Potential Strategy Research Articles

Photodynamic Therapy in Cancer: Principles, State of the Art, and Future Directions

Since its discovery more than 100 years ago, photodynamic therapy (PDT) has become a potent strategy for the treatment of many types of cancer [...]

Incremental versus saturation hypotheses for behavioral nudge in reducing sugar consumption.

This field experiment examined the efficacy of a behavioral nudge intervention towards lowering sugar intake in Indonesia. Specifically, two competing hypotheses were tested as to whether behavioral nudge played an additive role (i.e., the Incremental Hypothesis) or contributed to a ceiling effect (i.e., the Saturation Hypothesis) alongside social context and competition in a multimodal intervention program. This field experiment used a three-factorial mixed design involving 403 Indonesian participants based on power statistical analysis: 2 (sugar content nudge: lower sugar tea vs. regular sugar tea default) × 2 (social context: individual vs. group) × 2 (competition: absent vs. present). Nudging was the most powerful intervention in reducing sugar intake, but its effectiveness might be attenuated by social loafing even within Indonesia's collectivist culture. Competition did not work synergistically with nudging but was effective under the nonnudge condition. Our results are consistent with those of previous research showing that behavioral nudging has a stronger impact on behavioral change than nonnudge strategies. Contrary to some previous research, people in collectivist Indonesia did engage in social loafing: achievement motivation is not necessarily enhanced in a team of people in a collectivist culture. The Nudge × Competition interaction supports the saturation hypothesis in favor of behavioral nudging: using more than one intervention, when a potent strategy such as nudging is present, might result in diminishing returns that could reduce the overall benefit-cost profile of such multimodal intervention programs. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Quadripartite Evolutionary Game of Incentives for Green Retrofitting of Historical Buildings

Green retrofitting is a potent strategy to improve energy efficiency and support the cultural conservation of historical buildings. China has many historical buildings with significant potential for green retrofitting. Nevertheless, the Chinese green retrofit industry remains in its early stages due to the lack of a comprehensive promotion mechanism. Drawing upon evolutionary game theory, an evolutionary game model was formulated to analyze the interplay among governmental regulators, Energy Service Companies (ESCOs), the owners of historical buildings, and tourists. At an extreme disturbance intensity of 100%, a striking decline is observed in the likelihood of ESCOs maintaining the “green retrofit” strategy, with the probability dropping to a minimum of 24.68%. Under specific conditions however this interplay attains an optimal equilibrium state, denoted as (1,1,1,1). It is concluded that governmental regulators exhibit a greater degree of stability compared to other stakeholders, as they maintain their strategies despite external disturbances. Therefore, it is recommended that effective incentives and regulatory frameworks should consider the sensitivities of non-regulatory stakeholders to enhance the success of green retrofitting projects for historical buildings.

A Peptide-Copper Self-Assembled Nanoparticle for Enhanced Cuproptosis by Metabolic Reprogramming in Tumor Cells.

Cuproptosis is a type of metabolic cell death and exhibits great potential for cancer treatment. However, currently, most cuproptosis-based therapies are primarily effective in tumor cells reliant on mitochondrial respiration, limiting their broader application. The Warburg effect highlights that many tumors predominantly rely on glycolysis to meet their rapid metabolic demands, but glycolysis-dependent cells are less sensitive to copper ions than their mitochondrial-respiration-dependent counterparts, making it difficult to induce cuproptosis in these cells. Herein, we designed a copper-loaded peptide-based nanoparticle (MHRC@Cu) to enhance cuproptosis by metabolic reprogramming in a wider range of glycolysis-dependent tumor cells. Specifically, triggered by the acidic environment and laser irradiation, MHRC@Cu effectively released Cu2+ inside the cells. Then the peptide-conjugated probe (MHRC) reprogrammed glycolysis-dependent tumor cells, making them more dependent on mitochondrial respiration and increasing their sensitivity to copper ions. Additionally, the H2O2 generated by the photodynamic effect underwent Fenton reaction with Cu2+ in situ, producing highly toxic ·OH, which depleted GSH and disrupted copper efflux protein, thereby exacerbating copper deposition in cells. Through these synergistic mechanisms, MHRC@Cu significantly enhanced cuproptosis in glycolysis-dependent tumor cells, achieving up to 96% inhibition of tumor growth. This copper-loaded peptide-based nanoparticle offers a versatile and potent strategy for enhancing cuproptosis and may inspire the development of advanced self-assembled nanotherapeutic platforms.

