http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
- 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
- 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
RISS 인기검색어
- 검색키워드
- 저자 : Lu Xiaohang (검색결과 3 건)
- 무료
- 기관 내 무료
- 유료
-
Feifei Chen,Dunke Lu,Xiaohang Li 제어·로봇·시스템학회 2019 International Journal of Control, Automation, and Vol.17 No.7
This paper presents an integrated design of adaptive sliding mode observer and fault-tolerant control for aclass of one-sided Lipschitz Markovian jump systems with general uncertain transition rates. In the design process,an adaptive sliding mode observer is first constructed to estimate the states of the original system without knowingany information of the unknown input. Then a fault-tolerant control strategy is therefore proposed to stabilize theclosed-loop system against the unknown input. Sufficient conditions of the existences of the designed observer andcontroller are deduced in the forms of linear matrix inequalities. In the end, several examples are given to illustratethe effectiveness and make some comparisons with other results.
-
Gao Ran,Guo Wenjun,Fan Tianfei,Pang Junling,Hou Yangfeng,Feng Xiaohang,Li Bolun,Ge Weipeng,Fan Tianhui,Zhang Tiantian,Lu Jiakai,Jing He,Jin Mu,Yan Chen,Wang Jing 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-
Abdominal aortic aneurysm (AAA) is a permanent expansion of the abdominal aorta that has a high mortality but limited treatment options. Phosphodiesterase (PDE) 4 family members are cAMP-specific hydrolyzing enzymes and have four isoforms (PDE4A-PDE4D). Several pan-PDE4 inhibitors are used clinically. However, the regulation and function of PDE4 in AAA remain largely unknown. Herein, we showed that PDE4D expression is upregulated in human and angiotensin II-induced mouse AAA tissues using RT-PCR, western blotting, and immunohistochemical staining. Furthermore, smooth muscle cell (SMC)-specific Pde4d knockout mice showed significantly reduced vascular destabilization and AAA development in an experimental AAA model. The PDE4 inhibitor rolipram also suppressed vascular pathogenesis and AAA formation in mice. In addition, PDE4D deficiency inhibited caspase 3 cleavage and SMC apoptosis in vivo and in vitro, as shown by bulk RNA-seq, western blotting, flow cytometry and TUNEL staining. Mechanistic studies revealed that PDE4D promotes apoptosis by suppressing the activation of cAMP-activated protein kinase A (PKA) instead of the exchange protein directly activated by cAMP (Epac). Additionally, the phosphorylation of BCL2-antagonist of cell death (Bad) was reversed by PDE4D siRNA in vitro, which indicates that PDE4D regulates SMC apoptosis via the cAMP-PKA-pBad axis. Overall, these findings indicate that PDE4D upregulation in SMCs plays a causative role in AAA development and suggest that pharmacological inhibition of PDE4 may represent a potential therapeutic strategy.
-
Huang Jiazhen,Wei Wei,Kang Fuli,Tan Shuang,Li Yibing,Lu Xiaohang,Wang Ning 한국유전학회 2023 Genes & Genomics Vol.45 No.12
Background Cervical cancer, as one of the most common cancers in women, remains a major health threat worldwide. Annexin A3 (ANXA3), a component of the annexin family, is upregulated in numerous cancers, with no explicit role in cervical cancer. Objective This study aims to investigate the function of ANXA3 in cervical cancer. Methods Differential expression genes between the cervical cancer tissues of patients and the controls were analyzed in The Cancer Genome Atlas (TCGA) and Gene Expression Profiling Interactive Analysis (GEPIA) database. Using transfection approaches to either upregulate or downregulate ANXA3, its role in cell proliferation and chemosensitivity of human cervical cancer cell lines (HeLa and C33A) was evaluated. Furthermore, the binding activity between YAP1 and ANXA3 was also explored. Results Genomics analysis indicated that differential genes were mostly associated with cell cycle progression and DNA replication. ANXA3 was highly expressed in the cervical cancer tissues and closely linked to malignancy degree. Knockdown of ANXA3 in cervical cancer cells inhibited cell cycle progression. A similar result was observed in the reduction of cyclin D, CDK4, cyclin E, and CDK2 in cervical cancer cells with ANXA3 silencing. Cervical cancer cells obtained high sensitivity to cisplatin (DDP) when ANXA3 was downregulated. Conversely, these capabilities were the opposite in cervical cancer cells overexpressing ANXA3. Furthermore, the expression levels of ANXA3 and YAP1 were positively correlated. YAP1 upregulation was positively connected with malignant behaviors, which were reversed by ANXA3 downregulation. Conclusion In light of our findings, targeting ANXA3 expressed in cervical cancer might contribute to more potential therapeutic strategies.
연관 검색어 추천
이 검색어로 많이 본 자료
활용도 높은 자료
