21 results on '"Xiaoming Zhou"'
Search Results
2. Insight into binding of endogenous neurosteroid ligands to the sigma-1 receptor
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Chunting Fu, Yang Xiao, Xiaoming Zhou, and Ziyi Sun
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Science - Abstract
Abstract The sigma-1 receptor (σ1R) is a non-opioid membrane receptor, which responds to a diverse array of synthetic ligands to exert various pharmacological effects. Meanwhile, candidates for endogenous ligands of σ1R have also been identified. However, how endogenous ligands bind to σ1R remains unknown. Here, we present crystal structures of σ1R from Xenopus laevis (xlσ1R) bound to two endogenous neurosteroid ligands, progesterone (a putative antagonist) and dehydroepiandrosterone sulfate (DHEAS) (a putative agonist), at 2.15-3.09 Å resolutions. Both neurosteroids bind to a similar location in xlσ1R mainly through hydrophobic interactions, but surprisingly, with opposite binding orientations. DHEAS also forms hydrogen bonds with xlσ1R, whereas progesterone interacts indirectly with the receptor through water molecules near the binding site. Binding analyses are consistent with the xlσ1R-neurosteroid complex structures. Furthermore, molecular dynamics simulations and structural data reveal a potential water entry pathway. Our results provide insight into binding of two endogenous neurosteroid ligands to σ1R.
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- 2024
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3. Overexpression of COL11A1 confers tamoxifen resistance in breast cancer
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Chengxiao Fu, Shan Duan, Xiaoming Zhou, Yingcai Meng, and Xisha Chen
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Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,RC254-282 - Abstract
Abstract Breast cancer is the most commonly diagnosed malignancy and benefits from endocrine agents such as tamoxifen. However, the development of drug resistance in cancerous cells often leads to recurrence, thus limiting the therapeutic benefit. Identification of potential biomarkers that can predict response to tamoxifen and recognize patients who will clinically benefit from this therapy is urgently needed. In this study, we report that high collagen type XI alpha 1 (COL11A1) expression was associated with poor therapeutic response and prognosis in breast cancer patients treated with tamoxifen. To confirm the role of COL11A1 in the development of tamoxifen resistance, we established MCF-7/COL11A1 and T47D/COL11A1 cell lines, which stably expressed COL11A1. Compared with parental MCF-7 and T47D, MCF-7/COL11A1 and T47D/COL11A1 cells were more resistant to 4-OHT-induced growth inhibition. Moreover, the level of COL11A1 expression was upregulated in tamoxifen-resistant MCF-7/TamR and T47D/TamR cell lines, and depletion of COL11A1 markedly sensitized the cells to 4-OHT in vitro and in vivo. Interestingly, the level of estrogen receptor α (ERα) expression was elevated, probably due to the increased COL11A1 in TamR cells. In addition, knockdown of COL11A1 decreased the expression of ERα and its downstream target genes. Overall, our findings suggest that overexpressed COL11A1 contributes to tamoxifen resistance, and targeting COL11A1 holds great promise for reversing endocrine resistance.
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- 2024
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4. ‘Sultanina’ leaves increase their trehalose content in response to grapevine brown leaf spot infection by regulating the pentose and glucuronate interchange pathway
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Chuan Zhang, Haixia Zhong, Haoyu Chen, Nuerziya Yalimaimaiti, Ju Liang, Jiachen Duan, Yameng Yang, Songlin Zhang, Vivek Yadav, Xiaoming Zhou, Xinyu Wu, Fuchun Zhang, and Jingzhe Hao
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Grapevine brown leaf spot ,Transcriptome ,Trehalose content ,Pentose and glucuronate interchange pathway ,Response mechanism ,Plant ecology ,QK900-989 - Abstract
Since the first discovery of grapevine brown leaf spot disease in Turpan, Xinjiang, China, in 2007, it has been a common occurrence in grapevine-growing regions. Grapevine brown leaf spot seriously decreases fruit yield and has become one of the most important leaf diseases in the Turpan region. However, thus far, there have been no reports on the evaluation of grapevine germplasm resources for resistance to brown leaf spot disease. In addition, the response mechanism of grapevine leaves to brown leaf spot infection has not been revealed. To better understand the resistance of grapevine germplasm resources to brown leaf spot disease, we first evaluated resistance in grapevine varieties. On this basis, the most susceptible variety ‘Sultanina’ was selected as the experimental material for this study. Transcriptome analysis and carbohydrate content analysis were performed on ‘Sultanina’ leaves with different levels of disease susceptibility. As the severity of the disease increased, the content of fructose gradually decreased, while the content of trehalose gradually increased. Transcriptome data revealed that differentially expressed genes were enriched in the pentose and glucuronate interchange pathway. These results suggest that the sugar trehalose may play an important role in the response of ‘Sultanina’ leaves to brown leaf spot infection. In addition, the pentose and glucuronate interchange pathway may be involved in the response mechanism of brown leaf spot disease. Our work provides new insights into the mechanism of the ‘Sultanina’ leaf response to brown leaf spot infection.
