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Biomedical subjects

R Furrer

Publications and source records attributed to R Furrer.

At least 19 recordsLinked to original sources
PubMed1992

The effect of lowering faecal pH on the rate of proliferation of the normal colonic mucosa.

Epidemiological and animal studies suggest that faecal pH may be a risk factor for colorectal cancer with low faecal pH associated with a lower incidence of the disease. The aim of this study was to determine whether faecal pH (or dietary fibre) affects the short-term risk factors for colon cancer. Sixty-nine normal volunteers were randomized into three equal groups (A-C). They provided food records, faecal specimens and submitted to rectal biopsy for thymidine labelling studies before and after a 2-week intervention. Group A received a placebo of fruit juice. Group B, approximately 3.0 g d-1 sodium sulphate in juice. Group C, 30 g d-1 supplementary dietary fibre as wheat bran in bread. Age, sex, weight, height and intake of macronutrients and minerals were similar in the groups prior to intervention. Faecal pH was similar for the three groups before and was reduced in Group B after intervention (P = 0.001) with a relative reduction of 0.5 pH units. The labelling index for the three groups was similar prior to intervention; after, it was lowest in Group B with a relative reduction of 0.5% points, although this difference was not statistically significant. The results thus do not support the hypothesis that an acidification of faecal pH leads to a reduction in risk markers for colon cancer.

Adult↗
PubMed1990

Simulation of space adaptation syndrome on earth.

The three Spacelab D-1 Scientist Astronauts were exposed to a 1 1/2 h 3 g centrifuge run in the supine position, resulting in a linear 3 g acceleration in the x-direction. They used their space experience to evaluate their readapting to normal gravity and compared their observations with 'Space Adaptation Syndrome'. After the centrifuge runs, the vestibular visual system appeared to be modified in a very specific and reproducible manner. Readapting to the normal 1 g environment took at least 6 h. During this period there was a striking similarity to the astronaut's experience during adaptation to weightlessness in space. A series of vestibular tests were then performed, confirming these subjective findings.

Adaptation, Physiological↗
PubMed1989

Effect of calcium supplementation on mucosal cell proliferation in high risk patients for colon cancer.

Recent findings suggest that supplemental calcium could lower the abnormally high proliferation rate found in the colonic mucosa of subjects at high risk for colon cancer. In this double blind controlled study, this effect in volunteers previously operated upon for a colorectal adenocarcinoma was tested. Thirty subjects were randomised to receive either elemental calcium 1200 mg/day or a placebo. Mucosal proliferation was measured with tritiated thymidine labelling before and after the 30 day intervention period. Diets, faecal pH and the concentration of calcium and bile acids in the aqueous phase of feaces were also measured. Labelling index did not differ significantly in the two groups before intervention (placebo 4.0(2.4) v calcium 4.9(2.9), but the difference approached significance afterwards (4.4(2.4) v 6.5(3.4), p = 0.06). Individual changes occurring with intervention were tabulated and comparison of the means for the groups was not significant (delta = 0.3 vs delta = 1.8, p = 0.11). Calcium concentration, faecal pH and deoxycholic acid concentration increased in the calcium group (p = 0.02, 0.005 and 0.004 respectively). Calcium does not show any effect in decreasing colonic mucosal proliferation in this high risk group for colon cancer; it may increase faecal pH and the production of deoxycholic acid in the colon.

Aged↗
PubMed1988

Proliferative activity of rectal mucosa and soluble fecal bile acids in patients with normal colons and in patients with colonic polyps or cancer.

Rectal biopsies and fecal collections were obtained from a consecutive series of 34 outpatients prior to colonoscopy at a gastroenterology clinic. Subsequently, 14 were found to have no colonic pathology, 13 had adenomatous polyps, (3 of those had a previous history of colon cancer) and 7 were diagnosed with colon cancer. In confirmation of earlier studies the tritiated thymidine labelling index was higher in patients with tumors than in those without pathology (7.9% vs. 5.8% with P = 0.06). The patients with colonic tumors also had significantly higher levels of deoxycholic acid (P = 0.01) and lithocholic acid (P = 0.005) in the aqueous extract of their feces. This study shows that these biochemical measures may indicate colon cancer risk.

Bile Acids and Salts↗
PubMed1988

Effect of high fat consumption on cell proliferation activity of colorectal mucosa and on soluble faecal bile acids.

To assess the effect of fat consumption on the proliferation of the rectal mucosa, 30 normal volunteers (22 to 71 years) were randomly allocated to three groups: (a) basal low fat diet containing 30 g of fat per day; (b) the basal diet with doses of 30 g corn oil taken with each of the three meals: 120 g fat/day; (c) the basal diet with one dose of 90 g corn oil after the last meal: 120 g fat/day. Rectal biopsies were taken 15 cm from the anal verge after five days on the diets and mucosal cell proliferation was measured by labelling index (LI). The LI was significantly (p less than 0.01) higher in group (c) (9.2) than in group (a) (5.9), with group (b) intermediate (6.8). In multiple stepwise regression analysis, the data were best fitted with age and the variable indicating fat consumed as a bolus as predictors of LI (r2 = 0.39, p less than 0.001). In separate analyses the regression coefficient with age in the fat bolus group was 0.23, p less than 0.001. There was some tendency towards lower bile acids in the faecal water in group (a) than in groups (b) and (c) following the diets and between the bile acids and LI (for lithocholic acid r = 0.48, p = 0.01). These data show that dietary fat given as a bolus can lead to an increase in the proliferation of human colonic cells, possibly as a consequence of raised levels of cytotoxic acidic lipids in the faecal stream.

