Decorated-Induced Oxygen Vacancy Engineering for Ultra-Low Concentration Nonanal Sensing: A Case Study of La-Decorated Bi2O2CO3.

La-decorated Bi2O2CO3 (BCO-La) microspheres are synthesized using a facile wet chemical strategy for sensing low-concentration nonanal (C9H18O) at room temperature. These BCO-La gas sensors are applied to evaluate agricultural product quality, specifically for cooked rice. The sensitivity of the BCO-6La sensor significantly surpassed that of the pure BCO sensor, achieving a response value of 174.6 when detecting 30 ppm nonanal gas. Notably, the BCO-6La sensor demonstrated a faster response time (36 s) when exposed to 18 ppm of nonanal. Additionally, the selectivity toward nonanal gas detection is higher (approximately 4-24 times) compared to interfering gases (1-octanol, geranyl acetone, linalool, hexanal, 2-pentyfuran, and 1-octen-3-ol) during cooked rice quality detection. The gas sensing mechanism and the factors contributing to the enhanced sensing performance of the BCO-La microspheres are demonstrated through in situ FT-IR spectra and DFT analysis while the realistic detection scenario is carried out. In a broader context, the reported sensors here represent a novel platform for the detection and monitoring of gases released by agricultural products during storage.

Progress in the Pathogenesis of Diabetic Encephalopathy: The Key Role of Neuroinflammation.

Diabetic encephalopathy (DE) is a severe complication that occurs in the central nervous system (CNS) and leads to cognitive impairment. DE involves various pathophysiological processes, and its pathogenesis is still unclear. This review summarised current research on the pathogenesis of diabetic encephalopathy, which involves neuroinflammation, oxidative stress, iron homoeostasis, blood-brain barrier disruption, altered gut microbiota, insulin resistance, etc. Among these pathological mechanisms, neuroinflammation has been focused on. This paper summarises some of the molecular mechanisms involved in neuroinflammation, including the Mammalian Target of Rapamycin (mTOR), Lipocalin-2 (LCN-2), Pyroptosis, Advanced Glycosylation End Products (AGEs), and some common pro-inflammatory factors. In addition, we discuss recent advances in the study of potential therapeutic targets for the treatment of DE against neuroinflammation. The current research on the pathogenesis of DE is progressing slowly, and more research is needed in the future. Further study of neuroinflammation as a mechanism is conducive to the discovery of more effective treatments for DE in the future.

Amphiphilic Janus Graphene Oxide Acts as a Corrosion Inhibitor to Mitigate the Corrosion Caused by a 1 M HCl Solution on Mild Steel.

Great aqueous dispersibility, a large specific surface area, and high impermeability make graphene oxide (GO) the ideal candidate for a high-performance corrosion inhibitor. Numerous symmetrical modification methods have been reported to enhance the adsorption of GO on metal surfaces in various corrosive media. This work aims to investigate the enhancement and mechanism of unilateral hydrophobic modification on the corrosion inhibition performance of GO. In this study, amphiphilic Janus GO (JGO) was prepared by grafting hydrophobic alkyl chains on one side of GO, and its anticorrosion performance was evaluated via weight loss experiments and electrochemical tests. The results revealed that the corrosion inhibition efficiency for Q235 mild steel (MS) in a 1 M HCl aqueous solution of 25 ppm JGO (81.08%) was much higher than that of GO at the same concentration (22.12%). Furthermore, the Langmuir adsorption isotherm and computational study demonstrated that the synergistic effect of physical adsorption and chemical adsorption promoted the hydrophilic side of JGO close to the surface of the metal, and the dense protective layer was formed by the hydrophobic chains toward the corrosive medium, which effectively hindered the corrosion of MS by the acidic liquid. This study emphasizes the significant role of asymmetrically modified hydrophobic alkyl chains in improving the corrosion prevention performance of GO and provides a perspective for the structural design of GO-based corrosion inhibitors.

Bioinformatics analyses and experimental validation of ferroptosis-related genes in bronchopulmonary dysplasia pathogenesis.

