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Biomedical subjects

J S Han

Publications and source records attributed to J S Han.

At least 271 records · Page 15Linked to original sources
PubMed1990

[Evaluation of air-powder abrasive system on tooth abrasion].

The maintenance of good oral hygiene in patients with or without prosthesis has been one of the essential parts of the total oral health care. Recently a redesigned air-powder abrasive system was introduced to remove dental plaque and stain from tooth surfaces. This study was designed to evaluate effects of this device on the cementoenamel junction area quantitatively and qualitatively by using the Michigan Computer Graphic Coordinate Measuring system (MCGCMS) and scanning electron microscopy (SEM) after exposure to an air-powder abrasive device. A tooth specimen was exposed to a Cavi-Jet (Dentsply International Inc., York, PA) for 10, 30, 90 seconds intervals. The MCGCMS was utilized before and after treatment of the specimen at each time interval to measure the depth abrasion of the tooth material, and SEM pictures were taken after 90 seconds treatment of the specimen to evaluate surface characteristics. Following conclusions were drawn within the limits the confines of this study. 1. An air-powder abrasive device abrades cementum rapidly and should be used carefully below cementoenamel junction. 2. There was no significant change on the enamel surface quantitatively. 3. The MCGCMS reproduces and measures experimental points accurately.

Air↗
PubMed1990

Accelerated synthesis and release of angiotensin II in the rat brain during electroacupuncture tolerance.

Behavioural studies suggested that cerebral angiotensin II (AII) plays an important role in the development of tolerance to electroacupuncture (EA) analgesia. Observations made in this study revealed an increase in AII immunoreactivity (AII-ir) in both CSF and brain as well as an increase in the cerebral content of AI-ir in rats rendered tolerant to EA. The extracts of brain from rats receiving EA for 1h and 3h were subjected to gel filtration and the elution profile was compared with that of normal brain extract. There was a marked right shift of the AII peak from the large molecule precursor to the small molecule AII-ir. The latter peak showed the same retention time in HPLC system as that of AII. The results suggest that the acceleration of the synthesis and release of AII during a long-term EA stimulation might constitute one of the mechanisms for EA tolerance.

Acupuncture Analgesia↗
PubMed1989

Cholecystokinin-octapeptide antagonizes morphine analgesia in periaqueductal gray of the rat.

The analgesic effect of systemic morphine (5 mg/kg, s.c.) was dose-dependently antagonized by CCK-8 administered to the periaqueductal gray (PAG) of the rat. This effect could be reversed by proglumide, a CCK-receptor antagonist. The effect of morphine analgesia was potentiated by proglumide administered to PAG. These results are compatible with the notion that PAG is a strategic site where CCK-8 exerts an antiopioid activity.

Analgesia↗
PubMed1989

Cholecystokinin-8 suppressed 3H-etorphine binding to rat brain opiate receptors.

Radio receptor assay (RRA) was adopted to analyse the influence of CCK-8 on 3H-etorphine binding to opiate receptors in rat brain synaptosomal membranes (P2). In the competition experiment CCK-8 (1pM to 1 microM) suppressed the binding of 3H-etorphine. This effect was completely reversed by proglumide at 1 microM. Rosenthal analysis for saturation revealed two populations of 3H-etorphine binding sites. CCK-8 (1pM to 1 microM) inhibited 3H-etorphine binding to the high affinity sites by an increase in Kd (up to +235%) and decrease in Bmax (up to -80%) without significant changes in the Kd and Bmax of the low affinity sites. This effect of CCK-8 (10nM) was also completely reversed by proglumide at 1 microM. Unsulfated CCK-8 (100pM to 1 microM) produced only a slight increase in Kd of the high affinity sites (+64%) without affecting Bmax. The results suggest that CCK-8 might be capable of suppressing the high affinity opioid binding sites via the activation of CCK receptor.

Animals↗
PubMed1989

Effect of calcium ion on analgesia of opioid peptides.

