130,416 research outputs found
Extracellular Regulated Kinase Phosphorylates Mitofusin 1 to Control Mitochondrial Morphology and Apoptosis.
No full textMeSH term explosion and author rank improve expert recommendations
No full textInformation overload is an often-cited phenomenon that reduces the productivity, efficiency and efficacy of scientists. One challenge for scientists is to find appropriate collaborators in their research. The literature describes various solutions to the problem of expertise location, but most current approaches do not appear to be very suitable for expert recommendations in biomedical research. In this study, we present the development and initial evaluation of a vector space model-based algorithm to calculate researcher similarity using four inputs: 1) MeSH terms of publications; 2) MeSH terms and author rank; 3) exploded MeSH terms; and 4) exploded MeSH terms and author rank. We developed and evaluated the algorithm using a data set of 17,525 authors and their 22,542 papers. On average, our algorithms correctly predicted 2.5 of the top 5/10 coauthors of individual scientists. Exploded MeSH and author rank outperformed all other algorithms in accuracy, followed closely by MeSH and author rank. Our results show that the accuracy of MeSH term-based matching can be enhanced with other metadata such as author rank
Going Beyond Counting First Authors in Author Co-citation Analysis
No full textThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
"Closing the R&D Gap, Evaluating the Sources of R&D Spending"
No full textBoth spending and tax policies have been implemented in the United States with the goal of stimulating private sector research and development (R&D). Karier questions whether current R&D policy, especially the research and experimentation tax credit, can contribute to closing the gap between nondefense expenditures on R&D in the United States and such expenditures in other countries, such as Japan and Germany. He also explores possible changes to our current R&D policy to make it more effective.
Trichoplein/mitostatin regulates endoplasmic reticulum-mitochondria juxtaposition.
No full textTrichoplein/mitostatin (TpMs) is a keratin-binding protein that partly colocalizes with mitochondria and is often downregulated in epithelial cancers, but its function remains unclear. In this study, we report that TpMs regulates the tethering between mitochondria and endoplasmic reticulum (ER) in a Mitofusin 2 (Mfn2)-dependent manner. Subcellular fractionation and immunostaining show that TpMs is present at the interface between mitochondria and ER. The expression of TpMs leads to mitochondrial fragmentation and loosens tethering with ER, whereas its silencing has opposite effects. Functionally, the reduced tethering by TpMs inhibits apoptosis by Ca(2+)-dependent stimuli that require ER-mitochondria juxtaposition. Biochemical and genetic evidence support a model in which TpMs requires Mfn2 to modulate mitochondrial shape and tethering. Thus, TpMs is a new regulator of mitochondria-ER juxtaposition
Dispelling the Myths Behind First-author Citation Counts
No full textWe conducted a full-scale evaluative citation analysis study of scholars in the XML research field to explore just how different from each other author rankings resulting from different citation counting methods actually are, and to demonstrate the capability of emerging data and tools on the Web in supporting more realistic citation counting methods. Our results contest some common arguments for the continued
use of first-author citation counts in the evaluation of scholars, such as high correlations between author rankings by first-author citation counts and other citation
counting methods, and high costs of using more realistic citation counting methods that are not well-supported by the ISI databases. It is argued that increasingly available digital full text research papers make it possible for citation analysis studies to go beyond what the ISI databases have directly supported and to employ more
sophisticated methods
Scholarly Communication and Publishing Lunch and Learn Talk #11: The ULS Open Access Author Fee Fund
No full textAt the May 2014 talk, you will learn about the ULS Open Access Author Fee Fund--what it is, why we do it, how it works, and how the program is going so far
AIDS and endemic Kaposi's sarcoma development : comparison by histopathology, virology (HHV8/KSHV) and cytogenetics
No full textKaposi’s sarcoma (KS) is a highly and abnormally vascularized tumor-like lesion with spindle cells (SC) affecting the skin, lymphnodes and viscera which is found in four different clinico-epidemiological forms as Classic KS (CKS), Iatrogenic KS (IKS), Endemic KS (EKS) and AIDS-associated KS (AKS). All KS forms develop from early stages of patch/plaque to late, nodular tumors and are associated with Kaposi's sarcomaassociated herpesvirus or human herpesvirus-8 (KSHV/ HHV-8). HHV-8 is also associated with primary effusion lymphoma (PEL) and multicentric castleman's disease (MCD). Various studies favour an endothelial origin (CD34+) of the KS SC but whether of vascular (VEC) or lymphatic endothelial cell (LEC) origin has not been settled. The HHV-8 latency-associated nuclear antigen type 1 (LANA-1) protein is the most frequently expressed viral antigen in infected cells. KS is promoted by HIV infection mainly by the angiogenic and proinflammatory effects of HIV-Tat. Whether KS represents a predominantly monoclonal neoplastic cell proliferation or a hyperplastic, reactive polyclonal process is still controversial. Reports on cytogenetic and molecular genetic changes in KS are few indicating that initially KS may develop as a reactive polyclonal cell proliferation associated with chromosome instability, followed by clonal chromosome changes in later stages.In the present KS histopathological studies (paper I & V) by triple antibody immunofluorescence we observed that: (a) the frequency of LANA+/CD34+ cells