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Biomedical subjects

Yangsoo Jang

Publications and source records attributed to Yangsoo Jang.

At least 55 records · Page 3Linked to original sources
PubMed2005

Does a carbon ion-implanted surface reduce the restenosis rate of coronary stents?

BACKGROUND: Neointimal hyperplasia and resulting restenosis limit the long-term success of coronary stenting. Heavy metal ions induce an inflammatory and allergic reaction, and result in in-stent restenosis. However, a carbon ion-implanted surface might prevent heavy metal ions from diffusing into surrounding tissue. METHODS: 140 lesions in 140 patients with coronary lesions underwent implantation of carbon-implanted surface stents (Arthos(inert) stent group, n=70) or control stents (Arthos stent group, n=70). The primary end point was the in-stent restenosis and the secondary end point was the value of hs-CRP at 48 h and 6 months after coronary stenting. Clinical and angiographic follow-ups were performed at 6 months. RESULTS: The rate of in-stent restenosis was lower in the Arthos(inert) stent group (15.9%, 10/63) than in the Arthos stent group (20.9%, 13/62), but there were no significant differences between both groups (p=0.56). The value of hs-CRP at 48 h was lower in the Arthos(inert) stent group (13.9+/-13.4 mg/dl) than in the Arthos stent group (24.5+/-26.0 mg/dl) with significant differences (p=0.04). However, the differences between two groups were not statistically significant at 6 months (p=0.76). CONCLUSIONS: As compared with a standard coronary stent, a carbon ion-implanted stent shows no considerable benefit for the prevention of in-stent restenosis within the range of this study. Despite all the limitations of this study, a positive effect of a carbon ion-implanted stent in reducing inflammatory reaction after coronary revascularization seems likely.

Adult↗
PubMed2005

Transfection of mesenchymal stem cells with the FGF-2 gene improves their survival under hypoxic conditions.

Bone marrow mesenchymal stem cells (MSCs) have shown potential for cardiac repair following myocardial injury, but this approach is limited by their poor viability after transplantation. To reduce cell loss after transplantation, we introduced the fibroblast growth factor-2 (FGF-2) gene ex vivo before transplantation. The isolated MSCs produced colonies with a fibroblast-like morphology in 2 weeks; over 95% expressed CD71, and 28% expressed the cardiomyocyte-specific transcription factor, Nkx2.5, as well as a-skeletal actin, Nkx2.5, and GATA4. In hypoxic culture, the FGF-2-transfected MSCs (FGF-2-MSCs) secreted increased levels of FGF-2 and displayed a threefold increase in viability, as well as increased expression of the anti-apoptotic gene, Bcl2, and reduced DNA laddering. They had functional adrenergic receptors, like cardiomyocytes, and exposure to norepinephrine led to phosphorylation of ERK1/2. Viable cells persisted 4 weeks after implantation of 5.0 yen 105 FGF-2-MSCs into infarcted myocardia. Expression of cardiac troponin T (CTn T) and a voltage-gated Ca2+ channel (CaV2.1) increased, and new blood vessels formed. These data suggest that genetic modification of MSCs before transplantation could be useful for treating myocardial infarction and end-stage cardiac failure.

Animals↗
PubMed2005

Leptin induces hypertrophy via p38 mitogen-activated protein kinase in rat vascular smooth muscle cells.

The hypertrophy of vascular smooth muscle cells (VSMCs) is critical in vascular remodeling associated with hypertension, atherosclerosis, and restenosis. Recently, leptin has appeared to play a pivotal role in vascular remodeling. However, the mechanism by which leptin induces hypertrophy in vascular smooth muscle cells is still unknown. We studied the role of leptin as a potential hypertrophic factor in rat VSMCs. In the present study, leptin significantly increased [(3)H]leucine incorporation and the total protein/DNA ratio in VSMCs. The maximal hypertrophic effect was at 100ng/ml of leptin. Leptin induced phosphorylation and activation of p38 mitogen-activated protein (p38 MAP) kinase and of signal transducers and activators of transcription 3 in a concentration- and time-dependent manner. A p38 MAP kinase inhibitor SB203580 significantly inhibited leptin-induced hypertrophy, AG490 (a JAK2 inhibitor) partially inhibited it, and other MAP kinase inhibitors, PD98059 (an ERK inhibitor) and SP600125 (a JNK inhibitor), had no effect. These results indicate that leptin directly stimulates cellular hypertrophy via p38 MAP kinase in rat VSMCs.

