Highly Stable Pt/CeO2 Catalyst with Embedding Structure toward Water-Gas Shift Reaction.

Strong metal-support interaction (SMSI) has been extensively studied in heterogeneous catalysis because of its significance in stabilizing active metals and tuning catalytic performance, but the origin of SMSI is not fully revealed. Herein, by using Pt/CeO2 as a model catalyst, we report an embedding structure at the interface between Pt and (110) plane of CeO2, where Pt clusters (∼1.6 nm) are embedded into the lattice of ceria within 3-4 atomic layers. In contrast, this phenomenon is absent in the CeO2(100) support. This unique geometric structure, as an effective motivator, triggers more significant electron transfer from Pt clusters to CeO2(110) support accompanied by the formation of interfacial structure (Ptδ+-Ov-Ce3+), which plays a crucial role in stabilizing Pt nanoclusters. A comprehensive investigation based on experimental studies and theoretical calculations substantiates that the interfacial sites serve as the intrinsic active center toward water-gas shift reaction (WGSR), featuring a moderate strength CO activation adsorption and largely decreased energy barrier of H2O dissociation, accounting for the prominent catalytic activity of Pt/CeO2(110) (a reaction rate of 15.76 molCO gPt-1 h-1 and a turnover frequency value of 2.19 s-1 at 250 °C). In addition, the Pt/CeO2(110) catalyst shows a prominent durability within a 120 h time-on-stream test, far outperforming the Pt/CeO2(100) one, which demonstrates the advantages of this embedding structure for improving catalyst stability.

PCDH8 is a novel prognostic biomarker in thyroid cancer and promotes cell proliferation and viability.

Protocadherin 8 (PCDH8), a calcium-dependent transmembrane protein in the protocadherin family, regulates cell adhesion and signal transduction. While some studies have provided indirect evidence that PCDH8 has cancer-promoting properties, this association is controversial. In particular, its involvement in thyroid cancer (THCA) remains unclear. We aimed to elucidate the role of PCDH8 in THCA using bioinformatic analysis. Subsequently, the results were experimentally validated. The analysis conducted using the R programming language and online web tools explored PCDH8 expression levels, prognostic, and clinical implications, and its relationship with the tumor immune microenvironment in THCA. Furthermore, we examined the association between PCDH8 and co-expressed genes, highlighting their involvement in several biological processes relevant to THCA. The potential of PCDH8 as a therapeutic target for this pathology was also explored. Immunohistochemical (IHC) staining was performed on samples from 98 patients with THCA, and experimental validation was carried out. PCDH8 was significantly elevated in cancer tissues and associated with poor prognosis, several clinical factors, and immune cell and checkpoint abundance. Cox regression and survival analyses, together with Receiver Operating Curves (ROC) indicated that PCDH8 was an independent prognostic factor for THCA. Furthermore, PCDH8 impacts cell viability and proliferation, promoting tumorigenesis. Also, it influences tumor cell sensitivity to various drugs. Thus, PCDH8 might be a potential therapeutic target for THCA. IHC, cell culture, MTT, and colony formation experiments further confirmed our findings. This analysis provided insights into the potential carcinogenic role of PCDH8 in THCA, as it impacts cell viability and proliferation. Thus, PCDH8 might play an important role in its prognosis, immune infiltration, and diagnosis.

Association between visceral adipose tissue and asthma based on the NHANES and Mendelian randomization study.

BACKGROUND: Obesity is a crucial risk factor for asthma. Observational studies have examined the association between abdominal obesity and asthma symptoms. This study aimed to investigate the causal relationship between visceral adipose tissue (VAT) and asthma and its potential as an independent indicator. METHODS: This study utilized data from the National Health and Nutrition Examination Survey spanning 2011-8. Multivariable logistic regression and stratified variable selection were employed to identify associations between asthma and VAT. Moreover, a two-sample Mendelian randomization analysis, using 221 genetic variants as instrumental variables, was conducted to assess this relationship further. RESULTS: Our findings indicated that individuals with higher VAT levels were more likely to develop asthma. Visceral obesity remained a significant risk factor for asthma after adjusting for demographic characteristics. Genetic predictions suggest a positive association between VAT and an elevated risk of asthma (odds ratio [OR] = 1.393, 95% confidence interval [CI]: 1.266-1.534, and P = 1.43E-11). No significant polymorphisms were detected using the Mendelian randomization-Egger intercept test. CONCLUSIONS: This study presents potential evidence supporting the causal role of VAT in asthma development. Furthermore, the findings from the Mendelian randomization analysis further reinforce the relationship between VAT and asthma risk.

