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Biomedical subjects

J S Han

Publications and source records attributed to J S Han.

At least 145 records · Page 8Linked to original sources
PubMed1997

Idiopathic retroperitoneal fibrosis presented as an abdominal mass and nephrotic syndrome.

We present a 30-year-old male patient who was initially diagnosed as minimal change nephrotic syndrome, 5 years later, the patient developed a localized form of idiopathic retroperitoneal fibrosis (IRF). An elevated ESR and concomitant nephrotic syndrome in the patient suggested the immunologic nature of IRF, IRF has been reported in association with collagen diseases and rarely with proliferative and nonproliferative glomerulopathies. To our knowledge, the association between minimal change lesion (MC) and IRF has not been reported. Furthermore, the fact that IRF presented itself as an abdominal mass and lacked systemic symptoms was also unusual.

Adult↗
PubMed1997

[Correlation between motor paralysis and neurotoxicity induced by intrathecal dynorphin A (1-17) in rats].

Intrathecal(i.t.) injection of 10 microliters of dynorphin A(1-17) 20 nmol.L-1 per rat resulted in irreversible hind limb paralysis and suppression of the tail-flick reflex lasting for up to 40 h. The dual effects of dynorphin appeared 5-10 min after the i.t. administration. Histologic examination of the spinal cord in the rats demonstrated dead and/or dying and degenerated motor-neurons in the ventral horn located predominately in the lumbar segment(a 87.2% reduction of the number of motor neurons, P < 0.01) and also in a lesser degree in sacral segment(-69.6%, P < 0.05). The thoracic segment was essentially normal(-8.2%, P > 0.05).

Animals↗
PubMed1997

[Antagonistic effect of orphanin FQ on morphine analgesia in rat brain].

The discovery of a novel receptor-opioid receptor-like (ORL) receptor (1994) and its endogenous ligand-Orphanin FQ (OFQ) (1995) represented a new approach in the study of opioids and anti-opioids in CNS. Based on the high homology of ORL receptor and OFQ with their opioid family counterparts, as well as the high expression of ORL receptor mRNA and protein in the brain areas associated with nociception, the effect of OFQ on morphine induced analgesia in the rat brain was further investigated. The results showed that: (1) Intracerebroventricular (i.c.v.) injection of OFQ reversed the stress analgesia induced by i.c.v. injection of normal saline, which seems to be mediated by endogenous opioid peptides. (2) I.c.v. injection of OFQ dose-dependently antagonized morphine-induced analgesia dose-dependently. (3) I.c.v. injection of antisense oligodeoxynucleotide for the gene encoding ORL receptor to block the expression of ORL receptor in the CNS potentiated the analgesia induced by cumulative injection of morphine. The results suggest that OFQ seems to play a role of anti-opioid peptide in the rat brain.

Analgesics, Opioid↗
PubMed1997

[2 Hz and 100 Hz electroacupuncture accelerate the expression of genes encoding three opioid peptides in the rat brain].

Previous findings from this laboratory have shown that low (2 Hz) and high (100 Hz)-frequency electroacupuncture (EA) accelerated the release of different kinds of opioid peptides in the CNS. In the present study, we tried to elucidate whether EA of different frequencies would affect the transcription of genes encoding different opioid peptides. Digoxin-labeled antisense cRNA probes were used for in situ hybridization to detect the mRNA encoding preproenkephalin (PPE), preprodynorphin (PPD) and proopiomelanocortin (POMC) in the rat brain. The results showed that: (1) Neither 2 Hz nor 100 Hz EA altered the POMC mRNA level in the rat brain. (2) EA of the two frequencies induced a similar degree of increase of PPE mRNA in rostromedial reticular formation (gigantocellular, paragigantocellular and lateral reticular nucleus); whereas in supraoptic nucleus, suprachiasmatic nucleus, arcuate nucleus, paraventricular hypothalamic nucleus, ventromedial nucleus and the nucleus of lateral lemniscus, 2 Hz EA induced a higher PPE mRNA expression than 100 Hz EA. (3) 100 Hz EA markedly increased the PPD mRNA levels in supraoptic nucleus, paraventricular hypothalamic nucleus, ventromedial nucleus and parabrachial nucleus, while 2 Hz was without effect. Since de novo peptide synthesis is regarded as a natural outcome following accelerated peptide release, the present results substantiate our previous observation that EA of different frequencies exert different acceleratory effects on the release and synthesis of different opioid peptides in the central nervous system.

