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The present study examined plasma lipid profiles in thirty patients suffered from acute viral hepatitis. Patients' blood samples were collected at both the debut and recovery of diseases. Thirty sex and age matched normal subjects were included as controls. Plasma total triglycerides (TG), total cholesterol, high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), apolipoprotein AI (ApoAI), apolipoprotein B (ApoB), lipoprotein (a) (Lp(a)), blood coagulation status including prothrombin complex activity and activated partial tromboplastin time (APTT), and hepatic functions were determined by the automatic biochemical analytical instrument. It demonstrated that plasma levels of total cholesterol, HDL-C and apoAI were significantly lower in the patients at the acute phase of hepatitis than those in normal subjects, whereas plasma levels of TG and LDL-C were obviously higher in the patients than in normal subjects (P < 0.05). Moreover, we demonstrated that patients' plasma levels of total cholesterol, LDL-C, HDL-C and apoAI were lower at the active phase of the diseases than at the recovering phase, which indicating that acute liver damage could significant influence lipid metabolism in vivo. No pathological changes of blood coagulation status occurred in these patients during the study as all selected patients had moderate hepatitis. It may conclude that examinations of plasma lipid profile could be considered as a clinical index to reflect liver damage in the active phase of hepatitis. [ABSTRACT FROM AUTHOR]

We have developed the theoretical foundation and technical details of a migration method using a local-cosine-bases (LCB) beamlet propagator. A beamlet propagator for heterogeneous media based on local perturbation theory is derived, and a fast implementation method is constructed. The use of local background velocities and local perturbations results in a two-scale decomposition of beamlet propagators: a background propagator for large-scale structures and a local phase-screen correction for small-scale local perturbations. Because of its locally adaptive nature, the beamlet propagator can handle strong lateral velocity variations with improved accuracy. For high-efficiency migration, we use a table-driven method and apply some techniques of sparse matrix operations. Compared with the Fourier finite-difference and generalized screen propagator methods, the image quality and computational efficiency are similar. In some cases, we see fewer migration artifacts around and inside salt bodies with our method. We attribute this tO the better high-angle accuracy of beamlet propagators in strong-contrast media. Numerical tests using synthetic data sets of the SEG-EAGE 2D salt model, Marmousi model, and Sigsbee 2A model demonstrate its high accuracy and reasonable efficiency. Another special feature of LCB beamlet migration is the availability of information in the local wavenumber domain during migration, which can be used to correct acquisition aperture effect and for other processing. Compared to beamlet migration using the Gabor-Daubecbies frame (GDF) propagator, LCB migration is much more efficient because LCB is an orthonormal basis, whereas GDF has redundancy (usually greater than two) in the decomposition. [ABSTRACT FROM AUTHOR]

Objective: Angiogenic therapies in animals have demonstrated the development of new blood vessels within ischemic myocardium. However, results from clinical protein and gene angiogenic trials have been less impressive. The present study aimed to investigate the expression of angiogenic genes in human chronic ischemic myocardium and the influence of acute ischemia/cardioplegia and reperfusion on their expression. Methods: Myocardial biopsies were taken from chronic ischemic and nonischemic myocardium in 15 patients with stable angina pectoris during coronary bypass surgery. Tissue samples were evaluated by oligonucleotide microarray and quantitative real-time PCR for the expression of angiogenic factors. Results: There was identical baseline expression of VEGF-A and VEGF-C mRNA in chronic ischemic myocardium compared with nonischemic myocardium. Reperfusion increased the gene expression of VEGF-A and VEGF-C mRNA both in nonischemic and ischemic myocardium. VEGF-A protein was detected mainly in the extracellular matrix around the cardiomyocytes in ischemic myocardium. Conclusion: These data suggest that the nonconclusive VEGF gene therapy trials chronic coronary artery disease was not due to a preexisting upregulation of VEGF in chronic ischemic myocardium. There might be room for further therapeutic angiogenesis in chronic ischemic myocardium. [ABSTRACT FROM AUTHOR]

Background Hearing loss is highly prevalent in occupational populations, but it could be effectively prevented through early monitoring. There is still a lack of studies on the risk assessment of hearing loss. Objective To construct three risk assessment models for hearing loss in oil workers, and evaluate their performance to obtain the optimal one. Methods A cross-sectional study was conducted. Participants were 1 423 workers of an oil company who received the occupational health examination from 2018 to 2019 in the Jingxia Hospital of North China Petroleum Administration. Their general demographic data, audiometric test and laboratory test results were collected. Unconditional multivariable Logistic regression was used to explore the factors influencing hearing loss. Python was used to build the random forest, XG Boost, and BP neural network models with factors potentially associated with hearing loss determined based on a literature review and expert opinions incorporated. The discriminative ability of the models were evaluated using the receiver operating characteristic curve (ROC) , and the calibration ability of the model was tested using the calibration curve. Results The prevalence of hearing loss changed significantly according to age, gender, monthly household income, history of diabetes, labor intensity, physical exercise, ototoxic chemical exposure, sleep disturbance, shift, and high temperature exposure (P

