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Biomedical subjects

J G Shen

Publications and source records attributed to J G Shen.

6 recordsLinked to original sources

Novel sparse component analysis approach to free radical EPR spectra decomposition.

Free radicals play important roles in many physiological and pathological pathways in biological systems. These free radicals can be detected and quantified by their EPR spectra. The measured EPR spectra are often mixtures of pure spectra of several different free radicals and other chemicals. Blind source separation can be applied to estimate the pure spectra of interested free radicals. However, since the pure EPR spectra are often not independent of each other, the approach based on independent component analysis (ICA) cannot accurately extract the required spectra. In this paper, a novel sparse component analysis method for blind source separation, which exploits the sparsity of the EPR spectra, is presented to reliably extract the pure source spectra from their mixtures with high accuracy. This method has been applied to the analysis of EPR spectra of superoxide, hydroxyl, and nitric oxide free radicals, for both simulated data and real world ex vivo experiment. Compared to the traditional self-modeling method and our previous ICA-based blind source separation method, the proposed sparse component analysis approach gives much better results and can give perfect separation for mixtures of superoxide spectrum and hydroxyl spectrum in the ideal noise-free case. This method can also be used in other similar applications of quantitative spectroscopy analysis.

Algorithms↗

Free radical EPR spectroscopy analysis using blind source separation.

In this paper, we propose a novel approach for electron paramagnetic resonance (EPR) mixture spectra analysis based on blind source separation (BSS) technique. EPR spectrum of a free radical is often superimposed by overlapping spectra of other species. It is important and challenging to accurately identify and quantify the 'pure' spectra from such mixtures. In this study, an automated BSS method implementing independent component analysis is used to extract the components from mixed EPR spectra that contain overlapping components of different paramagnetic centers. To apply this method, there is no requirement to know the component spectra or the number of components in advance. The method is applied to analyze free radical EPR spectra which are collected from standard chemical system, cultured cell suspense, and ex vivo rat kidneys by spin trapping EPR technique. Results show that the BSS method proposed here is capable of identifying the component EPR spectra from mixtures with unknown compositions. The BSS technique can offer powerful aids in resolving spectral overlapping problems in general EPR spectroscopy analysis.

Algorithms↗

Chinonin, a novel drug against cardiomyocyte apoptosis induced by hypoxia and reoxygenation.

The inhibitory effects of Chinonin, a natural antioxidant extracted from a Chinese medicine, on apoptotic and necrotic cell death of cardiomyocytes in hypoxia-reoxygenation process were observed in this study. The possible mechanisms of Chinonin on scavenging reactive oxygen species and regulating apoptotic related genes bcl-2 and p53 were also investigated. Neonatal rat cardiomyocytes were subjected to 24-h hypoxia and 4-h reoxygenation. Cell death was evaluated by DNA electrophoresis on agarose gel, cell death ELISA and annexin-V-FLUOS/propidium iodide (PI) double staining cytometry. Hypoxia caused the increase of apoptotic rates and the release of lactate dehydrogenase (LDH), while reoxygenation not only further increased the apoptotic rates and leakage of LDH, but also induced necrosis of cardiomyocytes. In addition, hypoxia increased the levels of NO(2)(-)/NO(3)(-) and thiobarbituric acid reacted substances (TBARS), while reoxygenation decreased NO(2)(-)/NO(3)(-), but further increased TBARS in the cultured media. Moreover, hypoxia up-regulated the expression levels of bcl-2 and p53 proteins, while reoxygenation down-regulated bcl-2 and further up-regulated p53. Chinonin significantly decreased the rates of apoptotic and necrotic cardiomyocytes, and inhibited the leakage of LDH. It also diminished NO(2)(-)/NO(3)(-) and TBARS, down-regulated the expression level of p53 protein, and up-regulated bcl-2 protein, respectively. The results suggest that Chinonin has preventive effects against apoptotic and necrotic cell death and its protective mechanisms are related to the antioxidant properties of scavenging nitric oxide and oxygen free radicals, and the modulating effects on the expression levels of bcl-2 and p53 proteins.

Animals↗

[Mechanisms of yiqi tongluo pill on oxygen free radicals, nitric oxide and fibrinolysis in coronary heart diseases and hypertension patients].

OBJECTIVE: To clarify the mechanism of Yiqi Tongluo Pill (YQTLP) in treating coronary heart disease and hypertension. METHODS: The clinical effects of YQTLP on 97 coronary heart diseases (CHD) and hypertension patients, in comparing to the 92 patients treated with nitroglycerin was investigated. The changes of plasma lipid peroxide (LPO), superoxide dismutase (SOD), tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI) and nitric oxide (NO) were observed in the patients treated with YQTLP and nitroglycerin, which were compared to 30 healthy subjects. RESULTS: The levels of LPO and PAI increased and the levels of SOD, t-PA and NO decreased significantly in the patients. The clinical effects of YQTLP were better than that of nitroglycerin in the patients with unstable angina, while the effects of YQTLP were worse than that of nitroglycerin in the patients of hypertension and hypertension with CHD. YQTLP could decrease the levels of LPO and PAI and increase the levels of SOD, t-PA and NO significantly. The effects of YQTLP on t-PA and SOD were better than that of nitroglycerin. CONCLUSION: The protective mechanisms of YQTLP were related to inhibit lipid peroxidation, protect endothelium-derived relaxing factor and adjust the fibrinolytic activities.

Adult↗

Efficiency of Ginkgo biloba extract (EGb 761) in antioxidant protection against myocardial ischemia and reperfusion injury.

The cardio-protective mechanisms of EGb 761, an extract of Ginkgo biloba leaves, on myocardial ischemia-reperfusion injury were investigated using rabbits subjected to 30 minutes of regional cardiac ischemia and 120 min of reperfusion under anesthesia. Compared to the saline perfused group, EGb 761 treatment (10 mg/kg, injected into the coronary artery) significantly inhibited the increase in lipid peroxidation and maintained total and CuZn-SOD levels in both plasma and tissue during and at the end of reperfusion. Both the decrease in tissue type plasminogen activator (t-PA) and the increase in plasminogen activator inhibitor-1 (PAI-1) caused by ischemia-reperfusion were also significantly suppressed by EGb 761 treatment. Furthermore, the ultrastructure of the myocytes of the EGb 761 treated heart was slightly damaged after ischemia-reperfusion, while the control ischemic-reperfused hearts demonstrated severe histological damages such as swelling and vacuolization of the mitochondria. These results suggest that EGb 761 protects hearts by its antioxidant properties and by its ability to adjust fibrinolytic activity.

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