Biomedical subjects

Shing-Jong Lin

Publications and source records attributed to Shing-Jong Lin.

50 records · Page 3Linked to original sources

PubMed2003

Impact on the thrombogenicity of surface oxide properties of 316l stainless steel for biomedical applications.

Surface oxide film on cardiovascular devices could be one of the most critical factors that determine the degree of thrombosis. Previous studies have shown that metallic wire passivated with amorphous oxide film provides excellent corrosion and scratch resistance. Investigation was undertaken to see whether this oxide film, with its unique electrochemical properties, could reduce the development of thrombosis. Results show that amorphous oxide has higher value of time constant, lower open-circuit potential, and lower degree of thrombosis. These distinguished characteristics prove amorphous oxide to be the best candidate for the cardiovascular devices. Amorphous oxide film could be a potential solution to the thrombogenic problem of cardiovascular devices.

Animals↗

PubMed2003

Ginkgo biloba extract inhibits tumor necrosis factor-alpha-induced reactive oxygen species generation, transcription factor activation, and cell adhesion molecule expression in human aortic endothelial cells.

OBJECTIVE: This study was conducted to examination whether Ginkgo biloba extract (GBE), a Chinese herb with antioxidant activity, could reduce cytokine-induced monocyte/human aortic endothelial cell (HAEC) interaction, a pivotal early event in atherogenesis. METHODS AND RESULTS: Pretreatment of HAECs with GBE (50 and 100 microg/mL for 18 hours) significantly suppressed cellular binding between the human monocytic cell line U937 and tumor necrosis factor-alpha (TNF-alpha)-stimulated HAECs by using in vitro binding assay (68.7% and 60.1% inhibitions, respectively). Cell enzyme-linked immunosorbent assay and immunoblot analysis showed that GBE (50 microg/mL for 18 hours) significantly attenuated TNF-alpha-induced cell surface and total protein expression of vascular cellular adhesion molecule-1 and intracellular adhesion molecule-1 (63.5% and 69.2%, respectively; P<0.05). However, pretreatment with probucol (5 micromol/L for 18 hours) reduced the expression of vascular cellular adhesion molecule-1 but not intracellular adhesion molecule-1. Preincubation of HAECs with GBE or probucol significantly reduced intracellular reactive oxygen species formation induced by TNF-alpha (76.8% and 68.2% inhibitions, respectively; P<0.05). Electrophoretic mobility shift assay demonstrated that both GBE and probucol inhibited transcription factor nuclear factor-kappaB activation in TNF-alpha-stimulated HAECs (55.2% and 65.6% inhibitions, respectively) but only GBE could inhibit the TNF-alpha-stimulated activator protein 1 activation (45.1% inhibition, P<0.05). CONCLUSIONS: GBE could reduce cytokine-stimulated endothelial adhesiveness by downregulating intracellular reactive oxygen species formation, nuclear factor-kappaB and activator protein 1 activation, and adhesion molecule expression in HAECs, supporting the notion that the natural compound Ginkgo biloba may have potential implications in clinical atherosclerosis disease.

Aorta↗

PubMed2003

Expression of interleukin-1 beta and interleukin-1 receptor antagonist in oxLDL-treated human aortic smooth muscle cells and in the neointima of cholesterol-fed endothelia-denuded rabbits.

The migration of vascular smooth muscle cells (VSMCs) from the media to the intima and the proliferation of intimal VSMCs are key events in restenotic lesion development. These events, which are preceded and accompanied by inflammation, are modulated by the proinflammatory cytokine, interleukin-1 beta (IL-1 beta), which induces vascular smooth muscle cells to express adhesion molecules and to proliferate. IL-1 beta action is complex and regulated, in part, by its naturally occurring inhibitor, the IL-1 receptor antagonist (IL-1ra). Whether there was a temporal and spatial correlation between IL-1 beta and IL-1ra expression in, and release by, oxidized low density lipoproteins (oxLDL)-stimulated human aortic smooth muscle cells (HASMCs) was determined by using ELISA and Western blot. In addition, IL-1 beta and IL-1ra expression was detected in the neointima of endothelia-denuded cholesterol-fed New Zealand white rabbits by immunohistochemistry and Western blot. In HASMCs, oxLDL induced IL-beta and IL-1ra expression and release in a dose- and time-dependent manner. Treatment with 20 microg/ml oxLDL resulted in increased IL-1 beta release after 6 h, which peaked at 24 h, and in increased IL-1ra release, first seen after 12 h, but continuing to increase for at least 48 h. In the cells, IL-beta expression showed a similar pattern to release, whereas IL-1ra expression was seen in unstimulated cells and was not increased by oxLDL treatment. Confocal microscopy showed colocalization of IL-beta and IL-1ra expression in oxLDL-stimulated HASMCs. oxLDL caused significant induction of nuclear factor kappa B and activator protein-1 DNA binding activity in HASMCs (6.6- and 3.3-fold, respectively). In cholesterol-fed endothelia-denuded rabbits, the notably thickened intima showed significant IL-1 beta and IL-1ra expression. These results provide further support for the role of IL-1 system in the pathogenesis of restenosis. This is the first demonstration of IL-1 beta and IL-1ra expression and secretion of oxLDL-treated HASMCs and their expression in the rabbit neointima, suggesting that the smooth muscle cells of the intima are an important source of these factors.

