Biomedical subjects

Jong Dae Ji

Publications and source records attributed to Jong Dae Ji.

At least 19 recordsLinked to original sources

PubMed2007

The association between hyperuricemia and the Trp64Arg polymorphism of the beta-3 adrenergic receptor.

The object of this study was to determine the association of Trp64Arg polymorphism with hyperuricemia. This study is an age-matched, case-controlled study of 203 hyperuricemic and 203 normouricemic men. The frequency of genotypes was compared between the two groups. Possible confounding metabolic variables were included in a multiple logistic regression model for multivariate adjustment. The genotype frequencies of Trp64Trp, Trp64Arg, and Arg64Arg in hyperuricemic and normouricemic groups are respectively 130, 69, and 4 (64.0%, 34.0%, 2.0%) and 154, 45, and 4 (75.9%, 22.2%, 2.0%) (P = 0.029, Chi-square test). Simple logistic regression analysis indicated that the Trp64Arg genotype is significantly associated with hyperuricemia (OR = 1.816, 95% CI (1.167-2.827), P = 0.008). Multivariate analysis for controlling metabolic effects also showed a significant association with the occurrence of hyperuricemia (OR = 1.937, 95% CI (1.149-3.266), P = 0.013). Trp64Arg polymorphism of the beta-3 adrenergic receptor may be independently associated with hyperuricemia in males.

Adult↗

PubMed2007

Adjusted indirect comparison of celecoxib versus rofecoxib on cardiovascular risk.

To compare the magnitude of celecoxib versus rofecoxib on the cardiovascular risk. We performed adjusted indirect comparison of celecoxib versus rofecoxib for cardiovascular events using two data on The Adenomatous Polyp Prevention on Vioxx (APPROVe) trial and Adenoma Prevention with Celecoxib (APC) trial. Baseline characteristics of the patients and placebos were comparable in both trials, in terms of age, sex, hypertension, diabetes mellitus, smoking, and hypercholesterolemia. The overall incidence of cardiovascular events was similar in both groups (rofecoxib 48/1,287 versus celecoxib 48/1,356, p = 0.79). The relative risks (RRs) of all myocardial infarction or sudden death from cardiac causes were increased in both rofecoxib and celecoxib groups [rofecoxib versus placebo; RR 1.35, 95% confidence interval (CI) 1.07-1.69, p = 0.03, celecoxib versus placebo; RR 1.35, 95% CI 1.14-1.51, p = 0.01]. The RRs for cardiovascular events derived from the adjusted indirect comparisons of the two coxibs did not significantly differ from unity (celecoxib versus rofecoxib; RR 0.95, 95% CI 0.76-1.19, p = 0.67). The adjusted indirect comparison analysis shows that celecoxib and rofecoxib may have similarly effect of cardiovascular events when used for 3 years.

Adenoma↗

PubMed2006

Tumor necrosis factor-alpha promoter -308 A/G polymorphism and rheumatoid arthritis susceptibility: a metaanalysis.

OBJECTIVE: Tumor necrosis factor-alpha (TNF-alpha) promoter -308 A/G polymorphism has been reported to be associated with rheumatoid arthritis (RA) with inconsistent results. We investigated whether TNF-alpha -308 A/G polymorphism confers susceptibility to RA. METHODS: We conducted a random effect metaanalysis on the association of genotypes A/A (recessive effect), A/A + A/G (dominant effect), A allele, and A/A vs G/G genotypes of the TNF-alpha -308 polymorphisms with RA overall and within different ethnic populations. RESULTS: Fourteen studies, 10 of Europeans, 3 of Latin Americans, and one Asian, were included in this metaanalysis. An association between RA and the TNF-alpha -308 A allele was not found in the overall population (OR 1.005, 95% CI 0.715-1.412, p = 0.976). However, stratification by ethnicity indicated that the TNF-alpha A allele was significantly associated with RA in Latin Americans (OR 2.004, 95% CI 1.158-3.467, p = 0.013). Conversely, there was no association detected for the TNF-alpha A allele with RA patients from the European samples (OR 0.911, 95% CI 0.684-1.212, p = 0.520). The OR for the A/A + A/G genotype, the A/A genotypes, and the A/A vs G/G genotypes in samples overall and in each ethnic group showed a similar trend to those for the TNF-alpha A allele. CONCLUSION: This metaanalysis demonstrates that the TNF-alpha -308 A/G polymorphism may represent a significant risk factor for RA in Latin Americans, but not in Europeans.