PANoptosis Signaling Enables Broad Immune Response in Psoriasis: From Pathogenesis to New Therapeutic Strategies

BackgroundAccumulating evidence suggests that regulated cell death, such as pyroptosis, apoptosis, and necroptosis, is deeply involved in the pathogenesis of psoriasis. As a newly recognized form of systematic cell death, PANoptosis is involved in a variety of inflammatory disorders through amplifying inflammatory and immune cascades, but its role in psoriasis remains elusive. ObjectivesTo reveal the role of PANoptosis in psoriasis for a potential therapeutic strategy. MethodsMultitranscriptomic analysis and experimental validation were used to identify PANoptosis signaling in psoriasis. RNA-seq and scRNA-seq analyses were performed to establish a PANoptosis-mediated immune response in psoriasis, which revealed hub genes through WGCNA and predicted disulfiram as a potential drug. The effect and mechanism of disulfiram were verified in imiquimod (IMQ)-induced psoriasis. ResultsHere, we found a highlighted PANoptosis signature in psoriasis patients through multitranscriptomic analysis and experimental validation. Based on this, two distinct PANoptosis patterns (non/high) were identified, which were the options for clinical classification. The high-PANoptosis-related group had a higher response rate to immune cell infiltration (such as M1 macrophages and keratinocytes). Subsequently, WGCNA showed the hub genes (e.g., S100A12, CYCS, NOD2, STAT1, HSPA4, AIM2, MAPK7), which were significantly associated with clinical phenotype, PANoptosis signature, and identified immune response in psoriasis. Finally, we explored disulfiram (DSF) as a candidate drug for psoriasis through network pharmacology, which ameliorated IMQ-mediated psoriatic symptoms through antipyroptosis-mediated inflammation and enhanced apoptotic progression. By analyzing the specific ligandreceptor interaction pairs within and between cell lineages, we speculated that DSF might exert its effects by targeting keratinocytes directly or targeting M1 macrophages to downregulate the proliferation of keratinocytes. ConclusionsPANoptosis with its mediated immune cell infiltration provides a roadmap for research on the pathogenesis and therapeutic strategies of psoriasis.

Endothelial Cell Aging and Autophagy Dysregulation.

Entropy is a natural process that affects all living cells, including senescence, an irreversible physiological process that impairs cell homeostasis. Age is a significant factor in disease development, and the pathogenesis of endothelial cell aging is multifactorial. Autophagy dysfunction accelerates endothelial cell aging and cell death, while autophagy preserves endothelial cell youthfulness through intracellular homeostasis and gene expression regulation. Sirt, mTORC1, and AMPK are youthfulness genes that induce autophagy by inhibiting mTOR and upregulating FIP200/Atg13/ULK1. Aged endothelial cells have decreased levels of Lamin B1, γH2AX, Ki67, BrdU, PCNA, and SA β-Gal. Maintaining healthy young endothelial cells can prevent most cardiovascular diseases. Autophagy targeting is a potential future therapeutic strategy to modify endothelial cell age and potentially slow or reverse the aging process. This article provides state-of-the-art research on the role of autophagy in endothelial cell aging. Hypothesizing that autophagy dysregulation is associated with early endothelial cell dysfunction and further clinical sequelae, including atherosclerosis formation, leading to various cardiovascular diseases.

Dopamine-conjugated extracellular vesicles induce autophagy in Parkinson's disease.