Animals↗

PubMed2003

Asymmetrical dimethylarginine: a novel risk factor for coronary artery disease.

BACKGROUND: Asymmetrical dimethylarginine (ADMA) is an endogenous competitive inhibitor of nitric oxide synthase and has been associated with systemic atherosclerosis; however, the role of ADMA in patients with coronary artery disease (CAD) has not been investigated. HYPOTHESIS: The present study was designed to determine whether the plasma ADMA level predicts the presence of CAD independently, and whether the plasma ADMA level correlates with the extent and severity of coronary atherosclerosis. METHODS: In all, 97 consecutive patients with angina and positive exercise stress test were enrolled prospectively for coronary angiography. According to the result of angiography, the subjects were divided into two groups: Group I (n = 46): patients with normal coronary artery or mild CAD (< 50% stenosis of major coronary arteries); Group 2 (n = 51): patients with significant CAD (> or = 50% stenosis of majorcoronary arteries). Plasma levels of ADMA and L-arginine were determined by high-performance liquid chromatography. In addition, we used coronary atherosclerotic score to assess the extent and severity of CAD. RESULTS: The plasma levels of ADMA in Group 2 patients were significantly higher than those in Group 1 patients (0.66 +/- 0.17 microM vs. 0.44 +/- 0.09 microM, p < 0.001); these were accompanied by significantly lower plasma L-arginine/ADMA ratio in patients with significant CAD (Group 1 vs. 2: 194.0 +/- 55.3 vs. 136.7 +/- 50.3, p < 0.001). In a multivariate stepwise logistic regression analysis, both plasma ADMA level and plasma L-arginine/ADMA ratio were identified as independent predictors for CAD. Moreover, there were significant positive and negative correlations between coronary atherosclerotic score and plasma ADMA level as well as plasma L-arginine/ADMA ratio, respectively (plasma ADMA level: r = 0.518, p < 0.001; L-arginine/ADMA ratio: r = -0.430, p < 0.001). CONCLUSIONS: Both plasma ADMA level and plasma L-arginine/ADMA ratio were useful in predicting the presence of significant CAD and correlated significantly with the extent and severity of coronary atherosclerosis. Our findings suggest that plasma ADMA level may be a novel marker of CAD.

Aged↗

PubMed2003

Plasma levels of asymmetrical dimethylarginine and adverse cardiovascular events after percutaneous coronary intervention.

AIMS: We investigated the predictive value of plasma concentration of asymmetrical dimethylarginine (ADMA) on clinical outcome in patients undergoing percutaneous coronary intervention (PCI). METHODS AND RESULTS: One-hundred and fifty-three consecutive patients with stable angina and undergoing PCI were prospectively enrolled for clinical follow-up. Plasma ADMA levels were determined before procedure by high performance liquid chromatography. The major adverse cardiovascular events included cardiovascular death, myocardial infarction, and repeat revascularization of target vessels. Patients were grouped into tertiles according to their plasma ADMA levels. Over a follow-up period of 16 months (median), cardiovascular events occurred in 6 patients of tertile I (<0.50microM), in 17 patients of tertile II (0.50-0.62microM), and in 28 patients of tertile III (>0.62microM), P<0.001. By multivariate analysis, tertiles of ADMA levels were independently associated with a higher risk of adverse cardiovascular events after PCI (relative risk: tertile II vs I: 3.0 [1.2-7.7], P=0.022; tertile III vs I: 5.3 [2.2-12.9], P<0.001). Moreover, plasma ADMA level in the highest tertile also appeared as a significant risk factor of subsequent death and non-fatal myocardial infarction after PCI (tertile III vs I, P=0.04). CONCLUSION: Pre-procedural plasma ADMA levels may independently predict subsequent adverse cardiovascular events in patients undergoing PCI. Measurement of plasma ADMA levels could provide a rationale for risk stratification of patients by measuring ADMA levels before intervention.

