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Biomedical subjects

I S Song

Publications and source records attributed to I S Song.

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

Substance P induction of murine keratinocyte PAM 212 interleukin 1 production is mediated by the neurokinin 2 receptor (NK-2R).

The neurological system plays an important role in modulating some inflammatory skin diseases. Neuro-cutaneous interactions may be mediated by the release of neuropeptides such as substance P (SP) which activate immunocompetent cells in the skin by binding to high affinity neurokinin receptors (NKR). Since epidermal keratinocytes produce a variety of cytokines and are intimately associated with cutaneous sensory fibers, we tested the ability of these cells to participate in the cutaneous neuroimmune system by the secretion of potent cytokines such as interleukin 1 (IL-1) in response to released SP. RT-PCR studies demonstrated that cultured PAM 212 murine keratinocytes expressed mRNA for NK-2R but not NK-1R. Correspondingly, the addition of SP to these cells resulted in a rapid increase in intracellular Ca2+ levels that could be specifically blocked by an NK-2R antagonist. NK-2R was also shown in normal mouse epidermis by immunohistochemistry. SP augmented the expression of PAM 212 keratinocyte IL-1alpha mRNA in a dose and time dependent manner and this induction was inhibited by an NK-2R antagonist. Secretion of bioactive IL-1alpha by the PAM 212 keratinocytes was likewise stimulated by SP in a dose dependent manner. These data support the hypothesis that SP released from cutaneous sensory nerves contributes to neuroimmune inflammatory responses in the skin by modulating the expression and release of cytokines from epidermal keratinocytes.

Animals↗
PubMed2000

Incidence and prevalence of ulcerative colitis in the Songpa-Kangdong District, Seoul, Korea, 1986-1997.

BACKGROUND AND AIMS: Ulcerative colitis (UC) is regarded as a rare disease in developing countries, but accurate data are generally lacking. We performed the present study to evaluate the incidence and prevalence of UC in Korea. METHODS: A retrospective study was performed from 1986 to 1997 in the Songpa-Kangdong district of Seoul, Korea. To recruit UC patients as completely as possible, multiple information sources including all medical facilities in the study area and three referral centres located nearby, but outside the study area were used. The incidence and prevalence rates were adjusted using the 1997 Korean population statistics. RESULTS: During the study period, a total of 94 incident cases were identified, for an adjusted mean annual incidence rate of 0.68 per 100,000 inhabitants. On 31 December 1997, 91 patients with UC lived in the study area, giving an adjusted prevalence rate of 7.57 per 100,000 inhabitants. By using the Poisson regression analysis, the annual incidence rate increased significantly from 0.20 per 100,000 inhabitants in 1986-1988 to 1.23 per 100,000 inhabitants in 1995-1997 (P < 0.005). Patient age at diagnosis, the interval from onset of symptoms to diagnosis, and the disease extent at diagnosis were fairly constant throughout the study period. CONCLUSIONS: The incidence and prevalence of UC in our study area are still low compared with those of Western countries, but the incidence rate is steadily increasing.

Adult↗
PubMed2000

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↗
PubMed2000

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↗
PubMed2000

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↗
PubMed1999

VCAM-1 expression on human dermal microvascular endothelial cells is directly and specifically up-regulated by substance P.

Sensory nerves in skin are capable of releasing multiple neuropeptides, which modulate inflammatory responses by activating specific cutaneous target cells. Extravasation of particular subsets of leukocytes depends upon the regulated expression of cellular adhesion molecules such as VCAM-1 on microvascular endothelial cells. We examined the direct effect of cutaneous neuropeptides on the expression and function of human dermal microvascular endothelial cell (HDMEC) VCAM-1. A significant increase in VCAM-1 immunostaining of microvascular endothelium was observed in vivo following capsaicin application to human skin. Multiple cutaneous sensory C-fiber-released neuropeptides were evaluated for their ability to induce VCAM-1 cell surface expression on HDMEC. Only substance P (SP) was found to be capable of inducing HDMEC VCAM-1 expression. This SP-mediated VCAM-1 induction appeared to be a direct effect that did not require the release of other HDMEC-derived soluble factors. Increased HDMEC VCAM-1 mRNA expression was detected 1 h after the addition of SP, with peak mRNA increase at 6-9 h postinduction. FACS studies demonstrated a 6.5-fold increase in endothelial cell surface VCAM-1 expression detectable 16 h after addition of SP, which was specifically blocked by a neurokinin-1 receptor antagonist. Increased VCAM-1 cell surface expression on SP-treated HDMEC resulted in a 4-fold increase in the functional binding of 51Cr-labeled MOLT-4 T cells. These data indicate that SP is capable of directly and specifically up-regulating functional endothelial VCAM-1 expression and thus may play a key role in modulating certain inflammatory responses in the skin.

Capsaicin↗
PubMed1999

Effect of DA-6034, a derivative of flavonoid, on experimental animal models of inflammatory bowel disease.

