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Biomedical subjects

J S Han

Publications and source records attributed to J S Han.

At least 217 records · Page 12Linked to original sources
PubMed1993

Lectin histochemical study on the kidney of normal and streptozotocin-induced diabetic hamsters.

Lectin histochemical characteristics of the kidney of normal and streptozotocin (SZ)-induced diabetic APA hamsters were investigated. Paraffin sections of the kidney of animals killed at 1 and 3 months after SZ-injection were stained with the following 10 lectins: PNA, BPA, DBA, SBA, GSA-I, GSA-II, MPA, WGA, UEA-1 and Con A. Renal lectin binding characteristics of normal APA hamsters differed in some aspects from those in other species reported previously. In the kidney of SZ-induced diabetic APA hamsters, binding activities of some lectins increased in the affected Bowman's capsules and glomeruli as well as in degenerated epithelial cells of uriniferous tubules. Among them, GSA-II in particular exhibited strong binding activity to the degenerated epithelial cells of Bowman's capsules, distal convoluted tubules and collecting ducts.

Animals↗
PubMed1992

Influences of cholecystokinin octapeptide on phosphoinositide turnover in neonatal-rat brain cells.

Cholecystokinin octapeptide (CCK-8) has been shown to be coupled to phosphoinositide turnover in pancreatic acini as well as in a kind of neuroblastoma cell and a human embryonic cell line. Little is known, however, about its link with phosphatidylinositol breakdown in the brain. The brains (minus cerebella) from 1-2-day-old neonatal rats were enzymically dissociated into single cells. The intact cells were prelabelled by incubation with myo-[3H]inositol for 3 h, and were then stimulated with agonists in the presence of 10 mM-LiCl. Carbachol at 1 mM induced an increase in InsP3 labelling in brain cells (peak at 30 min, and then a gradual decrease), and a static accumulation of InsP with time, whereas the labelling of InsP2 remained essentially unchanged. A very similar time-response curve was obtained for 10 nM-CCK-8 in stimulating phosphoinositide turnover. The dose-response curve for incubated brain cells revealed that the formation of InsP3 increased when the concentration of CCK-8 was increased from 0.1 to 10 nM. A further increase in CCK-8 concentration to 100-1000 nM resulted in a gradual decrease in InsP3 formation. InsP and InsP2 levels stayed relatively stable. The production of InsP3 stimulated by 10 nM-CCK-8 was dose-dependently suppressed by the CCK-A antagonist Devazepide in the concentration range 1-10 nM; the effect declined when the concentration was further increased to 100-1000 nM. In contrast, the CCK-B antagonist L365,260 showed a sustained suppression of InsP3 production at concentrations above 0.1 nM, i.e. in the range 1-1000 nM. The results provide evidence that CCK-8 stimulates the turnover of phosphoinositide and increases InsP3 labelling in dissociated neonatal-rat brain cells, in which both CCK-A and CCK-B receptors seem to be involved.

Animals↗
PubMed1992

Further studies on interactions between periaqueductal gray, nucleus accumbens and habenula in antinociception.

Previous findings from this laboratory with the intracerebral microinjection technique suggested that the periaqueductal gray (PAG), nucleus accumbens, and habenula might constitute a unidirectional loop to play their roles in pain modulation. In the present study we demonstrate that intra-habenular injection of naloxone antagonizes the analgesia elicited by morphine injected into the periaqueductal gray (PAG) and that intra-accumbens injection of naloxone is capable of attenuating the analgesic effects of morphine injected into the habenula. These results indicate that the relationships between these nuclei may be more complex than the putative unidirectional loop.

Analysis of Variance↗
PubMed1992

Analgesia induced by electroacupuncture of different frequencies is mediated by different types of opioid receptors: another cross-tolerance study.