OBJECTIVE: We aimed to study the involvement of ferroptosis in the pathogenesis of bronchopulmonary dysplasia (BPD) by conducting bioinformatics analyses and identifying and validating the associated ferroptosis-related genes to explore new directions for treating BPD. METHODS: The dataset GSE32472 on BPD was downloaded from the public genome database. Using R language, differentially expressed genes (DEGs) between the BPD and normal group were screened. In the present study, we adopted weighted gene correlation network analysis (WGCNA) for identifying BPD-related gene modules and ferroptosis-related genes were extracted from FerrDb. Their results were intersected to obtain the hub genes. After that, to explore the hub gene-related signaling pathways, the hub genes were exposed to gene ontology enrichment analysis. With the purpose of verifying the mRNA expression of the hub genes, a single-gene gene set enrichment analysis and quantitative reverse transcription polymerase chain reaction were conducted. Immune cell infiltration in BPD was analyzed using the CIBERSORT inverse fold product algorithm. RESULTS: A total of 606 DEGs were screened. WGCNA provided the BPD-related gene module darkgreen4. The intersection of DEGs, intramodular genes, and ferroptosis-related genes revealed six ferroptosis-associated hub genes (ACSL1, GALNT14, WIPI1, MAPK14, PROK2, and CREB5). Receiver operating characteristic curve analysis demonstrated that the hub genes screened for BPD were of good diagnostic significance. According to the results of immune infiltration analysis, the proportions of CD8, CD4 naive, and memory resting T cells and M2 macrophage were elevated in the normal group, and the proportions of M0 macrophage, resting mast cell, and neutrophils were increased in the BPD group. CONCLUSIONS: A total of six ferroptosis-associated hub genes in BPD were identified in this study, and they may be potential new therapeutic targets for BPD.

Reconciling the Cooperative-Competitive Patterns among Tumor and Immune Cells for Triple-Negative Breast Cancer Treatment Using Multimodule Nanocomplexes.

Targeting the competitive-cooperative relationships among tumor cells and various immune cells can efficiently reverse the immune-dysfunction microenvironment to boost the immunotherapies for the triple-negative breast cancer treatment. Hence, a bacterial outer membrane vesicle-based nanocomplex is designed for specifically targeting malignant cells and immune cells to reconcile the relationships based on metabolic-immune crosstalk. By uniquely utilizing the property of charge-reversal polymers to realize function separation, the nanocomplexes could synergistically regulate tumor cells and immune cells. This approach could reshape the immunosuppressive competition-cooperation pattern into one that is immune-responsive, showcasing significant potential for inducing tumor remission in TNBC models.

Phosphorylation of IDH1 Facilitates Progestin Resistance in Endometrial Cancer.

The progestin regimen is one of the main therapeutic strategies for women with endometrial cancer who undergo conservative management. Although many patients respond well to initial therapy, progestin-refractory disease inevitably emerges, and the molecular basis underlying progestin resistance has not been comprehensively elucidated. Herein, they demonstrated progestin results in p38-dependent IDH1 Thr 77 phosphorylation (pT77-IDH1). pT77-IDH1 translocates into the nucleus and is recruited to chromatin through its interaction with OCT6. IDH1-produced α-ketoglutarate (αKG) then facilitates the activity of OCT6 to promote focal adhesion related target gene transcription to confer progestin resistance. Pharmacological inhibition of p38 or focal adhesion signaling sensitizes endometrial cancer cells to progestin in vivo. The study reveals p38-dependent pT77-IDH1 as a key mediator of progestin resistance and a promising target for improving the efficacy of progestin therapy.

Differential Impact of 0.01% and 0.05% Atropine Eyedrops on Ocular Surface in Young Adults.