Alleles↗

PubMed2006

Osteoarthritis susceptibility loci defined by genome scan meta-analysis.

Genome scans for osteoarthritis (OA) have yielded inconsistent results. The absence of replication of linkage might be due to lack of power of individual studies. A meta-analysis of the published data was performed to assess evidence for linkage of OA across genome scan studies. Three OA whole-genome scans including 893 families with 3,000 affected individuals were used for genome scan meta-analysis (GSMA). A total of 5 bins lie above 95% confidence level (P = 0.05) and 1 bin is above 99% confidence level (P = 0.01) in OA GSMA; bins 7.6 (7q34-7q36.3, Psumrnk = 0.0035), 11.3 (11p12-11q13.4), 6.3 (6p21.1-6q15), 2.8 (2q31.1-2q34) and 15.3 (15q21.3-15q26.1). The highest summed rank was observed at bin 7.6. In conclusion, the OA GSMA has shown chromosome 7q34-7q36.3 with the highest summed rank and four additional loci with significant summed ranks across studies.

Chromosomes, Human, Pair 7↗

PubMed2006

Association of TNF-alpha -308 G/A polymorphism with responsiveness to TNF-alpha-blockers in rheumatoid arthritis: a meta-analysis.

Tumor necrosis factor (TNF) antagonists are among the most effective therapies for rheumatoid arthritis (RA), yet not all patients show a response. Using meta-analysis, this present study was designed to investigate whether or not the TNF-alpha promoter -308 A/G polymorphism is associated with responsiveness to anti-TNF therapy in RA patients. We performed an exhaustive search for studies that examined the association of the TNF-alpha promoter -308 A/G polymorphism and responsiveness of anti-TNF therapy in RA using MEDLINE citations and manual review. Meta-analysis was performed for A allele carrier (genotypes A/A + A/G) between responders to anti-TNF therapy and a non-responder group in a random effects model. A total of 6 studies met the inclusion criteria. The number of patients in individual studies ranged from 33 to 123. There were 311 RA patients who were included in this meta-analysis. There was no heterogeneity between studies (I (2) = 0%, P = 0.42). The overall OR for the A allele carrier status was significantly decreased in the responder group (OR = 0.33, 95% confidence interval = 0.17-0.63, P = 0.0008). The frequency of the A allele carrier was 53/240 (22.1%) in responders and 32/71 (45.1%) in non-responders. Patients not responding to anti-TNF therapy showed an increased frequency of the A allele. The meta-analysis of the available data shows a significant association between the TNF-alpha promoter -308 A/G polymorphism and responsiveness to anti-TNF therapy, suggesting that the individuals with RA who carry the A allele have a poorer response to anti-TNF therapy than those with the G allele.

Antirheumatic Agents↗

PubMed2006

Prostaglandin E2 augments IL-10 signaling and function.

In inflamed joints of rheumatoid arthritis, PGE(2) is highly expressed, and IL-10 and IL-6 are also abundant. PGE(2) is a well-known activator of the cAMP signaling pathway, and there is functional cross-talk between cAMP signaling and the Jak-STAT signaling pathway. In this study, we evaluated the modulating effect of PGE(2) on STAT signaling and its biological function induced by IL-10 and IL-6, and elucidated its mechanism in THP-1 cells. STAT phosphorylation was determined by Western blot, and gene expression was analyzed using real-time PCR. Pretreatment with PGE(2) significantly augmented IL-10-induced STAT3 and STAT1 phosphorylation, as well as suppressors of cytokine signaling 3 (SOCS3) and IL-1R antagonist gene expression. In contrast, PGE(2) suppressed IL-6-induced phosphorylation of STAT3 and STAT1. These PGE(2)-induced modulating effects were largely reversed by actinomycin D. Pretreatment with dibutyryl cAMP augmented IL-10-induced, but did not change IL-6-induced STAT3 phosphorylation. Misoprostol, an EP2/3/4 agonist, and butaprost, an EP2 agonist, augmented IL-10-induced STAT3 phosphorylation and SOCS3 gene expression, but sulprostone, an EP1/3 agonist, had no effect. H89, a protein kinase A inhibitor, and LY294002, a PI3K inhibitor, diminished PGE(2)-mediated augmentation of IL-10-induced STAT3 phosphorylation. In this study, we found that PGE(2) selectively regulates cytokine signaling via increased intracellular cAMP levels and de novo gene expression, and these modulating effects may be mediated through EP2 or EP4 receptors. PGE(2) may modulate immune responses by alteration of cytokine signaling in THP-1 cells.