Aged↗

PubMed2003

Quantitative evaluation of thrombosis by electrochemical methodology.

Electrochemical reactions between blood and metal electrodes have been studied since 1928. Little is known about the actual current density induced during the reaction. In this study, an in situ continuous monitoring method was developed to detect the progress of thrombosis on an oxidized 316L stainless steel coil was deployed inside the artery. Three stages of current density were observed on a 316L wire passivated with polycrystalline oxide film. In contrast, no significant current density was detected for a wire passivated with amorphous oxide film. Results showed that this in situ electrochemical monitoring method is sensitive to the passivated film on the stainless steel coil and could provide efficient and reliable information on the control of thrombosis on cardiovascular devices.

Electrochemistry↗

PubMed2003

The prognostic value of circulating soluble cell adhesion molecules in patients with chronic congestive heart failure.

BACKGROUND: Circulating soluble (s) cell adhesion molecules (CAMs) are elevated in patients with congestive heart failure (CHF) and may play an important role in the pathogenesis of CHF by mediating the cell-cell interactions of the immune response. However, clinical data about the prognostic value of sCAMs are sparse. The purpose of this study is to determine whether various sCAMs can provide prognostic information in patients with CHF. METHODS: We measured circulating levels of three sCAMs (vascular cell adhesion molecule-1, intercellular adhesion molecule-1, and sP-selectin) in 74 patients with symptomatic chronic CHF and left ventricular ejection fraction (LVEF) <50%. We compared these levels with those of a group of 19 age-matched control subjects. Major adverse cardiac events (death, heart transplantation or hospitalization with worsening CHF) during a median follow-up period of 240 days were determined. RESULTS: The concentrations of the three sCAMs in the 74 patients with CHF were significantly associated with one another. Their levels were higher than those of the control subjects and increased with the severity of CHF. Significantly higher sCAM levels were noted in those patients who had major adverse cardiac events during the follow-up period. There were significant negative correlations between LVEF and sCAMs. However, only high levels of sP-selectin were found to be an independent significant predictor of CHF by Cox proportional hazards analysis. CONCLUSIONS: These findings indicate that the levels of these three sCAMs increase with the severity of CHF and are related to clinical outcomes. Among them, high levels of sP-selectin can provide prognostic information independently in patients with CHF.

Aged↗

PubMed2003

Prevalence of antilipemic drug use in Taiwan: analysis of a sampling cohort within the national health insurance.

BACKGROUND: Hyperlipidemia is a major risk factor of cardiovascular diseases. We investigated the utilization ofantilipemic drugs at the outpatient sector within the National Health Insurance in Taiwan. METHODS: We obtained the first cohort (n = 50,000) dataset from the National Health Insurance Research Database and analyzed the outpatient claim files of the cohort in 2000. The antilipemic drugs were defined as the drug items belonging to the group C10 (serum lipid reducing agents) of the Anatomical Therapeutic Chemical classification system. RESULTS: Among the cohort with 46,614 eligible people, 760 patients had ever received antilipemic drugs (prevalence: 1.6%). The group 60-69 years of age had the greatest age-specific prevalence (7.2%), followed by the group over 70 years of age (6.0%). There were more male than female patients, but female patients outnumbered male patients before the age of 49 years. The antilipemic drugs had been prescribed 3,850 times totally with 70,272 defined daily doses (DDDs). On an average, a patient with antilipemic therapy received 5.1 (+/- 4.5) prescriptions of antilipemic drugs in one year and a prescription contained 18.3 (+/- 11.5) DDDs. We measured 4.1 DDDs per 1,000 inhabitants per day for all antilipemic drug use in 2000. The statins and fibrates predominated the antilipemic drug use. While gemfibrozil was most popular in respect of recipients and prescription items, simvastatin had the largest amount of use in unit of DDDs. Diabetes mellitus co-existed in 37.8% of the patients with antilipemic therapy and the standardized morbidity ratio (SMR) was 3.34. The other concomitant diseases included essential hypertension (rate: 48.8%, SMR: 2.40) and other heart disease (rate: 30.7%, SMR: 2.36). CONCLUSIONS: Statins were the leading antilipemic drugs in Taiwan. The users of antilipemic drugs were more likely to have concomitant diabetes mellitus, hypertension and heart disease.

