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Biomedical subjects

C C Chang

Publications and source records attributed to C C Chang.

At least 469 records · Page 26Linked to original sources
PubMed1988

Neuromuscular block by verapamil and diltiazem and inhibition of acetylcholine release.

The effects of Ca2+-channel antagonists, verapamil, diltiazem and nifedipine, on the neuromuscular transmission were studied in the isolated mouse phrenic nerve-diaphragm preparations. All 3 drugs increased the twitch response evoked by direct single stimulation at 10-100 microM. The neuromuscular transmission at 0.1 Hz was blocked by verapamil and diltiazem, but not by nifedipine, only at very high concentrations (greater than or equal to 100 microM). In the time course of block, no endplate potential (e.p.p.) could be recorded, whenever the junction failed to elicit an action potential, suggesting that the block is due to an axonal conduction failure. Conduction block became apparent in both axon and muscle at low concentrations (greater than 10 microM) of verapamil and diltiazem at 100 Hz. When the safety margin of neuromuscular transmission was reduced by tubocurarine or low Ca2+ plus high Mg2+, verapamil and diltiazem, but not nifedipine, reduced the single twitch response to nerve stimulation at concentrations that did not cause axon conduction block. The inhibition was dependent on the frequency of nerve stimulation, enhanced by low-Ca2+ and antagonized by high-Ca2+. Verapamil (50 microM) inhibited the mean amplitude of the median size miniature e.p.p. by only 8%, whereas it increased the frequency by 4-5-fold and the proportion of both small and giant miniature e.p.p.s. The e.p.p. amplitude was inhibited by verapamil by about 67% in low-Ca2+ media and by about 38% in normal Tyrode. Similar but somewhat lesser effect was obtained with diltiazem. It is concluded that verapamil and diltiazem, but not nifedipine, inhibit the transmitter release.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1988

Purification and characterization of L-amino acid oxidase from the venom of Trimeresurus mucrosquamatus (Taiwan habu snake).

L-Amino acid oxidase (EC.1.4.3.2) was purified to homogeneity via four steps consisting of Sephadex G-100, CM-Toyopearl 650M, and first and second granulated hydroxyapatite column chromatographies. The mol. wt of the enzyme was 140,000 when estimated by analytical gel filtration and was 70,000 by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, suggesting that the enzyme is composed of two identical subunits. The enzyme has an absorption spectrum characteristic of flavoprotein, contains 2 moles of FMN per mole of enzyme and has an isoelectric point of 5.4. The enzyme oxidatively deaminated hydrophobic amino acids such as Leu, Met, Phe, and Tyr while basic amino acids except for Lys were also oxidized though at slower rates. This specificity was generally similar, with some exceptions, to that of the enzyme from Trimeresurus flavoviridis venom. For oxidative deamination of Leu, Km and maximum velocity of the enzyme were 1.17 mM and 9.9 units/mg, respectively, at pH 7.6. The activity was inhibited almost completely by heavy metal ions, some aromatic benzoates and sulfhydryl reagents but not by metal-chelating agents.

Amino Acid Oxidoreductases↗
PubMed1988

Effect of cholesterol epoxides on the inhibition of intercellular communication and on mutation induction in Chinese hamster V79 cells.

Cholesterol, cholesterol-5 alpha, 6 alpha-epoxide, cholesterol-5 beta, 6 beta-epoxide and cholestane-3 beta,5 alpha,6 beta-triol were tested for their ability to induce mutations at the Na+/K+-ATPase loci of the Chinese hamster V79 cells. None of these compounds induced ouabain-resistant mutations compared to the background mutation frequency in the control cells. These compounds were further tested for their ability to inhibit intercellular communication, using the Chinese hamster V79 cell metabolic cooperation assay. The diastereomeric epoxides and cholestane-triol, but not cholesterol, were found to be inhibitors of intercellular communication in a manner similar to other known tumor promoters.

Animals↗
PubMed1988

Tryptophan residue essential for activity of Naja naja atra phospholipase A2.

When Naja naja atra phospholipase A2, which contains three tryptophan residues at the 18th, 19th, and 61st positions, was oxidized with N-bromosuccinimide at pH 4.0, its activity decreased in a convex manner with increase in the extent of oxidation of tryptophan residues. The curve shape showed that the tryptophan residue oxidized last is most responsible for the activity. The order of accessibilities of the three tryptophan residues, which was analyzed according to the method reported previously (Mohri et al. (1876) J. Biochem. 100, 883-893), was Trp-61 greater than Trp-19 greater than Trp-18. Thus, Trp-18 was evaluated to be essential for activity. Difference spectra of phospholipase A2 produced by titrating with laurylphosphorylcholine in the presence of Ca2+, which are due in large part to perturbation of the tryptophan residue(s), were retained with phospholipase A2 derivatives containing 1.2 and 2.0 mol of tryptophan residues oxidized but not with the derivative containing 3.0 mol of tryptophan residues oxidized. Such observations led us to assume that Trp-18 is involved in the specific site that interacts with phospholipid.

Amino Acid Sequence↗
PubMed1988

Cell kinetics, DNA content and TSH receptor-adenylate cyclase system in differentiated thyroid cancer.

