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The oxygen evolution reaction (OER) underpins many aspects of energy storage and conversion in modern industry and technology, but which still be suffering from the dilemma of sluggish reaction kinetics and poor electrochemical performance. Different from the viewpoint of nanostructuring, this work focuses on an intriguing dynamic orbital hybridization approach to renormalize the disordering spin configuration in porous noble-metal-free metal-organic frameworks (MOFs) to accelerate the spin-dependent reaction kinetics in OER. Herein, we propose an extraordinary super-exchange interaction to reconfigure the domain direction of spin nets at porous MOFs through temporarily bonding with dynamic magnetic ions in electrolytes under alternating electromagnetic field stimulation, in which the spin renormalization from disordering low-spin state to high-spin state facilitates rapid water dissociation and optimal carrier migration, leading to a spin-dependent reaction pathway. Therefore, the spin-renormalized MOFs demonstrate a mass activity of 2,095.1 A gmetal-1 at an overpotential of 0.33 V, which is about 5.9 time of pristine ones. Our findings provide a insight into reconfiguring spin-related catalysts with ordering domain directions to accelerate the oxygen reaction kinetics.
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Single-molecule electrochemical science has advanced over the past decades and now extends well beyond molecular imaging, to molecular electronics functions such as rectification and amplification. Rectification is conceptually the simplest but has involved mostly challenging chemical synthesis of asymmetric molecular structures or asymmetric materials and geometry of the two enclosing electrodes. Here we propose an experimental and theoretical strategy for building and tuning in situ (in operando) rectification in two symmetric molecular structures in electrochemical environment. The molecules were designed to conduct electronically via either their lowest unoccupied molecular orbital (LUMO; electron transfer) or highest occupied molecular orbital (HOMO; "hole transfer"). We used a bipotentiostat to control separately the electrochemical potential of the tip and substrate electrodes of an electrochemical scanning tunneling microscope (EC-STM), which leads to independent energy alignment of the STM tip, the molecule, and the STM substrate. By creating an asymmetric energy alignment, we observed single-molecule rectification of each molecule within a voltage range of ±0.5 V. By varying both the dominating charge transporting LUMO or HOMO energy and the electrolyte concentration, we achieved tuning of the polarity as well as the amplitude of the rectification. We have extended an earlier proposed theory that predicts electrolyte-controlled rectification to rationalize all the observed in situ rectification features and found excellent agreement between theory and experiments. Our study thus offers a way toward building controllable single-molecule rectifying devices without involving asymmetric molecular structures.
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The performance of blue quantum dot light-emitting diodes (QLEDs) is limited by unbalanced charge injection, resulting from insufficient holes caused by low mobility or significant energy barriers. Here, we introduce an angular-shaped heteroarene based on cyclopentane[b]thiopyran (C8-SS) to modify the hole transport layer poly-N-vinylcarbazole (PVK), in blue QLEDs. C8-SS exhibits high hole mobility and conductivity due to the π···π and S···π interactions. Introducing C8-SS to PVK significantly enhanced hole mobility, increasing it by 2 orders of magnitude from 2.44 × 10-6 to 1.73 × 10-4 cm2 V-1 s-1. Benefiting from high mobility and conductivity, PVK:C8-SS-based QLEDs exhibit a low turn-on voltage (Von) of 3.2 V. More importantly, the optimized QLEDs achieve a high peak power efficiency (PE) of 7.13 lm/W, which is 2.65 times that of the control QLEDs. The as-proposed interface engineering provides a novel and effective strategy for achieving high-performance blue QLEDs in low-energy consumption lighting applications.
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Alloying-type anode materials provide high capacity for lithium-ion batteries; however, they suffer pulverization problems resulting from the volume change during cycling. Realizing the cycling reversibility of these anodes is therefore critical for sustaining their electrochemical performance. Here, we investigate the structural reversibility of Sn NPs during cycling at atomic-level resolution utilizing in situ high-resolution TEM. We observed a surprisingly near-perfect structural reversibility after a complete cycle. A three-step phase transition happens during lithiation, accompanied by the generation of a significant number of defects, grain boundaries, and up to 202% volume expansion. In subsequent delithiation, the volume, morphology, and crystallinity of the Sn NPs were restored to their initial state. Theoretical calculations show that compressive stress drives the removal of vacancies generated within the NPs during delithiation, therefore maintaining their intact morphology. This work demonstrates that removing vacancies during cycling can efficiently improve the structural reversibility of high-capacity anode materials.
