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Yu-Qing Liu

Publications and source records attributed to Yu-Qing Liu.

14 recordsLinked to original sources
PubMed2006

[Relationship between event-related potentials and brain injury].

Event-related potentials (ERPs) develop promptly as one kind of special evoked potentials. And it is one of the most effective methods to investigate human's cognition function in these years. P300 is the component of ERPs which is widely and maturately researched and has intimate relation with attention, memory and other high psychological activity. The evaluation of recognition change after brain injury is the focus of the research. With the development of relatively research, it is deemed that this technique has wide application perspective in many aspects such as forensic clinical medicine and forensic psychiatry.

Attention↗
PubMed2006

Epigallocathechin-3 gallate inhibits cardiac hypertrophy through blocking reactive oxidative species-dependent and -independent signal pathways.

Cardiac hypertrophy is a major cause of morbidity and mortality worldwide. Recent in vitro and in vivo studies have suggested that reactive oxygen species (ROS) may play an important role in cardiac hypertrophy. It was therefore thought to be of particular value to examine the effects of antioxidants on cardiac hypertrophy. Epigallocatechin-3-gallate (EGCG) is a major bioactive polyphenol present in green tea and a potent antioxidant. The current study was designed to test the hypothesis that EGCG inhibits cardiac hypertrophy in vitro and in vivo. In this study, we investigated the effects of EGCG on angiotensin II- (Ang II) and pressure-overload-induced cardiac hypertrophy. Our results showed that EGCG attenuated Ang II- and pressure-overload-mediated cardiac hypertrophy. Both reactive oxygen species generation and NADPH oxidase expressions induced by Ang II and pressure overload were suppressed by EGCG. The increased hypertension by pressure overload was almost completely blocked after EGCG treatment. Further studies showed that EGCG inhibited Ang II-induced NF-kappaB and AP-1 activation. Inhibition of the activity of NF-kappaB was through blocking ROS-dependent p38 and JNK signaling pathways, whereas inhibition of AP-1 activation was via blocking EGFR transactivation and its downstream events ERKs/PI3K/Akt/mTOR/p70(S6K). The combination of these actions resulted in repressing the reactivation of ANP and BNP, and ultimately preventing the progress of cardiac hypertrophy. These findings indicated that EGCG prevents the development of cardiac hypertrophy through ROS-dependent and -independent mechanisms involving inhibition of different intracellular signaling transductional pathways.

Angiotensin II↗
PubMed2006

Increase of CD4(+)CD25(+) T cells in Smad3(-/-) mice.

AIM: To investigate the changes of lymphocyte subpopulations, especially CD4(+)CD25(+) T regulatory cells in Smad3(-/-) mice. METHODS: Hematological changes and changes of lymphocyte subpopulations were detected in Smad3(-/-) mice using cell counter and flow cytometry, respectively, and compared to their littermate controls. RESULTS: The numbers of neutrophils and lymphocytes in peripheral blood were significantly increased in Smad3(-/-) mice compared to littermate controls. CD19(+) expressing cells in blood and spleen, and CD8(+) T cells in thymus were all markedly decreased in Smad3(-/-) mice. More important, Smad3(-/-) mice had an increased population of CD4(+)CD25(+) T cells in peripheral lymphoid tissues, including thymus, spleen, and lymph nodes. CONCLUSION: These observations suggest that the changes of lymphocyte subpopulations might play a role in susceptibility to inflammation of Smad3(-/-) mice.

Animals↗
PubMed2006

Experimental study of verapamil on the relaxation of isolated human corpus cavernosum tissues.

AIM: To evaluate the relaxant effect of verapamil on human corpus cavernosum in vitro and to assess the drug's potential as a treatment for erectile dysfunction (ED). METHODS: Preparations of the human corpus cavernosum were obtained from recently deceased young men who had had normal erectile function. The isometric tension and detailed curves were recorded when contractions induced by 10 micromol/L phenylephrine were reduced by different doses of verapamil or the vehicle control (sterile water). The tension of human corpus cavernosum preparations are described as a percentage of their top tension before adding verapamil or the vehicle. ANOVA and least significant difference tests were used for statistical analysis. RESULTS: Doses of 1 micromol/L, 10 micromol/L and 100 micromol/L verapamil resulted in relaxation of (35.28+/-7.96)%, (55.91+/-6.41)%, (85.68+/-4.16)% after 30 min, respectively. The vehicle control at the same time point produced relaxation of (-0.06+/-10.57)% (P<0.05). CONCLUSION: Verapamil is significantly effective in relaxing normal human corpus cavernous smooth muscle induced by phenylephrine in vitro and the relaxant effect depends on the concentration of verapamil.

