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H C Kim

Publications and source records attributed to H C Kim.

At least 91 records · Page 5Linked to original sources
PubMed2001

A case of glomerulonephritis in association with pyogenic liver abscess.

Glomerulonephritis associated with visceral abscess is being increasingly recognized. The association of glomerulonephritis with visceral suppuration in the absence of endocarditis was first described by Whitworth and associates. Abscesses were most frequently located in the respiratory tract but have been reported at numerous other sites, including appendix, uterus, aorto-femoral bypass graft and cutaneous wound. This report documents the apparently rare occurrence of glomerulonephritis with acute renal failure in association with pyogenic liver abscess. The need for awareness of glomerulonephritis as a cause of acute renal failure in pyogenic liver abscess is highlighted.

Aged↗
PubMed2001

hMLH1 and hMSH2 mutations in families with familial clustering of gastric cancer and hereditary non-polyposis colorectal cancer.

The pattern of hMLHI and hMSH2 mutations was assessed to identify the genetic correlation between hereditary gastric and colorectal cancers. Four disease groups and their healthy family members were assembled according to the presentation of gastric cancer: FG, familial clustering of gastric cancer (n = 32); CG, family with one or more colorectal and gastric cancers in first-degree relatives (n = 22); HS, seven HNPCC families corresponding to the Amsterdam criteria (AMS+) and 12 suspected HNPCC families which did not satisfy one of the criteria (AMS-), but no gastric cancer among first- and second-degree relatives (n = 19); and SG, sporadic gastric cancer (n = 33). In the CG group, three were included in AMS + and six in AMS- criteria. Peripheral blood was obtained from them to detect hMLHI and hMLH2 mutations using PCR-SSCP analysis and direct sequencing. The incidence of mutations was 9.4% in the FG group, 54.5% in the CG group, 31.6% in the HS group, and none in the SG group. The incidence, type, and number of the mutation were not different between the CG and HS groups. Thirty-four different mutations included 19 in hMLH1 and 15 in hMSH2. Gastric cancer was the most common extracolonic malignancy in HNPCC and suspected HNPCC families (9/28, 32.1%). The hMLH1 or hMSH2 mutation occurred in seven of 10 families with AMS+, whereas it occurred in four of 18 with AMS- (70% vs. 22.2%, P = .013). Five mutations in the hMLH1 and six mutations in the hMSH2 were exclusively found in families with gastric cancer. All three mutations in the FG group were in hMLHI and there was no mutation in their healthy family members. This study demonstrates that some familial clustering type of gastric cancer appears to be associated with hMLHI mutations thereby indicating a difference from the hereditary gastric cancer studies previously reported. In addition, hMLHI and hMSH2 mutations may impact the gastric cancer carcinogenesis in HNPCC or suspected HNPCC.

Adaptor Proteins, Signal Transducing↗
PubMed2001

Light, carbon dioxide, and octenol-baited mosquito trap and host-seeking activity evaluations for mosquitoes in a malarious area of the Republic of Korea.

Two field trials for commercially available and experimental mosquito traps variously baited with light, carbon dioxide, octenol, or combinations of these were evaluated in a malarious area at Paekyeon-Ri near Tongil-Chon (village) and Camp Greaves, Paju County, Kyonggi Province, Republic of Korea. The host-seeking activity for common mosquito species was determined using hourly aspirator collections from a human- and propane lantern-baited Shannon trap. The total number of mosquitoes and number of each species captured during the test were compared using 8 x 8 and 5 x 5 Latin square designs based on trap location. Significant differences were observed for the total number of mosquitoes collected in the 8 x 8 test, such that counterflow geometry (CFG) with CO2 > or = CFG with CO2 and octenol > or = Shannon trap > or = Mosquito Magnet with octenol > American Biophysics Corporation (ABC) light trap with light, CO2 (500 ml/min), and octenol > or = ABC light trap with light and dry ice > or = ABC light trap with light and CO2 > ABC light trap with light only. A concurrent 5 x 5 test found significant differences in trap catch, where Mosquito Magnet with octenol > New Jersey light trap > or = EPAR Mosquito Killer with CO2 > or = ABC light trap with light and dry ice > Centers for Disease Control (CDC) light trap (manufactured by John W. Hock) with light and octenol. Significant differences in trap catch were noted for several species including: Aedes vexans, Anopheles sinensis, An. yatsushiroensis, An. lesteri, Culex pipiens, and Cx. orientalis. Traps baited with octenol captured significantly fewer Cx. pipiens than those not baited with octenol. Likewise, no Cx. orientalis were captured in octenol-baited traps. Host-seeking activity showed a similar bimodal pattern for all species captured. Results from these field trap evaluations can significantly enhance surveillance efforts. Significantly greater numbers of mosquitoes were captured with mosquito traps using counterflow technology (e.g., Mosquito Magnet and CFG traps) when compared to standard light and carbon dioxide-baited traps. Additionally, field evaluations demonstrate that various traps can be utilized for isolation and detection of arboviruses and other pathogens.

