Shanghai Jiao Tong University

About: Shanghai Jiao Tong University is a education organization based out in Shanghai, Shanghai, China. It is known for research contribution in the topics: Population & Cancer. The organization has 157524 authors who have published 184620 publications receiving 3451038 citations. The organization is also known as: Shanghai Communications University & Shanghai Jiaotong University.

Transcription Factor Sp1 Expression Is a Significant Predictor of Survival in Human Gastric Cancer

Abstract: The transcription factor Sp1 regulates the expression of multiple genes. However, its expression and role in human tumor development and progression remain unclear. Using immunohistochemistry, we investigated Sp1 expression patterns in 86 cases of human gastric cancer having various clinicopathologic characteristics, 57 normal gastric tissue specimens, and 53 lymph node metastases. We found that Sp1 protein was expressed predominantly in the nuclei of cells located in the mucous neck region, whereas Sp1 expression was not detected either in the cells located toward the gastric pit (foveolar differentiation) or cells of the glandular epithelium (glandular differentiation). In sharp contrast, strong Sp1 expression was detected in tumor cells, whereas no or very weak Sp1 expression was detected in stromal cells and normal glandular cells surrounding or within the tumors. We also evaluated the effect of Sp1 expression on the survival of patients who have undergone surgical resection. The median survival duration in patients who had a tumor with negative, weak, and strong Sp1 expression was 43, 37, and 8 months, respectively (P = 0.0075). Next, Sp1 expression, stage, completeness of resection, age, and sex were entered into a Cox proportional hazard model. In multivariate analysis, Sp1 (P = 0.003) and stage (P < 0.001) were independently prognostic of survival. Therefore, normal and malignant gastric tissues have unique Sp1 expression patterns. Given the importance of Sp1 in the expression of multiple molecules key to tumor cell survival, growth, and angiogenesis, its disregulated expression and activation may play important roles in gastric cancer development and progression.

Effect of Cetane Number Improver on Heat Release Rate and Emissions of High Speed Diesel Engine Fueled with Ethanol-Diesel Blend Fuel

Abstract: The influence of cetane number improver on heat release rate and emissions of a high-speed diesel engine fueled with ethanol-diesel blend fuel was investigated.Different percentages of cetane number enhancer(0~0_0,0.2~0_0,0.4~0_0) were added to blends,and the engine tests were performed on a high speed diesel engine.The results show that the engine power decreases slightly; the thermal efficiency improves remarkably,and the NO_x and smoke emissions decrease simultaneously when diesel engine is fueled with blends.Besides, the engine power can be recovered,NO_x and smoke emissions are further reduced when cetane number improver is added to blends.By the combustion analysis,it can be found that the ignition delay prolongs;the total combustion duration shortens,and the maximum heat release rate increases for ethanol-diesel blend fuel when compared to diesel fuel; in addition,the combustion characteristics of ethanol-diesel blend fuel at large load may be recovered to diesel fuel by cetane number improver. However a large difference still exists at lower load.

Content-Centric Sparse Multicast Beamforming for Cache-Enabled Cloud RAN

Abstract: This paper presents a content-centric transmission design in a cloud radio access network (cloud RAN) by incorporating multicasting and caching. Users requesting a same content form a multicast group and are served by a same cluster of base stations (BSs) cooperatively. Each BS has a local cache and it acquires the requested contents either from its local cache or from the central processor (CP) via backhaul links. We investigate the dynamic content-centric BS clustering and multicast beamforming with respect to both channel condition and caching status. We first formulate a mixed-integer nonlinear programming problem of minimizing the weighted sum of backhaul cost and transmit power under the quality-of-service constraint for each multicast group. Theoretical analysis reveals that all the BSs caching a requested content can be included in the BS cluster of this content, regardless of the channel conditions. Then we reformulate an equivalent sparse multicast beamforming (SBF) problem. By adopting smoothed $\ell_0$-norm approximation and other techniques, the SBF problem is transformed into the difference of convex (DC) programs and effectively solved using the convex-concave procedure algorithms. Simulation results demonstrate significant advantage of the proposed content-centric transmission. The effects of three heuristic caching strategies are also evaluated.

METTL3-mediated N6-methyladenosine modification is critical for epithelial-mesenchymal transition and metastasis of gastric cancer

Abstract: As one of the most frequent chemical modifications in eukaryotic mRNAs, N6-methyladenosine (m6A) modification exerts important effects on mRNA stability, splicing, and translation. Recently, the regulatory role of m6A in tumorigenesis has been increasingly recognized. However, dysregulation of m6A and its functions in tumor epithelial-mesenchymal transition (EMT) and metastasis remain obscure. qRT-PCR and immunohistochemistry were used to evaluate the expression of methyltransferase-like 3 (METTL3) in gastric cancer (GC). The effects of METTL3 on GC metastasis were investigated through in vitro and in vivo assays. The mechanism of METTL3 action was explored through transcriptome-sequencing, m6A-sequencing, m6A methylated RNA immunoprecipitation quantitative reverse transcription polymerase chain reaction (MeRIP qRT-PCR), confocal immunofluorescent assay, luciferase reporter assay, co-immunoprecipitation, RNA immunoprecipitation and chromatin immunoprecipitation assay. Here, we show that METTL3, a major RNA N6-adenosine methyltransferase, was upregulated in GC. Clinically, elevated METTL3 level was predictive of poor prognosis. Functionally, we found that METTL3 was required for the EMT process in vitro and for metastasis in vivo. Mechanistically, we unveiled the METTL3-mediated m6A modification profile in GC cells for the first time and identified zinc finger MYM-type containing 1 (ZMYM1) as a bona fide m6A target of METTL3. The m6A modification of ZMYM1 mRNA by METTL3 enhanced its stability relying on the “reader” protein HuR (also known as ELAVL1) dependent pathway. In addition, ZMYM1 bound to and mediated the repression of E-cadherin promoter by recruiting the CtBP/LSD1/CoREST complex, thus facilitating the EMT program and metastasis. Collectively, our findings indicate the critical role of m6A modification in GC and uncover METTL3/ZMYM1/E-cadherin signaling as a potential therapeutic target in anti-metastatic strategy against GC.