Personalized Music Recommendation Based on Style Type

As Internet industry constantly develops and the computer penetration rate continues to grow, the number of online music platforms and music users has been able to increase year by year. With that comes more music choices, information overload has become a very prominent problem. Therefore, how to make users choose their favorite music more conveniently is one of the most challenging problems faced by online music recommendation systems. This paper bases on the existing recommendation system research and uses the collaborative filtering algorithm, proposes a music recommendation method from three perspectives: user attributes, music types and time migration. It is found that the online music recommendation from these three perspectives has a good effect, which can provide a reference for the construction of the current online music recommendation system and is also helpful to platform management practice

Vps41, a protein involved in lysosomal trafficking, interacts with caspase-8

Caspase-8 is a member of the cysteine-aspartic acid protease (caspase) family which plays a central role in apoptosis and development. We screened caspase-8 interacting proteins from mouse T-cell lymphoma and 7.5-day embryo cDNA libraries by yeast two-hybrid system and obtained eleven positive clones, including Vacuolar protein sorting 41 (Vps41), a protein involved in trafficking of proteins from the late Golgi to the vacuole. The interaction of Vps41 with caspase-8 was confirmed by co-immunoprecipitation (co-IP) and co-localization studies in HEK293T cells. Co-IP experiments also showed that Vps41 binds to the p18 subunit of caspase-8 through its WD40 region and RING-finger motif. Furthermore, we found that overexpression of Vps41 promotes Fas-induced apoptosis in A549 human lung adenocarcinoma cells. The cleavage of caspase-3, a caspase-8 downstream effector, was increased when cells were transfected with Vps41-overexpressing plasmid. Together, these results suggest a novel interaction of caspase-8 with Vps41 and provide a potential role of Vps41 beyond lysosomal trafficking

Perilipin1 deficiency in whole body or bone marrow-derived cells attenuates lesions in atherosclerosis-prone mice.

The objective of this study is to determine the role of perilipin 1 (Plin1) in whole body or bone marrow-derived cells on atherogenesis.Accumulated evidence have indicated the role of Plin1 in atherosclerosis, however, these findings are controversial. In this study, we showed that Plin1 was assembled and colocalized with CD68 in macrophages in atherosclerotic plaques of ApoE-/- mice. We further found 39% reduction of plaque size in the aortic roots of Plin1 and ApoE double knockout (Plin1-/-ApoE-/-) females compared with ApoE-/- female littermates. In order to verify whether this reduction was macrophage-specific, the bone marrow cells from wild-type or Plin1 deficient mice (Plin1-/-) were transplanted into LDL receptor deficient mice (LDLR-/-). Mice receiving Plin1-/- bone marrow cells showed also 49% reduction in aortic atherosclerotic lesions compared with LDLR-/- mice received wild-type bone marrow cells. In vitro experiments showed that Plin1-/- macrophages had decreased protein expression of CD36 translocase and an enhanced cholesterol ester hydrolysis upon aggregated-LDL loading, with unaltered expression of many other regulators of cholesterol metabolism, such as cellular lipases, and Plin2 and 3. Given the fundamental role of Plin1 in protecting LD lipids from lipase hydrolysis, it is reasonably speculated that the assembly of Plin1 in microphages might function to reduce lipolysis and hence increase lipid retention in ApoE-/- plaques, but this pro-atherosclerotic property would be abrogated on inactivation of Plin1.Plin1 deficiency in bone marrow-derived cells may be responsible for reduced atherosclerotic lesions in the mice

ATF3 induction prevents precocious activation of skeletal muscle stem cell by regulating H2B expression

Abstract Skeletal muscle stem cells (also called satellite cells, SCs) are important for maintaining muscle tissue homeostasis and damage-induced regeneration. However, it remains poorly understood how SCs enter cell cycle to become activated upon injury. Here we report that AP-1 family member ATF3 (Activating Transcription Factor 3) prevents SC premature activation. Atf3 is rapidly and transiently induced in SCs upon activation. Short-term deletion of Atf3 in SCs accelerates acute injury-induced regeneration, however, its long-term deletion exhausts the SC pool and thus impairs muscle regeneration. The Atf3 loss also provokes SC activation during voluntary exercise and enhances the activation during endurance exercise. Mechanistically, ATF3 directly activates the transcription of Histone 2B genes, whose reduction accelerates nucleosome displacement and gene transcription required for SC activation. Finally, the ATF3-dependent H2B expression also prevents genome instability and replicative senescence in SCs. Therefore, this study has revealed a previously unknown mechanism for preserving the SC population by actively suppressing precocious activation, in which ATF3 is a key regulator

MyoD- and FoxO3-mediated hotspot interaction orchestrates super-enhancer activity during myogenic differentiation

Super-enhancers (SEs) are cis-regulatory elements enriching lineage specific key transcription factors (TFs) to form hotspots. A paucity of identification and functional dissection promoted us to investigate SEs during myoblast differentiation. ChIP-seq analysis of histone marks leads to the uncovering of SEs which remodel progressively during the course of differentiation. Further analyses of TF ChIP-seq enable the definition of SE hotspots co-bound by the master TF, MyoD and other TFs, among which we perform in-depth dissection for MyoD/FoxO3 interaction in driving the hotspots formation and SE activation. Furthermore, using Myogenin as a model locus, we elucidate the hierarchical and complex interactions among hotspots during the differentiation, demonstrating SE function is propelled by the physical and functional cooperation among hotspots. Finally, we show MyoD and FoxO3 are key in orchestrating the Myogenin hotspots interaction and activation. Altogether our results identify muscle-specific SEs and provide mechanistic insights into the functionality of SE

Plasma cholesterol, triglyceride and body weight in ApoE-/- and Plin1-/-ApoE-/-mice after 12 weeks on western diet.

<p>*<i>p</i><0.05 for Plin1<b>-/-</b>ApoE<b>-/-</b> vs. ApoE<b>-/-</b>.</p><p>Plasma cholesterol, triglyceride and body weight in ApoE-/- and Plin1-/-ApoE-/-mice after 12 weeks on western diet.</p

The bone marrow cells from male Plin1-/- mice transplanted to female LDLR-/- mice reduce atherosclerotic lesion.

<p>(A) Representative photographs of aortic roots from LDLR<b>-/-</b> mice received bone marrow cells from Plin1+/+ and Plin1<b>-/-</b> mice respectively. (B) The mean lesion area (±SEM) in the aortic roots in mice transplanted with bone marrow cells from Plin1+/+ or Plin1<b>-/-</b> mice. ** <i>p</i> < 0.01 for Plin-/- vs. Plin+/+.</p

The cholesterol metabolism in macrophages.

<p>(A) Immunoblotting of CD36 and ABCA1 in peritoneal macrophages and foam cells and (B) The density of the protein band was quantitated. (C) Immunoblotting of HSL and ATGL in peritoneal macrophages and foam cells and (D) the density of the protein bands was quantitated. (E) The rate of cholesterol ester hydrolysis in peritoneal macrophages from Plin1+/+ and Plin1<b>-/-</b> mice. (F) Time-course of cholesterol efflux to ApoA-I in peritoneal macrophages from Plin1+/+ and Plin1<b>-/-</b> mice. * <i>p</i> < 0.05, ** <i>p</i> < 0.01 for Plin-/- vs. Plin+/+.</p