The cross-tolerance technique was used to analyze the receptor mechanisms of analgesia induced by electroacupuncture (EA) of 2 Hz, 100 Hz, or 2-15 Hz. (1) Rats were given EA stimulation of 2 Hz, 100 Hz and 2-15 Hz for 30 min with 30 min intervals successively. The percentage increase in tail-flick latency (TFL) was taken to indicate the intensity of EA analgesia. Rats made tolerant to repeated intrathecal injection of the mu-opioid agonist ohmefentanyl (OMF, 15 pmol, Q2h x 5) or the delta-opioid agonist DPDPE (10 nmol, Q2h x 5) showed a cross tolerance to both 2 Hz- and 2-15 Hz-, but not to 100 Hz-EA analgesia; and rats made tolerant to kappa-opioid agonist dynorphin-(1-13) (5 nmol, Q2h x 5) showed a cross-tolerance to 100 Hz- and 2-15 Hz-, but not to 2 Hz-EA analgesia; (2) Rats made tolerant to 2-15 Hz EA showed cross-tolerance to either 2 Hz- or 100 Hz-EA analgesia; (3) Rats made tolerant to either 2 Hz- or 100 Hz-EA were still reactive to 2-15 Hz-EA. The results indicate that 2 Hz-EA analgesia is mediated by mu- and delta-receptors, 100 Hz-EA analgesia by kappa-receptor, and 2-15 Hz-EA analgesia by combined action of mu-, delta- and kappa-receptors in the spinal cord of the rats.

Animals↗
PubMed1992

All three types of opioid receptors in the spinal cord are important for 2/15 Hz electroacupuncture analgesia.

The analgesic effect induced by 2/15 Hz electroacupuncture as shown by the increase in tail flick latency decreased steadily as electroacupuncture stimulation was given continuously for 6 h, showing the development of tolerance to electroacupuncture analgesia. These rats were then given an intrathecal (i.t.) injection of one of the following opioid agonists: the mu agonist, ohmefentanyl 7.5, 15 and 30 pmol, 10 min apart; the delta agonist, [D-Pen2,D-Pen5]enkephalin (DPDPE) 5, 10 and 20 nmol, 10 min apart and the kappa agonist, dynorphin-(1-13) 2.5, 5 and 10 nmol, 10 min apart, respectively. The analgesic effect induced by ohmefentanyl, DPDPE or dynorphin was dramatically reduced in rats rendered tolerant to 2/15 Hz electroacupuncture analgesia. Rats were injected i.t. with one of the three specific opioid antagonists: the mu antagonist, beta-funaltrexamine (beta-FNA) (5, 10 and 20 nmol), the delta antagonist, ICI174,864 (1, 2 and 4 nmol) and the kappa antagonist, nor-binaltorphimine (nor-BNI) (3.125, 6.25 and 12.5 nmol). It was found that analgesia induced by 2/15 Hz electroacupuncture stimulation was significantly and almost totally blocked by any one of the three opioid antagonists. These results suggest that all three types of opioid receptors, the mu, delta and kappa receptors in the spinal cord of the rat play important roles in mediating analgesia induced by electroacupuncture of 2/15 Hz.

Acupuncture Analgesia↗
PubMed1992

Centrally acting endogenous hypotensive substances in rats subjected to endotoxic shock.

Cerebroventricular perfusate (CVP) from rats subjected to endotoxic shock was infused into the lateral ventricle of the naive rat. This procedure produced a hypotensive response in the recipient rat which could be reversed by the intravenous injection of the opioid antagonist naltrexone. The degree of endotoxemic hypotension in the donor rat was attenuated by perfusing the cerebroventricular system with mock CSF. The results suggest the existence of endogenous hypotensive substances in rat central nervous system, possibly opioid in nature, which may play a critical role in the pathogenesis of endotoxic shock.

Animals↗
PubMed1992

Effects of various chemical compounds on spontaneous and hydrogen peroxide-induced reversion in strain TA104 of Salmonella typhimurium.

