Influential Publications in Ecological Economics: A Citation Analysis

We assessed the degree of influence of selected papers and books in ecological economics using citation analysis. We looked at both the internal influence of publications on the field of ecological economics and the external influence of those same publications on the broader academic community. We used four lists of papers and books for the analysis: (1) 92 papers nominated by the Ecological Economics (EE) Editorial Board; (2) 71 papers that were published in EE and that received 15 or more citations in all journals included in the Institute for Scientific Information (ISI) Citation Index; (3) 57 papers that had been cited in EE 15 or more times; and (4) 77 monographs and edited books that had been cited in EE 15 or more times. For each publication we counted the total number of ISI citations as well as the total number of citations in EE. We calculated the average number of citations/yr to each paper since its publication in both the ISI database and in EE, along with the percentage of the total ISI citations that were in EE. Ranking the degree of influence of the publications can be done in several ways, including using the number of ISI citations, the number of EE citations or both. We discuss both the internal and external influence of publications and show how these influences might be considered jointly. We display and analyze the results in several ways. By plotting the ISI citations against the EE citations we can identify those papers that are mainly influential in EE with some broader influence, those that are mainly influential in the broader literature but have also had influence on EE, and other patterns of influence. There are both overlaps and interesting lacunae among the four lists that give us a better picture of the real influence of publications in ecological economics versus perceptions of those publications' importance. By plotting the number of citations vs. date of publication, we can identify those publications that are projected to be most influential. Plots of the time series of citations over the 1990-2003 period show a generally increasing trend (contrary to what one would expect for an "average" paper) for the top papers. We suggest that this pattern of increasing citations (and thus influence) over time is one hallmark of a "foundational" paper.

Adaptable Group-Oriented Signature

A new type of signature is presented in this paper, named adaptable group-oriented signature. In contrast with traditional group-oriented signature, the new one laid a strong emphasis on how to improve the signer¡¯s efficiency. In fact, this new type of group-oriented signature can be seen as a type of designated verifier signature. In contrast with the ordinary designated verifier signature, it does not designate one member but several members to independently verify the signature. The designated members, who can independently verify the signature, come into a group. This scheme can ensure the anonymity of the verifiers. This type of signature can be used in such system that the compute resource is limited, such as the broadcast protocols of the mobile telephone in the mobile networks

Physical health and cognitive function independently contributed to functional disability among Chinese older adults: Data from two asian metropolises

10.4061/2011/960848Journal of Aging Research20111-

The G-protein-coupled estrogen receptor agonist G-1 suppresses proliferation of ovarian cancer cells by blocking tubulin polymerization.

The G-protein-coupled estrogen receptor 1 (GPER) has recently been reported to mediate the non-genomic action of estrogen in different types of cells and tissues. G-1 (1-[4-(6-bromobenzo[1,3] dioxol-5yl)-3a,4,5,9b-tetrahydro-3H-cyclopenta[c]quinolin-8-yl]-ethanone) was developed as a potent and selective agonist for GPER. G-1 has been shown to induce the expression of genes and activate pathways that facilitate cancer cell proliferation by activating GPER. Here we demonstrate that G-1 has an anticancer potential with a mechanism similar to vinca alkaloids, the commonly used chemotherapy drugs. We found that G-1 blocks tubulin polymerization and thereby interrupts microtubule assembly in ovarian cancer cells leading to the arrest of cell cycle in the prophase of mitosis and the suppression of ovarian cancer cell proliferation. G-1 treatment also induces apoptosis of ovarian cancer cells. The ability of G-1 to target microtubules to suppress ovarian cancer cell proliferation makes it a promising candidate drug for treatment of ovarian cancer

DCAF26, an Adaptor Protein of Cul4-Based E3, Is Essential for DNA Methylation in Neurospora crassa

