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Biomedical subjects

H J Liu

Publications and source records attributed to H J Liu.

At least 91 records · Page 5Linked to original sources
PubMed1987

The effect of DMSO on natural DNA conformation in enhancing transcription.

In the presence of 5% dimethylsulfoxide, 2.5 fold increase in vitro RNA synthesis rate by E. coli RNA polymerase was observed as superhelical pBR322 DNA was used as template. The effect of DMSO on DNA conformation was studied by: [i] measuring the dissociation constant of EtBr-DNA complex and the maximum EtBr binding site of EtBr in DNA which changed from 7.52 X 10(-7) M and 0.18 site per nucleotide to 9.61 X 10(-7) M and 0.156 site per nucleotide respectively when 10% DMSO was supplemented; and [ii] the increase of average linking number of pBR322 DNA in DMSO solution with topoisomerase I reaction. These results suggest that the stimulation of RNA synthesis may be caused by the easier initiation and elongation of RNA synthesis at some locally loosen regions of DNA affected by another torsionally more twisted counterpart regions in the DMSO microenvironment.

Animals↗
PubMed1987

Diazepam facilitates reflex bradycardia in conscious rats.

The effects of diazepam on cardiovascular function were assessed in conscious rats. Intravenous administration of diazepam (1-30 mg kg-1) produced a dose-dependent decrease in both the mean arterial pressure and the heart rate. Also, reflex bradycardia was produced in rats by intravenous infusion of adrenaline (1.25-2.5 micrograms kg-1). Intravenous pretreatment of the rats with diazepam, although causing no change in the adrenaline-induced pressor effect, did enhance the adrenaline-induced reflex bradycardia. However, the diazepam enhancement of adrenaline-induced reflex bradycardia was antagonized by pretreatment of rats with an intravenous dose of picrotoxin (an agent blocks chloride channels by binding to sites associated with the benzodiazepine-GABA-chloride channel macromolecular complex). The data indicate that diazepam acts through the benzodiazepine-GABA-chloride channel macromolecular complex within the central nervous system to facilitate reflex bradycardia mediated through baroreceptor reflexes in response to an acute increase in arterial pressure.

Animals↗
PubMed1985

Cholecystokinin-induced hypothermia: possible involvement of serotoninergic mechanisms in the rat hypothalamus.

The thermal effects of rats which were pretreated with 5,7-dihydroxytryptamine to deplete hypothalamic 5-hydroxytryptamine (5-HT) or with a 5-HT receptor blocker to intrahypothalamic administration of cholecystokinin (CCK) were compared with those of control rats. The CCK-induced hypothermic response was attenuated by pretreatment of the rats with either hypothalamic 5-HT depletion or receptor blockade. The reduction in the CCK hypothermia in the treated rats was due to the reduction of metabolic and vasomotor response. The data indicate that CCK may act on a 5-HT pathway within the hypothalamus to induce its hypothermia by promoting a reduction in metabolic heat production and an enhancement in heat loss in rats.

5,7-Dihydroxytryptamine↗
PubMed1985

Pharmacologic studies of the central action of zopiclone: effects on locomotor activity and brain monoamines in rats.

To investigate the effects of zopiclone on the central nervous system, we examined the effects of zopiclone on brain monoamines such as dopamine (DA), noradrenaline (NA) and serotonin (5-HT) and their metabolites such as homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA), as well as locomotor activity in comparison with those of nitrazepam and flurazepam. Zopiclone in a dose of 10 mg/kg (p.o.) significantly reduced it (p less than 0.01) in 30 min and the reduced locomotor activity persisted until 180 min. The reducing effect on locomotor activity by zopiclone was similar to that of nitrazepam and more potent than flurazepam. The effects of zopiclone on brain monoamines (MA) were examined. No significant changes in DA, NA and 5-HT were observed, but HVA and 5-HIAA were reduced. A fluorescent-histochemical study conducted simultaneously revealed almost the same results as the biochemical test results. From the facts that zopiclone inhibited locomotor activity in rats, and inhibited brain DA and 5-HT turnover, the mechanism of action of zopiclone in brain MA neurons seems to be similar to that of benzodiazepine derivatives.

