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Objective:To evaluate the effects of different pacing modes (unipolar/bipolar) under left bundle branch pacing(LBBP) on ventricular mechanical synchrony and myocardial work using the pressure-strain loop technique.Methods:Twenty-nine patients with LBBP due to symptomatic bradycardia were collected as LBBP group in Sun Yat-sen Memorial Hospital of Sun Yat-sen University from December 2018 to July 2020. Another 29 matched patients with right ventricular pacing (RVP) during the same period were also included as a RVP group. Each LBBP patient was programmed to different pacing modes (uni-/bio-polar) within 1 week after the operation.Under each pacing mode, the inter- and intra-ventricular mechanical synchronization were evaluated. Meanwhile, the global work index (GWI), global constructive work (GCW), global wasted work (GWW), and global work efficiency (GWE) were obtained by the left ventricular pressure-strain loops technique.Results:Compared with the RVP group, the mechanical synchrony in the LBBP group was significantly improved (all P<0.05). GWI, GCW, and GWE increased, while GWW decreased, and the differences were statistically significant (all P<0.05), there were no significant differences in ventricular mechanical synchronization, GWI, GCW, GWE, and GWW between unipolar and bipolar pacing in the LBBP group (all P>0.05), there were no significant differences in these parameters when increasing output voltage (all P>0.05). Conclusions:LBBP induces better mechanical synchronization and higher myocardial work efficiency than RVP. Different LBBP pacing modes do not affect ventricular mechanical synchronization and myocardial work efficiency.
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Objective To investigate the clinical value of vitamin D receptor ( VDR) gene polymorphism in lung cancer screening .Methods From January 2017 to September 2017 ,2000 lung cancer screening patients in the Fifth People's Hospital of Foshan were selected in the research .The VDR gene polymorphism was determined by phenol-chloroform method .DNA was extracted from the peripheral blood of patients ,different VDR genotypes [ Bsm1 bb and Bb),Apal(aa,Aa and AA)] were analyzed by univariate analysis to determine the correlation between lung cancer and VDR gene polymorphism and lung cancer incidence by multivariate non -conditional logistic regression analysis, thus to explore the relationship between different VDR genotypes and risk factors of lung cancer . Results The level of serum vitamin D in the non -lung cancer patients was (46.5 ±2.3) ng/L,which was signifi-cantly higher than (26.5 ±1.1)ng/L in the lung cancer patients (t=49.614,P=0.000).The Bsm1bp genotype, Apal aa genotype and Apal Aa genotype were the risk factors of lung cancer .The Bsm1bp and Apal Aa genotypes were independent risk factors of lung cancer .Conclusion The Bsm1 locus and Apal locus Aa genotype in VDR receptor are high risk population of lung cancer .Therefore,we should pay more attention to the clinical screening and avoid misdiagnosis and missed diagnosis .
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<p><b>OBJECTIVE</b>The purpose of this review was to delineate our current knowledge of the close relationship between the abundance of epicardial adipose tissue (EAT) and the risk of all major cardiovascular disease, especially atrial fibrillation (AF).</p><p><b>DATA SOURCES</b>The data analyzed in this review were mainly from articles reported in PubMed published from 1972 to 2014.</p><p><b>STUDY SELECTION</b>Original articles and critical reviews relevant to EAT and AF were selected.</p><p><b>RESULTS</b>EAT, a particular form of metabolically active visceral fat deposited around the heart, is being regarded as an important independent predictor of cardio-metabolic diseases. EAT is composed of smaller adipocytes than other visceral fat depots and functioned like brown adipose tissue (BAT) to protect adjacent tissues. Improving the understanding of EAT in AF genesis and maintenance may contribute to prevent AF and reduce the complications associated with AF.</p><p><b>CONCLUSION</b>The findings suggest that EAT associates with AF severity and the recurrence of AF after catheter ablation even after adjustment for AF risk factors, but the precise mechanisms are not fully elucidated.</p>
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Humans , Adipose Tissue , Pathology , Atrial Fibrillation , Cardiovascular Diseases , TherapeuticsABSTRACT
