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Objective: To solve the problems of poor accuracy and low sorting efficiency of the existing string fruits in robot sorting. Methods: Based on the structure of the high-speed parallel food sorting system, the improved SURF algorithm and the improved RANSAC algorithm were combined to locate the grab points of the food sorting robot, and a three-dimensional grab model was established to realize the automatic and stable grab of string fruits. Taking grapes as an example, the superiority and accuracy of the proposed method were verified by experiments. Results: Compared with the conventional method, the proposed method improved the average capture success rate by about 15.00% and the average capture time by 0.101 s. Conclusion: The food sorting robot can effectively improve the accuracy of the positioning of the holding points of string fruits, and has a high success rate.

Objective To investigate the role of proline-rich protein tyrosine kinase (Pyk2) in angiotensin Ⅱ(Ang Ⅱ)-induced cardiac hypertrophy and the underlying mechanism in rat. Methods Primary rat cardio-myocytes were isolated from rats and randomly divided into control group, Ang Ⅱ induction group (the dose of Ang Ⅱ was 100 nmol/L, cardiomyocytes were stimulated in the cell culture dish for 24 hours), Pyk2 inhibitor PF-431396 group (the dose of PF-431396 was 10 μmol/L, added to the cell culture dish 30 minutes in advance before Ang Ⅱ stimulation) and Ang Ⅱ induction group intervened by PF-431396 (the dose of Ang Ⅱ was 100 nmol/L, the dose of PF-431396 was 10 μmol/L). The size of cardiomyocytes was measured by α-actinin fluorescence staining. RT-qPCR was performed to detect the mRNA level of hypertrophic markers (ANP and β-MHC) in cardiomyocytes. The expressions of p-Pyk2, Pyk2 and p53 in cardiomyocytes were detected by Western blot analysis. Results Ang Ⅱ stimulation increased the surface area of cardiomyocytes and the mRNA level of hypertrophic markers(P＜0.05). In addition, the proteins of p-Pyk2 and p53 were increased(P＜0.05). However, after treatment of Pyk2 inhibitor PF-431396, moycardial hypertrophy was significantly improved and the protein level of Pyk2 and p53 decreased(P＜0.05). Conclusions Pyk2 promotes cardiomyocyte hypertrophy in rat induced by Ang Ⅱ through the p53 signaling pathway.

Although deep learning models show powerful performance, they are still easily deceived by adversarial samples. Some methods for generating adversarial samples have the drawback of high time loss, which is problematic for adversarial training, and the existing adversarial training methods are difficult to adapt to the dynamic nature of the model, so it is still challenging to study an efficient adversarial training method. In this paper, we propose an adversarial training method, the core of which is the improved adversarial sample generation method AGFAT for adversarial training and the improved dynamic adversarial training method AGFAT-DAT. AGFAT uses a word frequency-based approach to identify significant words, filter replacement candidates, and use an efficient semantic constraint module as a means to reduce the time of adversarial sample generation; AGFAT-DAT is a dynamic adversarial training approach that uses a cyclic attack on the model after adversarial training and generates adversarial samples for adversarial training again. It is demonstrated that the proposed method can significantly reduce the generation time of adversarial samples, and the adversarial-trained model can also effectively defend against other types of word-level adversarial attacks. [ABSTRACT FROM AUTHOR]

The FGF/FGFR signaling axis deregulation of the fibroblast growth factor receptor (FGFR) family is closely related to tumorigenesis, tumor progression and drug resistance to anticancer therapy. And fibroblast growth factor receptor 3 (FGFR3) is one member of this family. In this study, we aimed to investigate the effect of siRNA-induced knockdown of FGFR3 on the biological behaviors of intrahepatic cholangiocarcinoma (ICC). The expression levels of FGFR3 were determined in three intrahepatic cholangiocarcinoma cell lines RBE, HUCCT1 and HCCC9810 cell lines by Western blot. FGFR3 expression in RBE cell line was knocked down by siRNA. Our study found that knockdown of FGFR3 inhibited the migration, invasion and proliferation of ICC cells using Wound healing assay, Transwell migration and invasion assays and Cell proliferation assay. And significantly down-regulated the protein expression levels of MMP2, cyclinD1, and N Cadherin, but had no significant effect on MMP9, cyclinD3, vimentin, E-cadherin protein. In addition, we found that ERK/c-Myc presumably is its signaling pathway by bioinformatics analysis and Western blot verification. To sum up, knockdown of FGFR3 inhibited the migration, invasion and proliferation of ICC cells. It demonstrated that FGFR3 probably becomes a therapeutic target for ICC and increases the proportion of potentially curable intrahepatic cholangiocarcinoma patients treated with FGFR inhibitors. [ABSTRACT FROM AUTHOR]

