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  • 1
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    Helsinki: The United Nations University World Institute for Development Economics Research (UNU-WIDER)
    Publication Date: 2018-11-16
    Description: This paper examines the changing nature of occupational labour-market trends in South Africa and the resulting impact on wages. We observe high levels of demand for skilled labour that have intensified a trend already established before 1994. Over the period 2001-12 employment within the primary sectors collapsed, employment in the manufacturing sector did not increase, while employment in the tertiary sectors such as financial services and community services grew. High- and medium-skilled occupations such as managers, professionals, service and sales workers have seen significant growth while the number of low-skilled workers, and the proportion of medium-skilled workers in the primary and secondary sectors of the economy have declined. In addition, an analysis of occupation demand using a Katz-Murphy decomposition model further shows that within-sector shifts outweigh between-sector shifts in explaining changes in relative labour demand. Increasing demand for skilled labour has also fed into and changed the structure of wages, and therefore wage inequality. We follow the work by Firpo et al. (2011) in an attempt to explore the way in which the returns to certain tasks (rather than occupations) have changed over time. This approach emphasizes the influence of structural factors such as technology and trade, in the presence of increasingly routinized tasks and offshoring, on wages. We run quantile regressions which suggest that, when controlling for age/experience, race and education, jobs which involve automated or routine tasks and those without any face-to-face component (largely lower- to medium-skilled jobs) have seen declining wage levels over time.
    Keywords: E24 ; J21 ; J24 ; O14 ; O55 ; ddc:330 ; skills ; employment ; South Africa ; wages ; occupations
    Repository Name: EconStor: OA server of the German National Library of Economics - Leibniz Information Centre for Economics
    Language: English
    Type: doc-type:workingPaper
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  • 2
    Publication Date: 2015-09-30
    Description: Despite major advances in understanding the molecular and genetic basis of cancer, metastasis remains the cause of 〉90% of cancer-related mortality. Understanding metastasis initiation and progression is critical to developing new therapeutic strategies to treat and prevent metastatic disease. Prevailing theories hypothesize that metastases are seeded by rare tumour cells with unique properties, which may function like stem cells in their ability to initiate and propagate metastatic tumours. However, the identity of metastasis-initiating cells in human breast cancer remains elusive, and whether metastases are hierarchically organized is unknown. Here we show at the single-cell level that early stage metastatic cells possess a distinct stem-like gene expression signature. To identify and isolate metastatic cells from patient-derived xenograft models of human breast cancer, we developed a highly sensitive fluorescence-activated cell sorting (FACS)-based assay, which allowed us to enumerate metastatic cells in mouse peripheral tissues. We compared gene signatures in metastatic cells from tissues with low versus high metastatic burden. Metastatic cells from low-burden tissues were distinct owing to their increased expression of stem cell, epithelial-to-mesenchymal transition, pro-survival, and dormancy-associated genes. By contrast, metastatic cells from high-burden tissues were similar to primary tumour cells, which were more heterogeneous and expressed higher levels of luminal differentiation genes. Transplantation of stem-like metastatic cells from low-burden tissues showed that they have considerable tumour-initiating capacity, and can differentiate to produce luminal-like cancer cells. Progression to high metastatic burden was associated with increased proliferation and MYC expression, which could be attenuated by treatment with cyclin-dependent kinase (CDK) inhibitors. These findings support a hierarchical model for metastasis, in which metastases are initiated by stem-like cells that proliferate and differentiate to produce advanced metastatic disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4648562/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4648562/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lawson, Devon A -- Bhakta, Nirav R -- Kessenbrock, Kai -- Prummel, Karin D -- Yu, Ying -- Takai, Ken -- Zhou, Alicia -- Eyob, Henok -- Balakrishnan, Sanjeev -- Wang, Chih-Yang -- Yaswen, Paul -- Goga, Andrei -- Werb, Zena -- CA136717/CA/NCI NIH HHS/ -- CA180039/CA/NCI NIH HHS/ -- K23 HL116657/HL/NHLBI NIH HHS/ -- R01 CA136717/CA/NCI NIH HHS/ -- R01 CA180039/CA/NCI NIH HHS/ -- England -- Nature. 