<p><b>BACKGROUND</b>Atherosclerosis is a kind of disease with multiple risk factors, of which hyperlipidemia is a major classical risk factor resulting in its pathogenesis and development. The aim of this study was to determine the effects of short-term intensive atorvastatin (IA) therapy on vascular endothelial function and explore the possible mechanisms that may help to explain the clinical benefits from short-term intensive statin therapy.</p><p><b>METHODS</b>After exposure to high-fat diet (HFD) for 8 weeks, the animals were, respectively, treated with IA or low-dose atorvastatin (LA) for 5 days. Blood lipids, C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), nitric oxide (NO), endothelin-1 (ET-1), and endothelium-dependent vasorelaxation function were, respectively, measured. mRNA and protein expression of CRP, TNF-α, IL-6, macrophage chemoattractant protein-1 (MCP-1), and 5-lipoxygenase (5-LO) were also evaluated in pericarotid adipose tissue (PCAT) and cultured adipocytes.</p><p><b>RESULTS</b>HFD increased serum inflammatory factor levels; induced significant hyperlipidemia and endothelial dysfunction, including imbalance between NO and ET-1; enhanced inflammatory factors and 5-LO expression; and promoted macrophage infiltration into adipose tissue. Five-day IA therapy could significantly decrease serum inflammatory factor levels and their expression in PCAT; restore the balance between NO and ET-1; and improve endothelial function and macrophage infiltration without significant changes in blood lipids. However, all of the above were not observed in LA therapy. In vitro experiment found that lipopolysaccharide (LPS) enhanced the expression of inflammatory factors and 5-LO in cultured adipocytes, which could be attenuated by short-time (6 hours) treatment of high-dose (5 µmol/L) but not low-dose (0.5 µmol/L) atorvastatin. In addition, inhibiting 5-LO by Cinnamyl-3,4-dihydroxy-α-cyanocinnamate (CDC, a potent and direct 5-LO inhibitor) could significantly downregulate the above-mentioned gene expression in LPS-treated adipocytes.</p><p><b>CONCLUSION</b>Short-term IA therapy could significantly ameliorate endothelial dysfunction induced by HFD, which may be partly due to attenuating inflammation of PCAT through inhibiting 5-LO pathway.</p>
Subject(s)
Animals , Male , Rabbits , Adipose Tissue , Allergy and Immunology , Arachidonate 5-Lipoxygenase , Metabolism , Atorvastatin , Heptanoic Acids , Therapeutic Uses , Hyperlipidemias , Drug Therapy , Allergy and Immunology , Inflammation , Drug Therapy , Allergy and Immunology , Lipid Metabolism , Pyrroles , Therapeutic UsesABSTRACT
Objective To investigate the roles of phosphatidylinositol 3 kinase (PI3K) and phosphorylated Akt (P-Akt) in the pathogenesis of cervical squamous cell carcinoma and condyloma acuminatum.Methods Immunohistochemistry and Western blot were used to detect the expressions of PI3K and P-Akt in tissue specimens from the lesions of 30 cases of cervical squamous cell carcinoma,30 cases of condyloma acuminatum and the prepuce of 15 normal human controls.The average optical density and gray scale values were calculated and analyzed by t test and F test respectively.Results The expressions of PI3K and P-Akt were observed in only the basal layer of the epidermis of control specimens,but in the whole epidermis of condyloma acuminatum tissue specimens.Cervical squamous cell carcinoma tissue specimens displayed a stronger expression of PI3K and P-Akt compared with the control and condyloma acuminatum tissue specimens.As immunohistochemistry revealed,the average absorbance value for PI3K and P-Akt was 0.28 ±0.05 and 0.20 ± 0.07 respectively in cervical squamous cell carcinoma tissue specimens,0.22 ± 0.04 and 0.17 ± 0.03 respectively in condyloma acuminatum tissue specimens,and 0.16 ± 0.04 and 0.10 ± 0.02 respectively in the control tissue specimens; significant differences were observed in the expressions of PI3K and P-Akt among the three groups of tissue specimens (F =44.87,20.64,respectively,both P ＜ 0.01 ).The results of Western blot were consistent with those of immunohistochemistry,and there was a significant difference in the gray scale value for PI3K and P-Akt between cervical squamous cell carcinoma,condyloma acuminatum and control tissue specimens (3.48 ± 0.48 vs.1.99 ± 0.11 vs.1.00 ± 0.03,F=354.83,P＜ 0.01; 3.33 ± 0.26 vs.1.96 ± 0.11 vs.1.00 ± 0.03,F=302.33,P＜ 0.01 ).Conclusions The PI3K/Akt signaling pathway is abnormally activated in condyloma acuminatum and cervical squamous cell carcinoma,and human papilloma virus may cause the abnormal proliferation of infected epithelium likely by affecting the upregnlated expression of PI3K/P-Akt.
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AIM: To examine the relation between serum concentrations of interleukin-18, interleukin-10, interleukin-6 and acute coronary syndrome (ACS). METHODS: Serum concentrations of IL-18, IL-10, IL-6 were measured in 17 patients with acute myocardial infarction (AMI), 30 patients with unstable angina pectoris (UAP), 15 patients with stable angina pectoris (SAP) and 20 controls by enzyme-linked immunosorbent assay (ELISA) and radioimmunoassay (RIA).The relation between IL-18, IL-6 and IL-10 was compared. RESULTS: Serum concentrations of IL-18, IL-6 were significantly increased in the AMI and UAP groups in comparison with the SAP and control groups. Conversely, serum concentrations of IL-10 were significantly decreased in the AMI and UAP groups in comparison with the SAP and control groups. The correlation of concentrations of IL-18 and IL-6 had no significance; but the levels of IL-18 and IL-6 were negatively correlated with IL-10. CONCLUSION: Serum IL-18, IL-6 concentrations increase while serum IL-10 concentration decreases in patients with acute coronary syndromes. The inflammatory imbalance between IL-18, IL-6 and IL-10 may play an important role in the instability of atherosclerotic plaque.