F = Finance

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Urban demands for organic tomatoes in the Kathmandu Valley, Nepal

This paper presents the willingness to pay for organic tomatoes by the consumers in urban areas of Nepal. It further makes an analysis of consumer preferences to this vegetables using conjoint modeling

Quality information retrieval for the World Wide Web

The World Wide Web is an unregulated communication medium which exhibits very limited means of quality control. Quality assurance has become a key issue for many information retrieval services on the Internet, e.g. web search engines. This paper introduces some quality evaluation and assessment methods to assess the quality of web pages. The proposed quality evaluation mechanisms are based on a set of quality criteria which were extracted from a targeted user survey. A weighted algorithmic interpretation of the most significant user quoted quality criteria is proposed. In addition, the paper utilizes machine learning methods to produce a prediction of quality for web pages before they are downloaded. The set of quality criteria allows us to implement a web search engine with quality ranking schemes, leading to web crawlers which can crawl directly quality web pages. The proposed approaches produce some very promising results on a sizable web repository

Meeting the Sustainable Development Goals leads to lower world population growth

Here we show the extent to which the expected world population growth could be lowered by successfully implementing the recently agreed-upon Sustainable Development Goals (SDGs). The SDGs include specific quantitative targets on mortality, reproductive health, and education for all girls by 2030, measures that will directly and indirectly affect future demographic trends. Based on a multidimensional model of population dynamics that stratifies national populations by age, sex, and level of education with educational fertility and mortality differentials, we translate these goals into SDG population scenarios, resulting in population sizes between 8.2 and 8.7 billion in 2100. Because these results lie outside the 95% prediction range given by the 2015 United Nations probabilistic population projections, we complement the study with sensitivity analyses of these projections that suggest that those prediction intervals are too narrow because of uncertainty in baseline data, conservative assumptions on correlations, and the possibility of new policies influencing these trends. Although the analysis presented here rests on several assumptions about the implementation of the SDGs and the persistence of educational, fertility, and mortality differentials, it quantitatively illustrates the view that demography is not destiny and that policies can make a decisive difference. In particular, advances in female education and reproductive health can contribute greatly to reducing world population growth

Multi-Label Multi-Kernel Transfer Learning for Human Protein Subcellular Localization

Recent years have witnessed much progress in computational modelling for protein subcellular localization. However, the existing sequence-based predictive models demonstrate moderate or unsatisfactory performance, and the gene ontology (GO) based models may take the risk of performance overestimation for novel proteins. Furthermore, many human proteins have multiple subcellular locations, which renders the computational modelling more complicated. Up to the present, there are far few researches specialized for predicting the subcellular localization of human proteins that may reside in multiple cellular compartments. In this paper, we propose a multi-label multi-kernel transfer learning model for human protein subcellular localization (MLMK-TLM). MLMK-TLM proposes a multi-label confusion matrix, formally formulates three multi-labelling performance measures and adapts one-against-all multi-class probabilistic outputs to multi-label learning scenario, based on which to further extends our published work GO-TLM (gene ontology based transfer learning model for protein subcellular localization) and MK-TLM (multi-kernel transfer learning based on Chou's PseAAC formulation for protein submitochondria localization) for multiplex human protein subcellular localization. With the advantages of proper homolog knowledge transfer, comprehensive survey of model performance for novel protein and multi-labelling capability, MLMK-TLM will gain more practical applicability. The experiments on human protein benchmark dataset show that MLMK-TLM significantly outperforms the baseline model and demonstrates good multi-labelling ability for novel human proteins. Some findings (predictions) are validated by the latest Swiss-Prot database. The software can be freely downloaded at http://soft.synu.edu.cn/upload/msy.rar

Topology-Transparent Scheduling in Mobile Ad Hoc Networks Supporting Heterogeneous Quality of Service Guarantees

Transmission scheduling plays a critical role in mobile ad hoc networks. Many transmission scheduling algorithms have been proposed to maximize the spatial reuse and minimize the time-division multiple-access (TDMA) frame length. Most algorithms require information on the network topology and cannot adapt to the dynamic topology in mobile scenarios. To overcome this limitation, topology-transparent scheduling algorithms have been proposed. Most of them, based on Galois field theory, Latin square, and block design theory, assign time slots to users and guarantee that there is at least one collision-free slot in each frame for each user. To the best of our knowledge, none of these topology-transparent algorithms support multiple quality of service (QoS) requirements. In this paper, we exploit the variable-weight optical orthogonal codes (VW-OOC) to design a topology-transparent scheduling algorithm in wireless ad hoc networks with multiple QoS levels. We study the performance, in terms of minimum guaranteed throughput and average throughput, of our proposed algorithm analytically and by extensive simulations.published_or_final_versio

Anticipation and Adaptation in Particulate Matter Policy: The European Union, the Netherlands, and United States

