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Abstract Background The aberrant expression of phosphofructokinase-platelet (PFKP) plays a crucial role in the development of various human cancers by modifying diverse biological functions. However, the precise molecular mechanisms underlying the role of PFKP in head and neck squamous cell carcinoma (HNSCC) are not fully elucidated. Methods We assessed the expression levels of PFKP and c-Myc in tumor and adjacent normal tissues from 120 HNSCC patients. A series of in vitro and in vivo experiments were performed to explore the impact of the feedback loop between PFKP and c-Myc on HNSCC progression. Additionally, we explored the therapeutic effects of targeting PFKP and c-Myc in HNSCC using Patient-Derived Organoids (PDO), Cell Line-Derived Xenografts, and Patients-Derived Xenografts. Results Our findings indicated that PFKP is frequently upregulated in HNSCC tissues and cell lines, correlating with poor prognosis. Our in vitro and in vivo experiments demonstrate that elevated PFKP facilitates cell proliferation, angiogenesis, and metastasis in HNSCC. Mechanistically, PFKP increases the ERK-mediated stability of c-Myc, thereby driving progression of HNSCC. Moreover, c-Myc stimulates PFKP expression at the transcriptional level, thus forming a positive feedback loop between PFKP and c-Myc. Additionally, our multiple models demonstrate that co-targeting PFKP and c-Myc triggers synergistic anti-tumor effects in HNSCC. Conclusion Our study demonstrates the critical role of the PFKP/c-Myc positive feedback loop in driving HNSCC progression and suggests that simultaneously targeting PFKP and c-Myc may be a novel and effective therapeutic strategy for HNSCC.

Abstract Breast cancer (BC) remains a significant health concern for women globally, prompting the relentless pursuit of novel therapeutic modalities. As a traditional Chinese medicine, Boswellia carterii has been extensively used to treat various cancers, such as BC. However, the anti-BC effect and underlying mechanism of Boswellia carterii remain largely unclear. The aim of this study is to explore the therapeutic effect of Boswellia carterii n-hexane extract (BCHE) against BC as well as its underlying mechanism. The present study showed that BCHE significantly suppressed the viability of human BC cells. Moreover, BCHE exhibited potent anti-BC activity in vivo with no significant toxic effects. Additionally, BCHE induced ferroptosis via increased Transferrin expression and the intracellular accumulation of Fe2+, as well as decreased glutathione peroxidase 4 (GPX4) expression and the upregulation of reactive oxygen species (ROS)-induced lipid peroxidation in BC cells. In vivo experimental results also demonstrated that BCHE effectively induced ferroptosis through GPX4 downregulation and Transferrin upregulation in tumor-bearing mice. Overall, BCHE inhibited the growth of BC cells by inducing ferroptosis mediated by modulating the iron accumulation pathway and the lipid peroxidation pathway. Therefore, BCHE could serve as a potential ferroptosis-targeting drug for treating BC.

Abstract Background The dysregulated mechanistic target of rapamycin complex 1 (mTORC1) signaling plays a critical role in ferroptosis resistance and tumorigenesis. However, the precise underlying mechanisms still need to be fully understood. Methods Endoplasmic reticulum oxidoreductase 1 alpha (ERO1α) expression in mTORC1-activated mouse embryonic fibroblasts, cancer cells, and laryngeal squamous cell carcinoma (LSCC) clinical samples was examined by quantitative real-time PCR (qRT–PCR), western blotting, immunofluorescence (IF), and immunohistochemistry. Extensive in vitro and in vivo experiments were carried out to determine the role of ERO1α and its downstream target, member 11 of the solute carrier family 7 (SLC7A11), in mTORC1-mediated cell proliferation, angiogenesis, ferroptosis resistance, and tumor growth. The regulatory mechanism of ERO1α on SLC7A11 was investigated via RNA-sequencing, a cytokine array, an enzyme-linked immunosorbent assay, qRT–PCR, western blotting, IF, a luciferase reporter assay, and a chromatin immunoprecipitation assay. The combined therapeutic effect of ERO1α inhibition and the ferroptosis inducer imidazole ketone erastin (IKE) on mTORC1-activated cells was evaluated using cell line-derived xenografts, LSCC organoids, and LSCC patient-derived xenograft models. Results ERO1α is a functional downstream target of mTORC1. Elevated ERO1α induced ferroptosis resistance and exerted pro-oncogenic roles in mTORC1-activated cells via upregulation of SLC7A11. Mechanically, ERO1α stimulated the transcription of SLC7A11 by activating the interleukin-6 (IL-6)/signal transducer and activator of transcription 3 (STAT3) pathway. Moreover, ERO1α inhibition combined with treatment using the ferroptosis inducer IKE exhibited synergistic antitumor effects on mTORC1-activated tumors. Conclusions The ERO1α/IL-6/STAT3/SLC7A11 pathway is crucial for mTORC1-mediated ferroptosis resistance and tumor growth, and combining ERO1α inhibition with ferroptosis inducers is a novel and effective treatment for mTORC1-related tumors.

Abstract Background Although hepatitis B virus (HBV) infection is a major risk factor for hepatic cancer, the majority of HBV carriers do not develop this lethal disease. Additional molecular alterations are thus implicated in the process of liver tumorigenesis. Since phosphatase and tensin homolog (PTEN) is decreased in approximately half of liver cancers, we investigated the significance of PTEN deficiency in HBV-related hepatocarcinogenesis. Methods HBV-positive human liver cancer tissues were checked for PTEN expression. Transgenic HBV, Alb-Cre and Pten fl/fl mice were inter-crossed to generate WT, HBV, Pten −/− and HBV; Pten −/− mice. Immunoblotting, histological analysis and qRT-PCR were used to study these livers. Gp73 −/− mice were then mated with HBV; Pten −/− mice to illustrate the role of hepatic tumor biomarker golgi membrane protein 73 (GP73)/ golgi membrane protein 1 (GOLM1) in hepatic oncogenesis. Results Pten deletion and HBV transgene synergistically aggravated liver injury, inflammation, fibrosis and development of mixed hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC). GP73 was augmented in HBV; Pten −/− livers. Knockout of GP73 blunted the synergistic effect of deficient Pten and transgenic HBV on liver injury, inflammation, fibrosis and cancer development. Conclusions This mixed HCC-ICC mouse model mimics liver cancer patients harboring HBV infection and PTEN/AKT signaling pathway alteration. Targeting GP73 is a promising therapeutic strategy for cancer patients with HBV infection and PTEN alteration.