Adult↗
PubMed1987

The effect of fecapentaenes on nuclear aberrations in murine colonic epithelial cells.

Fecapentaenes, human fecal mutagens of bacterial origin, were intrarectally administered to mice in suppository form. Despite the strong, positive mutagenic response of fecanpentaenes using Ames tester strains TA 98 and TA 100, no increase in nuclear aberrations, taken as a measure of genotoxicity in colonic epithelial cells, was observed over control levels. In fecapentaene treated animals, however, the incidence of mitotic figures was increased above control levels to values comparable to those observed in mice treated with the known colon carcinogen, N-ethyl-N-nitrosourea. Thus, it would appear that fecapentaenes are not cytotoxic to murine colonic epithelia as judged by the nuclear aberration assay.

Animals↗
PubMed1986

Characterization of cytotoxic steroids in human faeces and their putative role in the etiology of human colonic cancer.

It has been shown previously that chemically induced nuclear abeerrations in the murine colon are correlated with the carcinogenicity of the respective chemicals. Consequently, the nuclear aberration assay was utilized for the identification of putatife carcinogens in human faeces. Human fecal samples were fractionated by several chromatographic methods, and the assay led to the isolation of two substances. A combination of spectroscopic (mass, nuclear magnetic resonance, ultraviolet, and infrared) and chromatographic (HPLC and GLC) methods showed that they are 5-alpha- cholestan-3-one (I) and cholest-4-en-3-one (II). A number of C-27-C-30 steroids isolated from closely related fractions of feces were inactive in this assay. Thus I and II could play a role in etiology of large bowel cancer in humans.

Animals↗
PubMed1986

Effects of calcium and pH on the mucosal damage produced by deoxycholic acid in the rat colon.

A single pass perfusion system was used in anaesthetised, restrained rats to examine the effect of changing the composition of the perfusion fluid on the damage caused to the colonic epithelium by deoxycholic acid. Damage to the colonic surface was monitored with light microscopy, transmission and scanning electron microscopy and with measurements of deoxyribonucleic acid and carbohydrate in the perfusate. New scoring techniques for monitoring alterations in surface epithelium of light microscopy sections were used. The damaging effect of 5 mM deoxycholic acid to the colonic epithelium is inhibited by lowering the pH of the perfusion fluid from 7.9 to 5.5, or by increasing the calcium concentration from 0 to 4 mM. This inhibition is shown to be because of a decreased amount of bile acid in solution. Thus it is not the total concentration of deoxycholic acid in the colon that is responsible for the colonic damage, but the concentration in solution. Although extrapolation to the human situation must be made with caution, the concentration of bile acid in solution in the faecal water may be more relevant to colonic mucosal damage than total bile acid concentration.

Animals↗
PubMed1985

Toxicity of orally administered fat to the colonic epithelium of mice.

C57BL/6J mice were given a gavage of from 0.1 to 0.4 ml beef tallow (BT) or corn oil (CO). The damaging effect of the orally administered fat boluses could be visualized 2-4 h later by instilling the excised animal colons with Trypan blue, a vital dye that stains non-viable cells. Microscopic examination of sections prepared at these times revealed that the tall columnar cells on the surface of the normal epithelium were replaced with cells demonstrating flattened, pleomorphic, pyknotic and fragmented nuclei. This phenomenon was quantitated by scoring 100 intercrypt epithelial zones between well-defined crypts. The maximum damage, affecting 25-45% of the epithelial zones, was seen at 2-4 h after treatment with 0.4 ml of BT or CO and the epithelium appeared normal with less than 10% damage at 12 h. The mitotic activity in the colonic crypts was unchanged up to 8 h and then showed a marked increase of 2- to 3-fold at 12-16 h. The severity of the epithelial damage and ensuing mitogenic response was related to the size of the fat bolus. These observations would suggest that the effects of any carcinogens present in the diet or formed in the feces could be enhanced if a fatty meal results in colonic damage and subsequent cell proliferation as we have observed in mice.

Animals↗
PubMed1979

Volatile N-nitrosamines in the urine of normal donors and of bladder cancer patients.

Volatile N-nitrosamines were detected in the urine of male volunteers with gas-liquid and high-pressure liquid chromatography interfaced to the thermal energy analyzer. Of 50 samples from normal males, 10 contained nitrosodimethylamine (0.02 to 0.10 micrograms/liter), 6 contained nitrosodiethylamine (0.02 to 3.10), 9 contained nitrosomorpholine (0.006 to 0.67), and none contained nitrosodibutylamine. Of 4 samples from bladder cancer patients, 2 contained nitrosodibutylamine (0.35 and 0.66). Cigarette smoking did not appear to be related to the pattern or amount of urinary volatile N-nitrosamines. The possibility that the N-nitrosamines arise from the diet or from endogenous production is considered.

Adult↗
PubMed1978

Non-volatile N-nitroso compounds in human feces.

A bacterial mutagen has been detected in ether extracts of freeze-dried feces of humans on Western diet. Several types of evidence suggest that nitroso compounds are present in human feces and the mutagen could be a nitroso compound. Ascorbic acid supplement in the diet reduces the levels of both the mutagens and nitroso compounds in the feces.

Ascorbic Acid↗