Role of the In-Situ-Formed Surface (Pt-S-O)-Ti Active Structure in SO2-Promoted C3H8 Combustion over a Pt/TiO2 Catalyst.

Typically, SO2 unavoidably deactivates catalysts in most heterogeneous catalytic oxidations. However, for Pt-based catalysts, SO2 exhibits an extraordinary boosting effect in propane catalytic oxidation, but the promotive mechanism remains contentious. In this study, an in situ-formed tactful (Pt-S-O)-Ti structure was concluded to be a key factor for Pt/TiO2 catalysts with a substantial SO2 tolerance ability. The experiments and theoretical calculations confirm that the high degree of hybridization and orbital coupling between Pt 5d and S 3p orbitals enable more charge transfer from Pt to S species, thus forming the (Pt-S-O)-Ti structure with the oxygen atom dissociated from the chemisorbed O2 adsorbed on oxygen vacancies. The active oxygen atom in the (Pt-S-O)-Ti active structure is a robust site for C3H8 adsorption, leading to a better C3H8 combustion performance. This work can provide insights into the rational design of chemical bonds for high SO2 tolerance catalysts, thereby improving economic and environmental benefits.

Rapid Ozone Decomposition over Water-activated Monolithic MoO3 /Graphdiyne Nanowalls under High Humidity.

Catalytic ozone (O3 ) decomposition at high relative humidity (RH) remains a great challenge due to the catalysts poison and deactivation under high humidity. Here, we firstly elaborate the role of water activation and the corresponding mechanism of the promoted O3 decomposition over the three-dimensional monolithic molybdenum oxide/graphdiyne (MoO3 /GDY) catalyst. The O3 decomposition over MoO3 /GDY reaches up to 100 % under high humid condition (75 % RH) at room temperature, which is 4.0 times as high as that of dry conditions, significantly surpasses other carbon-based MoO3 materials(≤7.1 %). The sp-hybridized carbon in GDY donates electrons to MoO3 along the C-O-Mo bond, facilitating water activation to form hydroxyl species. As a result, hydroxyl species dissociated from water act as new active sites, promoting the adsorption of O3 and the generation of new intermediate species (hydroxyl ⋅OH and superoxo ⋅O2 - ), which significantly lowers the energy barriers of O3 decomposition (0.57 eV lower than dry conditions).

circ_0006089 promotes gastric cancer growth, metastasis, glycolysis, and angiogenesis by regulating miR-361-3p/TGFB1.

Circular RNA (circRNA) participates in a variety of pathophysiological processes, including the development of gastric cancer (GC). However, the role of circ_0006089 in GC progression and its underlying molecular mechanism need to be further revealed. Quantitative real-time PCR was utilized for detecting circ_0006089, microRNA (miR)-361-3p and transforming growth factor-ß1 (TGFB1) expression. The interaction between miR-361-3p and circ_0006089 or TGFB1 was confirmed using a dual-luciferase reporter assay and an RNA immunoprecipitation (RIP) assay. Cell proliferation, metastasis, apoptosis, and angiogenesis were determined using colony formation assay, EdU assay, transwell assay, flow cytometry, and tube formation assay. Cell glycolysis was evaluated by detecting glucose consumption, lactate production, and ATP levels. In addition, western blot (WB) analysis was used to measure protein expression. Xenograft tumor models were used to assess the effect of circ_0006089 knockdown on GC tumorigenesis. circ_0006089 had been found to be upregulated in GC tissues and cells, and it could act as an miR-361-3p sponge. circ_0006089 knockdown suppressed GC proliferation, metastasis, glycolysis, angiogenesis, and increased apoptosis, while this effect could be revoked by miR-361-3p inhibitor. TGFB1 was targeted by miR-361-3p, and its overexpression reversed the effects of miR-361-3p on GC cell function. Also, circ_0006089 promoted TGFB1 expression via sponging miR-361-3p. Animal experiments showed that silenced circ_0006089 inhibited GC tumorigenesis through the miR-361-3p/TGFB1 pathway. Our results revealed that the circ_0006089/miR-361-3p/TGFB1 axis contributed to GC progression, confirming that circ_0006089 might be a potential therapeutic target for GC.

