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The large coercive electric field is the main obstacle for the application of wurtzite ferroelectrics in the memory devices. To explore the effective methods to reduce the coercive electric field of wurtzite ferroelectrics, in this work, after screening a series of possible candidates, (MC)1/(AlN)n (M = Ti, Zr) superlattices and anion P-doping are both chosen to regulate the switching energy barrier of wurtzite AlN based on the density functional theory calculations. It is found that the polarization switching energy barriers of wurtzite AlN gradually decrease by increasing the ratio of the MC (M = Ti, Zr) layer. When the ratio of the MC layer is up to 33%, the polarization switching energy barriers of (TiC)1/(AlN)n and (ZrC)1/(AlN)n are decreased by 68% and 55%, respectively, compared with that of pure wurtzite AlN. The anionic P-doping in AlN results in a 48% lower energy barrier. Also, the ferroelectric polarization in the designed superlattices and P-doped AlN is well maintained compared to pure AlN. Thus, the results show that the (MC)1/(AlN)n (M = Ti, Zr) superlattices and anion P-doping approaches are effective in improving the polarization switching properties of wurtzite AlN. [ABSTRACT FROM AUTHOR]

Objective: Dural arteriovenous fistulas (DAVFs) with deep venous drainage (DVD) (DAVFs-DVD) are characteristically associated with non-hemorrhagic neurological deficits, most notably cognitive impairment. Large studies have yet to thoroughly characterize these DAVFs. We conducted an analysis of the largest cohort of DAVFs-DVD to provide a comprehensive characterization of this specific subset. Methods: This study was a retrospective cohort analysis of 207 patients with DAVFs-DVD who were hospitalized at a single medical center between 2001 and 2022. Logistic regression was employed to identify angiographic features specific to DAVFs associated with cognitive impairment. Additionally, post-treatment outcomes were evaluated. Results: DAVFs-DVDs can be classified into two categories: the Galenic group, where arterial feeders drain directly into the vein of Galen (VoG), and the non-Galenic group, where arterial feeders drain into other veins or venous sinuses and indirectly flow into the VoG. Cognitive impairment accounting for 15.9% of all clinical presentations. We found that the overall rate of complete occlusion was 86.6%, while the overall rate of complications was 16.4%. Moreover, patients with DAVFs-DVD presenting with cognitive impairment were more likely to have straight sinus stenosis or occlusion, as well as DAVFs located at the midline. Conclusion: DAVFs-DVDs can be classified into two categories: the Galenic group and the non-Galenic group. Patients with DAVFs-DVD presenting with cognitive impairment were more likely to have straight sinus stenosis or occlusion, as well as DAVFs located at the midline. Venous hypertension of the deep venous system is a key angiographic feature of DAVFs associated with thalamic cognitive impairment. [ABSTRACT FROM AUTHOR]

This study aimed to investigate the protective effects of ginsenoside Rg1 on high-altitude hypoxia-induced acute lung injury (ALI) and elucidated its molecular targets and related pathways, specifically its association with the fluid shear stress pathway. Using a combination of bioinformatics analysis and both in vivo and in vitro experiments, we assessed the role of ginsenoside Rg1 in mitigating physiological and biochemical disturbances induced by hypoxia. In the in vivo experiments, we measured arterial blood gas parameters, levels of inflammatory cells and cytokines, erythrocyte and platelet parameters, and conducted histological analysis in rats. The in vitro experiments utilized human pulmonary microvascular endothelial cells (HPMECs) and A549 cells to examine cell viability, intracellular reactive oxygen species (ROS) and Ca2⁺ levels, and mitochondrial function. The results of the in vivo experiments demonstrate that ginsenoside Rg1 significantly increased arterial blood oxygen partial pressure and saturation, elevated arterial blood glucose levels, and stabilized respiratory and metabolic functions in rats. It also reduced inflammatory cells and cytokines, such as tumor necrosis factor-α and interleukin-6, and improved erythrocyte and platelet abnormalities, supporting its protective role through the regulation of the fluid shear stress pathway. Histological and ultrastructural analyses revealed that Rg1 significantly protected lung tissue structure and organelles. In vitro experiments further confirmed that Rg1 improved cell viability in HPMEC and A549 cells under hypoxic conditions, decreased intracellular ROS and Ca2⁺ levels, and enhanced mitochondrial function. These findings collectively demonstrate that ginsenoside Rg1 exerts significant protective effects against high-altitude hypoxia-induced ALI by enhancing oxygen delivery and utilization, reducing inflammatory responses, and maintaining cellular metabolism and vascular function. Notably, the protective effects of Rg1 are closely associated with the regulation of the fluid shear stress pathway, suggesting its potential for treating high-altitude hypoxia-related diseases. [ABSTRACT FROM AUTHOR]

