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Biomedical subjects

Yangsoo Jang

Publications and source records attributed to Yangsoo Jang.

At least 73 records · Page 4Linked to original sources

The impact of the preoperative severity of target-vessel stenosis on the short-term patency of radial artery grafts.

The fate of a grafted radial artery remains unknown. The purpose of this study was to determine whether the preoperative severity of stenosis of the target vessel influence short-term patency of radial artery (RA) grafts used as coronary artery bypass conduits. In 54 patients who had coronary artery bypass grafting (CABG) with RA grafts, RA patency was determined with multi-slice computed tomography (MSCT) 1 year after CABG. These patients were divided into three groups on the basis of the percentage of the target vessel stenosis: mild (< 60%, n=17), moderate (60% to 79%, n=19), and severe (>/= 80%, n=18). MSCT was also performed 1 week later to exclude early occlusion of RA grafts. In 3 patients, the MSCT failed to adequately discriminate the status of the RA graft due to poor image resolution. The overall incidence of RA occlusion was 23.5% (12 of 51) at 1 year in the entire population. The mild stenosis, moderate stenosis and severe stenosis group showed an occlusion rate of 50% (8 of 16), 23.5% (4 of 17) and 0% (0 of 18), respectively. The severe stenosis group had significantly lower rate of RA graft occlusion compared to the mild stenosis group (p < 0.001) and moderate stenosis group (p < 0.05). No difference in occlusion between grafts used for the different coronary artery branches could be demonstrated. Preoperative severity of the target coronary artery significantly affected the short-term RA grafts patency. Correct indication is the key factor for short-term RA patency.

Aged↗

Genetic analysis of the cardiac sodium channel gene SCN5A in Koreans with Brugada syndrome.

The SCN5A gene encodes the alpha subunit of the human cardiac voltage-gated sodium channel. Mutations in SCN5A are responsible for Brugada syndrome, an inherited cardiac disease that leads to idiopathic ventricular fibrillation (IVF) and sudden death. In this study, we screened nine individuals from a single family and 12 sporadic patients who were clinically diagnosed with Brugada syndrome. Using PCR-SSCP, DHPLC, and DNA sequencing analysis, we identified a novel single missense mutation associated with Brugada syndrome in the family and detected a C5607T polymorphism in Korean subjects. A single nucleotide substitution of G to A at nucleotide position 3934 changed the coding sense of exon 21 of the SCN5A from glycine to serine (G1262S) in segment 2 of domain III (DIII-S2). Four individuals in the family carried the identical mutation in the SCN5A gene, but none of the 12 sporadic patients did. This mutation was not found in 150 unrelated normal individuals. This finding is the first report of a novel mutation in SCN5A associated with Brugada syndrome in Koreans.

Base Sequence↗

Functional characterization of recombinant batroxobin, a snake venom thrombin-like enzyme, expressed from Pichia pastoris.

A thrombin-like enzyme of Bothrops atrox moojeni venom, batroxobin, specifically cleaves fibrinogen alpha chain, resulting in the formation of non-crosslinked fibrin clots. The cDNA encoding batroxobin was cloned, expressed in Pichia pastoris and the molecular function of purified recombinant protein was also characterized. The recombinant batroxobin had an apparent molecular weight of 33 kDa by SDS-PAGE analysis and biochemical activities similar to those of native batroxobin. The purified recombinant protein strongly converted fibrinogen into fibrin clot in vitro, and shortened bleeding time and whole blood coagulation time in vivo. However, it did not make any considerable alterations on other blood coagulation factors. Several lines of experimental evidence in this study suggest that the recombinant batroxobin is a potent pro-coagulant agent.

Amino Acid Sequence↗

Magnitude of left atrial V wave is the determinant of exercise capacity in patients with mitral stenosis.