The application of extracellular vesicles (EVs) as vehicles for anti-Parkinson's agents represents a significant advance, yet their clinical translation is hampered by challenges in efficient brain delivery and complex blood-brain barrier (BBB) targeting strategies. In this study, we engineered dopamine onto the surface of adipose-derived stem cell EVs (Dopa-EVs) utilizing a facile, two-step cross-linking approach. This engineering enhanced neuronal uptake of the EVs in primary neurons and neuroblastoma cells, a process shown to be competitively inhibited by dopamine pretreatment and dopamine receptor antibodies. Notably, Dopa-EVs demonstrated increased brain accumulation in mouse Parkinson's disease (PD) models. Therapeutically, Dopa-EVs administration led to the rescue of dopaminergic neuronal loss and amelioration of behavioural deficits in both 6-hydroxydopamine (6-OHDA) and α-Syn PFF-induced PD models. Furthermore, we observed that Dopa-EVs stimulated autophagy evidenced by the upregulation of Beclin-1 and LC3-II. These findings collectively indicate that surface modification of EVs with dopamine presents a potent strategy for targeting dopaminergic neurons in the brain. The remarkable therapeutic potential of Dopa-EVs, demonstrated in PD models, positions them as a highly promising candidate for PD treatment, offering a significant advance over current therapeutic modalities.

CK2B is a Prognostic Biomarker and a Potential Drug Target for Hepatocellular Carcinoma.

Although casein kinase II subunit beta (CK2B) was previously reported to be involved in human cancers, such as hepatocellular carcinoma (HCC), there has been no systematic assessment of CK2B in HCC. To assess the potential function of CK2B as a prognostic biomarker and possible druggable target in HCC. The Cancer Genome Atlas database was accessed to investigate the potential oncogenic and prognostic roles of CK2B in HCC. Diverse analytical methods were used to obtain a fuller understanding of CK2B, including CIBERSORT, The Tumor Immune Estimation Resource (TIMER), gene set enrichment analyses (GSEA), Kyoto Encyclopedia of Genes and Genomes (KEGG), and gene ontology (GO). Furthermore, the Comparative Toxicogenomic Database (CTD) was used to identify potential drugs to treat CK2B-overexpressing HCC. Patents for these drugs were reviewed using Patentscope® and Worldwide Espacenet®. Upregulated CK2B expression was markedly associated with more aggressive pathological features, including G3, G4 (vs. G1, G2), and T2, T3 (vs. T1). Kaplan-Meier survival curves indicated that patients with HCC with higher expression of CK2B had worse overall survival (P = 0.005), progression-free interval (P = 0.001), and disease-specific survival (P = 0.011). GO and KEGG analysis revealed that CK2B dysregulation affects mitotic chromosome condensation, protein stabilization and binding, regulation of signal transduction of p53 class mediator, and cancer-related pathways. GSEA identified six well-known pathways, including MAPK, WNT, Hedgehog, and TGFβ signaling pathways. Finally, CTD identified six compounds that might represent targeted drugs to treat HCC with CK2B overexpression. A review of patents indicated these compounds showed promising anticancer results; however, whether CK2B interacts with these drugs and improves drug outcomes for patients with HCC was not confirmed. CK2B is a biomarker for HCC prognosis and could be a potential new drug target. Moreover, the association between infiltrating immune cells and CK2B in the HCC tumor microenvironment might provide a solid basis for further investigation and a potent strategy for immunotherapy of HCC.

A Molecular‐Targeting Photosensitizer to Inhibit DNA Damage Repair System and Induce cGAS‐STING Pathway Activation for Photo‐Immunotherapy of Ovarian Cancer

AbstractPoly(ADP‐ribose) polymerase (PARP) inhibitors are commonly utilized in the clinical management of patients with platinum‐sensitive recurrent and late‐stage ovarian cancer, which constitutes a significant proportion of gynecological cancer‐related mortality. Nonetheless, the constraints of their monofunctional properties and limited therapeutic efficacy observed in advanced cancer cases necessitate the exploration of more potent therapeutic strategies for the management of ovarian cancer. The present study describes the development of QTABI, a PARP‐targeting photosensitizer capable of producing reactive oxygen species with light irradiation. Simultaneously, it exhibits significant inhibition of PARP activity, induction of deoxyribonucleic acid (DNA) damage, and consequent synthetic lethality. Furthermore, QTABI can effectively promote the accumulation of cytosolic DNA and activate the cyclicGMP‐AMP synthase (cGAS)‐stimulator of interferon gene (STING) pathway under light irradiation, thereby eliciting potent anti‐tumor immune responses and ultimately boosting anti‐cancer efficacy. Collectively, these findings suggest that QTABI is a multi‐functional photosensitizer, which targets the DNA‐damaging repair system and activates the cGAS‐STING pathway, offering a promising combination photo‐immunotherapy strategy for treating ovarian cancer.