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- 2024
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5. The glycyl-l-histidyl-l-lysine-Cu2+ tripeptide complex attenuates lung inflammation and fibrosis in silicosis by targeting peroxiredoxin 6
- Author
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Yiding Bian, Mingming Deng, Jia Liu, Jiaye Li, Qin Zhang, Zilin Wang, Liwei Liao, Jinrui Miao, Ruixia Li, Xiaoming Zhou, and Gang Hou
- Subjects
Silicosis ,GHK-Cu ,Oxidative stress ,Macrophage ,PRDX6 ,Medicine (General) ,R5-920 ,Biology (General) ,QH301-705.5 - Abstract
Silicosis is the most common type of pneumoconiosis, having a high incidence in workers chronically exposed to crystalline silica (CS). No specific medication exists for this condition. GHK, a tripeptide naturally occurring in human blood and urine, has antioxidant effects. We aimed to investigate the therapeutic effect of GHK-Cu on silicosis and its potential underlying molecular mechanism. An experimental silicosis mouse model was established to observe the effects of GHK-Cu on lung inflammation and fibrosis. Moreover, the effects of GHK-Cu on the alveolar macrophages (AM) were examined using the RAW264.7 cell line. Its molecular target, peroxiredoxin 6 (PRDX6), has been identified, and GHK-Cu can bind to PRDX6, thus attenuating lung inflammation and fibrosis in silicosis mice without significant systemic toxicity. These effects were partly related to the inhibition of the CS-induced oxidative stress in AM induced by GHK-Cu. Thus, our results suggest that GHK-Cu acts as a potential drug by attenuating alveolar macrophage oxidative stress. This, in turn, attenuates the progression of pulmonary inflammation and fibrosis, which provides a reference for the treatment of silicosis.
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- 2024
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6. Photochemical regulatory strategies for nucleic acid function and their biomedical applications
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Menglu Hu, Yihui Wang, and Xiaoming Zhou
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nucleic acid ,nucleic acid detection ,photoactivation ,photosensitive molecule ,Medical technology ,R855-855.5 ,Biotechnology ,TP248.13-248.65 - Abstract
Abstract Nucleic acids are not only essential biomolecules that drive critical life processes such as growth, development, reproduction, inheritance, and mutation, but also serve as significant markers for disease diagnosis, pathogen identification, and cancer screening. Nevertheless, several challenges have hindered the widespread use of nucleic acids in biomedicine, such as susceptibility to degradation, limited cellular uptake efficiency, potential toxicity, and uncontrollable activity. Photo‐regulation offers an effective solution to address these challenges. It allows for the precise control of nucleic acid structure and function and enhances the stability and safety of their application in biomedicine. In this review, we systematically review the structural characteristics of the three primary photosensitive groups commonly used in the regulation of nucleic acid molecules (i.e., photocleavable molecules, photoisomerization molecules, and photo‐crosslinking molecules) under light irradiation. Subsequently, recent research advances in the development and application of photo‐modulation strategies based on these photosensitive molecules in antisense oligonucleotides, RNA interference, nucleic acid amplification, and CRISPR/Cas systems are outlined. Finally, we discuss the challenges faced in the widespread application of these photo‐regulatory strategies and outline potential future directions for their development.
