Exploring Embeddings for Measuring Text Relatedness: Unveiling Sentiments and Relationships in Online Comments

After the COVID-19 pandemic caused internet usage to grow by 70%, there has been an increased number of people all across the world using social media. Applications like Twitter, Meta Threads, YouTube, and Reddit have become increasingly pervasive, leaving almost no digital space where public opinion is not expressed. This paper investigates sentiment and semantic relationships among comments across various social media platforms, as well as discusses the importance of shared opinions across these different media platforms, using word embeddings to analyze components in sentences and documents. It allows researchers, politicians, and business representatives to trace a path of shared sentiment among users across the world. This research paper presents multiple approaches that measure the relatedness of text extracted from user comments on these popular online platforms. By leveraging embeddings, which capture semantic relationships between words and help analyze sentiments across the web, we can uncover connections regarding public opinion as a whole. The study utilizes pre-existing datasets from YouTube, Reddit, Twitter, and more. We made use of popular natural language processing models like Bidirectional Encoder Representations from Transformers (BERT) to analyze sentiments and explore relationships between comment embeddings. Additionally, we aim to utilize clustering and Kl-divergence to find semantic relationships within these comment embeddings across various social media platforms. Our analysis will enable a deeper understanding of the interconnectedness of online comments and will investigate the notion of the internet functioning as a large interconnected brain.Comment: 6 pages, 5 figures, 3 tables, accepted to the Second International Conference on Informatics (ICI-2023

Data on the association of CMPK1 with clinicopathological features and biological effect in human epithelial ovarian cancer

Human epithelial ovarian cancer (EOC) is the most lethal gynecological disease. However, the molecular mechanisms by which transforming growth factor-β (TGF-β) regulates ovarian tumor progression markers remain unclear. The present data show cytidine monophosphate kinase (CMPK) as an EOC biomarker and are related to the article entitled “Cytidine monophosphate kinase is inhibited by the TGF-β signalling pathway through the upregulation of miR-130b-3p in human epithelial ovarian cancer” [1]. CMPK, as well as cystatin B [2] and β-2-microglobulin [3], is overexpressed in human epithelial-type ovarian tumors. CMPK is an enzyme required for nucleic acid biosynthesis [4] and is regulated by the TGF-β signaling pathway in EOC cells [1]. Furthermore, the data show the effect of CMPK-shRNA on EOC cell apoptosis and TGF-β-induced Smad2 phosphorylation. CMPK expression in two EOC cell lines OVCAR-3 and SK-OV-3 is regulated by multiple miRNAs and some of these miRNAs may affect EOC chemoresistance [5]. Keywords: TGF-β signaling, UMP/CMP kinase, Tissue microarray, Tumorigenesis, miRNA, Therapeutic targe

Crystal Plasticity Finite Element Method for Slip Systems Evolution Analysis of α/β Duplex Titanium Alloys during Quasi-Static Tensile Testing

The crystal plasticity finite element method, modeled on a realistic microstructure image, was developed to investigate the evolution of slip systems in grains of α/β titanium alloys during quasi-static tensile testing. By analyzing the data of slip evolution of simulation during the overall plastic deformation process, it was found that the prismatic slip systems in the α phase and the {112} <111> slip systems in the β phase played a leading role. By calculating the Schmid factors, it was found that the values calculated from the local stress, which was represented by major principal stress, were larger than the values calculated from the primary uniaxial tensile direction, which was due to the deviation of the local stress direction from the primary uniaxial tensile direction. Furthermore, the deviation of local stress of α phase was different from that of β phase, which was related to the deformation mechanism. During the deformation, the stress and strain were concentrated in the grains of the α phase, producing a driving effect on the neighboring grains of the β phase. Subsequently, the incompatible deformation produced the concentration of strain at the grain/interphase boundary, thus strengthening the grain interactions and leading to the deviation

Ballistic impact response of a heat-treated dual-phase Ti–5.2Mo–4.8Al–2.5Zr–1.7Cr alloy with hierarchical microstructure