Purpose: To evaluate the effect of low-concentration (0.01% and 0.05%) atropine eyedrops on ocular surface characteristics in young adults. Methods: Twenty-six myopic students aged 18 to 30 years were randomly assigned to receive either 0.01% or 0.05% atropine once nightly for 14 days, followed by cessation, with a ≥14-day interval between each administration. Assessments were conducted one, two, seven, and 14 days after using atropine with corresponding timepoints after atropine cessation. Tear meniscus height and first and average noninvasive keratograph tear film breakup time (NIKBUT-first, NIKBUT-average) were measured using Keratograph 5M, whereas the objective scatter index (OSI) was measured by OQAS II devices; the ocular surface disease index (OSDI) score was also obtained. Results: The mean OSI peaked after two days of administration of 0.05% atropine (ß = 0.51, P = 0.001), accompanied by significant decreases in NIKBUT-first (ß = -7.73, P < 0.001) and NIKBUT-average (ß = -8.10, P < 0.001); the OSDI peaked after 14 days (ß = 15.41, P < 0.001). The above parameters returned to baseline one week after atropine discontinuation (all P > 0.05). NIKBUT-first and NIKBUT-average reached their lowest points after 14 days of 0.01% atropine administration (NIKBUT-first: ß = -4.46, P = 0.005; NIKBUT-average: ß = -4.42, P = 0.001), but those significant changes were diminished once atropine treatment stopped. Conclusions: Young adult myopes experienced a significant but temporary impact on the ocular surface with 0.05% atropine administration, whereas 0.01% atropine had a minimal effect. Translational Relevance: The investigation of the ocular surface effects of different concentrations of atropine may inform evidence-based clinical decisions regarding myopia control in young adults.

Seaweed-inspired underwater anti-oil-fouling and anti-fogging coating with mechanical durability.

Ecofriendly fabrication of anti-oil-fouling materials is of interest. Surfaces with underwater superoleophobicity have been fabricated which exhibit limited mechanical durability and water resistance. In this study, we report on a bioinspired bilayer design of a transparent anti-oil-fouling coating. Seaweed surfaces show anti-oil-fouling in the sea due to its high surface hydration ability. Mussels can adhere tightly onto a surface with good stability in the sea by virtue of its levodopa-containing secretions. The surface layer was fabricated using a crosslinked combination of carboxymethyl cellulose (CMC) and sodium alginate (AlgS) inspired by seaweed, with the addition of calcium ions. Polydopamine (PDA), a derivative of levodopa, was used as the underlayer to enhance bonding strength and water resistance. Oil that adhered to the coated surface was spontaneously detached upon immersion in water. The mechanism underlying this anti-oil-fouling effect was elucidated using Gibbs free energy theory. The coating exhibited mechanical durability and water resistance. The coating is transparent and preserves the original color of the substrate. The coated glass showed stable anti-fogging and anti-frost performance. These coatings hold promise for a wide range of anti-oil-fouling applications.

Effect of myopia-control lenses on central and peripheral visual performance in myopic children.

PURPOSE: To evaluate the short-term effects of three myopia-control lenses, which impose peripheral myopic defocus while providing clear central vision, on central and peripheral visual performance in myopic children. METHODS: Twenty-one myopic children were enrolled in the study. Central visual performance was assessed using the quick contrast sensitivity function. Peripheral visual performance was evaluated by measuring peripheral contrast threshold and global motion perception, while subjects maintained fixation through the central portion of the lens. Single-vision spectacle lenses (SVL), spectacle lenses with highly aspherical lenslets (HAL) and defocus-incorporated soft contact (DISC) lenses were evaluated in random order, followed by orthokeratology (OK) lenses. All tests were performed monocularly on the right eye. RESULTS: The area under the log contrast sensitivity function (AULCSF) with DISC lenses was lower than that with SVL (1.14 vs. 1.40, p < 0.001) and HAL (1.14 vs. 1.33, p = 0.001). HAL increased the temporal visual field contrast threshold compared with OK lenses (p = 0.04), and OK lenses decreased the superior visual field contrast threshold compared with that of SVL (p = 0.04) and HAL (p = 0.005). HAL also increased the peripheral coherence threshold for identifying the contraction movement compared with OK lenses (p = 0.01). CONCLUSIONS: The short-term use of these optical interventions for myopia control exhibited measurable differences in central and peripheral visual performance. Relevant attention could be paid to these differences, especially when children switch to different treatments. DISC lenses exhibited worse central contrast sensitivity than SVL and HAL. Imposing peripheral defocus signals did not affect children's peripheral visual performance compared with SVL. However, considering the poorer peripheral visual performance provided by HAL, OK lenses are recommended for children if there are specific demands for global scene recognition and motion perception.

Performance improvement of underwater LIBS qualitative and quantitative analysis by irradiating with long nanosecond pulses.