Acupuncture Analgesia↗
PubMed1996

Cholecystokinin octapeptide reverses the kappa-opioid-receptor-mediated depression of calcium current in rat dorsal root ganglion neurons.

Although the cholecystokinin octapeptide (CCK-8) is reported to antagonize the kappa-opioid-receptor-mediated analgesic effect in spinal cord, its mechanism and sites of action remain obscure. In the present study, the whole-cell patch-clamp recording technique was employed to examine the effect of kappa-opioid agonist U50488H on voltage-gated calcium channels and the interaction between the CCK-8 and U50488H in acutely isolated rat dorsal root ganglion neurons. The results indicate that the calcium currents elicited in dorsal root ganglion neurons can be depressed by U50488H, an effect readily reversed by the kappa-opioid receptor antagonist Nor-BNI or by the antiopioid peptide CCK-8. The effect of the CCK-8 can be abolished by the CCK-B receptor antagonist, L365,260. While CCK-8 showed a potent opioid-reversal effect, it by itself exerted a slight inhibitory effect on calcium current. This novel observation in the dorsal root ganglion neurons indicates that CCK-8 can antagonize the kappa-opioid-receptor-mediated depressant effect on voltage-gated calcium current, and this antagonizing effect appears to be mediated via CCK-B receptor.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1996

Neurotoxic lesions of basolateral, but not central, amygdala interfere with Pavlovian second-order conditioning and reinforcer devaluation effects.

Considerable evidence suggests that various discrete nuclei within the amygdala complex are critically involved in the assignment of emotional significance or value to events through associative learning. Much of this evidence comes from aversive conditioning procedures. For example, lesions of either basolateral amygdala (ABL) or the central nucleus (CN) interfere with the acquisition or expression of conditioned fear. The present study examined the effects of selective neurotoxic lesions of either ABL or CN on the acquisition of positive incentive value by a conditioned stimulus (CS) with two appetitive Pavlovian conditioning procedures. In second-order conditioning experiments, rats first received light-food pairings intended to endow the light with reinforcing power. The acquired reinforcing power of the light was then measured by examining its ability to serve as a reinforcer for second-order conditioning of a tone when tone-light pairings were given in the absence of food. Acquisition of second-order conditioning was impaired in rats with ABL lesions but not in rats with CN lesions. In reinforcer devaluation procedures, conditioned responding of rats with ABL lesions was insensitive to postconditioning changes in the value of the reinforcer, whereas rats with CN lesions, like normal rats, were able to spontaneously adjust their CRs to the current value of the reinforcer. The results of both test procedures indicate that ABL, but not CN, is part of a system involved in CSs' acquisition of positive incentive value. Together with evidence that identifies a role for CN in certain changes in attentional processing of CSs in conditioning, these results suggest that separate amygdala subsystems contribute to a variety of processes inherent in associative learning.

Acoustic Stimulation↗
PubMed1996

Multiple forms of phospholipase D inhibitor from rat brain cytosol. Purification and characterization of heat-labile form.

Rat brain cytosol contains proteins that markedly inhibit the activity of partially purified brain membrane phospholipase D (PLD) stimulated by ADP-ribosylation factor (Arf) and phosphatidylinositol 4,5-bisphosphate (PIP2). Sequential chromatography of the brain cytosol yielded four inhibitor fractions, which exhibited different kinetics to heat treatment at 70 degrees C. Purification of the most heat-labile inhibitor to homogeneity yielded two preparations, which displayed apparent molecular masses of 150 kDa and 135 kDa, respectively, on SDS-polyacrylamide gels. Tryptic digests of the 150- and 135-kDa proteins yielded similar elution profiles on a C18 reverse-phase column, suggesting that the 135-kDa form is a truncated form of the 150-kDa form. Sequences of two tryptic peptides were determined. A data base search revealed no proteins with these sequences. The purified 150-kDa inhibitor negated the PLD activity stimulated by Arf, RhoA, or Cdc42. The concentration required for half-maximal inhibition was 0.4 nM. Concentration dependence on the 150-kDa inhibitor was not affected by changes in the concentrations of Arf, PIP2, or phosphatidylcholine used in the assays, suggesting that the inhibition is not due to competition with the activators or substrate for PLD. The purified inhibitor did not affect the PIP2-hydrolyzing activity of a phospholipase C isozyme that was measured with substrate vesicles of lipid composition identical with that used for the PLD assay. Thus, the mechanism of inhibition appears to be a specific allosteric modification of PLD rather than disruption of substrate vesicles.

