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Biomedical subjects

S W Mann

Publications and source records attributed to S W Mann.

11 recordsLinked to original sources
PubMed2003

Safety evaluation of functional ingredients.

Functional ingredients are a diverse group of compounds that are intended to produce a positive effect on the health of the consumer. The term "functional" is not meant to differentiate these ingredients from other ingredients historically consumed as part of the food supply that are indeed biologically active constituents, for example, nutrients. Indeed, all foods should be considered "functional". The term functional ingredient is meant to convey the function of these new ingredients, which is to produce a positive health outcome via physiological activity in the body. Functional ingredients encompass elements of drugs, nutrients and food additives. A framework for evaluation of the safety of functional ingredients utilizes an understanding of both the current regulatory frameworks in place as well as the characteristics that define these particular ingredients. The types of studies conducted and the data generated to support safety of functional ingredients is product-specific and can include compositional analysis, structure/toxicity analysis, evaluation of historical and intended exposure, animal studies, clinical/epidemiologic studies, and evaluation of special considerations such as potential for adverse food or drug interactions.

Animals↗
PubMed2000

A combined chronic toxicity/carcinogenicity study of sucralose in Sprague-Dawley rats.

The chronic toxicity and potential carcinogenicity of sucralose was evaluated by exposing Sprague-Dawley rats to dietary concentrations of this low-calorie sweetener both in utero and for up to 104 weeks following parturition. The rats assigned to the toxicity phase of this investigation were administered diets containing either 0% (control), 0.3% (3000 ppm), 1.0% (10,000 ppm) or 3.0% (30,000 ppm) sucralose. Each treatment group comprised 30 male and 30 female rats, of which 15 males and 15 females were sacrificed after 52 weeks of treatment. The surviving rats were killed following 78 weeks of sucralose administration. In the carcinogenicity phase of this investigation, groups of 50 male and 50 female rats were administered dietary sucralose at concentrations of 0% (control 1), 0% (control 2), 0.3%, 1.0% or 3.0% for 104 weeks. Evaluation of the data obtained from the two phases of this study showed that sucralose was not carcinogenic. Sucralose did not adversely affect the survival or clinical condition of the rats, and there were no toxicologically significant findings. Group mean body weight gain and food consumption were significantly decreased in a dose-dependent manner in sucralose-treated rats throughout the treatment period as compared to the controls. The primary effect of sucralose on food consumption, and secondarily on body weight gain, was established in later studies to be due to the fact that diets containing high concentrations of sucralose are unpalatable to rats. These subsequent studies established that the reduction of body weight gain seen in previous rat studies using sucralose in the diet at concentrations of 1% and below resulted from reduced food intake as a direct consequence of the unpalatable nature of sucralose. Similarly, at concentrations of 3% in the diet, it was shown that approximately 95% of the effect on body weight gain could be attributed to the reduction in food intake due to the reduced palatability of the diet, the remainder apparently due to a physiologic response to the high concentrations of non-digestible sucralose in the rats' diet. Complete toxicological evaluations of gavage studies with histopathological evaluations demonstrated that even at the 3% dietary level, toxicity was not responsible for the small body weight gain decrement. Gross and histopathologic examinations revealed that the administration of sucralose affected neither the types nor incidence of the tumours observed. The incidences of some non-neoplastic findings were statistically significantly increased in the sucralose treated groups relative to the controls. These included: renal pelvic epithelial hyperplasia in all female treatment groups, renal pelvic mineralization in females administered the intermediate or highest dietary concentrations of sucralose, adrenal cortical haemorrhagic degeneration in high-dose group female rats, and the histopathologic incidence of cataracts at necropsy in high-dose group male rats. The non-neoplastic findings that occurred were of no toxicological significance since they were either spontaneous findings commonly observed in aged rats of this strain or the physiological response to high dietary levels of a poorly absorbed compound.

Administration, Oral↗
PubMed2000

A carcinogenicity study of sucralose in the CD-1 mouse.