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- 2024
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7. Sustained generation of neurons destined for neocortex with oxidative metabolic upregulation upon filamin abrogation
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Caroline A. Kopsidas, Clara C. Lowe, Dennis P. McDaniel, Xiaoming Zhou, and Yuanyi Feng
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Developmental neuroscience ,Cellular neuroscience ,Science - Abstract
Summary: Neurons in the neocortex are generated during embryonic development. While the adult ventricular-subventricular zone (V-SVZ) contains cells with neural stem/progenitors’ characteristics, it remains unclear whether it has the capacity of producing neocortical neurons. Here, we show that generating neurons with transcriptomic resemblance to upper layer neocortical neurons continues in the V-SVZ of mouse models of a human condition known as periventricular heterotopia by abrogating Flna and Flnb. We found such surplus neurogenesis was associated with V-SVZ’s upregulation of oxidative phosphorylation, mitochondrial biogenesis, and vascular abundance. Additionally, spatial transcriptomics analyses showed V-SVZ’s neurogenic activation was coupled with transcriptional enrichment of genes in diverse pathways for energy metabolism, angiogenesis, cell signaling, synaptic transmission, and turnovers of nucleic acids and proteins in upper cortical layers. These findings support the potential of generating neocortical neurons in adulthood through boosting brain-wide vascular circulation, aerobic adenosine triphosphate synthesis, metabolic turnover, and neuronal activity.
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- 2024
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8. Astaxanthin attenuates cigarette smoke-induced small airway remodeling via the AKT1 signaling pathway
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Haidong Ding, Liming Yan, Yu Wang, Ye Lu, Mingming Deng, Yingxi Wang, Qiuyue Wang, and Xiaoming Zhou
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Chronic obstructive pulmonary disease ,Small airway remodeling ,Diseases of the respiratory system ,RC705-779 - Abstract
Abstract Background Astaxanthin (AXT) is a keto-carotenoid with a variety of biological functions, including antioxidant and antifibrotic effects. Small airway remodeling is the main pathology of chronic obstructive pulmonary disease (COPD) and is caused by epithelial-to-mesenchymal transition (EMT) and fibroblast differentiation and proliferation. Effective therapies are still lacking. This study aimed to investigate the role of AXT in small airway remodeling in COPD and its underlying mechanisms. Methods First, the model of COPD mice was established by cigarette smoke (CS) exposure combined with intraperitoneal injection of cigarette smoke extract (CSE). The effects of AXT on the morphology of CS combined with CSE -induced emphysema, EMT, and small airway remodeling by using Hematoxylin-eosin (H&E) staining, immunohistochemical staining, and western blot. In addition, in vitro experiments, the effects of AXT on CSE induced-EMT and fibroblast function were further explored. Next, to explore the specific mechanisms underlying the protective effects of AXT in COPD, potential targets of AXT in COPD were analyzed using network pharmacology. Finally, the possible mechanism was verified through molecular docking and in vitro experiments. Results AXT alleviated pulmonary emphysema, EMT, and small airway remodeling in a CS combined with CSE -induced mouse model. In addition, AXT inhibited the EMT process in airway cells and the differentiation and proliferation of fibroblasts. Mechanistically, AXT inhibited myofibroblast activation by directly binding to and suppressing the phosphorylation of AKT1. Therefore, our results show that AXT protects against small airway remodeling by inhibiting AKT1. Conclusions The present study identified and illustrated a new food function of AXT, indicating that AXT could be used in the therapy of COPD-induced small airway remodeling.
