Search

In order to obtain information about the activation of macrophages (M phi s) during photodynamic therapy (PDT), the influence of Photofrin II (Pf II) on the viability of thioglycollate-elicited murine M phi s and the subsequent generation of superoxide anion was studied. Irradiations were performed at an energy density of 5 J cm-2, a power density of 150 mW cm-2 and a wavelength of 405 nm. Viability of M phi s was assessed using the acridine orange-ethidium bromide assay. Superoxide anion generation was determined using ferricytochrome c (cyt c) and nitroblue tetrazolium (NBT) reduction. Our results indicate that the M phi s are highly susceptible to PDT as their viability is decreased to approximately 30% by 1 microgram ml-1 Pf II at the energy density indicated above. Within the first 30 min of addition of the photosensitizer, a reducing agent is generated intracellularly by the stimulation of the M phi s. An extracellular release of superoxide anion does not occur, as measured by the cyt c assay. Preincubation of the cells for 1 or 24 h with Pf II and a second challenge with phorbol myristate acetate (PMA) does not enhance the reduction of NBT. Thus, Pf II exerts an immediate effect on the M phi s which could be interpreted as a first step for subsequent reactions.

The traditional lane change trajectory prediction method has some problems such as large deviation of actual estimation and long prediction time. This paper proposes a lane change trajectory prediction method in the network of vehicles environment. Firstly, the hidden Markov model is used to classify the vehicle behavior in networked vehicle environment into three types: left lane change, right lane change and straight lane change. Secondly, according to the vehicle behavior, the lateral displacement is taken as the index to judge the safety state of the vehicle, and the lane-changing intention of the vehicle is analyzed by using the gradient lifting decision tree. Finally, the vehicle state vector is mapped to the social pool according to the result of lane change intention, combined with the vehicle speed and Angle, and the road network information, traffic control information, road traffic flow information, traffic control state information in the Internet of vehicles and real-time traffic environment information are used as lane change trajectory prediction data. Combined with vehicle state vector, lane change trajectory prediction is realized by multilayer perceptron. The experimental results show that the proposed method has a high degree of fitting with the actual trajectory under different time domain conditions, and the root mean square error of prediction is stable within 0.64, and the prediction time is short. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Bronchopulmonary dysplasia (BPD) is one of the most common chronic lung diseases in infants, but the ways to prevent and treat BPD are still very limited. We tried to find an effective method for treating BPD by studying the effect of fibroblast growth factor 18 (FGF18) on hyperoxia-induced lung injury in mice. MATERIALS AND METHODS: We placed newborn mice in high-oxygen environment (60-70%) and collected mouse lung tissue for histological examination at 3, 7, 14 and 21 days after birth. The correlation between FGF18 and BPD was studied by analyzing the expression of FGF18 in mouse lung tissue. In addition, we used exogenous FGF18 to stimulate primary mouse type II alveolar epithelial cells (AECs II), and detected changes in oxidative stress, inflammation and NF-κB signaling pathway activity of AECs II to analyze the effects of FGF18 on AECs II. RESULTS: From the 7th day after the birth of the mouse, the lung tissue of the hyperoxia-induced mice suffered significant lung injury relative to the control group. The expression of FGF18 in lung tissue induced by hyperoxia was lower than that in the control group. Cell viability of AECs II stimulated by exogenous FGF18 increased, and FGF18 also reduced oxidative stress and inflammation levels of AECs II and inhibited the AECs II injury caused by hyperoxia. NF-κB signaling pathway activity in hyperoxia-induced lung increased, while exogenous FGF18 could reduce the expression and phosphorylation of NF-κB p65 in AECs II. CONCLUSIONS: Hyperoxia-induced lung injury was accompanied by a decrease in FGF18. FGF18 can reduce oxidative stress and inflammation levels of AECs II by inhibiting the NF-κB signaling pathway, thereby reducing hyperoxia-induced cell injury. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The purpose of this study was to explore the influences of micro ribonucleic acid (miR)-708 on cerebral ischemia-reperfusion injury by regulating a disintegrin and metalloprotease 17 (ADAM17) in a targeted manner. MATERIALS AND METHODS: The rat model of middle cerebral artery occlusion (MCAO) was established, and the differentially expressed miR-NAs in the cerebral tissues of rats with ischemia-reperfusion injury were detected via sequencing. The research was performed in control group (PC12 cells received no treatment), inhibitor group (the expression of miR-708 in PC12 cells was down-regulated using miR-708 inhibitor), and interference + inhibitor group [PC12 cells were co-treated with miR-708 inhibitor and ADAM17 small interfering RNA (siRNA)]. Then, the expression of ADAM17 in cells, proliferation ability of cells, and number of apoptotic cells were detected in each group. RESULTS: A total of 225 differentially expressed miRNAs were obtained through miR-NA sequencing and bioinformatics analysis, of which miR-708, miR-169, miR-26, and miR-96 were highly expressed, whereas miR-122, miR-118, and miR-177 were lowly expressed in rats in ischemia-reperfusion group. Compared with that in control group, the level of miR-708 declined significantly in inhibitor group after treatment with miR-708 inhibitor. After treatment with miR-708 inhibitor, the protein expression level of ADAM17 in inhibitor group was evidently higher than that in control group, while its protein expression level in interference + inhibitor group was significantly decreased and restored, after interference of ADAM17 siRNA with protein expression. In comparison with control group, inhibitor group had increased apoptotic cells after miR-708 inhibitor treatment (p<0.05). Besides, after interference of ADAM17 siRNA with protein expression, there were a smaller number of apoptotic cells in interference + inhibitor group (p<0.05), showing mitigated apoptosis. Moreover, the proliferation ability of cells treated with miR-708 inhibitor in inhibitor group was weaker than that in control group (p<0.05), whereas the proliferation ability of cells in interference + inhibitor group was restored to a certain degree after ADAM17 siRNA interfered with the protein expression (p<0.05). CONCLUSIONS: MiR-708 can modulate ADAM17 in a targeted manner to affect cellular proliferation and apoptosis in cerebral ischemia-reperfusion injury. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The aim of this study was to explore the effect of myocardial infarction associated transcript 2 (Mirt2) and miR-101 on sepsis-induced myocardial injury in rats and its mechanism. MATERIALS AND METHODS: Sprague Dawley (SD) rats were divided into sham group, CLP group, CLP + adeno-associated virus (AAV)-lncRNA Mirt2 group, CLP + AAV-NC group and CLP + AAV-lncRNA Mirt2 + agomiR-101 group. Rat CLP model was constructed. PanoViewb1500 was used to detect left ventricular systolic blood pressure (LVSP), left ventricular end diastolic blood pressure (LVEDP), ejection fraction (EF) and fraction shortening (FS) values. Thereafter, Mirt2 and miR-101 expression levels were detected by real-time polymerase chain reaction (RT-PCR), myocardial pathological damage was detected by hematoxylin-eosin (HE) staining, and Interleukin-1β (IL-1β) expression was by immunohistochemical staining. Next, enzyme linked immunosorbent assay (ELISA) was performed to detect the levels of serum inflammatory factors, tumor necrosis factor α (TNF-α), IL-1β, Interleukin-6 (IL-6), myeloperoxidase (MPO), cardiac troponin I (cTn I) and creatine kinase isoenzyme (CK-MB). After that, Western blot was used to detect the expression of inflammatory factors and Phosphatidylinositol-3-kinases (PI3K)/protein-serine-threonine kinase (AKT) signaling pathway. Finally, Dual-Luciferase reporter gene assay was conducted to detect the relationship between Mirt2 and miR-101. RESULTS: Compared with those in the sham group, the cardiac function of the rats in the CLP group was significantly deteriorated, the cardiac structure was disordered, and the expression of pro-inflammatory related factors was significantly increased. Compared with those in CLP group, the cardiac function of the CLP + AAV-lncRNA Mirt2 group was alleviated, the PI3K/AKT signaling pathway was activated, the cardiac structure was slightly disordered, and the expression of pro-inflammatory related factors was reduced. To some extent, miR-101 could directly inhibit the effect of Mirt2. CONCLUSIONS: Mirt2 can silence miR-101 and inhibit myocardial inflammatory response in sepsis rats through the PI3K/AKT signaling pathway, thus improving cardiac structure and function [ABSTRACT FROM AUTHOR]

