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James W. Maas

Researcher at Washington University in St. Louis

Publications -  36
Citations -  3415

James W. Maas is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Normetanephrine & Homovanillic acid. The author has an hindex of 25, co-authored 36 publications receiving 3330 citations. Previous affiliations of James W. Maas include University of California, San Francisco.

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Pretreatment DST and hypothalamic-pituitary-adrenocortical function in depressed patients and comparison groups. A multicenter study.

TL;DR: Pretreatment measures of hypothalamic-pituitary-adrenocortical (HYPAC) function in depressed, manic, and healthy normal subjects showed that nonsuppression on the dexamethasone suppression test (DST) had less positive predictive value for major diagnostic category and was more frequent in normals than recently reported, although it was yet more Frequent in depressed patients.
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Catecholamine Metabolism, Depressive Illness, and Drug Response

TL;DR: Patients who responded best excreted greater quantities of normetanephrine and MHPG during drug treament, relative to the predrug period, and those patients who responded least well had a decrement in the excretion of these two metabolities.
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Biogenic Amines and Depression: Biochemical and Pharmacological Separation of Two Types of Depression

TL;DR: The biochemical heterogeneity of human depression has implications for both investigators and clinicians, and may account for disparate findings in biological studies of patients with affective disorders as discussed by the authors, which may explain the disparate findings.
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Genetic Elimination of Behavioral Sensitization in Mice Lacking Calmodulin-Stimulated Adenylyl Cyclases

TL;DR: It is shown that wild-type, AC1, AC8, or AC1&8 double knockout mice were indistinguishable in tests of acute pain, whereas behavioral responses to peripheral injection of two inflammatory stimuli, formalin and complete Freund's adjuvant, were reduced or abolished in AC1 &8 DKO mice.
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Mutations in the Gene PRRT2 Cause Paroxysmal Kinesigenic Dyskinesia with Infantile Convulsions

TL;DR: Four truncating mutations involving the gene PRRT2 in the vast majority of well-characterized families with PKD/IC are identified, leading ultimately to neuronal hyperexcitability that manifests in vivo as PKd/IC.