Search PubMed⌕ Search

Biomedical subjects

J S Han

Publications and source records attributed to J S Han.

At least 163 records · Page 9Linked to original sources
PubMed1996

[Transcriptional regulation by CREB and proteins of CREB family].

CREB (cAMP-responsive element binding protein), which can be activated after phosphorylation by protein kinase A, plays an important role in cAMP-induced gene expression. Several recent studies have suggested that a co-activator designated as CREB binding protein (CBP) is crucial in mediating the transcriptional activity of CREB. In nervous system, in addition to playing a role in neurotransmitter-induced gene transcription, CREB may take part in mediating neurotrophin signals that ultimately lead to such cellular responses as proliferation, differentiation and survival.

Activating Transcription Factor 1↗
PubMed1996

[Research progress on the glia cell line-derived neurotrophic factor].

Glia cell line-derived neurotrophic factor (GDNF) is a novel type of neurotrophic factor cloned in 1993. Recent research revealed that it may have potential application in the treatment of Parkinson's disease and motor neuron diseases. This short review summarized the character of the protein, gene structure, tissue distribution, and its physiological functions and pathological implications.

Animals↗
PubMed1995

Flow cytometric identification of cell surface markers on cultured human colonic cell lines using monoclonal antibodies.

BACKGROUND: The expression of tumor-associated cell surface antigens is a reflection of the state of cell differentiation of tumor cells in culture. METHOD: Monoclonal antibodies (MoAbs) against the tumor-associated antigens carcinoembryonic antigen (CEA) and CA19-9 and the extracellular matrix protein CD44 were used to label the cell surface of human colonic cells in culture. The binding of each antibody to its respective antigen was measured by fluorescence-activated flow cytometry and expressed as a percentage of positive cells. RESULTS: The human colon adenocarcinoma cell (HCAC) line, LS-180, showed strong binding with CEA (81%), CA 19-9 (87%), and CD44 (83%). LS-174t cells, a trypsinized variant of LS-180 cells, showed less binding with CEA (66%) and CA 19-9 (49%), but no binding with CD44. With cells from HCAC line HT-29, antigen expression was highly variable for CEA (13% +/- 18) and CD44 (31% +/- 35) but was consistently positive for CA19-9 (33% +/- 13). The expression of CEA in the Caco-2 cell line was weak (24%), whereas there was no expression of CA19-9 and CD44. Normal human colon fibroblast cells (CCD-18Co) did not recognize the monoclonal antibodies to CEA or CA 19-9, but were strongly positive with the CD44 antibody (97%). CONCLUSIONS: These results support the concept that the expression of the tumor associated markers CEA and CA19-9 and the cell surface marker CD44 on human colonic cell lines varies with the degree of cellular differentiation. Carcinoembryonic antigen and/or CA19-9 were expressed in all four human colon adenocarcinoma cell lines, but not in the normal colon fibroblast cells (CCD-18Co). Using these two MoAbs appeared to be a more reliable measure of the state of differentiation of human colon adenocarcinoma cells.

Antibodies, Monoclonal↗
PubMed1995

Cloning and expression of a cDNA for mu-class glutathione S-transferase from rabbit liver.

A mu-class glutathione S-transferase (GST) cDNA clone, pHMB1, from rabbit liver has been constructed, using a 748-base-pair fragment of GST Yb1 cDNA as a probe. The nucleotide sequence of pHMB1 has been determined, and the complete amino acid sequence has been deduced. Recombinant clone pHMB1 contains a cDNA insert of 1443 base pairs with 654 nucleotides of open reading frame, 33 nucleotides of 5'-untranslated region, and 756 nucleotides of 3'-untranslated region. The open reading frame encodes a polypeptide (rbGST mu I) comprising 218 amino acids with molecular weight of 25,417. Compared to published mu-class GST sequences, rbGST mu I is 73 and 77% identical to rat Yb1 and human GST4 in amino acid sequence, respectively. The pHMB1 was expressed in Escherichia coli using expression vector pIH821 and the expressed GST was purified as a single band on polyacrylamide gel electrophoresis by maltose- and glutathione-affinity column chromatography. Rabbit liver GST protein expressed by this system was catalytically active. The functional characterization was done on the expressed protein. The rabbit liver GST expressed in E. coli showed greater activity toward 1,2-dichloro-4-nitrobenzene than mu-class isozymes in rabbit hepatic tissue (T. Primiano and R.F. Novak (1993) Arch. Biochem. Biophys. 301, 404-410). Enzymatic activity of expressed protein toward the substrate 1-chloro-2,4-dinitrobenzene was inhibited by triethyltin bromide, Cibacron blue, triphenyltin chloride, bromosulfophthalein, and hematin. RNA blot hybridization demonstrated that the pHMB1 mRNA was well expressed in rabbit liver, brain, and kidney.