Hsa_circ_0001550 facilitates colorectal cancer progression through mediating microRNA-4262/nuclear casein kinase and cyclin-dependent kinase substrate 1 cascade.

BACKGROUND: Circular RNAs (circRNAs) play important roles in various malignancies, such as colorectal cancer (CRC). However, the function of hsa_circ_0001550 in CRC remains to be elucidated. METHODS: The expression levels of hsa_circ_0001550, microRNA (miR)-4262, and nuclear casein kinase and cyclin-dependent kinase substrate 1 (NUCKS1) were determined by real-time qPCR. Cell biological behaviors were evaluated via colony formation assay, transwell assay, flow cytometry, and sphere formation assays. The target relationship was validated via dual-luciferase reporter and RNA pull-down assays. Protein expression was analyzed by western blot. Xenograft tumor model was adopted to evaluate hsa_circ_0001550 function in vivo. RESULTS: Hsa_circ_0001550 enrichment was enhanced in CRC tissue specimens and cell lines. Hsa_circ_0001550 absence hindered CRC cell proliferation, metastasis, stemness, and caused apoptosis. Hsa_circ_0001550 targeted miR-4262, and hsa_circ_0001550 absence-caused impacts were diminished by anti-miR-4262. MiR-4262 targeted NUCKS1. Hsa_circ_0001550 had positive regulation on NUCKS1 expression. NUCKS1 overexpression overturned the influences of hsa_circ_0001550 silencingon CRC cell progression. Hsa_circ_0001550 interference notably blocked in vivo xenograft tumor growth. CONCLUSION: Hsa_circ_0001550 facilitated CRC progression by binding to miR-4262 to positively regulate NUCKS1 abundance.

A Stable and Conductive Covalent Organic Framework with Isolated Active Sites for Highly Selective Electroreduction of Carbon Dioxide to Acetate.

Electroreduction of CO2 to acetate provides a promising strategy to reduce CO2 emissions and store renewable energy, but acetate is usually a by-product. Here, we show a stable and conductive two-dimensional phthalocyanine-based covalent-organic framework (COF) as an electrocatalyst for reduction of CO2 to acetate with a single-product Faradaic efficiency (FE) of 90.3(2)% at -0.8 V (vs. RHE) and a current density of 12.5 mA cm-2 in 0.1 M KHCO3 solution. No obvious degradation was observed over 80 hours of continuous operation. Combined with the comparison of the properties of other catalysts with isolated metal active sites, theoretical calculations and in situ infrared spectroscopy revealed that the isolated copper-phthalocyanine active site with high electron density is conducive to the key step of C-C coupling of *CH3 with CO2 to produce acetate, and can avoid the coupling of *CO with *CO or *CHO to produce ethylene and ethanol.

Single-Product Faradaic Efficiency for Electrocatalytic of CO2 to CO at Current Density Larger than 1.2†A cm-2 in Neutral Aqueous Solution by a Single-Atom Nanozyme.

Electroreduction of CO2 to CO is a promising approach for the cycling use of CO2 , while it still suffers from impractical current density and durability. Here we report a single-atom nanozyme (Ni-N5 -C) that achieves industrial-scale performance for CO2 -to-CO conversion with a Faradaic efficiency (FE) exceeded 97 % over -0.8--2.4 V vs. RHE. The current density at -2.4 V vs. RHE reached a maximum of 1.23 A cm-2 (turnover frequency of 69.7 s-1 ) with an FE of 99.6 %. No obvious degradation was observed over 100 hours of continuous operation. Compared with the planar Ni-N4 site, the square-pyramidal Ni-N5 site has an increase and a decrease in the d z 2 ${{{\rm d}}_{{z}^{2}}}$ and dxz/yz orbital energy levels, respectively, as revealed by density functional theory calculations. Thus, the Ni-N5 catalytic site is more superior to activate CO2 molecule and reduce the energy barriers as well as promote the CO desorption, thus boosting the kinetic activation process and catalytic activity.

Highly Selective CO2 Electroreduction to C2H4 Using a Metal-Organic Framework with Dual Active Sites.

