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6. Performance comparison of two nucleic acid amplification systems for SARS‐CoV‐2 detection: A multi‐center study

Author

Mo, Chan, primary, Lo, Kamfai, additional, He, Ying, additional, Peng, Bo, additional, Guo, Feifan, additional, Zheng, Zhou, additional, Jiang, Ruiwei, additional, Cai, Yihua, additional, Li, Yumin, additional, Guo, Dongyue, additional, Zhang, Bing, additional, Ou, Tong, additional, Xiong, Dan, additional, and Zhang, Xiuming, additional

Published
2022
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9. Outbreak of acute respiratory disease caused by human adenovirus type 7 and human coronavirus‐229E in Zhejiang Province, China

Author

Liu, Shelan, primary, Cai, Jian, additional, Li, Yumin, additional, Ying, Lihong, additional, Li, Huan, additional, Zhu, An, additional, Li, Lin, additional, Zhu, Haiying, additional, Dong, Shengcao, additional, Ying, Ruyao, additional, Chan, Ta‐Chien, additional, Wu, Hanting, additional, Pan, Jinren, additional, and Chen, Yin, additional

Published
2022
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12. Prediction of progression of chronic atrophic gastritis with Helicobacter pylori and poor prognosis of gastric cancer by CYP3A4

Author

Zhang, Fan, Wang, Furong, Chen, Cong, Wang, Tianyu, Hu, Jike, Su, Ruiliang, Li, Xuemei, Gu, Baohong, Tang, Shaojun, Chen, Hao, Li, Yumin, Zhang, Fan, Wang, Furong, Chen, Cong, Wang, Tianyu, Hu, Jike, Su, Ruiliang, Li, Xuemei, Gu, Baohong, Tang, Shaojun, Chen, Hao, and Li, Yumin

Abstract

Background and Aim It has been well documented that Helicobacter pylori (H. pylori) infection is a risk factor for aggravating gastric mucosal atrophy. However, the exact molecular mechanism mediating this process is not fully elucidated. The purpose of this study was to identify biomarkers, which may predict the risk for progression of chronic atrophic gastritis (CAG) with H. pylori. Methods GSE27411 was downloaded from the Gene Expression Omnibus. The differentially expressed genes (DEGs) between H. pylori-infected samples without CAG and H. pylori-infected CAG samples were analyzed. Gene Ontology and pathway enrichment analyses were performed, followed by protein–protein interaction network construction. We used immunohistochemistry analysis to identify DEGs in 20 chronic gastritis, 20 CAG, and 22 gastric cancer (GC) specimens. Results A total of 303 upregulated and 26 downregulated DEGs were identified. The pathways enriched by upregulated DEGs were mainly related to fat digestion and absorption, peroxisome proliferator-activated receptor signaling pathway, and chemical carcinogenesis. Cytochrome P450, family 3, subfamily A, polypeptide 4 (CYP3A4) had the highest degrees in protein–protein interaction network. Moreover, the positive rates of CYP3A4 protein expression in chronic gastritis, CAG, and GC were 10% (2/20), 55% (11/20), and 77.3% (17/22), respectively (P < 0.001). The Kaplan–Meier analysis revealed that elevated expression of CYP3A4 was significantly associated with worse overall survival and first progression, respectively (P < 0.0001). Conclusion According to the findings of this study, the expression of CYP3A4 might be related to the potential carcinogenic transformation of CAG to GC. Therefore, CYP3A4 may be biomarkers to predict progression of CAG and poor prognosis of gastric cancer.