Amino Acid Sequence↗
PubMed1995

Different ARF domains are required for the activation of cholera toxin and phospholipase D.

ADP-ribosylation factors (ARFs), initially described as activators of cholera toxin ADP-ribosyltransferase activity, regulate intracellular vesicular membrane trafficking and stimulate a phospholipase D (PLD) isoform. ARF-like (ARL) proteins are structurally related to ARFs but do not activate cholera toxin and have relatively little effect on PLD. A new human ARL gene termed hARL1, which shares 57% amino acid identity with hARF1, was identified using a polymerase chain reaction-based cloning method. To determine whether different structural elements are responsible for the activation structural elements are responsible for the activation of the A subunit of cholera toxin and PLD, chimeric proteins were constructed by switching the amino-terminal 73 amino acids of ARF1 and ARL1. The recombinant rL73/F protein, in which the amino-terminal 73 amino acids of ARL1 replaced those of ARF1, activated the A subunit of cholera toxin, whereas the rF73/L protein, in which the NH2-terminal 73 amino acids of ARF1 replaced those of ARL1, was inactive. The two chimeric proteins had quite opposite effects on PLD activity. rF73/L activated PLD as effectively as rARF1, whereas rL73/F protein activated PLD only slightly. It appears that the amino-terminal region of ARF1 is not critical for its action as a GTP-dependent activator of cholera toxin, whereas it is necessary for activation of the putative effector enzyme, PLD.

ADP-Ribosylation Factor 1↗
PubMed1995

Loads in the spinal structures during lifting: development of a three-dimensional comprehensive biomechanical model.

Epidemiological studies have shown that loads imposed on the human spine during daily living play a significant role in the onset of low back pain. The loads applied to the lumbar spine are shared by a number of structures: muscles; posterior elements, including facets and ligaments; and the disc of a ligamentous motion segment. In vivo, it is not practical to determine forces in these structures using experimental techniques. Biomechanical models, based on an optimization technique of electromyographic activities of the trunk muscles, have been proposed to predict forces in the load transmitting structures. The mathematical models reported in the literature are based on information collected from a wide variety of sources, of which the subject that takes part in the experiment is only one. The present study describes techniques developed in our laboratory to collect from the subjects themselves all the data needed for the formulation of a biomechanical model. The results demonstrated that back lifting with 0 N (no load), 90 N, and 180 N in the hands created maximum external flexion moments respectively of 109.6 Nm, 137.9 Nm, and 161.7 Nm, at the L3-4 disc level. The corresponding external axial compression forces on the disc were 469.5 N, 511.8 N, and 601.5 N. The predicted disc compression varied from 3.4 to 5.0 times the body weight. In comparison to the static lifting mode, the dynamic lifting task caused an increase in the disc compression force ranging from 15.8% to 39.4% depending on the load being lifted (e.g., 3256 N for the dynamic mode vs. 2516 N for the static mode when the subject lifted 90 N). The salient features of the entire protocol developed by the authors and the need for further improvements are also presented.

Adult↗
PubMed1995

Hemorrhagic fever with renal syndrome caused by the Seoul virus.

The Seoul virus is an important etiologic agent in hemorrhagic fever with renal syndrome (HFRS), and infections with the Seoul virus are less severe than those with the Hantaan virus. However, the information on HFRS caused by the Seoul virus is limited in Korea. Retrospective clinical analysis was done on 30 patients with Seoul virus infection who had been diagnosed as having HFRS by clinical features and serologic testing by the plaque reduction neutralization test from 1986 to 1991 at the Seoul National University Hospital. They were compared with 69 patients with Hantaan virus infection. The Seoul virus was the etiologic agent in 25% of Korean HFRS and the major cause of HFRS during the summer season although infections occurred throughout the year. The Seoul virus infection had a milder degree of bleeding and renal derangement but had severer liver dysfunction than the Hantaan virus infection. Renal histopathologic findings revealed a milder degree of hemorrhage and vascular changes than cases involving Hantaan virus infection. The precise mechanisms of vascular dysfunction and organ involvement in Seoul virus infection, however, still remain to be explored.

