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  • 1
    Electronic Resource
    Electronic Resource
    Apolipoprotein(a) and cardiovascular disease in Type 2 (non-insulin-dependent) diabetic patients with and without diabetic nephropathy (1993)
    Springer
    Diabetologia 36 (1993), S. 438-444 
    Details
    ISSN: 1432-0428
    Keywords: Type 2 (non-insulin-dependent) diabetes mellitus ; diabetic nephropathy ; apolipoprotein(a) ; cardiovascular disease ; lipid metabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The relative mortality from cardiovascular disease is on average increased five-fold in Type 2 (non-insulin-dependent) diabetic patients with diabetic nephropathy compared to non-diabetic subjects. We assessed the possible contribution of dyslipidaemia in general and elevated serum apolipoprotein(a) (apo(a)) in particular. Type 2 diabetic patients with normo-, micro- and macroalbuminuria were compared with healthy subjects. Each group consisted of 37 subjects matched for age, sex and diabetes duration. Serum creatinine in the nephropathy group was 105 (54–740) Μmol/l. The prevalence of ischaemic heart disease (resting ECG, Minnesota, Rating Scale) was 57, 35, 19 and 2% in macro-, micro- and normoalbuminuric diabetic patients and healthy subjects, respectively. The prevalence of ischaemic heart disease was higher in all diabetic groups as compared to healthy subjects (p〈0.05), and higher in macroalbuminuric as compared to normoalbuminuric diabetic patients (p〈0.01). There was no significant difference between apo(a) in the four groups: 161 (10–1370), 191 (10–2080), 147 (10–942), 102 (10–1440) U/l (median (range)) in macro-, micro- and normoalbuminuric groups and healthy subjects. Serum total-cholesterol, HDL-cholesterol and LDL-cholesterol were not significantly different when comparing healthy subjects and each diabetic group. Apolipoprotein A-I was lower (p〈0.05) in all diabetic groups as compared to healthy subjects (nephropathy vs healthy subjects): 1.50±0.25 vs 1.69±0.32 g/l (mean ± SD). Triglyceride was higher (p〈0.05) in patients with nephropathy and microalbuminuria as compared to healthy subjects (nephropathy vs healthy subjects): 2.01 (0.66–14.7) vs 1.09 (0.41–2.75) mmol/l (median (range)). Apolipoprotein B was higher (p〈0.02) in patients with nephropathy as compared to the other three groups (nephropathy vs healthy subjects): 1.54±0.47 vs 1.33±0.30 g/l. In conclusion, our case-control study has confirmed that Type 2 diabetic patients with increased urinary albumin excretion frequently suffer from dyslipidaemia and cardiovascular disease. However, our study revealed no significant elevation in serum concentration of apo(a) in patients with diabetic nephropathy, but numbers were small.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00402281
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  • 2
    Electronic Resource
    Electronic Resource
    Plasma lipoproteins and renal function during simvastatin treatment in diabetic nephropathy (1992)
    Springer
    Diabetologia 35 (1992), S. 447-451 
    Details
    ISSN: 1432-0428
    Keywords: Plasma lipoproteins ; albuminuria ; diabetic nephropathy ; glomerular filtration rate ; Type 1 (insulin-dependent) diabetes mellitus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The aim of this study was to assess the effect of simvastatin on plasma lipoproteins and renal function in hypercholesterolaemic Type 1 (insulin-dependent) diabetic patients with diabetic nephropathy. Twenty-six hypercholesterolaemic (total cholesterol ≽ 5.5 mmol/l) Type 1 diabetic patients with nephropathy were enrolled in a double-blind randomized placebo-controlled study for 12 weeks. The active treatment group (n -14) received simvastatin (10–20 mg/day) for 12 weeks while the remaining 12 patients received treatment with placebo. The results during simvastatin treatment (baseline vs 12 weeks): total cholesterol 6.6 vs 4.8 mmol/1 (p 〈 0.01), LDL-cholesterol 4.25 vs 2.57 mmol/l (p 〈 0.01) and apolipoprotein B 1.37 vs 1.06 mmol/l (p 〈 0.01). HDL-cholesterol, and apolipoprotein A-I remained unchanged. Total cholesterol, LDL-cholesterol, HDL-cholesterol, apolipoprotein A–I, apolipoprotein B remained unchanged during placebo treatment. Albuminuria measured during the simvastatin and the placebo treatment (baseline vs 12 weeks) (the data are logarithmically transformed before analysis because of their positively skewed