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Hydrogen is being increasingly integrated into the international trade system as a clean and flexible energy carrier, motivated by the global energy transition and carbon neutrality objectives. The rapid expansion of the global hydrogen trade network has simultaneously exposed several sustainability challenges, including a centralized structure, overdependence on key countries, and limited resilience to external disruptions. Based on this, we develop a risk propagation model that incorporates the absorption capacity of nodes to simulate the propagation of supply shortage risks within the global hydrogen trade network. Furthermore, we propose a composite sustainability index constructed from structural, economic, and environmental resilience indicators, enabling a systematic assessment of the network’s sustainable development capacity under external shock scenarios. Findings indicate the following: (1) The global hydrogen trade network is undergoing a structural shift from a Western Europe-dominated unipolar configuration to a more polycentric pattern. Countries such as China and Singapore are emerging as key hubs linking Eurasian regions, with trade relationships among nations becoming increasingly dense and diversified. (2) Although supply shortage shocks trigger structural disturbances, economic losses, and risks of carbon rebound, their impacts are largely concentrated in a limited number of hub countries, with relatively limited disruption to the overall sustainability of the system. (3) Countries exhibit significant heterogeneity in structural, economic, and environmental resilience. Risk propagation demonstrates an uneven pattern characterized by hub-induced disruptions, chain-like transmission, and localized clustering. Accordingly, policy recommendations are proposed, including the establishment of a polycentric coordination mechanism, the enhancement of regional emergency coordination mechanisms, and the advancement of differentiated capacity-building efforts.

Light-induced halide segregation constrains the photovoltaic performance and stability of wide-bandgap perovskite solar cells and tandem cells. The implementation of an intermixed two-dimensional/three-dimensional heterostructure via solution post-treatment is a typical strategy to improve the efficiency and stability of perovskite solar cells. However, owing to the composition-dependent sensitivity of surface reconstruction, the conventional solution post-treatment is suboptimal for methylammonium-free and cesium/bromide-enriched wide-bandgap PSCs. To address this, we develop a generic three-dimensional to two-dimensional perovskite conversion approach to realize a preferential growth of wider dimensionality (n ≥ 2) atop wide-bandgap perovskite layers (1.78 eV). This technique involves depositing a well-defined MAPbI 3 thin layer through a vapor-assisted two-step process, followed by its conversion into a two-dimensional structure. Such a two-dimensional/three-dimensional heterostructure enables suppressed light-induced halide segregation, reduced non-radiative interfacial recombination, and facilitated charge extraction. The wide-bandgap perovskite solar cells demonstrate a champion power conversion efficiency of 19.6% and an open-circuit voltage of 1.32 V. By integrating with the thermal-stable FAPb 0.5 Sn 0.5 I 3 narrow-bandgap perovskites, our all-perovskite tandem solar cells exhibit a stabilized PCE of 28.1% and retain 90% of the initial performance after 855 hours of continuous 1-sun illumination. The conventional solution post-treatment is suboptimal for methylammonium-free and cesium/bromide-enriched wide-bandgap perovskite solar cells. Here, the authors develop a 3D-to-2D perovskite conversion approach for a preferential growth, achieving stabilized efficiency of 28.1% for tandem cells.

Due to the complex core–shell structure and variety of surface functional groups, the photoluminescence (PL) mechanism of carbon dots (CDs) remain unclear. o-Phenylenediamine (oPD), as one of the most common precursors for preparing red emissive CDs, has been extensively studied. Interestingly, most of the red emission CDs based on oPD have similar PL emission characteristics. Herein, we prepared six different oPD-based CDs and found that they had almost the same PL emission and absorption spectra after purification. Structural and spectral characterization indicated that they had similar carbon core structures but different surface polymer shells. Furthermore, single-molecule PL spectroscopy confirmed that the multi-modal emission of those CDs originated from the transitions of different vibrational energy levels of the same PL center in the carbon core. In addition, the phenomenon of “spectral splitting” of single-particle CDs was observed at low temperature, which confirmed these oPD-based CDs were unique materials with properties of both organic molecules and quantum dots. Finally, theoretical calculations revealed their potential polymerization mode and carbon core structure. Moreover, we proposed the PL mechanism of red-emitting CDs based on oPD precursors; that is, the carbon core regulates the PL emission, and the polymer shell regulates the PL intensity. Our work resolves the controversy on the PL mechanism of oPD-based red CDs. These findings provide a general guide for the mechanism exploration and structural analysis of other types of CDs.

