Research on the impact of the digital economy on the level of industrial structure: An empirical study of 280 cities in China.

As the digital revolution deepens, the digital economy (DE) is reshaping the global industrial structure (IS). This paper utilizes data from 280 Chinese cities between 2007 and 2020 to conduct an in-depth analysis of how DE propels the upgrading of IS and explores the role of human capital (HC) in this process. The research indicates that DE significantly fosters the optimization of IS. Additionally, it was discovered that the growth of HC plays a pivotal mediating role in this evolution, complementing existing research on the relationship between higher education and industrial upgrading. By adopting spatial econometric methods, this study unveils the spillover effects of DE in geographical space, identifying a positive influence on the industrial upgrading of surrounding regions. The paper also confirms the nonlinear characteristics of DE's impact on IS upgrading, which manifests as a pronounced inverted U-shaped trend, marking a novel discovery. Further findings suggest that in regions with more advanced artificial intelligence technologies, the impact of DE on industrial optimization is more significant, highlighting the role of regional disparities in the digital transformation. In conclusion, the paper proposes policy recommendations based on the research findings to facilitate the development of DE and the elevation of IS levels, thereby promoting high-quality economic growth.

Designing a medical information diagnosis platform with IoT integration.

In order to enhance the operational efficiency of the healthcare industry, this paper investigates a medical information diagnostic platform through the application of swarm and evolutionary algorithms. This paper begins with an analysis of the current development status of medical information diagnostic platforms based on Chat Generative Pre-trained Transformer (ChatGPT) and Internet of Things (IoT) technology. Subsequently, a comprehensive exploration of the advantages and disadvantages of swarm and evolutionary algorithms within the medical information diagnostic platform is presented. Further, the optimization of the swarm algorithm is achieved through reverse learning and Gaussian functions. The rationality and effectiveness of the proposed optimization algorithm are validated through horizontal comparative experiments. Experimental results demonstrate that the optimized model achieves favorable performance at the levels of minimum, average, and maximum algorithm fitness values. Additionally, preprocessing data in a 10 * 10 server configuration enhances the algorithm's fitness values. The minimum fitness value obtained by the optimized algorithm is 3.56, representing a 3 % improvement compared to the minimum value without sorting. In comparative experiments on algorithm stability, the optimized algorithm exhibits the best stability, with further enhancement observed when using sorting algorithms. Therefore, this paper not only provides a new perspective for the field of medical information diagnostics but also offers effective technical support for practical applications in medical information processing.

4-octyl itaconate improves the viability of D66H cells by regulating the KEAP1-NRF2-GCLC/HO-1 pathway.

As a novel nuclear factor E2-related factor 2 (NRF2) activator, the itaconate has shown significant therapeutic potential for oxidative stress diseases. However, its role in Vohwinkel syndrome in relation to the gap junction protein beta 2 (GJB2) mutation is still unclear. This study aimed at investigating the effect of 4-octyl itaconate (OI) on HaCaT and D66H cells and clarify its potential mechanism in vitro. The optimal concentration and treatment time of OI on HaCaT cells and D66H cells were determined by CCK-8 and LDH experiments. The effect of OI on cell proliferation was detected by EdU staining and FACS analysis of PI, while the apoptosis was evaluated by TUNEL staining and FACS analysis of Annexin V. The ROS staining was performed, and the levels of SOD, MDA, GSH and GSH/GSSG were detected to evaluate the effect of OI on oxidative damage induced by D66H-type mutation. CO-IP, Western blot, immunofluorescence and qPCR analyses were employed to detect the activation of KEAP1-NRF2-GCLC/HO-1 pathway by OI. Finally, sh-NRF2 was used to confirm the activation of this pathway by OI. Results showed that OI could improve the cell viability decreased by GJB2 gene mutation by regulating the balance between cell growth and apoptosis induced by oxidative damage. Furthermore, this alleviation process was regulated by the KEAP1-NRF2-HO-1/GCLC pathway. In conclusion, OI could improve the viability of HaCaT and D66H cells via regulating the KEAP1-NRF2-GCLC/HO-1 pathway, which provided a wide spectrum of potential targets for effective therapeutic treatments of Vohwinkel syndrome in the clinic.

Simultaneous carbon dioxide sequestration and nitrate removal by Chlorella vulgaris and Pseudomonas sp. consortium.

