First decay study of the very neutron-rich isotope Br-93

The decay of the mass-separated, very neutron-rich isotope Br-93 has been studied by gamma-spectroscopy. A level scheme of its daughter Kr-93 has been constructed. Level energies, gamma-ray branching ratios and multipolarities suggest spins and parities which are in accord with a smooth systematics of the N=57 isotones for Z less-equal 40, suggesting the N=56 shell closure still to be effective in Kr isotopes. So far, there is no indication of a progressive onset of deformation in neutron-rich Kr isotopes.The decay of the mass-separated, very neutron-rich isotope Br-93 has been studied by gamma-spectroscopy. A level scheme of its daughter Kr-93 has been constructed. Level energies, gamma-ray branching ratios and multipolarities suggest spins and parities which are in accord with a smooth systematics of the N=57 isotones for Z less-equal 40, suggesting the N=56 shell closure still to be effective in Kr isotopes. So far, there is no indication of a progressive onset of deformation in neutron-rich Kr isotopes

Mouse and rat ultrasonic vocalizations in neuroscience and neuropharmacology: State of the art and future applications

Mice and rats emit ultrasonic vocalizations (USVs), which may express their arousal and emotional states, to communicate with each other. There is continued scientific effort to better understand the functions of USVs as a central element of the rodent behavioral repertoire. However, studying USVs is not only important because of their ethological relevance, but also because they are widely applied as a behavioral readout in various fields of biomedical research. In mice and rats, a large number of experimental models of brain disorders exist and studying the emission of USVs in these models can provide valuable information about the health status of the animals and the effectiveness of possible interventions, both environmental and pharmacological. This review (i) provides an updated overview of the contexts in which ultrasonic calling behaviour of mice and rats has particularly high translational value, and (ii) gives some examples of novel approaches and tools used for the analysis of USVs in mice and rats, combining qualitative and quantitative methods. The relevance of age and sex differences as well as the importance of longitudinal evaluations of calling and non-calling behaviour is also discussed. Finally, the importance of assessing the communicative impact of USVs in the receiver, that is, through playback studies, is highlighted

Beta-decay of nuclei around Se-90. Search for signatures of a N=56 sub-shell closure relevant the r-process

Nuclear structure plays a significant role on the rapid neutron capture process (r-process) since shapes evolve with the emergence of shells and sub-shells. There was some indication in neighboring nuclei that we might find examples of a new N=56 sub-shell, which may give rise to a doubly magic Se-90 nucleus. Beta-decay half lives of nuclei around Se-90 have been measured to determine if this nucleus has in fact a doubly-magic character. The fragmentation of Xe-136 beam at the National Superconducting Cyclotron Laboratory at Michigan State University was used to create a cocktail of nuclei in the A=90 region. We have measured the half lives of twenty-two nuclei near the r-process path in the A=90 region. The half lives of As-88 and Se-90 have been measured for the first time. The values were compared with theoretical predictions in the search for nuclear-deformation signatures of a N=56 sub-shell, and its possible role in the emergence of a potential doubly-magic Se-90. The impact of such hypothesis on the synthesis of heavy nuclei, particularly in the production of Sr, Y and Zr elements was investigated with a weak r-process network. The new half lives agree with results obtained from a standard global QRPA model used in r-process calculations, indicating that Se-90 has a quadrupole shape incompatible with a closed N=56 sub-shell in this region. The impact of the measured Se-90 half-life in comparison with a former theoretical predication associated with a spherical half-life on the weak-r-process is shown to be strong

Neuroimaging Evidence of Major Morpho-Anatomical and Functional Abnormalities in the BTBR T+TF/J Mouse Model of Autism

BTBR T+tf/J (BTBR) mice display prominent behavioural deficits analogous to the defining symptoms of autism, a feature that has prompted a widespread use of the model in preclinical autism research. Because neuro-behavioural traits are described with respect to reference populations, multiple investigators have examined and described the behaviour of BTBR mice against that exhibited by C57BL/6J (B6), a mouse line characterised by high sociability and low self-grooming. In an attempt to probe the translational relevance of this comparison for autism research, we used Magnetic Resonance Imaging (MRI) to map in both strain multiple morpho-anatomical and functional neuroimaging readouts that have been extensively used in patient populations. Diffusion tensor tractography confirmed previous reports of callosal agenesis and lack of hippocampal commissure in BTBR mice, and revealed a concomitant rostro-caudal reorganisation of major cortical white matter bundles. Intact inter-hemispheric tracts were found in the anterior commissure, ventro-medial thalamus, and in a strain-specific white matter formation located above the third ventricle. BTBR also exhibited decreased fronto-cortical, occipital and thalamic gray matter volume and widespread reductions in cortical thickness with respect to control B6 mice. Foci of increased gray matter volume and thickness were observed in the medial prefrontal and insular cortex. Mapping of resting-state brain activity using cerebral blood volume weighted fMRI revealed reduced cortico-thalamic function together with foci of increased activity in the hypothalamus and dorsal hippocampus of BTBR mice. Collectively, our results show pronounced functional and structural abnormalities in the brain of BTBR mice with respect to control B6 mice. The large and widespread white and gray matter abnormalities observed do not appear to be representative of the neuroanatomical alterations typically observed in autistic patients. The presence of reduced fronto-cortical metabolism is of potential translational relevance, as this feature recapitulates previously-reported clinical observations

