650 research outputs found

    How the credit channel works: differentiating the bank lending channel and the balance sheet channel

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    The credit channel of monetary policy transmission operates through changes in lending. To examine this channel, we explore how movements in the real federal funds rate affect bank lending. Using data on individual loans from the Survey of Terms of Bank Lending, we are able to differentiate two ways the credit channel can work: by affecting overall bank lending (the bank lending channel) and by affecting the allocation of loans (the balance sheet channel). We find evidence consistent with the operation of both internal credit channels. During periods of tight monetary policy, banks adjust their stock of loans by reducing the maturity of loan originations and they reallocate their short-term loan supply from small firms to large firms. These results are stronger for large banks than for small banks.Monetary policy ; Bank loans

    Can the Market Add and Subtract? Mispricing in Tech Stock Carve-Outs

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    Recent equity carve-outs in US technology stocks appear to violate a basic premise of financial theory: identical assets have identical prices. In our 1998-2000 sample, holders of a share of company A are expected to receive x shares of company B, but the price of A is less than x times the price of B. A prominent example involves 3Com and Palm. Arbitrage does not eliminate these blatant mispricing due to short sale constraints, so that B is overpriced but expensive or impossible to sell short. Evidence from options prices shows that shorting costs are extremely high, eliminating exploitable arbitrage opportunities.

    No Sunshine When She’s Gone: The Shared Experiences of African American Men Who Have Undergone Divorce

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    The purpose of this transcendental phenomenological study is to chronicle the shared experiences of working-class/middle-class African American men who have gone through a divorce in Hampton Roads, Virginia. Vygotsky’s sociocultural theory of cognitive development, which highlights the essential roles of language and culture, and Kurt Lewin’s field theory, which suggests the field as a practical framework for researching divorce, guided this study. The research questions were as follows: How do working-class/middle-class African American men describe their experience with divorce? How do participants describe their initial understanding of the divorce process? How do participants describe the level of social support they received during the divorce process? How do participants describe the effect divorce had on their sense of self-actualization (motivation)? What benefits do participants describe that arose from going through their divorce? The participants were divorced African American men who were married for a minimum of two years. Data was collected through semi-structured interviews, focus groups, and cognitive representations. Data was analyzed utilizing Moustakas’ (1994) standards for transcendental phenomenology to synthesize the crux of the participants’ recollections. Two major themes emanated through data analysis: (a) divorce is a multifarious emotional ordeal that is exacerbated by a lack of knowledge of the divorce process, and (b) elevated levels of diverse post-traumatic growth and self-actualization in the wake of divorce due to high levels of social support. Data analysis revealed three subthemes of the primary theme - a convolution of feelings, a painful and horrific experience, and stress compounded by a negligible understanding of the divorce process. Two subthemes emerged from theme two: the importance of multi-layered social support and self-actualization as evidenced by positive post-divorce transformations

    Richard Askin and Towanann Payne in a Junior Recital

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    This is the program for the joint junior recital of tenor Richard Askin and soprano Towanann Payne. The recital was held on December 7, 1972, at 5:00. Cannon Lamont accompanied Askin on piano; Peggy Pearson accompanied Towanann Payne on piano

    The Enduring Importance of Animal Models in Understanding Periodontal Disease

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    Whereas no single animal model can reproduce the complexity of periodontitis, different aspects of the disease can be addressed by distinct models. Despite their limitations, animal models are essential for testing the biological significance of in vitro findings and for establishing cause-and-effect relationships relevant to clinical observations, which are typically correlative. We provide evidence that animal-based studies have generated a durable framework for dissecting the mechanistic basis of periodontitis. These studies have solidified the etiologic role of bacteria in initiating the inflammatory response that leads to periodontal bone loss and have identified key mediators (IL-1, TNF, prostaglandins, complement, RANKL) that induce inflammatory breakdown. Moreover, animal studies suggest that dysbiosis, rather than individual bacterial species, are important in initiating periodontal bone loss and have introduced the concept that organisms previously considered commensals can play important roles as accessory pathogens or pathobionts. These studies have also provided insight as to how systemic conditions, such as diabetes or leukocyte adhesion deficiency, contribute to tissue destruction. In addition, animal studies have identified and been useful in testing therapeutic targets

    The emerging oral pathogen, Filifactor alocis, modulates antimicrobial responses of primed human neutrophils.

