Fish oil in infancy protects against food allergy in Iceland-Results from a birth cohort study.

BACKGROUND: Consumption of oily fish or fish oil during pregnancy, lactation and infancy has been linked to a reduction in the development of allergic diseases in childhood. METHODS: In an observational study, Icelandic children (n = 1304) were prospectively followed from birth to 2.5 years with detailed questionnaires administered at birth and at 1 and 2 years of age, including questions about fish oil supplementation. Children with suspected food allergy were invited for physical examinations, allergic sensitization tests, and a double-blind, placebo-controlled food challenge if the allergy testing or clinical history indicated food allergy. The study investigated the development of sensitization to food and confirmed food allergy according to age and frequency of postnatal fish oil supplementation using proportional hazards modelling. RESULTS: The incidence of diagnosed food sensitization was significantly lower in children who received regular fish oil supplementation (relative risk: 0.51, 95% confidence interval: 0.32-0.82). The incidence of challenge-confirmed food allergy was also reduced, although not statistically significant (0.57, 0.30-1.12). Children who began to receive fish oil in their first half year of life were significantly more protected than those who began later (P = .045 for sensitization, P = .018 for allergy). Indicators of allergy severity decreased with increased fish oil consumption (P = .013). Adjusting for parent education and allergic family history did not change the results. CONCLUSION: Postnatal fish oil consumption is associated with decreased food sensitization and food allergies in infants and may provide an intervention strategy for allergy prevention.

IgE recognition patterns in peanut allergy are age dependent: perspectives of the EuroPrevall study.

BACKGROUND: We tested the hypothesis that specific molecular sensitization patterns correlate with the clinical data/manifestation in a European peanut-allergic population characterized under a common protocol. METHODS: Sixty-eight peanut-allergic subjects and 82 tolerant controls from 11 European countries were included. Allergy to peanut and lowest symptom-eliciting dose was established by double-blind placebo-controlled food challenge in all but anaphylactic subjects. Information of early or late (before or after 14 years of age) onset of peanut allergy was obtained from standardized questionnaires. IgE to peanut allergens rAra h 1-3, 6, 8-9, profilin and CCD was determined using ImmunoCAP. RESULTS: Seventy-eight percent of peanut allergics were sensitized to peanut extract and 90% to at least one peanut component. rAra h 2 was the sole major allergen for the peanut-allergic population. Geographical differences were observed for rAra h 8 and rAra h 9, which were major allergens for central/western and southern Europeans, respectively. Sensitization to rAra h 1 and 2 was exclusively observed in early-onset peanut allergy. Peanut-tolerant subjects were frequently sensitized to rAra h 8 or 9 but not to storage proteins. Sensitization to Ara h 2 ≥ 1.0 kUA /l conferred a 97% probability for a systemic reaction (P = 0.0002). Logistic regression revealed a significant influence of peanut extract sensitization and region on the occurrence of systemic reactions (P = 0.0185 and P = 0.0436, respectively). CONCLUSION: Sensitization to Ara h 1, 2 and 3 is usually acquired in childhood. IgE to Ara h 2 ≥ 1.0 kUA /l is significantly associated with the development of systemic reactions to peanut.

The present and future disease burden of hepatitis C virus (HCV) infection with today's treatment paradigm.

The disease burden of hepatitis C virus (HCV) is expected to increase as the infected population ages. A modelling approach was used to estimate the total number of viremic infections, diagnosed, treated and new infections in 2013. In addition, the model was used to estimate the change in the total number of HCV infections, the disease progression and mortality in 2013-2030. Finally, expert panel consensus was used to capture current treatment practices in each country. Using today's treatment paradigm, the total number of HCV infections is projected to decline or remain flat in all countries studied. However, in the same time period, the number of individuals with late-stage liver disease is projected to increase. This study concluded that the current treatment rate and efficacy are not sufficient to manage the disease burden of HCV. Thus, alternative strategies are required to keep the number of HCV individuals with advanced liver disease and liver-related deaths from increasing.