Animals↗
PubMed2005

The utility of multi-detector row spiral CT for detection of coronary artery stenoses.

Contrast-enhanced multi-detector row spiral computed tomography (MDCT) was introduced as a promising noninvasive method for vascular imaging. This study examined the accuracy of this technique for detecting significant coronary artery stenoses. Both MDCT(Sensation 16, Siemens, Germany, 12x0.75 mm collimation and 0.42 sec rotation speed, 120 kV, 500 effective mA, and 2.7 mm/rotation table-feed) and invasive coronary angiography (CAG) were performed on 61 patients (mean age 59.2+/-10, 44 men) who were suspected of having coronary artery disease. All patients were treated with atenolol (25-50 mg) prior to imaging and the heart rate was maintained below 65 beats per minutes during image acquisition. The images were reconstructed in the diastole around TI-400 ms with a 0.5 mm increment and a 1.0 mm thickness. All coronary arteries with a diameter of 2.0 mm or more were assessed for the presence of a stenosis (>50% luminal narrowing). Two independent radiologists who were unaware of the results of the invasive CAG evaluated the MDCT data, and the results were compared with those from the invasive CAG (interval 1-27, mean 11 days). An evaluation of the CT coronary angiogram (CTCA) was possible in 58 of the 61 patients (95%). Image acquisition of the major coronary arteries including the left main trunk was available in 229 out of 244 arteries. Invasive CAG showed that 35 out of 58 patients had significant coronary artery stenoses by. patient analysis of those who could be evaluated showed that CT coronary angiography correctly classified 30 out of 35 patients as having at least 1 coronary stenosis (sensitivity 85.7%, specificity 91.3%, positive predictive value 93.8%, negative predictive value 80.8%). By analyzing each coronary artery, CAG found 62 stenotic coronary arteries in the 229 coronary arteries that could be evaluated. MDCT correctly detected 50 out of 62 stenotic coronary arteries and an absence of stenosis was correctly identified in 156 out of 167 normal coronary arteries (sensitivity 80.6%, specificity 93.4%, positive predictive value 81.9%, negative predictive value 92.8%). The non-invasive technique of MDCT for examining the coronary artery appears to be a useful method for detecting coronary artery stenoses with a high accuracy particularly with the proximal portion and large arteries.

Aged↗
PubMed2005

The Src/PLC/PKC/MEK/ERK signaling pathway is involved in aortic smooth muscle cell proliferation induced by glycated LDL.

Low density lipoproteins (LDL) play important roles in the pathogenesis of atherosclerosis. Diabetes is associated with accelerated atherosclerosis leading to cardiovascular disease in diabetic patients. Although LDL stimulates the proliferation of arterial smooth muscle cells (SMC), the mechanisms are not fully understood. We examined the effects of native LDL and glycated LDL on the extracellular signal-regulated kinase (ERK) pathway. Addition of native and glycated LDL to rat aorta SMCs (RASMCs) stimulated ERK phosphorylation. ERK phosphorylation was not affected by exposure to the Ca2+ chelator BAPTA-AM but inhibition of protein kinase C (PKC) with GF109203X, inhibition of Src kinase with PP1 (5 microM) and inhibition of phospholipase C (PLC) with U73122/U73343 (5 microM) all reduced ERK phosphorylation in response to glycated LDL. In addition, pretreatment of the RASMCs with a cell-permeable mitogen-activated protein kinase kinase (MEK) inhibitor (PD98059, 5 microM) markedly decreased ERK phosphorylation in response to native and glycated LDL. These findings indicate that ERK phosphorylation in response to glycated LDL involves the activation of PKC, PLC, and MEK, but is independent of intracellular Ca2+.

Animals↗
PubMed2005

Self-expanding coronary stent (Radius) implantation with cutting balloon angioplasty.