DNA methylation is involved in gene silencing and genome stability in organisms from fungi to mammals. Genetic studies in Neurospora crassa previously showed that the CUL4-DDB1 E3 ubiquitin ligase regulates DNA methylation via histone H3K9 trimethylation. However, the substrate-specific adaptors of this ligase that are involved in the process were not known. Here, we show that, among the 16 DDB1- and Cul4-associated factors (DCAFs) encoded in the N. crassa genome, three interacted strongly with CUL4-DDB1 complexes. DNA methylation analyses of dcaf knockout mutants revealed that dcaf26 was required for all of the DNA methylation that we observed. In addition, histone H3K9 trimethylation was also eliminated in dcaf26KO mutants. Based on the finding that DCAF26 associates with DDB1 and the histone methyltransferase DIM-5, we propose that DCAF26 protein is the major adaptor subunit of the Cul4-DDB1-DCAF26 complex, which recruits DIM-5 to DNA regions to initiate H3K9 trimethylation and DNA methylation in N. crassa

A novel causal structure-based framework for comparing a basin-wide water–energy–food–ecology nexus applied to the data-limited Amu Darya and Syr Darya river basins

The previous comparative studies on watersheds were mostly based on the comparison of dispersive characteristics, which lacked systemicity and causality. We proposed a causal structure-based framework for basin comparison based on the Bayesian network (BN) and focus on the basin-scale water–energy–food–ecology (WEFE) nexus. We applied it to the Syr Darya River basin (SDB) and the Amu Darya River basin (ADB), of which poor water management caused the Aral Sea disaster. The causality of the nexus was effectively compared and universality of this framework was discussed. In terms of changes in the nexus, the sensitive factor for the water supplied to the Aral Sea changed from the agricultural development during the Soviet Union period to the disputes in the WEFE nexus after the disintegration. The water–energy contradiction of the SDB is more severe than that of the ADB, partly due to the higher upstream reservoir interception capacity. It further made management of the winter surplus water downstream of the SDB more controversial. Due to this, the water–food–ecology conflict between downstream countries may escalate and turn into a long-term chronic problem. Reducing water inflow to depressions and improving the planting structure prove beneficial to the Aral Sea ecology, and this effect of the SDB is more significant. The construction of reservoirs on the Panj River of the upstream ADB should be cautious to avoid an intense water–energy conflict such as the SDB's. It is also necessary to promote the water-saving drip irrigation and to strengthen the cooperation

The Hippo/YAP pathway interacts with EGFR signaling and HPV oncoproteins to regulate cervical cancer progression

The Hippo signaling pathway controls organ size and tumorigenesis through a kinase cascade that inactivates Yes-associated protein (YAP). Here, we show that YAP plays a central role in controlling the progression of cervical cancer. Our results suggest that YAP expression is associated with a poor prognosis for cervical cancer. TGF-α and amphiregulin (AREG), via EGFR, inhibit the Hippo signaling pathway and activate YAP to induce cervical cancer cell proliferation and migration. Activated YAP allows for up-regulation of TGF-α, AREG, and EGFR, forming a positive signaling loop to drive cervical cancer cell proliferation. HPV E6 protein, a major etiological molecule of cervical cancer, maintains high YAP protein levels in cervical cancer cells by preventing proteasome-dependent YAP degradation to drive cervical cancer cell proliferation. Results from human cervical cancer genomic databases and an accepted transgenic mouse model strongly support the clinical relevance of the discovered feed-forward signaling loop. Our study indicates that combined targeting of the Hippo and the ERBB signaling pathways represents a novel therapeutic strategy for prevention and treatment of cervical cancer

A role for the arginine methylation of Rad9 in checkpoint control and cellular sensitivity to DNA damage

The genome stability is maintained by coordinated action of DNA repairs and checkpoints, which delay progression through the cell cycle in response to DNA damage. Rad9 is conserved from yeast to human and functions in cell cycle checkpoint controls. Here, a regulatory mechanism for Rad9 function is reported. In this study Rad9 has been found to interact with and be methylated by protein arginine methyltransferase 5 (PRMT5). Arginine methylation of Rad9 plays a critical role in S/M and G2/M cell cycle checkpoints. The activation of the Rad9 downstream checkpoint effector Chk1 is impaired in cells only expressing a mutant Rad9 that cannot be methylated. Additionally, Rad9 methylation is also required for cellular resistance to DNA damaging stresses. In summary, we uncovered that arginine methylation is important for regulation of Rad9 function, and thus is a major element for maintaining genome integrity