Conversion from CO2 to C2H4 is important for the development of energy and the environment, but the high energy barrier of hydrogenation of the *CO intermediate and C-C coupling step tend to result in C1 compounds as the main product and thus restrict the generation of C2H4. Here, we report a metal-organic framework (denoted as PcCu-Cu-O), composed of 2,3,9,10,16,17,23,24-octahydroxyphthalo-cyaninato)copper(II) (PcCu-(OH)8) ligands and the square-planar CuO4 nodes, as the electrocatalyst for CO2 to C2H4. Compared with the discrete molecular copper-phthalocyanine (Faradaic efficiency (FE) of C2H4 = 25%), PcCu-Cu-O exhibits much higher performance for electrocatalytic reduction of CO2 to C2H4 with a FE of 50(1)% and a current density of 7.3 mA cm-2 at the potential of -1.2 V vs RHE in 0.1 M KHCO3 solution, representing the best performance reported to date. In-situ infrared spectroscopy and control experiments suggested that the enhanced electrochemical performance may be ascribed to the synergistic effect between the CuPc unit and the CuO4 unit, namely the CO on the CO-producing site (CuO4 site) can efficiently migrate and dimerize with the *CO intermediate adsorbed on the C2H4-producing site (CuPc), giving a lower C-C dimerization energy barrier.

NCAPH is upregulated in endometrial cancer and associated with poor clinicopathologic characteristics.

BACKGROUND: Recently, NCAPH (non-SMC condensin I complex subunit H), a regulatory subunit of the condensin complex, has captured our attention in various cancer studies. However, the function of NCAPH in endometrial cancer (EC) remains unclear. Our study aims to investigate the role of NCAPH in EC. METHODS: The expression of NCAPH in EC tissues and normal tissues was predicted by The Cancer Genome Atlas (TCGA). The Kaplan-Meier analysis was performed to evaluate the impact of NCAPH expression on EC patients' survival. Logistic regression was used to study the correlation of NCAPH expression with clinicopathologic characteristics. Molecular mechanisms behind NCAPH in EC were evaluated by Gene Set Enrichment Analysis, genetic mutations, copy number variation, and DNA methylation level. RESULTS: NCAPH was significantly upregulated in EC (p = 1e-24), and its expression level was significantly related to the more advanced International Federation of Gynecology & Obstetrics (FIGO) stage (stage IV vs. stage I: odd ratio.[OR] = 3.7), higher grade (poor vs. well & moderate: OR = 5.3), serous histology subtype (SEA vs. EEA: OR = 8.5), myometrial invasion (≥50 vs. < 50 invasion: OR = 1.8), metastasis (vs. no metastasis: OR = 2.5), and with-tumor status (vs. free of tumor: OR = 2.3) (all p were less than .05). The Gene Set Enrichment Analysis method indicated that MITOTIC_SPINDLE, G2M_CHECKPOINT, MYC_TARGETS_V1, E2F_TARGETS, MYC_TARGETS_V2, and MTORC1_SIGNALING were involved in the upregulated NCAPH group. NCAPH hypomethylation, amplified copy number variations and genetic mutations; all played a contributive role in NCAPH upregulation. CONCLUSIONS: These results reveal NCAPH functions as oncogene and promote the development of EC.

Suppressive Effect of Matrine on Tumor Invasion in N-Butyl-N-(4-Hydroxybutyl)Nitrosamine-Induced Urinary Bladder Carcinogenesis.

