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Biomedical subjects

K Huh

Publications and source records attributed to K Huh.

At least 37 records · Page 2Linked to original sources
PubMed2000

Memory deficits after bilateral anterior fornix infarction.

The authors report a patient who suddenly developed memory loss without any other focal neurologic deficits. Neuropsychological testing showed severe anterograde verbal and visual memory deficits that improved gradually over several months, but not to the point of the premorbid state. Brain MRI with diffusion-weighted imaging performed 3 days after onset revealed acute infarction involving the bilateral fornices and the right genu of the corpus callosum. The authors suggest that acute fornix infarction may cause anterograde memory deficits.

Cerebral Infarction↗
PubMed2000

Selective enhancement of non-NMDA receptor-mediated responses following induction of long-term potentiation in entorhinal cortex.

The contribution of NMDA receptors to the expression of long-term potentiation (LTP) is controversial. In entorhinal cortex (EC) previous studies reported either that LTP was exclusively expressed through NMDA receptors or that both NMDA and non-NMDA receptors were involved in LTP expression. To reexamine this issue, horizontal entorhinal cortical slices were prepared from adult rats and electrical stimulation was delivered in layer II/III, while field potential recordings were made in layer III. In the standard condition (2.5 mM Mg(++)), LTP was reliably induced by theta burst stimulation, but was blocked by 100 microM D-AP5, an NMDA receptor antagonist. This corroborates previous reports that NMDA receptor activation is required for induction of EC LTP. The field potential response was not affected by D-AP5, but completely blocked by 10 microM CNQX, a non-NMDA receptor antagonist. This indicates that the expression of LTP is mediated by non-NMDA receptors in the standard condition. LTP of NMDA receptor-mediated responses was tested by comparing NMDA responses before and after applying theta burst stimulation in medium containing low magnesium (0.4-1 mM). Theta burst stimulation induced 43.2+/-9.7% increase of non-NMDA responses (i.e., AP5-insensitive fast component) but 5.6+/-9.0% decrease of the NMDA receptor component (AP5-sensitive slow component). These results indicate that activation of NMDA receptors is critical for induction of LTP, but LTP expression is mediated by non-NMDA receptors in EC under these experimental conditions.

2-Amino-5-phosphonovalerate↗
PubMed2000

Cholinergic modulation of synaptic transmission and plasticity in entorhinal cortex and hippocampus of the rat.

Effects of cholinergic agents on synaptic transmission and plasticity were examined in entorhinal cortex and hippocampus. Bath application of carbachol (0.25-0.75 microM) induced transient depression of field potential responses in all cases tested (24/24 in layer III of medial entorhinal cortex slices and 24/24 in CA1 of hippocampal slices; 11.0+/-1.9% and 7.8+/-2.5%, respectively) and long-lasting potentiation in some cases (4/24 in entorhinal cortex and 12/24 in hippocampus; 33.7+/-3.7% and 32.1+/-9.9%, respectively, in successful cases). Carbachol (0.5 microM) induced transient depression, but not long-lasting potentiation, of N-methyl-D-aspartate receptor-mediated responses in entorhinal cortex. At 5 microM, carbachol induced transient depression only (55. 9+/-4.7% in entorhinal cortex and 41.4+/-2.9% in hippocampus), which was blocked by atropine. Paired-pulse facilitation was not altered during carbachol-induced potentiation but enhanced during carbachol-induced depression. These results suggest that the underlying mechanisms of carbachol-induced depression and potentiation are decreased transmitter release and selective enhancement of non-N-methyl-D-aspartate receptor-mediated responses, respectively. Long-term potentiation could be induced in the presence of 10 microM atropine by theta burst stimulation. The magnitude was significantly lower (15.2+/-5.2%, n=9) compared with control (37.2+/-6.1%, n=8) in entorhinal cortex, however. These results demonstrate similar, but not identical, cholinergic modulation of synaptic transmission and plasticity in entorhinal cortex and hippocampus.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed2000

4-Hydroxybenzaldehyde from Gastrodia elata B1. is active in the antioxidation and GABAergic neuromodulation of the rat brain.

