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AUSTIN -- If your community suffers a bioterroristic attack tomorrow, how prepared would your health care providers be? The answer may depend upon where you live, according to the September edition of Texas Medicine magazine, the official monthly news magazine of the Texas Medical Association. Texas Medicine reports that multi-faceted efforts are underway to shore up knowledge and resources to thwart the effects of a disease outbreak as a result of bioterrorism. Federal funds are flowing to Texas to augment research and preparedness for the day when such readiness will be needed -- and experts forecast it is a question of when, not if. "I think it's very likely that there will be biologic agents used against us by our enemies, " Ronald R. Blanck, DO, president of the University of North Texas Health Science Center and chair of TMA's Task Force on Bioterrorism, told Texas Medicine. "Is it going to happen? Yes. What's the organism going to be? I don't know." Part of the new federal money funded research to learn which Texas hospitals deemed themselves most ready for attack. Many hospitals proclaimed preparedness -- to an extent. "What the survey found was that the large hospitals seem to be better prepared than the smaller hospitals, " said David Morgan, MD, medical director of the Central Texas Poison Center at Scott & White Hospital and a member of the TMA bioterrorism task force. "The trauma hospitals are better prepared than the non-trauma hospitals." According to the magazine's reporting of the findings, many Texas hospitals are ready for an influx of 10 patients, but not prepared for a surge of hundreds, or more, of sick people all at once. "How do you handle a surge of 500 patients?" asked Ron Hilliard, RN, coordinator of the Texas Department of Health Bioterrorism Hospital Preparedness Program. He said the project's next step focuses on helping hospitals plan to handle a large-scale event. A second grant is beefing up the state's health infrastructure, which will benefit Texans regardless of bioterroristic threat. Approximately 70 percent of that money, for example, will help local health departments statewide detect, track, and investigate disease outbreaks. While public health efforts are underway, academic physicians are taking steps to increase the anti-bioterrorism arsenal as well. Texas Medicine reports that the Center for Biodefense was recently created at The University of Texas Medical Branch at Galveston, including a new laboratory where scientists will research some of the most virulent biological See TERROR, Page 8.
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Proliferating neoplastic cells to MP4 14, 15 this delay was interpreted to mean that inhibitions of punine nucleotide synthesis were not responsible for the lethal effects of the drug. We presently describe early and late effects on the punine nucleotides of cultured cells of mouse lymphoma L5 178Y produced by lethal exposure to MP and TG. A companion paper 16 ; describes the incorporation of MP into the nucleic acids of these cells in the form of TG nucleosides and correlates the extent of this incorporation with MP cytotoxicity. Warnick and Paterson 17, 18 ; demonstrated with LS l78Y cells that periods of punine starvation induced by MMPR metabolized to the S'-monophosphate, a potent inhibitor of punine nucleotide synthesis ; were not cytotoxic. Culture in medium containing 0.1 j MMMPR reduced cellular pools of punine nibonucleotides by 40% without affecting proliferation rates throughout a 6-day period 18 ; . After 18 hr of culture in medium with 0.5 zM MMPR, the punine nibonucleotide content and proliferation rates of these cells were reduced by 70 and 30%, respectively, but cell viability, determined by a cloning method, was not affected 18 ; . In the present study, limited exposure of LS178Y cells to MP under conditions that reduced the surviving fraction to 0.001 ; 16 ; caused substantial but temporary reductions in cellular punine ribonucleotides. When resuspended ii drug-free medium, cells underwent I to 2 divisions before lysis delayed cytotoxic response ; . Brief exposure of L5178Y cells to TG and -2'-deoxythioguanosine 16 ; also caused delayed cytotoxicity similar to that of MP, but perturbations of punine ribonucleotide pools during TG exposures were small relative to those caused by MP, in.
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