43 research outputs found
Long noncoding RNA microvascular invasion in hepatocellular carcinoma is an indicator of poor prognosis and a potential therapeutic target in gastric cancer
Background: Long noncoding RNAs (lncRNAs) have been shown to have a fundamental role in cancer initiation and development. LncRNA microvascular invasion in hepatocellular carcinoma (MVIH) has been identified as a potential prognostic marker in several cancers; however, its role in gastric cancer (GC) has not been elucidated.
Materials and Methods: A total of 152 tissue samples from patients underwent GC surgical resection in Linyi People's Hospital between 2007 and 2010 were collected. Quantitative real-time polymerase chain reaction was conducted to examine the expression level of lncRNA MVIH. The selection of clinically important cut-off scores for MVIH expression was based on receiver operating characteristic curve analysis. Then, the association between MVIH and GC clinicopathological parameters was analyzed. Moreover, univariate and multivariate Cox regression analysis were performed to reveal the relationship between MVIH and GC prognosis.
Results: GC tissues exhibited a higher lncRNA MVIH expression level than paired nontumoros tissues. High MVIH level was revealed to be associated with the T stage, tumor-node-metastasis (TNM) stage and lymphatic metastasis of GC. Specially, patients with high MVIH expression level showed significantly shorter overall survival rate and progression-free survival rate. Moreover, invasion depth, distant metastasis, TNM stage, and MVIH expression were identified as risk factors of GC poor prognosis on univariate Cox regression analyses. By further analyzing these factors with multivariate logistic regression, high MVIH, and distant metastasis were discovered to be independent risk factors of GC prognosis.
Conclusions: High MVIH is an independent risk factor of GC prognosis. LncRNA MVIH may serve as a potential therapeutic target and a prognostic marker of GC patients
Carbon Emission Estimation of Assembled Composite Concrete Beams during Construction
At present, the issue of carbon emissions from buildings has become a hot topic, and carbon emission reduction is also becoming a political and economic contest for countries. As a result, the government and researchers have gradually begun to attach great importance to the industrialization of low-carbon and energy-saving buildings. The rise of prefabricated buildings has promoted a major transformation of the construction methods in the construction industry, which is conducive to reducing the consumption of resources and energy, and of great significance in promoting the low-carbon emission reduction of industrial buildings. This article mainly studies the calculation model for carbon emissions of the three-stage life cycle of component production, logistics transportation, and on-site installation in the whole construction process of composite beams for prefabricated buildings. The construction of CG-2 composite beams in Fujian province, China, was taken as the example. Based on the life cycle assessment method, carbon emissions from the actual construction process of composite beams were evaluated, and that generated by the composite beam components during the transportation stage by using diesel, gasoline, and electric energy consumption methods were compared in detail. The results show that (1) the carbon emissions generated by composite beams during the production stage were relatively high, accounting for 80.8% of the total carbon emissions, while during the transport stage and installation stage, they only accounted for 7.6% and 11.6%, respectively; and (2) during the transportation stage with three different energy-consuming trucks, the carbon emissions from diesel fuel trucks were higher, reaching 186.05 kg, followed by gasoline trucks, which generated about 115.68 kg; electric trucks produced the lowest, only 12.24 kg
Viral Perturbation of Alternative Splicing of a Host Transcript Benefits Infection.
Pathogens disturb alternative splicing patterns of infected eukaryotic hosts. However, in plants it is unknown if this is incidental to infection or represents a pathogen-induced remodeling of host gene expression needed to support infection. Here, we compared changes in transcription and protein accumulation with changes in transcript splicing patterns in maize (Zea mays) infected with the globally important pathogen sugarcane mosaic virus (SCMV). Our results suggested that changes in alternative splicing play a major role in determining virus-induced proteomic changes. Focusing on maize phytoene synthase1 (ZmPSY1), which encodes the key regulatory enzyme in carotenoid biosynthesis, we found that although SCMV infection decreases total ZmPSY1 transcript accumulation, the proportion of splice variant T001 increases by later infection stages so that ZmPSY1 protein levels are maintained. We determined that ZmPSY1 has two leaf-specific transcripts, T001 and T003, distinguished by differences between the respective 3'-untranslated regions (UTRs). The shorter 3'-UTR of T001 makes it the more efficient mRNA. Nonsense ZmPSY1 mutants or virus-induced silencing of ZmPSY1 expression suppressed SCMV accumulation, attenuated symptoms, and decreased chloroplast damage. Thus, ZmPSY1 acts as a proviral host factor that is required for virus accumulation and pathogenesis. Taken together, our findings reveal that SCMV infection-modulated alternative splicing ensures that ZmPSY1 synthesis is sustained during infection, which supports efficient virus infection
Viral Perturbation of Alternative Splicing of a Host Transcript Benefits Infection.