To evaluate the effect of cutting balloon (CB) angioplasty on the outcome of self-expanding coronary stent implantation, we compared the results of Radius stent implantation using two predilation strategies. Seventy de novo lesions in 70 patients (60 men) were included in the study. Stenting was performed after conventional angioplasty (n = 38, group 1) or CB angioplasty (n = 32, group 2). In-stent restenosis (ISR) rates of each group were 39 and 10% at 6-month follow-up (p = 0.02). Major adverse cardiac events occurred in 20 and 11%, respectively (p = 0.25). Multivariate analysis revealed that ISR was predicted only by lesion length > or = 20 mm. In conclusion, CB angioplasty did not reduce ISR after Radius stent implantation, when other independent risk factors, such as lesion length, were taken into consideration.

Aged↗
PubMed2005

Can pro-brain natriuretic peptide be used as a noninvasive predictor of elevated left ventricular diastolic pressures in patients with normal systolic function?

OBJECTIVES: This study was sought to investigate whether plasma N-terminal pro-brain natriuretic peptide (proBNP) can help identify patients with an elevated left ventricular end-diastolic pressure (LVEDP) or filling pressures in patients with a normal systolic function. BACKGROUND: The proBNP is a good predictor of an elevated LVEDP in patients with a systolic dysfunction. However, whether proBNP can predict an elevated LVEDP in patients with a normal systolic function remains to be determined. METHODS: The LV pressures were measured by fluid-filled catheters in 216 patients (125 men, mean age 60 +/- 10 years) with a normal systolic function (ejection fraction 66% +/- 8%, range 50%-81%) who were undergoing diagnostic cardiac catheterization. The proBNP was sampled at the time of cardiac catheterization and was measured using a quantitative electrochemiluminescence immunoassay. RESULTS: The log-transformed proBNP levels correlated significantly with the LVEDP (r = 0.33, P = .001) and LV pre-A-wave pressure (pre-A pressure) (r = 0.31, P = .001). An elevated proBNP, defined as >315 pg/mL, predicted an LVEDP > or = 15 mm Hg with a sensitivity of 16% and a specificity of 95% as well as a pre-A pressure > or = 15 mm Hg with a sensitivity of 36% and a specificity of 95%. However, among the 93 patients with an LVEDP > or = 15 mm Hg, 77 (83%) patients had a normal proBNP concentration (< 315 pg/mL). CONCLUSION: The proBNP level showed weak correlations with the LVEDP and LV pre-A pressure in patients with a normal systolic function. Although high proBNP levels can predict an elevated LV diastolic pressure with high specificity, the sensitivity was quite low. Because the majority of patients with an elevated LVEDP had a normal proBNP, the proBNP level may not be suitable as a screening test for assessing LV filling pressures in the presence of normal systolic function.

Adult↗
PubMed2005

A beneficial effect of simvastatin on DNA damage in 242T allele of the NADPH oxidase p22phox in hypercholesterolemic patients.

BACKGROUND: The effect of simvastatin on DNA damage in hypercholesterolemic patients was investigated, and the relationship between the C242T polymorphism of the NADPH oxidase p22phox gene and the antioxidant effects of simvastatin was examined. METHODS: Simvastatin (20-40 mg /day) was administered for 8 weeks in 72 hypercholesterolemic patients. DNA damage in lymphocytes was quantified using single-cell gel electrophoresis (COMET assay) by measuring tail DNA (%), tail length (microm) and tail moment (tail length x % tail DNA/100). RESULTS: Simvastatin significantly reduced DNA damage as expressed by tail DNA (%, p< 0.001), tail length (mum, p<0.001) and tail moment on the DNA in lymphocytes (p<0.001) after 8 weeks. The frequencies of the C242T genotypes for CC, TC, and TT were 75.0%, 23.6% and 1.4% in the subjects. In the presence of the 242T allele, there were higher levels of baseline DNA damage and also a greater improvement in the DNA damage after 8 week simvastatin treatment compared with the CC homozygotes. CONCLUSION: Simvastatin significantly reduced DNA damage of hypercholesterolemic patients. This study showed that simvastatin has a beneficial effect on the improvement of DNA damage in patients with the 242T allele of NADPH oxidase p22phox gene.

Aged↗
PubMed2005

The case for strategic international alliances to harness nutritional genomics for public and personal health.

