38 research outputs found

    Foreign Savings, Financialization and Minsky: How External Capital Flows Pave the Way for Financial Instability in the Face of Increasing Risk

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    Minsky\u27s Financial Instability Hypothesis has not come without its fair share of criticism. Much ado about Minsky\u27s endogenous business cycle theory stems from a model where boom-time profit opportunities indelibly encourage firms to finance investment by leveraging their fixed capital assets against their internal liquidity. Opposition to Minsky often points to two distinct circumstances that might discourage the external finance of investment: a rise in effective demand and increasing risk. A rise in effective demand can increase the retained earnings of a firm providing more capital to internally finance investment and investment financed from retained earning is less risky than investment financed with debt. This has fueled criticism of Minsky\u27s framework as having controversial assumptions that discourage rather than encourage financial instability. This paper examines Minsky\u27s Financial Instability Hypothesis from a savings and debt point of view in order to determine whether or not Minsky\u27s financial crisis theory holds up to its critics. It looks at the peculiar role of foreign savings in creating an incentive for financialization and how that engenders financial instability. Moreover, I hope to display a theoretical argument that unifies much of the criticism of Minsky with the valuable contributions he has made to economic theory

    Age-Specific Estimates Indicate Potential Deleterious Capture Effects and Low Survival of Stocked Juvenile Colorado Pikeminnow (\u3ci\u3ePtychocheilus lucius\u3c/i\u3e)

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    Hatcheries and stocking programs have become necessary to repatriate or augment populations of imperiled fishes worldwide. Over nearly two decades, millions of endangered juvenile Colorado Pikeminnow Ptychocheilus lucius have been stocked into the San Juan River (Colorado, New Mexico, and Utah); however, recruitment of these individuals to adult life stages (age ā‰„6) remains low. Using a markā€“recapture data set collected from annual riverwide electrofishing efforts between 2003 and 2016, we investigated apparent survival and capture probabilities of stocked Colorado Pikeminnow to identify ageā€specific bottlenecks contributing to this lack of recruitment. With relatively high capture rates, which averaged between 0.34 and 0.39 for the first 2 years after an individual\u27s first encounter, our results indicated that survival was consistently less than 0.25 for young ageā€groups (i.e., ages 1ā€“3), and no appreciable increase in survival occurred until fish had been in the river for at least 3 years (i.e., age ā‰„4+). Although age and capture effects were confounded for most ageā€groups, capture appeared to reduce apparent survival for ageā€2 fish by approximately 50%. The confounding effects of age, a completely hatcheryā€origin population, and extensive environmental alterations to the San Juan River make it difficult to disentangle factors associated with this overall reduced juvenile survival

    Doctorsā€™ Pharma Industry Ties and Medicare Prescribing

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    Companies spend more than a billion dollars annually to market their treatments, and a significant portion is targeted at doctors. We found that having an industry interaction for a given drug was correlated with higher prescribing volume for that drug

    TOR Complex 2-Ypk1 Signaling Maintains Sphingolipid Homeostasis by Sensing and Regulating ROS Accumulation

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    Reactive oxygen species (ROS) are produced during normal metabolism and can function as signaling molecules. However, ROS at elevated levels can damage cells. Here, we identify the conserved target of rapamycin complex 2 (TORC2)/Ypk1 signaling module as an important regulator of ROS in the model eukaryotic organism, S.Ā cerevisiae. We show that TORC2/Ypk1 suppresses ROS produced both by mitochondria as well as by nonmitochondrial sources, including changes in acidification of the vacuole. Furthermore, we link vacuole-related ROS to sphingolipids, essential components of cellular membranes, whose synthesis is also controlled by TORC2/Ypk1 signaling. In total, our data reveal that TORC2/Ypk1 act within a homeostatic feedback loop to maintain sphingolipid levels and that ROS are a critical regulatory signal within this system. Thus, ROS sensing and signaling by TORC2/Ypk1 play a central physiological role in sphingolipid biosynthesis and in the maintenance of cell growth and viability

    The Effects of Lifetime Estrogen Exposure on Breast Epigenetic Age

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    BACKGROUND: Estrogens are thought to contribute to breast cancer risk through cell cycling and accelerated breast aging. We hypothesize that lifetime estrogen exposure drives early epigenetic breast aging observed in healthy women. In this study, we examined associations between hormonal factors and epigenetic aging measures in healthy breast tissues. METHODS: We extracted DNA from breast tissue specimens from 192 healthy female donors to the Susan G. Komen Tissue Bank at the Indiana University Simon Cancer Center. Methylation experiments were performed using the Illumina EPIC 850K array platform. Age-adjusted regression models were used to examine for associations between factors related to estrogen exposure and five DNA methylation-based estimates: Grim age, Pan-tissue age, Hannum age, Phenotypic age, and Skin and Blood Clock age. RESULTS: Women were aged 19ā€“90 years, with 95 pre-menopausal, and 97 nulliparous women. The age difference (Grim age - chronologic age) was higher at earlier ages close to menarche. We found significant associations between earlier age at menarche and age-adjusted accelerations according to the Grim clock, the Skin and Blood clock, and between higher body mass index (BMI) and age-adjusted accelerations in the Grim clock, Hannum clock, Phenotypic clock, and Skin and Blood clock. CONCLUSION: Earlier age at menarche and higher BMI are associated with elevations in DNA methylation-based age estimates in healthy breast tissues, suggesting that cumulative estrogen exposure drives breast epigenetic aging. IMPACT: Epigenetic clock measures may help advance inquiry into the relationship between accelerated breast tissue aging and an elevated incidence of breast cancer in younger women
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