Evaluation of a cefoxitin 30 microg disc on Iso-Sensitest agar for detection of methicillin-resistant Staphylococcus aureus.

OBJECTIVES: To evaluate the performance of a cefoxitin 30 microg disc on Iso-Sensitest agar, using a semi-confluent inoculum and overnight incubation at 35-36 degrees C, for detection of methicillin-resistant Staphylococcus aureus (MRSA). METHODS: A total of 457 S. aureus, including 190 MRSA of several defined PFGE types and a number of low-level resistant isolates, were tested with a cefoxitin 30 microg disc on Iso-Sensitest agar, using a semi-confluent inoculum and overnight incubation at 35-36 degrees C. This method was compared with the standard SRGA (Swedish Reference Group for Antibiotics) method (oxacillin 1 microg disc on Iso-Sensitest agar supplemented with 5% defibrinated horse blood, confluent growth and 24 h incubation in ambient air at 30 degrees C). RESULTS: The cefoxitin method was excellent, with a sensitivity of 100% and a specificity of 99% using an interpretative zone diameter of S > or = 29 mm and R < 29 mm. Its performance was much better than the SRGA method, which with this collection of difficult strains had a sensitivity of only 78% using the current breakpoint of S > or = 12 mm. CONCLUSION: We suggest that the cefoxitin method should replace that currently recommended by the SRGA for the detection of MRSA, and that it would fit well into BSAC methodology.

Radioprotection of salivary glands by amifostine in high-dose radioiodine treatment. Results of a double-blinded, placebo-controlled study in patients with differentiated thyroid cancer.

BACKGROUND AND PURPOSE: Parenchymal impairment of salivary glands following high-dose radioiodine treatment is a well-known side effect in general caused by free radicals. Therefore, the radioprotective effect of the radical scavenger amifostine was evaluated prospectively in patients receiving high-dose radioiodine treatment. PATIENTS AND METHODS: Parenchymal function was assessed by quantitative salivary gland scintigraphy performed in 50 patients with differentiated thyroid cancer prior to and 3 months after high-dose radioiodine treatment with either 3 GBq 131I (n = 21) or 6 GBq 131I (n = 29) in a double-blinded, placebo-controlled study. Twenty-five patients treated with 500 mg/m2 amifostine intravenously prior to high-dose radioiodine treatment were compared to 25 control patients receiving physiological saline solution. Xerostomia was graded according to WHO-criteria. RESULTS: In 25 control patients high-dose radioiodine treatment significantly (p < 0.001) reduced parenchymal function of parotid and submandibular glands by 40.2 +/- 14.1% and 39.9 +/- 15.3%, respectively. Nine out of these 25 patients developed Grade I and 2 Grade II xerostomia. In contrast, in 25 amifostine-treated patients there was no significant (p = 0.691) decrease in parenchymal function following high-dose radioiodine treatment, and xerostomia did not occur in any of them. CONCLUSION: Parenchymal damage of salivary glands induced by high-dose radioiodine treatment can be significantly reduced by amifostine which may improve quality of life of patients with differentiated thyroid cancer.

Pregnancy testing before high-dose radioiodine treatment: a case report.

This case emphasizes that negative urine pregnancy testing and a written declaration of the patient are not sufficient to safely exclude an early pregnancy. Serum pregnancy testing inherently has a diagnostic gap of about 1 wk following conception. We recommend sufficient contraception at least 1 mo before radioiodine treatment in women of childbearing age.

Radioprotection of salivary glands by S-2-(3-aminopropylamino)-ethylphosphorothioic (amifostine) obtained in a rabbit animal model.

