1.Effect of Xuebijing Injection on Extracellular Release of HMGB1 Induced by Endotoxin
Ming XU ; Zhaoxia SHUAI ; Guoqian CHEN
International Journal of Traditional Chinese Medicine 2009;31(5):393-394
Objective To investigate the effect of Xuebijing injection on release of high mobility group box 1 (HMGB1) in endotoxin-induced cells. Methods HMGB1 concentration and mRNA expression were analyzed by enzyme-linked immunosorbent assay (ELISA) and RT-PCR, respectively. The effects of Xuebijing injection with 2, 10 and 50 mg/ml on HMGB 1 concentration in the culture medium of 200 ng/ml lipopolysaccharide-induced macrophage-like RAW 264.7 cells and BRL-3A hepatocytes, and HMGB1 mRNA expression in lipopolysaccharide-induced macrophages were observed. Results 50 mg/ml Xuebijing injection significantly decreased HMGB1 concentration in the culture medium of lipopolysaccharide-induced macrophages and hepatocytes(P< 0.01), and inhibited HMGB1 mRNA expression in macrophages. Conclusion Xuebijing injection inhibits endotoxin-induced release of HMGB1.
2.A triage strategy in advanced ovarian cancer management based on multiple predictive models for R0 resection: a prospective cohort study.
Zheng FENG ; Hao WEN ; Zhaoxia JIANG ; Shuai LIU ; Xingzhu JU ; Xiaojun CHEN ; Lingfang XIA ; Junyan XU ; Rui BI ; Xiaohua WU
Journal of Gynecologic Oncology 2018;29(5):e65-
OBJECTIVE: To present the surgical outcomes of advanced epithelial ovarian cancer (AEOC) since the implementation of a personalized approach and to validate multiple predictive models for R0 resection. METHODS: Personalized strategies included: 1) Non-invasive model: preoperative clinico-radiological assessment according to Suidan criteria with a predictive score for all individuals. Patients with a score 0–2 were recommended for primary debulking surgery (PDS, group A), or otherwise were counseled on the choices of PDS, neoadjuvant chemotherapy (NAC, group B) or staging laparoscopy (S-LPS). 2) Minimally invasive model: S-LPS with a predictive index value (PIV) according to Fagotti. Individuals with a PIV < 8 underwent PDS (group C) or otherwise received NAC (group D). Intraoperative assessment (with Eisenkop, peritoneal cancer index [PCI], and Aletti scores) and surgical results were prospectively collected. RESULTS: Between September 2015 and August 2017, 161 pathologically confirmed epithelial ovarian cancer patients were included. A total of 52 (32.3%) patients had a predictive score of 0–2, and 109 (67.7%) patients had a score ≥ 3. Among these individuals, 41 (25.5%) patients received S-LPS. Finally, 110 (68.3%) patients underwent PDS (A+C), and 51 (31.7%) patients received NAC (B+D). The R0 resection rates in PDS and NAC patients were 56.4% and 60.8%, respectively. The area under the curve (AUC) of Suidan criteria was 0.548 for group (A+C). The AUC of Fagotti score was 0.702 for group C. The AUC of Eisenkop, PCI, and Aletti scores were 0.808, 0.797, and 0.524, respectively. CONCLUSION: The Suidan criteria were not effective in these AEOC patients. S-LPS was helpful in decision-making for PDS and should be endorsed in the future.
Area Under Curve
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Cohort Studies*
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Drug Therapy
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Humans
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Laparoscopy
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Ovarian Neoplasms*
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Prospective Studies*
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Research Design
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Triage*
3.Modeling CADASIL vascular pathologies with patient-derived induced pluripotent stem cells.
Chen LING ; Zunpeng LIU ; Moshi SONG ; Weiqi ZHANG ; Si WANG ; Xiaoqian LIU ; Shuai MA ; Shuhui SUN ; Lina FU ; Qun CHU ; Juan Carlos Izpisua BELMONTE ; Zhaoxia WANG ; Jing QU ; Yun YUAN ; Guang-Hui LIU
Protein & Cell 2019;10(4):249-271
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a rare hereditary cerebrovascular disease caused by a NOTCH3 mutation. However, the underlying cellular and molecular mechanisms remain unidentified. Here, we generated non-integrative induced pluripotent stem cells (iPSCs) from fibroblasts of a CADASIL patient harboring a heterozygous NOTCH3 mutation (c.3226C>T, p.R1076C). Vascular smooth muscle cells (VSMCs) differentiated from CADASIL-specific iPSCs showed gene expression changes associated with disease phenotypes, including activation of the NOTCH and NF-κB signaling pathway, cytoskeleton disorganization, and excessive cell proliferation. In comparison, these abnormalities were not observed in vascular endothelial cells (VECs) derived from the patient's iPSCs. Importantly, the abnormal upregulation of NF-κB target genes in CADASIL VSMCs was diminished by a NOTCH pathway inhibitor, providing a potential therapeutic strategy for CADASIL. Overall, using this iPSC-based disease model, our study identified clues for studying the pathogenic mechanisms of CADASIL and developing treatment strategies for this disease.