Deep factorization for speech signal

Various informative factors mixed in speech signals, leading to great difficulty when decoding any of the factors. An intuitive idea is to factorize each speech frame into individual informative factors, though it turns out to be highly difficult. Recently, we found that speaker traits, which were assumed to be long-term distributional properties, are actually short-time patterns, and can be learned by a carefully designed deep neural network (DNN). This discovery motivated a cascade deep factorization (CDF) framework that will be presented in this paper. The proposed framework infers speech factors in a sequential way, where factors previously inferred are used as conditional variables when inferring other factors. We will show that this approach can effectively factorize speech signals, and using these factors, the original speech spectrum can be recovered with a high accuracy. This factorization and reconstruction approach provides potential values for many speech processing tasks, e.g., speaker recognition and emotion recognition, as will be demonstrated in the paper.Comment: Accepted by ICASSP 2018. arXiv admin note: substantial text overlap with arXiv:1706.0177

p38MAPK plays a pivotal role in the development of acute respiratory distress syndrome

Acute respiratory distress syndrome (ARDS) is a life-threatening illness characterized by a complex pathophysiology, involving not only the respiratory system but also nonpulmonary distal organs. Although advances in the management of ARDS have led to a distinct improvement in ARDS-related mortality, ARDS is still a lifethreatening respiratory condition with long-term consequences. A better understanding of the pathophysiology of this condition will allow us to create a personalized treatment strategy for improving clinical outcomes. In this article, we present a general overview p38 mitogen-activated protein kinase (p38MAPK) and recent advances in understanding its functions. We consider the potential of the pharmacological targeting of p38MAPK pathways to treat ARDS

DNMT3a in the hippocampal CA1 is crucial in the acquisition of morphine self‐administration in rats

Drug‐reinforced excessive operant responding is one fundamental feature of long-lasting addiction‐like behaviors and relapse in animals. However, the transcriptional regulatory mechanisms responsible for the persistent drug‐specific (not natural rewards) operant behavior are not entirely clear. In this study, we demonstrate a key role for one of the de novo DNA methyltransferase, DNMT3a, in the acquisition of morphine self‐administration (SA) in rats. The expression of DNMT3a in the hippocampal CA1 region but not in the nucleus accumbens shell was significantly up‐regulated after 1‐ and 7‐day morphine SA (0.3 mg/kg/infusion) but not after the yoked morphine injection. On the other hand, saccharin SA did not affect the expression of DNMT3a or DNMT3b. DNMT inhibitor 5‐aza‐2‐deoxycytidine (5‐aza) microinjected into the hippocampal CA1 significantly attenuated the acquisition of morphine SA. Knockdown of DNMT3a also impaired the ability to acquire the morphine SA. Overall, these findings suggest that DNMT3a in the hippocampus plays an important role in the acquisition of morphine SA and may be a valid target to prevent the development of morphine addiction. Includes Supplemental informatio

Identification of a novel iron regulated basic helix-loop-helix protein involved in Fe homeostasis in Oryza sativa

<p>Abstract</p> <p>Background</p> <p>Iron (Fe) is the most limiting micronutrient element for crop production in alkaline soils. A number of transcription factors involved in regulating Fe uptake from soil and transport in plants have been identified. Analysis of transcriptome data from <it>Oryza sativa </it>grown under limiting Fe conditions reveals that transcript abundances of several genes encoding transcription factors are altered by Fe availability. These transcription factors are putative regulators of Fe deficiency responses.</p> <p>Results</p> <p>Transcript abundance of one nuclear located basic helix-loop-helix family transcription factor, <it>OsIRO3</it>, is up-regulated from 25- to 90-fold under Fe deficiency in both root and shoot respectively. The expression of <it>OsIRO3 </it>is specifically induced by Fe deficiency, and not by other micronutrient deficiencies. Transgenic rice plants over-expressing <it>OsIRO3 </it>were hypersensitive to Fe deficiency, indicating that the Fe deficiency response was compromised. Furthermore, the Fe concentration in shoots of transgenic rice plants over-expressing <it>OsIRO3 </it>was less than that in wild-type plants. Analysis of the transcript abundances of genes normally induced by Fe deficiency in <it>OsIRO3 </it>over-expressing plants indicated their induction was markedly suppressed.</p> <p>Conclusion</p> <p>A novel Fe regulated bHLH transcription factor (OsIRO3) that plays an important role for Fe homeostasis in rice was identified. The inhibitory effect of <it>OsIRO3 </it>over-expression on Fe deficiency response gene expression combined with hypersensitivity of <it>OsIRO3 </it>over-expression lines to low Fe suggest that OsIRO3 is a negative regulator of the Fe deficiency response in rice.</p

Post-treatment with the GLP-1 analogue liraglutide alleviate chronic inflammation and mitochondrial stress induced by Status epilepticus

Glucagon-like peptide-1(GLP-1) is a growth factor that has neuroprotective and anti-inflammatory properties. The protease resistant GLP-1 analogue liraglutide has been shown to be neuroprotective in previous studies in animal models of Alzheimer’s disease or Parkinson’s disease. Status epilepticus (SE) is a complex disorder, involving many underlying pathological processes, including excitotoxic and chronic inflammatory events. The present pilot study aims to investigate whether liraglutide alleviates the chronic inflammation response and mitochondrial stress induced by SE in the lithium-pilocarpine animal model. We found that treatment with 25nmol/kg. i.p. once-daily after the induction of SE for 7 days reduced chronic inflammation as shown by reduced numbers of activated microglia and astrocytes, and reduced levels of TNF-α and IL-1ß in the hippocampus. The mitochondrial stress marker BAX was reduced and the survival factor Bcl-2 was enhanced by liraglutide. Blood glucose levels were not affected by liraglutide. We show for the first time that liraglutide can reduce the chronic inflammation and mitochondrial stress induced by SE, and the results suggest that GLP-1 receptor agonists such as liraglutide have restorative and protective effects in the brain after SE and could serve as a potential treatment