Characteristics and problems of successful extension-related community clubs in Knox County, Tennessee, 1944-1977

Successful Knox County Community Clubs, organized prior to 1955 and active at the time of the study, were studied to compare and characterize the clubs and to Identify factors contributing to their success. Information was derived primarily from interviews with key members from selected clubs, also from interviews with other key people associated with selected clubs during periods studied, from review of records, club reports, minutes, scrapbooks, library materials, etc. Most clubs started because of special needs or interests of residents and because of the influence of Extension and other professionals. The East Tennessee Community Improvement Program influenced selected clubs\u27 start, and also their continuation through the time of the study. During the study period, 1944-1977, communities grew in population and farming declined. The major problems faced by clubs during the Formative Period, 1944-1954, were related to school, library and the need for community services; during Intermediate Years, 1955-1969, the problems mostly had to do with education, beautification, need for a community center, community services and parks and recreation; and in Recent Years, 1970-1977, basic club organization, land use planning and law enforcement were major problems. It was found that the clubs studied were successful in completing projects relating to specific community problems. They were receptive to help from Extension and other outside resources, and cooperated well with county government and other public and private organizations. Implications were drawn and recommendations made for use of the findings and for further study

The Narcotic Bowel Syndrome: Clinical Features, Pathophysiology, and Management

Narcotic bowel syndrome (NBS) is a subset of opioid bowel dysfunction that is characterized by chronic or frequently recurring abdominal pain that worsens with continued or escalating dosages of narcotics. This syndrome is under recognized and may be becoming more prevalent. This may be due in the United States to increases in using narcotics for chronic non-malignant painful disorders, and the development of maladaptive therapeutic interactions around its use. NBS can occur in patients with no prior gastrointestinal disorder who receive high dosages of narcotics after surgery or acute painful problems, among patients with functional GI disorders or other chronic gastrointestinal diseases who are managed by physicians unaware of the hyperalgesic effects of chronic opioids. The evidence for the enhanced pain perception is based on: a) activation of excitatory anti-analgesic pathways within a bimodal opioid regulation system, b) descending facilitation of pain at the Rostral Ventral Medulla and pain facilitation via dynorphin and CCK activation, and c) glial cell activation that produces morphine tolerance and enhances opioid induced pain. Treatment involves early recognition of the syndrome, an effective physician patient relationship, graded withdrawal of the narcotic according to a specified withdrawal program and the institution of medications to reduce withdrawal effects

Loose Groups of Galaxies in the Las Campanas Redshift Survey

A ``friends-of-friends'' percolation algorithm has been used to extract a catalogue of dn/n = 80 density enhancements (groups) from the six slices of the Las Campanas Redshift Survey (LCRS). The full catalogue contains 1495 groups and includes 35% of the LCRS galaxy sample. A clean sample of 394 groups has been derived by culling groups from the full sample which either are too close to a slice edge, have a crossing time greater than a Hubble time, have a corrected velocity dispersion of zero, or contain a 55-arcsec ``orphan'' (a galaxy with a mock redshift which was excluded from the original LCRS redshift catalogue due to its proximity to another galaxy -- i.e., within 55 arcsec). Median properties derived from the clean sample include: line-of-sight velocity dispersion sigma_los = 164km/s, crossing time t_cr = 0.10/H_0, harmonic radius R_h = 0.58/h Mpc, pairwise separation R_p = 0.64/h Mpc, virial mass M_vir = (1.90x10^13)/h M_sun, total group R-band luminosity L_tot = (1.30x10^11)/h^2 L_sun, and R-band mass-to-light ratio M/L = 171h M_sun/L_sun; the median number of observed members in a group is 3.Comment: 32 pages of text, 27 figures, 7 tables. Figures 1, 4, 6, 7, and 8 are in gif format. Tables 1 and 3 are in plain ASCII format (in paper source) and are also available at http://www-sdss.fnal.gov:8000/~dtucker/LCLG . Accepted for publication in the September 2000 issue of ApJ

Not All Side Effects Associated With Tricyclic Antidepressant Therapy Are True Side Effects

Patients with functional gastrointestinal (GI) disorders treated with tricyclic antidepressants may report non-GI symptoms. It is unclear whether these symptoms are side effects of the medication or reflect a general behavioral tendency to report symptoms. This study 1) evaluated whether a checklist of symptoms reported by patients prior to taking desipramine increased in number or worsened in severity after being on a tricyclic antidepressant (desipramine), and 2) assessed baseline factors that predispose patients to report symptoms

FMOS near-IR spectroscopy of Herschel selected galaxies: star formation rates, metallicity and dust attenuation at z~1