Abstract Background Usenamine A, a novel natural compound initially isolated from the lichen Usnea longissima, has exhibited promising efficacy against hepatoma in prior investigation. Nevertheless, the underlying mechanisms responsible for its antihepatoma effects remain unclear. Furthermore, the role of the AKT/mechanistic target of the rapamycin (mTOR)/signal transducer and activator of transcription 3 (STAT3)/inhibitor of differentiation/DNA binding 1 (ID1) signaling axis in hepatocellular carcinoma (HCC), and the potential anti-HCC effects of drugs targeting this pathway are not well understood. Methods CCK-8 assay was used to investigate the effects of usenamine A on the proliferation of human HCC cells. Moreover, the effects of usenamine A on the invasion ability of human HCC cells were evaluated by transwell assay. In addition, expression profiling analysis, quantitative real-time PCR, immunoblotting, immunohistochemistry (IHC) analysis, RNAi, immunoprecipitation, and chromatin immunoprecipitation (ChIP) assay were used to explore the effects of usenamine A on the newly identified AKT/mTOR/STAT3/ID1 signaling axis in human HCC cells. Results Usenamine A inhibited the proliferation and invasion of human HCC cell lines (HepG2 and SK-HEP-1). Through the analysis of gene expression profiling, we identified that usenamine A suppressed the expression of ID1 in human HCC cells. Furthermore, immunoprecipitation experiments revealed that usenamine A facilitated the degradation of the ID1 protein via the ubiquitin–proteasome pathway. Moreover, usenamine A inhibited the activity of STAT3 in human HCC cells. ChIP analysis demonstrated that STAT3 positively regulated ID1 expression at the transcriptional level in human HCC cells. The STAT3/ID1 axis played a role in mediating the anti-proliferative and anti-invasive impacts of usenamine A on human HCC cells. Additionally, usenamine A suppressed the STAT3/ID1 axis through AKT/mTOR signaling in human HCC cells. Conclusion Usenamine A displayed robust anti-HCC potential, partly attributed to its capacity to downregulate the AKT/mTOR/STAT3/ID1 signaling pathway and promote ubiquitin–proteasome-mediated ID1 degradation. Usenamine A has the potential to be developed as a therapeutic agent for HCC cases characterized by abnormal AKT/mTOR/STAT3/ID1 signaling, and targeting the AKT/mTOR/STAT3 signaling pathway may be a viable option for treating patients with HCC exhibiting elevated ID1 expression.

Th2-high asthma is characterized by elevated levels of type 2 cytokines, such as interleukin 13 (IL-13), and its prevalence has been increasing worldwide. Ferroptosis, a recently discovered type of programmed cell death, is involved in the pathological process of Th2-high asthma; however, the underlying mechanisms remain incompletely understood. In this study, we demonstrated that the serum level of malondialdehyde (MDA), an index of lipid peroxidation, positively correlated with IL-13 level and negatively correlated with the predicted forced expiratory volume in 1 s (FEV1%) in asthmatics. Furthermore, we showed that IL-13 facilitates ferroptosis by upregulating of suppressor of cytokine signaling 1 (SOCS1) through analyzing immortalized airway epithelial cells, human airway organoids, and the ovalbumin (OVA)-challenged asthma model. We identified that signal transducer and activator of transcription 6 (STAT6) promotes the transcription of SOCS1 upon IL-13 stimulation. Moreover, SOCS1, an E3 ubiquitin ligase, was found to bind to solute carrier family 7 member 11 (SLC7A11) and catalyze its ubiquitinated degradation, thereby promoting ferroptosis in airway epithelial cells. Last, we found that inhibiting SOCS1 can decrease ferroptosis in airway epithelial cells and alleviate airway hyperresponsiveness (AHR) in OVA-challenged wide-type mice, while SOCS1 overexpression exacerbated the above in OVA-challenged IL-13-knockout mice. Our findings reveal that the IL-13/STAT6/SOCS1/SLC7A11 pathway is a novel molecular mechanism for ferroptosis in Th2-high asthma, confirming that targeting ferroptosis in airway epithelial cells is a potential therapeutic strategy for Th2-high asthma.

The stem tips of Zizania latifolia at different development stages were used as research materials. The expression stability of nine candidate reference genes (ACT1, H2B, UBI, EF-1α, GAPDH, β-actin, 60S, SKIP and AQP) were evaluated using qRT-PCR. The data were analyzed with GeNorm and NormFinder software. Present results indicated that the expression of ACT1 was stable and that it could be used as the optimal reference gene for studying the development stage of gall formation. ACT1 was selected as the reference gene to verify the expression level of the correlative genes in the gall formation stage of Z. latifolia. Our results were consistent with the previous transcriptome sequencing results. This study revealed that ACT1 was the classic reference gene for the analysis of correlative genes in all of the gall development stages of Z. latifolia.

Abstract Background Aberrantly activated mammalian target of rapamycin complex 1 (mTORC1) plays a vital role in tumor angiogenesis, but its precise mechanisms are still unclear. Methods Micro-RNA-130b-3p (miR-130b-3p) expression in mTORC1-activated and control cells was examined by quantitative real-time PCR (qRT-PCR). MiR-130b-3p levels and their correlation with mTORC1 activity were evaluated by analyzing publicly available databases and in-house head and neck squamous cell carcinoma (HNSCC) tissues. The role of miR-130b-3p in mTORC1-mediated angiogenesis and tumor growth was examined using tube formation assay, chicken chorioallantoic membrane assay, cell line − derived xenograft models, and an HNSCC patient-derived xenograft (PDX) model. The regulatory mechanisms among signal transducer and activator of transcription 3 (STAT3), miR-130b-3p, and muscleblind-like protein 1 (MBNL1) were investigated via bioinformatics analyses, qRT-PCR, western blot, RNA immunoprecipitation, immunofluorescence, luciferase reporter assay, and chromatin immunoprecipitation assay. Results Elevated miR-130b-3p enhanced the angiogenic and tumorigenic abilities of mTORC1-activated cells both in vitro and in vivo. STAT3, a downstream effector of mTORC1, transactivated miR-130b-3p by direct binding promoter of the miR-130b gene. MBNL1 was identified as a direct target of miR-130b-3p. MBNL1 depletion rescued the compromised angiogenesis and tumor growth caused by miR-130b-3p inhibition. MiR-130b-3p levels were significantly upregulated and positively correlated with mTORC1 signaling in multiple cancers. MiR-130b-3p inhibition attenuated tumor angiogenesis and growth in an HNSCC PDX model. MBNL1 feedback inhibited STAT3 activation in mTORC1-activated cells. Conclusions The STAT3/miR-130b-3p/MBNL1 feedback loop plays a vital role in mTORC1-mediated angiogenesis and tumor progression. This pathway could be targeted for therapeutic intervention of mTORC1-related cancers.

