Reduced concentrations of several vitamins in normal weight patients with late-onset dementia of the Alzheimer type without vascular disease.

BACKGROUND: There is an uncertainty to what an extent initiation of late onset dementia of the Alzheimer type (DAT) is related to nutritional factors. OBJECTIVE: To find any differences in nutrient concentrations between women (75-85 y), well-nourished with moderate DAT, and a control group, all without vascular disease. DESIGN: A case control study assessing clinical, anthropometrical, biochemical and micronutrient characteristics of 20 DAT patients and 18 free-living healthy women. RESULTS: Significant differences (* = p < 0.05) were found for the following nutrients, given in sequence (Mean (SD)) for controls and DAT patients, respectively: Thiamine (nmol/L): 11.7 (6.9), 7.1(3.7)*; Blood thiamine diphosphate (nmol/L): 86.0 (12.5), 65.8 (27.5)*; Pyridoxal-5-phosphate 90.2 (14), 24.8 (3.3)*; Cobalamin (nmol/L) 435(263), 350 (264)*; Homocysteine (mmol/L) 14.7 (1.3), 18.5 (1.6)*; Ascorbic acid (mmol/L) 77.7 (28), 46.2 (25)*; alpha-tocopherol (mmol/L) 38.2 (9.2), 27.1 (11.5)*; Serum and blood thiamine mono-phosphate and ascorbic acid in cerebrospinal fluid were significantly different as well. Age, BMI, MMSE, MADRS, 'Vascular Score ' and a set of other biochemical parameters were similar between the groups. Using logistic regression analysis, models for predicting the presence of DAT all contained pyridoxal-5-phosphate, and CSF-protein, in combination with either one of variables, age, ascorbic acid, retinol, alpha-tocopherol, homocysteine, thiamin-diphosphate, CSF-thiamin. All the models give complete separation between DAT and controls. CONCLUSIONS: The presence of reduced concentrations of several vitamins in the DAT patients compared to the controls might indicate that these nutrients may contribute to the development of DAT.

[Clostridium difficile infection. The nosocomial aspect]. / Clostridium difficile-infeksjon. Det nosokomiale aspektet.

Clostridium difficile infection is discussed relatively rarely as a nosocomial problem in Norway. Epidemiological studies have shown Clostridium difficile diarrhoea to be frequently an antibiotica-associated nosocomial disease. We describe a material consisting of 22 patients with Clostridium difficile infection from a county hospital in Norway. The inclusion criteria were a clinical disease with diarrhoea and a positive test for Clostridium difficile toxin A and/or B in the faeces. 11 patients were or had been hospitalized for a short period in one specific medical ward when diagnosed. These and five other patients probably had a hospital-acquired Clostridium difficile infection. We discuss the nosocomial aspect and the clinical characteristics of the disease in our material.

Metabolism and transport of amino acids studied by immunocytochemistry.

The immunocytochemical method for demonstrating amino acids makes it possible to study accumulation and depletion of amino acids in individual tissue compartments resulting from experimental manipulations. We have incubated hippocampal slices in oxygenated Krebs solution, containing various additives, under basal conditions and during synaptic release of transmitters evoked by elevated K+ concentrations or by veratrine. Immunoreactivities for glutamate (Glu-LI), aspartate (Asp-LI), glutamine (Gln-LI), gamma-amino-butyrate (GABA-LI) and taurine (Tau-LI) have been demonstrated by specific antibodies after fixation of the slices in glutaraldehyde. Prolonged depolarisation depleted Glu-LI, Asp-LI and Gln-LI from nerve-ending-like structures. GABA-LI was less affected and Tau-LI not affected at all. The depletion of immunoreactivities could be prevented by metabolic precursors of transmitter amino acids, notably glutamine. This effect of glutamine was abolished by inhibiting glutaminase with diazooxonorleucine. Glu-LI, Asp-LI, GABA-LI and Gln-LI accumulated in astroglial cells during conditions of prolonged depolarization-induced release. The accumulation of GABA-LI in glia was strongly increased by inhibition of aminotransferases by aminooxyacetic acid. The described changes in Glu-LI were prevented by low Ca2+/high Mg2+, and promoted when the glial enzyme glutamine synthetase was inhibited by methionine sulfoximine. D-Aspartate, a metabolically inert competitive inhibitor/substrate for high affinity uptake of glutamate, inhibited the accumulation of Glu-LI in glia. The results confirm the biochemically derived theories on metabolic compartmentation in nervous tissue, and add knowledge on the dynamics of the cellular distribution of amino acids. They also indicate the possibilities offered by the present approach for studying metabolism and pharmacology at the cellular level.