The MuSe 2021 Multimodal Sentiment Analysis Challenge: sentiment, emotion, physiological-emotion, and stress

Multimodal Sentiment Analysis (MuSe) 2021 is a challenge focusing on the tasks of sentiment and emotion, as well as physiological-emotion and emotion-based stress recognition through more comprehensively integrating the audio-visual, language, and biological signal modalities. The purpose of MuSe 2021 is to bring together communities from different disciplines; mainly, the audio-visual emotion recognition community (signal-based), the sentiment analysis community (symbol-based), and the health informatics community. We present four distinct sub-challenges: MuSe-Wilder and MuSe-Stress which focus on continuous emotion (valence and arousal) prediction; MuSe-Sent, in which participants recognise five classes each for valence and arousal; and MuSe-Physio, in which the novel aspect of 'physiological-emotion' is to be predicted. For this year's challenge, we utilise the MuSe-CaR dataset focusing on user-generated reviews and introduce the Ulm-TSST dataset, which displays people in stressful depositions. This paper also provides detail on the state-of-the-art feature sets extracted from these datasets for utilisation by our baseline model, a Long Short-Term Memory-Recurrent Neural Network. For each sub-challenge, a competitive baseline for participants is set; namely, on test, we report a Concordance Correlation Coefficient (CCC) of .4616 CCC for MuSe-Wilder; .5088 CCC for MuSe-Stress, and .4908 CCC for MuSe-Physio. For MuSe-Sent an F1 score of 32.82% is obtained

Prepregnancy body mass index and risk of preterm birth: association heterogeneity by preterm subgroups

Background: To evaluate the association between prepregnancy body mass index (BMI) is associated with early vs. late and medically-induced vs. spontaneous preterm birth (PTB) subtypes. Methods: Using data from the Boston Birth Cohort, we examined associations of prepregnancy BMI with 189 early (<34 completed weeks) and 277 late (34–36 completed weeks) medically-induced PTBs and 320 early and 610 late spontaneous PTBs vs. 3281 term births (37–44 weeks) in multinomial regression. To assess for mediation by important pregnancy complications, we performed sequential models with and without hypertensive disorders of pregnancy, chorioamnionitis, and gestational diabetes. Results: Prevalence of prepregnancy obesity (BMI ≥ 30.0 kg/m2) was 28% among mothers with medically-induced PTBs, 18% among mothers with spontaneous PTBs, and 18% among mothers with term births (p = <0.001). After adjustment for demographic and known risk factors for PTB, prepregnancy obesity was associated with higher odds of both early [OR 1.78 (1.19, 2.66)] and late [OR 1.49 (1.09, 2.04)] medically-induced PTB. These effect estimates were attenuated with inclusion of hypertensive disorders of pregnancy and gestational diabetes. For spontaneous deliveries, prepregnancy obesity was associated with decreased odds of PTB (0.76 [0.58, 0.98]) and underweight was nearly associated with increased odds of PTB (1.46 [0.99, 2.16]). Conclusion: Prepregnancy obesity is associated with higher risk of medically-induced, but not spontaneous PTB. Hypertensive disorders of pregnancy and gestational diabetes appear to partially explain the association between prepregnancy obesity and early and late medically-induced PTB

CARAT: A novel method for allelic detection of DNA copy number changes using high density oligonucleotide arrays

