Improving Automatic Jazz Melody Generation by Transfer Learning Techniques

In this paper, we tackle the problem of transfer learning for Jazz automatic generation. Jazz is one of representative types of music, but the lack of Jazz data in the MIDI format hinders the construction of a generative model for Jazz. Transfer learning is an approach aiming to solve the problem of data insufficiency, so as to transfer the common feature from one domain to another. In view of its success in other machine learning problems, we investigate whether, and how much, it can help improve automatic music generation for under-resourced musical genres. Specifically, we use a recurrent variational autoencoder as the generative model, and use a genre-unspecified dataset as the source dataset and a Jazz-only dataset as the target dataset. Two transfer learning methods are evaluated using six levels of source-to-target data ratios. The first method is to train the model on the source dataset, and then fine-tune the resulting model parameters on the target dataset. The second method is to train the model on both the source and target datasets at the same time, but add genre labels to the latent vectors and use a genre classifier to improve Jazz generation. The evaluation results show that the second method seems to perform better overall, but it cannot take full advantage of the genre-unspecified dataset.Comment: 8 pages, Accepted to APSIPA ASC(Asia-Pacific Signal and Information Processing Association Annual Summit and Conference ) 201

Phyllanthus urinaria Induces Apoptosis in Human Osteosarcoma 143B Cells via Activation of Fas/FasL- and Mitochondria-Mediated Pathways

Phyllanthus urinaria (P. urinaria), in this study, was used for the treatment of human osteosarcoma cells, which is one of the tough malignancies with few therapeutic modalities. Herein, we demonstrated that P. urinaria inhibited human osteosarcoma 143B cells growth through an apoptotic extrinsic pathway to activate Fas receptor/ligand expression. Both intracellular and mitochondrial reactive oxygen species were increased to lead to alterations of mitochondrial membrane permeability and Bcl-2 family including upregulation of Bid, tBid, and Bax and downregulation of Bcl-2. P. urinaria triggered an intrinsic pathway and amplified the caspase cascade to induce apoptosis of 143B cells. However, upregulation of both intracellular and mitochondrial reactive oxygen species and the sequential membrane potential change were less pronounced in the mitochondrial respiratory-defective 143Bρ0 cells compared with the 143B cells. This study offers the evidence that mitochondria are essential for the anticancer mechanism induced by P. urinaria through both extrinsic and intrinsic pathways

Magnesium-enriched deep-sea water inhibits NLRP3 inflammasome activation and dampens inflammation.

The NLRP3 inflammasome is an essential component of the innate immune system, but excessive activation can lead to inflammatory diseases. Ion fluxes across the plasma membrane or from intracellular stores are known to regulate NLRP3 inflammasome activation. Deep-sea water (DSW) contains high concentrations of many mineral ions, which could potentially influence NLRP3 inflammasome activation. However, the impact of DSW on NLRP3 inflammasome activation has not been investigated. Here, we demonstrated that DSW with water hardness levels up to 500 mg/L did not affect cell viability or the expression of NLRP3 inflammasome components in macrophages derived from THP-1 cells. However, the DSW significantly inhibited IL-1β secretion and caspase-1 activation in response to NLRP3 activators such as nigericin, ATP, or monosodium urate (MSU) crystals. Mechanically, it was discovered that the presence of 5 mM magnesium ions (Mg2+), equivalent to the Mg2+ concentration found in the DSW with a water hardness of 500 mg/L, inhibits NLRP3 inflammasome activation. This indicates that Mg2+ contributes to the mechanism by which DSW mitigates NLRP3 inflammasome activation. Moreover, DSW administration effectively lessens MSU-triggered peritonitis in mice, a commonly used model for examining the impacts of NLRP3 inflammasome activation. These results show that DSW enriched with Mg2+ could potentially be beneficial in modulating NLRP3 inflammasome-associated diseases

A Vision-Based Driver Nighttime Assistance and Surveillance System Based on Intelligent Image Sensing Techniques and a Heterogamous Dual-Core Embedded System Architecture

This study proposes a vision-based intelligent nighttime driver assistance and surveillance system (VIDASS system) implemented by a set of embedded software components and modules, and integrates these modules to accomplish a component-based system framework on an embedded heterogamous dual-core platform. Therefore, this study develops and implements computer vision and sensing techniques of nighttime vehicle detection, collision warning determination, and traffic event recording. The proposed system processes the road-scene frames in front of the host car captured from CCD sensors mounted on the host vehicle. These vision-based sensing and processing technologies are integrated and implemented on an ARM-DSP heterogamous dual-core embedded platform. Peripheral devices, including image grabbing devices, communication modules, and other in-vehicle control devices, are also integrated to form an in-vehicle-embedded vision-based nighttime driver assistance and surveillance system

