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Biomedical subjects

A K Ho

Publications and source records attributed to A K Ho.

At least 145 records · Page 8Linked to original sources
PubMed1985

Differential effects of isoproterenol injections on the levels of pineal N-acetyltransferase, serum N-acetylserotonin and melatonin.

Rats housed under diurnal lighting conditions were either injected with isoproterenol (ISO), 0.5 mg/kg subcutaneous (SC) and sacrificed at different times up to 180 minutes afterwards, or injected with different doses of ISO (0.2 mg/kg to 5.0 mg/kg intraperitoneally (IP] and sacrificed 120 minutes later. Pineal N-acetyltransferase (NATase), serum N-acetylserotonin (NAS) and serum melatonin (MT) levels were determined. It was found that both pineal NATase and serum MT responded to the injection with peak increase at 120 minutes after the injection. This increase in pineal NATase and serum MT levels were also found to be dose-dependent. It was also observed that at 30 minutes after ISO injection, the serum MT level already demonstrated a significant increase which preceeded any increase in the pineal NATase activity. The underlying mechanism for this observation remains undetermined. Unlike serum MT and pineal NATase, there were no changes in serum NAS levels after injections of ISO at all the doses tested or up to 180 minutes after injection of the drug at 0.5 mg/kg dose SC. This suggests that serum NAS level is neither regulated by pineal NATase activity nor is the pineal gland the major source of NAS in circulation. This also indicates that serum NAS level is not influenced by beta-adrenergic stimulation.

Acetyltransferases↗
PubMed1985

Scheduled feeding and 24-hour rhythms of N-acetylserotonin and melatonin in rats.

Male rats, kept under a lighting condition of 14-h light, 10-h dark, were subjected to scheduled feeding regimens. Food was available either in the early light phase or the early dark phase. The 24-h rhythms of serum corticosterone and of N-acetylserotonin (NAS) and melatonin (MT) in the pineal and serum were determined. It was found that whereas serum corticosterone and NAS rhythms responded to the feeding schedules, the rhythms of pineal NAS and of serum and pineal MT remained synchronized with the light-dark cycle. These findings indicated that the pineal was not the major source of circulating NAS. Whereas environmental lighting was the dominant "Zeitgeber" for the NAS rhythms in the pineal and the MT rhythms in the pineal and serum, for serum NAS rhythm, food presentation was the stronger Zeitgeber.

Animals↗
PubMed1984

Relationship between pineal N-acetyltransferase activity, pineal melatonin and serum melatonin in rats under different lighting conditions.

Pineal N-acetyltransferase (NATase) activity has often been used as an indicator of pineal melatonin (MT) production, and the rhythms of pineal and serum MT levels are assumed to be parallel. However, these issues require further examination in view of some recent findings. In the present study, the 24-hour rhythms of pineal NATase, pineal MT content and serum MT concentrations were examined in groups of rats exposed to four artificial lighting regimens: (a) 16 h of light, 8 h of darkness (LD 16:8) for 2 weeks; (b) LD 12:12 for 2 weeks; (c) LD 4:20 for 2 weeks, and (d) LD 4:20 for 4 weeks. Under the above lighting conditions, the rhythms of pineal NATase, serum and pineal MT contents when tested demonstrated a closely parallel relationship. These results supported the idea that pineal NATase accurately reflected MT synthesis and that the rhythms of pineal and serum MT content were in phase under long and short photoperiods, in spite of extrapineal sites of MT synthesis. Further, the results also demonstrated that the timing of the MT peaks in the serum and the pineal may depend on the length of the adaptation period to the environmental lighting. When the rats were housed under a short photoperiod (LD 4:20), the peak MT levels appeared in the middle of the dark period after 2 weeks but shifted towards the end of the dark period after 4 weeks.

Acetyltransferases↗
PubMed1983

Differential effect of benserazide on catecholamine concentrations in the rat pineal, cerebral cortex and hypothalamus.

