| 1. |
- Guillemin, R., et al.
(author)
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Interplay of complex decay processes after argon 1s ionization
- 2018
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In: Physical Review A: covering atomic, molecular, and optical physics and quantum information. - : AMER PHYSICAL SOC. - 2469-9926 .- 2469-9934. ; 97:1
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Journal article (peer-reviewed)abstract
- Complex decay pathways involving radiative and nonradiative relaxation after deep core-level ionization in argon are disentangled by a unique combination of several synchrotron radiation-based spectroscopic techniques. In particular, by comparing the results obtained from electron-ion coincidence, photon-ion coincidence, and x-ray emission measurements, we are able to distinguish the final ionic states produced in the cascade decay involving K alpha and K beta radiative decay and final ionic states produced by nonradiative cascade decay. High-resolution Auger electron spectroscopy is then used as a complementary tool to identify the LMM transitions contributing to the cascade decay. Ab initio calculations are performed to identify the electronic states involved in the LMM decay.
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| 2. |
- Hadjikhani, Nouchine, 1966, et al.
(author)
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Bumetanide for autism: More eye contact, less amygdala activation
- 2018
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In: Scientific Reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 8:1
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Journal article (peer-reviewed)abstract
- We recently showed that constraining eye contact leads to exaggerated increase of amygdala activation in autism. Here, in a proof of concept pilot study, we demonstrate that administration of bumetanide (a NKCC1 chloride importer antagonist that restores GABAergic inhibition) normalizes the level of amygdala activation during constrained eye contact with dynamic emotional face stimuli in autism. In addition, eye-tracking data reveal that bumetanide administration increases the time spent in spontaneous eye gaze during in a free-viewing mode of the same face stimuli. In keeping with clinical trials, our data support the Excitatory/Inhibitory dysfunction hypothesis in autism, and indicate that bumetanide may improve specific aspects of social processing in autism. Future double-blind placebo controlled studies with larger cohorts of participants will help clarify the mechanisms of bumetanide action in autism. © 2018 The Author(s).
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| 3. |
- Lassalle, A., et al.
(author)
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Effect of visual stimuli of pain on empathy brain network in people with and without Autism Spectrum Disorder
- 2018
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In: European Journal of Neuroscience. - : Wiley. - 0953-816X .- 1460-9568. ; 48:6, s. 2333-2342
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Journal article (peer-reviewed)abstract
- The extent to which affective empathy is impaired in Autism Spectrum Disorder (ASD) remains unclear, as some-but not all-previous neuroimaging studies investigating empathy for pain in ASD have shown similar activation levels to those of neurotypicals individuals. These inconsistent results could be due to the use of different empathy-eliciting stimuli. While some studies used pictures of faces exhibiting a painful expression, others used pictures of limbs in painful situations. In this study, we used fMRI to compare activation in areas associated with empathy processing (empathy network) for these two types of stimuli in 31 participants (16 with ASD, 15 controls). We found a group difference in the inferior frontal gyrus (IFG) and the thalamus when participants viewed stimuli of limbs in painful situations, but not when they viewed face stimuli with a painful expression. Both groups of participants activated their empathy network more when viewing pictures of limbs in painful situations than when viewing pictures of faces with a painful expression; this increased activation for limbs versus faces was significantly enhanced in controls relative to ASD participants, especially in the secondary somatosensory cortex (SII). Our findings suggest that empathy defect of people with ASD is contingent upon the type of stimuli used, and may be related to the level of Mirror Neuron System involvement, as brain regions showing group differences (IFG, SII) underlie embodiment. We discuss the potential clinical implications of our findings in terms of developing interventions boosting the empathetic abilities of people with ASD.
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