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Microblogs are currently one of the most well-liked social platforms in China, and sentiment analysis of microblog texts can help further analyze the realization of their media value; however, the current task of sentiment analysis based on microblog information suffers from low accuracy due to the large size and high redundancy of microblog data, a microblog sentiment analysis method using Bidirectional Encoder Representation from Transformers (BERT)–Text Convolutional Neural Network (TextCNN)–Bidirectional Gate Recurrent Unit (BiGRU)–Multihead-Attention model in Spark big data environment is proposed. First, the Chinese pre-trained language model BERT is used to convert the input data into dynamic character-level word vectors; then, TextCNN is used to effectively obtain local features such as keywords and pool the filtered features; then, BiGRU is introduced to quickly capture more comprehensive semantic information; finally, a multi-headed attention mechanism is implemented to emphasize the most significant features in order to accomplish the sentiment classification of microblog information task precisely. By comparing the existing advanced models, the proposed model demonstrates an improvement of at least 4.99% and 0.05 in accuracy and F1-score evaluation indexes, respectively. This enhancement significantly enhances the accuracy of microblog sentiment analysis tasks and aids pertinent authorities in comprehending the inclination of individual’s attitude toward hot topics. Furthermore, it facilitates a prompt prediction of topic trends, enabling them to guide public opinion accordingly.

Enterovirus A71 (EV‐A71) is a highly contagious virus that poses a major threat to global health, representing the primary etiological agent for hand–foot and mouth disease (HFMD) and neurological complications. It has been established that interferon signaling is critical to establishing a robust antiviral state in host cells, mainly mediated through the antiviral effects of numerous interferon‐stimulated genes (ISGs). The host restriction factor SHFL is a novel ISG with broad antiviral activity against various viruses through diverse underlying molecular mechanisms. Although SHFL is widely acknowledged for its broad‐spectrum antiviral activity, it remains elusive whether SHFL inhibits EV‐A71. In this work, we validated that EV‐A71 triggers the upregulation of SHFL both in cell lines and in a mouse model. Knockdown and overexpression of SHFL in EVA71‐infected cells suggested that this factor could markedly suppress EV‐A71 replication. Our findings further revealed an intriguing mechanism of SHFL that it could interact with the nonstructural proteins 3Dpol of EV‐A71 and promoted the degradation of 3Dpol through the ubiquitin–proteasome pathway. Furthermore, the zinc‐finger domain and the 36 amino acids (164–199) of SHFL were crucial to the interaction between SHFL and EV‐A71 3Dpol. Overall, these findings broadened our understanding of the pivotal roles of SHFL in the interaction between the host and EV‐A71. [ABSTRACT FROM AUTHOR]

Generally, most miRNAs that were up-regulated during differentiation promoted adipogenesis, but our research indicated that up-regulation of miR-145 in porcine preadipocytes did not promote but inhibit adipogenesis. In this study, miR-145 was significantly up-regulated during porcine dedifferentiated fat (DFAT) cells differentiation. In miR-145 overexpressed DFAT cells, adipogenesis was inhibited and triglycerides accumulation was decreased after hormone stimulation (PCCAAT/enhancer-binding protein α (C/EBPα), and peroxisome proliferator-activated receptor γ2 (PPARγ2). These effects caused by miR-145 overexpression were mediated by Insulin receptor substrate 1 (IRS1) as a mechanism. These data suggested that induced miR-145 expression during differentiation could inhibit adipogenesis by targeting IRS1, and miR-145 may be novel agent for adipose tissue engineering.