Nutrigenomics is the study of how constituents of the diet interact with genes, and their products, to alter phenotype and, conversely, how genes and their products metabolise these constituents into nutrients, antinutrients, and bioactive compounds. Results from molecular and genetic epidemiological studies indicate that dietary unbalance can alter gene-nutrient interactions in ways that increase the risk of developing chronic disease. The interplay of human genetic variation and environmental factors will make identifying causative genes and nutrients a formidable, but not intractable, challenge. We provide specific recommendations for how to best meet this challenge and discuss the need for new methodologies and the use of comprehensive analyses of nutrient-genotype interactions involving large and diverse populations. The objective of the present paper is to stimulate discourse and collaboration among nutrigenomic researchers and stakeholders, a process that will lead to an increase in global health and wellness by reducing health disparities in developed and developing countries.

Animals↗
PubMed2005

Association of the 276G->T polymorphism of the adiponectin gene with cardiovascular disease risk factors in nondiabetic Koreans.

BACKGROUND: The adiponectin gene is known to modulate adiponectin concentrations and diabetes mellitus development. OBJECTIVE: We assessed whether adiponectin gene variants contribute to circulating adiponectin, insulin resistance (IR), or cardiovascular disease risk factors. DESIGN: Nondiabetic subjects [n = 902; x +/- SE age: 42.5 +/- 0.53 y; body mass index (BMI; in kg/m2): 24.7 +/- 0.11] were genotyped for 2 single-nucleotide polymorphisms (SNPs), 45T-->G and 276G-->T. RESULTS: After adjustment for age, sex, and BMI, subjects with the G allele for the SNP 276 had significantly higher concentrations of triacylglycerol and small dense LDL (sdLDL) and smaller LDL particle size than did T/T subjects. G/G subjects at SNP 276 had significantly lower plasma adiponectin and higher homeostasis model assessment (HOMA) of IR and urinary prostaglandin F2alpha than did T/T subjects. In the SNP 45-276 haplotype test, we also observed that subjects with the X/X haplotype had significantly higher plasma adiponectin after adjustment than did TG/TG or TG/X haplotype subjects. In the highest BMI group (BMI > or = 26), T/T subjects had lower HOMA-IR (P = 0.011) and higher plasma adiponectin (P = 0.026) at SNP 276 than did G/G or G/T subjects. These patterns were also seen for adiponectin in haplotype groups. However, no significant genotype effect for SNP 45T-->G was observed. CONCLUSIONS: The 276G-->T polymorphism of the adiponectin gene modulates circulating adiponectin and IR, particularly in obese states. G allele carriers also have higher oxidative stress, higher sdLDL concentrations, and smaller LDL particle size. Therefore, the presence of the G allele in the adiponectin gene at SNP 276 could be a significant contributor to higher cardiovascular disease risk in Koreans, independent of common environmental factors.

Adiponectin↗
PubMed2005

Small-diameter blood vessels engineered with bone marrow-derived cells.

OBJECTIVE: The objective of this study is to investigate if bone marrow-derived cells (BMCs) regenerate vascular tissues and improve patency in tissue-engineered small-diameter (internal diameter = 3 mm) vascular grafts. SUMMARY BACKGROUND DATA: BMCs have demonstrated the ability to differentiate into endothelial-like cells and vascular smooth muscle-like cells and may offer an alternative cell source for vascular tissue engineering. Thus, we tissue-engineered small-diameter vascular grafts with BMCs and decellularized arteries. METHODS: Canine BMCs were differentiated in vitro into smooth muscle alpha-actin/smooth muscle myosin heavy-chain-positive cells and von Willebrand factor/CD31-positive cells and seeded onto decellularized canine carotid arteries (internal diameter = 3 mm). The seeded grafts were implanted in cell donor dogs. The vascular-tissue regeneration and graft patency were investigated with immunohistochemistry and angiography, respectively. RESULTS: The vascular grafts seeded with BMCs remained patent for up to 8 weeks in the canine carotid artery interposition model, whereas nonseeded grafts occluded within 2 weeks. Within 8 weeks after implantation, the vascular grafts showed regeneration of the 3 elements of artery (endothelium, media, and adventitia). BMCs labeled with a fluorescent dye prior to implantation were detected in the retrieved vascular grafts, indicating that the BMCs participated in the vascular tissue regeneration. CONCLUSIONS: Here we show that BMCs have the potential to regenerate vascular tissues and improve patency in tissue-engineered small-diameter vascular grafts. This is the first report of a small-diameter neovessel engineered with BMCs as a cell source.

