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Your search keyword '"Li, Huangyuan"' showing total 226 results
Start Over Author "Li, Huangyuan" Publication Type Academic Journals
226 results on '"Li, Huangyuan"'

35. The risk of suicidal intention in severe mental illness: An ecological perspective.

Author

Lin, Yawen, Wei, Qinfei, Luo, Suping, Ye, Xiaoying, Zheng, Fuhao, Zheng, Liuyan, Lu, Xinyue, Li, Huangyuan, and Wu, Siying

Subjects
PSYCHIATRIC diagnosis, AGE distribution, SOCIAL factors, FAMILIES, ECOLOGICAL research, SUICIDAL ideation, RISK assessment, SEVERITY of illness index, CONCEPTUAL structures, SEX distribution, DESCRIPTIVE statistics, FACTOR analysis, RESEARCH funding, LOGISTIC regression analysis
Abstract

Objective: Guided by the ecosystem theory model framework, we aimed to explore the influence of three ecological dimensions (social, family and psychological factors) on suicidal intention in people with severe mental illness (SMI). We hypothesized that three factors influence suicidal intention, and that psychological factors may play a mediating role in the influence of social and family factors on suicidal intention. Methods: We collected 994 patients with SMI aged 18 and above from May 2021 to March 2022 in the Fourth Hospital of Fuzhou City. We used logistic regression to analyse the association between social, family, psychological factors and suicidal intention. Furthermore, we explored the mediating effects among the influencing factors. Results: Younger male patients with schizophrenia were more likely to have suicidal intention due to psychosocial family factors (p <.05). Social factors (poor interpersonal relations, social retreat, social activities outside the home), family factors (parental functions, activities within the family, family functions), psychological factors (anxiety, depression, interest in the outside world, overt aggression, lack of accountability and planning) were all independent risk factors for suicidal intention in patients. Mediation analysis showed anxiety and depression mediated the role of social and family factors on suicidal intention (p <.05). Conclusion: Social, family and psychological factors were important risk factors for suicidal intention, with anxiety and depression being partial mediators for suicidal intention. Therefore, interventions that enhance family and social functioning and reduce anxiety and depression may be effective in reducing suicidal intention in SMI. [ABSTRACT FROM AUTHOR]

Published
2023
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37. Evaluation of neurotoxicity and the role of oxidative stress of cobalt nanoparticles, titanium dioxide nanoparticles, and multiwall carbon nanotubes in Caenorhabditis elegans.

Author

Chen, Cheng, Chen, Jingrong, Lin, Xinpei, Yang, Jiafu, Qu, Huimin, Li, Lisong, Zhang, Duanyan, Wang, Wei, Chang, Xiangyu, Guo, Zhenkun, Cai, Ping, Yu, Guangxia, Shao, Wenya, Hu, Hong, Wu, Siying, Li, Huangyuan, Bornhorst, Julia, Aschner, Michael, and Zheng, Fuli

Subjects
CARBON nanotubes, OXIDATIVE stress, CAENORHABDITIS elegans, TITANIUM dioxide nanoparticles, ENVIRONMENTAL risk assessment, NEUROTOXICOLOGY
Abstract

The widespread use of nanomaterials in daily life has led to increased concern about their potential neurotoxicity. Therefore, it is particularly important to establish a simple and reproducible assessment system. Representative nanomaterials, including cobalt nanoparticles (CoNPs), titanium dioxide nanoparticles (TiO2-NPs), and multiwall carbon nanotubes (MWCNTs), were compared in terms of their neurotoxicity and underlying mechanisms. In 0, 25, 50, and 75 μg/ml of these nanomaterials, the survival, locomotion behaviors, acetylcholinesterase (AchE) activity, reactive oxygen species production, and glutathione-S transferase 4 (Gst-4) activation in wildtype and transgenic Caenorhabditis elegans (C. elegans) were evaluated. All nanomaterials induced an imbalance in oxidative stress, decreased the ratio of survival, impaired locomotion behaviors, as well as reduced the activity of AchE in C. elegans. Interestingly, CoNPs and MWCNTs activated Gst-4 , but not TiO2-NPs. The reactive oxygen species scavenger, N-acetyl- l -cysteine, alleviated oxidative stress and Gst-4 upregulation upon exposure to CoNPs and MWCNTs, and rescued the locomotion behaviors. MWCNTs caused the most severe damage, followed by CoNPs and TiO2-NPs. Furthermore, oxidative stress and subsequent activation of Gst-4 were involved in nanomaterials-induced neurotoxicity. Our study provides a comprehensive comparison of the neurotoxicity and mechanisms of typical nanomaterials, which could serve as a model for hazard assessment of environmental pollutants using C. elegans as an experimental model system. [ABSTRACT FROM AUTHOR]

Published
2023
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45. Oxidation and Antioxidation of Natural Products in the Model Organism Caenorhabditis elegans.