Adult↗
PubMed2006

Apolipoprotein E polymorphism influences lipid phenotypes in Chinese families with familial combined hyperlipidemia.

BACKGROUND: Apolipoprotein E (apoE) polymorphism is associated with changes in the lipoprotein profile of individuals with familial combined hyperlipidemia (FCHL), but its effects on the lipoprotein profiles of members of Chinese families with FCHL remain uncertain. METHODS AND RESULTS: 43 FCHL families (n=449) and 9 normolipidemic families (n=73) were recruited to assess the influence of apoE polymorphism on plasma lipids. The relative frequency of the epsilon4 allele in affected and unaffected FCHL relatives, spouses and normolipidemic members was 13.8%, 5.3%, 9.1% and 6.8%, respectively, with a significantly higher frequency in affected FCHL relatives, compared with unaffected FCHL relatives or normolipidemic members (p=0.0002 or p=0.029). In FCHL relatives, the apoE4 subset (E4/4 and E4/3) exhibited significantly higher levels of apoB, total cholesterol and low-density lipoprotein-cholesterol (LDL-C) than did the apoE3 (E3/3) subset, especially in women (all p<0.05), and there was significant elevation of LDL-C concentrations in men only (p<0.05). In men, the apoE2 (E3/2) subset indicated a decreased level of apoB and increased apoA1 compared with those in the apoE3 subset (p<0.05). CONCLUSIONS: ApoE polymorphism appears to be associated with variance of the lipoprotein phenotype in Chinese families with FCHL.

Adolescent↗
PubMed2005

Bcl-xL overexpression restricts gamma-radiation-induced apoptosis.

Bcl-xL belongs to a family of proteins which inhibit apoptosis in a number of stimuli including ionizing radiation. To better understand the effects and mechanisms of Bcl-xL on the apoptosis of lymphocytes and provide experimental basis to treat immune injury induced by radiation, we used normal human lymphoblastoid AHH-1 cells that were engineered to overexpress Bcl-xL proteins. Our results showed that overexpressed Bcl-xL reduced time-dependent increase of apoptosis induced by ionizing radiation. Reactive oxygen species (ROS) generation and Bax protein expression in the transfected AHH1-Bcl-xL cells were also lower compared to parental AHH-1 cells. Unexpectedly, the fluorescence intensity of Rhodomine 123 (Rh 123) for measuring mitochondrial membrane potential (MMP) did not change at all detected time points. These results possess a vital significance for insights into a new strategy for gene therapy of radiation-induced immune injury.

Apoptosis↗
PubMed2005

Biological impacts of "hot-spot" mutations of hepatitis B virus X proteins are genotype B and C differentiated.

AIM: To investigate the biological impacts of "hot-spot" mutations on genotype B and C HBV X proteins (HBx). METHODS: Five types of "hot-spot" mutations of genotype B or C HBV X genes, which sequentially lead to the amino acid substitutions of HBx as I127T, F132Y, K130M+V131I, I127T+K130M+V131I, or K130M+V131I+F132Y, respectively, were generated by means of site-directed mutagenesis. To evaluate the anti-proliferative effects, HBx or related mutants' expression vectors were transfected separately to the Chang cells by lipofectamine, and the cells were cultured in hygromycin selective medium for 14 d, drug-resistant colonies were fixed with cold methanol, stained with Giemsa dyes and scored (increase of the colonies indicated the reduction of the anti-proliferation activity, and vice versa). Different types of HBx expression vectors were co-transfected separately with the reporter plasmid pCMVbeta to Chang cells, which were lysed 48 h post-transfection and the intra-cellular beta-galactosidase activities were monitored (increase of the beta-galactosidase activities indicated the reduction of the transactivation activity, and vice versa). All data obtained were calculated by paired-samples t-test. RESULTS: As compared to standard genotype B HBx, mutants of I127T and I127T+K130M+V131I showed higher transactivation and anti-proliferative activities, while the mutants of F132Y, K130M+V131I, and K130M+V131I+F132Y showed lower activities. As compared to standard genotype C HBx, I127T mutant showed higher transactivation activity, while the other four types of mutants showed no differences. With regard to anti-proliferative activity, compared to standard genotype C HBx, F132Y and K130M+ V131I mutants showed lower activities, and K130M+V131I +F132Y mutant, on the other hand, showed higher activity, while the mutants of I127T and I127T+K130M+V131I showed no differences. CONCLUSION: "Hot-spot" mutations affect the anti-proliferation and transactivation activities of genotype B and/or C HBx, and the biological impacts of most "hot-spot" mutations on HBx are genotype B and C differentiated.