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Herein, we report a divergent synthesis of fluoroalkyl ketones through visible-light-induced reactions between readily available organoboronic esters and fluoroalkyl acylsilanes. Selective control of the reactivity of the in situ generated organoboronate complexes is the key to achieving divergent transformations. Under basic conditions, the organoboronate complexes undergo deboronative fluoride elimination, resulting in the formation of enol silyl ethers as intermediates that react with various electrophiles to generate defluorinated ketones as the products. Moreover, in combination with peroxide, a 1,2-shift of fluoroalkyl group is favored over deboronative fluoride elimination to generate ketal intermediates, leading to the formation of ketones as the products. This transition-metal-free reaction is operationally simple, and aryl, alkenyl, and alkyl boronic esters are all suitable substrates. The synthetic potential has been demonstrated by gram-scale reactions and facile synthesis of bioactive molecules including zifrosilone and its fluoroalkyl analogs.
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Donor-acceptor (D-A) conjugated systems have been extensively investigated and play important roles in organic electronics. Incorporating D-A structures into (hetero)cycloarenes endows them tunable electronic properties, while the well-defined cavity remains. However, the synthetic complexity of introducing electron-acceptor moieties into (hetero)cycloarenes limits their development and applications. In this paper, the first family of electronically tunable D-A heterocycloarenes (DAHCn, n = 1-5) based on pyrazine derivatives was facilely synthesized through cyclocondensation reaction from a tetraketone-functionalized heterocycloarene precursor prepared using the ketal-protection strategy. The effect of expanded conjugation and the inserted electron-withdrawing group on the electronic structures of the D-A heterocycloarenes was studied systematically by X-ray crystallographic analysis, various spectroscopic measurements, and theoretical calculations. Interestingly, the presence of an electron-withdrawing group polarizes the inner C(sp2)-H and significantly increases the binding affinities of D-A heterocycloarenes to the iodide anion. Meanwhile, the anion affinity can be further modulated by the type of attached substituents and the distance of polarization. More importantly, the dicyanopyrazine derivative DAHC3 shows the highest binding strength to the iodide ion as a 2:1 sandwich complex (logâ¯ß2 = 12.3 and ΔG = -69.1 kJ mol-1), which is the strongest iodide receptor using C(sp2)-H hydrogen bonding interactions reported to date. Our finding provides a new strategy to design and synthesize D-A heterocycloarenes and strong anion receptors.
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The anterior cingulate cortex (ACC) and visual cortex are integral components of the neurophysiological mechanisms underlying migraine, yet the impact of altered connectivity patterns between these regions on migraine treatment remains unknown. To elucidate this issue, we investigated the abnormal causal connectivity between the ACC and visual cortex in patients with migraine without aura (MwoA), based on the resting-state functional magnetic resonance imaging data, and its predictive ability for the efficacy of nonsteroidal anti-inflammatory drugs (NSAIDs). The results revealed increased causal connectivity from the bilateral ACC to the lingual gyrus (LG) and decreased connectivity in the opposite direction in nonresponders compared with the responders. Moreover, compared with the healthy controls, nonresponders exhibited heightened causal connectivity from the ACC to the LG, right inferior occipital gyrus (IOG) and left superior occipital gyrus, while connectivity patterns from the LG and right IOG to the ACC were diminished. Based on the observed abnormal connectivity patterns, the support vector machine (SVM) models showed that the area under the receiver operator characteristic curves for the ACC to LG, LG to ACC and bidirectional models were 0.857, 0.898, and 0.939, respectively. These findings indicate that neuroimaging markers of abnormal causal connectivity in the ACC-visual cortex circuit may facilitate clinical decision-making regarding NSAIDs administration for migraine management.
