Alternative Pseudo-Labeling for Semi-Supervised Automatic Speech Recognition

When labeled data is insufficient, semi-supervised learning with the pseudo-labeling technique can significantly improve the performance of automatic speech recognition. However, pseudo-labels are often noisy, containing numerous incorrect tokens. Taking noisy labels as ground-truth in the loss function results in suboptimal performance. Previous works attempted to mitigate this issue by either filtering out the nosiest pseudo-labels or improving the overall quality of pseudo-labels. While these methods are effective to some extent, it is unrealistic to entirely eliminate incorrect tokens in pseudo-labels. In this work, we propose a novel framework named alternative pseudo-labeling to tackle the issue of noisy pseudo-labels from the perspective of the training objective. The framework comprises several components. Firstly, a generalized CTC loss function is introduced to handle noisy pseudo-labels by accepting alternative tokens in the positions of incorrect tokens. Applying this loss function in pseudo-labeling requires detecting incorrect tokens in the predicted pseudo-labels. In this work, we adopt a confidence-based error detection method that identifies the incorrect tokens by comparing their confidence scores with a given threshold, thus necessitating the confidence score to be discriminative. Hence, the second proposed technique is the contrastive CTC loss function that widens the confidence gap between the correctly and incorrectly predicted tokens, thereby improving the error detection ability. Additionally, obtaining satisfactory performance with confidence-based error detection typically requires extensive threshold tuning. Instead, we propose an automatic thresholding method that uses labeled data as a proxy for determining the threshold, thus saving the pain of manual tuning.Comment: Accepted by IEEE/ACM Transactions on Audio, Speech and Language Processing (TASLP), 202

Neutrophil histamine contributes to inflammation in mycoplasma pneumonia

Mycoplasmas cause chronic inflammation and are implicated in asthma. Mast cells defend against mycoplasma infection and worsen allergic inflammation, which is mediated partly by histamine. To address the hypothesis that mycoplasma provokes histamine release, we exposed mice to Mycoplasma pulmonis, comparing responses in wild-type and mast cell–deficient KitW-sh/KitW-sh (W-sh) mice. Low histamine levels in uninfected W-sh mice confirmed the conventional wisdom that mast cells are principal sources of airway and serum histamine. Although mycoplasma did not release histamine acutely in wild-type airways, levels rose up to 50-fold above baseline 1 week after infection in mice heavily burdened with neutrophils. Surprisingly, histamine levels also rose profoundly in infected W-sh lungs, increasing in parallel with neutrophils and declining with neutrophil depletion. Furthermore, neutrophils from infected airway were highly enriched in histamine compared with naive neutrophils. In vitro, mycoplasma directly stimulated histamine production by naive neutrophils and strongly upregulated mRNA encoding histidine decarboxylase, the rate-limiting enzyme in histamine synthesis. In vivo, treatment with antihistamines pyrilamine or cimetidine decreased lung weight and severity of pneumonia and tracheobronchitis in infected W-sh mice. These findings suggest that neutrophils, provoked by mycoplasma, greatly expand their capacity to synthesize histamine, thereby contributing to lung and airway inflammation

Transcriptional Regulation of Enhancers Active in Protodomains of the Developing Cerebral Cortex

SummaryElucidating the genetic control of cerebral cortical (pallial) development is essential for understanding function, evolution, and disorders of the brain. Transcription factors (TFs) that embryonically regulate pallial regionalization are expressed in gradients, raising the question of how discrete domains are generated. We provide evidence that small enhancer elements active in protodomains integrate broad transcriptional information. CreERT2 and GFP expression from 14 different enhancer elements in stable transgenic mice allowed us to define a comprehensive regional fate map of the pallium. We explored transcriptional mechanisms that control the activity of the enhancers using informatics, in vivo occupancy by TFs that regulate cortical patterning (CoupTFI, Pax6, and Pbx1), and analysis of enhancer activity in Pax6 mutants. Overall, the results provide insights into how broadly expressed patterning TFs regulate the activity of small enhancer elements that drive gene expression in pallial protodomains that fate map to distinct cortical regions

Comparative proteomic analysis of pepper (Capsicum annuum L.) seedlings under selenium stress

Selenium (Se) is an essential trace element for human and animal health. Se fertilizer has been used to increase the Se content in crops to meet the Se requirements in humans and animals. To address the challenge of Se poisoning in plants, the mechanisms underlying Se-induced stress in plants must be understood. Here, to elucidate the effects of Se stress on the protein levels in pepper, we used an integrated approach involving tandem mass tag labeling, high performance liquid chromatography fractionation, and mass spectrometry-based analysis. A total of 4,693 proteins were identified, 3,938 of which yielded quantitative information. Among them, the expression of 172 proteins was up-regulated, and the expression of 28 proteins was down-regulated in the Se/mock treatment comparison. According to the above data, we performed a systematic bioinformatics analysis of all identified proteins and differentially expressed proteins (DEPs). The DEPs were most strongly associated with the terms “metabolic process,” “posttranslational modification, protein turnover, chaperones,” and “protein processing in endoplasmic reticulum” according to Gene Ontology, eukaryotic orthologous groups classification, and Kyoto Encyclopedia of Genes and Genomes enrichment analysis, respectively. Furthermore, several heat shock proteins were identified as DEPs. These results provide insights that may facilitate further studies on the pepper proteome expressed downstream of the Se stress response. Our data revealed that the responses of pepper to Se stress involve various pathways

Neutrophil histamine contributes to inflammation in mycoplasma pneumonia.

Mycoplasmas cause chronic inflammation and are implicated in asthma. Mast cells defend against mycoplasma infection and worsen allergic inflammation, which is mediated partly by histamine. To address the hypothesis that mycoplasma provokes histamine release, we exposed mice to Mycoplasma pulmonis, comparing responses in wild-type and mast cell-deficient KitW-sh/KitW-sh (W-sh) mice. Low histamine levels in uninfected W-sh mice confirmed the conventional wisdom that mast cells are principal sources of airway and serum histamine. Although mycoplasma did not release histamine acutely in wild-type airways, levels rose up to 50-fold above baseline 1 week after infection in mice heavily burdened with neutrophils. Surprisingly, histamine levels also rose profoundly in infected W-sh lungs, increasing in parallel with neutrophils and declining with neutrophil depletion. Furthermore, neutrophils from infected airway were highly enriched in histamine compared with naive neutrophils. In vitro, mycoplasma directly stimulated histamine production by naive neutrophils and strongly upregulated mRNA encoding histidine decarboxylase, the rate-limiting enzyme in histamine synthesis. In vivo, treatment with antihistamines pyrilamine or cimetidine decreased lung weight and severity of pneumonia and tracheobronchitis in infected W-sh mice. These findings suggest that neutrophils, provoked by mycoplasma, greatly expand their capacity to synthesize histamine, thereby contributing to lung and airway inflammation