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"Carman, Judith E"
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Singing our history, part II: the Civil War to World War II
In Part Two of a series, Carman presents an overview of American history as seen through vocal and choral repertoire. This installment covers the Civil War, settlement of what is now the Western United States and the resulting displacement of Native Americans, the influx of European immigrants, and World War I.
Journal Article
Singing Our History, Part III: World War II to the Present
Almost 400 years of the building of a great nation from a small band of like-minded Pilgrims to a multicultural society 300 million strong, from wilderness to cities, from the great western frontier to the frontier of space, from communication that took months by ship to instantaneous contact on the Internet, at war and at peace, in shame and glory - all is reflected in our heritage of art song. Francis Hopkinson's wish has come true: The arts have taken root and flourished among us.
Journal Article
Singing Our History: People and Events of American History Represented in American Art Song: PART I: 1620 TO THE CIVIL WAR
This article is the story of American history and the people and events that have been recorded or memorialized in poetry, prose, letters, speeches, and historical documents - and then set to music as art song, mostly by 20th-century American composers. The story is told chronologically by century and by events or movements within each century. This part covers the time period of 1620 to the Civil War.
Journal Article
IL-1 induces mitochondrial translocation of IRAK2 to suppress oxidative metabolism in adipocytes
Chronic inflammation is a common feature of obesity, with elevated cytokines such as interleukin-1 (IL-1) in the circulation and tissues. Here, we report an unconventional IL-1R–MyD88–IRAK2–PHB/OPA1 signaling axis that reprograms mitochondrial metabolism in adipocytes to exacerbate obesity. IL-1 induced recruitment of IRAK2 Myddosome to mitochondria outer membranes via recognition by TOM20, followed by TIMM50-guided translocation of IRAK2 into mitochondria inner membranes, to suppress oxidative phosphorylation and fatty acid oxidation, thereby attenuating energy expenditure. Adipocyte-specific MyD88 or IRAK2 deficiency reduced high-fat-diet-induced weight gain, increased energy expenditure and ameliorated insulin resistance, associated with a smaller adipocyte size and increased cristae formation. IRAK2 kinase inactivation also reduced high-fat diet-induced metabolic diseases. Mechanistically, IRAK2 suppressed respiratory super-complex formation via interaction with PHB1 and OPA1 upon stimulation of IL-1. Taken together, our results suggest that the IRAK2 Myddosome functions as a critical link between inflammation and metabolism, representing a novel therapeutic target for patients with obesity.
Obesity is often accompanied by chronic inflammation. Li and colleagues show that, in mice fed high-fat diets, IL-1 signaling in adipocytes induces an unconventional IRAK2 translocation to mitochondria and suppresses respiratory super-complex formation to alter mitochondrial function, and exacerbates obesity.
Journal Article