CircItgb5 promotes synthetic phenotype of pulmonary artery smooth muscle cells via interacting with miR-96-5p and Uba1 in monocrotaline-induced pulmonary arterial hypertension.

BACKGROUND: Pulmonary arterial hypertension (PAH) is a rare but fatal cardiopulmonary disease mainly characterized by pulmonary vascular remodeling. Aberrant expression of circRNAs has been reported to play a crucial role in pulmonary vascular remodeling. The existing literature predominantly centers on studies that examined the sponge mechanism of circRNAs. However, the mechanism of circRNAs in regulating PAH-related protein remains largely unknown. This study aimed to investigate the effect of circItgb5 on pulmonary vascular remodeling and the underlying functional mechanism. MATERIALS AND METHODS: High-throughput circRNAs sequencing was used to detect circItgb5 expression in control and PDGF-BB-treated pulmonary arterial smooth muscle cells (PASMCs). Localization of circItgb5 in PASMCs was determined via the fluorescence in situ hybridization assay. Sanger sequencing was applied to analyze the circularization of Itgb5. The identification of proteins interacting with circItgb5 was achieved through a RNA pull-down assay. To assess the impact of circItgb5 on PASMCs proliferation, an EdU assay was employed. Additionally, the cell cycle of PASMCs was examined using a flow cytometry assay. Western blotting was used to detect biomarkers associated with the phenotypic switch of PASMCs. Furthermore, a monocrotaline (MCT)-induced PAH rat model was established to explore the effect of silencing circItgb5 on pulmonary vascular remodeling. RESULTS: CircItgb5 was significantly upregulated in PDGF-BB-treated PASMCs and was predominately localized in the cytoplasm of PASMCs. In vivo experiments revealed that the knockdown of circItgb5 attenuated MCT-induced pulmonary vascular remodeling and right ventricular hypertrophy. In vitro experiments revealed that circItgb5 promoted the transition of PASMCs to synthetic phenotype. Mechanistically, circItgb5 sponged miR-96-5p to increase mTOR level and interacted with Uba1 protein to activate the Ube2n/Mdm2/ACE2 pathway. CONCLUSIONS: CircItgb5 promoted the transition of PASMCs to synthetic phenotype by interacting with miR-96-5p and Uba1 protein. Knockdown of circItgb5 mitigated pulmonary arterial pressure, pulmonary vascular remodeling and right ventricular hypertrophy. Overall, circItgb5 has the potential for application as a therapeutic target for PAH.

GDF15 affects venous thrombosis by promoting EndMT through smad2/p-smad2 pathway.

BACKGROUND: Endothelial-to-mesenchymal transition (EndMT) is a pathophysiological change in the vascular endothelium commonly seen in the cardiovascular system. Elevated serum Growth differiention factor 15 (GDF15) has been reported in VTE patients, but the relationship and mechanism between GDF15, EndMT and VTE are still unclear. METHODS: We performed a retrospective clinical study, and human serum GDF15 expression levels were detected. The mouse DVT model was established through subtotal ligation of the mouse inferior vena cava, and then we detected intimal changes and thrombi in the stenotic inferior vena cava by haematoxylin-eosin (HE) staining, Masson staining, and Sirius Red staining. The expression levels of GDF15 and SM22 were detected by immunohistochemistry and RT‒qPCR. Serum samples of mice were collected, and the expression level of GDF15 in serum was detected. Human umbilical vein endothelial cells (HUVECs) were stimulated with a cytokine mixture (TGF-ß1 + TNF-α + IL-1ß). The role and mechanism of GDF15 in EndMT and VTE were detected in HUVECs and in a DVT mice model. RESULTS: We found that serum GDF15 levels in both VTE patients and mouse DVT models were higher than those in the control group. EndMT was increased in the stenotic vascular tissue of mice. Further experiments showed that GDF15 could promote the EndMT of HUVECs and reduce their anticoagulation and antifibrinolytic ability through the smad2/p-smad2/snail pathway. Inhibition of mature GDF15 release can significantly reduce venous thrombotic fibre deposition in mice. CONCLUSIONS: GDF15 positively promotes EndMT through activation of the Smad2/psmad2/snail pathway, and inhibition of GDF15 expression can alleviate the EndMT process, further improving the coagulation and fibrinolytic function of endothelial cells and thus reducing the local fibre deposition of venous thrombi.

