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Hydropower is the largest renewable source of electricity generation. However, the construction and operation of hydropower plants may cause significant material footprints. This study provides a systems accounting framework for evaluating the life-cycle material footprint of a hydropower plant. It is based on the hybrid method as a combination of the process analysis and the input-output analysis. A case study for a typical pumped storage hydropower plant (NPSHP) is carried out to demonstrate the framework. 12 metals (bauxite and aluminum ores, copper ores, gold ores, iron ores, lead ores, nickel ores, PGM ores, silver ores, tin ores, uranium and thorium ores, zinc ores, and other non-ferrous metal ores) and 8 minerals (building stones, chemical and fertilizer minerals, clays and kaolin, gravel and sand, limestone & gypsum & chalk & dolomite, salt, slate, and other minerals) are included. The results can be helpful to promote a sustainable energy transition by incorporating material planetary boundaries into renewable energy systems.

The genomic variant features (mutations, deletions, structural variants, etc.) within gastric cancer impact its evolution and immunogenicity. The tumor has developed several coping strategies to respond to these changes by DNA repair and replication (DRR). However, the intrinsic relationship between the associated DRR-related genes and gastric cancer progression remained unknown. This study selected DRR-related genes with tumor mutation burden based on the TCGA (The Cancer Genome Atlas) database of gastric cancer transcriptome and mutation data. The prognosis model of seven genes (LAMA2, CREB3L3, SELP, ABCC9, CYP1B1, CDH2, and GAMT) was constructed by a univariate and LASSO regression analysis and divided into high-risk and low-risk groups with the median risk score. Survival analysis showed that overall survival (OS) was lower in the high-risk group than that in the low-risk group. Moreover, patients with gastric cancer in the high-risk group have worse survival in different subgroups, including age, gender, histological grade, and TNM stage. The nomogram that included risk scores for DRR-related genes could accurately foresee OS of patients with gastric cancer. Interestingly, the tumor mutation burden score was higher in the low-risk group than that in the high-risk group, and the risk score for DRR-related genes was negatively correlated with tumor mutation burden in gastric cancer. Next, we further combined the risk score and tumor mutation burden to evaluate the prognosis of gastric cancer patients. The low-risk cohort had a better prognosis than the high-risk cohort in the high tumor mutation burden subgroup. The number of mutation types in the high-risk group was lower than that in the low-risk group. In the immune microenvironment of gastric cancer, more naïve B cells, memory resting CD4+ T cells, Treg cells, monocytes cells, and resting mast cells were infiltrated in the high-risk group. At last, PD-L1 and IAP expressions were negatively correlated with the risk scores; patients with gastric cancer in the low-risk group showed better immunotherapy outcomes than those in the high-risk group. Overall, the DRR-related gene signature based on tumor mutation burden is a novel biomarker for prognostic and immunotherapy response in patients with gastric cancer.

Background. Colorectal cancer (CRC) is the third most common tumor worldwide. Aberrant N6-methyladenosine (m6A) modification can influence the progress of the CRC. Additionally, long noncoding RNA (lncRNA) plays a critical role in CRC and has a close relationship with m6A modification. However, the prognostic potential of m6A-related lncRNAs in CRC patients still remains to be clarified. Methods. We use “limma” R package, “glmnet” R package, and “survival” R package to screen m6A-related-lncRNAs with prognostic potential. Then, we comprehensively analysed and integrated the related lncRNAs in different TNM stages from TCGA database using the LASSO Cox regression. Meanwhile, the relationship between functional enrichment of m6A-related lncRNAs and immune microenvironment in CRC was also investigated using the TCGA database. A prognostic model was constructed and validated to determine the association between m6A-related lncRNAs in different TNM stages and the prognosis of CRC. Result. We demonstrated that three related m6A lncRNAs in different TNM stages were associated with the prognosis of CRC patients. Patients from the TCGA database were classified into the low-risk and the high-risk groups based on the expression of these lncRNAs. The patients in the low-risk group had longer overall survival than the patients in the high-risk group ( P < 0.001 ). We further constructed and validated a prognostic nomogram based on these genes with a C-index of 0.80. The receiver operating characteristic curves confirmed the predictive capacity of the model. Meanwhile, we also found that the low-risk group has the correlation with the dendritic cell (DC). Finally, we discovered the relationship between the m6A regulators and the three lncRNAs. Conclusion. The prognostic model based on three m6A-related lncRNAs exhibits superior predictive performance, providing a novel prognostic model for the clinical evaluation of CRC patients.