BACKGROUND: DNA copy number alterations are one of the main characteristics of the cancer cell karyotype and can contribute to the complex phenotype of these cells. These alterations can lead to gains in cellular oncogenes as well as losses in tumor suppressor genes and can span small intervals as well as involve entire chromosomes. The ability to accurately detect these changes is central to understanding how they impact the biology of the cell. RESULTS: We describe a novel algorithm called CARAT (Copy Number Analysis with Regression And Tree) that uses probe intensity information to infer copy number in an allele-specific manner from high density DNA oligonuceotide arrays designed to genotype over 100, 000 SNPs. Total and allele-specific copy number estimations using CARAT are independently evaluated for a subset of SNPs using quantitative PCR and allelic TaqMan reactions with several human breast cancer cell lines. The sensitivity and specificity of the algorithm are characterized using DNA samples containing differing numbers of X chromosomes as well as a test set of normal individuals. Results from the algorithm show a high degree of agreement with results from independent verification methods. CONCLUSION: Overall, CARAT automatically detects regions with copy number variations and assigns a significance score to each alteration as well as generating allele-specific output. When coupled with SNP genotype calls from the same array, CARAT provides additional detail into the structure of genome wide alterations that can contribute to allelic imbalance

MER 2023: Multi-label Learning, Modality Robustness, and Semi-Supervised Learning

Over the past few decades, multimodal emotion recognition has made remarkable progress with the development of deep learning. However, existing technologies are difficult to meet the demand for practical applications. To improve the robustness, we launch a Multimodal Emotion Recognition Challenge (MER 2023) to motivate global researchers to build innovative technologies that can further accelerate and foster research. For this year's challenge, we present three distinct sub-challenges: (1) MER-MULTI, in which participants recognize both discrete and dimensional emotions; (2) MER-NOISE, in which noise is added to test videos for modality robustness evaluation; (3) MER-SEMI, which provides large amounts of unlabeled samples for semi-supervised learning. In this paper, we test a variety of multimodal features and provide a competitive baseline for each sub-challenge. Our system achieves 77.57% on the F1 score and 0.82 on the mean squared error (MSE) for MER-MULTI, 69.82% on the F1 score and 1.12 on MSE for MER-NOISE, and 86.75% on the F1 score for MER-SEMI, respectively. Baseline code is available at https://github.com/zeroQiaoba/MER2023-Baseline

Improved detection of global copy number variation using high density, non-polymorphic oligonucleotide probes

<p>Abstract</p> <p>Background</p> <p>DNA sequence diversity within the human genome may be more greatly affected by copy number variations (CNVs) than single nucleotide polymorphisms (SNPs). Although the importance of CNVs in genome wide association studies (GWAS) is becoming widely accepted, the optimal methods for identifying these variants are still under evaluation. We have previously reported a comprehensive view of CNVs in the HapMap DNA collection using high density 500 K EA (Early Access) SNP genotyping arrays which revealed greater than 1,000 CNVs ranging in size from 1 kb to over 3 Mb. Although the arrays used most commonly for GWAS predominantly interrogate SNPs, CNV identification and detection does not necessarily require the use of DNA probes centered on polymorphic nucleotides and may even be hindered by the dependence on a successful SNP genotyping assay.</p> <p>Results</p> <p>In this study, we have designed and evaluated a high density array predicated on the use of non-polymorphic oligonucleotide probes for CNV detection. This approach effectively uncouples copy number detection from SNP genotyping and thus has the potential to significantly improve probe coverage for genome-wide CNV identification. This array, in conjunction with PCR-based, complexity-reduced DNA target, queries over 1.3 M independent NspI restriction enzyme fragments in the 200 bp to 1100 bp size range, which is a several fold increase in marker density as compared to the 500 K EA array. In addition, a novel algorithm was developed and validated to extract CNV regions and boundaries.</p> <p>Conclusion</p> <p>Using a well-characterized pair of DNA samples, close to 200 CNVs were identified, of which nearly 50% appear novel yet were independently validated using quantitative PCR. The results indicate that non-polymorphic probes provide a robust approach for CNV identification, and the increasing precision of CNV boundary delineation should allow a more complete analysis of their genomic organization.</p

The Src Family Kinases and Protein Kinase C Synergize to Mediate G q -dependent Platelet Activation

