Biomedical subjects

Ming-Jen Lu

Publications and source records attributed to Ming-Jen Lu.

6 recordsLinked to original sources

PubMed2006

Pericardial fluid and serum levels of vascular endothelial growth factor and endostatin in patients with or without coronary artery disease.

BACKGROUND/PURPOSE: Vascular endothelial growth factor (VEGF) and endostatin are related to ischemic heart disease. This study investigated pericardial fluid and serum levels of VEGF and endostatin in patients with or without ischemic heart disease. METHODS: A total of 39 patients (24 patients in the CAD group with significant coronary artery disease; 15 patients in the non-CAD group without coronary artery disease) undergoing open heart surgery were enrolled. In the CAD group, patients were classified according to good coronary collateralization (Group A; n = 11) or poor coronary collateralization (Group B; n = 13). Pericardial fluid and serum samples were obtained at the time of surgery. VEGF and endostatin were measured by enzyme-linked immunosorbent assay. RESULTS: The levels of endostatin in both serum and pericardial fluid were significantly lower in the CAD group than in the non-CAD group (130.5 +/- 37.3 ng/mL vs. 172.4 +/- 37.8 ng/mL and 119.0 +/- 25.0 ng/mL vs. 143.0 +/- 23.5 ng/mL). The concentration of serum VEGF in the CAD group (92.6 +/- 18.2 pg/mL) was significantly higher than that in the non-CAD group (75.2 +/- 22.3 pg/mL). The concentration of serum VEGF in Group A (100.1 +/- 20.7 pg/mL) was significantly higher than that in Group B (84.3 +/- 12.4 pg/mL). The levels of pericardial fluid VEGF, serum and pericardial fluid endostatin were not significantly different between Groups A and B. CONCLUSION: Patients with coronary artery disease have lower serum and pericardial fluid levels of endostatin and higher serum levels of VEGF. Serum level VEGF, but not endostatin, is associated with good or poor collateralization in patients with coronary artery disease.

Coronary Artery Disease↗

PubMed2005

A novel functional VKORC1 promoter polymorphism is associated with inter-individual and inter-ethnic differences in warfarin sensitivity.

Warfarin, a commonly prescribed anticoagulant, exhibited large inter-individual and inter-ethnic differences in the dose required for its anticoagulation effect. Asian populations, including Chinese, require a much lower maintenance dose than Caucasians, for which the mechanisms still remain unknown. We determined DNA sequence variants in CYP2C9 and VKORC1 in 16 Chinese patients having warfarin sensitivity (< or = 1.5 mg/day, n = 11) or resistance (> or = 6.0 mg/day, n = 5), 104 randomly selected Chinese patients receiving warfarin, 95 normal Chinese controls and 92 normal Caucasians. We identified three CYP2C9 variants, CYP2C9*3, T299A and P382L, in four warfarin-sensitive patients. A novel VKORC1 promoter polymorphism (-1639 G > A) presented in the homozygous form (genotype AA) was found in all warfarin-sensitive patients. The resistant patients were either AG or GG. Among the 104 randomly selected Chinese patients receiving warfarin, AA genotype also had lower dose than the AG/GG genotype (P < 0.0001). Frequencies of AA, AG and GG genotypes were comparable in Chinese patients receiving warfarin (79.7, 17.6 and 2.7%) and normal Chinese controls (82, 18 and 0%), but differed significantly from Caucasians (14, 47 and 39%) (P < 0.0001). The promoter polymorphism abolished the E-box consensus sequences and dual luciferase assay revealed that VOKRC1 promoter with the G allele had a 44% increase of activity when compared with the A allele. The differences in allele frequencies of A/G allele and its levels of VKORC1 promoter activity may underscore the inter-individual differences in warfarin dosage as well as inter-ethnic differences between Chinese and Caucasians.

Adult↗

PubMed2005

Spontaneous rupture of left ventricular true aneurysm.

The rupture of left ventricular true aneurysm is a rare event. We report the case of a 52-year-old man who presented to the emergency department with cardiac tamponade that was due to a ruptured left ventricular true aneurysm. An emergency operation was successfully performed to address this rare event.

Coronary Artery Bypass↗

PubMed2005

Carvedilol modulates the expression of hypoxia-inducible factor-1alpha and vascular endothelial growth factor in a rat model of volume-overload heart failure.

