The infection process of Colletotrichum truncatum on lentil

The fungus Colletotrichum truncatum (Schw.) Andrus and Moore causes lentil anthracnose, which is a major challenge to lentil production in Western Canada. The pathogen infects leaves and stems, resulting in defoliation, stem girdling, plant wilting, and possibly plant death. Two races, Ct0 and Ct1, have been identified in the pathogen population in Canada. However, the differences in the infection process between the two races have not been described in detail. Currently, several lentil cultivars, such as CDC Redberry, CDC Robin, CDC Rosetown, CDC Rouleau, and CDC Viceroy, have resistance against race Ct1, whereas there are no cultivars showing resistance to race Ct0. The objective of this study was to investigate differences in the infection process between race Ct0 and race Ct1 using the fully susceptible cultivar Eston and the race Ct1-resistant cultivar CDC Robin. Experiments on glass well slides showed that race Ct0 had no inherently different conidium germination rate compared to race Ct1, and that differences in conidium germination between the two races on lentil plants were the result of specific interactions between the two races and lentil resistance. Investigations of the infection process of the two races on detached and attached leaves of both lentil cultivars were conducted starting 12 h postinoculation (hpi) until 72 hpi, including conidium germination, appressorium formation, and leaf penetration. Results indicated that differences in virulence of the two races may be related to the ability of conidia to germinate and form appressoria, as well as the ability of primary infection hyphae to grow in response to cues from the lentil cultivars. Furthermore, resistance of lentil to isolates of race Ct1 appeared to involve an inhibition in and/or delay of the spread of primary infection hyphae inside the plant tissue. Results of infection studies of one isolate from each race on attached leaves did not completely agree with results of the same isolates on detached leaves. Based on this study, race Ct0 and race Ct1 do not appear to be classical physiological races, but may represent aggressive races or some intermediate forms

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

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

17β-Estradiol Enhances Breast Cancer Cell Motility and Invasion via Extra-Nuclear Activation of Actin-Binding Protein Ezrin

Estrogen promotes breast cancer metastasis. However, the detailed mechanism remains largely unknown. The actin binding protein ezrin is a key component in tumor metastasis and its over-expression is positively correlated to the poor outcome of breast cancer. In this study, we investigate the effects of 17β-estradiol (E2) on the activation of ezrin and its role in estrogen-dependent breast cancer cell movement. In T47-D breast cancer cells, E2 rapidly enhances ezrin phosphorylation at Thr567 in a time- and concentration-dependent manner. The signalling cascade implicated in this action involves estrogen receptor (ER) interaction with the non-receptor tyrosine kinase c-Src, which activates the phosphatidylinositol-3 kinase/Akt pathway and the small GTPase RhoA/Rho-associated kinase (ROCK-2) complex. E2 enhances the horizontal cell migration and invasion of T47-D breast cancer cells in three-dimensional matrices, which is reversed by transfection of cells with specific ezrin siRNAs. In conclusion, E2 promotes breast cancer cell movement and invasion by the activation of ezrin. These results provide novel insights into the effects of estrogen on breast cancer progression and highlight potential targets to treat endocrine-sensitive breast cancers