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Lisa M. Muglia

Researcher at Cincinnati Children's Hospital Medical Center

Publications -  21
Citations -  1717

Lisa M. Muglia is an academic researcher from Cincinnati Children's Hospital Medical Center. The author has contributed to research in topics: Adenylyl cyclase & Glucocorticoid. The author has an hindex of 16, co-authored 20 publications receiving 1485 citations. Previous affiliations of Lisa M. Muglia include Vanderbilt University & Washington University in St. Louis.

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Journal ArticleDOI

Genetic Associations with Gestational Duration and Spontaneous Preterm Birth

TL;DR: It is found that variants at the EBF1, EEFSEC, AGTR2, WNT4, ADCY5, and RAP2C loci were associated with gestational duration and variants atThe EBF 1, EE FSEC, and AG TR2 loci with preterm birth.
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Impaired synaptic plasticity and cAMP response element-binding protein activation in Ca2+/calmodulin-dependent protein kinase type IV/Gr-deficient mice.

TL;DR: An important role for CaMKIV/Gr in Ca2+-regulated neuronal gene transcription and synaptic plasticity is supported and the contribution of other signaling pathways may spare spatial memory of CaMK IV/Gr-deficient mice are suggested.
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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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Altered Stress-Induced Anxiety in Adenylyl Cyclase Type VIII-Deficient Mice

TL;DR: A novel role for AC8 in the modulation of anxiety is demonstrated as a compromise in calcium-stimulated AC activity in the hippocampus, hypothalamus, thalamus, and brainstem and the behavioral consequences of AC8 deficiency are evaluated.
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T-cell glucocorticoid receptor is required to suppress COX-2-mediated lethal immune activation.

TL;DR: It is indicated that glucocorticoid receptor suppression of COX-2 is crucial for curtailing lethal immune activation, and new therapeutic approaches for regulation of T-cell-mediated inflammatory diseases are suggested.