Ether fraction of G. elata methanol extract significantly inhibited the recovery time and severity induced by pentylenetetrazole (PTZ) treatment. Pretreatment of ether fraction of G. elata methanol extract successfully prevented diminution of brain GABA level in subconvulsive dose of PTZ-treated rats. 4-Hydroxybenzaldehyde, an analogue of p-hydroxybenzyl alcohol, showed an inhibitory effect on the GABA transaminase, and its inhibitory activity was higher than that of valproic acid, a known anticonvulsant. In the brain of PTZ-treated rats, brain lipid peroxidation was significantly increased, while it recovered to the control level after treatment with 4-hydroxybenzaldehyde. It may be concluded that antioxidation and positive modulation of GABAergic neuromodulation of 4-hydroxybenzaldehyde partially contribute to an antiepileptic and anticonvulsive activity of G. elata B1.

4-Aminobutyrate Transaminase↗
PubMed2000

Cisplatin-induced apoptotic cell death in mouse hybrid neurons is blocked by antioxidants through suppression of cisplatin-mediated accumulation of p53 but not of Fas/Fas ligand.

Peripheral neuropathy following cisplatin treatment is a major limiting factor in cisplatin chemotherapy of cancer patients. We investigated the pathomechanism underlying cisplatin neuropathy using a mouse dorsal root ganglion neuron-neuroblastoma hybrid cell line (N18D3) developed in our laboratory. DNA fragmentation, a characteristic feature of apoptosis, was induced in hybrid neurons following treatment with cisplatin. Accumulation of p53, Fas, and Fas ligand (Fas-L) was also demonstrated in these neurons. Preincubation with N-acetylcysteine (NAC), a precursor of glutathione, blocked cisplatin-induced apoptosis completely, whereas Trolox, a vitamin E analogue, blocked it partially. Cisplatin-induced p53 accumulation was suppressed by NAC treatment, whereas p53 accumulation was retarded by Trolox treatment. In contrast, neither NAC nor Trolox showed any inhibitory effect on cisplatin-induced Fas/Fas-L accumulation. These results suggest that the neuroprotective effects of antioxidants against cisplatin-induced neurotoxicity in hybrid neurons are mediated mainly through the inhibition of p53 accumulation but not of Fas/Fas-L accumulation by these antioxidants.

Acetylcysteine↗
PubMed1999

Protective effects of asiaticoside derivatives against beta-amyloid neurotoxicity.

Asiaticoside (AS) derivatives were tested for potential protective effects against Abeta-induced cell death. Of the 28 AS derivatives tested, asiatic acid (AA), asiaticoside 6 (AS6), and SM2 showed strong inhibition of Abeta-induced death of B103 cells at 1 microM. The three AS derivatives were further tested for their effects on free radical injury and apoptosis. All three AS derivatives reduced H(2)O(2)-induced cell death and lowered intracellular free radical concentration, but AA showed the strongest protection. In contrast, SM2 was the most effective blocker of staurosporine-induced apoptosis. These results suggest that the three AS derivatives block Abeta toxicity by acting through different cellular mechanisms. When applied to hippocampal slices, AA, SM2, and AS6 did not alter n-methyl-D-aspartic acid (NMDA) or non-NMDA receptor-mediated synaptic transmission, paired-pulse facilitation or induction of long-term potentiation in the field CA1. These results indicate that the three AS derivatives do not alter physiological properties of the hippocampus at the concentration that blocks Abeta-induced cell death. Therefore AS6, AA, and SM2 can be regarded as reasonable candidates for a therapeutic Alzheimer's disease drug that protects neurons from Abeta toxicity.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1999

Purification and partial peptide sequence analysis of the boar proacrosin binding protein.