Long nanosecond pulses have been proven to be efficient at enhancing underwater LIBS emission. However, the quantitative analytical capability of underwater long-pulse LIBS has yet to be further revealed. In this work, we investigated the spectral characteristics by irradiating with a laser pulse of 120 ns duration. The alkali and alkaline earth metals Li, K and Ca and the transition element Mn were selected for analysis. It is shown that obvious self-reversal structures were observed in the spectra at high concentrations, making the calibration curves saturated. Correction was performed using the approximate Voigt function fitting method, which significantly improves the linearity of the calibration curves. In addition to the target metal elements, atomic lines of the matrix elements H and O in water were also observed, which can serve as promising internal standards for quantitative analysis. A comparison of the quantification performance with and without the internal standards demonstrates that the use of the internal standards is conducive to improving the robustness of the calibration approaches with higher determination coefficients. More importantly, the underwater LIBS signal stability is improved by more than 3 times, and the prediction error for validation samples is reduced by 2-4 times. The present results suggest that long ns pulses are favorable to significantly improving the qualitative and quantitative performance of underwater single-pulse LIBS, enabling long-pulse LIBS to have great potential to be applied to underwater in situ chemical analysis.

Role of the P2 × 7 receptor in neurodegenerative diseases and its pharmacological properties.

Neurodegenerative diseases seriously affect patients' physical and mental health, reduce their quality of life, and impose a heavy burden on society. However, their treatment remains challenging. Therefore, exploring factors potentially related to the pathogenesis of neurodegenerative diseases and improving their diagnosis and treatment are urgently needed. Recent studies have shown that P2 × 7R plays a crucial role in regulating neurodegenerative diseases caused by neuroinflammation. P2 × 7R is an adenosine 5'-triphosphate ligand-gated cation channel receptor present in most tissues of the human body. An increase in P2 × 7R levels can affect the progression of neurodegenerative diseases, and the inhibition of P2 × 7R can alleviate neurodegenerative diseases. In this review, we comprehensively describe the biological characteristics (structure, distribution, and function) of this gene, focusing on its potential association with neurodegenerative diseases, and we discuss the pharmacological effects of drugs (P2 × 7R inhibitors) used to treat neurodegenerative diseases.

RNA 5-Methylcytosine regulators are associated with cell adhesion and predict prognosis of endometrial cancer.

Background: RNA methylation is a significant form of post-transcriptional modification that has been implicated in various diseases, including cancers. One prominent type of RNA methylation is 5-Methylcytosine (m5C), which primarily regulates RNA stability, transcription, and translation. However, the role of m5C-related gene regulation in cell adhesion within uterine corpus endometrial carcinoma (UCEC) remains unexplored. Therefore, the objective of this study was to investigate the association between RNA m5C methylation and UCEC and develop a prognostic predictive model to forecast survival outcomes in UCEC patients. Methods: The RNA datasets were acquired from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. The dataset was used to explore the interaction relationships of m5C regulators in UCEC. Unsupervised clustering analysis identified clusters with distinct m5C modification patterns. Different clusters underwent Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment level analysis to investigate the effects of pathways related to m5C methylation, which were further validated through in vitro cellular experiments. A prognostic predictive model was developed using the least absolute shrinkage and selection operator (LASSO) and multivariate regression analysis. Results: Two clusters with distinct m5C modification patterns were identified using unsupervised cluster analysis. Furthermore, the prognosis of cluster 2 was found to be worse. Enrichment analysis showed alterations in cell adhesion-related pathways in both clusters, as well as differences between the clusters. Through this analysis, we identified 25 genes with significant prognostic value. Finally, a prognostic predictive model comprising NSUN2 and YBX1 was constructed. Conclusions: In conclusion, diverse m5C modification patterns display distinct cell adhesion properties in UCEC, which are correlated with prognosis and offer significant potential as prognostic markers for UCEC assessment. We developed a prognostic predictive model to accurately predict the prognosis of UCEC.

Alternative Approach to Design and Optimization of High-Q Ring Resonators for Membrane-Free Acoustic Sensors.

