Analytical Methods
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2025
·
IF 2.6
Xiulei Xiong,Haihua Shen,Songnan Liu,Fei Rong,Jian Dong
To detect H2O2 and redox potential of an acute wound simultaneously, a SERS-active microneedle was fabricated by integrating H2O2 and redox potential SERS probes in two grooves of an acupuncture needle, respectively. When the SERS-active microneedle was inserted into tissues, an acute wound formed and the two SERS probes were brought into the wound to sense H2O2 and redox potential of the wound. The feasibility of the SERS-active microneedle was evaluated ex vivo and in vivo. Both sugar deficiency and sugar excess induce the increases of H2O2 and redox potential in most tissues. Short-term physiological disturbances eventually returned to normal levels in healthy organisms, and abnormal sugar intakes disrupt the normal physiological environment and induce stress response in all tissues. The SERS-active microneedle for detection of H2O2 and redox potential would become a powerful tool, used for collecting physiological signals in different tissues to elucidate the mechanisms of wound healing and redox-related diseases.
研究领域:
生物医学工程
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分析化学
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病理学
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DOI
PubMed
高影响因子
JOURNAL OF CHROMATOGRAPHY A
·
2024
·
IF 3.8
Lei Zhang,Xu Liu,Tenghui Jin,Jing Dong,Xiaodong Li,Youyi Zhang,Dongyang Liu
Some bile acids (BAs) were considered as biomarkers or have therapeutical effect on metabolic diseases. However, due to the existence of isomers and limitations in sensitivity, simultaneous quantification of multiple BAs remains a challenge. The aim of this study is to establish an accurate and sensitive method for the determination of multiple BAs with similar polarity. A LC-MS/MS analytical method capable of quantifying forty-five BAs simultaneously using nine stable isotope internal standards was developed and fully validated based on key isomers-oriented separation strategy. The method was further applied to analyze plasma samples to describe the dynamic profile of BAs after high glucose intake. The chromatography and mass spectrum conditions were optimized to enable the accurate quantification of forty-five BAs, while ensuring the lower limit of quantification between 0.05–10 ng/mL. The results of system suitability, linearity, dilution integrity, accuracy and precision demonstrated the good quantitative capacity and robustness of the method. A total of thirty-five BAs were quantified in plasma samples from twelve healthy Chinese individuals. The established method featured superior sensitivity and better separation efficiency compared to previous studies. Meanwhile, BAs exhibited correlations with glucose and insulin, suggesting their potential as biomarkers for metabolic disorders.
研究领域:
分析化学
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生物化学
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代谢组学
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临床化学
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PubMed
高影响因子
Nature Microbiology
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2025
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IF 19.4
Yuan Chen,Hullahalli Karthik,Huang Hao,Zhao Siqi,Wang Wenqing,Tian Xingyu,Li Xin,Xia Linya,Wang Yuchang,Pan Fei,Liang Ying,Xie Yurui,Li Yue,Fan Hongjie,Waldor Matthew K.,Ma Zhe
Proliferation of the emerging zoonotic pathogen Streptococcus equi subsp. zooepidemicus in the meninges is linked to mortality in pigs and morbidity in humans. The mechanisms underlying the remarkable capacity of hypervirulent S. zooepidemicus to proliferate in cerebrospinal fluid (CSF) are largely undefined. Here, using genetically barcoded S. zooepidemicus , we found that following systemic infection of mice, only ~1–10 S. zooepidemicus clones invade the meninges where they subsequently replicate ~10 7 -fold. Subsequent transposon insertion sequencing experiments, plus validation work with bacterial mannose phosphotransferase system (PTS man )-defective strains, identified the PTS man , which imports glucose, as essential for S. zooepidemicus proliferation in CSF. The S. zooepidemicus PTS man promoter confers species-specific constitutive transcription of PTS man , enabling glucose acquisition at low glucose concentrations and limiting activation of the stringent response, leading to pathogen replication in CSF. Our findings reveal how the rewiring of PTS man in the control of S. zooepidemicus metabolism enables this pathogen to adapt to and replicate in CSF during meningitis.
