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Biomedical subjects

J S Song

Publications and source records attributed to J S Song.

At least 19 recordsLinked to original sources
PubMed2006

Oxidative stress during peritoneal dialysis: implications in functional and structural changes in the membrane.

Progressive peritoneal fibrosis, membrane hyperpermeability, and ultrafiltration failure have been observed in patients on long-term peritoneal dialysis (PD). The present study tested the hypothesis that reactive oxygen species (ROS) generated by conventional PD solution (PDS) mediate functional and structural alterations of peritoneal membrane in vivo. Sprague-Dawley rats were randomized to control, PDS, PDS with an antioxidant, and PDS with an angiotensin II (Ang II) receptor blocker. Commercial PDS containing 3.86% glucose (20-30 ml) with or without N-acetylcystein (NAC) 10 mM or losartan 5 mg/kg was administered intraperitoneally twice a day for 12 weeks. Control rats received sham injection. Rats treated with PDS had significantly lower drain volume and D(4)/D(0) glucose, but higher D(4)/P(4) creatinine and increased membrane thickness and endothelial NOS (eNOS) expression compared to control rats. Omental transforming growth factor (TGF)-beta1, vascular endothelial growth factor (VEGF), collagen I, and heat-shock protein (hsp) 47 expression and lipid peroxide levels and dialysate VEGF and Ang II concentrations were significantly increased in rats treated with PDS compared to control. All of these changes were prevented by both NAC and losartan. In conclusion, the present study demonstrates that ROS generated by conventional PDS are, in large part, responsible for peritoneal fibrosis and membrane hyperpermeability. We suggest that antioxidants or Ang II receptor blockers may allow better preservation of the structural and functional integrity of the peritoneal membrane during long-term PD.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2006

Diagnostic yield of advanced colorectal neoplasia at colonoscopy, according to indications: an investigation from the Korean Association for the Study of Intestinal Diseases (KASID).

BACKGROUND AND STUDY AIMS: The factors that more accurately predict the detection of colorectal cancers and adenomas at colonoscopy are different. We conducted a prospective multicenter study to evaluate which indications were most closely associated with advanced colorectal neoplasm (CRN), including colorectal cancer, in a group of patients undergoing colonoscopy. PATIENTS AND METHODS: The 17 468 patients were enrolled in this study between July 2003 and March 2004, from 11 tertiary medical centers in Korea. They were recruited according to 11 itemized colonoscopic indications. The term "advanced adenoma" refers here to tubular adenomas of diameter of 11 mm or more, or to tubulovillous, villous, or severely dysplastic adenomas, irrespective of their size. Cancer was defined as the invasion of malignant cells beyond the muscularis mucosa. Advanced CRN was defined as advanced adenoma or invasive cancer. RESULTS: Advanced CRN was found in 1227/17 307 patients (1176 advanced adenomas plus 51 carcinomas, 7.1 %). According to univariate and multivariate analysis, the factors associated with advanced CRN included age >60 years (odds ratio (OR) 2.1, 95 % confidence interval (CI) 1.8 - 2.4, P < 0.0001), male gender (OR 2.1, 95 %CI 1.7 - 2.7, P < 0.0001), referral for colonoscopy from primary care physician (OR 3.1, 95 %CI 2.5 - 3.7, P < 0.0001), and several other indications (OR 1.8, 95 %CI 1.5 - 2.3, P < 0.001). The yield of colonoscopy for advanced CRN was lower (2.2 %) than expected in patients with iron-deficiency anemia (OR 0.5, 95 %CI 0.2 - 0.9, P = 0.03). CONCLUSIONS: Age, gender, and referral for colonoscopy from primary care physician constituted important independent predictors of advanced CRN in patients undergoing colonoscopy.

Adenoma↗
PubMed2005

The inhibitory effects of roflumilast on lipopolysaccharide-induced nitric oxide production in RAW264.7 cells are mediated by heme oxygenase-1 and its product carbon monoxide.