Helenalin Facilitates Reactive Oxygen Species-Mediated Apoptosis and Cell Cycle Arrest by Targeting Thioredoxin Reductase-1 in Human Prostate Cancer Cells.

BACKGROUND Helenalin is a pseudoguaianolide natural product with anti-cancer activities. This study investigated the underlying mechanism of the anti-prostate cancer effects of helenalin in vitro. MATERIAL AND METHODS CCK-8 assay was performed to detect the optimal concentrations of helenalin in DU145 and PC-3 cells. After exposure to helenalin and/or reactive oxygen species (ROS) inhibitor, ROS production was assessed by DCFH-DA staining. Thioredoxin reductase-1 (TrxR1) expression was detected by RT-qPCR and western blot. Moreover, apoptosis and cell cycle were evaluated by flow cytometry. Following TrxR1 knockdown or overexpression, TrxR1 expression, ROS generation, apoptosis, cell cycle, migration, and invasion were examined in cells co-treated with helenalin. RESULTS Helenalin distinctly repressed the viability of prostate cancer cells in a concentration-dependent manner. We chose 8 µM and 4 µM as the optimal concentrations of helenalin for DU145 and PC-3 cells, respectively. Helenalin treatment markedly triggered ROS production and lowered TrxR1 expression, which was ameliorated by ROS inhibitor. Exposure to helenalin facilitated apoptosis as well as G0/G1 cell cycle arrest, which was reversed by ROS inhibitor. Helenalin relieved the inhibitory effect of TrxR1 on ROS production. Furthermore, helenalin ameliorated the decrease in apoptosis rate and the shortening of G0/G1 phase as well as the increase in migration and invasion induced by TrxR1 overexpression. CONCLUSIONS Our findings revealed that helenalin accelerated ROS-mediated apoptosis and cell cycle arrest via targeting TrxR1 in human prostate cancer cells.

Inhibition of microRNA-500 has anti-cancer effect through its conditional downstream target of TFPI in human prostate cancer.

PURPOSE: We investigated the prognostic potential and regulatory mechanism of microRNA-500 (miR-500), and human gene of tissue factor pathway inhibitor (TFPI) in prostate cancer. METHODS: MiR-500 expression was assessed by qRT-PCR in prostate cancer cell lines and primary tumors. Cancer patients' clinicopathological factors and overall survival were analyzed according to endogenous miR-500 level. MiR-500 was downregulated in DU145 and VCaP cells. Its effect on prostate cancer proliferation, invasion in vitro, and tumorigenicity in vivo, were probed. Possible downstream target of miR-500, TFPI was assessed by luciferase assay and qRT-PCR in prostate cancer cells. In miR-500-downregulated DU145 and VCaP cells, TFPI was silenced to see whether it was directly involved in the regulation of miR-500 in prostate cancer. TFPI alone was either upregulated or downregulated in DU145 and VCaP cells. Their effect on prostate cancer development was further evaluated. RESULTS: MiR-500 is upregulated in both prostate cancer cells and primary tumors. In prostate cancer patients, high miR-500 expression is associated with poor prognosis and overall survival. In DU145 and VCaP cells, miR-500 downregulation inhibited cancer proliferation, invasion in vitro, and explant growth in vivo. TFPI was verified to be associated with miR-500 in prostate cancer. Downregulation of TFPI reversed anti-cancer effects of miR-500 downregulation in prostate cancer cells. However, neither TFPI upregulation nor downregulation alone had any functional impact on prostate cancer development. CONCLUSION: MiR-500 may be a potential biomarker and molecular target in prostate cancer. TFPI may conditionally regulate prostate cancer in miR-500-downregualted prostate cancer cells.

Leukemoid reaction in sarcomatoid renal cell carcinoma: a two-case report.

Leukemoid reaction is defined as reactive leukocytosis exceeding 40 × 109/l, with a significant increase in early neutrophil precursors, and can be a paraneoplastic manifestation of various malignant tumors. Leukemoid reaction is a sign for poor prognosis in solid tumors so is sarcomatoid renal cell carcinoma (SRCC) when compared to more differentiated histologies. Here, we are reporting two cases of leukemoid reaction after radical nephrectomy, both of which were diagnosed as SRCC pathologically. The operations were successful: no complications were observed and the patients were discharged in good condition. However, a few weeks later, the white blood cell (WBC) count gradually increased. Even though routine management was done immediately, the count was still elevating. A diagnosis of a leukemoid reaction was established and both of them died shortly thereafter. Due to the poor prognosis of most patients with malignant leukemoid reaction, leukemoid reaction may be a predictor of prognosis in patients with SRCC, but more data are needed.

