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After long-term oxidation and energy storage, broken coal body borehole walls and drainage shaft walls may cause spontaneous combustion during gas extraction. The high-temperature thermal shock caused by the spontaneous combustion of coal incurs thermal damage on adjacent coal, which, in turn, causes changes in the mechanical properties of the coal. However, only a few studies have been conducted in this context, which has limited our understanding of the thermal damage characteristics of coal bodies in such situations. This study aimed to experimentally investigate the correlation between the crack evolution law and the mechanical properties of coal bodies at different temperatures (50–300°C) using heat-force loading considering Ping Mei No. 10 coal mine as the research object. The results suggest that the coal body experiences a large amount of visible damage, and becomes increasingly complex. At 50–300°C, some indexes (such as longitudinal wave velocity, Poisson's ratio, compressive strength, elastic modulus, impact energy index, and pre-peak strain) are positively correlated with temperature. In addition, the dynamic failure time and temperature show a negative correlation, and the overall change slope is small. The relationship between each index and temperature at 200–300°C is opposite to that at 50–200°C, and the overall change slope is larger. Moreover, when the oxidation temperature exceeds 200°C, the destruction of the coal body changes from elastic brittleness to ductility-plasticity. High-temperature oxidation incurs irreversible thermal damage of coal. Hence, it is necessary to focus on the changes in mechanical properties of coal after a spontaneous combustion process is extinguished. [ABSTRACT FROM AUTHOR]

Purpose: To assess the impact of left ventricular (LV) diastolic dysfunction on left atrial (LA) phasic volume and function using dual-source CT (DSCT) and to find a viable alternative prognostic parameter of CT for LV diastolic dysfunction through quantitative evaluation of LA phasic volume and function in patients with LV diastolic dysfunction. Materials and Methods: Seventy-seven patients were examined using DSCT and Doppler echocardiography on the same day. Reservoir, conduit, and contractile function of LA were evaluated by measuring LA volume (LAV) during different cardiac phases and all parameters were normalized to body surface area (BSA). Patients were divided into four groups (normal, impaired relaxation, pseudonormal, and restrictive LV diastolic filling) according to echocardiographic findings. The LA phasic volume and function in different stages of LV diastolic function was compared using one-way ANOVA analysis. The correlations between indexed volume of LA (LAVi) and diastolic function in different stages of LV were evaluated using Spearman correlation analysis. Results: LA ejection fraction (LAEF), LA contraction, reservoir, and conduit function in patients in impaired relaxation group were not different from those in the normal group, but they were lower in patients in the pseudonormal and restrictive LV diastolic dysfunction groups (P < 0.05). For LA conduit function, there were no significant differences between the patients in the pseudonormal group and restrictive filling group (P = 0.195). There was a strong correlation between the indexed maximal left atrial volume (LAVmax, r = 0.85, P < 0.001), minimal left atrial volume (LAVmin, r = 0.91, P < 0.001), left atrial volume at the onset of P wave (LAVp, r = 0.84, P < 0.001), and different stages of LV diastolic function. The LAVi increased as the severity of LV diastolic dysfunction increased. Conclusions: LA remodeling takes place in patients with LV diastolic dysfunction. At the same time, LA phasic volume and function parameters evaluated by DSCT indicated the severity of the LV diastolic dysfunction. Quantitative analysis of LA phasic volume and function parameters using DSCT could be a viable alternative prognostic parameter of LV diastolic function. [ABSTRACT FROM AUTHOR]

