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Abstract Background and Aims Hepatocellular carcinoma (HCC) is a malignant tumour associated with high morbidity and mortality rates worldwide. Recently, TRPM8 was reported to play an important role in tumour progression. However, the precise role of TRPM8 in HCC remains unclear. In this study, we explored the expression levels, molecular functions and underlying mechanisms of TRPM8 in HCC. Methods Tissue samples were used to analyse the expression of TRPM8 to assess its diagnostic value for prognosis. Cell Counting Kit‐8, EdU and colony formation assays were performed to evaluate the effects of TRPM8 on cell proliferation, whereas the Transwell assay was used to assess cell migration and invasion. The role of TRPM8 in vivo was evaluated using a mouse subcutaneous xenograft tumour model. We performed PPI network analyses to understand the possible mechanisms of TRPM8 action. Results TRPM8 expression was decreased in HCC tissues and was correlated with histological grade and poor patient prognosis. Functionally, TRPM8 repressed the proliferation and metastasis of HCC cells both in vitro and in vivo by modulating the RTP3/STAT3 signalling pathway. Conclusion Our findings underscore the critical role of the TRPM8‐RTP3‐STAT3 axis in maintaining the malignant progression of HCC. Moreover, our study demonstrates that AD80 is involved in anti‐tumour processes by upregulating the expression of TRPM8.

Abstract Pediatric B-cell acute lymphoblastic leukemia (B-ALL) is a highly heterogeneous disease. According to large-scale RNA sequencing (RNA-seq) data, B-ALL patients can be divided into more than 10 subgroups. However, many genomic defects associated with resistance mechanisms have not yet been identified. As an individual clinical tool for molecular diagnostic risk classification, RNA-seq and gene expression pattern-based therapy could be potential upcoming strategies. In this study, we retrospectively analyzed the RNA-seq gene expression profiles of 45 children whose molecular diagnostic classifications were inconsistent with the response to chemotherapy. The relationship between the transcriptome and chemotherapy response was analyzed. Fusion gene identification was conducted for the included patients who did not have known high-risk associated fusion genes or gene mutations. The most frequently detected fusion gene pair in the high-risk group was the DHRSX duplication, which is a novel finding. Fusions involving ABL1, LMNB2, NFATC1, PAX5, and TTYH3 at onset were more frequently detected in the high-risk group, while fusions involving LFNG, TTYH3, and NFATC1 were frequently detected in the relapse group. According to the pathways involved, the underlying drug resistance mechanism is related to DNA methylation, autophagy, and protein metabolism. Overall, the implementation of an RNA-seq diagnostic system will identify activated markers associated with chemotherapy response, and guide future treatment adjustments.

Purpose: This study aims to identify the key factors influencing health-related quality of life (HRQoL) of pediatric acute myeloid leukemia (AML) patients following their initial diagnosis and examine their impact on the five-year survival prognosis. Methods: A chart review and follow-up were conducted for children with AML who participated in a prospective cohort study between 2017 and 2020. We identified factors influencing HRQoL through Pediatric Quality of Life Inventory™ (PedsQL™ 4.0), PedsQL™ Cancer Module 3.0 (CM 3.0) and PedsQL™ Family Impact Module 2.0 (FIM 2.0), as well as assessed the impact of impaired HRQoL on the overall outcomes of patients. Results: Sixty-four subjects enrolled in the study had complete HRQoL outcome data, and 61 of them completed the 5-year follow-up. In CM 3.0, age was positively associated with parental proxy reports (p = 0.040), whereas divorced families were negatively associated with child self-reports (p = 0.045). A positive medical history correlates with FIM 2.0 (p = 0.025). Residence (p = 0.046), the occupation of caregivers (p = 0.014), disease severity (p = 0.024), and the only child (p = 0.029) exhibited statistically significant associations with the impairment of HRQoL. Impaired HRQoL scores shown by the PedsQL™4.0 parent proxy report (p = 0.013) and FIM 2.0 (p = 0.011) were associated with a reduced 5-year survival rate. Conclusions: This study demonstrated that early impairment of HRQoL in pediatric acute myeloid leukemia patients has predictive value for long-term prognosis. Once validated, these findings may provide some guidance to clinicians treating children with AML.

