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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 5 (1978), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The mitotic rate in the crypts of Lieberkiihn of the descending colon and in dimethylhydrazine-induced adenocarcinomata of the descending colon of rat was measured using a stathmokinetic technique.2. Intraperitoneal injection of a small dose (10 jug/kg) of serotonin resulted in an increase in the tumour cell mitotic rate.3. Blockade of serotonin receptors by 2-bromolysergic acid diethylamide and depletion of tissue serotonin levels following injection of DL-6-fluorotryptophan both result in a decrease in the tumour cell mitotic rate.4. Treatment with serotonin, 2-bromolysergic acid diethylamide and DL-6-fluorotryptophan were all without effect on the colonic crypt cell mitotic rate.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 9 (1982), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Cell proliferation in the jejunal crypt epithelium of rat was measured using a stathmokinetic technique.2. Sodium butyrate was found to promote jejunal crypt cell proliferation.3. N6, 02'-Dibutyryl cyclic adenosine monophosphate (cAMP), N6-monobutyryl-cAMP and N6-monobutyryl-8-bromo-cAMP were found to inhibit cell proliferation when compared to sodium butyrate treated tissues.4. 8-Chlorophenylthio-cAMP was found to inhibit cell division when compared to untreated animals.5. O2'-Monobutyryl cAMP and 8-bromo-cAMP were not found to inhibit cell proliferation.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 3 (1976), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The influence of histamine and histamine receptor blockade on the mitotic rate in epithelial cell proliferation in epithelial cells lining the crypts of Lieberkühn in rat jejunum was studied.2. Histamine injection resulted in an increase in the mitotic rate. This increase in mitotic rate was blocked by metiamide but not by mepyramine.3. Prevention of histamine synthesis by α-methylhistidine administration did not alter the mitotic rate.4. The mechanism by which histamine may influence crypt cell proliferation and and possible role of cyclic GMP in this mediation are discussed.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 3 (1976), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. An in vivo stathmokinetic technique was used to determine the immediate effect of various adrenoceptor agonists and antagonists on the mitotic rate in the stratified squamous epithelium of the rat buccal mucosa.2. The mitotic rate increased significantly in rats treated with propranolol and with practolol, whereas the mitotic rate decreased significantly in rats treated with metaraminol. In animals treated with isoprenaline and phentolamine the mitotic rate did not differ significantly from the control value.3. The nature of the involvement of adrenergic mechanisms with cell proliferation is still uncertain but both α- and β-adrenergic mechanisms appear to be associated with the control of cell proliferation.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 2 (1975), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 〈list xml:id="l1" style="custom"〉1The influence of cholinoceptor stimulation and cholinoceptor blockade on the mitotic rate in epithelial cells lining the crypts of Lieberkühn in rat jejunum was studied.2Cholinoceptor stimulation, either by injection of carbachol or by inhibition of acetylcholinesterase enzymes resulted in an increase in the mitotic rate. This increase in mitotic rate was blocked by tubocurarine, but not by atropine or hexamethonium. Atropine by itself increased the mitotic rate whereas tubocurarine alone or hexamethonium alone decreased the mitotic rate.3The influence of atropine on crypt cell proliferation appears to involve an adrenergic mechanism since it is blocked by phentolamine.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 10 (1983), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The mitotic rates in the crypts of Lieberkühn of the proximal jejunum and descending colon of mouse, following different treatments, were measured using a stathmokinetic technique. Regression coefficients, representing mitotic rates, were then calculated by the method of least squares.2. Treatment with adrenaline, isoprenaline, phenylephrine, phentolamine, and yohimbine all resulted in decreased mitotic rate of jejunal and colonic crypt cells. Chemical sympathectomy and cryosympathectomy had a similar effect, and chemical sympathectomy was followed by a supersensitivity to clonidine.3. Intraperitoneal injection of metaraminol, clonidine, propranolol, prazosin, labetolol and simultaneous injection of propranolol and adrenaline all resulted in an increased rate of crypt cell proliferation in both jejunum and colon.4. A significant increase in mitotic rate was observed in both tissues at night. The amplitude of this diurnal variation was decreased in both jejunum and colon following chemical sympathectomy. In addition, the amplitude of this variation in jejunum was decreased after treatment with yohimbine or phentolamine.5. The results of the study suggest that the sympathetic nervous system stimulates epithelial cell proliferation in both the small and large intestine and that this effect is mediated by an α2-adrenoceptor. By contrast, stimulation of α1- and β-adrenoceptors is inhibitory to cell proliferation in these tissues.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 7 (1980), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Cell proliferation in the jejunal crypts, the colonic crypts and in dimethyl-hydrazine (DMH)-induced adenocarcinomata of rat colon was measured using a stathmokinetic technique.2. Dibutryl cyclic adenosine monophosphate (dibutyryl cAMP) was found to inhibit cell proliferation in colonic crypts and in colonic adenocarcinomata.3. Dibutryl cAMP at very high doses was found to inhibit jejunal crypt cell proliferation but at lower doses was found to accelerate jejunal crypt cell proliferation.4. Neither bilateral adrenalectomy nor chemical sympathectomy was found to abolish the ability of dibutryl cAMP to stimulate jejunal crypt cell proliferation.5. The present results are difficult to interpret in terms of known hormonal influences on cell proliferation in the tissues examined and of established actions, of these hormones on cyclic nucleotide metabolism in other tissues.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-0843
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The cytotoxicity of 5,6-dihydroxytryptamine (5,6-DHT), 5,7-dihydroxytryptamine (5,7-DHT), bromolysergic acid diethylamide (BOL), methysergide, and cyproheptadine, and also of 5,6-DHT together with either BOL, methysergide, or cyproheptadine in dimethylhydrazine-induced (DMH) carcinomata of rat colon was evaluated by estimating the percentage of necrotic cells in histological sections of tissues taken 15 h after injection of each of the drugs. In addition, the influence of methysergide and cyproheptadine on the tumour cell mitotic rate was estimated by means of a stathmokinetic technique. Both 5,6-DHT and 5,7-DHT were cytotoxic at each dose tested and for each of these agents the percentage of necrotic cells was directly correlated with the dose of drug used. BOL was not found to be cytotoxic to the colonic carcinomata, whereas both methysergide and cyproheptadine did cause detectable tumour cell necrosis. Methysergide was also found to accelerate tumour cell proliferation, whereas cyproheptadine did not. BOL competitively inhibited the cytotoxicity of 5,6-DHT and neither methysergide nor cyproheptadine potentiated the effect of 5,6 DHT.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 34 (1978), S. 249-249 
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Cell proliferation rates in the bases of the crypts of Lieberkuhn in the jejunum of rat were measured using a stathmokinetic technique. In rats subjected to recurring loud noise cell proliferation was more rapid than in rats not subjected to the noise.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Cancer chemotherapy and pharmacology 2 (1979), S. 137-138 
    ISSN: 1432-0843
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Previous studies have shown that several serotonin-related compounds are cytotoxic to dimethylhydrazine-induced carcinomata of the colon of rat. This paper reports the cytotoxicity of another serotonin-related compound, p-chloroamphetamine.
    Type of Medium: Electronic Resource
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