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C10H11ClN4O2, monoclinic, P21/c (no. 14), a = 12.7802(17) Å, b = 7.6211(12) Å, c = 12.0486(17) Å, β = 95.551(4)°, V = 1168.0(3) Å3, Z = 4, R gt(F) = 0.0562, wR ref(F 2) = 0.1172, T = 273(2) K.

C36H36N2 ${\mathrm{C}}_{36}{\mathrm{H}}_{36}{\mathrm{N}}_{2}$ O, orthorhombic, P212121 ${2}_{1}{2}_{1}{2}_{1}$ (no. 19), a = 11.849(2) Å, b = 14.373(3) Å, c = 17.183(3) Å, V = 2926.4(10) Å3 ${\mathrm{\mathring{\text{A}}}}^{3}$ , Z = 4, Rgt ${R}_{\mathrm{g}\mathrm{t}}$ (F) = 0.0514, w Rref ${R}_{\mathrm{r}\mathrm{e}\mathrm{f}}$ (F2 ${F}^{2}$ ) = 0.1272, T = 296(2) K.

Two-dimensional Ce-MOFs nanosheets were successfully constructed by using ceric ammonium nitrate as metal salt and 1, 3, 5-tris(4-carboxyphenyl)benzene (H3BTB) as organic ligand, together with the use of acetic acid as modulator.Acetic acid modulator shows significant effects on the morphology and crystallinity of Ce-MOFs. Ce-MOFs microspheres synthesized without acetic acid as modulator (named Ce-BTB-H0) are composed of highly cross-linked small nanosheets with low crystallinity and surface areas. On the contrary, Ce-MOFs synthesized with acetic acid (named Ce-BTB-H60) consist of dispersed nanosheets, and show improved crystallinity and higher surface areas than that of Ce-BTB-H0. Using blue LED as light source and oxygen as oxidant, two-dimensional Ce-MOFs nanosheets enable decarboxylation oxygenation of a variety of substituted phenylacetic acid to their corresponding benzaldehydes and benzyl alcoholsunder irradiation of blue LED in oxygen atmosphere at room temperature.Moreover, Ce-BTB-H60nanosheets show better photocatalytic performance due to their higher crystallinity, larger specific surface area and improved dispersity than that of Ce-BTB-H0.

Background: Programmed cell death plays an important role in neuronal injury and death after ischemic stroke (IS), leading to cellular glucose deficiency. Glucose deficiency can cause abnormal accumulation of cytotoxic disulfides, resulting in disulfidptosis. Ferroptosis, apoptosis, necroptosis, and autophagy inhibitors cannot inhibit this novel programmed cell death mechanism. Nevertheless, the potential mechanisms of disulfidptosis in IS remain unclear. Methods: The GSE16561 dataset was used to screen for differentially expressed disulfidptosis-related biomarkers (DE-DRBs). A correlation between the DE-DRBs was detected. The optimal machine-learning (ML) model and predictor molecules were determined. The GSE58294 dataset was used to verify the accuracy of the optimal ML model. The DE-DRB expression was detected in the blood of patients with IS. Based on IS models, experimental analyses were performed to verify DE-DRB expression and the correlation between DE-DRBs. Results: Leucine-rich pentatricopeptide repeat-containing (LRPPRC) and NADH dehydrogenase [ubiquinone] 1 alpha subcomplex subunit 11 (NDUFA11) were identified as DE-DRBs. The NADH: ubiquinone oxidoreductase core subunit S1 (NDUFS1) interacted with NDUFA11 and LRPPRC. The support vector machine (SVM) model was identified as the optimal ML model. The NDUFA11 expression level in the blood of patients with IS was 20.9% compared to that in normal controls. NDUFA11 expression was downregulated in the in vitro/in vivo models of IS. The number of formed complexes of NDUFS1 and NDUFA11 decreased in the in vitro/in vivo models of IS. Conclusion: This research suggests that NDUFA11 is a specific DRB for IS and demonstrates alterations in the disulfidptosis-related protein complexes NDUFS1-NDUFA11. [ABSTRACT FROM AUTHOR]