Abstract Background Damage in the ischemic core and penumbra after stroke affects patient prognosis. Microglia immediately respond to ischemic insult and initiate immune inflammation, playing an important role in the cellular injury after stroke. However, the microglial heterogeneity and the mechanisms involved remain unclear. Methods We first performed single-cell RNA-sequencing (scRNA-seq) and spatial transcriptomics (ST) on middle cerebral artery occlusion (MCAO) mice from three time points to determine stroke-associated microglial subclusters and their spatial distributions. Furthermore, the expression of microglial subcluster-specific marker genes and the localization of different microglial subclusters were verified on MCAO mice through RNAscope and immunofluorescence. Gene set variation analysis (GSVA) was performed to reveal functional characteristics of microglia sub-clusters. Additionally, ingenuity pathway analysis (IPA) was used to explore upstream regulators of microglial subclusters, which was confirmed by immunofluorescence, RT-qPCR, shRNA-mediated knockdown, and targeted metabolomics. Finally, the infarct size, neurological deficits, and neuronal apoptosis were evaluated in MCAO mice after manipulation of specific microglial subcluster. Results We discovered stroke-associated microglial subclusters in the brains of MCAO mice. We also identified novel marker genes of these microglial subclusters and defined these cells as ischemic core-associated (ICAM) and ischemic penumbra-associated (IPAM) microglia, according to their spatial distribution. ICAM, induced by damage-associated molecular patterns, are probably fueled by glycolysis, and exhibit increased pro-inflammatory cytokines and chemokines production. BACH1 is a key transcription factor driving ICAM generation. In contrast, glucocorticoids, which are enriched in the penumbra, likely trigger IPAM formation, which are presumably powered by the citrate cycle and oxidative phosphorylation and are characterized by moderate pro-inflammatory responses, inflammation-alleviating metabolic features, and myelinotrophic properties. Conclusions ICAM could induce excessive neuroinflammation, aggravating brain injury, whereas IPAM probably exhibit neuroprotective features, which could be essential for the homeostasis and survival of cells in the penumbra. Our findings provide a biological basis for targeting specific microglial subclusters as a potential therapeutic strategy for ischemic stroke.

Purpose: Acute lymphoblastic leukemia (ALL) is the most common type of cancer diagnosed in children. Despite cure rates of higher than 85 %, refractory or relapsed ALL still exhibits a bleak prognosis indicative of the dearth of treatment modalities specific for relapsed or refractory ALL. Prior research has implicated metabolic alterations in leukemia pathogenesis, and literature on the therapeutic efficacy of arsenic compounds targeting metabolic pathways in B-cell acute lymphoblastic leukemia (B-ALL) cells is scarce. Methods: A compound extracted from realgar, tetraarsenic tetrasulfide (As4S4), and its antitumor effects on B-ALL were experimentally examined in vitro and in vivo. Results: As4S4 apparently targets B-ALL cells by inducing specific cellular responses, including apoptosis, G2/M arrest, and ferroptosis. Interestingly, these effects are attributed to reactive oxygen species (ROS) accumulation, and increased ROS levels have been linked to both the mitochondria-dependent caspase cascade and the activation of p53 signaling. The ROS scavenger N-acetylcysteine (NAC) can counteract the effects of As4S4 treatment on Nalm-6 and RS4;11 cells. Specifically, by targeting Hexokinase-2 (HK2), As4S4 induces alterations in mitochondrial membrane potential and disrupts glucose metabolism, leading to ROS accumulation, and was shown to inhibit B-ALL cell proliferation in vitro and in vivo. Intriguingly, overexpression of HK2 can partially desensitize B-ALL cells to As4S4 treatment. Conclusion: Tetraarsenic tetrasulfide can regulate the Warburg effect by controlling HK2 expression, a finding that provides both new mechanistic insight into metabolic alterations and pharmacological evidence for the clinical treatment of B-ALL.

The wing is one of the most important parts of a bird's locomotor system and is the inspiration origination for bionic wing design. During wing motions, the wing shape is closely related to the rotation angles of wing bones. Therefore, the research on the law of bone movement in the process of wing movement can be good guidance for the design of the bionic morphing wing. In this paper, the skeletal posture of the peregrine falcon wing during the extension/flexion is studied to obtain critical data on skeletal posture. Since an elbow joint and a wrist joint rotate correlatively to drive a wing to flex/extend, the wing skeleton is simplified as a four-bar mechanism in this paper. The degree of reproduction of wing skeleton postures was quantitatively analyzed using the four-bar mechanism model, and the bionic wing skeleton was designed. It is found that the wing motions have been reproduced with high precision.