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Migraña sin Aura , Corteza Visual , Humanos , Giro del Cíngulo/diagnóstico por imagen , Imagen por Resonancia Magnética/métodos , Migraña sin Aura/patología , Corteza Visual/diagnóstico por imagen , Antiinflamatorios no Esteroideos/farmacología , Antiinflamatorios no Esteroideos/uso terapéutico , Antiinflamatorios , EncéfaloRESUMEN
Electrochemical growth of metal nanocrystals is pivotal for material synthesis, processing, and resource recovery. Understanding the heterogeneous interface between electrolyte and electrode is crucial for nanocrystal nucleation, but the influence of this interaction is still poorly understood. This study employs advanced in situ measurements to investigate the heterogeneous nucleation of metals on solid surfaces. By observing the copper nanocrystal electrodeposition, an interphase interaction-induced nucleation mechanism highly dependent on substrate surface energy is uncovered. It shows that a high-energy (HE) electrode tended to form a polycrystalline structure, while a low-energy (LE) electrode induced a monocrystalline structure. Raman and electrochemical characterizations confirmed that HE interface enhances the interphase interaction, reducing the nucleation barrier for the sturdy nanostructures. This leads to a 30.92-52.21% reduction in the crystal layer thickness and a 19.18-31.78% increase in the charge transfer capability, promoting the formation of a uniform and compact film. The structural compactness of the early nucleated crystals enhances the deposit stability for long-duration electrodeposition. This research not only inspires comprehension of physicochemical processes correlated with heterogeneous nucleation, but also paves a new avenue for high-quality synthesis and efficient recovery of metallic nanomaterials.
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With the development of high-throughput technologies, the accumulation of large amounts of multidimensional genomic data provides an excellent opportunity to study the multilevel biological regulatory relationships in cancer. Based on the hypothesis of competitive endogenous ribonucleic acid (RNA) (ceRNA) network, lncRNAs can eliminate the inhibition of microRNAs (miRNAs) on their target genes by binding to intracellular miRNA sites so as to improve the expression level of these target genes. However, previous studies on cancer expression mechanism are mostly based on individual or two-dimensional data, and lack of integration and analysis of various RNA-seq data, making it difficult to verify the complex biological relationships involved. To explore RNA expression patterns and potential molecular mechanisms of cancer, a network-regularized sparse orthogonal-regularized joint non-negative matrix factorization (NSOJNMF) algorithm is proposed, which combines the interaction relations among RNA-seq data in the way of network regularization and effectively prevents multicollinearity through sparse constraints and orthogonal regularization constraints to generate good modular sparse solutions. NSOJNMF algorithm is performed on the datasets of liver cancer and colon cancer, then ceRNA co-modules of them are recognized. The enrichment analysis of these modules shows that >90% of them are closely related to the occurrence and development of cancer. In addition, the ceRNA networks constructed by the ceRNA co-modules not only accurately mine the known correlations of the three RNA molecules but also further discover their potential biological associations, which may contribute to the exploration of the competitive relationships among multiple RNAs and the molecular mechanisms affecting tumor development.
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Neoplasias del Colon , MicroARNs , ARN Largo no Codificante , Neoplasias del Colon/genética , Regulación Neoplásica de la Expresión Génica , Redes Reguladoras de Genes , Genómica , Humanos , MicroARNs/genética , MicroARNs/metabolismo , ARN Largo no Codificante/genética , ARN Largo no Codificante/metabolismo , ARN Mensajero/genéticaRESUMEN
Demand for ultra-small, inexpensive, and high-accurate 3D shape measurement devices is growing rapidly, especially in the industrial and consumer electronics sectors. Phase shifting profilometry (PSP) is a powerful candidate due to its advantages of high accuracy, great resolution, and insensitivity to ambient light. As a key component in PSP, the projector used to generate the phase-shifting sinusoidal fringes must be ultra-small (several millimeters), low-cost, and simple to control. However, existing projection methods make it difficult to meet these requirements simultaneously. In this paper, we present a modern technique that can be used to fabricate the desired projector. A specifically designed device based on segmented liquid crystal display (SLCD) technology is used to display the projected patterns, and a cylindrical lens is used as the projection lens. The SLCD device can display four sets of specific filled binary patterns, each yielding a sinusoidal fringe, and all four sinusoidal fringes satisfy the four-step phase shift relation. 3D shape measurement experiments verify the performance of the projector. Considering that the size of SLCD devices can be reduced to a few millimeters, the proposed technique can be easily used to manufacture ultra-small, low-cost, and simple-to-control PSP projectors.