The factors that determine the anatomical variations of the coronary venous system (CVS) are poorly understood. The objective of this study was to evaluate the anatomical variations of the CVS in patients with coronary artery calcification. 196 patients underwent non-contrast CT and coronary CT angiography using 256-slice CT. All subjects were divided into four groups based on their coronary artery calcium score (CACS): 50 patients with CACS = 0 Agatston unit (AU), 52 patients with CACS = 1–100 AU, 44 patients with CACS = 101–400 AU, and 50 patients with CACS > 400 AU. The presence of the following cardiac veins was evaluated: the coronary sinus (CS), great cardiac vein (GCV), posterior interventricular vein (PIV), posterior vein of the left ventricle (PVLV), left marginal vein (LMV), anterior interventricular vein (AIV), and small cardiac vein (SCV). Vessel diameters were also measured. We found that the CS, GCV, PIV, and AIV were visualized in all patients, whereas the PVLV and LMV were identified in a certain proportion of patients: 98% and 96% in the CACS = 0 AU group, 100% and 78.8% in the CACS = 1–100 AU group, 93.2% and 77.3% in the CACS = 101–400 AU group, and 98% and 78% in the CACS > 400 AU group, respectively. The LMV was less often identified in the last three groups than in the first group (p < 0.05). The frequency of having either one PVLV or LMV was higher in the last three groups than in the first group (p < 0.05). No significant differences in vessel diameters were observed between the groups. It was concluded that patients with coronary artery calcification were less likely to have the LMV, which might hamper the left ventricular lead implantation in cardiac resynchronization therapy. [ABSTRACT FROM AUTHOR]

Purpose: To investigate the coronary venous system and its relation to adjacent structures using 256-slice computed tomography (CT). Materials and Methods: The study consisted of 102 patients who underwent coronary CT angiography (CTA) using 256-slice CT. For each patient, the coronary venous system and its relation to adjacent structures were evaluated. The appropriate locations and diameters of the posterior interventricular vein (PIV), posterior vein of the left ventricle (PVLV) and the left marginal vein (LMV) were detected. The paired student's t test was used to evaluate the difference between the diameter of the coronary sinus (CS) ostium in anteroposterior direction and that in superoinferior direction. Results: The CS, great cardiac vein (GCV), PIV, and anterior interventricular vein (AIV) were visualized in all cases. It was possible to evaluate at least one main vein with adequate caliber and regular course for cardiac resynchronization therapy (CRT) in 96.1% of these cases. The diameter of the CS ostium in superoinferior direction (11.7±2.1 mm) was larger than that in anteroposterior direction (9.0±2.0 mm) (t = 13.511, P<0.05). For the majority of the cases, the CS-GCV was located above the level of the mitral valve annulus (MVA), while the left circumflex coronary artery (LCX) was coursed between the CS-GCV and the MVA. LMV had more intersection with the circumflex or circumflex marginal than PVLV. Conclusion: 256-slice CT provides superior noninvasive evaluation of the coronary venous system which has important clinical implications. [ABSTRACT FROM AUTHOR]

Aims: Ischemic preconditioning (IPC) is a potent form of endogenous protection. However, IPC-induced cardioprotective effect is significantly blunted in insulin resistance-related diseases and the underlying mechanism is unclear. This study aimed to determine the role of glucose metabolism in IPC-reduced reperfusion injury. Methods: Normal or streptozotocin (STZ)-treated diabetic rats subjected to 2 cycles of 5 min ischemia/5 min reperfusion prior to myocardial ischemia (30 min)/reperfusion (3 h). Myocardial glucose uptake was determined by 18F-fluorodeoxyglucose-positron emission tomography (PET) scan and gamma-counter biodistribution assay. Results: IPC exerted significant cardioprotection and markedly improved myocardial glucose uptake 1 h after reperfusion (P<0.01) as evidenced by PET images and gamma-counter biodistribution assay in ischemia/reperfused rats. Meanwhile, myocardial translocation of glucose transporter 4 (GLUT4) to plasma membrane together with myocardial Akt and AMPK phosphorylation were significantly enhanced in preconditioned hearts. Intramyocardial injection of GLUT4 siRNA markedly decreased GLUT4 expression and blocked the cardioprotection of IPC as evidence by increased myocardial infarct size. Moreover, the PI3K inhibitor wortmannin significantly inhibited activation of Akt and AMPK, reduced GLUT4 translocation, glucose uptake and ultimately, depressed IPC-induced cardioprotection. Furthermore, IPC-afforded antiapoptotic effect was markedly blunted in STZ-treated diabetic rats. Exogenous insulin supplementation significantly improved glucose uptake via co-activation of myocardial AMPK and Akt and alleviated ischemia/reperfusion injury as evidenced by reduced myocardial apoptosis and infarction size in STZ-treated rats (P<0.05). Conclusions: The present study firstly examined the role of myocardial glucose metabolism during reperfusion in IPC using direct genetic modulation in vivo. Augmented glucose uptake via co-activation of myocardial AMPK and Akt in reperfused myocardium is essential to IPC-alleviated reperfusion injury. This intrinsic metabolic modulation and cardioprotective capacity are present in STZ-treated hearts and can be triggered by insulin. [ABSTRACT FROM AUTHOR]