The Src family kinases (SFKs) play essential roles in collagen- and von Willebrand factor (VWF)-mediated platelet activation. However, the roles of SFKs in G protein-coupled receptor-mediated platelet activation and the molecular mechanisms whereby SFKs are activated by G protein-coupled receptor stimulation are not fully understood. Here we show that the thrombin receptor protease-activated receptor 4 agonist peptide AYPGKF elicited SFK phosphorylation in P2Y12 deficient platelets but stimulated minimal SFK phosphorylation in platelets lacking Gq. We have previously shown that thrombin-induced SFK phosphorylation was inhibited by the calcium chelator 5,5′-dimethyl-bis-(o-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid (dimethyl-BAPTA). The calcium ionophore A23187 induced SFK phosphorylation in both wild-type and Gq deficient platelets. Together, these results indicate that SFK phosphorylation in response to thrombin receptor stimulation is downstream from Gq/Ca2+ signaling. Moreover, {"type":"entrez-nucleotide","attrs":{"text":"A23187","term_id":"833253","term_text":"A23187"}}A23187-induced thromboxane A2 synthesis, platelet aggregation, and secretion were inhibited by preincubation of platelets with a selective SFK inhibitor, PP2. AYPGKF-induced thromboxane A2 production in wild-type and P2Y12 deficient platelets was abolished by PP2, and AYPGKF-mediated P-selectin expression, integrin αIIbβ3 activation, and aggregation of P2Y12 deficient platelets were partially inhibited by the PKC inhibitor Ro-31-8220, PP2, dimethyl-BAPTA, or LY294002, but were abolished by Ro-31-8220 plus PP2, dimethyl-BAPTA, or LY294002. These data indicate that Ca2+/SFKs/PI3K and PKC represent two alternative signaling pathways mediating Gq-dependent platelet activation

Platelet Secretion and Hemostasis Require Syntaxin-binding Protein STXBP5

Genome-wide association studies (GWAS) have linked genes encoding several soluble NSF attachment protein receptor (SNARE) regulators to cardiovascular disease risk factors. Because these regulatory proteins may directly affect platelet secretion, we used SNARE-containing complexes to affinity purify potential regulators from human platelet extracts. Syntaxin-binding protein 5 (STXBP5; also known as tomosyn-1) was identified by mass spectrometry, and its expression in isolated platelets was confirmed by RT-PCR analysis. Coimmunoprecipitation studies showed that STXBP5 interacts with core secretion machinery complexes, such as syntaxin-11/SNAP23 heterodimers, and fractionation studies suggested that STXBP5 also interacts with the platelet cytoskeleton. Platelets from Stxbp5 KO mice had normal expression of other key secretory components; however, stimulation-dependent secretion from each of the 3 granule types was markedly defective. Secretion defects in STXBP5-deficient platelets were confirmed via lumi-aggregometry and FACS analysis for P-selectin and LAMP-1 exposure. Interestingly, STXBP5-deficient platelets had altered granule cargo levels, despite having normal morphology and granule numbers. Consistent with secretion and cargo deficiencies, Stxbp5 KO mice showed dramatic bleeding in the tail transection model and defective hemostasis in the FeCl3-induced carotid injury model. Transplantation experiments indicated that these defects were due to loss of STXBP5 in BM-derived cells. Our data demonstrate that STXBP5 is required for normal arterial hemostasis, due to its contributions to platelet granule cargo packaging and secretion

Autophagy Is Induced Upon Platelet Activation and Is Essential for Hemostasis and Thrombosis

