On realizability of pp-groups as Galois groups

In this article we survey and examine the realizability of $p$-groups as Galois groups over arbitrary fields. In particular we consider various cohomological criteria that lead to necessary and sufficient conditions for the realizability of such a group as a Galois group, the embedding problem (i.e., realizability over a given subextension), descriptions of such extensions, automatic realizations among $p$-groups, and related topics.Comment: In this version is added an example at the end of Section 6. Also, some mistakes are corrected and the references are update

Control of the bias tilt angles in nematic liquid crystals

This article may be downloaded for personal use only. Any other use requires prior permission of the author and AIP Publishing. This article appeared in S. V. Yablonskii, K. Nakayama, S. Okazaki, M. Ozaki, K. Yoshino, S. P. Palto, M. Yu. Baranovich, and A. S. Michailov, Journal of Applied Physics 85, 2556 (1999) and may be found at https://doi.org/10.1063/1.369574

Role of Four-Quark Operators in the Inclusive Λb\Lambda_b Decays

We compute by QCD sum rules the matrix elements of the relevant four-quark operators appearing in the expression of the $\Lambda_b$ inclusive decay rates at the order $1/m_b^3$. The results suggest that $1/m_b^3$ corrections are not responsible of the observed difference between the lifetime of $\Lambda_b$ and $B_d$.Comment: LaTex, 14 pages, 3 uuencoded postscript figure

Critical behavior of the two-dimensional N-component Landau-Ginzburg Hamiltonian with cubic anisotropy

We study the two-dimensional N-component Landau-Ginzburg Hamiltonian with cubic anisotropy. We compute and analyze the fixed-dimension perturbative expansion of the renormalization-group functions to four loops. The relations of these models with N-color Ashkin-Teller models, discrete cubic models, planar model with fourth order anisotropy, and structural phase transition in adsorbed monolayers are discussed. Our results for N=2 (XY model with cubic anisotropy) are compatible with the existence of a line of fixed points joining the Ising and the O(2) fixed points. Along this line the exponent $\eta$ has the constant value 1/4, while the exponent $\nu$ runs in a continuous and monotonic way from 1 to $\infty$ (from Ising to O(2)). For N\geq 3 we find a cubic fixed point in the region $u, v \geq 0$, which is marginally stable or unstable according to the sign of the perturbation. For the physical relevant case of N=3 we find the exponents $\eta=0.17(8)$ and $\nu=1.3(3)$ at the cubic transition.Comment: 14 pages, 9 figure

MMP-28 as a regulator of myelination

<p>Abstract</p> <p>Background</p> <p>Matrix metalloproteinase-28 (MMP-28) is a poorly understood member of the matrix metalloproteinase family. Metalloproteinases are important mediators in the development of the nervous system and can contribute to the maturation of the neural micro-environment.</p> <p>Results</p> <p>MMP-28 added to myelinating rat dorsal root ganglion (DRG) co-cultures reduces myelination and two antibodies targeted to MMP-28 (pAb180 and pAb183) are capable of binding MMP-28 and inhibiting its activity in a dose-dependent manner. Addition of 30 nM pAb180 or pAb183 to rat DRG cultures resulted in the 2.6 and 4.8 fold enhancement of myelination respectively while addition of MMP-28 to DRG co-cultures resulted in enhanced MAPK, ErbB2 and ErbB3 phosphorylation. MMP-28 protein expression was increased within demyelinated lesions of mouse experimental autoimmune encephalitis (EAE) and human multiple sclerosis lesions compared to surrounding normal tissue.</p> <p>Conclusion</p> <p>MMP-28 is upregulated in conditions of demyelination in vivo, induces signaling in vitro consistent with myelination inhibition and, neutralization of MMP-28 activity can enhance myelination in vitro. These results suggest inhibition of MMP-28 may be beneficial under conditions of dysmyelination.</p

Systemic proteasome inhibition triggers neurodegeneration in a transgenic mouse model expressing human α-synuclein under oligodendrocyte promoter: implications for multiple system atrophy

