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Biomedical subjects

H Rhim

Publications and source records attributed to H Rhim.

At least 19 recordsLinked to original sources
PubMed2006

Impaired long-term memory and long-term potentiation in N-type Ca2+ channel-deficient mice.

Voltage-dependent N-type Ca(2+) channels, along with the P/Q-type, have a crucial role in controlling the release of neurotransmitters or neuromodulators at presynaptic terminals. However, their role in hippocampus-dependent learning and memory has never been examined. Here, we investigated hippocampus-dependent learning and memory and synaptic plasticity at hippocampal CA3-CA1 synapses in mice deficient for the alpha(1B) subunit of N-type Ca(2+) channels. The mutant mice exhibited impaired learning and memory in the Morris water maze and the social transmission of food preference tasks. In particular, long-term memory was impaired in the mutant mice. Interestingly, among activity-dependent long-lasting synaptic changes, theta burst- or 200-Hz-stimulation-induced long-term potentiation (LTP) was decreased in the mutant, compared with the wild-type mice. This type of LTP is known to require brain-derived neurotrophic factor (BDNF). It was found that both BDNF-induced potentiation of field excitatory postsynaptic potentials and facilitation of the frequency of miniature excitatory postsynaptic currents (mEPSCs) were reduced in the mutant. Taken together, these results demonstrate that N-type Ca(2+) channels are required for hippocampus-dependent learning and memory, and certain forms of LTP.

Analysis of Variance↗
PubMed2005

Radiofrequency thermal ablation of hepatic tumors: pitfalls and challenges.

Image-guided radiofrequency (RF) thermal ablation has been accepted as a promising interventional technique to control unresectable hepatic tumors. One important key to maximize the efficacy of RF ablation is to adhere to the therapeutic guidelines and to avoid preventable pitfalls. There are also several challenges obstructing successful ablation: poor approach path; small sonic window during multiple overlapping ablations; incomplete ablation due to the heat sink effect; subcapsular mass (too exophytic or the mass is adjacent to the gastrointestinal tract); focal residual tumors; too isoechoic or small masses; and mistargeting to adjacent another lesion. Knowledge of these challenges and pitfalls in RF ablation is helpful for a successful ablation.

Catheter Ablation↗
PubMed2004

Omental torsion: CT features.

A 33-year-old male presented to the emergency department complaining of right upper quadrant pain and was initially diagnosed with acute cholecystitis. Abdominal computed tomography showed a whirling pattern of fatty streaks and vessels within the greater omentum, and surgery confirmed infarction of the omentum secondary to torsion. We report a case of surgically and pathologically proven omental torsion that demonstrated the typical whirling appearance on computed tomography.

Abdominal Pain↗
PubMed2004

Review of asian experience of thermal ablation techniques and clinical practice.

The field of image-guided tumour ablation has gained great attention from Asian physicians because it represents a safe and effective technique for many commonly seen tumours in this population, showing minimal morbidity and excellent local control rates. Based on the current survey data from Asian physicians who are currently performing image-guided tumour ablation, thermal ablation has been mainly performed for patients with unresectable liver tumours. Radiofrequency ablation has replaced many other local ablation techniques such as microwave or ethanol ablation in treating small focal hepatic tumours for the last 5 years. Surgery and transcatheter arterial chemoembolization also have a unique role as curative and palliative treatment options for patients with more extensive tumour burden. Although radiofrequency ablation represents a paradigm shift in local therapy, more sophisticated strategies to enhance the therapeutic efficacy are necessary and more randomized and controlled investigations to estimate its clinical benefit are warranted.

Asia↗
PubMed2002

Postsynaptic action mechanism of somatostatin on the membrane excitability in spinal substantia gelatinosa neurons of juvenile rats.