In the present study, a dual-phase Ti-5.2Mo-4.8Al-2.5Zr-1.7Cr alloy was hot-rolled at 980 °C with a thickness reduction of 65% and then heat-treated with the strategy of 920 °C/1 h/water quenching +550 °C/6 h/air cooling, and a hierarchical microstructure was prepared, which contained micro-scale equiaxed primary α phase (αp), sub-micro scale rod-like α phase (αr), nano-scale acicular secondary α phase (αs) and β matrix segmented by αs and αr. In addition, the dislocation densities of α phase and β phase were determined as 0.3652 × 1015/m2 and 2.2502 × 1015/m2, respectively. Contributing to αr and αs, the hierarchical microstructure exhibited higher strength (yield strength: 1228 MPa, ultimate tensile strength: 1389 MPa, dynamic compressive strength: 1661 ± 27 MPa). Simultaneously, αp and αr were helpful to the strain transfer, and thus the plasticity was maintained at a considerable level (elongation: 13.4 ± 0.2%, critical fracture strain: 18.9 ± 0.2%). Such hierarchical microstructure overcame the limitation of the strength-ductility trade-off to a certain extent and exhibited a superior combination of strength and ductility. The ballistic impact behavior of the titanium alloy plates with the thickness of 20.3 mm (1#), 19.3 mm (2#) and 18.4 mm (3#) against 7.62 mm armour piercing projectiles illustrated that as the titanium alloy thicknesses decreased from 20.3 mm to 18.4 mm, more ASB-induced cracks were formed near the rear face and connected to form catastrophic cracks in the 2# and the 3# titanium alloy plates, even resulting in the failure for the 3# titanium alloy plate. Ultimately, the 1# and 2# titanium alloy plates exhibited preferable ballistic impact properties

Dual Effects of N,N-dimethylformamide on Cell Proliferation and Apoptosis in Breast Cancer

N,N-dimethylformamide (DMF) has been widely used as an organic solvent in industries. DMF is a potential medication. However, the antitumorigenic role of DMF in breast cancer remains unclear. Here, we examined dose-dependent effects of DMF on proliferation and apoptosis in breast cancer MCF-7 and nontumorous MCF-12A cells. We found that DMF had a growth inhibitory effect in MCF-12A cells in a dose-dependent manner. By contrast, however, DMF had dual effects on cell proliferation and apoptosis in MCF-7 cells. DMF at a high dose (100 mM) significantly inhibited MCF-7 cell growth while at a low dose (1 mM) significantly stimulated MCF-7 cell growth (both P < .05). The inhibitory effect of DMF on cell proliferation was accompanied by the decrease of cyclin D1 and cyclin E1 protein expression, leading to the cell cycle arrest at the G0/G1 phase. Furthermore, a high-dose DMF significantly increased the number of early apoptotic cells by increasing cleaved caspase-9 and proapoptotic protein Bax expression and decreased the ratio of Bcl-xL/Bax ( P < .01). Thus, our data demonstrated for the first time that DMF has dual effects on breast cancer cell behaviors depending upon its dose. Caution must be warranted in determining its effective dose for targeting breast cancer

Physical interaction of STAT1 isoforms with TGF-β receptors leads to functional crosstalk between two signaling pathways in epithelial ovarian cancer

Abstract Background The signal transducer and activator of transcription (STAT) and transforming growth factor-β (TGF-β) signaling pathways play important roles in epithelial ovarian cancer (EOC). However, the mechanism of crosstalk between two pathways is not completely understood. Methods The expression of STAT1 protein was detected by tissue microarray and immunoblotting (IB). The interaction of STAT1 isoforms with TGF-β receptors was confirmed by immunoprecipitation and IB. The effect of TGF-β signaling on STAT1 activation was examined in EOC and non-tumorous HOSEpiC cells treated with TGF-β1 in the presence or absence of the inhibitor of TGF-β type I receptor. The gain-of-function and loss-of-function approaches were applied for detecting the role of STAT1 on EOC cell behaviours. Results The high level of STAT1 was observed in patients with high-grade serous EOC. STAT1 expression was higher in ovarian cancer cells than noncancerous cells. TGF-β1 activated the STAT1 pathway by inducing the phosphorylation of STAT1α on S727 residue. The full-length STAT1α and the truncated STAT1β directly interacted with TGF-β receptors (ALK1/ALK5 and TβRII), which was mediated by TGF-β1. STAT1α and STAT1β blocked the activation of the TGF-β1 signaling pathway in EOC cells by reducing Smad2 phosphorylation. STAT1 overexpression induced EOC cell proliferation, migration, and invasion; whereas its inhibition enhanced TGF-β1-induced phospho-Smad2 and suppressed EOC cell proliferation, migration, and invasion. Conclusions Our data unveil a novel insight into the molecular mechanism of crosstalk between the STAT1 and TGF-β signaling pathways, which affected the cancer cell behavior. Suppression of STAT1 may be a potential therapeutic strategy for targeting ovarian cancer