AIMS: This study was designed to investigate the mechanisms and suppressive effects of matrine on the development of urinary bladder cancers induced by N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) in rats. METHODS: Male Sprague-Dawley rats were given BBN (200 mg/rat) twice a week for a period of 8 weeks. Oral administration of matrine (50 and 100 mg/kg) was started 1 week before BBN exposure for 35 weeks. Half of each bladder was histopathologically analyzed and the remainder was extracted for protein analysis by Western blot. RESULTS: The bladders of BBN-treated rats demonstrated progression from epithelial hyperplasia to papillary urothelial neoplasia and even poorly differentiated invasive cancer. Matrine (50 and 100 mg/kg) treatment decreased the formation of large bladder tumors by 31.6 and 21.1%, respectively. An incidence of cancer cells was detected in rats given BBN [70% (14/20)] and matrine [50 mg/kg: 68.4% (13/19) and 100 mg/kg: 57.9% (11/19), respectively]. The frequency of invasive tumors in the matrine treatment groups [50 mg/kg: 15.4% (2/13), 100 mg/kg: 9.1% (1/11)] was significantly lower than in the BBN-alone group [57% (8/14)]. Furthermore, oral administration of matrine (50 and 100 mg/kg) markedly attenuated the BBN-induced upregulation of bladder cyclooxygenase-2 (COX-2) expression and the elevation of bladder cytosolic phospholipase A2 (cPLA2) levels. Although the contents of 15-prostaglandin dehydrogenase (PGDH), which degrades PGE2, were dramatically reduced by BBN, matrine exerted no effects on reduced PGDH contents. CONCLUSION: Our results suggest that matrine suppressed bladder tumor invasion in a rat model, and this might be primarily mediated through regulation of the protein contents, COX-2 and cPLA2 in the bladder.

Graphdiyne/metal oxide hybrid materials for efficient energy and environmental catalysis.

Graphdiyne (GDY)-based materials, owing to their unique structure and tunable electronic properties, exhibit great potential in the fields of catalysis, energy, environmental science, and beyond. In particular, GDY/metal oxide hybrid materials (GDY/MOs) have attracted extensive attention in energy and environmental catalysis. The interaction between GDY and metal oxides can increase the number of intrinsic active sites, facilitate charge transfer, and regulate the adsorption and desorption of intermediate species. In this review, we summarize the structure, synthesis, advanced characterization, small molecule activation mechanism and applications of GDY/MOs in energy conversion and environmental remediation. The intrinsic structure-activity relationship and corresponding reaction mechanism are highlighted. In particular, the activation mechanisms of reactant molecules (H2O, O2, N2, etc.) on GDY/MOs are systemically discussed. Finally, we outline some new perspectives of opportunities and challenges in developing GDY/MOs for efficient energy and environmental catalysis.

Clinical study of electroacupuncture on the recovery of gastrointestinal dysfunction after laparoscopic surgery for gastrointestinal cancer - study protocol for a randomized controlled trial.

BACKGROUND: Gastrointestinal dysfunction is one of the common complaints for patient post-surgery. Acupuncture has been employed to improve gastrointestinal function and sleeping quality and has confirmed clinical efficacy for emotional problems. This study aims to evaluate the clinical effect of electroacupuncture for postoperative rapid recovery. METHODS: This study design is a two-arm, parallel, double-blinded randomized controlled trial. 104 subjects, aged from 40 to 89 years old, diagnosed with gastrointestinal cancer undergoing laparoscopic surgery, will be divided into Interventional Group and Control Group. Patients of both groups receive perioperative care under the guidance of ERAS guidance. The Interventional Group receives electroacupuncture treatment starting from the first day post-surgery for a consecutive 5 days, whereas the Control Group receives placebo electroacupuncture treatment. The primary outcome will be the first flatus time whereas the secondary outcomes will be the first sign of borborygmus, recovery of defecation, laboratory tests and questionnaires including Self-rating anxiety scale, Ford Insomnia Response to Stress Test, TCM rating scale of Gastrointestinal symptoms and Gastrointestinal Symptoms Rating Scales. DISCUSSION: This study aims to provide timely intervention for post-laparoscopic patients with gastrointestinal tumour using the ERAS concept combined with electroacupuncture, observe the efficacy of this therapy in treating PGID, and contribute reliable scientific evidence for postoperative rapid recovery. TRIAL REGISTRATION: Chictr.org.cn Identifier: ChiCTR2300078710. Registered on 15th December 2023.

Tumor cells-derived exosomal circVCP promoted the progression of colorectal cancer by regulating macrophage M1/M2 polarization.