We used tight-seal, whole-cell recording in juvenile rat spinal slices to investigate the action of somatostatin on substantia gelatinosa neurons. Bath application of somatostatin caused a robust and repeatable hyperpolarization or outward current in substantia gelatinosa neurons. Somatostatin inhibited spontaneous action potentials in subpopulation of substantia gelatinosa neurons. The amplitude of dorsal root-evoked excitatory postsynaptic currents and the frequency of spontaneous excitatory postsynaptic currents were not affected by somatostatin. The current induced by somatostatin developed almost instantaneously and did not show any time-dependent inactivation. The current-voltage relationship exhibited inward rectification. The conductance of somatostatin-sensitive current increased with the concentration of external K(+). The reversal potentials in different external K(+) concentrations were close to the K(+) equilibrium potentials. The effect of somatostatin was dose-dependent, with an EC(50) of 113 nM. The somatostatin-sensitive current was blocked by low concentration of extracellular Ba(2+) but not by glibenclamide, an inhibitor of ATP-sensitive K(+) channels. Hyperpolarization-activated cation current in a subpopulation of substantia gelatinosa neurons was not affected by somatostatin. In neurons recorded with an internal solution containing GTPgammaS, somatostatin induced outward current and hyperpolarization that did not reverse on washing. When the spontaneous induction of outward current with GTPgammaS was greatest, somatostatin did not induce any outward currents. Furthermore, intracellular dialysis of GDPbetaS, a G-protein antagonist, abolished the effect of somatostatin. In addition, SST-sensitive neurons were fewer in slices incubated with pertussis toxin than in adjacent control slices incubated without pertussis toxin. These results suggest that somatostatin decreases the postsynaptic membrane excitability of substantia gelatinosa neurons by a pertussis toxin-sensitive G-protein-mediated activation of an inwardly rectifying K(+) conductance.

Age Factors↗
PubMed2001

Activation of caspase-8 in 3-deazaadenosine-induced apoptosis of U-937 cells occurs downstream of caspase-3 and caspase-9 without Fas receptor-ligand interaction.

3-Deazaadenosine (DZA), a cellular methylation blocker was reported to induce the caspase-3-like activities-dependent apoptosis in U-937 cells. In this study, we analyzed the activation pathway of the caspase cascade involved in the DZA-induced apoptosis using specific inhibitors of caspases. In the U-937 cells treated with DZA, cytochrome c release from mitochondria and subsequent activation of caspase-9, -8 and -3 were observed before the induction of apoptosis. zDEVD-Fmk, a specific inhibitor of caspase-3, and zLEHD-Fmk, a specific inhibitor of caspase-9, prevented the activation of caspase-8 but neither caspase-3 nor caspase-9, indicating that caspase-8 is downstream of both caspase-3 and caspase-9, which are activated by independent pathways. zVAD-Fmk, a universal inhibitor of caspases, kept the caspase-3 from being activated but not caspase-9. Moreover, ZB4, an antagonistic Fas-antibody, exerted no effect on the activation of caspase-8 and induction of apoptosis by DZA. In addition, zVAD-Fmk and mitochondrial permeability transition pore (MPTP) inhibitors such as cyclosporin A (CsA) and bongkrekic acid (BA) did not block the release of cytochrome c from mitochondria. Taken together, these results suggest that in the DZA-induced apoptosis, caspase-8 may serve as an executioner caspase and be activated downstream of both caspase-3 and caspase-9, independently of Fas receptor-ligand interaction. And caspase-3 seems to be activated by other caspses including IETDase-like enzyme and caspse-9 seems to be activated by cytochrome c released from mitochondria without the involvement of caspases and CsA- and BA- inhibitory MPTP.

Amino Acid Chloromethyl Ketones↗
PubMed2001

E3 ligase activity of RING finger proteins that interact with Hip-2, a human ubiquitin-conjugating enzyme.