Adolescent↗

PubMed2002

Long-term angiotensin-converting enzyme inhibition reduces plasma asymmetric dimethylarginine and improves endothelial nitric oxide bioavailability and coronary microvascular function in patients with syndrome X.

Angiotensin-converting enzyme (ACE) inhibition has been shown to improve clinical myocardial ischemia in patients with syndrome X (angina pectoris, positive treadmill exercise test, normal coronary angiograms, and no evidence of coronary spasm). This study was conducted to investigate the effects of long-term ACE inhibitors on endothelial nitric oxide (NO) metabolism and coronary microvascular function in patients with syndrome X. After a 2-week washout period, 20 patients with syndrome X were randomized to receive either enalapril, an ACE inhibitor, 5 mg twice daily (n = 10) or placebo (n = 10) in a double-blind design for 8 weeks. Another 6 age- and gender-matched subjects with negative treadmill exercise tests were also studied as controls. Compared with control subjects, patients with syndrome X had significantly reduced coronary flow reserve, reduced plasma levels of nitrate and nitrite (NOx), and a reduced plasma L-arginine to asymmetric dimethylarginine (ADMA) ratio (an index of systemic NO metabolism), as well as reduced endothelial function. These patients also had increased plasma levels of ADMA, which is an endogenous inhibitor of NO synthase and of von Willebrand factor, a marker of endothelial injury. Baseline characteristics including exercise performance and coronary flow reserve were similar between enalapril and placebo groups. After an 8-week treatment period, exercise duration (p = 0.001) and coronary flow reserve (p = 0.001) significantly improved with enalapril but not with placebo. Enalapril treatment, but not placebo, reduced plasma von Willebrand factor (p = 0.03) and ADMA levels (p = 0.01) and increased NOx levels (p = 0.01) and the ratio of L-arginine to ADMA (p <0.01). In patients with syndrome X, the plasma NOx level was positively and ADMA level inversely correlated with coronary flow reserve before and after the treatment. In conclusion, long-term ACE inhibitor treatment with enalapril improved coronary microvascular function as well as myocardial ischemia in patients with syndrome X. This may be related to the improvement of endothelial NO bioavailability with the reduction of plasma ADMA levels.

Aged↗

PubMed2002

Microsatellite polymorphism in promoter of heme oxygenase-1 gene is associated with susceptibility to coronary artery disease in type 2 diabetic patients.

Heme oxygenase is a rate-limiting enzyme in heme degradation, leading to the generation of free iron, biliverdin, and carbon monoxide. Induction of heme oxygenase-1 is implicated in the antioxidant defense mechanism and can modulate vascular function. To test the association of microsatellite polymorphism in the promoter region of human HO-1 gene with the risk of coronary artery disease (CAD) in type 2 diabetic patients, we examined the allele frequencies of (GT) (n) repeats in HO-1 gene in 474 patients with CAD and in 322 controls. A transient-transfection assay with HO-1 promoter/luciferase fusion constructs carrying various lengths of (GT) (n) repeats was performed to explore the regulatory effect of (GT) (n) repeats on HO-1 gene expression in cultured rat aortic smooth muscle cells. Serum thiobarbituric acid-reactive substances (TBARs), a measure of lipid peroxidation, was significantly higher in subjects carrying the L/L genotype (> or =32 repeats). Among type 2 diabetic subjects, the frequencies of the L alleles and proportion of genotypes with L alleles were significantly higher in those with CAD than in those without CAD. The adjusted odds ratio for CAD in type 2 diabetic patients with L alleles was 4.7 (95% confidence interval, 1.9-12.0, P=0.001). Transfection experiments in aortic smooth muscle cells revealed that HO-1 promoter/luciferase fusion constructs containing longer (GT) (n) repeats exhibited lower transcriptional activity. These results imply that the length polymorphism in the HO-1 gene promoter modulate the transcription of the gene in vascular cells. Type 2 diabetics carrying longer (GT) (n) repeats might have higher oxidative stress and increased susceptibility to the development of CAD.