Carbon dioxide and nitrogen oxides are the main components of fossil flue gas causing the most serious environmental problems. Developing a sustainable and green method to treat carbon dioxide and nitrogen oxides of flue gas is still challenging. Here, a co-cultured microalgae/bacteria system, Chlorella vulgaris and Pseudomonas sp., was developed for simultaneous sequestration of CO2 and removal of nitrogen oxides from flue gas, as well as producing valuable microalgae biomass. The co-cultured Chlorella vulgaris and Pseudomonas sp. showed the highest CO2 fixation and NO3--N removal rate of 0.482 g L-1d-1 and 129.6 mg L-1d-1, the total chlorophyll accumulation rate of 65.6 mg L-1 at the initial volume ratio of Chlorella vulgaris and Pseudomonas sp. as 1:10. The NO3--N removal rate can be increased to 183.5 mg L-1d-1 by continuous addition of 0.6 g L-1d-1 of glucose, which was 37% higher than that of co-culture system without the addition of glucose. Photosynthetic activity and carbonic anhydrase activity of Chlorella vulgaris were significantly increased when co-cultured with Pseudomonas sp. Excitation-emission matrix (EEM) fluorescence spectroscopy indicated that the humic acid-like substances released from Pseudomonas sp. could increase the growth of microalgae. This work provides an attractive way to simultaneously treatment of CO2 and NOX from flue gas to produce valuable microalgal biomass.

An eosinophil-Sos1-RAS axis licenses corticosteroid resistance in patients with allergic rhinitis.

BACKGROUND: Corticosteroid resistance (CR) is a serious disadvantage in treating many chronic inflammatory conditions. Eosinophils are the main inflammation cells in allergic reactions. Environmental pollution, such as PM2.5, is associated with the pathogenesis of allergic disorders. The objective of this study is to elucidate the mechanism by which the exposure to PM2.5 confers eosinophil CR status. METHODS: Patients with allergic rhinitis were recruited and assigned to corticosteroid sensitive (CS) and CR groups. Eosinophils were purified from nasal lavage fluids collected from patients with allergic rhinitis. A murine AR mouse model was developed with dust mite allergens and PM2.5 as the sensitization reagents. RESULTS: CR status was detected in about 60% eosinophil collected in patients with AR. Upon exposure to eosinophil activators, CS eosinophils released a large quantity of mediators, which was suppressed by the presence of steroids in the culture. CR eosinophils demonstrated resistance to steroidal therapy. RAS activation levels in eosinophils were higher in CR eosinophils than in CS eosinophils. Higher expression of the Son of sevenless-1 (Sos1) was detected in CR eosinophils, which formed a complex with RAS and glucocorticoidreceptor-α in CR eosinophils to prevent the binding between steroids and glucocorticoidreceptor-α. The presence of an Sos1 inhibitor dissociated glucocorticoid receptor-α from RAS/Sos1 complex, that restored the sensitivity to steroids in eosinophils. Administering the Sos1 inhibitor effectively attenuated the experimental allergic rhinitis. CONCLUSIONS: CR status was detected in approximately 1/3 eosinophils sampled from patients with allergic rhinitis. Sos1 was instrumental in the development and perseverance of CR in eosinophils. Sos1 inhibition restored sensitivity to steroids in CR eosinophils, which effectively reduced experimental allergic rhinitis.

Energy-Free, Singlet Oxygen-Based Chemodynamic Therapy for Selective Tumor Treatment without Dark Toxicity.

Traditional singlet oxygen-based antitumor therapies have been burdened with the necessity of external energy (e.g., light and ultrasound) and harmful dark toxicity. Ascorbate at the pharmacological concentration could accumulate hydrogen peroxide only in the tumor site. It is postulated that the concurrent delivery of ascorbate and nanoparticulate hypochlorous ion (ClO- ) could produce singlet oxygen at the tumor site as an energy-free, tumor-specific therapy. The ClO- is loaded in a hybrid core-shell nanocarrier consisting of a zeolitic imidazolate framework and amphiphilic poloxamer 188. Intracellular singlet oxygen production is verified in 4T1 cells by the cooperation between hybrid nanocarriers and ascorbate, which induces significant apoptotic cell death. Upon intravenous nanocarriers delivery plus intraperitoneal ascorbate administration to xenograft mice, the in vivo antitumor efficacy of this cooperative nanomedicine is demonstrated without noticeable side-effects. This work demonstrates a proof-of-concept of singlet oxygen-based chemodynamic therapy for selective tumor eradication, which produces a novel trigger-free, singlet oxygen-based cancer therapy without the side effects of traditional photodynamic and sonodynamic therapy.