Published
2020

20. Theoretical Studies on the Mechanism of Hydrolysis of Nitroguanidine by AM1 Method

Author

Li Yumin, Li Yong-Fu, and Xiao Heming

Subjects
Hydrolysis, chemistry.chemical_compound, Nitroguanidine, chemistry, Stereochemistry, General Chemical Engineering, General Chemistry, Medicinal chemistry
Abstract

The mechanism of hydrolysis of nitroguanidine has been studied theoretically. The molecular geometries have been fully optimized at AM1 level of theory for reagent, activated and product complexes for hydrolysis of nitroguanidine in neutral, acidic and alkaline media, respectively. In neutral and acidic media, both activated complexes have four-membered ring structures, and the reaction-coordinated eigenvectors show heavy-atom reorganization and proton transfer to be truly concerted in both cases. In alkaline medium, the hydrolysis also involves activated complex. The calculated activation energies for the hydrolysis of nitroguanidine in neutral, acidic and alkaline media are 278.2 kJ/mol, 330.2 kJ/mol and 213.0 kJ/mol, respectively. Der Mechanismus der Hydrolyse von Nitroguanidin wurde rechnerisch untersucht. Die Molekul-Geometrien wurden voll optimiert auf das Niveau der AM1-Theorie fur die reagierenden, aktivierten und Produkt-Komplexe der Hydrolyse des Nitroguanidins in neutralem, saurem und alkalischem Medium. In neutralem und saurem Medium haben die beiden aktivierten Komplexe eine 4-gliedrige Ringstruktur und die mit der Reaktion koordinierten Eigenvektoren zeigen Umordnung der schweren Atome und Protonenubertragung, was in beiden Fallen tatsachlich gleichzeitig verlaufen mus. Auch im alkalischen Medium entstehen bei der Hydrolyse aktivierte Komplexe. Die berechneten Aktivierungsenergien fur die Hydrolyse des Nitroguanidins in neutralem, saurem und alkalischem Medium betragen jeweils 278,2 kJ/mol, bzw. 330,2 kJ/mol, bzw. 213,0 kJ/mol. Le mecanisme d'hydrolyse de la nitroguanidine a ete etudie de facon theorique. Les geometries moleculaires ont ete totalement optimisees au niveau de la theorie AM1 pour les complexes reactants, actives et de produits pour l'hydrolyse de la nitroguanidine en milieu respectivement neutre, acide et alcalin. En milieu neutre et acide, les deux complexes actives ont des structures annulaires a 4 membres, et les vecteurs propres coordonnes a la reaction presentent une reorganisation des atomes lourds et un transfert de protons, ce qui doit effectivement se produire simultanement dans les deux cas. En milieu alcalin, l'hydrolyse englobe egalement un complexe active. Les energies d'activation calculees pour l'hydrolyse de nitroguanidine en milieux neutre, acide et alcalin sont respectivement de 278,2 kJ/mol, et 330 kJ/mol et 213,0 kJ/mol.

Published
1998

27. Current status and perspectives in environmental oncology.

Author

Liu J, Gan T, Hu W, and Li Y

Abstract

Cancer stands as a leading global cause of death, with its etiology characterized by complexity and multifaceted factors. Growing research indicates a strong correlation between environmental factors and cancer incidence, underscoring the critical importance of intervening in environmental risk factors to mitigate cancer occurrence. Despite this, specialized research institutions focusing on the intersection of environment and cancer remain scarce, with global investment in cancer prevention significantly trailing behind efforts in diagnosis and treatment. Against the backdrop of rapid global climate change, industrialization, urbanization, aging populations, and the globalization of lifestyles, we proposed the concept of Environmental Oncology (EO) to address these challenges. We discussed the rationale and necessity of developing EO and presented a comprehensive research framework focusing on cancer prevention and treatment. Future EO research will aim to identify cancer causes and implement early prevention strategies using advanced scientific technologies and methods. By emphasizing multidisciplinary collaboration and integrating molecular biology at the micro level, EO will explore the relationship between external and internal environments and cancer. EO will identify potential therapeutic targets by studying the pathways through which environmental exposures lead to carcinogenesis. EO will develop early warning systems and disseminate research findings by collecting big data, employing robust statistical models, and establishing research centers., Competing Interests: The authors declare no conflict of interest., (© 2024 The Author(s). Chronic Diseases and Translational Medicine published by John Wiley & Sons Ltd on behalf of Chinese Medical Association.)

Published
2024
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