Autophagy is important for maintaining cellular homeostasis, and thus its deficiency is implicated in a broad spectrum of human diseases. Its role in platelet function has only recently been examined. Our biochemical and imaging studies demonstrate that the core autophagy machinery exists in platelets, and that autophagy is constitutively active in resting platelets. Moreover, autophagy is induced upon platelet activation, as indicated by agonist-induced loss of the autophagy marker LC3II. Additional experiments, using inhibitors of platelet activation, proteases, and lysosomal acidification, as well as platelets from knockout mouse strains, show that agonist-induced LC3II loss is a consequence of platelet signaling cascades and requires proteases, acidic compartments, and membrane fusion. To assess the physiological role of platelet autophagy, we generated a mouse strain with a megakaryocyte- and platelet-specific deletion of Atg7, an enzyme required for LC3II production. Ex vivo analysis of platelets from these mice shows modest defects in aggregation and granule cargo packaging. Although these mice have normal platelet numbers and size distributions, they exhibit a robust bleeding diathesis in the tail-bleeding assay and a prolonged occlusion time in the FeCl3-induced carotid injury model. Our results demonstrate that autophagy occurs in platelets and is important for hemostasis and thrombosis

Torsion and accelerating expansion of the universe in quadratic gravitation

Several exact cosmological solutions of a metric-affine theory of gravity with two torsion functions are presented. These solutions give a essentially different explanation from the one in most of previous works to the cause of the accelerating cosmological expansion and the origin of the torsion of the spacetime. These solutions can be divided into two classes. The solutions in the first class define the critical points of a dynamical system representing an asymptotically stable de Sitter spacetime. The solutions in the second class have exact analytic expressions which have never been found in the literature. The acceleration equation of the universe in general relativity is only a special case of them. These solutions indicate that even in vacuum the spacetime can be endowed with torsion, which means that the torsion of the spacetime has an intrinsic nature and a geometric origin. In these solutions the acceleration of the cosmological expansion is due to either the scalar torsion or the pseudoscalar torsion function. Neither a cosmological constant nor dark energy is needed. It is the torsion of the spacetime that causes the accelerating expansion of the universe in vacuum. All the effects of the inflation, the acceleration and the phase transformation from deceleration to acceleration can be explained by these solutions. Furthermore, the energy and pressure of the matter without spin can produce the torsion of the spacetime and make the expansion of the universe decelerate as well as accelerate.Comment: 20 pages. arXiv admin note: text overlap with gr-qc/0604006, arXiv:1110.344

Expression of Regulatory Platelet MicroRNAs in Patients with Sickle Cell Disease

Background: Increased platelet activation in sickle cell disease (SCD) contributes to a state of hypercoagulability and confers a risk of thromboembolic complications. The role for post-transcriptional regulation of the platelet transcriptome by microRNAs (miRNAs) in SCD has not been previously explored. This is the first study to determine whether platelets from SCD exhibit an altered miRNA expression profile. Methods and Findings: We analyzed the expression of miRNAs isolated from platelets from a primary cohort (SCD = 19, controls = 10) and a validation cohort (SCD = 7, controls = 7) by hybridizing to the Agilent miRNA microarrays. A dramatic difference in miRNA expression profiles between patients and controls was noted in both cohorts separately. A total of 40 differentially expressed platelet miRNAs were identified as common in both cohorts (p-value 0.05, fold change>2) with 24 miRNAs downregulated. Interestingly, 14 of the 24 downregulated miRNAs were members of three families - miR-329, miR-376 and miR-154 - which localized to the epigenetically regulated, maternally imprinted chromosome 14q32 region. We validated the downregulated miRNAs, miR-376a and miR-409-3p, and an upregulated miR-1225-3p using qRT-PCR. Over-expression of the miR-1225-3p in the Meg01 cells was followed by mRNA expression profiling to identify mRNA targets. This resulted in significant transcriptional repression of 1605 transcripts. A combinatorial approach using Meg01 mRNA expression profiles following miR-1225-3p overexpression, a computational prediction analysis of miRNA target sequences and a previously published set of differentially expressed platelet transcripts from SCD patients, identified three novel platelet mRNA targets: PBXIP1, PLAGL2 and PHF20L1. Conclusions: We have identified significant differences in functionally active platelet miRNAs in patients with SCD as compared to controls. These data provide an important inventory of differentially expressed miRNAs in SCD patients and an experimental framework for future studies of miRNAs as regulators of biological pathways in platelets. © 2013 Jain et al