MicroRNA-361-5p (miR-361-5p) is a tumor suppressor miRNA that is dysregulated in several types of human cancer. However, the functional significance of miR-361-5p in hepatocellular carcinoma (HCC) is unclear. This study explored the biological function of miR-361-5p in regulating the progression of HCC and the underlying molecular mechanism. RT-qPCR analysis showed that miR-361-5p was downregulated in HCC tissues and cell lines. Functional analysis revealed that miR-361-5p acted as a tumor suppressor, inhibiting cell proliferation, migration, and invasion in HCC cell lines. Bioinformatics analyses identified Twist1 as a direct target of miR-361-5p, which was validated by dual-luciferase reporter assays, RT-qPCR, and western blotting. Rescue experiments indicated that Twist1 may mediate the tumor-suppressive effect of miR-361-5p in HCC cells, and this was supported by the effect of miR-361-5p on inhibiting the epithelial-mesenchymal transition (EMT) by targeting Twist1. This study is the first to suggest that miR-361-5p inhibits tumorigenesis and EMT in HCC by targeting Twist1. These findings are valuable for the diagnosis and clinical management of HCC. [ABSTRACT FROM AUTHOR]

Patent ductus arteriosus is the third most common congenital heart disease and resulted from the persistence of ductal patency after birth. Ductus arteriosus closure involves functional and structural remodeling, controlled by many factors. The changes in plasma protein levels associated with PDA closure are not known. Here we for the first time demonstrate six key differential plasma proteins in human patent ductus arteriosus patients using proteomic technology and present a model to illustrate the constriction and closure of ductus arteriosus. Differentially expressed proteins were analyzed by using isobaric tags for relative and absolute quantification and validated by enzyme‐linked immunosorbent assay in new samples. The proteomic data have been deposited to the ProteomeXchange Consortium via the PRIDE partner repository with the data set identifier PXD008568. We found 74 upregulated and 98 downregulated proteins in the plasma of patients with PDA. Five decreased proteins (platelet factor 4, fibrinogen, von Willebrand factor, collagen, and mannose binding lectin‐associated serine protease‐2) and one increased protein (fibronectin) may increase the risk of patent ductus arteriosus. Those proteins are closely related to platelet activation and coagulation cascades, complement mannan‐binding‐lectin, and other systemic signaling pathways. Our findings for the first time indicate that the differential proteins involved in different pathways may play key roles in the nonclosure of the ductus arteriosus in humans and may be developed as biomarkers for diagnosis. All those findings may be served as the basis of understanding the etiology and pathogenesis of patent ductus arteriosus. Ductus arteriosus closure involves functional and structural remodeling, controlled by many factors and we for the first time demonstrate six key differential plasma proteins in human patent ductus arteriosus patients using proteomic technology and present a model to illustrate the constriction and closure of ductus arteriosus. Those proteins are closely related to platelet activation and coagulation cascades, complement mannan‐binding‐lectin, and other systemic signaling pathways. Our findings for the first time indicate that the differential proteins involved in different pathways may play key roles in the nonclosure of the ductus arteriosus in humans and may be developed as biomarkers for diagnosis. All those findings may be served as the basis of understanding the etiology and pathogenesis of patent ductus arteriosus. [ABSTRACT FROM AUTHOR]