Author

Zhu, An, Zheng, Fuli, Zhang, Wenjing, Li, Ludi, Li, Yingzi, Hu, Hong, Wu, Yajiao, Bao, Wenqiang, Li, Guojun, Wang, Qi, and Li, Huangyuan

Subjects
NATURAL products, CAENORHABDITIS elegans, CAENORHABDITIS, DAMAGE models, DRUG target, OXIDATION, SMALL molecules, TISSUE culture
Abstract

Natural products are small molecules naturally produced by multiple sources such as plants, animals, fungi, bacteria and archaea. They exert both beneficial and detrimental effects by modulating biological targets and pathways involved in oxidative stress and antioxidant response. Natural products' oxidative or antioxidative properties are usually investigated in preclinical experimental models, including virtual computing simulations, cell and tissue cultures, rodent and nonhuman primate animal models, and human studies. Due to the renewal of the concept of experimental animals, especially the popularization of alternative 3R methods for reduction, replacement and refinement, many assessment experiments have been carried out in new alternative models. The model organism Caenorhabditis elegans has been used for medical research since Sydney Brenner revealed its genetics in 1974 and has been introduced into pharmacology and toxicology in the past two decades. The data from C. elegans have been satisfactorily correlated with traditional experimental models. In this review, we summarize the advantages of C. elegans in assessing oxidative and antioxidative properties of natural products and introduce methods to construct an oxidative damage model in C. elegans. The biomarkers and signaling pathways involved in the oxidative stress of C. elegans are summarized, as well as the oxidation and antioxidation in target organs of the muscle, nervous, digestive and reproductive systems. This review provides an overview of the oxidative and antioxidative properties of natural products based on the model organism C. elegans. [ABSTRACT FROM AUTHOR]

Published
2022
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48. Intercellular transfer of mitochondria via tunneling nanotubes protects against cobalt nanoparticle-induced neurotoxicity and mitochondrial damage.

Author

Zheng, Fuli, Luo, Zhousong, Lin, Xinpei, Wang, Wei, Aschner, Michael, Cai, Ping, Wang, Yuan-Liang, Shao, Wenya, Yu, Guangxia, Guo, Zhenkun, Wu, Siying, and Li, Huangyuan

Subjects
MITOCHONDRIA, NANOTUBES, NEUROTOXICOLOGY, COBALT, TUNNEL design & construction, REACTIVE oxygen species, TUBULINS, CELL survival
Abstract

Broad applications of cobalt nanoparticles (CoNPs) have raised increased concerns regarding their potential toxicity. However, the underlining mechanisms of their toxicity have yet to be characterized. Here, we demonstrated that CoNPs reduced cell viability and induced membrane leakage. CoNPs induced oxidative stress, as indicated by the generation of reactive oxygen species (ROS) secondary to the increased expression of hypoxia-induced factor 1 alpha. Moreover, CoNPs led to mitochondrial damage, including generation of mitochondrial ROS, reduction in ATP content, morphological damage and autophagy. Interestingly, exogenous mitochondria were observed between neurons and astrocytes upon CoNPs exposure. Concomitantly, tunneling nanotubes (TNTs)-like structures were observed between neurons and astrocytes upon CoNPs exposure. These structures were further verified to be TNTs as they were found to be F-actin rich and lacking tubulin. We then demonstrated that TNTs were utilized for mitochondrial transfer between neurons and astrocytes, suggesting a novel crosstalk phenomenon between these cells. Moreover, we found that the inhibition of TNTs (using actin-depolymerizing drug latrunculin B) intensified apoptosis triggered by CoNPs. Therefore, we demonstrate, for the first time, that the inhibition of intercellular mitochondrial transfer via TNTs aggravates CoNPs-induced cellular and mitochondrial toxicity in neuronal cells, implying a novel intercellular protection mechanism in response to nanoparticle exposure. [ABSTRACT FROM AUTHOR]

Published
2021
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