A large left atrial (LA) V wave can be observed in patients with pure mitral stenosis (MS) due to decreased LA compliance. Based on the hypothesis that exercise capacity may correlate with the magnitude of the LA V wave in patients with MS, symptom-limited exercise testing and right and left heart catheterization were performed in 28 patients. The results show that the magnitude of the LA V wave (p = 0.02) was the strongest predictor of the exercise duration, suggesting that LA compliance may be an important contributing factor in determination of exercise capacity in patients with MS.

Adult↗

Association of the gene polymorphisms of platelet glycoprotein Ia and IIb/IIIa with myocardial infarction and extent of coronary artery disease in the Korean population.

Platelet membrane receptor glycoproteins (GP) are essential for the platelet activation process, and the genetic polymorphisms in the genes that encode platelet glycoproteins have been proposed to influence the risk of acute coronary syndrome and atherosclerosis. In this study, we investigated the role of GPIa, HPA-1 and HPA-3 polymorphisms as putative risk factors for myocardial infarction (MI) and the extent of coronary artery disease. We selected 1,073 subjects who underwent coronary angiography; 242 had normal or minimal coronary atherosclerosis, and 831 patients had significant coronary artery disease (CAD). The genotype was determined by the methods of single base extension for C807T/G873A polymorphisms of GPIa, and restriction fragment length polymorphism for HPA-1 and HPA-3. The C807T and G873A polymorphisms of GPIa showed complete linkage in the Korean population. For HPA-1 gene polymorphism, only the HPA-1a/a (PlA1/A1) genotype was observed in 192 selected subjects from our study population. The distribution of GPIa (C807T/G873A) and HPA-3 genotypes did not differ significantly between normal subjects and CAD subjects. No significant association between MI and both gene polymorphisms was present. However, for the subgroup analysis of young male patients whose age was less than 56 years, the genotype frequency of HPA-3b/b was significantly lower in patients with MI compared to patients without a history of MI (7.5% vs. 20.0%, p=0.04). The odds ratio for HPA-3 b homozygosity versus the HPA-3a carrier was 0.32 (95% CI, 0.10- 0.99, p=0.04). Conclusively, HPA-3 polymorphism was associated with MI in Korean individuals younger than 56 years of age, but other polymorphisms of GP, which we studied, were not associated with both the extent of coronary atherosclerosis or MI.

Aged↗

Clinical and echocardiographic characteristics of pericardial effusion in patients who underwent echocardiographically guided pericardiocentesis: Yonsei Cardiovascular Center experience, 1993-2003.

Percutaneous pericardiocentesis guided by two-dimensional echocardiography was introduced in 1983 as an alternative to electrocardiographically or fluoroscopically guided puncture for the management of pericardial effusion. The objective of this study was to investigate echocardiographically (echo)- guided pericardiocenteses performed at Yonsei Cardiovascular Center from January 1, 1993 to December 31, 2003, and also to determine whether patient profiles, etiology, and practice patterns have changed over this 11-year period. The medical records of 272 patients were examined and a follow-up survey was conducted. Patient clinical profiles, etiology, echocardiographic findings, and procedural details were determined for 2 periods: January, 1993 through December, 1997 (period 1); and January 1998 through December, 2003 (period 2). During the 11-year study period, 291 therapeutic, echo-guided pericardiocenteses with pericardial catheter drainage were performed in 272 patients. The number of pericardiocentesis in period 2 was increased compared with period 1 (191 cases vs. 100 cases). The mean age at pericardiocentesis increased from 49 +/- 17 years in period 1 to 55 +/- 16 years in period 2 (p < 0.05). The procedural success rate was 99% overall with a major complication rate of 0.7% (2 cases of right ventricular free wall perforation which required emergency operation). Only one procedure-related mortality (< 30 days) was noted. Malignancy was the leading cause of a pericardial effusion requiring pericardiocentesis (45.6%). The incidence of pericardial effusion following cardiothoracic surgery and percutaneous coronary intervention procedures accounted for nearly 20% of all pericardiocenteses performed. Echo-guided pericardiocentesis has become a safe, standard practice for clinically significant pericardial effusion, in line with the changes of patients profiles over the 11 years of the study.

