Chemical catalytic upgrading of polyethylene terephthalate plastic waste into value-added materials, fuels and chemicals.

The substantial production of polyethylene terephthalate (PET) products, coupled with high abandonment rates, results in significant environmental pollution and resource wastage. This has prompted global attention to the development of rational strategies for PET waste treatment. In the context of renewability and sustainability, catalytic chemical technology provides an effective means to recycle and upcycle PET waste into valuable resources. In this review, we initially provide an overview of strategies employed in the thermocatalytic process to recycle PET waste into valuable carbon materials, fuels and typical refined chemicals. The effect of catalysts on the quality and quantity of specific products is highlighted. Next, we introduce the development of renewable-energy-driven electrocatalytic and photocatalytic systems for sustainable PET waste upcycling, focusing on rational catalysts, innovative catalytic system design, and corresponding underlying catalytic mechanisms. Moreover, we discuss advantages and disadvantages of three chemical catalytic strategies. Finally, existing limitations and outlook toward controllable selectivity and yield enhancement of value-added products and PET upvaluing technology for scale-up applications are proposed. This review aims to inspire the exploration of waste-to-treasure technologies for renewable-energy-driven waste management toward a circular economy.

An occluded cherry tomato recognition model based on improved YOLOv7.

The typical occlusion of cherry tomatoes in the natural environment is one of the most critical factors affecting the accurate picking of cherry tomato picking robots. To recognize occluded cherry tomatoes accurately and efficiently using deep convolutional neural networks, a new occluded cherry tomato recognition model DSP-YOLOv7-CA is proposed. Firstly, images of cherry tomatoes with different degrees of occlusion are acquired, four occlusion areas and four occlusion methods are defined, and a cherry tomato dataset (TOSL) is constructed. Then, based on YOLOv7, the convolution module of the original residual edges was replaced with null residual edges, depth-separable convolutional layers were added, and jump connections were added to reuse feature information. Then, a depth-separable convolutional layer is added to the SPPF module with fewer parameters to replace the original SPPCSPC module to solve the problem of loss of small target information by different pooled residual layers. Finally, a coordinate attention mechanism (CA) layer is introduced at the critical position of the enhanced feature extraction network to strengthen the attention to the occluded cherry tomato. The experimental results show that the DSP-YOLOv7-CA model outperforms other target detection models, with an average detection accuracy (mAP) of 98.86%, and the number of model parameters is reduced from 37.62MB to 33.71MB, which is better on the actual detection of cherry tomatoes with less than 95% occlusion. Relatively average results were obtained on detecting cherry tomatoes with a shade level higher than 95%, but such cherry tomatoes were not targeted for picking. The DSP-YOLOv7-CA model can accurately recognize the occluded cherry tomatoes in the natural environment, providing an effective solution for accurately picking cherry tomato picking robots.

Toward carbon neutrality: Uncovering constraints on critical minerals in the Chinese power system.

China has set up its ambitious carbon neutrality target, which mainly relies on significant energy-related carbon emissions reduction. As the largest important contributing sector, power sector must achieve energy transition, in which critical minerals will play an essential role. However, the potential supply and demand for these minerals are uncertain. This study aims to predict the cumulative demand for critical minerals in the power sector under different scenarios via dynamic material flow analysis (DMFA), including total demands, supplies and production capacities of different minerals. Then, these critical minerals are categorized into superior and scarce resources for further analysis so that more detailed results can be obtained. Results present that the total minerals supply will not meet the total minerals demand (74260 kt) in 2060. Serious resource shortages will occur for several key minerals, such as Cr, Cu, Mn, Ag, Te, Ga, and Co. In addition, the demand for renewable energy will be nearly fifty times higher than that of fossil fuels energy, implying more diversified demands for various minerals. Finally, several policy recommendations are proposed to help improve the overall resource efficiency, such as strategic reserves, material substitutions, and circular economy.

Can Elevated Pretreatment Serum Carcinoembryonic Antigen Levels Serve as a Potential Biomarker Guiding Adjuvant Chemotherapy in Rectal Cancer Patients With ypTis-3N0 After Neoadjuvant Radiotherapy and Surgery?