Dopaminergic modulation of affective and social deficits induced by prenatal glucocorticoid exposure

Prenatal stress or exposure to elevated levels of glucocorticoids (GCs) can impair specific neurobehavioral circuits leading to alterations in emotional processes later in life. In turn, emotional deficits may interfere with the quality and degree of social interaction. Here, by using a comprehensive behavioral approach in combination with the measurement of ultrasonic vocalizations, we show that in utero GC (iuGC)-exposed animals present increased immobility in the forced swimming test, pronounced anhedonic behavior (both anticipatory and consummatory), and an impairment in social interaction at different life stages. Importantly, we also found that social behavioral expression is highly dependent on the affective status of the partner. A profound reduction in mesolimbic dopaminergic transmission was found in iuGC animals, suggesting a key role for dopamine (DA) in the etiology of the observed behavioral deficits. Confirming this idea, we present evidence that a simple pharmacological approach—acute L-3,4-dihydroxyphenylacetic acid (L-DOPA) oral administration, is able to normalize DA levels in iuGC animals, with a concomitant amelioration of several dimensions of the emotional and social behaviors. Interestingly, L-DOPA effects in control individuals were not so straightforward; suggesting that both hypo- and hyperdopaminergia are detrimental in the context of such complex behaviors.This work was supported by a grant of Institute for the Study of Affective Neuroscience (ISAN) and Janssen Neurosciences Prize. SB and AJR have Fundacao para a Ciencia e Tecnologia (FCT) fellowships (SFRH/BD/89936/2012; SFRH/BPD/33611/2009)

Beta-decay half-lives and beta-delayed neutron emisison probabilities of nuclei in the region A. 110, relevant for the r-process

Measurements of the {beta}-decay properties of A {approx}< 110 r-process nuclei have been completed at the National Superconducting Cyclotron Laboratory, at Michigan State University. {beta}-decay half-lives for {sup 105}Y, {sup 106,107}Zr and {sup 108,111}Mo, along with ,B-delayed neutron emission probabilities of 104Y, 109,11OMo and upper limits for 105Y, 103-107Zr and 108,111 Mo have been measured for the first time. Studies on the basis of the quasi-random phase approximation are used to analyze the ground-state deformation of these nuclei

Isobaric analog states of neutron-rich nuclei. Doppler shift as a measurement tool for resonance excitation functions

We present a new approach for the measurement of resonance excitation functions of neutron-rich nuclei using Doppler shift information. Preliminary data from the first application of the method is presented in the spectroscopy studies of 7 He isobaric analog states in 7 Li.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/45815/1/10050_2005_Article_506014.pd

Meta-analysis of SHANK Mutations in Autism Spectrum Disorders: A Gradient of Severity in Cognitive Impairments.

International audienceSHANK genes code for scaffold proteins located at the post-synaptic density of glutamatergic synapses. In neurons, SHANK2 and SHANK3 have a positive effect on the induction and maturation of dendritic spines, whereas SHANK1 induces the enlargement of spine heads. Mutations in SHANK genes have been associated with autism spectrum disorders (ASD), but their prevalence and clinical relevance remain to be determined. Here, we performed a new screen and a meta-analysis of SHANK copy-number and coding-sequence variants in ASD. Copy-number variants were analyzed in 5,657 patients and 19,163 controls, coding-sequence variants were ascertained in 760 to 2,147 patients and 492 to 1,090 controls (depending on the gene), and, individuals carrying de novo or truncating SHANK mutations underwent an extensive clinical investigation. Copy-number variants and truncating mutations in SHANK genes were present in ∼1% of patients with ASD: mutations in SHANK1 were rare (0.04%) and present in males with normal IQ and autism; mutations in SHANK2 were present in 0.17% of patients with ASD and mild intellectual disability; mutations in SHANK3 were present in 0.69% of patients with ASD and up to 2.12% of the cases with moderate to profound intellectual disability. In summary, mutations of the SHANK genes were detected in the whole spectrum of autism with a gradient of severity in cognitive impairment. Given the rare frequency of SHANK1 and SHANK2 deleterious mutations, the clinical relevance of these genes remains to be ascertained. In contrast, the frequency and the penetrance of SHANK3 mutations in individuals with ASD and intellectual disability-more than 1 in 50-warrant its consideration for mutation screening in clinical practice