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Vibrational bruise is one of the most common mechanical damages of fruit under transportation. Transportation vibrational bruise prediction can provide important theoretical basis for reducing the bruise and package design. However, there is no related research about the vibrational bruise prediction of fruits. In this study, a vibrational bruise prediction model based on BP neural network was established to predict the vibrational bruise of harvested kiwifruit. The inputs of the prediction model included the vibrational acceleration, vibrational frequency and time, and this network model was trained using adaptive learning rate method based on momentum gradient descent, the vibrational bruise deformation of kiwifruit could be predicted. The results showed that the neural network model has a good prediction effect of vibrational bruise deformation, and the average relative error of predicting vibrational bruise of kiwifruit is 1.32%, and the average absolute error was 0.01, and R2 is 0. 9683. It can provide a weighable theoretical and data reference for the food storage and transportation. &nbsp

XLSX file - 623K, Genes that are upregulated or downregulated by BRG1.

The SWI/SNF chromatin-remodeling complex regulates gene expression and alters chromatin structures in an ATP-dependent manner. Recent sequencing efforts have shown mutations in BRG1 (SMARCA4), one of two mutually exclusive ATPase subunits in the complex, in a significant number of human lung tumor cell lines and primary non–small cell lung carcinoma (NSCLC) clinical specimens. To determine how BRG1 loss fuels tumor progression in NSCLC, molecular profiling was performed after restoration of BRG1 expression or treatment with a histone deacetylase inhibitor or a DNA methyltransferase (DNMT) inhibitor in a BRG1-deficient NSCLC cells. Importantly, validation studies from multiple cell lines revealed that BRG1 reexpression led to substantial changes in the expression of CDH1, CDH3, EHF, and RRAD that commonly undergo silencing by other epigenetic mechanisms during NSCLC development. Furthermore, treatment with DNMT inhibitors did not restore expression of these transcripts, indicating that this common mechanism of gene silencing did not account for their loss of expression. Collectively, BRG1 loss is an important mechanism for the epigenetic silencing of target genes during NSCLC development.Implications: Inactivation of the SWI/SNF complex provides a novel mechanism to induce gene silencing during NSCLC development. Mol Cancer Res; 12(4); 560–70. ©2014 AACR.

XLSX file - 90K, Genes upregulated by BRG1 or 5dAzaC.

Supplementary Figure S1. This supplementary figure shows that SNF5 KD in normal human fibroblasts does not alter mRNA levels of SWI/SNF components.

Table shows genes with significantly altered expression by RNA-seq after BRG1 or BRM knockout.

Malignant rhabdoid tumors (MRT), a pediatric cancer that most frequently appears in the kidney and brain, generally lack SNF5 (SMARCB1/INI1), a subunit of the SWI/SNF chromatin-remodeling complex. Recent studies have established that multiple SWI/SNF complexes exist due to the presence or absence of different complex members. Therefore, the effect of SNF5 loss upon SWI/SNF complex formation was investigated in human MRT cells. MRT cells and primary human tumors exhibited reduced levels of many complex proteins. Furthermore, reexpression of SNF5 increased SWI/SNF complex protein levels without concomitant increases in mRNA. Proteomic analysis, using mass spectrometry, of MRT cells before and after SNF5 reexpression indicated the recruitment of different components into the complex along with the expulsion of others. IP–Western blotting confirmed these results and demonstrated similar changes in other MRT cell lines. Finally, reduced expression of SNF5 in normal human fibroblasts led to altered levels of these same complex members. These data establish that SNF5 loss during MRT development alters the repertoire of available SWI/SNF complexes, generally disrupting those associated with cellular differentiation. These findings support a model where SNF5 inactivation blocks the conversion of growth-promoting SWI/SNF complexes to differentiation-inducing ones. Therefore, restoration of these complexes in tumors cells provides an attractive approach for the treatment of MRTs.Implications: SNF5 loss dramatically alters SWI/SNF complex composition and prevents formation of complexes required for cellular differentiation. Mol Cancer Res; 12(11); 1574–85. ©2014 AACR.