Amino Acid Sequence↗
PubMed2005

Isorhapontigenin, a new resveratrol analog, attenuates cardiac hypertrophy via blocking signaling transduction pathways.

Cardiac hypertrophy is a major cause of morbidity and mortality worldwide. The hypertrophic process is mediated, in part, by oxidative stress-mediated signaling pathways. We hypothesized that isorhapontigenin (ISO), a new resveratrol analog, inhibits cardiac hypertrophy by blocking oxidative stress and oxidative stress-mediated signaling pathways. We treated cardiomyocytes with angiotensin II (Ang II) with or without ISO and found that ISO inhibited Ang II-induced cardiac hypertrophy. These effects were associated with a decrease in the levels of reactive oxygen species and H2O2 and the content of intracellular malonaldehyde and an increase in the activities of superoxide dismutase and glutathione peroxidase. Ang II induced the phosphorylation of PKC, Erk1/2, JNK, and p38 in cardiomyocytes and such phosphorylation was inhibited by ISO. ISO also blocked the PKC-dependent PI3K-Akt-GSK3beta/p70S6K pathway. These effects lead to direct or indirect inhibition of NF-kappaB and AP-1 activation. Our results revealed that pretreatment with ISO significantly inhibited Ang II-mediated NF-kappaB through affecting the degradation and phosphorylation of IkappaBalpha and the activity of IKKbeta and AP-1 activation by influencing the expression of c-Fos and c-Jun proteins. In addition, we also established the molecular link between activation of PKC and MAPKs and activation of NF-kappaB and AP-1 in cardiomyocytes. We also found that ISO treatment significantly attenuated heart weight/body weight ratio by approximately 25%, decreased posterior wall thickness and left ventricle diastolic and systolic diameters, and increased 10% fractional shortening in an aortic-banded rat model. Furthermore, treatment with ISO significantly decreased cardiac myocyte size and systolic blood pressure. These findings suggest that ISO prevents the development of cardiac hypertrophy through an antioxidant mechanism involving inhibition of different intracellular signaling transduction pathways.

Angiotensin II↗
PubMed2005

Desensitization of T lymphocyte function by CXCR3 ligands in human hepatocellular carcinoma.

AIM: Despite the presence of lymphocyte infiltration, human hepatocellular carcinoma (HCC) is typically a rapidly progressive disease. The mechanism of regulation of lymphocyte migration is poorly understood. In this study, we investigated various factors regulating T cell migration in HCC patients. We examined serum CXC chemokine levels in HCC patients and demonstrated the production of CXC chemokines by HCC cell lines. We determined the effect of both HCC patient serum and tumor cell conditioned supernatant upon lymphocyte expression of chemokine receptor CXCR3 as well as lymphocyte migration. Lastly, we examined the chemotactic responses of lymphocytes derived from HCC patients. METHODS: The serum chemokines IP-10 (CXCL10) and Mig (CXCL9) levels were measured by cytometric bead array (CBA) and the tumor tissue IP-10 concentration was measured by ELISA. The surface expression of CXCR3 on lymphocytes was determined by flow cytometry. The migratory function of lymphocytes to the corresponding chemokines was assessed using an in vitro chemotactic assay. Phosphorylation of extracellular signal-regulated kinase (ERK) was determined by Western blot analysis. RESULTS: Increased levels of IP-10 and Mig were detected in HCC patient serum and culture supernatants of HCC cell lines. The IP-10 concentration in the tumor was significantly higher than that in the non-involved adjacent liver tissues. HCC cell lines secreted functional chemokines that induced a CXCR3-specific chemotactic response of lymphocytes. Furthermore, tumor-cell-derived chemokines induced initial rapid phosphorylation of lymphocyte ERK followed by later inhibition of ERK phosphorylation. The culture of normal lymphocytes with HCC cell line supernatants or medium containing serum from HCC patients resulted in a significant reduction in the proportion of lymphocytes exhibiting surface expression of CXCR3. The reduction in T cell expression of CXCR3 resulted in reduced migration toward the ligand IP-10, and both CD4+ and CD8+ T cells from HCC patients exhibited diminished chemotactic responses to IP-10 in vitro compared to T cells from healthy control subjects. CONCLUSION: This study demonstrates functional desensitization of the chemokine receptor CXCR3 in lymphocytes from HCC patients by CXCR3 ligands secreted by tumor cells. This may cause lymphocyte dysfunction and subsequently impaired immune defense against the tumor.

