Weanling F344 rats, which were fed a diet containing 10% chrysotile (B), were studied over their life-time to determine the effects of ingested asbestos on the colon. Control groups consisted of rats fed a diet containing a 10% nonnutritive cellulose or a standard laboratory rat diet. The pathological findings in the colons of 501 rats (189 on asbestos diet, 197 on fiber control diet, and 115 on standard control diet), are reported here. Epithelial tumors of the colon (eight adenocarcinomas and one adenoma) were found in nine of the rats on study. Four of the tumors were in asbestos-fed rats, two tumors were found in the non-nutritive cellulose controls, and three tumors were found in the standard laboratory rat diet controls. The probability (based on actuarial analysis) of developing adenoma or adenocarcinomas during the 32 months of the study were 7.4% for the asbestos-fed group, 3.5% for the fiber control diet and 4.0% on the standard control diet. In addition, one malignant mesothelioma of the type induced by intraperitoneally administered asbestos was found in the asbestos-fed group. Non-neoplastic lesions of the colon were also evaluated. The cumulative risk for development of any colon-associated lesion (non-neoplastic plus neoplastic lesions) was greatest for asbestos-fed rats (17.9%), compared to 13.6% for those fed the fiber control diet and 8.2% for those fed the standard control diet. The colon tissue levels of adenosine, 3'-5'-cyclic monophosphate (cAMP) were significantly lower in the animals fed asbestos compared to the control diets. Chrysotile fibers were seen by electronmicroscopy (e.m.) in six of ten ashed colon specimens of rats fed the asbestos diet. Although the differences in numbers of tumors between the animals fed asbestos and the controls were not statistically significant at the 5% level, we felt that the combination of observations including 1) evidence of increased probability of asbestos-fed animals to develop colon lesions in general; 2) evidence of a special type of mesothelioma in rats fed asbestos; 3) evidence for a cell regulator defect (lowered cAMP levels) in colon tissues of animals fed asbestos; and 4) evidence for asbestos fiber penetration of the colonic mucosa (e.m. studies) suggest that ingested asbestos is not inert in the colon.

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Abstract. Group A, B, and C rotaviruses were identified in 9% (96/1,048) of pig fecal specimens submitted to the Iowa State University Veterinary Diagnostic Laboratory during 1987 and 1988. Six of the rotaviruses were group B, 5 were group C, and the remaining 89% were group A. Of the rotavirus cases with more than 1 serotype, 5 were multiple group A serotypes, 1 involved a group A and B serotype, and 1 included 2 group C serotypes. A retrospective epidemiologic evaluation of pig diarrhea in herds of origin was done using data obtained from the accession records of the rotavirus and 88 matched nonrotavirus pig diarrhea control cases. Herds from which rotavirus cases were derived experienced lower morbidity, mortality, and case fatality rates than matched control herds. The incidence of diarrhea decreased rapidly among all pigs from birth to 3 weeks of age. The peak incidence for piglet diarrhea occurred in February, and a moderate rise occurred in AugustSeptember. Definitive evidence for transmissible gastroenteritis virus was found in 12% of nonrotavirus cases but none of the rotavirus cases in which it was sought. Other pathogenic microorganisms were identified less frequently and inconsistently.Since the discovery of a rotavirus as a cause of diarrhea in calves in 1969, 20 rotaviruses have been recognized as agents in diarrheic disease of swine, 41 and infection is widespread in pigs 4,39,41 In pigs and some other species, a very high incidence of infection may not be unusual. 41 Most rotavirus infections are subclinical in conventionally reared pigs, l1,13,23,41,42 and rotaviruses may be detected in apparently healthy pigs. 10,13,23,32,41,42 Virulence of rotavirus may be affected among other things by virus strain and dose, age of the pig, host environmental and nutritional factors, and concurrent infections. Nursing and weanling pigs experience the greatest morbidity and mortality from rotavirus infections 4,23,35,41 Observed interherd and interlitter rate variations may be the result of colostral antibody differences and the influences of other host, environmental, and agent factors. 40 For example, colostral antibodies have an important protective role for newborn Received for publication October 16, 1993. piglets, but colostrum is neither uniformly ingested nor of consistent protective value. 1 Likewise, the virulence of rotaviruses may be different, 43 and few field strains resemble prototype strains in RNA electropherotypes 15 Rotavirus infection has also been shown to induce villous atrophy and disease in gnotobiotic 4,[8][9][10][17][18][19]31,[36][37][38] and colostrum-deprived 10,17,19 neonatal pigs. The following report is the result of a retrospective epidemiological investigation. The objective of the study was to obtain an Iowa swine population perspective of rotavirus infection and the role of the virus in diarrheic disease as compared with other agents reported in the herds. The collaborative project utilized information obtained from specimens and the accompanying herd histories of ...

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Cell-mediated immunity (CMI) directed towards rat fetal cells was evaluated in Fischer F344 young inbred male rats having asbestos-induced peritoneal mesothelioma. The tumors were induced by exposure to Canadian chrysotile B fibers and the CMI delineated by the injury and destruction brought about to 6- to 10-day-old primary fetal cell cultures by the so-called educated peripheral blood lymphoid-cells (PBLC) obtained from the cancer-bearing rats. A significant cytotoxicity was found to be expressed by the PBLCs, suggesting that during the development of mesothelioma, a cellular retrodifferentiation occurs, thereby educating the effectors to recognize a common determinant existing in both the tumor and fetal cells. Educated PBLCs were produced from rats having endodermal tissue cancers (adenocarcinomas of the small bowel, colon and pancreas) and were found to also be cytotoxic to the fetal cultures, yet no injury was apparently inflicted upon cultured mesothelioma target cells by these effectors. These results suggested that the tumor education was specific and that probably a unique and different fetal component was being recognized by the effector cells obtained from the rats with lesions arising either in the mesodermal or endodermal tissue. Further support for this concept was the failure of an antibody, specific to an oncofetal protein existing in endodermal lesions, to apparently recognize any common oncogenic proteins in the mesothelioma. Preliminary studies have also been accomplished which suggests the existence of natural killing immune responses existing to the mesothelioma target cells.(ABSTRACT TRUNCATED AT 250 WORDS)