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Abstract Background Published data on whether post-stroke delirium (PSD) is an independent predictor of outcomes in patients with acute stroke are inconsistent and have not yet been synthesized and quantified via meta-analyses. Methods This systematic review and meta-analysis followed the Meta-analysis of Observational Studies in Epidemiology (MOOSE) and Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) guidelines. The study protocol involved a search of the PubMed, Embase, PsycINFO, and Medline databases from 1946 to November 1, 2023, of which prospective observational and case–control studies were included. The quality of the included studies was rated using the Newcastle Ottawa Scale. Pooled effect estimates calculated using a random-effects model were expressed as the odds ratios (ORs), hazard ratios (HRs), and standardized mean differences (SMDs) with 95% confidence intervals (CIs). The protocol was registered in PROSPERO (CRD42023472551). Results The search yielded 39 eligible articles comprising 3295 and 9643 patients with and without PSD, respectively. Thirty studies were high quality, while 9 had moderate quality. The primary analyses, adequately adjusting for predefined confounders, showed that PSD was significantly associated with mortality risk (average follow-up of 19.50 months; OR, 3.47; 95% CI, 2.35–5.12; I 2, 26.0%) and poor neurological function (average follow-up of 21.75 months; OR, 3.62; 95% CI, 2.15–6.09; I 2, 0). Secondary analyses, with or without inadequate adjustment, showed that PSD was significantly associated with prolonged hospital length of stay, increased risk of institutionalization, poor cognitive outcomes, and quality of life after discharge. Conclusions This systematic review and meta-analysis provides evidence that PSD was independently associated with mortality and poor neurological function after controlling for pre-specified confounders. The prevention of PSD remains a high clinical and research priority.

Abstract Objective This study aims to explore ADH4 expression in hepatocellular carcinoma (HCC), its prognostic impact, and its immune correlation to provide novel insights into HCC prognostication and treatment. Methods HCC prognostic marker genes were rigorously selected using GEO database, Lasso regression, GEPIA, Kaplan-Meier and pROC analyses. The expression of interested markers (ADH4, DNASE1L3, RDH16, LCAT, HGFAC) in HCC and adjacent tissues was assessed by Immunohistochemistry (IHC). We observed that ADH4 exhibited low expression levels in liver cancer tissues and high expression levels in normal liver tissues. However, the remaining four genes did not manifest any statistically significant differences between hepatocellular carcinoma (HCC) tissue and adjacent non-cancerous tissue. Consequently, ADH4 became the primary focus of our research. ADH4 expression was validated by signed-rank tests and unpaired Wilcoxon rank sum tests across pan-cancer and HCC datasets. Clinical significance and associations with clinicopathological variables were determined using Kaplan-Meier, logistic regression and Cox analyses on TCGA data. The ADH4-related immune responses were explored by Spearman correlation analysis using TIMER2 data. CD68, CD4, and CD19 protein levels were confirmed by IHC in HCC and non-cancerous tissues. Results ADH4 showed significant downregulation in various cancers, particularly in HCC. Moreover, low ADH4 expression was associated with clinicopathological variables and served as an independent prognostic marker for HCC patients. Additionally, ADH4 affects a variety of biochemical functions and may influence cancer development, prognosis, and treatment by binding to immune cells. Furthermore, at the immune level, the low expression pattern of ADH4 is TME-specific, indicating that ADH4 has the potential to be used as a target for cancer immunotherapy. Conclusion This study highlights the diagnostic, prognostic and immunomodulatory roles of ADH4 in HCC. ADH4 could serve as a valuable biomarker for HCC diagnosis and prognosis, as well as a potential target for immunotherapeutic interventions.

