Metabolic Pathways Associated With Glycogen Storage in Chronically Active and Normal Skeletal Muscle.

To determine the pathways used for glycogen synthesis in chronically active and normal muscle, muscles from C57B1/6J dy\sp{\rm 2J}/dy\sp{\rm 2J}(dy\sp{\rm 2J}) mice were evaluated biochemically and histochemically. The gastrocnemius muscle (GAST) of the dy\sp{\rm 2J} mouse, a chronically active muscle, contained twice as much glycogen and lactate as control GAST. The dy\sp{\rm 2J} triceps muscle (TRI), which is not chronically active, showed no elevation in glycogen content. An intraperitoneal injection of \sp{14}C-lactate resulted in increased incorporation of \sp{14}C into glycogen by dy\sp{\rm 2J} compared to control GAST. Both normal and dy\sp{\rm 2J} GAST incorporated \sp{14}C into glycogen in an in situ preparation, indicating direct glycogen synthesis from lactate. Autoradiography revealed that high glycogen containing muscle fibers in the dy\sp{\rm 2J} GAST have the highest capacity for glyconeogenesis. Glycogen synthase (GS), malic enzyme (ME) and phosphoenolpyruvate carboxykinase (PEPCK) are all elevated in dy\sp{\rm 2J} GAST, but not in dy\sp{\rm 2J} TRI compared to normal controls. High glycogen fibers in the dy\sp{\rm 2J} had higher activities of GS and ME than any other fibers. The variation in glycogen content along the length of single muscle fibers increased with increasing glycogen content. However, the variation was low enough in all fiber types to allow for a single histochemical section to be a good predictor of glycogen in that fiber. Glucose uptake and glycogen synthesis from glucose (glycogenesis) were elevated in chronically active muscles, in vivo and in vitro. The diaphragm muscle had the highest rates of glucose uptake and glycogenesis. Insulin stimulation of glucose uptake and glycogenesis were enhanced in chronically active muscles from dy\sp{\rm 2J} mice. Specific inhibitors of PEPCK inhibited glyconeogenesis in skeletal muscle, demonstrating the involvement of PEPCK. Previous contractile activity had no effect on glyconeogenic rates. Glyconeogenic rates were linearly dependent on substrate concentration and had a pH optimum of 6.6. Normal and chronically active muscles utilize both lactate and glucose for glycogen synthesis. Chronically active muscles store increased amounts of glycogen. The increased glycogen may provide the chronically active muscle with some additional resistance to fatigue

An Exploration of Professional Learning for Chief Diversity Officers in Higher Education

The purpose of the study is to understand the process of professional learning of Chief Diversity Officers (CDOs) who work in higher education. Professionals who become CDOs come from a variety of backgrounds and rely on professional experiences, along with “on-the-job” learning rather than pre-service education to navigate the role of a diversity executive. Cervero (2001) stated the importance of continued professional education to continue learning so that individuals develop and enhance their practice. Professional learning is important for diversity executives who are in higher education because there is no pre-service formal education program, and the profession is still developing a common body of knowledge. For this study, professional learning is framed as a combination of continuing professional education, the context of work, and individual experiences. Daley (2000) supports the combination of the three areas to have optimal learning in professions. This roundtable discussion is a discussion about a study conducted to explore the process of professional learning for CDOs working in higher education institutions. At the core of the study is the process of learning as professionals function as a diversity executive

Letter from Melvin J. Voigt and Robert L. Talmadge to Dr. M.C. Cunningham recommending construction of a new library

A letter from Melvin J. Voigt, Director of the Kansas State University Library, and Robert L. Talmadge, Acting Director of the University of Kansas Library, to Dr. Morton C. Cunningham, President of Fort Hays Kansas State College, recommending construction of a new library building for Forsyth Library.https://scholars.fhsu.edu/library_bldg/1079/thumbnail.jp

The Institute of Archaeology & Siegfried H. Horn Museum Newsletter Volume 42.3

Khirbat Safra 2021, Paul Gregor, Paul Ray, Robert Bates, Trisha Broy, and Talmadge Gerald Random Surveyhttps://digitalcommons.andrews.edu/iaham-news/1087/thumbnail.jp

