SCI 발표논문

전체 4,588편

882006

제1저자 김성한 · 교신저자 오명돈

, , , , , , , , ,
Outcome of inappropriate empirical antibiotic therapy in patients with Staphylococcus aureus bacteraemia: analytical strategy using propensity scores.
Clin Microbiol Infect. 2006;12(1):13-21.

Abstract
Patients with Staphylococcus aureus bacteraemia (SAB) who received either inappropriate or appropriate empirical therapy were compared by using two risk stratification models: (1) a cohort study using a propensity score to adjust for confounding by empirical treatment assignment; and (2) a propensity-matched case-control study. Inappropriate empirical therapy was modelled on the basis of patient characteristics, and included in the multivariate model to adjust for confounding. For case-matching analysis, patients with inappropriate empirical therapy (cases) were matched to those with appropriate empirical therapy (controls) on the basis of the propensity score (within 0.03 on a scale of 0-1). In total, 238 patients with SAB were enrolled in the cohort study. Characteristics associated with inappropriate empirical therapy were methicillin resistance, underlying haematological malignancy, no history of colonisation with methicillin-resistant S. aureus, and a long hospital stay before SAB. These variables were included in the propensity score, which had an area under the receiver operating characteristics curve of 85%. In the cohort study, SAB-related mortality was 39% (45/117) for inappropriate empirical therapy vs. 28% (34/121) for appropriate empirical therapy (odds ratio (OR) 1.60; 95% CI 0.93-2.76). After adjustment for independent predictors for mortality and the propensity score, inappropriate empirical therapy was not associated with mortality (adjusted OR 1.39; 95% CI 0.62-3.15). In the matched case-control study (50 pairs), SAB-related mortality was 32% (16/50) for inappropriate empirical therapy and 28% (14/50) for appropriate empirical therapy (McNemar's test; p 0.85; OR 1.15; 95% CI 0.51-2.64). In conclusion, inappropriate empirical therapy resulted in only a slight tendency towards increased mortality in patients with SAB.
PubMed IF 8.7 감염내과
872006

제1저자 김홍빈 · 교신저자 오명돈

, , , , , , , , , , , , , , ,
Prevalence and clinical implications of Staphylococcus aureus with a vancomycin MIC of 4 microg/ml in Korea.
Microb Drug Resist. 2006;12(1):33-8.

Abstract
In addition to vancomycin-intermediate Staphylococcus aureus (VISA), S. aureus with a vancomycin MIC of 4 microg/ml has been reported to be the cause of therapeutic failure. This study was designed to determine the prevalence of methicillin-resistant S. aureus (MRSA) with a vancomycin MIC of 4 microg/ml and to clarify the clinical characteristics of infections caused by these isolates. During the 8-week period from April to May, 2001, 27 hospitals participated in a nationwide surveillance program for VISA and vancomycin-resistant S. aureus (VRSA) in Korea. After screening on brain-heart infusion agar containing 4 microg/ml of vancomycin as previously described, 100 isolates with confluent growth were tested. The medical records of the patients involved were reviewed. Even though VISA or VRSA was not detected among 3,756 MRSA isolates, 18 (0.5%) had a vancomycin MIC of 4 microg/ml. The infections in 12 of these patients, excluding 5 that were colonized, were 8 chronic osteomyelitis, 1 surgical site infection, 1 pneumonia, 1 intra-abdominal infection, and 1 catheter-related infection. Although 11 cases were exposed to glycopeptides for a long time (median 56 days), the site of infection became culture-negative in only 1 case. Two patients died of their S. aureus infections. MRSA with a vancomycin MIC of 4 microg/ml was rare. Chronic osteomyelitis was the most common type of infection, and prolonged exposure to glycopeptides was associated with reduced susceptibility to vancomycin.
PubMed IF 1.8 감염내과
862006

제1저자 김인호 · 교신저자 김병국

, , , , , , , , , , ,
Comparative outcomes of reduced intensity and myeloablative allogeneic hematopoietic stem cell transplantation in patients under 50 with hematologic malignancies.
Clin Transplant. 2006;20(4):496-503.

Abstract
We have conducted a direct comparison of the outcomes of reduced intensity and myeloablative conditioning in younger adults with hematological malignancies<50 yr. One hundred and five patients received transplants from human leukocyte antigen (HLA)-matched donors, via either reduced intensity (n=35) or myeloablative conditioning (n=70). The median ages of the reduced intensity and myeloablative groups were 36 and 33 yr (p=0.014). Neutrophil engraftment (i.e. time to absolute neutrophil count>0.5x10(9)/L) occurred more rapidly in the reduced intensity group (median: 10 d; range: 0-21 d) than in the myeloablative group (median: 18 d; range: 11-38 d; p<0.0001). The incidence of grades 2-4 acute graft-vs.-host disease were similar between the reduced intensity and myeloablative groups, at 17% vs. 24% respectively (p=0.40). The cumulative incidence of day 100 non-relapse mortality was 18% in the reduced intensity group, and 21% in the myeloablative group (p=0.88). The overall two-yr survival rates were 43% in the reduced intensity group, and 35% in the myeloablative group (p=0.72). In conclusion, reduced intensity transplantation yielded outcomes comparable with those of myeloablative transplantation in patients under 50 with hematological malignancies.
PubMed IF 1.8 혈액종양내과
852006

제1저자 이근욱 · 교신저자 방영주

, , , , , , , , , , , ,
Antitumor activity of SK-7041, a novel histone deacetylase inhibitor, in human lung and breast cancer cells.
Anticancer Res. 2006;26(5A):3429-38.

Abstract
BACKGROUND A class of synthetic histone deacetylase (HDAC) inhibitors, which are hybrids of trichostatin A and MS-275 were previously developed. In this study, the antitumor effects of SK-7041, one of those novel HDAC inhibitors, was evaluated on lung and breast cancer cell lines.
MATERIALS AND METHODS Human lung and breast cancer cells, as well as normal human bronchial epithelial (NHBE) cells were treated with SK-7041, and results were compared with those of cells treated with suberoylanilide hydroxamic acid (SAHA).
RESULTS SK-7041 induced time-dependent histone hyperacetylation and showed more potent cytotoxicity than SAHA in cancer cells. These antiproliferative effects of SK-7041 were due to apoptotic cell death caused by G2/M-phase arrest and to a lesser extent to G1 arrest. Moreover, SK-7041 inhibited cancer cell proliferation more selectively than NHBE cell proliferation.
CONCLUSIONS These results suggest that SK-7041 may have potential anticancer activity.
PubMed IF 1.8 혈액종양내과
842006

제1저자 김광일 · 교신저자 김효수

, , , , , , , , , , ,
Beta-catenin overexpression augments angiogenesis and skeletal muscle regeneration through dual mechanism of vascular endothelial growth factor-mediated endothelial cell proliferation and progenitor cell mobilization.
Arterioscler Thromb Vasc Biol. 2006;26(1):91-8.