Monoacylglycerols (MAGs) are significant intermediate byproducts in the hydrolysis of oils and fats. The accumulation of MAGs not only reduces the quality and purity of the final products in biodiesel production and edible oil refining but also poses challenges for downstream separation processes. Therefore, the development of efficient biocatalysts for the specific MAG conversion is of great industrial importance. The lipase from Aspergillus oryzae (AOL) has shown potential for lipid modification; however, the wild-type enzyme (WT) suffers from poor solubility, tendency to aggregate, and low specific activity towards MAGs in aqueous systems, which severely restricts its practical application. In this study, a combinatorial protein engineering strategy was employed to overcome these limitations. We integrated fusion protein technology with rational design to enhance both the functional expression and catalytic efficiency of AOL. Firstly, the superfolder green fluorescent protein (sfGFP) was fused to the N-terminus of AOL. The results indicated that the sfGFP fusion tag significantly improved the solubility and stability of the enzyme, preventing the formation of inclusion bodies. The fusion protein sfGFP-AOL exhibited a MAG conversion rate of approximately 65%, confirming the positive impact of the fusion tag on enzyme developability. To further boost catalytic performance, site-directed mutagenesis was performed based on structural analysis. Among the variants, the mutant sfGFP-Y92Q emerged as the most potent candidate. In the MAG conversion, sfGFP-Y92Q achieved a conversion rate of 98%, which was not only significantly higher than that of sfGFP-AOL but also outperformed the widely used commercial immobilized lipase, Novozym 435 (~54%). Structural modeling and docking analysis revealed that the Y92Q mutation optimized the geometry of the active site. The substitution of Tyrosine with Glutamine at position 92 likely enlarged the substrate-binding pocket and altered the local electrostatic environment, thereby relieving steric hindrance and facilitating the access of the bulky MAG substrate to the catalytic center. In conclusion, this work demonstrates that the synergistic application of sfGFP fusion and rational point mutation (Y92Q) can dramatically transform the catalytic properties of AOL. The engineered sfGFP-Y92Q variant serves as a robust and highly efficient biocatalyst for MAG degradation. Its superior performance compared to commercial standards suggests immense potential for cost-effective applications in the bio-manufacturing of high-purity fatty acids and biodiesel, offering a greener alternative to traditional chemical processes.

This study aimed to investigate the role of long non-coding RNA (lncRNA) taurine up-regulated 1 (TUG1) in the development of ulcerative colitis (UC) and to explore the underlying mechanisms. A murine model of UC was induced by dextran sodium sulfate (DSS) exposure. The colonic epithelial YAMC cells were treated with TNF-α to simulate the inflammatory environment of intestinal epithelial cells (IECs). RNA pull-down and RIP assays were performed to analyze the interaction between TUG1 and HuR. Luciferase activity assay was conducted to evaluate the interaction between TUG1 and miR-29b-3p. Cell proliferation was evaluated by MTT assay. Cell apoptosis was assessed by flow cytometry and western blot analysis of apoptosis-related proteins. TUG1 overexpression promoted cell proliferation and inhibited cell apoptosis in the TNF-α-stimulated YAMC cells. The mechanistic analysis showed that TUG1 positively regulated the HuR/c-myc axis via its interaction with HuR, leading to upregulation of c-myc expression; meanwhile, TUG1 negatively regulated the miR-29b-3p/CDK2 signaling via binding to miR-29b-3p, leading to derepression of CDK2 expression. Further animal experiments showed that TUG1 overexpression attenuated UC progression in the DSS-induced UC in mice. Collectively, TUG1 inhibits IEC apoptosis and UC progression by regulating the balance of HuR and miR-29b-3p.