Adjuvants, Immunologic↗

PubMed2006

Osteoarthritis susceptibility loci defined by genome scan meta-analysis.

Genome scans for osteoarthritis (OA) have yielded inconsistent results. The absence of replication of linkage might be due to the lack of power of individual studies. A meta-analysis of published data was performed to assess evidence for linkage of OA across genome scan studies. Three OA whole-genome scans including 893 families with 3,000 affected individuals were used for genome scan meta-analysis (GSMA). A total of five bins lie above 95% confidence level (P=0.05) and one bin is above 99% confidence level (P=0.01) in OA GSMA; bins 7.6 (7q34-7q36.3, P (sumrnk) =0.0035), 11.3 (11p12-11q13.4), 6.3 (6p21.1-6q15), 2.8 (2q31.1-2q34) and 15.3 (15q21.3-15q26.1). The highest summed bin was bins 7.6. In conclusion, the OA GSMA has shown that chromosome 7q34-7q36.3 have the highest summed rank and four additional loci with significant summed ranks across studies.

Chromosomes, Human, Pair 7↗

PubMed2006

Meta-analysis of genome-wide linkage studies for bone mineral density.

Genome-wide linkage studies have shown several chromosome loci that may harbor genes that regulate bone mineral density (BMD), but results have been inconsistent. A meta-analysis was performed to assess evidence for linkage of BMD across whole genome scan studies. Eleven whole-genome scans of BMD or osteoporosis containing 3,097 families with 12,685 individuals were included in this genome scan meta-analysis (GSMA). For each study, 120 genomic bins of approximately 30 cM were defined and ranked according to maximum evidence for linkage within each bin. Bin ranks were weighted and summed across all studies. The summed rank for each bin was assessed empirically for significance using permutation methods. A total of seven bins lie above the 95% confidence level (P=0.05) and one bin was above the 99% confidence level (P=0.01) in the GSMA of eleven linkage studies: bins 16.1 (16pter-16p12.3, Psumrnk <0.01), 3.3 (3p22.2-3p14.1), 1.1 (1pter-1p36.22), 18.2 (18p11.23-18q12.2), 6.3 (6p21.1-6q15), 20.1 (20pter-20p12.3), and 18.1 (18pter-18p11.23). GSMA was performed with seven studies with linkage scores of LOD >1-1.85 for sensitivity test, confirming the linkage on chromosome 16p and 3p and revealing evidence of new linkage in bins 10.2 (10p14-10q11.21) and 22.2 (22q12.3-22pter). In conclusion, the meta-analysis of whole-genome linkage studies of BMD has shown chromosome 16pter-16p12.3 to have the greatest evidence of linkage as well as revealing evidence of linkage in chromosomes 1p, 3p, 6, 10, 18, 20p, and 22q across studies. This data may provide a basis with which to carry out targeted linkage and candidate gene studies particularly in these regions.

Bone Density↗

PubMed2006

Angiotensin-converting enzyme insertion/deletion polymorphism and systemic lupus erythematosus: a metaanalysis.