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In recent years, the interaction of intracellular organelles such as mitochondria and lysosomal functions has attracted increasing attention. Recent evidence suggests that mitochondrion-lysosomal contact plays a key role in regulating lysosomal biogenesis and maintaining cellular homeostasis. Myocardial ischemia and reperfusion will lead to corresponding changes in the autophagy flux in cardiomyocytes, and lysosomes are a key link in the process of autophagy, and the fusion of lysosomes and autophagosomes is an essential link in the occurrence of autophagy. Therefore, the function and homeostasis of lysosomes also undergo different changes during myocardial ischemia and reperfusion. Lysosomal-related biological factors and membrane proteins also play different roles. This article will review the mechanism of lysosomes in myocardial ischemia-reperfusion injury and the research progress of lysosomal-related proteins.
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The solid-solid insulation interface structure is a typical interface in extra-high-voltage power equipment, in which the multilayer epoxy resin material is a key component in the insulation structure of the power equipment, and the study of its interface characteristics is the most important. In this paper, epoxy-epoxy cross-linking interface specimens were prepared through experiments, and the degree of cross-linking between the interfaces was analyzed by changing the ratio of the curing agent and adding hydroxyl-terminated liquid nitrile rubber (HTBN) particles; it can be concluded that there exists a weak cross-linking reaction between the interfaces. The electrical tree measurement and alternating current (AC) breakdown test platform were set up, and three different cases of no interface, the electric field direction parallel to the interface, and the electric field direction perpendicular to the interface were tested, through which it was concluded that the existence of the interface inhibited the development of the electrical tree. For the three different cases of AC breakdown tested, it was concluded that the presence of an interface enhances the AC breakdown strength when the electric field direction is parallel to the interface and decreases the AC breakdown strength when the electric field direction is perpendicular to the interface through the interface, affecting the charge transport.
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Cardiomyocytes undergo a variety of cell death events during myocardial ischemiaâreperfusion injury (MIRI). Understanding the causes of cardiomyocyte mortality is critical for the prevention and treatment of MIRI. Among the various types of cell death, autosis is a recently identified type of autophagic cell death with distinct morphological and chemical characteristics. Autosis can be attenuated by autophagy inhibitors but not reversed by apoptosis or necrosis inhibitors. In recent years, it has been shown that during the late phase of reperfusion, autosis is activated, which exacerbates myocardial injury. This article describes the characteristics of autosis, autophagic cell death, and the relationship between autophagic cell death and autosis; reviews the mechanism of autosis in MIRI; and discusses its clinical significance.
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BACKGROUND: Interferon gene stimulator (Sting) is an indispensable adaptor protein that plays a crucial role in acute lung injury (ALI) induced by sepsis, and the PARP-1/NLRP3 signaling pathway may be an integral component of the inflammatory response mediated by Sting. However, the regulatory role of Sting in the PARP-1/NLRP3 pathway in ALI remains insufficiently elucidated. METHODS: Using lipopolysaccharide (LPS) to induce ALI in C57BL/6 mice and HUVEC cells, an in vivo and in vitro model was established. In vivo, Sting agonists and inhibitors were administered, while in vitro, Sting was knocked down using siRNA. ELISA was employed to quantify the levels of IL-1ß, IL-6, and TNF-α. TUNEL staining was conducted to assess cellular apoptosis, while co-immunoprecipitation was utilized to investigate the interaction between Sting and NLRP3. Expression levels of Sting, NLRP3, PARP-1, among others, were assessed via Western blotting and RT-qPCR. Lung HE staining and lung wet/dry ratio were evaluated in the in vivo mouse model. To validate the role of the PARP-1/NLRP3 signaling pathway, PARP-1 inhibitors were employed both in vivo and in vitro. RESULTS: In vitro experiments revealed that the Sting agonist group exacerbated LPS-induced pulmonary pathological damage, pulmonary edema, inflammatory response (increased levels of IL-6, TNF-α, and IL-1ß), and cellular injury, whereas the Sting inhibitor group significantly ameliorated the aforementioned injuries, with further improvement observed in the combination therapy of Sting inhibitor and PARP-1 inhibitor. Western blotting and RT-qPCR results demonstrated significant suppression of ICAM-1, VCAM-1, NLRP3, and PARP-1 expression in the Sting inhibitor group, with this reduction further enhanced in the Sting inhibitor + PARP-1 inhibitor treatment group, exhibiting opposite outcomes to the agonist. Furthermore, in vitro experiments using HUVEC cell lines validated these findings. CONCLUSIONS: Our study provides new insights into the roles of Sting and the PARP-1/NLRP3 signaling pathway in inflammatory responses, offering novel targets for the development of therapeutic interventions against inflammatory reactions.