The purpose of this study was to elucidate the changes of the TSH receptor-adenylate cyclase system in differentiated thyroid carcinomas, and their relationships with nuclear DNA content, cell kinetics and clinical stage. The results showed that the papillary carcinomas had an impaired TSH receptor-adenylate cyclase system. The production of cAMP stimulated by TSH was decreased when compared with non-cancerous tissue and high-affinity TSH receptors were reduced in number or even completely lost (nine in 24 cases). Follicular carcinomas also showed a reduction in, or even complete loss, of high-affinity TSH receptor (one in five cases). However, the responses to the stimulation of TSH, Gpp (NH)p and forskolin were not different from those in non-cancerous tissue. Papillary and follicular cancer cells showed more proliferative activity than those in non-cancerous tissue. Follicular carcinomas contained more hyperploid cells (DNA content greater than 2.5 C) than papillary carcinomas. There were no differences in cell kinetics, DNA content or the effects of Gpp (NH)p or forskolin on adenylate cyclase activity between those papillary carcinomas with high-affinity TSH receptor and those without. However, the presence of high-affinity TSH receptors had higher cAMP generation stimulated by TSH. The patients having papillary carcinomas in the absence of high-affinity TSH receptors were all in clinical stage III. These studies suggest that TSH receptors are the major sites influenced in the TSH receptor-adenylate cyclase system in papillary carcinomas. The TSH receptor-adenylate cyclase system of papillary carcinomas differs more from normal than does that of follicular carcinomas.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗
PubMed1988

Reversals of the neostigmine-induced tetanic fade and endplate potential run-down with respect to the autoregulation of transmitter release.

1. In order to shed more light on the role of presynaptic cholinoceptors in the modulation of transmitter release, the effects of tubocurarine, choline and hexamethonium on neostigmine-induced tetanic fade and run-down of endplate potentials (e.p.ps) in response to indirect stimulation with trains of pulses were studied in the intact and cut isolated phrenic nerve-diaphragm preparation of the mouse, respectively. 2. Tubocurarine, choline and hexamethonium reduced both the tetanic fade and e.p.p. run-down caused by neostigmine, despite the fact that they themselves also induced these two effects. 3. At a given degree of postsynaptic inhibition, choline and hexamethonium caused less e.p.p. run-down and reversed the neostigmine-induced tetanic fade and e.p.p. run-down better than tubocurarine. Moreover, the e.p.p. run-down caused by choline or hexamethonium, but not that induced by tubocurarine, was reciprocally reversed by neostigmine. 4. Tubocurarine, choline and hexamethonium significantly decreased the endplate depolarization induced by repetitive nerve stimulation in the presence of neostigmine. The remaining depolarization continued to grow during repetitive stimulation in the presence of choline or hexamethonium, but not, however, in the presence of tubocurarine; a finding which suggests that choline and hexamethonium but not tubocurarine may be displaced from the receptor by the accumulated acetylcholine. 5. The mutual reversal by neostigmine and cholinoceptor antagonists of e.p.p. run-down may implicate the presence of a positive (physiological) and a negative (pharmacological) feedback regulation for evoked transmitter release via nicotinic cholinoceptors in the mammalian motor nerve, depending on the concentration of acetylcholine within the synaptic cleft.

Animals↗
PubMed1988

A selective inhibitor of cAMP-specific phosphodiesterase, Ro 20-1724, has no effect on the quantal release of acetylcholine from the mouse phrenic nerve.

The indirect twitch response of the mouse isolated phrenic nerve-diaphragm preparation, partially paralysed by tubocurarine, was restored only by about 10% by Ro 20-1724 at 2 to 280 microM. The solvent vehicle, dimethylsulphoxide, also showed the same effect to a similar extent. Intracellular recordings with glass microelectrodes revealed that Ro 20-1724 (40 microM) affected neither the resting membrane potential, the amplitude and frequency of miniature endplate potentials nor the amplitude of nerve-impulse evoked endplate potentials recorded in curarized preparations. The result indicates that Ro 20-1724 at a concentration four times the IC50 of phosphodiesterase inhibition has no effect on the quantal release of acetylcholine from a mammalian motor nerve and suggests that cAMP has no modulatory effect on the transmitter release.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1988

Immunohistological evaluation of macrophage infiltrates in brain tumors. Correlation with peritumoral edema.

Peritumoral edema is one of the most serious complications of intracranial neoplasms; however, the exact pathogenesis of this condition is still unknown. To explore the effect of macrophages in brain tumors on the pathogenesis of peritumoral edema, 42 specimens of primary or metastatic brain tumors were studied. Frozen sections were examined by an immunoperoxidase staining technique with anti-Leu-M3 monoclonal antibody. Eight of 14 gliomas demonstrated Leu-M3-positive cell (macrophage) infiltration. The two glioblastomas showed a moderate or marked degree of macrophage infiltration. Twelve of 16 meningiomas demonstrated varying degrees of macrophage infiltration. All six metastatic brain tumors exhibited prominent macrophages in intra- and peritumoral tissues. Four acoustic neurinomas and two hemangioblastomas showed a slight to moderate degree of macrophage infiltration. Excellent correlation was found between the degree of macrophage infiltration seen on immunoperoxidase staining and the peritumoral edema detected on computerized tomography brain scans of patients with supratentorial tumors, especially meningiomas. Macrophages are known to secrete various substances (including arachidonate metabolites) that may interfere with vascular permeability. These data suggest that macrophages infiltrating brain tumors may play an important role in the pathogenesis of peritumoral edema.

Antibodies, Monoclonal↗