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24 results on '"Gu, Huajian"'

5. Fractalkine modulates pulmonary angiogenesis and tube formation by modulating CX3CR1 and growth factors in PVECs

Author

Liao Jun, Yang Xianwu, Yang Jiejie, Xiao Jingjing, Liu Xuyang, Zhuo Yingquan, Yang Jiafei, and Gu Huajian

Subjects
fractalkine, cx3cr1, hepatopulmonary syndrome, tube formation, macrophages, Biology (General), QH301-705.5
Abstract

This study aimed to investigate effects of pulmonary fractalkine (FKN/CX3CL1) on angiogenesis and tube formation. Tube forming capability of pulmonary vascular endothelial cells (PVECs) was evaluated. CCK-8 assay was used to evaluate proliferation of PVECs. RT-PCR assay was used to determine angiogenesis specific biomarkers. Western blot was applied to identify CX3CR1, Akt, phosphorylated Akt (p-Akt), Erk1/2, phosphorylated Erk1/2 (p-Erk1/2), vascular endothelial growth factor A (VEGFA), and inducible nitric oxide synthase (iNOS) expression. VEGF-A and platelet-derived growth factor (PDGF) levels were examined using ELISA. FKN was safe and triggered tube formation in PVECs. FKN significantly enhanced VEGF-A, PDGF, and iNOS gene transcription compared to the Control group (p < 0.05). CX3CR1 interfering (LV5-CX3CR1 shRNA) remarkably reduced CX3CR1 expression compared to those in LV5 blank group (p < 0.05). Ratios of p-Akt/Akt and p-Erk/Erk were significantly decreased in CX3CR1 shRNA-treated PVECs administered Akt inhibitor (or Erk inhibitor) and 10 ng/mL FKN compared to CX3CR1 shRNA-treated PVECs administered 10 ng/mL FKN (p < 0.05). FKN increased VEGF-A and iNOS expression through activating Akt/Erk pathway. FKN promoted VEGF-A/iNOS expression and triggered p-Akt/Akt and p-Erk/Erk pathway through modulating CX3CR1. FKN-treated macrophages enhanced activation of Akt/Erk pathway. FKN-treated macrophages enhanced PDGF and VEGF-1 expression in PVECs. FKN modulated pulmonary angiogenesis and tube formation through modulating CX3CR1 and growth factors and activating p-Akt/Akt and p-Erk/Erk signaling pathway.

Published
2023
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7. Whole-Course Intraperitoneal Robot-Assisted Choledochal Cyst Excision with a Hidden Incision in Children Under 1 Year Old.

Author

Zhuo, Yingquan, Yang, Xianwu, Du, Jun, Jiang, Hua, Sun, Xu, Chen, Guangtang, He, Kunfeng, Zhang, Wengqi, Liao, Jun, and Gu, Huajian

Abstract

Background: Whole-course intraperitoneal robot-assisted choledochal cyst resection in children under 1 year of age is controversial due to its technical challenges. Current Pfannenstiel incision is widely used in adults for its cosmetic effects but is rarely used in children. Materials and Methods: We conducted a prospective, single-center study to assess the feasibility, safety, and cosmesis of whole-course intraperitoneal robot-assisted choledochal cyst resection with Pfannenstiel incision in children under 1 year of age. Results: Ten patients were treated with our surgical protocol, and there was no conversion to laparotomy. The average total operation time was 223 minutes. The average duration of anesthesia was 260.2 minutes. The average docking time between the robot arm and Trocar was 17.5 minutes. The average intraoperative blood loss was 16 mL. No postoperative complications occurred in the 10 patients. The mean time to start drinking water after surgery was 2.4 days. The mean postoperative drainage tube removal time was 2.6 days. The average length of stay was 8.5 days. The scar assessment scale total scores of the 2 observers were (6.8 ± 1.23) and (7.4 ± 1.84), respectively. For every patient, there are only four abdominal surgery scars of which 75% of scars were hidden by underpants and 25% of scars were not covered. Conclusion: It is feasible and safe to perform whole-courses intraperitoneal robot-assisted choledochal cyst resection with Pfannenstiel incision in children under 1 year old. It also has a hidden incision effect and is worthy of promotion. [ABSTRACT FROM AUTHOR]

Published
2024
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12. Fluorescence in situ hybridization-based confirmation of acute graft-vs-host disease diagnosis following liver transplantation: A case report

Author

Hai-Tao Zhu, Jing-Jing Xiao, Li Haiyang, Jun Liao, Chao Lv, Gu Huajian, Zuo Shi, Di Wu, and Jin-Yu Ma

Subjects
Pathology, medicine.medical_specialty, Liver transplantation, medicine.diagnostic_test, business.industry, medicine.medical_treatment, Fluorescence in situ hybridization cytogenetics, Disease, Chimerism, Surgery, surgical procedures, operative, Graft-vs-host disease, Diagnosis, Case report, medicine, business, Host disease, Fluorescence in situ hybridization
Abstract