We investigate the properties (e.g. star formation rate, dust attentuation, stellar mass and metallicity) of a sample of infrared luminous galaxies at z \sim 1 via near-IR spectroscopy with Subaru-FMOS. Our sample consists of Herschel SPIRE and Spitzer MIPS selected sources in the COSMOS field with photometric redshifts in the range 0.7 < z-phot < 1.8, which have been targeted in 2 pointings (0.5 sq. deg.) with FMOS. We find a modest success rate for emission line detections, with candidate H{\alpha} emission lines detected for 57 of 168 SPIRE sources (34 per cent). By stacking the near-IR spectra we directly measure the mean Balmer decrement for the H{\alpha} and H{\beta} lines, finding a value of = 0.51\pm0.27 for = 10^12 Lsol sources at = 1.36. By comparing star formation rates estimated from the IR and from the dust uncorrected H{\alpha} line we find a strong relationship between dust attenuation and star formation rate. This relation is broadly consistent with that previously seen in star-forming galaxies at z ~ 0.1. Finally, we investigate the metallicity via the N2 ratio, finding that z ~ 1 IR-selected sources are indistinguishable from the local mass-metallicity relation. We also find a strong correlation between dust attentuation and metallicity, with the most metal-rich IR-sources experiencing the largest levels of dust attenuation.Comment: 13 pages, 7 figures, MNRAS accepte

The CARMA Paired Antenna Calibration System: Atmospheric Phase Correction for Millimeter Wave Interferometry and its Application to Mapping the Ultraluminous Galaxy Arp 193

Phase fluctuations introduced by the atmosphere are the main limiting factor in attaining diffraction limited performance in extended interferometric arrays at millimeter and submillimeter wavelengths. We report the results of C-PACS, the Combined Array for Research in Millimeter-Wave Astronomy Paired Antenna Calibration System. We present a systematic study of several hundred test observations taken during the 2009–2010 winter observing season where we utilize CARMA's eight 3.5 m antennas to monitor an atmospheric calibrator while simultaneously acquiring science observations with 6.1 and 10.4 m antennas on baselines ranging from a few hundred meters to ~2 km. We find that C-PACS is systematically successful at improving coherence on long baselines under a variety of atmospheric conditions. We find that the angular separation between the atmospheric calibrator and target source is the most important consideration, with consistently successful phase correction at CARMA requiring a suitable calibrator located ≾6° away from the science target. We show that cloud cover does not affect the success of C-PACS. We demonstrate C-PACS in typical use by applying it to the observations of the nearby very luminous infrared galaxy Arp 193 in ^(12)CO(2-1) at a linear resolution of ≈70 pc (0".12 × 0".18), 3 times better than previously published molecular maps of this galaxy. We resolve the molecular disk rotation kinematics and the molecular gas distribution and measure the gas surface densities and masses on 90 pc scales. We find that molecular gas constitutes ~30% of the dynamical mass in the inner 700 pc of this object with a surface density ~10^4 M_⊙ pc^(−2); we compare these properties to those of the starburst region of NGC 253

Quantum walk on circles in phase space

We propose a variation of the quantum walk on a circle in phase space by conjoining the Hadamard coin flip with simultaneous displacement of the walker's location in phase space and show that this generalization is a proper quantum walk albeit over multiple concentric circles in phase instead of just over one circle. We motivate the conjoining of Hadamard and displacement operations by showing that the Jaynes-Cummings model for coin+walker approximately yields this description in the dispersive limit. The quantum walk signature is evident in the phase distribution of the walker provided that appropriate pulse durations are applied for each coin flip.Comment: 10 pages, 5 figure

Signal transducer and activator of transcription 1 (STAT1) gain-of-function mutations and disseminated coccidioidomycosis and histoplasmosis

