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The human auditory system extracts rich linguistic abstractions from speech signals. Traditional approaches to understanding this complex process have used linear feature-encoding models, with limited success. Artificial neural networks excel in speech recognition tasks and offer promising computational models of speech processing. We used speech representations in state-of-the-art deep neural network (DNN) models to investigate neural coding from the auditory nerve to the speech cortex. Representations in hierarchical layers of the DNN correlated well with the neural activity throughout the ascending auditory system. Unsupervised speech models performed at least as well as other purely supervised or fine-tuned models. Deeper DNN layers were better correlated with the neural activity in the higher-order auditory cortex, with computations aligned with phonemic and syllabic structures in speech. Accordingly, DNN models trained on either English or Mandarin predicted cortical responses in native speakers of each language. These results reveal convergence between DNN model representations and the biological auditory pathway, offering new approaches for modeling neural coding in the auditory cortex.

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We have characterized a novel 21 amino acid-peptide derived from Antrum Mucosal Protein (AMP)-18 that mediates growth promotion of cultured normal epithelial cells and mitigates radiation-induced oral mucositis in animal models, while suppressing in vitro function of cancer cells. The objective of this study was to evaluate these dual potential therapeutic effects of AMP peptide in a clinically relevant animal model of head and neck cancer (HNC) by simultaneously assessing its effect on tumor growth and radiation-induced oral mucositis in an orthotopic model of HNC. Bioluminescent SCC-25 HNC cells were injected into the anterior tongue and tumors that formed were then subjected to focal radiation treatment. Tumor size was assessed using an in vivo imaging system, and the extent of oral mucositis was compared between animals treated with AMP peptide or vehicle (controls). Synergism between AMP peptide and radiation therapy was suggested by the finding that tumors in the AMP peptide/radiation therapy cohort demonstrated inhibited growth vs. radiation therapy-only treated tumors, while AMP peptide-treatment delayed the onset and reduced the severity of radiation therapy-induced oral mucositis. A differential effect on apoptosis appears to be one mechanism by which AMP-18 can stimulate growth and repair of injured mucosal epithelial cells while inhibiting proliferation of HNC cells. RNA microarray analysis identified pathways that are differentially targeted by AMP-18 in HNC vs. nontransformed cells. These observations confirm the notion that normal cells and tumor cells may respond differently to common biological stimuli, and that leveraging this finding in the case of AMP-18 may provide a clinically relevant opportunity.

The core-shell nanoparticles of Au@TiO2 were synthesised via a simple and flexible hydrothermal route. The structure and properties were characterised by X-ray diffraction, transmission electron microscopy, energy-dispersive X-ray spectroscopy, ultraviolet/visible diffuse reflectance spectra, photoluminescence spectra and Raman spectra. The photocatalytic activity and the photoelectrochemical behaviours were investigated. Compared to TiO2, Au@TiO2 exhibits superior photocatalytic activity and photoelectrochemical property. The enhanced properties of Au@TiO2 attributed to the Au core as electron trap to promote the separation of photogenerated charge carriers in the photocatalytic process, which was also confirmed by the results of electrochemical impedance spectra and photoluminescence. [ABSTRACT FROM AUTHOR]

In this work, g-C3N4/melem nanorods hybrids were synthesized via a rapid cooling process with H2SO4-assisted treatments of bulk g-C3N4. The results show that post treatment of pristine g-C3N4 using concentrated H2SO4 can produce a hybrid crystal structure containing both melem and g-C3N4. The melem nanorods were formed based on H2SO4 exfoliation, regrowth process and nanoplates roll-up mechanism through a rapid cooling process. The g-C3N4/melem nanorods hybrids exhibited efficient degradation of methyl orange and the efficiency was nearly 100% in 80 min, which presented much better than bulk g-C3N4 (giving a degradation efficiency of 67% in 80 min). The enhanced photocatalytic performance of g-C3N4/melem nanorods hybrids mainly originates from the synergistic effect of g-C3N4 and melem, which the g-C3N4/melem hybrids can improving the efficiency of photogenerated charge separation of g-C3N4. This study contributes towards an effective strategy for optimizing the crystalline structure and nanostructure of g-C3N4/melem hybrids to enhanced g-C3N4 photodegradation activity. [ABSTRACT FROM AUTHOR]

The pathogenesis of LPS-induced acute kidney injury (AKI) requires signaling through tumor necrosis factor-[alpha] (TNF) receptor 1 (TNFR 1), which within the kidney is primarily located in the endothelium. We showed previously that caspase inhibition protected mice against LPS-induced AKI and in parallel significantly inhibited LPS-induced renal inflammation. Therefore we hypothesized that caspase activation amplifies TNF-induced inflammation in renal endothelial cells (ECs). In cultured renal ECs, TNF induced apoptosis through a caspase-8-dependent pathway. TNF caused translocation of the p65 subunit of NF-KB to the nucleus, resulting in upregulation of inflammatory markers such as adhesion molecules ICAM-1 and VCAM-1. However, the broadspectrum caspase inhibitor Boc-D-fmk reduced NF-[kappa]B activation as assessed by gel shift assay, reduced phosphorylation of subunit I[kappa]B[alpha], and significantly inhibited TNF-induced expression of ICAM-1 and VCAM-1 as assessed by both real-time PCR and flow cytometry. Broad-spectrum caspase inhibition markedly inhibited neutrophil adherence to the TNF-activated endothelial monolayer, supporting the functional significance of this effect. Specific inhibitors of caspases-8 and -3, but not of caspase-1, reduced TNF-induced NF-[kappa]B activation. Caspase inhibition also reduced TNF-induced myosin light chain (MLC)-2 phosphorylation, and activation of upstream regulator RhoA. Consistent with this, MLC kinase (MLCK) inhibitor ML-7 reduced TNF-induced NF-[kappa]B activation. Thus caspase activation influences NF-[kappa]B signaling via its affect on cytoskeletal changes occurring through RhoA and MLCK pathways. These cell culture experiments support a role for caspase activation in TNF-induced inflammation in the renal endothelium, a key event in LPS-induced AKI. adhesion molecules; cytokines; sepsis; acute kidney injury; neutrophil

A stable polarization mode operation of long-wavelength tunable vertical-cavity surface-emitting lasers is demonstrated.