increased from early patch to late KS nodular lesions; (b) 30- 40% of the CD34+ SC were LANA- in both early and late KS, suggesting a continuous recruitment of noninfected endothelial cell into the KS lesion; (c) LANA+/CD34- cells were more frequent in early as compared to late KS and most of them expressed LEC markers such as LYVE-1 and D2-40, suggesting that the resident LECs represent an early target of primary HHV-8 infection; (d) LANA+/CD34-/LYVE-1+ cells decreased from early (25%) to late (4%) KS suggesting a phenotype switch from LEC to VEC; (e) the frequency of proliferating cells (Ki67+) was higher in early as compared to late KS stages and no significant difference in cell proliferation was observed between nodular AKS and EKS, suggesting that the growth of the usually more aggressive AKS tumors may reflect a higher rate of SC progenitor recruitment as compared to the slower growing EKS lesions, consistent with the observed increase in non-proliferative SC during KS (AKS) evolution to nodular stage; (f) infiltrating lymphocytes were LANA negative, whereas some CD68+ monocyte-macrophase appeared to be LANA+.To validate our results from LANA immunostaining, we established and optimized a semi-quantitative PCR assay for HHV-8 detection in formalin-fixed paraffin-embedded KS biopsies (paper III) and two different protocols for DNA extraction were compared namely the Chelex 100 and Qia-gene kit method. Our result indicate a better performance for Chelex-extracted DNA in paraffin embedded archival biopsies. In late, nodular stage of both AKS and EKS the virus load per unit tissue actin (HHV-8/actin) is higher than in early stages (patch/plaque), which corroborates our findings from double immunostaining for LANA and CD34 of the same cases. Thus these PCR results by serial dilutions of HHV-8 DNA show a correlation between virus load and progressive stages of KS development i.e. the increase in LANA+ SC and does not indicate an increase in viral content of individual tumor cells.With quantitative real time PCR on sera (paper II), we found higher HHV8 DNA load in AKS compared to EKS, patch compared to nodular KS and males compared to females as well as a significantly higher serum viral DNA load in KS compared to non-KS patients’ sera.AKS patient sera studied by ELISA for HIV-Tat antibodies showed that patients with high HHV8-DNA level had no or low levels of anti-Tat antibodies while patients with very low HHV8-DNA levels had several fold higher anti-Tat IgG titers. Analysis of these KS sera for epitope specificity showed reactivity to various Tat epitopes but not to the transcriptional (functional) epitopes 46-60 (TAR-binding region). To determine cytogenetic changes during the development of KS as well as possible differences between AKS and EKS we studied 27 KS (10 nodular AKS, 8 patch AKS, 8 nodular EKS and 1 patch EKS) cases by laser microdissection, global amplification of DNA and comparative genomic hybridization (paper IV). Deletion of Chromosome Y was detected in 20 of 23 male KS and was the only chromosomal deletion observed in early (patch) KS biopsies. Late AKS and EKS apart from random aberrations also showed recurrent chromosomal deletions of chromosome 16, 17, Y and a gain of chromosome 21. The deletion of chromosome 16 and Y was confirmed by interphase FISH on paraffin embedded sections. EKS had higher number of chromosomal abnormalities than AKS.In summary KS SC apparently represents a mixed pool endothelial cells including cells from both VEC and LEC the later being a possible early target for HHV-8 infection. Non-infected CD34+ progenitor cells appears to be continuously recruited to the developing KS lesion and locally infected during the development of KS. Serum HHV-8 DNA load is higher in AKS compared to EKS and HIV-Tat titers were inversely correlated to HHV-8 DNA load in AKS patients. Increased number of recurrent and sporadic chromosomal abnormalities found mostly in a subset of late nodular KS cases may indicate the onset of a clonal cell population (sarcoma).List of scientific papersI. Pyakurel P, Massambu C, Castanos-Velez E, Ericsson S, Kaaya E, Biberfeld P, Heiden T (2004). Human herpesvirus 8/Kaposi sarcoma herpesvirus cell association during evolution of Kaposi sarcoma. J Acquir Immune Defic Syndr. 36(2): 678-83. https://doi.org/10.1097/00126334-200406010-00004 II. Massambu C, Pyakurel P, Kaaya E, Enbom M, Urassa W, Demirhan I, Loewer J, Linde A, Chandra A, Heiden T, Doerr HW, Chandra P, Biberfeld P (2003). Serum HHV8 DNA and Tat antibodies in Kaposis sarcoma patients with and without HIV-1 infection. Anticancer Res. 23(3B): 2389-95. https://pubmed.ncbi.nlm.nih.gov/12894519 III. Pak F, Pyakural P, Kokhaei P, Kaaya E, Akbar Pourfathollah A, Selinova G, Biberfeld P (2005). HHV-8/KSHV during development of Kaposis sarcoma: evaluation by PCR and immunohistochemistry. J Cutan Pathol. 32(1): 21-7. https://doi.org/10.1111/j.0303-6987.2005.00256.x IV. Pyakurel P, Montag U, Castanos-Velez E, Kaaya E, Christensson B, Biberfeld P, Schrock E, Heiden T (2005). Kaposis sarcoma: CGH ctogenetic analysis of microdissected early and late stage biopsies. [Manuscript]V. Pyakurel P, Pak F, Mwakigonja AR, Kaaya E, Heiden T, Biberfeld P (2005). Recruitment of Kaposis sarcoma spindle cells during tumor development. [Manuscript]</p
The R&D Tax Incentives
No full textThis article sets out some background information and reflections of the author on the R&D tax incentive schemes included in the Common Corporate Tax Base (CCTB) Proposal. In particular the author analyzes the stimulus to private R&D through ad hoc tax incentives included in the CCTB Proposal and dives into the actual provisions included in the Proposal highlighting the most relevant issues connected with their design and interpretation. Moreover, the author explores the interaction between the CCTB Proposal and the granting by Member States of domestic R&D tax incentives
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