Prediction of human triglyceride concentration based on quantum genetic-partial least squares algorithm and fluorescence spectroscopy.

It is an important subject with practical significance in modern medical testing about how to obtain various indicators in blood effectively and conveniently. In this essay, the prediction model of triglyceride (TG) concentration was studied based on the fluorescence spectrum of human serum. Firstly, the concept of effective signal intensity was proposed based on the results of wavelet decomposition that the noise signals of spectrum was mainly distributed in the first and second detailed components, and 280 nm was selected as the optimal excitation wavelength for modeling. Secondly, the correlation between fluorescence spectra and triglyceride concentration was studied, which showed that derivative and wavelet decomposition can greatly reduce the multiple correlation of spectrum. Finally, prediction models of triglyceride (TG) concentration were established based on Quantum Genetic Algorithm and Partial Least Squares method, and the result showed that the wavelet decomposition spectral and derivative spectral had better prediction effects because of their lower multiple correlation and advanced resolution, and the Root Mean Square Error reaches to 0.077 mmol/L. In order to obtain the distribution of concentration information in the spectrum, the information density was defined, which indicated that the 3rd layer detailed wavelet decomposition spectrum contains more information of triglyceride concentration. The research results of this essay provide an important reference for the component concentration detection in complex system with multi-component.

Doping dependence of the phase diagram in one-dimensional extended Hubbard model: a functional renormalization group study.

Using functional renormalization group method, we studied the phase diagram of the one-dimensional extended Hubbard model at different dopings. At half filling, variety of states strongly compete with each other. These states include spin-density wave, charge-density wave, s-wave and p -wave superconductivity, phase separation, and an exotic bond-order wave. By doping, system favours superconductivity more than density waves. At 1/8 doping, a new area of extended s-wave superconductivity emerges between charge density wave and bond-order wave regions. If the system is doped to 1/4-doping, a new area of p -wave superconductivity emerges between charge-density wave and spin-density wave regions.

Activation of miR-34a-5p/Sirt1/p66shc pathway contributes to doxorubicin-induced cardiotoxicity.

The molecular mechanisms underlying anthracyclines-induced cardiotoxicity have not been well elucidated. MiRNAs were revealed dysregulated in the myocardium and plasma of rats received Dox treatment. MicroRNA-34a-5p (miR-34a-5p) was verified increased in the myocardium and plasma of Dox-treated rats, but was reversed in rats received Dox plus DEX treatments. Human miR-34a-5p was also observed increased in the plasma of patients with diffuse large B-cell lymphoma after 9- and 16-week epirubicin therapy. Up-regulation of miR-34a-5p was observed in Dox-induced rat cardiomyocyte H9c2 cells. MiR-34a-5p could augment Bax expression, but inhibited Bcl-2 expression, along with the increases of the activated caspase-3 and mitochondrial potentials in H9C2 cells. MiR-34a-5p was verified to modulate Sirt1 expression post-transcriptionally. In parallel to Sirt1 siRNA, miR-34a-5p could enhance p66shc expression, accompanied by increases of Bax and the activated caspase-3 and a decrease of Bcl-2 in H9c2 cells. Moreover, enforced expression of Sirt1 alleviated Dox-induced apoptosis of H9c2 cells, with suppressing levels of p66shc, Bax, the activated caspase-3 and miR-34a-5p, and enhancing Bcl-2 expression. Therefore, miR-34a-5p enhances cardiomyocyte apoptosis by targeting Sirt1, activation of miR-34a-5p/Sirt1/p66shc pathway contributes to Dox-induced cardiotoxicity, and blockage of this pathway represents a potential cardioprotective effect against anthracyclines.

CircRNA_000203 enhances the expression of fibrosis-associated genes by derepressing targets of miR-26b-5p, Col1a2 and CTGF, in cardiac fibroblasts.

