Design and Experimentation of a Machine Vision-Based Cucumber Quality Grader.

The North China type cucumber, characterized by its dense spines and top flowers, is susceptible to damage during the grading process, affecting its market value. Moreover, traditional manual grading methods are time-consuming and labor-intensive. To address these issues, this paper proposes a cucumber quality grader based on machine vision and deep learning. In the electromechanical aspect, a novel fixed tray type grading mechanism is designed to prevent damage to the vulnerable North China type cucumbers during the grading process. In the vision grading algorithm, a new convolutional neural network is introduced named MassNet, capable of predicting cucumber mass using only a top-view image. After obtaining the cucumber mass prediction, mass grading is achieved. Experimental validation includes assessing the electromechanical performance of the grader, comparing MassNet with different models in predicting cucumber mass, and evaluating the online grading performance of the integrated algorithm. Experimental results indicate that the designed cucumber quality grader achieves a maximum capacity of 2.3 t/hr. In comparison with AlexNet, MobileNet, and ResNet, MassNet demonstrates superior cucumber mass prediction, with a MAPE of 3.9% and RMSE of 6.7 g. In online mass grading experiments, the grading efficiency of the cucumber quality grader reaches 93%.

Inhibition of Japanese encephalitis virus proliferation by long non-coding RNA SUSAJ1 in PK-15 cells.

BACKGROUND: Japanese encephalitis virus is a mosquito-borne neurotropic flavivirus that causes acute viral encephalitis in humans. Pigs are crucial amplifier host of JEV. Recently, increasing evidence has shown that long non-coding RNAs (lncRNAs) play important roles in virus infection. METHODS: JEV proliferation was evaluated after overexpression or knockdown of lncRNA-SUSAJ1 using western blotting and reverse-transcription polymerase chain reaction (RT-PCR). C-C chemokine receptor type 1 (CCR1) was found to regulate the expression of lncRNA-SUSAJ1 by inhibitors screen. The expression of lncRNA-SUSAJ1 was detected using RT-PCR after overexpression or knockdown of transcription factor SP1. In addition, the enrichments of transcription factor SP1 on the promoter of lncRNA-SUSAJ1 were analyzed by chromatin immunoprecipitation. RESULTS: In this study, we demonstrated that swine lncRNA-SUSAJ1 could suppress JEV proliferation in PK-15 cells. We also found that CCR1 inhibited the expression of lncRNA-SUSAJ1 via the transcription factor SP1. In addition, knockdown of CCR1 could upregulated the expression of SP1 and lncRNA-SUSAJ1, resulting in resistance to JEV proliferation. CONCLUSIONS: These findings illustrate the importance of lncRNAs in virus proliferation, and reveal how this virus regulates lncRNAs in host cells to promote its proliferation.

OGG1 regulates the level of symmetric dimethylation of histone H4 arginine-3 by interacting with PRMT5.

OGG1 is the first enzyme in the base excision repair pathway (BER) responsible for repairing 8-oxoguanine DNA lesions. Recent studies found that OGG1 may also be involved in epigenetic regulation. In this study, we focused on the roles of OGG1 in histone modification. First, to study the effects of OGG1 on histone modification, the protein levels of symmetric dimethylation of histone H4 arginine-3 (H4R3me2s) were determined by western blot analysis following the knockdown or overexpression of OGG1. Second, the molecular mechanisms by which OGG1 regulates H4R3me2s were assessed by co-immunoprecipitation (CO-IP) assays in mouse embryonic fibroblast (MEF) wild-type (WT) and Ogg-/- cells. Finally, to verify the regulation of H4R3me2s by OGG1 on specific genes, chromatin immunoprecipitation (CHIP) was performed on MEF WT and Ogg-/- cells. We found that OGG1 affects PRMT5 binding on histone H4 and the formation of H4R3me2s via PRMT5. The methylation level of H4R3me2s was dramatically decreased in MEF Ogg-/- cells compared to WT cells. Knockdown of OGG1 by siRNA led to a decrease in H4R3me2s, while overexpression of OGG1 increased the level of H4R3me2s. OGG1 also interacted with PRMT5 and histone H4, and the interaction between PRMT5 and histone H4 was reduced in MEF Ogg-/- cells. Our data not only illustrate the important roles of OGG1 in histone modification, but also reveal the mechanism by which OGG1 affects PRMT5 binding on H4R3 resulting in the symmetrical dimethylation of histone H4 arginine-3.