Independent Commissioners' Role in CEO Tenure, Capital Intensity and Firm Size Tax Avoidance

Purpose: This research aims to understand the influence of CEO tenure, capital intensity, and company size on tax avoidance, with a focus on how these relationships are moderated by the proportion of independent commissioners in manufacturing companies listed on the Indonesia Stock Exchange (IDX) from 2017 to 2022. Methodology/approach: The study employs a purposive sampling strategy, selecting a total of 198 companies that meet the predefined criteria. The analysis relies on secondary data collected from the IDX website and utilizes panel data regression analysis on eViews 13.0 as the analytical technique. Findings: The data reveals that company size significantly affects tax avoidance, with larger firms tending to avoid tax less. Conversely, CEO tenure and capital intensity do not appear to impact tax avoidance significantly. The proportion of independent commissioners has a moderating effect on the relationship between firm size and tax avoidance, but not on the relationships between CEO tenure, capital intensity, and tax avoidance. Practical implications: These findings imply that corporate governance, represented by the proportion of independent commissioners, plays a crucial role in moderating the impact of company size on tax avoidance. However, its influence does not extend to the effect of CEO tenure and capital intensity on tax avoidance. This suggests that enhancing corporate governance practices could be a potent strategy for managing tax avoidance in large firms. Originality/value: This research contributes valuable insights into the factors influencing tax avoidance. It is unique in its use of independent commissioners as a proxy for corporate governance, testing its role in moderating the relationship between independent variables and tax avoidance. This is a departure from previous studies, which typically treat independent commissioners as independent variables.

Impact of Postsynthetic Modification on the Covalent Organic Framework (COF) Structures.

Covalent organic frameworks (COFs) have emerged as a versatile class of materials owing to their well-defined crystalline structures and inherent porosity. In the realm of COFs, their appeal lies in their customizable nature, which can be further enhanced by incorporating diverse functionalities. Postsynthetic modifications (PSMs) emerge as a potent strategy, facilitating the introduction of desired functionalities postsynthesis. A significant challenge in PSM pertains to preserving the crystallinity and porosity of the COFs. In this study, we aim to investigate the intricate interplay between PSM strategies and the resulting crystalline and porous structures of the COFs. The investigation delves into the diverse methodologies employed in PSMs, to elucidate their distinct influences on the crystallinity and porosity of the COFs. Through a comprehensive analysis of recent advancements and case studies, the study highlights the intricate relationships among PSM parameters, including reaction conditions, precursor selection, and functional groups, and their impact on the structural features of COFs. By understanding how PSM strategies can fine-tune the crystalline and porous characteristics of COFs, researchers can harness this knowledge to design COFs with tailored properties for specific applications, contributing to the advancement of functional materials in diverse fields. This work not only deepens our understanding of COFs but also provides valuable insights into the broader realm of PSM strategies for other solid materials.

Cooperative blockade of FLT3 and ALK synergistically suppresses growth of osteosarcoma.

Osteosarcoma is a common primary malignant bone tumor in children and young adults, with limited progress in improving survival rates for metastatic or recurrent cases. Kinase inhibitors have emerged as potential treatments for osteosarcoma due to the critical role kinases play in regulating cellular networks. However, single-agent kinase inhibitors often face challenges due to the activation of compensatory oncogenic signaling pathways, which can undermine treatment efficacy. In this study, a combination screening of FDA-approved kinase inhibitors was conducted in osteosarcoma cells. We identified the combination of ALK inhibitor and FLT3 inhibitor as a potent kinase-based therapeutic strategy for osteosarcoma. Our results showed that the combinatorial treatment synergistically suppressed osteosarcoma in cell lines, patient-derived organoids, and xenograft models. Mechanistically, the inhibition of FLT3 significantly promoted the activation of ALK, which subsequently enhanced its downstream PI3K/Akt and MAPK signaling pathways. The combinatorial use of an ALK inhibitor could reverse this process. Thus, our study demonstrates that the cooperative blockade of FLT3 and ALK synergistically suppresses osteosarcoma, providing a potential alternative for its treatment.