Radiation-induced intestinal injury is a common complication of radiotherapy for abdominal and pelvic malignancies. Due to its rapid proliferation, the small intestine is particularly sensitive to radiation, making it a critical factor limiting treatment. Ferulic acid (FA), a derivative of cinnamic acid, exhibits antioxidant, anti-inflammatory, and anti-radiation properties. In this study, we established a mouse model of radiation-induced intestinal injury using a dose of 11 Gy at a rate of 96.62 cGy/min. Our findings indicate that FA's protective effects against radiation-induced intestinal injury may be mediated through the parkinsonism-associated deglycase (DJ-1) nuclear factor erythroid 2-related factor 2 (Nrf2) and silent mating type information regulation 2 homolog 1 (Sirt1) nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-κB) NOD-like receptor family, pyrin domain containing 3 (NLRP3). FA was found to mitigate changes in oxidative stress indices and inflammatory factors induced by radiation, as well as to attenuate radiation-induced pathological alterations in the small intestine. Furthermore, FA enhanced the expression of DJ-1 and Nrf2 at both the transcriptional and protein levels, inhibited NLRP3 protein fluorescence intensity, and reduced the expression of NLRP3, interleukin-18 (IL-18), and interleukin-1 beta (IL-1β). Additionally, FA suppressed the transcription and translation of NF-κB, NLRP3, cysteine-aspartic acid protease-1 (Caspase-1), IL-18, and IL-1β by upregulating Sirt1, thereby alleviating radiation-induced inflammatory injury in the small intestine. Thus, FA holds promise as an effective therapeutic agent for ameliorating radiation-induced intestinal injury. [ABSTRACT FROM AUTHOR]

Intracellular biothiols, including cysteine (Cys), glutathione (GSH), and homocysteine (Hcy), play a critical role in many physiological and pathological processes. Among them, GSH is the most abundant non-protein mercaptan (1–10 mM) in cells, and the change in GSH concentration level is closely related to the occurrence of many diseases, such as Parkinson's disease, Alzheimer's disease, and neurological diseases. Fluorescent probes have attracted much attention due to their advantages of high specificity, high sensitivity, high selectivity, low cost, and high quantum yield. Methods that use optical probes for selective detection of GSH in vitro and in vivo are in high demand. In this paper, we reviewed the most recent five years of research on fluorescence probes for the detection of GSH, including the specific detection of GSH, dual-channel identification of GSH and other substances, and the detection of GSH and other biothiols. According to the type of fluorophore, we classified GSH fluorescent probes into eight classes, including BODIPY, 1,8-Naphthalimide, coumarin, xanthene, rhodamine, cyanine, benzothiazoles, and others. In addition, we roundly discuss the synthesis, detection mechanism, photophysical properties, and biological applications of fluorescent probes. We hope that this review will inspire the exploration of new fluorescent probes for GSH and other related analyses. [ABSTRACT FROM AUTHOR]

The disruption of hematopoietic and immune functions is a significant consequence of the long-term effects of radiation exposure. This study investigated the potential mechanisms by which ferulic acid (FA) acts as a radioprotective agent in mitigating radiation-induced immune damage. C57BL/6J mice were exposed to a dose of 6.0 Gy of 60Co γ irradiation. FA was administered at doses of 25, 50, and 100 mg/kg/d for 7 days before and 30 days following irradiation. We evaluated changes in peripheral blood cells, T and B lymphocytes, natural killer cells in the spleen, and hematopoietic stem/progenitor cells in the bone marrow (BM). Whole-genome transcriptome sequencing of BM was performed to explore potential mechanisms. FA administration resulted in a significant reduction in malonaldehyde levels (p < 0.0001), an increase in catalase and beta-nicotinamide adenine dinucleotide levels in serum (p < 0.05), and enhanced multipotent progenitors (p < 0.01) and common lymphoid progenitors (p < 0.05) in the BM. Additionally, there was an elevation in white blood cell levels, red blood cell levels, and hemoglobin levels in peripheral blood (p < 0.01). Transcriptome analysis indicated that FA reversed the radiation-induced expression of genes related to immunity and inflammation. Enzyme-linked immunosorbent assay experiments further demonstrated that FA reduced interleukin-6 levels in the BM and decreased JAK1, JAK2, and STAT3 protein content (p < 0.01). In conclusion, FA might mitigate hematopoietic and immune damage by modulating the JAK/STAT signaling pathway. [ABSTRACT FROM AUTHOR]

