Adapting sanitary inspections for the monitoring of small drinking water supplies in Iceland.

Sanitary inspections (SIs) are checklists of questions used to identify actual and potential sources and pathways of drinking water contamination. Though the importance of SI adaptation to local contexts is widely acknowledged, there is currently limited guidance on how this should be undertaken in practice. During this research, World Health Organization (WHO) draft template SI forms for spring and borehole supplies were adapted for use in Iceland based on a series of desk reviews and field tests, an approach which may guide other future SI adaptation processes. SI results were collected from 25 spring supplies and nine borehole supplies in three regions of Iceland using adapted SI forms. These results were combined with 10-year historical water quality data from the same supplies to explore potential relationships between both data sets. Binary logistic regression test results indicated a statistically significant association (P = 0.025; odds ratio (OR) 1.864, 95% CI 1.080-3.220) between SI Question 3 (Does ponding from surface water occur around the spring/borehole?) receiving a 'High' risk level assignment and at least one historical incidence of water quality noncompliance for the parameters heterotrophic plate count 22 °C, total coliforms, Escherichia coli, and turbidity at the same supply. The significant modifications applied to the starting template during the testing and development of the Icelandic SI form emphasises the importance of a robust adaptation process to ensure SI forms are appropriate for the local context. Results from the analysis of SI and water quality test results demonstrated the potential for these data sets to identify the primary risks at a supply. This information may then be used to direct remedial actions, especially when the amount of relevant data increases over time.

[Factor VQ50f) and prothrombin 20210 A mutations in an Icelandic apparently healthy population and patients suffering from venous thrombosis.].

INTRODUCTION: Inherited and aquired factors are important in the pathogenesis of thrombosis. Recent studies have demonstrated that mutations in the genes encoding coagulation factor V (FVQ506 or FVLeiden) and prothrombin (PT 20210 A) predispose to a markedly increased risk of venous thrombosis. FVQ506 is considered to be the most frequent cause of inherited venous thrombosis in Europeans and the allele frequency has been shown to be high. The aim of this study was to determine the allele frequency of the two mutations in an apparently healthy Icelandic population and patients suffering from venous thrombosis. MATERIAL AND METHODS: An apparently healthy Icelandic population and patients suffering from venous thrombosis were genotyped for the presence or absence of the FVQ506 and PT 20210 A mutations using PCR and restrictions fragment length polymorphisms. RESULTS: The allele frequency of FVQ506 was 0.0315 in the healthy population (n=159; 10 heterozygotes found). Fifteen of 99 patients with venous thrombosis were found to be heterozygous for FVQ506 (15.2%; allele frequency 0.071), significantly more when compared to controls (p<0.01). One apparently healthy individual (0.9%; n=108) and one of the patients (0.95%; n=99) were found to be heterozygous for PT 20210 A. CONCLUSION: The results demonstrate high prevalence of FVQ506 in the Icelandic population compared with many other European populations and that FVQ506 is commonly associated with venous thrombosis.

[Distribution of alpha1-antitrypsin phenotypes in Icelanders.].

Although the Z and S alleles causing alpha1-arantitrypsin deficiency are present at a high frequency in Northern Europeans, alpha1-arantitrypsin deficiency has never been identified in an Icelandic patient. In this study the frequency of the major alpha1-antitrypsin phenotypes M, F, S and Z, was determined in 511 unrelated Icelandic individuals by isoelectric focusing in polyacrylamide gel slabs. The frequencies of the alleles in this population were: M = 0.946; F = 0.006; S = 0.037; and Z = 0.011. The results demonstrate the presence of alpha1-arantitrypsin deficiency alleles in the Icelandic population at somewhat lower allele frequency than is found in the other Nordic populations.

Glucocorticoids enhance the gamma-interferon augmentation of human monocyte immunoglobulin G Fc receptor expression.

At physiologic and therapeutic concentrations, glucocorticoids decrease the number of Fc receptors for IgG (Fc gamma R) on human monocyte-like cell lines. In comparison, gamma-interferon (IFN-gamma) increases Fc gamma R expression on both human monocytes and monocyte-like cell lines. In this study, we examined the combined effects of glucocorticoids and IFN-gamma on human monocyte expression of the high affinity (72 kDa) Fc gamma R. Mononuclear cells prepared from heparinized venous blood of normal donors were treated for up to 90 hr with or without recombinant IFN-gamma and/or steroids. Monocyte Fc gamma R were measured by Scatchard analysis of the binding of human monomeric 125I-IgG1; indirect immunofluorescence plus flow cytometry, utilizing a monoclonal antibody (MoAb 32) which is specific for the high affinity Fc gamma R; and direct immunofluorescence using fluorescein isothiocyanate-labeled human monomeric IgG1 and flow cytometry quantitated using U-937 cells as a standard. Cultured monocytes incubated in the presence of both glucocorticoids and IFN-gamma for 18 hr had significantly higher (p less than 0.01) Fc gamma R levels than monocytes treated with IFN-gamma alone. The effect of combined treatment reached a plateau by 42 hr of incubation without increasing expression of other surface markers tested. Treatment with glucocorticoids alone did not consistently decrease monocyte Fc gamma R levels after either 18 or 42 hr of culture. Only glucocorticoids augmented the IFN-gamma increase in Fc gamma R; other steroids tested had no effect on IFN-gamma action. Furthermore, the effect was observed after treatment with only one type of interferon, IFN-gamma. These results describe a glucocorticoid immunoregulatory effect that may explain why combined IFN-gamma plus glucocorticoid treatment enhances mononuclear phagocyte Fc-mediated functions.