transformation; geometric mean (×/÷ antilog SE) is indicated) was 458 (×/÷ 1.58) vs 393 (×/÷ 1.61) and 481 (×/÷ 1.62) vs 368 (×/÷ 1.78 μg/min (NS). Glomerular filtration rate during simvastatin and placebo treatment (baseline vs 12 weeks) was 64 vs 63 and 72 vs 74 ml·min−1·1.73 m−2, respectively. Two patients receiving simvastatin treatment were withdrawn, one due to gastrointestinal side effects and one due to myalgia. In conclusion, our short-term study in Type 1 diabetic patients with diabetic nephropathy did not reveal any beneficial effect on albuminuria despite a striking lipid-lowering effect of simvastatin in diabetic nephropathy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02342442
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Mode of activation of hippocampal pyramidal cells by excitatory synapses on dendrites (1966)
    Springer
    Experimental brain research 2 (1966), S. 247-260 
    Details
    ISSN: 1432-1106
    Keywords: Synaptic excitation ; Hippocampus ; Pyramidal cells ; Dendritic activation ; Cat ; Rabbit
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Following selective activation of four afferent paths that terminate exclusively on dendrites, only a small proportion of pyramidal cells in the hippocampal fields CA1 and CA3 discharged impulses. Following a single afferent volley, an EPSP was never observed even in cells synaptically excited. On tetanic stimulation (about 10/sec), a large EPSP developed, but this was not a prerequisite for an action potential. Studies of the extracellular field potentials corresponding to the EPSP and the population spike potential, indicated that the EPSP was generated across the dendritic membrane and that the spike was initiated in the neighbouring part of the dendritic tree, propagating from there along the thicker dendrites towards the soma. This conduction had an average velocity of 0.4m/sec, and, presumably, a relatively low safety factor. In certain cases, the intrasomatic electrode recorded small all-or-nothing spikes which presumably were generated in the dendritic tree. These small spikes (D-spikes) invaded the soma only if assisted by some additional depolarization, for example by frequency potentiation of excitatory synapses. The results indicate two functional types of pyramidal dendrites, the conducting and the synaptic type.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00236716
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Location and identification of excitatory synapses on hippoeampal pyramidal cells (1966)
    Springer
    Experimental brain research 1 (1966), S. 236-248 
    Details
    ISSN: 1432-1106
    Keywords: Excitatory synapses ; Hippocampus ; Cat, Rabbit
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. In rabbits and cats anaesthetized by urethane-chloralose or pentobarbital sodium, stimulation of the commissural afferent pathway produced a negative field potential with maximal amplitude in the CA3 basal dendritic layer, and with a latency indicative of monosynaptic activation of excitatory synapses on the basal dendrites. 2. Mossy fibre stimulation resulted in a similar field potential restricted to the mossy fibre layer. Comparable negative field potentials were found in the layer of apical dendrites in CA1 in response to commissural and Schaffer collateral stimulation, suggesting a dendritic location of these synapses. 3. All negative field potentials grew in amplitude on tetanic stimulation, to produce large extracellular spikes, indicating their association with excitatory synaptic activity. 4. Usually, all pathways employed failed to produce EPSPs on single shock stimulation, in spite of their capability of discharging the cells, suggesting that the synaptic depolarization takes place at some distance from the soma. 5. Electron microscopy of degenerated commissural afferent fibres showed them to make contact with spines or the smooth surface of thin dendrites. The indentification of the postsynaptic element as pyramidal cell dendrite was ascertained. The mossy fibres end on ramified dendritic spines in CA3. 6. By comparison with normal electron micrographs, all the pathways, shown physiologically to be excitatory, terminate on thin dendrites, the contacts being of type 1.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00234344
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    Paper (German National Licenses)
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