Survival benefit of adjuvant chemotherapy (ACT) remained controversial in patients with stage II/III rectal cancer (RC) who received neoadjuvant therapy and surgery. This study aimed to investigate the guiding role of elevated pretreatment serum carcinoembryonic antigen (CEA) levels for receiving ACT in yield pathological Tis-3N0 (ypTis-3N0) RC patients after neoadjuvant radiotherapy and surgery. Between 2004 and 2015, 10,973 RC patients with ypTis-3N0 who received neoadjuvant radiotherapy and radical surgery were retrospectively analyzed using the Surveillance, Epidemiology, and End Results (SEER) database. Compared with CEA-normal group, elevated-CEA patients had worse 5-year CSS rate (90.1 vs 83.5%). The 5-year CSS rates were 86.3 and 87.4% for ypTis-3N0M0 patients with or without ACT, respectively. Patients receiving ACT had a comparable 5-year CSS rate compared to those who did not regardless of CEA levels in ypTis-3N0M0 RC patients (CEA elevation group: 76.4 vs. 83.5%, P = 0.305; CEA normal group: 90.0 vs. 90.1%, P = 0.943). Intriguingly, ypT3N0M0 RC patients with elevated CEA levels may benefit from ACT (5-year CSS: 69.1 vs. 82.9%, P = 0.045), while those with normal CEA levels did not (5-year CSS: 89.3 vs. 89.3%, P = 0.885). Multivariate Cox analysis demonstrated that ACT tended to be a protective factor in elevated-CEA ypT3N0M0 RC patients (HR = 0.633, 95% CI = 0.344-1.164, P = 0.141), while ACT was not associated with improved CSS in normal-CEA ypT3N0M0 RC patients (HR = 1.035, 95% CI = 0.487-2.202, P = 0.928). Elevated pretreatment serum CEA levels may serve as a promising biomarker guiding ACT in rectal cancer patients with ypT3N0M0.

miR-1301-3p Promotes Cell Proliferation and Facilitates Cell Cycle Progression via Targeting SIRT1 in Gastric Cancer.

So far, many existing evidences indicate that microRNAs (miRNA) are closely associated with the tumorigenesis and progression of various tumors. It has been reported that miR-1301-3p is abnormally expressed in several malignant tumors. However, the role of miR-1301-3p in gastric cancer (GC) remains unclear and is worth studying. Through qRT-PCR, the expression of miR-1301-3p and SIRT1 were detected in GC tissues and cells. The cell proliferation and cell cycle were measured through CCK-8 assay and clone formation assay. Dual luciferase reporter assay was used to determine the target of miR-1301-3p. Though tumorigenesis assay, we monitored the effect of miR-1301-3p on GC cell growth in vivo. miR-1301-3p was upregulated in GC tissues and cells in our study. Overexpression of miR-1301-3p accelerated GC cell proliferation, cell cycle progression and tumorigenesis. Notably, altering the expression miR-1301-3p caused deregulation of Cyclin D1, CDK4, c-Myc and P21. Furthermore, SIRT1 was the direct target of miR-1301-3p by luciferase reporter assay. After transfecting with miR-1301-3p inhibitor, we found that knockdown of SIRT1 could enhance the ability of proliferation. Our results identify miR-1301-3p as a novel potential therapeutic target that is associated with the tumorigenesis and progression of gastric cancer.

1.6 Million transactions replicate distributed PV market slowdown by COVID-19 lockdown.

Solar PV has seen a spectacular market development in recent years and has become a cost competitive source of electricity in many parts of the world. Yet, prospective observations show that the coronavirus pandemic could impact renewable energy projects, especially in the distributed market. Tracking and attributing the economic footprint of COVID-19 lockdowns in the photovoltaic sector poses a significant research challenge. Based on millions of financial transaction records and 44 thousand photovoltaic installation records, we tracked the spatio-temporal sale network of the distributed photovoltaic market and explored the extent of market slowdown. We found that a two-month lockdown duration can be assessed as a high-risk threshold value. When the lockdown duration exceeds the threshold value, the monthly value-added loss reaches 67.7%, and emission reduction capacity is cut by 64.2% over the whole year. We show that risks of a slowdown in PV deployment due to COVID-19 lockdowns can be mitigated by comprehensive incentive strategies for the distributed PV market amid market uncertainties.

Using Existing Infrastructure to Realize Low-Cost and Flexible Photovoltaic Power Generation in Areas with High-Power Demand in China.

