OPTICAL MATERIALS
·
2012
·
IF 2.023
Zhengwen Yang,Jialun Zhu,Dong Yan,Hangjun Wu,Rongfei Wang,Zhiguo Song,Xue Yu,Yong Yang,Dacheng Zhou,Zhaoyi Yin,Jianbei Qiu
Upconversion inverse opal photonic crystals based on a luminescent matrix of Yb, Er co-doped Y 2 Ti 2 O 7 were synthesized, and their photoluminescence was investigated. By comparing the spectra of the inverse opals with that of the reference sample, the contribution of photonic band gap effect to the upconversion emission was observed in the Y 2 Ti 2 O 7 : Yb, Er inverse opals. Intensity of the green or red upconversion emission from Er 3+ was depressed when the overlapping between the photonic band-gap and Er 3+ ions emission band occurs.
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高影响因子
Minerals
·
2024
·Vol. 14
·期 6
·534
·
IF 2.2
Chunhua Bai,Xiaoning Yang,Guanghui Li
The removal of low concentrations of rare-earth ions (e.g., Er(III)) from water has stimulated interest in the field of mineral processing and water treatment. Here, an ion-exchange and complexation-assisted precipitation method for the removal of low concentrations of Er(III) from water using heptadecyl-1,1-bisphosphonic acid (HBPA) was investigated. The results showed that effective cation-exchange between Er(III) ions and the bisphosphonate headgroup was achieved, and the solution pH abruptly decreased from 6.5 to around 3.1 at the first stage, which further led to the formation of less soluble Er(III) heptadecyl-1,1-bisphosphonate complexes. While low concentrations of Er(III) ions in water are typically treated by the addition of HBPA, followed by the addition of sodium bicarbonate (adjusting the pH to 6–8) and activate carbon, Er(III) ions could be efficiently removed from aqueous solution after about 30 min based on the cation-exchange and complexation-assisted precipitation method. Additionally, the removal of ultra trace amounts of Er(III) ions was not significantly affected by coexisting trace amounts of alkaline-earth metal ions (Mg2+, Ca2+and Sr2+). HBPA is an effective Er(III) chelator, which may be a potential and promising alternative technique to remove Er(III) ions from aqueous solutions.
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Cell Death & Disease
·
2025
·Vol. 16
·期 1
·1-15
·
IF 9.6
Cen Junjie,Zhao Dongliang,Shi Xin,Chen Jinlong,Zhou Hang,Liang Yanping,Gui Chengpeng,Chen Wei,Luo Junhang,Chen Xu
Renal cell carcinoma (RCC) remains a significant clinical challenge due to its increasing incidence and resistance to conventional therapy. This study identifies an unprecedented mechanism by which mesencephalic astrocyte-derived neurotrophic factor (MANF) contributes to RCC progression. From single-cell transcriptome, we observed a significant upregulation of MANF in RCC compared to its progenitor cells, the proximal tubular cells. Mechanistically, decreased N6-methyladenosine (m6A) modification on MANF mRNA, mediated by the upregulation of the m6A demethylase ALKBH5, led to reduced RNA degradation and increased MANF protein expression. Furthermore, while the common von Hippel-Lindau (VHL) deletion in RCC results in the accumulation of misfolded proteins and endoplasmic reticulum (ER) stress, increased MANF efficiently mitigated ER stress by binding to phosphorylated inositol-requiring enzyme-1 alpha (IRE1α) and inhibited its phosphorylation, indicating that MANF-mediated ER stress resistance compensates for the negative effects of VHL depletion and contributes to the survival of RCC. Our findings highlight a potential therapeutic strategy for RCC by targeting the m6A-mediated regulation, directly degrading MANF protein or inhibiting its function.