BACKGROUND: Impairment of salivary gland function following high-dose radioiodine treatment (HDRIT) is a well-recognized side effect of the treatment. Because differentiated thyroid cancer has an excellent prognosis, reduction of long-term side-effects is mandatory. Therefore, the aim of this study was to investigate the radioprotective effect of amifostine in a rabbit animal model. METHODS: Salivary gland scintigraphy was performed in a total of 16 New Zealand White rabbits. Uptake of 99-Tc-pertechnetate was calculated in percentage of injected activity as a quantitative measure of both salivary gland and thyroid function. Reproducibility of salivary gland scintigraphy was evaluated in one rabbit without any intervention. Fifteen rabbits were studied prior to and up to 6 months after high-dose radioiodine treatment applying 2 GBq 131I. Ten animals received 200 mg/kg amifostine prior to high-dose radioiodine therapy, and 5 served as controls. Salivary glands were examined histopathologically. RESULTS: Variation coefficient of parenchymal function was less than 3.8% in salivary glands. Prior to HDRIT, thyroid uptake was 0.417+/-0.373% and 0.421+/-0.241% in control and amifostine-treated rabbits, respectively. Four weeks after HDRIT, complete ablation of the thyroid was achieved in both groups. Prior to HDRIT, uptake of 99mTc-pertechnetate in salivary glands of five control rabbits was not significantly different from ten amifostine-treated rabbits. In control rabbits 6 months after HDRIT, parenchymal function was reduced significantly (p < 0.0001) by 75.3+/-5.3% and 53.6+/-17.4% in parotid and submandibular glands, respectively. In contrast, in amifostine-treated rabbits, parenchymal function was reduced by 10.6+/-3.4% and 6.5+/-4.3% (p > 0.05) in parotid and submandibular glands, respectively. Histopathologically, marked lipomatosis was observed in control animals but was negligible in amifostine-treated animals. CONCLUSION: Parenchymal damage in salivary glands induced by high-dose radioiodine treatment can be significantly reduced by amifostine in this rabbit animal model. This corresponds to data obtained in patients with differentiated thyroid cancer.

Salivary gland protection by amifostine in high-dose radioiodine therapy of differentiated thyroid cancer.

BACKGROUND: Salivary gland impairment following high-dose radioiodine treatment is a well-recognized side effect, in general caused by free radicals. Therefore, it seemed promising to evaluate the radioprotective effect of the radical scavenger amifostine in patients receiving high-dose radioiodine therapy. PATIENTS AND METHOD: Quantitative salivary gland scintigraphy using 100 to 120 MBq Tc-99m-pertechnetate was performed in 17 patients with differentiated thyroid cancer prior to and 3 months after radioiodine treatment with 6 GBq I-131. Eight patients were treated with 500 mg/m2 amifostine prior to high-dose radioiodine treatment and compared retrospectively with 9 control patients. Xerostomia was graded according to WHO criteria. RESULTS: In 9 control patients high-dose radioiodine treatment significantly (p < 0.01) reduced Tc-99m-pertechnetate uptake by 35.4 +/- 22.0% and 31.7 +/- 21.1% in parotid and submandibular glands, respectively. Of these 9 patients, 3 exhibited xerostomia Grade I (WHO). In contrast, in 8 amifostine-treated patients, there was no significant (p = 0.878) decrease in parenchymal function following high-dose radioiodine treatment, and xerostomia did not occur in any of them. CONCLUSION: Parenchymal damage in salivary glands induced by high-dose radioiodine treatment can be reduced significantly by amifostine. This may help to increase patients' quality of life in differentiated thyroid cancer.

Salivary gland protection by S-2-(3-aminopropylamino)-ethylphosphorothioic acid (amifostine) in high-dose radioiodine treatment: results obtained in a rabbit animal model and in a double-blind multi-arm trial.