Abstract Background There is a paucity of data regarding the prevalence of preoperative deep vein thrombosis (DVT) in patients with long bone (including femur, tibia and fibula) fractures of the lower limbs. We performed a meta-analysis to address the issue. Methods Electronic databases, including PubMed, EMBASE, the Web of Science, the Cochrane Library, the VIP database, CNKI, and the Wanfang database, were systematic searched for original articles that reported the prevalence of preoperative DVT in long bone fractures of the lower limbs from January 2016 to September 2021. The prevalence of preoperative DVT was pooled using random-effects models, and subgroups were established according to study type, detection method, sample size and fracture site. Results Twenty-three articles reporting on 18,119 patients were eligible. The overall pooled preoperative DVT prevalence was 24.1% (95% CI 19.3–28.8%). In different subgroups, the preoperative DVT prevalences were 18.2–27.3%, 15.2–28.6%, 23.1–24.9%, 18.2–26.0% and 23.2–23.4% for different study designs, sample sizes, age groups, detection methods and fracture sites, respectively. Conclusions Despite the heterogeneity among studies, this systematic review suggests that the prevalence of preoperative DVT, which may seriously affect the prognosis of patients, is high. Therefore, greater efforts should be devoted to the improvement of screening and prevention strategies for preoperative DVT in lower-extremity long bone fractures. Level of Evidence: Level III. Trial Registration The study was registered in the International Prospective Register of Systematic Reviews (PROSPERO) database with the registration number CRD42022324706.

Abstract Switch/sucrose-nonfermenting (SWI/SNF) complexes play a key role in chromatin remodeling. Recent studies have found that SMARCC2, as the core subunit of the fundamental module of the complex, plays a key role in its early assembly. In this study, we found a unique function of SMARCC2 in inhibiting the progression of glioblastoma by targeting the DKK1 signaling axis. Low expression of SMARCC2 is found in malignant glioblastoma (GBM) compared with low-grade gliomas. SMARCC2 knockout promoted the proliferation of glioblastoma cells, while its overexpression showed the opposite effect. Mechanistically, SMARCC2 negatively regulates transcription by dynamically regulating the chromatin structure and closing the promoter region of the target gene DKK1, which can be bound by the transcription factor EGR1. DKK1 knockdown significantly reduced the proliferation of glioblastoma cell lines by inhibiting the PI3K–AKT pathway. We also studied the functions of the SWIRM and SANT domains of SMARCC2 and found that the SWIRM domain plays a more important role in the complete chromatin remodeling function of SMARCC2. In addition, in vivo studies confirmed that overexpression of SMARCC2 could significantly inhibit the size of intracranial gliomas in situ in nude mice. Overall, this study shows that SMARCC2, as a tumor suppressor, inhibits the proliferation of glioblastoma by targeting the transcription of the oncogene DKK1 through chromatin remodeling, indicating that SMARCC2 is a potentially attractive therapeutic target in glioblastoma.

Zinc finger protein 384 ( ZNF384 ) encodes a C2H2-type zinc finger protein that can function as a transcription factor. ZNF384 rearrangement in acute lymphoblastic leukemia (ALL) was first reported in 2002. More than 19 different ZNF384 fusion partners have been detected in ALL. These include E1A-binding protein P300 ( EP300 ), CREB-binding protein ( CREBBP ), transcription factor 3 ( TCF3 ), TATA-box binding protein associated factor 15 ( TAF15 ), Ewing sarcoma breakpoint region 1 gene ( EWSR1 ), AT-rich interactive domain-containing protein 1B ( ARID1B ), SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily A, member 4 ( SMARCA4 ), SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily A, member 2 ( SMARCA2 ), synergin gamma ( SYNRG ), clathrin heavy chain ( CLTC ), bone morphogenic protein 2-inducible kinase ( BMP2K ), Nipped-B-like protein ( NIPBL ), A Kinase Anchoring Protein 8 ( AKAP8 ), Chromosome 11 Open Reading Frame 74 ( C11orf74 ), DEAD-Box Helicase 42 ( DDX42 ), ATP Synthase F1 Subunit Gamma ( ATP2C1 ), Euchromatic Histone Lysine Methyltransferase 1 ( EHMT1 ), Testic Expressed 41 ( TEX41 ), etc. Patients diagnosed with ALL harboring ZNF384 rearrangements commonly had a good prognosis. The mechanisms, performance, and features of different ZNF384 rearrangements in acute lymphoblastic leukemia have been well evaluated.