Inflammatory bowel disease (IBD) is a multifactorial disorder with unknown etiology and pathogenesis. DA-6034, 7-carboxymethyloxy-3', 4', 5-trimethoxy flavone, is a synthetic flavonoid known to possess anti-inflammatory activity. This study was performed to evaluate the oral therapeutic effect of DA-6034 in three experimental animal models of IBD: two chemical-induced IBD models of rats and the human leukocyte antigen (HLA)-B27 transgenic rat model known to develop spontaneous colitis without the use of exogenous agents. Acute chemical colitis was induced by intracolonic instillation of 1.2 ml of 4% acetic acid solution. Prednisolone (1 mg/kg), sulfasalazine (100 mg/kg) and DA-6034 (0.3 to approximately 3 mg/kg) were orally administered twice daily for 6 days in these rats. In addition, chronic chemical colitis was induced by intracolonic administration of trinitrobenzene sulfonic acid (TNBS) 30 mg in 50% ethanol and agents were orally administered for 6 or 20 days. In chemical-induced IBD models, all of these agents reduced the severity of colitis and specially, DA-6034 (3 mg/kg) showed more potent effect than other drugs in macroscopic lesion score. In HLA-B27 transgenic rats, DA-6034 (3 mg/kg) and prednisolone (0.5 mg/kg) were treated orally twice daily for 6 weeks. The HLA-B27 transgenic rats showed only mild colitis, compared with the chemical-induced colitis models. DA-6034 ameliorated the loose stool and decreased microscopic damage, which is the important indicator of this model. In conclusion, oral therapy of DA-6034 attenuated the macroscopic and histologic damages of the colon in all three experimental models of IBD, which suggest that DA-6034 could be a promising drug in the treatment of IBD.

Acetic Acid↗
PubMed1999

Different activity of ATP dependent transport across the canalicular membrane for tributylmethylammonium and triethylmethylammonium as a potential mechanism of the preferential biliary excretion for tributylmethylammonium in the rat.

PURPOSE: The mechanism(s) responsible for the significantly higher biliary excretion of tributyl methyl ammonium (TBuMA) than of triethyl methyl ammonium (TEMA) was investigated in canalicular liver plasma membrane vesicles (cLPM). METHODS: The uptake of [3H]TBuMA and [3H]TEMA into cLPM in the presence of a pH gradient or ATP was measured by a rapid filtration technique. RESULTS: The uptake of substrates into the vesicle was significantly increased by an outwardly directed pH gradient. The pH dependent uptake was saturable and cross-inhibited by the other organic cation, indicating that TEMA and TBuMA share a common transport mechanism. Kinetic analysis revealed the two compounds show similar characteristics for the pH-gradient dependent uptake. Thus, the organic cation/H+ exchange mechanism does not appear to explain the significant difference in biliary excretion of the organic cations. In the presence of ATP, however, uptake into cLPM was readily observed for TBuMA while TEMA uptake was negligible. Inhibition studies with typical P-glycoprotein substrates indicated the uptake may be mediated by the P-glycoprotein. CONCLUSIONS: Differences between TBuMA and TEMA in reactivity for an ATP dependent transport process, rather than for an organic cation/H+ exchanger, may be responsible for the markedly different biliary excretion of TBuMA and TEMA.

Adenosine Triphosphate↗
PubMed1999

Neutral endopeptidase expression and distribution in human skin and wounds.

Cutaneous sensory nerves mediate inflammation and wound healing by the release of neuropeptides such as substance P. Neutral endopeptidase is a cell surface enzyme that degrades substance P and thereby terminates its biologic actions. The distribution of neutral endopeptidase in normal skin and wounded human skin, however, has not been examined. The objectives of this study were to evaluate neutral endopeptidase expression in wounded and unwounded skin as well as in cells derived from human skin. Neutral endopeptidase was strikingly localized in normal skin by immunohistochemistry to keratinocytes of the epidermal basal layer, to hair follicles, eccrine and sebaceous glands as well as to endothelium of blood vessels and to large nerves. Standard incisional human wounds were studied at several time points between 1 h and 28 d after wounding. Staining for neutral endopeptidase was noted in the wound bed 6 h after wounding. In contrast to normal skin, staining of all the epidermal cell layers was noted in the migrating tongue of epithelium in l d wounds. Similar full-thickness staining was noted in 3 d and 7 d wounds in all layers of the new wound epithelium and in a "transition epithelium" near the wound edge. By 28 d post wounding neutral endopeptidase staining again was detected only in the basal layer of the epidermis. Neutral endopeptidase mRNA was detected in normal skin and wounds as well as cultured keratinocytes, fibroblasts and endothelial cells. Neutral endopeptidase enzymatic bioactivity was demonstrated in cultured keratinocytes. While it is known that several metalloproteinases important to tissue repair are produced by keratinocytes, this is the first evidence that keratinocytes produce neutral endopeptidase. Neutral endopeptidase may terminate the proinflammatory and mitogenic actions of neuropeptides in normal skin and wounds.