Adult↗
PubMed1995

Comparative study of the analgesic and paralytic effects induced by intrathecal dynorphin a in rats.

Intrathecal injection of dynorphin A produced dual effects on sensory and motor functions in the spinal cord of the rat. At a dose of 5 nmol, dynorphin A produced an increase in tail flick latency (TFL) as well as a reversible motor paralysis as assessed by change in the angle of inclined plane. At a dose of 10 or 20 nmol, dynorphin produced a motor paralysis lasting for up to 24 hours. The effect of dynorphin A on the sensory function of the spinal cord was shown by an increase in the vocalization threshold induced by electrical stimulation of the tail, at dose range of 1.25-10 nmol, with a quick onset (5 min) and relatively short duration (within 60 min). Unlike tail flick reaction which involves spinal motor function, tail stimulation-induced vocalization threshold is a relatively pure index for spinal nociceptive activities. The differential effect of dynorphin on sensory and motor function was supported by the evidence that (1) dynorphin-induced analgesic effect (increase in vocalization threshold) was naloxone reversible, whereas dynorphin-induced motor paralysis was naloxone resistant. (2) Nor-BNI, a specific antagonist for kappa opioid receptor, blocked the sensory effect of dynorphin, but had no influence on motor effect of dynorphin. It is thus concluded that dynorphin has both analgesic and paralytic effects in spinal cord. The analgesia shown by an increase of vocalization threshold is an opioid effect, most probably mediated by kappa opioid receptor; the paralytic effect, however, is a non-opioid effect. The increase of TFL induced by dynorphin involves both sensory (analgesia) and motor (paralysis) effects.

Analgesics↗
PubMed1995

Changes in the content of immunoreactive dynorphin in dorsal and ventral spinal cord of the rat in three different conditions.

Previous study in our group demonstrated that dynorphin exerted a significant analgesic effect in spinal cord, and electroacupuncture (EA) of high frequency (100 Hz) produced analgesia which was mediated by dynorphin released in spinal cord. However, no data are up to nowadays available for demonstrating either from anterior horn or from dorsal horn the dynorphin comes. Using radioimmunoassay, we found in the present study that ir-dynorphin content in dorsal horn was 10 times more than in anterior horn, which were 11.24 +/- 0.91 pmol/10 mg protein and 1.08 +/- 0.20 pmol/10 mg protein, respectively. Stimulation of 100 Hz EA for 30 min produced a significant increase of ir-dynorphin content in dorsal horn, in contrast, no change of ir-dynorphin content was found in anterior horn. For the meanwhile, a significant elevation of ir-dynorphin was induced by 100 Hz EA in cerebrospinal fluid. It is concluded according to these data that EA, as a stimulation in physiological condition, elevates the content of ir-dynorphin only in dorsal horn, and induces release of dynorphin in loci. The released dynorphin acts on dorsal horn to mediate the analgesia of EA.

Animals↗
PubMed1995

Hippocampal lesions disrupt decrements but not increments in conditioned stimulus processing.

Studies recording hippocampal neural activity show widespread registration of events during associative learning. Recent computational models of hippocampal function have stressed its role in attentional processes specified by well-developed modern theories of associative learning. These modeling efforts are largely aimed at accounting for the behavioral outcomes of damage to the hippocampal system in terms of underlying changes in information processing. Two experiments examined the effects of neurotoxic lesions of the hippocampus on changes in attentional processing of a conditioned stimulus (CS) in appetitive Pavlovian conditioning in rats. In Experiment 1, hippocampal lesions eliminated the reduction in associability of a CS usually produced by preexposure to that cue (latent inhibition). In Experiment 2, hippocampal lesions interfered with the loss in associability of a CS normally produced when that CS consistently predicts another event. In contrast, in Experiment 2, hippocampal lesions did not prevent the enhancement of CS associability when a previously consistent predictive relation between two events was made inconsistent. This research supports previous claims that the hippocampus is involved in regulating the processing of CSs in Pavlovian conditioning, and provides new evidence for a hippocampal role in decremental, but not incremental, changes in attention.