Abstract The China Energy Administration has issued policies to encourage energy storage to participate in the electric auxiliary service market, which will provide ideas for electric vehicle charging stations (EVCSs) to collectively participate in peak‐regulation and frequency modulation (FM). Taking into account the benefits of EVs participating in peak‐regulation and FM, this paper studies expansion planning for EVCSs. First, the orderly scheduling strategy of EVs under vehicle‐to‐grid (V2G) technology is established in this paper. And a peak regulation method is proposed to maximize the economic benefits of charging and discharging during peak and valley periods. Second, based on the temporal and spatial prediction model of EV charging demand, the expansion planning model of EVCSs is constructed considering the benefits of peak‐regulation and FM. Aiming at minimizing the comprehensive annual social cost of charging stations, the expansion site selection and capacity scheme of EVCSs are obtained. Finally, taking the 24 nodes in Xiangzhou District of Zhuhai City as an example, the location and capacity of the final annual expansion plan are obtained. And the influence of main control parameters on the results of the whole model and method is analysed in detail, the feasibility and effectiveness of the whole model and method are verified.

Why are lubricant-infused surfaces so effective at reducing drag in microfluidic flow? Here, authors reveal that infused nanostructured Teflon wrinkles induce large interfacial slip due to the spontaneous nucleation of surface nanobubbles, a mechanism likely to occur on most rough infused surfaces.

Background: Hereditary spherocytosis (HS) is an autosomal dominant (AD) and autosomal recessive (AR) disorder that is mostly caused by mutations of the erythrocyte membrane-related gene ANK1.Methods: Clinical and genetic testing data of 17 HS children with ANK1 gene mutations were retrospectively collected. Clinical manifestations and phenotypic analysis of HS were summarized based on our experience and literature review.Results: A total of 17 mutations of the ANK1 gene were identified from 17 probands (12 sporadic cases and five familial cases), including 15 novel mutations and two previously reported ones. Among the 15 novel variants of ANK1, there were four non-sense mutations, four frameshift mutations, three splicing mutations, three missense mutations and one in-frame deletion of three amino acids. In the present study, HS patients with mutations in membrane binding domains had significantly lower hemoglobin (Hb) levels and higher total bilirubin (T-Bil) levels than those with mutations in regulatory domains. After reviewing and analyzing all available published reports of Chinese HS patients carrying ANK1 mutations in PubMed and Chinese journals, there were no significant differences in Hb, Ret and T-Bil between different mutation types or mutation regions.Conclusion: Mutations of the ANK1 can be inherited or de novo. Clinical manifestations of HS in children caused by ANK1 mutations are similar to those of other types of hemolytic anemia. Our report expands the mutation spectrum of HS, thus providing references for clinical management and genetic counseling of HS.

IntroductionNecroptosis-related genes are essential for the advancement of IDH-wild-type GBM. However, the putative effects of necroptosis-related lncRNAs (nrlncRNAs) in IDH-wild-type GBM remain unknown.MethodsBy using the TCGA and GTEx databases, a nrlncRNA prognostic signature was created using LASSO Cox regression. The median risk score was used to categorize the patients into low and high-risk groups. To confirm the validity, univariate, multivariate Cox regression and ROC curves were used. Furthermore, by enrichment analysis, immune correlation analysis, and drug sensitivity analysis, the targeted lncRNAs were selected for further verification. As the highest upregulated expression in tumor than peritumor specimens, RP11-131L12.4 was selected for phenotype and functional experiments in primary GBM cells.ResultsSix lncRNAs were proved to be closely related to necroptosis in IDH-1-wild-type GBM, which were used to create a new signature. For 1-, 2-, and 3-year OS, the AUCs were 0.709, 0.645 and 0.694, respectively. Patients in the low-risk group had a better prognosis, stronger immune function activity, and more immune cell infiltration. In contrast, enrichment analysis revealed that the malignant phenotype was more prevalent in the high-risk group. In vitro experiments indicated that RP11-131L12.4 increased the tumor proliferation, migration and invasion, but decreased the necroptosis. Moreover, this nrlncRNA was also proved to be negatively associated with patient prognosis.ConclusionThe signature of nrlncRNAs may aid in the formulation of tailored and precise treatment for individuals with IDH-wild-type GBM. RP11-131L12.4 may play indispensable role in necroptosis suppression.

