Telepath: Understanding Users from a Human Vision Perspective in Large-Scale Recommender Systems

Designing an e-commerce recommender system that serves hundreds of millions of active users is a daunting challenge. From a human vision perspective, there're two key factors that affect users' behaviors: items' attractiveness and their matching degree with users' interests. This paper proposes Telepath, a vision-based bionic recommender system model, which understands users from such perspective. Telepath is a combination of a convolutional neural network (CNN), a recurrent neural network (RNN) and deep neural networks (DNNs). Its CNN subnetwork simulates the human vision system to extract key visual signals of items' attractiveness and generate corresponding activations. Its RNN and DNN subnetworks simulate cerebral cortex to understand users' interest based on the activations generated from browsed items. In practice, the Telepath model has been launched to JD's recommender system and advertising system. For one of the major item recommendation blocks on the JD app, click-through rate (CTR), gross merchandise value (GMV) and orders have increased 1.59%, 8.16% and 8.71% respectively. For several major ads publishers of JD demand-side platform, CTR, GMV and return on investment have increased 6.58%, 61.72% and 65.57% respectively by the first launch, and further increased 2.95%, 41.75% and 41.37% respectively by the second launch.Comment: 8 pages, 11 figures, 1 tabl

Functional complementation between FADD and RIP1 in embryos and lymphocytes.

FADD is a common adaptor shared by several death receptors for signalling apoptosis through recruitment and activation of caspase 8 (refs 1-3). Death receptors are essential for immune homeostasis, but dispensable during embryogenesis. Surprisingly, Fadd(-/-) mice die in utero and conditional deletion of FADD leads to impaired lymphocyte proliferation. How FADD regulates embryogenesis and lymphocyte responses has been a long-standing enigma. FADD could directly bind to RIP1 (also known as RIPK1), a serine/threonine kinase that mediates both necrosis and NF-κB activation. Here we show that Fadd(-/-) embryos contain raised levels of RIP1 and exhibit massive necrosis. To investigate a potential in vivo functional interaction between RIP1 and FADD, null alleles of RIP1 were crossed into Fadd(-/-) mice. Notably, RIP1 deficiency allowed normal embryogenesis of Fadd(-/-) mice. Conversely, the developmental defect of Rip1(-/-) lymphocytes was partially corrected by FADD deletion. Furthermore, RIP1 deficiency fully restored normal proliferation in Fadd(-/-) T cells but not in Fadd(-/-) B cells. Fadd(-/-)Rip1(-/-) double-knockout T cells are resistant to death induced by Fas or TNF-α and show reduced NF-κB activity. Therefore, our data demonstrate an unexpected cell-type-specific interplay between FADD and RIP1, which is critical for the regulation of apoptosis and necrosis during embryogenesis and lymphocyte function

In vitro and in vivo germ line potential of stem cells derived from newborn mouse skin

We previously reported that fetal porcine skin-derived stem cells were capable of differentiation into oocyte-like cells (OLCs). Here we report that newborn mice skin-derived stem cells are also capable of differentiating into early OLCs. Using stem cells from mice that are transgenic for Oct4 germline distal enhancer-GFP, germ cells resulting from their differentiation are expected to be GFP+. After differentiation, some GFP+ OLCs reached 40-45 μM and expressed oocyte markers. Flow cytometric analysis revealed that ∼0.3% of the freshly isolated skin cells were GFP+. The GFP-positive cells increased to ∼7% after differentiation, suggesting that the GFP+ cells could be of in vivo origin, but are more likely induced upon being cultured in vitro. To study the in vivo germ cell potential of skin-derived cells, they were aggregated with newborn ovarian cells, and transplanted under the kidney capsule of ovariectomized mice. GFP+ oocytes were identified within a subpopulation of follicles in the resulting growth. Our finding that early oocytes can be differentiated from mice skin-derived cells in defined medium may offer a new in vitro model to study germ cell formation and oogenesis. © 2011 Dyce et al

Proteomics-based analysis of differentially expressed proteins in the CXCR1-knockdown gastric carcinoma MKN45 cell line and its parental cell