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PubMed
高影响因子
PHYTOMEDICINE
·
2025
·
IF 8.3
Lifang Wei,Changhui Li,Daozheng Fang,Chi Zhang,Haipiao Huang,Jinru Wu,Lin Zheng,Yinghao Yin,Qiugu Chen,Shiying Huang,Jihang Chen,Jianping Chen
Background Tourette syndrome (TS) is a neuropsychiatric disorder that typically manifests in childhood. Currently, anti-psychotic drugs that aim to reduce dopaminergic hyperinnervation in the brain are recommended for TS. These drugs have been proven to increase the risk of extrapyramidal symptoms, which hinder their use. Gut microbiota has been shown to modulate dopamine (Da) metabolism along gut-brain axis and be relevant to the development of TS, and which may be a novel strategy for TS therapy. Xiao-Er-An-Shen Granule (XEASG) is a clinically prescribed herbal mixture that has demonstrated clinical efficacy in treating TS. The detailed mechanism of XEASG in alleviating TS symptoms through the gut-brain axis however remains incompletely understood. Purpose This study aimed to investigate the effect of XEASG on TS through regulating Da synthesis both in the brain and gut microbiota. Methods XEASG at doses of 2 and 4 g/kg/d was administered orally to 3,3’-iminodipropionitrile (IDPN)-induced TS model mice. Behavioral assessments, targeted metabolomics analysis, 16S rRNA sequencing and ELISA were employed to elucidate the therapeutic effects and mechanisms of XEASG for TS treatment. Results Data showed that XEASG treatment significantly alleviated IDPN-induced tic-like behavior in mice. XEASG significantly reduced Da level in the brain tissues of TS mice, resulting from down-regulated Da synthesis but up-regulated Da degradation. Aberrant Da metabolism was also found in serum and colon contents of TS mice, which was restored by XEASG treatment. Furthermore,16S rRNA sequence revealed that XEASG altered the microbial community composition. Finally, experimental validation confirmed that XEASG suppressed Da synthesis pathway by reducing tyrosine hydroxylase level in the gut microbiota. Conclusion Our findings reveal that XEASG alleviates TS via inhibiting Da synthesis in the brain and gut, which suggests that the regulation of Da through gut microbiota by XEASG could be a therapeutic strategy for TS treatment.
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PubMed
高影响因子
Nature Communications
·
2025
·
IF 15.7
Hu Xuewen,Zhou Tiantian,Cui Tiansi,Du Yuanjiao,Song Chunyu,Chang Weiping,Xiong Juan,Qin Jichao,Deng Lin,Ji Wei-Ke
Sigma Non-Opioid Intracellular Receptor 1 (SigmaR1) is a member of the sigma family of receptors that interacts with a variety of psychotomimetic drugs and is involved in a wide range of cellular and physiological functions. Despite its increasing importance in human physiology and disease, the subcellular localization of SigmaR1 and its molecular function remain poorly defined. Using endogenous tagging and cell fractionation, we show that SigmaR1 is a type II integral ER membrane protein that is specifically enriched at ER sheets. A short region at the N-terminus of SigmaR1 promotes its ER-sheet localization. Importantly, our biochemical studies demonstrate that SigmaR1 directly interacts with components of the translocon complex including TRAPα and Nicalin. In addition, we found that a β-barrel at the C-terminal of SigmaR1 binds phosphatidylcholine (PC), and the binding of PC strengthens the association of SigmaR1 with the translocon complex. SigmaR1 knockout systematically impaired cellular protein and lipid homeostasis, resulting in accumulation of lipid droplets in hepatocytes. Collectively, we propose that SigmaR1 is an auxiliary translocon factor that binds lipids to regulate protein and lipid droplet homeostasis, which may underlie the broad and vital roles of SigmaR1 in physiology and disease.
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高影响因子
MATERIALS CHEMISTRY AND PHYSICS
·
2014
·
IF 2.129
Yanhua Tong,Feng Cao,Jintian Yang,Minhong Xu,Chu Zheng,Xingyu Zhu,Di Chen,Min Zhang,Fan Huang,Jie Zhou,Lixiao Wang
Pristine and erbium-doped ZnS urchinlike hierarchical nanostructures were successfully synthesized via a chemical solution route. Morphologies of ZnS products have been controlled by adjusting sulfur source and the ratio of ethylene glycol to water by volume. The crystal structures, morphologies and chemical composition of samples were analyzed by X-ray powder diffraction, transmission electron microscopy and atomic emission spectrometry . The photoluminescence (PL) properties of samples were analyzed by spectrofluorometer. It was first found that its broad blue emission is originated not from zinc vacancies or just sulfur vacancies but from sulfur vacancies as well as extended sulfur-vacancy states. PL emission spectra of Er-doped ZnS urchinlike architectures indicated that Er doping can increase sulfur vacancies and extended sulfur-vacancy states. Photocatalytic experiments demonstrate that ZnS with 0.1 atomic% of Er 3+ performs the best photocatalytic activity . Photogenerated carriers transfer from outer surface to organic molecules and recombination inside ZnS were investigated by adsorbance and PL spectra, respectively. The results suggest that strong adsorptivity of Er-doped ZnS facilitates the transfer of photogenerated carriers from surface of ZnS to dye molecules; however, higher content of Er could in turn assists photogenerated electron–hole recombination inside ZnS.
