1.Comparison of stage Ⅰ bronchioloalveolar carcinoma and adenocarcinoma of the lung: clinical charteristics, recurrences, and survival
Bingqiang HAN ; Gening JIANG ; Jiaan DING ; Haifeng WANG ; Wenxin HE ; Peng ZHANG ; Ming LIU ; Nan SONG ; Zhiyi LIU
Chinese Journal of Thoracic and Cardiovascular Surgery 2010;26(4):244-246
Objective To compare the clinic characteristics, recurrences and prognosis in patients with stage Ⅰ bronchioloalveolar carcinoma (BAC) and adenocarcinoma of the lung. Methods The data of 56 patients with stage Ⅰ BAC and 169 patients with stage Ⅰ adenocarcinoma were analyzed retrospectively. Results The overall 1-, 3-, 5- year survival rates were 94.7%, 83.5% and 61.2%, respectively. Compared with adenocarcinoma of the lung, BAC showed a better survival rate(x2 =6.36, P =0.012). After surgery patients with BAC were prone to develop intrathoracic recurrence, and adenocarcinoma was equal between intrathoracic recurrence and extrathoracic metastasis. The rate of intrathoracic recurrence and extrathoracic metastasis between BAC and adenocarcinoma was significantly different (14/16 vs. 27/59, x2 =8.85, P=0.004). In both group, preoperative asymptomatic patients had better survival rate(x2 = 7.28, P = 0.007; x2 = 6.07, P = 0. 014). Univariate analysis indicated that sex, age(< 60 years and ≥60 years), location of tumor and smoking history did not significantly influence survival in patients with stage Ⅰ BAC or adenocarcinoma (P > 0.05). Conclusion The prognosis of stage Ⅰ BAC is superior to that of stage Ⅰ adenocarcinoma. BAC is prone to develop intrathoracic recurrence, and adenocarcinoma is equal between intrathoracic recurrence and extrathoracic metastasis. Early diagnosis of lung cancer could improve long-term survival.
2. Regulatory effect of faciogenital dysplasia 6 gene on hepatic stem cell differentiation
Qian XUE ; Jinfeng YANG ; Bing LI ; Tongchuan HE ; Bingqiang ZHANG
Chinese Journal of Hepatology 2017;25(4):268-272
Objective:
To investigate the regulatory effect of faciogenital dysplasia 6 (FGD6) gene on hepatic stem cell differentiation.
Methods:
FGD6 gene was selected for the co-intervention of target sequence, the AdEasy system was used for the construction of adenovirus vector and the packaging and multiplication of the recombinant adenovirus vector pSES-FGD6-siRNA, and the HP14.5 cells were infected. Immunofluorescence assay was used to measure the expression of FGD6 protein in HP14.5 cells, quantitative real-time PCR was used to measure the mRNA expression of FGD6, alpha-fetoprotein (AFP), and albumin (Alb), and Western blot was used to measure the protein expression of FGD6, AFP, and Alb. The empty pSES-Ad-RFP adenovirus vector was constructed as control in each group. All data were expressed as x±s, and a one-way analysis of variance was performed.
Results:
FGD6 protein was mainly expressed in the nucleus of HP14.5 cells. The pSES-FGD6-siRNA adenovirus vector was successfully constructed and it downregulated the expression of FGD6 gene and the mRNA and protein expression of AFP in HP14.5 cells and upregulated the mRNA and protein expression of Alb (
3.SOCS3 Attenuates GM-CSF/IFN-γ-Mediated Inflammation During Spontaneous Spinal Cord Regeneration.
Xuejie ZHANG ; Bingqiang HE ; Hui LI ; Yingjie WANG ; Yue ZHOU ; Wenjuan WANG ; Tiancheng SONG ; Nan DU ; Xingxing GU ; Yi LUO ; Yongjun WANG
Neuroscience Bulletin 2020;36(7):778-792
SOCS3, a feedback inhibitor of the JAK/STAT signal pathway, negatively regulates axonal regrowth and inflammation in the central nervous system (CNS). Here, we demonstrated a distinct role of SOCS3 in the injured spinal cord of the gecko following tail amputation. Severing the gecko spinal cord did not evoke an inflammatory cascade except for an injury-stimulated elevation of the granulocyte/macrophage colony-stimulating factor (GM-CSF) and interferon gamma (IFN-γ) cytokines. Simultaneously, the expression of SOCS3 was upregulated in microglia, and unexpectedly not in neurons. Enforced expression of SOCS3 was sufficient to suppress the GM-CSF/IFN-γ-driven inflammatory responses through its KIR domain by attenuating the activities of JAK1 and JAK2. SOCS3 was also linked to GM-CSF/IFN-γ-induced cross-tolerance. Transfection of adenovirus overexpressing SOCS3 in the injured cord resulted in a significant decrease of inflammatory cytokines. These results reveal a distinct role of SOCS3 in the regenerating spinal cord, and provide new hints for CNS repair in mammals.