Multifunctional Micelles Dually Responsive to Hypoxia and Singlet Oxygen: Enhanced Photodynamic Therapy via Interactively Triggered Photosensitizer Delivery.

Nanoparticulate antitumor photodynamic therapy (PDT) has been suffering from the limited dose accumulation in tumor. Herein, we report dually hypoxia- and singlet oxygen-responsive polymeric micelles to efficiently utilize the photosensitizer deposited in the disease site and hence facilely improve PDT's antitumor efficacy. Tailored methoxy poly(ethylene glycol)-azobenzene-poly(aspartic acid) copolymer conjugate with imidazole as the side chains was synthesized. The conjugate micelles (189 ± 19 nm) obtained by self-assembly could efficiently load a model photosensitizer, chlorin e6 (Ce6) with a loading of 4.1 ± 0.5% (w/w). The facilitated cellular uptake of micelles was achieved by the triggered azobenzene collapse that provoked poly(ethylene glycol) shedding; rapid Ce6 release was enabled by imidazole oxidation that induced micelle disassembly. In addition, the singlet oxygen-mediated cargo release not only addressed the limited diffusion range and short half-life of singlet oxygen but also decreased the oxygen level, which could in turn enhance internalization and increase the intracellular Ce6 concentration. The hypoxia-induced dePEGylation and singlet oxygen-triggered Ce6 release was demonstrated both in aqueous buffer and in Lewis lung carcinoma (LLC) cells. The cellular uptake study demonstrated that the dually responsive micelles could deliver significantly more Ce6 to the cells, which resulted in a substantially improved cytotoxicity. This concurred well with the superior in vivo antitumor ability of micelles in a LLC tumor-bearing mouse model. This study presented an intriguing nanoplatform to realize interactively triggered photosensitizer delivery and improved antitumor PDT efficacy.

In Situ Probing Intracellular Drug Release from Redox-Responsive Micelles by United FRET and AIE.

Redox-responsive micelles are versatile nanoplatforms for on-demand drug delivery, but the in situ evaluation of drug release is challenging. Fluorescence resonance energy transfer (FRET) technique shows potential for addressing this, while the aggregation-caused quenching effect limits the assay sensitivity. The aim of the current work is to combine aggregation-induced emission (AIE) probe with FRET to realize drug release assessment from micelles. Tetraphenylethene (TPE) is selected as AIE dye and curcumin (Cur) is chosen as the model drug as well as FRET receptor. The drug is covalently linked to a block copolymer via the disulfide bond linker and TPE is also chemically linked to the polymer via an amide bond; the obtained amphiphilic polymer conjugate self-assembles into micelles with a hydrodynamic size of ≈125 nm. Upon the supplement of glutathione or tris(2-carboxyethyl)phosphine) trigger (10 × 10-3 m), the drug release induces the fluorescence increase of both TPE and Cur. Accompanied with the FRET decay, absorption enhancement and particle size increase are observed. The same phenomenon is observed in MCF-7 cells. The FRET-AIE approach can be a useful addition to the spectrum of available methods for monitoring drug release from stimuli-responsive nanomedicine.

Large enhancements of NaYF4:Yb/Er/Gd nanorod upconversion emissions via coupling with localized surface plasmon of Au film.

Four-layered plasmonic structures of glass/Au/TiO2/NaYF4:Yb, Er, Gd nanorods were fabricated and tremendous improvement in upconversion luminescence (UCL) was observed under infrared 980 nm excitation. The TiO2 film was used as an oxide spacer. The emission intensity of the upconversion (UC) nanorods was strongly modulated by the thickness of the TiO2 layer. The extent of modulation depended on the separation distance between the Au layer and UC nanorods. A maximum UCL enhancement of 192-fold was observed for one green emission (540 nm) when a 10 nm-thick TiO2 film was used; 150-fold was observed for the other green emission (521 nm) at the same thickness of TiO2; and 105-fold was observed for the red emission (654 nm) when a 7.5 nm-thick TiO2 film was used. Alteration of the radiative decay rate was demonstrated for the first time in measurements of the decay times of UC nanorods positioned at various distances from the Au layer. The light interaction and coupling between metal Au and UC nanorods is numerically studied. The UCL mechanisms of multilayer plasmonic structures are discussed. Experimental results are explained and correspond well with those of theoretical calculations.