XLSX file - 71K, Genes upregulated by 5dAzaC or TSA.

XLSX file - 68K, Genes upregulated by BRG1 or TSA.

Supplementary Figure 1 shows BRG1 deficiency activates transcription of a subset of NRF2 target genes in second H358 BRG1 knockdown cell line; Supplementary Figure 2 shows western blot of BRG1 and BRM knockout samples used for RNA-seq.

XLSX file - 63K, Genes upregulated by any treatment.

PDF file - 4305K, Validation of gene expression for microarray and RGLS analyses; RGLS analysis of the A427 cell line.

XLSX file - 67K, Genes upregulated by TSA only.

Supplementary Figure 2. This figure shows additional characterization of global nucleosomal positioning changes in Brg1 KD cell lines.

Supplementary Table 2. Differentially expressed genes were identified between BRG1 mutant and BRG1 wild-type NSCLC cell lines, as described in Materials and Methods. Using an FDR threshold of .025, a total of 135 genes were down-regulated in the BRG1 mutant cell lines.

Supplementary Figure 3. This figure shows additional characterization of nucleosome positioning positions changes around transcription start sites in Brg1 KD cell lines.

Supplementary Figure 1. This figure shows validation of H358 and H441 Brg1 knockdown cell lines.

Supplementary Table and Figure Legends

Supplementary Figure 4. The figure shows kernal-smoothed data for nucleosome positioning about transcription start sites in the Brg1 KD human NSCLC cell line and in mouse SNF5 and Brg1 KO cells.

Supplementary Table 1. Differentially expressed genes were identified, as described in Material and Methods. Genes altered by BRG1 KD- Genes whose expression either increased or decreased in the H358 Brg1i.1 and H358 Brgi.2 cell lines; Upregulated and unregulated genes- We identified 316 genes that showed increased expression in both H358 Brg1i.1 and H358 Brg1i.2 cell lines. We also identified 300 genes that did not show altered expression in the Brg1i.2 cell line.

Supplementary Figure 5. This figure shows nucleosome positioning around 2 genes downregulated after Brg1 KD.

Cervical cancer is a common female malignancy worldwide, and the molecular mechanism of cervical tumorigenesis remains poorly understood. A large piece of evidence have demonstrated the important roles of long noncoding RNAs (lncRNAs) in tumorigenesis, cancer progression and drug resistance. In this study, we comprehensively analyzed the lncRNAs expression pattern in cervical cancer using RNA sequencing and microarray data from the cancer genome atlas, gene expression omnibus and Genotype Tissue Expression. Moreover, we assessed the correlation between lncRNA expression levels and cervical cancer patient's survival. We uncovered hundreds of lncRNAs that are upregulated or downregulated in cervical cancer tissues. Among these aberrantly lncRNAs, some are significantly associated with cervical patients' poorer prognosis, such as ALOX12-AS1 and LINC00173. ALOX12-AS1 expression is downregulated in cervical cancer, and over-expression of ALOX12-AS1 could inhibit cervical cancer cells proliferation in vitro. Further, mechanistically investigation revealed that ALOX12-AS1 could interact with AGO2 and sponge miR-3171, thereby antagonizing its' repression of tumor suppressor phosphatase and tensin homolog expression in cervical cancer cell. Taken together, this study provides lncRNA candidates in cervical cancer and highlights the critical role of ALOX12-AS1 in cervical cancer.