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- 2024
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9. HDAC6-selective inhibitor CAY10603 ameliorates cigarette smoke-induced small airway remodeling by regulating epithelial barrier dysfunction and reversing
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Qin Zhang, Liming Yan, Ye Lu, Xiaodong Liu, Yan Yin, Qiuyue Wang, Xiu Gu, and Xiaoming Zhou
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HDAC6 ,COPD ,Cigarette smoke ,Airway remodelling ,CAY10603 ,Diseases of the respiratory system ,RC705-779 - Abstract
Abstract Background Small airway remodelling is a vital characteristic of chronic obstructive pulmonary disease (COPD), which is mainly caused by epithelial barrier dysfunction and epithelial-mesenchymal transition (EMT). Recent studies have indicated that histone deacetylase 6 (HDAC6) plays an important role in the dysregulation of epithelial function. In this study, we investigated the therapeutic effects and underlying mechanisms of an inhibitor with high selectivity for HDAC6 in COPD. Methods Cigarette smoke (CS) exposure was used to establish a CS-induced COPD mouse model. CAY10603 at doses of 2.5 and 10 mg/kg was injected intraperitoneally on alternate days. The protective effects of CAY10603 against CS-induced emphysema, epithelial barrier function and small airway remodeling were evaluated using hematoxylin and eosin (H&E) staining, Masson’s trichrome staining, immunohistochemical staining, and western blot. The human lung bronchial epithelial cell line (HBE) was used to elucidate the underlying molecular mechanism of action of CAY10603. Results HDAC6 levels in the lung homogenates of CS-exposed mice were higher than that those in control mice. Compared to the CS group, the mean linear intercept (MLI) of the CAY10603 treatment group decreased and the mean alveolar number (MAN)increased. Collagen deposition was reduced in groups treated with CAY10603. The expression of α-SMA was markedly upregulated in the CS group, which was reversed by CAY10603 treatment. Conversely, E-cadherin expression in the CS group was further downregulated, which was reversed by CAY10603 treatment. CAY10603 affects the tight junction protein expression of ZO-1 and occludin. ZO-1 and occludin expression were markedly downregulated in the CS group. After CAY10603treatment, the protein expression level of ZO-1 and occludin increased significantly. In HBE cells, Cigarette smoke extract (CSE) increased HDAC6 levels. CAY10603 significantly attenuated the release of TGF-β1 induced by CSE. CAY10603 significantly increased the E-cadherin levels in TGF-β1 treated HBE cells, while concurrently attenuated α-SMA expression. This effect was achieved through the suppression of Smad2 and Smad3 phosphorylation. CAY10603 also inhibited TGF-β1 induced cell migration. Conclusions These findings suggested that CAY10603 inhibited CS induced small airway remodelling by regulating epithelial barrier dysfunction and reversing EMT via the TGF-β1/Smad2/3 signalling pathway.
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- 2024
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10. Causal association between atopic dermatitis and Parkinson's disease: A bidirectional Mendelian randomization study
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Taofeng Zhou, Baohao Wei, Yachun Hu, Xiaoming Zhou, Xiaoying Cai, and Xiaolei Shi
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atopic dermatitis ,causal association ,Mendelian randomization ,Parkinson's disease ,Neurosciences. Biological psychiatry. Neuropsychiatry ,RC321-571 - Abstract
Abstract Background Atopic dermatitis is one of the most common skin disorders. Evidence has suggested an association between skin disorders, such as atopic dermatitis, and Parkinson's disease (PD). However, whether atopic dermatitis has a causal effect on PD remains unknown. Methods The study aimed to determine whether their association between atopic dermatitis and PD is causal, using a bidirectional two‐sample Mendelian randomization method. Genetic variants from the public genome‐wide association studies for atopic dermatitis (n = 10788 cases and 30047 controls) were selected to evaluate their causal effects on the risk of PD (33,674 cases and 449,056 controls). The inverse variance weighted (IVW) method was used as the primary analysis. Results The IVW results indicated that atopic dermatitis was associated with decreased risk of PD {fixed effects: odds ratio [OR] [95% confidence interval (CI)]: .905 [.832–.986], p = .022; OR [95% CI]: .905 [.827–.991], p = .032}. However, we failed to detect the causal effects of PD on risk of atopic dermatitis in the reverse causation analysis. Conclusion This study indicated causal association of genetically proxied atopic dermatitis with the risk of PD. Future studies are warranted to explore the underlying mechanism and investigate the targeting effect of atopic dermatitis on PD.
