NDP52 SUMOylation contributes to low-dose X-rays-induced cardiac hypertrophy through PINK1/Parkin-mediated mitophagy via MUL1/SUMO2 signalling.

Radiation-induced heart damage caused by low-dose X-rays has a significant impact on tumour patients' prognosis, with cardiac hypertrophy being the most severe noncarcinogenic adverse effect. Our previous study demonstrated that mitophagy activation promoted cardiac hypertrophy, but the underlying mechanisms remained unclear. In the present study, PARL-IN-1 enhanced excessive hypertrophy of cardiomyocytes and exacerbated mitochondrial damage. Isobaric tags for relative and absolute quantification-based quantitative proteomics identified NDP52 as a crucial target mediating cardiac hypertrophy induced by low-dose X-rays. SUMOylation proteomics revealed that the SUMO E3 ligase MUL1 facilitated NDP52 SUMOylation through SUMO2. Co-IP coupled with LC-MS/MS identified a critical lysine residue at position 262 of NDP52 as the key site for SUMO2-mediated SUMOylation of NDP52. The point mutation plasmid NDP52K262R inhibited mitophagy under MUL1 overexpression, as evidenced by inhibition of LC3 interaction with NDP52, PINK1 and LAMP2A. A mitochondrial dissociation study revealed that NDP52K262R inhibited PINK1 targeting to endosomes early endosomal marker (EEA1), late/lysosome endosomal marker (LAMP2A) and recycling endosomal marker (RAB11), and laser confocal microscopy confirmed that NDP52K262R impaired the recruitment of mitochondria to the autophagic pathway through EEA1/RAB11 and ATG3, ATG5, ATG16L1 and STX17, but did not affect mitochondrial delivery to lysosomes via LAMP2A for degradation. In conclusion, our findings suggest that MUL1-mediated SUMOylation of NDP52 plays a crucial role in regulating mitophagy in the context of low-dose X-ray-induced cardiac hypertrophy. Two hundred sixty-second lysine of NDP52 is identified as a key SUMOylation site for low-dose X-ray promoting mitophagy activation and cardiac hypertrophy. Collectively, this study provides novel implications for the development of therapeutic strategies aimed at preventing the progression of cardiac hypertrophy induced by low-dose X-rays.

ESM1 enhances fatty acid synthesis and vascular mimicry in ovarian cancer by utilizing the PKM2-dependent warburg effect within the hypoxic tumor microenvironment.

BACKGROUND: The hypoxic tumor microenvironment is a key factor that promotes metabolic reprogramming and vascular mimicry (VM) in ovarian cancer (OC) patients. ESM1, a secreted protein, plays an important role in promoting proliferation and angiogenesis in OC. However, the role of ESM1 in metabolic reprogramming and VM in the hypoxic microenvironment in OC patients has not been determined. METHODS: Liquid chromatography coupled with tandem MS was used to analyze CAOV3 and OV90 cells. Interactions between ESM1, PKM2, UBA2, and SUMO1 were detected by GST pull-down, Co-IP, and molecular docking. The effects of the ESM1-PKM2 axis on cell glucose metabolism were analyzed based on an ECAR experiment. The biological effects of the signaling axis on OC cells were detected by tubule formation, transwell assay, RT‒PCR, Western blot, immunofluorescence, and in vivo xenograft tumor experiments. RESULTS: Our findings demonstrated that hypoxia induces the upregulation of ESM1 expression through the transcription of HIF-1α. ESM1 serves as a crucial mediator of the interaction between PKM2 and UBA2, facilitating the SUMOylation of PKM2 and the subsequent formation of PKM2 dimers. This process promotes the Warburg effect and facilitates the nuclear translocation of PKM2, ultimately leading to the phosphorylation of STAT3. These molecular events contribute to the promotion of ovarian cancer glycolysis and vasculogenic mimicry. Furthermore, our study revealed that Shikonin effectively inhibits the molecular interaction between ESM1 and PKM2, consequently preventing the formation of PKM2 dimers and thereby inhibiting ovarian cancer glycolysis, fatty acid synthesis and vasculogenic mimicry. CONCLUSION: Our findings demonstrated that hypoxia increases ESM1 expression through the transcriptional regulation of HIF-1α to induce dimerization via PKM2 SUMOylation, which promotes the OC Warburg effect and VM.