Loss of function of tuberous sclerosis complex 1 or 2 (TSC1 or TSC2) leads to the activation of mammalian target of rapamycin complex 1 (mTORC1). Hyperactivated mTORC1 plays a critical role in tumor growth, but the underlying mechanism is still not completely elucidated. Here, by analyzing Tsc1- or Tsc2-null mouse embryonic fibroblasts, rat Tsc2-null ELT3 cells, and human cancer cells, we present evidence for the involvement of epidermal growth factor receptor (EGFR) as a downstream target of mTORC1 in tumor growth. We show that mTORC1 leads to increased EGFR expression through upregulation of runt-related transcriptional factor 1 (RUNX1). Knockdown of EGFR impairs proliferation and tumoral growth of Tsc-deficient cells, while overexpression of EGFR promotes the proliferation of the control cells. Moreover, the mTOR signaling pathway has been shown to be positively correlated with EGFR in human cancers. In addition, we demonstrated that EGFR enhances cell growth through activation of signal transducer and activator of transcription 3 (STAT3). We conclude that activation of the RUNX1/EGFR/STAT3 signaling pathway contributes to tumorigenesis caused by hyperactivated mTORC1 and should be targeted for the treatment of mTORC1-related tumors, particularly TSC.

Drought is one of the most serious stresses affecting rice growth. Drought stress causes accelerated senescence, reduced fertility, and subsequent reductions in crop yield. Eukaryotic translation elongation factor EF1A is an important multifunctional protein that plays an essential role in the translation of eukaryotic proteins. In this study, we localized and cloned the OsEF1A gene in rice (Oryza sativa) in order to clarify its role in drought tolerance and yield. Subcellular localization revealed that it was mainly localized to the cell membrane, cytoskeleton and nucleus. Compared with the wild-type, OsEF1A overexpressing transgenic plants had significantly more tillers and grains per plant, resulting in a significantly higher yield. Increases in the relative water content and proline content were also observed in the transgenic seedlings under drought stress, with a decrease in the malondialdehyde content, all of which are representative of drought tolerance. Taken together, these findings suggest that OsEF1A plays a positive regulatory role in rice nutritional development under drought stress. These findings will help support future studies aimed at improving yield and stress tolerance in rice at the molecular level, paving the way for a new green revolution.

Abstract Angiogenesis is a key characteristic of asthma airway remodeling. By releasing cationic granule proteins, such as major basic protein (MBP), activated eosinophils play a prominent role in asthma, but the underlying mechanisms are still not fully understood. In this study, we demonstrated that fibroblast growth factor-binding protein 1 (FGFBP1) was dramatically upregulated in airway epithelial cell lines treated by poly-L-arginine (PLA), a mimic of MBP. Elevated FGFBP1 expression was also detected in asthma clinical samples, as well as in ovalbumin (OVA)-induced chronic asthma mouse models. PLA enhanced FGFBP1 expression through activation of the mechanistic target of rapamycin complex 1-signal transducer and activator of transcription 3 (mTORC1-STAT3) signaling pathway. STAT3 transactivated FGFBP1 by directly binding to the promoter of the FGFBP1 gene. Furthermore, we identified that FGFBP1 secreted by PLA-treated airway epithelial cells served as a proangiogenesis factor. Lastly, we found the mTORC1-STAT3-FGFBP1 signaling pathway was activated in an OVA-induced chronic asthma model with airway remodeling features. Rapamycin treatment alleviated respiratory symptoms and reduced angiogenesis in asthmatic mice. Therefore, activation of the mTORC1-STAT3-FGFBP1 pathway in the airway epithelium contributes to the progress of angiogenesis and should be targeted for the treatment of asthma.

Abstract As evidenced by the behavior of loss-of-function mutants of PTEN in the context of a gain-of-function mutation of AKT1, the PTEN-AKT1 signaling pathway plays a critical role in human cancers. In this study, we demonstrated that a deficiency in PTEN or activation of AKT1 potentiated the expression of platelet-derived growth factor receptor α (PDGFRα) based on studies on Pten−/− mouse embryonic fibroblasts, human cancer cell lines, the hepatic tissues of Pten conditional knockout mice, and human cancer tissues. Loss of PTEN enhanced PDGFRα expression via activation of the AKT1-CREB signaling cascade. CREB transactivated PDGFRα expression by direct binding of the promoter of the PDGFRα gene. Depletion of PDGFRα attenuated the tumorigenicity of Pten-null cells in nude mice. Moreover, the PI3K-AKT signaling pathway has been shown to positively correlate with PDGFRα expression in multiple cancers. Augmented PDGFRα was associated with poor survival of cancer patients. Lastly, combination treatment with the AKT inhibitor MK-2206 and the PDGFR inhibitor CP-673451 displayed synergistic anti-tumor effects. Therefore, activation of the AKT1-CREB-PDGFRα signaling pathway contributes to the tumor growth induced by PTEN deficiency and should be targeted for cancer treatment.

AbstractThe physical property heterogeneity of tight sandstones was mainly caused by complex alteration of various diagenesis combinations during burial process. However, diagenetic evolution of different diagenesis combinations which generally result in the strong difference and heterogeneity of physical property and pore structure is rarely well understood. The Middle Permian lower Shihezi Formation is one of the most important tight gas sandstone reservoirs in the Hangjinqi area of Ordos Basin, China. The reservoir heterogeneity of lower Shihezi Formation, which was caused by the differential diagenesis combination, is crucial to efficient exploration and development. Evolution mechanism of differential diagenesis combination and its effect on the reservoir quality in the tight lower Shihezi Formation sandstone in the Hangjinqi area of Ordos Basin was investigated by means of thin-section description, cathodoluminescence (CL) imaging, X-ray diffraction (XRD), scanning electron microscopy (SEM), and homogenization temperature of fluid inclusions. The lower Shihezi Formation sandstones can be divided into four diagenesis combination types according to the reservoir characteristics and diagenetic relationship. The main diagenetic sequence was mechanical compaction-chlorite rim-early pore-filling calcite cementation-dissolution-authigenic kaolinite-quartz cementation-late calcite cementation. Differential diagenesis combination was mainly controlled by the petrological characteristics, microfacies, and fault. Low content of rock fragment and high content of detrital quartz were beneficial to the compaction resistance and cementation. The moderate content of pore-filling calcite was conducive to pore space protection and feldspar dissolution. The faults control dissolution and differential diagenesis combination by influencing the migration of acid fluids. Moderate compaction-moderate cementation-moderate dissolution type (BBB type) and weak compaction-moderate cementation-strong dissolution type (CBA type) were in favour of high-quality reservoir development.

