Electron backscattering from stacking faults in SiC by means of \textit{ab initio} quantum transport calculations

We study coherent backscattering phenomena from single and multiple stacking faults (SFs) in 3C- and 4H-SiC within density functional theory quantum transport calculations. We show that SFs give rise to highly dispersive bands within both the valance and conduction bands that can be distinguished for their enhanced density of states at particular wave number subspaces. The consequent localized perturbation potential significantly scatters the propagating electron waves and strongly increases the resistance for $n$-doped systems. We argue that resonant scattering from SFs should be one of the principal degrading mechanisms for device operation in silicon carbide.Comment: 5 pages, 4 figure

Publisher's Note: Defect Influence on Heteroepitaxial 3C-SiC Young's Modulus [Electrochem. Solid-State Lett., 14, H161 (2011)]

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Inferior vena cava distensibility from subcostal and trans-hepatic imaging using both M-mode or artificial intelligence: a prospective study on mechanically ventilated patients

Background: Variation of inferior vena cava (IVC) is used to predict fluid-responsiveness, but the IVC visualization with standard sagittal approach (SC, subcostal) cannot be always achieved. In such cases, coronal trans-hepatic (TH) window may offer an alternative, but the interchangeability of IVC measurements in SC and TH is not fully established. Furthermore, artificial intelligence (AI) with automated border detection may be of clinical value but it needs validation. Methods: Prospective observational validation study in mechanically ventilated patients with pressure-controlled mode. Primary outcome was the IVC distensibility (IVC-DI) in SC and TH imaging, with measurements taken both in M-Mode or with AI software. We calculated mean bias, limits of agreement (LoA), and intra-class correlation (ICC) coefficient. Results: Thirty-three patients were included. Feasibility rate was 87.9% and 81.8% for SC and TH visualization, respectively. Comparing imaging from the same anatomical site acquired with different modalities (M-Mode vs AI), we found the following IVC-DI differences: (1) SC: mean bias − 3.1%, LoA [− 20.1; 13.9], ICC = 0.65; (2) TH: mean bias − 2.0%, LoA [− 19.3; 15.4], ICC = 0.65. When comparing the results obtained from the same modality but from different sites (SC vs TH), IVC-DI differences were: (3) M-Mode: mean bias 1.1%, LoA [− 6.9; 9.1], ICC = 0.54; (4) AI: mean bias 2.0%, LoA [− 25.7; 29.7], ICC = 0.32. Conclusions: In patients mechanically ventilated, AI software shows good accuracy (modest overestimation) and moderate correlation as compared to M-mode assessment of IVC-DI, both for SC and TH windows. However, precision seems suboptimal with wide LoA. The comparison of M-Mode or AI between different sites yields similar results but with weaker correlation. Trial registration Reference protocol: 53/2022/PO, approved on 21/03/202

Synapsin III Regulates Dopaminergic Neuron Development in Vertebrates

Attention deficit and hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by alterations in the mesocorticolimbic and nigrostriatal dopaminergic pathways. Polymorphisms in the Synapsin III (Syn III) gene can associate with ADHD onset and even affect the therapeutic response to the gold standard ADHD medication, methylphenidate (MPH), a monoamine transporter inhibitor whose efficacy appears related with the stimulation of brain-derived neurotrophic factor (BDNF). Interestingly, we previously showed that MPH can bind Syn III, which can regulate neuronal development. These observations suggest that Syn III polymorphism may impinge on ADHD onset and response to therapy by affecting BDNF-dependent dopaminergic neuron development. Here, by studying zebrafish embryos exposed to Syn III gene knock-down (KD), Syn III knock-out (ko) mice and human induced pluripotent stem cells (iPSCs)-derived neurons subjected to Syn III RNA interference, we found that Syn III governs the earliest stages of dopaminergic neurons development and that this function is conserved in vertebrates. We also observed that in mammals Syn III exerts this function acting upstream of brain-derived neurotrophic factor (BDNF)- and cAMP-dependent protein kinase 5 (Cdk5)-stimulated dendrite development. Collectively, these findings own significant implications for deciphering the biological basis of ADHD

Modulation by chronic stress and ketamine of ionotropic AMPA/NMDA and metabotropic glutamate receptors in the rat hippocampus

Converging clinical and preclinical evidence has shown that dysfunction of the glutamate system is a core feature of major depressive disorder. In this context, the N-methyl-d-aspartate (NMDA) receptor antagonist ketamine has raised growing interest as fast acting antidepressant. Using the chronic mild stress (CMS) rat model of depression, performed in male rats, we aimed at analyzing whether hippocampal specific changes in subunit expression and regulation of \u3b1-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) or NMDA ionotropic receptors and in metabotropic glutamate receptors could be associated with behavioral vulnerability/resilience to CMS. We also assessed whether acute ketamine (10 mg/kg) was able to dampen the alterations in CMS vulnerable animals. Although chronic stress and ketamine had no effect on ionotropic glutamate receptors mRNAs (expression, RNA editing and splicing), we found selective modulations in their protein expression, phosphorylation and localization at synaptic membranes. AMPA GluA2 expression at synaptic membranes was significantly increased only in CMS resilient rats (although a trend was found also in vulnerable animals), while its phosphorylation at Ser880 was higher in both CMS resilient and vulnerable rats, a change partially dampened by ketamine. In the hippocampus from all stressed groups, despite NMDA receptor expression levels were reduced in total extract, the levels of GluN2B-containing NMDA receptors were remarkably increased in synaptic membranes. Finally, mGlu2 underwent a selective downregulation in stress vulnerable animals, which was completely restored by acute ketamine. Overall, these results are in line with a hypofunction of activity-dependent glutamatergic synaptic transmission induced by chronic stress exposure in all the animals, as suggested by the alterations of ionotropic glutamate receptors expression and localization at synaptic level. At the same time, the selective modulation of mGlu2 receptor, confirms its previously hypothesized functional role in regulating stress vulnerability and, for the first time here, suggests a mGlu2 involvement in the fast antidepressant effect of ketamine

Glutamatergic Reinnervation and Assembly of Glutamatergic Synapses in Adult Rat Skeletal Muscle Occurs at Cholinergic Endplates

After denervation of adult rat abdominal muscles, the postsynaptic apparatus of neuromuscular junctions (NMJs) retains its original architecture and clustering of acetylcholine receptors (AChRs). When descending fibers of the spinal cord are surgically diverted to this muscle by a nerve grafting procedure, supraspinal glutamatergic neurons can innervate muscle fibers and restore motor function; the newly formed NMJs switch from a cholinergic to a glutamatergic-type synapse. We show here that regenerating nerve endings contact the fibers in an area occupied by cholinergic endplates. These NMJs are morphologically indistinguishable from those in controls, but they differ in the subunit composition of AChRs. Moreover, by immunofluorescence and immunoelectron microscopy, new NMJs express glutamatergic synapse markers. The \u3b1-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor subunit GluR1 partially colocalizes with AChRs, and vesicular glutamate transporter 2 is localized in the presynaptic compartment. Immunoprecipitation analysis of membranes from reinnervated muscle showed that AMPA receptor subunits GluR1 and GluR2 coimmunoprecipitate with rapsyn, the AChR-anchoring protein at the NMJ. Taken together, these results indicate that cholinergic endplates can be targeted by new glutamatergic projections and that the clustering of AMPA receptors occurs there