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991.
David A. Cheresh 《Cancer metastasis reviews》1991,10(1):3-10
Summary Human melanoma represents one of the most metastatic cancers in man. The capacity of melanoma cells to invade a variety of tissues and extracellular matrices is, in part, due to their repertoire of adhesion receptors. To this end, human melanoma cells express multiple integrin cell adhesion receptors among these is the vitronectin receptor, v3. This adhesion receptor enables melanoma cells to attach to a wide variety of extracellular matrix components containing the sequence Arg-Gly-Asp. This review will focus on the biosynthetic, biochemical and biological properties of this receptor expressed on the surface of human melanoma cells. 相似文献
992.
G. J. Molderings G. Weißenborn E. Schlicker J. Likungu M. Göthert 《Naunyn-Schmiedeberg's archives of pharmacology》1992,346(1):46-50
Summary The human saphenous vein was used to examine whether presynaptic histamine receptors can modulate noradrenaline release and, if so, to determine their pharmacological characteristics. Strips of this blood vessel were incubated with [3H]noradrenaline and subsequently superfused with physiological salt solution containing desipramine and corticosterone. Electrically (2 Hz) evoked 3H overflow was inhibited by histamine and the H3 receptor agonist R-(–)--methylhistamine. Histamine-induced inhibition of electrically evoked tritium overflow was not affected by 2-adrenoceptor blockade by rauwolscine. S-(+)--methylhistamine (up to 10 mol/l) as well as the histamine H1 and H2 receptor agonists 2-(2-thiazolyl)ethylamine (up to 3 mol/l) and dimaprit (up to 30 mol/l), respectively, were ineffective. The selective histamine H3 receptor antagonist thioperamide abolished the inhibitory effect of histamine. The histamine H2 and H1 receptor antagonists ranitidine and pheniramine, respectively, did not affect the histamine-induced inhibition of evoked tritium overflow. The present results are compatible with the suggestion that the sympathetic nerves of the human saphenous vein are endowed with inhibitory presynaptic histamine receptors of the H3 class.
Send offprint requests to M. Gothert at the above address 相似文献
993.
Summary The effects of 5-methoxytryptamine and 5-hydroxytryptamine (5-HT) on both basal and electrically evoked outflow of tritium were studied in guinea-pig myenteric plexus preparations preincubated with [3H]-choline.
Basal outflow. 5-Methoxytryptamine caused a transient and calcium-dependent increase in basal outflow of [3H]acetylcholine that was abolished by tetrodotoxin. Ondansetron (1 mol/1) did not affect the stimulatory response of 5-methoxytryptamine but ICS 205-930 (1 and 3 mol/1) produced parallel rightward displacements of the concentration-response curve to 5-methoxytryptamine. The PKB value for ICS 205-930 was 6.6 suggesting an involvement of 5-HT4 receptors. 5-HT caused an increase in basal outflow of [3H]acetylcholine and a biphasic concentration-response curve was obtained. The maximal response of the first phase to 5-HT (release of 0.98% of tissue tritium) and the maximal response to 5-methoxytryptamine (0.94% of tissue tritium) were similar but 5-methoxytryptamine (-log EC50: 6.9) was less potent than 5-HT (-log EC50 of the high affinity component: 7.9). ICS 205-930 (0.01–1.0 mol/1) acted as a competitive antagonist against the low affinity component of the 5-HT concentration-response curve with a pA2 value of 8.0. It is concluded that stimulation of both 5-HT4 receptors (by 5-methoxytryptamine and submicromolar concentrations of 5-HT) and 5-HT3 receptors (by micromolar concentrations of 5-HT) causes a release of acetylcholine which in turn leads to smooth muscle contraction.
