Jun-Ki Min

Bio: Jun-Ki Min is an academic researcher from Catholic University of Korea. The author has contributed to research in topics: Arthritis & T cell. The author has an hindex of 36, co-authored 111 publications receiving 3079 citations. Previous affiliations of Jun-Ki Min include The Catholic University of America.

Vascular endothelial growth factor levels in the serum and synovial fluid of patients with rheumatoid arthritis.

Abstract: Objective To determine the vascular endothelial growth factor (VEGF) concentr ations in serum and synovial fluid (SF) from patients with rheumatoid arthritis (RA) and to search for relationships between VEGF levels and clinical and labor ato ry variables. Methods We measured VEGF levels using an e n z y m e - l i n ked immunosorbent assay. Serum samples were obtained from 99 RA pat i e n t s , 49 osteoart h ritis (OA ) p at i e n t s , and 80 normal contro l s . Paired samples of serum and SF wer e collected from 32 patients with RA and 15 with OA. Results The mean serum VEGF concentr ation was 590.1 pg/ml for RA patients,286.7 pg/ml for OA patients,and 265.8 pg/ml in controls. The serum VEGF concentration was significantly higher in the RA patients than in the OA patients or the controls (both p< 0.001). Further more, the VEGF levels in SF from RA patients were significantly higher than in SF from OA patients (p =0 . 0 1 7 ) . However, there was no correlation be tween VEGF levels in serum and SF from the same RA patients. The serum VEGF concentration was corr e l at e d with the ESR, serum CRP concentra tion, serum rheumatoid factor , number of tender and swollen joints, Modified Health Assessment Questionnair e, and p atient and physician global assess ments of disease activity in RA patients. Conclusion These results suggest that VEGF level is related to RA disease activity, sug gesting that VEGF may play some role in the pathogenesis of RA.

CT features of systemic lupus erythematosus in patients with acute abdominal pain: emphasis on ischemic bowel disease.

Abstract: PURPOSE: To evaluate the computed tomographic (CT) features of systemic lupus erythematosus (SLE) in patients with acute abdominal pain. Special emphasis was placed on the analysis of ischemic bowel disease. MATERIALS AND METHODS: The authors retrospectively reviewed the images from 39 abdominal CT examinations performed in 33 patients with SLE and acute abdominal pain. Images were evaluated for bowel wall changes, mesenteric changes, fluid collection, retroperitoneal lymphadenopathy, peritoneal enhancement, and hepatomegaly as well as for changes in other abdominal organs. Ischemic bowel disease was diagnosed if at least three of the following signs were seen: bowel wall thickening, target sign, dilatation of intestinal segments, engorgement of mesenteric vessels, and increased attenuation of mesenteric fat. RESULTS: Thirty-one (79%) of the 39 examinations had CT findings diagnostic of ischemic bowel disease, including symmetric bowel wall thickening (n = 29), target sign (n = 26), and mesenteric vascula...

Lupus mesenteric vasculitis can cause acute abdominal pain in patients with SLE.

Abstract: Lupus mesenteric vasculitis (LMV) is a unique clinical entity found in patients who present with gastrointestinal manifestations of systemic lupus erythematosus, and is the main cause of acute abdominal pain in these patients. LMV usually presents as acute abdominal pain with sudden onset, severe intensity and diffuse localization. Other causes of abdominal pain, such as acute gastroenteritis, peptic ulcers, acute pancreatitis, peritonitis, and other reasons for abdominal surgery should be ruled out. Prompt and accurate diagnosis of LMV is critical to ensure implementation of appropriate immunosuppressive therapy and avoidance of unnecessary surgical intervention. The pathology of LMV comprises immune-complex deposition and complement activation, with subsequent submucosal edema, leukocytoclastic vasculitis and thrombus formation; most of these changes are confined to small mesenteric vessels. Abdominal CT is the most useful tool for diagnosing LMV, which is characterized by the presence of target signs, comb signs, and other associated findings. The presence of autoantibodies against phospholipids and endothelial cells might provide information about the likelihood of recurrence of LMV. Immediate, high-dose, intravenous steroid therapy can lead to a favorable outcome and prevent serious complications such as bowel ischemia, necrosis and perforation.

Enhanced T cell proliferative response to type II collagen and synthetic peptide CII (255-274) in patients with rheumatoid arthritis.