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- 2024
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11. Integrated omics-based exploration for temperature stress resilience: An approach to smart grape breeding strategies
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Vivek Yadav, Haixia Zhong, Manish Kumar Patel, Songlin Zhang, Xiaoming Zhou, Chuan Zhang, Jing Zhang, Jingyi Su, Fuchun Zhang, and Xinyu Wu
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Grapevine ,Abiotic stress ,Omics ,Resistance ,Smart breeding ,Plant ecology ,QK900-989 - Abstract
Crop resilience measures must be strengthened in response to the global climate impact. Temperature stress exacerbates the impact on crop growth and grain yield, threatening the sustainability of grapevine production and dependent wine industries. Grape (Vitis spp.) is one of the most widely cultivated fruit crops in the world, as well as the most economically important fruit. However, grape yield and quality are highly dependent on environmental conditions, particularly temperature stress. Understanding the molecular mechanisms that control grapevine responses to environmental stresses and the development of stress-resilient varieties have markedly advanced through the rapid evolution of high-throughput sequencing technologies, state-of-the-art multi-omics analytic platforms, and automated phenotyping facilities. In the current review, we summarized recent genomic progress and omics-based breakthroughs in grapes that have contributed to abiotic stress tolerance via genetic strategies during the last decades. Furthermore, we delve into prospective challenges and opportunities pertaining to the use of multi-omics-based breeding strategies aimed at designing climate-resilient grape varieties. Advances in highly efficient de novo or re-domestication histories, as well as the characterization of numerous trait genes using various omics tools, are also discussed. By describing the underlying mechanisms of crop adaptability and future breeding strategies to meet demand due to population bursts in the following decades while keeping climate change in mind, the information will offer potential solutions for sustainable grape and wine businesses.
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- 2024
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12. Proteomic analyses of urinary exosomes identify novel potential biomarkers for early diagnosis of sickle cell nephropathy, a sex-based study
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Balamurugan Packialakshmi, Emily Limerick, Hans C. Ackerman, Xionghao Lin, Sergei Nekhai, James D. Oliver, Ian J. Stewart, Mark A. Knepper, Courtney Fitzhugh, and Xiaoming Zhou
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heparanase ,cathepsin C ,α2-macroglobulin ,sarcoplasmic endoplasmic Ca2+ ATPase-3 ,albuminuria ,sex difference ,Physiology ,QP1-981 - Abstract
Sickle cell nephropathy (SCN) is a leading cause of morbidity and mortality in sickle cell disease (SCD). Early intervention is crucial for mitigating its effects. However, current diagnostic methods rely on generic tests and may not detect SCN until irreversible renal damage occurs. Therefore, specific biomarkers for early diagnosis of SCN are needed. Urinary exosomes, membrane-bound vesicles secreted by renal podocytes and epithelial cells, contain both common and cell type-specific membrane and cytosolic proteins, reflecting the physiologic and pathophysiologic states of the kidney. Using proteomics, we analyzed the proteomes of urinary exosomes from humanized SCD mice at 2 months (without albuminuria) and 4 months (with albuminuria) of age. Excretion of 164 proteins were significantly increased and 176 proteins was significantly decreased in the exosomes when mice developed albuminuria. Based on the relevance to SCD, chronic kidney disease and Western blot confirmation in mice, we analyzed protein abundance of heparanase, cathepsin C, α2-macroglobulin and sarcoplasmic endoplasmic Ca2+ ATPase-3 (SERCA3) in the urinary exosomes and urine of 18 SCD subjects without albuminuria and 12 subjects with albuminuria using Western blot analyses. Both male and female subjects increased or tended to increase the excretion of these proteins in their urinary exosomes upon developing albuminuria, but female subjects demonstrated stronger correlations between the excretion of these proteins and urine albumin creatinine ratio (UACR) compared to male subjects. In contrast, exosomal excretion of Tamm-Horsfall protein, β-actin and SHP-1 was independent of albuminuria. These findings provide a foundation for a time-course study to determine whether increases in the levels of these proteins precede the onset of albuminuria in patients, which will help determine the potential of these proteins as biomarkers for early detection of SCN.