The tumour suppressor ARF is specifically required for p53 activation under oncogenic stress (1-6). Recent studies showed that p53 activation mediated by ARF, but not that induced by DNA damage, acts as a major protection against tumorigenesis in vivo under certain biological settings (7,8), suggesting that the ARF-p53 axis has more fundamental functions in tumour suppression than originally thought. Because ARF is a very stable protein in most human cell lines, it has been widely assumed that ARF induction is mediated mainly at the transcriptional level and that activation of the ARF-p53 pathway by oncogenes is a much slower and largely irreversible process by comparison with p53 activation after DNA damage. Here we report that ARF is very unstable in normal human cells but that its degradation is inhibited in cancerous cells. Through biochemical purification, we identified a specific ubiquitin ligase for ARF and named it ULF. ULF interacts with ARF both in vitro and in vivo and promotes the lysine-independent ubiquitylation and degradation of ARF. ULF knockdown stabilizes ARF in normal human cells, triggering ARF-dependent, p53-mediated growth arrest. Moreover, nucleophosmin (NPM) and c-Myc, both of which are commonly overexpressed in cancer cells, are capable of abrogating ULF-mediated ARF ubiquitylation through distinct mechanisms, and thereby promote ARF stabilization in cancer cells. These findings reveal the dynamic feature of the ARF-p53 pathway and suggest that transcription-independent mechanisms are critically involved in ARF regulation during responses to oncogenic stress., Although recent studies have demonstrated that ARF turnover can occur through ubiquitylation and proteasomal degradation, the identity of the E3 ligase responsible for ARF degradation and its biological significance are [...]

In order to make cotton spunlaced nonwoven keeping well air permeability and a certain waterrepellent effect at the same, atmospheric pressure plasma technology was adopted. Hexamethyldisiloxane was used as monomer for the study of cotton spunlaced nonwoven single water-repellent modification experiment. After modification, hydrophobic surface layer was formed on the surface of nonwoven sample. water-repellent theory of modified nonwoven surface was analyzed combining with lotus effect. Infrared spectroscopy test results showed that hydrophobic groups like Si--CH3, Si--C and so on were generated on the modified surface. Water contact angle of the modified nonwoven was tested and it could be reached 157° on the treated surface in maximum. The surface without treatment were infiltrated and showed excellent single water-repellent effect. When modified nonwoven sample was treated by friction and placed for different time, the water contact angle was not changed too much. The water-repellent property of modified nonwoven was stable. It is considered that cotton spunlaced nonwoven after modified by atmospheric pressure plasma technology with hexamethyldisiloxane as monomer has excellent single water-repellent property. [ABSTRACT FROM AUTHOR]

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.cell.2005.03.037 Byline: Delin Chen (1), Ning Kon (1), Muyang Li (1), Wenzhu Zhang (1), Jun Qin (2), Wei Gu Abstract: Although the importance of the ARF tumor suppressor in p53 regulation is well established, numerous studies indicate that ARF also suppresses cell growth in a p53/Mdm2-independent manner. To understand the mechanism of ARF-mediated tumor suppression, we identified a ubiquitin ligase, ARF-BP1, as a key factor associated with ARF in vivo. ARF-BP1 harbors a signature HECT motif, and its ubiquitin ligase activity is inhibited by ARF. Notably, inactivation of ARF-BP1, but not Mdm2, suppresses the growth of p53 null cells in a manner reminiscent of ARF induction. Surprisingly, in p53 wild-type cells, ARF-BP1 directly binds and ubiquitinates p53, and inactivation of endogenous ARF-BP1 is crucial for ARF-mediated p53 stabilization. Thus, our study modifies the current view of ARF-mediated p53 activation and reveals that ARF-BP1 is a critical mediator of both the p53-independent and p53-dependent tumor suppressor functions of ARF. As such, ARF-BP1 may serve as a potential target for therapeutic intervention in tumors regardless of p53 status. Author Affiliation: (1) Institute for Cancer Genetics, Department of Pathology, College of Physicians and Surgeons, Columbia University, 1150 St. Nicholas Avenue, New York, New York 10032 (2) Departments of Biochemistry and Cell Biology, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030 Article History: Received 13 September 2004; Revised 24 February 2005; Accepted 30 March 2005 Article Note: (miscellaneous) Published: June 30, 2005

Results demonstrate that mammalian Sir2alpha interacts with p53 inhibiting deacetylation of p53 as well as enhancing acetylation of p53 in vivo. Data also suggest that Sir2alpha represses p53-dependent apoptosis during DNA damage and oxidative stress.