Impairment of Myocardial and Skeletal Mitochondria in Mice with Viral Myocarditis and Their Correlation / 华中科技大学学报（医学）（英德文版）

In order to investigate the impairment of mitochondrial membrane phospholipid localization and DNA3867 (mtDNA3867) deletion and the correlation between cardiac and skeletal muscle cells in mice with viral myocarditis, 50 BALB/c mice were divided into two groups randomly. In experimental group (n=40), the mice were intraperitoneally injected with 0.1 mL Eagle liquid with CVB3 (TCID50=108), while in the control group (n=10), the mice were subjected to equal volume of Eagle liquid. The impairment of mitochondrial membrane phospholipid localization and mtDNA3867 deletion rate of cardiac and skeletal muscle were detected separately at day 3, 11 and 24 after injection. The correlation of mitochondrial membrane phospholipid localization and mtDNA3867 deletion rate between cardiac and skeletal muscle cells cells was analyzed using Spearman method. At the day 3 after injection, in both cardiac and skeletal muscle cells, mtDNA3867 deletion rate was significantly higher in experimental group than in control group (P＜0.05), but the localization of mitochondrial membrane phospholipid showed no difference between two groups (P＞0.05). At day 11 after injection, the mtDNA3867 deletion rate of both cells in experimental group was increased to the peak level (P＜0.05), and the impairment of mitochondrial membrane phospholipid localization of both cells also increased markedly in experimental group as compared with control group (P＞0.05). At the day 24 after injection, the impairment of mitochondrial membrane phospholipid localization and mtDNA3867 deletion of both cells showed a recovery tendency, but still severer than those at the day 3 after injection (P＜0.05). The impairment of mitochondrial membrane phospholipid localization and mtDNA3867 deletion were consistent and synchronistic between cardiac and skeletal muscle cells, and showed good correlations (P＜0.05). The impairment of mitochondria plays an important role in the pathogenesis of viral myocardifis, and the skeletal muscle cells might act as a peripheral "window" to reflect the mitochondrial damage of cardiac myocytes.

The correlation between insulin sensitivity and human erythrocyte memberane phospholipid in elderly diabetic patients / 中华老年医学杂志

ObjectiveTo study the correlation between human erythrocyte membrane phospholipid profile and insulin sensitivity in elderly diabetic patients. MethodsThe levels of phosphatidylcholine (PC), phosphatidylserine(PS),phosphatidtlinostiol(PI),phosphatidylethanolamine(PE),the maximum erythrocyte deformation index(DImax) , the maximum erythrocyte aggregation index(AImax) and glucose disposal contant Ki (KITT) were measured in 32 cases of elderly diabetics and 30 healthy old subjects. ResultsThe KITT was lower in diabetic patients than in normal controls (P

In Vitro Analysis of Apoptotic Cell Death Using Proton Nuclear Magnetic Resonance Spectroscopy / 대한암학회지

PURPOSES: Cells undergoing apoptosis display profound morphologic and biochemical changes in the nucleus and cytoplasm, loss of membrane phospholipid asymmetry, resulting in the exposure of phosphatidylserine (PS) at the surface of the cell, membrane blebbing, and decreased membrane microviscosity. Proton nuclear magnetic resonance spectroscopy ('H NMR spectroscopy) is able to detect the mobile fraction of lipids contained in the cell, and thus is sensitive to membrane fluidity modifications related to lipid composition changes. We have used 'H NMR spectroscopy in HL-60 cell line to detect and characterize the changes in plasma membrane lipid associated with apoptotic cell death. MATERIALS AND METHODS: We performed annexin-FITC and propidium iodide dual fluorescence flow cytometry, DNA gel electrophoresis, and obtained 200 MHz 'H NMR spectra of the HL-60 cell cultures before and at 6, 12, 18, 24, 36 and 48 hours after the addition of doxorubicin (100 ng/mL). RESULTS: The onset of apoptosis is accompanied by a greater than four fold increase in signal intensity ratio of the membrane lipid methylene (-CH2) resonance (at 1.2 ppm) to the methyl (-CH3) resonance (at 0.9 ppm). The quantitative relationship between apoptosis and the H NMR signal intensity was determined by fluorescein-annexin V flow cytometry, and showed that increases in the CH2/CH3 resonance signal intensity ratio paralleled the surface expression of PS as an early marker of apoptosis ( y =0.80, N 18 samples). The gradual decrease in the ratio of choline resonance (at 3.2 ppm) to CH3 signal intensity after 12 hours in the time course' experiment is directly proportional to the percentage of apoptotic cells ( y =0.96, N=18 samples). CONCLUSIONS: Monitoring of the CH2 and choline resonance signal intensity may therefore be useful in detecting apoptosis. Further studies using various stimuli to induce apoptotic cell death will be necessary to better determine the capabilities of 'H NMR spectroscopy for the detection and estimation of apoptosis in vitro.

Mechanism of M-current modulation by neural transmitters / 第二军医大学学报

M channel, a voltage-dependent potassium channel, has been found in a variety of neurons. It is activated near the threshold of neuron action potential,producing a primary K~+ current, namely the M-current. The M-current can be modulated by many neurotransmitters and hormones, which can influence neuron excitability, conduction and neurotransmitter release. This review discusses the signal transduction pathway from G_~ q/11 activation to intracellular calcium, membrane phospholipid and phosphokinase, and explains the mechanism of M-current modulation by neurotransmitters.