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关键词： Filter parameter training   Sub-band   Convolutional neural network   High energy frequency   Low energy feature vanishing  

摘要： Although Convolutional Neural Networks (CNNs) architecture based learning systems have shown impressive results in the performance of numerous classification tasks, their effectiveness has been limited in certain cases of acoustic based classification. This vulnerability is particularly evident in the acoustic event classification tasks using spectral features. For example, spectral based features may suffer from a typical normalization process when it is fed to a neural network for training since the magnitudes in high-frequency band are inadvertently attenuated even though they may yet contain useful discriminant features. Although some research efforts try to mitigate this problem by introducing a multi-band approach for attaining salient and stable features, it requires empirically preset frequency bands to separate the spectral features. Being heuristic, however, this process is difficult to ensure the consistency required for high correlation between manually separated features and good classification performance. In this paper, we propose a novel filter parameter modeling framework performing optimized frequency sub-band separation via CNN based end-to-end training for achieving high acoustic event classification performance. In particular, the filter response characteristics, namely, cut-off frequencies and damping ratio for roll off are considered as added learning parameters to the CNN architecture for the proposed end-to-end learning framework so that the filter's frequency response is optimized for producing salient features. The proposed training process is shown to not only automatically select the filter parameters for multi-band frequency separation but also guarantee high correlation between the resulting sub-band features and accurate classification performance. (C) 2020 Elsevier Ltd. All rights reserved.

关键词： PCB153   Apoptosis   Pituitary   PI3K/Akt   NF-kappa B   p21/p53  

摘要： Polychlorinated biphenyls (PCBs) are persistent pollutants involved in human tumorigenesis. PCB153 is a ubiquitous non-dioxin-like PCB with proliferative and anti-apoptotic effects. To explore the impact of PCB153 in the survival of pituitary cells, we exposed murine pituitary primary cells to PCB153 10 mu M for 24 h. Apoptosis was assessed by RT-qPCR, Western-blot, immunoprecipitation, caspase activity, and immunofluorescence. We found that PCB153 decreased pituitary apoptosis through both the extrinsic and intrinsic pathways. PCB153 reduced the level of the pro-apoptotic protein p38-MAPK. Otherwise, PCB153 activated PI3K/Akt and Erk1/2 pathways and enhanced the expression and nuclear translocation of NF-kappa B. Cotreatments with specific inhibitors revealed that only PI3K/Akt changed the caspase-3 expression and NF-kappa B activation induced by PCB153. Also, PCB153 decreased the expression of the pro-apoptotic and pro-senescent cyclins p53 and p21. In summary, exposure to PCB153 leads to a downregulation of apoptosis in the pituitary driven by a PI3K/Akt-mediated activation of NF-kappa B.

关键词： neuroprotection   preconditioning   ischaemia   hypoxia   HIF-1   glucose  

摘要： Preconditioning tissue with sublethal ischaemia or hypoxia can confer tolerance (protection) against subsequent ischaemic challenge. In vitro ischaemic preconditioning (IPC) is typically achieved through oxygen glucose deprivation (OGD), whereas hypoxic preconditioning (HPC) involves oxygen deprivation (OD) alone. Here, we report the effects of preconditioning of OGD, OD or glucose deprivation (GD) in ischaemic tolerance models with PC12 cells and primary rat neurons. PC12 cells preconditioned (4 h) with GD or OGD, but not OD, prior to reperfusion (24 h) then ischaemic challenge (OGD 6 h), showed greater mitochondria! activity, reduced cytotoxicity and decreased apoptosis, compared to sham preconditioned PC12 cells. Furthermore, 4 h preconditioning with reduced glucose (0.565 giL, reduced from 4.5 g/L) conferred protective effects, but not for higher concentrations (1.125 or 2.25 g/L). Preconditioning (4 h) with OGD, but not OD or GD, induced stabilization of hypoxia inducible factor 1 alpha (HIF1 alpha) and upregulation of HIF1 downstream genes (Vegf, Glutl, Pfkfb3 and Ldha). In primary rat neurons, only OGD preconditioning (4 h) conferred neuroprotection. OGD preconditioning (4 h) induced stabilization of HIF1 alpha and upregulation of HIF1 downstream genes (Vegf, Phd2 and Bnip3). In conclusion, OGD preconditioning (4 h) followed by 24 h reperfusion induced ischaemic tolerance (against OGD, 6 h) in both PC12 cells and primary rat neurons. The OGD preconditioning protection is associated with HIF1 alpha stabilization and upregulation of HIF1 downstream gene expression. GD preconditioning (4 h) leads to protection in PC12 cells, but not in neurons. This GD preconditioning-induced protection was not associated with HIF1 alpha stabilization. (C) 2020 IBRO. Published by Elsevier Ltd. All rights reserved.

关键词： Sickle cell disease   Malnutrition   Nutrition   Africa  

关键词： Quercetin   Cadmium   Autophagy   Lysosome   TFEB  

摘要： Autophagy dysregulation plays a pivotal role in cadmium (Cd)-induced nephrotoxicity. Quercetin (Qu), a flavonoid antioxidant with autophagy-enhancing effect, has protective effect on Cd-induced toxicity, but whether it can prevent Cd-induced nephrotoxicity via restoration of autophagy remains unknown. Here, primary rat proximal tubular (rPT) cells were exposed to Cd and/or Qu in vitro to clarify this issue. Data first showed that Cdimpaired autophagic flux was markedly alleviated by Qu, including decreased levels of autophagy marker proteins and recovery of autophagosome-lysosome fusion targeted for lysosomes. Meanwhile, Cd-induced lysosomal alkalization due to v-ATPases inhibition was prominently recovered by Qu. Accordingly, Qu enhanced Cddiminished lysosomal degradation capacity and lysosome-related gene transcription levels. Notably, Qu improved Cd-inhibited TFEB nuclear translocation and its gene transcription level. Furthermore, data showed that the restoration of Cd-impaired autophagy-lysosome pathway and resultant alleviation of cytotoxicity by Qu are TFEB-dependent using TFEB gene silencing and overexpression technologies. In summary, these data provide novel evidences that the protective action of Qu against Cd-induced autophagy inhibition is attributed to its restoration of lysosomal dysfunction, which is dependent on TFEB.

摘要： In this issue of Blood, Pal et al demonstrate that heme released during hemolysis inhibits human plasma B-cell differentiation, but this pathway was inhibited in B cells from alloimmunized patients with sickle cell disease (SCD). Thus, insensitivity to heme inhibition in B cells may be a potential alloimmunization risk factor.(1)