628 research outputs found

    The Education of Real Estate Salespeople and the Value of the Firm

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    In order to protect the public, most states require salespeople and brokers to meet specific licensing requirements, typically in the form of classroom instruction and/or successful completion of an examination. Frequently, however, many real estate brokers require their sales staff to undertake education that exceeds these minimum requirements. In this study, we derive a theoretical model that shows how optimally-timed, firm provided education that exceeds legal minimums can increase staff productivity, reduce litigation risks and perhaps raise and/or maximize the expected value of the firm.

    The Capitalization of Seller Paid Consessions

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    Using a hedonic pricing model, we analyze the capitalization of total seller paid discount points and closing costs into the price of a house. We hypothesize that sellers are concerned about the sales price net of total seller paid concessions (SPNC), rather than the exact terms of the transaction. Since the SPNC is easily ascertained in the negotiation process, we further hypothesize that total seller paid concessions (TSPC) are fully capitalized into the sales price. To test this hypothesis, sales price is regressed on a set of control variables including TSPC. In this framework, TSPC will be positive and not significantly different from one if concessions are fully capitalized. The empirical results provide support for the capitalization hypothesis. Negotiation strategies and study limitations follow from the empirical results.

    Alterations in cellular metabolism modulate CD1d-mediated NKT-cell responses

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    Natural killer T (NKT) cells play a critical role in the host's innate immune response. CD1d-mediated presentation of glycolipid antigens to NKT cells has been established; however, the mechanisms by which NKT cells recognize infected or cancerous cells remain unclear. 5′-AMP activated protein kinase (AMPK) is a master regulator of lipogenic pathways. We hypothesized that activation of AMPK during infection and malignancy could alter the repertoire of antigens presented by CD1d and serve as a danger signal to NKT cells. In this study, we examined the effect of alterations in metabolism on CD1d-mediated antigen presentation to NKT cells and found that an infection with lymphocytic choriomeningitis virus rapidly increased CD1d-mediated antigen presentation. Hypoxia inducible factors (HIF) enhance T-cell effector functions during infection, therefore antigen presenting cells pretreated with pharmacological agents that inhibit glycolysis, induce HIF and activate AMPK were assessed for their ability to induce NKT-cell responses. Pretreatment with 2-deoxyglucose, cobalt chloride, AICAR and metformin significantly enhanced CD1d-mediated NKT-cell activation. In addition, NKT cells preferentially respond to malignant B cells and B-cell lymphomas express HIF-1α. These data suggest that targeting cellular metabolism may serve as a novel means of inducing innate immune responses

    Changes in river water temperature between 1980 and 2012 in Yongan watershed, eastern China: Magnitude, drivers and models

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    Climate warming is expected to have major impacts on river water quality, water column/hyporheic zone biogeochemistry and aquatic ecosystems. A quantitative understanding of spatio-temporal air (Ta) and water (Tw) temperature dynamics is required to guide river management and to facilitate adaptations to climate change. This study determined the magnitude, drivers and models for increasing Tw in three river segments of the Yongan watershed in eastern China. Over the 1980-2012 period, Tw in the watershed increased by 0.029-0.046°Cyr-1 due to a ~0.050°Cyr-1 increase of Ta and changes in local human activities (e.g., increasing developed land and population density and decreasing forest area). A standardized multiple regression model was developed for predicting annual Tw (R2=0.88-0.91) and identifying/partitioning the impact of the principal drivers on increasing Tw:Ta (76±1%), local human activities (14±2%), and water discharge (10±1%). After normalizing water discharge, climate warming and local human activities were estimated to contribute 81-95% and 5-19% of the observed rising Tw, respectively. Models forecast a 0.32-1.76°C increase in Tw by 2050 compared with the 2000-2012 baseline condition based on four future scenarios. Heterogeneity of warming rates existed across seasons and river segments, with the lower flow river and dry season demonstrating a more pronounced response to climate warming and human activities. Rising Tw due to changes in climate, local human activities and hydrology has a considerable potential to aggravate river water quality degradation and coastal water eutrophication in summer. Thus it should be carefully considered in developing watershed management strategies in response to climate change