Acquired resistance to BRAF inhibitor vemurafenib is frequently observed in metastatic colorectal cancer (CRC), and it is a thorny issue that results in treatment failure. As adaptive responses for vemurafenib treatment, a series of cellular bypasses are response for the adaptive feedback reactivation of ERK signaling, which warrant further investigation.We identified ARF1 (ADP-ribosylation factor 1) as a novel regulator of both vemurafenib resistance and cancer metastasis, its molecular mechanism and potential inhibitor were investigated in this study.DIA-based quantitative proteomics and RNA-seq were performed to systematic analyze the profiling of vemurafenib-resistant RKO cells (RKO-VR) and highly invasive RKO cells (RKO-I8), respectively. Co‑immunoprecipitation assay was performed to detect the interaction of ARF1 and IQGAP1 (IQ-domain GTPase activating protein 1). An ELISA-based drug screen system on FDA-approved drug library was established to screen the compounds against the interaction of ARF1-IQGAP1.The biological functions of ARF1 and LY2835219 were determined by transwell, western blotting, Annexin V-FITC/PI staining and in vivo experimental metastasis assays.We found that ARF1 strongly interacted with IQGAP1 to activate ERK signaling in VR and I8 CRC cells. Deletion of IQGAP1 or inactivation of ARF1 (ARF-T48S) restored the invasive ability induced by ARF1. As ARF1-IQGAP1 interaction is essential for ERK activation, we screened LY2835219 as novel inhibitor of ARF1-IQGAP1 interaction, which inactivated ERK signaling and suppressed CRC metastasis and vemurafenib-resistance in vitro and in vivo with no observed side effect. Furthermore, LY2835219 in combined treatment with vemurafenib exerted significantly inhibitory effect on ARF1-mediated cancer metastasis than used independently.This study uncovers that ARF1-IQGAP1 interaction-mediated ERK signaling reactivation is critical for vemurafenib resistance and cancer metastasis, and that LY2835219 is a promising therapeutic agent for CRC both as a single agent and in combination with vemurafenib.

Hyaluronic acid (HA) intra-articular injection after arthroscopic knee surgery has been widely applied but its efficacy and safety remain controversial. The aim of this systematic review is to analyze the efficacy and safety of HA intra-articular injection after arthroscopic knee surgery, and to compare the efficacy of HA with different molecular weights.We conducted a systematic literature search in PubMed, Embase, Google scholar and the Cochrane library from inception to 16 September 2022 for English-written articles, in order to identify randomized controlled trials that evaluated the clinical efficacy and/or safety of HA intra-articular injection after arthroscopic knee surgery. Then we meta-analyzed the outcomes of patients given intra-articular HA injections postoperatively and control patients. We also evaluated the influence of HA with different molecular weights. In every calculation, sensitive analysis was performed. The visual analogue scale (VAS) for pain, Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) and adverse events were selected as the primary outcome measurements, while Lysholm, International Knee Documentation Committee (IKDC) and Tegner score were selected as the secondary outcome measurements. Publication bias of every outcome was evaluated using egger test.Fifteen studies involving 951 knees were included and 12 of them were used to performed the meta-analysis. The results showed no significant difference between the HA group and control group according to VAS, whether assessed at less (P = 0.90) or more than 6 months (P = 0.55). Besides, there were no statistical differences between the HA group and control group according to subgroup analysis (Ps = 0.77, 0.91 and 0.81 in anterior cruciate ligament reconstruction, meniscectomy and overall groups, respectively). Compared to control group, the overall effect of WOMAC score showed no significant differences (P = 0.25), nor did in two subgroups (P = 0.37 and P = 0.22). Outcomes measured by Lysholm (P = 0.13), IKDC (P = 0.86) and Tegner (P = 0.42) scores showed no significant differences, either. The analysis of the risk of adverse events indicated no increase in HA groups (P = 0.06). We found no significant differences between high- and low-molecular-weight HA at 6 (P = 0.96) or 12 months (P = 0.93) postoperatively. Two studies failed to pass the sensitive analysis and the reasons were discussed detailly and acceptable publication bias was observed.Although HA injection after arthroscopic knee surgery is safe, the available evidence does not support its efficacy in pain relief and functional recovery. Therefore, the application of HA injection after arthroscopic knee surgery is not recommended.