M2 macrophage-derived paracrine factor TNFSF13 affects the fibrogenic alterations in endothelial cells and cardiac fibroblasts by mediating the NF-κB and Akt pathway.

Heart failure remains a global threaten to public health, cardiac fibrosis being a crucial event during the development and progression of heart failure. Reportedly, M2 macrophages might affect endothelial cell (ECs) and fibroblast proliferation and functions through paracrine signaling, participating in myocardial fibrosis. In this study, differentially expressed paracrine factors between M0/1 and M2 macrophages were analyzed and the expression of TNFSF13 was most significant in M2 macrophages. Culture medium (CM) of M2 (M2 CM) coculture to ECs and cardiac fibroblasts (CFbs) significantly promoted the cell proliferation of ECs and CFbs, respectively, and elevated α-smooth muscle actin (α-SMA), collagen I, and vimentin levels within both cell lines; moreover, M2 CM-induced changes in ECs and CFbs were partially abolished by TNFSF13 knockdown in M2 macrophages. Lastly, the NF-κB and Akt signaling pathways were proved to participate in TNFSF13-mediated M2 CM effects on ECs and CFbs. In conclusion, TNFSF13, a paracrine factor upregulated in M2 macrophages, could mediate the promotive effects of M2 CM on EC and CFb proliferation and fibrogenic alterations.

Global air pollution exposure and congenital anomalies: an updated systematic review and meta-analysis of epidemiological studies.

A systematic review and meta-analysis was conducted to evaluate recent epidemiological evidence on the association of air pollution with congenital anomalies (CAs). Of 11,014 records, 49 were finally included in this meta-analysis. Per 10 µg/m3 increase in air pollutant, PM10 exposure during the 1st month of pregnancy and at the first trimester (T1) was associated with increased overall CAs. Further, exposure to PM10 was associated with congenital heart disease (OR = 1.055, 95% CI: 1.035, 1.074) and patent ductus arteriosus (OR = 1.094, 95% CI: 1.020, 1.168) at T1, with chromosomal anomalies during the entire pregnancy and with nervous system anomalies when exposure occurred 3 months prior to pregnancy, during the 1st, 2nd months of pregnancy and at T1. Besides, a significant association with overall CAs was observed for a combined exposure of PM10 and SO2 during the 1st month of gestation (OR: 1.101, 95% CI: 1.023, 1.180). A combined exposure of PM10 and CO was also associated with tetralogy of Fallot during 3-8 weeks of gestation (OR: 1.016, 95% CI: 1.005, 1.027). No significant associations were observed between PM2.5, NO2, and O3 exposure and CAs.

LACC1: A critical involvement in macrophage immunometabolism.

Laccase domain-containing 1 (LACC1) protein is an enzyme highly expressed in inflammatory macrophages, and studies have shown that it has a key role in diseases such as inflammatory bowel disease, arthritis, and microbial infections. Therefore, in this review, we focus on LACC1-mediated catalysis. In detail, LACC1 converts l-CITrulline (l-CIT) to l-ORNithine (l-ORN) and isocyanic acid in mice and humans and acts as a bridge between proinflammatory nitric oxide synthase (NOS2) and polyamine immunometabolism, thus exerting anti-inflammatory and antibacterial effects. Considering the actions of LACC1, targeting LACC1 may be a potent therapeutic avenue for inflammation-related diseases and microbial infection diseases.

Hydrogen sulfide ameliorates abdominal aorta coarctation-induced myocardial fibrosis by inhibiting pyroptosis through regulating eukaryotic translation initiation factor 2α phosphorylation and activating PI3K/AKT1 pathway.

