Overexpression of AtBMI1C, a Polycomb Group Protein Gene, Accelerates Flowering in Arabidopsis

Polycomb group protein (PcG)-mediated gene silencing is emerging as an essential developmental regulatory mechanism in eukaryotic organisms. PcGs inactivate or maintain the silenced state of their target chromatin by forming complexes, including Polycomb Repressive Complex 1 (PRC1) and 2 (PRC2). Three PRC2 complexes have been identified and characterized in Arabidopsis; of these, the EMF and VRN complexes suppress flowering by catalyzing the trimethylation of lysine 27 on histone H3 of FLOWER LOCUS T (FT) and FLOWER LOCUS C (FLC). However, little is known about the role of PRC1 in regulating the floral transition, although AtRING1A, AtRING1B, AtBMI1A, and AtBMI1B are believed to regulate shoot apical meristem and embryonic development as components of PRC1. Moreover, among the five RING finger PcGs in the Arabidopsis genome, four have been characterized. Here, we report that the fifth, AtBMI1C, is a novel, ubiquitously expressed nuclear PcG protein and part of PRC1, which is evolutionarily conserved with Psc and BMI1. Overexpression of AtBMI1C caused increased H2A monoubiquitination and flowering defects in Arabidopsis. Both the suppression of FLC and activation of FT were observed in AtBMI1C-overexpressing lines, resulting in early flowering. No change in the H3K27me3 level in FLC chromatin was detected in an AtBMI1C-overexpressing line. Our results suggest that AtBMI1C participates in flowering time control by regulating the expression of FLC; moreover, the repression of FLC by AtBMI1C is not due to the activity of PRC2. Instead, it is likely the result of PRC1 activity, into which AtBMI1C is integrated

A 60-year record of 129I in Taal Lake sediments (Philippines): Influenceof human nuclear activities at low latitude region

The influence of human nuclear activities on environmental radioactivity is not well known at low latitude regions that are distant from nuclear test sites and nuclear facilities. A sediment core collected from Taal Lake in the central Philippines was analyzed for 129I and 127I to investigate this influence in a low-latitude terrestrial system. A baseline of 129I/127I atomic ratios was established at (2.04e5.14) * 10-12&nbsp;in the pre-nuclear era in this region. Controlled by the northeasterly equatorial trade winds, increased 129I/127I ratios of (20.1e69.3) * 10-12 suggest that atmospheric nuclear weapons tests at the Pacific Proving Grounds in the central Pacific Ocean was the major source of 129I in the sediment during 1956-1962. The 129I/127I ratios, up to 157.5*10-12 after 1964, indicate a strong influence by European nuclear fuel reprocessing plants. The East Asian Winter Monsoon is found to be the dominant driving force in the atmospheric dispersion of radioactive iodine (129I) from the European nuclear fuel reprocessing plants to Southeast Asia, which is also important for dispersion of other airborne pollutants from the middle-high to low latitude regions. A significant 129I/127I peak at 42.8 cm in the Taal Lake core appears to be the signal of the Chernobyl accident in 1986. In addition, volcanic activities are reflected in the iodine isotope profiles in the sediment core, suggesting the potential of using iodine isotopes as an indicator of volcanic eruptions.<br style="line-height: normal; text-align: -webkit-auto; text-size-adjust: auto;" /

An Improvement of Global Error Bound for the Generalized Nonlinear Complementarity Problem over a Polyhedral Cone

We consider the global error bound for the generalized nonlinear complementarity problem over a polyhedral cone (GNCP). By a new technique, we establish an easier computed global error bound for the GNCP under weaker conditions, which improves the result obtained by for GNCP

Quantitative Systems Pharmacological Analysis of Drugs of Abuse Reveals the Pleiotropy of Their Targets and the Effector Role of mTORC1

Existing treatments against drug addiction are often ineffective due to the complexity of the networks of protein-drug and protein-protein interactions (PPIs) that mediate the development of drug addiction and related neurobiological disorders. There is an urgent need for understanding the molecular mechanisms that underlie drug addiction toward designing novel preventive or therapeutic strategies. The rapidly accumulating data on addictive drugs and their targets as well as advances in machine learning methods and computing technology now present an opportunity to systematically mine existing data and draw inferences on potential new strategies. To this aim, we carried out a comprehensive analysis of cellular pathways implicated in a diverse set of 50 drugs of abuse using quantitative systems pharmacology methods. The analysis of the drug/ligand-target interactions compiled in DrugBank and STITCH databases revealed 142 known and 48 newly predicted targets, which have been further analyzed to identify the KEGG pathways enriched at different stages of drug addiction cycle, as well as those implicated in cell signaling and regulation events associated with drug abuse. Apart from synaptic neurotransmission pathways detected as upstream signaling modules that “sense” the early effects of drugs of abuse, pathways involved in neuroplasticity are distinguished as determinants of neuronal morphological changes. Notably, many signaling pathways converge on important targets such as mTORC1. The latter emerges as a universal effector of the persistent restructuring of neurons in response to continued use of drugs of abuse