The analgesic effect produced by subcutaneous injection (SC) of morphine was antagonized by intracerebroventricular (ICV) but not intrathecal (ITH) injection of CaCl2. While ITH CaCl2 was devoid of any effect on the analgesia induced by ITH morphine, it did antagonize the analgesic effect produced by ITH injection of dynorphin A or (D-Pen2,D-Pen5)-enkephalin (DPDPE). In accordance with this, the uptake of 45Ca by synaptosomes prepared from the dorsal column of rat spinal cord was suppressed by dynorphin A or DPDPE, but not by morphine. The results imply that different kinds of opioid ligands might have different mechanisms of action at discrete areas of the CNS. Blockade of neuronal Ca2+ uptake may serve as an important mechanism for morphine analgesia in the brain as well as DPDPE and dynorphin A analgesia in the spinal cord.

Analgesia↗
PubMed1989

Involvement of arcuate nucleus of hypothalamus in the descending pathway from nucleus accumbens to periaqueductal grey subserving an antinociceptive effect.

The present study was performed to explore the possible involvement of the arcuate nucleus of hypothalamus (ARH) and beta-endorphinergic pathway in the connection from nucleus accumbens to periaqueductal grey (PAG). It was found that the analgesic effect of morphine administered to nucleus accumbens of the rabbit was significantly attenuated by the antiserum against beta-endorphin (beta-EP) injected into PAG. The antagonistic effect was totally abolished by lesioning of the ARH. However, in the rabbit with ARH lesioning, no significant change in basal nociceptive threshold was seen nor was there any significant change in the efficacy of analgesia induced by injecting morphine into nucleus accumbens. The latter effect was attenuated by intra-PAG-administered naloxone, as in the normal control rabbits. These results indicate that (1) ARH and its efferent beta-endorphinergic fibers are involved in the descending pathway from the nucleus accumbens to PAG, subserving an antinociceptive effect, (2) endogenous opioid peptides other than beta-EP seem to play an equally important role in mediating analgesia.

Analgesia↗
PubMed1989

[High and low frequency electroacupuncture analgesia are mediated by different types of opioid receptors at spinal level: a cross tolerance study].

Previous studies have shown that rats subjected to low or high frequency electroacupuncture (EA) stimulation release enkephalins or dynorphins respectively to produce analgesia. This conclusion was tested in the present study by using cross tolerance technique for further analysing their receptor mechanisms. The main results were as follows: (1) In rats subjected to 2 Hz EA for 6 h, there was a gradual decrease in the analgesic effect, leading to a state of tolerance to 2 Hz EA analgesia. These rats, however, still responded to 100 Hz EA. Likewise, rats made tolerant to 100 Hz EA were still effective to 2 Hz EA stimulation, showing not significant cross tolerance between 2 Hz and 100 Hz EA analgesia. (2) Rats made-tolerant to 100 Hz EA analgesia showed a diminished response to intrathecal dynorphin A (1-13), a kappa agonist, whereas the analgesic effect of the delta agonist [D-Pen2, D-pen5] enkephalin (DPDPE) remained intact. (3) Rats made tolerant to 2 Hz EA analgesia showed a cross tolerance to DPDPE, but not to dynorphin A (1-13). Results obtained from aforementioned cross tolerance studies suggest that 2 Hz and 100 Hz EA analgesia are mediated by delta and kappa opioid receptors, respectively, at the spinal cord of the rat.

Acupuncture Analgesia↗
PubMed1989

[Antagonism of morphine analgesia and electroacupuncture analgesia by cholecystokinin octapeptide (CCK-8) administered in periaqueductal gray (PAG) of the rabbits].

We have reported that intracerebroventricular (i. c. v.) injection of 1-4 ng of CCK-8 to the rat produced a remarkable antagonistic effect on morphine analgesia. In order to study the species specificity and the site of action, CCK-8 was microinjected into the PAG of the rabbit, and its influence on morphine analgesia and electroacupuncture analgesia was observed. The latency of the escape response (ERL) to radiant heat focused on the snout was measured as an index of the pain threshold. Microinjections were made via cannulae chronically implanted into the PAG. The drug solutions were delivered in a volume of 1 microliter, at a speed of 0.125 microliter/min. The ERL was measured for a period of 60 or 70 minutes at 10 min intervals. 1. CCK-8 administered unilaterally to the PAG of the rabbit at a dose of 3 ng antagonized the analgesia induced by morphine (4 mg/kg, i. v.) by 73% (P less than 0.001), and reduced the analgesic effect of electroacupuncture by 67% (P less than 0.001). These effects were dose-dependent within the range from 1.5 ng to 6.0 ng. The effect of CCK-8 was reversed by CCK receptor blocker proglumide (4 microliters, intra-PAG injection). Unsulfated CCK-8 (CCK-us) had no effect in this regard. These results indicate that in the PAG of the rabbit, exogenously administered CCK-8 was capable of antagonizing opioid analgesia by the activation of CCK receptors. 2. Two groups of rabbits were given with morphine (2 mg/kg, i. v.) and simultaneous injection of CCK-8 antiserum (CCK-AS, 1 microliter) or normal rabbit serum (NRS) into the PAG.(ABSTRACT TRUNCATED AT 250 WORDS)

