Search PubMed⌕ Search

Biomedical subjects

H C Jung

Publications and source records attributed to H C Jung.

At least 37 records · Page 2Linked to original sources

Prediction of the clinical course of Behçet's colitis according to macroscopic classification by colonoscopy.

BACKGROUND AND STUDY AIMS: The lesions in Behçet's colitis show aphthoid or punched-out ulceration, but the macroscopic types of lesion found have not been defined. To predict the clinical outcome in patients with Behçet's colitis according to the colonoscopic findings, we classified the characteristic colonic ulcers, evaluated the efficacy of medical treatment on colonoscopic lesions, and calculated the operation rates and recurrence rates relative to the macroscopic types. PATIENTS AND METHODS: The medical records and colonoscopic photographs of 50 patients with Behçet's colitis were reviewed. The colonic lesions were examined by colonoscopy in patients with Behçet's disease and gastrointestinal symptoms. The colonoscopic findings were categorized into three types of ulceration: volcano-like, geographic, and aphthous. The efficacy of medical treatment was assessed by follow-up colonoscopy or double-contrast barium enema four to eight weeks after treatment, and recurrence of the lesions was evaluated during the follow-up periods. Cumulative surgery rates were obtained using the Kaplan-Meier method. RESULTS: The macroscopic classification of colonic ulcers identified 25 of 50 patients (50%) with volcano-type lesions, 11 (22%) with the geographic type, and 14 (28%) with the aphthous type. The rates of complete remission after medical treatment and surgery, respectively, were six of 25 (24%) and 13 of 25 (52%) with volcano-type ulcerations; eight of 11 (73%) and one of 11 (9%) with the geographic type; and nine of 14 (64%) and two of 14 (14%) with the aphthous type. The endoscopic and clinical recurrence rates were nine of 19 (47%) in volcano-type ulcerations, one of nine (11%) in the geographic type, and one of 11 (9%) in the aphthous type. CONCLUSION: Volcano-type ulcerations in Behçet's colitis showed a less favorable response to medical treatment, a more frequent requirement for surgery, and more frequent recurrences than the geographic and aphthous types of ulcerations.

Adult↗

Apoptosis of human gastric epithelial cells via caspase-3 activation in response to Helicobacter pylori infection: possible involvement of neutrophils through tumor necrosis factor alpha and soluble Fas ligands.

BACKGROUND: Infection with Helicobacter pylori activates a proinflammatory gene program in human gastric epithelial cells and neutrophils and is associated with significant epithelial cell damage, including an increased level of apoptosis. We evaluated whether immune mediators produced by neutrophils could modulate gastric epithelial cell apoptosis in response to H. pylori infection. METHODS: After gastric epithelial cells were infected with H. pylori in the presence of immune mediators, including tumor necrosis factor alpha (TNF-alpha) and Fas ligand (FasL), apoptosis and caspase-3 activity were assessed. The neutrophils were obtained from healthy volunteers, and Western blot for FasL and quantitative reverse transcription polymerase chain reaction for TNF-alpha transcripts were performed. Fas expression in gastric epithelial cells was explored by flow cytometric analysis. RESULTS: Activation of caspase-3 was first apparent 12 h after bacterial infection, and the phenotypic expression of apoptosis was first apparent 18 h after bacterial infection. The extent of apoptosis was similar in cases of cagA+ cytotoxin+, cagA+ cytotoxin-, cagA- cytotoxin- H. pylori-infected gastric epithelial cells. Approximately 20% of the Hs746T cells expressed Fas within 24 h of H. pylori infection. The soluble FasL was upregulated in neutrophils after treatment with H. pylori-soluble proteins for 24 and 48 h. The addition of TNF-alpha and the soluble form of FasL, produced by neutrophils, significantly increased H. pylori-infected cell apoptosis and caspase-3 activation. However, the combination of these two immune mediators showed only an additive increase. CONCLUSION: These results suggest that H. pylori-induced gastric epithelial cell apoptosis and caspase-3 activation can be modulated by the immune response of neutrophils.

Apoptosis↗

Bacterial cell surface display of an enzyme library for selective screening of improved cellulase variants.