Animals↗
PubMed2005

Insulin resistance is associated with arterial stiffness in nondiabetic hypertensives independent of metabolic status.

We sought to determine whether insulin resistance (IR) is related to arterial stiffness in nondiabetic hypertensive patients, independent of metabolic status and gender. IR has been associated with increased arterial stiffness in patients with diabetes. In nondiabetic hypertensive patients, the correlation between IR and arterial stiffness has yet to be investigated. We enrolled 284 nondiabetic patients who were being treated for hypertension. At the time of enrollment, the patients underwent a baseline laboratory assessment including homeostatic model assessment (HOMA) IR index and pulse wave velocity (PWV). The HOMA IR index is used as a marker of IR, and brachial to ankle PWV (baPWV) was used as a marker of arterial stiffness. Of the 284 study subjects, 121 were classified as having metabolic syndrome. The patients with metabolic syndrome were older than the non-metabolic syndrome patients (55.4+/-10.7 vs. 52.1+/-11.6 years, p=0.013), but there was no gender difference between the two groups. The average baPWV was significantly higher in the patients with metabolic syndrome (1,506+/-235 vs. 1,435+/-211 cm/s, p=0.009). The HOMA index was independently associated with an increase in arterial stiffness (r=0.548, p<0.001) after controlling for age, systolic blood pressure (SBP), heart rate, medication and gender. The independent association of HOMA with arterial stiffness was demonstrated in subgroup analysis, regardless of the metabolic status and gender. In conclusion, increased IR was associated with arterial stiffness, independent of age, baseline SBP, gender and heart rate. This independent association of IR was demonstrated regardless of gender and metabolic status.

Adult↗
PubMed2005

Endovascular therapy combined with immunosuppressive treatment for occlusive arterial disease in patients with Takayasu's arteritis.

PURPOSE: To evaluate the feasibility and efficacy of endovascular therapy combined with immunosuppression for the treatment of arterial occlusive disease in patients with Takayasu's arteritis (TA). METHODS: From January 1998 to June 2003, 25 patients (22 women; age 37.8+/-15.5 years) with TA were treated with angioplasty for symptomatic lesions or with a hemodynamically significant aortic narrowing. The patients with active disease, defined as an increase in inflammatory markers (e.g., erythrocyte sedimentation rate [ESR]), were treated with immunosuppressive agents before intervention. Angioplasty was performed after the ESR had been normalized. RESULTS: In the 25 patients, 58 vascular territories (7 aortic, 9 carotid, 3 vertebral, 11 subclavian, 2 superior mesenteric, 18 renal, 4 iliac, and 4 coronary arteries) were treated with angioplasty only (19 lesions) or with stents (39 lesions). The mean ESR when the vascular lesions were initially diagnosed was 35.6+/-26.2 mm/h, which fell to 18.5+/-7.8 mm/h after immunosuppressive therapy. The endovascular procedure was performed successfully in 52 (90%) of 58 lesions. During the mean 23.7+/-18.4-month follow-up, 9 (17%) treated segments restenosed; 4 were treated with repeat angioplasty. The overall cumulative primary clinical success rate was 82%; secondary clinical success was 90%. CONCLUSIONS: Endovascular therapy for stenotic lesions in patients with TA is safe and effective when disease activity is strictly controlled with immunosuppressive treatment.

Adolescent↗
PubMed2005

Hemostatic efficacy of hydrophilic wound dressing after transradial catheterization.

Here, we evaluate the efficacy of the Clo-Sur PAD nonwoven hydrophilic wound dressing (HWD) on hemostasis in an arterial-access site after transradial percutaneous coronary angiography compared with the RadiStop compression device (CD). Eighty patients who had undergone transradial coronary angiography with or without intravascular ultrasound were randomly assigned to the HWD or CD group. The time required to achieve hemostasis was measured, and the incidence of vascular complications was assessed. No significant differences in clinical and procedural characteristics were observed between the HWD group (n = 40) and the CD group (n = 40). A significant reduction in the time required to achieve hemostasis (58.7 +/- 32.6 minutes versus 131.3 +/- 59.1 minutes; p < 0.001) was associated with the use of HWD. The incidence of vascular complications was similar in both groups (5% for HWD versus 2.5% for CD; p = 0.500). No major complications, such as large hematoma or acute radial occlusion, occurred in the HWD group. In conclusion, HWD represents a safe alternative to the compression method. Hemostasis can be achieved more quickly using HWD, with no increase in access site complications, as compared to CD.