The shale oil reservoir of the Lucaogou Formation in the Jimsar Sag has undergone tectonic movement, regional deposition and complex diagenesis processes. Therefore, various reservoir space types and complex combination patterns of pores have developed, resulting in an intricate pore throat structure. The complex pore throat structure brings great challenges to the classification and evaluation of reservoirs and the efficient development of shale oil. The methods of scanning electron microscopy, high-pressure mercury injection, low-temperature adsorption experiments and thin-slice analysis were used in this study. Mineral, petrology, pore throat structure and evolution process characteristics of the shale oil reservoir were analyzed and discussed qualitatively and quantitatively. Based on these studies, the evolution characteristics and formation mechanisms of different pore throat structures were revealed, and four progressions were made. The reservoir space of the Lucaogou Formation is mainly composed of residual intergranular pores, dissolved pores, intercrystalline pores and fractures. Four types of pore throat structures in the shale oil reservoir of the Lucaogou Formation were quantitatively characterized. Furthermore, the primary pore throat structure was controlled by a sedimentary environment. The pores and throats were reduced and blocked by compaction and cementation, which deteriorates the physical properties of the reservoirs. However, the dissolution of early carbonate, feldspar and tuffaceous minerals and a small amount of carbonate cements by organic acids are the key factors to improve the pore throat structure of the reservoirs. The genetic evolution model of pore throat structures in the shale oil reservoir of the Lucaogou Formation are divided into two types. The large-pore medium-fine throat and medium-pore medium-throat reservoirs are mainly located in the delta front-shallow lake facies and are characterized by the diagenetic assemblage types of weak compaction–weak carbonate cementation–strong dissolution, early medium compaction–medium calcite and dolomite cementation–weak dissolution. The medium-pore fine throats and fine-pore fine throats are mainly developed in shallow lakes and semi-deep lakes. They are characterized by the diagenetic assemblage type of strong compaction–strong calcite cementation–weak dissolution diagenesis. This study provides a comprehensive understanding of the pore throat structure and the genetic mechanism of a complex shale oil reservoir and benefits the exploration and development of shale oil.

The effect of long noncoding RNAs (lncRNAs) on crop yield is unknown. Here, the authors show overexpression of a lncRNA, transcribed from the antisense strand of the previously discovered gene cluster LRK, can upregulate LRK genes’ expression, change histone modification status of LRK1, and increase rice grain yield.

Shale gas accumulates in reservoirs that have favorable characteristics and associated organic geochemistry. The Wufeng-Longmaxi formation of Well Yucan-6 in Southeast Chongqing, SW China was used as a representative example to analyze the organic geochemical and reservoir characteristics of various shale intervals. Total organic carbon (TOC), vitrinite reflectance (Ro), rock pyrolysis, scanning electron microscopy (SEM), and nitrogen adsorption analyses were conducted, and a vertical coupling variation law was established. Results showed the following: the Wufeng-Longmaxi formation shale contains kerogen types I and II2; the average TOC value at the bottom of the formation is 3.04% (and the average value overall is 0.78%); the average Ro value is 1.94%; the organic matter is in a post mature thermal evolutionary stage; the shale minerals are mainly quartz and clay; and the pores are mainly intergranular, intragranular dissolved pores, organic matter pores and micro fractures. In addition, the average specific surface area (BET) of the shale is 5.171 m2/g; micropores account for 4.46% of the total volume; the specific surface area reaches 14.6%; and mesopores and macropores are the main pore spaces. There is a positive correlation between TOC and the quartz content of Wufeng-Longmaxi shale, and porosity is positively correlated with the clay mineral content. It is known that organic pores and the specific area develop more favorably when the clay mineral content is higher because the adsorption capacity is enhanced. In addition, as shale with a high clay mineral content and high TOC content promotes the formation of a large number of nanopores, it has a strong adsorption capacity. Therefore, the most favorable interval for shale gas exploration and development in this well is the shale that has a high TOC content, high clay mineral content, and a suitable quartz content. The findings of this study can help to better identify shale reservoirs and predict the sweet point in shale gas exploration and development.

68Ga-DOTA-TATE has been successfully applied in the diagnosis of clinical neuroendocrine tumors，but its short half-life limits its widespread use. This study aimed to develop [18F]AlF-NOTA-TATE to meet the clinical demands of patients with neuroendocrine tumors (NETs) for diagnosis and treatment evaluation. A new column chromatography purification method for [18F]AlF-NOTA-TATE was developed and automated synthesis was performed using a clinical single-vessel multi-functional fluorine synthesis module. The lipophilicity, in vitro stability，and pharmacokinetics of [18F]AlF-NOTA-TATE were studied，and biodistribution experiments and PET/CT imaging of nude mice with NCI-H69 (SSTR2 positive expression) small cell lung cancer were conducted，followed by preliminary clinical evaluation on three patients with neuroendocrine tumors. The new column chromatography purification method for [18F]AlF-NOTA-TATE was simple，which was synthesized in a short time with higher than 95% of radiochemical purity and，less than 3% of.ethanol content. Pharmacokinetic and biodistribution experiments in BALB/c mice showed rapid blood clearance of the drug and renal metabolism. PET/CT imaging of tumor-bearing mice showed specific uptake of the radiotracer in SSTR-positive tumors. Preliminary clinical application showed that [18F]AlF-NOTA-TATE is well targeted in patients with long retention time and can provide better image quality. The column chromatography method for the preparation of [18F]AlF-NOTA-TATE was simple and had high radiochemical purity. Preliminary clinical results suggested that [18F]AlF-NOTA-TATE has further value for clinical research.

Abstract In order to improve the measurement accuracy of mutual inductance parameters of transmission lines in the environment of double circuit power lines without power outage, this paper establishes simulation models for measuring mutual inductance parameters of transmission lines using the different frequency method in two modes: equal and unequal zero sequence self‐parameters of two circuit lines, using a parallel zero sequence coupling model of double circuit power lines. In the article, simulation analysis is conducted on the line parameters with a coupling coefficient between 0.4 and 0.6 and a line length of 20–50 km. In order to further verify the correctness of the simulation model and measurement methods, a test bench was established based on the principle of line mutual inductance parameter testing in a laboratory dual circuit line without a power outage environment for experimental testing. By comparing the test values under experimental conditions with the standard values, it has been proven that the model and method can meet the actual measurement requirements of engineering.