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    Almost 50% of the adult population older than 30 years of age suffers from some form of periodontitis, a chronic inflammatory disease of the periodontal tissue caused by microbial subversion of the host immune response. Neutrophils are the most abundant leukocyte present in the oral mucosa. In periodontitis, periodontal pathogens have developed strategies to evade neutrophil antimicrobial responses and promote bacterial growth. Among these oral pathogens is Filifactor alocis which can modulate neutrophils’ antimicrobial responses by preventing phagosome maturation. During inflammation, neutrophils that reach the gingival tissue are primed by cytokines and chemokines. However, the response of primed human neutrophils to F. alocis is currently unknown. To address this gap in knowledge, human neutrophils were primed with TNF-α, an established priming agent, and the kinetics of phagocytosis and intracellular ROS production in response to serum opsonized F. alocis were tested. Our results showed a significant increase in phagocytosis of F. alocisby TNF-α-primed neutrophils compared to unprimed cells. However, the significant increase in bacteria uptake was not accompanied by increased ROS production. F. alocis significantly downregulated the respiratory burst response in human neutrophils independently of priming with TNF-α. Interestingly, priming of neutrophils with IL-8 did not result in a significant increase in phagocytosis of F. alocis, but IL-8-primed neutrophils did have a similar ROS phenotype to TNF-α-primed neutrophils. This suggests dome ability of F. alcois to modulate the phagocytic ability of IL-8-primed neutrophils. Future studies will aim to characterize F. alocis’ virulence factors that modulate neutrophil responses

    Developing Learning-Based Models for Occupant Centric Control

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    Pathway analysis for intracellular Porphyromonas gingivalis using a strain ATCC 33277 specific database

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    <p>Abstract</p> <p>Background</p> <p><it>Porphyromonas gingivalis </it>is a Gram-negative intracellular pathogen associated with periodontal disease. We have previously reported on whole-cell quantitative proteomic analyses to investigate the differential expression of virulence factors as the organism transitions from an extracellular to intracellular lifestyle. The original results with the invasive strain <it>P. gingivalis </it>ATCC 33277 were obtained using the genome sequence available at the time, strain W83 [GenBank: <ext-link ext-link-id="AE015924" ext-link-type="gen">AE015924</ext-link>]. We present here a re-processed dataset using the recently published genome annotation specific for strain ATCC 33277 [GenBank: <ext-link ext-link-id="AP009380" ext-link-type="gen">AP009380</ext-link>] and an analysis of differential abundance based on metabolic pathways rather than individual proteins.</p> <p>Results</p> <p>Qualitative detection was observed for 1266 proteins using the strain ATCC 33277 annotation for 18 hour internalized <it>P. gingivalis </it>within human gingival epithelial cells and controls exposed to gingival cell culture medium, an improvement of 7% over the W83 annotation. Internalized cells showed increased abundance of proteins in the energy pathway from asparagine/aspartate amino acids to ATP. The pathway producing one short chain fatty acid, propionate, showed increased abundance, while that of another, butyrate, trended towards decreased abundance. The translational machinery, including ribosomal proteins and tRNA synthetases, showed a significant increase in protein relative abundance, as did proteins responsible for transcription.</p> <p>Conclusion</p> <p>Use of the ATCC 33277 specific genome annotation resulted in improved proteome coverage with respect to the number of proteins observed both qualitatively in terms of protein identifications and quantitatively in terms of the number of calculated abundance ratios. Pathway analysis showed a significant increase in overall protein synthetic and transcriptional machinery in the absence of significant growth. These results suggest that the interior of host cells provides a more energy rich environment compared to the extracellular milieu. Shifts in the production of cytotoxic fatty acids by intracellular <it>P. gingivalis </it>may play a role in virulence. Moreover, despite extensive genomic re-arrangements between strains W83 and 33277, there is sufficient sequence similarity at the peptide level for proteomic abundance trends to be largely accurate when using the heterologous strain annotated genome as the reference for database searching.</p
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