Pathogens disturb alternative splicing patterns of infected eukaryotic hosts. However, in plants it is unknown if this is incidental to infection or represents a pathogen-induced remodeling of host gene expression needed to support infection. Here, we compared changes in transcription and protein accumulation with changes in transcript splicing patterns in maize (Zea mays) infected with the globally important pathogen sugarcane mosaic virus (SCMV). Our results suggested that changes in alternative splicing play a major role in determining virus-induced proteomic changes. Focusing on maize phytoene synthase1 (ZmPSY1), which encodes the key regulatory enzyme in carotenoid biosynthesis, we found that although SCMV infection decreases total ZmPSY1 transcript accumulation, the proportion of splice variant T001 increases by later infection stages so that ZmPSY1 protein levels are maintained. We determined that ZmPSY1 has two leaf-specific transcripts, T001 and T003, distinguished by differences between the respective 3'-untranslated regions (UTRs). The shorter 3'-UTR of T001 makes it the more efficient mRNA. Nonsense ZmPSY1 mutants or virus-induced silencing of ZmPSY1 expression suppressed SCMV accumulation, attenuated symptoms, and decreased chloroplast damage. Thus, ZmPSY1 acts as a proviral host factor that is required for virus accumulation and pathogenesis. Taken together, our findings reveal that SCMV infection-modulated alternative splicing ensures that ZmPSY1 synthesis is sustained during infection, which supports efficient virus infection
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Maize phenylalanine ammonia-lyases contribute to resistance to Sugarcane mosaic virus infection, most likely through positive regulation of salicylic acid accumulation.
Sugarcane mosaic virus (SCMV) is a pathogen of worldwide importance that causes dwarf mosaic disease on maize (Zea mays). Until now, few maize genes/proteins have been shown to be involved in resistance to SCMV. In this study, we characterized the role of maize phenylalanine ammonia-lyases (ZmPALs) in accumulation of the defence signal salicylic acid (SA) and in resistance to virus infection. SCMV infection significantly increased SA accumulation and expression of SA-responsive pathogenesis-related protein genes (PRs). Interestingly, exogenous SA treatment decreased SCMV accumulation and enhanced resistance. Both reverse transcription-coupled quantitative PCR and RNA-Seq data confirmed that expression levels of at least four ZmPAL genes were significantly up-regulated upon SCMV infection. Knockdown of ZmPAL expression led to enhanced SCMV infection symptom severity and virus multiplication, and simultaneously resulted in decreased SA accumulation and PR gene expression. Intriguingly, application of exogenous SA to SCMV-infected ZmPAL-silenced maize plants decreased SCMV accumulation, showing that ZmPALs are required for SA-mediated resistance to SCMV infection. In addition, lignin measurements and metabolomic analysis showed that ZmPALs are also involved in SCMV-induced lignin accumulation and synthesis of other secondary metabolites via the phenylpropanoid pathway. In summary, our results indicate that ZmPALs are required for SA accumulation in maize and are involved in resistance to virus infection by limiting virus accumulation and moderating symptom severity
Knockdown of <i>CCP1</i> in maize plants compromises SA biosynthesis and decreases <i>ZmPR1</i> and <i>ZmPR5</i> expressions.
A) Appearance of maize plants silenced for CCP1 gene expression at 7 dpi. B) The contents of SA in the CMV-CCP1-inoculated or the CMV-GUS-inoculated maize plants at 7 d post challenge inoculation with SCMV or Mock. C) and D) Relative expression of ZmPR1 (C) and ZmPR5 (D) in the CMV-CCP1-inoculated or the CMV-GUS-inoculated maize plants. Three independent experiments were conducted with at least three biological replicates per treatment. Error bars represented the means ±SE. Significant differences between CMV-GUS and CMV-CCP1 infected plants are indicated (*, P P P P t test analysis.</p
The double mutant virus SCMV-NIa-Pro<sub>K230A, D234A</sub>-GFP fails to induce CCP1 gene expression and activates PLCP activity.
A) RT-qPCR analysis of the relative accumulation levels of SCMV RNA in the SCMV-GFP- or SCMV-NIa-ProK230A, D234A-GFP- infected first systemically leaves at 8 dpi. B) Immunoblotting analysis of SCMV CP accumulation in the first systemically infected maize leaves. C) RT-qPCR analysis of the relative accumulation levels of CCP1 in the mock, SCMV-GFP- or SCMV-NIa-ProK230A, D234A-GFP- infected first systemically leaves. D) Immunoblotting analysis of CCP1 accumulation and activity-based protein profiling (ABPP) analysis of the protease activities of maize PLCPs in the first systemically infected leaves at 8 dpi. E) The contents of SA in the mock, SCMV-GFP- or SCMV-NIa-ProK230A, D234A-GFP- infected first systemically leaves. F) RT-qPCR analysis of the relative accumulation levels of PR1 and PR5 in the mock, SCMV-GFP- or SCMV-NIa-ProK230A, D234A-GFP- infected first systemically leaves. Error bars represent the means ± SE. Statistical differences (*, P P P P t test analysis. Three independent experiments are conducted.</p
Excel spreadsheet containing, in separate sheets, the underlying numerical data and statistical analysis for Figs 1A, 1D, 1E, 2B, 2E, 3B, 3C, 3D, 5A, 5D, 7B, 7C, 8A, 8C, 8E, 8F, S1A, S1B, S3, S4, S5A, S5B, S5C and S5D.
Excel spreadsheet containing, in separate sheets, the underlying numerical data and statistical analysis for Figs 1A, 1D, 1E, 2B, 2E, 3B, 3C, 3D, 5A, 5D, 7B, 7C, 8A, 8C, 8E, 8F, S1A, S1B, S3, S4, S5A, S5B, S5C and S5D.</p