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OBJECTIVE: γδ T cells are a distinct subset of unconventional T cells, which link innate and adaptive immunity by secreting cytokines and interacting with other immune cells, thereby modulating immune responses. As the first line of host defense, γδ T cells are essential for mucosal homeostasis and immune surveillance. When abnormally activated or impaired, γδ T cells can contribute to pathogenic processes. Accumulating evidence has revealed substantial impacts of γδ T cells on the pathogenesis of cancers, infections, and immune-inflammatory diseases. γδ T cells exhibit dual roles in cancers, promoting or inhibiting tumor growth, depending on their phenotypes and the clinical stage of cancers. During infections, γδ T cells exert high cytotoxic activity in infectious diseases, which is essential for combating bacterial and viral infections by recognizing foreign antigens and activating other immune cells. γδ T cells are also implicated in the onset and progression of immune-inflammatory diseases. However, the specific involvement and underlying mechanisms of γδ T cells in oral diseases have not been systematically discussed. METHODS: We conducted a systematic literature review using the PubMed/MEDLINE databases to identify and analyze relevant literature on the roles of γδ T cells in oral diseases. RESULTS: The literature review revealed that γδ T cells play a pivotal role in maintaining oral mucosal homeostasis and are involved in the pathogenesis of oral cancers, periodontal diseases, graft-versus-host disease (GVHD), oral lichen planus (OLP), and oral candidiasis. γδ T cells mainly influence various pathophysiological processes, such as anti-tumor activity, eradication of infection, and immune response regulation. CONCLUSION: This review focuses on the involvement of γδ T cells in oral diseases, with a particular emphasis on the main functions and underlying mechanisms by which γδ T cells influence the pathogenesis and progression of these conditions. This review underscores the potential of γδ T cells as therapeutic targets in managing oral health issues.
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Enfermedades de la Boca , Humanos , Enfermedades de la Boca/inmunología , Animales , Receptores de Antígenos de Linfocitos T gamma-delta/inmunología , Receptores de Antígenos de Linfocitos T gamma-delta/metabolismo , Linfocitos Intraepiteliales/inmunología , Enfermedad Injerto contra Huésped/inmunología , Linfocitos T/inmunologíaRESUMEN
A series of thiopyran-fused polycyclic aromatic hydrocarbons (PAHs) have been straightforwardly synthesized from 2,5-di(1-en-3-ynyl)thiophene-containing precursors via one-pot ring-expansion and 6-endo cyclization reactions. The reaction monitoring and the density function theoretical calculation suggest that the ring-expansion reaction occurs prior to 6-endo cyclization. Moreover, the absorption profiles of the thiopyran-fused PAHs suggest that the π-conjugation extension on the side of the cyclopentadiene ring in the cyclopenta[b]thiochromene core is predominant in prolonging the effective conjugation length, while the effect from extension on the other side is negligible. Furthermore, all of the thiopyran-fused PAHs exhibit halochromic properties. Upon the addition of trifluoromethanesulfonic acid, fluorescence "off-on" switches can be found for these thiopyran-fused PAHs. Therefore, this work not only provides a new synthetic approach for one-pot ring-expansion and 6-endo cyclization reactions but also expands the diversity of thiopyran-fused PAHs.
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Three new donor-acceptor-donor (D-A-D) architecture regioisomers comprising a large planar electron-withdrawing core tribenzo[a,c,i]phenazine and two identical electron-donating triphenylamines with different substitution patterns were designed and synthesized. Employing this regioisomerization strategy, the intramolecular charge-transfer interactions are effectively tuned and result in a significant bathochromic shift of photoluminescence maximum over 100 nm, which induces the corresponding emission band extending into the near-infrared region as well as giving a high solid-state quantum yield of 25%. Meanwhile, it is found that the supramolecular interactions of this series of regioisomers with planar electron-donor pyrene are greatly affected by the substitution pattern.