This study aimed to assess the effects of exogenous hydrogen sulfide (H2S) on abdominal aorta coarctation (AAC) induced myocardial fibrosis (MF) and autophagy in rats. Forty-four Sprague-Dawley rats were randomly divided into control group, AAC group, AAC + H2S group, and H2S control group. After a model of rats with AAC was built surgically, AAC + H2S group and H2S group were injected intraperitoneally with H2S (100 µmol/kg) daily. The rats in the control group and the AAC group were injected with the same amount of PBS. We observed that H2S can improve left ventricular function and the deposition of myocardial collagen fibers, inhibit pyroptosis, down-regulate the expression of P-eif2α in myocardial tissue, and inhibit cell autophagy by activating the phosphatidylinositol 3-kinase (PI3K)/AKT1 signaling pathway (p < 0.05). In addition, angiotensin II (1 µM) H9c2 cardiomyocytes were injured in vitro experiments, and it was also observed that pyroptosis was inhibited after H2S (400 µmol/kg) intervention, the expression of P-eif2α in cardiomyocytes was significantly down-regulated, and the PI3K/AKT1 signaling pathway was activated at the same time. Therefore, increasing the expression of P-eif2α reverses the activation of the PI3K/AKT1 signaling pathway by H2S. In conclusion, these findings suggest that exogenous H2S can ameliorate MF in rats with AAC by inhibiting pyroptosis, and the mechanism may be associated with inhibiting the phosphorylation of eif2α and activating the PI3K/AKT1 signaling pathway to inhibit excessive cell autophagy.

The expression of Hexokinase 2 and its hub genes are correlated with the prognosis in glioma.

BACKGROUND: Hexokinase 2 (HK2) is an enzyme that catalyses the conversion of glucose to glucose-6-phosphate, which has been found to be associated with malignant tumour growth. However, the potential immunological and clinical significance of HK2, especially in terms of prognostic prediction for patients with glioma, has not been fully elucidated. METHODS: To investigate the expression, immunological and clinical significance of HK2 in patients with glioma, several databases, including ONCOMINE, TIMER2.0, GEPIA, CGGA, UCSC, LinkedOmics, Metascape, STRING, GSCA, and TISIDB, as well as biochemical, cellular, and pathological analyses, were used in this study. In addition, we performed univariate, multivariate Cox regression and nomogram analyses of the hub genes positively and negatively correlated with HK2 to explore the potential regulatory mechanism in the initiation and development of glioma. RESULTS: Our results demonstrated that HK2 was highly expressed in most malignant cancers. HK2 expression was significantly higher in lower grade glioma (LGG) and glioblastoma (GBM) than in adjacent normal tissue. In addition, HK2 expression was significantly correlated with clinical parameters, histological manifestations, and prognosis in glioma patients. Specifically, the data from The Cancer Genome Atlas downloaded from UCSC Xena database analysis showed that high expression of HK2 was strongly associated with poor prognosis in glioma patients. The LinkedOmics database indicated that HK2-related genes were mainly enriched in immune-related cells. In LGG and GBM tissues, HK2 expression is usually correlated with recognized immune checkpoints and the abundance of multiple immune infiltrates. Similarly, the Metascape database revealed that HK2-related genes were mainly enriched and annotated in immune-related pathways and immune cells. Further investigations also confirmed that the inhibition of HK2 expression remarkably suppressed metastasis and vasculogenic mimicry (VM) formation in glioma cells through regulating the gene expression of inflammatory and immune modulators. CONCLUSION: HK2 expression was closely associated with the malignant properties of glioma through activating multiple immune-related signalling pathways to regulate immune responses and the infiltration of immune cells. Thus, HK2 and its hub genes may be a potential target for the treatment of glioma.

A novel mechanism of Smads/miR-675/TGFßR1 axis modulating the proliferation and remodeling of mouse cardiac fibroblasts.

Cardiac fibroblasts (CFs) can over-proliferate during the progression of cardiac fibrosis, accompanied by a net accumulation of extracellular matrix proteins. Based on the profibrotic actions of transforming growth factor beta 1 (TGFß1), investigating the mechanisms of TGFß1 function in CFs may provide new directions to treatment for cardiac fibrosis. microRNAs (miRNAs) could control CFs proliferation or remodeling via binding to 3'-untranslated region of messenger RNA (mRNA) to negatively regulate gene expression. In the present study, we downloaded several microarray analyses results from GEO attempting to identify miRNAs and possible downstream targets that may be involved in TGF-ß1 function in CFs and to detect the cellular and molecular functions of the identified miRNA-mRNA axis. Here, we identified miR-675 as a downregulated miRNA by TGFß1 by bioinformatics analyses and experimental verification. Upon TGFß1 stimulation, the protein levels of Α-SMAΑ-SMA, collagen I, and POSTN, and the secreted collagen in the cell culture supernatant significantly increased, whereas the miR-675 expression decreased. Smads mediate TGFß1-induced suppression on miR-675 via binding miR-675 promoter region. miR-675 overexpression could inhibit, whereas miR-675 inhibition could enhance TGFß1-induced mouse CFs (MCF) remodeling and proliferation. TGFß receptor 1 (TGFßR1), a critical receptor in TGFß1/Smad signaling, is a direct downstream target of miR-675. TGFßR1 overexpression significantly reverses the effect of miR-675 overexpression on MCF remodeling and proliferation. In summary, miR-675 targets TGFßR1 to attenuate TGFß1-induced MCF remodeling and proliferation. We demonstrate a novel mechanism of the Smads/miR-675/TGFßR1 axis modulating TGFß1-induced MCF remodeling and proliferation.