Electrically evoked outflow. This outflow of [3H]acetylcholine was concentration-dependently inhibited by both 5-methoxytryptamine and 5-HT. ICS 205-930 (1 mol/1) reinforced the inhibitory effect of 5-methoxytryptamine but not that of 5-HT. In the presence of methiothepine (0.1 mol/1) 5-methoxytryptamine enhanced the evoked outflow of [3H]acetylcholine, an effect which was attenuated by 3 mol/1 ICS 205-930. These results suggest that 5-methoxytryptamine may both inhibit (via 5-HT1 receptors) and facilitate (via 5-HT4 receptors) the evoked release of acetylcholine from guinea-pig myenteric neurones. The facilitatory action is unmasked when the 5-HT1 receptor is blocked by methiothepine.
Send offprint requests to H. Kilbinger at the above address 相似文献
994.
Maria L. Anthony Kevin P. R. Gartland Christopher R. Beddell John C. Lindon Jeremy K. Nicholson 《Archives of toxicology》1992,66(8):525-537
The acute toxicological effects of the nephrotoxic antibiotic cephaloridine (CPH, 0–1500 mg/kg) in male Fischer 344 (F344) rats, have been investigated over 48 h using clinical chemistry, histopathology and proton nuclear magnetic resonance (1H NMR) spectroscopy of urine and plasma. High field (400 and 600 MHz)1H NMR urinalysis revealed increased excretion of lactic acid, acetoacetate, alanine, valine, lysine, glutamine and glutamate and a severe, time-dependent glycosuria. A major change observed in urine of CPH-treated animals was the dose-dependent increase in HB which may relate to altered energy metabolism. CPH also caused dose-dependent decreases in the urinary excretion of hippurate, allantoin and protein (conventional assay). This abnormal metabolic profile is consistent with a functional defect in the S1/S2 regions of the proximal tubule, and was confirmed by histologypost mortem. Functional changes observed included elevations in blood urea nitrogen (BUN) and urine flow rate (UFR) and dose-related decreases in urine osmolality. Spin-echo1H NMR spectroscopic analysis of lyophilised plasma, reconstituted with2H2O revealed an abnormal phase modulation of the methyl signal from free alanine and it is postulated that this is due to the release of transaminases from damaged tissue which via a reversible conversion to pyruvate, cause variable deuteration of alanine at the -CH position. This observation suggests that1H NMR spectral patterns are also dependent on the level of plasma transaminases and this may provide a novel indicator of tissue damage. 相似文献
995.
Dr. I. Wessler C. Apel M. Garmsen A. Klein 《Journal of molecular medicine (Berlin, Germany)》1992,70(3-4):182-189
Summary The effects of nicotine receptor agonists on the release of [3H]acetylcholine from the phrenic nerve, the small intestine and the trachea were investigated to characterize neuronal nicotine receptors within the peripheral nervous system. Contraction of the indirectly-stimulated hemidiaphragm was recorded to investigate desensitization of the postsynaptic muscular nicotine receptors. Nicotine, cytisine, 1,1-dimethyl-4-phenylpiperazinium and 2-(4-aminophenyl)-ethyl-trimethyl-ammoniumiodide caused a concentration-dependent (0.1–30 M) increase in evoked [3H]acetylcholine release from the phrenic nerve, whereby bell-shaped concentration-response curves were obtained. The rank order of decreasing potency was: nicotine > cytisine > 1,1-dimethyl-4-phenylpiperazinium > 2-(4-aminophenyl)-ethyl-trimethyl-ammoniumiodide. The presynaptic effects of nicotine depended strongly on the exposure time: facilitation occurred after a short 20 s exposure and inhibition after a 3 min exposure, whereas nicotine no longer affected evoked [3H]acetylcholine release after a 15 min exposure. Pre-exposure (40 min) of the phrenic nerve to 0.3 M nicotine prevented any subsequent modulatory effect of a high nicotine concentration. In contrast, the contraction of the indirectly-stimulated hemidiaphragm remained unaffected in the presence of 0.3–30 M nicotine, but a concentration of 1 mM nicotine abolished skeletal muscle contraction. Nicotine (10 M) produced a substantial release of [3H]acetylcholine in the small intestine but not in the isolated trachea. The present experiments show presynaptic nicotine receptors at the phrenic nerve, which, under appropriate conditions, can mediate facilitation of evoked transmitter release. These neuronal receptors appear more sensitive to desensitizing conditions than the postsynaptic muscular nicotine receptors. Nicotine also mediates a transient release of acetylcholine in the myenteric plexus but not in the trachea, and as a consequence, applied nicotine preferentially activates smooth muscle activity in the intestine.Abbreviations DMPP
1,1-dimethyl-4-phenylpiperazinium
- PAPETA
2-(4-aminophenyl)-ethyl-trimethylammoniumiodiderine of [3H]acetylcholine release 相似文献
996.