OBJECTIVE: To explore the effects of lamivudine on cell proliferation of liver cancer and expressions of HBsAg, HBeAg, and MMP-9 in hepatoma cells. MATERIALS AND METHODS: In the intervention group, HepG2.2.15 cells were cultured with lamivudine at 100, 200, and 300 μmol/L for 24 hours, 48 hours, and 72 hours. In the control group, HepG2.2.15 cells were cultured without lamivudine. MTT assay was used to assess the proliferative activity of cells after the intervention by lamivudine for 24 hours, 48 hours, and 72 hours. ELISA was used to measure the expression levels of HBsAg, HBeAg, and MMP-9 after the intervention by lamivudine for 48 hours and 72 hours. RESULTS: There was no significant difference between the intervention group and the control group in the proliferation activity of cells (p>0.05). After 48 hours and 72 hours of intervention by lamivudine, the expressions of MMP-9, HBsAg, and HBeAg in the control group were statistically lower than those in the intervention groups with lamivudine at 100 μmol/L, 200 μmol/L, and 300 μmol/L (p<0.05). The expressions of MMP-9, HBsAg, and HBeAg in HepG2.2.15 gradually decreased with the increase of intervention concentration and intervention time of lamivudine (p<0.05). CONCLUSIONS: Lamivudine cannot directly inhibit the proliferation of liver cancer cells, but it can reduce the expressions of MMP-9, HBsAg, and HBeAg in hepatoma cells, inhibit the replication of HBV disease in hepatoma cells, and suppress tumor growth. [ABSTRACT FROM AUTHOR]

In aquaculture, almost all images collected of an aquaculture scene contain reflections, which often affect the results and accuracy of machine vision. Classifying these images and obtaining images of interest are key to subsequent image processing. The purpose of this study was to identify useful images and remove images that had a substantial effect on the results of image processing for computer vision in aquaculture. In this study, a method for classification of reflective frames based on image texture and a support vector machine (SVM) was proposed for an actual aquaculture site. Objectives of this study were to: (1) develop an algorithm to improve the speed of the method and to ensure that the method has a high classification accuracy, (2) design an algorithm to improve the intelligence and adaptability of the classification, and (3) demonstrate the performance of the method. The results show that the average classification accuracy, false positive rate, and false negative rate for two types of reflective frames (type I and II) were 96.34%, 4.65%, and 2.23%, respectively. In addition, the running time was very low (1.25 s). This strategy also displayed considerable adaptability and could be used to obtain useful images or remove images that have substantial effects on the accuracy of image processing results, thereby improving the applicability of computer vision in aquaculture. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To investigate the expression and correlation of B-cell lymphoma- 2 (Bcl-2) and Bax in the parotid gland after leading duct ligation in rat. MATERIALS AND METHODS: Atrophy of the right parotid was induced by ligating the right Stensen's duct of rats. Immunohistochemical labeling was performed to study the changes in number and distribution of Bcl-2 and Bax in each step of glandular atrophy, and every group at 1, 3, 5, 7, 14, 21, 30, 60, 90, 150, 180 days after ligation. RESULTS: Bcl-2 and Bax showed a low level of expression in normal glandular tissues. At different time points after the ligation of the main duct, Bcl-2 was highly expressed in the duct cells, and the absorbance value reached a peak value at 21 day (3.02+0.10). The 1 D expression of Bax was found in some of the cells in the 3 D, and the expression of Bax reached the peak (1.99+0.10), and the expression of Bcl-2 and Bax were decreased in some cells. Bcl-2/Bax ratio increased at 1-day and 21-day, and then decreased and stabilized. CONCLUSIONS: The expression of Bax and Bcl-2 after ligation of the parotid gland is closely related to the process of the parotid gland atrophy. [ABSTRACT FROM AUTHOR]