1.Probation into Analytic-Chemistry Bilingual Teaching
Gang YI ; Yurong YAN ; Shijia DING
Chinese Journal of Medical Education Research 2005;0(06):-
Beginning with the authors' experience in analytic-chemistry bilingual teaching,this article probes into some problems of analytic-chemistry in undergraduate education.And the authors give some beneficial suggestions in the teaching material construction,teachers training and teaching quality control.
2.Discussion on Innovation in the Experiment Teaching of Analytical Chemistry
Shijia DING ; Gang YI ; Yurong YAN
Chinese Journal of Medical Education Research 2005;0(05):-
The present situation and problems in experiment teaching of analytical chemistry were explained,and innovation was explored and practiced in the faculty of laboratory medicine,including the opitimization of teaching contents,teaching methods and score system evaluation reformation.
3.Discussion on Improving Teaching Quality in Sanitary Chemistry
Yurong YAN ; Gang YI ; Shijia DING
Chinese Journal of Medical Education Research 2006;0(09):-
The academic teaching quality and experimental teaching quality of sanitary chemistry will be improved,through enriching the teacher with specialized knowledge and cultivating the creative ability of thacher and updating the teaching methods.
4.Teaching exploration of sample preparation and separation in proteomics course for postgraduates
Yurong YAN ; Lan ZHOU ; Shijia DING ; Zongyin QIU
Chinese Journal of Medical Education Research 2012;(12):1254-1256
Sample preparation and separation is a very crucial and complicated process in proteomics research.Based on the actual condition of university and students,this article explored the way to improve the teaching quality of sample preparation and separation in proteomics course for medical post-graduates aiming at cultivating and enhancing the students' scientific thought,making them have a better understanding of the rules,technologies,strategies in sample preparation and separation procedure.
5.Real-time virtual navigation system combined with CEUS guided radiofrequency ablation therapy of neonatal or recurrent hepatocellular carcinoma lesions
Qian XU ; Shuzhi LIN ; Shijia DONG ; Jinyu WU ; Wei YANG ; Wei WU ; Kun YAN ; Minhua CHEN
Chinese Journal of Medical Imaging Technology 2018;34(5):701-704
Objective To investigate the value of real-time virtual navigation system (RVS) combined with CEUS in guiding radiofrequency ablation (RFA) therapy of neonatal or recurrent lesions of hepatocellular carcinoma (HCC).Methods Totally 111 patients with neonatal or recurrent lesions of HCC after RFA therapy were enrolled.Seventy-eight patients with 86 lesions (77 neonatal lesions and 9 recurrent lesions) underwent RFA guided by RVS combined with CEUS (RVS combined with CEUS group),and 33 patients with 38 lesions (26 neonatal lesions and 12 recurrent lesions) underwent RFA guided by CEUS alone (control group).The precise localization,inactivation rate and local recurrence rate between the two groups were compared.Results Eighty-four lesions (84/86,97.67%) in RVS combined with CEUS group and 25 lesions (25/38,65.79%) in control group were clearly showed and localized (P<0.001).One month after RFA therapy,the tumor inactivation rate in RVS combined with CEUS group and control group was 95.35 % (82/86) and 76.31% (29/38),respectively (P=0.003).The local recurrence rate in RVS combined with CEUS group was 8.14% (7/86),while was 36.84% (14/38) in control group (x2 =15.434,P<0.001).Conclusion RVS combined with CEUS guidance can improve the accurate position rate and early inactivation rate of RFA therapy for neonatal or recurrent lesions of HCC.
