E-MFNN: an emotion-multimodal fusion neural network framework for emotion recognition.

Emotional recognition is a pivotal research domain in computer and cognitive science. Recent advancements have led to various emotion recognition methods, leveraging data from diverse sources like speech, facial expressions, electroencephalogram (EEG), electrocardiogram, and eye tracking (ET). This article introduces a novel emotion recognition framework, primarily targeting the analysis of users' psychological reactions and stimuli. It is important to note that the stimuli eliciting emotional responses are as critical as the responses themselves. Hence, our approach synergizes stimulus data with physical and physiological signals, pioneering a multimodal method for emotional cognition. Our proposed framework unites stimulus source data with physiological signals, aiming to enhance the accuracy and robustness of emotion recognition through data integration. We initiated an emotional cognition experiment to gather EEG and ET data alongside recording emotional responses. Building on this, we developed the Emotion-Multimodal Fusion Neural Network (E-MFNN), optimized for multimodal data fusion to process both stimulus and physiological data. We conducted extensive comparisons between our framework's outcomes and those from existing models, also assessing various algorithmic approaches within our framework. This comparison underscores our framework's efficacy in multimodal emotion recognition. The source code is publicly available at https://figshare.com/s/8833d837871c78542b29.

Exosomal miR-485-3p derived from pancreatic ductal epithelial cells inhibits pancreatic cancer metastasis through targeting PAK1.

BACKGROUND: Cell competition is an important feature in pancreatic cancer (PC) progression, but the underlying mechanism remains elusive. This study aims to explore the role of exosomes derived from normal pancreatic ductal epithelial cells involved in PC progression. METHODS: PC cells and pancreatic stellate cells (PSCs) were treated with exosomes isolated from pancreatic ductal epithelial cells. Cell proliferation was assessed by CCK8 assays. Cell migration and invasion were assessed by Transwell assays. PC and matched adjacent non-tumor tissue specimens were obtained from 46 patients pathologically diagnosed with PC at Peking University First Hospital from 2013 to 2017. Tissue miR-485-3p and p21-activated kinase-1 (PAK1) expression was examined by real-time polymerase chain reaction (RT-PCR), and the relationship of the two was analyzed using Pearman's product-moment correlation. The clinical significance of miR-485-3p was analyzed using the Chi-square test, Wilcoxon rank-sum test, and Fisher exact probability, respectively. The binding of miR-485-3p to PAK1 5'-untranslated region (5'-UTR) was examined by luciferase assay. PC cells were xenografted into nude mice as a PC metastasis model. RESULTS: Exosomes from pancreatic ductal epithelial cells suppressed PC cell migration and invasion as well as the secretion and migration of PSCs. MiR-485-3p was enriched in the exosomes of pancreatic ductal epithelial cells but deficient in those of PC cells and PSCs, in accordance with the lower level in PSCs and PC cells than that in pancreatic ductal cells. And the mature miR-485-3p could be delivered into these cells by the exosomes secreted by normal pancreatic duct cells, to inhibit PC cell migration and invasion. Clinical data analysis showed that miR-485-3p was significantly decreased in PC tissues (P < 0.05) and was negatively associated with lymphovascular invasion (P = 0.044). As a direct target of miR-485-3p, PAK1 was found to exert an inhibitory effect on PC cells, and there was a significantly negative correlation between the expression levels of miR-485-3p and PAK1 (r = -0.6525, P < 0.0001) in PC tissues. Moreover, miR-485-3p could suppress PC metastasis in vivo by targeting p21-activated kinase-1. CONCLUSIONS: Exosomal miR-485-3p delivered by normal pancreatic ductal epithelial cells into PC cells inhibits PC metastasis by directly targeting PAK1. The restoration of miR-485-3p by exosomes or some other vehicle might be a novel approach for PC treatment.

BRM transcriptionally regulates miR-302a-3p to target SOCS5/STAT3 signaling axis to potentiate pancreatic cancer metastasis.