This study develops a new concept involving using the existing infrastructure for photovoltaic (PV) generation to reduce the costs associated with increased land use and to avoid curtailment due to the mismatch between power supply and demand. We establish a method to estimate the technological potential and economic performance of the PV systems deployed in coal-fired power plants in China. The potential capacity of the examined 1,082 units in China reaches 4 GWe, which is equivalent to 32% of China's newly installed distributed PV capacity in 2019. A total of 87% of PV systems achieve plant-side grid parity compared with desulfurized coal benchmark electricity prices. To the best of our knowledge, this is the first study that investigates the use of rooftops and coal storage sheds in power plants to facilitate low-cost, flexible PV power generation, thus opening a new channel for future PV generation development.

Downregulation of NUSAP1 suppresses cell proliferation, migration, and invasion via inhibiting mTORC1 signalling pathway in gastric cancer.

Gastric cancer (GC) is one of the most common causes of cancer-related death worldwide, and outstanding biomarkers for therapeutic targets or predicting GC survival are still lacking. Increasing evidence indicated that nucleolar and spindle associated protein 1 (NUSAP1) involved in regulating the progression of various cancers; however, its specific role in GC remained unclear. In this study, we found that NUSAP1 was upregulated in the GC tissues and cell lines via analysing data from The Cancer Genome Atlas (TCGA), gene expression omnibus (GEO), qRT-PCR, and western blot assays. Patients with high NUSAP1 expression levels showed shorter free-progression survival (FPS), larger tumour size, and higher lymphatic metastasis rate compared with those with low NUSAP1 expression. Further functional experiments revealed knockdown of NUSAP1 could inhibit the growth, migration, and invasion of GC cells in vitro and vivo. Additionally, silencing NUSAP1 induced G0/G1 phase arrest, apoptosis, and suppressed the epithelial-mesenchymal transition (EMT) process. Finally, we performed gene set enrichment analysis (GSEA) and observed NUSAP1 was positive with mTORC1 signalling pathway, which was verified by the subsequent immunoblotting. In conclusion, our findings suggested that NUSAP1 contributed to GC progression and may act as a potential therapeutic target for GC. SIGNIFICANCE OF THE STUDY: Our results firstly illuminated that NUSAP1 expression was significantly upregulated in GC tissues and predicted poor FPS. Silencing it could attenuate GC progression via inhibiting mTORC1 signalling pathway. Hence, NUSAP1 may act as a promising therapy target for GC.

STRA6 exerts oncogenic role in gastric tumorigenesis by acting as a crucial target of miR-873.

BACKGROUND: Increasing evidence shows that stimulated by retinoic acid 6 (STRA6) participates in regulating multiple cancers. However, the biological roles of STRA6 in gastric cancer (GC) remain unknown. This study aimed to investigate the biological function of STRA6 and reveal the underlying mechanism of its dysregulation in GC. METHODS: The expression level of STRA6 was detected through quantitative real-time PCR and Western blot analysis. The effects of STRA6 on the proliferation of GC cells were studied through CCK-8 proliferation, colony formation and 5-ethynyl-2'-deoxyuridine (EdU) assays. The effects of STRA6 on migration and invasion were detected via wound healing and Transwell assays. Upstream miRNAs, which might regulate STRA6 expression, was predicted through bioinformatics analysis. Their interaction was further confirmed through dual-luciferase reporter assays and rescue experiments. RESULTS: STRA6 was up-regulated in GC and enhanced the proliferation and metastasis of GC cells in vitro and in vivo. STRA6 knockdown could inhibit the Wnt/ß-catenin signalling pathway. STRA6 was confirmed as an miR-873 target, which acted as a tumour suppressor in GC. Rescue assays showed that the repressing effect of miR-873 could be partially reversed by overexpressing STRA6. CONCLUSIONS: STRA6 is down-regulated by miR-873 and plays an oncogenic role by activating Wnt/ß-catenin signalling in GC.

Adenosquamous Carcinoma of the Stomach: A Population-based Study from the SEER Database.

