164 research outputs found
Massive Decaying Tau Neutrino and Big Bang Nucleosynthesis
Comparing Big Bang Nucleosynthesis predictions with the light element
abundances inferred from observational data, we can obtain the strong
constraints on some neutrino properties, e.g. number of neutrino species, mass,
lifetime. Recently the deuterium abundances were measured in high red-shift QSO
absorption systems. It is expected that they are close to the primordial
values, however, two groups have reported inconsistent values which are
different in one order of magnitude. In this paper we show how we can constrain
on neutrino mass and its lifetime in each case when we adopt either high
or low deuterium data. We find that if 0.01 \sec
\lesssim \tau_{\nutau} \lesssim 1 \sec and 10\mev \lesssim m_{\nutau}
\lesssim 24\mev, the theoretical predictions agree with the low D/H
abundances. On the other hand if we adopt the high D/H abundances, we obtain
the upper bound of neutrino mass, m_{\nutau}\lesssim 20 \mev.Comment: 11 pages, using LATEX and four postscript figure
Superheavy Dark Matter and Thermal Inflation
The thermal inflation is the most plausible mechanism that solves the
cosmological moduli problem naturally. We discuss relic abundance of superheavy
particle in the presence of the thermal inflation assuming that its
lifetime is longer than the age of the universe, and show that the long-lived
particle of mass -- GeV may form a part of the dark
matter in the present universe in a wide region of parameter space of the
thermal inflation model. The superheavy dark matter of mass GeV
may be interesting in particular, since its decay may account for the observed
ultra high-energy cosmic rays if the lifetime of the particle is
sufficiently long.Comment: 13 pages (RevTex file) including 8 figures, revised version to be
published in Physical Review
Big Bang Nucleosynthesis and Lepton Number Asymmetry in the Universe
Recently it is reported that there is the discrepancy between big bang
nucleosynthesis theory and observations (BBN crisis). We show that BBN
predictions agree with the primordial abundances of light elements, He4, D, He3
and Li7 inferred from the observational data if an electron neutrino has a net
chemical potential xi_{nu_e} due to lepton asymmetry. We estimate that
xi_{nu_e} = 0.043^{+0.040}_{-0.040} (95% C.L.) and Omega_bh^2 =
0.015^{+0.006}_{-0.003} (95% C.L.).Comment: 10 pages, using AAS LATEX and three postscript figure
RNAseq Analyses Identify Tumor Necrosis Factor-Mediated Inflammation as a Major Abnormality in ALS Spinal Cord
ALS is a rapidly progressive, devastating neurodegenerative illness of adults that produces disabling weakness and spasticity arising from death of lower and upper motor neurons. No meaningful therapies exist to slow ALS progression, and molecular insights into pathogenesis and progression are sorely needed. In that context, we used high-depth, next generation RNA sequencing (RNAseq, Illumina) to define gene network abnormalities in RNA samples depleted of rRNA and isolated from cervical spinal cord sections of 7 ALS and 8 CTL samples. We aligned \u3e50 million 2X150 bp paired-end sequences/sample to the hg19 human genome and applied three different algorithms (Cuffdiff2, DEseq2, EdgeR) for identification of differentially expressed genes (DEG’s). Ingenuity Pathways Analysis (IPA) and Weighted Gene Co-expression Network Analysis (WGCNA) identified inflammatory processes as significantly elevated in our ALS samples, with tumor necrosis factor (TNF) found to be a major pathway regulator (IPA) and TNFα-induced protein 2 (TNFAIP2) as a major network “hub” gene (WGCNA). Using the oPOSSUM algorithm, we analyzed transcription factors (TF) controlling expression of the nine DEG/hub genes in the ALS samples and identified TF’s involved in inflammation (NFkB, REL, NFkB1) and macrophage function (NR1H2::RXRA heterodimer). Transient expression in human iPSC-derived motor neurons of TNFAIP2 (also a DEG identified by all three algorithms) reduced cell viability and induced caspase 3/7 activation. Using high-density RNAseq, multiple algorithms for DEG identification, and an unsupervised gene co-expression network approach, we identified significant elevation of inflammatory processes in ALS spinal cord with TNF as a major regulatory molecule. Overexpression of the DEG TNFAIP2 in human motor neurons, the population most vulnerable to die in ALS, increased cell death and caspase 3/7 activation. We propose that therapies targeted to reduce inflammatory TNFα signaling may be helpful in ALS patients
Models of Networked Analysis at Regional Centres for LHC Experiments (MONARC), Phase 2 Report, 24th March 2000
Expression and Function of Serotonin 2A and 2B Receptors in the Mammalian Respiratory Network
Neurons of the respiratory network in the lower brainstem express a variety of serotonin receptors (5-HTRs) that act primarily through adenylyl cyclase. However, there is one receptor family including 5-HT2A, 5-HT2B, and 5-HT2C receptors that are directed towards protein kinase C (PKC). In contrast to 5-HT2ARs, expression and function of 5-HT2BRs within the respiratory network are still unclear. 5-HT2BR utilizes a Gq-mediated signaling cascade involving calcium and leading to activation of phospholipase C and IP3/DAG pathways. Based on previous studies, this signal pathway appears to mediate excitatory actions on respiration. In the present study, we analyzed receptor expression in pontine and medullary regions of the respiratory network both at the transcriptional and translational level using quantitative RT-PCR and self-made as well as commercially available antibodies, respectively. In addition we measured effects of selective agonists and antagonists for 5-HT2ARs and 5-HT2BRs given intra-arterially on phrenic nerve discharges in juvenile rats using the perfused brainstem preparation. The drugs caused significant changes in discharge activity. Co-administration of both agonists revealed a dominance of the 5-HT2BR. Given the nature of the signaling pathways, we investigated whether intracellular calcium may explain effects observed in the respiratory network. Taken together, the results of this study suggest a significant role of both receptors in respiratory network modulation
