Linking Mid-century Concentration Targets to Long-Term Climate Change Outcomes

We present a framework that could inform the choice of an interim (mid-21st century) target in the making of climate mitigation policy. The idea of interim targets for greenhouse gas concentration has been proposed previously as a way to bridge short- and long-term climate targets, address concerns about the rate of temperature change, and provide guidance in planning for energy infrastructure while scientific understanding improves and long-term climate goals are negotiated. Our analysis relates a wide range of mid-century equivalent CO2 (eCO2) concentrations to rates of temperature increase as well as total long-term temperature increases, accounts for uncertainties in the carbon cycle and the climate response (including climate sensitivity, ocean diffusivity, and aerosol forcing), and provides a rough measure of the economic feasibility of different emissions pathways. Our results show, for example, that for a roughly 50% likelihood of limiting long-term warming to 20C above the pre-industrial level, and with the constraint that global emissions should not have to be reduced by more than 2.5%/year, the mid-century concentration needs to remain below about 470 ppm eCO2 (including only the Kyoto gases and defined relative to a year 2000 baseline). For a roughly 83% likelihood of achieving the same temperature goal, the mid-century target needs to be about 440 ppm. These targets require that emissions between 2010 and 2050 average to approximately the current level and the 1990 level, respectively. Our framework illustrates how delay in emissions reductions in the near term forecloses options in the long term. Finally, we demonstrate how near-term reductions of CO2 from a particular source, deforestation, can significantly facilitate the achievement of long-term temperature goals

The effect of surface and Coulomb interaction on the liquid-gas phase transition of finite nuclei

By means of the Furnstahl, Serot and Tang's model, the effects of surface tension and Coulomb interaction on the liquid-gas phase transition for finite nuclei are investigated. A limit pressure p-lim above which the liquid-gas phase transition cannot take place has been found. It is found that comparing to the Coulomb interaction, the contribution of surface tension is dominate in low temperature regions. The binodal surface is also addressed.Comment: LaTex, 8 pages with 6 fig

Molecular evidence of the haploid origin in wheat (Triticum aestivum L.) with Aegilops kotschyi cytoplasm and whole genome expression profiling after haploidization

Aegiolops kotschyi cytoplasmic male sterile system often results in part of haploid plants in wheat (Triticum aestivum L.). To elucidate the origin of haploid, 235 wheat microsatellite (SSR) primers were randomly selected and screened for polymorphism between haploid (2n = 3x = 21 ABD) and its parents, male-sterile line YM21 (2n = 6x = 42 AABBDD) and male fertile restorer YM2 (2n = 6x = 42 AABBDD). About 200 SSR markers yielded clear bands from denatured PAGE, of which 180 markers have identifiable amplification patterns, and 20 markers (around 8%) resulted in different amplification products between the haploid and the restorer, YM2. There were no SSR markers that were found to be distinguishable between the haploid and the male sterile line YM21. In addition, different distribution of HMW-GS between endosperm and seedlings from the same seeds further confirmed that the haploid genomes were inherited from the maternal parent. After haploidization, 1.7% and 0.91% of total sites were up- and down-regulated exceeding twofold in the shoot and the root of haploid, respectively, and most of the differentially expressed loci were up/down-regulated about twofold. Out of the sensitive loci in haploid, 94 loci in the shoot, 72 loci in the root can be classified into three functional subdivisions: biological process, cellular component and molecular function, respectively

Sumoylation of LAP1 is involved in the HDAC4-mediated repression of COX-2 transcription