Background: Congenital infection of Toxoplasma gondii is an important factor causing birth defects. The neural stem cells (NSCs) are found to be one of the target cells for the parasite during development of the brain. As a key virulence factor of the parasite that hijacks host cellular functions, ROP18 has been demonstrated to mediate the inhibition of host innate and adaptive immune responses through specific binding different host immunity related molecules. However, its pathogenic actions in NSCs remain elusive. Results: In the present study, ROP18 recombinant adenovirus (Ad-ROP18) was constructed and used to infect C17.2 NSCs. After 3d- or 5d-culture in differentiation medium, the differentiation of C17.2 NSCs and the activity of the Wnt/β-catenin signaling pathway were detected. The results showed that the protein level of βIII-tubulin, a marker of neurons, in the Ad-ROP18-transfected C17.2 NSCs was significantly decreased, indicating that the differentiation of C17.2 NSCs was inhibited by the ROP18. The β-catenin level in the Ad-ROP18-transfected C17.2 NSCs was found to be lower than that in the Ad group. Also, neurogenin1 (Ngn1) and neurogenin2 (Ngn2) were downregulated significantly (P < 0.05) in the Ad-ROP18-transfected C17.2 NSCs compared to the Ad group. Accordingly, the TOP flash/FOP flash dual-luciferase report system showed that the transfection of Ad-ROP18 decreased the Wnt/β- catenin pathway activity in the C17.2 NSCs. Conclusions: The inhibition effect of the ROP18 from T. gondii (TgROP18) on the neuronal differentiation of C17.2 NSCs was at least partly mediated through inhibiting the activity of the Wnt/β-catenin signaling pathway, eventually resulting in the downregulation of Ngn1 and Ngn2. The findings help to better understand potential mechanisms of brain pathology induced by TgROP18. [ABSTRACT FROM AUTHOR]

Gene expression signals involved in ischemic injury, extracellular matrix composition and fibrosis defined by global mRNA profiling of the human left ventricular myocardium. The mechanism(s) by which acute and chronic myocardial ischemia translate into the characteristic features of ischemic cardiomyopathy is unresolved at present. We hypothesized that such translation relates to modification of specific gene expression programs during acute and chronic ischemic insults to the myocardium. Global mRNA expression profiles by Affymetrix HG&#95;U133A GeneChip analysis on 33 samples was performed on non-failing human left ventricular myocardium during acute and chronic ischemia in 6 patients undergoing coronary artery by-pass grafting. Results were confirmed by real-time quantitative RT-PCR in 14 patients and supported by histology and immunohistochemistry analyses. Acute ischemia elicited an acute inflammatory response including IL-6, IL-8, MCP-1, VCAM-1 and CYR-61 with an attenuated increase of IL-6 and IL-8 in chronic ischemic myocardium compared to normal myocardium. High mRNA expression of connective tissue growth factor (CTGF) was present in chronic ischemic myocardium with a high degree of correlation between CTGF and mRNA expression of specific genes (e.g. thrombospondin 4, collagen type Ialpha2, versican, adlican, latent transforming growth factor beta binding protein 2 and fibronectin) involved in extracellular matrix remodelling. In conclusion, acute inflammatory induction (e.g. IL-8, IL-6, VCAM-1 and MCP-1) and an acute phase CCN family gene with effects on matrix interactions (CYR-61) might play important roles in the coupling between acute ischemic episodes and chronic myocardial remodelling. In addition, the findings support an important role of CTGF signalling in chronic extracellular matrix remodelling in chronic coronary artery disease.

Aims: Increased plasma concentrations of B-type natriuretic peptide (BNP) and its precursor (proBNP) provide important prognostic information in patients presenting with acute coronary syndromes. Although a majority of these patients undergo early invasive assessment, the effects of coronary angiography per se on plasma BNP and proBNP concentrations are not known. We therefore sought to determine whether coronary angiography and ventriculography affect the cardiac secretion of these prognostic markers., Methods and Results: Blood samples were collected before and two minutes after coronary angiography and ventriculography in patients with or without coronary artery disease (CAD) and normal left ventricular ejection fraction. In patients with suspected CAD and normal left ventricular ejection fraction, the plasma proBNP concentration transiently increased from 11 pmol/l (range 1-67 pmol/l) to 19 pmol/l (range 5-102 pmol/l, n=29,P<0.0001) two minutes after coronary angiography and ventriculography. The increase was similar in patients with or without CAD, although patients with stable CAD displayed higher plasma BNP and proBNP concentrations at baseline. In contrast, plasma BNP concentrations did not change after coronary angiography and ventriculography., Conclusion: Coronary angiography induces a transient increase in cardiac proBNP secretion. Blood sampling for plasma proBNP measurements in patient stratification and prognosis estimation should consequently be avoided immediately after coronary angiography.