研究领域:
材料科学
·
光学
·
纳米技术
·
化学
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高影响因子
JOURNAL OF MATERIALS SCIENCE-MATERIALS IN ELECTRONICS
·
2020
·Vol. 31
·期 21
·18370-18380
·
IF 2.22
Yun Xiangyan,Zhou Jun,Zhu Yaohui,Molokeev Maxim S.,Jia Yetong,Wei Chao,Xu Denghui,Sun Jiayue
The discovery of stable and highly sensitive up-conversion (UC) phosphors using the fluorescence intensity ratio (FIR) is a significant challenge in the field of optical temperature sensor. Er 3+ /Ho 3+ /Tm 3+ -doped LiYbMo 2 O 8 UC phosphors with excellent luminescence properties were successfully synthesized through a high-temperature solid-state reaction, and the crystal structure and UC luminescence properties were discussed in detail. The UC process has been investigated by spectra pump power dependence and further explained via the energy level diagram. All emission processes about Er 3+ ions and Ho 3+ ions are two-photon processes and the blue emission process about Tm 3+ ions is a combination of two-photon process and three-photon process. Thermal sensing performances depended on FIR technology were estimated and the sensitivities of LiYb 1− x Mo2O8: x Ln 3+ included absolute sensitivity ( S a ) and relative sensitivity ( S r ) can produce particular change rules with the temperature, which can serve as excellent candidates for applications in optical temperature sensing. With the increase of temperature, the maximum values of S r of LiYb 1− x Mo 2 O 8 : x Ln 3+ are 1.16% K −1 (0.05Er 3+ ), 0.25% K −1 (0.01Ho 3+ ), and 0.51% K −1 (0.01Tm 3+ ), respectively. In addition, the S a value of LiYb 0.95 Mo 2 O 8 :0.05Er 3+ phosphor will reach the maximum (1.08% K −1 ) at 475 K, while the maximum values of S a of LiYb 0.99 Mo 2 O 8 :0.01Ho 3+ and LiYb 0.99 Mo 2 O 8 :0.01Tm 3+ are 0.16% K −1 , 0.14% K −1 .
研究领域:
材料科学
·
光学
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International Journal of Biological Sciences
·
2026
·Vol. 22
·期 12
·6363
·
IF 11.7
Ziyang Ding,Sisi Wang,Junhui Chen,Yali Song,Zhou Zhu,Haibo Tong,Ashok Iyaswamy,Peng Chen,Xu Wei,Wei Zhang,Jigang Wang,Chuanbin Yang,Yulin Feng
Oridonin is a bioactive diterpenoid derived from the widely used traditional Chinese medicinal herb Rabdosia rubescens , exhibits broad-spectrum anti-cancer activity, with several derivatives currently in clinical trials. However, the molecular mechanism underlying its anticancer effects, especially its direct target proteins, remain to be fully elucidated. Here, we found that Oridonin promoted intracellular reactive oxygen species (ROS) accumulation, which in turn induced endoplasmic reticulum (ER) stress-mediated apoptosis. Moreover, ER stress was instrumental in inducing autophagy after Oridonin treatment, while blockade of autophagy further exacerbated Oridonin-induced cytotoxicity. Notably, using activity-based protein profiling (ABPP), we identified the anti-oxidant enzyme Peroxiredoxin 1 (PRDX1) as a key direct covalent target of Oridonin. By binding to Cysteine 173 of PRDX1, Oridonin increased intracellular ROS levels. Furthermore, PRDX1 over-expression mitigated, whereas PRDX1 knockdown potentiated, Oridonin-induced ROS accumulation, autophagy, and subsequently apoptosis. Overall, our results indicate that PRDX1 is a direct covalent binding target mediating Oridonin-induced apoptosis. These findings not only provide fresh insights into the core mechanism of Oridonin-induced cytotoxicity, but also highlight PRDX1 as a potential therapeutic target for renal cancer drug development.