What Is the Impact of Baseline Inflammatory and Hemostatic Indicators with the Risk of Mortality in Severe Inpatients with COVID-19: A Retrospective Study.

The purpose of the study was to investigate baseline inflammatory, hemostatic indicators and new-onset deep vein thrombosis (DVT) with the risk of mortality in COVID-19 inpatients. In this single-center study, a total of 401 COVID-19 patients hospitalized in Sir Run Run Shaw Hospital, Zhejiang University School of Medicine were enrolled from December 1, 2022 to January 31, 2023. The basic information, first laboratory examination results, imaging examination, and outcome-related indicators were compared between patients in the moderate and severe subgroups. We found that baseline D-dimer and baseline absolute neutrophil count (ANC) levels were associated with new-onset DVT and death in severe hospitalized patients with COVID-19. The odds ratio (OR) of baseline D-dimer and baseline ANC with mortality was 1.18 (95% confidence interval [CI], 1.08-1.28; P < .001) and 1.13 (95% CI, 1.06-1.21; P < .001). Baseline ANC was associated with the risk of death in severe hospitalized COVID-19 patients, irrespective of the DVT status. In addition, a significantly higher serum neutrophil activity was observed in severe COVID-19 inpatients with DVT or those deceased during hospital stay. New-onset DVT partially mediated the association between baseline D-dimer (indirect effect: 0.011, estimated mediating proportion: 67.0%), baseline ANC (indirect effect: 0.006, estimated mediating proportion: 48.7%), and mortality in severe hospitalized patients with COVID-19. In summary, baseline D-dimer and baseline absolute neutrophil count (ANC) levels were associated with the mortality in severe hospitalized patients with COVID-19, especially DVT inpatients. New-onset DVT partially mediated the association between baseline D-dimer, baseline ANC, and mortality in severe hospitalized patients with COVID-19.

Hyperhomocysteinemia is associated with the risk of venous thromboembolism in patients with mental illness: a case-control study.

Objective: The risk of venous thromboembolism in patients with mental illness has been insufficiently addressed. This study aimed to assess the correlation between hyperhomocysteinemia and venous thromboembolism prevalence among this population. Methods: Patients with a diagnosis of mental illness and concurrent venous thromboembolism, admitted to Sir Run Run Shaw Hospital at Zhejiang University School of Medicine between January 2014 and December 2021, were included in the venous thromboembolism group. The control group, approximately twice the size, comprised individuals with mental illness but without venous thromboembolism. Basic clinical data were gathered for both cohorts. Results: In psychiatric patients, elevated D-dimer levels(OR=5.60,95% CI 3.28-10.00), hyperhomocysteinemia (OR=2.37,95% CI 1.10-5.14), and hyperprolactinemia(OR= 2.68,95% CI 1.12-6.42)were significant risk factors for venous thromboembolism. According to further subgroup analyses, hyperhomocysteinemia is a significant risk factor associated with pulmonary embolism, with an OR of 5.08 (95% CI 1.20-21.48). An interaction effect between gender and homocysteine level was found, with a p-interaction of 0.022. A subsequent analysis confirmed the association between hyperhomocysteinemia and venous thromboembolism in female psychiatric patients, with an OR of 3.34 (95% CI 1.68-6.65), indicating that hyperhomocysteinemia is a significant risk factor for venous thromboembolism in women. Conclusion: Patients with psychiatric disorders were found to have an elevated risk of venous thromboembolism, which was associated with increased levels of D-dimer, hyperprolactinemia, and hyperhomocysteinemia. A strong correlation between hyperhomocysteinemia and pulmonary embolism was identified in patients with mental illnesses. Furthermore, the study revealed that female psychiatric patients with hyperhomocysteinemia constituted a high-risk group for venous thromboembolism. This finding holds significant clinical implications, suggesting that early preventative measures could be implemented for this high-risk population to reduce the incidence of thromboembolic events during hospitalization for psychiatric patients.

