Plasmodynamic synthesis of product based on aluminum in the oxygen atmosphere of a reactor-chamber

In this paper, the possibility is shown to synthesize oxide aluminum using a high-speed electro discharge plasma jet. The synthesized products were characterized by X-Ray diffractometry and transmission electron microscopy

Значимые личности в истории города Юрги Кемеровской области

В данной статье впервые даётся авторский взгляд на то, кого из юргинцев можно отнести к наиболее значимым личностям в истории города Юрги Кемеровской области. Предлагается перечень лиц с короткой характеристикой причины их включения. Делается вывод о малоизученности многих вопросов этой темы и её научной перспективности

Novel genetic loci associated with hippocampal volume

The hippocampal formation is a brain structure integrally involved in episodic memory, spatial navigation, cognition and stress responsiveness. Structural abnormalities in hippocampal volume and shape are found in several common neuropsychiatric disorders. To identify the genetic underpinnings of hippocampal structure here we perform a genome-wide association study (GWAS) of 33,536 individuals and discover six independent loci significantly associated with hippocampal volume, four of them novel. Of the novel loci, three lie within genes (ASTN2, DPP4 and MAST4) and one is found 200 kb upstream of SHH. A hippocampal subfield analysis shows that a locus within the MSRB3 gene shows evidence of a localized effect along the dentate gyrus, subiculum, CA1 and fissure. Further, we show that genetic variants associated with decreased hippocampal volume are also associated with increased risk for Alzheimer's disease (rg =-0.155). Our findings suggest novel biological pathways through which human genetic variation influences hippocampal volume and risk for neuropsychiatric illness

Genetic architecture of subcortical brain structures in 38,851 individuals

Subcortical brain structures are integral to motion, consciousness, emotions and learning. We identified common genetic variation related to the volumes of the nucleus accumbens, amygdala, brainstem, caudate nucleus, globus pallidus, putamen and thalamus, using genome-wide association analyses in almost 40,000 individuals from CHARGE, ENIGMA and UK Biobank. We show that variability in subcortical volumes is heritable, and identify 48 significantly associated loci (40 novel at the time of analysis). Annotation of these loci by utilizing gene expression, methylation and neuropathological data identified 199 genes putatively implicated in neurodevelopment, synaptic signaling, axonal transport, apoptosis, inflammation/infection and susceptibility to neurological disorders. This set of genes is significantly enriched for Drosophila orthologs associated with neurodevelopmental phenotypes, suggesting evolutionarily conserved mechanisms. Our findings uncover novel biology and potential drug targets underlying brain development and disease

Genetic architecture of subcortical brain structures in 38,851 individuals

Subcortical brain structures are integral to motion, consciousness, emotions and learning. We identified common genetic variation related to the volumes of the nucleus accumbens, amygdala, brainstem, caudate nucleus, globus pallidus, putamen and thalamus, using genome-wide association analyses in almost 40,000 individuals from CHARGE, ENIGMA and UK Biobank. We show that variability in subcortical volumes is heritable, and identify 48 significantly associated loci (40 novel at the time of analysis). Annotation of these loci by utilizing gene expression, methylation and neuropathological data identified 199 genes putatively implicated in neurodevelopment, synaptic signaling, axonal transport, apoptosis, inflammation/infection and susceptibility to neurological disorders. This set of genes is significantly enriched for Drosophila orthologs associated with neurodevelopmental phenotypes, suggesting evolutionarily conserved mechanisms. Our findings uncover novel biology and potential drug targets underlying brain development and disease

Novel genetic loci underlying human intracranial volume identified through genome-wide association

Intracranial volume reflects the maximally attained brain size during development, and remains stable with loss of tissue in late life. It is highly heritable, but the underlying genes remain largely undetermined. In a genome-wide association study of 32,438 adults, we discovered five novel loci for intracranial volume and confirmed two known signals. Four of the loci are also associated with adult human stature, but these remained associated with intracranial volume after adjusting for height. We found a high genetic correlation with child head circumference (ρgenetic=0.748), which indicated a similar genetic background and allowed for the identification of four additional loci through meta-analysis (Ncombined = 37,345). Variants for intracranial volume were also related to childhood and adult cognitive function, Parkinson’s disease, and enriched near genes involved in growth pathways including PI3K–AKT signaling. These findings identify biological underpinnings of intracranial volume and provide genetic support for theories on brain reserve and brain overgrowth

The coming decade of digital brain research: a vision for neuroscience at the intersection of technology and computing

In recent years, brain research has indisputably entered a new epoch, driven by substantial methodological advances and digitally enabled data integration and modelling at multiple scales— from molecules to the whole brain. Major advances are emerging at the intersection of neuroscience with technology and computing. This new science of the brain combines high-quality research, data integration across multiple scales, a new culture of multidisciplinary large-scale collaboration and translation into applications. As pioneered in Europe’s Human Brain Project (HBP), a systematic approach will be essential for meeting the coming decade’s pressing medical and technological challenges. The aims of this paper are to: develop a concept for the coming decade of digital brain research, discuss this new concept with the research community at large, to identify points of convergence, and derive therefrom scientific common goals; provide a scientific framework for the current and future development of EBRAINS, a research infrastructure resulting from the HBP’s work; inform and engage stakeholders, funding organisations and research institutions regarding future digital brain research; identify and address the transformational potential of comprehensive brain models for artificial intelligence, including machine learning and deep learning; outline a collaborative approach that integrates reflection, dialogues and societal engagement on ethical and societal opportunities and challenges as part of future neuroscience research

Towards understanding the pathogenesis of polyglutamine disorders: mRNA and protein expression, proteolytic cleavage and proteasomal degradation

Huntington´s Disease (HD), spinocerebellar ataxia type 3 (SCA3) and 7 (SCA7) belong to a group of neurodegenerative diseases caused by an expansion of CAG trinucleotide repeats in the coding region of the affected genes. The CAG-expansion is translated into an expanded polyglutamine (poly-Q) stretch, altering the conformation of the mutant protein. In an expression analysis in human brain a widespread neuronal expression of ataxin-7 (a7) throughout the brain was identified, but a7 was not enriched at all sites of pathology. Three different mouse models for SCA7, expressing mutant or normal a7 either throughout the brain or exclusively in Purkinje cells or rod photoreceptors, respectively, were generated. In all models, a fragment of mutant a7 accumulated and formed inclusions. The mutant poly-Q protein in HD-huntingtin (htt) forms also intranuclear inclusions. For this protein the cleavage site and the responsible protease were identified. The cellular reaction to aggregated poly-Q protein was studied in SCA7 mouse brain and human SCA3 brain. Surprisingly, only in a minority of inclusions all elements thought to be essential for proteasomal degradation were assembled: no more than 30 % of inclusions displayed immunoreactivity against the 20S catalytical core of the proteasome, whereas most inclusions contained 19S antigens, suggesting an attempt to unfold aggregated protein. To test the hypothesis of an impairment of proteasomal degradation in poly-Q expressing cells, a proteasome reporter system was generated to study proteasomal degradation in vivo. An impairment of proteasomal degradation was shown with this construct. In summary, the cleavage of mutant poly-Q proteins is giving rise to fragments prone to aggregation. An altered degradation pathway involving an impaired unfolding and degradation are features shared by different poly-Q disorders and are potential targets for therapeutic interventions in neurodegenerative diseases