Since differentiated thyroid cancer has an excellent prognosis, reduction of long-term side effects of high-dose radioiodine treatment (HD-RIT), i.e. salivary gland impairment is important. Thus, radioprotective effects of amifostine were studied. Salivary gland function was quantified by scintigraphy both in rabbits and patients. Fifteen rabbits were studied prior to and up to 6 months after HD-RIT applying 2 GBq 131I. Ten animals received 200 mg/kg amifostine prior to HD-RIT, and five served as controls. Animals were examined histopathologically. Fifty patients with differentiated thyroid cancer were evaluated prospectively prior to and 3 months after HD-RIT with either 3 or 6 GBq 131I in a double-blind, placebo-controlled study. Twenty-five patients were treated with 500 mg/m2 amifostine intravenously prior to HD-RIT, and 25 patients receiving physiological saline solution served as controls. Complete ablation of the thyroid was achieved in all rabbits four weeks after HD-RIT. In control rabbits 6 months after HD-RIT parenchymal function was reduced significantly (p < 0.0001) by 75.3 +/- 5.3% and 53.6 +/- 17.4% in parotid and submandibular glands, respectively. In contrast, in amifostine-treated rabbits parenchymal function was not significantly reduced. Histopathologically, marked lipomatosis was observed in control animals but was negligible in amifostine-treated animals. In control patients, salivary gland function was significantly (p < 0.001) reduced by 40.2 +/- 14.1% and 39.9 +/- 15.3% in parotid and submandibular glands, respectively, three months after HD-RIT, and 11 patients developed xerostomia. In 25 amifostine-treated patients, salivary gland function was not significantly reduced (p = 0.691), and xerostomia did not occur. Thus, parenchymal damage in salivary glands induced by high-dose radioiodine therapy can be reduced significantly by amifostine. This may improve quality of life of patients with differentiated thyroid cancer.

Salivary gland protection by amifostine in high-dose radioiodine treatment: results of a double-blind placebo-controlled study.

PURPOSE: Salivary gland impairment is a well-recognized side effect following high-dose radioiodine treatment (HD-RIT). Since differentiated thyroid cancer has a good prognosis, reduction of long-term side effects is important. Therefore, the effect of amifostine was studied in HD-RIT. PATIENTS AND METHODS: Parenchymal function was assessed by quantitative salivary gland scintigraphy performed prospectively in 50 patients with differentiated thyroid cancer before and 3 months after HD-RIT with either 3 GBq iodine ((131)I) (n=21) or 6 GBq (131)I (n=29) in a double-blind, placebo-controlled study. Twenty-five patients were treated with 500 mg/m2 amifostine intravenously before HD-RIT and 25 patients served as controls, who received physiologic saline solution. Xerostomia was graded according to World Health Organization (WHO) criteria. RESULTS: Before HD-RIT in 25 control patients, uptake of technetium-99m (99mTc)-pertechnetate was 0.45%+/-0.16% and 0.42%+/-0.16% in parotid and submandibular glands, respectively. Three months after HD-RIT, parenchymal function was significantly (P < .001) reduced by 40.2%+/-14.1% and 39.9%+/-15.3% in parotid and submandibular glands, respectively. Nine control patients developed grade I and two grade II xerostomia. In 25 amifostine-treated patients, uptake of 99mTc-pertechnetate was 0.46%+/-0.16% and 0.43%+/-0.17% in parotid and submandibular glands, respectively. Three months after HD-RIT, parenchymal function of salivary glands was not significantly altered (P=.691) and xerostomia did not occur in any of these patients. CONCLUSION: Parenchymal damage in salivary glands caused by HD-RIT can significantly be reduced by amifostine, which may improve the quality of life of patients with differentiated thyroid cancer.

Radioprotection of salivary glands by amifostine in high-dose radioiodine therapy.

UNLABELLED: Salivary gland impairment after high-dose radioiodine treatment is well recognized. Because differentiated thyroid cancer has a good prognosis, reduction of long-term side effects is important. This study investigated the radioprotective effects of amifostine in animals and humans receiving high-dose radioiodine therapy. METHODS: Quantitative salivary gland scintigraphy was performed in five rabbits before and up to 3 mo after high-dose radioiodine therapy applying 1 GBq 131I. Three animals received 200 mg/kg amifostine before high-dose radioiodine therapy, and two served as controls. All animals were examined histopathologically. Quantitative salivary gland scintigraphy also was performed in 17 patients with differentiated thyroid cancer before and 3 mo after high-dose radioiodine therapy with 6 GBq 131I. Eight patients were treated with 500 mg/m2 amifostine before high-dose radioiodine therapy, and nine served as controls. RESULTS: In two control rabbits, high-dose radioiodine therapy significantly reduced parenchymal function by 63% and 46% in parotid and submandibular glands, respectively. In contrast, there was no significant decrease in parenchymal function in amifostine-treated animals. Histopathologically, lipomatosis was observed in control animals but was negligible in amifostine-treated animals. Similar findings were observed in differentiated thyroid cancer patients. In nine control patients, high-dose radioiodine therapy significantly (p < 0.01) reduced parenchymal function by 37% and 31% in parotid and submandibular glands, respectively. Three patients exhibited Grade I (World Health Organization) xerostomia. In contrast, there was no significant decrease in parenchymal function in amifostine-treated patients and no incidence of xerostomia. CONCLUSION: Parenchymal damage in salivary glands induced by high-dose radioiodine therapy can be reduced significantly by amifostine. This may increase the quality of life of patients with differentiated thyroid cancer.