Background: Currently, no licensed therapy can thoroughly eradicate hepatitis B virus (HBV) from the body, including interferon α and inhibitors of HBV reverse-transcription. Small interfering RNA (siRNA) seem to be a promising tool for treating HBV, but had no effect on the pre-existing HBV covalently closed circular DNA. Because it is very difficult to thoroughly eradicate HBV with unique siRNAs, upgrading the immune response is the best method for fighting HBV infection. Here, we aim to explore the immune response of transgenic mice to HBV vaccination after long-term treatment with siRNAs and develop a therapeutic approach that combines siRNAs with immunopotentiators. Methodology/Principal Findings: To explore the response of transgenic mice to hepatitis B vaccine, innate and acquired immunity were detected after long-term treatment with siRNAs and vaccination. Antiviral cytokines and level of anti-hepatitis B surface antigen antibody (HBsAg-Ab) were measured after three injections of hepatitis B vaccine. Results: Functional analyses indicated that toll-like receptor-mediated innate immune responses were reinforced, and antiviral cytokines were significantly increased, especially in the pSilencer4.1/HBV groups. Analysis of CD80+/CD86+ dendritic cells in the mouse liver indicated that dendritic cell antigen presentation was strengthened. Furthermore, the siRNA-treated transgenic mice could produce detectable HBsAg-Ab after vaccination, especially in the CpG oligonucleotide vaccine group. Conclusions/Significance: For the first time, our studies demonstrate that siRNAs with CpG HBV vaccine could strengthen the immune response and break the immune tolerance status of transgenic mice to HBV. Thus, siRNAs and HBV vaccine could provide a sharp double-edged sword against chronic HBV infection. [ABSTRACT FROM AUTHOR]

Reactive aldehydes can initiate protein oxidative damage which may contribute to heart senescence. Sirtuin 1 (SIRT1) is considered to be a potential interventional target for I/R injury management in the elderly. We hypothesized that aldehyde mediated carbonyl stress increases susceptibility of aged hearts to ischemia/reperfusion (I/R) injury, and elucidate the underlying mechanisms with a focus on SIRT1. Male C57BL/6 young (4-6 mo) and aged (22-24 mo) mice were subjected to myocardial I/R. Cardiac aldehyde dehydrogenase (ALDH2), SIRT1 activity and protein carbonyls were assessed. Our data revealed that aged heart exhibited increased endogenous aldehyde/carbonyl stress due to impaired ALDH2 activity concomitant with blunted SIRT1 activity (P<0.05). Exogenous toxic aldehydes (4-HNE) exposure in isolated cardiomyocyte verified that aldehyde-induced carbonyl modification on SIRT1 impaired SIRT1 activity leading to worse hypoxia/reoxygenation (H/R) injury, which could all be rescued by Alda-1 (ALDH2 activator) (all P<0.05). However, SIRT1 inhibitor blocked the protective effect of Alda-1 on H/R cardiomyocyte. Interestingly, myocardial I/R leads to higher carbonylation but lower activity of SIRT1 in aged hearts than that seen in young hearts (P<0.05). The application of Alda-1 significantly reduced the carbonylation on SIRT1 and markedly improved the tolerance to in vivo I/R injury in aged hearts, but failed to protect Sirt1+/− knockout mice against myocardial I/R injury. This was verified by Alda-1 treatment improved postischemic contractile function recovery in ex vivo perfused aged but not in Sirt1+/− hearts. Thus, aldehyde/carbonyl stress is accelerated in aging heart. These results provide a new insight that impaired cardiac SIRT1 activity by carbonyl stress plays a critical role in the increased susceptibility of aged heart to I/R injury. ALDH2 activation can restore this aging-related myocardial ischemic intolerance. [ABSTRACT FROM AUTHOR]