Adult↗

Antiproliferative mechanisms of raxofelast (IRFI-016) in H2O2-stimulated rat aortic smooth muscle cells.

Reactive oxygen species-mediated cellular injury is involved in the pathogenesis of many diseases, including those affecting the cardiovascular system, such as myocardial ischemia-reperfusion injury, inflammation, and atheroscleosis. Raxofelast (IRFI-016; (+/-)-5-acetoxy-2, 3-dihydro-4, 6, 7-trimethyl-2-benzofuran-acetic acid) was designed with the aim of maximizing the antioxidant potency of phenols chemically related to vitamin E. The antioxidant activity of raxofelast has been convincingly demonstrated in several in vitro studies and in various models of ischemia-reperfusion injury. In this study, the antiproliferative effects of raxofelast were investigated to determine whether transduction signals and protooncogenes are affected in H(2)O(2)-stimulated rat aortic smooth muscle cells. In a tetrazolium-based colorimetric assay, the proliferation of rat aortic smooth muscle cells was increased by 3-fold in 0.1% fetal bovine serum/Dulbecco's modified Eagle's medium (DMEM) containing 500 microM H(2)O(2), indicating that exogenous 500 microM H(2)O(2) was a growth stimulator of rat aortic smooth muscle cells. Exogenous H(2)O(2) significantly activated extracellular signal-regulated kinases (ERKs) activity within 30 min and raxofelast inhibited the ERKs activation dose dependently in 500 microM H(2)O(2)-stimulated rat aortic smooth muscle cells (IC(50): 200 microM). Raxofelast reduced the intracellular reactive oxygen species generated by exogenous H(2)O(2) in a dose-dependent manner. In 500 microM H(2)O(2)-stimulated rat aortic smooth muscle cells, raxofelast dramatically attenuated the activation of mitogen-activating protein kinase (MAPK)/ERK kinase 1, 2 (MEK1,2) and protein kinase C (PKC) without affecting Ras expression. Induction of c-myc mRNA was significantly reduced dose dependently up to 100 microM by raxofelast in concentrations. These data indicate that the antiproliferative effects of raxofelast in H(2)O(2)-stimulated rat aortic smooth muscle cells may involve the suppression of intracellular reactive oxygen species formation and the inhibition of ERKs by inactivation through PKC and MEK1,2 and down-regulation of c-myc expression, regardless of Ras activation.

Animals↗

Overlapping vs. one long stenting in long coronary lesions.

Intervention of long coronary lesions remains problematic, and optimal treatment strategy is yet to be determined. Despite advancement of stent technology, data are few regarding the efficacy of overlapping stents vs. a single long stent in long coronary lesions. This study was performed to evaluate the results of those strategies for long coronary lesions and to determine the predictors of in-stent restenosis (ISR). Sixty-four lesions (> 20 mm) in 64 patients were treated with either one long stent (group 1, n = 32) or two overlapping stents (group 2, n = 32). Overlapping stents were used at tortuous or calcified lesions and at lesions with diameter discrepancy or significant dissection. Immediate results, follow-up clinical and angiographic outcomes, and predictors of ISR were evaluated. Procedures were successful in all patients in both groups. Clinical and angiographic follow-ups were performed in 54 (84%) cases and 50 (78%) cases, respectively. During the follow-up, major adverse cardiac event occurred in 36% of group 1 and 29% of group 2 (P = 0.56). Six-month ISR rates were 39% in group 1 and 41% in group 2 (P = 0.91). Age (>/= 65 years old) was an independent risk factor of ISR (54% vs. 23%; OR = 4.4; P = 0.04), and distal reference diameter (RD) of less than 2.5 mm tended to predict ISR in multivariate analysis (60% vs. 25%; OR = 3.5; P = 0.06). In conclusion, stent overlapping can be used with outcome similar to that of one long stent in long coronary lesions. The optimal result may be obtained by considering the patient's age and the distal vessel diameter of the lesion.