Background: An increasing number of studies had shown that tertiary lymphoid structure (TLS) plays an important role in tumor progression. However, the prognostic role of TLS in various tumors remains controversial. This meta-analysis aims to investigate the clinicopathological and prognostic values of TLS in solid tumors. Methods: A systematic search was conducted in PubMed, EMBASE and Cochrane Library undated to November 2, 2020. Odds ratios of clinical parameters, hazard ratio (HR) of overall survival (OS), relapse-free survival (RFS), disease-free survival (DFS) and relapse rate were calculated in order to evaluate the relationship between TLS expression and clinicopathological or prognostic values in different tumors. Result: 27 eligible studies including 6647 patients with different types of tumors were analyzed. High TLS expression was associated with a longer OS (HR = 0.66, 95% CI: 0.50 - 0.86, P = 0.002) and RFS (HR = 0.61, 95% CI: 0.47 - 0.79, P = 0.0001). Moreover, high TLS levels in tumor were associated with a low risk of recurrence (HR = 0.43, 95% CI: 0.32 - 0.57, P < 0.0001). However, there was no relationship between TLS expression and DFS. Meanwhile, high TLS expression was associated with smaller tumor size (P < 0.00001) and higher tumor infiltrating lymphocytes (TILs). Furthermore, the subgroup analysis showed high TLS expression that may be associated with a lower clinical grading and N stage in breast cancer and colorectal cancer. Conclusion: High TLS expression is associated with the longer OS and RFS in solid tumors, and a lower risk of cancer relapse. Meanwhile, high TLS expression is also associated with a smaller tumor size, higher infiltration of TILs, lower clinical grading and N stage in the tumor. Therefore, high TLS expression in the tumor is a favorable prognostic biomarker for solid tumor patients.

Transcription-induced chimeric RNAs are an emerging area of research into molecular signatures for disease biomarker and therapeutic target development. Despite their importance, little is known for chimeric RNAs-relevant roles and the underlying mechanisms for cancer pathogenesis and progression. Here we describe a unique ASTN2-PAPPA(antisense) chimeric RNA (A-P-as chiRNA) that could be the first reported chimeric RNA derived from the splicing of exons and intron antisense of two neighboring genes, respectively. Aberrant A-P-as chiRNA level in ESCC tissues was associated with tumor progression and patients' outcome. In vitro and in vivo studies demonstrated that A-P-as chiRNA aggravated ESCC metastasis and enhanced stemness through modulating OCT4. Mechanistic studies demonstrated that ERK5-mediated non-canonical PAF1 activity was required for A-P-as chiRNA-induced cancer malignancy. The study defined an undocumented function of chimeric RNAs in aggravating cancer stemness and metastasis.

Smoking is one of the most impactful lifestyle-related risk factors in many cancer types including esophageal squamous cell carcinoma (ESCC). As the major component of tobacco and e-cigarettes, nicotine is not only responsible for addiction to smoking but also a carcinogen. Here we report that nicotine enhances ESCC cancer malignancy and tumor-initiating capacity by interacting with cholinergic receptor nicotinic alpha 7 subunit (CHRNA7) and subsequently activating the JAK2/STAT3 signaling pathway. We found that aberrant CHRNA7 expression can serve as an independent prognostic factor for ESCC patients. In multiple ESCC mouse models, dextromethorphan and metformin synergistically repressed nicotine-enhanced cancer-initiating cells (CIC) properties and inhibited ESCC progression. Mechanistically, dextromethorphan non-competitively inhibited nicotine binding to CHRNA7 while metformin downregulated CHRNA7 expression by antagonizing nicotine-induced promoter DNA hypomethylation of CHRNA7. Since dextromethorphan and metformin are two safe FDA-approved drugs with minimal undesirable side-effects, the combination of these drugs has a high potential as either a preventive and/or a therapeutic strategy against nicotine-promoted ESCC and perhaps other nicotine-sensitive cancer types as well.