OBJECTIVES: Heme oxygenase-1 (HO-1) is an enzyme that degrades heme into biliverdin, free iron, and carbon monoxide (CO). This enzyme is known to have cytoprotective and anti-inflammatory effects. In this study, we investigated whether roflumilast, a newly developed specific phosphodiesterase 4 (PDE4) inhibitor, mediates some of its anti-inflammatory effects by blocking nitric oxide (NO) and tumor necrosis factor alpha (TNF-alpha) via the induction of HO-1 expression in macrophages. METHODS: The expression of iNOS and HO-1 was analyzed by western blot analysis. The production of NO and TNF-alpha was assayed by Greiss and ELISA, respectively. RESULTS: Roflumilast markedly suppressed LPS-induced NO and TNF-alpha production and these phenomena were correlated with the induction of HO-1 protein levels. Moreover, the inhibitory effects of roflumilast on NO production were abrogated by a HO-1 inhibitor and a CO scavenger. Tricarbonyldichlrororuthenium(II) dimer, a CO releasing molecule significantly suppressed NO production. CONCLUSIONS: These results suggested that roflumilast exerts its anti-inflammatory effects in macrophages through a novel mechanism that involves the action of HO-1 and its product, CO.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed2005

Dissemination of transferable CTX-M-type extended-spectrum beta-lactamase-producing Escherichia coli in Korea.

AIMS: Among 365 Escherichia coli isolated in 2003, 31 cefotaxime-resistant isolates were obtained from clinical specimens taken from adults hospitalized in Busan, Korea. Six extended-spectrum beta-lactamase (ESBL)-producing isolates were investigated further to determine the mechanism of resistance. METHODS AND RESULTS: These isolates were analysed by antibiotic susceptibility testing, pI determination, plasmid profiles, transconjugation test, PCR-restriction fragment length polymorphism (RFLP), enterobacterial repetitive consensus (ERIC)-PCR and DNA sequencing. All six of these isolates were found to contain the CTX-M-type ESBL genes. Five clinical isolates and their transconjugants produced CTX-M-3. One clinical isolate (K17391) and its transconjugant (trcK17391) produced CTX-M-15. Five clinical isolates also produced another TEM-1. One clinical isolate (K12776) also contained another TEM-52. CTX-M-3 ESBL gene was responsible for the resistance to piperacillin, cephalothin, cefotaxime, cefepime and aztreonam. CTX-M-15 or TEM-52 was especially responsible for the resistance to ceftazidime. CONCLUSIONS: These results appear to represent the in vivo evolution of CTX-M-type beta-lactamase genes (bla(CTX-M-3) --> bla(CTX-M-15)) under the selective pressure of antimicrobial therapy (especially ceftazidime). PCR-RFLP is a reliable method to discriminate CTX-M-15 gene from CTX-M-3 gene. ERIC-PCR analysis revealed that dissemination of CTX-M-3 was not due to a clonal outbreak of a resistant strain but to the intra-species spread of resistance to piperacillin, cephalothin, cefotaxime, cefepime and aztreonam in Korea. SIGNIFICANCE AND IMPACT OF THE STUDY: This is the first report of the occurrence of CTX-M-1 cluster ESBLs in Korea. A more comprehensive survey of these ESBL types from Korea is urgently needed because of the in vivo evolution of CTX-M-15 from CTX-M-3. The emergence of these CTX-M-type ESBLs suggests that diagnostic laboratories should screen for ESBLs with ceftazidime as well as cefotaxime; they should still perform clavulanate synergy tests on resistant isolates.

Adult↗
PubMed2004

Investigation of extended-spectrum beta-lactamases produced by clinical isolates of Klebsiella pneumoniae and Escherichia coli in Korea.

AIMS: Isolates obtained from various regions in Korea in 2002 were identified and their susceptibility to extended-spectrum cephalosporins, monobactams and/or cephamycins was studied along with any production of extended-spectrum beta-lactamases (ESBLs). METHODS AND RESULTS: Bacteria identified by the conventional techniques and Vitek GNI card were Klebsiella pneumoniae and Escherichia coli. Using disk diffusion and double-disk synergy tests, we found that 39.2% of strains produced ESBLs. About 52% of isolates transferred resistance to ceftazidime by conjugation. Banding patterns of PCR amplification with the designed primers showed that 837- and 259-bp fragments specific to bla(TEM) genes were amplified in 63.3% of strains. 929- and 231-bp fragments (bla(SHV)), 847- and 520-bp fragments (bla(CMY)), 597- and 858-bp fragments (bla(CTX-M)) were amplified in 61.5, 17.3 and 7.7% of strains respectively. About 51.9% of strains contained more than two types of beta-lactamase genes. Especially, one strain contained bla(TEM), bla(CMY) and bla(CTX-M) genes. SIGNIFICANCE: Resistance mechanisms to beta-lactams, comprising mostly ESBL production, lead to the resistance against even recently developed beta-lactams in enterobacteria, which is now a serious threat to antibiotic therapy. The high prevalence of bla(CMY) genes and multidrug-resistant genes may also make therapeutic failure and lack of eradiation of these strains by extended-spectrum cephalosporins or cephamycins.