Abstract
OBJECTIVE Beta-catenin plays a critical role in directing cell fate during embryogenesis, and uncontrollable activation leads to cancers, suggesting its importance in cell survival and proliferation. However, little is known regarding its role in endothelial cell (EC) and skeletal muscle proliferation and progenitor cell mobilization.
METHODS AND RESULTS Beta-catenin enhanced ECs proliferation, protected ECs from apoptosis, and increased the capillary forming capabilities, which was completely blocked by inhibition of its nuclear translocation. In addition, the increased proliferation by beta-catenin was associated with increased expression of cyclin E2. In skeletal myocytes, beta-catenin overexpression increased proliferation with cyclin D1 expression, decreased apoptosis, and induced hypertrophy. Furthermore, beta-catenin induced the expression of vascular endothelial growth factor (VEGF) in skeletal myocytes, resulting in EC proliferation. In a mouse hindlimb ischemia model, beta-catenin significantly increased recovery of blood perfusion, capillary density along with enhanced VEGF expression, and the number of proliferating ECs and myocytes. Local delivery of beta-catenin also promoted angiogenic progenitor cell mobilization and increased the number of satellite cells.
CONCLUSIONS Beta-catenin may be an important modulator of angiogenesis and myocyte regeneration not only by directly enhancing proliferation and survival of ECs and skeletal myocytes but also by inducing VEGF expression and promoting angiogenic progenitor cell mobilization and muscle progenitor cell activation.
PubMed IF 8.8 순환기내과
832006

제1저자 명선정 · 교신저자 윤정환

, , , , , , ,
Diffuse infiltrative hepatocellular carcinomas in a hepatitis B-endemic area: diagnostic and therapeutic impediments.
Hepatogastroenterology. 2006;53(68):266-70.

Abstract
BACKGROUND/AIMS Clinical features of diffuse infiltrative hepatocellular carcinoma (D-HCC) are distinct from those of mass-forming HCCs, and also dependent on etiologic viruses. Moreover, despite a regular HCC-surveillance in those with chronic liver diseases, patients sometimes present with advanced D-HCCs. Thus, in the present study, we were to assess the risk factors, mode of diagnosis and prognosis of D-HCCs in a hepatitis B virus-endemic area.
METHODOLOGY From January to June 2003, 35 patients who had been newly diagnosed as having D-HCC were enrolled. Their clinical characteristics were compared with those with other types of HCCs, who had been enrolled during the same period. Survival rates were analyzed using Kaplan-Meier method and Cox proportional hazard model.
RESULTS D-HCC patients were younger and more commonly positive for HBsAg than those with other types of HCCs. During a regular follow-up, these tumors were not readily detectable in ultrasonography. Transarterial chemoembolization was beneficial in patients with good liver function as compared to supportive care, while this was not evident in those with poor hepatic reserve.
CONCLUSIONS D-HCCs are not readily diagnosed using ultrasonography. These tumors are mostly resistant to treatment, while transarterial chemoembolization might be applied in patients with good liver function.
PubMed IF 0.696 소화기내과
822006

제1저자 이춘택 · 교신저자 이춘택

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In vivo imaging of adenovirus transduction and enhanced therapeutic efficacy of combination therapy with conditionally replicating adenovirus and adenovirus-p27.
Cancer Res. 2006;66(1):372-7.

Abstract
Gene therapy is hampered by poor gene transfer to the tumor mass. We previously proposed a combination adenoviral gene therapy containing a conditionally replicating adenovirus (CRAD) expressing mutant E1 (delta24RGD) and a replication-defective E1-deleted adenovirus to enhance the efficiency of gene transfer. Mutant E1 expressed by delta24RGD enables the replication of replication-defective adenoviruses in tumors when cancer cells are co-infected with both viruses. In this study, gene transfer rates in xenografts tumors were monitored by bioluminescence in cells infected with the replication-defective adenovirus-luciferase (ad-luc). Tumor masses treated with CRAD + ad-luc showed dramatically stronger and more prolonged luciferase expression than ad-luc-treated tumors and this expression spread through the entire tumor mass without significant systemic spread. Transduction with CRAD + replication-defective adenovirus-p27 increased the expression of p27 by 24-fold versus transduction with ad-p27 alone. Treatment of a lung cancer cell line and of established lung cancer xenografts with CRAD + adenovirus-p27 also induced stronger growth suppression than treatment with either virus alone. These findings confirm the selective replication of E1-deleted adenovirus containing a therapeutic gene due to the presence of mutant E1 produced by delta24RGD in tumors. Moreover, this replication increased the therapeutic gene transfer rate and enhanced its antitumor effects.
PubMed IF 22.6 호흡기내과
812006

제1저자 정현승 · 교신저자 박경수

, , , , , , , , ,
Resistin is secreted from macrophages in atheromas and promotes atherosclerosis.
Cardiovasc Res. 2006;69(1):76-85.

Abstract
OBJECTIVE Resistin belongs to a family of cysteine-rich secreted polypeptides that are mainly produced by monocytes/macrophages in humans. Recently, high concentrations of resistin were shown to induce vascular endothelial dysfunction and vascular smooth muscle cell proliferation. We examined if resistin was secreted from macrophages locally in atheromas and if it affected vascular cell function in human.
METHODS AND RESULTS Immunohistochemical staining of human vessels showed that aortic aneurysms exhibited resistin-positive staining areas along macrophage infiltration, while normal arteries and veins did not. Co-localization of resistin and CD68 (a marker for macrophages) was observed in immunofluorescent double staining of aneurysms. Resistin mRNA was expressed much higher in cultured monocytes/macrophages than in human vascular smooth muscle cells (VSMCs) and human umbilical venous endothelial cells (HUVECs). This suggested that the resistin in aneurysms originates from macrophages within the vessels. To determine the effects of resistin on atherosclerosis, HUVECs and human VSMCs were incubated with resistin (10-100 ng/mL for 4 approximately 24 h). In HUVECs, plasminogen activator inhibitor (PAI)-1 release was assayed by ELISA, while the PAI-1 and endothelin (ET)-1 mRNA levels were analyzed by Northern blotting. Both were increased significantly with resistin treatment by factors of 1.3-2.5 (p<0.05). Migratory activity of VSMCs measured by scratched wound assay also increased significantly (1.6 times, p<0.05). In summary, macrophages infiltrating atherosclerotic aneurysms secrete resistin, and resistin affects endothelial function and VSMC migration.
CONCLUSIONS Resistin secreted from macrophages may contribute to atherogenesis by virtue of its effects on vascular endothelial cells and smooth muscle cells in humans.
PubMed IF 12.5 내분비대사내과
802005

제1저자 김상균 · 교신저자 정현채

, , , ,
Inhibition of proinflammatory cytokine expression by NF-kappaB (p65) antisense oligonucleotide in Helicobacter pylori-infected mice.
Helicobacter. 2005;10(6):559-66.