2015 Oct 1;526(7571):131-5. doi: 10.1038/nature15260. Epub 2015 Sep 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy, University of California, San Francisco, California 94143, USA. ; Department of Medicine, University of California, San Francisco, California 94143, USA. ; Department of Cell and Tissue Biology, University of California, San Francisco, California 94143, USA. ; Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan. ; Department of Cell and Molecular Biology, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26416748" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/drug therapy/genetics/*pathology ; Cell Cycle/drug effects ; Cell Differentiation/drug effects/genetics ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Separation ; Cell Transformation, Neoplastic/drug effects/pathology ; Cyclin-Dependent Kinases/antagonists & inhibitors ; Disease Models, Animal ; *Disease Progression ; Epithelial Cells/drug effects/pathology ; Epithelial-Mesenchymal Transition/genetics ; Flow Cytometry ; Gene Expression Profiling ; Genes, myc/genetics ; Humans ; Mesoderm/metabolism/pathology ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Neoplasm Metastasis/drug therapy/*pathology ; Neoplastic Stem Cells/drug effects/metabolism/*pathology ; *Single-Cell Analysis ; Xenograft Model Antitumor Assays
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 1994-04-15
    Description: A complementation strategy was developed to define the signaling pathways activated by the Bcr-Abl tyrosine kinase. Transformation inactive point mutants of Bcr-Abl were tested for complementation with c-Myc. Single point mutations in the Src-homology 2 (SH2) domain, the major tyrosine autophosphorylation site of the kinase domain, and the Grb-2 binding site in the Bcr region impaired the transformation of fibroblasts by Bcr-Abl. Hyperexpression of c-Myc efficiently restored transformation activity only to the Bcr-Abl SH2 mutant. These data support a model in which Bcr-Abl activates at least two independent pathways for transformation. This strategy may be useful for discerning signaling pathways activated by other oncogenes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Afar, D E -- Goga, A -- McLaughlin, J -- Witte, O N -- Sawyers, C L -- CA 01551/CA/NCI NIH HHS/ -- CA 53867/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Apr 15;264(5157):424-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, University of California-Los Angeles 90024-1489.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8153630" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Animals ; Base Sequence ; Binding Sites ; Cell Line ; *Cell Transformation, Neoplastic ; Fusion Proteins, bcr-abl/*genetics/physiology ; GRB2 Adaptor Protein ; Gene Expression ; *Genes, abl ; *Genes, myc ; Genetic Complementation Test ; Molecular Sequence Data ; Phosphorylation ; Point Mutation ; Proteins/metabolism ; Proto-Oncogene Proteins c-myc/genetics/physiology ; Rats ; Retroviridae/physiology ; Signal Transduction ; Transfection ; Tyrosine/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2015-12-01
    Description: Genome-wide association studies have identified over 70 single-nucleotide polymorphisms (SNPs) associated with breast cancer. A subset of these SNPs are associated with quantitative expression of nearby genes, but the functional effects of the majority remain unknown. We hypothesized that some risk SNPs may regulate alternative splicing. Using RNA-sequencing data from breast tumors and germline genotypes from The Cancer Genome Atlas, we tested the association between each risk SNP genotype and exon-, exon–exon junction- or transcript-specific expression of nearby genes. Six SNPs were associated with differential transcript expression of seven nearby genes at FDR 〈 0.05 ( BABAM1 , DCLRE1B/PHTF1 , PEX14 , RAD51L1, SRGAP2D and STXBP4 ). We next developed a Bayesian approach to evaluate, for each SNP, the overlap between the signal of association with breast cancer and the signal of association with alternative splicing. At one locus ( SRGAP2D ), this method eliminated the possibility that the breast cancer risk and the alternate splicing event were due to the same causal SNP. Lastly, at two loci, we identified the likely causal SNP for the alternative splicing event, and at one, functionally validated the effect of that SNP on alternative splicing using a minigene reporter assay. Our results suggest that the regulation of differential transcript isoform expression is the functional mechanism of some breast cancer risk SNPs and that we can use these associations to identify causal SNPs, target genes and the specific transcripts that may mediate breast cancer risk.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
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  • 5
    Publication Date: 2019
    Description: This study aims to analyze and assess studies published from 1992 to 2019 and listed in the Web of Science (WOS) and Current Contents (CC) databases, and to identify agricultural abandonment by application of remote sensing (RS) optical and microwave data. We selected 73 studies by applying structured queries in a field tag form and Boolean operators in the WOS portal and by expert analysis. An expert assessment yielded the topical picture concerning the definitions and criteria for the identification of abandoned agricultural land (AAL). The analysis also showed the absence of similar field research, which serves not only for validation, but also for understanding the process of agricultural abandonment. The benefit of the fusion of optical and radar data, which supports the application of Sentinel-1 and Sentinel-2 data, is also evident. Knowledge attained from the literary sources indicated that there exists, in the world literature, a well-covered problem of abandonment identification or biomass estimation, as well as missing works dealing with the assessment of the natural accretion of biomass in AAL.