M. Duran R. J. A. Wanders J. P. de Jager L. Dorland L. Bruinvis D. Ketting L. Ijlst F. J. van Sprang 《European journal of pediatrics》1991,150(3):190-195
Two siblings were found to be affected by longchain 3-hydroxyacyl-CoA dehydrogenase deficiency, one of which died suddenly and unexpectedly on the 3rd day of life suffering from extreme hypoketotic hypoglycaemia. The younger sibling started to have feeding problems, lowered consciousness, and liver dysfunction at the age of 5 months. Her urine contained large amounts of C6–C14 3-hydroxydicarboxylic acids and conjugated 3-hydroxyoctanoic acid, as verified by gas chromatography/mass spectrometry. Plasma long-chain acylcarnitine was increased. A clue to the diagnosis was given by the results of a phenylpropionic acid loading test. This revealed small, but significant amounts of conjugated 3-hydroxyphenylpropionic acid (phenylhydracrylic acid) in the patient's urine. Subsequently, the activity of long-chain 3-hydroxyacyl-CoA dehydrogenase was found to be deficient in cultured skin fibroblasts. Based on the findings obtained by a medium-chain triglyceride load, a diet enriched in this type of fat was prescribed. On this regimen the patient started to thrive, signs of cardiomyopathy disappeared, and her liver function normalized. 相似文献
997.
Integration in trigeminal premotor interneurones in the cat 总被引:1,自引:0,他引:1
K. Å. Olsson K.-G. Westberg 《Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale》1991,84(1):115-124
Seventy-one (n = 71) premotor interneurones have been localized by extracellular recordings within the subnucleus-gamma of the oral nucleus of the spinal trigeminal tract (NVspo-gamma) in nineteen chloralose anaesthetized cats. The neurons were antidromically activated by microstimulation (minimum = 3 microA) applied to the digastric motoneurone subnucleus of the trigeminal motor nucleus. Fifty-one (n = 51) of the interneurones were discharged from the ipsi- and nineteen (n = 19) from the contralateral digastric subnucleus. One neurone out of four tested was antidromically activated from both stimulation sites suggesting a bifurcated axon. The identified premotor neurones had a unique convergence profile of oral and perioral primary afferents. Latency calculations indicated that at least 55% of these interneurones were monosynaptically activated by low stimulus strength applied to the inferior alveolar (minimum = 1.0 T) and/or the lingual nerve (minimum = 1.0 T). The thresholds for evoking the neuronal discharges coincided statistically with those required to evoke a jaw opening reflex response by stimulation of the same nerves. It is suggested that the specific group of NVspo-gamma interneurones under different contexts mediates the disynaptic reflex and participates in the centrally and reflexly evoked "patterning" adjustments of the digastric jaw opening motoneurones during ongoing jaw movements. A companion paper reports the convergence of descending cortical, tectal and ascending cervical inputs, as well as of oro-facial and neck primary afferent inputs onto an unselected population of interneurones in the NVspo-gamma (Westberg and Olsson 1991). 相似文献
998.