Abstract
BACKGROUND Helicobacter pylori induces the expression of proinflammatory cytokines in vitro by activating nuclear factor-kappaB, a transcriptional regulator. However, it has not been clarified whether H. pylori-induced proinflammatory cytokines are also mediated through nuclear factor-kappaB in vivo. The aim of this study was to evaluate the role of nuclear factor-kappaB on the expressions of proinflammatory cytokines in H. pylori-infected mice.
MATERIALS AND METHODS We evaluated nuclear factor-kappaB (p65) activation in the H. pylori-infected gastric mucosa of mice by immunofluorescent staining using antip65 polyclonal antibody, and the expressions of proinflammatory cytokines with inhibition of nuclear factor-kappaB pathway by using phosphorothioate antisense and sense oligonucleotide against the nuclear factor-kappaB (p65).
RESULTS In the H. pylori-infected gastric mucosa of mice, immunofluorescent staining using antip65 polyclonal antibody showed nuclear factor-kappaB (p65) activation, which was particularly localized to epithelial cells. Tumor necrosis factor-alpha and interleukin-1beta concentrations in gastric mucosa by enzyme-linked immunosorbent assay (ELISA) were elevated in the infected group versus the uninfected group. Pretreatment with nuclear factor-kappaB (p65) antisense oligonucleotide inhibited the activation of nuclear factor-kappaB and the expressions of tumor necrosis factor-alpha and interleukin-1beta in H. pylori-infected gastric mucosa. Sense oligonucleotide did not influence on the expression of proinflammatory cytokines.
CONCLUSIONS H. pylori infection was found to activate the expressions of proinflammatory cytokines via nuclear factor-kappaB in vivo, and this may play an important role in the initiation of H. pylori-induced gastric inflammation.
PubMed IF 4.6 소화기내과
792005

제1저자 김태민 · 교신저자 허대석

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Local tumor invasiveness is more predictive of survival than International Prognostic Index in stage I(E)/II(E) extranodal NK/T-cell lymphoma, nasal type.
Blood. 2005;106(12):3785-90.

Abstract
This study was launched to determine the prognostic significance of local tumor invasiveness (LTI) in 114 patients diagnosed with stage I(E)/II(E) extranodal natural killer (NK)/T-cell lymphoma, nasal type (NTCL). LTI was defined as bony invasion or destruction or tumor invasion of the skin. Complete remission (CR), overall survival (OS), and disease-free survival (DFS) were compared between each group according to LTI, Ann Arbor stage, and International Prognostic Index (IPI). LTI was observed in 23 patients. Using multivariate analysis, factors associated with low probability of CR were the presence of LTI (P < .001), the presence of B symptoms (P = .003), and single-modality chemotherapy (P = .045). The presence of LTI (relative risk [RR] = 8.4, 95% confidence interval [CI] 3.9-17.9; P < .001) and high IPI score (RR = 2.8, 95% CI 1.2-6.8; P = .019) were also predictive of OS. The presence of LTI (RR = 7.3, 95% CI 3.2-16.5; P < .001) was an independently significant factor for reduced DFS. Ann Arbor staging system did not predict CR, OS, or DFS but IPI did have predictive power with regard to survival outcome. LTI is the most important prognostic factor in predicting low probability of CR and reduced OS and DFS in nasal stage I(E)/II(E) NTCL.
PubMed IF 23.9 혈액종양내과
782005

제1저자 신찬수 · 교신저자 신찬수

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Dominant negative N-cadherin inhibits osteoclast differentiation by interfering with beta-catenin regulation of RANKL, independent of cell-cell adhesion.
J Bone Miner Res. 2005;20(12):2200-12.

Abstract
UNLABELLED We studied the effects of dominant negative N-cadherin (NCadDeltaC) expression in ST2 cells on their ability to support osteoclastogenesis. Expression of NCadDeltaC in ST2 cells did not decrease cell-to-cell adhesion but significantly reduced osteoclast formation when co-cultured with BMMs. NCadDeltaC inhibited beta-catenin/TCF signaling, resulting in decreased RANKL expression, which could contribute to the reduced osteoclast formation.
INTRODUCTION Cadherin is a calcium-dependent cell adhesion molecule that plays major roles during embryonic development and morphogenesis. Classic cadherins interact with beta-catenin, which is also involved in the Wnt signaling pathway. We tested whether disruption of N-cadherin function in stromal cells by dominant negative N-cadherin affects their ability to support osteoclastogenesis by altering heterotypic interaction with osteoclast precursors.
MATERIALS AND METHODS ST2 cells were transduced with retrovirus encoding extracellular domain-truncated, dominant negative N-cadherin (NCadDeltaC) and co-cultured with bone marrow macrophages (BMMs) to study the ability to support osteoclastogenesis. As a downstream target of NCadDeltaC, beta-catenin/T-cell factor (TCF) transcriptional activity was analyzed using TOPflash reporter construct. Real-time RT-PCR analysis and RANKL-luciferase reporter assays were performed to study the effects of NCadDeltaC on the osteoprotegerin (OPG)/RANKL system.
RESULTS Immunoblotting analysis showed that primary bone marrow stromal cells, ST2 cells, and BMMs expressed N-cadherin. Retroviral expression of NCadDeltaC in ST2 cells did not significantly inhibit cell adhesion but markedly impaired the formation of TRACP(+) osteoclasts (>40%) when co-cultured with BMMs. However, the inhibition of osteoclastogenesis was not reproduced by neutralizing antibody against N-cadherin. Expression of NCadDeltaC, however, strongly suppressed beta-catenin/TCF transcriptional activity in ST2 cells, which was rescued by constitutively active beta-catenin adenovirus (Ad DeltaN46 beta-catenin) or constitutively active TCF mutant (pCS2-VP16DeltabetaXTCF-3). As a potential downstream target of Wnt signaling, we found that the expression of RANKL was reduced in ST2 cells expressing NCadDeltaC. Moreover, Wnt-3A, Ad DeltaN46 beta-catenin, and VP16DeltabetaXTCF-3 increased the expression of RANKL and enhanced the transcriptional activity of mouse RANKL promoter in ST2 cells.
CONCLUSIONS Our data suggest that expression of dominant negative N-cadherin in ST2 cells suppressed osteoclastogenesis by interfering with beta-catenin regulation of RANKL independent of cell-cell adhesion.
PubMed IF 6.5 내분비대사내과
772005

제1저자 김상완 · 교신저자 신찬수

, , , , , ,
Early changes in biochemical markers of bone turnover predict bone mineral density response to antiresorptive therapy in Korean postmenopausal women with osteoporosis.
Endocr J. 2005;52(6):667-74.