Indispensable role of lipoprotein bound-ApoE in adipogenesis and endocytosis induced by postprandial TRL.

Diet-associated obesity is coexisted with postprandial hypertriglyceridemia that indicates increased number of triglyceride-rich lipoproteins (TRL). This study aimed to investigate the effect of postprandial TRL-bound apolipoprotein E (ApoE) on adipogenesis and potential mechanisms. 3T3-L1 cells were cultured with (i) human TRL (h-TRL) with or without insulin, or (ii) TRL from wild type mice (WT-TRL) or ApoE knock-out mice (EKO-TRL) and insulin. The differentiating adipocytes were incubated with different kinds of TRL labeled by red fluorescence and confocal microscopy was performed. Receptor associated protein (RAP), heparin or both were added to inhibit low density lipoprotein receptor family receptors, heparan sulfate proteoglycan or both, respectively. With the aid of insulin, postprandial h-TRL or WT-TRL, instead of EKO-TRL, successfully induced adipogenesis. Confocal microscopy revealed red fluorescence in the differentiating adipocytes treated with h-TRL or WT-TRL, but not with EKO-TRL. RAP markedly reduced red fluorescence within the differentiating adipocytes, while heparin had little impact. The low density lipoprotein receptor related protein 1 protein showed upward trend with the increase of TRL concentrations. Taken together, lipoprotein-bound ApoE was required in both postprandial TRL-induced adipogenesis and TRL endocytosis by the differentiating adipocytes, the latter could be partially through low density lipoprotein receptor family dependent-pathway.

Dynamics of the diversity and structure of the overall and nitrifying microbial community in activated sludge along gradient copper exposures.

Diversity and composition of the microbial community, especially the nitrifiers, are essential to the treatment efficiency of wastewater in activated sludge systems. Heavy metals commonly present in the wastewater influent such as Cu can alter the community structure of nitrifiers and lower their activity. However, the dynamics of microbial community along a gradient of metal exposure have largely been unexplored, partially due to the limitations in traditional molecular methods. This study explored the dynamics regarding the diversity and community structures of overall and nitrifying microbial communities in activated sludge under intermittent Cu gradient loadings using Illumina sequencing. We created a new local nitrifying bacterial database for sequence BLAST searches. High Cu loadings (>10.9 mg/L) impoverished microbial diversity and altered the microbial community. Overall, Proteobacteria was the predominant phylum in the activated sludge system, in which Zoogloea, Thauera, and Dechloromonas (genera within the Rhodocyclaceae family of the Beta-proteobacteria class) were the dominant genera in the presence of Cu. The abundance of unclassified bacteria at the phylum level increased substantially with increasing Cu loadings. Nitrosomonas and Nitrospira were the predominant nitrifiers. The nitrifying bacterial community changed through increasing abundance and shifting to Cu-tolerant species to reduce the toxic effects of Cu. Our local nitrifying bacterial database helped to improve the resolution of bacterial identification. Our results provide insights into the dynamics of microbial community in response to various metal concentrations in activated sludge systems and improve our understanding regarding the effect of metals on wastewater treatment efficiency.

Blockade of PD-1 and CTLA-4: A potent immunotherapeutic approach for hepatocellular carcinoma.

