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10 results on '"Qin, Xinfang"'

2. Sparse Coding of Deep Residual Descriptors for Vein Recognition

Author

Shen, Zhengwen, Qin, Xinfang, Pan, Zaiyu, Wang, Jun, Goos, Gerhard, Founding Editor, Hartmanis, Juris, Founding Editor, Bertino, Elisa, Editorial Board Member, Gao, Wen, Editorial Board Member, Steffen, Bernhard, Editorial Board Member, Yung, Moti, Editorial Board Member, Jia, Wei, editor, Kang, Wenxiong, editor, Pan, Zaiyu, editor, Ben, Xianye, editor, Bian, Zhengfu, editor, Yu, Shiqi, editor, He, Zhaofeng, editor, and Wang, Jun, editor

Published
2023
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7. Nanobody-Based Bispecific Neutralizer for Shiga Toxin-Producing E. coli

Author

Afd Chemical Biology and Drug Discovery, Chemical Biology and Drug Discovery, Lu, Zhongkai, Liu, Zhicheng, Li, Xia, Qin, Xinfang, Hong, Haofei, Zhou, Zhifang, Pieters, Roland J., Shi, Jie, Wu, Zhimeng, Afd Chemical Biology and Drug Discovery, Chemical Biology and Drug Discovery, Lu, Zhongkai, Liu, Zhicheng, Li, Xia, Qin, Xinfang, Hong, Haofei, Zhou, Zhifang, Pieters, Roland J., Shi, Jie, and Wu, Zhimeng

Published
2022

8. Repurposing the Pentameric B-Subunit of Shiga Toxin for Gb3-Targeted Immunotherapy of Colorectal Cancer by Rhamnose Conjugation

Author

Afd Chemical Biology and Drug Discovery, Chemical Biology and Drug Discovery, Liu, Zhicheng, Li, Xia, Lu, Zhongkai, Qin, Xinfang, Hong, Haofei, Zhou, Zhifang, Pieters, Roland J., Shi, Jie, Wu, Zhimeng, Afd Chemical Biology and Drug Discovery, Chemical Biology and Drug Discovery, Liu, Zhicheng, Li, Xia, Lu, Zhongkai, Qin, Xinfang, Hong, Haofei, Zhou, Zhifang, Pieters, Roland J., Shi, Jie, and Wu, Zhimeng

Published
2022

9. Nanobody-Based Bispecific Neutralizer for Shiga Toxin-Producing

Author

Lu, Zhongkai, Liu, Zhicheng, Li, Xia, Qin, Xinfang, Hong, Haofei, Zhou, Zhifang, Pieters, Roland J., Shi, Jie, Wu, Zhimeng, Afd Chemical Biology and Drug Discovery, Chemical Biology and Drug Discovery, Afd Chemical Biology and Drug Discovery, and Chemical Biology and Drug Discovery

Subjects
STEC, Infectious Diseases, Shiga-Toxigenic Escherichia coli, intimin, Hemolytic-Uremic Syndrome, Humans, Gb3, Shiga toxin, Shiga Toxins, bispecific nanobody, Escherichia coli Infections, Shiga Toxin
Abstract

Currently, no specific therapeutics are available for foodborne Shiga toxin-producing Escherichia coli (STEC) infections that cause severe gastroenteritis and life-threatening complications of hemolytic uremic syndrome (HUS). As STEC attachment to intestinal epithelium might increase the host absorption of Shiga toxins and severity of the disease, we were inspired to develop a bispecific neutralizer capable of blocking its Shiga toxin and adhesin intimin simultaneously. Two nanobodies against the B subunit of Shiga toxin 2 (Stx2B) and the C terminus of Intimin (IntC280) were genetically fused together as the bispecific neutralizer, and it can be efficiently produced in a conventional E. coli expression system. We demonstrated that each of the nanobody modules in the bispecific format showed increased antigen binding capability and was able to functionally neutralize the binding of Stx2B or IntC280 to the respective host receptors even in the presence of the two virulence factors together. Moreover, the bispecific neutralizer was relatively stable to harsh storage conditions and gastrointestinal pH extremes. Taking into account its easy and economical production and superior pharmaceutical properties, we believe that a nanobody-based bispecific neutralizer would be more favorable and practical to be developed as a therapeutic to fight STEC in the developing world.

Published
2022

10. Clinical and pathological correlation between urinary exosome miR-223 and IgAN patients.

Author

Song J, Qin X, Li H, Huang G, and Bi H

Subjects
Humans, Biomarkers urine, Urinary Tract, Exosomes genetics, Exosomes metabolism, Exosomes pathology, Glomerulonephritis, IGA genetics, Glomerulonephritis, IGA pathology, MicroRNAs
Abstract

Objective: To investigate the association between urine exosome miR-223 and clinical markers with pathological severity of IgA nephropathy (IgAN) in order to offer a new perspective for the evaluation of IgAN patients., Materials and Methods: Western blotting and transmission electron microscopy were used to identify the exosomes collected and isolated from subjects' urine. qRT-PCR was then performed to determine the expression level of miR-223. Following that, the relationship between miR-223 expression, clinical markers, and the severity of pathology in IgAN patients was examined., Results: (1) Urine can be used to isolate exosomes since its marker protein was visible by Western blotting, and its size and structure were observable using transmission electron microscopy. (2) Expression levels of miR-223 in urinary exosomes were much higher in IgAN patients than in healthy subjects, and these were also positively correlated with creatinine (Cr) (rho = 0.396; p = 0.006), blood urea nitrogen (BUN) (rho = 0.371; p = 0.011), 24-hour urinary microalbumin (24hU-mALB) (rho = 0.341; p = 0.036), mesangial cell proliferation (rho = 0.359; p = 0.014), glomerular segmental sclerosis (rho = 0.417; p = 0.004), cell/fibroblast crescents (rho = 0.612; p = 0.000), glomerulosclerosis, and renal interstitial fibrosis (rho = 0.331; p = 0.025)., Conclusion: In urine exosomes, miR-223 might be considered a non-invasive biomarker for the assessment of IgAN disease progression.

Published
2023
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