Buffers and Duality

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/60252/1/Reprint97Jacobs.pd

BMQ

BMQ: Boston Medical Quarterly was published from 1950-1966 by the Boston University School of Medicine and the Massachusetts Memorial Hospitals. Pages 49-52, v17n2, provided courtesy of Howard Gotlieb Archival Research Center

THE ICEBERG METAPHOR OF EDUCATIONAL TELECOMMUNICATIONS : HISTORY AND APPLICATION

ミシガン大学ICS(相互伝達・模擬実験)グループは1984年以来コンピューター媒介による模擬実験を行って来た。実験の成果の一つとして、アイスバーグ・メタファー(氷山隠喩)と呼ばれる教育的遠距離通信に関する概念的モデルを創り出したことがあげられる。このモデルは10年以上に渡り何千人もの学生によって現場でテストされ、その結果この隠喩の中心的主題は不変であり、その一方で広範囲におよぶ教育的模擬実験を促進する柔軟性を備えていることが分かった。このモデルは、K-12、遠距離教育、高等教育などへ応用するための教育技術導入の道を模索している教育者には有益となるはずである。当論文はアイスバーグ・メタファーの発展を述べると共に、それがサーバー側と教室内の双方に関するテレコミュニケーション(遠距離通信)研究にどのような影響を与え得るかについて考察するものである。The Interactive Communications & Simulations (ICS) group at the University of Michigan has operated computer-mediated simulations since 1984. One outcome of our experience was the development of a conceptual model for educational telecommunications called the Iceberg Metaphor. This model has been field-tested by thousands of students for over a decade, and the central themes of this metaphor have remained constant while retaining the flexibility to facilitate a wide range of educational simulations. This model should prove useful to educators who are exploring ways to use instructional technologies for K-12, distance, and higher education applications. This paper describes the development of the Iceberg Metaphor and examines how it influences telecommunications projects on both the server side and in the classroom

Evaluation of menogaril in renal cell carcinoma

The Southwest Oncology Group (SWOG) studied the response rate and toxicity of menogaril (200 mg/m 2 i.v. q 28 days) in patients with advanced metastatic renal cell carcinoma. During the early stage of the trial two partial responses were seen in the first 20 treated patients, and an additional 36 evaluable patients were studied. Three of 56 (5%) evaluable patients achieved partial responses. Significant white cell toxicity was observed. Mild or moderate degrees of thrombocytopenia, gastrointestinal side effects, alopecia and phlebitis occurred. No cardiac toxicity was noted. The low response rate suggests that menogaril in this dose schedule has no role in the treatment of patients with advanced metastatic renal cancer.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/45344/1/10637_2004_Article_BF00171987.pd

Young Adults, Mortality, and Employment

This study assessed the relationship between employment status and mortality over a two-year period among a nationally representative sample of young adults aged 18–24 years (n=121,478, representing over 21 million US young adults)

Health Indicators Among Unemployed and Employed Young Adults

Research on the prevalence of health indicators by employment status among young US adults is limited. We analyzed data from a nationally representative sample of young adults aged 18 to 24 years to document the prevalence of five health behaviors (cigarette smoking, risky drinking, leisure-time physical activity, and fruit and French fries consumption) by employment status

Antimicrobial Resistance among Campylobacter Strains, United States, 1997–2001

We summarize antimicrobial resistance surveillance data in human and chicken isolates of Campylobacter. Isolates were from a sentinel county study from 1989 through 1990 and from nine state health departments participating in National Antimicrobial Resistance Monitoring System for enteric bacteria (NARMS) from 1997 through 2001. None of the 297 C. jejuni or C. coli isolates tested from 1989 through 1990 was ciprofloxacin-resistant. From 1997 through 2001, a total of 1,553 human Campylobacter isolates were characterized: 1,471 (95%) were C. jejuni, 63 (4%) were C. coli, and 19 (1%) were other Campylobacter species. The prevalence of ciprofloxacin-resistant Campylobacter was 13% (28 of 217) in 1997 and 19% (75 of 384) in 2001; erythromycin resistance was 2% (4 of 217) in 1997 and 2% (8 of 384) in 2001. Ciprofloxacin-resistant Campylobacter was isolated from 10% of 180 chicken products purchased from grocery stores in three states in 1999. Ciprofloxacin resistance has emerged among Campylobacter since 1990 and has increased in prevalence since 1997

Caenorhabditis elegans Semi-Automated Liquid Screen Reveals a Specialized Role for the Chemotaxis Gene cheB2 in Pseudomonas aeruginosa Virulence