Ginsenoside Rb1 induces hepatic stellate cell ferroptosis to alleviate liver fibrosis via the BECN1/SLC7A11 axis.

Liver fibrosis is primarily driven by the activation of hepatic stellate cells (HSCs), a process associated with ferroptosis. Ginsenoside Rb1 (GRb1), a major active component extracted from Panax ginseng, inhibits HSC activation. However, the potential role of GRb1 in mediating HSC ferroptosis remains unclear. This study examined the effect of GRb1 on liver fibrosis both in vivo and in vitro, using CCl4-induced liver fibrosis mouse model and primary HSCs, LX-2 cells. The findings revealed that GRb1 effectively inactivated HSCs in vitro, reducing alpha-smooth muscle actin (α-SMA) and Type I collagen (Col1A1) levels. Moreover, GRb1 significantly alleviated CCl4-induced liver fibrosis in vivo. From a mechanistic standpoint, the ferroptosis pathway appeared to be central to the antifibrotic effects of GRb1. Specifically, GRb1 promoted HSC ferroptosis both in vivo and in vitro, characterized by increased glutathione depletion, malondialdehyde production, iron overload, and accumulation of reactive oxygen species (ROS). Intriguingly, GRb1 increased Beclin 1 (BECN1) levels and decreased the System Xc-key subunit SLC7A11. Further experiments showed that BECN1 silencing inhibited GRb1-induced effects on HSC ferroptosis and mitigated the reduction of SLC7A11 caused by GRb1. Moreover, BECN1 could directly interact with SLC7A11, initiating HSC ferroptosis. In conclusion, the suppression of BECN1 counteracted the effects of GRb1 on HSC inactivation both in vivo and in vitro. Overall, this study highlights the novel role of GRb1 in inducing HSC ferroptosis and promoting HSC inactivation, at least partly through its modulation of BECN1 and SLC7A11.

Effects of non-pharmacological interventions on pain in wound patients during dressing change: A systematic review.

BACKGROUND: Changes to the wound dressing frequently cause pain. Some adverse side effects of pharmacologic pain management may cause problems or even impede wound healing. There is no systematic study of non-pharmacologic therapies for pain during wound dressing changes, despite the gradual promotion of non-pharmacologic pain reduction methods. OBJECTIVES: To give clinical wound pain management a new direction, locating and assessing non-pharmacological interventions regarding pain brought on by wound dressing changes are necessary. METHOD: The researchers conducted a comprehensive literature review on non-pharmacological interventions for pain during wound dressing changes across five databases: PubMed, Web of Science, Medline, Embase, and the Cochrane Library spanning the period from January 2010 to September 2022. The evaluation of literature and data extraction was carried out independently by two researchers, and in cases of disagreement, a third researcher participated in the deliberation. To assess the risk of bias in the literature, the researchers utilised the Cochrane Handbook for Reviews of Interventions, version 5.1.0. RESULTS: In total, 951 people were involved in 11 investigations covering seven non-pharmacological therapies. For pain triggered by dressing changes, virtual reality (VR) distraction, auditory and visual distractions, foot reflexology, religious and spiritual care, and guided imaging demonstrated partially positive effects, with hypnosis therapy and jaw relaxation perhaps having a weak effect. CONCLUSION: The key to managing wounds is pain management. According to our review, there is some indication that non-pharmacologic interventions can help patients feel less discomfort when having their wound dressings changed. However, the evidence supporting this view is weak. It needs to be corroborated by future research studies with multicentre and large samples. To promote and use various non-pharmacologic interventions in the future, it is also necessary to build standardised and homogenised paths for their implementation.

Lycopene from tomatoes and tomato products exerts renoprotective effects by ameliorating oxidative stress, apoptosis, pyroptosis, fibrosis, and inflammatory injury in calcium oxalate nephrolithiasis: the underlying mechanisms.

