necessaria un'accurata stima in real time della quota di volo. Il Radgyro è un velivolo dedicato a survey multiparametrici, capace di trasportare strumentazione pari ad un payload massimo di 120 kg, tra cui quattro spettrometri gamma NaI(Tl). Una stazione inerziale con ricevitore integrato GNSS (Global Navigation Satellite System) restituisce l'assetto del velivolo con una frequenza massima di 400 Hz. Il velivolo è dotato di un network di tre ricevitori GNSS posizionati alle estremità della carena del velivolo. Un altimetro radar a 24 GHz rileva la quota con una frequenza di 60 Hz. La misura di pressione e temperatura consente di ricavare la quota barometrica a 2 Hz. Con l'obiettivo di studiare le incertezze associate alle misure della quota di volo acquisite dagli altimetri in relazione ai dati GNSS, sono stati realizzati tre voli sul mare in un range di altezze comprese tra 31 m e 249 m, per un totale di 4702 secondi di volo effettivo. Al termine dello studio è possibile concludere che l'errore complessivo delle abbondanze di K, U e Th aumenta di 7.7%, 0.5% e 2.7% rispettivamente, a causa delle incertezze della quota di volo

Neonatal stroke in mice causes long-term changes in neuronal notch-2 expression that may contribute to prolonged injury

Background and Purpose: Notch receptors (1–4) are membrane proteins that, on ligand stilumation, release their cytoplasmic domains to serve as transcription factors. Notch-2 promotes proliferation both during development and cancer, but its role in response to ischemic injury is less well understood. The purpose of this study was to understand whether Notch-2 is induced after neonatal stroke and to investigate its functional relevance.Methods: P12 CD1 mice were subjected to permanent unilateral (right-sided) double ligation of the common carotid artery.Results: Neonatal ischemia induces a progressive brain injury with prolonged apoptosis and Notch-2 up-regulation. Notch-2 expression was induced shortly after injury in hippocampal areas with elevated c-fos activation and increased cell death. Long-term induction of Notch-2 also occurred in CA1 and CA3 in and around areas of cell death, and had a distinct pattern of expression as compared to Notch-1. In vitro oxygen glucose deprivation treatment showed a similar increase in Notch-2 in apoptotic cells. In vitro gain of function experiments, using an active form of Notch-2, show that Notch-2 induction is neurotoxic to a comparable extent as oxygen glucose deprivation treatment.Conclusions: These results suggest that Notch-2 up-regulation after neonatal ischemia is detrimental to neuronal survival

Engrailed protects mouse midbrain dopaminergic neurons against mitochondrial complex I insults

International audienceMice heterozygous for homeobox gene Engrailed-1 display progressive loss of mesencephalic dopaminergic (mDA) neurons. We report that exogenous Engrailed-1 and Engrailed-2 (collectively Engrailed) protect mDA neurons from 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a mitochondrial complex I toxin used to model PD in animals. Engrailed enhances the translation of nuclear-encoded mRNAs for two key complex I subunits, Ndufs1 and Ndufs3, and increases complex I activity. Accordingly, in vivo protection against MPTP by Engrailed is antagonized by Ndufs1 siRNA. An association between Engrailed and complex I is further confirmed by the reduced expression of Ndufs1 and Ndufs3 in the substantia nigra pars compacta of Engrailed-1 heterozygous mice. Engrailed also confers in vivo protection against 6-hydroxydopamine and α-synuclein-A30P. Finally, the unilateral infusion of Engrailed into the midbrain increases striatal dopamine content resulting in contralateral amphetamine-induced turning. Therefore, Engrailed is both a survival factor for adult mDA neurons and a regulator of their physiological activity

Autism-Relevant Social Abnormalities and Cognitive Deficits in Engrailed-2 Knockout Mice

ENGRAILED 2 (En2), a homeobox transcription factor, functions as a patterning gene in the early development and connectivity of rodent hindbrain and cerebellum, and regulates neurogenesis and development of monoaminergic pathways. To further understand the neurobiological functions of En2, we conducted neuroanatomical expression profiling of En2 wildtype mice. RTQPCR assays demonstrated that En2 is expressed in adult brain structures including the somatosensory cortex, hippocampus, striatum, thalamus, hypothalamus and brainstem. Human genetic studies indicate that EN2 is associated with autism. To determine the consequences of En2 mutations on mouse behaviors, including outcomes potentially relevant to autism, we conducted comprehensive phenotyping of social, communication, repetitive, and cognitive behaviors. En2 null mutants exhibited robust deficits in reciprocal social interactions as juveniles and adults, and absence of sociability in adults, replicated in two independent cohorts. Fear conditioning and water maze learning were impaired in En2 null mutants. High immobility in the forced swim test, reduced prepulse inhibition, mild motor coordination impairments and reduced grip strength were detected in En2 null mutants. No genotype differences were found on measures of ultrasonic vocalizations in social contexts, and no stereotyped or repetitive behaviors were observed. Developmental milestones, general health, olfactory abilities, exploratory locomotor activity, anxiety-like behaviors and pain responses did not differ across genotypes, indicating that the behavioral abnormalities detected in En2 null mutants were not attributable to physical or procedural confounds. Our findings provide new insight into the role of En2 in complex behaviors and suggest that disturbances in En2 signaling may contribute to neuropsychiatric disorders marked by social and cognitive deficits, including autism spectrum disorders