關於探討教師專業能力發展對於教學效能之影響，以往研究較少同時整合外在因素與內在因素；本研究採取行銷導向的觀點，將教師視為學校組織的內部顧客，整合內部行銷策略為外在因素、教學信念為內在因素，以探討內部行銷、教學信念、教師專業發展與教學效能之關係。本研究以國民中學332位教師為研究對象進行實證問卷調查，資料分析方法為結構方程模式。研究結論發現：內部行銷與教學信念對於教師專業發展有顯著正向的影響；教師專業發展對教學效能有顯著正向的影響；並且更進一步驗證教師專業發展的中介效果，內部行銷與教學信念能夠經由教師專業發展的中介轉化機制，進而有助於提升教學效能。最後提出供學校組織參考之實務建議及未來研究建議。 Little research explores the effects of external and internal factors on teacher professional development and teaching effectiveness. Based on the marketing-oriented perspective, this study regards teachers as internal customers in school organizations. This study integrates internal marketing strategies as external factors and teaching beliefs as internal factors to explore the relationships between internal marketing, teaching belief, teachers' professional development, and teaching effectiveness. This study employs a quantitative survey method to collect data from 332 teachers in junior high schools. The data analysis method is structural equation modelling. The results indicate that internal marketing and teaching belief have significantly positive influences on teaching effectiveness. Professional development has a significantly positive influence on teaching effectiveness. The mediating role of professional development is further demonstrated in the relationships between internal marketing, teaching belief, and teaching effectiveness. This study provides specific suggestions to educational organizations and future research.

In order to adapt to the current rapid development of aerospace，automotive，and high-end equipment manufacturing industries，using graphene quantum dots (GQDs) with unique properties as the second phase additive，Ni-based nanocomposite coatings were prepared by supercritical pulse electrodeposition technology.The effect of pulse frequency on the microstructure，corrosion resistance，microhardness，wear resistance and other properties of composite coatings under supercritical conditions was investigated.Results showed that when the pulse frequency was 2 000 Hz under supercritical conditions，the microstructure of the prepared coating was densified and uniform，with better sphericity.XRD results showed that supercritical conditions could change the preferred orientation of crystallization and the appropriate pulse frequency could refine the coating grains and reduce the grain size.At a pulse frequency of 2 000 Hz under supercritical conditions，the properties of the prepared coating were more excellent.Electrochemical experiments showed that it had the largest capacitive arc radius，the highest self-corrosion potential，the lowest corrosion current density，and the largest capacitive modulus，so the coating had the most excellent corrosion resistance.The coating prepared at 2 000 Hz pulse frequency had the highest microhardness，reaching 835.4 HV2 N，and had the best wear resistance with a wear scar cross-sectional area of the coating of 1 582 μm2.The microhardness and wear scar cross-sectional area were 126%，107%，121%and 134%，and 47.6%，57.1%，71.5%and 44.3%of the coatings prepared with pulse frequencies of 100，1 000，3 000 Hz and under room temperature and pressure，respectively.Under supercritical conditions，the graphene quantum dot composite coating prepared at a pulse frequency of 2 000 Hz had excellent corrosion resistance and wear resistance.

The efficacy of immune checkpoint inhibitors (ICIs) on KRAS-mutant advanced non-small cell lung cancer (NSCLC) remains controversial. This retrospective study compared the effects of ICIs treatment and chemotherapy on the prognosis of patients with KRAS-mutant advanced NSCLC and different mutant subtypes in the real world. The study included 95 patients with KRAS-mutant advanced NSCLC. Patients treated with first-line ICIs plus platinum-containing chemotherapy had better progression-free survival (PFS) (7.4 vs 4.5 months, P = 0.035) and overall survival (OS) (24.1 vs 13.2 months, P = 0.007) than those receiving platinum-containing chemotherapy alone, and second-line ICI monotherapy was associated with better PFS (4.8 vs 3.0 months, P = 0.043) and OS (18.0 vs 13.8 months, P = 0.013) than chemotherapy monotherapy. There was no significant difference in PFS (5.267 vs 6.734 months, P = 0.969) and OS (19.933 vs 20.933 months, P = 0.808) between patients with KRAS-mutant and KRAS-wild-type NSCLC treated with ICIs or between KRAS G12C and KRAS non-G12C patients (PFS: 8.1 vs 4.8 months, P = 0.307; OS: 21.3 vs 21.8 months, P = 0.434). In summary, patients with advanced NSCLC with KRAS mutations can benefit from ICIs, but no difference between KRAS mutant subtypes was observed.