Abstract. Background:. Carotid intima-media thickness (IMT) and diameter, stiffness, and wave reflections, are independent and important clinical biomarkers and risk predictors for cardiovascular diseases. The purpose of the present study was to establish nationwide reference values of carotid properties for healthy Chinese adults and to explore potential clinical determinants. Methods:. A total of 3053 healthy Han Chinese adults (1922 women) aged 18–79 years were enrolled at 28 collaborating tertiary centers throughout China between April 2021 and July 2022. The real-time tracking of common carotid artery walls was achieved by the radio frequency (RF) ultrasound system. The IMT, diameter, compliance coefficient, β stiffness, local pulse wave velocity (PWV), local systolic blood pressure, augmented pressure (AP), and augmentation index (AIx) were then automatically measured and reported. Data were stratified by age groups and sex. The relationships between age and carotid property parameters were analyzed by Jonckheere–Terpstra test and simple linear regressions. The major clinical determinants of carotid properties were identified by Pearson’s correlation, multiple linear regression, and analyses of covariance. Results:. All the parameters of carotid properties demonstrated significantly age-related trajectories. Women showed thinner IMT, smaller carotid diameter, larger AP, and AIx than men. The β stiffness and PWV were significantly higher in men than women before forties, but the differences reversed after that. The increase rate of carotid IMT (5.5 μm/year in women and 5.8 μm/year in men) and diameter (0.03 mm/year in both men and women) were similar between men and women. For the stiffness and wave reflections, women showed significantly larger age-related variations than men as demonstrated by steeper regression slopes (all P for age by sex interaction

Introduction: Whole-genome duplication (WGD) is one of the most sudden and dramatic events rarely reported in invertebrates, but its occurrence can lead to physiological, morphological, and behavioral diversification. WGD has also never been reported in barnacles, which is one of the most unique groups of crustaceans with extremely speciallized morphology (calcareous shells) and habits (intertidal sessile lifestyle). Objectives: To investigate whether WGD has occurred in barnacles and examine its potential role in driving the adaptive evolution and diversification of barnacles. Methods: Based on a newly sequenced and assembled chromosome-level barnacle genome, a novel WGD event has been identified in barnacles through a comprehensive analysis of interchromosomal synteny, the Hox gene cluster, and synonymous substitution distribution. Results: We provide ample evidences for WGD in the barnacle genomes. Comparative genomic analysis indicates that this WGD event predates the divergence of Thoracicalcarea, occurring more than 247 million years ago. The retained ohnologs from the WGD are primarily enriched in various pathways related to environmental information processing, shedding light on the adaptive evolution and diversification of intertidal sessile lifestyle. In addition, transcriptomic analyses show that most of these ohnologs were differentially expressed following the ebb of tide. And the cytochrome P450 ohnologs with differential expression patterns are subject to subfunctionalization and/or neofunctionalization for intertidal adaptation. Besides WGD, parallel evolution underlying intertidal adaptation has also occurred in barnacles. Conclusion: This study revealed an ancient WGD event in the barnacle genomes, which is potentially associated with the origin and diversification of thoracican barnacles, and may have contributed to the adaptive evolution of their intertidal sessile lifestyle.

Abstract The Final Year Project (FYP) is one of the most important courses for every undergraduate student, and the effective operation of the FYPs in higher education still faces challenges, such as uneven resource distribution and limited efficiency. This study reports a mixed-methods approach to study the impact of a student-centered FYP allocation mechanism on student performance. This research aims to investigate how aligning students’ FYP choices with their interests can inspire motivation and enhance academic performance. More importantly, this mechanism improves students’ academic resilience, enabling them to navigate unexpected contextual factors. The study’s findings take into account various aspects, including student satisfaction with the allocation process, future improvement methods, and the relationship between interest and context. The outcomes observed in this study support our hypotheses, indicating the improvements in students’ academic performance as well as the pass and completion rates. Moreover, this research contributes to ‘resilience theory’ by exploring students’ adaptability to contextual changes and their enhancement of academic resilience. This study proposes recommendations for cultivating a dynamic student-centered classroom environment. Future work could pay attention to addressing the limitations of this study, exploring other factors influencing FYP allocation, and integrating more quantitative measures for a comprehensive assessment of its impact.

Heat treatment is an important factor affecting the stability of the protein emulsion. This paper investigated the effects of different heat treatment temperature (30, 50, 70, 80 and 90 ℃, 30 min) on the physicochemical properties of tuna protein emulsion. The results showed that the emulsifying property of the heat-treated protein emulsion changed significantly compared with those without heat treatment (P

This case report describes a 62-year-old male with a notable medical history, including surgically treated bladder cancer and the suspicion of metastatic disease. He underwent 18F-FDG PET/CT imaging as part of the initial diagnostic workup, which identified several marginally hypodense hepatic lesions. These lesions exhibited metabolic activity that was slightly lower than the surrounding hepatic parenchyma, raising concerns for metastatic involvement. Subsequent 18F-DOTATATE PET/CT imaging significantly expanded the diagnostic perspective by identifying multiple somatostatin receptor (SSTR)-positive lesions, not only in the liver but also in lymph nodes and bones. This marked an important diagnostic advancement over the initial FDG PET/CT findings, showcasing the superior sensitivity of 18F-DOTATATE PET/CT in detecting SSTR-expressing tumors. Pathological evaluation after these imaging studies confirmed the diagnosis of a rectal neuroendocrine tumor (NET) with extensive hepatic metastasis, altering the clinical management and therapeutic approach for the patient. This case underscores the pivotal role of integrating 18F-DOTATATE and FDG PET/CT in the diagnostic and therapeutic management of neuroendocrine tumors, highlighting the complementary nature of these imaging modalities. The findings advocate for the use of 18F-DOTATATE PET/CT in cases where NETs are suspected, particularly for its enhanced sensitivity in detecting SSTR-positive lesions across various sites, thereby facilitating a more comprehensive disease assessment and informed therapeutic planning.