6.Regulatory effect of C12ORF66 on viability of MYCN amplified high-risk neuroblastoma cells
Anna JIA ; Shijia ZHAN ; Xuan ZHANG ; Jinxin GUO ; Yongbo YU ; Yongli GUO ; Yan CHANG
Basic & Clinical Medicine 2024;44(3):288-294
Objective To explore the effect of open reading frame 66(C12ORF66)located at chromosome 12 on the viability of MYCN amplified NB cell lines.Methods DDatasets GSE16476 and GSE49710 in R2 database were analyzed for expression level of C12ORF66 in MYCN amplified and MYCN non-amplified NB cells and its potential correlation with the prognosis of pediatric patients.C12ORF66 mRNA expression level in normal tissue immortalized cell lines,MYCN amplified and MYCN non-amplified cell lines were detected by RT-qRCR.Transient or stable knockdown of C12ORF66 cell lines were constructed to compare the difference in real time cellular analysis(RTCA),colony formation,Ki67 positive cells between the control group and the C12ORF66 knockdown group.Results By analyzing R2 datasets,C12ORF66 level in MYCN amplified samples was significantly higher than that in MYCN non-amplified samples,and the expression of C12ORF66 was negatively correlated with the prognosis of pediatric patients(P<0.05).C12ORF66 highly expressed in MYCN-amplified BE(2)-C and SK-N-BE(2)cell lines than in MYCN non-amplified CHLA-255 and SH-SY5Y cell lines(P<0.001).Transient or stable knockdown of C12ORF66 resulted in significant slow down of proliferation of MYCN amplified NB cells(P<0.001),the colony formation ability was significantly reduced(P<0.001),and the proportion of Ki67 positive cells was significantly decreased(P<0.05).Conclusions C12ORF66 was highly expressed in MYCN amplified clinical NB samples and cell lines which is believed to be correlated with poor prognosis of pediatric patients.C12ORF66 knockdown signifi-cantly inhibits cell viability of NB cells.
7.SIRT7 antagonizes human stem cell aging as a heterochromatin stabilizer.
Shijia BI ; Zunpeng LIU ; Zeming WU ; Zehua WANG ; Xiaoqian LIU ; Si WANG ; Jie REN ; Yan YAO ; Weiqi ZHANG ; Moshi SONG ; Guang-Hui LIU ; Jing QU
Protein & Cell 2020;11(7):483-504
SIRT7, a sirtuin family member implicated in aging and disease, is a regulator of metabolism and stress responses. It remains elusive how human somatic stem cell populations might be impacted by SIRT7. Here, we found that SIRT7 expression declines during human mesenchymal stem cell (hMSC) aging and that SIRT7 deficiency accelerates senescence. Mechanistically, SIRT7 forms a complex with nuclear lamina proteins and heterochromatin proteins, thus maintaining the repressive state of heterochromatin at nuclear periphery. Accordingly, deficiency of SIRT7 results in loss of heterochromatin, de-repression of the LINE1 retrotransposon (LINE1), and activation of innate immune signaling via the cGAS-STING pathway. These aging-associated cellular defects were reversed by overexpression of heterochromatin proteins or treatment with a LINE1 targeted reverse-transcriptase inhibitor. Together, these findings highlight how SIRT7 safeguards chromatin architecture to control innate immune regulation and ensure geroprotection during stem cell aging.
8.The role of phosphatidylcholine 34:1 in the occurrence, development and treatment of ulcerative colitis.
Tengjie YU ; Zhihao ZHOU ; Shijia LIU ; Changjian LI ; Zhi-Wei ZHANG ; Yong ZHANG ; Wei JIN ; Keanqi LIU ; Shuying MAO ; Lei ZHU ; Lin XIE ; Guangji WANG ; Yan LIANG
Acta Pharmaceutica Sinica B 2023;13(3):1231-1245
Lipid homeostasis is considered to be related to intestinal metabolic balance, while its role in the pathogenesis and treatment of ulcerative colitis (UC) remains largely unexplored. The present study aimed to identify the target lipids related to the occurrence, development and treatment of UC by comparing the lipidomics of UC patients, mice and colonic organoids with the corresponding healthy controls. Here, multi-dimensional lipidomics based on LC-QTOF/MS, LC-MS/MS and iMScope systems were constructed and used to decipher the alteration of lipidomic profiles. The results indicated that UC patients and mice were often accompanied by dysregulation of lipid homeostasis, in which triglycerides and phosphatidylcholines were significantly reduced. Notably, phosphatidylcholine 34:1 (PC34:1) was characterized by high abundance and closely correlation with UC disease. Our results also revealed that down-regulation of PC synthase PCYT1α and Pemt caused by UC modeling was the main factor leading to the reduction of PC34:1, and exogenous PC34:1 could greatly enhance the fumarate level via inhibiting the transformation of glutamate to N-acetylglutamate, thus exerting an anti-UC effect. Collectively, our study not only supplies common technologies and strategies for exploring lipid metabolism in mammals, but also provides opportunities for the discovery of therapeutic agents and biomarkers of UC.