Senator James O. Eastland; Herman E. Talmadge; Bob Dole; Dick Clark; Edward Zorinsky; Walter D. Huddleston; S.I. Hayakawa; James B. Allen; Dick Stone; Hubert H. Humphrey; John Melcher; George McGovern; Carl T. Curtis; Milton Young; Patrick Leahy; Jesse Helms; & Richard Lugar to President Jimmy Carter, 20 October 1977

Copy typed letter signed dated 20 October 1977 from Eastland; Herman E. Talmadge; Bob Dole; Dick Clark; Edward Zorinsky; Walter D. Huddleston; S.I. Hayakawa; James B. Allen; Dick Stone; Hubert H. Humphrey; John Melcher; George McGovern; Carl T. Curtis; Milton Young; Patrick Leahy; Jesse Helms; & Richard Lugar to Carter, re: agricultural exports, farm prices, Commodity Credit Corporation; 2 pages.https://egrove.olemiss.edu/joecorr_h/1075/thumbnail.jp

Senator James O. Eastland; Herman E. Talmadge; Bob Dole; George McGovern; James B. Allen; Milton Young; Jesse Helms; Patrick Leahy; Henry Bellmon; S.I. Hayakawa; Carl T. Curtis; Richard Lugar; John Melcher; & Dick Clark to President Jimmy Carter, 14 October 1977

Copy typed letter signed dated 14 October 1977 from Eastland; Herman E. Talmadge; Bob Dole; George McGovern; James B. Allen; Milton Young; Jesse Helms; Patrick Leahy; Henry Bellmon; S.I. Hayakawa; Carl T. Curtis; Richard Lugar; John Melcher; & Dick Clark to Carter, re: New Orleans strike of International Longshoremens Association, grain exports; 2 pages.https://egrove.olemiss.edu/joecorr_h/1069/thumbnail.jp

Bob Dole, [Carl T. Curtis, Herman E. Talmadge, James O. Eastland, S.I. Hykawa possibly] to President Jimmy Carter, 31 January 1978

Copy typed letter signed dated 31 January 1978 from Bob Dole, [Curtis, Talmadge, Eastland, Hykawa possibly] to Carter, re: European Community trade negotiations, soybeans.https://egrove.olemiss.edu/joecorr_h/1090/thumbnail.jp

Depressed Neuromuscular Transmission Causes Weakness in Mice Lacking BK Potassium Channels

Mice lacking functional large-conductance voltage- and Ca2+-activated K+ channels (BK channels) are viable but have motor deficits including ataxia and weakness. The cause of weakness is unknown. In this study, we discovered, in vivo, that skeletal muscle in mice lacking BK channels (BK−/−) was weak in response to nerve stimulation but not to direct muscle stimulation, suggesting a failure of neuromuscular transmission. Voltage-clamp studies of the BK−/− neuromuscular junction (NMJ) revealed a reduction in evoked endplate current amplitude and the frequency of spontaneous vesicle release compared with WT littermates. Responses to 50-Hz stimulation indicated a reduced probability of vesicle release in BK−/− mice, suggestive of lower presynaptic Ca2+ entry. Pharmacological block of BK channels in WT NMJs did not affect NMJ function, surprisingly suggesting that the reduced vesicle release in BK−/− NMJs was not due to loss of BK channel–mediated K+ current. Possible explanations for our data include an effect of BK channels on development of the NMJ, a role for BK channels in regulating presynaptic Ca2+ current or the effectiveness of Ca2+ in triggering release. Consistent with reduced Ca2+ entry or effectiveness of Ca2+ in triggering release, use of 3,4-diaminopyridine to widen action potentials normalized evoked release in BK−/− mice to WT levels. Intraperitoneal application of 3,4-diaminopyridine fully restored in vivo nerve-stimulated muscle force in BK−/− mice. Our work demonstrates that mice lacking BK channels have weakness due to a defect in vesicle release at the NMJ