Boar proacrosin binding protein has been purified and the partial peptide sequence of the CNBr-digested proacrosin binding protein has been determined. Proacrosin binding protein was purified as a proacrosin and proacrosin binding protein complex from the acid extracts of boar spermatozoa through gel filtration. After the proacrosin binding protein was dissociated from proacrosin by freeze-thaw method, the proacrosin binding protein was purified through gel filtration. Fractions containing the proacrosin binding protein were pooled and were concentrated by lyophilization and then subjected to CNBr digestion. Four major CNBr-digested peptides were subjected to N-terminal peptide sequencing. All four showed the same N-terminus sequence.

Acrosin↗
PubMed1999

Inhibitory effects of constituents of Gastrodia elata Bl. on glutamate-induced apoptosis in IMR-32 human neuroblastoma cells.

The inhibitory effects of the constituents of Gastrodia elata Bl. (GE) on glutamate-induced apoptosis in human neuronal cells were investigated using IMR32 human neuroblastoma cells. Glutamate (GLU) induced DNA fragmentation, a hallmark of apoptosis, in a dose-dependent manner. GLU also induced a slow and sustained increase in intracellular Ca2+ concentration. Treatment with EGTA, an extracellular Ca2+ chelator, in a nominal Ca2+-free buffer solution abolished the GLU-induced intracellular Ca2+ increase, indicating that GLU stimulated Ca2+ influx pathway in the IMR32 cells. BAPTA, an intracellular Ca2+ chelator, significantly inhibited the GLU-induced apoptosis assessed by the flow cytometry measuring hypodiploid DNA content indicative of apoptosis, implying that intracellular Ca2+ rise may mediate the apoptotic action of GLU. Vanillin (VAN) and p-hydroxybenzaldehyde (p-HB), known constituents of GE, significantly inhibited both intracellular Ca2+ rise and apoptosis induced by GLU. These results suggest that the apoptosis-inhibitory actions of the constituents of GE may account, at least in part, for the basis of their antiepileptic activities. These results further suggest that intracellular Ca2+ signaling pathway may be a molecular target of the constituents of GE.

Antineoplastic Agents, Phytogenic↗
PubMed1999

Nuclear factor kappa B-mediated kainate neurotoxicity in the rat and hamster hippocampus.

Administration of the excitotoxin kainate produces seizure activity and selective neuronal death in various brain areas. We examined the degeneration pattern of hippocampal neurons following systemic injections of kainate in the hamster and the rat. As reported, treatment with kainate resulted in severe neuronal loss in the hilus and CA3 in the rat. While the hilar neurons were also highly vulnerable to kainate in the hamster, neurons in the CA1 area, but not CA3, were highly sensitive to kainate. In both animals, immunoreactivity to anti-p50 nuclear factor kappa B antibody was increased in nuclei of the hilar neurons within 4 h following administration of kainate. Kainate treatment also increased the nuclear factor kappa B immunoreactivity in hamster CA1 neurons and rat CA3 neurons 24 h later. Neurons showing intense nuclear factor kappa B signal were stained with acid fuchsin. Kainate also increased DNA binding activity of p50 and p65 nuclear factor kappa B in the nuclear extract of the hippocampal formation as analysed by electrophoretic mobility shift assay in the hamster, suggesting that activation of nuclear factor kappa B may contribute to kainate-induced hippocampal degeneration. Administration of 100 nmol dizocilpine maleate 3 h prior to kainate attenuated kainate-induced activation of nuclear factor kappa B and neuronal death in CA1 in the hamster. The present study provides evidence that the differential vulnerability of neurons in the rat and the hamster hippocampus to kainate is partly mediated by mechanisms involving N-methyl-D-aspartate-dependent activation of nuclear factor kappa B.

Animals↗
PubMed1999

Homocyst(e)ine and atherosclerosis in patients on chronic hemodialysis.

