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Biomedical subjects

C C Ho

Publications and source records attributed to C C Ho.

50 records · Page 3Linked to original sources
PubMed1985

A novel method of transport for thyroxine (T4), cortisol, thyroid stimulating hormone (TSH), parathormone (PTH), and insulin.

A simple and convenient method of transport of serum in the form of protein disc on water resistant medium is described. The method was used to study the stability of thyroxine (T4), cortisol, thyroid stimulating hormone (TSH), parathormone (PTH) and insulin. The mean recoveries of these hormones were between 98 and 100%. The standard deviations of duplicates of assays for protein disc samples were comparable to that of serum samples except in assays using enzyme immunoassay techniques. The correlation coefficients of the results between the serum and protein disc samples were satisfactory ranging from 0.86-0.99. The proposed method could be used for interlaboratory referral of serum.

Desiccation↗
PubMed1980

Ethanol-sedative hypnotic interactions: in vitro studies on Na-K-activated adenosine triphosphatase.

The combined in vitro effects of ethanol wih methaqualone, phenobarbital, pyrazole or disulfiram were studied using rat brain microsomal NA-K-ATPase. Methaqualone and phenobarbital, either alone or in combination with ethanol, showed a dose-dependent inhibition of Na-K-ATPase activity. Kinetic studies showed that the inhibitory effects were competitive with the respect to K+ and uncompetitive with respect to MgATP for phenobarbital either alone or in combination with ethanol. Methaqualone showed a noncompetitive type of inhibition with respect to K+, whereas a mixed type of inhibition was seen in combinations with ethanol. Furthermore, methaqualone either alone or in combination with ethanol also showed an uncompetitive type of inhibition with respect to MgATP. The dose-dependent inhibition of brain Na-K-ATPase activity by disulfiram was independent of K+ and additive in combination with ethanol. Pyrazole showed no effect on brain Na-K-ATPase activity. The inhibitions by phenobarbital and methaqualone, either alone or in combination with ethanol, were significantly greater at low K+ (1 mM) and high Na+ (100-200 mM). A greater inhibition by these drugs was also obtained when Na+ is low (5 mM) and K+ is high (15 mM). The inhibition by these drugs appears to depend on K+ and Na/K ratio in the reaction medium. The combined effects of ethanol and the other CNS depressants on brains Na-K-ATPase may be important to their interaction toxicities.

Animals↗
PubMed1979

Toxic interactions of ethanol with other central depressants: antagonism by naloxone to narcosis and lethality.

The effects of naloxone on narcosis and/or lethality induced by diazepam, lithium, methaqualone and phenobarbital either alone or in combination with ethanol were studied in mice. Interaction toxicities between ethanol and the various psychotropic drugs were dose-dependent and so was the degree of antagonism by naloxone. Treatment with phenobarbital (10 mg/kg) or methaqualone (50 mg/kg) or lithium (4 meq/kg) prolonged the narcosis induced by ethanol (5 g/kg) by 45, 269 and 107% respectively. Naloxone (10 mg/kg) shortened the ethanol (5 g/kg) induced narcosis by 38%. Naloxone (10 mg/kg) also shortened narcosis induced by ethanol (5 g/kg) in combination with phenobarbital (10 mg/kg) or methaqualone (50 mg/kg) or lithium (2meq/kg) by 31, 12 and 38% respectively. At 10 mg/kg of naloxone, the LD50 due to methaqualone was increased from 240 mg/kg to 416 mg/kg, and the LD50 due to ethanol was increased from 9.2 g/kg to 10.8 g/kg. Multiple injections of naloxone significantly (p less than 0.01) protected against the lethality of phenobarbital but not that of lithium. These findings provide further evidence of naloxone antagonism towards various CNS depressants.

Animals↗
PubMed1978

Potentiation of lithium toxicity by ethanol in rats and mice.

The effects of ethanol treatments, both acute (single, intraperitoneal) and chronic (forced drinking of ethanol for 10 mo), on the distribution, excretion of lithium and urine output were studied in rats. Retention of lithium induced by ethanol appeared to be responsible for the potentiation of lithium toxicity. The potential hazard in the interaction between lithium and ethanol is discussed.