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- 2024
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13. Association between sarcopenia and multimorbidity among middle-aged and older adults in China: Findings from the China Health and Retirement Longitudinal Study
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Mingming Deng, Ye Lu, Xuelian Li, Xiaoming Zhou, and Gang Hou
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Sarcopenia ,Possible sarcopenia ,Multimorbidity ,Middle-aged and older adults ,Medicine ,Biology (General) ,QH301-705.5 - Abstract
Background: Little is known about the association between sarcopenia and multimorbidity among middle-aged and older adults. This study investigated whether sarcopenia is associated with multimorbidity in middle-aged and older Chinese individuals. Materials and methods: A total of 12,760 participants from China Health and Retirement Longitudinal Study (CHARLS) 2015, with data on 14 specified chronic diseases and sarcopenia status were included in the cross-sectional analysis. A total of 7345 participants without multimorbidity from the CHARLS 2015 were included and followed up in 2018 in the longitudinal analysis. Logistic regression models were used in a cross-sectional investigation to assess the association between sarcopenia status and multimorbidity. In a longitudinal analysis, the relationships between sarcopenia status and multimorbidity were investigated using Cox proportional hazards models. Results: Multimorbidity was prevalent in the no sarcopenia, possible sarcopenia, and sarcopenia groups at 38.8 % (3765/9713), 56.6 % (1199/2118), and 48.5 % (451/929), respectively. Multivariable regression revealed that both possible sarcopenia (β = 0.088, P
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- 2024
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14. Synthesis of 3,4-Disubstituted Maleimide Derivatives via Phosphine-Catalyzed Isomerization of α-Succinimide-Substituted Allenoates Cascade γ′-Addition with Aryl Imines
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Zhenzhen Gao, Xiaoming Zhou, Baoshen Nie, Hanchong Lu, Xiaotong Chen, Jiahui Wu, Xuekun Wang, and Lei Li
- Subjects
phosphine-catalyzed ,γ′-addition ,isomerization ,allenoates ,3,4-disubstituted maleimides ,Biology (General) ,QH301-705.5 ,Chemistry ,QD1-999 - Abstract
3,4-disubstituted maleimides find wide applications in various pharmacologically active compounds. This study presents a highly effective approach for synthesizing derivatives of 3,4-disubstituted maleimides through the direct isomerization of α-succinimide-substituted allenoates, followed by a cascade γ′-addition and aryl imines using PR3 as a catalyst. The resulting series of 3,4-disubstituted maleimides exhibited excellent stereoselectivities, achieving yields of up to 86%. To our knowledge, the phosphine-mediated γ′-addition reaction of allenoates is seldom reported.
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- 2024
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15. Phosphine-Catalyzed γ′-Carbon 1,6-Conjugate Addition of α-Succinimide Substituted Allenoates with Para-Quinone Methides: Synthesis of 4-Diarylmethylated 3,4-Disubstituted Maleimides
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Zhenzhen Gao, Xiaoming Zhou, Dandan Liu, Baoshen Nie, Hanchong Lu, Xiaotong Chen, Jiahui Wu, Lei Li, and Xuekun Wang
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phosphine-catalyzed ,allenoates ,1,6-conjugate addition ,para-quinone methides ,Organic chemistry ,QD241-441 - Abstract
In this paper, an interesting γ′-carbon 1,6-conjugate addition for phosphine-catalyzed α-succinimide substituted allenoates has been disclosed. A wide array of substrates was found to participate in the reaction, resulting in the production of diverse 4-diarylmethylated 3,4-disubstituted maleimides with satisfactory to outstanding yields. Furthermore, a plausible mechanism for the reaction was proposed by the investigators.
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- 2024
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16. TREM2 Alleviates Subarachnoid Hemorrhage-Induced Brain Injury through Attenuating Neuroinflammation and Programmed Cell Death in Vivo and in Vitro
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Jiaqiang Liu, Zihuan Zhang, Mengliang Zhou, Shizhang Ling, Xiaoming Zhou, Bin Yuan, Xintong Zhao, Min Qi, Yanling Han, Feiyun Qin, and Zhenbao Li
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subarachnoid hemorrhage ,trem2 ,neuroinflammatory ,pyroptosis ,apoptosis ,Biochemistry ,QD415-436 ,Biology (General) ,QH301-705.5 - Abstract
Background: Apoptosis and pyroptosis are two types of programmed cell death related to the neuroinflammatory reaction after subarachnoid hemorrhage (SAH). Research indicates that triggering receptor expressed on myeloid cells 2 (TREM2) can regulate the SAH-induced inflammatory response. However, whether TREM2 regulates programmed cell death (apoptosis and pyroptosis) remains to be clarified. The purpose of the present study was to investigate the effects of TREM2 on cell death in SAH. Methods: SAH was induced in adult male C57BL/6J mice by endovascular perforation. An in-vitro cellular model of SAH was established by treating cocultured BV2 microglia and HT22 neuronal cells with oxyhemoglobin. TREM2 overexpression or knockdown was carried out by intraventricular lentivirus injection at 7 d before SAH induction in mice or lentiviral transfection, respectively. Neurobehavioral tests as well as western blot, reverse transcription–quantitative polymerase chain reaction (RT-qPCR), immunofluorescence, Evans blue (EB) staining, Nissl staining, and flow cytometry assays were performed to investigate the neuroprotective role of TREM2 after SAH. Results: After SAH, the TREM2 mRNA and protein levels were elevated in SAH mice, exhibiting a peak at 72 h. TREM2 overexpression improved the SAH-induced neurological deficits in mice, while TREM2 knockdown worsened them. In the brains of mice with TREM2 overexpression, less neuronal death and more neuronal survival were detected at 72 h post SAH. Meanwhile, TREM2 overexpression showed an inhibitory effect on microglial activation, neutrophil infiltration, and the expression of cell death marker proteins. Consistent results were obtained in vitro. Conclusions: Our research indicates the important role of TREM2 on cell death after SAH, suggesting that targeting TREM2 might be an effective approach for treating SAH.
