Committed emissions from existing energy infrastructure jeopardize 1.5 °C climate target.

Net anthropogenic emissions of carbon dioxide (CO2) must approach zero by mid-century (2050) in order to stabilize the global mean temperature at the level targeted by international efforts1-5. Yet continued expansion of fossil-fuel-burning energy infrastructure implies already 'committed' future CO2 emissions6-13. Here we use detailed datasets of existing fossil-fuel energy infrastructure in 2018 to estimate regional and sectoral patterns of committed CO2 emissions, the sensitivity of such emissions to assumed operating lifetimes and schedules, and the economic value of the associated infrastructure. We estimate that, if operated as historically, existing infrastructure will cumulatively emit about 658 gigatonnes of CO2 (with a range of 226 to 1,479 gigatonnes CO2, depending on the lifetimes and utilization rates assumed). More than half of these emissions are predicted to come from the electricity sector; infrastructure in China, the USA and the 28 member states of the European Union represents approximately 41 per cent, 9 per cent and 7 per cent of the total, respectively. If built, proposed power plants (planned, permitted or under construction) would emit roughly an extra 188 (range 37-427) gigatonnes CO2. Committed emissions from existing and proposed energy infrastructure (about 846 gigatonnes CO2) thus represent more than the entire carbon budget that remains if mean warming is to be limited to 1.5 degrees Celsius (°C) with a probability of 66 to 50 per cent (420-580 gigatonnes CO2)5, and perhaps two-thirds of the remaining carbon budget if mean warming is to be limited to less than 2 °C (1,170-1,500 gigatonnes CO2)5. The remaining carbon budget estimates are varied and nuanced14,15, and depend on the climate target and the availability of large-scale negative emissions16. Nevertheless, our estimates suggest that little or no new CO2-emitting infrastructure can be commissioned, and that existing infrastructure may need to be retired early (or be retrofitted with carbon capture and storage technology) in order to meet the Paris Agreement climate goals17. Given the asset value per tonne of committed emissions, we suggest that the most cost-effective premature infrastructure retirements will be in the electricity and industry sectors, if non-emitting alternatives are available and affordable4,18

K-Connected Cores Computation in Large Dual Networks

© 2018, The Author(s). Computing k- cores is a fundamental and important graph problem, which can be applied in many areas, such as community detection, network visualization, and network topology analysis. Due to the complex relationship between different entities, dual graph widely exists in the applications. A dual graph contains a physical graph and a conceptual graph, both of which have the same vertex set. Given that there exist no previous studies on the k- core in dual graphs, we formulate a k-connected core (k- CCO) model in dual graphs. A k- CCO is a k- core in the conceptual graph, and also connected in the physical graph. Given a dual graph and an integer k, we propose a polynomial time algorithm for computing all k- CCOs. We also propose three algorithms for computing all maximum-connected cores (MCCO), which are the existing k- CCOs such that a (k+ 1) -CCO does not exist. We further study a subgraph search problem, which is computing a k- CCO that contains a set of query vertices. We propose an index-based approach to efficiently answer the query for any given parameter k. We conduct extensive experiments on six real-world datasets and four synthetic datasets. The experimental results demonstrate the effectiveness and efficiency of our proposed algorithms

(E)-N′-(Furan-2-ylmethyl­ene)-4-(quinolin-8-yl­oxy)butanohydrazide

In the title mol­ecule, C18H17N3O3, the dihedral angle between the mean planes of the furan ring and the quinoline group is 77.4 (2)°. In the crystal structure, inter­molecular N—H⋯N hydrogen bonds link the mol­ecules into centrosymmetric dimers

Prospects of CPCP violation in Λ\Lambda decay with polarized electron beam at STCF

Based on $1.89 \times 10^8$ $J/\psi \rightarrow \Lambda \bar{\Lambda}$ Monte Carlo (MC) events produced from a longitudinally-polarized electron beam, the sensitivity of $CP$ violation of $\Lambda$ decay is studied with fast simulation software. In addition, the $J/\psi \rightarrow \Lambda \bar{\Lambda}$ decay can also be used as a process to optimize the detector response using the interface provided by the fast simulation software. In the future, STCF is expected to obtain 3.4 trillion $J/\psi$ events, and the statistical sensitivity of $CP$ violation of $\Lambda$ decay via $J/\psi \rightarrow \Lambda \bar{\Lambda}$ process is expected to reach $\mathcal O$~$(10^{-5})$ when the electron beam polarization is 80\%

Effects of triazolodiazepine on the production of interleukin-6 from murine spleen cells and rabbit synovial cells in vitro

Interleukin-6 (IL-6) is a multifunctional cytokine that regulates the immune response, acute phase anaphylactic reaction, and haematopoiesis. Lipopolysaccharide (6–24 μg/ml) significantly induced IL-6 release from murine spleen cells. In cultured rabbit synovial cells interleukin-1 (IL-1, 1–10 U/ml) induced IL-6 production in a concentration-dependent manner. Triazolodiazepine (Tri) is a hetrazepine platelet-activating factor antagonist. In this study we found that Tri (0.1–10 μmol/l) exerted strong inhibitory effects on LPS stimulated IL-6 production in murine spleen cells. Kinetic studies showed that the inhibition of IL-6 release was time-independent. In rabbit synovial cells Tri also reduced IL-6 release induced by IL-1 and tumour necrosis factor. Inhibition of cytokine production by Tri may partially explain its wide and strong anti-inflammatory effects

Ghrelin Stimulates Hepatocyte Proliferation via Regulating Cell Cycle Through GSK3β/Β-Catenin Signaling Pathway