The bacterial surface display method was used to selectively screen for improved variants of carboxymethyl cellulase (CMCase). A library of mutated CMCase genes generated by DNA shuffling was fused to the ice nucleation protein (Inp) gene so that the resulting fusion proteins would be displayed on the bacterial cell surface. Some cells displaying mutant proteins grew more rapidly on carboxymethyl cellulose plates than controls, forming heterogeneous colonies. In contrast, cells displaying the nonmutated parent CMCase formed uniform tiny colonies. These variations in growth rate were assumed to result from altered availability of glucose caused by differences in the activity of variant CMCases at the cell surface. Staining assays indicate that large, rapidly growing colonies have increased CMCase activity. Increased CMCase activity was confirmed by assaying the specific activities of cell extracts after the expression of unfused forms of the variant genes in the cytoplasm. The best-evolved CMCases showed about a 5- and 2.2-fold increase in activity in the fused and free forms, respectively. Sequencing of nine evolved CMCase variant genes showed that most amino acid substitutions occurred within the catalytic domain of the enzyme. These results demonstrate that the bacterial surface display of enzyme libraries provides a direct way to correlate evolved enzyme activity with cell growth rates. This technique will provide a useful technology platform for directed evolution and high-throughput screening of industrial enzymes, including hydrolases.

Amino Acid Substitution↗

Helicobacter pylori in dental plaque and saliva.

BACKGROUND: About half of the world population is infected with H. pylori, but the transmission and the source of this infection are still unclear. Recently, dental plaque (DP) and saliva have been implicated as possible sources of H. pylori infection. This study was done to investigate the detection rates of H. pylori in the DP and saliva by use of PCR depending on H. pylori infection state of gastric mucosa. METHODS: In 46 subjects, gastric H. pylori colonization was evaluated with CLO test, microscopy of Gram stained mucosal smear, culture and histology after modified Giemsa staining in the antrum and body, respectively. A patient was regarded as H. pylori positive if one or more of the four aforementioned test methods demonstrated H. pylori colonization of the gastric mucosa. For detection of H. pylori in the DP and saliva, PCR assay was done with ET4-U and ET4-L primers. To estimate the sensitivity and specificity of this PCR, H. pylori positivity was evaluated in the antrum and body, separately. RESULTS: The sensitivity of mucosal PCR was 50.0% (27/54) and the specificity 86.8% (33/38). When a subject was regarded as H. pyloi positive, if either antrum or body mucosal H. pylori was is positive, the positive rate of mucosal PCR was 62.1% (18 subjects) in the 29 H. pylori-positive and 17.6% (3 subjects) in the 17 H. pylori-negative subjects. DP PCR was positive in 2 of 29 H. pylori-positive subjects (6.9%) and none in the 17 H. pylori-negative (0%). Saliva PCR was positive in 4 of 14 H. pylori-positive subjects (28.6%) and none of 6 H. pylori-negative (0%). CONCLUSION: The detection rates of H. pylori in DP and saliva by PCR were rather low, 6.9% and 28.6%, respectively, and these rates might have been underestimated by low sensitivity of the PCR method used in this study. However, the results that H. pylori was found in the DP and saliva suggest that the oral cavity can perform a role as a reservoir of H. pylori in Korea.

Dental Plaque↗

Eradication of Helicobacter pylori infection did not lead to cure of duodenal mucosa-associated lymphoid tissue lymphoma.

Duodenal mucosa-associated lymphoid tissue (MALT) lymphoma is very rare, and little is known about its clinical course or association with Helicobacter pylori infection. This report describes the case of a 76-year-old man with a polypoid mass in the duodenal bulb, diagnosed as low-grade MALT lymphoma. H. pylori infection in the duodenal mucosa was confirmed by histology with silver stain. Endoscopic examination showed that the gross lesion regressed after the eradication of H. pylori despite its histopathologic persistence. Ten months later, however, cervical and intraperitoneal lymphadenopathy and bone marrow involvement was observed, and the pathologic diagnosis of the cervical lymph node was identical with that of the duodenal lesion.

Aged↗

Homofermentative production of D- or L-lactate in metabolically engineered Escherichia coli RR1.