Shared heritability of attention-deficit/hyperactivity disorder and autism spectrum disorder
Attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) are both highly heritable neurodevelopmental disorders. Evidence indicates both disorders co-occur with a high frequency, in 20–50% of children with ADHD meeting criteria for ASD and in 30-80% of ASD children meeting criteria for ADHD. This review will provide an overview on all available studies [family based, twin, candidate gene, linkage, and genome wide association (GWA) studies] shedding light on the role of shared genetic underpinnings of ADHD and ASD. It is concluded that family and twin studies do provide support for the hypothesis that ADHD and ASD originate from partly similar familial/genetic factors. Only a few candidate gene studies, linkage studies and GWA studies have specifically addressed this co-occurrence, pinpointing to some promising pleiotropic genes, loci and single nucleotide polymorphisms (SNPs), but the research field is in urgent need for better designed and powered studies to tackle this complex issue. We propose that future studies examining shared familial etiological factors for ADHD and ASD use a family-based design in which the same phenotypic (ADHD and ASD), candidate endophenotypic, and environmental measurements are obtained from all family members. Multivariate multi-level models are probably best suited for the statistical analysis
Blueprint for a minimal photoautotrophic cell: conserved and variable genes in Synechococcus elongatus PCC 7942
Background:
Simpler biological systems should be easier to understand and to engineer towards pre-defined goals. One way to achieve biological simplicity is through genome minimization. Here we looked for genomic islands in the fresh water cyanobacteria Synechococcus elongatus PCC 7942 (genome size 2.7 Mb) that could be used as targets for deletion. We also looked for conserved genes that might be essential for cell survival.Results:
By using a combination of methods we identified 170 xenologs, 136 ORFans and 1401 core genes in the genome of S. elongatus PCC 7942. These represent 6.5%, 5.2% and 53.6% of the annotated genes respectively. We considered that genes in genomic islands could be found if they showed a combination of: a) unusual G+C content; b) unusual phylogenetic similarity; and/or c) a small number of the highly iterated palindrome 1 (HIP1) motif plus an unusual codon usage. The origin of the largest genomic island by horizontal gene transfer (HGT) could be corroborated by lack of coverage among metagenomic sequences from a fresh water microbialite. Evidence is also presented that xenologous genes tend to cluster in operons. Interestingly, most genes coding for proteins with a diguanylate cyclase domain are predicted to be xenologs, suggesting a role for horizontal gene transfer in the evolution of Synechococcus sensory systems.Conclusions:
Our estimates of genomic islands in PCC 7942 are larger than those predicted by other published methods like SIGI-HMM. Our results set a guide to non-essential genes in S. elongatus PCC 7942 indicating a path towards the engineering of a model photoautotrophic bacterial cell.Financial support was provided by grants BFU2009-12895-C02-01/BMC
(Ministerio de Ciencia e Innovación, Spain), the European Community’s
Seventh Framework Programme (FP7/2007-2013) under grant agreement
number 212894 and Prometeo/2009/092 (Conselleria d’Educació, Generalitat
Valenciana, Spain) to A. Moya. Work in the FdlC laboratory was supported by
grants BFU2008-00995/BMC (Spanish Ministry of Education), RD06/0008/1012
(RETICS research network,
Instituto de Salud Carlos III, Spanish Ministry of Health) and LSHM-CT-
2005_019023 (European VI Framework Program). Dr. González-Domenech
was supported by grant from the University of Granada. LD, thanks to
financial support from Facultad de Ciencias, Universidad Nacional Autónoma
de México
The role of inflammation in epilepsy.
Epilepsy is the third most common chronic brain disorder, and is characterized by an enduring predisposition to generate seizures. Despite progress in pharmacological and surgical treatments of epilepsy, relatively little is known about the processes leading to the generation of individual seizures, and about the mechanisms whereby a healthy brain is rendered epileptic. These gaps in our knowledge hamper the development of better preventive treatments and cures for the approximately 30% of epilepsy cases that prove resistant to current therapies. Here, we focus on the rapidly growing body of evidence that supports the involvement of inflammatory mediators-released by brain cells and peripheral immune cells-in both the origin of individual seizures and the epileptogenic process. We first describe aspects of brain inflammation and immunity, before exploring the evidence from clinical and experimental studies for a relationship between inflammation and epilepsy. Subsequently, we discuss how seizures cause inflammation, and whether such inflammation, in turn, influences the occurrence and severity of seizures, and seizure-related neuronal death. Further insight into the complex role of inflammation in the generation and exacerbation of epilepsy should yield new molecular targets for the design of antiepileptic drugs, which might not only inhibit the symptoms of this disorder, but also prevent or abrogate disease pathogenesis
Opioid tolerance in methadone maintenance treatment: comparison of methadone and levomethadone in long-term treatment
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