The NF-E2–related factor 2 (referred to as NRF2) transcription factor binds antioxidant responsive elements within the promoters of cytoprotective genes to induce their expression. Next-generation sequencing studies in lung cancer have shown a significant number of activating mutations within the NRF2 signaling pathway. Mutations in components of the SWI/SNF chromatin-remodeling complex, a general regulator of transcription using either BRG1 or BRM as the catalytic subunit, also frequently occur in lung cancers. Importantly, low BRG1 expression levels in primary human NSCLC correlated with increased NRF2-target gene expression. Here, we show that loss of SWI/SNF complex function activated a subset of NRF2-mediated transcriptional targets. Using a series of isogenic NSCLC lines with reduced or depleted BRG1 and/or BRM expression, we observed significantly increased expression of the NRF2-target genes HMOX1 and GSTM4. In contrast, expression of the NRF2 target genes NQO1 and GCLM modestly increased following BRM reduction. Chromatin immunoprecipitation showed that BRG1 knockdown led to increased NRF2 binding at its respective ARE sites in the HMOX1 promoter but not in NQO1 and GCLM. Our data demonstrate that loss of BRG1 or BRM in lung cancer results in activation of the NRF2/KEAP1 pathway and HMOX1 expression. Therefore, we provide an additional molecular explanation for why patients harboring BRG1 or BRM mutations show poor prognoses. A better understanding of this mechanism may yield novel insights into the design of targeted treatment modalities. Implications: Our study identifies a novel mechanism for how mutations in the SMARCA4 gene may drive progression of human lung adenocarcinomas.

Background: Carcinoma ex pleomorphic adenoma (CXPA), a very rare malignancy found mostly in the major salivary glands, has no established standardized treatment. Case presentation: This report describes a 67-year-old male with advanced CXPA who was effectively treated by anlotinib. Pleomorphic adenoma of the submandibular gland was first diagnosed in 1976 after a surgical resection of a mass underneath the jaw. The patient underwent re-excision 3 years later due to a recurrent pleomorphic adenoma. CXPA was first diagnosed in 2016 after a surgical removal of the left submandibular mass. A lung nodule was found on a chest CT scan in January 2018. Following a CT-guided lung biopsy that demonstrated findings consistent with pulmonary metastasis, the patient underwent local therapy (microwave ablation and radioactive seed implantation) but suffered a recurrence of disease approximately 6 months later. Anlotinib was administered orally at a dose of 12 mg daily on a 2 weeks on/1 week off schedule. A partial response was observed after two cycles of treatment. The disease remains in continued partial response after completion of his sixth cycle. Conclusion: This is the first report for anlotinib in treating CXPA. Further pre-clinical and clinical studies are needed to validate the efficacy and safety of anlotinib in the treatment of CXPA.

Math anxiety is a common correlate of math performance for adults. Research on young children’s emotional reactions to math is limited, but critical for determining how math anxiety develops. Students (N = 244) completed math measures (i.e., number comparison, arithmetic fluency, and math problem solving) and math anxiety assessments twice, in grade 2 (Mage = 7.10) and a year later in grade 3. Math anxiety was significantly related to arithmetic fluency, but not to others. Longitudinally, arithmetic fluency in grade 2 predicted the change in math anxiety from grades 2 to 3, but not vice versa. The growth in math anxiety was related to arithmetic fluency for students with higher working memory scores, but this moderation effect of working memory was not significant after a multiple-comparisons correction. In sum, these findings are consistent with the view that math anxiety develops in some children in response to their experiences with mathematics.