Acupuncture Analgesia↗
PubMed1989

[Antagonism to morphine analgesia and involvement in morphine tolerance of angiotensin II in periaqueductal gray of the rabbits].

The stainless steel cannulas were implanted to male rabbits of 2.0-2.6 kg, under Na-pentobarbital anaesthesia with the aid of a stereotaxic instrument. Co-ordinates of the locations of the implantations were P 9.5, LR 1.0, H 10.0 mm (under outer surface of the skull) on both sides of periaqueductal gray (PAG). After 1 wk, nociception was assessed by measuring the latency of the escape response (ERL) elicited by strong radiant heat focused on the nose of rabbits. The analgesic effect of morphine (4 mg/kg, iv) was blocked by injecting angiotensin II (AII, 0.1 microgram) into PAG (P less than 0.01, ANOVA), but not by injecting the same dose of AII into the vicinity of PAG (P greater than 0.05, ANOVA). Morphine tolerance was induced by iv infusion of morphine for 2 d, the dose being 50 mg/(kg.8 h) on d 1 and 75 mg/(kg.8 h) on d 2. On d 3, the degree of tolerance was checked by the analgesia induced by iv morphine 4 mg/kg. Tolerance was partly reversed by injecting AII anti-serum 2 microliters into PAG(P less than 0.01, ANOVA). The results suggest that AII in PAG is antagonistic to morphine analgesia and is involved in the development of morphine tolerance.

Angiotensin II↗
PubMed1989

[Antagonistic effects of angiotensin II and morphine on synaptosomal calcium uptake].

Behavioral observations have repeatedly shown that the analgesic effect of morphine can be antagonized by intracerebroventricular injection of angiotensin I (A I), although mechanisms underlying the action were obscure. Since a prevention of Ca2+ uptake into the nerve terminals was considered as one of the mechanisms for morphine analgesia, we examined the effect of A I and morphine on the 45Ca uptake by rat brain synaptosomal preparations. Morphine of 10(-8)-10(-6) mol/L produced a dose-related suppression on synaptosomal 45Ca uptake, which was completely reversed by the opioid antagonist naloxone of 10(-6) mol/L. A I of 10(-8)-10(-6) mol/L, on the contrary, enhanced 45Ca uptake. This effect was totally abolished by saralasin, a A I antagonist, at 10(-6) mol/L. When synaptosomal preparations were incubated in a mixture of morphine (10(-6) mol/L) and A I (10(-8)-10(-6) mol/L), the effect of morphine was almost completely reversed. The results suggest that the distinct effect of A I may account for, at least in part, the antagonistic effect of A I on morphine analgesia.

Angiotensin II↗
PubMed1989

[Accelerated angiotensinogen gene expression in the rat brain made tolerant to morphine or electroacupuncture stimulation].

The aim of the present study was to explore whether the expression of angiotensinogen (Ang) gene was accelerated during the development of morphine tolerance or electroacupuncture tolerance. The total rat brain RNA was extracted by phenol, and dot blot hybridization with synthetic Ang oligo-DNA was adopted for measuring Ang mRNA. Autoradiographic examination revealed a marked increase in Ang mRNA in rats receiving multiple injections of morphine or continuous electroacupuncture (EA) stimulation for several hours. The integrated O.D. (I.O.D.) of the hybridized dots revealed a 1-fold and 8-fold increase in Ang mNRA in rats receiving morphine injection for 1 and 4 days, respectively, and a 5-fold and 13-fold increase in rats receiving 3 and 6h EA stimulation, respectively. The results suggest that transcription of Ang gene in rat brain can be accelerated within 3-4h by continuous morphine or EA stimulation and that a longer lasting stimulation resulted in a stronger gene expression.

Acupuncture Therapy↗