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Simulations of lithium (Li) impurity transport behaviour with a liquid lithium divertor on the EAST tokamak have been performed using the fluid code EMC3-EIRENE and the Monte Carlo code ITCD. The interactions between particles and the wall surface, like the gyration-induced scrape-off effect, sheath acceleration, kinetic self-sputtering and reflection, are typically ignored or simplified in fluid models. In order to uncover the impacts of the scrape-off effect, sheath acceleration, kinetic self-sputtering and reflection on Li distribution, detailed analysis of the density distributions of Li1+ and Li2+ ions at the divertor region have been carried out by ITCD modelling. The newly-upgraded ITCD code can principally reproduce the distribution patterns of Li ions as well as EMC3-EIRENE under identical plasma conditions on EAST. However, due to the scrape-off effect and sheath acceleration, the densities of Li1+ and Li2+ ions simulated by ITCD are evidently reduced compared to the EMC3-EIRENE simulations. The kinetic self-sputtering by redeposited Li particles in ITCD can increase the densities of the Li ions. Moreover, the kinetic reflection database calculated by SRIM code has been employed by ITCD, which leads to an increase in the Li densities compared to the reflection approach used in EMC3-EIRENE. Overall, by adding the aforesaid physical effects in ITCD, the total number of Li ions shows an obvious reduction compared to the EMC3-EIRENE modelling.

In recent years, with the changes in living standards and dietary structure, the incidence of non-alcoholic fatty liver disease has been increasing year by year in China, and the incidence rate in the general population is as high as 29.81%. An increasingly epidemiological evidence suggests that non-alcoholic fatty liver disease has become one of the causes of increasing liver cirrhosis and liver cancer. However, its etiology and pathogenesis are complex and have not yet been fully elucidated. Therefore, establishing an appropriate non-alcoholic fatty liver disease animal models for pre-clinical research is essential to elucidate its pathogenesis. This article summarizes the latest research progress of non-alcoholic fatty liver disease animal models, which are common at home and abroad in recent years.近年来，随着生活水平和饮食结构的改变，非酒精性脂肪性肝病的发病率呈逐年上升的趋势，在一般人群中的发病率高达29.81%。越来越多的流行病学证据表明，非酒精性脂肪性肝病已成为日益增长的肝硬化和肝癌的原因之一。但其病因和发病机制复杂，至今尚未完全阐明。构建非酒精性脂肪性肝病合适的动物模型进行临床前研究，对于阐明其发病机制至关重要。现就近年来国内外常见的非酒精性脂肪性肝病动物模型的最新研究进展进行综述。.

The purpose of this study was to explore the clinical significance and biological function of long noncoding RNA CASC9 (CASC9) in esophageal squamous cell carcinoma (ESCC).Quantitative Real-time PCR (qRT-PCR) was used to determine the expression of CASC9 in ESCC tissues and cell lines. Receiver operating characteristic curves were used to evaluate the sensitivity and specificity of CASC9. The correlation between the CASC9 levels and the clinicopathological factors of the patients was also analyzed. Then, the survival was assessed by the Kaplan-Meier method and proportional hazards model. The effects of CASC9 on ESCC cells were evaluated by Cell Counting Kit-8 (CCK-8), migration and invasion. Finally, several EMT markers expression was detected by Western blot.We found that CASC9 was significantly upregulated in ESCC cell lines and clinical tissues. The CASC9 levels discriminated ESCC tissues from normal tissues with an area under the ROC curve (AUC) of 0.813. In addition, there is statistical significance between CASC9 expression level and tumor stage, lymph nodes metastasis, and clinical stage. Kaplan-Meier analysis indicated that high CASC9 expression had a significant impact on overall survival (p = 0.014) and disease-free survival (p = 0.0025). Moreover, CASC9 expression was an independent prognostic marker of overall survival and disease-free survival in a multivariate analysis. In vitro assay indicated that inhibition of CASC9 could suppress proliferation, migration, and invasion in ESCC. Further mechanistic studies found that aberrant CASC9 expression could modulate the expression levels of markers of EMT.Our data highlight the pivotal role of CASC9 as a novel diagnostic, prognostic biomarker and a potential therapeutic target of ESCC.

