Objective To elucidate the molecular mechanism of sirtuin-3 (SIRT3) in regulating mitochondrial biogenesis in human renal tubular epithelial cells. Methods Cells were stimulated with different concentrations of H₂O₂ and divided into four groups: control (NC), 50 μmol/L H₂O₂, 110 μmol/L H₂O₂ and 150 μmol/L H₂O₂. SIRT3 protein expression was then measured. SIRT3 was knocked down with siRNA, and cells were further assigned to five groups: control (NC), negative-control siRNA (NCsi), SIRT3-siRNA (siSIRT3), NCsi+H₂O₂, and siSIRT3+H₂O₂. After 24 h, cellular adenosine triphosphate (ATP) and mitochondrial superoxide anion (O₂•⁻) levels were determined, together with mitochondrial expression of SIRT3, peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), nuclear respiratory factor 1 (NRF1), mitochondrial transcription factor A (TFAM), superoxide dismutase 2 (SOD2), acetylated-SOD2 and adenosine monophosphate activated protein kinase α1 (AMPKα1). Results The 110 and 150 μmol/L H₂O₂ decreased SIRT3 protein (both P<0.05). ATP and mitochondrial O₂•⁻ did not differ between NC and NCsi groups (both P>0.05). Compared to the NCsi group, the siSIRT3 group exhibited elevated O₂•⁻ level, decreased SIRT3 protein and increased expression levels of SOD2 and acetylated SOD2 protein (all P<0.05). Compared to the NCsi group, the NCsi+H₂O₂ group exhibited decreased cellular ATP levels, elevated mitochondrial O₂•⁻ levels, and reduced protein expression levels of SIRT3, SOD2, TFAM, AMPKα1, PGC-1α and NRF1 (all P<0.05). Compared with the siSIRT3 group, the siSIRT3+H₂O₂ group showed a decrease in cellular ATP levels, an increase in mitochondrial O₂•⁻ levels, a decrease in SIRT3, SOD2, TFAM, AMPKα1, PGC-1α and NRF1 protein expression levels and a decrease in acetylated SOD2 protein expression levels (all P<0.05). Compared with the NCsi+H₂O₂ group, the siSIRT3+H₂O₂ group showed a decrease in cellular ATP levels, an increase in mitochondrial O₂•⁻ levels, a decrease in SIRT3, AMPKα1, PGC-1α and NRF1, TFAM protein expression levels, and an increase in SOD2 and acetylated SOD2 protein expression levels (all P<0.05). Conclusions SIRT3 promotes mitochondrial biogenesis in tubular epithelial cells via the AMPK/PGC-1α/NRF1/TFAM axis, representing a key mechanism through which SIRT3 ameliorates oxidative stress-induced mitochondrial dysfunction.

Aerosol removal using flame-retardant atomized fixatives, as a major means of aerosol control, has achieved remarkable results in the field of nuclear facility decommissioning and decontamination. Traditional atomized fixatives for aerosol removal have deficiencies in high-temperature resistance and flame retardancy, rendering them inadequate for operational scenarios involving high temperatures and flammability encountered during nuclear decommissioning. This paper investigates the current development of flame-retardant atomized fixatives for aerosol removal both domestically and internationally and presents a preliminary exploration of this technology. The experiments showed that atomized fixatives modified with flame-retardant properties not only maintained excellent aerosol capture efficiency, but also exhibited significantly improved flame-retardant performance. This confirmed the technical feasibility of the proposed approach. Finally, suggestions and reflections are proposed for the development of this technology and its application in nuclear facility decommissioning.

OBJECTIVE To predict and validate the mechanisms of Chaiqi yigan granules （CQYG） improving hepatocellular carcinoma （HCC）. METHODS The signaling pathways of CQYG intervention in HCC were predicted using network pharmacology. A mice model of transplanted hepatocellular carcinoma was established by injecting H22 hepatoma cells into the axilla. Successfully modeled mice were randomly divided into model group （normal saline）， sorafenib group （positive control， 50 mg/kg）， and CQYG low-， medium- and high-dose groups （24.83， 49.66， 99.32 g/kg）， with 10 mice in each group. Mice in each group were administered the corresponding drug solution or normal saline intragastrically， once a day， for 14 consecutive days. After last administration， pathological morphological changes in the tumor tissues of mice were observed in each group. Immunohistochemical staining was performed to detect the expression of the nuclear proliferation antigen Ki-67 in tumor tissues of mice. Western blot assay was used to measure the expression of proteins related to epithelial-mesenchymal transition （EMT） [N-cadherin， E-cadherin， Vimentin， matrix metalloproteinase 7 （MMP7）] and the mitogen-activated protein kinase （MAPK） signaling pathway [p38 MAPK， phosphorylated p38 MAPK， c-Jun N-terminal kinase （JNK）， phosphorylated JNK， extracellular regulated protein kinase 1/2 （ERK1/2）， phosphorylated ERK1/2] in tumor tissue of mice. RESULTS Network pharmacology analysis revealed that metabolic pathways， pathways in cancer， and the MAPK signaling pathway were key signaling pathways through which CQYG exert their anti-hepatocellular carcinoma effects. In animal experiments， the tumor tissues of mice in the model group exhibited dense tumor cells and vigorous growth. Compared with model group， CQYG high-dose group showed a decreased density of tumor cells in the tumor tissues of mice. Moreover， the expression levels of Ki-67， N-cadherin， MMP7 and Vimentin proteins， along with the phosphorylation levels of ERK1/2 and JNK proteins， were all significantly reduced （ P ＜0.05）. The expression level of E-cadherin protein was significantly increased （ P ＜0.05）， the phosphorylation level of p38 MAPK protein was increased， the difference was not statistically significant （ P ＞0.05）. CONCLUSIONS CQYG can inhibit EMT by regulating the MAPK signaling pathway， thereby suppressing tumor cell invasion and metastasis and ultimately exerting a therapeutic effect in improving HCC.