Membrane-free acoustic sensors based on new principle and structure are becoming a research hotspot, because of many advantages, e.g., their wide bandwidth and high sensitivity. It is proposed that a membrane-free acoustic sensor employs a semi-buried optical waveguide ring resonator (SOWRR) as a sensing element. Using air as the upper cladding medium, the excited evanescent field in the air cladding medium would be modulated by acoustic wave. On this basis, the acoustic sensing model is established. Taking high Q factor and resonance depth as design criteria, the optimal design parameters are given. The optimal values of the air/SiO2: Ge/SiO2 waveguide resonator length and coupling spacing are obtained as 50 mm and 5.6 µm, respectively. The Q factor of the waveguide resonator of this size is as high as 8.33 × 106. The theoretical simulation indicates that the frequency response ranges from 1 Hz to 1.58 MHz and that the minimum detectable sound pressure is 7.48 µPa using a laser with linewidth of 1 kHz. Because of its advantages of wide bandwidth and high sensitivity, the membrane-free sensor is expected to become one of the most promising candidates for the next-generation acoustic sensor.

Microenvironment-Responsive Metal-Phenolic Nanozyme Release Platform with Antibacterial, ROS Scavenging, and Osteogenesis for Periodontitis.

Periodontitis is a chronic inflammatory disease deriving from dental plaque, characterized by the excessive accumulation of reactive oxygen species (ROS), matrix metalloproteinase (MMP) and other substances, resulting in the destruction of periodontal tissues. At present, the main therapeutic modalities, such as local mechanical debridement and antibiotic delivery, are not only difficult to solve the intractable bacterial biofilm effectively but also tricky to ameliorate the excessive inflammatory response as well as regenerate the impaired periodontal tissues. Herein, we have proposed the TM/BHT/CuTA hydrogel system formed by the self-assembly of the copper-based nanozyme (copper tannic acid coordination nanosheets, CuTA NSs) and the triglycerol monostearate/2,6-di-tert-butyl-4-methylphenol (TM/BHT) hydrogel. The negatively charged TM/BHT/CuTA can retain at the inflammation sites with a positive charge through electrostatic adsorption and hydrolyze in response to the increasing MMP of periodontitis, realizing the on-demand release of the CuTA nanozyme. The released CuTA nanozyme has antibacterial and antiplaque properties. Meanwhile, as a metal-phenolic nanozyme, it can scavenge multiple ROS by simulating the cascade process of superoxide dismutase (SOD) and catalase (CAT). Further, the CuTA nanozyme can modulate the macrophage polarization from M1 phenotype to M2 phenotype through the Nrf2/NF-κB pathway, which reduces the pro-inflammatory cytokines, increases the anti-inflammatory cytokines, and promotes the expression of osteogenetic genes successively, thus relieving the inflammation and accelerating the tissue regeneration of periodontitis. Altogether, this multifunctional nanozyme on-demand release platform (TM/BHT/CuTA) provides a desirable strategy for the treatment of periodontitis.

Pleiotropic Microenvironment Remodeling Micelles for Cerebral Ischemia-Reperfusion Injury Therapy by Inhibiting Neuronal Ferroptosis and Glial Overactivation.

Reperfusion injury presents a significant obstacle to neuronal survival following successful recanalization in ischemic stroke, which is characterized by intricate pathophysiological processes comprising numerous interconnected pathways. Oxidative stress-induced neuronal ferroptosis and the overactivation of glial cells play important roles in this phenomenon. In this study, we developed a targeted cross-linked micelle loaded with idebenone to rescue the ischemic penumbra by inhibiting neuronal ferroptosis and glial overactivation. In rat models, the CREKA peptide-modified micelles accumulate in the damaged brain via binding to microthrombi in the ipsilateral microvessels. Upon reactive oxygen species (ROS) stimulation, diselenide bonds within the micelles are transformed to hydrophilic seleninic acids, enabling synchronized ROS consumption and responsive drug release. The released idebenone scavenges ROS, prevents oxidative stress-induced neuronal ferroptosis, attenuates glial overactivation, and suppresses pro-inflammatory factors secretion, thereby modulating the inflammatory microenvironment. Finally, this micelle significantly reinforces neuronal survival, reduces infarct volume, and improves behavioral function compared to the control groups. This pleiotropic therapeutic micelle provides a proof-of-concept of remodeling the lesion microenvironment by inhibiting neuronal ferroptosis and glial overactivation to treat cerebral ischemia-reperfusion injury.

The first record of Trichotanypus Kieffer (Diptera, Chironomidae: Podonominae) in the Tibet Plateau of China, with description of a new species.