Animals↗
PubMed2000

Human RNA lariat debranching enzyme cDNA complements the phenotypes of Saccharomyces cerevisiae dbr1 and Schizosaccharomyces pombe dbr1 mutants.

The cDNA encoding the human RNA lariat debranching enzyme (hDBR1) was identified and cloned by searching the Expressed Sequence Tag (EST) database and screening a HeLa cDNA library, based on predicted amino acid sequence homologies with the Saccharomyces cerevisiae, Schizosaccharomyces pombe and Caenorhabditis elegans debranching enzymes. The hDBR1 cDNA expressed in Escherichia coli showed debranching activity in vitro and was also shown to be functional in an interspecies specific complementation experiment. hDBR1 cDNA in a S. cerevisiae expression vector complemented the intron accumulation phenotype of a S. cerevisiae dbr1 null mutant. Integration of the cDNA for hDBR1 into the ura4 locus of S. pombe also complemented both the intron accumulation and slow growth phenotypes of a S. pombe dbr1 null mutant strain. Comparison of the amino acid sequence of hDBR1 with the other DBR protein sequences showed several conserved regions, with 40, 44 and 43% identity to the S. cerevisiae, S. pombe and C. elegans debranching enzymes, respectively.

Amino Acid Sequence↗
PubMed2000

Applicability of carcinoembryonic antigen-specific monoclonal antibodies to radioimmunoguided surgery for human colorectal carcinoma.

Two carcinoembryonic antigen (CEA)-specific monoclonal antibodies (MAbs), PR1A3 and T84.66, were tested to determine whether they could accurately localize colorectal carcinoma and therefore be applicable in radioimmunoguided surgery (RIGS). Twenty-one tumors by three human colorectal carcinoma cell lines with various levels of CEA expression (KM-12c, C75, and Clone A) were successfully implanted in the intra-abdominal organs of 15 nude mice. The tumors was localized using a portable radioisotope detector (Neoprobe 1000) 48 h after injection of radiolabeled MAbs (10 mCi/mouse) when the precordial counts were <20 per 2 s. Histopathological identification of radiolabeled MAbs were also performed using immunohistochemistry and microautoradiography. Radioactivity counted on a portable radioisotope detector correlated well with that on a gamma counter. The distribution in the blood was significantly greater than in other organs (P < 0.001). Localization indices of the tumor in various organs was from 1.1 to 8.5 in the PR1A3-pretreated mice and 3.0 to 8.6 in the T84.66-pretreated mice. Silver grains and immune staining were distributed in the tumor cells of the PR1A3-pretreated mice, whereas they were in the necrotic debris as well as the tumor cells of the T84.66-pretreated mice. There were significantly more silver grains in the liver in the T84.66-pretreated mice than in the PR1A3-pretreated mice (P = 0.004). The sensitivity and specificity of tumor localization by RIGS were 71.4 and 91.4% in the PR1A3-pretreated mice, whereas they were 60 and 76% in the T84.66-pretreated mice. A study using specific anti-CEA MAbs suggested PR1A3 as an efficient immune probe for RIGS in colorectal carcinoma with a low rate of false-positive detection.

Animals↗
PubMed2000

Phenidone prevents kainate-induced neurotoxicity via antioxidant mechanisms.

