Debt maturity, risk, and asymmetric information

We test the implications of Flannery’s (1986) and Diamond’s (1991) models concerning the effects of risk and asymmetric information in determining debt maturity, and we examine the overall importance of informational asymmetries in debt maturity choices. We employ data from more than 6,000 commercial loans from 53 large U.S. banks. Our results for low-risk firms are consistent with the predictions of both theoretical models, but our findings for high-risk firms conflict with the predictions of Diamond’s model and with much of the empirical literature. Our findings also suggest a strong quantitative role for asymmetric information in explaining debt maturity.

Why do borrowers pledge collateral? new empirical evidence on the role of asymmetric information

An important theoretical literature motivates collateral as a mechanism that mitigates adverse selection, credit rationing, and other inefficiencies that arise when borrowers hold ex ante private information. There is no clear empirical evidence regarding the central implication of this literature—that a reduction in asymmetric information reduces the incidence of collateral. We exploit exogenous variation in lender information related to the adoption of an information technology that reduces ex ante private information, and compare collateral outcomes before and after adoption. Our results are consistent with this central implication of the private-information models and support the empirical importance of this theory.

Does Function Follow Organizational Form? Evidence From the Lending Practices of Large and Small Banks

Theories based on incomplete contracting suggest that small organizations may do better than large organizations in activities that require the processing of soft information. We explore this idea in the context of bank lending to small firms, an activity that is typically thought of as relying heavily on soft information. We find that large banks are less willing than small banks to lend to informationally 'difficult' credits, such as firms that do not keep formal financial records. Moreover, controlling for the endogeneity of bank-firm matching, large banks lend at a greater distance, interact more impersonally with their borrowers, have shorter and less exclusive relationships, and do not alleviate credit constraints as effectively. All of this is consistent with small banks being better able to collect and act on soft information than large banks.

Does Function Follow Organzizational Form? Evidence From the Lending Practices of Large and Small Banks

Theories based on incomplete contracting suggest that small organizations may do better than large organizations in activities that require the processing of soft information. We explore this idea in the context of bank lending to small firms, an activity that is typically thought of as relying heavily on soft information. We find that large banks are less willing than small banks to lend to informationally “difficult†credits, such as firms that do not keep formal financial records. Moreover, controlling for the endogeneity of bank-firm matching, large banks lend at a greater distance, interact more impersonally with their borrowers, have shorter and less exclusive relationships, and do not alleviate credit constraints as effectively. All of this is consistent with small banks being better able to collect and act on soft information than large banks. The opinions in this paper do not necessarily reflect those of the Federal Reserve Board or its staff. This work has been supported by the National Science Foundation (Rajan, Stein), and the George J. Stigler Center for Study of the State and Economy (Rajan). Thanks also to seminar participants at Yale, the Federal Reserve Bank of New York, Tulane, Babson, the University of Illinois, the Federal Reserve Bank of Chicago Bank Structure Conference, the NBER and the Western Finance Association meetings, as well as to Abhijit Banerjee, Michael Kremer, David Scharfstein, Andrei Shleifer, Greg Udell, Christopher Udry and James Weston for helpful comments and suggestions.

Metabolomics of ApcMin/+ mice genetically susceptible to intestinal cancer

BACKGROUND: To determine how diets high in saturated fat could increase polyp formation in the mouse model of intestinal neoplasia, Apc( Min/+ ), we conducted large-scale metabolome analysis and association study of colon and small intestine polyp formation from plasma and liver samples of Apc( Min/+ ) vs. wild-type littermates, kept on low vs. high-fat diet. Label-free mass spectrometry was used to quantify untargeted plasma and acyl-CoA liver compounds, respectively. Differences in contrasts of interest were analyzed statistically by unsupervised and supervised modeling approaches, namely Principal Component Analysis and Linear Model of analysis of variance. Correlation between plasma metabolite concentrations and polyp numbers was analyzed with a zero-inflated Generalized Linear Model. RESULTS: Plasma metabolome in parallel to promotion of tumor development comprises a clearly distinct profile in Apc( Min/+ ) mice vs. wild type littermates, which is further altered by high-fat diet. Further, functional metabolomics pathway and network analyses in Apc( Min/+ ) mice on high-fat diet revealed associations between polyp formation and plasma metabolic compounds including those involved in amino-acids metabolism as well as nicotinamide and hippuric acid metabolic pathways. Finally, we also show changes in liver acyl-CoA profiles, which may result from a combination of Apc( Min/+ )-mediated tumor progression and high fat diet. The biological significance of these findings is discussed in the context of intestinal cancer progression. CONCLUSIONS: These studies show that high-throughput metabolomics combined with appropriate statistical modeling and large scale functional approaches can be used to monitor and infer changes and interactions in the metabolome and genome of the host under controlled experimental conditions. Further these studies demonstrate the impact of diet on metabolic pathways and its relation to intestinal cancer progression. Based on our results, metabolic signatures and metabolic pathways of polyposis and intestinal carcinoma have been identified, which may serve as useful targets for the development of therapeutic interventions