    Electronic ISSN: 2072-4292
    Topics: Architecture, Civil Engineering, Surveying , Geography
    Published by MDPI
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  • 6
    Publication Date: 2012-10-09
    Description: The endoplasmic reticulum (ER) is the primary organelle for folding and maturation of secretory and transmembrane proteins. Inability to meet protein-folding demand leads to "ER stress," and activates IRE1alpha, an ER transmembrane kinase-endoribonuclease (RNase). IRE1alpha promotes adaptation through splicing Xbp1 mRNA or apoptosis through incompletely understood mechanisms. Here, we found that sustained IRE1alpha RNase activation caused rapid decay of select microRNAs (miRs -17, -34a, -96, and -125b) that normally repress translation of Caspase-2 mRNA, and thus sharply elevates protein levels of this initiator protease of the mitochondrial apoptotic pathway. In cell-free systems, recombinant IRE1alpha endonucleolytically cleaved microRNA precursors at sites distinct from DICER. Thus, IRE1alpha regulates translation of a proapoptotic protein through terminating microRNA biogenesis, and noncoding RNAs are part of the ER stress response.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3742121/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3742121/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Upton, John-Paul -- Wang, Likun -- Han, Dan -- Wang, Eric S -- Huskey, Noelle E -- Lim, Lionel -- Truitt, Morgan -- McManus, Michael T -- Ruggero, Davide -- Goga, Andrei -- Papa, Feroz R -- Oakes, Scott A -- DK063720/DK/NIDDK NIH HHS/ -- DP2 OD001925/OD/NIH HHS/ -- DP2OD001925/OD/NIH HHS/ -- GM080783/GM/NIGMS NIH HHS/ -- P30 DK063720/DK/NIDDK NIH HHS/ -- R01 CA136577/CA/NCI NIH HHS/ -- R01 CA136717/CA/NCI NIH HHS/ -- R01 CA140456/CA/NCI NIH HHS/ -- R01 CA154916/CA/NCI NIH HHS/ -- R01 DK080955/DK/NIDDK NIH HHS/ -- R01 GM080783/GM/NIGMS NIH HHS/ -- R01CA136577/CA/NCI NIH HHS/ -- R01CA136717/CA/NCI NIH HHS/ -- R01CA140456/CA/NCI NIH HHS/ -- R01CA154916/CA/NCI NIH HHS/ -- R01DK080955/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Nov 9;338(6108):818-22. doi: 10.1126/science.1226191. Epub 2012 Oct 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of California, San Francisco, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23042294" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions ; Animals ; Apoptosis ; Brefeldin A/pharmacology ; Caspase 2/*genetics/*metabolism ; Cell-Free System ; Cells, Cultured ; Cysteine Endopeptidases/*genetics/*metabolism ; Down-Regulation ; Endoplasmic Reticulum/metabolism ; *Endoplasmic Reticulum Stress ; Endoribonucleases/chemistry/genetics/*metabolism ; Enzyme Activation ; HEK293 Cells ; Humans ; Mice ; Mice, Knockout ; MicroRNAs/*metabolism ; Mutant Proteins ; Protein Biosynthesis ; Protein-Serine-Threonine Kinases/chemistry/genetics/*metabolism ; RNA Stability ; RNA, Messenger/genetics/metabolism ; Up-Regulation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2018-02-10
    Description: Lichens and mosses often share the same environmental conditions where they compete for substrate and other essential factors. Lichens use secondary metabolites as allelochemicals to repel surrounding plants and potential rivals. In mosses, endoreduplication leads to the occurrence of various ploidy levels in the same individual and has been suggested as an adaptation to abiotic stresses. Here, we show that also biotic factors such as usnic acid, an allelochemical produced by lichens, directly influenced the level of ploidy in mosses. Application of usnic acid changed the nuclei proportion and significantly enhanced the endoreduplication index in two moss species, Physcomitrella patens and Pohlia drummondii . These investigations add a new aspect on secondary metabolites of lichens which count as biotic factors and affect ploidy levels in mosses. Lichens use secondary metabolites as allelochemicals to repel surrounding plants and potential rivals. In mosses, endoreduplication leads to the occurrence of various ploidy levels in the same individual and has been suggested as an adaptation to abiotic stresses. Here, we show that also biotic factors such as usnic acid, an allelochemical produced by lichens, directly influenced the level of ploidy in mosses.