In experiments designed to determine which active oxygen species contribute to hydrogen peroxide (HP)-induced reversion in strain TA104 of Salmonella typhimurium, 1,10-phenanthroline (an iron chelator, which prevents the formation of hydroxyl radicals from HP and DNA-bound iron by the Fenton reaction), sodium azide (a singlet oxygen scavenger), and potassium iodide (an hydroxyl radical scavenger) inhibited HP-induced reversion. These results indicate that hydroxyl radicals generated from HP by the Fenton reaction, and perhaps singlet oxygen, contribute to HP-induced reversion in TA104. However, reduced glutathione (reduces Fe3+ to Fe2+ and/or HP to water), diethyldithiocarbamic acid (an inhibitor of superoxide dismutase), diethyl maleate (a glutathione scavenger), and 3-amino-1,2,4-triazole (an inhibitor of catalase) did not inhibit HP-induced reversion in TA104. Thus, superoxide radical anions and HP itself do not appear to be the cause of HP-induced reversion in this strain. In experiments on the effect of 5 common dietary compounds (beta-carotene, retinoic acid, and vitamins A, C and E), chlorophyllin (CHL), and ergothioneine, the frequency of revertants in TA104 increased above the spontaneous frequency in the presence of beta-carotene or vitamin C (about 2-fold) or vitamin A (about 3-fold). The 5 dietary antimutagens and CHL did not inhibit HP-induced reversion in TA104. However, L-ergothioneine inhibited HP-induced reversion in this strain. Therefore, it is likely that L-ergothioneine is a scavenger of hydroxyl radicals or an inhibitor of their formation, and perhaps of singlet oxygen, at the concentrations tested in TA104.

Ascorbic Acid↗
PubMed1992

Mobilization of calcium from intracellular store as a possible mechanism underlying the anti-opioid effect of angiotensin II.

Angiotensin II (AII), injected intracerebroventricularly, has been shown to antagonize opioid analgesia. The mechanism for this was obscure. In the neuroblastoma X glioma NG 108-15 hybrid cell line, the K(+)-induced increase in [Ca2+]i can be suppressed by the delta opioid agonist [D-Pen2, D-Pen5]enkephalin (DPDPE) at 0.01-1 microM, an effect completely reversed by the opioid antagonist naloxone. Angiotensin II (AII) at concentrations of 0.1 and 1 microM mobilized free Ca2+ from an intracellular pool, and this effect was antagonized by the AII receptor antagonist saralasin. All (1 microM) had no significant effect on the increase in [Ca2+]i induced by K+, but it blocked the suppressive effect of DPDPE on the K(+)-induced [Ca2+]i increase. The results indicate that mobilization of intracellular calcium may underlie the anti-opioid effect of AII.

Angiotensin II↗
PubMed1992

Naloxone blocks opioid peptide release in N. accumbens and amygdala elicited by morphine injected into periaqueductal gray.

It has been proposed that a serial, unidirectional circuit from the PAG to the N. accumbens and the amygdala are involved in antinociception and that enkephalins (ENK) and beta-endorphin (beta-EP) act as neurotransmitters in this circuitry. In the present study, we measured the release of ENK and beta-EP by simultaneous push-pull perfusion of the N. accumbens and amygdala after microinjection of morphine into the PAG. Morphine administration elicited an increase in immunoreactive ENK and beta-EP in both the N. accumbens and the amygdala, which was antagonized in each nucleus by perfusion with naloxone. These data suggest that the three nuclei were not serially connected and that they may take part in one and the same antinociceptive system with an "all or none" character.

Amygdala↗
PubMed1992

Neurochemical and morphological evidence of an antinociceptive neural pathway from nucleus raphe dorsalis to nucleus accumbens in the rabbit.

Previous studies using a pharmacological approach suggested a neural pathway emanating from the periaqueductal gray (PAG) to the nucleus accumbens relevant to antinociception. This was investigated with neurochemical and histochemical methods in the present study. Push-pull perfusion and radioimmunoassay were used to measure the release of immunoreactive-(ir) enkephalin (ir-ENK) and ir-beta-endorphin (ir-beta-EP) in the nucleus accumbens after microinjection of morphine into the PAG and the nucleus raphe dorsalis (NRD) of the rabbit. Morphine administration elicited an increase in ir-ENK and ir-beta-EP in the nucleus accumbens. Horseradish peroxidase (HRP) retrograde tracing in combination with 5-hydroxytryptamine (5-HT) immunocytochemistry revealed a serotonergic projection from the NRD and ventral PAG to the nucleus accumbens in the rabbit. About 7% of the serotonin-positive cells in the NRD and ventral PAG send fibers directly to the nucleus accumbens, with an ipsilateral dominance. These results indicate the existence of a serotonergic pathway from the NRD to the N. accumbens involved in opioid analgesia.

