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- Moss, B, et al.
(författare)
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The determination of ecological status in shallow lakes - a tested system (ECOFRAME) for implementation of the European Water Framework Directive
- 2003
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Ingår i: Aquatic Conservation: Marine and Freshwater Ecosystems. - : Wiley. - 1052-7613. ; 13:6, s. 507-549
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Tidskriftsartikel (refereegranskat)abstract
- 1. The European Water Framework Directive requires the determination of ecological status in European fresh and saline waters. This is to be through the establishment of a typology of surface water bodies, the determination of reference (high status) conditions in each element (ecotype) of the typology and of lower grades of status (good, moderate, poor and bad) for each ecotype. It then requires classification of the status of the water bodies and their restoration to at least 'good status' in a specified period. 2. Though there are many methods for assessing water quality, none has the scope of that defined in the Directive. The provisions of the Directive require a wide range of variables to be measured and give only general guidance as to how systems of classification should be established. This raises issues of comparability across States and of the costs of making the determinations. 3. Using expert workshops and subsequent field testing, a practicable pan-European typology and classification system has been developed for shallow lakes, which can easily be extended to all lakes. It is parsimonious in its choice of determinands, but based on current limnological understanding and therefore as cost-effective as possible. 4. A core typology is described, which can be expanded easily in particular States to meet local conditions. The core includes 48 ecotypes across the entire European climate gradient and incorporates climate, lake area, geology of the catchment and conductivity. 5. The classification system is founded on a liberal interpretation of Annexes in the Directive and uses variables that are inexpensive to measure and ecologically relevant. The need for taxonomic expertise is minimized. 6. The scheme has been through eight iterations, two of which were tested in the field on tranches of 66 lakes. The final version, Version 8, is offered for operational testing and further refinement by statutory authorities.
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| 2. |
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| 3. |
- Ristow, M, et al.
(författare)
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Frataxin deficiency in pancreatic islets causes diabetes due to loss of beta cell mass
- 2003
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Ingår i: Journal of Clinical Investigation. - 0021-9738. ; 112:4, s. 527-534
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Tidskriftsartikel (refereegranskat)abstract
- Diabetes is caused by an absolute (type 1) or relative (type 2) deficiency of insulin-producing beta cells. We have disrupted expression of the mitochondrial protein frataxin selectively in pancreatic beta cells. Mice were born healthy but subsequently developed impaired glucose tolerance progressing to overt diabetes mellitus. These observations were explained by impairment of insulin secretion due to a loss of beta cell mass in knockout animals. This phenotype was preceded by elevated levels of reactive oxygen species in knockout islets, an increased frequency of apoptosis, and a decreased number of proliferating beta cells. Hence, disruption of the frataxin gene in pancreatic beta cells causes diabetes following cellular growth arrest and apoptosis, paralleled by an increase in reactive oxygen species in islets. These observations might provide insight into the deterioration of beta cell function observed in different subtypes of diabetes in humans.
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| 4. |
- Shoenfeld, Y, et al.
(författare)
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Prevalence and clinical correlations of antibodies against six beta 2-glycoprotein-I-related peptides in the antiphospholipid syndrome
- 2003
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Ingår i: Journal of Clinical Immunology. - 0271-9142. ; 23:5, s. 377-383
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Tidskriftsartikel (refereegranskat)abstract
- Two-hundred ninety five patients with the antiphospholipid syndrome (APS) were studied for the presence of antibodies against six anti-beta2GPI-related peptides Abs. The prevalence of a wide spectrum of clinical and laboratory parameters of APS was evaluated in all patients, and correlated with the presence of each anti-beta2GPI peptide antibody. The rates of the various antipeptides Abs ranged from 18.0 to 63.7%. Altogether, 87.1% of the patients had antibody reactivity against at least one of the six beta2GPI-related peptides. A high degree of simultaneous reactivity against several beta2GPI-peptides was found. Positive and negative correlations were found between several antipeptides Abs and the rates of thrombosis and fetal loss. Our results point to a heterogeneous activity of antiphospholipid Abs in APS patients, directed, often concurrently, against various epitopes of the beta2GPI molecule. Evaluation of APS patients for the presence of specific antipeptides Abs may be of a value in predicting the risk for future thrombotic and obstetrical complication, as well as for specific therapeutic purposes.
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