Anti-Bacterial Agents↗
PubMed2003

Inhibition of angiogenesis by antibody blocking the action of proangiogenic high-molecular-weight kininogen.

Previously we demonstrated that domain 5 (D5) of high-molecular-weight kininogen (HK) inhibits neovascularization in the chicken chorioallantoic membrane (CAM) assay and further found that kallikrein cleaved HK (HKa) inhibited FGF2-and VEGF-induced neovascularization, and thus was antiangiogenic. In this study, we sought to demonstrate whether uncleaved HK stimulates neovascularization and thus is proangiogenic. The chick chorioallantoic membrane was used as an in ovo assay of angiogenesis. Low-molecular-weight kininogen stimulates angiogenesis, indicating that D5 is not involved. Bradykinin stimulates neovascularization equally to HK and LK and is likely to be responsible for the effect of HK. A murine monoclonal antibody to HK (C11C1) also recognizes a similar component in chicken plasma as detected by surface plasmon resonance. Angiogenesis induced by FGF2 and VEGF is inhibited by this monoclonal antibody and is a more potent inhibitor of neovascularization induced by VEGF than an integrin alphavbeta3 antibody (LM 609). Our postulate that C11C1 inhibits the stimulation of angiogenesis by HK was confirmed when either C11C1 or D5 completely inhibited angiogenesis in the CAM induced by HK. Growth of human fibrosarcoma (HT-1080) on the CAM was inhibited by GST-D5 and C11C1. These results indicate HK is proangiogenic probably by releasing bradykinin and that a monoclonal antibody directed to HK could serve as an antiangiogenic agent with a potential for inhibiting tumor angiogenesis and other angiogenesis-mediated disorders.

Allantois↗
PubMed2002

Gamma-interferon and soluble interleukin 2 receptor in tuberculous pleural effusion.

To analysis the difference between systemic and local pleural T cell response in pulmonary tuberculosis, we analyzed interferon (IFN)-gamma and soluble interleukin-2 receptor (sIL-2R) in peripheral blood mononuclear cells (PBMC) culture supernatants and in pleural effusion (PE). We also investigated the association of pleural INF-gamma and sIL-2R levels with development of residual pleural thickening (RPT). The subjects in this study included patients with active pulmonary tuberculosis with or without PE (n = 46), those with nontuberculous PE (n = 32), and healthy tuberculin reactors (n = 20). Measurement of IFN-gamma and sIL-2R were made by ELISA. In pulmonary tuberculosis, IFN-gamma and sIL-2R concentrations in PBMC culture supernatants were lower than those of healthy tuberculin reactors (IFN-gamma; 258.4 +/-111.5 pg/mL versus 2792.5 +/-633.2 pg/mL, sIL-2R; 1465.0 +/-144.4 pg/mL versus 4777.1 +/-178.5 pg/mL, p < 0.05), whereas IFN-gamma and sIL-2R concentrations in PE were higher than those from nontuberculous pleural effusion (IFN-gamma; 1154.4 +/-252.4 pg/mL versus 292.0 +/-68.9 pg/mL, sIL-2R; 9805.2 +/-978.9 pg/mL versus 3426.7 +/-695.6 g/mL, p < 0.05). IFN-gamma and sIL-2R in PBMC culture supernatants were significantly lower in tuberculat patients with PE than those without PE, and the patients with a high value of IFN-gamma or sIL-2R in PE showed a low value of IFN-gamma or sIL-2R in PBMC culture supernatant, respectively. Patients with RPT had significantly higher IFN-gamma and sIL-2R values in their PE compared with those without RPT. These findings suggest that diminished systemic Th1 response in tuberculosis results from the accumulation of activated Th1 cell to the disease site, and that levels of IFN-gamma and sIL-2R in PE are useful posttreatment markers of RPT.