    Electronic ISSN: 2045-7758
    Topics: Biology
    Published by Wiley
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  • 8
    Publication Date: 2012-08-01
    Description: Malignant glioma, the most common primary brain tumor, is generally incurable. Although phosphatidylinositol-3-kinase (PI3K) signaling features prominently in glioma, inhibitors generally block proliferation rather than induce apoptosis. Starting with an inhibitor of both lipid and protein kinases that induced prominent apoptosis and that failed early clinical development because of its broad target profile and overall toxicity, we identified protein kinase targets, the blockade of which showed selective synthetic lethality when combined with PI3K inhibitors. Prioritizing protein kinase targets for which there are clinical inhibitors, we demonstrate that cyclin-dependent kinase (CDK)1/2 inhibitors, siRNAs against CDK1/2, and the clinical CDK1/2 inhibitor roscovitine all cooperated with the PI3K inhibitor PIK-90, blocking the antiapoptotic protein Survivin and driving cell death. In addition, overexpression of CDKs partially blocked some of the apoptosis caused by PIK-75. Roscovitine and PIK-90, in combination, were well tolerated in vivo and acted in a synthetic-lethal manner to induce apoptosis in human glioblastoma xenografts. We also tested clinical Akt and CDK inhibitors, demonstrating induction of apoptosis in vitro and providing a preclinical rationale to test this combination therapy in patients.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 9
    Publication Date: 2012-04-25
    Description: A family of conserved serine/threonine kinases known as cyclin-dependent kinases (CDKs) drives orderly cell cycle progression in mammalian cells. Prior studies have suggested that CDK2 regulates S-phase entry and progression, and frequently shows increased activity in a wide spectrum of human tumors. Genetic KO/knockdown approaches, however, have suggested that lack of CDK2 protein does not prevent cellular proliferation, both during somatic development in mice as well as in human cancer cell lines. Here, we use an alternative, chemical-genetic approach to achieve specific inhibition of CDK2 kinase activity in cells. We directly compare small-molecule inhibition of CDK2 kinase activity with siRNA knockdown and show that small-molecule inhibition results in marked defects in proliferation of nontransformed cells, whereas siRNA knockdown does not, highlighting the differences between these two approaches. In addition, CDK2 inhibition drastically diminishes anchorage-independent growth of human cancer cells and cells transformed with various oncogenes. Our results establish that CDK2 activity is necessary for normal mammalian cell cycle progression and suggest that it might be a useful therapeutic target for treating cancer.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 10
    Publication Date: 2017-03-22
    Description: The mammary gland consists of an adipose tissue that, in a process called branching morphogenesis, is invaded by a ductal epithelial network comprising basal and luminal epithelial cells. Stem and progenitor cells drive mammary growth, and their proliferation is regulated by multiple extracellular cues. One of the key regulatory pathways...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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