ObjectiveGastrodia elata has evolved ecological types with shortened rhizome internodes and diversified flower and fruit coloration in response to different altitudes. Studying the genetic mechanisms of different ecotype germplasm is significant for guiding variety breeding in different cultivation areas. MethodsThe bHLH gene family was identified based on the whole-genome datasets of G. elata f. elata and G. elata f. glauca. Subsequently， the gene family members were subject to analysis， including gene structure， chromosomal localization， cis-acting elements， gene synteny， and phylogeny. Combined with transcriptome data and quantitative Real-time PCR， the expression patterns of bHLH genes in the stems of the different G. elata ecotype germplasm were analyzed. Finally， correlation analysis was conducted between gene expression patterns and color to obtain the key bHLH genes regulating the color formation of stem. ResultsA total of 63 bHLH genes were identified in both G elata f. elata and G. elata f. glauca， unevenly distributed across 17 chromosomes and clustered into 16 subfamilies， with significant expansion in some family members. Obvious inversions of bHLH genes on the same chromosome and interchromosomal translocations were detected in the two ecotype germplasm. Among these genes， 12 bHLH genes （such as bHLH62-3 and bHLH74） were associated with the bright yellow color of G elata f. elata stem， while 9 bHLH genes （such as PIL13， UNE12， and bHLH130） were correlated with the red color of G. elata f. glauca stem. Compared to G. elata f. glauca， the bHLH48 expression level was significantly higher in flowers and scale leaves of G elata f. elata， and the bHLH62-3 expression level was significantly higher in all organs of G elata f. elata. ConclusionsFunctional pathway divergence of the bHLH family members has occurred across different chromosomes in G elata f. elata and G. elata f. glauca. Through synergism or antagonism with other genes， 21 bHLH genes participate in the coloration metabolic pathway regulation of stems， flowers， and fruits. Specifically， bHLH62-3 is involved in regulating stem color differentiation in the anthocyanin biosynthesis pathway of G. elata， thus relevant to the color formation of stem. Additionally， GebHLH48 positively regulates flowering-related pathways to promote the early-flowering phenotype of G. elata f. elata. These findings have laid the foundation for analyzing the genetic regulatory mechanisms underlying the color formation of the G. elata stem.

ObjectiveGastrodia elata has evolved ecological types with shortened rhizome internodes and diversified flower and fruit coloration in response to different altitudes. Studying the genetic mechanisms of different ecotype germplasm is significant for guiding variety breeding in different cultivation areas. MethodsThe bHLH gene family was identified based on the whole-genome datasets of G. elata f. elata and G. elata f. glauca. Subsequently， the gene family members were subject to analysis， including gene structure， chromosomal localization， cis-acting elements， gene synteny， and phylogeny. Combined with transcriptome data and quantitative Real-time PCR， the expression patterns of bHLH genes in the stems of the different G. elata ecotype germplasm were analyzed. Finally， correlation analysis was conducted between gene expression patterns and color to obtain the key bHLH genes regulating the color formation of stem. ResultsA total of 63 bHLH genes were identified in both G elata f. elata and G. elata f. glauca， unevenly distributed across 17 chromosomes and clustered into 16 subfamilies， with significant expansion in some family members. Obvious inversions of bHLH genes on the same chromosome and interchromosomal translocations were detected in the two ecotype germplasm. Among these genes， 12 bHLH genes （such as bHLH62-3 and bHLH74） were associated with the bright yellow color of G elata f. elata stem， while 9 bHLH genes （such as PIL13， UNE12， and bHLH130） were correlated with the red color of G. elata f. glauca stem. Compared to G. elata f. glauca， the bHLH48 expression level was significantly higher in flowers and scale leaves of G elata f. elata， and the bHLH62-3 expression level was significantly higher in all organs of G elata f. elata. ConclusionsFunctional pathway divergence of the bHLH family members has occurred across different chromosomes in G elata f. elata and G. elata f. glauca. Through synergism or antagonism with other genes， 21 bHLH genes participate in the coloration metabolic pathway regulation of stems， flowers， and fruits. Specifically， bHLH62-3 is involved in regulating stem color differentiation in the anthocyanin biosynthesis pathway of G. elata， thus relevant to the color formation of stem. Additionally， GebHLH48 positively regulates flowering-related pathways to promote the early-flowering phenotype of G. elata f. elata. These findings have laid the foundation for analyzing the genetic regulatory mechanisms underlying the color formation of the G. elata stem.