To identify the active components of honeybee venom in production of inflammation and pain-related behaviors, five major peptidergic subfractions were separated, purified and identified from the whole honeybee venom. Among them, four active peptidergic components were characterized as apamin, mast-cell degranulating peptide (MCDP), phospholipase A(2) (PLA(2))-related peptide and melittin, respectively. All five subfractions were effective in production of local inflammatory responses (paw edema) in rats although the efficacies were different. Among the five identified subfractions, only MCDP, PLA(2)-related peptide and melittin were able to produce ongoing pain-related behaviors shown as paw flinches, while only apamin and melittin were potent to produce both thermal and mechanical hypersensitivity. As shown in our previous report, melittin was the most potent polypeptide in production of local inflammation as well as ongoing pain and hypersensitivity. To further explore the peripheral mechanisms underlying melittin-induced nociception and hypersensitivity, a single dose of capsazepine, a blocker of thermal nociceptor transient receptor potential vanilloid receptor 1, was treated s.c. prior to or after melittin administration. The results showed that both pre- and post-treatment of capsazepine could significantly prevent and suppress the melittin-induced ongoing nociceptive responses and thermal hypersensitivity, but were without influencing mechanical hypersensitivity. The present results suggest that the naturally occurring peptidergic substances of the whole honeybee venom have various pharmacological potencies to produce local inflammation, nociception and pain hypersensitivity in mammals, and among the five identified reverse-phase high pressure liquid chromatography subfractions (four polypeptides), melittin, a polypeptide occupying over 50% of the whole honeybee venom, plays a central role in production of local inflammation, nociception and hyperalgesia or allodynia following the experimental honeybee's sting. Peripheral transient receptor potential vanilloid receptor 1 is likely to be involved in melittin-produced ongoing pain and heat hyperalgesia, but not mechanical hyperalgesia, in rats.

The high temperature low cycle fatigue tests of 1Cr11Ni2W2MoV are conducted under total axial straincontrol. The specimens are tested under fully reversed strain. The relationships of cyclic strain-life, stress-strain and stress-life are analyzed. Manson-Coffin method and a new method based on power transformation theory are evaluated by the low cycle fatigue data. The results showed that two methods can effective predict low cycle fatigue life of 1Cr11Ni2W2MoV at 360 °C. Prediction accuracy within ± 1.65 times scatter band. The life prediction capability of new methods proves more effective and accurate than Manson-Coffin method. The new method has smaller standard deviation than Manson-Coffin method. Manson-Coffin method and new method have standard deviations of 0.32 and 0.18 respectively.

Using reverse transcriptase-polymerase chain reaction (RT-PCR) the changes of the angiotensin II receptor subtype 1-a (AT1a) and 1-b (AT1b) mRNA levels were examined in hypertrophied ventricles caused by ventral aorta-caval fistula of SD rats. The results show as follows. (1) Three days after operation, the ventricular weight increased significantly, whereas the level of AT1a and AT1b mRNA in both ventricles remained unchanged. (2) Twelve days after operation, the weight increase of both ventricles was more evident, the levels of AT1a and AT1b mRNA in the right ventricle increased (by 62.6% and 72.0%), as compared with control. In the left ventricle, on the other hand, the level of AT1a mRNA increased by 79.0%, while the level of AT1b mRNA showed no obvious increase. (3) Thirty-five days after operation, the levels of AT1a and AT1b mRNA in both ventricles increased still more significant, (i.e., 70.0% and 83.9% in the right and 96.5% and 86.9% in the left). Moreover, 12 d and 35 d after operation, the level of AT1a mRNA was higher than that of AT1b mRNA in both ventricles. (4) There was a positive correlation between the degree of ventricular hypertrophy with the level of AT1 mRNA in ventricular myocardium (r = 0.6168-0.8223). The results suggest that the increased mRNA expression of AT1 in myocardial hypertrophy caused by volume overload may be a mechanism underlying the increased responsiveness of hypertrophic myocardial cells to Ang II, and a difference in the expression between AT1a and AT1b mRNAs in myocardial hypertrophy may be related to the different physiological or pathophysiological roles of Ang II, mediated by the two subtypes of AT1.

To determine the contribution of cardiac renin-angiotensin system (RAS) to the physiological myocardial hypertrophy induced by swimming training and the relationship between locally produced and circulating RAS, both ventricular and plasma angiotensin (Ang) I and II contents, ventricular angiotensin converting enzyme (ACE) and plasma renin activity (PRA) were detected by means of radioimmunoassay and biochemical method. It was shown that after 5 weeks of swimming, the ventricular wet weight to body weight ratio (V/Bwt) and Ang II in both left and right ventricles and ACE activity increased markedly as compared with the controls (P0.05). Furthermore, significantly positive correlation was found between the ventricular Ang II and V/Bwt (r = 0.7721, P0.001), while the plasma Ang I and II and PRA remained at the control level. No correlation was found between plasma Ang II and V/Bwt. These above findings suggest that cardiac RAS may play an important role in physiological myocardial hypertrophy and to a large extent is in dependent on circulating RAS.