C-X-C chemokine receptor types 1 (CXCR1), a cell-surface G-protein-coupled receptor has been found to be associated with tumorigenesis, development, and progression of some tumors. Previously, we have found that CXCR1 overexpression is associated with late-stage gastric adenocarcinoma. We also have demonstrated that knockdown of CXCR1 could inhibit cell proliferation in vitro and in vivo. In this study, we compared the changes of protein expression profile between gastric carcinoma MKN45 cell line and CXCR1-knockdown MKN45 cell line by 2D electrophoresis. Among the 101 quantified proteins, 29 spots were significantly different, among which 13 were downregulated and 16 were up-regulated after CXCR1 knockdown. These proteins were further identified by mass spectrometry analysis. Among them, several up-regulated proteins such as hCG2020155, Keratin8, heterogeneous nuclear ribonucleoprotein C (C1/C2), and several downregulated proteins such as Sorcin, heat shock protein 27, serpin B6 isoform b, and heterogeneous nuclear ribonucleoprotein K were confirmed. These proteins are related to cell cycle, the transcription regulation, cell adherence, cellular metabolism, drug resistance, and so on. These results provide an additional support to the hypothesis that CXCR1 might play an important role in proliferation, invasion, metastasis, and prognosis, and drug resistance of gastric carcinoma

Along-strike segmentation of the South China Sea margin imposed by inherited pre-rift basement structures

Multibeam bathymetric, seismic and borehole data are used to investigate a large-scale strike-slip structure, the Baiyun-Liwan Fault Zone, in the northern South China Sea. This fault zone comprises NW- to NE-striking faults and negative flower structures that were generated by oblique extensional displacement. Notably, the interpreted data reveals that the Baiyun-Liwan Fault Zone was active during the Cenozoic, recording intense magmatism, and accommodating significant intraplate deformation during progressive continental rifting and ocean spreading. It bounds two distinct crustal segments and played a significant role in segmenting the northern margin of the South China Sea. The geometry of faults and strata within the Baiyun-Liwan Fault Zone also controlled local sediment routing and depocentre evolution during the Cenozoic. As basement and syn-rift structures change markedly across the Baiyun-Liwan Fault Zone, we propose this structure to be inherited from a lithospheric-scale fault zone separating the Mesozoic arc from forearc-related terrains. We therefore stress the importance of pre-existing structures in the development of rifted margins, with the example provided by the Baiyun-Liwan Fault Zone having profound implications for palaeogeographic reconstructions in the South China Sea. At present, the Baiyun-Liwan Fault Zone is incised by the Pearl River Canyon and eroded by recurrent submarine landslides, forming a major area of sediment bypass towards the abyssal plain

Emerging role of ferroptosis-related circular RNA in tumor metastasis

Tumor metastasis is an important factor that contributes to the poor prognosis of patients with tumors. Therefore, to solve this problem, research on the mechanism of metastasis is essential. Ferroptosis, a new mode of cell death, is characterized by membrane damage due to lipid peroxidation caused by iron overload. Many studies have shown that excessive ferroptosis can affect tumor metastasis and thus inhibit tumor progression. Recently, circular RNA (circRNA), a type of non-coding RNA, has been shown to be associated with the progression of ferroptosis, thus influencing tumor development. However, the specific mechanisms by which circRNAs affect the progression of ferroptosis and their roles in tumor metastasis are not known. In this review, we systematically discuss the role of circRNAs in regulating tumor ferroptosis and their mechanism of action through sponging miRNAS in various tumors, thereby impacting metastasis. This review helps elucidate the relationship and role of ferroptosis-related circRNAs in tumor metastasis and may provide future researchers with new ideas and directions for targeted therapies

HLA-B*35-Px–mediated acceleration of HIV-1 infection by increased inhibitory immunoregulatory impulses

A subset of HLA-B*35 alleles, B*35-Px, are strongly associated with accelerated HIV-1 disease progression for reasons that are not understood. Interestingly, the alternative set of B*35 subtypes, B*35-PY, have no detectable impact on HIV-1 disease outcomes, even though they can present identical HIV-1 epitopes as B*35-Px molecules. Thus, the differential impact of these alleles on HIV-1 disease progression may be unrelated to interactions with HIV-1–specific CD8+ T cells. Here, we show that the B*35-Px molecule B*3503 binds with greater affinity to immunoglobulin-like transcript 4 (ILT4), an inhibitory MHC class I receptor expressed on dendritic cells, than does the B*35-PY molecule B*3501, even though these two B*35 molecules differ by only one amino acid and present identical HIV-1 epitopes. The preferential recognition of B*3503 by ILT4 was associated with significantly stronger dendritic cell dysfunction in in vitro functional assays. Moreover, HIV-1–infected carriers of B*3503 had poor dendritic cell functional properties in ex vivo assessments when compared with carriers of the B*3501 allele. Differential interactions between HLA class I allele subtypes and immunoregulatory MHC class I receptors on dendritic cells thus provide a novel perspective for the understanding of MHC class I associations with HIV-1 disease progression and for the manipulation of host immunity against HIV-1