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  • Articles: DFG German National Licenses  (2)
  • 1985-1989  (2)
  • Polyoxyethylene cholesteryl ethers  (1)
  • diabetes mellitus  (1)
  • 1
    ISSN: 1432-0428
    Keywords: Renal kallikrein ; urinary kallikrein excretion ; diabetes mellitus ; hypertension ; nephropathy ; plasma aldosterone concentration ; plasma renin activity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We measured the 24-h excretion of urinary kallikrein in 27 patients with Type 2 (non-insulin-dependent) diabetes and in 10 normal control subjects. Mean (± SD) kallikrein excretion in diabetic patients with nephropathy (6.2±2.4 naphthyl units (NU)/day,n=13) was significantly lower than in control subjects (12.8±3.4NU/day,p〈0.01) and in diabetic patients without nephropathy (9.4±3.4NU/day,n=14,p〈0.05). Kallikrein excretion in hypertensive diabetic patients with nephropathy (5.1±1.6 NU/day,n=8) was significantly lower (p〈0.05) than in normotensive patients with nephropathy (8.3±2.1 NU/day,n=5). There were no significant differences in kallikrein excretion rate (24-h excretion of urinary kallikrein/24-h creatinine clearance) among control subjects (9.9±4.3 NU/ml), diabetic patients with (9.0±3.2 NU/ml) and without (9.3±3.5 NU/ml) nephropathy. However, kallikrein excretion rate in hypertensive diabetic patients with nephropathy (7.7±3.3 NU/ml) was significantly lower (p〈0.05) than in normotensive diabetic patients with nephropathy (11.8 ±2.0 NU/ml,n=10). Respective basal and post-stimulated (with intravenous furosemide 40 mg plus 60 min ambulation) plasma aldosterone concentrations measured in control subjects and in hypertensive diabetic patients with nephropathy were similar and increased to the same extent in the 2 groups (5.5±3.2 versus 5.3±3.2 and 9.3±2.6 versus 10.5±3.4 ng/ml), although the respective plasma renin activity tended to be lower in diabetic patients than in control subjects (0.7±0.6 versus 1.3±0.9 and 1.8±1.8 versus 3.0±2.6 ng−1 · ml−1 · h−1). The results indicate that urinary kallikrein excretion is decreased in hypertensive diabetic patients with nephropathy, and that the decrease might not be attributable to an altered renin-aldosterone system.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Colloid & polymer science 267 (1989), S. 201-208 
    ISSN: 1435-1536
    Keywords: Polyoxyethylene cholesteryl ethers ; liposome ; membrane-lysis ; membrane fluidity ; activation energy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics
    Notes: Abstract In order to deduce the mechanisms of hemolysis induced with the nonionic surfactants, polyoxyethylene cholesteryl ethers, C27H45(OCH2CH2) n OH (n=8, 25, 30, 50) and polyoxyethylene dihydrocholesteryl ethers, C27H47(OCH2CH2) n OH (n=15, 30, 50), the interaction of these surfactants with the liposomal membrane as a simple model membrane was investigated in terms of a leakage of the entrapped marker, and a change of the membrane fluidity. The time-courses of the marker leakage were characterized with two kinetic parameters, the initial induction period and the apparent first-order rate constant. The polyoxyethylene chain length was an important factor in the membrane-lytic activities, and the maximal rate as well as the maximal amount of the marker leakage was observed with n=25–30 in these surfactants series. However, the apparent activation energies derived from the two kinetic parameters increased almost linearly with the hydrophilic chain length. The used surfactants tended to fluidize the liposomal membrane in the concentration ranges of surfactants where the marker leakage is not at all or only slightly induced — but with the higher concentration of the cholesteryl derivatives, the apparent fluidity was significantly reduced. From these observations, the mechanisms of the membrane-lysis are discussed.
    Type of Medium: Electronic Resource
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