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Introduction: Colorectal adenomas and other types of polyps are commonly used as end points or risk factors in epidemiologic studies. However, it is not known how accurately patients are able to self-report the presence or absence of adenomas following colonoscopy. Methods: Participants in the Colon Cancer Family Registry provided self-reports of recent colorectal cancer (CRC) screening activity, and whether or not they had ever been told they had a polyp. Positive and negative predictive values for polyp self-report were calculated by comparing medical records with selfreports from 488 participants.

The effect of insulin on epidermal growth factor (EGF)- and transforming growth factor-alpha (TGF alpha)-induced cell proliferation was examined in primary cultures of gastric surface mucous epithelial cells by using changes in cell counts and DNA as indices of cell growth. With 1.0% fetal bovine serum and Dulbecco's modified Eagle medium (low-serum DMEM) there was no effect of bovine insulin (0.1-10.0 micrograms/ml) on cell growth. Higher doses of insulin (20.0 micrograms/ml) in low-serum DMEM were able to stimulate growth of these cells compared with controls. In low-serum DMEM with no insulin the lowest effective dose of EGF or TGF alpha for stimulating cell growth was 10 nM and 5 nM, respectively. In low-serum DMEM containing 2.5 micrograms/ml insulin there was a dose-dependent increase in cell growth with EGF and TFG alpha at concentrations of 0.5-10.0 nM. The addition of insulin alone at 2.5 micrograms/ml, EGF alone at 2 nM, or TGF alpha alone at 2 nM in serum-free DMEM media had no effect on gastric surface mucous cell DNA. In serum-free DMEM media with 2.5 micrograms/ml insulin, the addition of 2 nM EGF or 2 nM TGF alpha caused an increase in both cell counts and DNA of 1.80- and 3.50-fold, respectively. The present study demonstrates that insulin, at concentrations that are not mitogenic, will enhance the proliferative effects of EGF and TGF alpha on the growth of primary cultures of guinea pig gastric surface mucous epithelial cells.

Guinea pigs were given a daily oral dose of 400 μg/kg of omeprazole or the omeprazole vehicle for 6 weeks. At weekly intervals, the animal and stomach weights were recorded, the nonfasted serum gastrins measured, and the total number of gastric fundic epithelial cells were isolated and counted. Gastric mucous epithelial cells were enriched from the total gastric fundic cell population and cultured for 6 days in the absence or presence of hormones (epidermal growth factor and pentagastrin). We found that omeprazole treatment for 1–6 weeks significantly (p < 0.05) increased the stomach weight, the nonfasted serum gastrin levels, and the total number of isolated gastric fundic and mucous epithelial cells over control animals. A significant (p < 0.05) increase was also found in the basal and hormone-stimulated cultured growth rates of gastric mucous epithelial cells isolated from the stomachs of omeprazole-treated animals as compared with gastric mucous cells from control animals. We conclude that oral omeprazole treatment of guinea pigs will cause a specific increase in the gastric mucous cell population as well as increase the in vitro cultured gastric mucous cell basal and hormone-stimulated growth rates.

Summary The pathogenesis of R. tsutsugamushi in infected suckling and weanling mice was studied by the use of fluorescein-labeled antibodies. Although the areas of involvement differed with the route of inoculation, rickettsial antigen was observed primarily in connective tissues of mesenchymal origin. X-irradiation increased the mortality, shortened the incubation period and intensified the antigenic involvement. Rickettsiae could be found by infectivity titrations but not by fluorescent antibody staining in mice infected up to a year before. Attempts to cause a recrudescence by the use of various stresses were unsuccessful.