We investigated metabolic engineering of fermentation pathways in Escherichia coli for production of optically pure D- or L-lactate. Several pta mutant strains were examined, and a pta mutant of E. coli RR1 which was deficient in the phosphotransacetylase of the Pta-AckA pathway was found to metabolize glucose to D-lactate and to produce a small amount of succinate by-product under anaerobic conditions. An additional mutation in ppc made the mutant produce D-lactate like a homofermentative lactic acid bacterium. When the pta ppc double mutant was grown to higher biomass concentrations under aerobic conditions before it shifted to the anaerobic phase of D-lactate production, more than 62.2 g of D-lactate per liter was produced in 60 h, and the volumetric productivity was 1.04 g/liter/h. To examine whether the blocked acetate flux could be reoriented to a nonindigenous L-lactate pathway, an L-lactate dehydrogenase gene from Lactobacillus casei was introduced into a pta ldhA strain which lacked phosphotransacetylase and D-lactate dehydrogenase. This recombinant strain was able to metabolize glucose to L-lactate as the major fermentation product, and up to 45 g of L-lactate per liter was produced in 67 h. These results demonstrate that the central fermentation metabolism of E. coli can be reoriented to the production of D-lactate, an indigenous fermentation product, or to the production of L-lactate, a nonindigenous fermentation product.

Acetate Kinase↗

A precipitation reaction found in patients with hepatitis C as a marker for the purification of virus-like particles.

Even after the molecular cloning of the hepatitis C virus (HCV), an HCV-specific precipitation reaction has not yet been identified. We attempted to develop a precipitation system exclusively for anti-HCV-positive sera as a first step in finding an HCV-specific antigen and HCV-associated particles. In some patients being in a final stage of different liver diseases, we found sera (179/132,761; designated 'a-CK') which specifically precipitated with anti-HCV- and HCV-RNA-positive sera (designated 'CK'). When CK-positive sera were searched for in patients with various liver diseases using standard a-CK-positive plasma, CK was detected in 420 (57.9%) of 726 anti-HCV-positive sera and in none of the 1,630 anti-HCV-negative ones. The nature of CK and a-CK has not been fully clarified yet; CK demonstrated inter-betagamma mobility, whereas a-CK showed beta-globulin mobility; CK was not detected in cryoprecipitate, but HCV RNA was present in precipitates of CK-positive plasma incubated with one that was a-CK positive. Transmission electron microscopy revealed two size ranges of particles in the precipitate of CK- and a-CK-positive plasmas, 23-38 nm and 48-65 nm. We have found a novel precipitation system which is exclusive to anti-HCV-positive sera and which specifically precipitates an HCV-RNA-containing serum fraction and particles. This system can be useful for the purification and characterization of the circulating particles. Furthermore, it may be a new approach to the nature of HCV-RNA-carrying material.

Centrifugation↗

Establishment of BALB/c mice model infected with Helicobacter pylori.

OBJECTIVES: Considering the geographic differences in the prevalence of virulence factors such as CagA or VacA of H. pylori isolated from Korean adults compared with those from western countries, the establishment of a mouse model infected with H. pylori isolated from Korean adults is needed to investigate the pathogenesis and to develop vaccines against H. pylori infection in Korea. The aim of this study was to establish the BALB/c mouse model infected with H. pylori isolated from Korean. METHODS: Six-week-old BALB/c mice were inoculated intragastrically with 10(9) CFU of H. pylori. Loss of glandular architecture, erosions and infiltration of inflammatory cells within the lamina propria compared with normal gastric mucosa were scrutinized. Evidence for H. pylori infection was assessed by rapid urease test of gastric mucosa and by microscopic examination using the H & E stain and Warthin-Starry silver stain. RESULTS: Rapid urease test was positive in 55% of all inoculated mice. Definite histologic changes and the evidence of H. pylori colonization were observed in the H. pylori infected group. Significant infiltration of inflammatory cells was observed 6 weeks after the last inoculation and the level of serum IgG against H. pylori was increased from 2 weeks after the last inoculation. CONCLUSIONS: The H. pylori isolated freshly from Korean adults could colonize the stomach of BALB/c mice and induce pathologic alterations that mimics human gastric diseases. This model would facilitate the investigations for the pathogenetic mechanisms of H. pylori infection.

Adult↗

Single dose pharmacokinetics of HEPP, a new anticonvulsant in normal healthy volunteers.