Acculmulating evidence indicates that a marked generation of oxygen free radicals derived from the metabolism of arachidonic acid causes neurodegeneration. Recently, we have demonstrated that the novel antioxidant actions mediated by phenidone, a dual inhibitor of cyclooxygenase/lipoxygenase pathways, may play a crucial role in preventing neuroexcitotoxicity in vitro [Neurosci. Lett. 272 (1999) 91], and that phenidone significantly attenuates kainic acid (KA)-induced seizures via inhibiting the synthesis of Fos-related antigen protein [Brain Res. 782 (1998) 337]. In order to extend our understanding of the pharmacological intervention of phenidone, we evaluated the antioxidant activity of this compound in vivo in the present study. In order to better understand the significance of a blockade of both the cyclooxygenase and lipoxygenase pathways, we studied the effects of aspirin (ASP; a non-selective inhibitor of cyclooxygenase), NS-398 (a selective inhibitor of cyclooxygenase-2), esculetin (an inhibitor of lipoxygenase) and phenidone on lipid peroxidation, protein oxidation, and glutathione (GSH) status in the rat hippocampus after KA administration. ASP (7.5 or 15 mg/kg), NS-398 (10 or 20 mg/kg), esculetin (5 or 10 mg/kg) or phenidone (25, 50 or 100 mg/kg) was administered orally five times every 12 h before the injection of KA (10 mg/kg, i.p.). The KA-induced toxic behavioral signs, oxidative stress (lipid peroxidation and protein oxidation), impairment of GSH status, and the loss of hippocampal neurons were dose-dependently attenuated by the phenidone, NS-398+esculetin, and ASP+esculetin. However, ASP, NS-398 and esculetin alone failed to protect against the neurotoxicities induced by KA. Therefore, the results suggest that protection by blockade of both cyclooxygenase and lipoxygenase pathways against KA-induced neuroexcitotoxicity is via antioxidant actions. However, a novel anticonvulsant/neuroprotective effect mediated by phenidone remains to be further characterized.

Animals↗
PubMed2000

Dual effects of dextromethorphan on cocaine-induced conditioned place preference in mice.

Dextromethorphan (DM) at supra-antitussive doses might produce psychotomimetic effects in humans. In order to understand the underlying mechanisms responsible for the behavior induced by DM, we examined the effects of DM on cocaine-induced conditioned place preference (CPP) and locomotor pattern in mice, and Fos-related antigen immunoreactivity (FRA-IR) in the striatal complex (nucleus accumbens and striatum) of the mouse brain. The effects of DM (20 and 40 mg/kg, i.p.) on the CPP for 2.5, 5, 10, and 20 mg cocaine/kg, i.p. were assessed. Pretreatment with DM dose-dependently decreased the CPP for 20 mg cocaine/kg. Similarly, pretreatment with DM appeared to reduce the CPP for 10 mg cocaine/kg, but increase the CPP for 5 mg cocaine/kg. This finding was more pronounced for 2.5 mg cocaine/kg; DM significantly increased the CPP for 2.5 mg cocaine/kg in a dose-related manner. Furthermore, these results were correlated with alterations in the locomotor pattern (marginal activity) and FRA-IR in the striatal complex. Thus, our results suggest that DM exhibits a biphasic effect on the cocaine-induced CPP and locomotor pattern.

Animals↗
PubMed2000

An immunocytochemical study of mitochondrial manganese-superoxide dismutase in the rat hippocampus after kainate administration.

We examined the immunocytochemical distribution of mitochondrial Mn-superoxide dismutase (SOD-2) in the rat hippocampus after systemic injection of kainic acid (KA), in order to understand SOD-2-responsible antioxidant defense mechanism during the neurodegenerative process. SOD-2 immunostaining was more intense in CA3 pyramidal neurons than in CA1 neurons in the normal hippocampus. The immunoreactivity in region CA1 was reduced without significant neuronal losses within 12 h of KA injection. The CA1 and CA3 neurons lost their immunoreactivity, whereas SOD-2-positive glia-like cells proliferated, mainly throughout the CA1 sector, and had intense immunoreactivity 3 and 7 days after KA injection. This immunocytochemical distribution of SOD-2-positive non-neuronal elements was similar to that of glial fibrillary acidic protein (GFAP) and S-100 protein-positive cells. Activated microglial cells selectively marked with lectin occurred in the areas affected by the KA-induced lesion. Double-labeling immunocytochemistry showed the co-localization of SOD-2-positive non-neuronal cells and GFAP or S-100 protein-like immunoreactivity in the same cells. This suggests that astroglial cells mobilized to synthesize of SOD-2 protein in a response to KA toxicity designed to reduce the oxidative damage.

Animals↗
PubMed2000

No evidence of Peutz-Jeghers syndrome gene LKB1 involvement in left-sided colorectal carcinomas.

LKB1 serine/threonine kinase is a gene for Peutz-Jeghers cancer predisposition syndrome. Most studies have detected a low frequency of LKB1 defects in sporadic cancer. A notable exception is a recent report describing frequent, mostly missense type, LKB1 mutations in Korean distal colorectal tumors. To clarify the role of LKB1 in colon cancer, we scrutinized 50 left-sided Korean and Finnish specimens. No somatic mutations were found. The seven Korean somatic missense mutations reported previously were functionally analyzed, and five were found not to alter LKB1 kinase activity. One of these changes was found to be a germ-line polymorphism. LKB1 involvement in distal colorectal cancer is not common.