Adolescent↗
PubMed2002

Relation of airway reactivity and sensitivity with bronchial pathology in asthma.

Airway hyperresponsiveness in asthmatics, which may result from inflammation or remodeling, is expressed as the concentration of methacholine that causes a 20% fall in FEV1 in the concentration-response curve (PC20). A decrease in PC20 may be due to a steeper curve (hyperreactivity) and/or a curve shift to the left (hypersensitivity). Our purpose was to analyze the relation of airway sensitivity and reactivity to airway pathological changes. The PC6, as sensitivity parameter, and the slope between PC20 and PC40 as reactivity parameter, were calculated. Total and differential cell counts in the bronchoalveolar lavage fluid, and percentage of epithelial shedding, basement membrane thickness, and submucosal thickness on bronchial biopsy, were measured. The PC6 showed a correlation with the baseline FEV1%. The slope was significantly correlated with the basement membrane thickness, and also demonstrated a strong association with submucosal thickness. The PC20 showed a correlation with the baseline FEV1% and the degree of epithelial shedding. These results suggest that the airway sensitivity and reactivity measurements reflect the degree of airway caliber and remodeling, respectively.

Adolescent↗
PubMed2001

Observation of a (6)(LambdaLambda)He double hypernucleus.

A double-hyperfragment event has been found in a hybrid-emulsion experiment. It is identified uniquely as the sequential decay of ( 6)(LambdaLambda)He emitted from a Xi(-) hyperon nuclear capture at rest. The mass of ( 6)(LambdaLambda)He and the Lambda-Lambda interaction energy DeltaB(LambdaLambda) have been measured for the first time devoid of the ambiguities due to the possibilities of excited states. The value of DeltaB(LambdaLambda) is 1.01+/-0.20(+0.18)(-0.11) MeV. This demonstrates that the Lambda-Lambda interaction is weakly attractive.

Journal Article↗
PubMed2001

Lead treatment in vitro at early developmental stage of bone marrow-derived macrophages enhances NO production through IL-1beta and IL-6 but not TNF-alpha.

Lead (Pb(2+)) is known to decrease or block nitric oxide (NO) production by mature macrophages (mphi). Bone marrow cells were treated with various doses of lead in vitro and the morphological and functional changes were observed. Bone marrow cells were treated with various doses of lead (1, 10, 20 and 50 microM) at the start of culture with mphi growth factor (CSF-1), and after 6-7 days of culture, the resultant mphi (bone marrow-derived mphi, BMDM) showed decreased NO production. Unexpectedly, BMDM from the lowest does of lead treatment (1.0 microM) showed increased NO production. The increased NO production was due to increased expression of the iNOS gene and concurrent enhanced transcript levels of proinflammatory cytokines such as IL-1beta and IL-6, but not TNF-alpha. Lead treatment on mature BMDM showed decreased NO production in a dose-dependent manner. These results suggest that a low dose of lead affects developmental characteristics of BMDM through different proinflammatory cytokines, and the lead effects on precursor cells of mphi and mature mphi are different.

Animals↗
PubMed2001

The usefulness of serum transferrin receptor and ferritin for assessing anemia in rheumatoid arthritis: comparison with bone marrow iron study.

OBJECTIVES: This study was aimed at investigating the usefulness of serum transferrin receptor (sTfR) and ferritin in anemic patients with rheumatoid arthritis (RA) compared with bone marrow storage iron and other tests for anemia. METHODS: Fifty-five anemic RA patients underwent anemia study. Bone marrow iron stain was performed in 18 patients. sTfR and serum ferritin levels were compared with bone marrow iron stores. RESULTS: (1) Mean sTfR concentration was 2.63+/-1.91 mg/L, (2) sTfR correlated with most indicators of anemia, (3) sTfR showed no correlation with CRP and ESR, whereas ferritin did, and (4) sTfR was higher in the "iron depleted" subgroup than in the "iron nondepleted" subgroup in bone marrow study. CONCLUSION: The measurement of sTfR and ferritin is useful in finding the cause of anemia in RA and is a possible substitute for invasive bone marrow iron study.