To identify proteins that interact with Huntingtin-interacting protein-2 (Hip-2), a ubiquitin-conjugating enzyme, a yeast two-hybrid screen system was used to isolate five positive clones. Sequence analyses showed that, with one exception, all Hip-2-interacting proteins contained the RING finger motifs. The interaction of Hip-2 with RNF2, one of the clones, was further confirmed through in vitro and in vivo experiments. Mutations in the RING domain of RNF2 prevented the clone from binding to Hip-2, an indication that the RING domain is the binding determinant. RNF2 showed a ubiquitin ligase (E3) activity in the presence of Hip-2, suggesting that a subset of RING finger proteins may have roles as E3s.

Amino Acid Sequence↗
PubMed2001

Effect of ginsenosides on voltage-dependent Ca(2+) channel subtypes in bovine chromaffin cells.

In previous reports we have shown that ginsenosides inhibit high threshold voltage-dependent Ca(2+) channels in neuronal cells. However, these studies did not show whether ginsenosides-induced inhibition of Ca(2+) currents discriminates among the various Ca(2+) channel subtypes, although it is known that there are at least five different Ca(2+) channel subtypes in neuronal cells. In this study we investigated the effect of ginsenosides on high threshold voltage-dependent Ca(2+) channel subtypes using their selective Ca(2+) channel blockers nimodipine (L-type), omega-conotoxin GVIA (N-type), or omega-agatoxin IVA (P-type) in bovine chromaffin cells. We could observe that ginsenosides inhibited high threshold voltage-dependent Ca(2+) currents in a dose-dependent manner. The IC(50) was about 120 microgram/ml. Nimodipine had no effect on ginsenosides response. However, the effect of ginsenosides on Ca(2+) currents was reduced by omega-conotoxin GVIA, omega-agatoxin IVA, and mixture of nimodipine, omega-conotoxin GVIA, and omega-agatoxin IVA. These data suggest that ginsenosides are negatively coupled to three types of calcium channels in bovine chromaffin cell, including an omega-conotoxin GVIA-sensitive (N-type) channel, an omega-agatoxin IVA-sensitive (P-type) channel and nimodipine/omega-conotoxin GVIA/omega-agatoxin VIA-resistant (presumptive Q-type) channel. Thus, the selective regulation of voltage-dependent Ca(2+) subtypes by ginsenosides in bovine chromaffin cell could be the cellular basis of antistress effects induced by ginseng.

Animals↗
PubMed2001

Essential techniques for successful radio-frequency thermal ablation of malignant hepatic tumors.

Radio-frequency thermal ablation is one of the most promising minimally invasive techniques for the treatment of nonresectable hepatic tumors. Essential technical tips to successful radio-frequency ablation therapy were collected from five international experts. They were organized into five categories: understanding the mechanisms and principles of radio-frequency ablation, modulation of tissue physiologic characteristics to increase tumor destruction, strategies of overlapping ablations, strategies to improve ablation according to tumor location, and imaging strategies after ablation to ensure adequate therapy. Established factors for optimal ablation, as well as emerging technical tips, are addressed with illustrations in each section. These essential tips will be very helpful for physicians performing radio-frequency ablation of hepatic tumors.

Catheter Ablation↗
PubMed2001

Treatment of acute cholecystitis in non-critically ill patients at high surgical risk: comparison of clinical outcomes after gallbladder aspiration and after percutaneous cholecystostomy.