Background Colorectal cancer (CRC) is the third most prevalent cancer globally. In the treatment of CRC, surgical resection is commonly adopted, and neoadjuvant chemotherapy or immunotherapy is mainly administered for patients with advanced disease. However, despite the developments in the field of cancer treatment, the mortality rate of CRC has remained high. Therefore, novel treatments for CRC need to be explored. Astragalus membranaceus, commonly known in China as Huangqi (HQ), a traditional Chinese medicine, has been reported to be a potential antitumorigenic agent. This study aimed to investigate the mechanisms of action of HQ. Methods Active ingredients and putative targets of HQ were obtained through a comprehensive search of the Traditional Chinese Medicine Systems Pharmacology database. CRC-related targets were retrieved from the GeneCards database and then overlapping targets were acquired. After visualization of the compound-disease network and protein-protein interaction (PPI) network, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses of the overlapping genes were performed. Additionally, HCT116 cells were treated with the active components of HQ at a 20-µM concentration. Cell Counting Kit-8 was used to detect cell activity, and real-time quantitative polymerase chain reaction was carried out to detect the expression of genes downstream of the interleukin (IL)-17 signaling pathway. Results A PPI network comprising 177 nodes and 318 edges was obtained. The GO analysis of the overlapping genes showed enrichment in response to lipopolysaccharide and oxidative process. For the KEGG analysis, the AGE-RAGE signaling pathway and inflammation-related pathways, such as the IL-17 and tumor necrosis factor (TNF) signaling pathways, were enriched. The in vitro experiments showed that HQ promoted the apoptosis of CRC cells by inhibiting the expression of the CCL2, CXCL8, CXCL10, and PTGS2 genes. Conclusions This study systematically revealed the multitarget mechanism of HQ in CRC through a network pharmacology approach. We verified that HQ promotes CRC cell death via the IL-17 signaling pathway. This finding provides indications for further mechanistic studies and the development of HQ as a potential treatment for CRC patients.

Hydropower is the largest renewable source of electricity generation, the carbon emissions of which have attracted a lot attention. However, the system boundaries of existing studies are either incomplete or inaccurate. Therefore, this study provides a systems accounting framework for evaluating both the direct and indirect carbon emissions from a hydropower plant. It is based on the hybrid method as a combination of the process analysis and the input-output analysis. To demonstrate the framework, a case study for a typical pumped storage hydropower plant (NPSHP) is carried out. The total carbon emissions are estimated as 5828.39 kt in the life-cycle of the case system. The end-of-use stage causes the largest carbon emissions (38.4%), followed by the construction stage (34.5%), the operation stage (25.6%), and the preparation stage (1.5%). The direct carbon emissions are mainly released from sediments in the end-of-use stage and the surface of reservoirs in the operation stage (94.8%). The indirect carbon emissions are 2.8 times higher than the direct carbon emissions. The material, machinery, energy, and service inputs respectively account for 7.1%, 14.7%, 15.9%, and 62.3% of the total indirect carbon emissions by the case system. The indicator of EGOC (electricity generation on carbon emission) for the NPSHP is calculated as 26.06 g CO2-eq./kWh, which is lower than that of most other power plants.

Background: Zeste White 10 interactor (ZW10 interactor, ZWINT) is a centromeric complex required for a mitotic spindle checkpoint. According to previous studies, it was overexpressed in people with recurrent tumors. However, the expression of ZWINT in breast cancer has not been thoroughly studied. In addition, the correlations of ZWINT to prognosis in breast cancer remain unclear. Methods: In this study, the expression of ZWINT in different types of tumors was analyzed based on the Oncomine database, and the effect of ZWINT expression on clinical prognosis was evaluated by Kaplan- Meier plotter. Results: In breast cancer, lung cancer, sarcoma, ovarian cancer, bladder cancer, liver cancer and cervical cancer, the expression of ZWINT was higher than that in normal tissues, but in gastric cancer, prostate cancer, myeloma, renal cancer and pancreatic cancer, the expression of ZWINT was lower. In addition, a meta-analysis of 22 cancer database studies found that the ZWINT gene was over-expressed in breast cancer tissues compared with normal tissues (P=4.05×10 −6 ). Through the survival analysis of Kaplan-Meier plotter, it is found that the high expression of ZWINT is related to the worse overall survival (OS) [hazard ratio (HR) =1.73, 95% confidence interval (CI): 1.39–2.51, P=5.4×10 −7 ], RFS (HR =1.68, 95% CI: 1.51– 1.88, P −16 ) and distant metastasis-free survival (DMFS) (HR =1.55, 95% CI: 1.28–1.89, P=7.9×10 −6 ) in all BC patients. Conclusions: Our results strongly suggest that over expression of ZWINT is closely related to poor prognosis of breast cancer. ZWINT may be a prognostic biomarker for the treatment of BC.

