89 research outputs found

    The Zoning in and the Zoning out of the Elderly: Emerging Community and Communication Patterns

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    Increasingly, senior only residences are zoning seniors out of mainstream residential areas and into segregated living and mature communities. Senior gated communities are variations on a theme of gated communities in which lifestyle is packaged and sold. Active adult retirement communities exclude the young and offer active lifestyle living, with diverse levels of senior living choices. Such an approach contrasts with policies designed to encourage aging in place. It is also distinct from Golden Age Zoning districts designed to allow affordable housing for senior citizens in a public/private partnership. Some towns have zoned public parks to establish areas for children distinct from the elderly. Simultaneously, more and more older adults are embracing the modern media environment. According to the Pew Research Center, baby boomers and seniors are the fastest growing group of social networking website users to connect with family, friends from the past, and seeking information and support with medical issues. This paper explores the person/place relationship and issues associated with design for the social needs of an aging in a media filled world

    Glucagon receptor family in GtoPdb v.2023.1

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    The glucagon family of receptors (nomenclature as agreed by the NC-IUPHAR Subcommittee on the Glucagon receptor family [165]) are activated by the endogenous peptide (27-44 aa) hormones glucagon, glucagon-like peptide 1, glucagon-like peptide 2, glucose-dependent insulinotropic polypeptide (also known as gastric inhibitory polypeptide), GHRH and secretin. One common precursor (GCG) generates glucagon, glucagon-like peptide 1 and glucagon-like peptide 2 peptides [121]. For a recent review on the current understanding of the structures of GLP-1 and GLP-1R, the molecular basis of their interaction, and the associated signaling events see de Graaf et al., 2016 [90]

    Glucagon receptor family (version 2019.4) in the IUPHAR/BPS Guide to Pharmacology Database

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    The glucagon family of receptors (nomenclature as agreed by the NC-IUPHAR Subcommittee on the Glucagon receptor family [159]) are activated by the endogenous peptide (27-44 aa) hormones glucagon, glucagon-like peptide 1, glucagon-like peptide 2, glucose-dependent insulinotropic polypeptide (also known as gastric inhibitory polypeptide), GHRH and secretin. One common precursor (GCG) generates glucagon, glucagon-like peptide 1 and glucagon-like peptide 2 peptides [116]. For a recent review on review the current understanding of the structures of GLP-1 and GLP-1R, the molecular basis of their interaction, and the signaling events associated with it, see de Graaf et al., 2016 [87]

    Glucagon receptor family in GtoPdb v.2021.3

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    The glucagon family of receptors (nomenclature as agreed by the NC-IUPHAR Subcommittee on the Glucagon receptor family [162]) are activated by the endogenous peptide (27-44 aa) hormones glucagon, glucagon-like peptide 1, glucagon-like peptide 2, glucose-dependent insulinotropic polypeptide (also known as gastric inhibitory polypeptide), GHRH and secretin. One common precursor (GCG) generates glucagon, glucagon-like peptide 1 and glucagon-like peptide 2 peptides [119]. For a recent review on the current understanding of the structures of GLP-1 and GLP-1R, the molecular basis of their interaction, and the associated signaling events see de Graaf et al., 2016 [89]

    Reproducibility of histopathological findings in experimental pathology of the mouse: a sorry tail

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    Reproducibility of in vivo\textit{in vivo} research using the mouse as a model organism depends on many factors, including experimental design, strain or stock, experimental protocols, and methods of data evaluation. Gross and histopathology are often the endpoints of such research and there is increasing concern about the accuracy and reproducibility of diagnoses in the literature. To reproduce histopathological results, the pathology protocol, including necropsy methods and slide preparation, should be followed by interpretation of the slides by a pathologist familiar with reading mouse slides and familiar with the consensus medical nomenclature used in mouse pathology. Likewise, it is important that pathologists are consulted as reviewers of manuscripts where histopathology is a key part of the investigation. The absence of pathology expertise in planning, executing and reviewing in vivo\textit{in vivo} research using mice leads to questionable pathology-based findings and conclusions from studies, even in high-impact journals. We discuss the various aspects of this problem, give some examples from the literature and suggest solutions.This work was supported in part by US National Institutes of Health grants R01 AR049288, CA089713 and R21 AR063781 (to J.P.S.) and by The Warden and Fellows of Robinson College, Cambridge (to P.N.S.)

    Mudança organizacional: uma abordagem preliminar

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    Pojav konvergence: tehnologija, industrija in regulacija

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    GATEWAY MEDIATED INTERSYSTEM CROSSING IN C2H2C_{2}H_{2}

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    Author Institution: Department of Chemistry, Massachusetts Institute of Technology; Department of Chemistry, University of California at Santa BarbaraLaser Excited Metastable (LEM) Spectra of C2H2C_{2}H_{2} indicate that a single vibrational level of the T3T_{3} surface couples the 3ν33\nu_{3} level of the S1S_{1} surface to a dense manifold of T1T_{1} and T2T_{2} states. In the proposed coupling mechanism, Gateway Mediated Intersystem Crossing (GMISC), the spin-orbit matrix element between the 3ν3  S13\nu_{3}\;S_{1} state and one near-degenerate vibrational level of the T3T_{3} state is much larger than the direct interaction between 3ν3  S13\nu_{3}\;S_{1} and any other T1T_{1} or T2T_{2} level. This is due to a near degeneracy between the S1S_{1} and T3T_{3} vibrational states and a nearby S1−T3S_{1}-T_{3} surface crossing. The S1S_{1} state interacts with the background triplet states indirectly through T3T_{3} via T3∼T2,1T_{3} \sim T_{2,1} matrix elements. Evidence for this mechanism includes a shift between the LIF and LEM spectra, an interference effect near J=5J = 5 in LEM spectrum, and the strength of the LEM signal for the 3ν33\nu_{3} band relative to other bands in the Aˉ−Xˉ\bar{A}-\bar{X} band system. Other experiments in which S1∼(T3,2,1,S0)S_{1} \sim (T_{3,2,1,} S_{0}) interactions were observed will be discussed in the context of the GMISC model
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