The pharmacokinetics and the dose proportionality of a new anticonvulsant compound, HEPP (D,L-3-hydroxy-3-ethyl-3-phenylpropionamide) was studied in healthy male volunteers as part of the pharmacological evaluation for new drugs. Study was performed administering doses of 250, 375, 500 and 625 mg of HEPP to six male volunteers. Blood and urine samples were collected for 72 h postdose and analysed by HPLC. Results showed that in man HEPP is rapidly absorbed from the gastrointestinal tract. Tmax values were between 1.5 and 6.0 h. Plasma mean terminal half-life after the different doses ranged between 15.83 and 27.62 h with an overall harmonic mean value of 22.8. The mean AUC0-infinity and Cmax increased linearly with doses of 250, 375 and 500 mg but not with the dose of 625 mg. The amount of unchanged drug excreted in urine was between 3 and 6% of administered dose which shows an extensive metabolism of the drug.

Administration, Oral↗

Synergy between Entamoeba histolytica and Escherichia coli in the induction of cytokine gene expression in human colon epithelial cells.

Entamoeba histolytica induces the expression and secretion of interleukin 8 (IL-8) by cultured colon epithelial cells. We assessed the array of cytokine genes expressed by human colon epithelial cells in response to co-culture with E. histolytica trophozoites and tested the hypothesis that enteric bacteria may alter the E. histolytica-induced expression of such genes. HT-29 colon epithelial cells were co-cultured with E. histolytica trophozoites in the presence or absence of Escherichia coli. Cytokine gene expression was assessed by quantitative reverse-transcription polymerase chain reaction (RT-PCR). IL-8 mRNA in colon epithelial cells was up-regulated following exposure to E. histolytica and this was paralleled by increased IL-8 secretion. Granulocyte-macrophage colony-stimulating factor (GM-CSF) and IL-1alpha/beta mRNAs were also up-regulated in these cells. When HT-29 cells were co-cultured with E. coli DH5alpha and E. histolytica there was a synergistic increase in the expression of IL-8, IL-1alpha, and GM-CSF. These results suggest that enteric bacteria may significantly affect early proinflammatory signals produced in host tissues in response to E. histolytica infection.

Animals↗

Expression of carboxymethylcellulase on the surface of Escherichia coli using Pseudomonas syringae ice nucleation protein.

Ice-nucleation protein (INP), an outer membrane protein from Pseudomonas syringae, is able to catalyze the ice crystal formation of supercooled water. It was exploited for anchoring of Bacillus subtilis carboxymethylcellulase (CMCase) on the surface of Escherichia coli. A surface anchoring vector, pGINP21M, was created that contains the multicloning sites including BamHI, SmaI and EcoRI at the end of the 3' flanking region encoding the C-terminus of INP instead of the stop codon for subcloning the foreign genes. The CMCase gene was in-frame subcloned for making INP-CMCase fusion proteins. The ability of this vector for directing the actual synthesis of INP-CMCase fusion proteins was confirmed by Western blotting analysis. CMCase targeted on the surface of cells was verified by measuring whole cell CMCase activity and ice-nucleation activity. CMCase activity was mainly detected on the cell surface whereas no enzyme activity was detected in the culture supernatant. Ice-nucleation activity was also maintained even if an INP-CMCase hybrid was made. This means that the fusion protein is functionally expressed and has its biological conformation on the surface. INP-CMCase fusion proteins were stable in the stationary phase. INP deleted of the repeating domain, thus producing no ice-nucleation activity, could also direct CMCase on the cell surface. This suggests that it has the secretion and targeting signal to the outer membrane.

Bacterial Outer Membrane Proteins↗

Surface display of Zymomonas mobilis levansucrase by using the ice-nucleation protein of Pseudomonas syringae.

The ice-nucleation protein (Inp) is a glycosyl phosphatidylinositol-anchored outer membrane protein found in some Gram-negative bacteria. Using Pseudomonas syringae inp as an anchoring motif, we investigated the functional display of a foreign protein, Zymomonas mobilis levansucrase (LevU), on the surface of Escherichia coli. The cells expressing Inp-LevU were found to retain both the ice-nucleation and whole-cell levansucrase enzyme activities, indicating the functional expression of Inp-LevU hybrid protein on the cell surface. The surface localization was further verified by immunofluorescence microscopy, fluorescence-activated cell sorting flow cytometry and immunogold electron microscopical examination. No growth inhibition or changes in the outer membrane integrity were observed upon the induction of fusion protein synthesis. Viability of the cells was also maintained over 48 hours in the stationary phase. Surface-displayed levansucrases were found to be resistant to the externally added proteases unless the cells were treated with EDTA. When the levansucrase-displayed cells were used as the enzyme source, levan (44 g/L) was efficiently synthesized from sucrose (130 g/L) with 34% (wt/wt) conversion yield, generating glucose (65 g/L) as a by-product.