Cancer is a major global public health problem with high morbidity. Depression is known to be a high-frequency complication of cancer diseases that decreases patients’ life quality and increases the mortality rate. Therefore, antidepressants are often used as a complementary treatment during cancer therapy. During recent decades, various studies have shown that the combination of antidepressants and anticancer drugs increases treatment efficiency. In recent years, further emerging evidence has suggested that the modulation of autophagy serves as one of the primary anticancer mechanisms for antidepressants to suppress tumor growth. In this review, we introduce the anticancer potential of antidepressants, including tricyclic antidepressants (TCAs), tetracyclic antidepressants (TeCAs), selective serotonin reuptake inhibitors (SSRIs), and serotonin-norepinephrine reuptake inhibitors (SNRIs). In particular, we focus on their autophagy-modulating mechanisms for regulating autophagosome formation and lysosomal degradation. We also discuss the prospect of repurposing antidepressants as anticancer agents. It is promising to repurpose antidepressants for cancer therapy in the future.

The further practical applications of halide perovskite quantum dots (QDs) are blocked by problems of instability and nonradiative Auger recombination manifested as photoluminescence blinking. Here, single core/shell structured perovskite semiconductor QDs are successfully fabricated by capping CsPbBr3 QD core with CdS shell. It is demonstrated that CsPbBr3/CdS core/shell QDs exhibit ultrahigh chemical stability and nonblinking photoluminescence with high quantum yield due to the reduced electronic traps within the core/shell structure. Efficiency of amplified spontaneous emission exhibits obvious enhancement compared to that of pure CsPbBr3 QDs, originating from the mitigated competition between stimulated emission and suppressed nonradiative biexciton Auger recombination. Furthermore, low‐threshold whispering‐gallery‐mode lasing with a high‐quality factor is achieved by incorporating CsPbBr3/CdS QDs into microtubule resonators. Density functional theory (DFT)‐based first‐principles calculations are also performed to reveal the atomic interface structure, which supports the existence of CsPbBr3/CdS structure. An interesting feature of spatially separated charge density at CsPbBr3/CdS interface is found, which may greatly contribute to the suppressed Auger recombination. The results provide a practical approach to improve the stability and suppress the blinking of halide perovskite QDs, which may pave the way for future applications for various optoelectronic devices. Single CsPbBr3/CdS core/shell quantum dots are successfully fabricated and demonstrated by combining materials synthesis, characterization, optical measurements, and first‐principles calculations, which show ultrahigh stability and nonblinking photoluminescence with high quantum yield. Exotic interfacial electronic structures within the core/shell structures contribute to their interesting physical behaviors, such as low‐threshold whispering‐gallery‐mode lasing.

Colorectal cancer (CRC) is the second leading cause of cancer-related death worldwide. It is important to discover new therapeutic regimens for treating CRC. Depression is known to be an important complication of cancer diseases. Repurposing antidepressants into anticancer drugs and exploring the combinational efficacy of antidepressants and chemotherapy are potentially good options for developing CRC treatment regimens. In this study, sertraline, an antidepressant drug, and paclitaxel, an anticancer drug, were chosen to study their antitumor effects in the treatment of colorectal cancer, alone or in combination, and to explore their underlying mechanisms. The data showed that sertraline exerted a dose-dependent cytotoxic effect on MC38 and CT26 colorectal cancer cell lines with IC50 values of 10.53 μM and 7.47 μM, respectively. Furthermore, sertraline synergistically sensitized chemotherapeutic agent paclitaxel efficacy in CRC cells with combination index (CI) values at various concentrations consistently lower than 1. Sertraline remarkably augmented paclitaxel-induced autophagy by increasing autophagosome formation indicated by elevated LC3-II/I ratio and promoting autophagic flux by degrading autophagy cargo receptor SQSTM1/p62, which may explain the synergistically cytotoxic effect of sertraline and paclitaxel combination therapy on CRC cells. This study provides important evidence to support repurposing sertraline as an anticancer agent and suggests a novel combinational regimen for effectively treating CRC as well as in the simultaneous treatment of CRC and depression.