CEBPB, one of the CEBP family members, is a crucial regulator of gene expression during innate immunity, inflammatory responses and adipogenesis. In this study, the EGF-induced increase of CEBPB mRNA is shown to be coincident with the decrease of COX-2 mRNA. We identified that all of the individual CEBPB isoforms, LAP1, LAP2 and LIP, attenuate EGF-induced COX-2 promoter activity. Although increased sumoylation of both LAP1 and LAP2 is observed during the lagging stage of EGF treatment, only the sumoylated LAP1, but not the sumoylated LAP2, is responsible for COX-2 gene repression. In addition, EGF treatment can regulate the nucleocytoplasmic redistribution of HDAC4 and SUMO1. We further demonstrated by loss-of- and gain-of-function approaches that HDAC4 can be a negative regulator while inactivating COX-2 transcription. The sumoylation mutant LAP1, LAP1K174A, exhibits an attenuated ability to interact with HDAC4, and increased COX-2 promoter activity. Furthermore, the in vivo DNA binding assay demonstrated that LAP1K174A and CEBPDK120A, sumoylation-defective CEBPD mutants, attenuate the binding of HDAC4 on the COX-2 promoter. In light of the above, our data suggest that the suCEBPD and suLAP1 are involved in the repression of COX-2 transcription through the recruitment of HDAC4

Lipids driving protein structure? Evolutionary adaptations in Kir channels

Many eukaryotic channels, transporters and receptors are activated by phosphatidyl inositol bisphosphate (PIP(2)) in the membrane, and every member of the eukaryotic inward rectifier potassium (Kir) channel family requires membrane PIP(2) for activity. In contrast, a bacterial homolog (KirBac1.1) is specifically inhibited by PIP(2). We speculate that a key evolutionary adaptation in eukaryotic channels is the insertion of additional linkers between trans-membrane and cytoplasmic domains, revealed by new crystal structures, that convert PIP(2) inhibition to activation. Such an adaptation may reflect a novel evolutionary drive to protein structure,; one that was necessary to permit channel function within the highly negatively charged membranes that evolved in the eukaryotic lineage

Milk fat globule-epidermal growth factor-factor VIII downregulates interleukin-17 expression in sepsis by modulating STAT3 activation

BACKGROUND: Milk fat globule-epidermal growth factor-factor VIII (MFG-E8) is a secretory glycoprotein with a known role in inflammation. In sepsis, interleukin (IL)-17 acts as a proinflammatory cytokine to exaggerate systemic inflammation. We hypothesize that MFG-E8 downregulates IL-17 expression in sepsis. METHODS: Sepsis was induced in 8-week-old male C57BL/6 mice by cecal ligation and puncture (CLP). Recombinant mouse MFG-E8 (rmMFG-E8) at a dosage of 20 mug/kg body weight or phosphate-buffered saline was concurrently injected. After 10 hours, blood and spleen samples were harvested for analysis. For in vitro studies, splenocytes isolated from healthy mice pretreated with rmMFG-E8 and splenocytes from MFG-E8 knockout (mfge8-/-) mice were stimulated with phorbol 12-myristate 13-acetate (PMA) and ionomycin, followed by measurement of IL-17 expression with either quantitative PCR or enzyme-linked immunosorbent assay. RESULTS: At 10 hours after CLP, rmMFG-E8 inhibited the elevated levels of IL-17 protein in serum by 31%, compared with the vehicle. In the spleen, rmMFG-E8 reduced the upregulated IL-17 mRNA and protein levels by 81% and 51%, respectively. This correlated with a significant reduction in organ injury markers AST and ALT in sepsis after administration of rmMFG-E8. In vitro treatment of splenocytes isolated from healthy mice with rmMFG-E8 showed significant downregulation in PMA/ionomycin-induced IL-17 expression. In contrast, CD4 T-cells from mfge8-/- mice showed significant upregulation of IL-17 compared with wild-type mice. The phosphorylated level of signal transducer and activator of transcription 3 (STAT3) was downregulated in spleen tissue of septic mice treated with rmMFG-E8. Conversely, mfge8-/- mice showed increased phosphorylated STAT3 compared with wild-type mice after sepsis. CONCLUSION: Our findings demonstrate MFG-E8-mediated downregulation of IL-17 expression, implicating its potential as a novel therapeutic agent against sepsis

AICAR attenuates organ injury and inflammatory response after intestinal ischemia and reperfusion

