826 research outputs found

    Money in monetary policy design: monetary cross-checking in the New-Keynesian model

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    In the New-Keynesian model, optimal interest rate policy under uncertainty is formulated without reference to monetary aggregates as long as certain standard assumptions on the distributions of unobservables are satisfied. The model has been criticized for failing to explain common trends in money growth and inflation, and that therefore money should be used as a cross-check in policy formulation (see Lucas (2007)). We show that the New-Keynesian model can explain such trends if one allows for the possibility of persistent central bank misperceptions. Such misperceptions motivate the search for policies that include additional robustness checks. In earlier work, we proposed an interest rate rule that is near-optimal in normal times but includes a cross-check with monetary information. In case of unusual monetary trends, interest rates are adjusted. In this paper, we show in detail how to derive the appropriate magnitude of the interest rate adjustment following a significant cross-check with monetary information, when the New-Keynesian model is the central bank’s preferred model. The cross-check is shown to be effective in offsetting persistent deviations of inflation due to central bank misperceptions. Keywords: Monetary Policy, New-Keynesian Model, Money, Quantity Theory, European Central Bank, Policy Under Uncertaint

    Hypoxia stimulates proximal tubular cell matrix production via a TGF-β1-independent mechanism

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    Hypoxia stimulates proximal tubular cell matrix production via a TGF-β1-independent mechanism. Tubulointerstitial fibrosis is characterized by tubular basement membrane thickening and accumulation of interstitial extracellular matrix (ECM). Since chronic low-grade hypoxia has been implicated in the pathogenesis of fibrosis and proximal tubular epithelial cells (PTE) are sensitive to oxygen deprivation, we hypothesized that hypoxia may stimulate ECM accumulation. In human PTE, hypoxia (1% 02, 24 hr) increased total collagen production (15%), decreased MMP-2 activity (55% ± 13%; control = 100%) and increased tissue inhibitor of metalloproteinase-1 (TIMP-1) protein. Collagen IV mRNA levels decreased while collagen I mRNA increased, suggesting induction of interstitial collagen. Hypoxia-induced changes persisted on re-oxygenation with increased expression of TIMP mRNAs. A potential mediator for these effects is transforming growth factor-β1 (TGF-β1, a major pro-fibrogenic factor produced by PTE. Although hypoxia stimulated TGF-β production (2- to 3-fold), neutralizing anti-TGF-β1 antibody did not abolish the hypoxia-induced changes in gelatinase activity, TIMP-1, collagen IV or collagen I mRNA expression, implying that TGF-β1 is not the mediator. Furthermore, exogenous TGF-β1 (0 to 10 ng/ml) did not mimic hypoxia, as it stimulated MMP-2 activity and increased the expression of collagen IV, collagen I and TIMP-1 mRNA. The data suggest that hypoxia may be an important pro-fibrogenic stimulus independent of TGF-β1

    The Need to Decide If All Estrogens Are Intrinsically Similar

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    We used gene expression profiling to investigate whether the molecular effects induced by estrogens of different provenance are intrinsically similar. In this article we show that the physiologic estrogen 17β-estradiol, the phytoestrogen genistein, and the synthetic estrogen diethylstilbestrol alter the expression of the same 179 genes in the intact immature mouse uterus under conditions where each chemical has produced an equivalent gravimetric and histologic uterotrophic effect, using the standard 3-day assay protocol. Data are also presented indicating the limitations associated with comparison of gene expression profiles for different chemicals at times before the uterotrophic effects are fully realized. We conclude that the case has yet to be made for regarding synthetic estrogens as presenting a unique human hazard compared with phytoestrogens and physiologic estrogens

    A Theory of Natural Addiction

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    Economic theories of rational addiction aim to describe consumer behavior in the presence of habit-forming goods. We provide a biological foundation for this body of work by formally specifying conditions under which it is optimal to form a habit. We demonstrate the empirical validity of our thesis with an in-depth review and synthesis of the biomedical literature concerning the action of opiates in the mammalian brain and their eects on behavior. Our results lend credence to many of the unconventional behavioral assumptions employed by theories of rational addiction, including adjacent complementarity and the importance of cues, attention, and self-control in determining the behavior of addicts. We oer evidence for the special case of the opiates that "harmful" addiction is the manifestation of a mismatch between behavioral algorithms encoded in the human genome and the expanded menu of choices faced by consumers in the modern world

    Relationship between gene co-expression and probe localization on microarray slides

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    BACKGROUND: Microarray technology allows simultaneous measurement of thousands of genes in a single experiment. This is a potentially useful tool for evaluating co-expression of genes and extraction of useful functional and chromosomal structural information about genes. RESULTS: In this work we studied the association between the co-expression of genes, their location on the chromosome and their location on the microarray slides by analyzing a number of eukaryotic expression datasets, derived from the S. cerevisiae, C. elegans, and D. melanogaster. We find that in several different yeast microarray experiments the distribution of the number of gene pairs with correlated expression profiles as a function of chromosomal spacing is peaked at short separations and has two superimposed periodicities. The longer periodicity has a spacing of 22 genes (~42 Kb), and the shorter periodicity is 2 genes (~4 Kb). CONCLUSION: The relative positioning of DNA probes on microarray slides and source plates introduces subtle but significant correlations between pairs of genes. Careful consideration of this spatial artifact is important for analysis of microarray expression data. It is particularly relevant to recent microarray analyses that suggest that co-expressed genes cluster along chromosomes or are spaced by multiples of a fixed number of genes along the chromosome
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