Segmentation of blood vessels becomes an essential step in computer aided diagnosis system for the diseases in several departments of ophthalmology, neurosurgery, oncology, cardiology, and laryngology. Aiming at the problem of insufficient segmentation of small blood vessels by existing methods, a novel method based on multi-module fusion residual neural network model (MF2ResU-Net) was proposed. In the proposed networks, to obtain refined features of vessels, three cascade connected U-Net networks were employed as main networks. To deal with the problem of over-fitting, residual paths were used in main networks. In the blocks of U-Net in MF2ResU-Net, in order to remove the semantic difference in low-level and high-level, shortcut connections were used to combine the encoder layers and decoder layers in the blocks. Furthermore, atrous spatial pyramid pooling was embedded between the encoder and decoder to achieve multi-scale feature of blood vessels. During the training of the networks, to deal with the imbalance between background and foreground, a novel joint loss function was proposed based on the dice and cost- sensitive, which could greatly reduce the impact of unbalance in classes of samples. In experiment section, two retinal datasets, DRIVE and CHASE DB1, were used to test our method, and experiments showed that MF2ResU-Net was superior to existing methods on the criteria of sensitivity (Sen), specificity (Spe), accuracy (Acc), and area under curve (AUC), the values of which are 0.8013 and 0.8102, 0.9842 and 0.9809, 0.9700 and 0.9776, and 0.9797 and 0.9837 respectively for DRIVE and CHASE DB1. The results of experiments demonstrated the effectiveness and robustness of the model in the segmentation of complex curvature and small blood vessels.

Thyroid cancer is the most common endocrine malignancy, and its incidence continues to rise. For clinicians with cancer patients, choosing and interpreting diagnostic laboratory studies has become increasingly important. Previously, changes in plasma free mitochondrial DNA levels have been found in colorectal, breast, lung, and urinary cancers, and have demonstrated diagnostic value. In this study, we investigated whether the occurrence and development of thyroid cancer might be predicted using mtDNA copy number (ND1), mtDNA integrity (ND4/ND1) and levels of cell-free nDNA (GAPDH). We analyzed ND1, ND4, and GAPDH levels in plasma and blood cells from 75 patients with thyroid cancer, 40 patients with nodular goiter, and 107 normal controls using real-time PCR. Although both the thyroid nodule and thyroid cancer patients had significantly increased ND1 levels, the ND4/ND1 ratio in the thyroid cancer group was higher than the thyroid nodule group (P < 0.05), and significantly higher than the normal control group (P < 0.01). Plasma levels of nuclear DNA (GAPDH) in the thyroid cancer group were also higher compared to normal (P < 0.05). These results indicate that increased intactness of plasma free mtDNA is associated with increased levels of plasma cell-free nDNA, and that the ND4/ ND1 ratio has the potential to be a new detection indicator in thyroid cancer. Furthermore, we classified thyroid cancer patients according to clinical data including age, tumor size, and metastasis. We found significantly higher levels of GAPDH in malignant tissues. Because ND4/ND1 correlated with plasma GAPDH in the plasma studies, this also suggests a potential relationship between ND4 intactness and thyroid tumor tissue size. Taken together, our findings suggest a tumor-specific process involving increased release of intact mtDNA, detectable in the plasma, which differentiates normal patients from patients with thyroid cancer.

Gastritis cystica profunda (GCP) is a rare lesion characterized by hyperplasia and cystic dilatation of the gastric glands in the submucosal layer. Here we report seven cases of GCP. The patients are 5 women and 2 men with a mean age of 62 (range, 42-82) years at the time of diagnosis. The patients presented with abdominal distension, sour regurgitation, and heartburn. One case had the previous gastric surgery and the other six cases had no special history. The lesions were located in the fundus (4/7), corpus (1/7), cardia (1/7), and antrum (1/7). Endoscopic analysis revealed pedunculated polyps, or a dome-shaped polyp. Histologically, all cases showed dilated tubular glands, mainly located in the submucosa, among the muscularis mucosa, and occasionally in the lamina propria. The glands were lined by bland single columnar epithelium with infolding features in some areas. Mitotic activity and marked cellular atypia were not present. The stroma in some cases was mildly edematous with infiltrated lymphocytes and plasma cells. There was no epithelial dysplasia in the overlying mucosa. Immunohistochemically, the Ki-67 index was < 1%. P53 immunostaining was generally characterized as wild type in all cases. Based on the morphology of the glands and the cells and the possible mechanism of hyperplasia and cystic dilatation of the gastric glands, it is easy to differentiate GCP from a well-differentiated adenocarcinoma.