Abstract
Biochemical markers of bone turnover have been suggested to be useful in monitoring the efficacy of antiresorptive therapy. In this study, we investigated the predictive value of bone turnover markers to determine short-term response in bone mineral density (BMD) and to identify nonresponders in 138 postmenopausal women (mean age 58 years) with osteoporosis given with either hormone thearpy (HT) or alendronate. Urinary type I collagen N-telopeptide (NTx) and serum osteocalcin (OC) at baseline, 3, and 6 months after treatment as well as spine and femoral neck BMD at baseline and 12 months were measured. Significant decreases in both NTx and OC were evident in women on treatment with antiresorptive agents as early as 3 months (p<0.01). Percent change of NTx at 3 months correlated with the percent change of spinal BMD at 12 months of treatment. When bone turnover markers were stratified by tertiles, the average rate of lumbar spine BMD gain increased significantly with increasing tertiles of baseline value (p<0.05) and percent change (p<0.05) of urinary NTx at 3 month of treatment. In terms of BMD response, urinary NTx at 3 months decreased significantly more in BMD responders group than in nonresponders group. Logistic regression analysis demonstrated that percent change of NTx at 3 months is an independent predictor to identify BMD nonresponders, defined as those whose BMD gain remained within the precision error range of dual energy X-ray absorptiometer (DXA). We conclude that biochemical markers of bone turnover, especially percent change in urinary NTx levels, can be used to determine BMD response to antiresorptive therapy in Korean postmenopausal women with osteoporosis.
PubMed IF 2.5 내분비대사내과
762005

제1저자 한대희 · 교신저자 이재호

, , ,
Resolution of residual pleural disease according to time course in tuberculous pleurisy during and after the termination of antituberculosis medication.
Chest. 2005;128(5):3240-5.

Abstract
STUDY OBJECTIVES To assess the resolution of pleural disease in patients with tuberculous pleurisy (TP) during and after antituberculosis medication.
DESIGN An observational, prospective, longitudinal study.
SETTING University-affiliated general hospital in Seoul, Korea.
PATIENTS AND METHODS Chest radiographs of 85 adult TP patients were followed up prospectively from diagnosis to 24 months after the start of medication. The extent of pleural disease, synonymous with the radiographic term, pleural opacity (PO), was evaluated at regular intervals according to a size scale. Additionally, following completion of 6 months of therapy, residual PO (RPO) was determined by either measurement of the widest width of the opacity, if loculated, or at the superior level of the hemidiaphragm.
RESULTS Seventy-seven patients had a PO graded > or = 2 at the initial presentation. At 6, 9, and 24 months, the number of patients with these grades declined. At these time periods, there were 14, 8, and 7 patients, respectively, remaining with this classification. RPO > 10 mm at 24 months was considered indicative of significant residual pleural disease. During the period after 6 months of antituberculosis medication, the number of patients with RPO > or = 10 mm declined from 43 patients at 6 months to 21 patients at 24 months. The presence of loculation on an initial chest decubitus view was associated with significant RPO at 24 months (p = 0.009).
CONCLUSION In TP patients, improvement of RPO often occurred even after completion of 6 months of antituberculosis medication up to 24 months. A loculated PO at initial presentation, but not initial PO size, was a predictor of significant RPO at 24 months.
PubMed IF 9.8 호흡기내과
752005

제1저자 백한주 · 교신저자 송영욱

, , , , , ,
Osteopenia in men with mild and severe ankylosing spondylitis.
Rheumatol Int. 2005;26(1):30-4.

Abstract
We investigated the frequency and distribution of osteopenia according to the clinical severity in ankylosing spondylitis (AS). Bone mass was measured in men with mild (n = 45) and severe AS (n = 31) with dual-energy X-ray absorptiometry (DEXA). Definition of clinical severity was based on the Schober's test. Osteopenia was commonly detected (48% in mild AS and 39% severe AS) and, in mild disease, more frequently observed at the lumbar spine than any of the proximal femur sites. In severe AS, however, the frequency of osteopenia at the femoral neck and Ward's triangle was as high as at the lumbar spine. Both bone mineral density and T-scores in severe disease were lower than in mild disease at the femur neck, Ward's triangle, and total proximal femur, but not in the lumbar spine. The progression of osteopenia may be reflected more reliably at proximal femur sites than at the lumbar spine.
PubMed IF 3.5 류마티스내과
742005

제1저자 황진혁 · 교신저자 김용태

, , , , , , , , , ,
Spontaneous activation of pancreas trypsinogen in heat shock protein 70.1 knock-out mice.
Pancreas. 2005;31(4):332-6.

Abstract
OBJECTIVES Heat shock proteins (Hsp's) protect cellular proteins in response to injury, and the role of Hsp70 in experimental pancreatitis was recently described. To find out the possible role of Hsp70 in pancreatitis, we used Hsp70 knock-out mice (Hsp70.1-/-) and wild-type mice (Hsp70.1+/+).
METHODS We studied enzymes activities, Hsp70 protein levels, and histologies in cerulein-induced pancreatitis of Hsp70.1-/- and Hsp70.1+/+ mice.
RESULTS In the basal state, Hsp70 protein levels were higher in Hsp70.1+/+ than in Hsp70.1-/- mice, and trypsin activity was higher in Hsp70.1-/- than in Hsp70.1+/+ mice. The zymogen/lysosome ratio of cathepsin B activity before cerulein injection was higher in Hsp70.1-/- than in Hsp70.1+/+ mice. The expression level of Hsp70 in the pancreas increased in both of Hsp70.1-/- and Hsp70.1+/+ mice after hyperthermia because of the Hsp70.3 gene left intact in Hsp70.1-/- mice. After cerulein hyperstimulation, trypsin activity increased 2-fold in Hsp70.1+/+ mice, but cerulein did not further increase basally elevated trypsin activity in Hsp70.1-/- mice. Hyperthermia pretreatment not only blocked cerulein-induced trypsinogen activation, pancreatic edema, and vacuolization in Hsp70.1+/+ mice, but also decreased basally elevated trypsin activity in Hsp70.1-/- mice.
CONCLUSIONS Hsp70 can be responsible for inhibition of cerulein-induced pancreatitis and prevention of spontaneous trypsinogen activation in mice by inhibiting the colocalization of zymogen and lysosomal enzymes.
PubMed IF 2.2 소화기내과
732005