9.Clinical Features and Prognosis of t(8;21) AML Patients in China: A Multicenter Retrospective Study.
Dan GONG ; Wei LI ; Liang-Ding HU ; Jian-Min LUO ; Jian-Liang SHEN ; Mei-Yun FANG ; Qing-Ming YANG ; Heng-Xiang WANG ; Xiao-Yan KE ; Hui-Ren CHEN ; Zhao WANG ; Hui LIU ; Feng LIU ; Yi-Gai MA ; Jing-Wen WANG ; Hong-Hua LI ; Quan-Shun WANG ; Yu JING ; Xiao-Ning GAO ; Li-Ping DOU ; Yong-Hui LI ; Li YU
Journal of Experimental Hematology 2017;25(4):980-986
OBJECTIVETo summarize the clinical characteristics of peripheral blood, immune phenotypes, fusion genes and cytogenetics of patients with t(8;21) acute myeloid leukemia(AML) through the retrospective analysis of 586 patients with t(8;21) AML from 15 blood disease research centers in Northern area of China.
METHODSThe factors affecting prognosis of patients with t(8;21) AML were investigated by using univariate and multivariate COX regression.
RESULTSThe immune type of t(8;21) AML patients was mainly with HLA-DR, CD117, CD34, MPO, CD38, CD13and CD33(>95%), part of them with CD19and CD56; the most common accompanied mutation of t(8;21) AML patients was C-KIT mutation (37.8%); in addition to t(8;21) ectopic, the most common chromosomal abnormality was sex chromosome deletions (38.9%). The univariate analysis revealed a significant survival superiority of OS and PFS in t(8;21) AML patients of WBC≤3.5×10/L without C-KIT mutation, the newly diagnosed ones achieved HSCT(P<0.05), only survival superiority on OS in t(8;21) AML patients with extramedullary infiltration and CD19 positive; the results of multivariate analysis showed a significant survival superiority on OS and PFS in t(8;21) AML patients with WBC≤3.5×10/L(P<0.05).
CONCLUSIONThe clinical features of t(8;21) AML patients in China are similar to those in other countries, WBC≤3.5×10/L is a good prognostic factor while the C-KIT mutation is a poor one in t(8;21) AML patients.
10.A novel inhibitor of ARfl and ARv7 induces protein degradation to overcome enzalutamide resistance in advanced prostate cancer.
Yan LI ; Ya CHU ; Guangjiang SHI ; Xiaobin WANG ; Wanli YE ; Chun SHAN ; Dajia WANG ; Di ZHANG ; Wei HE ; Jingwei JIANG ; Shuqian MA ; Yuhong HAN ; Zhili ZHAO ; Shijia DU ; Zhen CHEN ; Zhiyu LI ; Yong YANG ; Chen WANG ; Xi XU ; Hongxi WU
Acta Pharmaceutica Sinica B 2022;12(11):4165-4179
Enzalutamide (ENZ) is a second-generation androgen receptor (AR) antagonist used for the treatment of castration-resistant prostate cancer (CRPC) and reportedly prolongs survival time within a year of starting therapy. However, CRPC patients can develop ENZ resistance (ENZR), mainly driven by abnormal reactivation of AR signaling, involving increased expression of the full-length AR (ARfl) or dominantly active androgen receptor splice variant 7 (ARv7) and ARfl/ARv7 heterodimers. There is currently no efficient treatment for ENZR in CRPC. Herein, a small molecule LLU-206 was rationally designed based on the ENZ structure and exhibited potent inhibition of both ARfl and constitutively active ARv7 to inhibit PCa proliferation and suppress ENZR in CRPC. Mechanically, LLU-206 promoted ARfl/ARv7 protein degradation and decreased ARfl/ARv7 heterodimers through mouse double minute 2-mediated ubiquitination. Finally, LLU-206 exhibited favorable pharmacokinetic properties with poor permeability across the blood-brain barrier, leading to a lower prevalence of adverse effects, including seizure and neurotoxicity, than ENZ-based therapies. In a nutshell, our findings demonstrated that LLU-206 could effectively inhibit ARfl/ARv7-driven CRPC by dual-targeting of ARfl/ARv7 heterodimers and protein degradation, providing new insights for the design of new-generation AR inhibitors to overcome ARfl/ARv7-driven CRPC.