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- 2024
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17. Multiphysics Coupling Modeling and Simulation of Electrostatic Sensors for Gas Path Monitoring.
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Manthar Ali, Jiaxin He, Maria Muzamil Memon, Asif Ali, and Xiaoming Zhou
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- 2024
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18. CFL-IDS: An Effective Clustered Federated Learning Framework for Industrial Internet of Things Intrusion Detection.
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Yao Shan, Yu Yao, Xiaoming Zhou, Tong Zhao, Bo Hu, and Lei Wang
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- 2024
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19. Cooperative multi-task assignment modeling of UAV based on particle swarm optimization.
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Xiaoming Zhou and Kun Yang
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- 2024
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20. Networked Industrial Control Device Asset Identification Method Based on Improved Decision Tree.
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Wei Yang, Yushan Fang, Xiaoming Zhou, Yijia Shen, Wenjie Zhang, and Yu Yao
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- 2024
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21. Proteomic analyses of urinary exosomes identify novel potential biomarkers for early diagnosis of sickle cell nephropathy, a sex-based study.
- Author
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Packialakshmi, Balamurugan, Limerick, Emily, Ackerman, Hans C., Xionghao Lin, Nekhai, Sergei, Oliver III, James D., Stewart, Ian J., Knepper, Mark A., Fitzhugh, Courtney, and Xiaoming Zhou
- Subjects
DIABETIC nephropathies ,EXOSOMES ,PROTEOMICS ,UROMODULIN ,KIDNEY diseases ,SICKLE cell anemia - Abstract
Sickle cell nephropathy (SCN) is a leading cause of morbidity and mortality in sickle cell disease (SCD). Early intervention is crucial for mitigating its effects. However, current diagnostic methods rely on generic tests and may not detect SCN until irreversible renal damage occurs. Therefore, specific biomarkers for early diagnosis of SCN are needed. Urinary exosomes, membrane-bound vesicles secreted by renal podocytes and epithelial cells, contain both common and cell type-specific membrane and cytosolic proteins, reflecting the physiologic and pathophysiologic states of the kidney. Using proteomics, we analyzed the proteomes of urinary exosomes from humanized SCD mice at 2 months (without albuminuria) and 4 months (with albuminuria) of age. Excretion of 164 proteins were significantly increased and 176 proteins was significantly decreased in the exosomes when mice developed albuminuria. Based on the relevance to SCD, chronic kidney disease and Western blot confirmation in mice, we analyzed protein abundance of heparanase, cathepsin C, α2-macroglobulin and sarcoplasmic endoplasmic Ca2+ ATPase-3 (SERCA3) in the urinary exosomes and urine of 18 SCD subjects without albuminuria and 12 subjects with albuminuria using Western blot analyses. Both male and female subjects increased or tended to increase the excretion of these proteins in their urinary exosomes upon developing albuminuria, but female subjects demonstrated stronger correlations between the excretion of these proteins and urine albumin creatinine ratio (UACR) compared to male subjects. In contrast, exosomal excretion of Tamm-Horsfall protein, β-actin and SHP-1 was independent of albuminuria. These findings provide a foundation for a time-course study to determine whether increases in the levels of these proteins precede the onset of albuminuria in patients, which will help determine the potential of these proteins as biomarkers for early detection of SCN. [ABSTRACT FROM AUTHOR]
- Published
- 2024
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