Abstract Background The aim of this study was to quantitatively summarize the available evidence on the association of breastfeeding with the risk of childhood cancer. Methods A literature search of PubMed and Embase databases was performed to identify eligible observational studies published from inception to July 17, 2020. The categorical and dose-response meta-analysis was conducted by pooling relative risk (RR) or odds ratio (OR) estimates with 95% confidence intervals (CIs). Potential sources of heterogeneity were detected by meta-regression and stratification analysis. Sensitivity analysis and publication bias test were also carried out. Results Forty-five articles involving 475,579 individuals were included in the meta-analysis. Among the thirty-three studies on the association between breastfeeding and risk of childhood leukemia, the pooled risk estimates were 0.77 (95% CI, 0.65–0.91) and 0.77 (95% CI 0.63–0.94) for ever versus non/occasional breastfeeding and longest versus shortest breastfeeding duration group, respectively. There was clear indication for non-linear dose-response relationship between breastfeeding duration and the risk of childhood leukemia (P non-linear

Ischemic stroke is the second leading cause of death worldwide with limited medications and neuroinflammation was recognized as a critical player in the progression of stroke, but how to control the overactive neuroinflammation is still a long-standing challenge. Here, we designed a novel SIRT6 activator MDL-811 which remarkably inhibited inflammatory response in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages and primary mouse microglia, which were abolished by silencing SIRT6. RNA-seq screening identified the forkhead box C1 (Foxc1) is a key gene evoked by MDL-811 stimulation and is required for the anti-inflammatory effects of MDL-811. We found MDL-811-activated SIRT6 directly interacted with enhancer of zeste homolog 2 (EZH2) and promoted deacetylation of EZH2 which could bind to the promoter of Foxc1 and upregulate its expression to modulate inflammation. Moreover, our data demonstrated that MDL-811 not only ameliorated sickness behaviors in neuroinflammatory mice induced by LPS, but also markedly reduced the brain injury in ischemic stroke mice in addition to promoting long-term functional recovery. Importantly, MDL-811 also exhibited strong anti-inflammatory effects in human monocytes isolated from ischemic stroke patients, underlying an interesting translational perspective. Taken together, MDL-811 could be an alternative therapeutic candidate for ischemic stroke and other brain disorders associated with neuroinflammation.

Abstract Cisplatin resistance is frequently occurred in ovarian cancer therapy, understanding its regulatory mechanisms is critical for developing novel treatment methods and drugs. Here, we found ovarian cancer patients with low FAM83B levels had shorter survival time, tissues with cisplatin resistance also had low FAM83B levels, suggesting FAM83B might inhibit cisplatin resistance. FAM83B overexpression inhibits cisplatin resistance showed in increased ovarian cancer cell proliferation and growth rate, and reduced apoptosis rate, while FAM83B knockdown promotes cisplatin resistance. Mechanism analysis showed FAM83B interacted with APC to inhibit Wnt pathway activity, causing ovarian cancer cisplatin resistance. We also found FAM83B levels were negative with Wnt pathway activity in clinic samples, confirming FAM83B inhibited Wnt pathway activity. In summary, we found FAM83B inhibits ovarian cancer cisplatin resistance through inhibiting Wnt pathway, providing a new target for ovarian cancer therapy.