제1저자 방수미 · 교신저자 박선양

, , , , , , , , , , , ,
High-dose therapy and autologous stem cell transplantation in Korean patients with aggressive T/NK-cell lymphoma.
Leuk Lymphoma. 2005;46(11):1599-1604.

Abstract
The proportion of aggressive T/NK-cell lymphoma in Korea is larger than in the West, and it shows a lower response to conventional chemotherapy and poorer survival than diffuse large B-cell lymphoma. This study was undertaken to evaluate the response rate and survival and to document the prognostic factors in patients with T/NK-cell lymphoma who have undergone high-dose therapy (HDT). Eligibility for the study was a mature T/NK-cell lymphoma with initially poor risk (as high or high intermediate risk on age-adjusted International Prognostic Index) or relapsed cases. Twenty-eight patients from 6 centers were reviewed retrospectively. The M : F ratio was 20:8, and median age was 36 years (range 16--60 years). Twelve patients had unspecified peripheral T-cell lymphomas, 7 anaplastic large-cell lymphomas, 6 nasal T/NK-cell lymphomas, and 3 angioimmunoblastic T-cell lymphomas. Disease status at transplant were initially poor risk in 15, chemosensitive relapse in 8 and chemo-resistant relapse in 5 patients, respectively. A complete response (CR) after HDT comprised 20 patients, including 16 with continued CR. Absolute neutrophil count ( > 500/microl) recovered at a median 11 days after autologous stem cell transplantation in 26 patients. Two therapy-related mortalities occurred. Estimated 3-year event-free survival and overall survival (OS) (+/- SE) were 24+/- 9 and 42+/- 10 months, respectively. Only CR status after HDT influenced OS (P=0.000). Therefore, an initial approach with effective induction and HDT may result in a better outcome in T/NK-cell lymphoma.
PubMed IF 2.1 혈액종양내과
722005

제1저자 김경아 · 교신저자 이효석

, , , ,
15d-Deoxy-Delta12,14-prostaglandin J2 modulates collagen type I synthesis in human hepatic stellate cells by inducing oxidative stress.
Prostaglandins Leukot Essent Fatty Acids. 2005;73(5):361-7.

Abstract
15 deoxy-Delta(12,14)-prostaglandin(2) (15d-PGJ(2)) is known to inhibit the proliferation of hepatic stellate cells (HSCs), major cellular components that cause hepatic fibrosis, in vitro. It also induces oxidative stress, which results in hepatic myofibroblast death. On the other hand, oxidative stress generally induces HSC proliferation and collagen synthesis in vitro, and liver fibrogenesis in vivo. In this study, we evaluated the effects of 15d-PGJ(2) at various concentrations on the viability and collagen synthesis of HSCs. 15d-PGJ(2) increased intracellular reactive oxygen species (ROS), and reduced the viability of human HSCs at concentrations 5 microM by inducing apoptotic cell death. In addition, the antioxidants alpha-tocopherol and N-acetylcysteine (NAC) blocked 15d-PGJ(2)-induced HSC death. Collagen I synthesis was increased 1.5-fold by 0.5 microM 15d-PGJ(2) treatment, but was reduced to 30% of the control level by 10 microM 15d-PGJ(2), and NAC pretreatment prevented these changes in collagen production by 15d-PGJ(2). We conclude that 15d-PGJ(2) may either induce or prevent hepatic fibrogenesis depending on its concentration.
PubMed IF 2.4 소화기내과
712005

제1저자 윤영순 · 교신저자 임재준

, , , , , , ,
Impact of fluoroquinolones on the diagnosis of pulmonary tuberculosis initially treated as bacterial pneumonia.
Int J Tuberc Lung Dis. 2005;9(11):1215-9.

Abstract
OBJECTIVE The excellent in vitro activity of fluoroquinolones against Mycobacterium tuberculosis has raised concerns about the delayed diagnosis of pulmonary tuberculosis (PTB) initially misdiagnosed as pneumonia. The aim of this study was to assess the effect of empiric fluoroquinolone therapy on delays in diagnosis in patients with PTB initially misdiagnosed as bacterial pneumonia.
DESIGN Patients with PTB initially treated as having community-acquired pneumonia and treated with fluoroquinolones for more than 5 consecutive days, from January 2000 to December 2004, were enrolled. As a control group, TB patients initially treated with nonfluoroquinolone antibiotics were enrolled. We reviewed the clinical data and compared treatment responses between the two groups.
RESULTS Nine patients in the fluoroquinolone group and 19 patients in the non-fluoroquinolone group were enrolled. In the fluoroquinolone group, eight patients (89%) improved clinically or radiographically, whereas only eight patients (42%) in the non-fluoroquinolone group improved (P = 0.04). The delay in initiation of anti-tuberculosis medication was longer in the fluoroquinolone group than in the non-fluoroquinolone group (43.1 - 40.0 vs. 18.7 +/- 16.9 days, P = 0.04).
CONCLUSION Delay in the initiation of anti-tuberculosis treatment is possible in patients administered fluoroquinolone and initially misdiagnosed as having bacterial pneumonia.
PubMed IF 3.6 호흡기내과
702005

제1저자 곽금연 · 교신저자 윤정환

, , , , , , ,
Detection of response-predicting mutations in the kinase domain of the epidermal growth factor receptor gene in cholangiocarcinomas.
J Cancer Res Clin Oncol. 2005;131(10):649-52.