The potential carcinogenicity of sucralose was evaluated by feeding groups of 52 male and 52 female CD-1 mice a diet containing sucralose at 0.3% (3000 ppm), 1.0% (10,000 ppm) or 3.0% (30,000 ppm) for 104 weeks. A group of 72 male and 72 female mice received diet without sucralose and served as controls. Week 1 achieved doses ranging from 543 to 5870mg/kg body weight/day in the low-dose males and high-dose females, respectively. Sucralose had no adverse effect on survival. No significant changes attributable to sucralose were found in the clinical condition or behaviour of the mice. Organ weights and the gross appearance of tissues were unaffected by treatment. The mean erythrocyte counts of females receiving the highest dietary concentration were slightly, but statistically significantly, lower than those of the controls after 104 weeks of treatment. Group mean body weight gain at the highest dietary concentration of sucralose was significantly less than that of the control in mice of both sexes. Food consumption, after correction for sucralose content, was lower for female mice, but not statistically significant. Water consumption for male mice receiving the highest dietary concentration was approximately 9% higher than that of the controls. There were statistically significant increases in the incidence of several non-neoplastic findings, but these were not considered to be related to sucralose administration. Treatment with sucralose did not increase the incidence of any tumour or influence the types of tumours observed. It was concluded that sucralose is not carcinogenic in CD-1 mice. The body weight gain and erythrocyte observations at the 3.0% dietary level were of limited biological significance as they were not accompanied by any histopathologic finding and had no impact on survival. The remaining dose levels were judged to have no effects.

Administration, Oral↗
PubMed1987

Introduction of an ion selective sodium and potassium analyser in a paediatric intensive care unit: our experience over a 3-year period.

We describe our approach, policy and experience in establishing a sodium and potassium analyser for use by medical and laboratory staff in a satellite laboratory adjacent to a paediatric intensive care unit. The effects on patient care are difficult to quantify, but are felt to be beneficial. A reduction in 'out of hours' laboratory workload and significant financial savings have been achieved.

Child, Preschool↗
PubMed1983

Mutagenic evaluations of four rubber accelerators in a battery of in vitro mutagenic assays.

The mutagenic/carcinogenic potential of four commercial accelerators were evaluated using a battery of in vitro assays. All of these compounds were mutagenic in one or more assays. Positive responses were noted in the Escherichia coli pol A+/pol A- DNA repair, mouse lymphoma L5178Y TK+/- forward mutation, BALB/3T3 cell transformation, and CHO cell chromosome aberration assays. In contrast to previous studies of accelerators, no mutagenic response was observed in the E coli WP2 uvrA- assay or in any of the Salmonella typhimurium strains tested. These studies have indicated that rubber accelerators should be regarded as potential human health hazards and that further in vitro and in vivo studies are needed to assess the potential genetic hazards of this large class of chemicals.

Benzothiazoles↗
PubMed1979

Hepatic prolyl hydroxylase and collagen synthesis in patients with alcoholic liver disease.

Hepatic prolyl hydroxylase activity and collagen synthesis were measured in patients with alcoholic liver disease to determine the feasibility of using the enzyme prolyl hydroxylase as a marker of hepatic fibrogenesis. Alcoholic patients with liver histopathology consistent with normal, steatosis, alcoholic hepatitis, early cirrhosis, or advanced cirrhosis were analysed for liver prolyl hydroxylase activity and in vitro collagen synthesis. Prolyl hydroxylase activity and the rate of in vitro collagen synthesis were correlated when these parameters were measured in samples of the same liver biopsy. Mean prolyl hydroxylase activity was significantly raised in all groups of alcoholic patients with alcoholic liver disease, except those with steatosis, when compared with alcoholic patients with normal morphology. Alcoholic patients with early cirrhosis had enzyme activity (mean +/- SE: 1.367 +/-0.162 mU/mg protein) significantly raised over all other groups. Mean enzyme activity was less raised (0.985 +/- 0.097 mU/mg protein) in patients with advanced cirrhosis. The percentage of collagen synthesis in patients with early or advanced cirrhosis was also raised compared with alcoholic patients with normal morphology. Prolyl hydroxylase activity and the rate of collagen synthesis are significantly correlated (r=0.62). These findings suggest that hepatic prolyl hydroxylase activity is a useful indicator of hepatic fibrogenesis and its measurement on available liver biopsy tissue should be a potent diagnostic tool reflecting active fibrogenesis and predicting progression of alcoholic liverdisease.

Adult↗