OBJECTIVE: This study was performed to compare the clinical outcome after gallbladder aspiration with that after percutaneous cholecystostomy in non-critically ill patients with acute cholecystitis who were at high risk from surgery. MATERIALS AND METHODS: Medical records of 53 consecutive non-critically ill, high-surgical-risk patients admitted with acute cholecystitis between July 1995 and July 1999 were reviewed. Thirty-one had gallbladder aspiration and 22 had percutaneous cholecystostomy. The primary outcome measure of clinical response within 72 hr and the secondary outcome measures of overall positive response rate, complication rate, time to resolution, and rate of recurrence of acute cholecystitis were compared between the two groups. RESULTS: Gallbladder aspiration and percutaneous cholecystostomy were technically successful in 30 (97%) and 21 (97%) patients, respectively; of these, 23 (77%) and 19 (90%) patients responded clinically within 72 hr (p > 0.2). Complications occurred in three patients (12%) after percutaneous cholecystostomy and in none after gallbladder aspiration (p < 0.05). No significant difference was noted in the other secondary outcome measures of the two groups. CONCLUSION: We found no significant difference in the clinical outcomes of gallbladder aspiration and percutaneous cholecystostomy in the treatment of acute cholecystitis in high-surgical-risk patients who are not critically ill. However, we found gallbladder aspiration to be significantly safer. Therefore, gallbladder aspiration should be the procedure of choice in high-risk patients with acute cholecystitis who are not critically ill, and percutaneous cholecystectomy should be reserved as a salvage procedure if gallbladder aspiration is technically or clinically unsuccessful.

Acute Disease↗
PubMed2001

Tumor recurrence after radiofrequency thermal ablation of hepatic tumors: spectrum of findings on dual-phase contrast-enhanced CT.

OBJECTIVE: We conducted this study to determine the spectrum of CT findings of tumor recurrence after radiofrequency ablation of primary and secondary malignant hepatic tumors. MATERIALS AND METHODS: Twenty-five patients, 10 with hepatocellular carcinoma (HCC) and 15 patients with metastases who developed tumor recurrence after radiofrequency ablation of hepatic neoplasms, formed the study population. Three observers reviewed the CT scans of these patients and evaluated the location (local intrahepatic, remote intrahepatic, or extrahepatic) of all recurrent lesions and the morphology and enhancement characteristics of local intrahepatic recurrences. RESULTS: Local intrahepatic recurrences were seen in nine patients (90%) and 11 patients (73%); remote intrahepatic recurrences, in five patients (50%) and seven patients (45%); and extrahepatic recurrences, in zero and six patients (40%) with recurrent HCC and recurrent metastases, respectively. Of the 12 nodules of local intrahepatic recurrences in HCC and the 24 in metastases, the patterns of local intrahepatic recurrences were of nodular, halo, and gross enlargement types in eight (67%) and nine (38%), four (33%) and six (38%), and zero and nine (37%) nodules in HCC and hepatic metastases, respectively. The number of local intrahepatic recurrent lesions enhancing in the arterial phase was significantly greater in HCC. CONCLUSION: Tumor recurrences occurred at intra- and extrahepatic sites after radiofrequency ablation of hepatic neoplasms. The local intrahepatic recurrences appeared in three patterns: nodular, halo, or gross enlargement. The sites of recurrence and the morphologic patterns of local intrahepatic tumor recurrence differed between primary and secondary hepatic neoplasms.

Carcinoma, Hepatocellular↗
PubMed2000

Intracellular calcium mobilization induces immediate early gene pip92 via Src and mitogen-activated protein kinase in immortalized hippocampal cells.

Regulation of intracellular calcium levels plays a central role in cell survival, proliferation, and differentiation. A cell-permeable, tumor-promoting thapsigargin elevates the intracellular calcium levels by inhibiting endoplasmic reticulum Ca(2+)-ATPase. The Src-tyrosine kinase family is involved in a broad range of cellular responses ranging from cell growth and cytoskeletal rearrangement to differentiation. The immediate early gene pip92 is induced in neuronal cell death as well as cell growth and differentiation. To resolve the molecular mechanism of cell growth by intracellular calcium mobilization, we have examined the effect of thapsigargin and subsequent intracellular calcium influx on pip92 expression in immortalized rat hippocampal H19-7 cells. An increase of intracellular calcium ion levels induced by thapsigargin stimulated the expression of pip92 in H19-7 cells. Transient transfection of the cells with kinase-inactive mitogen-activated protein kinase kinase (MEK) and Src kinase or pretreatment with the chemical MEK inhibitor PD98059 significantly inhibited pip92 expression induced by thapsigargin. When constitutively active v-Src or MEK was overexpressed, the transcriptional activity of the pip92 gene was markedly increased. Dominant inhibitory Raf-1 blocked the transcriptional activity of pip92 induced by thapsigargin. The transcription factor Elk1 is activated during thapsigargin-induced pip92 expression. Taken together, these results suggest that an increase of intracellular calcium ion levels by thapsigargin stimulates the pip92 expression via Raf-MEK-extracellular signal-regulated protein kinase- as well as Src kinase-dependent signaling pathways.