Abstract
PURPOSE Epidermal growth factor receptor (EGFR) signalings have recently been implicated in the genesis and progression of cholangiocarcinomas. Thus, the EGFR kinase inhibitor appears to be promising in the treatment of this cancer. The response-predicting mutations in the tyrosine kinase domain of EGFR gene have recently been detected in non-small cell lung cancers. This study was, therefore, to investigate if these mutations are also found in cholangiocarcinomas.
METHODS Twenty-two consecutive cholangiocarcinoma patients who underwent surgical resection were enrolled. Their resected paraffin-embedded cholangiocarcinoma specimens were used for mutation analysis, which was performed by DNA sequencing of exons 18, 19 and 21 in the EGFR gene. Clinical characteristics were compared between each group according to the presence or absence of mutations.
RESULTS Three patients (13.6%) harbored EGFR mutations. All the mutations found were deletions in exon 19. Mutations were more common in intra-hepatic or poorly differentiated tumors. Differences in age, sex, stage at diagnosis and survival were not observed between mutation-positive and -negative patients.
CONCLUSIONS This study, for the first time, demonstrates that a subset of cholangiocarcinoma patients has response-predicting EGFR mutations. Therefore, a highly selected application of the EGFR kinase inhibitor would be therapeutically effective in these patients.
PubMed IF 3.3 소화기내과
692005

제1저자 류지곤 · 교신저자 윤용범

, , , , , , , , , , , , , , , , ,
Clinical features of chronic pancreatitis in Korea: a multicenter nationwide study.
Digestion. 2005;72(4):207-11.

Abstract
BACKGROUND/AIMS No reliable nationwide clinical data about chronic pancreatitis (CP) was available in Korea. The etiology and clinical features of CP were investigated using a multicenter nationwide study.
METHODS 814 cases of CP were enrolled retrospectively over the past 4 years at 13 hospitals. The following data were obtained from all patients: etiology, symptoms, complications, and surgery.
RESULT Alcohol (64.3%) was the major cause of CP and idiopathic CP (20.8%) was the second most common form. Mean patient age was 50.6 years and the male:female ratio was 6:1 (24:1 for alcoholic CP vs. 2:1 in idiopathic CP, p < 0.001). Diabetes (31.6%), pseudocysts (28.4%), biliary stricture (13.9%), and pancreatic ascites (6.6%) were the main complications. Of these, diabetes (35 vs. 26%) and pseudocyst (33.7 vs. 21.9%) were more frequent in alcoholic than in idiopathic CP. Pancreatic cancer developed in 25 patients (3.1%) during follow-up and their mean age was 59.1 years.
CONCLUSIONS In Korea, alcohol is the most common etiology of CP. Moreover, diabetes and pseudocysts are frequent complications, especially in alcoholic CP, and pancreatic cancer development is not infrequent.
PubMed IF 3.4 소화기내과
682005

제1저자 김덕겸 · 교신저자 임재준

, , , , , ,
Clinical characteristics and treatment responses of tuberculosis in patients with malignancy receiving anticancer chemotherapy.
Chest. 2005;128(4):2218-22.

Abstract
STUDY OBJECTIVES The aim of this study was to elucidate the clinical characteristics and treatment responses of tuberculosis developing in patients receiving anticancer chemotherapy.
DESIGN Retrospective case-control study.
SETTING The Seoul National University Hospital, a tertiary referral hospital in South Korea.
PATIENTS From January 1, 2000, to July 31, 2004, patients with tuberculosis detected during the course of anticancer chemotherapy were enrolled as cases. Age- and sex-matched tuberculosis patients without any malignant disease were selected as control subjects.
MEASUREMENTS AND RESULTS Twenty-four patients and 48 control subjects were enrolled. Their mean +/- SD age was 56.3 +/- 14.3 years, and the male-to-female ratio was 3:1. The most common malignancy was gastric cancer (43%). Lymphoma (17%), lung cancer (8%), and head and neck cancer (8%) were also common. In both groups, the lung was the most common site of tuberculosis involvement (87.8% and 79.2%, retrospectively). The presence of scar tissue suggesting old tuberculosis on radiography was more common in patients with tuberculosis receiving anticancer chemotherapy (66.7% vs 43.8%, p = 0.07). No difference in radiographic severity was observed between groups. A regimen based on first-line antituberculosis drugs was started in all subjects. Frequency of completion of the expected antituberculosis chemotherapy was lower in patients with tuberculosis developing with anticancer chemotherapy (58.3% vs 79.2%, p = 0.02), but it was not different after excluding the loss due to progression of underlying malignancies. Bacteriologic/radiographic responses to treatment and toxicity of antituberculosis medication sufficient to change or stop treatment were not different in both groups.
CONCLUSIONS With regard to radiographic and clinical responses to antituberculosis treatment, tuberculosis developing during anticancer chemotherapy is not clinically different from tuberculosis developing in ordinary situations. Findings in this study suggest that anticancer chemotherapy is not an obstacle in treating tuberculosis.
PubMed IF 9.8 호흡기내과
672005

제1저자 김상균 · 교신저자 방영주

, , , , , , ,
The endogenous ratio of Smad2 and Smad3 influences the cytostatic function of Smad3.
Mol Biol Cell. 2005;16(10):4672-83.

Abstract
Although Smad2 and Smad3, critical transcriptional mediators of transforming growth factor-beta (TGF-beta) signaling, are supposed to play a role in the TGF-beta cytostatic program, it remains unclear whether TGF-beta delivers cytostatic signals through both Smads equally or through either differentially. Here, we report that TGF-beta cytostatic signals rely on a Smad3-, but not a Smad2-, dependent pathway and that the intensity of TGF-beta cytostatic signals can be modulated by changing the endogenous ratio of Smad3 to Smad2. Depleting endogenous Smad3 by RNA interference sufficiently interfered with TGF-beta cytostatic actions in various TGF-beta-sensitive cell lines, whereas raising the relative endogenous ratio of Smad3 to Smad2, by depleting Smad2, markedly enhanced TGF-beta cytostatic response. Consistently, Smad3 activation and its transcriptional activity upon TGF-beta stimulation were facilitated in Smad2-depleted cells relative to controls. Most significantly, a single event of increasing this ratio by Smad2 depletion was sufficient to restore TGF-beta cytostatic action in cells resistant to TGF-beta. These findings suggest a new important determinant of sensitivity to TGF-beta cytostatic signaling.
PubMed IF 3 혈액종양내과
662005

제1저자 이재호 · 교신저자 이재호

, , ,
Diagnostic and therapeutic problems of pulmonary tuberculosis in elderly patients.
J Korean Med Sci. 2005;20(5):784-9.