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CELL DEATH AND DIFFERENTIATION
·
2026
·
IF 13.6
Sun Ya-Zhou,Li Xin-Yan,Wang Jia,Zeng Meng-Liu,Qu Wei-Yi,Cheng Xu,Luo Lei,Wang Wei,Yang Juan,Zhang Jun,Tian Han,Zhang Peng,She Zhi-Gang,Li Hongliang,Zhang Xiao-Jing
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are severe conditions lacking specific pharmacological treatments. Endoplasmic reticulum (ER) stress plays a pivotal role in their pathophysiology, yet the precise regulatory mechanisms remain elusive. In this study, we identify the E3 ubiquitin ligase ring finger protein 5 (RNF5) as a critical driver of ALI/ARDS. RNF5 is markedly upregulated in response to ALI and significantly exacerbates lung injury by stabilizing HSPA5 (heat shock protein family A member 5), a master regulator of the unfolded protein response (UPR). Notably, in vivo Rnf5 ablation effectively attenuated pulmonary edema, inflammatory cell infiltration, and apoptosis, whereas lung-specific Rnf5 overexpression worsened inflammation and cell death in mice. Mechanistically, RNF5 interacts with HSPA5 and competitively blocks its binding to PERK, facilitating PERK release. Furthermore, RNF5 promotes the retro-translocation of HSPA5 from the ER lumen to the cytosol. In the cytosol, RNF5 mediates the K6- and K63-linked polyubiquitination of HSPA5, enhancing its thermal stability and preventing its re-entry into the ER. This spatial sequestration sustains the persistent dissociation of the PERK-HSPA5 complex, leading to the hyperactivation of the pro-apoptotic and pro-inflammatory PERK-eIF2α-CHOP signaling cascade. The ability of RNF5 to promote ALI is strictly dependent on its E3 ligase activity. In conclusion, our findings uncover a compartment-specific regulatory mechanism of HSPA5, suggesting that the RNF5-HSPA5-PERK axis represents a promising therapeutic target for ALI/ARDS.
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JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
·
2024
·
IF 5.7
Quanwei Li,Pan Guo,Shaofeng Wang,Luna Su,Wenlan Yu,Jianying Guo,Liammei Hu,Hui Zhang,Jiaqiang Pan,Zhaoxin Tang,Jianzhao Liao
As an efficient alternative copper (Cu) source, copper nanoparticles (nano-Cu) have been widely supplemented into animal-producing food. Therefore, it is necessary to assess the effect of nano-Cu exposure on the biological health risk. Recently, the toxic effects of nano-Cu have been confirmed but the underlying mechanism remains unclear. This study reveals the impact of nano-Cu on endoplasmic reticulum autophagy (ER-phagy) in chicken hepatocytes and further identifies Drp1 and its downstream gene FAM134B as crucial regulators of nano-Cu-induced hepatotoxicity. Nano-Cu exposure can induce Cu ion overaccumulation and pathological injury in the liver, trigger excessive mitochondrial fission and mitochondria-associated membrane (MAM) integrity damage, and activate ER-phagy in vivo and in vitro. Interestingly, the knockdown of Drp1 markedly decreases the expression of FAM134B induced by nano-Cu. Furthermore, the expression levels of ATL3, CCPG1, SEC62, TEX264, and LC3II/LC3I induced by nano-Cu exposure are decreased by inhibiting the expression of Drp1. Simultaneously, the inhibition of FAM134B effectively alleviates nano-Cu-induced ER-phagy by downregulating the expression of ATL3, CCPG1, SEC62, TEX264, and LC3II/LC3I. Overall, these results suggest that Drp1-mediated impairment of MAM integrity leads to ER-phagy as a novel molecular mechanism involved in the regulation of nano-Cu-induced hepatotoxicity. These findings provide new ideas for future research on the mechanism of nano-Cu-induced hepatotoxicity.
