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Biomedical subjects

Weihong Liu

Publications and source records attributed to Weihong Liu.

7 recordsLinked to original sources

Differential expression of the mechanosensitive potassium channel TREK-1 in epicardial and endocardial myocytes in rat ventricle.

Mechanoelectric feedback (MEF) is the process by which mechanical forces on the myocardium induce electrical responses. It is thought that MEF is important in controlling the beat to beat force of contraction in the ventricle, in response to fluctuations in load, and it may also play a role in controlling the dispersion of repolarization. The transduction mechanism for MEF is via stretch sensitive ion channels in the surface membrane of myocytes. Two types of stretch sensitive channels have been described; a non-selective cation channel, and a potassium selective channel. TREK-1 is a member of the recently cloned tandem pore potassium channels that has been shown to be mechanosensitive and to be expressed in rat heart. Here we report that the gene expression level of TREK-1, quantified using real-time RT-PCR against glyceraldehyde phosphate dehydrogenase (GAPDH) as a comparator gene, was found to be 0.34 +/- 0.14 in endocardial cells compared to 0.02 +/- 0.02 in epicardial cells (P < 0.05). To confirm that this is reflected in a different current density, whole cell TREK-1 currents, activated by chloroform, were recorded with patch clamp techniques in epicardial and endocardial cells. TREK-1 current density in epicardial and endocardial cells was 0.21 +/- 0.06 pA/pF and 0.8 +/- 0.27 pA/pF, respectively (P</= 0.05). We discuss the implications of this differential expression of TREK-1 for controlling action potential repolarization when the myocardium is stretched. We hypothesize that the gene expression of TREK-1 is controlled by the different amounts of stretch experienced by muscle cells across the ventricular wall.

Animals↗

Chiral effect on a self-assembling bicopper complex.

A bicopper complex was prepared with chiral ligands. The self-assembly of the complex in trans-decalin differed greatly for the racemic and nonracemic ligands. With the latter the resulting gel formed at a lower concentration and exhibited a higher thermal transition temperature. A large optical activity was found in the nonracemic bicopper complex, which was used to probe the process of filament formation, i.e., the aggregation-dissociation process. The material with nonracemic ligands may form a longer nanoscopic filament.

Journal Article↗

c-Jun N-terminal kinase contributes to apoptotic synergy induced by tumor necrosis factor-related apoptosis-inducing ligand plus DNA damage in chemoresistant, p53 inactive mesothelioma cells.

Apoptotic resistance of cancer cells may be overcome by the combination of treatments that activate the two major apoptotic pathways: (i) the death receptor pathway activated by death ligands and (ii) the DNA damage pathway activated by chemotherapy. We have previously shown that mesothelioma cells, resistant to most treatments, are sensitive to the combination of the death ligand tumor necrosis factor-related apoptosis inducing ligand (TRAIL/Apo2L) plus chemotherapy. We investigated a possible role for c-Jun N-terminal kinase (JNK) in the synergistic effect, knowing that JNK can be activated separately by TRAIL and by DNA damage. We chose to study the M28 and REN human mesothelioma cell lines, which are p53-inactivated, to avoid an interaction between p53 and JNK. We showed that JNK was activated by TRAIL and by etoposide and that the activation was enhanced by the combination of the two treatments. We found this activation to be caspase-independent. To inhibit the JNK pathway, we used either dominant-negative constructs of JNK1 and JNK2 (compared with dominant-negative caspase 9) or a chemical inhibitor of the JNK pathway (SP600125). In cells treated with TRAIL plus etoposide, JNK inhibition increased cell survival and decreased apoptosis significantly. In transfected M28 cells, the effect of JNK inhibition was as great as that of the dominant-negative caspase 9 construct. We conclude that JNK contributes to the synergistic effect of TRAIL combined with DNA damage by mediating signals independent of p53 leading to apoptosis.

Anthracenes↗

[Changes of prostaglandin E2 levels in periapical exudates after root canal treatment].

OBJECTIVE: The aim of this study was to examine the levels of prostaglandin E2 in periapical exudates before and after root canal treatment. METHODS: Periapical exudates specimens were quantitatively sampled from root canals of 25 teeth at consecutive treatment visits, and the concentration of prostaglandin E2 in each sample was determined using a commercial kit. RESULTS: The mean prostaglandin E2 levels significantly decreased after the endodontic therapy. Significant correlations between the levels of prostaglandin E2 and the clinical features of periapical periodontitis were also found in this study. CONCLUSION: The results suggest that the level of prostaglandin E2 in periapical exudates reflects the state of periapical periodontitis.