Hyperhomocyst(e)inemia is an established risk factor for atherosclerosis. We performed this study to identify the correlating variables and risk factors for atherosclerosis, as measured by the atherosclerotic score (AS), and to determine the relative risk for cardiovascular disease in relation to plasma homocyst(e)ine levels in patients on chronic hemodialysis. We evaluated and measured 61 patients on chronic hemodialysis for clinical and biochemical parameters including atherosclerotic score (AS) and plasma homocyst(e)ine. We divided patients into high and low groups, first, by the mean AS, and second, by the median value of plasma total homocyst(e)ine levels. Then we compared the variables between the two groups. Out of the 61 patients, the median plasma total homocyst(e)ine level was 24.4 micromol/L (mean+/-SD, 27.7+/-17.4; range, 9.8-127.4 micromol/L), and the median AS was 5 (mean+/-SD, 6.2+/-2.8; range, 3-13) out of a possible 20 points. AS was significantly correlated with plasma total homocyst(e)ine levels (r=0.37) and age (r=0.67). Through multivariate analysis, plasma total homocyst(e)ine level and age were determined as significant risk factors for the high-AS group (p<0.05). However, plasma total homocyst(e)ine level did not correlate with age (p>0.05). Eighteen of the 61 patients, presented with cardiovascular disease until the present study, had an AS>6. Cardiovascular disease was found more often in the high-homocyst(e)ine group (>24.4 micromol/L) than in the low-homocyst(e)ine group (odds ratio, 9.3; 95% confidence interval, 2.3-37.4). Regardless of age, hyperhomocyst(e)inemia (especially homocyst(e)ine levels >24.4 micromol/L) is a risk factor that can be modified for the development of cardiovascular disease in patients on chronic hemodialysis.

Adolescent↗
PubMed1998

Dopaminergic influences on the P300 abnormality in Parkinson's disease.

This study was designed to evaluate the contribution of central dopaminergic mechanisms to the P300 event-related potential (P300) abnormality in Parkinson's disease. We measured the P300 in 37 non-demented patients with Parkinson's disease (19 de novo and 18 levodopa-treated) and 15 age-matched healthy volunteers. The P300 measurement was repeated in 14 de novo patients, after 6-12 months levodopa therapy. The severity of parkinsonian symptom was assessed using the UPDRS-motor scale. De novo patients showed prolonged P300 latency compared with levodopa-treated patients, as well as healthy volunteers. The levodopa therapy for 6-12 months significantly shortened the P300 latency and reduced the UPDRS-motor examination score in de novo patients. However, the percent changes in the P300 latency were not correlated with those in the UPDRS-motor examination score. These results indicate that the central dopaminergic mechanisms apart from those responsible for motor symptoms, may contribute to the P300 abnormality in Parkinson's disease.

Acoustic Stimulation↗
PubMed1998

Role of the hepatic xanthine oxidase in thyroid dysfunction: effect of thyroid hormones in oxidative stress in rat liver.

The effect of thyroid hormones on the hepatic xanthine oxidase activity was studied in rats after the intraperitoneal injections of comthyroid (triiodotyronine:thyroxine = 1:4) at 0.3 mg/kg for 3 consecutive days. The aim of this study was to understand the precise mechanism of hyperthyroidism induced by oxidative stress. The concentration of lipid peroxides determined indirectly by the measurement of thiobarbituric acid reactants was increased in comthyroid treated rats. The hepatic glutathione content was decreased in comthyroid injected rat compared to the euthyroid state. It was also observed that the increment of xanthine oxidase activity has a profound role in oxygen radicals generation system in comthyroid treated rat. These findings suggest that the enhanced xanthine oxidase activity and depleting glutathione content in comthyroid treated rats result in pathophysiological oxidative stress including an increment of hepatic lipid peroxidation.

Animals↗
PubMed1998

Structure-activity relationships of gagaminine and its derivatives on the inhibition of hepatic aldehyde oxidase activity and lipid peroxidation.

