Presence of mutation m.14484T>C in a Chinese family with maternally inherited essential hypertension but no expression of LHON.

Essential hypertension (EH, MIM 145500) is the most common cardiovascular disease and affects one-quarter of the world's adult population. Families with EH in a mode of maternal transmission have been occasionally observed in clinical settings and suggested an involvement of mitochondrial DNA (mtDNA) mutation. We aimed to characterize the role of mtDNA mutation in EH. We reported a large Han Chinese family with a maternally inherited EH and an extraordinarily high percentage of sudden death mainly in affected females. Analysis of the entire mtDNA genome of the proband identified a homoplasmic primary mutation m.14484T>C for Leber's hereditary optic neuropathy (LHON), along with several variants indicating haplogroup F1 status. Intriguingly, no maternal member in this family had LHON though they all harbored m.14484T>C. The arterial stiffness of the members carrying mutation m.14484T>C was significantly increased than that of non-maternal members without this mutation. No environmental factor (including age, sex, smoking, diabetes, hyperlipidemia) was correlated with the decreased aortic elastic properties observed in affected members. Mitochondrial respiration rate and membrane potential (ΔΨ(m)) were significantly reduced in lymphoblastoid cell lines established from affected members carrying m.14484T>C when compared to control cell lines (P<0.05). There was an elevation of reactive oxygen species and a compensatory increase of mitochondrial mass in mutant cell lines. Our results suggest that m.14484T>C causes EH under certain circumstance. This study provides a paradigm for diverse phenotypes of the primary LHON mutation and suggests for the necessity of routine cardiac evaluation in patients with the primary LHON mutation.

[Myocardial protective effects of luteolin on isolated rat heart in hypothermic preservation].

OBJECTIVE: To investigate the protective effect of luteolin on isolated rat heart in hypothermic preservation. METHODS: Forty male SD rats were randomly divided into 4 groups (n = 10): control group, luteolin low-dose group (7.5 micromol/L), middle-dose group (15 micromol/L) and high dose group (30 micromol/L). Langendorff model of isolated rat heart was used. After 30 min basal perfusion, the hearts were stored in University of Wisconsin solution (UW solution) at 4 degrees C with luteolin (7.5, 15 and 30 micromol/L) or without luteolin for 12 h and followed by 60 min reperfusion. The recovery of cardiac contractile and diastolic function, coronary flow (CF), creatine kinase (CK) leakage in the coronary effluent, myocardial water content were determined. The myocardial ultrastructure was also observed. RESULTS: The results revealed that luteolin improved the recovery of left ventricular peak systolic pressure and +/- dp/dtmax dose-dependently and increased coronary flow. The leakage of creatine kinase in the coronary effluent was significantly reduced in luteolin-added hearts. Impairment of myocardial ultrastructure after 12 h hypothermic preservation was obviously alleviated in hearts luteolin-added group compared with that in control group. There were no differences between the groups in myocardial water contents. CONCLUSION: Luteolin as a supplementation in cardiac preservation solution can significantly improve the hypothermic preservation effects on rat heart and have myocardial protection effect, especially in luteolin-added with 30 micromol/L.

In vitro model of bacterial biofilm formation on polyvinyl chloride biomaterial.

The aim of the study was to establish an in vitro model of Staphylococcus epidermidis biofilms on polyvinyl chloride (PVC) material, and to investigate bacterial biofilm formation and its structure using the combined approach of confocal laser scanning microscope (CLSM) and scanning electron microscope (SEM). Staphylococcus epidermidis bacteria (stain RP62A) were incubated with PVC pieces in Tris buffered saline to form biofilms. Biofilm formation was examined at 6, 12, 18, 24, 30, and 48 h. Thicknesses of these biofilms and the number, and percentage of viable cells in biofilms were measured. CT scan images of biofilms were obtained using CLSM and environmental SEM. The results of this study showed that Staphylococcus epidermidis biofilm is a highly organized multi-cellular structure. The biofilm is constituted of large number of viable and dead bacterial cells. Bacterial biofilm formation on the surface of PVC material was found to be a dynamic process with maximal thickness being attained at 12-18 h. These biofilms became mature by 24 h. There was significant difference in the percentage of viable cells along with interior, middle, and outer layers of biofilms (P < 0.05). Staphylococcus epidermidis biofilm is sophisticated in structure and the combination method involving CLSM and SEM was ideal for investigation of biofilms on PVC material.

[Expressions of epithelial growth factor receptor and E-cadherin in esophageal carcinoma and their correlation].

BACKGROUND & OBJECTIVE: Up-regulation of epithelial growth factor receptor (EGFR) and down-regulation of E-cadherin are correlated with genesis, progression, invasion, and metastasis of tumor; however,their expressions,especially their association,in esophageal carcinoma have seldom been reported. This study was to detect expressions of EGFR and E-cadherin in esophageal carcinoma, and to analyze their relationship. METHODS: Expressions of EGFR and E-cadherin in 50 specimens of esophageal squamous carcinoma and 8 specimens of esophageal adenocarcinoma were detected by immunohistochemistry. RESULTS: Positive rates of EGFR, and E-cadherin in esophageal squamous carcinoma were 72.0% (36/50), and 22.0% (11/50); while those in esophageal adenocarcinoma were 75.0% (6/8), and 25% (2/8). Positive rates of EGFR in esophageal squamous carcinoma of grades I, II, and III were 63.6%, 75.0%, and 81.3%, respectively. The expression of EGFR negatively correlated with that of E-cadherin (r=-0.341, P=0.008). CONCLUSION: The expression of EGFR in esophageal carcinoma is increased, while that of E-cadherin is decreased;down-regulation of E-cadherin may be associated with up-regulation of EGFR.