Is Kidney Stone Associated with Thyroid Disease? The United States National Health and Nutrition Examination Survey 2007­2018

BACKGROUND: Kidney stones and thyroid disease are two common diseases in the general population, with multiple common risk factors. The associations between kidney stones and thyroid disease are unclear. AIM: This study aims to assess the association between 'once had a thyroid disease' and the odds of kidney stones. METHODS: Adult participants from the National Health and Nutrition Examination Survey (NHANES) 2007-2018 with reliable kidney stone and thyroid disease data were included. Adjusting for age, gender, race, education level, and marital status, diabetes, hypertension, gout, angina pectoris, stroke, and asthma, logistic regression was used to examine the relationship between kidney stones and thyroid illness. RESULTS: Using stratified analysis, the association between thyroid illness and kidney stones was investigated further. Among the participants, 4.9% had kidney stones, and 10.1% had thyroid disease. Kidney stone was associated with thyroid disease (OR=1.441, (95% CI:1.294-1.604), p <0.01), which remained significant (OR=1.166, (95% CI:1.041-1.305), p <0.01) after adjustments with age, gender, race, education level and marital status, diabetes, hypertension, gout, angina pectoris, stroke, and asthma. Stratified by blood lead, blood cadmium, and blood urea nitrogen levels in the human body, the odds of kidney stones still increased with once having a previous thyroid disease. CONCLUSIONS: In this large nationally representative survey over 10 years, kidney stone was strongly associated with thyroid disease. In this cross-sectional study, we explored the association between thyroid disease and kidney stones, which may help clinicians intervene in them early.

Integrated bioinformatics combined with machine learning to analyze shared biomarkers and pathways in psoriasis and cervical squamous cell carcinoma.

Background: Psoriasis extends beyond its dermatological inflammatory manifestations, encompassing systemic inflammation. Existing studies have indicated a potential risk of cervical cancer among patients with psoriasis, suggesting a potential mechanism of co-morbidity. This study aims to explore the key genes, pathways, and immune cells that may link psoriasis and cervical squamous cell carcinoma (CESC). Methods: The cervical squamous cell carcinoma dataset (GSE63514) was downloaded from the Gene Expression Omnibus (GEO). Two psoriasis-related datasets (GSE13355 and GSE14905) were merged into one comprehensive dataset after removing batch effects. Differentially expressed genes were identified using Limma and co-expression network analysis (WGCNA), and machine learning random forest algorithm (RF) was used to screen the hub genes. We analyzed relevant gene enrichment pathways using GO and KEGG, and immune cell infiltration in psoriasis and CESC samples using CIBERSORT. The miRNA-mRNA and TFs-mRNA regulatory networks were then constructed using Cytoscape, and the biomarkers for psoriasis and CESC were determined. Potential drug targets were obtained from the cMAP database, and biomarker expression levels in hela and psoriatic cell models were quantified by RT-qPCR. Results: In this study, we identified 27 key genes associated with psoriasis and cervical squamous cell carcinoma. NCAPH, UHRF1, CDCA2, CENPN and MELK were identified as hub genes using the Random Forest machine learning algorithm. Chromosome mitotic region segregation, nucleotide binding and DNA methylation are the major enrichment pathways for common DEGs in the mitotic cell cycle. Then we analyzed immune cell infiltration in psoriasis and cervical squamous cell carcinoma samples using CIBERSORT. Meanwhile, we used the cMAP database to identify ten small molecule compounds that interact with the central gene as drug candidates for treatment. By analyzing miRNA-mRNA and TFs-mRNA regulatory networks, we identified three miRNAs and nine transcription factors closely associated with five key genes and validated their expression in external validation datasets and clinical samples. Finally, we examined the diagnostic effects with ROC curves, and performed experimental validation in hela and psoriatic cell models. Conclusions: We identified five biomarkers, NCAPH, UHRF1, CDCA2, CENPN, and MELK, which may play important roles in the common pathogenesis of psoriasis and cervical squamous cell carcinoma, furthermore predict potential therapeutic agents. These findings open up new perspectives for the diagnosis and treatment of psoriasis and squamous cell carcinoma of the cervix.