Abstract: Objective To determine the presence of specific immune recognition of type II collagen (CII) and its immunodominant epitope CII (255–274) in patients with rheumatoid arthritis (RA). Methods T cell proliferative responses to bovine CII and a synthetic peptide encompassing CII (255–274) in peripheral blood mononuclear cells (PBMC) and synovial fluid mononuclear cells (SFMC) from RA patients, and in PBMC from osteoarthritis (OA) patients and healthy controls were assayed by mixed lymphocyte culture. Results The stimulation index (SI) and the number of positive (SI ≥2) T cell responses to CII were higher in RA patients (n = 106) than in OA patients (n = 26) and healthy controls (n = 34). T cell responses to CII (255–274) were also enhanced in RA patients and correlated well with those to CII. In SFMC, positive responses to CII or CII (255–274) were detected in 61.9% of 42 RA patients. T cell responses to CII in SFMC were stronger and more prevalent than peripheral responses. The SI and positive responses to CII were higher in early RA than in late RA. Levels of IgG antibodies to CII in synovial fluid inversely correlated with T cell responses to CII. Conclusion T cell responses to CII or CII (255–274) were enhanced in RA, especially in early disease. Synthetic peptide CII (255–274), as well as native CII, could be recognized as immunogenic antigens by T cells, particularly in the synovial fluid. These observations suggest that CII-reactive T cells play an important role in the pathogenesis of RA. Peripheral tolerance induction using CII (255–274) might be useful in the treatment of RA.

Vascular Endothelial Growth Factor and Angiogenesis

Abstract: Angiogenesis is a hallmark of wound healing, the menstrual cycle, cancer, and various ischemic and inflammatory diseases. A rich variety of pro- and antiangiogenic molecules have already been discovered. Vascular endothelial growth factor (VEGF) is an interesting inducer of angiogenesis and lymphangiogenesis, because it is a highly specific mitogen for endothelial cells. Signal transduction involves binding to tyrosine kinase receptors and results in endothelial cell proliferation, migration, and new vessel formation. In this article, the role of VEGF in physiological and pathological processes is reviewed. We also discuss how modulation of VEGF expression creates new therapeutic possibilities and describe recent developments in this field.

The role of synovitis in pathophysiology and clinical symptoms of osteoarthritis

Abstract: Osteoarthritis (OA), one of the most common rheumatic disorders, is characterized by cartilage breakdown and by synovial inflammation that is directly linked to clinical symptoms such as joint swelling, synovitis and inflammatory pain The gold-standard method for detecting synovitis is histological analysis of samples obtained by biopsy, but the noninvasive imaging techniques MRI and ultrasonography might also perform well The inflammation of the synovial membrane that occurs in both the early and late phases of OA is associated with alterations in the adjacent cartilage that are similar to those seen in rheumatoid arthritis Catabolic and proinflammatory mediators such as cytokines, nitric oxide, prostaglandin E(2) and neuropeptides are produced by the inflamed synovium and alter the balance of cartilage matrix degradation and repair, leading to excess production of the proteolytic enzymes responsible for cartilage breakdown Cartilage alteration in turn amplifies synovial inflammation, creating a vicious circle As synovitis is associated with clinical symptoms and also reflects joint degradation in OA, synovium-targeted therapy could help alleviate the symptoms of the disease and perhaps also prevent structural progression

Molecular Mechanisms RegulatinG Th1 Immune Responses

Abstract: The T helper lymphocyte is responsible for orchestrating the appropriate immune response to a wide variety of pathogens. The recognition of the polarized T helper cell subsets Th1 and Th2 has led to an understanding of the role of these cells in coordinating a variety of immune responses, both in responses to pathogens and in autoimmune and allergic disease. Here, we discuss the mechanisms that control lineage commitment to the Th1 phenotype. What has recently emerged is a rich understanding of the cytokines, receptors, signal transduction pathways, and transcription factors involved in Th1 differentiation. Although the picture is still incomplete, the basic pathways leading to Th1 differentiation can now be understood in in vitro and a number of infection and disease models.

Collagen-induced arthritis

Abstract: The collagen-induced arthritis (CIA) mouse model is the most commonly studied autoimmune model of rheumatoid arthritis. Autoimmune arthritis is induced in this model by immunization with an emulsion of complete Freund's adjuvant and type II collagen (CII). This protocol describes the steps necessary for acquisition, handling and preparation of CII, as well as selection of mouse strains, proper immunization technique and evaluation of the arthritis incidence and severity. Typically, the first signs of arthritis appear in this model 21–28 days after immunization, and identification of the arthritic limbs is not difficult. Using the protocol described, the investigator should be able to reproducibly induce a high incidence of CIA in various strains of genetically susceptible mice as well as learn how to critically evaluate the pathology of the disease. The total time for the preparation of reagents and the immunization of ten mice is about 1.5 h.

Evidence that cytokines play a role in rheumatoid arthritis

Abstract: A large number of cytokines are active in the joints of patients with rheumatoid arthritis (RA). It is now clear that these cytokines play a fundamental role in the processes that cause inflammation, articular destruction, and the comorbidities associated with RA. Following the success of TNF-α blockade as a treatment for RA, other cytokines now offer alternative targets for therapeutic intervention or might be useful as predictive biomarkers of disease. In this Review, we discuss the biologic contribution and therapeutic potential of the major cytokine families to RA pathology, focusing on molecules contained within the TNF-α, IL-1, IL-6, IL-23, and IL-2 families.