Novel (Cr,V)-ZrSiO4 jewel green pigments with near-infrared reflection performance were prepared at a low temperature of 900 °C. Effects of Cr/Si mole ratio on phase composition, microstructure, Vis–NIR reflection performance, optical properties and thermal stability were studied. The results show that with the increase of Cr/Si mole ratio from 0 to 0.4, the color of the pigment changes from blue to jewel green and then to dark green. When the Cr/Si mole ratio is 0.2, the (Cr,V)-ZrSiO4 jewel green pigment shows the best comprehensive properties, which has rendering performance (L* = 56.69, a* = −18.52, b* = −9.28), thermal stability, and near-infrared reflection performance. The properties especially excellent near-infrared reflection performance make it promising functional pigment in heat insulation. Resumen: Se prepararon nuevos pigmentos verde joya (Cr,V)-ZrSiO4 con rendimiento por reflejo en el infrarrojo cercano a una temperatura baja de 900 ̊C. Se estudiaron los efectos de la relación molar Cr/Si sobre la composición de fase, la microestructura, el rendimiento de reflexión Vis-NIR, las propiedades ópticas y la estabilidad térmica. Los resultados muestran que con el aumento de la relación molar Cr/Si de 0 a 0,4, el color del pigmento cambia de azul a verde joya y luego a verde oscuro. Cuando la relación molar Cr/Si es 0.2, el pigmento verde joya (Cr,V)-ZrSiO4 muestra las mejores propiedades integrales, que tiene rendimiento de renderizado (L* = 56.69, a* = -18.52, b* = -9.28), estabilidad térmica y rendimiento de reflexión en el infrarrojo cercano. Las propiedades especialmente excelente rendimiento de reflexión en el infrarrojo cercano lo convierten en un pigmento funcional prometedor en el aislamiento térmico.

Abstract BAZ2A, an epigenetic regulatory factor that affects ribosomal RNA transcription, has been shown to be highly expressed in several cancers and promotes tumor cell migration. This study explored the expression and mechanism of BAZ2A in tumorigenesis at the pan-cancer level. The Cancer Genome Atlas, Gene Expression Omnibus databases and TIMER2.0, cBioPortal and other tools were used to analyze the level of expression of BAZ2A in various tumor tissues and to examine the relationship between BAZ2A and survival, prognosis, mutation and immune invasion. In vitro experiments were performed to assess the function of BAZ2A in cancer cells. Using combined transcriptome and proteome analysis, we examined the possible mechanism of BAZ2A in tumors. BAZ2A exhibited high expression levels in multiple tumor tissues and displayed a significant association with cancer patient prognosis. The main type of BAZ2A genetic variation in cancer is gene mutation. Downregulation of BAZ2A inhibited proliferation, migration, and invasion and promoted apoptosis in LM6 liver cancer cell. The mechanism of BAZ2A in cancer development may involve lipid metabolism. These results help expand our understanding of BAZ2A in tumorigenesis and development and suggest BAZ2A may serve as a prognostic and diagnostic factor in several cancers.

This study aimed to investigate the prognostic value of the Naples Prognostic Score (NPS) in patients with locally advanced cervical cancer (LACC) who received curative concurrent chemoradiotherapy (CCRT). Clinicopathological data from 213 (training set) and 106 (validation set) LACC cases undergoing CCRT were retrospectively analyzed. The receiver operating characteristic curve (ROC) was used to compare the predictive ability of NPS and other indicators for survival. Cox proportional hazard regression was conducted for overall survival (OS) and progression-free survival (PFS). A prediction model using a nomogram was developed with independent prognostic factors in the training set and validated in the validation set. The 5-year OS for the NPS = 1, 2, and 3 groups was 56.8%, 45.4%, and 28.9% (P < 0.001), and the 5-year PFS for the NPS = 1, 2, and 3 groups was 44.9%, 36.7%, and 28.4% (P = 0.001), respectively. NPS showed better predictive ability for OS and PFS compared to other indicators. Multivariate regression analysis identified NPS as an independent prognostic factor for OS (P < 0.001) and PFS (P < 0.001). A predictive nomogram based on NPS was established and validated. The C-indexes of the nomogram in the training set were 0.722 for OS and 0.683 for PFS, while in the validation set the C-indexes were 0.731 for OS and 0.693 for PFS. This study confirmed that preoperative NPS could serve as a useful independent prognostic factor in LACC patients treated with CCRT.

Vibriosis is one of the most serious diseases that commonly occurs in aquatic animals, thus, shaping a steady inherited resistance trait in organisms has received the highest priority in aquaculture. Whereas, the mechanisms underlying the development of such a resistance trait are mostly elusive. In this study, we constructed vibriosis-resistant and susceptible families of the Pacific white shrimp Litopenaeus vannamei after four generations of artificial selection. Microbiome sequencing indicated that shrimp can successfully develop a colonization resistance trait against Vibrio infections. This trait was characterized by a microbial community structure with specific enrichment of a single probiotic species (namely Shewanella algae), and notably, its formation was inheritable and might be memorized by host epigenetic remodeling. Regardless of the infection status, a group of genes was specifically activated in the resistant family through disruption of complete methylation. Specifically, hypo-methylation and hyper-expression of genes related to lactate dehydrogenase (LDH) and iron homeostasis might provide rich sources of specific carbon (lactate) and ions for the colonization of S. algae, which directly results in the reduction of Vibrio load in shrimp. Lactate feeding increased the survival of shrimp, while knockdown of LDH gene decreased the survival when shrimp was infected by Vibrio pathogens. In addition, treatment of shrimp with the methyltransferase inhibitor 5-azacytidine resulted in upregulations of LDH and some protein processing genes, significant enrichment of S. algae, and simultaneous reduction of Vibrio in shrimp. Our results suggest that the colonization resistance can be memorized as epigenetic information by the host, which has played a pivotal role in vibriosis resistance. The findings of this study will aid in disease control and the selection of superior lines of shrimp with high disease resistance.