Multiple system atrophy (MSA) is a progressive late onset neurodegenerative α-synucleinopathy with unclear pathogenesis. Recent genetic and pathological studies support a central role of α-synuclein (αSYN) in MSA pathogenesis. Oligodendroglial cytoplasmic inclusions of fibrillar αSYN and dysfunction of the ubiquitin–proteasome system are suggestive of proteolytic stress in this disorder. To address the possible pathogenic role of oligodendroglial αSYN accumulation and proteolytic failure in MSA we applied systemic proteasome inhibition (PSI) in transgenic mice with oligodendroglial human αSYN expression and determined the presence of MSA-like neurodegeneration in this model as compared to wild-type mice. PSI induced open field motor disability in transgenic αSYN mice but not in wild-type mice. The motor phenotype corresponded to progressive and selective neuronal loss in the striatonigral and olivopontocerebellar systems of PSI-treated transgenic αSYN mice. In contrast no neurodegeneration was detected in PSI-treated wild-type controls. PSI treatment of transgenic αSYN mice was associated with significant ultrastructural alterations including accumulation of fibrillar human αSYN in the cytoplasm of oligodendroglia, which resulted in myelin disruption and demyelination characterized by increased g-ratio. The oligodendroglial and myelin pathology was accompanied by axonal degeneration evidenced by signs of mitochondrial stress and dysfunctional axonal transport in the affected neurites. In summary, we provide new evidence supporting a primary role of proteolytic failure and suggesting a neurodegenerative pathomechanism related to disturbed oligodendroglial/myelin trophic support in the pathogenesis of MSA

Transgenic Overexpression of the Type I Isoform of Neuregulin 1 Affects Working Memory and Hippocampal Oscillations but not Long-term Potentiation

Neuregulin 1 (NRG1) is a growth factor involved in neurodevelopment and plasticity. It is a schizophrenia candidate gene, and hippocampal expression of the NRG1 type I isoform is increased in the disorder. We have studied transgenic mice overexpressing NRG1 type I (NRG1tg-type I) and their wild-type littermates and measured hippocampal electrophysiological and behavioral phenotypes. Young NRG1tg-type I mice showed normal memory performance, but in older NRG1tg-type I mice, hippocampus-dependent spatial working memory was selectively impaired. Hippocampal slice preparations from NRG1tg-type I mice exhibited a reduced frequency of carbachol-induced gamma oscillations and an increased tendency to epileptiform activity. Long-term potentiation in NRG1tg-type I mice was normal. The results provide evidence that NRG1 type I impacts on hippocampal function and circuitry. The effects are likely mediated via inhibitory interneurons and may be relevant to the involvement of NRG1 in schizophrenia. However, the findings, in concert with those from other genetic and pharmacological manipulations of NRG1, emphasize the complex and pleiotropic nature of the gene, even with regard to a single isoform

Schizophrenia-associated HapICE haplotype is associated with increased NRG1 type III expression and high nucleotide diversity

Excitement and controversy have followed neuregulin (NRG1) since its discovery as a putative schizophrenia susceptibility gene; however, the mechanism of action of the associated risk haplotype (HapICE) has not been identified, and specific genetic variations, which may increase risk to schizophrenia have remained elusive. Using a postmortem brain cohort from 37 schizophrenia cases and 37 controls, we resequenced upstream of the type I–IV promoters, and the HapICE repeat regions in intron 1. Relative abundance of seven NRG1 mRNA transcripts in the prefrontal cortex were determined and compared across diagnostic and genotypic groups. We identified 26 novel DNA variants and showed an increased novel variant load in cases compared with controls (χ2=7.815; P=0.05). The average nucleotide diversity (θ=10.0 × 10−4) was approximately twofold higher than that previously reported for BDNF, indicating that NRG1 may be particularly prone to genetic change. A greater nucleotide diversity was observed in the HapICE linkage disequilibrium block in schizophrenia cases (θ(case)=13.2 × 10−4; θ(control)=10.0 × 10−4). The specific HapICE risk haplotype was associated with increased type III mRNA (F=3.76, P=0.028), which in turn, was correlated with an earlier age of onset (r=−0.343, P=0.038). We found a novel intronic five-SNP haplotype ∼730 kb upstream of the type I promoter and determined that this region functions as transcriptional enhancer that is suppressed by SRY. We propose that the HapICE risk haplotype increases expression of the most brain-abundant form of NRG1, which in turn, elicits an earlier clinical presentation, thus providing a novel mechanism through which this genetic association may increase risk of schizophrenia