Background: The impairment of the cardiovascular system by fluoride has attracted public health concern, and its toxic effects on ECs have garnered extensive research attention. However, epidemiological clues of fluoride induced cardiovascular injury are limited. The function of ECs is crucial for the early diagnosis of CVD, yet mechanisms through which fluoride disrupts endothelial function are still unclear., Purpose: To investigate the relationship between fluoride exposure and hypertension in population by epidemiological investigation. To explore the potential mechanism of functional injury of ECs induced by fluoride., Result: Epidemiological studies have shown that the risk of hypertension in study population increased with the increased of urinary fluoride concentration [OR = 1.565, 95%CI (1.143, 2.142)]. In rat model with fluorosis alongside a model of fluoride induced ECs injury, NaF led to anti-adhesion of ECs and barrier dysfunction. Notably, the expression levels of eNOS and NO were found to be decreased, while the expression levels of ACE, vWF, ICAM-1, VCAM-1 and ET-1 were elevated. Our findings also indicated that NaF induced oxidative stress in ECs, evidenced by significant increased in ROS and MDA levels and decreased protein expression of GPx4 and SOD activity. It was further found that NaF activated the p53/miR-200c-3p signaling axis via ROS, leading to endothelial dysfunction., Conclusion: This study found that fluoride exposure was a risk factor for hypertension. In addition, fluoride could cause ECs dysfunction by inducing oxidative stress and activating p53/miR-200c-3p. These findings were helpful to further understand the mechanism of fluoride induced cardiovascular system injury and provide a theoretical basis for fluoride induced cardiovascular system injury., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2025 Elsevier Inc. All rights reserved.)

Background: Intracranial dural arteriovenous fistulas (DAVFs) are rare lesions, making it challenging to fully understand and improve their management. Globally, only two major large-scale studies have focused on DAVFs. This report outlines the design of the DREAM-INI (Dural arteriovenous fistula research and management in China) project and provides an overview of the 1101-patient cohort it includes., Methods: Patient data were sourced from the DREAM-INI database, a retrospective, single-center observational study conducted from January 2001 to December 2022, encompassing a total of 1101 DAVF patients., Results: The cohort consists of 367 patients diagnosed with Borden type I DAVFs, 172 patients with Borden type II fistulas, and 562 patients with Borden type III fistulas. 565 patients exhibited flow-related symptoms, 176 patients presented with intracranial hemorrhage, and 275 patients had non-hemorrhagic neurological deficits. A large proportion of patients (95.6%, 1053/1101) underwent treatment through endovascular embolization (83.7%, 922/1101), surgery (8.7%, 96/1101), or multimodal therapy (3.2%, 35/1101). The overall immediate angiographic cure rate was 85.2% (897/1053 treated cases), and the rate of treatment-related permanent neurological morbidity was 3.4% (45/1328 total procedures). The median duration from the final treatment to the last follow-up for DAVF was 39 months. The predictive factors for aggressive symptoms, initial angiographic cure, and complications in DAVFs have also been preliminarily explored., Conclusions: With over 1100 patients, DREAM-INI represents a large and relatively well-documented registry of DAVF patient data in China and even globally. This database will enable numerous future studies, further advancing our understanding of this rare disease., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2025. No commercial re-use. See rights and permissions. Published by BMJ Group.)

Abstract: The effects of different radiation doses on T and B lymphocyte functional subsets and the changes of immune cells and immune molecules were observed in mice at different times post-irradiation to provide a theoretical basis for the changes of immune cells affected by radiation. In this study, the changes of T and B immune cells and immune-related molecules were observed at 1, 3, 7, 14, and 21 d after single irradiation of 2 Gy, 4 Gy, and 6 Gy. The results showed that white blood cells (WBC), lymphocytes (LYMPH), and lymphocyte percentage (LYMPH%) in peripheral blood of mice were significantly reduced and reached the lowest point 3 d after irradiation. Flow cytometry results showed that the percentages of CD3+T and CD8+/CD3+T lymphocytes in spleen and thymus were significantly decreased, and the percentages of CD19+B lymphocytes in spleen and CD4+/CD3+T lymphocytes in thymus were also decreased. However, the percentages of splenic NK cells, CD4+/CD3+T cells, and CD4+/CD8+ ratios in spleen and thymus were increased. Most of the indicators fell to the lowest or highest point 3 d after irradiation, indicating that immune function was suppressed at this time. From 7 to 21 d after irradiation, most immune cells gradually recovered. Single irradiation of 2 Gy, 4 Gy, and 6 Gy increased the contents of IL-1β, IL-2, IL-6, IL-17, TNF-α, TGF-β, and IFN-γ in serum of mice and decreased the contents of anti-inflammatory factors IL-4 and IL-10. The serum levels of immunoglobulin IgA, IgG, IgM and complement C3, C4 were significantly increased after irradiation. Our study showed that a single dose of 2 Gy, 4 Gy, and 6 Gy induced immunosuppression in mice, and maximum immunosuppression was achieved 3 d after irradiation. At this time, CD19+B lymphocytes were the most sensitive, followed by CD3+T lymphocytes, and NK cells were the most resistant. The radiosensitivity of CD8+/CD3+T lymphocytes was slightly higher than that of CD4+/CD3+T lymphocytes., (Copyright © 2025 Health Physics Society.)