Colonic production of butyrate in patients with previous colonic cancer during long-term treatment with dietary fibre (Plantago ovata seeds).

BACKGROUND: Butyrate has antineoplastic properties against colorectal cancer cells and is the preferred oxidative substrate for colonocytes. Like acetate and propionate (short-chain fatty acids; SCFAs), butyrate is produced by colonic fermentation of dietary fibre. METHODS: Twenty patients resected for colorectal cancer were treated with 20 g/day of the fibre Plantago ovata seeds for 3 months, which increased the intake of fibre by 17.9 +/- 0.8 g/day, from basal levels of 19.2 +/- 1.7 g/day; 17 patients completed the study. Faecal samples were obtained on eight occasions, twice before treatment, and monthly three times during and three time after treatment. RESULTS: One month of fibre therapy increased faecal concentrations of butyrate by 42 +/- 12% (from 13.2 +/- 1.2 to 19.3 +/- 3.0 mmol/l; P < 10(-4)), acetate by 25 +/- 6% (P < 10(-4)), propionate by 28 +/- 9% (P = 0.01), and total SCFAs by 25 +/- 6% (P < 10 (-4)). Concentrations were increased during the 3-month fibre treatment but reversed to pretreatment levels within 1 to 2 months after cessation of fibre supplementation. The relative concentration (ratio) of butyrate was not altered owing to a simultaneous increase in acetate and propionate. Faecal pH decreased initially but was normalized after 2 months of fibre supplements. Fibre therapy increased the 24-h productions of butyrate by 47 +/- 10% (P < 10(-4)) and acetate by 50 +/- 7% (P < 10(-4)) in 16.6% faecal homogenates with added P. ovata seeds (20mg/ml), but SCFA productions returned to pretreatment levels after discontinuation of additional fibre intakes. CONCLUSIONS: Oral intake of P. ovata seeds adapted the colonic flora to increase the production of butyrate (and acetate) from this fibre and increased faecal concentrations of butyrate by 42% in patients resected for colonic cancer. The effects depended on continuity of treatment.

Quantitative salivary gland scintigraphy in the diagnosis of parenchymal damage after treatment with radioiodine.

This study was undertaken to quantify salivary gland parenchymal damage after radioiodine treatment with a standard protective regimen of ascorbic acid. Altogether, 106 patients underwent quantitative salivary gland scintigraphy with 99Tcm-pertechnetate prior to and 3 months after radioiodine therapy. Parenchymal function was quantified by calculating 99Tcm-pertechnetate uptake 13 min post-injection. Patients received 131I doses ranging from 400 MBq to 24 GBq (cumulative). Among the patients who received large doses of 131I, severe parenchymal destruction could be visually analysed as well as quantitatively evaluated. In contrast, after low-dose radioiodine treatment, mild parenchymal impairment was demonstrated by quantitative evaluation only. In conclusion, standardized quantitative salivary gland scintigraphy is essential for the reliable detection of mild parenchymal malfunction. Despite the standard protection regimen using ascorbic acid as a sialogogue, radioiodine therapy induces loss of salivary gland parenchymal function even with low doses of 131I.

Kinetic studies on the metabolism of short-chain fatty acids and glucose by isolated rat colonocytes.

