Value of acoustic cardiography in the clinical diagnosis of coronary heart disease.

BACKGROUND: To investigate the clinical value of acoustic cardiography in the diagnosis of coronary artery disease (CAD) and post-percutaneous coronary intervention (PCI) early asymptomatic left ventricular systolic dysfunction. METHODS: Inpatients in the department of cardiology were included in the research (n = 315); including 180 patients with angina pectoris and 135 patients with acute anterior wall myocardial infarction after emergency PCI did not present with signs and symptoms of heart failure. Color Doppler echocardiography, brain natriuretic peptide, acoustic cardiography examination were performed. The patients were divided into four groups: non-CAD group (n = 60), CAD group (n = 120), MIREF group (EF% < 50%, n = 75), and MINEF group (EF% ≥ 50%, n = 60). RESULTS: Acoustic cardiography parameters EMATc, systolic dysfunction index, S3 strength and S4 strength in the MIREF group were higher than those in MINEF group (p < .05), and the MINEF group was higher than CAD group (p < .05). S3 strength (area under the curve [AUC] 0.67, 95% CI 0.585-0.755, p < .001) and S4 strength (AUC 0.617, 95% CI 0.536-0.698, p = .011) are useful in the diagnosis of CAD. S3 strength (AUC 0.942, 95% CI 0.807-0.978, p < .001) was superior to other indicators in the diagnosis of early left ventricular systolic dysfunction after myocardial infarction. CONCLUSION: S4 combined with STT standard change can improve the diagnosis of CAD. Acoustic cardiography can be used as a non-invasive, rapid, effective, and simple method for the diagnosis of asymptomatic left ventricular systolic dysfunction in the early stage after myocardial infarction.

Possible role of DNA polymerase beta in protecting human bronchial epithelial cells against cytotoxicity of hydroquinone.

OBJECTIVE: To explore the toxicological mechanism of hydroquinone in human bronchial epithelial cells and to investigate whether DNA polymerase beta is involved in protecting cells from damage caused by hydroquinone. METHODS: DNA polymerase beta knock-down cell line was established via RNA interference as an experimental group. Normal human bronchial epithelial cells and cells transfected with the empty vector of pEGFP-C1 were used as controls. Cells were treated with different concentrations of hydroquinone (ranged from 10 micromol/L to 120 micromol/L) for 4 hours. MTT assay and Comet assay [single-cell gel electrophoresis (SCGE)] were performed respectively to detect the toxicity of hydroquinone. RESULTS: MTT assay showed that DNA polymerase beta knock-down cells treated with different concentrations of hydroquinone had a lower absorbance value at 490 nm than the control cells in a dose-dependant manner. Comet assay revealed that different concentrations of hydroquinone caused more severe DNA damage in DNA polymerase beta knock-down cell line than in control cells and there was no significant difference in the two control groups. CONCLUSIONS: Hydroquinone has significant toxicity to human bronchial epithelial cells and causes DNA damage. DNA polymerase beta knock-down cell line appears more sensitive to hydroquinone than the control cells. The results suggest that DNA polymerase beta is involved in protecting cells from damage caused by hydroquinone.

[hPARP1 genetic polymorphism in southern Chinese Han and Miao populations].

OBJECTIVE: To study hPARP1 genetic polymorphism in southern Chinese Han and Miao populations. METHODS: Blood samples from 187 and 210 southern healthy Han and Miao populations were collected. The mutations of exons 12,13,16 and 17 of hPARP1 gene were investigated by PCR-single-strand conformation polymorphism(SSCP). RESULTS: Fragments of 253 bp,313 bp,175 bp,362 bp within exons 12,13,16 and 17 respectively of hPARP1 gene were amplified by multiple PCR. An SSCP variant in exons 12,13,16 and 17 of PARP1 gene in 187 healthy Han and 210 healthy Miao individuals was identified. Seven single-base substitutions compared with the sequence of PARP1 gene were identified: a T to C transition in exon 12 (Phe548Ser), a G to T transition in exon 13 (Ala683Ser), a G to T transition in exon 16 (Asp798Tyr), and a A to G transition in exon 17 (His808Arg). CONCLUSION: There were polymorphism sites in exons 12,13,16,17 of hPARP1 gene in southern Chinese Han and Miao populations; these results may be useful for the establishment of PARP1 genotyping, and these newly described PARP1 alleles would be advantageous indicators for population studies.

