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  • Wetlands  (6)
  • coupled transport  (4)
  • glucose  (4)
  • linkage analysis  (4)
  • loop diuretics  (4)
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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Regional environmental change 1 (1999), S. 47-57 
    ISSN: 1436-378X
    Keywords: Key words Meta-analysis ; Contingent valuation ; Wetlands ; Ecosystem functions
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Energy, Environment Protection, Nuclear Power Engineering
    Notes: Abstract There is growing interest in the potential for producing generally applicable models for valuing non-market environmental services which do not rely upon expensive and time-consuming survey work, but rather extrapolate results from previous studies. This paper presents a meta-analysis for the use and non-use values generated by wetlands across North America and Europe. The study assesses the socio-economic values attributable to the hydrological, biogeochemical and ecological functions provided by such complex environmental assets. The clustering of multiple values derived from single studies is examined through the application of multilevel modelling methods allowing for the hierarchical structure of such data.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 24 (1983), S. 231-237 
    ISSN: 1432-0428
    Keywords: Insulin ; Type 2 diabetes ; oscillations ; pulsations ; man ; vagotomy ; pacemaker ; atropine ; naloxone ; phentolamine ; propranolol ; glucose ; tolbutamide ; sodium salicylate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Plasma insulin and glucose concentrations were examined in man in a basal state from central venous samples taken at 1-min intervals for up to 2.5 h. Normal subjects have insulin oscillations of mean period 14 min (significant autocorrelation, p 〈 0.0001) with changes in concentration of 40% over 7 min. The pulsation frequency was stable through cholinergic, endorphin, α-adrenergic or β-adrenergic blockade, or small pertubations with glucose or insulin. Stimulation of insulin secretion by intravenous glucose, tolbutamide or sodium salicylate increased the amplitude of the insulin oscillations while the frequency remained stable. Patients with a truncal vagotomy or after Whipple's operation had longer-term oscillations of 33 and 37 min periodicity (autocorrelation: p 〈 0.0001), with insulin-associated glucose swings four times larger than those of normal subjects. Type 2 (non-insulin-dependent) diabetic patients had a similarly increased insulin-associated glucose swing of six times that seen in normal subjects. The hypothesis is proposed that the 14-min cycle of insulin production is controlled by a ‘pacemaker’ which assists glucose homeostasis. The longer 33–37-min oscillations, seen in those with denervation, may arise from a limit-cycle of the feedback loop between insulin from the B cells and glucose from the liver. The vagus may provide hierarchical control of insulin release.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0428
    Keywords: Insulin ; glucose ; insulin resistance ; man ; glucotoxicity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In vitro and in vivo studies have suggested that metabolic deterioration can be induced by hyperglycaemia per se. The effect of 53 h of 2.2 mg glucose · kg ideal body weight−1· min−1 was examined in four normal male subjects. This produced overnight hyperglycaemia of 6.0 mmol/l on the two nights of the study compared with 4.7 mmol/l on the control night (p〈0.05). In response there was a sustained, two-fold increase in basal plasma insulin (p〈0.005) and C-peptide (p〈0.05) levels. After two days of hyperglycaemia an increased Beta-cell response was demonstrated in response to an additional glucose infusion stimulus (estimated Beta-cell function median of 84% on the control day to 100% after two days glucose infusion). Plasma insulin and C-peptide responses to a 10.0 mmol/l hyperglycaemic clamp increased over the two days of the study (insulin from median 48 mU/l to 73 mU/l and C-peptide from median 2.0 pmol/ml to 2.6 pmol/ml). Glucose tolerance to the additional glucose infusion stimulus improved, suggesting that the increased insulin response during hyperglycaemia was enhancing peripheral glucose uptake. The calculated peripheral insulin sensitivity was unchanged during the hyperglycaemic clamp. Thus, in response to the two days of basal hyperglycaemia, both the basal and stimulated Beta-cell responses were enhanced and there was no evidence for ‘glucose toxicity’ to the Beta-cells.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-0428
    Keywords: Glucagon-like peptide-1 receptor ; non-insulin-dependent diabetes mellitus ; maturity onset diabetes of the young ; polymerase chain reaction ; linkage analysis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Glucagon-like peptide-1 (GLP-1) is a hormone derived from the preproglucagon molecule that is secreted by intestinal L cells and stimulates insulin secretion from betacells. The GLP-1 receptor is a candidate gene for diabetes mellitus, as mutations may induce the impaired insulin response that is a characteristic feature of NIDDM. To study the relationship between the GLP-1 receptor gene and NIDDM, linkage of a microsatellite polymorphism flanking the GLP-1 receptor gene with diabetes was investigated in three Caucasian families with MODY and in the nuclear families of 12 NIDDM probands. A cumulative LOD score −8.50 excludes linkage in these MODY pedigrees. A LOD score of −1.24 in the NIDDM nuclear pedigrees makes linkage improbable. Mutations in or near the GLP-1 receptor gene are unlikely to be the major cause of the inherited predisposition to NIDDM in Caucasian pedigrees, but we cannot exclude a role for this locus in a polygenic model or a major role in some pedigrees.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 31 (1988), S. 407-414 