Animals↗
PubMed1995

Critical role of the capsaicin-sensitive nerve fibers in the development of the causalgic symptoms produced by transecting some but not all of the nerves innervating the rat tail.

We investigated the role of capsaicin-sensitive small diameter fibers in the development of the thermal and mechanical allodynia in a new rat model for neuropathic pain, produced by transecting some but not all of the nerves innervating the tail. Capsaicin (50 mg/kg, s.c.) injected neonatally prior to the nerve injury produced thermal hypoalgesia in the tail the degree of which was variable across individual rats, presumably as a result of variable degeneration of the small diameter fibers. When subjected to the nerve injury, the animals with moderate thermal hypoalgesia exhibited signs of pain (e.g., tail flick) to normally innocuous mechanical stimuli applied to the tail with von Frey hairs (4.9 mN or 19.6 mN bending force), but not to thermal stimuli given by immersion of the tail into cold (4 degrees C) or warm (40 degrees C) water. The animals with marked thermal hypoalgesia, on the other hand, exhibited no signs of pain either to the mechanical or to the thermal stimuli. These results suggest that the capsaicin-sensitive fibers are critical in the development of both the mechanical and thermal allodynia. It is hypothesized that the destruction of A delta- and C-nociceptive fibers by capsaicin prevented activities induced in these fibers by the nerve injury from producing a central sensitization and thus allodynia.

Animals↗
PubMed1995

Cholecystokinin octapeptide reverses mu-opioid-receptor-mediated inhibition of calcium current in rat dorsal root ganglion neurons.

Cholecystokinin octapeptide (CCK-8) is reported to antagonize the analgesic effect produced by mu- and kappa- but not delta-opioid agonist in spinal cord. However, the mechanisms of interaction remain obscure. In the present study, whole-cell patch-clamp recording was performed on acutely isolated rat dorsal root ganglion (DRG) neurons to evaluate the effects of the highly specific mu-opioid agonist ohmefentanyl and the delta-opioid agonist DPDPE on voltage-gated calcium channels and the possible interaction between CCK-8 receptor and mu- or delta-opioid receptor. The results indicated that ohmefentanyl, but not DPDPE, can suppress the voltage-gated calcium currents elicited in DRG neurons, an effect readily reversed by naloxone or by the antiopioid peptide CCK-8. The effect of CCK-8 can in turn be abolished by the CCK-B receptor antagonist L365,260. CCK-8 used by itself has no enhancing effect, but rather a depressant effect, on calcium currents. However, used simultaneously with ohmefentanyl, CCK-8 shows a clear-cut reversal of depression of the mu-opioid. We conclude that the depressant effect produced by mu-opioid on voltage-gated calcium current in DRG neurons can be antagonized by CCK-8 through CCK-B receptor located in the same neuron. The delta-opioid DPDPE has no direct effect on the voltage-gated calcium current in DRG neurons.

Animals↗
PubMed1995

[Progress in the study of the central ACTH receptors].

In addition to pituitary gland, adrenocorticotropic hormone (ACTH) was also found to exist in the neurons of the central nervous system (CNS). ACTH-containing neurons project their fibers to the broad areas of CNS. ACTH-related peptides play many roles in CNS. In recent years, the study about the central ACTH receptors has been made a great progress. It has been realized that the binding sites of ACTH exist in extensive regions of CNS. In the four types of currently cloned ACTH receptors (melanocortin receptors), two of them (MC3R and MC4R) are prevalent in the CNS.

Animals↗
PubMed1994

Spinal serotonin IA and IC/2 receptors mediate supraspinal mu opioid-induced analgesia.

Intracerebroventricular (i.c.v.) injection of highly selective mu opioid receptor agonist ohmefentanyl (OMF) to rats produced dose-dependent antinociception as assessed with the tail flick test. This analgesia could be blocked by intrathecal (i.t.) injection of the 5-HT1A receptor antagonist spiperone or the 5-HT1C/2 receptor antagonist mianserin, but not by the 5-HT2 receptor antagonist 1-NP or the 5-HT3 receptor antagonist ICS 205-930. The results suggest that the descending 5-HT system is involved in mediating spinal mu opioid analgesia via spinal 5-HT1A and 5-HT1C/2 receptors.

Analgesia↗