Generic medications offer substantial potential cost savings to health systems compared to their branded counterparts. In Europe and the US, they are only approved if they are bioequivalent to the respective originator product. Nevertheless, the lack of clinical outcomes is sometimes used as the reason for hesitancy in prescribing generics. We performed an observational retrospective study on 17 branded vs. generic pharmaceutical substances for the treatment of hypertension/heart failure, hyperlipidemia, and diabetes mellitus in a dataset of 9,413,620 insured persons, representing nearly the full population of Austria, from 2007 to 2012. We compared generic vs. branded medications using hazard ratios for all-cause death and major adverse cardiac and cardiovascular events (MACCE) as outcomes of interest. Using patient demographics, health characteristics from hospitalization records, and pharmacy records as covariates, we controlled for confounding in Cox models through inverse probability of treatment weighting (IPTW) using high-dimensional propensity scores. We observed that the unadjusted hazard ratios strongly favor generic drugs for all three pooled treatment indications (hypertension/heart failure, hyperlipidemia, diabetes mellitus), but were attenuated towards unity with increasingly larger covariate sets used for confounding control. We found that after IPTW adjustment the generic formulation was associated with significantly fewer deaths in 10 of 17 investigated drugs, and with fewer MACCE in 11 of 17 investigated drugs. This result favoring generic drugs was also present in a number of sub-analyses based on gender, prior disease status, and treatment discontinuation. E-value sensitivity analyses suggested that only strong unmeasured confounding could fully explain away the observed results. In conclusion, generic medications were at least similar, and in some cases superior, to their branded counterparts regarding mortality and major cardiovascular events.

Alendronate and raloxifene are among the most popular anti-osteoporosis medications. However, there is a lack of head-to-head comparative effectiveness studies comparing the two treatments. We conducted a retrospective large-scale multicenter study encompassing over 300 million patients across nine databases encoded in the Observational Medical Outcomes Partnership (OMOP) Common Data Model (CDM). The primary outcome was the incidence of osteoporotic hip fracture, while secondary outcomes were vertebral fracture, atypical femoral fracture (AFF), osteonecrosis of the jaw (ONJ), and esophageal cancer. We used propensity score trimming and stratification based on an expansive propensity score model with all pre-treatment patient characteritistcs. We accounted for unmeasured confounding using negative control outcomes to estimate and adjust for residual systematic bias in each data source. We identified 283,586 alendronate patients and 40,463 raloxifene patients. There were 7.48 hip fracture, 8.18 vertebral fracture, 1.14 AFF, 0.21 esophageal cancer and 0.09 ONJ events per 1,000 person-years in the alendronate cohort and 6.62, 7.36, 0.69, 0.22 and 0.06 events per 1,000 person-years, respectively, in the raloxifene cohort. Alendronate and raloxifene have a similar hip fracture risk (hazard ratio [HR] 1.03, 95% confidence interval [CI] 0.94–1.13), but alendronate users are more likely to have vertebral fractures (HR 1.07, 95% CI 1.01–1.14). Alendronate has higher risk for AFF (HR 1.51, 95% CI 1.23–1.84) but similar risk for esophageal cancer (HR 0.95, 95% CI 0.53–1.70), and ONJ (HR 1.62, 95% CI 0.78–3.34). We demonstrated substantial control of measured confounding by propensity score adjustment, and minimal residual systematic bias through negative control experiments, lending credibility to our effect estimates. Raloxifene is as effective as alendronate and may remain an option in the prevention of osteoporotic fracture.