Abstract Background Bone marrow mesenchymal stem cells (BMSCs) have been used as important cell-based tools for clinical applications. Oxidative stress-induced apoptosis causes a low survival rate after transplantation, and the underlying mechanisms remain unknown. The endoplasmic reticulum (ER) and mitochondria are vital organelles regulated by adenosine monophosphate (AMP)-activated protein kinase (AMPK), especially during oxidative stress injury. Melatonin exerts an antioxidant effect by scavenging free radicals. Here, we aimed to explore whether cytoprotective melatonin relieves ER stress-mediated mitochondrial dysfunction through AMPK in BMSCs after oxidative stress injury. Methods Mouse BMSCs were isolated and exposed to H2O2 in the absence or presence of melatonin. Thereafter, cell damage, oxidative stress levels, mitochondrial function, AMPK activity, ER stress-related proteins, and apoptotic markers were measured. Additionally, the involvement of AMPK and ER stress in the melatonin-mediated protection of BMSCs against H2O2-induced injury was investigated using pharmacologic agonists and inhibitors. Results Melatonin improved cell survival and restored mitochondrial function. Moreover, melatonin intimately regulated the phosphorylation of AMPK and molecules associated with ER stress pathways. AMPK activation and ER stress inhibition following melatonin administration improved the mitochondrial membrane potential (MMP), reduced mitochondria-initiated oxidative damage, and ultimately suppressed apoptotic signaling pathways in BMSCs. Cotreatment with N-acetyl-l-cysteine (NAC) significantly enhanced the antioxidant effect of melatonin. Importantly, pharmacological AMPK activation/ER stress inhibition promoted melatonin-induced cytoprotection, while pharmacological AMPK inactivation/ER stress induction conferred resistance to the effect of melatonin against H2O2 insult. Conclusions Our data also reveal a new, potentially therapeutic mechanism by which melatonin protects BMSCs from oxidative stress-mediated mitochondrial apoptosis, possibly by regulating the AMPK-ER stress pathway.

TAGAP gene variants are linked to human autoimmunity. Here the authors identify TAGAP as a Dectin-1 and EphB2-binding protein mediating antifungal innate immune signaling and cytokine production, and demonstrate TAGAP in non-T cells promotes Th17 response in mouse models of infection and autoimmunity.

With the rapid development of electric vehicle (EV) technology under the background of double carbon, a reasonable evaluation of the network planning of EV charging stations is conducive to the long-term stable development of the EV industry. Therefore, this paper proposes a comprehensive evaluation system and method for EV charging networks under the traffic network and power grid coupling. First, an EV travel model is developed based on the travel probability matrix to analyze the spatial and temporal characteristics of EVs. Secondly, the coupling relationship among users, charging network, road network, and the power grid is analyzed, four criteria of user feedback, charging network operation, road network operation impact, and power grid operation impact are proposed, and corresponding evaluation indexes are constructed under each criterion to form a comprehensive evaluation index system. Furthermore, the Analytic Hierarchy Process (AHP) and entropy weighting method are used to assign weights to the index layer and the criterion layer respectively, and the improved TOPSIS evaluation method is used to quantitatively analyze the impact of charging networks on different subjects for comprehensive evaluation. Finally, through the comprehensive evaluation of different charging network planning schemes, the effectiveness of the comprehensive evaluation method and model proposed in this paper is verified, which can provide a reference basis for the planning and improvement of EV charging station networks.

Summary: Vascular smooth muscle cells (VSMCs) have been widely recognized as key players in regulating blood-brain barrier (BBB) function, and their roles are unclear in ischemic stroke. Myosin phosphatase target subunit 1 (MYPT1) is essential for VSMC contraction and maintaining healthy vasculature. We generated VSMC-specific MYPT1 knockout (MYPT1SMKO) mice and cultured VSMCs infected with Lv-shMYPT1 to explore phenotypic switching of VSMCs and the accompanied impacts on BBB integrity. We found that MYPT1 deficiency induced phenotypic switching of synthetic VSMCs, which aggravated BBB disruption. Proteomic analysis identified evolutionarily conserved signaling intermediates in Toll pathways (ECSIT) as a downstream molecule that promotes activation of synthetic VSMCs and contributed to IL-6 expression. Knocking down ECSIT rescued phenotypic switching of VSMCs and BBB disruption. Additionally, inhibition of IL-6 decreased BBB permeability. These findings reveal that MYPT1 deficiency activated phenotypic switching of synthetic VSMCs and induced BBB disruption through ECSIT-IL-6 signaling after ischemic stroke.