Design and Detection of Cyanide Raman Tag pH-Responsive SERS Probes

As one of the most important parameters of biochemical analysis and detection, the pH value plays a very important role in cell function, food preservation and production, soil and water sources, and other applications. This makes it increasingly important to explore pH detection methods in depth. In this paper, a pH-responsive SERS probe based on the cyano Raman Tag was designed to realize pH sensing detection through the influence of the pH value of analytes on the displacement of the cyano Raman peak in the SERS probe. This cyano Raman tag exhibited not only excellent sensitivity in the liner range of pH 3.0–9.0 with a limit of detection (LOD) of pH 0.33, but also the anti-interference performance and stability (the relative standard deviation (RSD) was calculated to be 6.68%, n = 5). These results indicated that this pH SERS probe with the Raman cyano tag can provide new research ideas for future biological detection, bioimaging, and environmental detection

Additional file 2: of Physical interaction of STAT1 isoforms with TGF-β receptors leads to functional crosstalk between two signaling pathways in epithelial ovarian cancer

Figure S1. STAT1 expression in human epithelial-type ovarian tumors. Tissue microarray shows the immunohistochemical (IHC) staining of pSTAT1-Y701, pSTAT1-S727, and total STAT1 in serous, mucinous, endometrioid, transitional cell, and metastatic tumors. Figure S2. STAT1 expression in ovarian surface epithelial cells. a STAT1 mRNA expression detected by quantitative RT-PCR. b STAT1 protein expression detected by immunoblotting. c Densitometric analysis of the gels. Figure S3. Effect of TGF-β1 on the phosphorylation of STAT1. (DOCX 1304 kb

Pyridoxine 5′-phosphate oxidase is a novel therapeutic target and regulated by the TGF-β signalling pathway in epithelial ovarian cancer

Abstract Pyridoxine 5′-phosphate oxidase (PNPO) is an enzyme that converts pyridoxine 5′-phosphate into pyridoxal 5′-phosphate (PLP), an active form of vitamin B6 implicated in several types of cancer. However, the role of PNPO and its regulatory mechanism in epithelial ovarian cancer (EOC) are unknown. In the present study, PNPO expression in human ovarian tumour tissue and its association with the clinicopathological features of patients with EOC were examined. Further, the biological function of PNPO in EOC cells and in xenograft was evaluated. We demonstrated for the first time that PNPO was overexpressed in human EOC. Knockdown of PNPO induced EOC cell apoptosis, arrested cell cycle at G2/M phase, decreased cell proliferation, migration and invasion. Xenografts of PNPO-shRNA-expressing cells into the nude mouse attenuated tumour growth. PNPO at mRNA and protein levels in EOC cells was decreased after transforming growth factor-β1 (TGF-β1) treatment. The inhibitory effect of TGF-β1 on PNPO expression was abolished in the presence of SB-431542, a TGF-β type I receptor kinase inhibitor. Moreover, we found that TGF-β1-mediated PNPO expression was at least in part through the upregulation of miR-143-3p. These data indicate a mechanism underlying PNPO regulation by the TGF-β signalling pathway. Furthermore, PLP administration reduced PNPO expression and decreased EOC cell proliferation, suggesting a feedback loop between PLP and PNPO. Thus, our findings reveal that PNPO can serve as a novel tissue biomarker of EOC and may be a potential target for therapeutic intervention

Additional file 1: of Physical interaction of STAT1 isoforms with TGF-β receptors leads to functional crosstalk between two signaling pathways in epithelial ovarian cancer

Table S1. PCR primer and siRNA sequence used in experiments. Table S2. Comparison of pSTAT1-Y701, pSTAT1-S727, and STAT1 immunostaining in the ovarian tissues. Table S3. The expression of pSTAT1-Y701, pSTAT1-S727, and STAT1 in human ovarian tissues. (DOCX 50 kb