研究领域:
微生物学
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传染病学
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细菌致病机制
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代谢调控
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PubMed
高影响因子
Signal Transduction and Targeted Therapy
·
2025
·Vol. 10
·期 1
·1-20
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IF 52.7
Ma Xiao,Chen Jiao,Wang Fang,Fan Xinzou,Li Zhenhong,Liang Hantian,Cheng Hao,Nan Fang,Lin Yubin,Song Xiaoshuang,Zhang Jianan,Gao Fan,Zhang Wei,Jin Wenwen,Zhang Huiyuan,Tong Jiyu,Jiang Hong,Zhou Xikun,Zou Qiang,Hu Hongbo,Tong Aiping,Chen WanJun,Zhang Dunfang
The intake of sugars, especially glucose and fructose, has significantly increased with the change of lifestyle. Excessive intake of sugar has been proven to be associated with tumors and inflammatory diseases. Fructose directly mediates innate immune responses; however, whether it can directly regulate T-cell immunity remains unknown. We show that high fructose consumption accelerates the development of inflammatory bowel disease (IBD) by promoting the generation of T helper 1 (Th1) and T helper 17 (Th17) cells. It was demonstrated that fructose promotes the differentiation of Th1 and Th17 cells directly by enhancing mechanistic target of rapamycin complex 1 (mTORC1) activation through the glutamine metabolism-dependent pathway. Reactive oxygen species (ROS)-induced activation of transforming growth factor-β (TGF-β) is also involved in fructose-induced Th17 cell generation. Moreover, metformin can reverse Th1 and Th17 cell generation induced by fructose by suppressing mTORC1 activation and reducing ROS-mediated TGF-β activation. Finally, we identified metformin as an in vivo therapeutic drug for relieving high fructose consumption-induced T-cell inflammation and colitis aggravation. Our study revealed a previously unknown adverse effect of high fructose consumption in disrupting immune homeostasis and exacerbating IBD by directly promoting T-cell immunity, and showed metformin is a potential therapeutic for reversing the T cell immune imbalance caused by long-term high fructose consumption.
研究领域:
免疫学
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营养学
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细胞生物学
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代谢
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胃肠病学
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药理学
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PubMed
高影响因子
Biomaterials Science
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2024
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IF 5.8
Yu Xia,Ming-Kang Zhang,Jing-Jie Ye,Mei-ting Niu,Xin-yi Dai,Zi-yang Wang,Zhi-ling He,Jun Feng
Metabolic disorders of cancer cells create opportunities for metabolic interventions aimed at selectively eliminating cancer cells. Nevertheless, achieving this goal is challenging due to cellular plasticity and metabolic heterogeneity of cancer cells. This study presents a dual-drug-loaded, macrophage membrane-coated polymeric nanovesicle designed to reprogram cancer metabolism with high specificity through integrated extracellular and intracellular interventions. This nanoformulation can target cancer cells and largely reduce their glucose intake, while the fate of intracellular glucose internalized otherwise is redirected at the specially introduced oxidation reaction instead of inherent cancer glycolysis. Meanwhile, it inhibits cellular citrate intake, further reinforcing metabolic intervention. Furthermore, the nanoformulation causes not only H2O2 production but also NADPH down-regulation, intensifying Redox damages to cancer cells. Consequently, this nanoformulation displays highly selective toxicity to cancer cells and minimal harms to normal cells mainly due to metabolic vulnerability of the former. Once administrated into tumor-bearing mice, this nanoformulation is found to induce the transformation of pro-tumor tumor associated macrophages into the tumor-suppressive phenotype and completely inhibit tumor growth with favourable biosafety.
研究领域:
癌症生物学
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纳米技术
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药物科学
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生物医学工程
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高影响因子
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