BACKGROUND: Colorectal cancer (CRC) is among the most frequent tumors of the digestive tract and the second leading cause of cancer death worldwide. Tumor-associated macrophages (TAMs) are one of the most critical immune cells in the tumor microenvironment, which closely interact with tumor cells to promote tumor incidence and progression. However, the precise mechanism of action between CRC cells and TAMs polarization is still being investigated. METHODS: Transmission electronic microscopy (TEM), NanoSight and western blotting were used to characterize exosomes (Exo) isolated from the culture medium of CRC cells. The cellular uptake and internalization of Exo were detected by confocal laser scanning microscopy. M1/ M2 phenotype markers expression were examined by ELISA and flow cytometry. Cell migration, invasion and proliferation were determined by transwell and CCK-8 assay, respectively. A xenograft tumor model was established to explore the role of circVCP in vivo. The target genes of circVCP or miR-9-5p were predicted by StarBase2.0. The target association among miR-9-5p and circVCP or NRP1 was confirmed using the luciferase assay and RNA-pull down assay. RESULTS: circVCP was highly accumulated in exosomes derived from plasma of CRC patients and CRC cells. Additionally, exosomal circVCP derived from CRC cells promoted cell proliferation, migration and invasion by regulating the miR-9-5p/NRP1 axis, and induced macrophage M2 polarization and inhibited macrophage M1 polarization. CONCLUSIONS: Over-expressed exosomal circVCP promoted the progression of CRC by regulating macrophage M1/M2 polarization through miR-9-5p/NRP1 axis. CircVCP may be a diagnostic biomarker and potential target for CRC therapy.

Circ-CCS regulates oxaliplatin resistance via targeting miR-874-3p/HK2 axis in colorectal cancer.

BACKGROUND: Colorectal cancer (CRC) is a malignancy that threatens the patient's life. Previous reports showed that circular RNAs (circRNAs) can affect CRC development. Herein, we demonstrated the characters of circular RNA copper chaperone for superoxide dismutase (circ-CCS) in CRC tissues and cells. METHODS: Circ-CCS, CCS mRNA, microRNA-874-3p (miR-874-3p) and hexokinase 2 (HK2) were indicated by qRT-PCR and western blot in CRC. The cell roles were examined. Additionally, the interaction between miR-874-3p and circ-CCS or HK2 was forecasted by the bioinformatics method and assessed by dual-luciferase reporter assay. Finally, the mouse test was implemented to demonstrate the effect of circ-CCS in vivo. RESULTS: Circ-CCS and HK2 were increased, whereas miR-874-3p was diminished in CRC. Circ-CCS lack subdued the IC50 value of oxaliplatin, cell proliferation, migration, invasion and glycolysis metabolism in CRC cells, while it endorsed cell apoptosis. Furthermore, miR-874-3p was validated as having a tumor repressive effect in CRC cells by restraining HK2. The results also showed that HK2 could regulate the development of CRC. In mechanism, circ-CCS targeted miR-874-3p to control HK2. In addition, circ-CCS knock-down also attenuated tumor growth in mice. CONCLUSION: Circ-CCS expedited CRC through miR-874-3p/HK2.

The role of PYCR1 in inhibiting 5-fluorouracil-induced ferroptosis and apoptosis through SLC25A10 in colorectal cancer.

Although PYCR1 is a well-recognized oncogenic gene for malignant tumors, the causal relationship of its expression with malignant growth and cytotoxic chemotherapeutics remains unclear. Therefore, this study aimed to clarify the role of PYCR1 and its interaction with SLC25A10 in a chemotherapeutic agent 5-fluorouracil (5-FU)'s toxicity to colorectal cancer cells. PYCR1 and SLC25A10 expressions were detected in The Cancer Genome Atlas database and colon adenocarcinoma (COAD) clinical samples. PYCR1 upregulation was associated with SLC25A10 expression and poor prognosis, and its high expression indicated decreased survival rates in patients with COAD. PYCR1 overexpression inhibited lipid reactive oxygen species production and promoted SLC25A10 expression in colorectal cancer cells. PYCR1 silencing enhanced the antitumor effects of 5-FU. Ferroptosis inhibitor deferoxamine suppressed the antitumor effects of PYCR1 silencing, whereas ferroptosis inducer erastin inhibited the protumor effects of PYCR1 overexpression. SLC25A10 overexpression reversed the antitumor effects of PYCR1 silencing in vitro and inhibited the antitumor effects of erastin in vivo. Therefore, PYCR1 is an oncogenic gene that promotes colorectal tumor growth and desensitizes colorectal cancer cells to 5-FU cytotoxicity by preventing apoptosis and ferroptosis.