The Efficacy of Combined “Oral Simvastatin Plus Narrowband UVB Phototherapy” Than “Phototherapy Alone” in Treating Skin Lesions in Patients with Vitiligo, a Double-Blind Add-On Randomized Controlled Clinical Trial

Background: A tailored therapy for vitiligo is crucial in enhancing patients' quality of life and decreasing the associated dimensions. In addition, statins play a significant function in modulating the immune system. Objectives: This study investigated the efficacy of oral simvastatin in treating skin lesions in patients with vitiligo. Methods: This interventional randomized clinical trial enrolled 50 vitiligo patients referred to Shahid Faghihi Hospital in Shiraz (Iran) in 2015. Participants were divided into control and intervention groups using block randomization. Participants in the control group received “NB-UVB phototherapy plus placebo,” and those in the intervention group received “NB-UVB phototherapy with 40, 60, and 80 mg simvastatin by a monthly increase in the drug dosage”. A reduction in the Vitiligo Area Scoring Index (VASI) score and side effects were measured for four months, and the results were compared between the two groups. Results: At the start of the study, the mean score for the disease severity was equal for both groups (P ˃ 0.05). However, the disease severity was significantly reduced in the following stages of the study in the simvastatin group compared to the placebo group (P = 0.0001). Conclusions: Oral simvastatin enhances the photothermal outcomes while exerting trivial side effects. Thus, combining oral simvastatin with phototherapy is recommended as a potent strategy for treating patients with vitiligo.

Sumac liposomes/mesenchymal stem cells fight methotrexate-induced nephrotoxicity in rats via regulating Nrf-2/Keap-1/HO-1 and apoptotic signaling pathways.

Methotrexate (MTX) is commonly employed in cancer treatment, but its clinical use is restricted due to the MTX-associated renal injury. This study investigates the combined potential of Rhus coriaria (sumac) and bone marrow mesenchymal stem cells (BMMSCs) against MTX-induced nephrotoxicity in rats. The high-resolution-liquid chromatography-mass spectrometry (HR-LC-MS) of sumac extract tentatively identified 22 phytochemicals, mostly flavonoids, anthocyanins, and steroids. Preparation of sumac liposomes attained a suitable particle size of 3041.33 ± 339.42 nm, a polydispersity index of 0.208 ± 0.086, and an encapsulation efficiency of 84.92 ± 3.47%. Rat BMMSCs were injected into the tail vein of the experimental rats (0.5 × 106 cells, intravenous [iv]) of seven treated groups. The experimental design relies on either pre- or posttreatment of rats with intraperitoneal (IP) sumac liposomes (SL) (200 mg/kg, daily with a dose of MTX (300 µg/kg/14 days). The histopathological examination and serum analysis of creatinine and urea revealed good results, besides regulating levels of oxidative stress and inflammatory markers. Additionally, a significant decrease in the gene expression levels of B-Cell Lymphoma 2 (Bcl-2) and caspases-3 and -9, a remarkable increase in the Bcl-2 Associated X-Protein (Bax), nuclear factor erythroid 2-related factor 2 (Nrf2), and heme-oxygenase 1 expression, and a downregulation of Kelch-like ECH-associated protein 1 (Keap1). Collectively, the coadministration of SL with BMMSCs might be a potent therapeutic strategy for attenuation of MTX-induced renal damage. The network pharmacology analysis identified the involved key hub genes as KEAP1, Nrf2, HMOX1, mitogen-activated protein kinase (MAPK1), nuclear factor-kappa B (NF-KB), interleukin-1 beta (IL-1B), and caspase-3. The docking results revealed strong binding affinities of 7-O-methyl-cyanidin-3-O-(2″-galloyl)-galactoside with Keap1 and amentoflavone with MAPK. These insights pave the way for future experimental validation and therapeutic development of sumac-based phytoconstituents against MTX-induced nephrotoxicity.