Traditional charging stations have a single function, which usually does not consider the construction of energy storage facilities, and it is difficult to promote the consumption of new energy. With the gradual increase in the number of new energy vehicles (NEVs), to give full play to the complementary advantages of source-load resources and provide safe, efficient, and economical energy supply services, this paper proposes the optimal operation strategy of a PV-charging-hydrogenation composite energy station (CES) that considers demand response (DR). Firstly, the operation mode of the CES is analyzed, and the CES model, including a photovoltaic power generation system, fuel cell, hydrogen production, hydrogen storage, hydrogenation, and charging, is established. The purpose is to provide energy supply services for electric vehicles (EVs) and hydrogen fuel cell vehicles (HFCVs) at the same time. Secondly, according to the travel law of EVs and HFCVs, the distribution of charging demand and hydrogenation demand at different periods of the day is simulated by the Monte Carlo method. On this basis, the following two demand response models are established: charging load demand response based on the price elasticity matrix and interruptible load demand response based on incentives. Finally, a multi-objective optimal operation model considering DR is proposed to minimize the comprehensive operating cost and load fluctuation of CES, and the maximum–minimum method and analytic hierarchy process (AHP) are used to transform this into a linearly weighted single-objective function, which is solved via an improved moth–flame optimization algorithm (IMFO). Through the simulation examples, operation results in four different scenarios are obtained. Compared with a situation not considering DR, the operation strategy proposed in this paper can reduce the comprehensive operation cost of CES by CNY 1051.5 and reduce the load fluctuation by 17.8%, which verifies the effectiveness of the proposed model. In addition, the impact of solar radiation and energy recharge demand changes on operations was also studied, and the resulting data show that CES operations were more sensitive to energy recharge demand changes.

Significant developments have been observed in recent years, in the field of deep part exploration in the Bozhong Sag, Bohai Bay Basin in eastern China. The BZ19-6 large condensate gas field, the largest gas field in the Bohai Bay Basin, was discovered for the first time in a typical oil-type basin. The proven oil and gas geological reserves in the deeply buried hills of the Archean metamorphic rocks, amount to approximately 3×108 tons of oil equivalent. However, the phase behavior and genetic mechanisms of hydrocarbon fluids are still unclear. In this study, the phase diagram identification method and various empirical statistical methods, such as the block diagram method, φ1 parameter method, rank number method, and Z-factor method were implemented to comprehensively identify the phase behavior types of the BZ19-6 condensate gas reservoir. The genetic mechanism of the BZ19-6 condensate gas reservoir was investigated in detail through analyses of physical properties of the fluid at high temperatures and pressures, organic geochemical characteristics of condensate oil and gas, and regional tectonic background. Consequently, this study is shown as follows: (1) The BZ19-6 condensate gas reservoir is a part of a secondary condensate gas reservoir with oil rings, formed synthetically since the Neogene period due to multiple factors, such as retrograde evaporation from deep burial and high temperature, inorganic CO2 charging from the deep mantle, and late natural gas invasion. (2) The hydrocarbon accumulation process of the BZ19-6 condensate gas reservoir is as follows: First, a large amount of oil is accumulated at the end of the lower Minghuazhen deposition (5 Ma BP); second, a large amount of natural gas is generated in the deep-source kitchen and mantle-derived inorganic CO2 charged into the early formed oil reservoirs at the end of the upper Minghuazhen deposition (2 Ma BP). As a result, the content of gaseous hydrocarbons in the hydrocarbon system of the reservoir increased, which led to large amounts of liquid hydrocarbons dissolved in gaseous hydrocarbons and significantly reduced the critical temperature of the hydrocarbon system. Therefore, existing secondary condensate gas reservoirs are formed when the critical temperature is lower than the formation temperature and it enters the critical condensate temperature range.

Typical dolomite reservoirs exist in the upper assemblage of the Ordovician Majiagou Formation in the southeastern Sulige gas field, Ordos Basin, however, the current understanding of dolomite genesis needs to be clarified. This study confirms the dolomitization characteristics, diagenetic environment, and genesis of dolomite through the use of core observations, thin section identification, and geochemical data (carbon and oxygen stable isotopes, strontium isotopes, and major and trace element contents). The results showed that dolomite samples from the study area includes micritic dolomite, powder crystal dolomite, and micrite to powder crystal dolomite, in which the main reservoir space consisted of intergranular pores, intercrystalline pores and various dissolved pores. The δ 13 C value of the dolomite samples ranged from −7.26‰ to1.28‰ with an average of −0.45‰, which is equivalent to that of seawater during the Ordovician. The δ 18 O value ranged from −9.94‰ to −6.32‰ with an average of −7.86‰, which is clearly more negative than that of the Ordovician seawater. The 87 Sr/ 86 Sr ratio varied from 0.70867 to 0.71033 with an average of 0.70946, which is significantly more positive than that of Ordovician seawater. The Mg/Ca ratio was lower than that of the seawater and close to 1:1. Overall, all of the samples were characterized by high Fe and Mn contents, while low Sr and Na contents. These results clearly indicate that the dolomitized fluid was closely related to seawater or a sea-source fluid. Furthermore, the restored paleosalinity, paleotemperature, and paleodepth also indicate that the dolomite was formed in a marine reducing environment. Combined with the petrological characteristics and geochemical indicators, two dolomitization models (mixed water dolomitization and burial dolomitization) were established for the upper assemblage of the Ordovician Majiagou Formation in southeastern Sulige gas field. We infer that mixed water dolomitization was dominant before the Carboniferous, whereas burial dolomitization was dominant after the Early Permian.