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Alleviating myocardial ischemia-reperfusion injury (MIRI) plays a critical role in the prognosis and improvement of cardiac function following acute myocardial infarction. Pyroptosis is a newly identified form of cell death that has been implicated in the regulation of MIRI. In our study, H9c2 cells and SD rats were transfected using a recombinant adenovirus vector carrying cFLIPL , and the transfection was conducted for 3 days. Subsequently, H9c2 cells were subjected to 4 h of hypoxia followed by 12 h of reoxygenation to simulate an in vitro ischemia-reperfusion model. SD rats underwent 30 min of ischemia followed by 2 h of reperfusion to establish an MIRI model. Our findings revealed a notable decrease in cFLIPL expression in response to ischemia/reperfusion (I/R) and hypoxia/reoxygenation (H/R) injuries. Overexpression of cFLIPL can inhibit pyroptosis, reducing myocardial infarction area in vivo, and enhancing H9c2 cell viability in vitro. I/R and H/R injuries induced the upregulation of ASC, cleaved Caspase 1, NLRP3, GSDMD-N, IL-1ß, and IL-18 proteins, promoting cell apoptosis. Our research indicates that cFLIPL may suppress pyroptosis by strategically binding with Caspase 1, inhibiting the release of inflammatory cytokines and preventing cell membrane rupture. Therefore, cFLIPL could potentially serve as a promising target for alleviating MIRI by suppressing the pyroptotic pathway.
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Daño por Reperfusión Miocárdica , Daño por Reperfusión , Ratas , Animales , Daño por Reperfusión Miocárdica/metabolismo , Piroptosis , Caspasa 1/metabolismo , Ratas Sprague-Dawley , Proteínas Reguladoras de la Apoptosis/metabolismo , Isquemia/metabolismo , Hipoxia/metabolismo , Daño por Reperfusión/metabolismo , Miocitos Cardíacos/metabolismoRESUMEN
Nanoceria have demonstrated a wide array of catalytic activity similar to natural enzymes, holding considerable significance in the colorimetric detection of alkaline phosphatase (ALP), which is a biomarker of various biological disorders. However, the issues of physiological stability and formation of protein corona, which are strongly related to their surface chemistry, limit their practical application. In this work, CeO2 nanoparticles characterized by enhanced dimensional uniformity and specific surface area were synthesized, followed by encapsulation with various polymers to further increase catalytic activity and physiological stability. Notably, the CeO2 nanoparticles encapsulated within each polymer exhibited improved catalytic characteristics, with PAA-capped CeO2 exhibiting the highest performance. We further demonstrated that the PAA-CeO2 obtained with enhanced catalytic activity was attributed to an increase in surface negative charge. PAA-CeO2 enabled the quantitative assessment of AA activity within a wide concentration range of 10 to 60 µM, with a detection limit of 0.111 µM. Similarly, it allowed for the evaluation of alkaline phosphatase activity throughout a broad range of 10 to 80 U/L, with a detection limit of 0.12 U/L. These detection limits provided adequate sensitivity for the practical detection of ALP in human serum.
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BACKGROUND: Oral lichen planus (OLP) is a common T cell-mediated oral mucosal immune inflammatory disease. Intraepithelial lymphocytes (IELs) are a unique subset of T cells that play an important role in regulating immune response. This study aims to investigate the phenotype and the differentiation mechanism of IELs in OLP. METHODS: The expression of CD4, CD8α, CD8ß, T-helper-inducing POZ/Krueppel-like factor (ThPOK), and RUNX family transcription factor 3 (Runx3) in the epithelium and peripheral blood mononuclear cells (PBMCs) of OLP was determined by immunofluorescence and immunohistochemistry. Then, the correlations among them were analyzed. Naïve CD4+ T cells were sorted from blood of OLP patients and stimulated with retinoic acid (RA) and transforming growth factor-ß1 (TGF-ß1). Then the expression of CD4, CD8α, CD8ß, ThPOK, and Runx3 was investigated by immunocytochemistry. RESULTS: CD8α expression and CD8αα+ cells were upregulated in the epithelium of OLP, whereas they were downregulated in PBMCs of OLP. CD8ß was not expressed in the epithelium of OLP. CD4, CD8α, and Runx3 expression and CD4+CD8α+ cells were increased, whereas ThPOK expression was decreased in the epithelium of OLP. CD8α expression was positively correlated with Runx3 expression, whereas ThPOK expression was negatively correlated with Runx3 expression. After RA and TGF-ß1 stimulation, CD8α and Runx3 expression was upregulated, and ThPOK expression was downregulated in naïve CD4+ T cells. CONCLUSION: CD4+CD8αα+ IELs may be the dominant phenotype of IELs in OLP, and the differentiation of CD4+CD8αα+ IELs in OLP is negatively regulated by ThPOK and positively regulated by Runx3.