Abstract
To identify differences in the clinical, radiologic, and microbiologic features of pulmonary tuberculosis (TB) in the young (<64 yr) and elderly (> or =65 yr), we performed a retrospective analysis of the medical charts and chest radiographs of 207 young and 119 elderly pulmonary TB patients. Hemoptysis and a febrile sense were more frequent in the young, whereas weakness, dyspnea, anorexia, and mental change were more frequent in the elderly. Elderly patients showed higher frequencies of cardiovascular and chronic lung diseases, whereas the young showed a higher proportion of underlying liver disease. In addition, chest radiography showed a significantly higher frequency of mid or lower lung involvement by TB lesions in the elderly (10.6% vs. 22.7%, p<0.05). Lesions were frequently misdiagnosed as pneumonia or lung cancer in the elderly. However, there was no difference between these two groups in terms of sputum acid-fast bacilli positivity. The elderly showed a higher frequency of adverse drug reactions (18.5% vs. 40.7%, p<0.05), and higher TB-related mortality (1.3% vs. 11.1%, p<0.05). In conclusion this study showed that young and elderly pulmonary TB patients have similar microbiologic features; however, the elderly showed higher frequencies of atypical clinical and radiologic presentations, adverse drug reactions, and higher TB-related mortality.
PubMed IF 3.2 호흡기내과
652005

제1저자 강은하 · 교신저자 이은봉

, , , , , ,
Interstitial lung disease in patients with polymyositis, dermatomyositis and amyopathic dermatomyositis.
Rheumatology (Oxford). 2005;44(10):1282-6.

Abstract
OBJECTIVE To assess the prevalence, characteristics and prognostic factors of interstitial lung disease (ILD) in Korean patients with polymyositis (PM), dermatomyositis (DM) and amyopathic dermatomyositis (ADM).
METHODS We reviewed the medical records of 72 consecutive PM and DM patients, including six patients with ADM, who were seen at the Rheumatology Clinic of Seoul National University Hospital between 1984 and 2003.
RESULTS Twenty-nine PM/DM patients (40.3%) developed ILD. Anti-Jo-1 antibody and arthralgia were associated with the presence of ILD (P = 0.022 and P = 0.041, respectively), whereas dysphagia was more frequently found in patients without ILD (P = 0.041). Lung biopsies revealed diffuse alveolar damage (DAD) (n = 2), usual interstitial pneumonia (UIP) with DAD (n = 2), UIP (n = 1), and non-specific interstitial pneumonia (n = 2). Of the 29 patients, 11 (37.9%) died. The mean survival time in ILD patients was significantly shorter than in those without ILD (13.8+/-1.8 vs 19.2+/-0.9 yr, P = 0.017). Poor survival in ILD patients was associated with a Hamman-Rich-like presentation (P = 0.0000), ADM features (P = 0.0001) and an initial forced vital capacity (FVC) < or =60% (P = 0.024).
CONCLUSIONS ILD was observed in 40.3% of Korean PM/DM patients and was associated with poor survival. A Hamman-Rich-like presentation, ADM features and an initial FVC < or =60% were associated with poor survival in ILD.
PubMed IF 4.7 류마티스내과
642005

제1저자 조영민 · 교신저자 이홍규

, , , , , ,
Association between polymorphisms in the nuclear respiratory factor 1 gene and type 2 diabetes mellitus in the Korean population.
Diabetologia. 2005;48(10):2033-8.

Abstract
AIMS/HYPOTHESIS Dysfunction in mitochondrial oxidative phosphorylation plays a central role in insulin resistance and type 2 diabetes. Nuclear respiratory factor 1 (NRF1) is a transcription factor that acts on nuclear genes encoding respiratory subunits and components of the mitochondrial transcription and replication machinery. Thus, we investigated its genetic association with type 2 diabetes.
METHODS The NRF1 gene was sequenced to identify polymorphisms in 24 Korean DNA samples and then common variants were genotyped in 766 patients with type 2 diabetes and 303 non-diabetic subjects.
RESULTS Twelve single nucleotide polymorphisms and one insertion/deletion polymorphism were identified. Six common variants among them were genotyped in a larger study. Although three individual polymorphisms appeared to be associated with type 2 diabetes (g.-46350insdel A, g.+141G>T and g.+54529A>G), the effects were only marginal. However, a haplotype (H2) was associated with a decreased risk of type 2 diabetes and another haplotype (H4) was associated with an increased risk of type 2 diabetes (p values for the Haplo. Score test were 0.009 and 0.004, respectively).
CONCLUSIONS/INTERPRETATION We demonstrated that two common haplotypes of NRF1 gene are associated with type 2 diabetes in the Korean population.
PubMed IF 10.4 내분비대사내과
632005

제1저자 Shin HD · 교신저자 박경수

, , , , , , ,
Association of a polymorphism in the gene encoding phosphoenolpyruvate carboxykinase 1 with high-density lipoprotein and triglyceride levels.
Diabetologia. 2005;48(10):2025-32.

Abstract
AIMS/HYPOTHESIS Phosphoenolpyruvate carboxykinase (PCK) is the key enzyme involved in the regulation of gluconeogenesis. The aim of this study was to identify genetic polymorphisms in potential candidate genes for type 2 diabetes by sequencing all exons in the PCK genes (PCK1 and PCK2), and examining the association with type 2 diabetes and diabetic phenotypes in a Korean population (775 type 2 diabetic patients and 316 normal control subjects).
MATERIALS AND METHODS Twenty-two polymorphisms in PCK1 and PCK2 were identified in a Korean population (n=24) by direct DNA sequencing. The TaqMan genotyping method was applied for genotyping the remainder of the study population. Associations of PCK polymorphisms with the risk of type 2 diabetes and diabetic phenotypes were analysed using logistic and multiple regressions, adjusting for age, sex and BMI.
RESULTS Although no significant associations between the genetic polymorphisms in PCK genes and the risk of type 2 diabetes were detected, in further haplotype analysis, one of the common haplotypes, PCK1 ht3, revealed susceptibility to type 2 diabetes (p=0.006). One 3' untranslated region (UTR) single nucleotide polymorphism (SNP) also showed an association with HDL levels among non-diabetic control subjects: individuals homozygous for the major allele (T/T) had the lowest HDL level (1.11+/-0.32 mmol/l), heterozygotes (T/C) had an intermediate level (1.27+/-0.37 mmol/l), and those homozygous for the minor allele (C/C) had the highest level (1.39+/-0.28 mmol/l) (p=0.000003). This 3' UTR SNP was also associated with triglyceride levels, with a lower triglyceride level observed among individuals who were homozygous for the minor allele (C/C) than among those who were not.
CONCLUSIONS/INTERPRETATION The strong genetic association of HDL and triglyceride levels with variation/haplotype information identified in this study would be useful for further genetic epidemiological studies of this important gene.
PubMed IF 10.4 내분비대사내과
622005

제1저자 이광혁 · 교신저자 류지곤

, , , , ,
Mutation analysis of SPINK1 and CFTR gene in Korean patients with alcoholic chronic pancreatitis.
Dig Dis Sci. 2005;50(10):1852-6.