Purpose: Gastric adenosquamous carcinoma (ASC) is a rare pathological type with poorly understood clinicopathological features. The purpose of this study is to identify the characteristics of gastric ASC patients. Methods: Using the Surveillance, Epidemiology, and End Results (SEER) database (2000 to 2014), patients with ASC (N=93) or adenocarcinoma (AC) (N=41794) of the stomach were included. The epidemiology, tumor features, treatment, and outcomes between these two groups were compared. Results: The incidences of ASC from 1983 to 2014 [annual percentage change (APC) = -3.5%, 95% confidence interval (CI) -4.9 to -2.1] and AC from 1973-2014 [APC = -1.8%, 95%CI -2.0 to -1.6] decreased over time. Compared to AC cases, patients with ASC were more likely to present poor differentiation (74.2% vs 52.4%) and later summary stage (distant: 46.2% vs 33.6%) or later T stage (T4: 15.1%% vs 9.0%). Besides, the proportion of patients with distant metastasis (33.3% vs 23.9%), and chemotherapy (44.1% vs 34.0%) in ASC group was higher. The Kaplan-Meier analyses showed ASC cases had worse overall survival (OS) (p=0.017) than that of AC after propensity score matching (PSM), but not the cancer-specific survival (CSS) (p=0.849). The further subgroup analyses suggested no statistical significance between gastric ASC patients and AC patients for CSS. The multivariate cox proportional hazard analyses indicated that patients with distant summary stage (HR=2.11, p=0.014), no surgery (HR=2.22, p=0.016), and no/unknown chemotherapy (HR=3.33, p<0.001) were associated with poor OS for ASC population alone. However, for CSS, only ASC cases with no/unknown chemotherapy (HR=2.22, p=0.018) indicated worse outcomes. Conclusions: Gastric ASC presented more aggressive clinicopathologic characteristics and poorer OS compared with AC. The localized/regional summary stages and undergoing surgery suggested favorable OS for gastric ASC patients. ASC cases receiving chemotherary showed both better OS and CSS.

Association of TP73-AS1 gene polymorphisms with the risk and survival of gastric cancer in a Chinese Han Population.

It was investigated that TP73-AS1(TP73 antisense RNA 1) could function as an oncogene in gastric cancer (GC). The expression and function of long noncoding RNAs (lncRNAs) could be impacted by single nucleotide polymorphisms (SNPs), which are related to cancer susceptibility and prognosis. This study was to reveal the association between lncRNAs TP73-AS1 polymorphisms (rs1181865 A > G, rs9800 G > C, rs3737589 A > G, rs2298222 G > A, rs7515164 C > A) and GC in 1000 GC cases and 1000 controls in a Chinese Han population. Rs3737589 G allele had significant associations with the increasing risk of GC (G vs. A: p = .005). Rs3737589 variant genotypes (AG + GG) were related to an increased risk of GC in the elder population (age ≥60), females, nonsmokers, nondrinkers, individuals living in urban, and individuals without family history of GC in stratified analyses. Rs3737589 variant genotypes (AG + GG) were related to the advanced depth of tumor invasion (T3 + T4). Besides, we found that GC patients with AG or GG genotype of rs3737589 had poorer overall survival (OS) than those with AA genotype (p < .05). Our findings showed that the lncRNA TP73-AS1 rs3737589 polymorphism might increase the risk of GC, and rs3737589 polymorphism could be a potential biomarker to predict the prognosis of GC patients.

miR-1254 inhibits cell proliferation, migration, and invasion by down-regulating Smurf1 in gastric cancer.

Gastric cancer (GC) is one of the most frequent malignancies, and increasing evidence supports the contribution of microRNA (miRNAs) to cancer progression. miR-1254 has been confirmed to participate in the regulation of various cancers, while the function of miR-1254 in GC remains unknown. In this study, we investigated the role of miR-1254 in GC. The expression of miR-1254 was detected in human GC specimens and cell lines by miRNA RT-PCR. The effects of miR-1254 on GC proliferation were determined by CCK-8 proliferation assays, colony formation assays, 5-ethynyl-2'-deoxyuridine (EdU) incorporation, and cell-cycle assays. The ability of migration and invasion was examined by transwell and wound-healing assay. Dual Luciferase reporter assay was used to validate the interaction of miR-1254 with its target gene. The xenograft mouse models were conducted to investigate the effects of miR-1254 in vivo. The signaling pathways and epithelial-mesenchymal transition (EMT)-related proteins were detected with western blot. The results showed that miR-1254 inhibited the proliferation, migration and invasion in vitro and suppressed tumorigenesis in vivo. Smurf1 was shown to be the direct target of miR-1254. Overexpressing Smurf1 could partially counteract the effects caused by miR-1254. Similarly, the effects of the miR-1254-inhibitor were also rescued by Smurf1-shRNA. Furthermore, we found that miR-1254 inhibited EMT and decreased the PI3K/AKT signaling pathway through downregulating Smurf1. In summary, overexpression of miR-1254 could suppress proliferation, migration, invasion, and EMT via PI3K/AKT signaling pathways by downregulation of Smurf1 in GC, which suggests a potential therapeutic target for GC.