Trichotanypus hani sp. nov. is described here based on the male, pupa and larva collected in the Tibet Plateau. The new species is characteristic by the elongated posterolateral heel of gonostylus in the male, bifid thoracic horn in the pupa and 8-10 mandible teeth in the larva. This is the first formal record of Trichotanypus from East Asia, indeed the first far-outside the circum-Arctic area.

LC-MS/MS-Based Serum Metabolomics and Transcriptome Analyses for the Mechanism of Augmented Renal Clearance.

Augmented Renal Clearance (ARC) refers to the increased renal clearance of circulating solute in critically ill patients. In this study, the analytical research method of transcriptomics combined with metabolomics was used to study the pathogenesis of ARC at the transcriptional and metabolic levels. In transcriptomics, 534 samples from 5 datasets in the Gene Expression Omnibus database were analyzed and 834 differential genes associated with ARC were obtained. In metabolomics, we used Ultra-Performance Liquid Chromatography-Quadrupole Time-of-Flight Mass Spectrometry to determine the non-targeted metabolites of 102 samples after matching propensity scores, and obtained 45 differential metabolites associated with ARC. The results of the combined analysis showed that purine metabolism, arginine biosynthesis, and arachidonic acid metabolism were changed in patients with ARC. We speculate that the occurrence of ARC may be related to the alteration of renal blood perfusion by LTB4R, ARG1, ALOX5, arginine and prostaglandins E2 through inflammatory response, as well as the effects of CA4, PFKFB2, PFKFB3, PRKACB, NMDAR, glutamate and cAMP on renal capillary wall permeability.

Glucose-induced CRL4COP1-p53 axis amplifies glycometabolism to drive tumorigenesis.

The diabetes-cancer association remains underexplained. Here, we describe a glucose-signaling axis that reinforces glucose uptake and glycolysis to consolidate the Warburg effect and overcome tumor suppression. Specifically, glucose-dependent CK2 O-GlcNAcylation impedes its phosphorylation of CSN2, a modification required for the deneddylase CSN to sequester Cullin RING ligase 4 (CRL4). Glucose, therefore, elicits CSN-CRL4 dissociation to assemble the CRL4COP1 E3 ligase, which targets p53 to derepress glycolytic enzymes. A genetic or pharmacologic disruption of the O-GlcNAc-CK2-CSN2-CRL4COP1 axis abrogates glucose-induced p53 degradation and cancer cell proliferation. Diet-induced overnutrition upregulates the CRL4COP1-p53 axis to promote PyMT-induced mammary tumorigenesis in wild type but not in mammary-gland-specific p53 knockout mice. These effects of overnutrition are reversed by P28, an investigational peptide inhibitor of COP1-p53 interaction. Thus, glycometabolism self-amplifies via a glucose-induced post-translational modification cascade culminating in CRL4COP1-mediated p53 degradation. Such mutation-independent p53 checkpoint bypass may represent the carcinogenic origin and targetable vulnerability of hyperglycemia-driven cancer.

Structural insights into neurokinin 3 receptor activation by endogenous and analogue peptide agonists.

Neurokinin 3 receptor (NK3R) is a tachykinin receptor essential for the hypothalamic-pituitary-gonadal axis. The endogenous peptide agonist neurokinin B (NKB) preferentially activates NK3R, while substance P (SP) binds preferentially to NK1R. In addition, the SP analogue senktide more potently activates NK3R than NKB and SP. However, the mechanisms of preferential binding of peptide and NK3R activation remain elusive. Herein, we determined the cryogenic electron microscopy (cryo-EM) structures of the NK3R-Gq complex bound to NKB, SP and senktide. The three NK3R-Gq/peptide complexes utilize a class of noncanonical receptor activation mechanisms. Combining the structural analysis and functional assay illustrated that the consensus C-termini of the three peptide agonists share a conserved binding mode to NK3R, while the divergent N-termini of the peptides confer the preferential binding of the agonist to NK3R. In addition, the specific interactions between the N-terminus of senktide and the N-terminus and extracellular loops (ECL2 and ECL3) of NK3R lead to the improved activation displayed by senktide compared to SP and NKB. These findings pave the way to understand tachykinin receptor subtype selectivity and provide ideas to rationally develop drugs targeting NK3R.