Animals↗
PubMed1982

[Suppressive effects of lisuride on the synthesis, release and metabolism of dopamine in rat brain].

Effects of lisuride, a central dopaminergic agonist of the ergot type, on the biosynthesis, release and metabolism of dopamine at the dopaminergic nerve terminals of the rat brain were studied under several experimental conditions. 1) In the rat whose impulse flow of dopamine neurons and the activity of aromatic amino acid decarboxylase were inhibited by the pretreatment with gamma-butyrolactone and with 3-hydroxybenzylhydrazine (NDS 1015), respectively, DOPA formation in the neostriatum and limbic forebrain were decreased significantly by the s.c. administration of lisuride at the dosage known to be ineffective on the postsynaptic dopamine receptor. 2) When it was measured by the accumulation of 3-methoxytyramine in the neostriatum and limbic forebrain of pargyline (MAO inhibitor)-pretreated rats, lisuride at the low dosage caused the inhibition of not only the spontaneous release of dopamine from the nerve terminal to the synaptic cleft, but also the release induced with methamphetamine. 3) In the rat whose dopamine biosynthesis was inhibited with alpha-methyl-p-tyrosine, lisuride caused the suppression of dopamine metabolism, resulting in significant increases of dopamine histofluorescence in the nucleus caudatus, olfactory tubercle and median eminence. As to the effect on dopamine histofluorescence, apomorphine at 1 mg/kg was equipotent to lisuride at 50 micrograms/kg. It was concluded from these results that lisuride administered at low dosage interacts preferentially with the presynaptic dopamine receptor, hereby causing the suppressive effects on the tyrosine hydroxylase reaction and the dopamine release mechanism in the dopamine nerve terminals of the brain.

Animals↗
PubMed1980

Altitude convulsion threshold and time to altitude convulsion in gold thioglucose obese mice.

Gold thioglucose-induced hypothalamic obesity caused a higher altitude convulsion threshold and a decrease in the time to altitude convulsion. The average altitude convulsion threshold for the obese mice was 151 torr (38,500 ft). In contrast, the average value for the controls was 131 torr (41,500 ft). It was also observed that at 206 torr (32,000 ft), the average time until altitude convulsion of the obese mice was 69 s; at 179 torr (35,000 ft), 27 s; at 141 torr (40,000 ft), 17 s; at 111 torr (45,000 ft), 10 s; at 87 torr (50,000 ft), 9 s; and at 69 torr (55,000 ft), 8 s. On the other hand, the average control time until altitude convulsion at the above-mentioned altitudes was 97, 37, 26, 11, 9, and 8 s, respectively. Moreover, the average accumulation of fat between pleura and lungs in obese mice was 154 (Table I) or 181 mg (Table II), while the value of the control group was only 72 to 67 mg. Such an increase of fat accumulation in the thoracic cage could decrease the tidal volume. The altitude convulsion threshold and the time until altitude convulsion might thus be changed. The time until altitude convulsion may be regarded as a convenient objective measure of altitude tolerance in mice.

Altitude↗
PubMed1975

Influence of hypothalamic hyperphagia on tolerance of lung to explosive decompression.

A study was made of the effect of hypothalamic hyperphagia on the tolerance of lung to explosive decompression in male Long-Evans rats. The control and hypothalamic hyperphagic rats were explosively decompressed together from 1 atm to an ambient pressure of 30 min Hg in 0.04s. The hypothalamic-lesiones rats gained from 252 g average weight to 460 g, a 82% gain. The respective figures for the controls. were from 248 g to 336 g and 36%. It was also observed that a considerable amount of fat was accumulated between pleura and lungs in experimental animals. The average accumulation of fat between pleura and lungs in experimental rats was 3.23 g, while the value of the control group was only 0.42 g. The difference was statistically significant. Such an increase of fat accumulation in the thoracic cage could decrease the tidal volume. The severity of decompression-induced pulmonary hemorrages might thus be decreased. On the other hand, it also seems possible that the soft fat cushion between pleura and lungs might damp the bruising of the pulmonary tissue against the resistant thoracic wall to a certain extent, thus resulting in a decreased susceptibility to decompression-induced lung damage. Besides , the mortality in obese rats undergoing explosive decompression was also significantly lower than that of the controls

Adaptation, Physiological↗