The effect of benserazide, an aromatic L-amino acid decarboxylase inhibitor, has been investigated simultaneously on the noradrenaline content of the pineal, hypothalamus and cerebral cortex of the rat. The dopamine concentration of the hypothalamus was investigated in the same animals. Benserazide had no effect on pineal noradrenaline content throughout the light phase and the early part of the dark phase but caused a drastic reduction in the latter part of the dark period. The drug had no significant effect on noradrenaline or dopamine contents of the hypothalamus. Benserazide treatment caused a large reduction in the noradrenaline content of the cerebral cortex throughout 24 hr. However, this effect is unlikely to be due to a differential penetration of benserazide into the brain areas as a similar degree of decarboxylase inhibition was observed in all three tissues.

Animals↗
PubMed1983

Cholinergic urticaria: acetylcholine-receptor-dependent immediate-type hypersensitivity reaction to copper.

A patient with cholinergic urticaria syndrome was found to have an unusually large number of muscarinic cholinergic receptors in the urticarial sites. The amplification of these receptors may account for her heightened sensitivity to acetylcholine discharge following exercise, heat, and emotion. The acetylcholine presumably acts directly on the mast-cell membrane to initiate histamine release and thereby punctate urticaria. In addition, an otherwise occult sensitivity to copper was detected with a 48 h contact patch test to the metal followed by an exercise challenge. Under these conditions, the patch test site developed hives after the autonomic stress stimulus of exercise but showed nothing on conventional patch testing before exercise. Such "cholinergic patch testing" is recommended for the demonstration of other examples of antigen enhancement of acetylcholine-mediated reactions.

Acetylcholine↗
PubMed1982

Effect of benserazide on the levels of pineal 5-hydroxytryptamine, melatonin synthesising enzymes and serum melatonin.

The effect of benserazide, an aromatic L-amino acid decarboxylase inhibitor, has been investigated on pineal 5-hydroxytryptamine content, melatonin synthesising enzyme activities and serum melatonin concn. Increasing doses of benserazide caused increasing reductions in the pineal content of 5-hydroxytryptamine. Dark phase serum melatonin concns were also greatly reduced. The drug abolished the diurnal rhythm of hydroxyindole-O-methyltransferase by increasing the light period activities and decreasing the night levels of this enzyme. Pineal N-acetyltransferase was unaffected. It is concluded that benserazide probably inhibits melatonin synthesis by preventing the formation of the substrate, 5-hydroxytryptamine.

Acetylserotonin O-Methyltransferase↗
PubMed1981

Differential effect of benserazide (Ro4-4602) on the concentration of indoleamines in rat pineal and hypothalamus.

1 Low doses (50 and 80 mg/kg) of benserazide (Ro4-4602), an aromatic amino acid decarboxylase inhibitor, markedly reduced 5-hydroxytryptamine and melatonin in the rat pineal gland without affecting hypothalamic 5-hydroxytryptamine. 2 This differential effect shows that inhibition of the pineal gland decarboxylase activity is possible, and confirms that the rat pineal gland is accessible to peripherally acting agents.

Animals↗
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↗
PubMed1978

Activity sampling in two nursing home foodservice systems.

Activity sampling was conducted in the foodservice department of two Wisconsin skilled care nursing homes with bed capacities between 100 and 160. Two seven-day sampling periods about one month apart were conducted in each home with 100 random observations being made each day. Analysis of variance of data indicated that the modified activity sampling technique was reliable in analyzing activities of personnel in nursing home foodservice systems with similar organizational and operational characteristics. In both homes, approximately 81, 9, and 10% of total labor time were spent in direct work, indirect work, and delays, respectively. Mean labor minutes per meal equivalent served (7.48 in Home X and 7.43 in Home Y) were similar. The consistent values for minutes per meal equivalent from Monday through Friday suggest that future activity sampling studies in nursing homes could be less than seven days. When evaluating staffing patterns in nursing home foodservice systems, consideration should be given to both quantitative indexes (minutes per meal, food cost per meal, labor cost per meal and qualitative indexes (sensory, microbial, and nutrient quality of food served), as well as to employee and resident satisfaction with the system.

Analysis of Variance↗