[Study on the adaptive reaction of low dose hydroquinone inducement in human embryo lung fibroblasts cells].

OBJECTIVE: To study the adaptive reaction and its possible mechanisms in eukaryotic cells, the oxidize of adaptive mode was established by studying the dose-effect relation of inducing the adaptive reaction. METHODS: Human embryo lung fibroblasts (HLF) were attacked 1 hour by 80.0 micromol/L concentration respectively after using a different concentration HQ to pretreat the 12 hours. The adaptive reaction of a low concentration HQ inducement was observed by combining the micronucleus test, the comet test and the cell cycle change. RESULTS: The results showed that, in cellular viability, HLF induced by pretreated with HQ at 0.001 micromol/L and 0.0 micromol/L appeared to be tolerated when retreated by the following 80.0 micromol/L concentration of HQ. Compared with control respectively, the micronucleus rate and abnormal nuclei rate increased obviously by pretreatment with HQ concentration from 0.5 micromol/L to 80 micromol/L in HLF. Phenomena of cells with tails appeared, tail length and percentage of cells with tails increased significantly in HLF (P < 0.01). From 0.1 micromol/L pretreatment dose on, proportion of DNA lesion cells belonged to three and four grade increase gradually by the dose increasing. G2 phase arrest and cell numbers decreasing in G1. When compared with only high dose attack respectively, micronucleus rate, abnormal nuclei rate, tail length, percentage of cells with tails decreased significantly. proportion of severely damaged cells descended markedly by pretreatment with HQ from 0 micromol/L from 0.1 micromol/L in HLF (P < 0.05). It showed that there was a dose-related increase in the rate of micronucleus or abnormal nuclei, tail length and in percentage of cells with tails after pretreatment with HQ from 0 micromol/L to 80 micromol/L in HLF (P < 0.05). CONCLUSION: HLF induced by pretreated with HQ at low concentration appeared to adaptive reaction when retreated by high concentration of HQ.

[Low concentration of hydroquinone-induced adaptive response in hPARP-1 protein normal and deficient cells].

OBJECTIVE: To investigate whether or not adaptive response of hPARP-1 protein normal and deficient cells is induced by low dose of hydroquinone (HQ), and to analyze the relationship between the adaptive response and micronuclei formation, and cell cycle alteration in human embryo lung fibroblasts (HLF), so as to elucidate the mechanism of adaptive response. METHODS: HLF, HLFC and HLFP cells pretreated with low concentration were retreated by high concentration of HQ. Cellular viability, the rate of micronuclei and abnormal nuclei, cell cycle and DNA strand break were determined. RESULTS: The tolerance to 80.0 micromol/L concentration of HQ was enhanced when HLF, HLFC and HLFP cells were pretreated with HQ from 0.001 - 0.050 micromol/L. There were varying degrees of micronuclei and abnormal nuclei in three cells pretreated with low concentration of HQ and then retreated with high concentration of HQ; the cell numbers of G1, G2, S phase in cell cycle were obviously different. When compared with only high attack dose, the micronuclei rate and abnormal nuclei rate of HLF, HLFC and HLFP decreased by pretreatment with HQ at high concentration (P < 0.05), meanwhile increased by pretreatment with HQ at low concentration (P < 0.05). HLF, HLFC and HLFP showed blockage in G2 phase when pretreated with HQ at 0 approximately 0.05 micromol/L, but HLFP showed blockage in G1 phase, and in S phase at 1.0 and 2.0 micromol/L. CONCLUSION: The level of adaptive response of hPARP-1 protein deficient cells was lower than normal cell, suggesting that hPARP-1 protein may play an important role in the adaptive response of cells, which may be related with the regulation of cell cycle.