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

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

A Mouse Model of Huntington’s Disease Shows Altered Ultrastructure of Transverse Tubules in Skeletal Muscle Fibers

Huntington’s disease (HD) is a fatal and progressive condition with severe debilitating motor defects and muscle weakness. Although classically recognized as a neurodegenerative disorder, there is increasing evidence of cell autonomous toxicity in skeletal muscle. We recently demonstrated that skeletal muscle fibers from the R6/2 model mouse of HD have a decrease in specific membrane capacitance, suggesting a loss of transverse tubule (t-tubule) membrane in R6/2 muscle. A previous report also indicated that Cav1.1 current was reduced in R6/2 skeletal muscle, suggesting defects in excitation–contraction (EC) coupling. Thus, we hypothesized that a loss and/or disruption of the skeletal muscle t-tubule system contributes to changes in EC coupling in R6/2 skeletal muscle. We used live-cell imaging with multiphoton confocal microscopy and transmission electron microscopy to assess the t-tubule architecture in late-stage R6/2 muscle and found no significant differences in the t-tubule system density, regularity, or integrity. However, electron microscopy images revealed that the cross-sectional area of t-tubules at the triad were 25% smaller in R6/2 compared with age-matched control skeletal muscle. Computer simulation revealed that the resulting decrease in the R6/2 t-tubule luminal conductance contributed to, but did not fully explain, the reduced R6/2 membrane capacitance. Analyses of bridging integrator-1 (Bin1), which plays a primary role in t-tubule formation, revealed decreased Bin1 protein levels and aberrant splicing of Bin1 mRNA in R6/2 muscle. Additionally, the distance between the t-tubule and sarcoplasmic reticulum was wider in R6/2 compared with control muscle, which was associated with a decrease in junctophilin 1 and 2 mRNA levels. Altogether, these findings can help explain dysregulated EC coupling and motor impairment in Huntington’s disease

Idiopathic interstitial pneumonia: Do community and academic physicians agree on diagnosis?

Rationale: Treatment and prognoses of diffuse parenchymal lung diseases (DPLDs) varies by diagnosis. Obtaining a uniform diagnosis among observers is difficult. Objectives: Evaluate diagnostic agreement between academic and community-based physicians for patients with DPLDs, and determine if an interactive approach between clinicians, radiologists, and pathologists improved diagnostic agreement in community and academic centers. Methods: Retrospective review of 39 patients with DPLD. A total of 19 participants reviewed cases at 2 community locations and 1 academic location. Information from the history, physical examination, pulmonary function testing, high-resolution computed tomography, and surgical lung biopsy was collected. Data were presented in the same sequential fashion to three groups of physicians on separate days. Measurements and Main Results: Each observer’s diagnosis was coded into one of eight categories. A statistic allowing formultiple raters was used to assess agreement in diagnosis. Interactions between clinicians, radiologists, and pathologists improved interobserver agreement at both community and academic sites; however, final agreement was better within academic centers (Kappa= 0.55–0.71) than within community centers (Kappa=0.32–0.44). Clinically significant disagreement was present between academic and communitybased physicians (Kappa=0.11–0.56). Community physicians were more likely to assign a final diagnosis of idiopathic pulmonary fibrosis compared with academic physicians. Conclusions: Significant disagreement exists in the diagnosis of DPLD between physicians based in communities compared with those in academic centers. Wherever possible, patients should be referred to centers with expertise in diffuse parenchymal lung disorders to help clarify the diagnosis and provide suggestions regarding treatment options.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/91941/1/2007 AJRCCM Idiopathic interstitial pneumonia - Do community and academic physicians agree on diagnosis.pd

Grupo Comunitário de Porto Alegre - Leigos para o Desenvolvimento

Comunicação apresentada no 3º Encontro Conhecimento e Cooperação, INA, Lisboa, 17 de setembro de 201