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  • 1
    Electronic Resource
    Electronic Resource
    Effect of dexamethasone on insulin sensitivity, islet amyloid polypeptide and insulin secretion in humans (1993)
    Springer
    Diabetologia 36 (1993), S. 84-87 
    Details
    ISSN: 1432-0428
    Keywords: Islet amyloid polypeptide ; insulin ; dexamethasone ; insulin resistance ; Type 2 (non-insulin-dependent) diabetes mellitus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The response of islet amyloid polypeptide and insulin and their molar ratios were investigated in eight healthy volunteers before and after treatment with dexamethasone by oral and frequently-sampled intravenous glucose tolerance tests. Following dexamethasone treatment the insulin sensitivity index decreased significantly from 6.5±1.3 to 4.1±1.0 (μU·ml−1·min−1, p〈0.05. The area under the curve representing above-basal levels of insulin during oral glucose tolerance test increased significantly following dexamethasone treatment from 48132±9736 to 82230±14846 pmol·l−1·3 h−1, p〈0.05, the area under the curve of islet amyloid polypeptide increased from 1308±183 to 2448±501 pmol·l−1·3h−1, p〈0.05. The overall insulin/islet amyloid polypeptide molar ratios calculated from the area under the curve during the 3-h period of the oral glucose tolerance test was not significantly different before and after dexamethasone treatment (42±5 vs 40±4). During the oral glucose tolerance test the insulin/islet amyloid polypeptide ratio increased significantly from baseline to 30 min (p〈0.05), then declined towards initial values before and after dexamethasone treatment. In conclusion, dexamethasone induced a significant decrease in insulin sensivity and a significant increase in insulin secretion during the oral glucose tolerance test. However, in contrast to previous animal experiments we did not find a change in the insulin/islet amyloid polypeptide ratio before and after dexamethasone treatment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00399099
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  • 2
    Electronic Resource
    Electronic Resource
    Role of islet amyloid polypeptide secretion in insulin-resistant humans (1994)
    Springer
    Diabetologia 37 (1994), S. 188-194 
    Details
    ISSN: 1432-0428
    Keywords: Key words Islet amyloid polypeptide release, insulin secretion, insulin resistance, essential hypertension, obesity.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Although it is generally accepted that islet amyloid polypeptide is cosecreted with insulin, relatively few data on its kinetics are available. We therefore studied the dynamics of islet amyloid polypeptide release following oral and frequently sampled intravenous glucose tolerance tests in comparison to insulin and C-peptide using mathematical model techniques in 14 control subjects, 10 obese and 11 hypertensive patients. The fractional clearance rate of islet amyloid polypeptide (0.034±0.004 min–1 in control subjects, 0.058±0.008 in the obese and 0.050±0.008 in the hypertensive patients) was significantly different (p〈0.01) in each group compared with that of insulin (0.14±0.03 min–1) and similar to that of C-peptide (0.061±0.007 min–1), at least in the insulin-resistant subjects. Based on the insulin sensitivity index derived from the minimal model analysis of intravenous glucose tolerance test data, both the hypertensive (2.4±0.4 min–1/(µU/ml); p〈0.0005) and the obese (2.7±0.5; p〈0.001) patients demonstrated severe insulin resistance compared to control subjects (8.1±1.3). Marked insulin hypersecretion was found in the hypertensive (57.6±5.2 nmol·l–1 in 180 min; p〈0.001) and obese (60.8±10.1; p〈0.003) patients in comparison with control subjects (32.4±3.2). The release of islet amyloid polypeptide was significantly higher in the hypertensive (83.1±16.6 pmol/l in 180 min; p〈0.02) and obese (78.6±13.1; p〈0.005) patients than in control subjects (40.5±6.4). No correlation was found between islet amyloid polypeptide release and the insulin sensitivity index in any group. We conclude that, due to a significantly slower clearance of islet amyloid polypeptide in comparison to insulin, reliance on molar ratios between these two peptides might be misleading in the interpretation of islet amyloid polypeptide secretion especially under non-steady-state conditions. [Diabetologia (1994) 37: 188–194]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050092
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  • 3
    Electronic Resource
    Electronic Resource
    Effects of captopril treatment versus placebo on renal function in type 2 diabetic patients with microalbuminuria: a long-term study (1994)
    Springer
    Journal of molecular medicine 72 (1994), S. 961-966 
    Details
    ISSN: 1432-1440
    Keywords: Angiotensin-converting enzyme inhibitor ; Type 2 diabetes mellitus ; Microalbuminuria
