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  • 1
    Electronic Resource
    Electronic Resource
    Observed correlations between aftershock spatial distribution and earthquake fault lengths (2000)
    Oxford UK : Blackwell Science Ltd
    Terra nova 12 (2000), S. 0 
    Details
    ISSN: 1365-3121
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Geosciences
    Notes: We observe the spatial distributions of the magnitude of aftershocks following the six earthquakes of focal depth shallower than 20 km with magnitude more than 5.0 from 1983 to 1987 in Japan. The upper limit of the aftershock magnitude is examined as a function of the distance from mainshock hypocentre. The observed spatial distributions of the upper limit are bimodal, with a tendency of the upper limit to decrease as the distance from mainshock hypocentre increases. Moreover, we observe the correlations between the aftershock spatial distribution and earthquake fault length. We focus on the largest aftershocks in each of two aftershock sequences constituting the bimodal distribution. The distances of the two largest aftershocks from the mainshock hypocentre are equal to the fault lengths of shallow earthquakes in Japan and to the maximum earthquake fault lengths.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-3121.2000.00329.x
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Spatial Distribution of Aftershocks and the Fractal Structure of Active Fault Systems (2000)
    Springer
    Pure and applied geophysics 157 (2000), S. 575-588 
    Details
    ISSN: 1420-9136
    Keywords: Key Words: Aftershock, active fault system, fractal, fractal dimension, spatial distribution.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Geosciences , Physics
    Notes: Abstract —The relationship between the fractal dimensions of aftershock spatial distribution and of pre-existing fracture systems is examined. Fourteen main shocks occurring in Japan were followed by aftershocks, and the aftershocks occurred in swarms around the main shock. Epicentral distributions of the aftershocks exhibit fractal properties, and the fractal dimensions are estimated by using correlation integral. Observable pre-existing active fault systems in the fourteen aftershock regions have fractal structures, and the fractal dimensions are estimated by using the box-counting method. The estimated fractal dimensions derive positive correlation, showing independence from the main-shock magnitude. The correlation shows that aftershock distributions become less clustered with increasing fractal dimensions of the active fault system. That is, the clusters of the aftershocks are constrained under the fractal properties of the pre-existing active fault systems. If the fractal dimension of the active fault system is the upper limit value of the fractal dimension of the actual fracture geometries of rocks, then the clustering aftershocks manifest completely random and unpredictable distribution.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00001108
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Simple tandem repeat DNA polymorphism in the human glycogen synthase gene is associated with NIDDM in Japanese subjects (1994)
    Springer
    Diabetologia 37 (1994), S. 536-539 
    Details
    ISSN: 1432-0428
    Keywords: Key words NIDDM, glycogen synthase, DNA polymorphism, genetics, hypertension.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We investigated the possible association between alleles of a simple tandem repeat DNA polymorphism in the human glycogen synthase gene and non-obese non-insulin-dependent diabetes (NIDDM) in Japanese subjects. Nine alleles (−4G, −3G, −2G, −1G, 0G, 1G, 2G, 3G, and 4G) were identified in the study group of 164 patients with NIDDM and 115 non-diabetic subjects. The overall frequency distribution of the glycogen synthase gene alleles was significantly different between the two groups (p =0.0316). The 2G allele was found more frequently in patients with NIDDM than in non-diabetic subjects (17.7 % vs 8.7 %, p =0.0016). These results suggest that the 2G allele could be a genetic marker of NIDDM in Japanese subjects. [Diabetologia (1994) 37: 536–539]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050144
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Islet amyloid polypeptide amide causes peripheral insulin resistance in vivo in dogs (1990)
    Springer
    Diabetologia 33 (1990), S. 118-120 
    Details
    ISSN: 1432-0428
    Keywords: Islet amyloid polypeptide ; amylin ; amidation ; invivo effect ; insulin resistance ; diabetes mellitus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Islet amyloid polypeptide is a 37 amino acid hormone-like peptide which is the major protein component of islet amyloid deposits commonly found in patients with Type 2 (non-insulin-dependent) diabetes mellitus. Recent studies indicate that a physiologically active form of this peptide appears to be carboxyamidated and secreted from the insulin-producing beta cell. In order to clarify the possible in vivo actions of islet amyloid polypeptide, we have studied the effects of synthesized islet amyloid polypeptide-amide on peripheral glucose utilization by performing hyperinsulinaemic euglycaemic glucose clamp studies on dogs. Exogenously administered islet amyloid polypeptide-amide (an infusion from 1.0 to 100 μg·kg−1·h−1, over 2 h) inhibited the insulin-stimulated glucose disposal rate in a dose dependent manner. Twenty-five μg·kg−1·h−1 of islet amyloid polypeptide-amide infused via a peripheral vein significantly lowered the glucose disposal rate by 20% (from 17.4±1.7 to 14.4±1.7 mg·kg−1·min−1, n = 5, p〈0.01). These findings suggest that islet amyloid polypeptide-amide causes peripheral insulin resistance in vivo.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00401051
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Plasma islet amyloid polypeptide (Amylin) levels and their responses to oral glucose in Type 2 (non-insulin-dependent) diabetic patients (1991)
    Springer
    Diabetologia 34 (1991), S. 129-132 
    Details
    ISSN: 1432-0428
    Keywords: Islet amyloid polypeptide ; amylin ; diabetes mellitus ; fasting concentration ; oral glucose tolerance test
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Fasting plasma islet amyloid polypeptide concentrations and their responses to an oral glucose load were determined in non-diabetic control subjects and patients with abnormal glucose tolerance in relation to the responses of insulin or C-peptide. Plasma islet amyloid polypeptide was measured by radioimmunoassay. In the non-diabetic control subjects, fasting plasma islet amyloid polypeptide was 6.4±0.5 fmol/ml (mean ± SEM) and was about 1/7 less in molar basis than in insulin. The fasting islet amyloid polypeptide level rose in obese patients and fell in patients with Type 1 (insulin-dependent) diabetes mellitus. In non-obese patients with impaired glucose tolerance and Type 2 (non-insulin-dependent) diabetic patients without insulin therapy, the level was equal to that of the control subjects, but a low concentration of islet amyloid polypeptide relative to insulin or C-peptide was observed in the non-obese Type 2 diabetic group. The patterns of plasma islet amyloid polypeptide responses after oral glucose were similar to those of insulin or C-peptide. However, compared to non-obese patients, a hyper-response of islet amyloid polypeptide relative to C-peptide was noted in obese patients who had a hyper-response of insulin relative to C-peptide. This study suggests that basal hypo-secretion of islet amyloid polypeptide relative to insulin exists in non-obese Type 2 diabetes and that circulating islet amyloid polypeptide may act physiologically with insulin to modulate the glucose metabolism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00500385
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    Paper (German National Licenses)
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