BACKGROUND/AIMS: Although the interest in colonic mucosal metabolism of short-chain fatty acids is steadily increasing, the kinetic parameters Vmax (maximum velocity) and Km (Michaelis constant) of the complete oxidation of these acids into CO2 by colonic epithelial cells have not previously been determined. METHODS: Isolated rat colonocytes were incubated in the presence of a concentration range of 14C-labeled acetate, propionate, butyrate, and glucose. Oxidation rates were obtained by quantifying the production of 14CO2. Vmax and Km were calculated by computer-fitting of the data to a Michaelis-Menten plot. RESULTS: The apparent Vmax values were similar comparing acetate, propionate, and butyrate (1.114 +/- 0.061, 0.991 +/- 0.072, and 1.007 +/- 0.070 mumol/min.g, respectively), but significantly lower for glucose (0.339 +/- 0.022 mumol/min.g). The corresponding Km values were all different and in the order of butyrate (0.184 +/- 0.017 mmol/L) < propionate (0.339 +/- 0.025 mmol/L) < acetate (0.487 +/- 0.019 mmol/L) < glucose (0.777 +/- 0.051 mmol/L). In substrate competition experiments, butyrate caused a strong noncompetitive inhibition of acetate oxidation and a mixed type of inhibition of propionate oxidation. Propionate inhibited the oxidation of acetate noncompetitively and that of butyrate competitively. Acetate only slightly inhibited the oxidation of propionate and butyrate. CONCLUSIONS: Colonic epithelial cells seem to utilize short-chain fatty acids in a preferential order of butyrate > propionate > acetate. Oxidation of propionate or acetate, however, may provide the energy needed for cellular functions if the metabolism of butyrate is impaired or the luminal supply is limited.

Colonic fermentation of ispaghula, wheat bran, glucose, and albumin to short-chain fatty acids and ammonia evaluated in vitro in 50 subjects.

The production of short-chain fatty acids and ammonia was measured in 16.6% fecal homogenates from 50 subjects incubated at 37 degrees C for 6 and 24 hours. All 50 homogenates produced ammonia and short-chain fatty acids of any chain length (C2-C5). Incubation for 24 hours with dietary fiber (ispaghula husk or wheat bran), albumin, or glucose (10 mg/mL) increased the short-chain fatty acid production (43.6 +/- 2.8, 45.4 +/- 2.0, 60.3 +/- 3.2, and 65.8 +/- 3.1 mmol/L, respectively) compared with controls (21.4 +/- 1.3 mmol/L). The degradation of different substrates was associated with the production of different amounts of ammonia and short-chain fatty acids. Ispaghula, wheat bran, albumin, and glucose were fermented to acetate (> 2 mmol/L; 24-hour incubations) in 86%, 96%, 98%, and 98% of the homogenates, to propionate in 80%, 76%, 100%, and 68%, and to butyrate in 32%, 94%, 88%, and 54% of the homogenates, respectively. Isobutyrate, valerate, and isovalerate were produced from albumin in all (100%) of the homogenates, but only in 2 to 4% of the homogenates incubated with ispaghula or glucose. Ammonia was always (100%) produced after the addition of albumin and always (98%) consumed (assimilated) when glucose was fermented. Surgery (sigmoid or right- or left-sided colonic resection) did not change the pattern of ammonia and short-chain fatty acid production from these substrates. This study suggests that the different colonic flora from a large number of subjects share general biochemical characteristics, which metabolize different substrates to specific patterns of ammonia and short-chain fatty acids.

Fecal ammonia in patients with adenomatous polyps and cancer of the colon.