Improving cancer immunotherapy in prostate cancer by modulating T cell function through targeting the galectin-1

Our study aimed to elucidate the role of Galectin-1 (Gal-1) role in the immunosuppressive tumor microenvironment (TME) of prostate cancer (PCa). Our previous findings demonstrated a correlation between elevated Gal-1 expression and advanced PCa stages. In this study, we also observed that Gal-1 is expressed around the tumor stroma and its expression level is associated with PCa progression. We identified that Gal-1 could be secreted by PCa cells, and secreted Gal-1 has the potential to induce T cell apoptosis. Gal-1 knockdown or inhibition of Gal-1 function by LLS30 suppresses T cell apoptosis resulting in increased intratumoral T cell infiltration. Importantly, LLS30 treatment significantly improved the antitumor efficacy of anti-PD-1 in vivo. Mechanistically, LLS30 binds to the carbohydrate recognition domain (CRD) of Gal-1, disrupting its binding to CD45 leading to the suppression of T cell apoptosis. In addition, RNA-seq analysis revealed a novel mechanism of action for LLS30, linking its tumor-intrinsic oncogenic effects to anti-tumor immunity. These findings suggested that tumor-derived Gal-1 contributes to the immunosuppressive TME in PCa by inducing apoptosis in effector T cells. Targeting Gal-1 with LLS30 may offer a strategy to enhance anti-tumor immunity and improve immunotherapy

Pluripotency maintenance of amniotic fluid-derived stem cells cultured on biomaterials

The stem cell fates of pluripotency and differentiation are regulated by not only soluble biological cues but also insoluble biochemical cues (i.e., extracellular matrix (ECM)) and the physical cues of cell culture biomaterials (i.e., elasticity). We investigated the maintenance of pluripotency and the differentiation lineages of human amniotic fluid-derived stem cells (hAFSCs) cultured on poly(vinyl alcohol-co-itaconic acid) (PVA) hydrogels grafted with several types of ECM and corresponding oligopeptides in expansion medium. hAFSCs cultured on soft PVA hydrogels (12.2 kPa) that were grafted with oligopeptides derived from fibronectin and vitronectin showed high pluripotency, which was evaluated by Oct4, Sox2 and Nanog expression. The hAFSCs grown on soft PVA hydrogels (12.2 kPa) grafted with each oligopeptide showed higher pluripotency, as assessed by Oct4 and Nanog expression, than hAFSCs grown on stiff PVA hydrogels (25.3 kPa) grafted with the same oligopeptides and a much higher pluripotency than those grown on rigid tissue-culture polystyrene dishes. Soft biomaterials appeared to be adequate to maintain the pluripotency of hAFSCs. Surprisingly, hAFSCs that showed higher pluripotency on PVA hydrogels grafted with oligopeptides derived from fibronectin and vitronectin also expressed higher levels of early differentiation markers for three germ layers in expansion medium. This result suggests that hAFSCs are heterogeneous and that this population contains highly pluripotent stem cells and stem cells that can be easily differentiated

Dominance of Tau Burden in Cortical Over Subcortical Regions Mediates Glymphatic Activity and Clinical Severity in PSP

Background: Progressive supranuclear palsy (PSP) is a tauopathy that involves subcortical regions but also extends to cortical areas. The clinical impact of different tau protein sites and their influence on glymphatic dysfunction have not been investigated. Patients and Methods: Participants (n = 55; 65.6 ± 7.1 years; 29 women) with PSP (n = 32) and age-matched normal controls (NCs; n = 23) underwent 18F-Florzolotau tau PET, MRI, PSP Rating Scale (PSPRS), and Mini-Mental State Examination. Cerebellar gray matter (GM) and parametric estimation of reference signal intensity were used as references for tau burden measured by SUV ratios. Glymphatic activity was measured by diffusion tensor image analysis along the perivascular space (DTI-ALPS). Results: Parametric estimation of reference signal intensity is a better reference than cerebellar GM to distinguish tau burden between PSP and NCs. PSP patients showed higher cortical and subcortical tau SUV ratios than NCs (P < 0.001 and <0.001). Cortical and subcortical tau deposition correlated with PSPRS, UPDRS, and Mini-Mental State Examination scores (all P’s < 0.05). Cortical tau deposition was further associated with the DTI-ALPS index and frontal-temporal-parietal GM atrophy. The DTI-ALPS indexes showed a significantly negative correlation with the PSPRS total scores (P < 0.01). Finally, parietal and occipital lobe tau depositions showed mediating effects between the DTI-ALPS index and PSPRS score. Conclusions: Cortical tau deposition is associated with glymphatic dysfunction and plays a role in mediating glymphatic dysfunction and clinical severity. Our results provide a possible explanation for the worsening of clinical severity in patients with PSP