SUMMARYPaneth cells are important contributors to the intestinal antimicrobial barrier through synthesis and release of antimicrobial peptides and proteins. Animal studies indicate that Paneth cell numbers, location and granule morphology are altered by infection and zinc status. We examined human tissue to determine whether Paneth cell numbers, distribution or granule morphology are altered in infective, inflammatory and nutritional disorders. Archival sections from infective disorders (giardiasis, cryptosporidiosis, HIV, helminth infection) were compared with active inflammatory conditions (coeliac, Crohn's and graft-versus -host diseases) and histologically normal tissues. A subset of tissues was studied by electron microscopy and TUNEL staining for apoptosis. Human defensin-5 (HD5) peptide and mRNA was analysed by immunohistochemistry, in situ hybridization and quantitative reverse transcription polymerase chain reaction. Sections from a tropical population cohort study were then analysed to determine the relationship of granule depletion to infection, nutritional status and plasma zinc concentration. In HIV-related cryptosporidiosis, but not other disorders, Paneth cells were reduced in number and markedly depleted of granules. Paneth cell granule depletion was associated with reduced HD5 immunoreactivity, but this was not due to apoptosis and there was no reduction in mRNA transcripts. In the tropical population studied, depletion of granules was associated with reduced body mass index, reduced plasma zinc levels and HIV infection. Paneth cell granules in human small intestine may be depleted in response to infective and nutritional stress. We postulate that this is one mechanism through which zinc status influences host susceptibility to intestinal infection.

BackgroundThere is a growing volume of research to offer improvements in nutritional care for people with dementia living in nursing homes. Whilst a number of interventions have been identified to support food and drink intake, there has been no systematic research to understand the factors for improving nutritional care from the perspectives of all those delivering care in nursing homes. The aim of this study was to develop a research informed model for understanding the complex nutritional problems associated with eating and drinking for people with dementia.MethodsWe conducted nine focus groups and five semi-structured interviews with those involved or who have a level of responsibility for providing food and drink and nutritional care in nursing homes (nurses, care workers, catering assistants, dietitians, speech and language therapists) and family carers. The resulting conceptual model was developed by eliciting care-related processes, thus supporting credibility from the perspective of the end-users.ResultsThe seven identified domain areas were person-centred nutritional care (the overarching theme); availability of food and drink; tools, resources and environment; relationship to others when eating and drinking; participation in activities; consistency of care and provision of information.ConclusionsThis collaboratively developed, person-centred model can support the design of new education and training tools and be readily translated into existing programmes. Further research is needed to evaluate whether these evidence-informed approaches have been implemented successfully and adopted into practice and policy contexts and can demonstrate effectiveness for people living with dementia.

1. Urea kinetics were measured by using prime/intermittent oral doses of [15N15N]urea in five healthy men taking formula diets adequate in energy and containing either 70 or 35 g of protein/day. In some studies the low-protein diet was supplemented with non-starch polysaccharides in the form of ispaghula husk or ripe bananas. 2. On the 70 g of protein/day diet urea production was 132% of intake. Only 54% of the urea produced was excreted in the urine with 46% being salvaged in the colon; 90% of the salvaged nitrogen was retained in the metabolic nitrogen pool. 3. On the 35 g of protein/day diet the small decrease in urea production rate compared with that on the 70 g of protein/day diet was not significant, but only 36% of the urea produced was excreted in urine, with the majority, 64%, being salvaged. 4. The extent of urea-nitrogen salvaging on the 35 g of protein/day diet was similar in magnitude to the decrease in nitrogen intake, with the effect that the sum of intake and salvaged nitrogen did not differ between the 35 and the 70 g of protein/day diets. This implies that quantitative control is exerted over the rate at which urea nitrogen is salvaged. 5. The addition of non-starch polysaccharides to the 35 g of protein/day diet had a demonstrable effect upon faecal weight and composition, but did not exert any significant influence upon urea kinetics.(ABSTRACT TRUNCATED AT 250 WORDS)

The gastrointestinal handling and metabolism of [1-13C]palmitic acid given as the free fatty acid was examined in six healthy women by measuring the excretion of 13C-label in stool and in breath as 13CO2. The gastrointestinal handling of [1-13C]palmitic acid was compared with the apparent absorption of dietary lipid by measuring lipid losses in stool. The variation both within and between subjects was determined by repeating the study in the same individuals on separate occasions. The time course for excretion of label in stool over the five-day study period followed a common pattern, with most of the label excreted over the first two days of the stool collection. 13C-Label excreted in stool over the five-day study period was 14.3 +/- 9.8% of that administered and on repeating the trial was 31.6 +/- 24.7% (not significantly different due to variability); there was poor agreement within subjects. Lipid excreted in stool expressed as a percentage of ingested lipid was 5.2 +/- 4.4% in Trial 1 and 5.9 +/- 4.0% in Trial 2, and was the same in each individual on repeating the trial. There was no clear relationship between the excretion of 13C-label and lipid in stool (Trial 1: R = -0.43, P > 0.40; Trial 2: R = -0.02, P > 0.97). On the first occasion, 22.0 +/- 4.5% of the administered label was excreted on breath over the 15-h study period and on repeating the trial was 15.8 +/- 9.5% (not significantly different) with poor repeatability in a given individual.(ABSTRACT TRUNCATED AT 250 WORDS)

The gastrointestinal handling and metabolic disposal of [1-13 C]palmitic acid, [1-13 C]stearic acid and [1-13 C]oleic acid administered within a lipid-casein-glucose-sucrose emulsion were examined in normal healthy women by determining both the amount and nature of the 13 C label in stool and label excreted on breath as 13 CO 2 . The greatest excretion of 13 C label in stool was in the stearic acid trial (9 . 2 % of administered dose) whilst comparatively little label was observed in stool in either the palmitic acid (1 . 2 % of administered dose) or oleic acid (1 . 9 % of administered dose) trials. In both the palmitic acid and oleic acid trials, all of the label in stool was identified as being present in the form in which it was administered (i.e. [13 C]palmitic acid in the palmitic acid trial and [13 C]oleic acid in the oleic acid trial). In contrast, only 87 % of the label in the stool in the stearic acid trial was identified as [13 C]stearic acid, the remainder was identified as [ C]stearic acid within the gastrointestinal tract. Small, but statistically significant, differences were observed in the time course of recovery of 13 C label on breath over the initial 9 h of the study period (oleic acid ¼ palmitic acid > stearic acid). However, when calculated over the 24 h study period, the recovery of the label as 13 CO 2 was similar in all three trials (approximately 25 % of absorbed dose). These results support the view that chain length and degree of unsaturation may influence the gastrointestinal handling and immediate metabolic disposal of these fatty acids even when presented within an emulsion. Fatty acids: Postprandial lipid metabolism: Stable isotopes