Efficient Dendritic Cell Activation by a Layered Double Hydroxide‐Loaded Dual Adjuvant Cocktail

AbstractOne of the main goals of present vaccine investigations is to develop a potent and efficient adjuvant strategy. The combination of multiple agonists to different pattern recognition receptor families offers great opportunities to achieve strong immune responses in a synergy manner. Here, we employed layered double hydroxide nanomaterials with BSA coating (LB) to integrate CpG and 3pRNA dual adjuvant cocktail, together with ovalbumin antigen. With LB loading, CpG and 3pRNA led to a quick internalization and enhanced induction of dendritic cell (DC) maturation. Meanwhile, this nanoadjuvant cocktail facilitated antigen crosspresenting in activated DCs. Taken together, these results may inspire the investigation of agonists combination and LDH‐based nanoadjuvants.

Antibiotic-Augmented Chemodynamic Therapy for Treatment of Helicobacter pylori Infection in the Dynamic Stomach Environment.

Helicobacter pylori (H. pylori) is one of the main causes of peptic ulcer disease and gastric cancer. The overuse of antibiotics leads to bacterial drug resistance and disruption to the gut microbiome. Herein, a nanoparticle (TA-FeHMSN@Amox) was developed, comprising amoxicillin (Amox)-loaded iron-engineered hollow mesoporous silica as the core and a metal-polyphenol shell formed by tannic acid (TA) and Fe3+. In acidic stomach conditions, TA-FeHMSN@Amox generates bactericidal ·OH through Fenton/Fenton-like reactions of the degraded product Fe2+ and hydrogen peroxide (H2O2) at the infection site, achieving chemodynamic therapy (CDT). Moreover, released amoxicillin enhances therapeutic efficacy by impeding the self-repair of the bacterial cell wall damaged by CDT, overcoming the limitations of ineffective CDT under conditions lacking sufficient acidity and H2O2. The acidity-responsive CDT combined with reduced antibiotic usage ensures superior in vivo therapeutic efficacy and biocompatibility with intestinal flora, providing a highly potent strategy for treating H. pylori infections in the dynamic stomach environment.

Repositioning of aripiprazole, an anti‑psychotic drug, to sensitize the chemotherapy of pancreatic cancer.

Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy with limited therapeutic options. Cisplatin is a primary chemotherapeutic agent utilized in combination with other drugs or radiotherapy for PDAC treatment. However, the severe side effects of cisplatin often necessitate discontinuation of therapy and drug resistance in tumor cells poses significant clinical challenges. Therefore, the development of effective therapeutic strategies is imperative. The present study investigated whether repositioning of the antipsychotic drug aripiprazole could sensitize the anticancer activity of cisplatin in pancreatic cancer at doses calculated by the combination index. The findings indicated that aripiprazole combined with cisplatin to suppress pancreatic cancer cell growth. Notably, the combination notably increased the expression of apoptosis markers, including cleaved caspase‑3, compared with cisplatin alone. Additionally, this combination effectively decreased XIAP and MCL‑1 expression via mitochondrial membrane potential change as revealed by JC‑1 assay, thereby inducing apoptosis. Furthermore, in fluid shear stress assay, the combination of aripiprazole and cisplatin notably inhibited cell adhesion and tumor spheroid formation. Mechanistically, phospho‑kinase array profiles showed that the enhanced anticancer efficacy of the combination treatment could be attributed to the inhibition of STAT3 signaling, which led to a significant reduction in tumor growth in a pancreatic cancer animal model. The results showed that the repositioning of aripiprazole inhibits cancer cell growth by blocking the STAT3 signaling pathway and effectively enhancing cisplatin‑induced apoptosis, thereby suggesting that the combination of aripiprazole and cisplatin may be a potent chemotherapeutic strategy for the treatment of pancreatic cancer.

Electronic Structure Modulating of W18O49 Nanospheres by Niobium Doping for Efficient Hydrogen Evolution Reaction.