Aged↗

The prevalence and clinical predictors of atherosclerotic renal artery stenosis in patients undergoing coronary angiography.

Renal artery stenosis is an important cause of secondary hypertension as well as ischemic nephropathy. The purpose of this study was to determine the clinical predictors in patients with renal artery stenosis in a population referred for coronary angiography. From March 1998 to July 1999, 1459 patients undergoing coronary angiography for various indications were routinely screened for renal artery stenosis by undergoing abdominal aortography. Coronary angiography, carotid angiography, and abdominal aortography was performed via either the radial or the femoral approach. The data were analyzed retrospectively. Out of 1459 patients undergoing abdominal aortography, 158 (10.8%) were found to have significant renal artery stenosis with 24 of the patients having bilateral stenosis. Significant coronary artery diseases were found in 994 of the 1459 study population (68.1%), with 134 (13.5%) of these patients having concomitant renal artery stenosis. Multivariate logistic regression showed that extracranial carotid artery stenosis odds ratio [(OR) 4.89 (95% confidence interval 2.57-9.33), P < 0.001], peripheral artery disease [OR 4.64 (2.65-9.33), P < 0.001], renal insufficiency [OR 2.68 (1.43-5.02), P = 0.002], significant coronary artery disease [OR 2.01 (1.12-3.59), P = 0.019], hypercholesterolemia [OR 1.92 (1.07-3.43), P = 0.028], hypertension [OR 1.85 (1.16-2.95), P = 0.010], and old age (> 60 years) [OR 1.64 (1.01-2.64), P = 0.044] were significant clinical predictors of renovascular disease. The prevalence of indolent atherosclerotic renal artery stenosis is relatively high in selected groups of patients with high clincial risk factors for this underdiagnosed disease. Renal artery stenosis should be highly suspected in patients who have these risk factors because early detection of this disease may reverse the progression to chronic renal failure and end-stage renal disease.

Adult↗

Purification and molecular cloning of a novel serine protease from the centipede, Scolopendra subspinipes mutilans.

A novel serine protease, named as scolonase, was purified and characterized from the tissue of the Korean centipede, Scolopendra subspinipes mutilans. Purified scolonase showed an apparent molecular weight of 25 kDa on sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis and an isoelectric point of 4.8 on isoelectric focusing gel. Scolonase was able to preferentially hydrolyze arginine over lysine at the cleavage site among the several synthetic peptide substrates. Scolonase has also a potent fibrinolytic activity by converting human Glu-plasminogen to activated plasmin due to the specific cleavage of the molecule at the peptide bond Arg(561)-Val(562). The enzyme activity of scolonase was completely inhibited by phenylmethanesulfonyl fluoride and difluorophosphate. The cDNA encoding scolonase was cloned from the cDNA library of the centipede constructed with oligonucleotide probe, which was designed on the basis of the N-terminal amino acid sequence of scolonase. The deduced complete amino acid sequence of scolonase demonstrated that the protein is composed of 277 amino acids including 33 amino acids as a leader sequence, and that it has significant sequence homology with other serine proteases.

Amino Acid Sequence↗

Phospholipase C-delta1 rescues intracellular Ca2+ overload in ischemic heart and hypoxic neonatal cardiomyocytes.

Ischemia and simulated ischemic conditions cause intracellular Ca2+ overload in the myocardium. The relationship between ischemia injury and Ca2+ overload has not been fully characterized. The aim of the present study was to investigate the expression and characteristics of PLC isozymes in myocardial infarction-induced cardiac remodeling and heart failure. In normal rat heart tissue, PLC-delta1 (about 44 ng/mg of heart tissue) was most abundant isozymes compared to PLC-gamma1 (6.8 ng/mg) and PLC-beta1 (0.4 ng/mg). In ischemic heart and hypoxic neonatal cardiomyocytes, PLC-delta1, but not PLC-beta1 and PLC-gamma1, was selectively degraded, a response that could be inhibited by the calpain inhibitor, calpastatin, and by the caspase inhibitor, zVAD-fmk. Overexpression of the PLC-delta1 in hypoxic neonatal cardiomyocytes rescued intracellular Ca2+ overload by ischemic conditions. In the border zone and scar region of infarcted myocardium, and in hypoxic neonatal cardiomyocytes, the selective degradation of PLC-delta1 by the calcium sensitive proteases may play important roles in intracellular Ca2+ regulations under the ischemic conditions. It is suggested that PLC isozyme-changes may contribute to the alterations in calcium homeostasis in myocardial ischemia.