Administration, Oral↗
PubMed1977

Thiocardenolides II: synthesis and pharmacological evaluation of 3beta-thioacetyl-14beta-hydroxy-5beta-card-20(22)-enolide.

The synthesis of a 3beta-thioacetylcardenolide is described. The thioacetate exhibited effects similar to those seen with digitoxigenin acetate on the isolated frog and guinea pig hearts at 1 X 10(-7) dilution. In the intact rat heart, the lethal dose was 5 mg/kg for the thioacetate and 2.5 mg/kg for digitoxigenin acetate. The thioacetate inhibited sodium- and potassium-activated adenosine triphosphatase to the same extent as digitoxigenin, but it was somewhat less inhibitory than digitoxigenin acetate.

Adenosine Triphosphatases↗
PubMed1977

Chromosome stability in CHO cells.

The established cell line derived many years ago from Chinese hamster ovary (CHO cells) has been studied for the extent of chromosomal variation. Because this cell line is used extensively for genetic studies, the contribution of chromosome variability to genetic variability has also been examined. The quasidiploid CHO cells were found to have a banded karyotype somewhat altered from that of the Chinese hamster from which the line was derived. However, most of the genome could be accounted for among the rearranged marker chromosomes. In addition, the CHO line was found to have a relatively stable karyotype, the same basic karyotype being found in a majority of the uncloned cells, as well as in most cells of several but not all independent clones. Many, but not all, mutant cell lines derived from CHO also showed the same basic karyotype. Quasitetraploid cells, derived either spontaneously or by Sendai-virus-induced fusion, showed considerably more variation resulting in loss or gain of whole chromosomes, rearrangement of chromosomes, and appearance of new "marker" chromosomes.

Cell Line↗
PubMedDate not supplied

Rhein affects arylamine N-acetyltransferase activity in Helicobacter pylori from peptic ulcer patients.

Arylamine N-acetyltransferase (NAT) activities with 2-aminofluorene and p-aminobenzoic acid were determined in the bacterium Helicobacter pylori collected from peptic ulcer patients. Cytosols or suspensions of H. pylori with or without specific concentrations of rhein co-treatment showed different percentages of 2-aminofluorene and p-aminobenzoic acid acetylation. The data indicate that there was decreased NAT activity associated with increased levels of rhein in H. pylori cytosols. Inhibition of growth studies from H. pylori demonstrated that rhein elicited dose-dependent bacteriostatic activity in H. pylori cultures: i.e. the greater the concentration of rhein, the greater the inhibition of growth to H. pylori. For the cytosol and intact bacteria examination, the apparent values of Km and Vmax were decreased after co-treatment with 40 microM rhein. This report is the first demonstration of rhein inhibition of arylamine N-acetyltransferase activity and rhein inhibition of growth in the bacterium H. pylori.

4-Aminobenzoic Acid↗
PubMedDate not supplied

Interactions between methaqualone and ethanol in rats and mice during acute and chronic states.

1. The effects of acute and chronic treatment of methaqualone on ethanol preference, the rate of disappearance of ethanol and on toxicity were studied in mice and rats. 2. Acute treatment with methaqualone showed a dose-dependent suppression in the voluntary intake of ethanol in C57Bl/6J mice in rats. No significant change in ethanol intake was observed during chronic methaqualone treatment and withdrawal. 3. Methaqualone pretreatment significantly (P less than 0.005) delayed the disappearance of ethanol in the blood and brain over a period of 50 and 200 min after a loading dose of 2.0 g/kg, i.p., of ethanol. 4. Methaqualone pretreatment at doses of 140 and 200 mg/kg significantly increased ethanol toxicity by 11% and 28%, respectively. Co-administration of ethanol using 6.0, 7.0 and 8.0 g/kg also reduced the LD50 of methaqualone by 19%, 24% and 40%, respectively. 5. Chronic administration with ethanol decreased the toxicity due to methaqualone. Potentiation of ethanol toxicity by methaqualone may be of clinical importance in view of the narrow range of safety margin of ethanol.

Alcohol Drinking↗