Several mechanisms underlying nephrolithiasis, one of the most common urological diseases, involve calcium oxalate formation, including oxidative stress, inflammatory reactions, fibrosis, pyroptosis, and apoptosis. Although lycopene has strong antioxidant activity, its protective effects against CaOx-induced injury have not yet been reported. This study aimed to systematically investigate the protective effects of lycopene and explore its mechanisms and molecular targets. Crystal deposition, renal function, oxidative stress, inflammatory response, fibrosis, pyroptosis, and apoptosis were assessed to evaluate the renoprotective effects of lycopene against crystal formation in a CaOx rat model and oxalate-stimulated NRK-52E and HK-2 cells. Lycopene markedly ameliorated crystal deposition, restored renal function, and suppressed kidney injury by reducing oxidative stress, apoptosis, inflammation, fibrosis, and pyroptosis in the rats. In cell models, lycopene pretreatment reversed reactive oxygen species increase, apoptotic damage, intracellular lactate dehydrogenase release, cytotoxicity, pyroptosis, and extracellular matrix deposition. Network pharmacology and proteomic analyses were performed to identify lycopene target proteins under CaOx-exposed conditions, and the results showed that Trappc4 might be a pivotal target gene for lycopene, as identified by cellular thermal shift assay and surface plasmon resonance analyses. Based on molecular docking, molecular dynamics simulations, alanine scanning mutagenesis, and saturation mutagenesis, we observed that lycopene directly interacts with Trappc4 via hydrophobic bonds, which may be attributed to the PHE4 and PHE142 residues, preventing ERK1/2 or elevating AMPK signaling pathway phosphorylation events. In conclusion, lycopene might ameliorate oxalate-induced renal tubular epithelial cell injury via the Trappc4/ERK1/2/AMPK pathway, indicating its potential for the treatment of nephrolithiasis.

NanoSHP099-Targeted SHP2 Inhibition Boosts Ly6Clow Monocytes/Macrophages Differentiation to Accelerate Thrombolysis.

Tumor-associated thrombus (TAT) accounts for a high proportion of venous thromboembolism. Traditional thrombolysis and anticoagulation methods are not effective due to various complications and contraindications, which can easily lead to patients dying from TAT rather than the tumor itself. These clinical issues demonstrate the need to research diverse pathways for adjuvant thrombolysis in antitumor therapy. Previously, the phenotypic and functional transformation of monocytes/macrophages is widely reported to be involved in intratribal collagen regulation. This study finds that myeloid deficiency of the oncogene SHP2 sensitizes Ly6Clow monocyte/macrophage differentiation and can alleviate thrombus organization by increasing thrombolytic Matrix metalloproteinase (MMP) 2/9 activities. Moreover, pharmacologic inhibition by SHP099, examined in mouse lung metastatic tumor models, reduces tumor and thrombi burden in tumor metastatic lung tissues. Furthermore, SHP099 increases intrathrombus Ly6Clow monocyte/macrophage infiltration and exhibits thrombolytic function at high concentrations. To improve the thrombolytic effect of SHP099, NanoSHP099 is constructed to achieve the specific delivery of SHP099. NanoSHP099 is identified to be simultaneously enriched in tumor and thrombus foci, exerting dual tumor-suppression and thrombolysis effects. NanoSHP099 presents a superior thrombus dissolution effect than that of the same dosage of SHP099 because of the higher Ly6Clow monocyte/macrophage proportion and MMP2/MMP9 collagenolytic activities in organized thrombi.

Bi3.64Mo0.36O6.55 nanoparticles anchored in BiOI: A p-n heterojunction photocatalyst to enhance water purification.

Selective constructing of heterojunctions enables directional electron-hole migration and favorable charge separation. In this study, a novel p-n junction Bi3.64Mo0.36O6.55 (BMO) nanoparticles anchored in BiOI construct by hydrothermal and subsequent in-situ synthesis. The construction of tight heterojunctions that enhance the characteristic absorption of visible light by Bi3.64Mo0.36O6.55/BiOI (BIMO) and expose more reactive sites can be used to facilitate the rapid degradation of antibiotics (Tetracycline, TC), endocrine disruptors (Bisphenol A, BPA) and dyes in water. In addition, the BIMO catalyst maintained the rapid degradation rate of TC despite the interference of inorganic anions and aqueous substrates. The charge transfer pathways and radical species between the heterojunction components were investigated. In addition, the intermediates and toxicological analysis showed that TC was further mineralized and the small molecule products were generated significantly less toxic and less contaminated. In conclusion, this study synthesized photocatalysts based on p-n heterojunctions, which have potential applications for the degradation of TC.

Construction of a novel double S-scheme structure WO3/g-C3N4/BiOI: Enhanced photocatalytic performance for antibacterial activity.

