2,501 research outputs found

    Too Many to Fail: Against Community Bank Deregulation

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    Since the 2008 financial crisis, policymakers and scholars have fixated on the problem of “too-big-to-fail” banks. This fixation, however, overlooks the historically dominant pattern in banking crises: the contemporaneous failure of many small institutions. We call this blind spot the “too-many-to-fail” problem and document how its neglect has skewed the past decade of financial regulation. In particular, we argue that, for so- called community banks, there has been a pronounced and unjustifiable shift toward deregulation, culminating in sweeping regulatory rollbacks in the Economic Growth, Regulatory Relief, and Consumer Protection Act of 2018. As this Article demonstrates, this deregulatory trend rests on three myths. First, that community banks do not contribute to systemic risk and were not central to the 2008 crisis. Second, that the Dodd-Frank Act imposed regulatory burdens that threaten the survival of the community bank sector. And third, that community banks cannot remain viable without special subsidies or regulatory advantages. While these claims have gained near- universal acceptance among legal scholars and policymakers, none of them withstands scrutiny. Contrary to the conventional wisdom, community banks were key participants in the 2008 crisis, were not uniquely burdened by postcrisis reforms, and continue to thrive economically. Dispelling these myths about the community bank sector leads to the conclusion that diligent oversight of community banks is necessary to preserve financial stability. Accordingly, this Article recommends a reversal of the community bank deregulatory trend and proposes affirmative reforms, including enhanced supervision and macroprudential stress tests, that would help mitigate systemic risks in the community bank sector

    Iterative Temporal Motion Planning for Hybrid Systems in Partially Unknown Environments

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    This paper considers the problem of motion planning for a hybrid robotic system with complex and nonlinear dynamics in a partially unknown environment given a temporal logic specification. We employ a multi-layered synergistic framework that can deal with general robot dynamics and combine it with an iterative planning strategy. Our work allows us to deal with the unknown environmental restrictions only when they are discovered and without the need to repeat the computation that is related to the temporal logic specification. In addition, we define a metric for satisfaction of a specification. We use this metric to plan a trajectory that satisfies the specification as closely as possible in cases in which the discovered constraint in the environment renders the specification unsatisfiable. We demonstrate the efficacy of our framework on a simulation of a hybrid second-order car-like robot moving in an office environment with unknown obstacles. The results show that our framework is successful in generating a trajectory whose satisfaction measure of the specification is optimal. They also show that, when new obstacles are discovered, the reinitialization of our framework is computationally inexpensive

    Histone H3K36 methylation regulates pre-mRNA splicing in Saccharomyces cerevisiae

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    Co-transcriptional splicing takes place in the context of a highly dynamic chromatin architecture, yet the role of chromatin restructuring in coordinating transcription with RNA splicing has not been fully resolved. To further define the contribution of histone modifications to pre-mRNA splicing in Saccharomyces cerevisiae, we probed a library of histone point mutants using a reporter to monitor pre-mRNA splicing. We found that mutation of H3 lysine 36 (H3K36) – a residue methylated by Set2 during transcription elongation – exhibited phenotypes similar to those of pre-mRNA splicing mutants. We identified genetic interactions between genes encoding RNA splicing factors and genes encoding the H3K36 methyltransferase Set2 and the demethylase Jhd1 as well as point mutations of H3K36 that block methylation. Consistent with the genetic interactions, deletion of SET2, mutations modifying the catalytic activity of Set2 or H3K36 point mutations significantly altered expression of our reporter and reduced splicing of endogenous introns. These effects were dependent on the association of Set2 with RNA polymerase II and H3K36 dimethylation. Additionally, we found that deletion of SET2 reduces the association of the U2 and U5 snRNPs with chromatin. Thus, our study provides the first evidence that H3K36 methylation plays a role in co-transcriptional RNA splicing in yeast

    MGARD+: Optimizing Multilevel Methods for Error-Bounded Scientific Data Reduction

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    Nowadays, data reduction is becoming increasingly important in dealing with the large amounts of scientific data. Existing multilevel compression algorithms offer a promising way to manage scientific data at scale but may suffer from relatively low performance and reduction quality. In this paper, we propose MGARD+, a multilevel data reduction and refactoring framework drawing on previous multilevel methods, to achieve high-performance data decomposition and high-quality error-bounded lossy compression. Our contributions are four-fold: 1) We propose to leverage a level-wise coefficient quantization method, which uses different error tolerances to quantize the multilevel coefficients. 2) We propose an adaptive decomposition method which treats the multilevel decomposition as a preconditioner and terminates the decomposition process at an appropriate level. 3) We leverage a set of algorithmic optimization strategies to significantly improve the performance of multilevel decomposition/recompositing. 4) We evaluate our proposed method using four real-world scientific datasets and compare with several state-of-the-art lossy compressors. Experiments demonstrate that our optimizations improve the decomposition/recompositing performance of the existing multilevel method by up to 70Ă—70 \times70x, and the proposed compression method can improve compression ratio by up to 2Ă—2 \times2x compared with other state-of-the-art error-bounded lossy compressors under the same level of data distortion