Bandages, Hydrocolloid↗
PubMed2004

Dominant negative insulin-like growth factor-1 receptor inhibits neointimal formation through suppression of vascular smooth muscle cell migration and proliferation, and induction of apoptosis.

Blocking of the IGF-1 signaling pathway targeting the IGF-1 receptor (IGF-1R) provides a potential treatment strategy for restenosis. In this study, we have examined the effects of a dominant negative IGF-1R (IGF-1Rt) on primary rat VSMCs in vitro and on injured rat carotid artery in vivo. Ad/IGF-1Rt infection inhibited VSMC migration and proliferation, and it also induced apoptosis by inhibiting phosphorylation of Akt and phosphorylation of ERK1/2. Consistent with the anti-proliferative and apoptotic effects in vitro, the Ad/IGF-1Rt infection markedly reduced neointimal formation in carotid injury model. Ad/IGF-1Rt treated carotid arteries exhibited a suppressed proliferation index, PCNA expression, and also were stained positive for TUNEL assay. These results indicate that a dominant negative IGF-1R has the potential to reduce neointimal formation of injured rats' carotid arteries. The delivery of dominant negative IGF-1R by adenoviral or other vectors may provide a useful strategy for inhibiting restenosis after angioplasty.

Angioplasty, Balloon↗
PubMed2004

Thiamine attenuates hypoxia-induced cell death in cultured neonatal rat cardiomyocytes.

Previous studies have demonstrated that thiamine (vitamin B1) has a cytoprotective effect against ischemic damage to the heart, and that heat shock protein 70 (Hsp70) is capable of protecting cardiac cells from lethal ischemia/hypoxia. We show here that thiamine has a cytoprotective effect on cultured neonatal rat cardiomyocytes under hypoxic insult, and also protects the cardiomyocytes against hypoxia-induced apoptosis; caspase-3 activation, PARP cleavage and DNA fragmentation are all inhibited. Moreover, it increases the level of Hsp70 protein in the cardiomyocytes even under prolonged hypoxic stress and its effects on hypoxia-induced cardiac cell death are antagonized by an Hsp70 inhibitor. These results suggest that the cytoprotective effect of thiamine in cardiomyocytes under hypoxic stress is due to its ability to induce Hsp70.

Animals↗
PubMed2004

Percutaneous interventional treatment of extracranial vertebral artery stenosis with coronary stents.

Stenosis of extracranial vertebral artery (VA) is not an infrequent lesion, and it can pose a significant clinical problem. However, the standard treatment for a significant VA stenosis has still not been established. Here in this study, we report our experiences of VA stenting in 25 patients (age 56.2 +/- 15.2 years, male 76%). The patients had comorbidities as follows: DM (36%), hypertension (64%), Takayasu's (12%) and Behcet's diseases (4%). There were combined involvement of other vessels such as the coronary artery (72%), carotid artery (36%), subclavian artery (32%) and the contralateral vertebral artery (24%). Indications for stenting were prior stroke or symptoms related to vertebrobasilar ischemia in 11 patients, and an asymptomatic but angiographically significant stenosis (> 70% stenosis) in 14 patients. Twenty-three balloon-expandable stents and two self-expandable stents were deployed. A drug-eluting coronary stent and distal balloon protection device were each used in one case. A technically successful procedure was achieved in all patients. The baseline reference diameter was 4.7 +/- 1.3 mm, minimal luminal diameter (MLD) 1.0 +/- 0.6 mm (diameter stenosis 77.8 +/- 12.5%) and lesion length 6.4 +/- 3.9 mm. After stenting and adjuvant dilation, the MLD was increased to 4.5 +/- 0.9 mm (diameter stenosis 3.1 +/- 17.9%). There were no procedure-related complications. During the further follow-up period of 25 (3-49) months, no stroke or death occurred. Restenosis was observed in 4 (30.8%) of 13 eligible patients. In conclusion, VA stenting is feasible with a high degree of technical success, and this treatment is associated with a relatively low incidence of procedure-related complications. However, a relative high rate of in-stent restenosis remains as a problem to be resolved.

Adult↗