Anemia, Iron-Deficiency↗
PubMed2001

Distribution and cytokine production of CD4 and CD8 T-lymphocyte subsets in patients with acute asthma attacks.

BACKGROUND: The activation of T cells and the elevation of Th2-type cytokines have been observed in asthmatic patients, but the relative role of CD4 and CD8 T cell is still unclear. OBJECTIVE: To investigate the role of T cell subset in patients with acute asthma attacks, we analyzed the distribution, activation status, and cytokine production of CD4 and CD8 cells. METHODS: The percentages of the CD4 and CD8 cell in peripheral blood (PB) and bronchoalveolar lavage (BAL) fluid were analyzed by flow cytometry. The cytokines (IL-4, IL-5, and IFN-gamma) and soluble IL-2 receptor (sIL-2R) were measured by ELISA in culture supernatants of CD4 and CD8 cells purified from PB. RESULTS: The CD4/CD8 ratio in PB of asthmatic patients was significantly higher than that of controls, which was significantly reduced after treatment. In contrast, there was a tendency to high percentage of CD8 cells in asthmatic patients as compared with controls in BAL, which resulted in a decreased CD4/CD8 ratio. Comparing the T cell subsets in BAL with paired PB in asthma, the CD4 cells were higher in PB, but CD8 cells were higher in BAL. The IL-4, IL-5, and sIL-2R produced by CD4 cells were significantly higher than those produced by CD8 cells in asthmatic patients. CONCLUSIONS: Our results provide evidence that activated CD4 T cells increase and produce type 2 cytokines in PB, but CD8 T cell are more sequestrated than CD4 T cells in the airway during an acute asthma attack.

Acute Disease↗
PubMed2001

Clinical effects of pranlukast, an oral leukotriene receptor antagonist, in mild-to-moderate asthma: a 4 week randomized multicentre controlled trial.

OBJECTIVE: Leukotriene antagonists are increasingly used in asthma management. Pranlukast is a new, orally active, selective inhibitor of CysLt1 leukotriene receptor. The present clinical trial was performed to study the effect and safety of pranlukast in mild-to-moderate asthma. METHODOLOGY: A randomized, double-blind, placebo-controlled, parallel group study was performed in eight medical centres in Korea. Mild-to-moderate asthma patients who had been treated with beta2-agonists and/or inhaled corticosteroids were studied. The patients' symptoms were evaluated by asthma diary and twice-daily peak flow monitoring. RESULTS: Of the 206 patients enrolled, 197 were eligible for analysis. The pranlukast group (n = 98) showed statistically significant improvement in asthma symptoms, including asthma attack rate, daily living score, and morning and evening asthma scores. Pranlukast significantly reduced the consumption of beta2-agonist. Compared with the placebo group, forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV1) were not significantly higher in the pranlukast group. Morning and evening peak expiratory flow (PEF) were significantly increased after pranlukast treatment at weeks 2 and 4 (380.8 +/- 10.1 L/min at baseline, 394.5 +/- 10.1 at week 2, 396.3 +/- 10.4 at week 4). There were no serious adverse reactions. CONCLUSION: Pranlukast, an oral leukotriene antagonist, was well tolerated and was effective for the management of mild-to-moderate asthma.

Adrenergic beta-Agonists↗
PubMed2001

Occupational asthma due to formaldehyde.

Formaldehyde is a low molecular weight chemical and can elicit acute and chronic health related problems. Most of the inhaled formaldehyde is retained in the upper respiratory tract due to its extraordinary solubility. Therefore, cases of formaldehyde-induced occupational asthma are sporadic despite its widespread use in industrial processes. We herein report upon a case of occupational asthma due to formaldehyde, which was confirmed by workplace challenge including working environmental assessments, and by formaldehyde inhalation challenge using a specially designed closed-circuit apparatus. To investigate the possible involvement of an IgE-mediated mechanism, both in vitro and in vivo tests were done. IgE antibody specific for formaldehyde-human serum albumin conjugate (F-HSA) was not detected by ELISA, and no specific cutaneous reactivity to F-HSA was noted by either skin prick or intradermal test. The patient was diagnosed with formaldehyde-induced occupational asthma not associated with an IgE mediated mechanism.