Blood vessels in tumors often exhibit abnormal morphology and function, which promotes the growth, metastasis and resistance of tumors to conventional therapies. Therefore, vascular normalization is an emerging strategy to enhance the effectiveness of radiotherapy and chemotherapy when used in combination; however, there is a lack of evidence regarding the optimal schedule for the co-administration of anti-angiogenic and chemotherapeutic drugs. Scheduling treatment is important as the period for normalization is transient, also known as the 'time window'; however, no biomarker has been identified to detect this window. In the present study, recombinant human endostatin (rhES) was employed as an anti-angiogenic agent in xenograft tumor tissue in mice. Following rhES or control (saline) treatment, the density and integrity of tumor vessels were detected by immunofluorescence staining for cluster of differentiation 31 and α-smooth muscle actin; the level of hypoxia in tumor tissue was examined by immunohistochemistry with pimonidazole; the necrotic area was evaluated by hematoxylin and eosin staining; and the level of thrombospondin-1 (TSP-1) in plasma was tested by ELISA. The Cell Counting Kit-8 assay was also used to evaluate the effect of rhES on the proliferation of colon carcinoma SW620 cells. A 'time window' normalized vasculature was determined between day 4 and 6 following rhES treatment, and accompanied by a decrease in hypoxia in tumor tissue. Decreasing plasma TSP-1 levels were consistent with changes in vascular morphology and hypoxia, which exhibited features of normalization. In addition, rhES had no effect on the proliferation of SW620 cells, suggesting that the reduction in TSP-1 was associated with increased oxygen content during vascular normalization, rather than inhibited cell proliferation. In conclusion, TSP-1 may be a potential biomarker for predicting the normalization window of colon cancer vessels.

Simple Summary Excessive angiogenesis is a distinct feature of colorectal cancer (CRC) and plays a pivotal role in tumor development and metastasis. Therefore, it is essential to clarify the underlying mechanism of angiogenesis. In this study, we found that the level of proline-, glutamic acid, and leucine-rich protein 1 (PELP1) was positively correlated with microvessel density (MVD). In vitro and in vivo assays further showed PELP1 regulated angiogenesis via the Signal transducer and activator of transcription 3 (STAT3)/Vascular endothelial growth factor (VEGFA). Notably, we found that inhibition of PELP1 enhanced the efficacy of chemotherapy due to vascular normalization. Thus, targeting of PELP1 may be a potentially therapeutic strategy for CRC. Abstract Abnormal angiogenesis is one of the important hallmarks of colorectal cancer as well as other solid tumors. Optimally, anti-angiogenesis therapy could restrain malignant angiogenesis to control tumor expansion. PELP1 is as a scaffolding oncogenic protein in a variety of cancer types, but its involvement in angiogenesis is unknown. In this study, PELP1 was found to be abnormally upregulated and highly coincidental with increased MVD in CRC. Further, treatment with conditioned medium (CM) from PELP1 knockdown CRC cells remarkably arrested the function of human umbilical vein endothelial cells (HUVECs) compared to those treated with CM from wildtype cells. Mechanistically, the STAT3/VEGFA axis was found to mediate PELP1-induced angiogenetic phenotypes of HUVECs. Moreover, suppression of PELP1 reduced tumor growth and angiogenesis in vivo accompanied by inactivation of STAT3/VEGFA pathway. Notably, in vivo, PELP1 suppression could enhance the efficacy of chemotherapy, which is caused by the normalization of vessels. Collectively, our findings provide a preclinical proof of concept that targeting PELP1 to decrease STAT3/VEGFA-mediated angiogenesis and improve responses to chemotherapy due to normalization of vessels. Given the newly defined contribution to angiogenesis of PELP1, targeting PELP1 may be a potentially ideal therapeutic strategy for CRC as well as other solid tumors.