The correlation between high intakes of protein and high incidence of human colonic cancer is unexplained. Appreciable amounts of ammonia are generated in the large bowel through bacterial degradation of proteins and peptides, and experimental studies indicate that ammonia may select for neoplastic growth. Fecal concentrations of ammonia did not differ among 17 patients with former colonic adenomas [40.6 +/- 4.5 (SE) mM], 17 patients with former colonic cancer (51.4 +/- 3.9 mM), and 16 healthy controls (46.4 +/- 6.1 mM). By use of an in vitro fecal incubation system, possible alterations in bacterial fermentation and formation of ammonia were investigated. Fecal suspensions were incubated for 6 and 24 hours with and without addition of fermentable substrates (ispaghula husk, wheat bran, albumin, and glucose; 10 mg/ml). The in vitro production of ammonia in unsupplemented fecal homogenates from both groups of patients was comparable with the production found in homogenates from healthy controls, and the response to fermentable substrates was similar in all three groups. Addition of albumin caused a marked increase in the production of ammonia, and addition of glucose increased bacterial assimilation of ammonia considerably. These well-known characteristics of bacterial metabolism of ammonia apparently did not differ between healthy individuals and patients investigated more than three months after colonoscopic polypectomy or colonic cancer resection.

Colonic fermentation of dietary fibre to short chain fatty acids in patients with adenomatous polyps and colonic cancer.

Short chain (C2-C6) fatty acids are produced in the colon through bacterial fermentation of mainly dietary fibre. Butyrate (C4) possesses antineoplastic effects on human colon carcinoma cells, and epidemiological studies indicate that high fibre diets may reduce the incidence of colorectal cancer. The role of dietary fibre during colorectal carcinogenesis might therefore be related to its fermentation to butyrate. Faecal concentrations of total short chain fatty acids and concentrations and ratios of the individual C2-C6 fatty acids did not differ between 16 healthy controls, 17 patients with colonic adenomas, and 17 patients with colonic cancer. Comparison of the molar production velocities (mmol/l.hour) of total and individual short chain fatty acids from glucose, ispagula, wheat bran, and albumin in six and 24 hour faecal incubations showed no differences. The ratio of butyrate production to total short chain fatty acid production from fibre, however, was reduced in patients with colonic cancer and adenomas compared with healthy controls (ispagula, six hours: 6.4, 7.6, and 11.5% respectively, p = 0.005 and 24 hour: 9.1, 9.9, and 15.4%, p = 0.002; wheat bran, six hours: 9.9, 10.2, and 14.7% respectively, p = 0.06 and 24 hours: 15.1, 16.8, and 21.0%, p = 0.01). It may be that the low ratios of colonic butyrate formation combined with low fibre diets increase the risk of colonic neoplasia.

Application of P-31 nuclear magnetic resonance spectroscopy to a new experimental kidney perfusion model using cadaveric porcine kidneys from slaughterhouse.

Larger NMR magnets with relatively high field strengths have become available recently, allowing the application of magnetic resonance spectroscopy (MRS) in larger mammalian organs. The aim of this study was to develop and test a new and simple kidney perfusion model from slaughterhouse swine using a new 4.7-tesla/40-cm diameter system, with the intention behind to provide a human-like mammalian experimental kidney perfusion model, and to avoid sensitive in vivo animal experiments on higher-developed mammalians, 35 pig kidneys obtained 10-15 min post mortem were studied to evaluate and define conditions for optimum metabolic preservation with the following perfusion protocols: (1) immediate plegia with cold Collins solution, 1-3 h cold storage, P-31 MRS; (2) immediate plegia, 1-3 h cold storage, blood reperfusion, P-31 MRS; (3) immediate blood reperfusion, plegia, 1-3 h cold storage, blood reperfusion, P-31 MRS; (4) immediate blood reperfusion, plegia, 24 h cold storage, blood reperfusion, P-31 MRS, P-31 MRS at 81 MHz with a double-tuned surface coil yielded the following results: [table: see text] Blood flow showed a weak correlation with beta-ATP/inorganic phosphate in protocols 3 and 4 of r = 0.64. Repeated reperfusion and ischemia experiments of this model allowed the on-line observation of the metabolic response of the energy phosphate pattern for several hours. In conclusion, slaughterhouse-harvested swine kidneys lend themselves to a simple, low-cost in vitro perfusion model, provided they are reperfused with arterial blood immediately after harvesting.(ABSTRACT TRUNCATED AT 250 WORDS)