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Ying Zhu,Hao-liang Zhang,Qi-ying Wang,Min-jing Chen,Lin-bo Liu 한국분자세포생물학회 2018 Molecules and cells Vol.41 No.2
microRNA (miR)-612 shows anticancer activity in several types of cancers, yet its function in melanoma is still unclear. This study was undertaken to investigate the expression of miR-612 and its biological relevance in melanoma cell growth, invasion, and tumorigenesis. The expression and prognostic significance of miR-612 in melanoma were examined. The effects of miR-612 overexpression on cell proliferation, colony formation, tumorigenesis, and invasion were determined. Rescue experiments were conducted to identify the functional target gene(s) of miR-612. miR-612 was significantly downregulated in melanoma tissues compared to adjacent normal tissues. Low miR-612 expression was significantly associated with melanoma thickness, lymph node metastasis, and shorter overall, and disease-free survival of patients. Overexpression of miR-612 significantly decreased cell proliferation, colony formation, and invasion of SK-MEL-28 and A375 melanoma cells. In vivo tumorigenic studies confirmed that miR-612 overexpression retarded the growth of A375 xenograft tumors, which was coupled with a decline in the percentage of Ki-67-positive proliferating cells. Mechanistically, miR-612 targeted Espin in melanoma cells. Overexpression of Espin counteracted the suppressive effects of miR-612 on melanoma cell proliferation, invasion, and tumorigenesis. A significant inverse correlation (r = -0.376, P = 0.018) was observed between miR-612 and Espin protein expression in melanoma tissues. In addition, overexpression of miR-612 and knockdown of Espin significantly increased the sensitivity of melanoma cells to doxorubicin. Collectively, miR-612 suppresses the aggressive phenotype of melanoma cells through downregulation of Espin. Delivery of miR-612 may represent a novel therapeutic strategy against melanoma.
Hao, Li-Ying,H. Park, Ju,Ye, Dan IET 2016 IET control theory & applications Vol.10 No.3
<P>This study proposes an integral sliding mode control (ISMC) scheme for a class of uncertain non-linear systems subject to actuator faults including outage. It is noted that traditional ISMC method cannot handle actuator outage. To tackle the problem, matrix full-rank factorisation technique and adaptive mechanism are incorporated. Based on the above technique, two novel integral sliding surfaces using construction methods I and II are then introduced and existence conditions of sliding modes are given in terms of linear matrix inequalities, in which less conservativeness and better robustness against actuator faults are obtained using construction method II than I. The fuzzy logic systems are applied to approximate the bounds of unknown non-linear functions. Furthermore, an integral sliding mode controller, without an fault detection and isolation mechanism, is synthesised to guarantee the asymptotic stability and the robustness of the closed-loop system against actuator faults and non-linearities from the every beginning. Finally, simulation results for a model of B747-100/200 aircraft confirm the effectiveness of the proposed control method.</P>
Ying-Ying Hung,Yun-Ching Fu,Hao-Ji Wei,I-Chen Tsai,Clayton Chi-Chang Chen 대한영상의학회 2013 Korean Journal of Radiology Vol.14 No.5
Double aortic arch with an atretic left arch distal to the origin of left subclavian artery was diagnosed with multidetector row computed tomography (MDCT) in two children with dysphagia. This rare type of complete vascular ring is clinically important because it may be confused with right aortic arch in mirror imaging. Anatomic details of this rare type of complete vascular ring demonstrated on MDCT facilitated appropriate surgical treatment.
Ying-Hao Liu,Qian Gong,Yi-Kai Wang,Wei-Bing Shuang 대한배뇨장애요실금학회 2023 International Neurourology Journal Vol.27 No.2
Purpose: The main treatment options of neurogenic bladder remains catheterization and long-term oral medications. Metabolic interventions have shown good therapeutic results in many diseases. To date, no studies have characterized the metabolites of the detrusor muscle during neurogenic bladder. Using metabolomics, new muscle metabolomic signatures were identified to reveal the temporal metabolic profile of muscle during disease progression. Methods: We used 42 Sprague-Dawley rats (200±20 g, males) for T10 segmental spinal cord injury modeling and collected detrusor tissue and performed nontargeted metabolomics after sham surgery, 30-minute, 6-hour, 12-hour, 24-hour, 5-day, and 2-week postmodelling, to identify the dysregulated metabolic pathways and key metabolites. Results: By comparing mzCloud, mzVault, MassList, we identified a total of 1,271 metabolites and enriched a total of 12 metabolism-related pathways with significant differences (P<0.05) based on Kyoto Encyclopedia of Genes and Genomes analysis. Metabolites in several differential metabolic pathways such as ascorbate and aldarate metabolism, Steroid hormone biosynthesis, and carbon metabolism are altered in a regular manner before and after ridge shock. Conclusions: Our study is the first time-based metabolomic study of rat forced urinary muscle after traumatic spinal cord injury, and we identified multiple differential metabolic pathways during injury that may improve long-term management strategies for neurogenic bladder and reduce costs in long-term treatment.