Intestinal ischemia and reperfusion (I/R) is encountered in various clinical conditions and contributes to multiorgan failure and mortality as high as 60% to 80%. Intestinal I/R not only injures the intestine, but affects remote organs such as the lung leading to acute lung injury. The development of novel and effective therapies for intestinal I/R are critical for the improvement of patient outcome. AICAR (5-aminoimidazole-4-carboxyamide ribonucleoside) is a cell-permeable compound that has been shown to possess antiinflammatory effects. The objective is to determine that treatment with AICAR attenuates intestinal I/R injury and subsequent acute lung injury (ALI). Male Sprague Dawley rats (275 to 325 g) underwent intestinal I/R injury with blockage of the superior mesenteric artery for 90 min and subsequent reperfusion. At the initiation of reperfusion, vehicle or AICAR (30 mg/kg BW) was given intravenously (IV) for 30 min. At 4 h after reperfusion, blood and tissues were collected for further analyses. Treatment with AICAR significantly decreased the gut damage score and the water content, indicating improvement in histological integrity. The treatment also attenuated tissue injury and proinflammatory cytokines, and reduced bacterial translocation to the gut. AICAR administration after intestinal I/R maintained lung integrity, attenuated neutrophil chemotaxis and infiltration to the lungs and decreased lung levels of tumor necrosis factor (TNF)-alpha and interleukin (IL)-6. Inflammatory mediators, lung-inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) proteins, were decreased in the lungs and lung apoptosis was significantly reduced after AICAR treatment. These data indicate that AICAR could be developed as an effective and novel therapeutic for intestinal I/R and subsequent ALI

Drying of the Qaidam basin and its controlling factors deduced from core SG-1

Abstract HKT-ISTP 2013 B

Stimulation of Wnt/beta-catenin signaling pathway with Wnt agonist reduces organ injury after hemorrhagic shock

BACKGROUND: Hemorrhagic shock is a leading cause of morbidity and mortality in surgery and trauma patients. Despite a large number of preclinical trials conducted to develop therapeutic strategies against hemorrhagic shock, there is still an unmet need for effective therapy for hemorrhage patients. Wnt/beta-catenin signaling controls developmental processes and cellular regeneration owing to its central role in cell survival and proliferation. We therefore hypothesized that the activation of Wnt signaling reduces systemic injury caused by hemorrhagic shock. METHODS: Adult male Sprague-Dawley rats underwent hemorrhagic shock by controlled bleeding of the femoral artery to maintain a mean arterial pressure of 30 mm Hg for 90 minutes, followed by resuscitation with crystalloid equal to two times the shed blood volume. After resuscitation, animals were infused with Wnt agonist (5 mg/kg) or vehicle (20% dimethyl sulfoxide in saline). Blood and tissue samples were collected 6 hours after resuscitation for analysis. RESULTS: Hemorrhagic shock increased serum levels of aspartate aminotransferase, lactate, and lactate dehydrogenase. Treatment with Wnt agonist significantly reduced these levels by 40%, 36%, and 77%, respectively. Wnt agonist also decreased blood urea nitrogen and creatinine by 34% and 56%, respectively. The treatment reduced lung myeloperoxidase activity and interleukin 6 messenger RNA by 55% and 68%, respectively, and significantly improved lung histology. Wnt agonist treatment increased Bcl-2 protein to sham values and decreased cleaved caspase 3 by 46%, indicating attenuation of hemorrhage-induced apoptosis in the lungs. Hemorrhage resulted in significant reductions of A-catenin protein levels in the lungs as well as down-regulation of a Wnt target gene, cyclin D1, while Wnt agonist treatment preserved these levels. CONCLUSION: The administration of Wnt agonist attenuated hemorrhage-induced organ injury, inflammation, and apoptosis. This was correlated with the preservation of the Wnt signaling pathway. Thus, Wnt/beta-catenin activation could be protective in hemorrhagic shock. Copyright (C) 2015 Wolters Kluwer Health, Inc. All rights reserved