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We evaluated the renal effect of long-term antihypertensive treatment (12 months) with the angiotensin-converting enzyme inhibitor captopril compared to placebo in 15 type 2 diabetic patients with microalbuminuria. The patients were randomly allocated to captopril (n = 9) or placebo (n = 6). After 1-year therapy no significant decrease in blood pressure was demonstrated with captopril (139 ± 17/80 ± 9 versus 138±13/76±6 mmHg) or placebo (138 ± 9/75 ± 6 versus 135 ± 14/79 ±10 mmHg). Only in a small hypertensive subgroup (n = 4) treated with captopril did we find a significant reduction in blood pressure (154 ± 2/88 ± 1 versus 142 ± 7/78 ± 5 mmHg,P 〈 0.05). The urinary albumin excretion rate did not change significantly either in the captopril group (95.6 mg/24 h, 25th percentile 138.4, 75th percentile 25.1; versus 127.8 mg/24 h, 25th percentile 29.3, 75th percentile 222) or in the placebo group (99.2 mg/24 h, 25th percentile 58.5, 75th percentile 125.8; versus 120.9 mg/24 h, 25th percentile 62.1, 75th percentile 179.7). There were also no alterations in renal blood flow or filtration rate. In the hypertensive subgroup treated with captopril a reduction in urinary albumin excretion rate after 3 and 6 months of treatment was observed (captopril 73.4 versus 24 and 41 mg/24 h,P 〈 0.05), but not after 12 months. Triglyceride and cholesterol levels remained constant before and after treatment while glycosylated hemoglobin decreased significantly after 12 months captopril (7.8 ± 0.9 versus 6.9 ± 0.7 mg%,P 〈 0.03). We conclude that in patients with type 2 diabetes with microalbuminuria angiotensin-converting enzyme inhibitors may have protective renal effects in so far as a lack of increase in urinary albumin excretion is equivalent to low progression in renal disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00577736
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  • 4
    Electronic Resource
    Electronic Resource
    XIX Symposium of the International Association for Comparative Research on Leukemia and Related Diseases (1998)
    Springer
    Journal of cancer research and clinical oncology 124 (1998), S. 220-230 
    Details
    ISSN: 1432-1335
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004320050158
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  • 5
    Electronic Resource
    Electronic Resource
    Versuche über die Dauer der postmortalen Erregbarkeit der Muskulatur verschiedener Fischarten bei Sauerstoffmangel (1919)
    Springer
    Pflügers Archiv 173 (1919), S. 400-421 
    Details
    ISSN: 1432-2013
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01722118
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  • 6
    Electronic Resource
    Electronic Resource
    Long-term treatment with nifedipine reduces urinary albumin excretion and glomerular filtration rate in normotensive type 1 diabetic patients with microalbuminuria (1994)
    Springer
    Acta diabetologica 31 (1994), S. 14-18 
    Details
    ISSN: 1432-5233
    Keywords: Microalbuminuria ; Calcium channel blockers ; Nifedipine ; Type 1 diabetes ; Diabetic nephropathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aim of the present study was to investigate the renal effects of long-term treatment with the calcium channel blocker nifedipine in normotensive type 1 diabetic patients with microalbuminuria. In a randomized, double-blind trial, 15 type 1 diabetic patients were treated with either nifedipine (n=8; dosage 30 mg/day) or placebo (n=7) for 12 months. At baseline and after 6 and 12 months of therapy, the albumin excretion rate (UAER, radioimmunoassay), glomerular filtration rate (GFR, chromium 51 ethylenediamine tetra-acetic acid clearance) and renal plasma flow (RPF, iodine 125 hippuran clearance) were determined. Nifedipine treatment caused a significant reduction of UAER after 6 and 12 months (median, Q1/Q3 in mg/24 h): baseline 84 (65/163); 6 months 35 (23/90),P〈0.02; 12 months 39 (15/79),P〈0.05. GFR was significantly decreased by nifedipine treatment (baseline 157±15, 6 months 122±8, 12 months 111±47 ml/min;P〈0.05, mean ± SEM), whereas RPF remained constant. Nifedipine treatment did not influence systolic (baseline 121±7, 12 months 124±2 mmHg, mean ± SEM) or diastolic (baseline 72±2, 12 months 74±3 mmHg) arterial blood pressure. With placebo treatment no significant alterations of UAER, GFR, RPF and arterial blood pressure were observed. Metabolic control was constant throughout the whole study period. Thus, 1 year's treatment with nifedipine reduces the UAER and GFR in normotensive type 1 diabetic patients without influencing the systemic arterial blood pressure. The data, however, do not present a recommendation for the general use of nifedipine in these patients as the exact intrarenal mechanism of calcium channel blockers in humans remains to be established.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00580754
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  • 7
    Electronic Resource
    Electronic Resource
    Intracellular expression of CD61 precedes surface expression (1999)
    Springer
    Annals of hematology 78 (1999), S. 472-474 
    Details
    ISSN: 1432-0584
    Keywords: Key words AML ; FAB-M7 ; Acute megakaryoblastic leukemia ; Cytoplasmic CD61
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  We report a case of acute myeloid leukemia which we have classified as acute megakaryoblastic leukemia because of intracytoplasmic expression of CD61. Light microscopy demonstrated agranular blasts which, by cytochemical staining, were negative for myeloperoxidase. Using flow cytometry, the blast cells were seen to be positive for HLA-DR, CD7, CD13, CD33, and CD34, thus revealing their myeloid origin. Immunophenotyping on fixed blood smears additionally showed positive reaction with the CD61 antibody, demonstrating the megakaryoblastic differentiation of the blasts. After permeabilization of the cell membrane, the intracytoplasmic CD61 expression was confirmed by flow cytometry. Cytogenetic analysis disclosed a del(7)(q21–22). Our findings suggest that cytoplasmic expression of CD61 may precede the cell-surface expression of this antigen and should therefore be investigated in all cases of acute leukemias with undifferentiated morphology and negative cytochemistry to set apart early FAB-M7 from FAB-M0.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002770050601
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