Adolescent↗

Validation of a quantitative method for real time PCR kinetics.

Real time RT-PCR is the most sensitive method for quantitation of gene expression levels. The accuracy can be dependent on the mathematical model on which the quantitative methods are based. The generally accepted mathematical model assumes that amplification efficiencies are equal at the exponential phase of the reactions for the same amplicon. However, no methods are available to test the assumptions regarding amplification efficiency before one starts the real time PCR quantitation. Here we further develop and test the validity of a new mathematical model which dynamically fits real time PCR data with good correlation (R(2)=0.9995+/-0.002, n=50). The method is capable of measuring cycle-by-cycle PCR amplification efficiencies and demonstrates that these change dynamically. Validation of the method revealed the intrinsic relationship between the initial amount of gene transcript and kinetic parameters. A new quantitative method is proposed which represents a simple but accurate quantitative method.

Animals↗

A new quantitative method of real time reverse transcription polymerase chain reaction assay based on simulation of polymerase chain reaction kinetics.

Real-time reverse transcription (RT) PCR is currently the most sensitive method for the detection of low-abundance mRNAs. Two relative quantitative methods have been adopted: the standard curve method and the comparative C(T) method. The latter is used when the amplification efficiency of a reference gene is equal to that of the target gene; otherwise the standard curve method is applied. Based on the simulation of kinetic process of real-time PCR, we have developed a new method for quantitation and normalization of gene transcripts. In our method, the amplification efficiency for each individual reaction is calculated from the kinetic curve, and the initial amount of gene transcript is derived and normalized. Simulation demonstrated that our method is more accurate than the comparative C(T) method and would save more time than the relative standard curve method. We have used the new method to quantify gene expression levels of nine two-pore potassium channels. The relative levels of gene expression revealed by our quantitative method were broadly consistent with those estimated by routine RT-PCR, but the results also showed that amplification efficiencies varied from gene to gene and from sample to sample. Our method provides a simple and accurate approach to quantifying gene expression level with the advantages that neither construction of standard curve nor validation experiments are needed.

Animals↗

[Effects of fetal anoxia and acidosis on superoxide dismutase].

OBJECTIVE: To analyze the effects of fetal anoxia, respiratory and metabolic acidosis on the activity of antioxidation in fetal distress. METHODS: Blood samples were taken from umbilical artery in 386 neonates for blood gas analysis and detection of the concentration of superoxide dismutase (SOD). Normal situation, anoxia, acidosis, respiratory acidosis, metabolic acidosis and mixed acidosis were diagnosed in all neonates according to the results of blood gas values, and the neonate asphyxia was diagnosed according to the Apgar scores (one minute). The effect of anoxia and acidosis to SOD were analyzed with multiple factor analysis of variation. RESULTS: (1) Among the all 386 cases, 317 were normal, 31 with anoxia, 17 with acidosis, and 21 with both anoxia and acidosis. Among the total cases of acidosis, 8 respiratory, 21 metabolic, and 9 mixed acidosis. (2) The plasma levels of SOD of umbilical artery blood in anoxia, acidosis, both anoxia and acidosis, and normal sitution were (118.5 +/- 7.1) mmol/L, (122.0 +/- 11.4) mmol/L, (140.0 +/- 7.0) mmol/L, and (98.5 +/- 2.6) mmol/L, respectively. The results of unvariate analysis of variance showed that anoxia: F = 4.999 (P < 0.05), acidosis: F = 7.025 (P < 0.01), and both anoxia and acidosis: F = 0.013 (P > 0.05). (3) The plasma levels of SOD with respiratory acidosis, metabolic acidosis and mixed acidosis were (127.3 +/- 18.4) mmol/L, (126.0 +/- 8.1) mmol/L, (150.0 +/- 10.4) mmol/L. The results of univariate analysis of variance showed that respiratory acidosis: F = 4.404 (P < 0.05), metabolic acidosis: F = 3.965 (P < 0.05), and mixed acidosis: F = 0.015 (P > 0.05). CONCLUSION: The superoxidation and antioxidation can be effected by factors like anoxia and acidosis, respiratory acidosis and metabolic acidosis. However, the mechanisms of these effects are different. There is additive, but not synergistic effects among them.

Acidosis↗