Chronic Alcohol Causes Alteration of Lipidome Profiling in Brain

Much efforts have been tried to clarify the molecular mechanism of alcohol-induced brain damage from the perspective of genome and protein; however, the effect of chronic alcohol exposure on global lipid profiling of brain is unclear. In the present study, by using Q-TOF/MS-based lipidomics approach, we investigated the comprehensive lipidome profiling of brain from the rats orally administrated with alcohol daily, continuously for one year. Through systematically analysis of all lipids in prefrontal cortex (PFC) and striatum region, we found that long-term alcohol exposure profoundly modified brain lipidome profiling. Notably, three kinds of lipid classes, glycerophospholipid (GP), glycerolipid (GL) and fatty acyls (FA), were significantly increased in these two brain regions. Interestingly, most of the modified lipids were involved in synthetic pathways of endoplasmic reticulum (ER), which may result in ER stress-related metabolic disruption. Moreover, alcohol-modified lipid species displayed long length of carbon chain with high degree of unsaturation. Taken together, our results firstly present that chronic alcohol exposure markedly modifies brain lipidomic profiling, which may activate ER stress and eventually result in neurotoxicity. These findings provide a new insight into the mechanism of alcohol-related brain damage.Peer reviewe

Comprehensive summary of solid oxide fuel cell control : a state-of-the-art review

Hydrogen energy is a promising renewable resource for the sustainable development of society. As a key member of the fuel cell (FC) family, the solid oxide fuel cell (SOFC) has attracted a lot of attention because of characteristics such as having various sources as fuel and high energy conversion efficiency, and being pollution-free. SOFC is a highly coupled, nonlinear, and multivariable complex system, and thus it is very important to design an appropriate control strategy for an SOFC system to ensure its safe, reliable, and efficient operation. This paper undertakes a comprehensive review and detailed summary of the state-of-the-art control approaches of SOFC. These approaches are divided into eight categories of control: proportional integral differential (PID), adaptive (APC), robust, model predictive (MPC), fuzzy logic (FLC), fault-tolerant (FTC), intelligent and observer-based. The SOFC control approaches are carefully evaluated in terms of objective, design, application/scenario, robustness, complexity, and accuracy. Finally, five perspectives are proposed for future research directions

Ekonomski rast i emisija ugljika u Kini: Kuznetsova krivulja prostorne ekonometrije

Economic development has largely contributed to the increment of CO2 emission. This study uses spatial econometric models to investigate the relationship between economic growth and carbon emission in China with data of 30 provinces of China during the period of 2000 to 2012. Results show that the relationship between carbon emission and economic growth in China during the recent decade has the development tendency toward an inverse U-shaped curve, approximately confirming the carbon emission’s Kuznets curve hypothesis in China. There exists a significant spatial correlation between carbon emission and economic growth,implying that carbon emission in a province may be influenced by economic growth in adjacent provinces. When economic growth reaches 279.91 million Yuan/km2 GDP (at a comparable price in 2000), the contradiction between economic growth and carbon emission begins to be gradually alleviated. These findings provide new insights and valuable information for reducing carbon emissions in China.Gospodarski razvoj uvelike je pridonio povećanju emisije CO2. Ova studija koristi prostorne ekonometrijske modele za istraživanje odnosa između gospodarskog rasta i emisije ugljika u Kini s podacima iz 30 pokrajina Kine u razdoblju od 2000. do 2012. godine. Rezultati pokazuju da tijekom posljednjeg desetljeća odnos emisije ugljika i gospodarskog rasta u Kini ima tendenciju razvoja prema inverznoj krivulji U-oblika, približno potvrđujući hipotezu Kuznetsove krivulje emisije ugljika u Kini. Postoji značajna prostorna povezanost između emisije ugljika i ekonomskog rasta, što implicira da na emisiju ugljika u pokrajini može utjecati gospodarski rast u susjednim pokrajinama. Nakon što je ekonomski rast dosegnuo omjer od 279,91 milijuna Yuan/km2 BDP-a (usporediva cijena u 2000. godini), kontradikcija između gospodarskog rasta i emisije ugljika počinje se postupno ublažavati. Ovi rezultati pružaju nove uvide i vrijedne informacije kako reducirati emisije ugljika u Kini

Multi-biological functions of intermedin in diseases

Intermedin (IMD) is a member of the calcitonin gene-related peptide (CGRP)/calcitonin (CT) superfamily, and it is expressed extensively throughout the body. The typical receptors for IMD are complexes composed of calcitonin receptor-like receptor (CLR) and receptor activity-modifying protein (RAMP), which leads to a biased activation towards Gαs. As a diagnostic and prognostic biomarker, IMD regulates the initiation and metastasis of multiple tumors. Additionally, IMD functions as a proangiogenic factor that can restrain excessive vascular budding and facilitate the expansion of blood vessel lumen, ultimately resulting in the fusion of blood vessels. IMD has protective roles in various diseases, including ischemia-reperfusion injury, metabolic disease, cardiovascular diseases and inflammatory diseases. This review systematically elucidates IMD’s expression, structure, related receptors and signal pathway, as well as its comprehensive functions in the context of acute kidney injury, obesity, diabetes, heart failure and sepsis. However, the precise formation process of IMD short peptides in vivo and their downstream signaling pathway have not been fully elucidated yet. Further in-depth studies are need to translate IMD research into clinical applications