Jiangsu Vocational College of Medicine

Practical solutions are important in meeting the educational needs of patients and their caregivers. Using mobile technology offers a tremendous opportunity to teach specific skills to patients and/or to caregivers. This study aimed to develop a mobile-based application to support patients and their caregivers in meeting the tracheal suctioning information needs of patients with tracheostomies. The "ASSURE Instructional Design Model" was used to develop the material. This model enables the mobile-based application to be developed stepwise, which consists of 6 stages. The designing and development process of the mobile-based application requires following each step carefully, collaborating with different teams, obtaining the expert opinions and learners' feedback, as well as revising the material until it reaches the desired form. This article reports the design and development process of the mobile-based application by using the ASSURE Model and provides guidelines for researchers willing to study in this field.

GbF3H acts as a hierarchical switch that suppresses NtFLS1 but activates NtFLS2, thereby diverting flavonoid flux away from flavonols and toward isoflavonoids in transgenic tobacco. Flavanone 3-hydroxylase (F3H) is a key branch-point enzyme in the flavonoid biosynthesis, catalyzing the hydroxylation of naringenin to dihydrokaempferol and thereby directing metabolic flux into distinct flavonoid branches. In this study, we employed an integrated approach combining bioinformatic, molecular characterization, and transgenic techniques to elucidate the function and regulatory role of F3H in Ginkgo biloba. The cloned GbF3H encodes a cytoplasm-localized hydrophobic acidic protein of 369 amino acids, containing the conserved DIOX_N and 2OG-FeII_Oxy domains characteristic of 2-oxoglutarate-dependent dioxygenases. Expression profiling revealed that GbF3H transcripts were most abundant in immature fruits, ovulate strobili, and juvenile leaves, and were significantly modulated by different nitrogen forms and abscisic acid (ABA). Heterologous overexpression of GbF3H in tobacco (Nicotiana tabacum cv. K326) substantially reshaped the flavonoid metabolome, characterized by the pronounced upregulation in isoflavonoids and concomitant downregulation in flavonols. Concurrent transcriptomic analysis demonstrated that GbF3H overexpression suppressed key flavonoid biosynthetic genes (Nt4CL, NtFLS1, and NtUFGT), while differentially regulating NtFLS2, indicating a hierarchical regulatory mechanism governing the flavonoid metabolic network. Collectively, these results establish GbF3H as a central switch of flavonoid metabolic flux partitioning in G. biloba, providing crucial mechanistic insights for understanding the regulation of flavonoid biosynthesis and providing a basis for future metabolic engineering strategies.

Extracellular vesicles (EVs) are promising drug-delivery vehicles owing to their biocompatibility and low immunogenicity. Genetic engineering of a membrane-bound EV-sorting scaffold protein empowers EVs by installing targeting moieties on the surface and enriching therapeutic cargo in the lumen. However, the choice of scaffold proteins with simple structures and short sequences is limited. Here, we conduct mass spectrometry-based proteomic studies and identify ENPP1 as a superior scaffold protein. Furthermore, we show that a truncated 144-amino acid variant, EN144, efficiently loads diverse therapeutic cargoes and outperforms conventional scaffolds. By fusing EN144 to the IL-6 decoy receptor gp130, we create engineered decoy EVs that potently inhibit inflammatory IL-6 trans-signaling. In mouse models, these EVs reduce inflammation, improve survival in sepsis, and, when targeted to cartilage, alleviate tissue damage in osteoarthritis. Our work establishes EN144 as a minimal, high-performance scaffold for EV engineering and demonstrates its broad therapeutic potential for inflammatory diseases.