Bacterial Outer Membrane Proteins↗

Interleukin-8 expression by human neutrophils activated by Helicobacter pylori soluble proteins.

BACKGROUND: Helicobacter pylori soluble proteins may serve as chemoattractants for neutrophils. Once extravasated and attracted to the gastric mucosa, neutrophils themselves may be a source of interleukin-8 (IL-8), further amplifying the inflammatory response. We evaluated IL-8 expression and the activation of human neutrophils by H. pylori products. METHODS: After neutrophils had been stimulated with H. pylori culture supernatant, IL-8 mRNA expression was assessed by quantitative reverse transcription polymerase chain reaction, using synthetic standard RNA at 0, 1, 2, 4, and 9 h. The amount of IL-8 protein was measured by enzyme-linked immunosorbent assay (ELISA). Lymphocyte function-associated antigen-1beta (LFA-1beta) (CD18) expression was determined with flow cytometry, and myeloperoxidase secretion was analyzed with ELISA. After acetohydroxamic acid (AHA) and/or N-tert-butoxycarbonyl-methionyl-leucyl-phenylalanine (BOC-MLP) was added to H. pylori culture supernatant, IL-8 ELISA was analyzed for 9 h. RESULTS: IL-8 mRNA expression by stimulated neutrophils was 16 to 67 times greater than by controls, peaking at 2 h after stimulation. The amount of IL-8 protein was markedly increased at 4 h after stimulation. H. pylori culture supernatant enhanced LFA-1beta expression and myeloperoxidase secretion by neutrophils. AHA and/or BOC-MLP decreased IL-8 production at 2-4 h after stimulation. CONCLUSIONS: H. pylori-induced neutrophil recruitment may be mediated via IL-8 expressed by neutrophils activated by H. pylori soluble proteins. This may explain the gastric mucosal inflammatory response to the non-invasive organism.

CD18 Antigens↗

Helicobacter pylori reinfection rate and duodenal ulcer recurrence in Korea.

In the short term, the eradication of Helicobacter pylori in patients with duodenal ulcer (DU) is deemed to be clearly effective; the long-term effectiveness apparently depends on the H. pylori reinfection rate. We conducted the present study to investigate the rates of H. pylori reinfection and DU recurrence in 45 patients previously cured of DU in whom H. pylori had been eradicated. These patients underwent gastroscopy and tests for H. pylori at least 1 year after eradication. In a control group comprising 31 patients with DU who were not treated with H. pylori eradication regimen, the DU recurrence rate was checked annually for 4 years. Twenty of 45 patients (44.4%) in whom the mean follow-up period was 3.5 years were again found to be H. pylori positive, and the reinfection rate was 12.8% per year. DU recurred in 8 of these 20 (40%) but not in any nonreinfected patients. In the control group, the DU recurrence rate was 61% within 1 year, 81% within 2 years, 84% within 3 years, and 90% within 4 years. The respective recurrence rates in the 45 patients in whom the bacteria had been eradicated were 0%, 4%, 13%, and 18%. The H. pylori reinfection rate was as high as 12.8% per year in Korea, but in that the DU recurrence rate is significantly lower (p < 0.01; odds ratio, 129.5) in the H. pylori-eradicated group than in the control group, the eradication of H. pylori in DU patients is effective over the long term (at least 4 years).

Adolescent↗

Cytokine genes are down-regulated when attachment of Entamoeba histolytica to HT-29 colon epithelial cells is prevented.

