Core Polarization Effects in (p,p′) Reactions

McManus, Hugh

doi:10.1007/978-1-4684-8337-6_31

Cited by 2 publications

(3 citation statements)

References 15 publications

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“…Metal binding to the a7 161-172 domain Terbium ions replace calcium in most metal binding proteins/peptides (Rubsamen et al, 1976a,b;McManus et al, 1990;D'Souza et al, 1994), and Tb3+-protein complexes can be detected by fluorescence resonance energy transfer from these sites. The synthetic peptide a7 160-174, which comprises a full loop V, contains two determined in the absence and presence of calcium, were indistinguishable.…”

Section: Resultsmentioning

confidence: 99%

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Identification of calcium binding sites that regulate potentiation of a neuronal nicotinic acetylcholine receptor.

et al. 1996

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The divalent cation calcium potentiates the physiological response of neuronal nicotinic receptors to agonists by enhancing ionic current amplitudes, apparent agonist affinity and cooperativity. Here we show that mutations in several consensus Ca2+ binding sequences from the N‐terminal domain of the neuronal alpha 7 nicotinic acetylcholine receptor alter Ca2+ potentiation of the alpha 7‐V201–5HT3 chimera. Mutations E18Q or E44Q abolish calcium‐enhanced agonist affinity but preserve the calcium increase of plateau current amplitudes and cooperativity. On the other hand, mutations of amino acids belonging to the 12 amino acid canonical domain (alpha 7 161–172) alter all features of potentiation by enhancing (D163, S169), reducing (E161, S165, Y167) or abolishing (E172) calcium effects on ionic current amplitudes and agonist affinity. Introduction of the alpha 7 161–172 domain in the calcium insensitive 5‐hydroxytryptamine (5HT3) serotoninergic receptor results in a receptor activated by 5HT and potentiated by calcium. In vitro terbium fluorescence studies with an alpha 7 160–174 peptide further show that mutation E172Q also alters in vitro calcium binding. Data are consistent with the occurrence of distinct categories of regulatory calcium binding sites, among which the highly conserved (alpha 7 161–172) domain may simultaneously contribute to calcium and agonist binding.

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Section: Resultsmentioning

confidence: 99%

“…Fluorescence measurements were performed, as described in McManus et al (1990), in 10 mM Tris-HCl buffer (pH 7.2) on a Perkin Elmer LS-5B spectrofluorimeter, with an excitation wavelength of 285 nm.…”

Section: Fluorescence Measurementsmentioning

confidence: 99%

Identification of calcium binding sites that regulate potentiation of a neuronal nicotinic acetylcholine receptor.

et al. 1996

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“…In August 2015, St. Luke's Family Medicine Residency Program in Bethlehem decided to study its resident burnout and wellness in preparation for a faculty development on physician burnout. Residents were assessed with the abbreviated Maslach Burnout Inventory (aMBI) [23,29,30]. The aMBI assesses the following three components: emotional exhaustion, depersonalization, and personal accomplishment.…”

Section: Curriculummentioning

confidence: 99%

Implementing Wellness Curriculum in Residency

Lam¹,

Black²

2019

Contemporary Topics in Graduate Medical Education

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Transitions from medical school training to residency and then on to practice can be very challenging. An important but often overlooked aspect of medical education is the development of strategies to improve and sustain individual well-being so that trainees can successfully complete their training and transition into practice. In this chapter, we will be discussing ways in which physician and trainee well-being can be objectively assessed through the use of a burnout and work engagement index, as well as components of a wellness curriculum that can help to maintain and improve physician well-being across the continuum of training. Establishing a framework and wellness curriculum can help to prevent physician burnout and improve physician and trainee work engagement and well-being.

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Core Polarization Effects in (p,p′) Reactions

Cited by 2 publications

References 15 publications

Identification of calcium binding sites that regulate potentiation of a neuronal nicotinic acetylcholine receptor.

Identification of calcium binding sites that regulate potentiation of a neuronal nicotinic acetylcholine receptor.

Implementing Wellness Curriculum in Residency

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