Background/Aims: Obesity is associated with a reduction in ghrelin, a 28 aa gastric hormone. Whether reduced ghrelin contributes to the impaired proliferation of hepatocytes associated with obesity-related steatosis remains largely unknown. Here we examined the effects of ghrelin on the proliferation of hepatocytes derived from lean and obese mice. Methods: AML 12 cells or hepatocytes isolated from mice fed normal chow diet (NCD) or high fat diet (HFD) were used. Effects of ghrelin on hepatocyte proliferation were detected with CCK8 assay and EdU staining. Cell cycle was analyzed by flow cytometry. Levels of proliferation markers was examined by Western blot. Results: Growth hormone secretagogue receptor 1a (GHS-R1a) mRNA and protein were present in hepatocytes. Levels of GHS-R1a were increased upon ghrelin treatment. Ghrelin significantly increased hepatocyte proliferation measured by Cell Counting Kit-8(CCK8) assay and EdU staining in a dose- and time-dependent manner. Proportion of cells in S phase was markedly increased upon treatment with ghrelin. Ghrelin significantly increased levels of proliferating cell nuclear antigen (PCNA) and cyclin D1, while reducing p27 in hepatocytes from mice fed NCD or HFD. Deletion of GHS-R1a completely abolished the effects of ghrelin in cultured hepatocytes. Ghrelin stimulated the phosphorylation of glycogen synthase kinase 3 beta (GSK3β), leading to subsequent increase of nuclear β-catenin in hepatocytes derived from lean and obese mice. This effect was dependent on the GHS-R1a. Conclusion: Ghrelin activates GHS-R1a to stimulate hepatocyte proliferation via GSK3/β-catenin signaling pathway

Effects of esculentoside A on turnour necrosis factor production by mice peritoneal macrophages

Esculentoside A (EsA) is a saponin isolated from the roots of Phytolacca esculenta. Previous experiments showed that it had strong anti-inflammatory effects. Tumour necrosis factor (TNF) is an important inflammatory mediator. In order to study the mechanism of the anti-inflammatory effect of EsA, it was determined whether TNF production from macrophages was altered by EsA under lipopolysaccharide (LPS) stimulated conditions. EsA was found to decrease both extracellular and cell associated TNF production in a dose dependent manner at concentrations higher than 1 μmol/l EsA. Previous studies have showed that EsA reduced the releasing of platelet activating factor (PAF) from rat macrophages. The reducing effects of EsA on the release of TNF and PAF may explain its anti-inflammatory effect

Disitamab Vedotin plus anti-PD-1 antibody show good efficacy in refractory primary urethral cancer with low HER2 expression: a case report

Primary urethral carcinoma (PUC) has a low incidence, but with high aggressiveness. Most of the patients are found in late stage, with poor prognosis. At present, chemotherapy is still the main treatment for metastatic PUC, but it has limited effect. Here, we report a case of metastatic PUC with low HER2 expression that developed disease progression after multiline therapy including chemotherapy, programmed death-1 (PD-1) inhibitors and multi-targeted receptor tyrosine kinase (RTK) inhibitor. After receiving Disitamab Vedotin(a novel antibody drug conjugate, ADC) and toripalimab (a PD-1 inhibitor), the patient achieved persistent PR, and the PFS exceeded 12 months up to now. Our report indicates that, despite the patient of metastatic PUC has low expression of HER2, it is still possible to benefit from Disitamab Vedotin combined with PD-1 inhibitor, which may reverse the drug resistance of PD-1 inhibitor and chemotherapy to a certain extent. But larger sample studies are needed to determine the efficacy of this treatment strategy and its impact on survival

Regulation of non-classical immune parameters in immune thrombocytopenic purpura mice by a spleen-invigorating, qi-replenishing and blood-containing formula

AbstractObjectiveThis study investigated the regulatory effect of non-classical immune parameters on immune thrombocytopenic purpura (ITP) mice by a spleen-invigorating, qi-replenishing and blood-containing formula (SQBF).MethodA total of 80 BALB/c mice were randomly divided into four equal groups (20 mice each): control group, model group, prednisone group and spleen-invigorating, qi-replenishing and blood-containing (SQBF) group. Mice in the model group, prednisone group, and SQBF group were administered anti-platelet serum to induce ITP. The dynamic variations of platelet counts in ITP mice were measured with an automatic blood analyzer before modeling and 48 h, and 8, 12 and 15 days following APS injection. Levels of β-endorphin (β-EP), vasoactive intestinal peptide (VIP) and salivary IgA (SIgA) were detected by enzyme-linked immunosorbent assay (ELISA) on 15th day of experiment.ResultsSQBF enhanced peripheral blood platelet counts in ITP mice similar to that of prednisone, and both groups showed a statistically significant response compared with the model group (P < .01). The SQBF significantly decreased β-EP levels compared with the model and prednisone intervention groups (P < .05), significantly increased the levels of VIP and SIgA in ITP mice compared with the model group (P < .05) and had significant protective effects on the thymus of ITP mice compared with the model group (P < .01).ConclusionsThe SQBF had a similar effect to prednisone with regards to enhancing peripheral blood platelet counts in ITP mice. Furthermore, it decreased β-EP levels and increased VIP and SIgA, and protected the thymus. This shows that, on base of the brain-gut axis functions, some non-classical immune vascular active factors or neurotransmitters are also involved in immune responses, and also have relationship with the onset of ITP and bleeding and/or hemostasis. It needs further study to determine whether a change in these active factors is related to immediate hemostasis