Adult↗
PubMed2005

Pathways to caspase activation.

Apoptosis or programmed cell death is an active form of cell death which is essential for tissue homeostasis. Many proteins are involved in the molecular signal transduction of apoptosis. The caspase enzymes, a family of specific cysteine proteases, play a central role in cell death machinery. In this review, we mainly discuss the current understanding of several pathways to activate caspases and some key proteins related to these pathways.

Animals↗
PubMed2005

A novel approach to estimate in vitro antibacterial potency of Chinese medicine using a concentration-killing curve method.

The antibacterial pharmacodynamics against E. coli of Chinese medicine (CM) Rhizoma coptidis (Coptis Root) and its formula Sanhuang, and the control antibiotics enoxacin, were analyzed by a concentration-killing curve (CKC) approach, and the novel parameters BC50 and r for antibacterial potency were proposed. Using the agar plate method, about 400 cells of E. coli were evenly inoculated into LB agar plates containing a series of different concentrations of CM or antibiotic, and after a 24 hour incubation at 37 degrees C, all the viable colonies were enumerated. This resulted in a sigmoid concentration-killing curve , in which No, that could be closely fitted (R2 > 0.9) with the function: N = 1 + e(r(x-BC50))/N0 in which N0, BC50 and r represent meaningfully inoculums size, median bactericidal concentration, and bactericidal intensity, respectively. N modeled the survival of colony-forming units on each plate (CFU/plate) in a concentration series x of the drug. The CKC was symmetrical about its single inflexion (BC50, N0/2). Therefore theoretically, 2BC50 can replace MBC (minimum bactericidal concentration). BC1 = BC50 + r/ln(N0-1), the drug concentration at r which only one colony survived, was the least critical value of MBC in CKC. The parameters 2BC50 and BC1 agreed more closely with the definition of MBC, and were little affected by either the biochemical basis of the antibacterial or the inoculum's size (200-400 CFU/plate), and were determined by a multi-point curve. As a result, these were more accurate, reproducible and practical as metrics than was the endpoint of MBC. The two-dimensional CKC, involving BC50 and r, captures the intrinsic dynamics of the antibacterial effect of CM/strain versus concentration, and it is consistent with the Logistic equation of the bacterial growth curve in the format. This verified approach has considerable value as a tool for the accurate and proper administration of CM. The CKC of CM, different from that of antibiotics, is likely to be the resultant force of each ingredient in certain CM, which provides a clue to solve the problem of antibiotic resistance.

Coptis↗
PubMed2004

In vitro genotoxicity of exhaust emissions of diesel and gasoline engine vehicles operated on a unified driving cycle.

Acetone extracts of engine exhaust particulate matter (PM) and of vapor-phase semi-volatile organic compounds (SVOCs) collected from a set of 1998-2000 model year normal emitter diesel engine automobile or light trucks and from a set of 1982-1996 normal emitter gasoline engine automobiles or light trucks operated on the California Unified Driving Cycle at 22 [degree]C were assayed for in vitro genotoxic activities. Gasoline and diesel PM were comparably positive mutagens for Salmonella typhimurium strains YG1024 and YG1029 on a mass of PM extract basis with diesel higher on a mileage basis; gasoline SVOC was more active than diesel on an extracted-mass basis, with diesel SVOC more active on a mileage basis. For chromosomal damage indicated by micronucleus induction in Chinese hamster lung fibroblasts (V79 cells), diesel PM expressed about one-tenth that of gasoline PM on a mass of extract basis, but was comparably active on a mileage basis; diesel SVOC was inactive. For DNA damage in V79 cells indicated by the single cell gel electrophoresis (SCGE) assay, gasoline PM was positive while diesel PM was active at the higher doses; gasoline SVOC was active with toxicity preventing measurement at high doses, while diesel SVOC was inactive at all but the highest dose.

Air Pollutants↗