Hydrogen, known for its high energy density and environmental benefits, serves as a prime substitute for fossil fuels. Nonetheless, the hydrogen evolution reaction (HER), essential in electrolysis, encounters challenges with slow kinetics and significant overpotential, which elevate costs and reduce efficiency. Thus, developing efficient electrocatalysts to reduce HER overpotential is vital to enhance hydrogen production efficiency and minimize energy consumption. Adjusting the electronic structure of transition metal oxides via elemental doping is a potent strategy to improve the effectiveness of electrocatalysts for hydrogen evolution. In this work, we synthesized a set of niobium-doped tungsten oxides (Nbx-W18O49) under anoxic conditions using a straightforward "one-pot" solvothermal approach. After doping Nb, the oxygen vacancy content inside W18O49 was increased, which induced a synergistic effect with the active sites of tungsten. In acidic environments, the hydrogen evolution activity of the Nb0.6-W18O49 electrocatalyst is second only by 20 wt % Pt/C. It attains a current density of -10 mA cm-2 at an overpotential of 102 mV. By comparison with W18O49, Nb0.4-W18O49 and Nb0.5-W18O49, Nb0.6-W18O49 demonstrates a reduced charge transfer resistance, which significantly enhances its conductivity and the speed of electron movement across interfaces. Coupled with this feature are notably faster HER kinetics. Additionally, it exhibits excellent stability, meaning it maintains its performance and structural integrity over prolonged periods and under various operational conditions. This article provides a new perspective for discovering inexpensive and efficient hydrogen evolution electrocatalyst materials.

Nanotech‐Enhanced Chemical Energy Storage with DNA

AbstractDNA nanotechnology has revolutionized materials science by harnessing DNA's programmable properties. DNA serves as a versatile biotemplate, facilitating the creation of novel materials such as electrode materials and DNA hydrogels for electrolytes and membranes. These advancements have significantly boosted the performance of energy storage devices. DNA biotemplates not only enhance supercapacitor capacitance and increase Li–S battery cycling stability but also improve metal ion transport in perovskite solar cells, enhancing power conversion efficiency. Additionally, DNA's addressable nature allows precise enzyme positioning in biofuel cells, enhancing enzyme cascade efficiency. Overall, DNA nanotechnology offers a potent strategy for enhancing electrochemical device performance and stability through structural engineering.

Systematic multiomics analysis and in vitro experiments suggest that ITGA5 could serve as a promising therapeutic target for ccRCC

BackgroundIntegrin alpha 5 (ITGA5) was previously confirmed to be related to prognosis in several cancer types; however, its function in clear cell renal cell carcinoma (ccRCC) and how this molecule regulates tumor progression and the tumor microenvironment (TME) remain to be elucidated.MethodsWe investigated the prognostic implications of ITGA5 with a machine learning model and evaluated biological behaviors of different levels of ITGA5 expression in vitro. Bioinformatic analysis was performed to explain the comprehensive effect of ITGA5 on the TME and drug sensitivity.ResultsWe constructed a machine learning model to elaborate the prognostic implication of ITGA5. As tumorigenesis of ccRCC was tightly relevant with several mutant genes, we investigated the correlation between ITGA5 expression and frequent mutations and found ITGA5 upregulation in VHL mutant ccRCC (P = 0.016). Through overexpressing, silencing, and blocking ITGA5, we verified the role of ITGA5 in promoting ccRCC adverse biological activities; and the potential functions of ITGA5 in ccRCC were bioinformatically demonstrated, summarizing as cell proliferation, migration, and angiogenesis. The localization of ITGA5 primarily in endothelia and macrophages further verified its magnitude in angiogenesis and aroused our excavation in ITGA5 regulation of immune infiltration landscape. Generally, ITGA5-high ccRCC presented an immunosuppressive TME by inducing a lower level of CD8 + T cell infiltration. For the last part we predicted drug sensitivity relevant to ITGA5 and concluded that a joint medication of ITGA5 inhibitors and VEGFR-target drugs (including sunitinib, axitinib, pazopanib, and motesanib) might be a promising therapeutic strategy.ConclusionOur findings clarified the adverse outcome induced by high expression of ITGA5 in ccRCC patients. In vitro experiments and bioinformatical analysis identified ITGA5 function as predominantly cell proliferation, migration, angiogenesis, and macrophage recruitment. Further, we predicted immune infiltration and medication sensitivity regulation by ITGA5 and proposed a joint use of ITGA5 inhibitors and anti-angiogenetic drugs as a potential potent therapeutic strategy.