BACKGROUND Although acute graft-vs-host disease (aGvHD) is a rare complication of liver transplantation, it is poorly understood and has an extremely high mortality rate. No standardized diagnostic criteria or treatment regimens currently exist. CASE SUMMARY The present study investigated the etiology, diagnosis, and treatment of aGvHD following liver transplantation. Presentation, diagnosis, disease course, histology, and treatment of an aGvHD case are reported, and associated literature is reviewed. A 64-year-old female required LTx due to primary biliary cirrhosis. The donor was a 12-year-old male. Three weeks following liver transplantation, the recipient developed pyrexia, diarrhea, rashes, and antibiotic-unresponsive pancytopenia. Clinical symptoms together with laboratory investigations suggested a diagnosis of aGvHD, which was confirmed via peripheral blood fluorescent in situ hybridization. Donor XY chromosome fluorescent in situ hybridization indicating early chimerism achieved 93% sensitivity in the detection of GvHD. Existing immunosuppressants were discontinued, and high-dose intravenous methylprednisolone was initiated along with antibiotics. While diarrhea resolved, the patient’s general condition continued to deteriorate until demise due to multi-system organ failure at 37 d post-liver transplantation. This case illustrates the life-threatening nature of aGvHD. CONCLUSION Herein, we have summarized a post-LTx aGvHD case and reviewed associated literature in order to increase awareness and provide potentially risk-mitigating recommendations.

Published
2021

16. CX3CR1 regulates angiogenesis and activation of pro-angiogenic factors and triggers macrophage accumulation in experimental hepatopulmonary syndrome model

Author

Yang Xianwu, Gu Huajian, Wu Changhao, Zuo Shi, Jun Liao, Ran Xun, Gu Lelin, Xiansong Feng, Li Haiyang, and Haiyuan Liu

Subjects
Male, 0301 basic medicine, MAPK/ERK pathway, Angiogenesis, CX3C Chemokine Receptor 1, Mice, 03 medical and health sciences, 0302 clinical medicine, CX3CR1, Animals, Medicine, Macrophage, CX3CL1, Protein kinase B, Neovascularization, Pathologic, Hepatology, biology, business.industry, Macrophages, Gastroenterology, Mice, Inbred C57BL, Disease Models, Animal, 030104 developmental biology, 030220 oncology & carcinogenesis, biology.protein, Cancer research, Immunohistochemistry, business, Platelet-derived growth factor receptor, Hepatopulmonary Syndrome
Abstract

Objective Prevalence of hepatopulmonary syndrome (HPS) ranges from 4% to 47% in patients with cirrhosis. This study aimed to explore possible relationship between CX3CR1 and angiogenesis or macrophage accumulation in pathological process of HPS. Material and methods Wide-type C57Bl/6 mice were divided into WT-sham, WT-common bile duct ligation (WT-CBDL), WT-CBDL plus antibody (WT-CBDL + Ab) and WT-CBDL plus Bevacizumab. The CX3CR1GFP/GFP mice were grouping into CX3CR1 GFP/GFP-sham, CX3CR1 GFP/GFP-CBDL and CX3CR1 GFP/GFP-CBDL + Bevacizumab group. Intrapulmonary expression of Akt, pAkt, ERK, pERK, iNOS, VEGF, PDGF was measured using biological technology. Hematoxylin-eosin (H&E) staining and immunohistochemical analysis were used to evaluate changes of pulmonary tissues including pathological abnormality, angiogenesis and macrophage accumulation. Results Blockade CX3CR1 pathway inhibited angiogenesis, macrophage accumulation and pathological changes of lung tissues. Blockade of CX3CR1 pathway reduced pAkt, pERK, iNOS, PDGF and VEGF activation. CX3CR1 contributed to the process of angiogenesis and activate the pro-angiogenic factors. CX3CR1 deficiency obviously reduced the macrophage accumulation. Inhibition of VEGF by Bevacizumab improved intrapulmonary angiogenesis and pathological changes of lung tissues. Inhibition of VEGF by Bevacizumab retarded the production of pAKt, PDGF, and iNOS. Inhibition of VEGF by Bevacizumab reduced CX3CL1 production. Conclusion CX3CR1 could regulate the angiogenesis and activation of pro-angiogenic factors, including pAKT, pERK, iNOS, VEGF and PDGF in the process of hepato-pulmonary syndrome. Moreover, CX3CR1 could also contribute to the macrophage accumulation.

Published
2021

20. Effect of sodium silicate on the performance of high fluidity potassium and magnesium phosphate cement paste.

Author

GU Huajian, YANG Jianming, WU Qing, and WANG Qi

Abstract

This paper investigated the influence of sodium silicate on the mechanical and physical performance and microstructure of high fluidity potassium and magnesium phosphate cement(MKPC) through testing its paste fluidity, strength, temperature change, volume deformation, water resistance and micromorphology. The results indicated that water glass solution can greatly increase the fluidity of MKPC without losing the characteristics of fast hardening and early strength, at the same time, it can increase strength, make the structure denser and improve the water resistance. [ABSTRACT FROM AUTHOR]

Published
2019

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