Aged↗

PubMed2002

Clinical and angiographic determinants of adverse cardiac events in patients with stent restenosis.

Patients with angiographically proven stent restenoses do not necessarily develop adverse cardiac events. Which clinical, procedural, or angiographic parameters relate to the development of adverse cardiac events among these patients has not been determined. This study included 155 patients (167 stented lesions) with angiographically proven restenosis (> or = 50% diameter stenosis) within the stent or at its margins in routine follow-up angiograms that was obtained at 6.5 +/- 3.6 months after successful stenting. Thirty-six patients (22%) had adverse cardiac events (including unstable angina necessitating target lesion revascularization, acute myocardial infarction, or cardiac death) during follow-up and 119 patients (78%) were event-free. These two groups of patients were compared to determine the parameters related to adverse cardiac events. Univariate determinants of adverse events included hypertension (P = 0.023), unstable angina at initial presentation (P = 0.002), target lesion in proximal left anterior descending artery (P = 0.041), TIMI grade 0-2 flow in follow-up angiograms (p < 0.001), impaired left ventricular function at follow-up (P = 0.002), follow-up minimal lumen diameter < or = 0.6 mm (P = 0.003), follow-up diameter stenosis > 75% (P = 0.005), late loss > 2 mm (P = 0.01), and loss index > 1.127 (P < 0.001). Multivariate analysis demonstrated hypertension (odds ratio, OR, = 3.6; P = 0.019), unstable angina at initial presentation (OR = 2.6; P = 0.007), TIMI grade 0-2 flow at follow-up (OR = 2.8; P = 0.05), impaired LV function at follow-up (OR = 4.2; P = 0.004), and loss index > 1.127 (OR = 3.6; P = 0.017) as independent risk factors for adverse cardiac events. Classification and regression tree analysis identified loss index > 1.127 and impaired LV function as the two strongest determinant of adverse cardiac event. Therefore, hypertensive patients whose initial clinical presentation were unstable angina should be managed carefully to optimize the angiographic results and, most importantly, followed up more closely for development of impaired LV function after coronary stenting in order to prevent the occurrence of adverse cardiac event at follow-up.

Aged↗

PubMed2002

Effects of Ginkgo biloba extract on the proliferation of vascular smooth muscle cells in vitro and on intimal thickening and interleukin-1beta expression after balloon injury in cholesterol-fed rabbits in vivo.

Restenosis may develop in response to cytokine activation and smooth muscle cell proliferation. Ginkgo biloba extract (EGb) has been used to treat cardiovascular and cerebrovascular diseases. In the present study, the effects of EGb on the growth of cultured vascular smooth muscle cells (VSMC), as well as on the expression of interleukin-1beta (IL-1beta) and the intimal response in balloon-injured arteries of cholesterol-fed rabbits, were investigated. Using bromodeoxyuridine incorporation as an index of cell proliferation, EGb was found to inhibit serum-induced mitogenesis of cultured rat aorta VSMC in a dose-dependent manner. In vivo, EGb and probucol ( positive control) reduced the atheroma area in thoracic aortas of male New Zealand white rabbits fed a 2% cholesterol diet for 6 weeks with balloon denudation of the abdominal aorta being performed at the end of the third week. Intimal hyperplasia, expressed as the intimal/medial area ratio, in the abdominal aortas was significantly inhibited in the both the EGb group (0.61 +/- 0.06) and the probucol group (0.55 +/- 0.03) compared to the C group (0.87 +/- 0.02). In the balloon-injured abdominal aorta, both EGb and probucol significantly reduced IL-1beta mRNA and protein expression and the percentage of proliferating cells. The inhibitory effects of EGb on the intimal response might be attributed to its antioxidant capacity. EGb may have therapeutic potential for the prevention of restenosis after angioplasty.

Angioplasty, Balloon↗

PubMed2002

Magnolol attenuates VCAM-1 expression in vitro in TNF-alpha-treated human aortic endothelial cells and in vivo in the aorta of cholesterol-fed rabbits.