ADP-Ribosylation Factors↗
PubMed1996

Anatomical basis for a fasciocutaneous flap from the hypothenar eminence of the hand.

Thirty-two fresh cadaver hands were perfused with a silicone rubber compound (Microfil) and dissected to explore the vascular and neural anatomy of the hypothenar eminence, in order to assess the possibility for free or pedicled island flaps from this area. In five specimens Microfil was selectively injected into the ulnar palmar digital artery of the little finger to determine the skin territory nourished by this artery. The hypothenar eminence was divided into three territories according to the type of nutrient artery supplying each territory. Among the three territories, the distal half of the ulnar aspect of the hypothenar eminence (approximately 3 x 2 cm), located over the abductor and flexor digiti minimi muscles, had a constant vascular and neural supply from the ulnar palmar digital artery of the little finger and the dorsal or palmar cutaneous branch of the ulnar nerve. This fasciocutaneous area provides a new and feasible donor site for free or pedicled island skin flaps to repair palmar skin defects of the fingers.

Aged↗
PubMed1996

Evaluation of urine acidification by urine anion gap and urine osmolal gap in chronic metabolic acidosis.

To investigate the clinical significance of urine anion gap and urine osmolal gap as indirect markers of urine acidification in chronic metabolic acidosis, we evaluated urine ammonium (NH4+), net acid excretion (NAE), urine anion gap (Na(+) + K(+) - Cl-), and urine osmolal gap (urine osmolality - [2(Na(+) + K(+)) + urea]) in 24 patients with chronic renal failure (CRF), eight patients with classic distal renal tubular acidosis (dRTA), and eight NH4Cl-loaded normal controls (NCs). Urine NH4+ excretion was lower (P < 0.001) in the CRF (5.4 +/- 0.6 mmol/d) and dRTA (19.2 +/- 2.7 mmol/d) patients than in the NCs (52.6 +/- 3.7 mmol/d); NAE was also lower (P < 0.001) in the CRF (9.8 +/- 1.6 mmol/d) and dRTA (16.7 +/- 4.7 mmol/d) patients than in the NCs (79.4 +/- 4.7 mmol/d). Urine anion gap was higher (P < 0.001) in the CRF (24.7 +/- 2.2 mmol/L) and dRTA (36.7 +/- 7.7 mmol/L) patients than in the NCs (-16.2 +/- 5.5 mmol/L). Urine osmolal gap was lower (P < 0.05) in the dRTA patients (129.7 +/- 17.0 mmol/L) than in the NCs (319.7 +/- 58.4 mmol/L). When the data from all subjects were pooled, urine anion gap correlated inversely with urine NH4+ (r = -0.70, P < 0.001) and with NAE (r = -0.83, P < 0.001), and urine osmolal gap correlated positively with urine NH4+ (r = 0.69, P < 0.01) and with NAE (r = 0.71, P < 0.05). We conclude that impaired urine acidification in CRF and dRTA patients is associated with an increase in urine anion gap and a decrease in urine osmolal gap, and that both urine anion gap and urine osmolal gap correlate well with NAE as well as with urine NH4+.

Acid-Base Equilibrium↗
PubMed1996

Cholecystokinin octapeptide reverses the inhibitory effect induced by electroacupuncture on C-fiber evoked discharges.

Extracellular single unit recordings were made from spinal dorsal horn wide dynamic range neurons in spinal transected, urethane-anesthetized rats. The unit discharges elicited by noxious electrical stimulation of the hind paw were suppressed by electroacupuncture (15 Hz, 0.3 ms, 3 mA, 30 min) placed at the hind leg points (S-36 and SP-6). Local spinal superfusion with naloxone (20 micrograms/15 microliters) or CCK-8 (10 ng/15 microliters) attenuated, whereas CCK-B receptor antagonist L365,260 (2.5 micrograms/15 microliters) enhanced the electroacupuncture effect. These findings provide further evidence for the notion that CCK-8, in the spinal cord, functions as an antiopioid substrate that antagonizes opioid- or electroacupuncture-induced analgesia.