研究领域:
毒理学
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细胞生物学
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分子生物学
·
兽医学
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高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
·
2025
·
IF 5.4
Maohui Liu,Jiawei Chen,Zubing Zhou,Jiexin Wang,Guangsen Li,Jinghui Xie,Lingmiao Wen,Huan Wang,Rong Gan,Peihai Zhang,Yanju Gong,Weijun Ding
Ethnopharmacological Relevance Er-Chen Decoction (ECD), a classic traditional Chinese medicine (TCM) formula, is clinically indicated for dispelling dampness and resolving phlegm. It has been widely used in the management of phlegm‒dampness syndrome, including obesity, with a long-standing clinical application history in improving obesity-related male infertility. Although its therapeutic efficacy has been validated through long-term clinical practice, the underlying molecular mechanisms remain incompletely understood. Aim This study aimed to investigate the molecular mechanisms by which ECD ameliorates obesity-related spermatogenic dysfunction (SD) through the SIRT1/p53 signaling axis. Materials and Methods A mouse model of diet-induced obesity was established by feeding a high-fat diet (HFD) for 8 weeks. Subsequently, obese mice were randomly assigned to receive interventions with ECD (low-, medium-, or high-dose) or L-carnitine (positive control) for 3 weeks. Sperm functional parameters were evaluated to assess obesity-related SD. A combination of network pharmacology analysis, molecular docking, biochemical assays, hematoxylin‒eosin (HE) staining, Oil Red O staining, transmission electron microscopy (TEM), quantitative real-time polymerase chain reaction (RT‒qPCR), immunofluorescence (IF) staining, immunohistochemical (IHC) staining, Western blotting (WB), and transcriptomic analysis was employed to dissect the molecular mechanisms underlying the protective effects of the ECD against obesity-related SD. Additionally, the bioactive components of ECD were characterized using extensive targeted mass spectrometry. Results Medium-dose ECD (ECD-M) significantly reduced body weight and lipid accumulation in HFD-induced obese mice. Notably, compared with the HFD group, the ECD-M group presented a 50% reduction in the abnormal sperm percentage (p < 0.01), along with a 60% increase in sperm concentration (p < 0.01), and showed an upward trend in both sperm progressive motility and sperm motility. Furthermore, ECD-M significantly upregulated the expression of the tight junction (TJ) proteins Occludin (p < 0.001) and β-catenin (p < 0.05), thereby restoring the integrity of the blood‒testis barrier (BTB). Mechanistically, ECD not only reversed lipid-induced inhibition of SIRT1 but also suppressed p53 acetylation, leading to a significant decrease in the ratios of cleaved caspase-3/caspase-3 (p < 0.05) and Bax/Bcl-2 (p < 0.0001) in testicular tissues. These effects collectively alleviated mitochondria-mediated apoptosis in the testes of obese mice. Conclusion ECD alleviates mitochondria-mediated apoptosis in testicular tissues by regulating the SIRT1/p53 axis, thereby mitigating obesity-related SD. These findings highlight ECD as a potential therapeutic agent for the management of obesity-related male infertility.
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ACS Applied Materials & Interfaces
·
2024
·
IF 8.3
Haoqun Zeng,Xi Chen,Jianyu Ling,Hongpeng Zhang,Yu Tong,Kewei Zhang,Mingzhe Zhang
The enhancement of the spin–orbit torque (SOT) effect through the integration of intrinsic inverse spin galvanic effect spin–orbit torque and spin Hall effect spin–orbit torque is fundamentally dependent on the structural and material properties of the ferromagnets. Consequently, the synthesis of ferromagnets with superior structural integrity and material characteristics is of paramount importance. In this study, a gas–liquid chemical reaction, in conjunction with ultrasonic crushing, was employed to synthesize few-layer MoS2:Er nanosheets. X-ray diffraction, X-ray photoelectron spectroscopy, and energy-dispersive spectroscopy analyses confirm the successful substitution of Mo4+ by Er3+ through doping within the MoS2 lattice. Vibrating sample magnetometry and MT measurements indicate that MoS2:Er exhibits room-temperature ferromagnetism (RTFM), with the underlying mechanism elucidated through first-principles calculations. Furthermore, the unique electron density of states at the Fermi level suggests the presence of ferromagnetism in MoS2:Er. A wedge-shaped Pt/MoS2:Er/Au structure was fabricated and subsequently evaluated for current-induced SOT switching, as well as for its memcapacitor and memristor characteristics. The precession of a magnetic moment in three-dimensional space was successfully simulated by solving the Landau–Lifshitz–Gilbert–Slonczewski equation using the Mumax.
研究领域:
自旋电子学
·
纳米材料
·
凝聚态物理
·
材料科学
·
忆阻器件
·
铁磁半导体
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