The Effect of Co-Culture with Different Pichia kluyveri and Saccharomyces cerevisiae on Volatile Compound and Characteristic Fingerprints of Mulberry Wine.

In this study, changes in volatile compounds co-fermented by different Pichia kluyveri with Saccharomyces cerevisiae were analyzed using GC-IMS and compared with S. cerevisiae fermentation, to investigate the production of aroma in mulberry wine during the fermentation process. A total of 61 compounds were accurately identified, including 21 esters, 10 alcohols, 8 aldehydes, 6 ketones, and 19 other volatiles. Compared with the single strain fermentation (S. cerevisiae), the content of 2-methylpropyl acetate, allyl Isothiocyanate, ethyl crotonate, isobutyl propanoate, and butyl 2-methylbutanoate, co-fermentation groups (S. cerevisiae with different P. kluyveri) showed a significant decrease. Alcohols, aldehydes, ketones, and organic acid were lower in both the F(S-P1) and F(S-P2) groups than in the F(S) group throughout fermentation. The 2-methylpentanoic acid only was contained in the F(S) group. The co-fermentation with different P. kluyveri could also be well distinguished. The content of Benzaldehyde and 4-methylphenol in the F(S-P1) group was significantly lower than that in the F(S-P2) group. The PCA results revealed effective differentiation of mulberry wine fermented by different fermentation strains from GC-IMS. The result showed that P. kluyveri could establish a new flavor system for mulberry wine, which plays a crucial role in enhancing the flavor of fruit wine.

Denoising of three-dimensional fast spin echo magnetic resonance images of knee joints using spatial-variant noise-relevant residual learning of convolution neural network.

PURPOSE: Two-dimensional (2D) fast spin echo (FSE) techniques play a central role in the clinical magnetic resonance imaging (MRI) of knee joints. Moreover, three-dimensional (3D) FSE provides high-isotropic-resolution magnetic resonance (MR) images of knee joints, but it has a reduced signal-to-noise ratio compared to 2D FSE. Deep-learning denoising methods are a promising approach for denoising MR images, but they are often trained using synthetic noise due to challenges in obtaining true noise distributions for MR images. In this study, inherent true noise information from two number of excitations (2-NEX) acquisition was used to develop a deep-learning model based on residual learning of convolutional neural network (CNN), and this model was used to suppress the noise in 3D FSE MR images of knee joints. METHODS: A deep learning-based denoising method was developed. The proposed CNN used two-step residual learning over parallel transporting and residual blocks and was designed to comprehensively learn real noise features from 2-NEX training data. RESULTS: The results of an ablation study validated the network design. The new method achieved improved denoising performance of 3D FSE knee MR images compared with current state-of-the-art methods, based on the peak signal-to-noise ratio and structural similarity index measure. The improved image quality after denoising using the new method was verified by radiological evaluation. CONCLUSION: A deep CNN using the inherent spatial-varying noise information in 2-NEX acquisitions was developed. This method showed promise for clinical MRI assessments of the knee, and has potential applications for the assessment of other anatomical structures.

Long non­coding RNA PLK1S1 was associated with renal cell carcinoma progression by interacting with microRNA­653 and altering C­X­C chemokine receptor 5 expression.

Renal cell carcinoma (RCC) is the most common type of renal cancer. Long non­coding RNA (lncRNA) has been reported to play a vital role in the development and progression of various types of cancer type. However, the underlying molecular mechanisms of PLK1S1 in regulating RCC progression remain unclear. In the present study, PLK1S1 was upregulated in RCC tissues and cells, and PLK1S1 expression was also significantly elevated in stage IV RCC tissues. Kaplan­Meier analysis showed that patients with high PLK1S1 expression had a shorter overall survival time compared with those with low PLK1S1 expression. Moreover, bioinformatics analysis and luciferase reporter assay demonstrated that PLK1S1 inhibited microRNA (miR)­653 expression by direct interaction. Functional analyses demonstrated that a miR­653 inhibitor promoted short hairpin PLK1S1­attenuated cell proliferation, invasion and sorafenib resistance of RCC cells. In addition, C­X­C motif chemokine receptors 5 (CXCR5) was identified as an effector of PLK1S1/miR­653­mediated tumorigenesis and drug resistance in RCC cells. Lastly, xenograft experiments demonstrated that PLK1S1 knockdown inhibited tumor growth in vivo. Reverse transcription­quantitative PCR and western blot analysis revealed that PLK1S1 knockdown upregulated the expression level of miR­653, whilst downregulating the expression level of CXCR5. In conclusion, the present study revealed that PLK1S1 promoted tumor progression and sorafenib resistance in RCC through regulation of the miR­653/CXCR5 axis, which may offer a novel treatment strategy for patients with RCC.

Silencing circular RNA VANGL1 inhibits progression of bladder cancer by regulating miR-1184/IGFBP2 axis.

Circular RNA VANGL1 (circVANGL1) is generated from two exons of the Van Gogh-like 1 (VANGL1) gene and serves as a tumor promoter by sponging certain microRNAs (miRNAs). However, the role of circVANGL1 in bladder cancer (BC) is still unclear. So, in order to investigate the role of circVANGL1 in BC, quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was employed to evaluate the circVANGL1 expression in tumor tissues from BC patients and in BC cell lines. Small interfering RNA against circVANGL1 was constructed and stably transfected into human bladder epithelium immortalized cells (SV-HUC). Cell invasion and migration were detected in Transwell chambers, cell proliferation was determined by CCK8 assays, and tumorigenesis in nude mice was examined to assess the effect of circVANGL1 in BC. Subcellular localization of circVANGL1 was confirmed by fluorescence in situ hybridization. The interactive relationships among circVANGL1, miRNA, and relative proteins were confirmed by luciferase reporter assays. The results showed that circVANGL1 was upregulated in both BC tissues and cell lines. Silencing the expression of circVANGL1 suppressed cell invasion, migration, and proliferation during in vitro experiments. Mechanistically, we demonstrated that circVANGL1 upregulated the expression of miR-1184 target gene insulin-like growth factor-binding protein 2 (IGFBP2) by sponging miR-1184, which promoted the aggressive biological behaviors of BC. Taken together, our results indicate that circVANGL1 acts as a tumor promoter through the novel circVANGL1/miR-1184/IGFBP2 axis. Hopefully, our study will provide new ideas for the clinical treatment of BC.