Animals↗
PubMed1996

[Frequency dependence of substance P release by electroacupuncture in rat spinal cord].

Previous studies in our laboratory have shown that electroacupuncture (EA) using different frequencies produced differential opioid peptides release in the spinal cord of rats and human beings. In the present study we observed the frequency dependence of substance P (SP) release from rat spinal cord, with the frequencies of EA set at 2, 4, 8, 15, 30 and 100 Hz. The spinal perfusate was collected in 3 periods of 30 min before, during and after EA, and the immunoreactive SP (SP-ir) was measured by radioimmunoassay (RIA). The effectiveness of EA-induced analgesia was assessed by tail flick latency (TFL). Rats showing an increase of TFL over 40% was considered as EA responder. The results showed that in the responders, SP-ir in spinal perfusate showed a moderate decrease during 2 Hz EA, (P < 0.01 compared with baseline level), no change in the 4 Hz EA group, and a marked increase during 8, 15, 30 and 100 Hz EA (P < 0.01), with maximal increase occurring at 15 Hz (P < 0.001). The above results suggest that EA may induce upward or downward modulation in SP-ir release depending on the frequency of EA. However in the non-responder rats no change in spinal fluid SP-ir content was observed. This suggests that changes in SP-ir release have same causal relation with the analgesia induced by EA stimulation.

Acupuncture Analgesia↗
PubMed1996

[Angiotensin II release and anti-electroacupuncture analgesia in spinal cord].

Changes in the content of angiotensin II (A II) immunoreactivity (ir) in rat spinal perfusate induced by electroacupuncture (EA) stimulation of different frequencies were measured by radioimmunoassay (RIA). The results were analyzed in relation to the role of opioid receptor. (1) 2 Hz EA produced a 20% (P > 0.05) decrease in A II -ir content in the spinal perfusate. 15 Hz EA produced an even more decrease (62%, P < 0.01), whereas 100 Hz produced a significant increase (65%, P < 0.05). (2) The release in spinal A II -ir produced by 15 Hz EA was reversed by the opioid antagonist naloxone to a of 125% highter than that of the control (P < 0.05), suggesting that 15 Hz EA may accelerate the release of endogenous opioids to suppress the release of A II. (3) This was substantiated by the finding that intrathecal (i.t.) injection of the selective mu agonist ohmefentanyl produced a dramatic suppression (20%, P < 0.05) of A II release, but not by delta and kappa agonist. (4) Intrathecal injection of salarasin, the angiotensin receptor antagonist, produced a significant potentiation of the analgesia produced by 100 Hz EA, but not that produced by 2 or 15 Hz EA. It is concluded that 15 Hz EA may induce the release of endogenous opioids acting on mu opioid receptor so as to suppress A II release, and that 100 Hz EA may accelerate the release of A II serving as a brake for 100 Hz EA-induced analgensia. Removal of the brake by angiotensin antagonist may be advised as an adjunct for the potentiation of 100 Hz EA-induced analgesia.

Acupuncture Analgesia↗
PubMed1996

[Current status of the application of patch-clamp technique and its combinations with other techniques].

The Patch-clamp technique, as an advanced electrophysiological technique, has been widely used for research in the life science research field. A recent trend is to combine this technique with other techniques, such as the Fura-2 microfluorimetry for measuring the concentration of Ca2+, electrochemical detection with carbon-fiber electrode (i.e. amperometric detection or amperometry), and single-cell reverse transcription of RNA followed by the polymerase chain reaction (RT-PCR). This article is to summarize the current status of the use of patch-clamp technique and its combinations with other techniques in solving problems related with transmembrane signal transduction in neurobiology.

Animals↗
PubMed1996

[The discovery of a novel opioid-receptor-like receptor and its endogenous ligand].

A novel member of the opioid receptor family (orphan ORL receptor) was cloned in 1994, followed by the discovery of its endogenous ligand OFQ or nociceptin in 1995. ORL receptor has 50% homology with conventional opioid receptor, and OFQ is structurally homologous with dynorphin A. Whether the two systems are functionally antagonistic or synergistic with each other is a subject of future research.

Amino Acid Sequence↗