In order to determine the structure-activity relationships for antioxidative effects of gagaminine, a steroidal alkaloid isolated from the roots of Cynanchum wilfordi (Asclepiadaceae), two derivatives identified as sarcostin and penupogenin were prepared from gagaminine by hydrolysis and reduction. These compounds were evaluated for the inhibitory effects on the aldehyde oxidase activity and on lipid peroxidation in vitro. Furthermore, their effects were compared with those of gagaminine and the related compounds, cinnamic acid and nicotinic acid. The results of this study prove that the cinnamoyl group in the structure of gagaminine is critical in inhibition of the aldehyde oxidase activity while the nicotinoyl group may be necessary for anti-lipid peroxidation of the compound.

Aldehyde Oxidoreductases↗
PubMed1998

Therapeutic effect of rebamipide on ammonia-induced gastric mucosal hemorrhagic lesion in rats.

Rebamipide, 2-(4-chlorobenzoylamino)-3-[2(1H)-quinolinone-4-yl]-propionic acid, a novel antipeptic ulcer agent, has been reported to prevent various acute experimental gastric mucosal lesions and to accelerate the healing of chronic ulcers. Therapeutic effect of rebamipide was investigated with regard to the inhibitory effect on xanthine oxidase activity and type conversion of the enzyme which play a profound role in oxygen radicals generation system. Intraperitoneal administration of rebamipide at 60 mg/kg body weight reduced the xanthine oxidase activity, lipid peroxide content in ammonia induced hemorrhagic lesion. These results suggest that the therapeutic effect of rebamipide on gastric mucosal lesion may be in part due to the inhibitory activity of xanthine oxidase and type conversion rate of the enzyme.

Alanine↗
PubMed1998

Molecular analysis of prion protein gene (PRNP) in Korean patients with Creutzfeldt-Jakob disease.

Creutzfeldt-Jakob disease (CJD), a relatively uncommon human dementia, is caused by an unconventional slow infectious agent. Several cases of CJD, clinically or histopathologically diagnosed, have been reported in Korea. In order to confirm the diagnosis of CJD and also differential diagnosis of sporadic and familial types of CJD in Korea, we studied two patients who had symptoms of CJD. The histopathological and immunohistochemical studies showed spongiform neurodegeneration and expression of abnormal isoform of prion protein (PrPSc) in astrocytes. Thus, these two patients were diagnosed CJD. To investigate whether these patients were sporadic or familial type of CJD, the molecular analyses of the prion protein gene (PRNP) were done by restriction fragment length polymorphism (RFLP) and DNA sequencing. In the cases of a healthy Korean and two CJD patients, no point mutation was detected in the known hot spots (178, 180, 200, 210, and 232) and they exhibited wild type PRNP sequences. We concluded that both patients have a sporadic type of CJD, but not familial type.

Base Sequence↗
PubMed1998

Prevalence of viral hepatitis markers in Korean patients with hepatocellular carcinoma.

The positive rates of hepatitis B surface antigen (HBsAg) and antibody to hepatitis C virus (anti-HCV) were analyzed according to year, sex, age, and serum ALT levels in 1,370 patients with hepatocellular carcinoma (HCC) who visited the Korea Cancer Center Hospital between January 1989 and December 1994. The positive rate of HBsAg was 68.8 to 76.0% per year in patients with HCC, while that of anti-HCV was 3.2 to 9.8% per year. No sex predominance was found in the positive rates of HBsAg and anti-HCV. HBsAg positivity was distributed mostly in the 41 to 50 age group, whereas anti-HCV positivity was distributed mostly in the over 50 age group. Higher positive rate of anti-HCV was observed in HCC patients with serum ALT levels above the normal range than in those with serum ALT levels within the normal range. However, elevated serum ALT levels above the normal range was not related to the positive rate of HBsAg. The relatively low prevalence of anti-HCV in patients with HCC suggests that the role of HCV infection in the development of HCC lower than that of HBV infection in Korea. However, our results suggest that HCV is another potent risk factor for HCC even in HBV endemic areas.

Adolescent↗