Immune checkpoints (ICPs) can promote tumor growth and prevent immunity-induced cancer cell apoptosis. Fortunately, targeting ICPs, such as programmed cell death 1 (PD-1) or cytotoxic T lymphocyte associated protein 4 (CTLA-4), has achieved great success in the past few years and has gradually become an effective treatment for cancers, including hepatocellular carcinoma (HCC). However, many patients do not respond to ICP therapy due to acquired resistance and recurrence. Therefore, clarifying the specific mechanisms of ICP in the development of HCC is very important for enhancing the efficacy of anti-PD-1 and anti-CTLA-4 therapy. In particular, antigen presentation and interferon-γ (IFN-γ) signaling were reported to be involved in the development of resistance. In this review, we have explained the role and regulatory mechanisms of ICP therapy in HCC pathology. Moreover, we have also elaborated on combinations of ICP inhibitors and other treatments to enhance the antitumor effect. Collectively, recent advances in the pharmacological targeting of ICPs provide insights for the development of a novel alternative treatment for HCC.

Research progress on the role of p53 in pulmonary arterial hypertension.

PURPOSE OF REVIEW: Pulmonary arterial hypertension (PAH) is a devastating disease characterized by increased pulmonary vascular resistance and pulmonary arterial pressure. At present, the definitive pathology of PAH has not been elucidated and its effective treatment remains lacking. Despite PAHs having multiple pathogeneses, the cancer-like characteristics of cells have been considered the main reason for PAH progression. RECENT FINDINGS: p53 protein, an important tumor suppressor, regulates a multitude of gene expressions to maintain normal cellular functions and suppress the progression of malignant tumors. Recently, p53 has been found to exert multiple biological effects on cardiovascular diseases. Since PAH shares similar metabolic features with cancer cells, the regulatory roles of p53 in PAH are mainly the induction of cell cycle, inhibition of cell proliferation, and promotion of apoptosis. SUMMARY: This paper summarized the advanced findings on the molecular mechanisms and regulatory functions of p53 in PAH, aiming to reveal the potential therapeutic targets for PAH.

Integration of artificial intelligence performance prediction and learning analytics to improve student learning in online engineering course.

As a cutting-edge field of artificial intelligence in education (AIEd) that depends on advanced computing technologies, AI performance prediction model is widely used to identify at-risk students that tend to fail, establish student-centered learning pathways, and optimize instructional design and development. A majority of the existing AI prediction models focus on the development and optimization of the accuracy of AI algorithms rather than applying AI models to provide student with in-time and continuous feedback and improve the students' learning quality. To fill this gap, this research integrated an AI performance prediction model with learning analytics approaches with a goal to improve student learning effects in a collaborative learning context. Quasi-experimental research was conducted in an online engineering course to examine the differences of students' collaborative learning effect with and without the support of the integrated approach. Results showed that the integrated approach increased student engagement, improved collaborative learning performances, and strengthen student satisfactions about learning. This research made contributions to proposing an integrated approach of AI models and learning analytics (LA) feedback and providing paradigmatic implications for future development of AI-driven learning analytics.

L1CAM promotes vasculogenic mimicry formation by miR-143-3p-induced expression of hexokinase 2 in glioma.

In recent decades, antiangiogenic therapy, which blocks the supply of oxygen and nutrition to tumor cells, has become a promising clinical strategy for the treatment of patients with tumors. However, recent studies revealed that vasculogenic mimicry (VM), which is the process by which vascular morphological structures are formed by highly invasive tumor cells, has been considered a potential factor for the failure of antiangiogenic therapy in patients with tumors. Thus, inhibition of VM formation might be a potential target for improving the outcome of antiangiogenic strategies. However, the mechanism underlying VM formation is still incompletely elucidated. Herein, we report that L1CAM might be a critical regulator of VM formation in glioma, and might be associated with the resistance of glioma to antiangiogenic therapy. We found that the tumor-invasion and tube-formation capabilities of L1CAM-overexpressing cells were significantly enhanced in vitro and in vivo. In addition, the results indicated that miR-143-3p, which might directly target the 3'UTR of the hexokinase 2 (HK2) gene to regulate its protein expression, was subsequently involved in L1CAM-mediated VM formation by glioma cells. Further study revealed that the regulation of MMP2, MMP9, and VEGFA expression was involved in this process. Moreover, we identified that activation of the downstream PI3K/AKT signaling pathway of the L1CAM/HK2 cascade is critical for VM formation by glioma cells. Furthermore, we found that the combined treatment of anti-L1CAM neutralizing monoclonal antibody and bevacizumab increases efficacy beyond that of bevacizumab alone, and suppresses glioma growth in vivo, indicating that the inhibition of L1CAM-mediated VM formation might efficiently improve the effect of antiangiogenic treatment for glioma patients. Together, our findings demonstrated a critical role of L1CAM in regulating VM formation in glioma, and that L1CAM might be a potential target for ameliorating tumor resistance to antiangiogenic therapy in glioma patients.