    ISSN: 1432-0428
    Keywords: Genetics ; Type 2 (non-insulin-dependent) diabetes ; linkage analysis ; restriction fragment length polymorphism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In the last five years, genetic markers for a large number of diseases have been localised using linkage analysis of DNA polymorphisms in affected families. The site of the genetic defect or defects leading to Type 2 (non-insulin-dependent) diabetes mellitus, a common illness with a major genetic component, remains unknown. This is due, at least in part, to the lack of large well-defined Type 2 diabetic pedigrees suitable for linkage analysis. There are several features of the disease which make large pedigrees difficult to find. The late age of onset of most probands means that informative older generations are often dead, while there is difficulty in detecting disease in younger generations. The diagnostic criteria for diabetes are, as yet, dependent on an arbitrary cut-off along a continuum of plasma glucose. The high prevalence of the disease may also produce problems as, in any given family, diabetogenic genes may be contributed by more than one parent. Varieties of the disease with a well-defined inheritance, such as maturity onset diabetes of youth, are more suitable for linkage analysis but might be due to defects at a different gene locus. Despite these difficulties, once large well-defined pedigrees have been found, linkage analysis using both candidate genes and random highly polymorphic markers is the strategy most likely to find genetic markers for the disease.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-0428
    Keywords: Genetics ; Type 2 (non-insulin-dependent) diabetes ; insulin receptor ; linkage analysis ; maturity onset diabetes of the young
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The possibility of linkage between the human insulin receptor gene locus and diabetes was examined in three Type 2 (non-insulin-dependent) diabetic families and one family with maturity onset diabetes of the young. Insulin receptor gene haplotypes were established using BglII, Rsal and Sstl restriction enzyme digests of genomic DNA from all available family members. The digested DNA was subjected to agarose gel electrophoresis, Southern blotted, and hybridised to 32P-labelled human insulin receptor gene cDNA. In the pedigree with maturity onset diabetes of the young, formal linkage analysis allowed exclusion of close linkage between the insulin receptor locus and diabetes (logarithm of the odds for linkage versus non-linkage was −5.35 at recombination fraction of 0.01). This confirms the absence of linkage between insulin receptor and diabetes which has been reported in two similar pedigrees. In the three Type 2 diabetic families there were a minimum of 4 recombinants between the insulin receptor locus and diabetes, which makes a direct role for insulin receptor defects unlikely. The importance of using realistic estimates of penetrance when performing linkage analysis in a disease with a late age of onset is emphasised. In contrast to the one previous linkage analysis study of the insulin receptor gene, no specific association of diabetes with the rare Sstl Sl(-) allele was observed in either the maturity onset diabetes of the young or the Type 2 diabetic families.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-0428
    Keywords: Maturity-onset diabetes of the young ; glucokinase ; adenosine deaminase ; pituitary adenylate cyclase-activation polypeptide receptor ; hexokinase II ; glucagon-like peptide-1 receptor ; polymerase chain reaction ; linkage analysis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Maturity-onset diabetes of the young (MODY) is a form of non-insulin-dependent diabetes mellitus characterised by an early age of onset and an autosomal dominant mode of inheritance. Only a proportion of cases are due to mutations in the glucokinase gene. We have studied five Caucasian MODY families, including the first MODY family to be described, with five candidate genes implicated in regulation of insulin secretion. The affected subjects showed more marked hyperglycaemia than that found in subjects with glucokinase mutations. We assessed polymorphic markers close to the genes for glucokinase, hexokinase II, adenosine deaminase, pituitary adenylate cyclase-activating polypeptide receptor, and glucagon-like peptide-1 receptor. Linkage analysis with diabetes gave cumulative log of the odds (LOD) scores of less than -3, implying that mutations in these genes are unlikely to provide a major genetic contribution to this form of MODY.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-0428
    Keywords: β-cell function ; insulin resistance ; mathematical model ; intravenous glucose tolerance test ; glucose clamp ; insulin receptors ; Type 2 diabetes ; insulin ; glucose