The evolution of particulate matter (PM) air quality policy in the European Union and in the United States between 1970 and the present has been atypical. The US government and the European Commission have mandated scheduled reviews of PM policy over the past three decades and have updated that policy to new scientific information on multiple occasions. The use of planned adaptation over such a long period and in this manner, as a means to deal with uncertainty, has not often been reproduced in air quality policy. Furthermore, particulate matter policy in the EU and US does not conform to the commonly held perception that the EU’s environmental policies are, by and large, more precautionary than the respective policies in the United States. The US decisions to adopt air quality standards for PM10 and PM2.5, in 1987 and 1997 respectively, led those in the EU by approximately nine years. An analysis of the comparative stringency of the PM standards in the US and EU shows that the PM2.5 standard the US implemented in 1997 is more stringent than the standards that have been proposed in the EU by the European Commission and the European Parliament. In September this year, the US repealed their annual standard for PM10. Prior to that, however, the annual PM10 standard the EU implemented in 1999 was more stringent than the one the US adopted in 1987. The daily PM10 standards in the EU and US are of similar stringency. In the Appendix, these comparisons in stringency are discussed in more detail. The differences between the EU and US policies are remarkable because they are based on the same science and therefore reflect dissimilar processes of interpreting that science and the uncertainties inherent in it. The two cases themselves focus on the sciencepolicy interfaces for their respective governing bodies. The EU case also looks at the science-policy interface in the Netherlands. The US case also examines policies for sulfur dioxides that relate to the PM policies. The remainder of this summary discusses how characteristics of the science-policy interfaces may have led to the differences in outcomes

Physiological roles of taurine in heart and muscle

Taurine (aminoethane sulfonic acid) is an ubiquitous compound, found in very high concentrations in heart and muscle. Although taurine is classified as an amino acid, it does not participate in peptide bond formation. Nonetheless, the amino group of taurine is involved in a number of important conjugation reactions as well as in the scavenging of hypochlorous acid. Because taurine is a fairly inert compound, it is an ideal modulator of basic processes, such as osmotic pressure, cation homeostasis, enzyme activity, receptor regulation, cell development and cell signalling. The present review discusses several physiological functions of taurine. First, the observation that taurine depletion leads to the development of a cardiomyopathy indicates a role for taurine in the maintenance of normal contractile function. Evidence is provided that this function of taurine is mediated by changes in the activity of key Ca2+ transporters and the modulation Ca2+ sensitivity of the myofibrils. Second, in some species, taurine is an established osmoregulator, however, in mammalian heart the osmoregulatory function of taurine has recently been questioned. Third, taurine functions as an indirect regulator of oxidative stress. Although this action of taurine has been widely discussed, its mechanism of action is unclear. A potential mechanism for the antioxidant activity of taurine is discussed. Fourth, taurine stabilizes membranes through direct interactions with phospholipids. However, its inhibition of the enzyme, phospholipid N-methyltransferase, alters the phosphatidylcholine and phosphatidylethanolamine content of membranes, which in turn affects the function of key proteins within the membrane. Finally, taurine serves as a modulator of protein kinases and phosphatases within the cardiomyocyte. The mechanism of this action has not been studied. Taurine is a chemically simple compound, but it has profound effects on cells. This has led to the suggestion that taurine is an essential or semi-essential nutrient for many mammals

Signal transducer and activator of transcription 2 deficiency is a novel disorder of mitochondrial fission

Defects of mitochondrial dynamics are emerging causes of neurological disease. In two children presenting with severe neurological deterioration following viral infection we identified a novel homozygous STAT2 mutation, c.1836C4A (p.Cys612Ter), using whole exome sequencing. In muscle and fibroblasts from these patients, and a third unrelated STAT2-deficient patient, we observed extremely elongated mitochondria. Western blot analysis revealed absence of the STAT2 protein and that the mitochondrial fission protein DRP1 (encoded by DNM1L) is inactive, as shown by its phosphorylation state. All three patients harboured 15 decreased levels of DRP1 phosphorylated at serine residue 616 (P-DRP1S616), a post-translational modification known to activate DRP1, and increased levels of DRP1 phosphorylated at serine 637 (P-DRP1S637), associated with the inactive state of the DRP1 GTPase. Knockdown of STAT2 in SHSY5Y cells recapitulated the fission defect, with elongated mitochondria and decreased PDRP1 S616 levels. Furthermore the mitochondrial fission defect in patient fibroblasts was rescued following lentiviral transduction with wild-type STAT2 in all three patients, with normalization of mitochondrial length and increased P-DRP1S616 levels. Taken 20 together, these findings implicate STAT2 as a novel regulator of DRP1 phosphorylation at serine 616, and thus of mitochondrial fission, and suggest that there are interactions between immunity and mitochondria. This is the first study to link the innate immune system to mitochondrial dynamics and morphology. We hypothesize that variability in JAK-STAT signalling may contribute to the phenotypic heterogeneity of mitochondrial disease, and may explain why some patients with underlying mitochondrial disease decompensate after seemingly trivial viral infections. Modulating JAK-STAT activity may represent a novel 25 therapeutic avenue for mitochondrial diseases, which remain largely untreatable. This may also be relevant for more common neurodegenerative diseases, including Alzheimer’s, Huntington’s and Parkinson’s diseases, in which abnormalities of mitochondrial morphology have been implicated in disease pathogenesis