Animals↗
PubMed1992

Accelerated expression of cholecystokinin gene in the brain of rats rendered tolerant to morphine.

Results from behavioural studies have shown that central cholecystokinin octapeptide (CCK-8) is a powerful antagonist against opioid effects and that an increased release of central CCK-8 plays an important role in the mechanisms of tolerance to morphine analgesia. No information is available concerning the rate of biosynthesis of CCK-8 in response to chronic morphine administration. Blot hybridization experiments made in the present study revealed a marked increase in preproCCK mRNA in the brain of rats receiving chronic morphine treatment for 1, 3 and 6 days, showing an increment of 52% (p < 0.05), 62% (p < 0.05) and 97% (p < 0.01) respectively. The results suggest that an acceleration of the expression of the CCK gene during long-term morphine treatment might constitute one of the mechanisms for morphine tolerance.

Animals↗
PubMed1992

CT-based geometric data of human spine musculature. Part I. Japanese patients with chronic low back pain.

Mechanical factors are considered to play a dominant role in low back problems. Various spinal structures, including muscles, act in unison to resist the external load, including the body segments. An estimation of the forces in these requires a knowledge of the orientation, location, and area of cross-section of the muscles to complete the information for the formulation of a truly three-dimensional biomechanical mathematical model of the spine in the lumbar region. Computed tomography scans of 10 Japanese patients suffering from chronic low back pain were obtained to determine the geometric data of the abdominal and back muscles from the 12th thoracic vertebral to the first sacral vertebral level. The mean age +/- 1 SD of the group was 40.1 +/- 14.12 years (range, 24-70), 573 +/- 88.5 N of body weight (range, 441-705), and 1.63 +/- 0.09 m tall (range, 1.44-1.74). The geometric parameters quantified were the line of action, and the centroid and physiologic area of cross-section of each muscle as a function of the spinal level. The effective/physiological area of cross-section of each muscle changed along the length of the spine because of the change in the line of action of the muscle. The centroidal approach adopted for quantifying the lines of action of various muscles was found unsuitable for the abdominal muscles, excluding the rectus abdominis, because of the associated anatomic complexities. Alternatives are proposed to complete the data base. The application of the data for the formulation of a truly three-dimensional biomechanical model of the spine at the L3-4 level is briefly presented. Application to nonlinear optimization-based force predictions in various spinal structures is discussed.

Adult↗
PubMed1992

Kinetics of urea and water permeability activation by vasopressin in rat terminal IMCD.

The vasopressin-regulated urea carrier and the vasopressin-regulated water channel are distinct transporters present in the apical membrane of the inner medullary collecting duct (IMCD) cells. To assess whether these transporters may be activated by common mechanisms, we investigated the time course of increase of urea and water permeability in response to vasopressin in isolated perfused terminal IMCD segments. The permeability responses were determined through the use of a specially designed continuous-flow fluorometer for rapid analysis of collected tubule fluid samples. The time courses of activation of the two transporters by vasopressin were virtually identical. Both urea and water permeability displayed a rapid initial increase for the first 10 min followed by a slower secondary response lasting at least 30 additional min. The lag periods between vasopressin addition and the initial rise in permeability were the same for urea (34.2 +/- 8.8 s) and water (34.8 +/- 8.9 s) transport activation. Furthermore, the initial rate of permeability increase (normalized by the total increase) was not significantly different for the two transport processes. The lag periods for the increase in urea permeability in response to 8-bromoadenosine 3',5'-cyclic monophosphate and vasopressin were not significantly different. The results are consistent with the view that the rate-limiting step in vasopressin-induced activation is the same for both the urea carrier and water channel and may lie at a step beyond generation of adenosine 3',5'-cyclic monophosphate.

Animals↗
PubMed1992

Encephalomyocarditis (EMC) virus-induced myocarditis by different virus variants and mouse strains.

