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The article explores the potential dangers associated with commodities trading terms and conditions stipulated in the Uniform Commercial Code (UCC), both when used in the context of coal trading and in the setting of a more traditional supply contract in the U.S. It also examines the calculation of damages stipulated under Article 2 of the UCC. The arguable gaps and conflicts in the treatment and determination of such damages in the UCC are addressed. It examines whether and to what extent the typical coal trading terms and conditions address or solve any such ambiguities.

Application of Microencapsulation for Toxicology Studies. II. Toxicity of Microencapsulated Trichloroethylene in Fischer 344 Rats. MELNICK, R. L., JAMESON, C. W., GOEHL, T. J., MARONPOT, R. R., COLLINS, B. J., GREENWELL, A., HARRINGTON, F. W., WILSON, R. E., TOMAS-ZEWSKI, K. E., AND AGARWAL, D. K. (1987). . , 432–442. Gelatin–sorbitol microcapsules containing 44.1% trichloroethylene (TCE) were prepared and mixed in NIH-07 rodent meal diet and provided at microcapsule concentrations of 0 (untreated control group), 1.25,2.5, 5.0, or 10% (equivalent to 0, 0.55, 1.10, 2.21, or 4.41% TCE, respectively) to groups of 10 male F344 rats for 14 days. An additional control group received diets containing 5% empty capsules. For comparisons, TCE dissolved in corn oil was administered by gavage to different groups of 10 male rats for 14 consecutive days at dose levels adjusted to correspond to those in the feed study. Treatment-related deaths occurred only in the highest dose group of the gavage study. Body weight gain and feed consumption were reduced in high-dose groups of both the feed and gavage studies. There was no measurable loss of TCE in feed sampled from the cages during the study. Dose-related increases in organ (liver and kidney) weight/body weight ratios, individual cell necrosis in the liver, and hepatic microsomal NADPH cytochrome re-ductase and peroxisomal palmitoyl-CoA oxidase and catalase activities were found in both the dosed-fed and gavage groups. Induction of cytochrome -450 occurred only in the dosed-feed study. There were no significant compound-related pathologic lesions observed in the kidneys, the only other organ examined microscopically. Differences in lethality, cytochrome -450 levels, and induction of microsomal or peroxisomal enzyme activities were attributed to differences in the method of dosing (gavage versus dosed-feed). The demonstration of no significant loss of TCE from the feed and of similar toxic effects produced by microencapsulated TCE via feed and TCE in corn oil via gavage indicate that microencapsulation can provide an excellent alternative exposure route for studying the oral toxicological properties of volatile chemicals, such as TCE, in rats. [ABSTRACT FROM PUBLISHER]

Interactions between Bromobenzene Dose, Glutathione Concentrations, and Organ Toxicities in Single- and Multiple-Treatment Studies. KLUWE, W. M., MARONPOT, R. R., GREENWELL, A., AND HARRINGTON, F. (1984). . 4, 1019–1028. A single oral dose of 4.0 mmol/kg bromobenzene transiently depleted hepatic and renal reduced nonprotein sulfhydryl group (NPS) concentrations, caused hepatocellular necrosis, and increased serum glutamic-pyruvic transaminase activity in male Fischer 344 rats. The depletion of NPS had partially reversed by 24 hr, and NPS concentrations were approximately twice normal values by 48 hr post-treatment When the effects of single and repeated (once dairy for 2, 4, or 10 days) treatments with 4.0 mmol/kg were compared, it was apparent that the severity of hepatotoxicity lessened and the percentage depletions of hepatic and renal NPS concentrations decreased with increasing length of bromobenzene treatment There were essentially no signs of toxicity following the tenth treatment with 4.0 mmol/kg. Single-treatment studies indicated the following dose-response; 2.0 mmol/kg bromobenzene depleted liver NPS and was hepatotoxic 0.5 mmol/ kg caused a lesser depletion of liver NPS and was not (overtly) hepatotoxic, and 0.0625 mmol/ kg was the maximum dose that did not deplete liver NPS. The responses to single and multiple (ten) treatments with these representative doses were compared. Liver injury was observed after a single but not after the tenth daily treatment with 2.0 mmol/kg. Both the single and the tenth administrations of 2.0 mmol/kg depleted hepatic NPS, but the precentage of depletion was greater after the first than after the tenth dose. Liver injury was not detected with lower dose regimens. The patterns of NPS depletion in liver and kidney were similar after single or muliple (ten) treatments. The minimum NPS concentrations produced, however, were lower after single than after multiple treatments. The molar amounts of liver NPS depleted after the tenth treatment appeared to be equivalent to or greater than those after the first but prior bromobenzene exposure resulted in a higher concentration of tissue NPS being present at the time of the final treatment. Thus, the minimum tissue concentrations of NPS were greater after multiple treatments than after single treatments, despite the loss of equivalent amounts of NPS. It is concluded from these studies that repeated treatment produces resistance to bromobenzene hepatotoxicity. This protective adaptation may be due to a chemically induced increase in liver glutathione concentration [ABSTRACT FROM PUBLISHER]

BACKGROUND. Ionizing radiation is frequently used for the treatment of malignancy. Sequelae of therapeutic radiation frequently present clinical problems in the form of poor wound healing and easy injury of treated tissue in response to mild trauma. OBJECTIVE. We describe a radiation-impaired wound healing model in guinea pigs, developed to determine the effect of cutaneous irradiation on wound contraction. METHODS. Guinea pigs were anesthetized and a flap of skin was isolated and treated with x-rays to 18 Gy. Circular wounds of identical size were made in Irradiated and control skin, and average wound size was recorded. RESULTS. Our results demonstrate that a statistically significant wound healing deficit is produced in open wounds by surface irradiation of skin. CONCLUSION. Radiation of skin results in slower healing of open wounds, and provides an in vivo system for evaluation of topical dressings and growth factors in radiation-impaired wounds. [ABSTRACT FROM AUTHOR]