AMP-Activated Protein Kinase Kinases↗
PubMed2000

Protection by a manganese porphyrin of endogenous peroxynitrite-induced death of glial cells via inhibition of mitochondrial transmembrane potential decrease.

In the cerebral ischemic penumbra, progressive metabolic deterioration eventually leads to death of glial cells. The exact mechanism for the death of glial cells is unclear. Here we report that under glucose-deprived conditions immunostimulated glial cells rapidly underwent death via production of large amounts of peroxynitrite. The cell-permeable Mn(III)tetrakis(N-methyl-4'-pyridyl)porphyrin (MnTMPyP) caused a concentration-dependent attenuation of the increased death in glucose-deprived immunostimulated glial cells. The structurally related compound H(2)TMPyP, which lacks metals, did not attenuate this augmented cell death. MnTMPyP prevented the elevation in nitrotyrosine immunoreactivity (a marker of ONOO(-)) in glucose-deprived immunostimulated glial cells. In glucose-deprived glial cells, MnTMPyP also completely blocked the augmented death and nitrotyrosine immunoreactivity induced by the ONOO(-)-producing reagent 3-morpholinosydnonimine (SIN-1). The mitochondrial transmembrane potential (MTP), as measured using the dye JC-1, was rapidly decreased in immunostimulated or SIN-1-treated glial cells deprived of glucose. MnTMPyP, but not H(2)TMPyP, blocked the depolarization of MTP in those glial cells. The present data, at least in part, provide evidence for how glial cells die in the postischemic and/or recurrent ischemic brain.

Animals↗
PubMed2000

Efficiency of combined colonoscopy and computed tomography for diagnosis of colonic actinomycosis: a retrospective evaluation of eight consecutive patients.

The preoperative diagnosis of colonic actinomycosis is accurate in fewer than 20% of patients. Colonoscopy and computed tomography (CT) findings were analyzed to ascertain their diagnostic value and their role in determining therapeutic modality and outcome. Before and after treatment we retrospectively evaluated eight consecutive patients with colonic actinomycosis, all of whom were women with a previous history of intrauterine contraceptive device use. Median follow-up period was 20 months (7-57). Localized nodules were found in all cases by colonoscopy; half of these nodules included umbilication at the apex. The colonic mucosa demonstrated normal to moderate inflammation as well as hyperemia and edema. Mucosal ulceration was found in only one case. All cases showed some degree of stenosis. These findings differ from those in other inflammatory or neoplastic diseases of the colon. Abdominopelvic CT revealed extramural involvement of heterogeneous lesions all cases. Contrast enhancement also indicated severe thickening of the colonic wall (7-20 mm) with focal and dense enhancement in six cases. Seven of eight patients required surgery for diagnostic or therapeutic purposes. Complete resolution was determined using both colonoscopy and CT. As more than half of these cases could have been safely managed using an adequate antibiotic treatment, diagnostic studies indicating a high likelihood of colonic actinomycosis should be evaluated to avoid unnecessary surgeries carried out for diagnostic purposes. A combination of colonoscopy and CT appears to be important for both diagnosis and management because of their compensatory findings of mucosal and extramucosal lesions, respectively.

Actinomycosis↗
PubMed2000

Prolonged exposure to cigarette smoke blocks the neurotoxicity induced by kainic acid in rats.

We examined the effects of cigarette smoke (CS) on three parameters associated with kainic acid (KA)-induced neurotoxicity: seizure activity, cell loss in the hippocampus, and increased Fos-related antigen (FRA) expression. Animals were exposed to the main stream of CS from 15 Kentucky 2R1F research cigarettes containing 28.6 mg tar and 1.74 mg nicotine per cigarette, for 10 min a day, 6 days per week, for 4 weeks, using an automatic smoking machine. KA administration (10 mg/kg, i.p.) produced robust behavioral convulsions lasting 4-5 h. Pre-exposure to CS significantly reduced the seizures, mortality, and severe loss of cells in regions CA1 and CA3 of the hippocampus after KA administration. Consistently, pre-exposure to CS significantly attenuated the KA-induced increased FRA immunoreactivity in the hippocampus. In contrast, pretreatment with central nicotinic antagonist, mecamylamine (2 or 10 mg/kg, i.p.) blocked the neuroprotective effects mediated by CS in a dose-dependent manner. These results indicate that CS exposure provides neuroprotection against the KA insult via nicotinic receptor activation.

Animals↗