ObjectiveThis study aimed to investigate the role of ficolin-2 (FCN2) in the development and course of hepatocellular carcinoma (HCC) and to contribute to the evolution of innovative HCC therapeutics.MethodsOncomine, GEPIA (Gene Expression Profiling Interactive Analysis), TISIDB (Tumor Immune System Interactions and Drug Bank database), UALCAN (University of Alabama at Birmingham Cancer data analysis portal), UCSC (University of California, Santa Cruz), R package, the Kaplan–Meier technique, Cox regression analysis, LinkedOmics, Pearson’s correlation, and a nomogram were used to investigate the prognostic value of FCN2 in HCC. Co-expressed genes were screened. A protein–protein interaction network was created using the STRING database. Finally, immunohistochemistry was performed to establish the expression of FCN2 in HCC tissues. A pan-cancer study centered on HCC-related molecular analysis was also conducted to look for a link between FCN2 and immune infiltration, immune modulators, and chemokine receptors.ResultsIn HCC tissues, the expression of FCN2 was observed to be lower than that in normal tissues. This was connected to the HCC marker alpha-fetoprotein, showing that FCN2 is involved in the development and progression of cancer. FCN2 may act through Staphylococcus aureus infection, lectins, and other pathways. Furthermore, at the immune level, the expression of FCN2 in HCC was associated with some immune cell infiltration, immunomodulators, and chemokine receptors.ConclusionFCN2 may be an immune checkpoint inhibitor for HCC, creating a breakthrough in the treatment of HCC.

In recent years, with the global response to the emission reduction pressure caused by climate change, global awareness of green hydrogen has progressively grown. Electrolysis of water is the only way to create green hydrogen. Among them, one of the semi-reactions of the electrolysis of water is the oxygen evolution reaction (OER). One of the bottlenecks limiting the total energy efficiency of green hydrogen production from water electrolysis is its intricate four-electron transfer process. Developing highly efficient oxygen evolution catalysts is essential to increasing the efficiency of the water electrolysis process. Therefore, researchers have been exploring high-performance OER catalysts. In recent years, heterostructured electrocatalysts have shown surprisingly good performance in OER processes due to their unique structural characteristics, including synergistic effects, strain effects, and electronic interactions. This paper reviews the reaction mechanism of the OER in various pH environments, highlights the advantages of heterostructure catalysts, and provides an overview of OER heterostructure electrocatalysts. This review focuses mainly on the overall facilitating effect of heterostructures on the OER process. The aim is to emphasize the advantages of heterostructure catalysts over one-component catalysts. The paper discusses the preparation of heterostructures and explores the relationship between their structures and electrochemical properties. By providing new insights into the interfacial chemistry of OER heterostructure electrocatalysts, this review sheds light on the future opportunities and challenges for developing OER heterostructure catalysts, both in terms of fundamental understanding and practical applications. [ABSTRACT FROM AUTHOR]

The Dlk1-Dio3 domain is important for normal embryonic growth and development. The heart is the earliest developing and functioning organ of the embryo. In this study, we constructed a transcriptional termination model by inserting termination sequences and clarified that the lack of long non-coding RNA (lncRNA) expression in the Dlk1-Dio3 domain caused the death of maternal insertion mutant (MKI) and homozygous mutant (HOMO) mice starting from E13.5. Parental insertion mutants (PKI) can be born and grow normally. Macroscopically, dying MKI and HOMO embryos showed phenomena such as embryonic edema and reduced heart rate. Hematoxylin and eosin (H.E.) staining showed thinning of the myocardium in MKI and HOMO embryos. In situ hybridization (IHC) and quantitative reverse-transcription polymerase chain reaction (qRT-PCR) showed downregulation of lncGtl2, Rian, and Mirg expression in MKI and HOMO hearts. The results of single-cell RNA sequencing (scRNA-Seq) analysis indicated that the lack of lncRNA expression in the Dlk1-Dio3 domain led to reduced proliferation of epicardial cells and may be an important cause of cardiac dysplasia. In conclusion, this study demonstrates that Dlk1-Dio3 domain lncRNAs play an integral role in ventricular development. [ABSTRACT FROM AUTHOR]