Intrahepatic cholangiocarcinoma (ICC) is an aggressive type of cancer, and its incidence and mortality rates are increasing worldwide. Mortalin is a highly conserved chaperone protein involved in multiple pathological and physiological processes, including anti-apoptosis, carcinogenesis and metastasis. The Bcl-2 family of proteins can be divided into pro-survival and pro-apoptotic members, including B-cell lymphoma 2 (Bcl-2) and Bcl-2-like protein 4 (Bax). The aim of the present study was to investigate the association between mortalin, Bcl-2 and Bax, as well as the prognostic significance of the combined expression of mortalin, Bcl-2 and Bax in ICC. Immunohistochemistry was used to determine the expression of mortalin, Bcl-2 and Bax in 116 ICC samples and to assess the association between expression of 3 markers and clinicopathological features of ICC patients. This revealed that ICC tumor tissues overexpressed mortalin and Bcl-2 and exhibited low expression of Bax in ICC tumor tissues compared with that in corresponding peritumoral samples. According to Pearson's correlation coefficient analysis, high expression of mortalin in ICC was positively correlated with Bcl-2 expression and negatively correlated with Bax expression. Furthermore, multiple linear regression analysis demonstrated that mortalin was positively associated with Bcl-2, but not with Bax, in patients with ICC. Patients with ICC exhibiting high expression of mortalin/Bcl-2 or low expression of Bax were closely associated with a malignant ICC phenotype, a relatively low overall survival rate and a high recurrence rate. Multivariate analysis indicated that mortalin and Bcl-2 were independent prognostic indicators for ICC patients. Meanwhile, the concomitant overexpression of mortalin and Bcl-2 and the low expression of Bax were independent markers for predicting a relatively poor prognosis of ICC. The overexpression of mortalin and Bcl-2 and/or the low expression of Bax are implicated in the anti-apoptotic effect and tumor progression of ICC. Mortalin or Bcl-2, or a combination of mortalin, Bcl-2 and Bax may be used to predict the prognosis of ICC, as well as potential therapeutic targets. [ABSTRACT FROM AUTHOR]

The immunoproteasome is a multicatalytic protease complex in all eukaryotic cells, which plays a key role in regulating essential cellular processes. However, the role of immunoproteasome subunit β2i in regulation of cardiac fibrosis and inflammation in deoxycorticosterone-acetate (DOCA)/salt mice remains unknown. Wild-type (WT) and β2i knockout (KO) mice were subjected to uninephrectomy and DOCA/salt treatment for 21 days. Blood pressure was measured by the tail-cuff system. Cardiac function and remodeling were examined by echocardiography, hematoxylin-eosin (H&E) and Masson's trichrome staining. The gene and protein expressions were detected by quantitative real-time PCR, and Western blot analysis. After 21 days, DOCA/salt treatment significantly up-regulated the expression of β2i mRNA and protein in the hearts. Moreover, systolic blood pressure and heart weight/body weight (HW/BW) ratio were significantly higher in DOCA/salt mice than in sham groups, and these effects were markedly reversed in β2i knockout mice. Importantly, DOCA/salt-induced cardiac fibrosis, inflammation and the expression of collagen I, collagen III, α-SMA, IL-1β, IL-6 and TNF-α in the wild-type hearts, which were markedly attenuated by β2i knockout. These beneficial effects were due, at least in part, to the inhibition of IκBα/NF-κB and TGF-β1/Smad2/3 signaling pathways. Collectively, these findings indicate that knockout of β2i ameliorates DOCA/salt-induced cardiac fibrosis and inflammation, and may be a novel potential therapeutic target for hypertensive heart diseases. [ABSTRACT FROM AUTHOR]

We have modified the mitral repair technique in infants and small children by using autologous pericardial strips to treat mitral regurgitation resulting from a dilated mitral annulus. Our results demonstrate that this technique maintains stability and flexibility of the mitral annulus and decreases the risk of mitral stenosis. [ABSTRACT FROM AUTHOR]