Abstract
Several genetic mutations have been reported to increase susceptibility to chronic pancreatitis. However, their roles in alcoholic chronic pancreatitis are controversial. We investigated the prevalence of SPINK1 N34S and new CFTR Q1352H mutations in alcoholic chronic pancreatitis in Korea. Forty-three patients with alcoholic chronic pancreatitis were enrolled and 35 healthy individuals served as controls. The SPINK1 N34S mutation was detected by the PCR-RFLP technique. The CFTR Q1352H mutation was examined with PCR direct sequencing. Mean age of chronic pancreatitis and control groups was 53.2 and 51.3 years, respectively. A SPINK1 N34S was detected as a heterozygote in one (2.4%) patient with alcoholic chronic pancreatitis and a heterozygote CFTR Q1352H was detected in one other patient. In the control population, neither SPINK1 nor CFTR mutation was detected. This study shows that SPINK1 N34S and CFTR Q1352H mutations are uncommon and do not play an important role in chronic alcoholic pancreatitis in Korea.
PubMed IF 2.8 소화기내과
612005

제1저자 김광일 · 교신저자 구본권

, , , , , , , , , , ,
Long-term clinical outcomes of dissections after intracoronary beta-radiation with rhenium-188-diethylene triamine penta-acetic acid-filled balloon system.
Int J Cardiol. 2005;104(2):190-6.

Abstract
BACKGROUND Intracoronary radiation with a rhenium-188 ((188)Re)-filled balloon is safe and efficiently reduces restenosis, but there is a potential risk of a (188)Re-filled balloon induced dissection. Little is known about the effect of radiation on dissection resolution and the late clinical outcome of dissection after brachytherapy.
METHODS After successful catheter-based treatments of de novo or restenotic lesion, 256 patients were randomly assigned to the radiation or control group. The (188)Re-filled balloon system was designed to deliver 17.6 Gy in 1.0-mm tissue depth.
RESULTS Dissections were identified in 15 patients among the 138 patients of the radiation group (10.9%). Additional stents were deployed in 10 patients to cover the flow-limiting dissection. Binary restenosis rate (53.3% vs. 16.3%, p=0.001) and target vessel revascularization (TVR) rate (53.3% vs. 11.1%, p<0.001) were significantly higher in patients with the dissection at 9 months. Geographic miss (GM) was identified in 4 of the 10 patients who underwent additional stenting. Binary restenosis rate in the GM group (100%; 4 of 4 patients) was significantly higher than the non-GM group (33.3%; 2 of 6 patients, p=0.02). Long-term follow-up of the patients with dissections who had not undergone TVR (n=7, mean follow-up duration: 640.7+/-387.3 days) has demonstrated persistent unhealed dissections.
CONCLUSIONS Intracoronary radiation impairs the healing process after vessel injury and residual dissection after brachytherapy leads to adverse clinical outcomes, which was mainly due to GM in case of stent implantation.
PubMed IF 3.3 순환기내과
602005

제1저자 김성한 · 교신저자 오명돈

, , , , , , , , , , , ,
Clinical responses to smallpox vaccine in vaccinia-naive and previously vaccinated populations: undiluted and diluted Lancy-Vaxina vaccine in a single-blind, randomized, prospective trial.
J Infect Dis. 2005;192(6):1066-70.

Abstract
We conducted a single-blind, randomized trial of 2 dilutions (1:1 or 1:10) of Lancy-Vaxina vaccine (Berna Biotech) in vaccinia-naive persons (n=36) and persons previously vaccinated >25 years ago (n=76). All vaccinees responded successfully to the vaccination. There were no significant differences in the size of the skin lesions, the number of adverse events, the amount of viral shedding, or the level of antibody responses between the undiluted (n=56) and diluted (n = 56) vaccine groups. Compared with vaccinia-naive persons, previously vaccinated persons exhibited significantly smaller and more rapidly evolving skin lesions and fewer adverse events. Previously vaccinated persons had significantly higher neutralizing antibody levels before the administration of the study vaccine than vaccinia-naive persons, and viral shedding from lesions in previously vaccinated persons was lower and diminished more rapidly than from lesions in vaccinia-naive persons.
PubMed IF 4.1 감염내과
592005

제1저자 윤창환 · 교신저자 김효수,박영배

, , , , , , , , , , , , ,
Synergistic neovascularization by mixed transplantation of early endothelial progenitor cells and late outgrowth endothelial cells: the role of angiogenic cytokines and matrix metalloproteinases.
Circulation. 2005;112(11):1618-27.

Abstract
BACKGROUND Two types of cells are cultured from the human peripheral blood, early endothelial progenitor cells (EPCs) and outgrowth endothelial cells (OECs), as previously reported. Here, we further characterize these cells, especially with respect to their different origins and functions both in vitro and in vivo. We also investigated whether the combination of these different cell types shows synergism during neovascularization.
METHODS AND RESULTS Early EPCs were heterogeneously made up of both CD14+ monocyte-derived cells, which secrete cytokines, and CD14(-)-derived cells, which contain high levels of (CD34+)KDR+ cells. OECs were cultured almost exclusively from CD14- cells, not CD14+ cells, and were distinct from mature endothelial cells in terms of proliferation potential, KDR+ expression level, and telomerase activity. A portion of cells from CD14- cells and early EPCs produced rapidly proliferating, capillary-forming cells in both the Matrigel plug and the ischemic hind limb similar to OECs. Early EPCs and OECs expressed receptors for vascular endothelial growth factor and interleukin-8, cytokines secreted by early EPCs. There was a differential increase in matrix metalloproteinases (MMPs): MMP-9 in early EPCs and MMP-2 in OECs. In vitro, the angiogenic capability of the 2 cell types was augmented by mutual interaction through cytokines and MMPs. Injection of a mixture of the 2 cells resulted in superior neovascularization in vivo to any single-cell-type transplantation.
CONCLUSIONS Distinct origins of the different types of EPCs exist that have different functions in neovascularization. Mixed transplantation of these cells results in synergistic neovascularization through cytokines and MMPs.
PubMed IF 41.3 순환기내과

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