Animals↗

The -1131T-->C polymorphism in the apolipoprotein A5 gene is associated with postprandial hypertriacylglycerolemia; elevated small, dense LDL concentrations; and oxidative stress in nonobese Korean men.

BACKGROUND: Apolipoprotein A5 plays an important role in modulating triacylglycerol metabolism in experimental animal models. OBJECTIVE: The objective was to determine associations of the common apolipoprotein A5 gene (APOA5) -1131T-->C polymorphism with postprandial lipemic response and other cardiovascular disease risk factors in humans. DESIGN: Healthy, nonobese subjects [n = 158; mean (+/-SEM) age: 33.8 +/- 1.2 y; body mass index (in kg/m(2)): 23.3 +/- 0.3] were subdivided into 3 genotype groups: TT (n = 85), TC (n = 56), and CC (n = 17). We measured fasting and postprandial lipid concentrations, lipid peroxidation, C-reactive protein concentrations, and DNA damage. RESULTS: Fasting triacylglycerol concentrations in carriers of the C allele were higher (P < 0.05) than in carriers of the TT genotype. No other significant genotype-related differences were observed for any of the other baseline measures. After consumption of a mixed meal, carriers of the C allele had significantly greater increases in total chylomicron and VLDL triacylglycerol than did subjects with the TT genotype. Moreover, carriers of the C allele had higher dense LDL, serum C-reactive protein, and urinary 8-epi-prostaglandin F(2alpha) concentrations and more lymphocyte DNA damage. Conversely, we did not find significant genotype-related differences in postprandial glucose, insulin, or free fatty acid measures. CONCLUSIONS: Our data confirm the genetic modulation of serum fasting triacylglycerol concentrations by the APOA5 gene polymorphism and extend this observation to postprandial triacylglycerol concentrations and to markers of oxidation and inflammation. The presence of the C allele in the APOA5 promoter region at position 1131 could be a significant factor contributing to higher cardiovascular disease risk in Koreans independently of common environmental factors.

Adult↗

Comparison of a percutaneous separate stent endograft and a conventional thoracic stent-graft for endovascular repair of type B aortic dissection.

PURPOSE: To compare the immediate and midterm outcomes of aortic dissection repair with a separate stent endograft (SSE) versus a conventionally constructed thoracic stent-graft. METHODS: The records of 35 patients treated for type B aortic dissection from September 1997 to April 2003 were reviewed. Seventeen patients (12 men; mean age 58.8+/-11.6 years) underwent endovascular repair with a separate stent endograft (SSE), a custom-made device with a reduced profile suitable for percutaneous introduction through a 12-F sheath. Eighteen patients (10 men; mean age 56.1+/-12.8 years) underwent treatment with a conventional custom-made stent-graft. RESULTS: Angiographic success was achieved in 13/17 (76.5%) of the SSE-treated patients and 12/18 (66.7%) for the conventional device group (p=0.521). Clinical success (complete obliteration/thrombosis of the false lumen) was achieved in 12/17 (70.6%) and 11/18 (61.1%), respectively (p=0.555). There were 2 cases of stent-graft movement during deployment and 2 access site complications in the conventional stent-graft group, whereas the SSE patients had no complications. Except for 2 conventional stent-graft patients who were lost to follow-up, all patients are alive at a mean 19.5+/-11.6 months for the SSE group and 34.2+/-21.5 months for the conventional stent-graft patients. CONCLUSIONS: The separate stent endograft can be deployed percutaneously without the need for blood pressure reduction, achieving accurate deployment without migration. In this small clinical experience, patients treated with the SSE had no access site complications and demonstrated midterm results comparable to the conventional stent-graft cohort, suggesting the possible usefulness of this device for the treatment of thoracic aortic dissection.