In recent years, the threat to human health from bacteria in wastewater has attracted attention, and photocatalytic technology has emerged as a promising strategy for inactivating bacteria in water. Therefore, it is of great research value to develop a novel high-efficiency photocatalytic system with the visible light response. We successfully designed a double S-scheme heterojunction composite WO3/g-C3N4/BiOI (WCB) in this paper. The preparation of WCB composites was demonstrated by a series of characterizations, including X-ray diffraction (XRD), X-ray photoelectron spectroscopy (XPS), Fourier transform infrared spectroscopy (FT-IR) and transmission electron microscopy (TEM). The antibacterial effects of photocatalysts against representative Gram-negative strain Escherichia coli (E. coli) and Gram-positive strain Staphylococcus aureus (S. aureus) were tested under LED light irradiation. The novel photocatalyst presented excellent antibacterial properties, inactivating E. coli in 12 min and S. aureus in 20 min. The bacterial cell inactivation process was studied by scanning electron microscopy (SEM) and Confocal Laser Scanning Microscopy (CLSM). Active species capture experiments show that the active species present in the WCB composites in the process of inactivating bacteria are h+, e-, OH and O2-. In conclusion, the synthesized double S-scheme WCB photocatalyst exhibits remarkable photocatalytic antibacterial activity under LED light and has broad prospects for practical application in water antibacterial treatment.

A novel Z-type heterojunction Bi3O4Cl/Bi4O5I2 photocatalytic composite with broad-spectrum antibacterial activity and degradation properties.

At present, the sustainable development of humans is facing health problems and ecological imbalance caused by environmental pollution. To solve the bacteria, antibiotics and other pollutants in wastewater, Bi3O4Cl and Bi4O5I2 with appropriate bandgap width were selected to prepare Z-type heterojunction Bi3O4Cl/Bi4O5I2 photocatalytic materials by calcination method. Under LED light, the best sample Bi3O4Cl/Bi4O5I2-4 could completely inactivate Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus) in 30 min, Bacillus subtilis (B. subtilis) and Pseudomonas aeruginosa (P. aeruginosa) in 20 min, and degrade 70.6% of tetracycline (TC) and 97.4% of Rhodamine B (RhB). Photocurrent and electrochemical impedance tests (EIS) confirmed the high photocurrent response and low charge transfer resistance in the Bi3O4Cl/Bi4O5I2. The photocatalytic antibacterial and degradation mechanism of Z-type Bi3O4Cl/Bi4O5I2 heterojunction was verified by capture experiments. Thus, this study provides a compact and efficient photocatalyst with broad-spectrum antibacterial activity and degradation properties.

Fabrication of n-p ß-Bi2O3@BiOI core/shell photocatalytic heterostructure for the removal of bacteria and bisphenol A under LED light.

A novel n-p ß-Bi2O3@BiOI core/shell heterostructure was successfully constructed by a facile ultrasonication method. SEM, TEM, XRD and XPS confirmed the core/shell structure. UV-vis indicated the composite had good absorption of visible light. Photocurrent and electrochemical impedance analysis (EIS) revealed effective electron (e-) and hole (h+) separation efficiency in the core/shell hybrid structure, which induced a significantly improved photocatalytic activity. The ß-Bi2O3@BiOI photocatalyst effectively treated with Escherichia coli (E. coli), Staphylococcus aureus (S. aureus) and bisphenol A (BPA) under LED light, and presented better photocatalytic antibacterial performance than ß-Bi2O3 and BiOI. Trapping experiment revealed that h+ played an important role in photocatalytic reaction. The present work provided a novel LED light-activated photocatalyst that was efficient for antibacterial application.

Constructing an S-scheme CuBi2O4/Bi4O5I2 heterojunction for lightemittingdiode-driven pollutant degradation and bacterial inactivation.