Objective To investigate the effects of metformin on the proliferation, apoptosis and migration ability of human hepatocellular carcinoma cells HCCLM3. Methods HCCLM3 cells were treated with different concentrations of metformin. Cell proliferation was assessed by CCK-8 assay. The expression of related apoptosis genes, Bax and Bcl-2 were determined by RT-PCR. Cell migration was determined by scratch experiment. Results Metformin decreased the proliferation of HCCLM3 cells in a dose-dependent and time-dependent manner and the cell proliferation inhibition rate was significantly higher than the control group (P < 0.05) . The migration of HCCLM3 was inhibited when the concentration of metformin reaches 10mmol/L. The expression of Bax mRNA was up-regulated, while Bcl-2 was down-regulated after 48h treated. Conclusion Metformin can inhibit HCCLM3 cell proliferation and migration, and affect the expression of apoptosis related gene Bax and Bcl-2 in a concentration and time-dependent manner. [ABSTRACT FROM AUTHOR]

To understand the mechanism of NaHSO3 as a photosynthetic accelerator on rapeseed, the effects of NaHSO3 on growth, nitrogen metabolism and photosynthetic characteristics of Brassica napus cultivar Zhuangshuang 11 were investigated in liquid solution added with NaHSO3 at the concentration of 0-0.08 mmol/L. Results showed that with 0. 02 mmolL NaHSO3, plant height increased by 21.0%, 28.4% and 40.4% respectively after 10, 15 and 20 days. Their fresh weight and root length were also increased but not significantly different to the control. With 0. 08 mmolL NaHSO3, root length was significantly decreased by 15.1 - 16.5% after 10-15 days. Contents of chlorophyll b and total chlorophyll in rapeseed seedlings significantly increased under all concentrations of NaHSO3 treatments. Increase of chlorophyll a was observed only at 0.02 mmol/L NaHSO3 treatment, and the highest contents of chlorophyll b and total chlorophyll were also achieved. After NaHSO3 treatment, photosynthetic rate (Pn), light saturation point (LCP) and apparent quantum efficiency (AQY) increased significantly, while photorespiration rate (Rp), intercellular concentration of CO2(Ci) and transpiration rate (Tr) declined significantly. With a higher maximum light energy conversion rate (Fv/Fm) and actual light energy conversion rate n) and a lower non - photochemical quenching coefficient (NPQ), the low concentration of NaHSO3 resulted in an increasing of the share of light energy which was used to describing photochemical transfer. The activity of nitrate reductase (NR) and glutamine synthetase (SR) increased after NaHSO3 treatment. In conclusion, NaHSO3 improved the photosynthesis through the increase of chlorophyll b content, which led to a higher efficiency of electronic absorption and transportation. [ABSTRACT FROM AUTHOR]

Aim:To investigate the role of extracellular signal-regulated kinases (ERKs) in sevoflurane post-conditioning induced cardioprotection in vitro.Methods:Isolated rat hearts were subjected to 30 min ischemia followed by 120 min reperfusion (I/R). Sevoflurane post-conditioning was carried out by administration of O2-enriched gas mixture with 3% sevoflurane (SEVO) for 15 min from the onset of reperfusion. Cardiac functions, myocardial infarct size, myocardial ATP and NAD+ contents, mitochondrial ultrastructure, and anti-apototic and anti-oncosis protein levels were measured.Results:Sevoflurane post-conditioning significantly improved the heart function, decreased infarct size and mitochondria damage, and increased myocardial ATP and NAD+ content in the I/R hearts. Furthermore, sevoflurane post-conditioning significantly increased the levels of p-ERK and p-p70S6K, decreased the levels of porimin, caspase-8, cleaved caspase-3, and cytosolic cytochrome c in the I/R hearts. Co-administration of the ERK1/2 inhibitor PD98059 (20 μmol/L) abolished the sevoflurane-induced protective effects against myocardial I/R.Conclusion:Sevoflurane post-conditioning protects isolated rat hearts against myocardial I/R injury and inhibits cell oncosis and apoptosis via activation of the ERK1/2 pathway. [ABSTRACT FROM AUTHOR]