Previous research papers on urban water resources accounting were confined to the perspectives of production and consumption, ignoring the perspective of income. This paper proposes a systems framework to analyze the income, production, and consumption-based water uses and underlying driving forces of a city based on the methods of multi-scale input-output analysis and structural decomposition analysis. A case study is performed for Shanghai as a megacity. The results show that the income, production and consumption-based water uses of Shanghai had decreased from 5.70 billion m

Inspired by the strict constraint ratio (relatively low variability) between carbon (C), nitrogen (N), and phosphorus (P) in global soils and soil microbial biomass, our study explores the biogeographic distribution of C:N:P stoichiometric ratios in soils and soil microbial biomass in China and seeks to identify areas with similar ratios. Our study also attempts to determine the impacts of soil and soil microbial biomass C:N:P in China and the factors determining the ratio. The element concentrations may vary in each phylogenetic group of soils and soil microbial communities in China’s terrestrial ecosystems, as they do in global terrestrial ecosystems. However, on average, the C:N:P ratios for soil (66:5:1) and soil microbial biomass (22:2:1) are highly constrained within China. Soil microbial biomass C, N, and P concentrations have relatively weak internal stability, while soil microbial biomass C:N, C:P, and N:P ratios do not have internal stability at the national scale and in different terrestrial ecosystems of China. Unlike plant N:P, which can be used as the basis for evaluations of nutrient restrictions, the use of soil or soil microbial biomass N:P to evaluate soil nutrients is not universal. Latitude is the main factor influencing the patterns of soil C, N, and P. Longitude is the main factor determining the patterns of soil microbial biomass C, N, and P. pH is the main nonzonal factor affecting the patterns of soil and soil microbial biomass C, N, and P. The findings of this study are helpful in understanding the spatial pattern of soils and soil microbial biomass and their influencing factors in regions with complex ecosystems.

Background. Gastric cancer (GC) is the third leading cause of cancer death worldwide with complicated molecular and cellular heterogeneity. Iron metabolism and ferroptosis play crucial roles in the pathogenesis of GC. However, the prognostic role and immunotherapy biomarker potential of ferroptosis-related genes (FRGs) in GC still remains to be clarified. Methods. We comprehensively analyzed the prognosis of different expression FRGs, based on gastric carcinoma patients in the TCGA cohort. The functional enrichment and immune microenvironment associated with these genes in gastric cancer were investigated. The prognostic model was constructed to clarify the relation between FRGs and the prognosis of GC. Meanwhile, the ceRNA network of FRGs in the prognostic model was performed to explore the regulatory mechanisms. Results. Gastric carcinoma patients were classified into the A, B, and C FRGClusters with different features based on 19 prognostic ferroptosis-related differentially expressed genes in the TCGA database. To quantify the FRG characteristics of individual patients, FRGScore was constructed. And the research shows the GC patients with higher FRGScore had worse survival outcome. Moreover, thirteen prognostic ferroptosis-related differentially expressed genes (DEGs) were selected to construct a prognostic model for GC survival outcome with a superior accuracy in this research. And we also found that FRG RiskScore can be an independent biomarker for the prognosis of GC patients. Interestingly, GC patients with lower RiskScore had less immune dysfunction and were more likely to respond to immunotherapy according to TIDE value analysis. Finally, a ceRNA network based on FRGs in the prognostic model was analyzed to show the concrete regulation mechanisms. Conclusions. The ferroptosis-related gene risk signature has a superior potent in predicting GC prognosis and acts as the biomarkers for immunotherapy, which may provide a reference in clinic.

Chimeric RNAs (chiRNAs) play many previously unrecognized roles in different diseases including cancer. They can not only be used as biomarkers for diagnosis and prognosis of various diseases but also serve as potential therapeutic targets. In order to better understand the roles of chiRNAs in pathogenesis, we inserted human sequences into mouse genome and established a knockin mouse model of the tamoxifen-inducible expression of ASTN2-PAPPA antisense chimeric RNA (A-PaschiRNA). Mice carrying the A-PaschiRNA knockin gene do not display any apparent abnormalities in growth, fertility, histological, hematopoietic, and biochemical indices. Using this model, we dissected the role of A-PaschiRNA in chemical carcinogen 4-nitroquinoline 1-oxide (4NQO)-induced carcinogenesis of esophageal squamous cell carcinoma (ESCC). To our knowledge, we are the first to generate a chiRNA knockin mouse model using the Cre-loxP system. The model could be used to explore the roles of chiRNA in pathogenesis and potential targeted therapies.