A Correction to this paper has been published: https://doi.org/10.1038/s41389-021-00303-4

TiO2 possesses a wide forbidden band of about 3.2 eV, which severely limits its visible light absorption efficiency. In this work, copper nitride (Cu3N) films were prepared by magnetron sputtering at different gas flow ratios. The structure of the films was tested by scanning electron microscope, X-ray diffractometer, and X-ray photoelectron spectroscope. Optical properties were investigated by UV-vis spectrophotometer and fluorescence spectrometer. Results show that the Cu3N crystal possesses a typical anti-ReO3 crystal structure, and the ratio of nitrogen and Cu atoms of the Cu3N films was adjusted by changing the gas flow ratio. The Cu3N films possess an optical band gap of about 2.0 eV and energy gap of about 2.5 eV and exhibit excellent photocatalytic activity for degrading methyl orange (degradation ratio of 99.5% in 30 min). The photocatalytic activity of Cu3N mainly originates from vacancies in the crystal and Cu self-doping. This work provides a route to broaden the forbidden band width of photocatalytic materials and increase their photoresponse range.

Cu3N/MoS2 heterojunction was prepared through magnetron sputtering, and its optical band gap was investigated. Results showed that the prepared Cu3N/MoS2 heterojunction had a clear surface heterojunction structure, uniform surface grains, and no evident cracks. The optical band gap (1.98 eV) of Cu3N/MoS2 heterojunction was obtained by analyzing the ultraviolet-visible transmission spectrum. The valence and conduction band offsets of Cu3N/MoS2 heterojunction were 1.42 and 0.82 eV, respectively. The Cu3N film and multilayer MoS2 formed a type-II heterojunction. After the two materials adhered to form the heterojunction, the interface electrons flowed from MoS2 to Cu3N because the latter had higher Fermi level than the former. This behavior caused the formation of additional electrons in the Cu3N and MoS2 layers and the change in optical band gap, which was conducive to the charge separation of electrons in MoS2 or MoS2 holes. The prepared Cu3N/MoS2 heterojunction has potential application in various high-performance photoelectric devices, such as photocatalysts and photodetectors.

Background: Undetectable occult liver metastases block the long-term survival of pancreatic ductal adenocarcinoma (PDAC). This study aimed to develop a radiomics-based model to predict occult liver metastases and assess its prognostic capacity for survival. Materials and methods: Patients who underwent surgical resection and were pathologically proven with PDAC were recruited retrospectively from five tertiary hospitals between January 2015 and December 2020. Radiomics features were extracted from tumors, and the radiomics-based model was developed in the training cohort using LASSO-logistic regression. The model's performance was assessed in the internal and external validation cohorts using the area under the receiver operating curve (AUC). Subsequently, the association of the model's risk stratification with progression-free survival (PFS) and overall survival (OS) was then statistically examined using Cox regression analysis and the log-rank test. Results: A total of 438 patients [mean (SD) age, 62.0 (10.0) years; 255 (58.2%) male] were divided into the training cohort (n=235), internal validation cohort (n =100), and external validation cohort (n =103). The radiomics-based model yielded an AUC of 0.73 (95% CI: 0.66-0.80), 0.72 (95% CI: 0.62-0.80), and 0.71 (95% CI: 0.61-0.80) in the training, internal validation, and external validation cohorts, respectively, which were higher than the preoperative clinical model. The model's risk stratification was an independent predictor of PFS (all P <0.05) and OS (all P <0.05). Furthermore, patients in the high-risk group stratified by the model consistently had a significantly shorter PFS and OS at each TNM stage (all P <0.05). Conclusion: The proposed radiomics-based model provided a promising tool to predict occult liver metastases and had a great significance in prognosis. [ABSTRACT FROM AUTHOR]