Pseudomonas aeruginosa is an opportunistic human pathogen that causes infections in a variety of animal and plant hosts. Caenorhabditis elegans is a simple model with which one can identify bacterial virulence genes. Previous studies with C. elegans have shown that depending on the growth medium, P. aeruginosa provokes different pathologies: slow or fast killing, lethal paralysis and red death. In this study, we developed a high-throughput semi-automated liquid-based assay such that an entire genome can readily be scanned for virulence genes in a short time period. We screened a 2,200-member STM mutant library generated in a cystic fibrosis airway P. aeruginosa isolate, TBCF10839. Twelve mutants were isolated each showing at least 70% attenuation in C. elegans killing. The selected mutants had insertions in regulatory genes, such as a histidine kinase sensor of two-component systems and a member of the AraC family, or in genes involved in adherence or chemotaxis. One mutant had an insertion in a cheB gene homologue, encoding a methylesterase involved in chemotaxis (CheB2). The cheB2 mutant was tested in a murine lung infection model and found to have a highly attenuated virulence. The cheB2 gene is part of the chemotactic gene cluster II, which was shown to be required for an optimal mobility in vitro. In P. aeruginosa, the main player in chemotaxis and mobility is the chemotactic gene cluster I, including cheB1. We show that, in contrast to the cheB2 mutant, a cheB1 mutant is not attenuated for virulence in C. elegans whereas in vitro motility and chemotaxis are severely impaired. We conclude that the virulence defect of the cheB2 mutant is not linked with a global motility defect but that instead the cheB2 gene is involved in a specific chemotactic response, which takes place during infection and is required for P. aeruginosa pathogenicity

Atlas of prostate cancer heritability in European and African-American men pinpoints tissue-specific regulation.

Although genome-wide association studies have identified over 100 risk loci that explain ∼33% of familial risk for prostate cancer (PrCa), their functional effects on risk remain largely unknown. Here we use genotype data from 59,089 men of European and African American ancestries combined with cell-type-specific epigenetic data to build a genomic atlas of single-nucleotide polymorphism (SNP) heritability in PrCa. We find significant differences in heritability between variants in prostate-relevant epigenetic marks defined in normal versus tumour tissue as well as between tissue and cell lines. The majority of SNP heritability lies in regions marked by H3k27 acetylation in prostate adenoc7arcinoma cell line (LNCaP) or by DNaseI hypersensitive sites in cancer cell lines. We find a high degree of similarity between European and African American ancestries suggesting a similar genetic architecture from common variation underlying PrCa risk. Our findings showcase the power of integrating functional annotation with genetic data to understand the genetic basis of PrCa.This work was supported by NIH fellowship F32 GM106584 (AG), NIH grants R01 MH101244(A.G.), R01 CA188392 (B.P.), U01 CA194393(B.P.), R01 GM107427 (M.L.F.), R01 CA193910 (M.L.F./M.P.) and Prostate Cancer Foundation Challenge Award (M.L.F./M.P.). This study makes use of data generated by the Wellcome Trust Case Control Consortium and the Wellcome Trust Sanger Institute. A full list of the investigators who contributed to the generation of the Wellcome Trust Case Control Consortium data is available on www.wtccc.org.uk. Funding for the Wellcome Trust Case Control Consortium project was provided by the Wellcome Trust under award 076113. This study makes use of data generated by the UK10K Consortium. A full list of the investigators who contributed to the generation of the data is available online (http://www.UK10K.org). The PRACTICAL consortium was supported by the following grants: European Commission's Seventh Framework Programme grant agreement n° 223175 (HEALTH-F2-2009-223175), Cancer Research UK Grants C5047/A7357, C1287/A10118, C5047/A3354, C5047/A10692, C16913/A6135 and The National Institute of Health (NIH) Cancer Post-Cancer GWAS initiative Grant: no. 1 U19 CA 148537-01 (the GAME-ON initiative); Cancer Research UK (C1287/A10118, C1287/A 10710, C12292/A11174, C1281/A12014, C5047/A8384, C5047/A15007 and C5047/A10692), the National Institutes of Health (CA128978) and Post-Cancer GWAS initiative (1U19 CA148537, 1U19 CA148065 and 1U19 CA148112—the GAME-ON initiative), the Department of Defense (W81XWH-10-1-0341), A Linneus Centre (Contract ID 70867902), Swedish Research Council (grant no K2010-70X-20430-04-3), the Swedish Cancer Foundation (grant no 09-0677), grants RO1CA056678, RO1CA082664 and RO1CA092579 from the US National Cancer Institute, National Institutes of Health; US National Cancer Institute (R01CA72818); support from The National Health and Medical Research Council, Australia (126402, 209057, 251533, 396414, 450104, 504700, 504702, 504715, 623204, 940394 and 614296); NIH grants CA63464, CA54281 and CA098758; US National Cancer Institute (R01CA128813, PI: J.Y. Park); Bulgarian National Science Fund, Ministry of Education and Science (contract DOO-119/2009; DUNK01/2–2009; DFNI-B01/28/2012); Cancer Research UK grants [C8197/A10123] and [C8197/A10865]; grant code G0500966/75466; NIHR Health Technology Assessment Programme (projects 96/20/06 and 96/20/99); Cancer Research UK grant number C522/A8649, Medical Research Council of England grant number G0500966, ID 75466 and The NCRI, UK; The US Dept of Defense award W81XWH-04-1-0280; Australia Project Grant [390130, 1009458] and Enabling Grant [614296 to APCB]; the Prostate Cancer Foundation of Australia (Project Grant [PG7] and Research infrastructure grant [to APCB]); NIH grant R01 CA092447; Vanderbilt-Ingram Cancer Center (P30 CA68485); Cancer Research UK [C490/A10124] and supported by the UK National Institute for Health Research Biomedical Research Centre at the University of Cambridge; Competitive Research Funding of the Tampere University Hospital (9N069 and X51003); Award Number P30CA042014 from the National Cancer Institute.This is the final version of the article. It first appeared from Nature Publishing Group via http://dx.doi.org/0.1038/ncomms1097