OBJECTIVE: To explore whether insertion (I) and deletion (D) polymorphisms within intron 16 of the angiotensin-converting enzyme (ACE) gene confer susceptibility to systemic lupus erythematosus (SLE) and lupus nephritis (LN). METHODS: We surveyed studies of ACE I/D polymorphism and SLE using Medline and manual searches. We conducted a metaanalysis of the DD genotype (recessive effect), DD and DI genotype (dominant effect), and D allele of the ACE overall and in each ethnic population. We performed a metaanalysis of ACE I/D polymorphism in SLE and LN. RESULTS: Thirteen comparison studies were included in our metaanalysis consisting of 1411 patients with SLE and 1551 controls. We found no association of ACE I/D polymorphism with SLE in the total sample and by ethnic groups. There was a trend for association of the DD genotype (OR 1.212, 95% CI 0.966-1.520, p = 0.097) and the D allele with SLE in Caucasian patients (OR 1.157, 95% CI 0.991-1.349, p = 0.064); however, this was not statistically significant. The metaanalysis also showed no association of the ACE I/D polymorphisms with LN. CONCLUSION: This metaanalysis of 2962 subjects showed there is a lack of association of the ACE I/D polymorphism with SLE and LN.

Adult↗

PubMed2005

Ankylosing spondylitis susceptibility loci defined by genome-search meta-analysis.

In genome scans of ankylosing spondylitis (AS), with the exception of the HLA loci, linkage has not been easy to replicate across studies. We applied the genome-search meta-analysis (GSMA) method to genome scans of AS and spondyloarthropathy (SpA) to assess evidence for linkage across studies. Three AS genome scans and one SpA scan including 430 families with 1,048 affected individuals were used. All four original genome scans mainly analyzed Caucasian families. Seven bins had both Psumrnk and Pord<0.05, suggesting these bins most likely contain AS-linked loci; bin 6.2, 6.1, 6.3, 16.3, 19.2, 17.1, and 16.4. The GSMA produced significant genome-wide evidence for linkage on chromosome 6p22.3-6p21.1 (Psumrnk=0.000003), including the HLA locus. In addition to the HLA-B27 locus, strong linkage evidence was found on chromosome 6p25.3-6p22.3 (Psumrnk=0.0013) and 6p21.1-6p15 (Psumrnk=0.043). In the GSMA of four genome scans including one SpA study, the bin 9.4 (9q21.32-9q33.1) was newly found for linkage (Psumrnk=0.043, Pord=0.013). This GSMA added the evidence of the HLA loci as the greatest susceptibility factor to AS and showed evidences of chromosome 6, 16q, 19, 17p, and 9q as non-HLA susceptibility loci.

Chromosomes, Human, Pair 6↗

PubMed2005

Scleroderma associated with ANCA-associated vasculitis.

We have recently reported on two cases of scleroderma patients with ANCA-associated vasculitis for the first time in Korea. In order to explore the nature of this disease combination, we pooled together all the previously known cases and statistically analyzed them. Out of the 50 selected cases, survival analysis was done for comparison of the scleroderma disease period and the clinical factors associated with ANCA-associated vasculitis (AAV). Kaplan-Meier analysis revealed that patients having anti-topoisomerase antibody (anti-Scl-70) and, probably, PR-3 ANCA are at a higher risk for developing AAV than patients without both anti-topoisomerase antibody and anti-centromere antibody (ACA), and patients with MPO-ANCA. Multivariate Cox regression analysis revealed having anti-topoisomerase antibody as a risk factor for developing AAV [OR 3.1 (95% CI 1.11-8.55), P=0.031]. We suggest that having anti-topoisomerase antibodies may play a role among scleroderma patients in developing AAV.

Adult↗

PubMed2005

Scleroderma associated with ANCA-associated vasculitis.

Scleroderma and ANCA-associated vasculitides (AAV), such as microscopic polyangiitis, are distinct disease entities, but are rarely known to coexist with each other. We have reported on two cases of scleroderma patients for the first time in Korea, and these patients were initially known to have only limited type scleroderma with pulmonary fibrosis, but eventually they were found to be ANCA-positive with the associated clinical features of vasculitis. Both were treated with high-dose steroids and cyclophosphamide and remitted without major sequelae. When scleroderma patients exhibit atypical features such as normotensive renal failure with signs of active inflammation, the possibility of AAV should always be considered.

Antibodies, Antineutrophil Cytoplasmic↗

PubMed2005

15-Deoxy-delta12,14-PGJ2 inhibits IL-6-induced Stat3 phosphorylation in lymphocytes.