MiR-592 Promotes Gastric Cancer Proliferation, Migration, and Invasion Through the PI3K/AKT and MAPK/ERK Signaling Pathways by Targeting Spry2.

BACKGROUND/AIMS: Gastric cancer (GC) is one of the most prevalent digestive malignancies. MicroRNAs (miRNAs) are involved in multiple cellular processes, including oncogenesis, and miR-592 itself participates in many malignancies; however, its role in GC remains unknown. In this study, we investigated the expression and molecular mechanisms of miR-592 in GC. METHODS: Quantitative real-time PCR and immunohistochemistry were performed to determine the expression of miR-592 and its putative targets in human tissues and cell lines. Proliferation, migration, and invasion were evaluated by Cell Counting Kit-8, population doubling time, colony formation, Transwell, and wound-healing assays in transfected GC cells in vitro. A dual-luciferase reporter assay was used to determine whether miR-592 could directly bind its target. A tumorigenesis assay was used to study whether miR-592 affected GC growth in vivo. Proteins involved in signaling pathways and the epithelial-mesenchymal transition (EMT) were detected with western blot. RESULTS: The ectopic expression of miR-592 promoted GC proliferation, migration, and invasion in vitro and facilitated tumorigenesis in vivo. Spry2 was a direct target of miR-592 and Spry2 overexpression partially counteracted the effects of miR-592. miR-592 induced the EMT and promoted its progression in GC via the PI3K/AKT and MAPK/ERK signaling pathways by inhibiting Spry2. CONCLUSIONS: Overexpression of miR-592 promotes GC proliferation, migration, and invasion and induces the EMT via the PI3K/AKT and MAPK/ERK signaling pathways by inhibiting Spry2, suggesting a potential therapeutic target for GC.

MicroRNA-let-7a regulates cell autophagy by targeting Rictor in gastric cancer cell lines MGC-803 and SGC-7901.

miR-let-7a is the most widely studied miRNA, whose functions have been well-established by scientists in both carcinogenesis and progression of human cancer, including gastric cancer (GC). However, to date there is a lack of information concerning the relationship between miR-let-7a and cellular autophagy. Using western blotting and immunofluorescence, we determined that upregulation of miR-let-7a led to increased cellular autophagic level, whereas miR-let-7a suppression decreased autophagy activity in GC cells. To further elucidate the mechanisms underlying this, we screened potential targets of miR-let-7a using bioinformatics analyses, validated by a series of assays. Our results indicated that Rptor independent companion of mTOR complex 2 (Rictor) was a direct target of miR-let-7a. In addition, rescue experiments in vitro showed that miR-let-7a promoted cellular autophagic level by inhibiting Rictor expression in GC cells. Furthermore, as an upstream executor of Akt-mTOR signaling pathway, we found that Rictor elaborated its effect on autophagy by phosphorylating Akt and mTOR, and this regulatory process could also be mediated by miR-let-7a. Taken together, our results present a novel role for miR-let-7a in GC which modulates autophagy by targeting Rictor, following the regulation of Akt-mTOR signal pathway.

Polymorphisms in lncRNA PTENP1 and the Risk of Gastric Cancer in a Chinese Population.

Long noncoding RNA (lncRNA) phosphatase and tensin homolog pseudogene 1 (PTENP1) is significantly downregulated in gastric cancer (GC), playing critical roles in GC progression. However, the association between PTENP1 genetic variants and GC risk has not yet been reported. Using TaqMan technology, three lncRNA PTENP1 tag single nucleotide polymorphisms (tagSNPs) (rs7853346 C>G, rs865005 C>T, and rs10971638 G>A) were genotyped in 768 GC patients and 768 cancer-free controls in a Chinese population. We found that subjects with rs7853346 G allele had a remarkably decreased risk of GC, compared with those carrying C allele (P = 0.011 in an additive model, P = 0.033 after Bonferroni's correction). The further stratified analyses showed that the link between variant genotypes of rs7853346 and decreased GC risk was more obvious in older subjects (≥60 years), nonsmokers, nondrinkers, and subjects without family history of GC. We also found that relative PTENP1 mRNA expression levels were higher in rs7853346 CG/GG genotype carriers than those with common genotype in both GC and normal tissues (P < 0.05). Besides, bioinformatics analyses revealed that rs7853346 may change the local folding structure and alter the target microRNAs (miRNAs) of PTENP1. In conclusion, our results suggested that lncRNA PTENP1 polymorphism rs7853346 may predict GC susceptibility.