Adult↗

Expanding false lumen in the abdominal aorta 5 years after endovascular repair of a type B aortic dissection: successful exclusion of 3 distal re-entry sites.

PURPOSE: To report endovascular treatment of an expanding aneurysmal false lumen several years after successful stent-graft deployment in the descending thoracic aorta for type B aortic dissection. CASE REPORT: A 54-year-old woman who had a stent-graft placed at the entry site of a type B aortic dissection 5 years prior presented with abdominal discomfort and palpable abdominal mass. Successful remodeling of the thoracic aorta was demonstrated by computed tomography; however, a false lumen aneurysm in the abdominal aorta had expanded from 4.8 to 6.5 cm and caused symptoms. She was successfully treated with 3 additional stent-grafts at 3 re-entry sites. Six months after the procedure, the false lumen aneurysm was completely excluded. CONCLUSIONS: Endovascular repair of the re-entry sites can prevent further expansion of false lumen aneurysm, which occurs in some patients with type B dissection treated with stent-grafts.

Aneurysm, False↗

Preventative effects of rosiglitazone on restenosis after coronary stent implantation in patients with type 2 diabetes.

OBJECTIVE: Despite the popularity of coronary stenting in coronary artery disease (CAD), restenosis remains a challenging clinical problem. This study evaluated the efficacy of rosiglitazone for preventing in-stent restenosis in type 2 diabetic patients. RESEARCH DESIGN AND METHODS: We conducted a prospective, randomized, case-controlled trial involving 95 diabetic patients with CAD who were randomly assigned to either the control or rosiglitazone group (48 and 47 patients, respectively). Quantitative coronary angiography (QCA) was performed at study entry and again at 6-month follow-up. The primary end point was the restenosis rate, which was determined by QCA. RESULTS: Eighty-three patients (45 patients with 55 lesions in the control group and 38 patients with 51 lesions in the rosiglitazone group) completed follow-up angiography. Rosiglitazone treatment for 6 months reduced fasting insulin concentration. The high-sensitivity C-reactive protein concentration was significantly reduced in the rosiglitazone group compared with that in the control group (from 2.92 +/- 1.98 to 0.62 +/- 0.44 mg/l, P < 0.001 vs. from 2.01 +/- 1.33 to 1.79 +/- 1.22 mg/l, P = NS). However, the baseline and follow-up glucose and lipid concentrations were not different between two groups. The rate of in-stent restenosis was significantly reduced in the rosiglitazone group compared with the control group (for stent lesions: 17.6 vs. 38.2%, P = 0.030). The rosiglitazone group had a significantly lower degree of diameter stenosis (23.0 +/- 23.4% vs. 40.9 +/- 31.9%, P = 0.004) compared with the control group. CONCLUSIONS: We demonstrated that treatment with rosiglitazone significantly reduces in-stent restenosis in diabetic patients with CAD who underwent coronary stent implantation.

Adult↗

Solution structure of a novel disintegrin, salmosin, from Agkistrondon halys venom.