Aged↗
PubMed1999

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↗
PubMed1999

Association of plasma fibrinogen concentration with vascular access failure in hemodialysis patients.

BACKGROUND: Elevated plasma fibrinogen is an important risk factor for coronary artery disease in the general population and patients with chronic renal failure. High plasma fibrinogen may trigger thrombus formation in arteriovenous fistulas. We performed a prospective, cohort study to evaluate the association of plasma fibrinogen concentration with vascular access failure in patients undergoing long-term haemodialysis. METHODS: Between September 1989 and October 1995, 144 patients underwent a vascular access operation. In March 1997, 102 patients (56 M, 46 F) who had been followed up for more than 18 months (median; 37 months, range; 18-102 months) were included in the study. The median age of the patients was 52 years (range; 19-78 years). In 35 patients, renal disease was secondary to diabetes mellitus. The type of vascular access was a polytetrafluoroethylene (PTFE) graft in 17 patients. Seventy-seven patients received recombinant human erythropoietin (r-HuEPO) therapy during the follow-up period. Plasma fibrinogen, albumin, total cholesterol, hematocrit, platelets and creatinine were measured at the time of operation. Vascular access failure was defined as the occurrence of complications requiring transluminal angioplasty, thrombolytic therapy or surgical repair. RESULTS: Thirty-eight patients had at least one vascular access failure and the incidence was 0.3 (range; 0-2.4) episodes per patient-year. The survival rate of vascular access was 78% (native fistula; 80%, PTFE graft; 71%) after 12 months and 70% (native fistula; 73%, PTFE graft; 51%) after 24 months. Older age, a PTFE graft, r-HuEPO therapy, higher hematocrit, lower albumin and higher fibrinogen levels were significantly associated with vascular access failure, whereas gender, diabetes mellitus, total cholesterol and platelet count were not. Plasma fibrinogen was inversely correlated with albumin (r=-0.38, P=0.001). The cumulative vascular access survival was significantly lower in patients with high plasma fibrinogen levels (> or = 460 mg/dl) compared with patients with low levels (< 460 mg/dl) (P=0.007). Independent risk factors for vascular access failure analysed by Cox's proportional hazards model were older age (RR; 1.36 by 10-year increment), higher fibrinogen level (RR; 1.20 by 100 mg/dl increment), PTFE graft (RR; 2.28) and r-HuEPO therapy (RR; 3.79). CONCLUSION: High plasma fibrinogen level is an independent risk factor for vascular access failure in haemodialysis patients.

Adult↗
PubMed1999

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↗
PubMed1999

Percutaneously implantable catheter-port system for chemotherapeutic infusion through the hepatic artery.

OBJECTIVE: The goal of this study was to determine the feasibility and outcomes of percutaneously implantable catheter-port system placement in the hepatic artery for the purpose of intraarterial chemotherapeutic infusion. CONCLUSION: Percutaneously implantable catheter-port system placement is safe and technically feasible for use in the hepatic artery. The implantation procedure is less invasive than surgical implantation of similar port systems.

Antineoplastic Agents↗
PubMed1999

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↗
PubMed1998

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↗
PubMed1998

Leukotriene D4-induced contraction of cat esophageal and lower esophageal sphincter circular smooth muscle.

BACKGROUND & AIMS: In esophageal circular muscle, acetylcholine activates phosphatidylcholine-specific phospholipases C and D and phospholipase A2, producing diacylglycerol and arachidonic acid, which cause contraction by interacting synergistically to activate protein kinase C. In a model of acute esophagitis, leukotriene D4 (LTD4) contributes to acetylcholine-induced contraction. We examined intracellular signaling in LTD4-induced contraction. METHODS: Esophageal and lower esophageal sphincter (LES) cells, isolated by enzymatic digestion, were contracted by LTD4 in the absence or presence of inhibitors. Permeabilization by saponin allowed use of G-protein antibodies and heparin. RESULTS: Esophageal contraction was inhibited by pertussis toxin, Gi3 antibodies, D609 (phosphatidylcholine-specific phospholipase C inhibitor), propranolol (phospholipase D pathway inhibitor), and chelerythrine (protein kinase C antagonist) but not W7 (calmodulin antagonist). LES contraction was unaffected by pertussis toxin. It was inhibited by Gq antibodies, U-73122 (phosphatidylinositol-specific phospholipase C inhibitor), heparin (inositol 1,4,5-trisphosphate inhibitor), and W7 and reduced by D609. CONCLUSIONS: In the esophagus, LTD4 activates a protein kinase C-dependent pathway through pertussis toxin-sensitive Gi3 proteins and phosphatidylcholine-specific phospholipase. In the LES, LTD4 activates a calmodulin-dependent pathway through pertussis toxin-insensitive Gq proteins and phosphatidylinositol-specific phospholipase C. The intracellular pathways activated by LTD4 in the esophagus and the LES are similar to those activated by acetylcholine and other agonists.

Animals↗