With the intensification of global climate change and the depletion of fossil fuels, renewable energy represented by photovoltaic power generation has become the key alternative form of energy for the transformation of electric energy. Driven by policy support and market demand, China’s photovoltaic industry is developing rapidly, but it also faces the problems of efficiency differentiation and unequal resource allocation. This research focuses on the development efficiency, influencing factors, and future trend prediction of China’s photovoltaic industry, selects data of 37 listed Chinese photovoltaic enterprises from 2018 to 2023, uses Windows DEA model to evaluate enterprise efficiency, analyzes the influencing factors through a Tobit regression model, and predicts the future development trend with the help of a BP neural network method. The findings show that overall efficiency of the domestic photovoltaic industry increased steadily from 2018 to 2023 at an average of 0.31–0.46 under average annual growth of about 8%. There are significant differences in the efficiency performance of enterprises located in various industrial chain positions. The efficiency of the silicon chip link leads, while there is a large room for improvement in the battery link. In terms of influencing factors, GDP of the enterprise location has a positive role in promoting the efficiency of photovoltaic enterprises, electricity consumption and government subsidies negatively impact photovoltaic efficiency, and the installed capacity of power generation has a significantly positive effect on efficiency. The prediction results show that the efficiency of China’s photovoltaic industry is expected to grow, but there is clear differentiation between industrial chains. This study provides theoretical basis and decision support for optimizing resource allocation of the photovoltaic industry, enhancing international competitiveness, and helping this industry’s sustainable development in China. Finally, this paper offers targeted suggestions to improve the power generation efficiency of the photovoltaic industry and to promote the transformation of the power industry toward a cleaner direction.

Protein acylation represents a class of metabolism-dependent post-translational modifications that are increasingly recognized as emerging regulatory components implicated in the molecular mechanisms associated with sleep disorders. Accumulating experimental evidence indicates that diverse acylation modifications-including acetylation, lactylation, crotonylation, succinylation, and lipid-type modifications such as palmitoylation and myristoylation-may influence circadian clock proteins, neurotrophic factors, synaptic scaffolding molecules, and mitochondrial energy metabolism. Importantly, most lysine acylation events occur at low global stoichiometry under physiological conditions, whereas pathological metabolic states may induce relative enrichment at specific functional sites rather than widespread high-occupancy modification. These acylation events have been linked to oxidative stress, neuroinflammation, and circadian disruption in preclinical studies, while robust causal and quantitative evidence in humans remains limited. This review synthesizes current mechanistic insights, emphasizes emerging conceptual advances, and outlines key challenges and future directions for translational research in sleep medicine.

​ Altered homeostasis of the ocular surface microenvironment is a hallmark of dry eye disease (DED). The alpha-7 nicotinic acetylcholine receptor (α7nAChR) plays a key role in DED pathophysiology. In this study, we established a rabbit model of DED using scopolamine hydrobromide (Scop) to determine the effect of electroacupuncture (EA) on ocular surface damage in DED and to explore its underlying mechanisms.​ Methods: New Zealand White rabbits (1.5-2.0 kg) were subcutaneously administered Scop for 21 days prior to EA treatment. After 35 days, the homeostasis of the ocular surface microenvironment was evaluated using the Schirmer I test (SIT), tear break-up time (BUT), corneal fluorescein (FL) staining, and measurement of tear osmolarity. The expression levels of ACh, α7nAChR, and high mobility group box 1 (HMGB1) were detected via histopathological examination of the cornea, lacrimal glands, and conjunctiva, combined with immunohistochemistry and western blotting. Additionally, protein chip technology was used to determine the expression levels of downstream factors.​ Results: EA stimulation significantly improved the homeostasis of the ocular surface microenvironment, as evidenced by increased SIT values and BUT, reduced corneal FL intensity, and decreased tear osmolarity. It also alleviated pathological damage to the cornea, conjunctiva, and lacrimal glands; upregulated the expression of ACh and α7nAChR; and downregulated the expression of HMGB1 and related inflammatory factors. However, these changes were reversed following administration of α-Bungarotoxin.​ Conclusion: EA stimulation improves ocular surface homeostasis and reduces inflammation in DED, potentially via activation of the α7nAChR signaling pathway, which in turn inhibits the expression of HMGB1 and inflammatory factors.​.