Background: Impaired signaling in the IFN-g/IL-12 pathway causes susceptibility to severe disseminated infections with mycobacteria and dimorphic yeasts. Dominant gain-of-function mutations in signal transducer and activator of transcription 1 (STAT1) have been associated with chronic mucocutaneous candidiasis. Objective: We sought to identify the molecular defect in patients with disseminated dimorphic yeast infections. Methods: PBMCs, EBV-transformed B cells, and transfected U3A cell lines were studied for IFN-g/IL-12 pathway function. STAT1 was sequenced in probands and available relatives. Interferon-induced STAT1 phosphorylation, transcriptional responses, protein-protein interactions, target gene activation, and function were investigated. Results: We identified 5 patients with disseminated Coccidioides immitis or Histoplasma capsulatum with heterozygous missense mutations in the STAT1 coiled-coil or DNA-binding domains. These are dominant gain-of-function mutations causing enhanced STAT1 phosphorylation, delayed dephosphorylation, enhanced DNA binding and transactivation, and enhanced interaction with protein inhibitor of activated STAT1. The mutations caused enhanced IFN-g–induced gene expression, but we found impaired responses to IFN-g restimulation. Conclusion: Gain-of-function mutations in STAT1 predispose to invasive, severe, disseminated dimorphic yeast infections, likely through aberrant regulation of IFN-g–mediated inflammationFil: Sampaio, Elizabeth P.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados Unidos. Instituto Oswaldo Cruz. Laboratorio de Leprologia; BrasilFil: Hsu, Amy P.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados UnidosFil: Pechacek, Joseph. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados UnidosFil: Hannelore I.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados Unidos. Erasmus Medical Center. Department of Medical Microbiology and Infectious Disease; Países BajosFil: Dias, Dalton L.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados UnidosFil: Paulson, Michelle L.. Clinical Research Directorate/CMRP; Estados UnidosFil: Chandrasekaran, Prabha. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados UnidosFil: Rosen, Lindsey B.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados UnidosFil: Carvalho, Daniel S.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados Unidos. Instituto Oswaldo Cruz, Laboratorio de Leprologia; BrasilFil: Ding, Li. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados UnidosFil: Vinh, Donald C.. McGill University Health Centre. Division of Infectious Diseases; CanadáFil: Browne, Sarah K.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados UnidosFil: Datta, Shrimati. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Allergic Diseases. Allergic Inflammation Unit; Estados UnidosFil: Milner, Joshua D.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Allergic Diseases. Allergic Inflammation Unit; Estados UnidosFil: Kuhns, Douglas B.. Clinical Services Program; Estados UnidosFil: Long Priel, Debra A.. Clinical Services Program; Estados UnidosFil: Sadat, Mohammed A.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Host Defenses. Infectious Diseases Susceptibility Unit; Estados UnidosFil: Shiloh, Michael. University of Texas. Southwestern Medical Center. Division of Infectious Diseases; Estados UnidosFil: De Marco, Brendan. University of Texas. Southwestern Medical Center. Division of Infectious Diseases; Estados UnidosFil: Alvares, Michael. University of Texas. Southwestern Medical Center. Division of Allergy and Immunology; Estados UnidosFil: Gillman, Jason W.. University of Texas. Southwestern Medical Center. Division of Infectious Diseases; Estados UnidosFil: Ramarathnam, Vivek. University of Texas. Southwestern Medical Center. Division of Infectious Diseases; Estados UnidosFil: de la Morena, Maite. University of Texas. Southwestern Medical Center. Division of Allergy and Immunology; Estados UnidosFil: Bezrodnik, Liliana. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños "Ricardo Gutierrez"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Moreira, Ileana. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños "Ricardo Gutierrez"; ArgentinaFil: Uzel, Gulbu. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados UnidosFil: Johnson, Daniel. University of Chicago. Comer Children; Estados UnidosFil: Spalding, Christine. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados UnidosFil: Zerbe, Christa S.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados UnidosFil: Wiley, Henry. National Eye Institute. Clinical Trials Branch; Estados UnidosFil: Greenberg, David E.. University of Texas. Southwestern Medical Center. Division of Infectious Diseases; Estados UnidosFil: Hoover, Susan E.. University of Arizona. College of Medicine. Valley Fever Center for Excellence; Estados UnidosFil: Rosenzweig, Sergio D.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Host Defenses Infectious Diseases Susceptibility Unit; Estados Unidos. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Primary Immunodeficiency Clinic; Estados UnidosFil: Galgiani, John N.. University of Arizona. College of Medicine. Valley Fever Center for Excellence; Estados UnidosFil: Holland, Steven M.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados Unido

Peptidases compartmentalized to the Ascaris suum intestinal lumen and apical intestinal membrane

The nematode intestine is a tissue of interest for developing new methods of therapy and control of parasitic nematodes. However, biological details of intestinal cell functions remain obscure, as do the proteins and molecular functions located on the apical intestinal membrane (AIM), and within the intestinal lumen (IL) of nematodes. Accordingly, methods were developed to gain a comprehensive identification of peptidases that function in the intestinal tract of adult female Ascaris suum. Peptidase activity was detected in multiple fractions of the A. suum intestine under pH conditions ranging from 5.0 to 8.0. Peptidase class inhibitors were used to characterize these activities. The fractions included whole lysates, membrane enriched fractions, and physiological- and 4 molar urea-perfusates of the intestinal lumen. Concanavalin A (ConA) was confirmed to bind to the AIM, and intestinal proteins affinity isolated on ConA-beads were compared to proteins from membrane and perfusate fractions by mass spectrometry. Twenty-nine predicted peptidases were identified including aspartic, cysteine, and serine peptidases, and an unexpectedly high number (16) of metallopeptidases. Many of these proteins co-localized to multiple fractions, providing independent support for localization to specific intestinal compartments, including the IL and AIM. This unique perfusion model produced the most comprehensive view of likely digestive peptidases that function in these intestinal compartments of A. suum, or any nematode. This model offers a means to directly determine functions of these proteins in the A. suum intestine and, more generally, deduce the wide array functions that exist in these cellular compartments of the nematode intestine