Metabolomics of ApcMin/+\u3c/sup\u3e Mice Genetically Susceptible to Intestinal Cancer

Background: To determine how diets high in saturated fat could increase polyp formation in the mouse model of intestinal neoplasia, ApcMin/+, we conducted large-scale metabolome analysis and association study of colon and small intestine polyp formation from plasma and liver samples of ApcMin/+ vs. wild-type littermates, kept on low vs. high-fat diet. Label-free mass spectrometry was used to quantify untargeted plasma and acyl-CoA liver compounds, respectively. Differences in contrasts of interest were analyzed statistically by unsupervised and supervised modeling approaches, namely Principal Component Analysis and Linear Model of analysis of variance. Correlation between plasma metabolite concentrations and polyp numbers was analyzed with a zero-inflated Generalized Linear Model.Results: Plasma metabolome in parallel to promotion of tumor development comprises a clearly distinct profile in ApcMin/+ mice vs. wild type littermates, which is further altered by high-fat diet. Further, functional metabolomics pathway and network analyses in ApcMin/+ mice on high-fat diet revealed associations between polyp formation and plasma metabolic compounds including those involved in amino-acids metabolism as well as nicotinamide and hippuric acid metabolic pathways. Finally, we also show changes in liver acyl-CoA profiles, which may result from a combination of ApcMin/+-mediated tumor progression and high fat diet. The biological significance of these findings is discussed in the context of intestinal cancer progression.Conclusions: These studies show that high-throughput metabolomics combined with appropriate statistical modeling and large scale functional approaches can be used to monitor and infer changes and interactions in the metabolome and genome of the host under controlled experimental conditions. Further these studies demonstrate the impact of diet on metabolic pathways and its relation to intestinal cancer progression. Based on our results, metabolic signatures and metabolic pathways of polyposis and intestinal carcinoma have been identified, which may serve as useful targets for the development of therapeutic interventions. © 2014 Dazard et al.; licensee BioMed Central Ltd

Quality of Life in Endometrial Cancer Survivors: What Does Obesity Have to Do with It?

Objective. Most women with type I endometrial cancer (EC) are obese, increasing the risk of morbidity and mortality in this population. The study objective was to evaluate the impact of obesity on quality of life (QOL) and general health status in EC survivors with early-stage disease. Methods. A prospective ancillary analysis of stage I/II EC survivors. The association of BMI with QOL questionnaire variables measured with the functional assessment of cancer therapy (subscales: physical (PWB), functional (FWB), social, and emotional well-being) and the physical (PCS) and mental component summary subscales of the short-form medical outcomes survey was determined. Results. 152 women completed both questionnaires; 81% were obese. After multiple linear regression, BMI was inversely associated with PWB (P = .001), FWB (P = 0.048), and PCS (P = .001). Conclusions. Despite the good prognosis associated with early-stage EC, QOL, and physical health are not optimized in obese survivors. This paper highlights the importance of incorporating health-related QOL assessments and obesity interventions during the survivorship period

Complex multimorbidity and health outcomes in older adult cancer survivors

Objective: To characterize complex multimorbidity among cancer survivors and evaluate the association between cancer survivorship, time since cancer diagnosis, and self-reported fair/poor health, self-rated worse health in 2 years, and 2-year mortality. Methods: We used the 2010–2012 Health and Retirement Study. Cancer survivors were individuals who reported a (nonskin) cancer diagnosis 2 years or more before the interview. We defined complex multimorbidity as the co-occurrence of chronic conditions, functional limitations, and/or geriatric syndromes. In addition to descriptive analyses, we used logistic regression to evaluate the independent association between cancer survivor status and health outcomes. We also examined whether cancer survivorship differed by the number of years since diagnosis. Results: Among 15,808 older adults (age ≥50 years), 11.8% were cancer survivors. Compared with cancer-free individuals, a greater percentage of cancer survivors had complex multimorbidity: co-occurring chronic conditions, functional limitations, and geriatric syndromes. Cancer survivorship was significantly associated with self-reported fair/poor health, self-rated worse health in 2 years, and 2-year mortality. These effects declined with the number of years since diagnosis for fair/ poor health and mortality but not for self-rated worse health. Conclusion: Cancer survivor status is independently associated with more complex multimorbidity, and with worse health outcomes. These effects attenuate with time, except for patient perception of being in worse health