Rui-Juan Xin
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Rui-Juan Xin has a total of 11 co-authors. Here are the top co-authors by number of shared publications:
- Feihu Bai
Department of Gastroenterology, The Second Affiliated Hospital of Hainan Medical University, Haikou, China
2 shared publications - Fang-Rui Hu
Department of Gastroenterology, People’s Hospital of Ningxia Hui Autonomous Region, Yinchuan, Ningxia Hui Autonomous Region, China
1 shared publication - Li Yao
Department of Laboratory Medicine The Second People's Hospital of Lianyungang Lianyungang China
1 shared publication Lirong Mo
Department of Basic Medicine, Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region 750004, P.R. China
1 shared publicationMengna Jiu
Department of Gastroenterology, Ankang Central Hospital, Ankang, Shanxi 725000, P.R. China
1 shared publication- Ming Luo
Department of Hepatobiliary Oncology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, State Key Laboratory of Druggability Evaluation and Systematic Translational Medicine, Tianjin Key Laboratory of Digestive Cancer, Tianjin’s Clinical Research Center for Cancer, Tianjin, China
1 shared publication
Latest Publications
- 3 August 2022
- Published by Taylor & Francis in Expert Review of Gastroenterology & Hepatology
- Vol. 16 (8) , 797-807
Altered gut microbiota is associated with sleep disturbances in patients with minimal hepatic encephalopathy caused by hepatitis B-related liver cirrhosis
Increasing spread by SARS-CoV-2 Omicron variants challenges existing vaccines and broadly reactive neutralizing antibodies (bNAbs) against COVID-19. Here we determine the diversity, potency, breadth and structural insights of bNAbs derived from memory B cells of BNT162b2-vaccinee after homogeneous Omicron BA.1 breakthrough infection. The infection activates diverse memory B cell clonotypes for generating potent class I/II or III bNAbs with new epitopes mapped to receptor-binding domain (RBD). The top eight bNAbs neutralize wildtype and BA.1 potently but display divergent IgH/IgL sequences and neuralization profiles against other variants of concern (VOCs). Two of them (P2D9 and P3E6) belonging to class III NAbs display comparable potency against BA.4/BA.5, although structural analysis reveals distinct modes of action. P3E6 neutralizes all variants tested through a unique bivalent interaction with two RBDs. Our findings provide new insights into hybrid immunity on BNT162b2-induced diverse memory B cells in response to Omicron breakthrough infection for generating diverse bNAbs with distinct structural basis.
- 3 August 2022
- Published by Taylor & Francis in Expert Review of Gastroenterology & Hepatology
- Vol. 16 (8) , 797-807
Altered gut microbiota is associated with sleep disturbances in patients with minimal hepatic encephalopathy caused by hepatitis B-related liver cirrhosis
Increasing spread by SARS-CoV-2 Omicron variants challenges existing vaccines and broadly reactive neutralizing antibodies (bNAbs) against COVID-19. Here we determine the diversity, potency, breadth and structural insights of bNAbs derived from memory B cells of BNT162b2-vaccinee after homogeneous Omicron BA.1 breakthrough infection. The infection activates diverse memory B cell clonotypes for generating potent class I/II or III bNAbs with new epitopes mapped to receptor-binding domain (RBD). The top eight bNAbs neutralize wildtype and BA.1 potently but display divergent IgH/IgL sequences and neuralization profiles against other variants of concern (VOCs). Two of them (P2D9 and P3E6) belonging to class III NAbs display comparable potency against BA.4/BA.5, although structural analysis reveals distinct modes of action. P3E6 neutralizes all variants tested through a unique bivalent interaction with two RBDs. Our findings provide new insights into hybrid immunity on BNT162b2-induced diverse memory B cells in response to Omicron breakthrough infection for generating diverse bNAbs with distinct structural basis.
- Open Access
- 19 April 2018
- Published by Spandidos Publications in Molecular Medicine Reports
- Vol. 17 (6) , 8145-8152
miR‑29a‑3p represses proliferation and metastasis of gastric cancer cells via attenuating HAS3 levels
MicroRNA‑29a (miR‑29a) has recently been in the spotlight as a tumor suppressor whose encoding gene is frequently suppressed in cancers. The aim of the present study was to investigate the biological functions and underlying molecular mechanism by which miR‑29a‑3p suppresses gastric cancer peritoneum metastasis. Cell proliferation, colony‑forming, wound healing and Transwell migration assays were performed in the present study. MiR‑29a‑3p expression was markedly decreased in gastric cancer cell lines with stronger metastatic potential. Silencing miR‑29a‑3p expression promoted gastric cancer cell proliferation, colony‑forming, migration and invasion. By contrast, overexpression of miR‑29a‑3p inhibited these biological phenotypes. In addition, it was revealed that miR‑29a‑3p functioned through downregulating hyaluronan synthase 3 expression. Collectively, dysregulated miR‑29a‑3p expression in gastric cancer cells was associated with malignant properties primarily relevant to migration and metastasis. The results suggest that miR‑29a‑3p may be a potential therapeutic target for gastric cancer.
- 19 April 2018
- Published by Spandidos Publications in Molecular Medicine Reports
- Vol. 17 (6) , 8145-8152
Open AccessmiR‑29a‑3p represses proliferation and metastasis of gastric cancer cells via attenuating HAS3 levels
MicroRNA‑29a (miR‑29a) has recently been in the spotlight as a tumor suppressor whose encoding gene is frequently suppressed in cancers. The aim of the present study was to investigate the biological functions and underlying molecular mechanism by which miR‑29a‑3p suppresses gastric cancer peritoneum metastasis. Cell proliferation, colony‑forming, wound healing and Transwell migration assays were performed in the present study. MiR‑29a‑3p expression was markedly decreased in gastric cancer cell lines with stronger metastatic potential. Silencing miR‑29a‑3p expression promoted gastric cancer cell proliferation, colony‑forming, migration and invasion. By contrast, overexpression of miR‑29a‑3p inhibited these biological phenotypes. In addition, it was revealed that miR‑29a‑3p functioned through downregulating hyaluronan synthase 3 expression. Collectively, dysregulated miR‑29a‑3p expression in gastric cancer cells was associated with malignant properties primarily relevant to migration and metastasis. The results suggest that miR‑29a‑3p may be a potential therapeutic target for gastric cancer.