Speech emotion recognition is a vital and challenging task that the feature extraction plays a significant role in the SER performance. With the development of deep learning, we put our eyes on the structure of end-to-end and authenticate the algorithm that is extraordinary effective. In this paper, we introduce a novel architecture ADRNN (dilated CNN with residual block and BiLSTM based on the attention mechanism) to apply for the speech emotion recognition which can take advantage of the strengths of diverse networks and overcome the shortcomings of utilizing alone, and are evaluated in the popular IEMOCAP database and Berlin EMODB corpus. Dilated CNN can assist the model to acquire more receptive fields than using the pooling layer. Then, the skip connection can keep more historic info from the shallow layer and BiLSTM layer are adopted to learn long-term dependencies from the learned local features. And we utilize the attention mechanism to enhance further extraction of speech features. Furthermore, we improve the loss function to apply softmax together with the center loss that achieves better classification performance. As emotional dialogues are transformed of the spectrograms, we pick up the values of the 3-D Log-Mel spectrums from raw signals and put them into our proposed algorithm and obtain a notable performance to get the 74.96% unweighted accuracy in the speaker-dependent and the 69.32% unweighted accuracy in the speaker-independent experiment. It is better than the 64.74% from previous state-of-the-art methods in the spontaneous emotional speech of the IEMOCAP database. In addition, we propose the networks that achieve recognition accuracies of 90.78% and 85.39% on Berlin EMODB of speaker-dependent and speaker-independent experiment respectively, which are better than the accuracy of 88.30% and 82.82% obtained by previous work. For validating the robustness and generalization, we also make an experiment for cross-corpus between above databases and get the preferable 63.84% recognition accuracy in final. INDEX TERMS 3-D Log-Mel, dilated CNN, residual block, center loss, BiLSTM, attention mechanism.

Mammalian metallothionein-2A (MT2A) has received considerable attention in recent years due to its crucial pathophysiological role in anti-oxidant, anti-apoptosis, detoxification and anti-inflammation. For many years, most studies evaluating the effects of MT2A have focused on reactive oxygen species (ROS), as second messengers that lead to oxidative stress injury of cells and tissues. Recent studies have highlighted that oxidative stress could activate mitogen-activated protein kinases (MAPKs), and MT2A, as a mediator of MAPKs, to regulate the pathogenesis of various diseases. However, the molecule mechanism of MT2A remains elusive. A deeper understanding of the functional, biochemical and molecular characteristics of MT2A would be identified, in order to bring new opportunities for oxidative stress therapy.

Brood parasites and predators pose different threats to passerines that may favour the evolution of enemy-specific defence strategies. Furthermore, potential sex-specific variation in parental investment may be manifested in differences between male and female nest defence behaviour. We investigated these hypotheses in Oriental reed warblers (Acrocephalus orientalis), by recording sex- and stage-specific (nests with eggs or nestlings) responses to stuffed dummies placed at their nests. Warblers showed the highest level of aggression to the co-occurring parasite, the common cuckoo (Cuculus canorus), colour morph (grey), but showed reluctance to mob or attack the co-occurring nest predator, the magpie (Pica pica). There was a sex difference in rate of body attacks towards rufous morph common cuckoo, sparrowhawk (Accipiter nisus) (locally absent parasite and predator, respectively) and the spotted dove (Streptopelia chinensis) (locally present, harmless species), with females showing better ability to distinguish between these species than males.

ObjectiveTo reveal the prevalence and molecular characterization of (δβ)0‐thalassemia [(δβ)0‐thal] and hereditary persistence of fetal hemoglobin (HPFH) in the Chinese Zhuang population.MethodsA total of 105 subjects with fetal hemoglobin (Hb F) level ≥5% from 14 204 unrelated ones were selected for the study. Multiplex ligation dependent probe amplification was firstly used to analyze dosage changes of the β‐globin gene cluster for associated with (δβ)0‐thal and HPFH mutations. The gap polymerase chain reaction was then performed to identify the deletions using the respective flanking primers. Hematologic data were recorded and correlated with the molecular findings.ResultsTwenty‐one (0.15%) subjects were diagnosed with Chinese Gγ(Aγδβ)0‐thal. Nine (0.06%) were diagnosed with Southeast Asia HPFH (SEA‐HPFH) deletion. Seventy‐five (0.53%) cases remained uncharacterized. Three genotypes for Chinese Gγ(Aγδβ)0‐thal and SEA‐HPFH deletion were identified, respectively. The genotype‐phenotype relationships were discussed.ConclusionOur study for the first time demonstrated that (δβ)0 and HPFH were not rare events, and molecular characterized Gγ(Aγδβ)0‐thal and HFPH mutations in the Chinese Zhuang population. The findings in our study will be useful in genetic counseling and prenatal diagnostic service of β‐thalassemia in this populations.

Bone morphogenetic protein (BMP) and Rho kinase signaling pathways exert counter regulatory effects on pulmonary artery smooth muscle cell (PASMC) proliferation in pulmonary artery hypertension (PAH). To elucidate the mechanism of this interaction, the present study tested whether Rho kinase activated by platelet derived growth factor-BB (PDGF-BB) enhances PASMC proliferation by suppressing the nuclear translocation of Smad1 induced by BMP-2. BMP-2 was used to activate the Smad1 signaling pathway and PDGF-BB was used to activate the Rho kinase signaling pathway when cells were pretreated with or without Rho-associated protein kinase (ROCK) inhibitor Y-27632 or dual specificity mitogen-activated protein kinase kinase (MEK) 1 and 2 inhibitor U0126. Western blotting was used to determine the expression of the components of the Rho signaling pathway, and the expression of various variants of phosphorylated mothers against decapentaplegic homolog (p-Smad)1 in the cytoplasm and nucleus. Immunofluorescent staining was used to observe subcellular distribution of p-Smad1. A cell counting kit was used to analyze cell proliferation. Active RhoA/Rho kinase signaling and decreased nuclear translocation of Smad1 were found in primary cultured PASMCs from the rat model of PAH compared with the control PASMCs. Treatment with BMP-2 significantly increased nuclear accumulation of Smad1 and inhibited the proliferation of PASMCs. However, pretreatment with PDGF-BB significantly decreased the nuclear accumulation of Smad1 induced by BMP-2 and enhanced the proliferation of PASMCs. Furthermore, pretreatment with Y-27632 or U0126 was found to restore the nuclear translocation of Smad1 suppressed by PDGF-BB and decrease the proliferation of PASMCs. In conclusion, the present study suggested that Rho kinase activated by PDGF-BB suppressed BMP-2-induced nuclear translocation of Smad1 via the MEK/mitogen-activated protein kinase and enhanced BMP-2-inhibited proliferation of PASMCs.