Auditory neuropathy spectrum disorder (ANSD) is an auditory dysfunction disorder characterized by impaired speech comprehension. Its etiology is complex and can be broadly categorized into genetic and non-genetic factors. TMEM43 mutation is identified as a causative factor in ANSD. While some studies have been conducted using animal models, its pathogenic mechanisms in humans remain unclear. TMEM43 is predominantly expressed in cochlear glia-like support cells (GLSs) and plays a vital role in gap junction intercellular communication. In this work, we utilized induced pluripotent stem cells from an ANSD patient carrying the TMEM43 gene mutation c.1114C>T (p.Arg372Ter) and directed their differentiation toward GLSs to investigate the effect of TMEM43 mutation on the function of gap junctions in cochlear GLSs in vitro. Reduced expression of genes associated with GLSs characteristics and reduced gap junction intercellular communication in TMEM43 mutant cell lines were observed compared to controls. Transcriptome analysis revealed that differentially expressed genes were significantly enriched in pathways related to cell proliferation, differentiation, extracellular space and adhesion. Furthermore, significant alterations were noted in the PI3K-Akt signaling pathway and the calcium signaling pathway, which could potentially influence gap junction function and contribute to hearing loss. In summary, our study based on patient-derived iPSCs sheds new light on the molecular mechanisms by which TMEM43 mutations may lead to ANSD. These mutations could result in developmental defects in GLSs and a diminished capacity for gap junction function, which may be implicated in the auditory deficits observed in ANSD patients. Our study explored the pathological effects of the TMEM43 mutation and its causal relationship with ANSD using a patient-derived iPSC-based GLSs model, providing a foundation for future mechanistic studies and potential drug screening efforts. [ABSTRACT FROM AUTHOR]

Background: Chronic obstructive pulmonary disease (COPD) is a chronic and progressive lung disease. Disulfidptosis-related genes (DRGs) may be involved in the pathogenesis of COPD. From the perspective of predictive, preventive, and personalized medicine (PPPM), clarifying the role of disulfidptosis in the development of COPD could provide a opportunity for primary prediction, targeted prevention, and personalized treatment of the disease. Methods: We analyzed the expression profiles of DRGs and immune cell infiltration in COPD patients by using the GSE38974 dataset. According to the DRGs, molecular clusters and related immune cell infiltration levels were explored in individuals with COPD. Next, co-expression modules and cluster-specific differentially expressed genes were identified by the Weighted Gene Co-expression Network Analysis (WGCNA). Comparing the performance of the random forest (RF), support vector machine (SVM), generalized linear model (GLM), and eXtreme Gradient Boosting (XGB), we constructed the ptimal machine learning model. Results: DE-DRGs, differential immune cells and two clusters were identified. Notable difference in DRGs, immune cell populations, biological processes, and pathway behaviors were noted among the two clusters. Besides, significant differences in DRGs, immune cells, biological functions, and pathway activities were observed between the two clusters.A nomogram was created to aid in the practical application of clinical procedures. The SVM model achieved the best results in differentiating COPD patients across various clusters. Following that, we identified the top five genes as predictor genes via SVM model. These five genes related to the model were strongly linked to traits of the individuals with COPD. Conclusion: Our study demonstrated the relationship between disulfidptosis and COPD and established an optimal machine-learning model to evaluate the subtypes and traits of COPD. DRGs serve as a target for future predictive diagnostics, targeted prevention, and individualized therapy in COPD, facilitating the transition from reactive medical services to PPPM in the management of the disease. [ABSTRACT FROM AUTHOR]