Human infection with avian-origin H5N6 influenza a virus after exposure to slaughtered poultry.

Exposure to poultry in live poultry markets is strongly associated with human infection with avian influenza virus. To effectively prevent the transmission of viruses from live poultry to humans, people have been forced to change their living habits from purchasing live poultry for consumption to purchasing freshly slaughtered poultry after the permanent closure of live poultry markets in China. In this study, we reported a case of human infection by the H5N6 virus in Hangzhou after exposure to a freshly slaughtered chicken, defying the traditional hypothesis that human infection requires a history of exposure to live poultry and indicating a novel route of infection. Rapid genomic characterization of H5N6 influenza A variants from the patient and the associated environment suggested that these viral variants were of avian origin, belonged to clade 2.3.4.4b H5 and were adapting to the human host after infection. Comparative analysis of the local H5N6 genomes showed that viral contamination in the associated environment and the poultry market was complex. Considering this case of H5N6 infection, conducting surveillance for any possible new avian influenza virus reassortment spillover to humans or other animal species is critical, and awareness of the risk of exposure to possible viral variants from infected slaughtered poultry or the associated environment must be seriously improved.Highlights We reported the first case of human infection with avian-origin influenza A (H5N6) virus in Zhejiang Province, southeastern China.Rapid genomic characterization of H5N6 influenza A variants from a patient and the associated environment suggested that these viral variants were of avian origin and were adapting to the human host after infection.Comparative analysis of the H5N6 genomes showed that viral contamination in the associated environment and poultry market was complex.Considering this case of H5N6 infection, the risk of exposure to possible viral variants from infected slaughtered poultry or the associated environment must be seriously considered.

Nonfunctionalized polydimethyl siloxane superhydrophobic surfaces based on hydrophobic-hydrophilic interactions.

Superhydrophobic surfaces based on polydimethyl siloxane (PDMS) were fabricated using a 50:50 PDMS-poly(ethylene glycol) (PEG) blend. PDMS was mixed with PEG, and incomplete phase separation yielded a hierarchic structure. The phase-separated mixture was annealed at a temperature close to the crystallization temperature of the PEG. The PEG crystals were formed isothermally at the PDMS/PEG interface, leading to an engineered surface with PDMS spherulites. The resulting roughness of the surface was studied by scanning electron microscopy (SEM) and atomic force microscopy (AFM). The PDMS spherulites, a few micrometers in diameter observed from SEM images, were found to have an undulated (rippled) surface with nanometer-sized features. The combination of micrometer- and nanometer-sized surface features created a fractal surface and increased the water contact angle (WCA) of PDMS more than 60°, resulting in a superhydrophobic PDMS surface with WCA of >160°. The active surface layer for the superhydrophobicity was approximately 100 µm thick, illustrating that the material had bulk superhydrophobicity compared to conventional fluorocarbon or fluorinated coated rough surfaces. Theoretical analysis of the fractal surface indicates that the constructed surface has a fractal dimension of 2.5, which corresponds to the Apollonian sphere packing.

Host Delipidation Mediated by Bacterial Effectors.

Protein lipidation, the covalent attachment of a lipid moiety to a target protein, plays a critical role in many cellular processes in eukaryotic cells. Bacterial pathogens secrete various effectors to subvert the host signaling pathway as a mechanism of microbial pathogenesis. An increasing number of effectors from diverse bacterial pathogens function as cysteine proteases to cause irreversible delipidation of host lipidated proteins. This in turn results in disruption of crucial lipidation-mediated host signal transduction, thereby enabling pathogen survival and replication. In this review, we discuss the role of the bacterial effectors in interactions with the host and highlight our knowledge of irreversible host delipidation, with a focus on the common concerted biochemical mechanisms of the bacterial effectors.

A novel biomarker, MRPS12 functions as a potential oncogene in ovarian cancer and is a promising prognostic candidate.