Chronic obstructive pulmonary disease (COPD) is the most common chronic respiratory disease around the world, and pharmacotherapy is the foremost treatment method currently. In recent decades, with the rapid development of bronchoscopic interventional therapy, endoscopic physical ablation technology presents a therapeutic effect in treating COPD, with few treatment-related side effects, showing excellent application prospects in treating COPD. Since ablation techniques in this field are emerging technologies with low patient acceptance, they are not widely used in the clinical treatment of COPD. This article reviews the development process of physical ablation techniques. Moreover, their current application status and the prospects in the field of COPD treatment are also summarized and analyzed. We hope to promote the application of physical ablation in the clinical treatment of COPD and provide practical references and a theoretical basis for the clinical treatment of COPD.

Curcumin (Cur), a natural polyphenolic compound extracted from the rhizomes of plants belonging to the Zingiberaceae and Araceae families, has attracted considerable interest for its remarkable antioxidant, anti-inflammatory, antibacterial, and anticancer activities. Extensive studies have focused on its potential in treating various diseases, including cancers, neurodegenerative diseases, inflammation, and autoimmune disorders. However, its clinical application has been hampered by inherent physicochemical challenges, such as poor aqueous solubility, short half-life, and low bioavailability. To address these challenges, nanodrug delivery systems have been developed to improve the pharmacokinetic and pharmacodynamic profiles of curcumin, thereby enhancing its therapeutic efficacy. This review summarizes the pharmacological activities and underlying mechanisms of curcumin, encompassing its antioxidant, anti-inflammatory, anticancer, antiviral, and antibacterial effects. Furthermore, it highlights the significant advancements achieved through the development of curcumin-based nanomedicines. By synthesizing current findings, this review aims to provide insights that may inspire innovative strategies for the future design and broader applications of curcumin nanomedicines.

Bone remodeling is essential for maintaining skeletal integrity and mineral homeostasis and depends on the coordinated activities of osteoclasts, osteoblasts, and osteocytes. Osteoclast-mediated bone resorption must remain closely coupled with osteoblast-mediated bone formation, while osteocytes continuously sense mechanical loading and changes in the local and systemic environment. Reactive oxygen species are involved in these physiological processes, particularly in the regulation of osteoclast differentiation and osteoblast function. Once oxidative stress exceeds the capacity of cellular antioxidant systems, however, this balance may be disturbed, leading to enhanced bone resorption, impaired bone formation, and deterioration of bone quality. In recent years, ferroptosis has attracted increasing attention in studies of bone metabolism. Ferroptosis is characterized by iron-dependent accumulation of lipid peroxides, but ferroptosis-related alterations in bone tissue may occur before obvious cell death becomes detectable. Changes in the labile iron pool, membrane lipid composition, antioxidant capacity, and mitochondrial metabolism can already influence the biological behavior of bone cells at an earlier stage. On this basis, ferroptosis susceptibility may provide a useful way to describe a reversible metabolic state in which cells become increasingly vulnerable to lipid peroxidation while widespread membrane damage and terminal cell death have not yet occurred. Such a state should not be identified by a single molecular marker. A more appropriate assessment would combine changes in intracellular iron handling, lipid peroxidation, antioxidant defense, cell viability, bone-cell function, and the response to ferroptosis-related interventions. Measurements of Fe²⁺ or the labile iron pool, C11-BODIPY oxidation, 4-HNE and MDA, GPX4 activity or expression, GSH/GSSG balance, LDH release, and PI staining may therefore provide complementary information when interpreted together with functional changes and rescue experiments. Several metabolic processes may contribute to the development of ferroptosis susceptibility in the bone. Disturbances in iron uptake, ferritin storage, ferritinophagy, and ferroportin-mediated iron export can increase the availability of redox-active iron. At the same time, ACSL4- and LPCAT3-dependent incorporation of polyunsaturated fatty acids into membrane phospholipids increases the pool of oxidizable lipid substrates. Reduced activity of the system Xc^--GSH-GPX4 pathway further weakens the ability of cells to remove lipid hydroperoxides, while FSP1-CoQ and mitochondrial DHODH-CoQ systems provide additional antioxidant protection. Mitochondrial dysfunction, inflammation, and abnormalities in calcium-phosphate and endocrine regulation may further increase this metabolic pressure. Importantly, the consequences are unlikely to be identical among bone-cell populations. In osteoclasts, increased iron availability and oxidative stress may strengthen RANKL-NFATc1-associated differentiation and resorptive activity. In osteoblasts, persistent lipid peroxidation may interfere with RUNX2-related differentiation, collagen synthesis, matrix production, and mineralization before extensive cell loss occurs. Osteocytes, because of their long lifespan and specialized location within the mineralized matrix, may be particularly sensitive to chronic metabolic stress, resulting in impaired mechanosensing and disturbed RANKL- or FGF23-related feedback. Evidence linking these changes with osteoporosis, diabetes-related bone disorders, chronic kidney disease-mineral and bone disorder, inflammatory bone loss, and particle-induced osteolysis is increasing, although the strength of evidence differs among disease models. Changes in ROS, MDA, GPX4, or other individual indicators alone are insufficient to demonstrate ferroptosis-related susceptibility, and stronger conclusions require evidence of iron dependence, lipid peroxidation, temporal sequence, and reversibility. Emerging single-cell, spatial, proteomic, lipidomic, and metabolomic approaches may help identify susceptible cell populations and bone-remodeling regions more precisely, although the mineralized matrix and the effects of sample processing remain important technical limitations. Overall, ferroptosis susceptibility may represent an intermediate metabolic state linking disturbances in iron and redox homeostasis with progressive uncoupling of bone resorption and formation. Clarifying its cell-specific features, temporal development, and reversible window may improve our understanding of how chronic metabolic stress contributes to bone remodeling disorders and may also provide a basis for earlier and more targeted intervention.