Effect and mechanism of HMG-CoA reductase inhibitor on the improvement of elderly essential hypertension-induced vascular endothelial function impairment based on the JAK/STAT pathway.

OBJECTIVE: Our research was designed to figure out the influence and mechanism of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor on the improvement of elderly essential hypertension-induced vascular endothelial function impairment based on the JAK/STAT pathway. METHODS: Eighty-six elderly patients with essential hypertension were randomized into a control group (oral Amlodipine Besylate Tablets) and an observation group (oral Amlodipine Besylate Tablets + HMG-CoA reductase inhibitor atorvastatin calcium). Patients in both groups were treated with the drug for 12 weeks. Blood pressure, serum levels of inflammatory factors, and vascular endothelial function indicators, and levels of blood lipids were measured. The modeled rats were treated with atorvastatin calcium and a JAK/STAT pathway inhibitor (AG490), and the levels of cardiac function-related indices, left ventricular mass index, lipid levels, serum inflammatory factors and vascular endothelial function-related indices were detected in each group. RESULTS: HMG-CoA reductase inhibitor improved blood pressure levels, lipid levels, serum inflammatory factor levels and cardiac function in elderly patients with essential hypertension. Both HMG-CoA reductase inhibitor and AG490 improved blood pressure levels, lipid levels, serum inflammatory factor levels and cardiac function in SHR rats. Both HMG-CoA reductase inhibitor and AG490 decreased p-JAK2/JAK2 and p-STAT3/STAT3 expression levels. CONCLUSION: Our study demonstrates that HMG-CoA reductase inhibitor improves elderly essential hypertension-induced vascular endothelial function impairment by blocking the JAK/STAT pathway.

EduNER: a Chinese named entity recognition dataset for education research.

A high-quality domain-oriented dataset is crucial for the domain-specific named entity recognition (NER) task. In this study, we introduce a novel education-oriented Chinese NER dataset (EduNER). To provide representative and diverse training data, we collect data from multiple sources, including textbooks, academic papers, and education-related web pages. The collected documents span ten years (2012-2021). A team of domain experts is invited to accomplish the education NER schema definition, and a group of trained annotators is hired to complete the annotation. A collaborative labeling platform is built for accelerating human annotation. The constructed EduNER dataset includes 16 entity types, 11k+ sentences, and 35,731 entities. We conduct a thorough statistical analysis of EduNER and summarize its distinctive characteristics by comparing it with eight open-domain or domain-specific NER datasets. Sixteen state-of-the-art models are further utilized for NER tasks validation. The experimental results can enlighten further exploration. To the best of our knowledge, EduNER is the first publicly available dataset for NER task in the education domain, which may promote the development of education-oriented NER models.

Examining the effect of a genetic algorithm-enabled grouping method on collaborative performances, processes, and perceptions.

Group formation is a critical factor which influences collaborative processes and performances in computer-supported collaborative learning (CSCL). Automatic grouping has been widely used to generate groups with heterogeneous attributes and to maximize the diversity of students' characteristics within a group. But there are two dominant challenges that automatic grouping methods need to address, namely the barriers of uneven group size problem, and the inaccessibility of student characteristics. This research proposes an optimized, genetic algorithm-based grouping method that includes a conceptual model and an algorithm module to address these challenges. Through a quasi-experiment research, we compare collaborative groups' performance, processes, and perceptions in China's higher education. The results indicate that the experimental groups outperform the traditional grouping methods (i.e., random groups and student-formed groups) in terms of final performances, collaborative processes, and student perceptions. Based on the results, we propose implications for implementation of automatic grouping methods, and the use of collaborative analytics methods in CSCL.