ABSTRACT: Ovarian cancer (OC) is the leading cause of gynecological cancer deaths. Extraordinary histologic and genetic heterogeneity presents as great hurdle to OC's diagnosis and treatment. MRPS12 (Mitochondrial Ribosomal Protein S12), encoding a 28S subunit protein, controls the decoding fidelity and susceptibility to aminoglycoside antibiotics. Our study aims to investigate the clinical significance and potential mechanism of MRPS12 in OC.Oncomine, Tumor Immune Estimation Resource database (TIMER), and GEPIA databases were utilized to explore the expression level of MRPS12 in OC and normal tissues. Kaplan-Meier plotter was used to evaluate the influence of MRPS12 expression on OC patients' survival. The potential biologic function and immune infiltration of MRPS12 in OC were analyzed by GSEA (Gene set enrichment analysis) and TIMER database, respectively.MRPS12 was significantly highly expressed in OC (P < .05) compared with normal ovarian tissues. Its overexpression was also significantly related with poor overall survival in advanced FIGO stage (III+IV) patients, in serous OC and in those patients with TP53 mutation (P < .05). GSEA showed that HALLMARK_G2M_CHECKPOINT, BIOCARTA_CELLCYCLE_PATHWAY, HALLMARK_PI3K_AKT_MTOR_SIGNALING, BIOCARTA_P53_PATHWAY were significantly enriched in high-MRPS12-expression phenotype. MRPS12 expression was positively correlated with the infiltration of macrophages and neutrophils in OC.These results reveal that MRPS12 could function as a potential oncogene and serve as a promising prognostic candidate in OC.

Effect of Anti-Infective Reconstituted Bone Xenograft Combined with External Fixator on Serum CRP and PCT Levels and Prognosis of Patients with Bone Infection after Lower Extremity Long Bone Trauma.

Bone infection is one of the common complications of orthopedic surgery. After bone trauma occurs in the human body, the infection of Staphylococcus aureus and Gram-negative bacteria into the fracture area can lead to double infection of the soft tissue and bone tissue at the fracture site, leading to a variety of complications, mostly in the lower extremities. Bone infection easily causes bone destruction, bone nonunion, and bone defect, seriously affecting the quality of life of patients. The traditional treatment method of bone infection is to control the infection first and then repair the bone graft, but this method has a long course, poor efficacy, and high disability rate. In this study, anti-infective reconstituted bone xenograft (ARBX) combined with external fixation was used to treat patients with posttraumatic bone infections of the long bones of the lower extremities, to explore its efficacy, and to analyze its effects on serum CRP, PCT levels, and prognosis. Our results showed that ARBX combined with the external fixator had a good effect on the treatment of patients with bone infection after lower extremity long bone trauma, which could effectively enhance the repair and functional recovery of the limb bone, significantly alleviate the infection degree of patients, reduce the inflammatory response of the body, and have a good prognosis.

Incorporating redox-sensitive nanogels into bioabsorbable nanofibrous membrane to acquire ROS-balance capacity for skin regeneration.

Facing the high incidence of skin diseases, it is urgent to develop functional materials with high bioactivity for wound healing, where reactive oxygen species (ROS) play an important role in the wound healing process mainly via adjustment of immune response and neovasculation. In this study, we developed a kind of bioabsorbable materials with ROS-mediation capacity for skin disease therapy. Firstly, redox-sensitive poly(N-isopropylacrylamide-acrylic acid) (PNA) nanogels were synthesized by radical emulsion polymerization method using a disulfide molecule as crosslinker. The resulting nanogels were then incorporated into the nanofibrous membrane of poly(l-lactic acid) (PLLA) via airbrushing approach to offer bioabsorbable membrane with redox-sensitive ROS-balance capacity. In vitro biological evaluation indicated that the PNA-contained bioabsorbable membrane improved cell adhesion and proliferation compared to the native PLLA membrane. In vivo study using mouse wound skin model demonstrated that PNA-doped nanofibrous membranes could promote the wound healing process, where the disulfide bonds in them were able to adjust the ROS level in the wound skin for mediation of redox potential to achieve higher wound healing efficacy.