Polarized Secretion of Drosophila EGFR Ligand from Photoreceptor Neurons Is Controlled by ER Localization of the Ligand-Processing Machinery

Trafficking within the endoplasmic reticulum and specialized localization of the intra-membrane protease Rhomboid regulate EGF ligand-dependent signaling in Drosophila photoreceptor axon termini

ЧАСТОТА ВЫЯВЛЕНИЯ СЕРОЛОГИЧЕСКИХ МАРКЕРОВ ВИРУСНЫХ ГЕПАТИТОВ В И D СРЕДИ УСЛОВНО ЗДОРОВОГО НАСЕЛЕНИЯ РЕСПУБЛИКИ ТЫВА

Aim: to estimate prevalence of markers, genetic diversity, risk factors of HBV and HDV infections in all age groups among healthy population in Republic Tyva. Serum samples obtained from healthy population in Republic Tyva (N = 1086) were tested (aged from birth to older 60 years). The markers of HBV and HDV infections were determined by enzyme immunoassay and PCR. HBsAg was detected in 7,7% (84/1086), anti-HBc — in 47,8% (519/1086) and HBeAg — in 0,3% (3/1086) cases. Prevalence of HBsAg in children under 9 years was 1,3%, no positive results of anti-HDV were determined among children aged up to 9 year. Prevalence of anti-HDV among HBsAg-positive individuals of healthy population was 32,1% (27/84). HBV DNA was detected in 2,9% (31/1086) cases; HDV RNA — in 32,1% (14/84) HBsAg-positive individuals. The obtained data showed high prevalence of HBV ang HDV infections among healthy population of Republic Tyva. Thus, it is necessary to extend screening program in this region to improve viral hepatitis surveillance and diagnostics. The sharp decline in the prevalence of these infections in children up to 9 years in the surveyed endemic region is an evidence of effective protection against HBV and HDV with vaccination against hepatitis B. Цель работы: оценить распространенность маркеров, генетическое разнообразие, факторы риска инфицирования вирусами HBV и HDV во всех возрастных группах детского и взрослого условно здорового населения Республики Тыва. Исследованы образцы сывороток крови, полученные от условно здорового населения Республики Тыва (N = 1086), от новорожденных до лиц старше 60 лет. Маркеры инфицирования HBV и HDV определяли методом ИФА и ПЦР. HBsAg был определен в 7,7% (84/1086), anti-HBc — в 47,8% (519/1086) и HBeAg — в 0,3% (3/1086) случаях. Частота выявления anti-HDV среди HBsAg-положительных лиц из группы условно здорового населения составила 32,1% (27/84). HBV DNA была определена в 2,9% (31/1086) случаях; HDV RNA была обнаружена у 32,1% (14/84) HBsAg-положительных лиц. Среди детей до 9 лет частота выявления HBsAg составила 1,3%, в этой возрастной группе не было выявлено ни одного образца сыворотки крови с наличием anti-HDV. Полученные нами данные свидетельствуют о высоком уровне инфицирования HBV и HDV условно здорового населения Республики Тыва, что указывает на необходимость расширения скрининговых программ в данном регионе для усовершенствования диагностики вирусных гепатитов и надзора за этими инфекциями. Резкое снижение распространенности данных инфекций среди детей до 9 лет в обследованном эндемичном регионе является свидетельством эффективной защиты от HBV и HDV с помощью вакцинации против гепатита В.