Circular RNAs (circRNAs) participate in regulating gene expression in diverse biological and pathological processes. The present study aimed to investigate the mechanism underlying the modulation of circRNA_000203 on expressions of fibrosis-associated genes in cardiac fibroblasts. CircRNA_000203 was shown upregulated in the diabetic mouse myocardium and in Ang-II-induced mouse cardiac fibroblasts. Enforced-expression of circRNA_000203 could increase expressions of Col1a2, Col3a1 and α-SMA in mouse cardiac fibroblasts. RNA pull-down and RT-qPCR assay indicated that circRNA_000203 could specifically sponge miR-26b-5p. Dual luciferase reporter assay revealed that miR-26b-5p interacted with 3'UTRs of Col1a2 and CTGF, and circ_000203 could block the interactions of miR-26b-5p and 3'UTRs of Col1a2 and CTGF. Transfection of miR-26b-5p could post-transcriptionaly inhibit expressions of Col1a2 and CTGF, accompanied with the suppressions of Col3a1 and α-SMA in cardiac fibroblasts. Additionally, over-expression of circRNA_000203 could eliminate the anti-fibrosis effect of miR-26b-5p in cardiac fibroblasts. Together, our results reveal that suppressing the function of miR-26b-5p contributes to the pro-fibrosis effect of circRNA_000203 in cardiac fibroblasts.

Myocyte-specific enhancer factor 2C: a novel target gene of miR-214-3p in suppressing angiotensin II-induced cardiomyocyte hypertrophy.

The role of microRNA-214-3p (miR-214-3p) in cardiac hypertrophy was not well illustrated. The present study aimed to investigate the expression and potential target of miR-214-3p in angiotensin II (Ang-II)-induced mouse cardiac hypertrophy. In mice with either Ang-II infusion or transverse aortic constriction (TAC) model, miR-214-3p expression was markedly decreased in the hypertrophic myocardium. Down-regulation of miR-214-3p was observed in the myocardium of patients with cardiac hypertrophy. Expression of miR-214-3p was upregulated in Ang-II-induced hypertrophic neonatal mouse ventricular cardiomyocytes. Cardiac hypertrophy was attenuated in Ang-II-infused mice by tail vein injection of miR-214-3p. Moreover, miR-214-3p inhibited the expression of atrial natriuretic peptide (ANP) and ß-myosin heavy chain (MHC) in Ang-II-treated mouse cardiomyocytes in vitro. Myocyte-specific enhancer factor 2C (MEF2C), which was increased in Ang-II-induced hypertrophic mouse myocardium and cardiomyocytes, was identified as a target gene of miR-214-3p. Functionally, miR-214-3p mimic, consistent with MEF2C siRNA, inhibited cell size increase and protein expression of ANP and ß-MHC in Ang-II-treated mouse cardiomyocytes. The NF-κB signal pathway was verified to mediate Ang-II-induced miR-214-3p expression in cardiomyocytes. Taken together, our results revealed that MEF2C is a novel target of miR-214-3p, and attenuation of miR-214-3p expression may contribute to MEF2Cexpressionin cardiac hypertrophy.

Targeting EZH1 and EZH2 contributes to the suppression of fibrosis-associated genes by miR-214-3p in cardiac myofibroblasts.