Animals↗
PubMed2000

Evidence that ginsenosides prevent the development of opioid tolerance at the central nervous system.

The analgesic effect of ginsenosides or morphine was first determined following intrathecal (i.t.) administration in rat tail-flick test. The effect of chronic i.t. co-administration of ginsenosides with morphine on the development of opioid tolerance were also examined using rat tail-flick test. Administration of ginsenosides (i.t.) produced a weak antinociception in a dose-dependent manner. Administration of morphine (i.t.) also produced antinociception in a dose-dependent manner. The ED50 was 1.20 microg (1.14-1.29 microg). However, acute i.t. co-administration of ginsenosides with morphine was not additive in antinociception. Repeated i.t. co-administration of 200 microg ginsenosides with 10 microg morphine inhibited the development of tolerance induced by 10 microg morphine in rat tail-flick test, although i.t. co-administration of 50 or 100 microg ginsenosides with morphine was without effect. In conclusion, these results indicate that i.t. administered ginsenosides produce an antinociception in rat tail-flick test and also prevent opioid tolerance caused by chronic treatment with morphine at the spinal sites.

Analgesics, Opioid↗
PubMed2000

Rapid increase in immunoreactivity to GFAP in astrocytes in vitro induced by acidic pH is mediated by calcium influx and calpain I.

In higher vertebrates, reactive gliosis resulting from injury to the central nervous system (CNS) is characterized by a rapid increase in immunoreactivity (IR) to glial fibrillary acidic protein (GFAP). Little is known about the extracellular signals that initiate the increase in GFAP-IR following CNS injury. We demonstrated recently [T.H. Oh, G.J. Markelonis, J.R. Von Visger, B. Baik, M.T. Shipley, Acidic pH rapidly increases immunoreactivity of glial fibrillary acidic protein in cultured astrocytes, Glia 13 (1995) 319-322] that a rapid increase in GFAP-IR can be evoked in mature astrocyte cultures by exposing the cells to an acidic medium. We investigated the intracellular pathway(s) involved in initiating increased GFAP-IR, a hallmark of reactive astrocytes. The increase in GFAP-IR produced by exposure to acidic medium was blocked by pretreatment with nickel ions, by such blockers of L-type calcium channels as nifedipine, verapamil and diltiazem, by calpain inhibitor I, or by the intracellular calcium chelator, BAPTA-AM. At physiological pH, treatment with the calcium ionophore, A23187, resulted in increased GFAP-IR which could be blocked by pretreatment with calpain inhibitor I. Astrocytes exposed to low pH exhibited a marked increase in a GFAP fragment with a molecular weight of 48 kDa. In astrocytes exposed to acidic medium, alpha-fodrin, a selective endogenous substrate of calpain, was also found to be hydrolyzed producing fragments with molecular weights of 120-150 kDa. As anticipated, pretreatment with calpain inhibitor I prevented the proteolytic degradation of both GFAP and alpha-fodrin in these samples. These results suggest that the initial increase in GFAP-IR after CNS injury appears to be linked to Ca(++) influx, and is mediated further by a proteolytic process that seemingly involves the activation of the calcium-dependent protease, calpain I.

Acids↗
PubMed2000

Role of tumor necrosis factor-alpha in neuronal and glial apoptosis after spinal cord injury.