Brahma (BRM) has recently been documented as a significant predictor of pancreatic cancer (PC) metastasis. This study aimed to further elucidate molecular mechanism by which BRM promotes PC metastasis. We found that silencing BRM reduced PC cell migration and invasion both in vivo and in vitro, accompanied by reduced level of miR-302a-3p. BRM positively regulated the transcription of miR-302a-3p, which acted as a metastasis-promoting miRNA in PC cells. miR-302a-3p directly targeted SOCS5 to boost STAT3 phosphorylation and induce the transcription of STAT3 target genes. Furthermore, miR-302a-3p level was higher in tissue and plasma samples derived from PC patients, and was significantly associated with worse clinical pathological features. In xenograft models, inhibiting miR-302a-3p was synergistically lethal in BRM-silenced PC cells. In conclusion, our results suggest that transcriptional regulation of miR-302a-3p by BRM potentiates PC metastasis by epigenetically suppressing SOCS5 expression and activating STAT3 signaling. These new findings provide potential therapeutic avenues for preventing PC-associated death.

A primary retroperitoneal anaplastic lymphoma kinase-positive anaplastic large cell lymphoma with tumor thrombosis.

Anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL) is a T cell subtype of non-Hodgkin's lymphoma (NHL). Typically, lymphoma rarely infiltrates vascular structure. In this article, we present a case of retroperitoneal ALK-positive ALCL with splenic venous tumor thrombosis. A 62-year-old patient presented to our institute with the symptoms of epigastric pain, abdominal distension, and reduced bowel movement. Physical examination indicated no enlarged peripheral lymph nodes or abdominal mass. Laboratory workup revealed granulocytosis, abnormal coagulation function, and normal level of lactic dehydrogenase (LDH). Contrast-enhanced computed tomography (CT) showed a retroperitoneal mass with involvement of pancreas and duodenum and formation of splenic venous tumor thrombus. Ultrasonography-guided retroperitoneal lesion biopsy confirmed the diagnosis of ALK-positive ALCL. The patient was able to tolerate oral intake after two cycles of chemotherapy and showed no sign of lymphoma by positron emission tomography (PET)-CT after the fourth cycle of chemotherapy. In spite of its rarity, lymphoma should be taken into account as a differential diagnosis of other malignancies with tumor thrombosis.

[Construction of a recombinant HVT virus expressing the HA gene of avian influenza virus H5N1 via Rde/ET recombination system].

OBJECTIVE: In recent years,manipulation of large herpesvirus genomes has been facilitated by using bacterial artificial chromosome (BAC) vectors. We have previously reported the construction of the BAC clones (HVT BACs) of herpesvirus of turkey (HVT). With these BAC clones in hand,we manipulated the genome of HVT by utilizing Red/ET recombination system, and developed a biologically safe live vaccine based on the HVT BACs. METHOD: In this two-step approach, we first transformed the plasmid pRedET into the DH10B competent cells that carried the HVT BACs,and added inducer L-arabinose into the cells. We prepared the cells into competent cells and electroporated the linear rpsL-neo counter-selection/selection cassette flanked by the 50 bp long homology arms into the cells. So the functional cassette was inserted into the U(S)2 locus. Only colonies carrying the modified BAC would survive Kanamycin selection on the agar plates. The successful integration of the rpsL-neo cassette was monitored by PCR and Streptomycin selection, for the insertion of rpsL-neo cassette cells will become Streptomycin sensitive. Secondly, in the same way, we replaced the rpsL-neo cassette with the hemagglutinin (HA) gene of (HPAIV) A/Goose/ Guangdong/1/96(H5N1) flanked by the same homology arms. Only colonies which lost the rpsL-neo cassette will grow on Streptomycin containing plates. RESULTS: Finally, we obtained many colonies of which the HA gene of the AIV was inserted into the U(S)2 locus to be modified of HVT. And we reconstituted one recombinant virus from transfecting one of these BAC clones DNA into chick embryo fibroblasts (CEFs). CONCLUSION: We achieved one rescued recombinant virus which designated as rHVT-HA3. The H5 subtype HA gene expression in this recombinant virus rHVT-HA3 was confirmed by immunofluorescence assay.