Journal Article Tumors Induced in Mice by N-Methyl-N-formylhydrazine of the False Morel Gyromitra esculenta Get access Bela Toth, Bela Toth 2The Eppley Institute for Research in Cancer, University of Nebraska Medical Center, 42d St. and Dewey Ave., Omaha, Nebr. 68105. Search for other works by this author on: Oxford Academic PubMed Google Scholar Donald Nagel Donald Nagel 2The Eppley Institute for Research in Cancer, University of Nebraska Medical Center, 42d St. and Dewey Ave., Omaha, Nebr. 68105. 3We thank Dr. Kashinath Patil of this Institute for the statistical analysis and Mrs. Connie Anderson for the technical assistance. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 60, Issue 1, January 1978, Pages 201–204, https://doi.org/10.1093/jnci/60.1.201 Published: 01 January 1978 Article history Received: 05 May 1977 Accepted: 29 July 1977 Published: 01 January 1978
A 0.05% solution of trimethylhydrazine hydrochloride (TMH) administered for a lifetime in drinking water to outbred Swiss albino mice, beginning at 6 weeks of age, induced tumors of blood vessels, lungs, and kidneys. The tumor incidences in these tissues in untreated controls were 5, 22, and 0%, whereas in the treated groups the corresponding tumor incidences increased to 85, 44, and 6%, respectively. Histopathologically, tumors were classified as angiosarcomas of blood vessels and adenomas of the lungs and kidneys. The study thus demonstrated the tumorigenicity of TMH. Contrary to expectation, the chemical structure modification apparently failed to alter qualitatively the tumorigenic response.
ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTSynthesis and structural verification of novel olefinic derivatives of bicyclo[2.2.2]octane. Intermediates in the synthesis of bridged morphinan-like compoundsVictoria F. Roche, Edward B. Roche, and Donald L. NagelCite this: J. Org. Chem. 1982, 47, 7, 1368–1371Publication Date (Print):March 1, 1982Publication History Published online1 May 2002Published inissue 1 March 1982https://doi.org/10.1021/jo00346a049RIGHTS & PERMISSIONSArticle Views101Altmetric-Citations6LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InReddit PDF (569 KB) Get e-Alerts Get e-Alerts
Journal Article Tumor Induction With Trimethylhydrazine Hydrochloride in the Syrian Golden Hamster Get access Bela Toth, Bela Toth Search for other works by this author on: Oxford Academic PubMed Google Scholar Donald Nagel Donald Nagel Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 59, Issue 2, August 1977, Pages 431–433, https://doi.org/10.1093/jnci/59.2.431 Published: 01 August 1977 Article history Received: 29 November 1976 Accepted: 08 February 1977 Published: 01 August 1977
In 110 well-trained participants of a 1000-km running competition lasting for 20 days hematological parameters, iron metabolism, and their respective changes during the race were investigated. Thirty-nine men and 11 women were accustomed to wholesome vegetarian food (lacto-ovovegetarian), 52 men and 8 women consumed a conventional western diet. In each group 50% of the runners finished the race.
Functionally active antithrombin can be quantified by chromogenic substrate assays utilizing the heparin cofactor activity of antithrombin and the inhibition rates of thrombin or of activated factor X (FXa). Thrombin-based assays but not FXa-based assays may overestimate the antithrombin activity due to their sensitivity toward heparin cofactor II. We focused on the question whether an overestimation of antithrombin activity by thrombin-based assays involves the risk of misdiagnosing antithrombin-deficient individuals as being non-deficient. We determined antithrombin using two thrombin-based assays and one FXa-based assay in 27 plasma samples from patients with acquired antithrombin deficiency spiked with lepirudin, in antithrombin-deficient plasma and in mixtures of antithrombin-deficient plasma and normal plasma. We also measured antithrombin in healthy subjects, in patients with inherited and acquired antithrombin deficiency and in patients under high-dose heparin treatment. At therapeutic final concentrations of lepirudin, antithrombin activities were considerably overestimated by the thrombin-based assays but not by the FXa-based assay. The residual antithrombin activities in antithrombin-deficient plasma determined by the thrombin-based assays were markedly higher than the corresponding values obtained with the FXa-based assay. The thrombin-based assays also overestimated antithrombin activity in patients under high-dose heparin. However, the degree of overestimation in the range between 50 and 100 IU/dl was too low to misidentify individuals with inherited or acquired antithrombin deficiency as normal. We conclude that functionally active antithrombin can be reliably determined using FXa-based chromogenic substrate assays in all settings examined. Thrombin-based assays must not be used in patients under treatment with hirudin or other direct thrombin inhibitors.
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