Optimization of Sputtering Process for Medium Entropy Alloy Nanotwinned CoCrFeNi Thin Films by Taguchi Method.

We demonstrate a systematic study optimizing the properties of CoCrFeNi medium entropy alloy (MEA) thin films by tuning the deposition parameters of the pulsed direct current (DC) magnetron sputtering process. The chemical composition and microstructure of thin films were studied with energy dispersive X-ray spectroscopy (EDS), an X-ray diffractometer (XRD) and a transmission electron microscope (TEM). Abundant nanotwins and the dual face-centered cubic-hexagonal close-packed (FCC-HCP) phases were formed in some specimens. The Taguchi experimental method and analysis of variance (ANOVA) were applied to find the optimized parameters. The control factors are five deposition parameters: substrate bias, substrate temperature, working pressure, rotation speed and pulsed frequency. According to the signal-to-noise ratio results, the optimized parameters for low electrical resistivity (98.2 ± 0.8 µΩ·cm), low surface roughness (0.5 ± 0.1 nm) and high hardness (9.3 ± 0.2 GPa) were achieved and verified with confirmed experiments.

A case study of distribution and characteristics of microplastics in surface water and sediments of the seas around Shenzhen, southern coastal area of China.

Microplastics (MPs), known to cause environmental pollution, is attracting a growing attention worldwide owing to their extensive existence and potential risks to biota. The marginal sea areas are suspected to be especially susceptible to MPs pollution. Unfortunately, data on MPs in the surface water and sediments ecosystems are still limited, particularly in the southern coastal areas of China. The study was successfully utilized to explore the distribution and characteristics of MPs below 5 mm collected from 14 sites in the seas around Shenzhen, a typical special economic zone of China. MPs were detected in both surface water and sediments with concentrations ranging from 3.8 to 7.8 items per liter and 2.6 × 103 to 10.0 × 103 items per kilogram, respectively. The highest abundance of MPs appeared in S5/S9 and S14 in surface water and sediments, respectively. Fiber and film with small particle size (<0.5 mm) were identified as typical and abundant MPs type among all samples. In addition, polyethylene (PE) was considered as dominant forms of MPs in surface water and sediment samples. Results from this study indicated a positive correlation with abundance of MPs and urbanization rate, which also showed an evident difference of MPs in different urban functional areas. Based on the types and quantity of detected MPs, we assessed the risk of MPs pollution in this study area, and the ecological risk category of MPs was at a high level. Importantly, our work might be employed as a potential information so as to better understand MPs pollution, source tracing and ecological risk assessment, which enhances the possibility of achieving effective control and supervision of MPs pollution in southern coastal aera of China.

Impact of the COVID-19 Pandemic on ST-Elevation Myocardial Infarction Management in Hunan Province, China: A Multi-Center Observational Study.

Background: This study aimed to investigate the impact of the COVID-19 pandemic on ST-segment elevation myocardial infarction (STEMI) care in China. Methods: We conducted a multicenter, retrospective cohort study in Hunan province (adjacent to the epidemic center), China. Consecutive patients presenting with STEMI within 12 h of symptom onset and receiving primary percutaneous coronary intervention, pharmaco-invasive strategy and only thrombolytic treatment, were enrolled from January 23, 2020 to April 8, 2020 (COVID-19 era group). The same data were also collected for the equivalent period of 2019 (pre-COVID-19 era group). Results: A total of 610 patients with STEMI (COVID-19 era group n = 286, pre-COVID-19 era group n = 324) were included. There was a decline in the number of STEMI admissions by 10.5% and STEMI-related PCI procedures by 12.7% in 2020 compared with the equivalent period of 2019. The key time intervals including time from symptom onset to first medical contact, symptom onset to door, door-to-balloon, symptom onset to balloon and symptom onset to thrombolysis showed no significant difference between these two groups. There were no significant differences for in-hospital death and major adverse cardiovascular events between these two groups. Conclusion: During the COVID-19 pandemic outbreak in China, we observed a decline in the number of STEMI admissions and STEMI-related PCI procedures. However, the key quality indicators of STEMI care were not significantly affected. Restructuring health services during the COVID-19 pandemic has not significantly adversely influenced the in-hospital outcomes.