Thomas H. Kent
University of Iowa
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Featured researches published by Thomas H. Kent.
Annals of Internal Medicine | 1975
Thomas J. Stemper; Thomas H. Kent; Robert W. Summers
A kindred contained at least 10 members with single or multiple juvenile polyps of the stomach and large intestine. Several additional polyps had both adenomatous and juvenile features. Eleven members of the kindred have had gastrointestinal carcinoma of the stomach, duodenum, pancreas, or proximal colon. The pattern of inheritance in this kindred suggests either a single or two closely linked autosomal dominant determinants for gastrointestinal carcinoma and polyposis. Management of this kindred is complicated due to the occurrence of gastrointestinal carcinoma without polyposis.
Experimental Biology and Medicine | 1972
Thomas H. Kent; Lawrence J. Fischer; Rose Marr
Summary Bacterial type β-glucuronidase activity is absent in human feces at birth and increases in human and rat feces with age. In rats there is an association of glucuronidase activity with increases in anaerobic flora. Antibiotics which reduce the anaerobic flora eliminate enzyme activity from rat cecal content in vivo and in cultures. Gross cultures of rat cecal content produce glucuronidase only under anaerobic conditions and enzyme production rapidly diminishes in the absence of substrate (glucuronide). Isolation of individual organisms that released glucuronidase into the media was difficult and required maintenance of strict anaerobic conditions and substrate in the media. A variety of anaerobes were found to produce the enzyme.
Annals of Internal Medicine | 1971
Charles D. Gerson; Thomas H. Kent; Jnan R. Saha; Naveed Siddiqi; John Lindenbaum
Abstract Forty-one former Peace Corps volunteers previously living in India or Pakistan for 18 to 24 months were studied after they had returned to the United States. Most noted cessation of diarrh...
Gastroenterology | 1973
Lawrence Poulakos; Thomas H. Kent
Abstract A technique for simultaneous and independent measurement of gastric emptying and small intestinal propulsion in rats was developed and utilized to describe these parameters in 24-hr fasted and fed rats. The differing emission energies of the radioisotopes 51 Cr and 125 I allowed separate determination of the distribution of Na 2 51 CrO 4 and 125 I-polyvinylpyrrolidone at various times after simultaneous intragastric and/or intraduodenal administration of these nonabsorbable markers. Gastric emptying of isotopes was exponential in both groups but much more rapid in fasted than fed rats. There was also a considerable difference in distribution in the small intestine between fasted and fed rats after intragastric administration of the markers with the bulk of the marker moving faster in fasted animals. After intraduodenal administration of the markers, the distribution in the small intestine was quite similar for fasted and fed rats. In contrast to the distribution of radioisotope, the rate of movement of the leading edge of activity in the small intestine was not greatly influenced by gastric emptying.
Radiation Research | 1968
Thomas H. Kent; James W. Osborne; Carolee M. Wende
Striking changes occurred in mid-small intestinal and cecal flora of rats after exposure to 1400 R of whole-body irradiation or 2000 R of intestinal irradiation delivered at 250 kVp and 30 mA. The changes reached a maximum 3 days after irradiation. A consistent 100- to 10,000-fold increase in coliforms and enterococci occurred at both sites, and similar increases in proteus occurred in most animals. The normally predominant lactobacilli decreased slightly in numbers or remained unchanged. Other organisms participated less constantly in the overgrowth. Massive bacterial invasion of the severely injured small intestinal mucosa did not occur. There was no difference in bacterial invasion of mesenteric lymph nodes, spleen, liver, or heart blood between control and irradiated animals. The bacterial overgrowth in the intestines was effectively prevented by orally administered neomycin-polymyxin B-bacitracin without altering mortality. The findings indicate that massive intestinal flora changes occur in rats wit...
Experimental Biology and Medicine | 1969
Thomas H. Kent; Robert W. Summers; Lawrence DenBesten; James C. Swaner; Marilynn Hrouda
Summary Rats with weight loss resulting from surgically created self-filling upper small intestinal blind loops had increased numbers of Escherichia coli and bacteroides in the blind loop, mid-small intestine, and cecum. Counts of other organisms were not significantly elevated. Treatment with neomycin-polymyxin-bacitracin or lincomycin resulted in weight gain, reduced fecal fat excretion, and reduction of bacteroides but not E. coli counts in the blind loop and small intestine. Mixed cultures from blind loops of untreated rats and isolates of bacteroides decon-jugated glycocholic acid in vitro, while mixed cultures from blind loops of treated rats or small intestine of normal rats and isolates of E. coli did not. The findings suggest that bacteroides are the important organisms producing steatorrhea in the rat blind-loop syndrome.
Digestive Diseases and Sciences | 1964
Kenneth A. Hubel; Luke Faber; Thomas H. Kent; James A. Clifton; Edward E. Mason
SummaryIn controlled studies to determine the effect of gastric freezing in patients, the following was found:1.Microscopically the gastric mucosa showed mild degenerative changes with minimal reactive inflammation and foveolar hyperplasia. No necrosis was seen.2.Serum amylase, glutamic oxalacetic transaminase, and leucine aminopeptidase did not rise. This suggested that no appreciable injury to the liver or pancreas occurred.3.Vitamin B12 absorption did not decrease. The apparent increase in absorption that occurred was probably experimental artifact.4.Studies of gastric acid secretion using the maximum histamine and maximum insulin responses (maximum 30-min. output) suggested that injury to the mucosal nerve supply played a role in the reduction of acid secretion that follows gastric freezing.
International Journal of Radiation Biology | 1963
Kedar N. Prasad; G. Mark Kollmorgen; Thomas H. Kent; James W. Osborne
Summaryβ-mercaptoethylamine (MEA) given intraperitoneally 15 min before x-irradiation or clamping of the mesenteric vessel during x-irradiation of the exteriorized ileum and jejunum in rats reduced mortality, body-weight loss in survivors, and histological damage as compared with irradiated controls. When animals which received 1800 r and MEA were compared on a mortality and histopathological basis with those exposed to 1400 r with no drug treatment, the responses were very similar. Thus, with this method for evaluation, MEA reduced the effect of the x-ray exposure dose by about 20 per cent. MEA and clamping were not effective with x-ray exposure doses of 2200 r and above and 3000 r and above respectively. The combination of the two treatments had a substantial additive protective effect. It resulted in 67 per cent survival at the exposure dose of 3500 r where neither treatment by itself was effective, but became completely ineffective at 4500 r and above.
Evaluation & the Health Professions | 1987
Thomas H. Kent; Mark A. Albanese
Two types of computer-administered unit quizzes in a systematic pathology course for second-year medical students were compared. Quizzes composed of questions selected on the basis of a students ability (tailored or adaptive testing) had higher correlations with the final examination than did quizzes composed of questions randomly selectedfrom topic areas (conventional testing). Further, tailored tests obtained optimum correlations with 25% fewer test items.
Experimental Biology and Medicine | 1968
Thomas H. Kent; W. Edmund Farrar
Summary Guinea pigs made highly susceptible to intravenous endotoxin with a sublethal dose of CCl4 were not more susceptible to the lethal infection induced by penicillin when the increased susceptibility to endotoxin occurred at the time of the infection induced by penicillin. However, during the recovery phase of CCl4 damage mortality from penicillin was reduced. A mild degree of resistance to the lethal effect of endotoxin did not protect guinea pigs from the lethal effect of penicillin.