Highly Selective Hydrogenation of Unsaturated Aldehydes in Aqueous Phase.

Chemoselective hydrogenation of carbonyl in unsaturated aldehydes is a significant process in the chemical industry, in which the development of aqueous-phase reaction systems as a substitution to organic ones is challenging. Herein, we report Ir atomic cluster catalysts anchored onto WO3-x nanorods via a reduction treatment at various temperatures (denoted as Ir/WOx-T, T = 200, 300, 400, and 500 °C), which accelerates the chemoselective hydrogenation of carbonyl groups in aqueous solutions. The optimal catalyst Ir/WOx-300 exhibits exceptional activity (TOF value: 1313.7 min-1) and chemoselectivity toward cinnamaldehyde (CAL) hydrogenation to cinnamyl alcohol (COL) (yield: ∼98.0%) in water medium, which is, to the best of our knowledge, the highest level compared with previously reported heterogeneous catalysts in liquid-phase reaction. Ac-HAADF-STEM, XAFS, and XPS verify the formation of interface structure (Irδ+-Ov-W5+ (0 ≤ δ ≤ 4); Ov denotes oxygen vacancy) induced by metal-support interaction and the largest concentration of interfacial Ir (Irδ+) in Ir/WOx-300. In situ studies (Raman, FT-IR), isotopic labeling measurements combined with DFT calculations substantiate that the hydrogenation of the C=O group consists of two pathways: water-mediated hydrogenation (predominant) and direct hydrogenation via H2 dissociation (secondary). In the former case, W5+-Ov site accelerates the activation adsorption of H2O, while Ir0 site facilitates the H-H bond cleavage of H2 and Irδ+ promotes the CAL adsorption. H2O molecule, as the source of hydrogen species, participates directly in the hydrogenation of the carbonyl group through a hydrogen-bonded network, with a largely reduced energy barrier relative to the H2 dissociation path. This work demonstrates a green catalytic route that breaks the activity-selectivity trade-off toward the selective hydrogenation of unsaturated aldehydes, which shows great potential in heterogeneous catalysis.

RARRES1 identified by comprehensive bioinformatic analysis and experimental validation as a promising biomarker in Skin Cutaneous Melanoma.

Skin cutaneous melanoma (SKCM) is a highly malignant form of skin cancer, known for its unfavorable prognosis and elevated mortality rate. RARRES1, a gene responsive to retinoic acid receptors, displays varied functions in various cancer types. However, the specific role and underlying mechanisms of RARRES1 in SKCM are still unclear. GSE15605 was utilized to analyze the expression of RARRES1 in SKCM. Subsequently, the TCGA and GEO databases were employed to investigate the relationships between RARRES1 and clinicopathological parameters, as well as the prognostic implications and diagnostic efficacy of RARRES1 in SKCM. GO, KEGG, and GSEA analyses were conducted to explore the potential functions of RARRES1. Furthermore, the associations between RARRES1 and immune infiltration were examined. Genomic alterations and promoter methylation levels of RARRES1 in SKCM were assessed using cBioPortal, UALCAN, and the GEO database. Finally, RARRES1 expression in SKCM was validated through immunohistochemistry, and its functional role in SKCM progression was elucidated via in vivo and in vitro experiments. We found that RARRES1 was downregulated in SKCM compared with normal tissues, and this low expression was associated with worse clinicopathological features and poor prognosis of SKCM. The diagnostic efficacy of RARRES1, as determined by ROC analysis, was 0.732. Through GO, KEGG, and GSEA enrichment analysis, we identified 30 correlated genes and pathways that were mainly enriched in the tumor immune microenvironment, proliferation, apoptosis, and autophagy. Additionally, RARRES1 expression was found to be positively related to the infiltration of various immune cells in SKCM, particularly macrophages and T helper cells, among others. Analysis of genomic alterations and promoter methylation revealed that shallow deletion and hypermethylation of the RARRES1 promoter could lead to reduced RARRES1 expression. IHC validation confirmed the downregulation of RARRES1 in SKCM. Moreover, overexpression of RARRES1 inhibited the proliferation and migration of A375 cells, promoted apoptosis, and inhibited autophagic flux. In the mouse xenograft model, RARRES1 overexpression also suppressed SKCM tumor growth. Collectively, these findings suggest that RARRES1 may function as a suppressor and could potentially serve as a prognostic biomarker and therapeutic target for SKCM.