The mode of occurrence of encephalomyocarditis (EMC) virus-induced myocarditis in mice was pathologically and virologically investigated using 2 virus variants (highly diabetogenic EMC-D and non-diabetogenic EMC-B) and 2 mouse strains (diabetes-susceptible BALB/c and diabetes-resistant C57BL/6). Mice were inoculated with 10(5) PFU/head of the virus intraperitoneally and observed up to 7 days post inoculation (7DPI). As compared with EMC-B-infected BALB/c and EMC-D-infected C57BL/6 mice, EMC-D-infected BALB/c mice developed marked myocarditis and exhibited a heart virus titer of more than 100 times above that of the others after 4DPI. Electron microscopically, small aggregations of virus-like particles, with 20-25 nm in diameter, were found in the cytoplasm of degenerated cardiomyocytes showing mitochondrial and myofibrillar degeneration in EMC-D-infected BALB/c mice.

Animals↗
PubMed1992

Experimental tests of three-dimensional model of urinary concentrating mechanism.

Recently, a new model of the urinary concentrating process has been proposed that takes into account the three-dimensional architecture of the renal medulla. Under the assumptions of the model, computer simulations predicted significant axial osmolality gradients in the inner medulla without active transport by the inner medullary loop of Henle. Two of the model assumptions (which constitute hypotheses for this study) were: (1) the osmotic water permeability of the initial part of the inner medullary collecting duct (initial IMCD) is very low even in the presence of vasopressin; and (2) there is significant lateral separation of structures such that thin descending limbs are far from the collecting ducts at the same inner medullary level. The first hypothesis was addressed by perfusing rat initial IMCD segments in vitro and measuring osmotic water permeability. With the osmotic gradient oriented as predicted by the model (lumen greater than bath), vasopressin increased the osmotic water permeability from 286 to 852 microns/s. Three additional series of experiments confirmed the high water permeability in the presence of vasopressin. The second hypothesis was addressed by morphometric analysis of histologic cross-sections of the rat renal medulla. Mean distances of descending limbs to the nearest adjacent collecting duct were very small throughout the inner medulla (less than 6 microns) and substantially less than in the outer medulla (28 microns). It was concluded that the data are inconsistent with both hypotheses and therefore do not support the feasibility of the "three-dimensional" model of the renal inner medulla. The axial distributions of loops of Henle and collecting ducts in the rat renal medulla are also reported.

Animals↗
PubMed1992

[Induction of Fos-like protein in the rat spinal cord following electroacupuncture stimulation].

The expression of the c-fos proto-oncogene has been regarded as a marker for noxious stimulation. We now report that electroacupuncture (EA) stimulation (100 Hz, 0.3 ms, 1-2-3 mA, 30 min) delivered into the acupoint Sanyinjiao (SP6) could also induce the c-fos expression in the rat spinal cord as demonstrated by immunohistochemical technique using antibody against the c-fos protein product Fos. In rats receiving EA stimulation, numerous cells with Fos-like immunoreactivity (FLI) were observed in both dorsal and ventral horn of the spinal cord with dense labelling in laminae III and IV of the ipsilateral side. Only scattered FLI cells were found in laminae I and II. In contrast, FLI evoked by noxious stimulation (5% formalin injected at the hindfoot subcutaneously) was shown mainly in laminae I and II, rather than in III and IV. The c-fos expression was very low in control animals receiving neither formalin nor EA administration. The present study indicates that the site specificity of the c-fos expression induced by EA is different from that evoked by noxious stimulation. The possibility that EA-induced Fos protein might participate in acupuncture analgesia is currently under investigation.

Animals↗
PubMed1992

Morphometric study on the renal glomeruli of streptozotocin (SZ)-induced diabetic APA hamsters.

Morphometrical analysis was done on the renal glomeruli of streptozotocin (SZ)-induced diabetic and control APA hamsters. In coincidence with the histopathological and ultrastructural findings, the areas of whole glomerulus (WG) and mesangial region (MR) were significantly larger in diabetic animals than in controls at 1 and 3 months after SZ-injection (1 and 3MAI). The area of capillary lumen in diabetic animals was larger than that in controls at 1MAI but it became similar between both groups at 3MAI probably due to an increase in the area of MR. The thickness of basement membrane was significantly larger in diabetic animals than in controls at 3MAI. The present morphometrical findings, together with histological and ultrastructural ones, suggest that SZ-induced diabetic APA hamsters are useful as a model system for the investigation of focal and segmental glomerulosclerosis.

Animals↗