Disintegrins are potent inhibitors of both platelet aggregation and integrin-dependent cell adhesion. A new disintegrin, salmosin, isolated from the venom of the Korean snake Agkistrodon halys brevicaudus, has been characterized by mass spectrometry and NMR spectroscopy, and its in vitro biological activity has been assessed. The IC(50) value of the purified salmosin was determined to be 2.2 nM in an assay for the inhibition of glycoprotein IIb-IIIa/fibrinogen interaction. Salmosin also inhibited the bovine capillary endothelial cell proliferation induced by bFGF in a dose-dependent manner. The NMR solution structures were well converged with a root-mean-square deviation of 0.76 A for backbone atoms among the 20 lowest energy structures, except for the arginylglycylaspartic acid (RGD) loop. The structure revealed that the conserved RGD motif with an unusual finger shape is distal from the rigid core of the C-terminal domain. Furthermore, even though the RGD motif did not interact with the hydrophobic core of the protein, it was stabilized by a network of molecular contacts through a small antiparallel beta-sheet comprising residues of Ile46-Ala50 and Asp54-Tyr58. Last, the electrostatic charge distribution on the surface of salmosin differs dramatically from that of other disintegrin proteins in that there is a cluster of negatively charged residues in close proximity to the RGD loop.

Amino Acid Sequence↗

Inhibitory effect of the salmosin gene transferred by cationic liposomes on the progression of B16BL6 tumors.

Salmosin is a novel disintegrin containing the Arg-Gly-Asp sequence that significantly inhibits platelet aggregation, basic fibroblast growth factor-induced endothelial cell proliferation, and tumor progression by antagonizing integrin-mediated cell interactions. Previously, it was shown that daily administration of salmosin was able to inhibit tumor-derived angiogenesis and adherence and proliferation of tumor cells, resulting in suppression of tumor progression. However, it is very difficult to maintain a therapeutic level of salmosin in the blood by systemic administration of the protein. Hence, an alternative strategy for antiangiogenic cancer therapy, based on the in vivo expression of the salmosin gene administered with cationic liposomes, was investigated. The salmosin peptides expressed in vitro inhibited the proliferation of bovine capillary endothelial cells in a dose-dependent manner, presumably as a result of inhibition of cell adhesion mediated via alpha(v)beta(3) integrin. Subcutaneous administration of the salmosin gene resulted in systemic expression of the gene product and concomitant inhibition of the growth of B16BL6 melanoma cells. Suppression of pulmonary metastases, verified by experimental and spontaneous metastasis models in mice, also resulted from salmosin gene treatment. These results suggest that administration of the salmosin gene complexed to cationic liposomes is effective in maintaining antiangiogenic salmosin at an effective therapeutic level and may be clinically applicable to anticancer gene therapy.

Animals↗

Visceral fat accumulation determines postprandial lipemic response, lipid peroxidation, DNA damage, and endothelial dysfunction in nonobese Korean men.

Visceral fat has been associated with multiple cardiovascular disease (CVD) risk factors. The aim of this study was to identify anthropometrical measures most closely associated with some well-known CVD risk factors. Because most Asians at risk have normal body mass index (BMI) according to Western standards, we studied healthy nonobese Korean males (n = 102; age: 36.5 +/- 0.8 years, BMI: 23.8 +/- 0.2 kg/m2). Visceral fat area (VFA) at the fourth lumbar vertebra was associated with increased postprandial triglyceride (TG) response (r = 0.53, P < 0.001) and with plasma malondialdehyde (MDA) (r = 0.36, P < 0.01) and PGF2alpha (r = 0.24, P < 0.05). When matched for BMI and age, men with high VFA (HVFA) (>/=100 cm2; n = 27) had higher blood pressure (P < 0.01), increased consumption of cigarettes (P < 0.01), and lower ratio of energy expenditure to calorie intake (P < 0.01) as compared with low VFA men (<100 cm2; n = 27). Men with HVFA showed higher TG, glucose, and insulin responses following fat and oral glucose tolerance tests respectively higher plasma concentrations of MDA (P < 0.001), urinary PGF2alpha (P < 0.05), and lymphocytes deoxyribonucleic acid tail moments (P < 0.01). Conversely, HVFA was associated with lower testosterone, insulin-like growth factor-1, and brachial artery flow-mediated dilation (P < 0.001). In conclusion, our data indicate that visceral fat accumulation, even in nonobese men, is a major factor contributing to increased CVD risk.

Adipose Tissue↗