BackgroundInsulin-like Growth Factor-1 (IGF-1) plays a crucial role in the growth and metabolic functions of various tissues and cells in the body. Recently, there has been increased attention to the association between IGF-1 and osteoarthritis (OA). However, there is controversy in current research regarding the correlation between IGF-1 levels and OA. Furthermore, the specific manner in which Body Mass Index (BMI), a key risk factor for OA, mediates the impact of IGF-1 levels on OA remains unclear.ObjectThis study aimed to investigate the bidirectional causal link between IGF-1 levels and OA in four body regions, and to explore how BMI influences the impact of IGF-1 on these types of OA.MethodTwo-sample Mendelian Randomization (MR) and its combined forms were utilized to investigate the bidirectional relationship between IGF-1 levels and four types of OA, as well as the mediating role of BMI in the impact of IGF-1 levels on OA. Data from various Genome-Wide Association Studies (GWAS) and multiple analytical methods, including inverse variance weighted, MR-Egger regression, and weighted median were utilized. Sensitivity analyses, such as MR-Egger intercept, Cochran Q test, leave-one-out, and MR-PRESSO, were conducted to ensure the robustness of the results.ResultsHigher IGF-1 levels are correlated with an increased risk for knee (OR, 1.07; 95% CI, 1.01–1.03; p = 1.49e-01; q = 9.86e-03), hip (OR, 1.13; 95% CI, 1.06–1.20; p = 7.61e-05; q = 7.44e-05), and hand OA (OR, 1.09; 95% CI, 1.01–1.17; p = 1.88e-02; q = 1.15e-02), but not spine OA but not spine OA (OR, 1.05; 95% CI, 0.99–1.10; p = 9.20e-02; q = 5.52e-02). Different types of OA do not affect IGF-1 levels. BMI mediates the increase in OA risk associated with higher IGF-1, including indirect spine OA risk through BMI.ConclusionThe study elucidates the bidirectional causality between IGF-1 levels and OA in various body parts, highlighting BMI’s mediating role in the impact of IGF-1 levels on OA. This provides valuable insights for OA prevention, diagnosis, and treatment strategies. Future research will expand our study to include a broader spectrum of ethnicities and explore the underlying mechanisms involved.

BackgroundAllergic rhinitis (AR) is a complex disease in which gene-environment interactions contribute to its pathogenesis. Epigenetic modifications, such as N6-methyladenosine (m6A) modification of mRNA, play important roles in regulating gene expression in multiple physiological and pathological processes. However, the function of m6A modification in AR and the inflammatory response is poorly understood.MethodsWe used the ovalbumin (OVA) and aluminum hydroxide to induce an AR mouse model. Nasal symptoms, histopathology, and serum cytokines were examined. We performed combined m6A and RNA sequencing to analyze changes in m6A modification profiles. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and methylated RNA immunoprecipitation sequencing qPCR (MeRIP-qPCR) were used to verify differential methylation of mRNAs and the m6A methylation level. Knockdown or inhibition of Alkbh5 in nasal mucosa of mice was mediated by lentiviral infection or IOX1 treatment.ResultsWe showed that m6A was enriched in a group of genes involved in MAPK signaling pathway. Moreover, we identified a MAPK pathway involving Map3k8, Erk2, and Nfκb1 that may play a role in the disrupted inflammatory response associated with nasal inflammation. The m6A eraser, Alkbh5, was highly expressed in the nasal mucosa of AR model mice. Furthermore, knockdown of Alkbh5 expression by lentiviral infection resulted in high MAPK pathway activity and a significant nasal mucosa inflammatory response. Our findings indicate that ALKBH5-mediated m6A dysregulation likely contributes to a nasal inflammatory response via the MAPK pathway.ConclusionTogether, our data show that m6A dysregulation mediated by ALKBH5, is likely to contribute to inflammation of the nasal mucosa via the MAPK signaling pathway, suggesting that ALKBH5 is a potential biomarker for AR treatment.

Abstract Phototherapeutic nanoplatforms that combine photodynamic therapy (PDT) and photothermal therapy (PTT) with the guidance of photoacoustic (PA) imaging are an effective strategy for the treatment of tumors, but establishing a universal method for this strategy has been challenging. In this study, we present a supramolecular assembly strategy based on Förster resonance energy transfer to construct a supramolecular nanostructured phototherapeutic agent (PcDA) via the anion and cation supramolecular interaction between two water‐soluble phthalocyanine ramifications, PcD and PcA. This approach promotes the absorption of energy, thus enhancing the generation of reactive oxygen species (ROS) and heat by PcDA, improving its therapeutic efficacy, and overcoming the low photon utilization efficiency of conventional PSs. Notably, after the intravenous injection of PcDA, neoplastic sites could be clearly visualized using PA imaging, with a PA signal‐to‐liver ratio as high as 11.9. Due to these unique features, PcDA exhibits excellent antitumor efficacy in a preclinical model at a low dose of light irradiation. This study thus offers a general approach for the development of efficient phototherapeutic agents based on the simultaneous effect of PDT and PTT against tumors with the assistance of PA imaging.

Chinese philosophy understood through the key philosophical terms has been made familiar to Western readers by first “Christianizing” it, and then by “Orientalizing” it. Many of new translations of these canonical texts are uncritically perpetuating the same formula for rendering key philosophical terms proffered in the earlier efforts at cultural translation. Those who are working with the Master of Confucianism in China reconsider the Confucian values and attempt to interpret Confucianism in Chinese philosophical context. This paper employs the qualia structure (Pustejovsky 1991) to verify the validation of three important Confucian concepts, rén (仁), lǐ(礼) and dé (德), of the total 92 Confucian conceptual terms from The Analects (Lúnyǚ,《论语》) and Tao-Te Ching (Dàodéjīng,《道德经》) as the case studies. The qualia structure investigates the semantic information of the core characters in both source and target text which can effectively clarify the correspondence in Chinese-English translation in that the equivalent semantic information can be regarded as the equivalent translation. Furthermore, through this research, misunderstandings can be avoided and foreigners will find it easy to understand Chinese culture.

Background: This study aimed to show a 3-year trajectory of physical performance among Chinese elderly in Beijing communities and explore the associations between new adverse events during the 3-year follow-up period and decreased physical performance. Methods: A longitudinal observational study included baseline data and transitional information of physical performance from 456 community elders (mean age 67.3 ± 4.9 years, female 43.2 %) at a 3-year follow-up. The Mini-Mental State Examination (MMSE) and the Short Physical Performance Battery (SPPB) were used to measure cognition and physical performance, respectively. The number of chronic diseases, cognitive impairment, malnutrition, depression, knee pain, falls, and frailty were the principal independent variables in multivariate logistic regression analysis. Results: The proportion of the elderly with poor physical performance (26.97 %) increased to 42.11 % and the proportion of those with good physical performance (44.96 %) dropped to 30.48 % after the three-year follow-up. As for physical performance transitions, 39.47 % of the elderly progressed to a worsening physical status. After adjustment for covariates, only new onset cognitive impairment (OR: 5.17; 95%CI: 2.01–14.54; P = 0.001) was associated with physical performance deterioration. Conclusion: Cognitive impairment is an independent risk factor for decreased physical performance in elderly people. Active interventions targeted at cognitive impairment could help promote healthy aging.