[Purpose]To analyze the trends of incidence and age of onset of ovarian cancer in can-cer registration areas of Jiangsu Province from 2009 to 2019.[Methods]Based on data reported by 16 cancer registries in Jiangsu Province,the average annual change percentage(AAPC)of ovarian cancer crude rate(CR),age-standardized incidence rate by Chinese standard population(ASIRC),proportion of cases in people over 60 years old of age were calculated by Joinpoint software.The linear regression model was used to calculate the trend of the mean age of onset and the standardi-zed average age of onset.The change trend of ovarian cancer incidence rate among people born in different periods using the birth cohort from 1929 to 2019.[Results]The CR(AAPC=4.18％,P＜0.001)and ASIRC(AAPC=2.11％,P=0.010)of ovarian cancer from 2009 to 2019 showed a significant increasing trend.The CR of ovarian cancer in urban areas was higher than that in rural areas,however,the CR in rural areas showed a significant upward trend(AAPC=4.85％,P＜0.05),while it was not significantly changed in urban areas.The incidence of ovarian cancer first increased and then decreased with age,and peaked at the age group of 60～69 years old.From 2009 to 2019,the incidence trend of different age groups varied,but the age group over 50 years showed an up-ward trend,and the upward trend became more significantly as age increased.From 2009 to 2019,the crude mean age of onset and the standardized mean age of onset in Jiangsu Province showed a significant upward trend,with an average annual increase of 0.572 years and 0.380 years,respectively(P＜0.05).The average age of onset in both urban and rural areas showed a sig-nificant upward trend,and the annual increase in urban areas was higher than that in rural areas.However,there was no significant change in rural areas after adjusting the population composi-tion.Compared with 2009,the standardized age proportion of ovarian cancer in Jiangsu Province in 2019 showed a backward trend.Standardized proportion of ovarian cancer among people over 60 years old showed a significant upward trend(AAPC=2.78％,P=0.010).[Conclusion]From 2009 to 2019,the incidence rate of ovarian cancer in Jiangsu Province showed an upward trend.Compared with urban areas,the increase in rural areas was more pronounced.The average age of onset of ovarian cancer has shifted later with the increasing cases in older individuals.

Thoracic anesthesia with spontaneous respiration represents a form of precision anesthesia meticulously customized to individual patients.Considering the more stringent requirements this anesthesia approach imposes on the regulation of respiratory function,the writing group of the"Consensus of Experts on the Management of Thoracic Anesthesia with Spontaneous Respiration"has formulated elaborate guidelines regarding indications and contraindications,preoperative evaluation,anesthesia implementation,common complications,and treatment strategies.This was accomplished by referencing relevant domestic and international literature and integrating it with actual clinical requirements.The objective is to standardize the rational application of this anesthesia method.