Background: The use of two or more drugs carries the potential risk of drug–drug interactions (DDIs), which may result in adverse reactions. Some human immunodeficiency virus (HIV)‐infected patients who receive antiretroviral therapy (ART) may require general anesthesia with propofol (PRL) before undergoing surgical treatment. Both PRL and ART drugs may lead to neuronal dysfunction, which can be accompanied by energy metabolism disorders. Neurons take in glucose mainly through glucose transporter 3 (Glut3) which is specifically expressed on the cell membranes of neurons. However, to date, no study has examined whether the DDIs of PRL and ART drugs interfere with glucose metabolism and Glut3 expression in neurons. Methods: An in vitro model was constructed using the primary cultures of neurons. PRL and ART drugs (EFV, AZT, and 3TC), were added at different concentrations (low, medium, and high). The neurons were exposed to the drugs for 1, 4, 8, and 12 h. The optimal drug concentration and exposure time were selected. The cellular survival rate, glucose concentration, electrophysiology, and the expression of Glut3 were detected. Results: There were no significant changes in the cellular survival rates of the neurons that were exposed to both PRL and ART drugs at low concentrations for 1 h. However, the survival rates of the neurons decreased significantly as the drug concentrations and durations increased. The glucose concentration of the neurons that were exposed to both PRL and the ART drugs was significantly decreased. The glucose concentration of the neurons was not affected by any individual drug. The amplitude of the action potential and the expression of Glut3 were decreased in the neurons that were exposed to both PRL and ART drugs. Conclusions: The main adverse reactions induced by the DDIs between PRL and the ART drugs were decreased glucose metabolism and neuronal damage, which were caused by inhibiting the expression of Glut3. More importantly, we found that decreases in glucose metabolism predated neuronal damage. [ABSTRACT FROM AUTHOR]

C10H11ClN4O2, monoclinic, P21/c (no. 14), a = 12.7802(17) Å, b = 7.6211(12) Å, c = 12.0486(17) Å, β = 95.551(4)°, V = 1168.0(3) Å3, Z = 4, Rgt(F) = 0.0562, wRref(F2) = 0.1172, T = 273(2) K. [ABSTRACT FROM AUTHOR]

Electrochemical C–C and C–N coupling reactions with the conversion of abundant and inexpensive small molecules, such as CO2 and nitrogen‐containing species, are considered a promising route for increasing the value of CO2 reduction products. The development of high‐performance catalysts is the key to the both electrocatalytic reactions. In this review, we present a systematic summary of the reaction systems for electrocatalytic CO2 reduction, along with the coupling mechanisms of C–C and C–N bonds over outstanding electrocatalytic materials recently developed. The key intermediate species and reaction pathways related to the coupling as well as the catalyst‐structure relationship will be also discussed, aiming to provide insights and guidance for designing efficient CO2 reduction systems. [ABSTRACT FROM AUTHOR]

Compared to the Haber–Bosch (H–B) process for ammonia synthesis with massive emission of greenhouse CO2 and necessary harsh reaction conditions, the electrocatalytic NO3− reduction (NO3RR) for ammonia synthesis under ambient temperature and pressure driven by renewable electricity has attracted great attention. NO3RR is also a promising route to construct nitrogen cycles utilizing NOx produced from industrial and agricultural operations. Cu‐based catalyst is one of the most promising platforms for this reaction. This perspective shows the latest understanding and research advances on the NO3RR by Cu‐based electrocatalysts. Through a deep analysis on the rate‐limiting step of NO3RR, the strategies of overcoming the deactivation and enhancing the performance of Cu‐based catalysts are discussed. The great significance of synergistic NOx and H activation in promoting the key kinetic step of electrocatalytic NO3RR by single‐atom, oxide, bimetallic of Cu on the catalytic reaction site construction with tunable adsorption of N‐containing intermediate and active H is stressed. Also, future challenges and perspectives toward coupling reaction of nitrate reduction catalyzed by Cu‐based catalysts are proposed. This perspective can move forward the future research on electrocatalytic NO3RR to ammonia synthesis over advanced Cu‐based electrocatalysts. [ABSTRACT FROM AUTHOR]