The CuBi2O4/Bi4O5I2 S-scheme heterojunction structure was constructed by a hydrothermal and subsequent calcination route. The combination of CuBi2O4 and Bi4O5I2 produced excellent photocatalytic performance under an LED light. A series of technical characterizations, including X-ray diffraction (XRD), scanning electron microscopy (SEM) and X-ray photoelectron spectroscopy (XPS), were used to determine the successful construction of S-scheme CuBi2O4/Bi4O5I2 composites. The improvement of photogenerated carrier separation efficiency helped to achieve the best photocatalytic performance of 37% CuBi2O4/Bi4O5I2, which can degrade tetracycline (TC) to 81.67% in 90 min, and completely inactivate Escherichia coli (E. coli) in 20 min and Staphylococcus aureus (S. aureus) in 40 min. The effects of some key parameters (such as the concentration of pollutants, the amount of catalyst, pH value of a solution, various inorganic anions and various water substrates) and the possible degradation path of tetracycline were systematically studied. Finally, the removal of pollutants and inactivation of bacterial mechanisms based on the S-scheme heterojunction (CuBi2O4/Bi4O5I2) was proposed. This study provides insight into the synthesis of S-scheme heterojunction photocatalysts, which can efficiently degrade organic pollutants and inactivate bacteria under LED light irradiation.

Organoids in lung cancer: A teenager with infinite growth potential.

Despite the rapid advancement in lung cancer research, morbidity and mortality remain high in recent years. Therefore, deeper learning of the underlying molecular mechanisms of pathogenesis and discovery of novel effective therapeutic strategies of treatment in lung cancer research are around the corner. Among these, applying an efficient and reliable preclinical model would be a critical step that exists throughout the whole process. Traditional 2D models used in lung cancer research, including lung cancer cell lines and cell-derived xenograft models, cannot recapitulate the situations of patients due to the lack of a tumor microenvironment or tumor heterogeneity. Organoids, newly developed 3D in vitro structures, more comprehensively imitate the architecture, interaction and genetics of human organs. Cancer organoids, especially those derived from individual patients, can better resemble primary tumor tissues and thus have a greater potential for making breakthroughs in future cancer studies. Here, we mainly review recent advances in the methodologies and applications of lung cancer organoids, which are just developing but have huge potential.

Development and validation of a novel necroptosis-related score to improve the outcomes of clear cell renal cell carcinoma.

Necroptosis has been indicated as a key regulator of tumor progression. However, the prognostic regulatory role of necroptosis in clear cell renal cell carcinoma (ccRCC) needs to be further investigated. In this study, necroptosis-related subtypes were identified by mining the public cohort (n = 530) obtained from The Cancer Genome Atlas. By applying Principal Component Analysis (PCA), the necroptosis-related scores (N-Score) were developed to assess the prognosis procession of ccRCC. The results were further validated by an external clinical cohort (n = 116) obtained from the First Affiliated Hospital of Wenzhou Medical University. It has been found that N-Score could precisely distinguish the prognostic outcomes of patients as an independent risk factor (Hazard ratio = 4.990, 95% confidence interval (CI) = 2.007-12.403, p < 0.001). In addition, changes in N-Score were associated with differences in tumor mutational burden as well as immune infiltration characterization. Moreover, higher N-Scores were also correlated significantly molecular drug sensitivity and stronger immune checkpoint activity. Notably, the prognosis of ccRCC could be effectively guided by combining the N-Scores and external clinical indicators. In conclusion, N-Scores could be served as a robust and effective biomarker to improve the prognosis outcomes and targeted therapy of ccRCC.

Facile synthesis CQDs/SnO2-x/BiOI heterojunction photocatalyst to effectively degrade pollutants and antibacterial under LED light.

To remove multitudinous pollutants from wastewater, the design of a highly efficient and multifunctional photocatalyst is necessary. A novel CQDs/SnO2-x/BiOI photocatalyst (named CSnBI composite) was prepared by combining carbon quantum dots (CQDs), large specific surface area SnO2-x nanocrystals and BiOI nanocrystals to obtain a compact hybrid structure. TEM and Raman techniques confirmed the structure of CSnBI composite. The photocurrent and EIS showed that the photoexcited electron-hole pairs separation efficiency was improved. As anticipated, novel CSnBI photocatalyst can successfully remove tetracycline, methyl orange, E. coli (Escherichia coli) and S. aureus under a LED light due to the hybridization contaction among CQDs, SnO2-x and BiOI. The mechanism showed that the introduction of CQDs promoted visible light absorption and efficient separation of photogenerated carriers of SnO2-x/BiOI heterojunction. The capture experiment and related measurements showed that h+, •O2- and •OH are active species in the photocatalytic process. This study gave a novel case for facile construction of photocatalysts with tight hybrid structure.