In In the field of garbage intelligent identification, similar garbage are difficult to be effectively detected due to different kinds of characteristics. This paper proposes a Skip-YOLO model for garbage detection in real life through the visual analysis of feature mapping in different neural networks. First of all, the receptive field of the model is enlarged through the large-size convolution kernel, which enhanced the shallow information of images. Secondly, the high-dimensional feature mappings of garbage is extracted by dense convolutional blocks. The sensitivity of similar features in the same type of garbage is enhanced by strengthening the sharing of shallow low semantics and deep high semantics information. Finally, the multi-scale high-dimensional feature mappings is integrated and sent to the YOLO layer to predict the type and location of garbage. Experimental results show that compared with the YOLOv3, the overall detection precision is increased by 22.5%, and the average recall rate is increased by 18.6%. In qualitative comparison, it successfully detects domestic garbage in complex multi-scenes. In addition, our approach alleviates the overfitting problem of deep residual blocks. The application case of waste sorting production line is used to further highlight the model generalization performance of our method.

Immunotherapy of malignant tumor is a verified and crucial anti-tumor strategy to help patients with cancer for prolonging prognostic survival. It is a novel anticancer tactics that activates the immune system to discern and damage cancer cells, thereby prevent them from proliferating. However, immunotherapy still faces many challenges in view of clinical efficacy and safety issues. Various nanomaterials, especially gold nanoparticles (AuNPs), have been developed not only for anticancer treatment but also for delivering antitumor drugs or combining other treatment strategies. Recently, some studies have focused on AuNPs for enhancing cancer immunotherapy. In this review, we summarized how AuNPs applicated as immune agents, drug carriers or combinations with other immunotherapies for anticancer treatment. AuNPs can not only act as immune regulators but also deliver immune drugs for cancer. Therefore, AuNPs are candidates for enhancing the efficiency and safety of cancer immunotherapy.

Background Recent studies have reported the involvement of microRNA-29 (miR-29) family members in human cancers through their ability to regulate cellular functions. The present study investigated biological function of miR-29b in colorectal cancer (CRC). Methods CRC tissues and adjacent normal tissues were collected and the expression of ETV4 and miR-29b in the tissues were identified. The relationship between ETV4 and miR-29b or ETV4 expression and the EGFR promoter was identified using dual-luciferase reporter gene and CHIP assays. The proliferation, invasion, migration, and apoptosis of CRC HCT116 cells were assayed using MTT assay, Scratch test, Transwell assay, and flow cytometry, respectively. Also, expression of epithelial-mesenchymal transition (EMT) markers, angiogenic factors, and vasculogenic mimicry formation were evaluated using RT-qPCR and Western blot. Results ETV4 was upregulated, while miR-29b expression was decreased in CRC tissues. ETV4 was identified as a target gene of miR-29b, which in turn inactivated the ERK signaling pathway by targeting ETV4 and inhibiting EGFR transcription. Transfection with miR-29b mimic, siRNA-ETV4, or ERK signaling pathway inhibitor U0126 increased expression of E-cadherin and TSP-1, and CRC cell apoptosis, yet reduced expression of ERK1/2, MMP-2, MMP-9, Vimentin, and VEGF, as well as inhibiting EMT, angiogenesis, and CRC cell migration and invasion. The EMT, angiogenesis and cancer progression induced by miR-29b inhibitor were reversed by siRNA-mediated ETV4 silencing. Conclusions miR-29b suppresses angiogenesis and EMT in CRC via the ETV4/ERK/EGFR axis.

The scanning electron microscope (SEM) is widely used in the analysis and research of materials, including fracture analysis, microstructure morphology, and nanomaterial analysis. With the rapid development of materials science and computer vision technology, the level of detection technology is constantly improving. In this paper, the deep learning method is used to intelligently identify microcracks in the microscopic morphology of SEM image. A deep learning model based on image level is selected to reduce the interference of other complex microscopic topography, and a detection method with dense continuous bounding boxes suitable for SEM images is proposed. The dense and continuous bounding boxes were used to obtain the local features of the cracks and rotating the bounding boxes to reduce the feature differences between the bounding boxes. Finally, the bounding boxes with filled regression were used to highlight the microcrack detection effect. The results show that the detection accuracy of our approach reached 71.12%, and the highest mIOU reached 64.13%. Also, microcracks in different magnifications and in different backgrounds were detected successfully. open access