16 research outputs found

    Lending to Low- and Moderate-Income Borrowers: The Impact of Lender Board Composition, Stakeholder Outreach, and Regulatory Environment

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    Increasing homeownership has been a long-standing public policy goal in the United States (Rohe & Watson, 2007). Historically low- and moderate-income borrowers and minority groups have had a more difficult time gaining access to the mortgage lending market (Marsico, 2005). The market for mortgage lending is large, complex, and subject to a patchwork of regulations. It has also undergone significant changes over the last few decades. This study explores how organizational level factors (i.e., board composition with respect to community influentials and stakeholder outreach) and institutional factors influence rates of lending to low- and moderate-income borrowers. A two level hierarchical model including both fixed and random effects was used to analyze publicly available data provided by lenders under the Home Mortgage Disclosure Act. The results of the study were mixed. Higher peer levels of lending as well as being subject to the Community Reinvestment Act were associated with increased lending to low- and moderate-income borrowers. A greater number of activities toward certain stakeholders, surprisingly, was associated with a decrease in rates of lending to low- and moderate-income borrowers. There was no support for the presence of community influentials on the board affecting rates of lending to low- and moderate-income borrowers

    Reflections

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    An Allosteric Anti-tryptase Antibody for the Treatment of Mast Cell-Mediated Severe Asthma

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    Severe asthma patients with low type 2 inflammation derive less clinical benefit from therapies targeting type 2 cytokines and represent an unmet need. We show that mast cell tryptase is elevated in severe asthma patients independent of type 2 biomarker status. Active β-tryptase allele count correlates with blood tryptase levels, and asthma patients carrying more active alleles benefit less from anti-IgE treatment. We generated a noncompetitive inhibitory antibody against human β-tryptase, which dissociates active tetramers into inactive monomers. A 2.15 Å crystal structure of a β-tryptase/antibody complex coupled with biochemical studies reveal the molecular basis for allosteric destabilization of small and large interfaces required for tetramerization. This anti-tryptase antibody potently blocks tryptase enzymatic activity in a humanized mouse model, reducing IgE-mediated systemic anaphylaxis, and inhibits airway tryptase in Ascaris-sensitized cynomolgus monkeys with favorable pharmacokinetics. These data provide a foundation for developing anti-tryptase as a clinical therapy for severe asthma
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