15-deoxy-delta(12,14)-PGJ(2)(15d-PGJ(2)) is a natural ligand that activates the peroxisome proliferators-activated receptor (PPAR) gamma, a member of nuclear receptor family implicated in regulation of lipid metabolism and adipocyte differentiation. Recent studies have shown that 15d-PGJ(2) is the potent anti-inflammatory agent functioning via PPARgamma-dependent and -independent mechanisms. Most postulated mechanisms for anti-inflammatory action of PPARgamma agonists are involved in inhibiting NF-kappaB signaling pathway. We examined the possibility that IL-6 signaling via the Jak-Stat pathway is modulated by 15d-PGJ(2) in lymphocytes and also examined whether the inhibition of IL-6 signaling is dependent of PPARgamma. 15d-PGJ(2) blocked IL-6 induced Stat1 and Stat3 activation in primary human lymphocytes, Jurkat cells and immortalized rheumatoid arthritis B cells. Inhibition of IL-6 signaling was induced rapidly within 15 min after treatment of 15d-PGJ(2). Other PPARgamma-agonists, such as troglitazone and ciglitazone, did not inhibit IL-6 signaling, indicating that 15d-PGJ(2) affect the IL-6-induced Jak-Stat signaling pathway via PPARgamma-independent mechanism. Although cycloheximide reversed 15d-PGJ(2)-mediated inhibition of Stat3 activation, actinomycin D had no effect on 15d-PGJ(2)-mediated inhibition of IL-6 signaling, indicating that inhibition of IL-6 signaling occur independent of de novo gene expression. These results show that 15d-PGJ(2) specifically inhibit Jak-Stat signaling pathway in lymphocytes, and suggest that 15d-PGJ(2) may regulate inflammatory reactions through the modulation of different signaling pathway other than NF-kappaB in lymphocytes.

Arthritis, Rheumatoid↗

PubMed2005

The prevalence of metabolic syndrome in patients with gout: a multicenter study.

It has been suggested that hyperuricemia and possibly gout are associated with the metabolic syndrome, but there have been no direct studies. This study was undertaken to obtain the prevalence of the metabolic syndrome in patients with gout and to compare it with those from the general population studies. This was a 4-institutional case-historical control study composed of 168 patients with gout. We assessed the prevalence of metabolic syndrome according to the ATP III criteria and compared the prevalence with that of the historical controls. To elucidate the factors in gout that were associated with metabolic syndrome, a multivariate analysis was done. The age-adjusted prevalence of metabolic syndrome in gout patients was 43.6%, which was significantly higher than that of the Korean control population (5.2%) from the previous studies. Patients with gout had more components of metabolic syndrome than did the controls. Body mass index (BMI, OR = 1.357 (95%CI 1.111-1.657)) and high density lipoprotein (HDL, OR = 0.774 (95%CI 0.705-0.850)) were the variables most significantly associated with the occurrence of metabolic syndrome in gout, but alcohol consumption did not show such associations. Gout is associated with the metabolic syndrome, and furthermore, obesity and dyslipidemia were the factors most associated with the syndrome in these patients.

Adult↗

PubMed2005

Relapsing polychondritis with aortitis without valvular involvement.

Relapsing polychondritis is a multisystemic disease of unknown etiology that mainly involves the cartilaginous portions of the ear, nose, and trachea. Occasionally, there is involvement of the cardiovascular system, which usually results in severe morbidity and mortality. The most common manifestation of cardiovascular involvement is aortic root dilation resulting in aortic regurgitation. We describe the first case in Korea, a 51-year-old woman with relapsing polychondritis with aortitis, but without aortic valve involvement. She presented only with complaints of abdominal pain, and was successfully treated with corticosteroids and methotrexate.

Abdominal Pain↗

PubMed2004

Interleukin-1 receptor antagonist gene polymorphism and rheumatoid arthritis.