BACKGROUND: The use of beta-blockers has emerged as a beneficial treatment for congestive heart failure. Hypoxia-inducible factor-1alpha (HIF-1alpha) is tightly regulated in the ventricular myocardium. However, the expression of HIF-1alpha in chronic heart failure resulting from volume overload and after treatment with beta-blocker is little known. METHODS AND RESULTS: To test the hypothesis that HIF-1alpha plays a role in the failing myocardium because of volume overload, an aorta-caval shunt was created for 4 weeks in adult Sprague-Dawley rats to induce volume-overload heart failure. Carvedilol at 50 mg/kg body weight per day after surgery was given. The heart weight and body weight ratio increased from 2.6 +/- 0.3 in the sham group to 3.9 +/- 0.7 (P < .001) in the shunt group. Left ventricular end-diastolic dimension increased from 6.5 +/- 0.5 mm to 8.7 +/- 0.6 mm (P < .001). Treatment with carvedilol in the shunt group reversed the heart weight and ventricular dimension to the baseline values. Western blot showed that HIF-1alpha, vascular endothelial growth factor (VEGF), and brain natriuretic peptide (BNP) proteins were upregulated and nerve growth factor-beta (NGF-beta) downregulated in the shunt group. Real-time polymerase chain reaction showed that mRNA of HIF-1alpha, VEGF, and BNP increased and mRNA of NGF-beta decreased in the shunt group. Treatment with carvedilol reversed both protein and mRNA of HIF-1alpha, VEGF, BNP, and NGF-beta to the baseline values. Increased immunohistochemical labeling of HIF-1alpha, VEGF, and BNP in the ventricular myocardium was observed in the shunt group and carvedilol again normalized the labeling. CONCLUSION: HIF-1alpha and VEGF mRNA and protein expression were upregulated in the rat model of volume-overload heart failure. Treatment with carvedilol is associated with a reversal of abnormal regulation of HIF-1alpha and VEGF in the failing ventricular myocardium.

Adrenergic beta-Antagonists↗

PubMed2005

Temporal and spatial expression of hypoxia-inducible factor-1alpha and vascular endothelial growth factor in a rat model of myocardial ischemia with or without reperfusion.

BACKGROUND AND PURPOSE: Although hypoxia-inducible factor-1alpha (HIF-1alpha) plays a major role in the prevention of myocardial ischemia, the temporal and spatial patterns of expression of HIF-1alpha in myocardial ischemia-reperfusion are not well known. This study examined the role of HIF-1alpha and vascular endothelial growth factor (VEGF) in myocardial ischemia-reperfusion. METHODS: Adult Wistar rats were studied after ligation of the left anterior descending coronary artery (LAD) for 30 min and then after reperfusion. HIF-1alpha and VEGF were measured immediately after relief of occlusion and at 30 min, 1, 3, 6, and 24 h after reperfusion. HIF-1alpha and VEGF proteins were also measured 6 h after permanent occlusion of the LAD. RESULTS: HIF-1alpha and VEGF mRNA increased 1.8- and 1.4-fold, respectively, immediately after relief of occlusion and reached a maximum of 4.3- and 2.3-fold, respectively, at 3 h after reperfusion and remained elevated up to 24 h. HIF-1alpha and VEGF proteins increased immediately after relief of ischemia. HIF-1alpha protein significantly increased from 0.5 h to 24 h after reperfusion and VEGF protein significantly increased from 1 h to 6 h after reperfusion compared to the sham control. Administration of HIF-1alpha antisense oligonucleotide before ligation of the LAD significantly inhibited VEGF protein expression induced by ischemia-reperfusion. Immunohistochemical study showed increased immunoreactivity of HIF-1alpha and VEGF in the jeopardized myocardium after ischemia-reperfusion. HIF-1alpha and VEGF proteins were increased at 6 h after permanent occlusion of the LAD. CONCLUSIONS: This study demonstrated that HIF-1alpha and VEGF were co-induced in a temporal and spatial pattern after ischemia-reperfusion in the rat ventricular myocardium.

Animals↗

PubMed2003

Spontaneous cardiac rupture.

An 83-year-old woman had a sudden onset of loss of consciousness with no detectable blood pressure. Pulseless electrical activity was present in the electrocardiogram and massive pericardial effusion was found by echocardiography. Emergent subxiphoid pericardiotomy and drainage was immediately performed to release the cardiac tamponade at bedside and was followed by rushing the patient to the operating room for exploration. As a result a ruptured hole was identified on the posterior-lateral wall of the left ventricle and the defect was successfully repaired. The patient had an uneventful postoperative recovery and received postoperative study by cardiac catheterization, which disclosed coronary artery disease.

Aged↗