Frog motoneurons were intracellularly labelled with cobaltic lysine in the brachial and the lumbar segments of the spinal cord, and the material was processed for light microscopy in serial sections. With the aid of the neuron reconstruction system NEUTRACE, the dendritic tree of neurons was reconstructed and the length and surface area of dendrites measured. The surface of somata was determined with the prolate - oblate average ellipsoid calculation. Corrections were made for shrinkage and for optical distortion. The mean surface area of somata was 6710 microm2; lumbar motoneurons were slightly larger than brachial motoneurons. The mean length of the combined dendritic tree of brachial neurons was 29 408 microm and that of lumbar neurons 46 806 microm. The mean surface area was 127 335 microm2 in brachial neurons, and 168 063 microm2 in lumbar neurons. The soma - dendrite surface area ratio was 3 - 5% in most cases. Dendrites with a diameter of = 1.0 microm constituted approximately 75% of the combined dendritic length in most of the neurons. Unlike in the cat, there was no correlation between the size of stem dendrites and the extent of daughter branches. From the synaptic density estimated in earlier electron microscope investigations of frog motoneuron dendrites (Antal et al., J. Neurocytol., 15, 303 - 310, 1986; 21, 34 - 49, 1992), and from the present data, the number of synapses on the dendritic tree was calculated. The calculations indicated 26 949 synapses on the smallest and 61 519 synapses on the largest neuron if the synaptic density was multiplied by the length of the dendritic tree. If the synaptic density was multiplied by the surface area of the dendritic tree the calculation yielded 23 337 synapses for the smallest and 60 682 synapses for the largest neuron. More than 60% of the combined surface area of dendrites was >600 microm from the soma. This suggests that about two-thirds of the synapses impinged upon distant dendrites >600 microm from the soma. The efficacy of synapses at these large distances is investigated on model neurons in the accompanying paper (Wolf et al., Eur. J. Neurosci., 4 1013 - 1021, 1992). 相似文献
999.
Ph. Cornu J. Benavides B. Scatton J. -J. Hauw J. Philippon' 《Acta neurochirurgica》1992,119(1-4):146-152
Summary The density of 3 (peripheral type benzodiazepine) binding sites, a marker of reactive and tumoural cells, has been measured in different types of human brain tumours; 3 sites were quantified autoradiographically in sections from biopsy or autopsy specimens labelled with the specific radioligand3H-PK 11195. Compared to normal brain parenchyma, up to 12-fold increase in 3 site densities were found in appparently viable areas of high grade astrocytoma and glioblastoma specimens, whereas more limited increases (2 to 3-fold) in this marker were observed in areas of necrosis. Low grade gliomas (astrocytomas) and meningiomas exhibited only moderate increases (2 to 3-fold) in this autoradiographic marker. Metastases of lung or kidney origin were characterized by greatly elevated (up to 20-fold) 3 site densities as compared to normal brain parenchyma. In every case, there was a good spatial correspondence between the histopathological limits of the tumour and the anatomical location of the increase in 3 site densities. These results suggest that 3 site densities in human brain tumours reflect their proliferative activity and point to a possible future usefulness of positron or gamma-ray emitting 3 site ligands for the clinical investigation and detection of human brain proliferative diseases. 相似文献
1000.
Summary The effects of interleukin-1 (IL-1), forskolin, and tumor necrosis factor (TNF-) on tissue plasminogen activator (t-PA) activity were studied in the human osteoblastic osteosarcoma cell line, G292. t-PA activity was measured in the cell media using the chromogenic substrate, S-2251. After a 24 hour incubation period, IL-1 increased t-PA in a dose-dependent manner. The effect of IL-1 at 10.0 U/ml was partially inhibited in the presence of indomethacin. Forskolin (1.0 M) increased t-PA activity after 24 hours with the effects of combined treatment of IL-1 (1.0 U/ml, 10.0 U/ml) and forskolin being apparently additive in nature. TNF- (10-8–10-7 M) also produced increased t-PA activity in the cell medial after a 24 hour incubation period. These results suggest that the cytokines, IL-1 and TNF-, can increase t-PA activity in G292 cells and that there is both a cAMP-dependent as well as a cAMP-independent pathway involved in the regulation of this osteoblastic cell function. 相似文献