The aim of this study was to evaluate the association of polymorphism in IL-1 receptor antagonist (IL-1RA) gene intron 2 with susceptibility to rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) and their clinical features. Polymerase chain reaction of a genomic DNA was used to determine genotypes of the IL-1RA in 138 RA, 93 SLE, and 127 healthy control subjects. The frequency of IL-1RA allele 2 (IL-1RN*2) was lower in RA patients (2.5%) than in control subjects (7.1%) (odds ratio 0.34, 95% confidence interval 0.13-0.88, P=0.02). There was a significant difference in genotype and allele distribution between RA patients and controls. However, it did not differ between SLE patients and controls. In SLE and RA patients, there was no significant difference in clinical and laboratory findings concerning IL-1RA polymorphisms. In conclusion, our data suggest that IL-1RA gene polymorphism is not responsible for specific clinical characteristics in RA and SLE but that IL-1RN*2 is relevant in the susceptibility to RA, suggesting a protective role of IL-1RN*2 in the pathogenesis of RA.

Adolescent↗

PubMed2003

The biallelic variable number of tandem repeats of the tumor necrosis factor receptor 2 promoter in systemic lupus erythematosus.

The objective of this study was to investigate whether the variable number of tandem repeats (VNTR) of the tumor necrosis factor receptor 2 (TNFR2) promoter is associated with susceptibility to systemic lupus erythematosus (SLE) and its clinical phenotypes. A biallelic VNTR within a 42-bp region in the TNFR2 gene promoter was determined by polymerase chain reaction in 88 SLE patients and 95 healthy control subjects. Clinical manifestations were analyzed in each patient and correlated with the genotypes. When the TNFR2 promoter VNTR was compared between Korean and Caucasian healthy controls with respect to allele frequencies, there was a significant difference (alleles 1 and 2: 39, 151 in Koreans vs 60, 138 in Caucasians, respectively; chi-squared test 4.38; 2 df; P=0.036). The genotype distribution of the TNFR2 promoter VNTR did not differ between SLE patients and control subjects (1.1, 1.2, and 2.2 genotypes 7, 14, 67 vs 5, 29, and 61 controls, respectively; chi-squared test 5.19; 2 df; P=0.061). According to the TNFR2 promoter genotypes in the lupus patients, clinically there was no significant difference in age at onset, anti-dsDNA titer, C4 level, systemic lupus erythematosus disease activity index (SLEDAI), Systemic Lupus International Collaborating Clinics/American College of Rheumatology (SLICC/ACR) damage index, or autoantibodies. However, the 1.1 genotype group showed the lowest C3 level and more frequent renal involvement than the 1.2 and 2.2 genotype groups. In conclusion, an ethnic difference in the TNFR2 promoter VNTR has been found and the biallelic VNTR of the TNFR2 promoter may be associated with clinical phenotypes in SLE.

Adolescent↗

PubMed2002

Predictors of bone mineral density and osteoporosis in patients attending a rheumatology outpatient clinic.

The aim of this study was to evaluate determinants of bone mineral density (BMD) and osteoporosis in patients attending our rheumatology outpatient clinic. A cross-sectional analysis of 320 patients with rheumatism (248 noninflammatory and 72 inflammatory arthropathies) was done. Bone mineral density was measured in the lumbar spine (posteroanterior and lateral views) using dual-energy X-ray absorptiometry. Single and multiple analyses were used to assess associations between BMD and potential risk factors including age, height, weight, body mass index (BMI), alkaline phosphatase (ALP), calcium (Ca), phosphorous (P), magnesium (Mg), spot urine calcium/creatinine (Ca/Cr) ratio, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), total cumulative dose and mean daily dosage of prednisolone, and duration of therapy. In these patients, there were significant correlations between BMD and age (r = -0.372, P = 0.000), height (r = 0.308, P = 0.000), weight (r = 0.145, P = 0.011), and ALP (r = -0.262, P = 0.000). By multiple regression analysis, age and ALP were found to be significant predictors of BMD (r(2) = 0.253, P < 0.01). Two hundred eighty-three of the patients had osteoporosis. Multiple logistic regression analysis showed that age and ALP were significant determinants for osteoporosis. These observations suggest that age and ALP were the major determinants of BMD and osteoporosis in these patients, suggesting a contribution of increased bone metabolism to loss of bone in cases of rheumatism.

Aged↗