Adult↗
PubMed2001

A case of hypothermia combined with systemic lupus erythematosus.

Systemic lupus erythematosus(SLE) is a prototypic autoimmune disease affecting various organ systems. Hypothermia is a rare manifestation of SLE. We experienced a case of SLE combined with hypothermia. A 36-year-old woman, who had been diagnosed as SLE 3 days before admission, admitted complaining of mental confusion. After admission, her body temperature, initially 36.1 degrees C, became 32.6 degrees C. Her core body temperature was less than 35.0 degrees C. Despite of warming with heating lamp and blankets, her core temperature did not reach 35.0 degrees C during 18 hours. Ten days later, her temperature exceeded 36.0 degrees C.

Adrenal Cortex Hormones↗
PubMed2001

Mucin secretion in the rat tracheal epithelial cells by epidermal growth factor and Pseudomonas aeruginosa extracts.

BACKGROUND: Hypersecretion of mucin due to goblet cell hyperplasia is frequently encountered in many chronic airway diseases, such as chronic bronchitis, bronchiectasis, bronchial asthma and cystic fibrosis. Even in normal individuals, viral infection or bacterial pneumonia frequently provoke huge amounts of bronchial secretions which may cause airway obstruction. The production of mucin was regulated by epidermal growth factor (EGF) in vitro. To know whether this EGF system regulates mucin secretion in vivo and Pseudomonas also stimulates the mucin secretion by the same pathway, we studied these relationships in the cultured rat tracheal epithelial cells. METHODS: Rat tracheal epithelial cells were obtained by pronase dissociation from the male Fisher 344 rats. When cells became confluent, they were divided into 6 groups and stimulated with either EGF for 24 hours or Pseudomonas extracts for 12 hours with or without selective EGF-R tyrosine kinase inhibitor tyrphostin AG1478. RESULTS: We found that both EGF and Pseudomonas extracts phosphorylated the tyrosine residue in the EGF receptor from the rat tracheal epithelial cells and this tyrosine phosphorylation was nearly completely blocked by selective EGF-R tyrosine kinase inhibitor tyrphostin AG1478. The mucin secretion was also stimulated by either EGF or Pseudomonas extracts but more strong secretion of mucin and MUC5AC gene expression in the rat tracheal epithelial cell was done by Pseudomonas extracts. CONCLUSION: These data suggest that Pseudomonas secretes the mucin by way of the EGF receptor and MUC5AC gene expression and the inhibitors of EGF receptor tyrosine phosphorylation would be useful to prevent the huge production of mucin due to Pseudomonas aeruginosa lung infection.

Animals↗
PubMed2000

The Src homology 2 domain of Vav is required for its compartmentation to the plasma membrane and activation of c-Jun NH(2)-terminal kinase 1.

Vav is a hematopoietic cell-specific guanine nucleotide exchange factor (GEF) whose activation is mediated by receptor engagement. The relationship of Vav localization to its function is presently unclear. We found that Vav redistributes to the plasma membrane in response to Fcin receptor I (FcinRI) engagement. The redistribution of Vav was mediated by its Src homology 2 (SH2) domain and required Syk activity. The FcinRI and Vav were found to colocalize and were recruited to glycosphingolipid-enriched microdomains (GEMs). The scaffold protein, linker for activation of T cells (LAT), and Rac1 (a target of Vav activity) were constitutively present in GEMs. Expression of an SH2 domain-containing COOH-terminal fragment of Vav inhibited Vav phosphorylation and movement to the GEMs but had no effect on the tyrosine phosphorylation of the adaptor protein, SLP-76 (SH2 domain-containing leukocyte protein of 76 kD), and LAT. However, assembly of the multiprotein complex containing these proteins was inhibited. In addition, FcinRI-dependent activation of c-Jun NH(2)-terminal kinase 1 (JNK1) was also inhibited. Thus, Vav localization to the plasma membrane is mediated by its SH2 domain and may serve to regulate downstream effectors like JNK1.

Adaptor Proteins, Signal Transducing↗