The role of microRNA-214-3p (miR-214-3p) in cardiac fibrosis was not well illustrated. The present study aimed to investigate the expression and potential target of miR-214-3p in angiotensin II (Ang-II)-induced cardiac fibrosis. MiR-214-3p was markedly decreased in the fibrotic myocardium of a mouse Ang-II infusion model, but was upregulated in Ang-II-treated mouse myofibroblasts. Cardiac fibrosis was shown attenuated in Ang-II-infused mice received tail vein injection of miR-214-3p agomir. Consistently, miR-214-3p inhibited the expression of Col1a1 and Col3a1 in mouse myofibroblasts in vitro. MiR-214-3p could bind the 3'-UTRs of enhancer of zeste homolog 1 (EZH1) and -2, and suppressed EZH1 and -2 expressions at the transcriptional level. Functionally, miR-214-3p mimic, in parallel to EZH1 siRNA and EZH2 siRNA, could enhance peroxisome proliferator-activated receptor-γ (PPAR-γ) expression and inhibited the expression of Col1a1 and Col3a1 in myofibroblasts. In addition, enforced expression of EZH1 and -2, and knockdown of PPAR-γ resulted in the increase of Col1a1 and Col3a1 in myofibroblasts. Moreover, the NF-κB signal pathway was verified to mediate Ang-II-induced miR-214-3p expression in myofibroblasts. Taken together, our results revealed that EZH1 and -2 were novel targets of miR-214-3p, and miR-214-3p might be one potential miRNA for the prevention of cardiac fibrosis.

Hsp90aa1: a novel target gene of miR-1 in cardiac ischemia/reperfusion injury.

The role of microRNA-1 (miR-1) in ischemia/reperfusion (I/R)-induced injury is not well illustrated. The present study aimed to investigate the expression and potential target of miR-1 in the myocardium of a rat model of I/R. The apoptosis of cardiomyocytes in the ischemic rat myocardium increased on day 1, then attenuated on day 3 and day 7 post-I/R. Heat shot protein 90 (Hsp90) aa1 mRNA expression was decreased post-I/R, and Hsp90aa1 protein level was decreased on day1 post-I/R, but was reversed on day 3 and day 7 post-I/R. MiR-1 was downregulated post-I/R, and repression of miR-1 in cultured neonatal rat ventricular cells (NRVCs) led to an increase of Bcl-2 and decreases of Bax and active caspase-3. Dual luciferase reporter assays revealed that miR-1 interacted with the 310-315 nt site at the 3'UTR of Hsp90aa1, and miR-1 was verified to inhibit Hsp90aa1 expression at the posttranscriptional level. Over-expression of Hsp90aa1 could attenuate oxygen-glucose deprivation (OGD)-induced apoptosis of NRVCs. Additionally, miR-1 mimic, in parallel to Hsp90aa1 siRNA, could enhance OGD-induced apoptosis of NRVCs. Taken together, our results reveal that Hsp90aa1 is a novel target of miR-1, and repression of miR-1 may contribute to the recovery of Hsp90aa1 during myocardial I/R.

[The long-term effect and associated factors of double embolization of bronchial artery in patients with lung tuberculosis and hemoptysis].

OBJECTIVE: To investigate the long-term effect and the key factors associated with relapse of double embolization of bronchial artery in patients with lung tuberculosis and hemoptysis. METHODS: Fifty patients with lung tuberculosis and hemoptysis receiving the radiography and double embolization of bronchial artery (BAG + BAE) had been followed up for two years. The causes for hemoptysis relapse was determined, followed by specific treatment, and the effect was evaluated. Among them, 37 were males, 13 females, with the age of 8-75 years (mean age 47.6 years). RESULTS: The 2 year follow-up showed that the cure rate and the effective rate were 62% (31/50) and 94% (47/50) respectively. In a short term after embolization, hemoptysis relapsed in 9 cases, the major causes being active tuberculosis and secondary bronchiectasis complicated with infection. Other responsible factors included missed-embolization of bronchial artery and remaining blood supply from systemic circulation. In mid and long term follow-up, hemoptysis relapsed in 10 cases, the major causes being secondary pulmonary mycotic infection and recurrence of tuberculosis. CONCLUSIONS: The long term result of double embolization of bronchial artery in patients with lung tuberculosis and hemoptysis was significant. It could prevent the danger from massive hemoptysis, and therefore allows the medical therapy for tuberculosis. Embolization of bronchial artery is effective for hemostasis, while etiologic therapy aimed at removing the infection leading to chronic inflammation is the cure for tuberculosis and hemoptysis.