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The steady-state basal plasma glucose and insulin concentrations are determined by their interaction in a feedback loop. A computer-solved model has been used to predict the homeostatic concentrations which arise from varying degrees of β-cell deficiency and insulin resistance. Comparison of a patient's fasting values with the model's predictions allows a quantitative assessment of the contributions of insulin resistance and deficient β-cell function to the fasting hyperglycaemia (homeostasis model assessment, HOMA). The accuracy and precision of the estimate have been determined by comparison with independent measures of insulin resistance and β-cell function using hyperglycaemic and euglycaemic clamps and an intravenous glucose tolerance test. The estimate of insulin resistance obtained by homeostasis model assessment correlated with estimates obtained by use of the euglycaemic clamp (Rs = 0.88, p 〈 0.0001), the fasting insulin concentration (Rs = 0.81, p 〈 0.0001), and the hyperglycaemic clamp, (Rs = 0.69, p 〈 0.01). There was no correlation with any aspect of insulin-receptor binding. The estimate of deficient β-cell function obtained by homeostasis model assessment correlated with that derived using the hyperglycaemic clamp (Rs = 0.61, p 〈 0.01) and with the estimate from the intravenous glucose tolerance test (Rs = 0.64, p 〈 0.05). The low precision of the estimates from the model (coefficients of variation: 31% for insulin resistance and 32% for β-cell deficit) limits its use, but the correlation of the model's estimates with patient data accords with the hypothesis that basal glucose and insulin interactions are largely determined by a simple feed back loop.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-0428
    Keywords: Basal insulin secretion ; adrenalin ; alpha blockade ; glucose ; insulinoma ; malignant insulinoma ; proinsulin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Basal insulin secretion has been thought to be via a different mechanism from stimulated insulin secretion, partly because it is not similarly suppressed by adrenalin. However, adrenalin normally causes hyperglycaemia, but if it is infused while the plasma glucose is kept constant there is marked suppression of insulin secretion. Sympathetic stimulation modulates basal insulin secretion, and alpha adrenergic blockade impaired the suppression of insulin secretion in response to hypoglycaemia. Four of five benign insulinomas had marked suppression of insulin secretion by adrenalin, but one malignant and one benign insulinoma had little suppression. Both had a raised proportion of their basal plasma insulin as proinsulin, and the impaired suppression of secretion by adrenalin probably signified an undifferentiated tumour.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Environmental management 11 (1987), S. 823-836 
    ISSN: 1432-1009
    Keywords: Backfilling ; Mitigation ; Wetlands ; Louisiana ; Dredging
    Source: Springer Online Journal Archives 1860-2000
    Topics: Energy, Environment Protection, Nuclear Power Engineering
    Notes: Abstract Returning canal spoil banks into canals, or backfilling, is used in Louisiana marshes to mitigate damage caused by dredging for oil and gas extraction. We evaluated 33 canals backfilled through July 1984 to assess the success of habitat restoration. We determined restoration success by examining canal depth, vegetation recolonization, and regraded spoil bank soils after backfilling. Restoration success depended on: marsh type, canal location, canal age, marsh soil characteristics, the presence or absence of a plug at the canal mouth, whether mitigation was on- or off-site, and dredge operator performance. Backfilling reduced median canal depth from 2.4 to 1.1 m, restored marsh vegetation on the backfilled spoil bank, but did not restore emergent marsh vegetation in the canal because of the lack of sufficient spoil material to fill the canal and time. Median percentage of cover of marsh vegetation on the canal spoil banks was 51.6%. Median percentage of cover in the canal was 0.7%. The organic matter and water content of spoil bank soils were restored to values intermediate between spoil bank levels and predredging marsh conditions. The average percentage of cover of marsh vegetation on backfilled spoil banks was highest in intermediate marshes (68.6%) and lowest in fresh (34.7%) and salt marshes (33.9%). Average canal depth was greatest in intermediate marshes (1.50 m) and least in fresh marshes (0.85 m). Canals backfilled in the Chenier Plain of western Louisiana were shallower (average depth = 0.61 m) than in the eastern Deltaic Plain (mean depth range = 1.08 to 1.30 m), probably because of differences in sediment type, lower subsidence rate, and lower tidal exchange in the Chenier Plain. Canals backfilled in marshes with more organic soils were deeper, probably as a result of greater loss of spoil volume caused by oxidation of soil organic matter. Canals ten or more years old at the time of backfilling had shallower depths after backfilling. Depths varied widely among canals backfilled within ten years of dredging. Canal size showed no relationship to canal depth or amount of vegetation reestablished. Plugged canals contained more marsh reestablished in the canal and much greater chance of colonization by submerged aquatic vegetation compared with unplugged canals. Dredge operator skill was important in leveling spoil banks to allow vegetation reestablishment. Wide variation in dredge performance led to differing success of vegetation restoration. Complete reestablishment of the vegetation was not a necessary condition for successful restoration. In addition to providing vegetation reestablishment, backfilling canals resulted in shallow water areas with higher habitat value for benthos, fish, and waterfowl than unfilled canals. Spoil bank removal also may help restore water flow patterns over the marsh surface. Increased backfilling for wetland mitigation and restoration is recommended.
    Type of Medium: Electronic Resource
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