Alzheimer's disease (AD) is a global medical challenge. Studies have shown that neurotoxicity caused by pathological aggregation of β-amyloid (Aβ) is an important factor leading to AD. Therefore, inhibiting the pathological aggregation of Aβ is the key to treating AD. The recombinant human HspB5-ACD structural domain protein (AHspB5) prepared by our group in the previous period has been shown to have anti-amyloid aggregation effects, but its inability to penetrate biological membranes has limited its development. In this study, we prepared a recombinant fusion protein (T-AHspB5) of TAT and AHspB5. In vitro experiments showed that T-AHspB5 inhibited the formation of Aβ1–42 protofibrils and had the ability to penetrate the blood-brain barrier; in cellular experiments, T-AHspB5 prevented Aβ1–42-induced oxidative stress damage, apoptosis, and inflammatory responses in neuronal cells, and its mechanism of action was related to microglia activation and mitochondria-dependent apoptotic pathway. In animal experiments, T-AHspB5 improved memory and cognitive dysfunction and inhibited pathological changes of AD in APP/PS1 mice. In conclusion, this paper is expected to reveal the intervention mechanism and biological effect of T-AHspB5 on pathological aggregation of Aβ1–42, provide a new pathway for the treatment of AD, and lay the foundation for the future development and application of T-AHspB5.

Insulin-like peptide (ILP) is a member of the insulin superfamily with evolutionary conservation and is one of the most important factors affecting animal life activities. In this study, a full-length of ILP1 gene in Pacific white shrimp, Litopenaeus vannamei, was cloned, and the mRNA length consisted of 812 bp with an open reading frame (ORF) of 543 bp, encoding 180 amino acids. Sequence analysis showed that the predicted molecular weight of LvILP1 protein was 20.81 kDa, and the theoretical isoelectric point was 9.45 and the instability coefficient was 96.20. There was a signal peptide, no transmembrane structure. It was deduced that it was located outside the cell and is an alkaline unstable secreted protein. Structure prediction found that LvILP1 protein had the conserved IlGF domain of the insulin superfamily, which was composed of the N-terminal signal peptide, B-chain, C-peptide and A-chain, as well as six conserved cysteine sites and two cleavage sites. Phylogenetic analysis found that LvILP1 was most closely related to ILP7 in Penaeus monodon, and clustered with ILP1 of Crustaceans to form a branch, and then clustered with ILP7 of Invertebrate, Relaxin, Insulin and Insulin-like growth factor (IGF) of vertebrate; ILP7 of Invertebrate was evolutionarily closest to outgroup sea anemone ILP1, suggesting that it may be more similar to the ancestor gene of the insulin superfamily. Transcription factor prediction found that the possible transcription factors of LvILP1 are Forkhead box protein O3 (FoxO3), Glucocorticoid receptor (GR), CAAT region/enhancer binding protein (C/EBP) and Signal transduction and transcription activator protein (STAT); The protein interaction analysis found that LvILP1 interacted with Insulin receptor (IR) on the cell membrane, nerve signaling molecules (VGLUT1, SYT 1_3), Glycoprotein hormone beta 5 (GPHB5), Bursicon alpha, etc. By analyzing the biological function analysis of these transcription factors and interacting proteins, it is speculated that LvILP1 may play an important role in regulating shrimp growth and development, response to hormonal stimulation, nervous system homeostasis, carbohydrate homeostasis, postmolt tissue remodeling and reproductive development. The analysis showed that LvILP1 was expressed in the early developmental stage of shrimp, and expressed in all tissues of adults, but the expression level in the eye stalk was the highest. This study provides important information for in-depth understanding of the structure, evolution, function and expression of ILP in shrimp, as well as clues for molecular breeding and healthy farming of shrimp.

Abstract Background Kernel dehydration is an important factor for the mechanized harvest in maize. Kernel moisture content (KMC) and kernel dehydration rate (KDR) are important indicators for kernel dehydration. Although quantitative trait loci and genes related to KMC have been identified, where most of them only focus on the KMC at harvest, these are still far from sufficient to explain all genetic variations, and the relevant regulatory mechanisms are still unclear. In this study, we tried to reveal the key proteins and metabolites related to kernel dehydration in proteome and metabolome levels. Moreover, we preliminarily explored the relevant metabolic pathways that affect kernel dehydration combined proteome and metabolome. These results could accelerate the development of further mechanized maize technologies. Results In this study, three maize inbred lines (KB182, KB207, and KB020) with different KMC and KDR were subjected to proteomic analysis 35, 42, and 49 days after pollination (DAP). In total, 8,358 proteins were quantified, and 2,779 of them were differentially expressed proteins in different inbred lines or at different stages. By comparative analysis, K-means cluster, and weighted gene co-expression network analysis based on the proteome data, some important proteins were identified, which are involved in carbohydrate metabolism, stress and defense response, lipid metabolism, and seed development. Through metabolomics analysis of KB182 and KB020 kernels at 42 DAP, 18 significantly different metabolites, including glucose, fructose, proline, and glycerol, were identified. Conclusions In sum, we inferred that kernel dehydration could be regulated through carbohydrate metabolism, antioxidant systems, and late embryogenesis abundant protein and heat shock protein expression, all of which were considered as important regulatory factors during kernel dehydration process. These results shed light on kernel dehydration and provide new insights into developing cultivars with low moisture content.

The bleeding circuit is important for dropping the dc-bus voltage to safe voltage when electric vehicles (EVs) encounter an emergency. However, the bleeding circuit may be bulky and heavy to ensure that the total discharge operation can be completed in the specified time (5 seconds). In order to reduce the volume and weight of the bleeding circuit, this paper proposes a maximum discharge power method that can maintain the discharge power of the bleeding resistor and windings at the maximum discharge power. The mechanism and disadvantage of traditional uncontrolled rectification (UR) method is analyzed for illustrating the necessity of reducing the bleeding resistor at first. Then, the proposed maximum discharge power is developed based on the established power flow model. For the sake of improving the tracking performance and dynamic performance of the discharge power, an adaptive sliding mode power control (ASMPC) is proposed with the adaptive reaching law, which can effectively reduce the chatting effect on inner current loop. Finally, the proposed strategy is validated on a permanent magnet synchronous motor drive used for EVs, and the results show that the proposed discharge method can not only reduce the bleeding resistor size and weight but also improve the dynamic characteristics.