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Learn about the most recent theoretical and practical advances in radar signal processing using tools and techniques from compressive sensing. Providing a broad perspective that fully demonstrates the impact of these tools, the accessible and tutorial-like chapters cover topics such as clutter rejection, CFAR detection, adaptive beamforming, random arrays for radar, space-time adaptive processing, and MIMO radar. Each chapter includes coverage of theoretical principles, a detailed review of current knowledge, and discussion of key applications, and also highlights the potential benefits of using compressed sensing algorithms. A unified notation and numerous cross-references between chapters make it easy to explore different topics side by side. Written by leading experts from both academia and industry, this is the ideal text for researchers, graduate students and industry professionals working in signal processing and radar.
Rasd2 is a striatal GTP-binding protein that modulates Akt and mTOR signaling cascades, well known to be highly vulnerable pathways in psychiatric disorders.
We investigated the association of Rasd2 and its genetic variation with a series of prefronto-striatal phenotypes related to psychosis in rodents and humans.
We want to provide evidence that Rasd2 controls the vulnerability to schizophrenia-related behavior induced by psychothomimetic drugs in mice. Moreover, we aim to find genetic variations within the Rasd2 gene that influence a series of brain schizophrenia-related phenotypes in human.
Rasd2 knockout mice were employed to evaluate schizophrenia-like behaviors induced by psychotomimetic drugs like amphetamine and phencyclidine. Furthermore, we investigated if RASD2genetic variations in humans are associated with mRNA expression in post-mortem prefrontal cortex, as well as prefrontal and striatal grey matter volume and physiology during working memory as measured with MRI in healthy subjects. Finally, we assessed RASD2mRNA expression levels in post-mortem brains of patients with schizophrenia and bipolar disorder.
We found that both psychotomimetics triggered greater vulnerability to motor stimulation and to prepulse inhibition deficits in Rasd2 mutants. In humans, we found that a genetic variation (rs6518956) within RASD2 predicts prefrontal mRNA expression as well as prefrontal grey matter volume and prefronto-striatal activity during working memory. Finally, we reported that RASD2 mRNA expression is slightly reduced in post-mortem prefrontal cortex of patients with schizophrenia.
Collectively, our data suggests that RASD2represents a gene of potential interest in psychiatric disorders for its ability to modulate prefronto-striatal phenotypes related to schizophrenia.