    Enzymes Are Enriched in Bacterial Essential Genes

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    Essential genes, those indispensable for the survival of an organism, play a key role in the emerging field, synthetic biology. Characterization of functions encoded by essential genes not only has important practical implications, such as in identifying antibiotic drug targets, but can also enhance our understanding of basic biology, such as functions needed to support cellular life. Enzymes are critical for almost all cellular activities. However, essential genes have not been systematically examined from the aspect of enzymes and the chemical reactions that they catalyze. Here, by comprehensively analyzing essential genes in 14 bacterial genomes in which large-scale gene essentiality screens have been performed, we found that enzymes are enriched in essential genes. Essential enzymes have overrepresented ligases (especially those forming carbon-oxygen bonds and carbon-nitrogen bonds), nucleotidyltransferases and phosphotransferases, while have underrepresented oxidoreductases. Furthermore, essential enzymes tend to associate with more gene ontology domains. These results, from the aspect of chemical reactions, provide further insights into the understanding of functions needed to support natural cellular life, as well as synthetic cells, and provide additional parameters that can be integrated into gene essentiality prediction algorithms

    Economic Analysis of Labor Markets and Labor Law: An Institutional/Industrial Relations Perspective

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    Contribution of copy number variants to schizophrenia from a genome-wide study of 41,321 subjects

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    Copy number variants (CNVs) have been strongly implicated in the genetic etiology of schizophrenia (SCZ). However, genome-wide investigation of the contribution of CNV to risk has been hampered by limited sample sizes. We sought to address this obstacle by applying a centralized analysis pipeline to a SCZ cohort of 21,094 cases and 20,227 controls. A global enrichment of CNV burden was observed in cases (OR=1.11, P=5.7×10−15), which persisted after excluding loci implicated in previous studies (OR=1.07, P=1.7 ×10−6). CNV burden was enriched for genes associated with synaptic function (OR = 1.68, P = 2.8 ×10−11) and neurobehavioral phenotypes in mouse (OR = 1.18, P= 7.3 ×10−5). Genome-wide significant evidence was obtained for eight loci, including 1q21.1, 2p16.3 (NRXN1), 3q29, 7q11.2, 15q13.3, distal 16p11.2, proximal 16p11.2 and 22q11.2. Suggestive support was found for eight additional candidate susceptibility and protective loci, which consisted predominantly of CNVs mediated by non-allelic homologous recombination

    No Reliable Association between Runs of Homozygosity and Schizophrenia in a Well-Powered Replication Study

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    It is well known that inbreeding increases the risk of recessive monogenic diseases, but it is less certain whether it contributes to the etiology of complex diseases such as schizophrenia. One way to estimate the effects of inbreeding is to examine the association between disease diagnosis and genome-wide autozygosity estimated using runs of homozygosity (ROH) in genome-wide single nucleotide polymorphism arrays. Using data for schizophrenia from the Psychiatric Genomics Consortium (n = 21,868), Keller et al. (2012) estimated that the odds of developing schizophrenia increased by approximately 17% for every additional percent of the genome that is autozygous (β = 16.1, CI(β) = [6.93, 25.7], Z = 3.44, p = 0.0006). Here we describe replication results from 22 independent schizophrenia case-control datasets from the Psychiatric Genomics Consortium (n = 39,830). Using the same ROH calling thresholds and procedures as Keller et al. (2012), we were unable to replicate the significant association between ROH burden and schizophrenia in the independent PGC phase II data, although the effect was in the predicted direction, and the combined (original + replication) dataset yielded an attenuated but significant relationship between Froh and schizophrenia (β = 4.86,CI(β) = [0.90,8.83],Z = 2.40,p = 0.02). Since Keller et al. (2012), several studies reported inconsistent association of ROH burden with complex traits, particularly in case-control data. These conflicting results might suggest that the effects of autozygosity are confounded by various factors, such as socioeconomic status, education, urbanicity, and religiosity, which may be associated with both real inbreeding and the outcome measures of interest

    Genetic correlation between amyotrophic lateral sclerosis and schizophrenia

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    A. Palotie on työryhmän Schizophrenia Working Grp Psychiat jäsen.We have previously shown higher-than-expected rates of schizophrenia in relatives of patients with amyotrophic lateral sclerosis (ALS), suggesting an aetiological relationship between the diseases. Here, we investigate the genetic relationship between ALS and schizophrenia using genome-wide association study data from over 100,000 unique individuals. Using linkage disequilibrium score regression, we estimate the genetic correlation between ALS and schizophrenia to be 14.3% (7.05-21.6; P = 1 x 10(-4)) with schizophrenia polygenic risk scores explaining up to 0.12% of the variance in ALS (P = 8.4 x 10(-7)). A modest increase in comorbidity of ALS and schizophrenia is expected given these findings (odds ratio 1.08-1.26) but this would require very large studies to observe epidemiologically. We identify five potential novel ALS-associated loci using conditional false discovery rate analysis. It is likely that shared neurobiological mechanisms between these two disorders will engender novel hypotheses in future preclinical and clinical studies.Peer reviewe
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