    The acyl-CoA Synthetase, pudgy, Promotes Sleep and Is Required for the Homeostatic Response to Sleep Deprivation

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    The regulation of sleep and the response to sleep deprivation rely on multiple biochemical pathways. A critical connection is the link between sleep and metabolism. Metabolic changes can disrupt sleep, and conversely decreased sleep can alter the metabolic environment. There is building evidence that lipid metabolism, in particular, is a critical part of mounting the homeostatic response to sleep deprivation. We have evaluated an acyl-CoA synthetase, pudgy (pdgy), for its role in sleep and response to sleep deprivation. When pdgy transcript levels are decreased through transposable element disruption of the gene, mutant flies showed lower total sleep times and increased sleep fragmentation at night compared to genetic controls. Consistent with disrupted sleep, mutant flies had a decreased lifespan compared to controls. pdgy disrupted fatty acid handling as pdgy mutants showed increased sensitivity to starvation and exhibited lower fat stores. Moreover, the response to sleep deprivation is reduced when compared to a control flies. When we decreased the transcript levels for pdgy using RNAi, the response to sleep deprivation was decreased compared to background controls. In addition, when the pdgy transcription is rescued throughout the fly, the response to sleep deprivation is restored. These data demonstrate that the regulation and function of acyl-CoA synthetase plays a critical role in regulating sleep and the response to sleep deprivation. Endocrine and metabolic signals that alter transcript levels of pdgy impact sleep regulation or interfere with the homeostatic response to sleep deprivation

    Stereotactic radiosurgery for single brain metastases from non-small cell lung cancer: progression of extracranial disease correlates with distant intracranial failure

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    BackgroundLimited data exist regarding management of patients with a single brain lesion with extracranial disease due to non-small cell lung cancer (NSCLC).MethodsEighty-eight consecutive patients with a single brain lesion from NSCLC in the presence of extracranial disease were treated with stereotactic radiosurgery (SRS) alone. Local control (LC), distant intracranial failure (DIF), overall survival (OS), and toxicity were assessed. The logrank test was used to identify prognostic variables.ResultsMedian OS was 10.6 months. One-year DIF was 61%; LC 89%. Treatments were delivered in 1-5 fractions to median BED10 = 60Gy. Five patients developed radionecrosis. Factors associated with shortened OS included poor performance status (PS) (p = 0.0002) and higher Recursive Partitioning Analysis class (p = 0.017). For patients with PS 0, median survival was 22 months. DIF was associated with systemic disease status (progressive vs. stable) (p = 0.0001), as was BED (p = 0.021) on univariate analysis, but only systemic disease (p = 0.0008) on multivariate analysis.ConclusionsThis study identifies a patient population that may have durable intracranial control after treatment with SRS alone. These data support the need for prospective studies to optimize patient selection for up-front SRS and to characterize the impact of DIF on patients’ quality of life

    Stereotactic radiosurgery for single brain metastases from non-small cell lung cancer: progression of extracranial disease correlates with distant intracranial failure

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    BackgroundLimited data exist regarding management of patients with a single brain lesion with extracranial disease due to non-small cell lung cancer (NSCLC).MethodsEighty-eight consecutive patients with a single brain lesion from NSCLC in the presence of extracranial disease were treated with stereotactic radiosurgery (SRS) alone. Local control (LC), distant intracranial failure (DIF), overall survival (OS), and toxicity were assessed. The logrank test was used to identify prognostic variables.ResultsMedian OS was 10.6 months. One-year DIF was 61%; LC 89%. Treatments were delivered in 1-5 fractions to median BED10 = 60Gy. Five patients developed radionecrosis. Factors associated with shortened OS included poor performance status (PS) (p = 0.0002) and higher Recursive Partitioning Analysis class (p = 0.017). For patients with PS 0, median survival was 22 months. DIF was associated with systemic disease status (progressive vs. stable) (p = 0.0001), as was BED (p = 0.021) on univariate analysis, but only systemic disease (p = 0.0008) on multivariate analysis.ConclusionsThis study identifies a patient population that may have durable intracranial control after treatment with SRS alone. These data support the need for prospective studies to optimize patient selection for up-front SRS and to characterize the impact of DIF on patients’ quality of life
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