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  • 1
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    FEBS Letters 202 (1986), S. 245-250 
    ISSN: 0014-5793
    Keywords: (Bovine spleen) ; Heme protein ; Myeloperoxidase
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    FEBS Letters 214 (1987), S. 111-116 
    ISSN: 0014-5793
    Keywords: (Bovine spleen) ; Heme-protein ; Myeloperoxidase ; NMR
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    FEBS Letters 184 (1985), S. 52-55 
    ISSN: 0014-5793
    Keywords: Myeloperoxidase ; Raman spectrum
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochimica et Biophysica Acta (BBA)/Protein Structure and Molecular 1076 (1991), S. 317-320 
    ISSN: 0167-4838
    Keywords: Cyanide complex ; EPR ; Enzyme catalysis ; Halide ; Myeloperoxidase
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochimica et Biophysica Acta (BBA)/Protein Structure and Molecular 873 (1986), S. 62-72 
    ISSN: 0167-4838
    Keywords: (Bovine spleen) ; Circular dichroism ; Magnetic circular dichroism ; Myeloperoxidase ; Spleen green hemeprotein
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Urological research 25 (1997), S. 207-211 
    ISSN: 1434-0879
    Keywords: Outflow obstruction ; Rat bladder ; Ischemia ; Detrusor function ; Atherosclerosis ; Benign prostatic hyperplasia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We investigated the effects of ischemia induced by ligation of the bilateral internal iliac arteries following partial outlet obstruction on changes in detrusor function in rat. Rats were divided into three groups: sham-operated control rats, rats with partial outlet obstruction, and rats with obstruction + ischemia. Bladder function was studied by the in vitro organ bath technique 7 days after surgery. The weight of the bladder was significantly increased in both the obstruction and obstruction + ischemia groups. The obstruction + ischemia group exhibited a greater increase in weight. The passive length-tension relationship of detrusor muscle strips showed that tissue elasticity was decreased and the active length-tension relationship demonstrated that the peak response was observed at a shorter tissue length in the obstruction + ischemia group compared with the other two groups. There was no difference in the passive and active length-tension relationships between the control group and the obstruction group. The contractile response to various kinds of stimulation (field stimulation, bethanechol, ATP, and KCl) increased in the obstruction group and decreased in the obstruction + ischemia group. These findings suggest that partial outflow obstruction alone increased bladder contractility in response to stimuli. However, ischemia reduced the contractility and elasticity of the bladder wall.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Urological research 28 (2000), S. 141-146 
    ISSN: 1434-0879
    Keywords: Key words Kidney ; Nitric oxide ; Ischemia-reperfusion injury ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In this study we attempted to clarify the release of nitric oxide (NO) and its role in the ischemia-reperfusion rat kidney. After right nephrectomy, male Wistar rats were divided into four groups: one sham operated and three groups who underwent ischemia (30 min) and reperfusion of the left renal artery. Thirty minutes prior to ischemia-reperfusion, two groups were injected intraperitoneally with 10 and 30 mg/kg of NG-nitro-l-arginine methylester (L-NAME). Real-time monitoring of blood flow and NO release in the rat kidney was measured with a laser Doppler flowmeter and an NO-selective electrode, respectively. Serum creatinine and blood urea nitrogen (BUN) levels were measured 1 and 7 days after the induction of ischemia-reperfusion. Clamping of the renal artery decreased blood flow to 1–5% of the basal level measured before clamping. After removal of the clip, the blood flow of the 30 mg/kg L-NAME rats was significantly lower than that of the controls. Immediately following the clipping of the renal artery, NO release rapidly increased. After removing the clip, NO release immediately returned to three-quarters of the basal level. Serum creatinine and BUN levels of the ischemia-reperfusion rats were slightly but not significantly higher and those of 30 mg L-NAME rats were significantly higher than those of the control or ischemia-reperfusion rats 1 day and 7 days after ischemia-reperfusion. Our data suggest that NO acts as a cytoprotective agent in ischemia-reperfusion injury of the rat kidney.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Urological research 25 (1997), S. 193-197 
    ISSN: 1434-0879
    Keywords: Release of outflow obstruction ; Rat bladder ; Detrusor function ; Benign prostatic hyperplasia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Detrusor dysfunction does not recover in some patients with benign prostatic hyperplasia (BPH) even after prostate resection. ‘We studied the functional restoration of the rat bladder after release of short- or long-term outflow obstruction. Bladder function was assessed by in vivo infusion cystometry and an in vitro organ bath technique. There were no significant differences in bladder weight and contractile strength induced by stimuli in detrusor muscle strips from obstructed rats and age-matched control rats. After short-term obstruction the whole bladder pressure generated in vitro by field stimulation, bethanechol, ATP, and KCl completely recovered to control levels. In contrast, after long-term obstruction, the whole bladder pressure in response to field stimulation remained significantly lower than in controls. Infusion cystometry variables, including the pressure at which micturition was induced, maximal voiding pressure, capacity, and residual urine volume, were similar between controls and rats subjected to short-term obstruction. However, the maximal voiding pressure after long-term obstruction was significantly less than that of controls.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1420-908X
    Keywords: Cartilage ; Arthritis ; Nitric oxide ; Interleukin-1
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To determine the role of nitric oxide (NO) in the inhibition of aggrecan synthesis, we measured levels of NO produced by bovine chondrocytes from different layers of articular cartilage in the presence of interleukin-1 (IL-1). Chondrocytes from the superficial layer showed a large increase in NO synthesis in response to IL-1. Although chondrocytes from the deep layer also produced NO in response to IL-1, the amount was less than that from the superficial layer. Enhanced NO production evoked by IL-1 was accompanied by a significant inhibition of aggrecan synthesis. These data suggest that chondrocytes in both superficial and deep layer of articular cartilage inhibit aggrecan synthesis with IL-1 via NO production. In addition, superficial layer cells respond to lower amounts of IL-1 with respect to NO-production and inhibition of proteoglycan synthesis.
    Type of Medium: Electronic Resource
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