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- 저자 : Jinjin Liang (검색결과 3 건)
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Investigation on Micro-Milling of Ti–6Al–4V Alloy by PCD Slotting-Tools
Jinjin Han,Xiuqing Hao,Liang Li,Li Zhong,Guolong Zhao,Ning He 한국정밀공학회 2020 International Journal of Precision Engineering and Vol.21 No.2
Ti–6Al–4V is characterized by various protruding characteristics and has been found extensive applications in aerospace, biomedical device industries and other fields. However, these properties in turn bring about the increase in cutting forces, make the chips intractable to control and also shorten the tool service life, etc. A preliminary exploration of micro-milling of Ti–6Al–4V by PCD slotting-tool (MST-PCD) was launched in this paper. The most prominent advantage was the PCD slotting-tools could reach a higher linear velocity even the spindle speed was lower, which can strongly ensure the strength and stiffness of micro cutters and suppress the vibration occurrence due to the high spindle speed. The machining processes of using PCD slotting-tool and carbide micro-end mill (MEM-WC) was compared in detail. The wear experiments were conducted to confirm the effectiveness and advantage of MST-PCD. The cutting forces and surface quality, as well as the effects of tool wear on these output responses were investigated. Then model establishment and multi-objective parameter optimization were performed based on the orthogonal experiment results. Finally, verification experiments were also carried out to confirm the effectiveness of the developed models and MST-PCD. The findings in this paper can also be applied to other difficult-to-machine materials.
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Multiple Smooth Support Vector Machine with FCM Clustering in Hidden Space
Xian-wei Zhang,Jinjin Liang 보안공학연구지원센터 2016 International Journal of Grid and Distributed Comp Vol.9 No.9
A multiple smooth model is proposed by smoothing technique and piecewise technique for large scale data. Mapping the training data to the hidden space with a hidden function, the proposed model divides the original data into several subclasses by Fuzzy C Means (FCM), whose initial cluster centers are selected by samples with large density indexes; derives the smooth differentiable model by utilizing the entropy function to replace the plus function of the slack vector, and introduces linking rules to combine results of subclasses. Simulations demonstrate that the obtained algorithm maintains good classification accuracies, reduces the training time and hardly varies with kernel parameters.
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Melatonin Attenuates Mitochondrial Damage in Aristolochic Acid-Induced Acute Kidney Injury
Sun Jian,Pan Jinjin,Liu Qinlong,Cheng Jizhong,Tang Qing,Ji Yuke,Cheng Ke,wang Rui,Liu Liang,Wang Dingyou,Wu Na,Zheng Xu,Li Junxia,Zhang Xueyan,Zhu Zhilong,Ding Yanchun,Zheng Feng,Li Jia,Zhang Ying,Yua 한국응용약물학회 2023 Biomolecules & Therapeutics(구 응용약물학회지) Vol.31 No.1
Aristolochic acid (AA), extracted from Aristolochiaceae plants, plays an essential role in traditional herbal medicines and is used for different diseases. However, AA has been found to be nephrotoxic and is known to cause aristolochic acid nephropathy (AAN). AA-induced acute kidney injury (AKI) is a syndrome in AAN with a high morbidity that manifests mitochondrial damage as a key part of its pathological progression. Melatonin primarily serves as a mitochondria-targeted antioxidant. However, its mitochondrial protective role in AA-induced AKI is barely reported. In this study, mice were administrated 2.5 mg/kg AA to induce AKI. Melatonin reduced the increase in Upro and Scr and attenuated the necrosis and atrophy of renal proximal tubules in mice exposed to AA. Melatonin suppressed ROS generation, MDA levels and iNOS expression and increased SOD activities in vivo and in vitro. Intriguingly, the in vivo study revealed that melatonin decreased mitochondrial fragmentation in renal proximal tubular cells and increased ATP levels in kidney tissues in response to AA. In vitro, melatonin restored the mitochondrial membrane potential (MMP) in NRK-52E and HK-2 cells and led to an elevation in ATP levels. Confocal immunofluorescence data showed that puncta containing Mito-tracker and GFP-LC3A/B were reduced, thereby impeding the mitophagy of tubular epithelial cells. Furthermore, melatonin decreased LC3A/B-II expression and increased p62 expression. The apoptosis of tubular epithelial cells induced by AA was decreased. Therefore, our findings revealed that melatonin could prevent AA-induced AKI by attenuating mitochondrial damage, which may provide a potential therapeutic method for renal AA toxicity.
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