We investigated the role of tumor necrosis factor (TNF)-alpha in the onset of neuronal and glial apoptosis after traumatic spinal cord crush injury in rats. A few TUNEL-positive cells were first observed within and surrounding the lesion area 4 h after injury, with the largest number observed 24-48 h after injury. Double-labeling of cells using cell type-specific markers revealed that TUNEL-positive cells were either neurons or oligodendrocytes. One hour after injury, an intense immunoreactivity to TNF-alpha was observed in neurons and glial cells in the lesion area, but also seen in cells several mm from the lesion site rostrally and caudally. The level of nitric oxide (NO) also significantly increased in the spinal cord 4 h after injury. The injection of a neutralizing antibody against TNF-alpha into the lesion site several min after injury significantly reduced both the level of NO observed 4 h thereafter as well as the number of apoptotic cells observed 24 h after spinal cord trauma. An inhibitor of nitric oxide synthase (NOS), N(G)-monomethyl-l-arginine acetate (l-NMMA), also reduced the number of apoptotic cells. This reduction of apoptotic cells was associated with a decrease in DNA laddering on agarose gel electrophoresis. These results suggest that: (i) TNF-alpha may function as an external signal initiating apoptosis in neurons and oligodendrocytes after spinal cord injury; and (ii) TNF-alpha-initiated apoptosis may be mediated in part by NO as produced by a NOS expressed in response to TNF-alpha.

Animals↗
PubMed2000

Correlation between structure of Bcl-2 and its inhibitory function of JNK and caspase activity in dopaminergic neuronal apoptosis.

To examine the correlation between the structure of Bcl-2 and its inhibitory function of c-Jun N-terminal kinase (JNK) and caspase activity, we established a dopaminergic neuronal cell line, MN9D overexpressing Bcl-2 (MN9D/Bcl-2) or its structural mutants. The mutants comprised a point mutation in the BH1 (G145A; MN9D/BH1) or BH2 (W188A; MN9D/BH2) domain and a deletion mutation in the C-terminal (MN9D/C22), BH3 (MN9D/BH3), or BH4 (MN9D/BH4) domain. As determined by the TUNEL (terminal deoxynucleotidyltransferase nick end-labeling) and MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] reduction assay, apoptotic death of MN9D/Neo cells reached 80-90% within 24 h in response to 1 microM staurosporine. Upon staurosporine treatment, JNK activity increased six- to sevenfold over the basal level within 2-4 h. Treatment of MN9D/Neo with both staurosporine and a caspase inhibitor, Z-VAD, attenuated cell death without suppressing JNK activation. Both staurosporine-induced cell death and JNK activation were attenuated in MN9D/Bcl-2. As determined by cleavage of poly(ADP-ribose) polymerase into 85 kDa, Bcl-2 blocked caspase activity as well. When cells overexpressing one of the Bcl-2 mutants were treated with staurosporine, death was attenuated in MN9D/BH1, MN9D/BH2, and MN9D/C22 but not in MN9D/BH3 and MN9D/BH4. Similarly, both JNK and caspase activation were blocked in MN9D/BH1, MN9D/BH2, and MN9D/C22, whereas they were not suppressed in MN9D/BH3 and MN9D/BH4. Taken together, our data indicate that there exists a close structural and functional correlation of Bcl-2 to JNK and caspase activity in staurosporine-induced dopaminergic neuronal cell death.

Apoptosis↗
PubMed2000

Helical CT cholangiography with oral cholecystographic contrast material.

Twenty asymptomatic volunteers underwent helical computed tomographic (CT) cholangiography 10-12 hours after ingesting iopanoic acid. Three observers assessed the images for the extent of bile duct visualization and image quality. The common bile duct and common hepatic duct were adequately visualized in 19 (95%) subjects. Helical CT cholangiography with oral cholecystographic contrast material is feasible and deserves further clinical studies.

Administration, Oral↗