Entamoeba histolytica can cause invasive disease by disruption of the intestinal barriers and subsequent lysis of the intestinal cells. Adherence to and contact dependent killing of host cells requires the galactose inhibitable lectin. To elucidate the mechanism whereby E. histolytica influences host defence, the authors assessed the change of proinflammatory cytokine genes expressed by colon epithelial cells in response to co-culture with E. histolytica trophozoites and carbohydrates, including galactose, N-acetyl-galactosamine or N-acetyl-lactosamine, which prevented E. histolytica from attaching to epithelial cells. After HT-29 human colon epithelial cells were co-cultured with E. histolytica trophozoites in the presence or absence of carbohydrates (0.1-100 mM), RNA was extracted from the epithelial cells by an acid guanidinium thiocyanate-phenol-chloroform method. Cytokine gene expression was assessed by quantitative RT-PCR using a synthetic internal standard, and proteins were determined by ELISA. IL-8 mRNA expressed by HT-29 cells in response to E. histolytica trophozoites was downregulated in the presence of galactose, N-acetylgalactosamine or N-acetyl-lactosamine (0.1-100 mM), and this was paralleled by decreased IL-8 protein secretion. GM-CSF and IL-1 alpha/beta mRNAs were also downregulated in those cells in the presence of these agents. These results suggest that the expression of proinflammatory cytokine genes could be inhibited by preventing E. histolytica from attaching to the host's colon epithelial cells.

Animals↗

Helicobacter pylori induces an array of pro-inflammatory cytokines in human gastric epithelial cells: quantification of mRNA for interleukin-8, -1 alpha/beta, granulocyte-macrophage colony-stimulating factor, monocyte chemoattractant protein-1 and tumour necrosis factor-alpha.

Despite the fact that Helicobacter pylori is known to be non-invasive, mucosal infiltration of inflammatory cells have been observed in the gastric mucosa. The exact pathogenesis of such an inflammatory reaction has not been well defined. We explored the repertoire of cytokine genes expressed in human gastric epithelial cells in response to coculture with H. pylori. After gastric epithelial cells, SNU-5 and KATO III, were infected with H. pylori, expression of several cytokine genes was assessed using quantitative reverse transcription polymerase chain reaction. Interleukin (IL)-8, -1 alpha and -1 beta mRNA were expressed in both gastric epithelial cells throughout the entire infection period. In SNU-5, IL-1 alpha and IL-8 mRNA were expressed at 1 h, reached a peak level at 4 h and then decreased. Interleukin-1 beta mRNA was expressed less frequently than IL-1 alpha, or IL-8 mRNA. In SNU-5 cells, granulocyte-macrophage colony-stimulating factor (GM-CSF), monocyte chemoattractant protein-1 (MCP-1), and tumour necrosis factor-alpha (TNF-alpha) mRNA were expressed at 9 h, but was not expressed in KATO III. Gene expression paralleled the amount of IL-8 protein measured by enzyme-linked immunoabsorbent assay (ELISA). Interleukin-8 mRNA expression was not observed in KATO III cells infected with Campylobacter fetus ssp. fetus, Campylobacter jejuni or Escherichia coli. IL-8 mRNA expression was increased not only in gastric epithelial cells but also in non-gastric cells infected with H. pylori. These results suggest that an inflammatory reaction induced by H. pylori may be initially triggered by an array of pro-inflammatory cytokines expressed by infected gastric epithelial cells.

Campylobacter Infections↗

GM-CSF production by epithelial cell line: upregulation by ultraviolet A.

It was demonstrated that UVB increases synthesis and expression of IL-1 alpha and GM-CSF by keratinocytes. Upregulation of GM-CSF by UVB is reported to be mediated by IL-1 alpha. However, regulation of IL-1 alpha and GM-CSF by UVA is not well-known. The purpose of the present study was to evaluate the effects of UVA on IL-1 alpha and GM-CSF production. Here we used a competitive RT-PCR for measuring cytokine gene expression in an epidermal cell line after UVA irradiation. IL-1 alpha and GM-CSF mRNA did not show any change at 1 h and 6 h following exposure to UVA. After UVA irradiation, however, IL-1 alpha mRNA decreased and GM-CSF mRNA increased at 24 h and the level of GM-CSF in culture supernatant increased at 24 h and 48 h. Addition of antihuman IL-1 alpha neutralizing antibody to UVA irradiated cells did not prevent the increase of GM-CSF mRNA expression. These results suggest that UVA radiation may induce GM-CSF production through an IL-1 alpha independent pathway.

Antibodies↗