1. In a previous study, we showed that magnolol, a potent antioxidant derived from a Chinese herb, attenuates monocyte chemotactic protein-1 (MCP-1) expression and intimal hyperplasia in the balloon-injured aorta of cholesterol-fed rabbits. Expression of cell adhesion molecules by the arterial endothelium and the attachment of leukocytes to the endothelium may play a major role in atherosclerosis. In the present study, the effects of magnolol on the expression of endothelial-leukocyte adhesion molecules and the activation of nuclear factor kappa B (NF-kappa B) in tumour necrosis factor-alpha (TNF-alpha)-treated human aortic endothelial cells (HAECs) were investigated. 2. Pretreatment of HAECs with magnolol (5 microM) significantly suppressed the TNF-alpha-induced expression of vascular cell adhesion molecule-1 (VCAM-1) (64.8+/-1.9%), but had no effect on the expression of intercellular cell adhesion molecule-1 and endothelial cell selectin. 3. Magnolol (5 and 10 microM) significantly reduced the binding of the human monocytic cell line, U937, to TNF-alpha-stimulated HAECs (58.4 and 56.4% inhibition, respectively). Gel shift assays using the (32)P-labelled NF-kappa B consensus sequence as probe showed that magnolol pretreatment reduced the density of the shifted bands seen after TNF-alpha-induced activation. Immunoblot analysis and immunofluorescence staining of nuclear extracts demonstrated a 58% reduction in the amount of NF-kappa B p65 in the nuclei in magnolol-treated HAECs. Magnolol also attenuated intracellular H(2)O(2) generation in both control and TNF-alpha treated HAECs. 4. Furthermore, in vivo, magnolol attenuates the intimal thickening and TNF-alpha and VCAM-1 protein expression seen in the thoracic aortas of cholesterol-fed rabbits. 5. Taken together, these data demonstrate that magnolol inhibits TNF-alpha-induced nuclear translocation of NF-kappa B p65 and thereby suppresses expression of VCAM-1, resulting in reduced adhesion of leukocytes. These results suggest that magnolol has anti-inflammatory properties and may play important roles in the prevention of atherosclerosis and inflammatory responses in vivo.

Animals↗

PubMed2002

Modified quantitative detection of apoptosis in coronary atherosclerosis.

BACKGROUND: Apoptosis, or programmed cell death, is a physiological cell death process that allows a tissue or organ to remove unwanted cells and responsible for the maintenance of stable cell numbers in tissues even in primary atherosclerotic or restenotic lesion of coronary artery. Previous studies on the apoptosis of coronary atherosclerosis are usually prone to run into qualitative description without the aid of "quantitative" evaluation. To eliminate such subjective errors, we have designed a triple immunofluorescent stain assessed by digital camera and computer-aided analysis system so that the actual quantitative apoptotic expression of coronary atherosclerotic development can be more precisely evaluated. METHODS: Specimens of coronary artery were obtained from consecutive patients undergoing coronary endarterectomy or cardiac transplantation. Twenty-seven blocks of paraffin tissue specimens from 16 patients were analyzed. According to the American Heart Association (AHA) classification of atherosclerotic lesion, type I, II, III lesions were defined as early lesions and the other three types: IV, V, and VI as advanced lesions. Apoptosis and cell types were recognized simultaneously by triple immunofluorescent stain combined with Hoechst, Terminal deoxynucleotidyl transferase-mediated dUTP Nick End-Labeling (TUNEL) and smooth muscle cell (SMC) marker staining. Apoptotic index deduced from TUNEL-positive nucleus number divided by Hoechst-positive nucleus number. Apoptotic cell-type index deduced from TUNEL-positive nuclei, which are surrounded by cell type fluorescent marker, divided by total TUNEL-positive nuclei. RESULTS: Fourteen early lesions and 13 advanced lesions of tissue specimens were analyzed in this study. The mean apoptotic index of early lesions was 2.60 +/- 1.72%, which is significantly lower than that of the advanced lesions (7.42 +/- 3.07%). The apoptosis between the tapering portion and lesion portion obtained from 10 coronary endarterectomy specimens was also significantly different (2.59 +/- 1.90% vs 8.10 +/- 3.20%). In either early or advanced lesions, the predominant cell type of apoptosis was SMC. CONCLUSIONS: The identical counting and quantification analytic method we designed is more accurate and quantitative than the traditional investigation in detecting and affirming the "homeostasis" role of apoptosis in the atherosclerotic pathogenesis process of coronary artery disease.

Adolescent↗