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Effects of Rad51 on Survival of A549 Cells
Yu, Sha-Sha,Tu, Yi,Xu, Lin-Lin,Tao, Xue-Qin,Xu, Shan,Wang, Shan-Shan,Xiong, Yi-Feng,Mei, Jin-Hong Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.1
Rad51, a key factor in the homologous recombination pathway for the DNA double-strand break repair, plays a vital role in genesis of non-small-cell lung cancer (NSCLC). In recent years, more and more studies indicate that high expression of Rad51 is of great relevance to resistance of NSCLC to chemotherapeutic agents and ionizing radiation. However, the underlying molecular mechanisms are poorly understood. In this study, we investigated the role of single Rad51 on cell viability in vitro. Our results show that depletion of endogenous Rad51 is sufficient to inhibit the growth of the A549 lung cancer cell line, by accumulating cells in G1 phase and inducing cell death. We conclude that independent Rad51 expression is critical to the survival of A549 cells and can be an independent prognostic factor in NSCLC patients.
Yi-Sheng Liu,Ming-Ching Ou,Yi-Shan Tsai,Xi-Zhang Lin,Chien-Kuo Wang,Hong-Ming Tsai,Ming-Tsung Chuang 대한영상의학회 2015 Korean Journal of Radiology Vol.16 No.1
To retrospectively compare treatment of hepatocellular carcinoma (HCC) with transarterial chemoembolization (TACE) using gelatin sponges or microspheres plus lipiodol-doxorubicin vs. doxorubicin-loaded drug-eluting beads (DEB). A total of 158 patients with HCC received TACE from November 2010 to November 2011 were enrolled in this study, including 64 (40.5%) received TACE with lipiodol-doxorubicin and gelatin sponges (group A), 41 (25.9%) received TACE with lipiodol-doxorubicin and microspheres (group B), and 53 (33.5%) received TACE with doxorubicin-loaded DEB (group C). Tumor response and adverse events (AEs) were evaluated. No significant difference was found at baseline among the three groups. The doxorubicin dosage in group C wassignificantly (p < 0.001) higher compared to the dose used in groups A or B (median, 50 mg vs. 31 mg or 25 mg). Significantly (p < 0.001) more patients in group C achieved complete response compared to those in groups A or B (32.1% vs. 6.3% or 2.4%). Significantly (p < 0.001) less patients in group C had progressive disease compared to those in groups A or B (34.0% vs. 57.8% or 68.3%). Minor AEs were more common in groups A and B compared to group C, with rates of 54.7%, 34.1%, and 5.7%, respectively. In patients with HCC, TACE with DEB offers better safety and efficacy profiles compared to either TACE with gelatin sponges or TACE with microspheres.
( Ming Yi Zhao ),( Ming Hua Yang ),( Liang Chun Yang ),( Yan Yu ),( Min Xie ),( Shan Zhu ),( Rui Kang ),( Dao Lin Tang ),( Zhi Gang Jiang ),( Wu Zhou Yuan ),( Xiu Shan Wu ),( Li Zhi Cao ) 생화학분자생물학회(구 한국생화학분자생물학회) 2011 BMB Reports Vol.44 No.9
HMGB1 is associated with human cancers and is an activator of autophagy which mediates chemotherapy resistance. We here show that the mRNA levels of HMGB1 are high in leukemia cells and it is involved in the progression of childhood chronic myeloid leukemia (CML). HMGB1 decreases the sensitivity of human myeloid leukemia cells K562 to anti-cancer drug induced death through up-regulating the autophagy pathway, which is confirmed by the observation with an increase in fusion of autophagosomes and autophagolysosomes. When overexpressing HMGB1, both mRNA levels of Beclin-1, VSP34 and UVRAG which are key genes involved in mammalian autophagy and protein levels of p-Bcl-2 and LC3-II are increased. Luciferase assays document that over-expression of HMGB1 increases the transcriptional activity of JNK and ERK, which may be silenced by siRNA. The results suggest that HMGB1 regulates JNK and ERK required for autophagy, which provides a potential drug target for therapeutic interventions in childhood CML. [BMB reports 2011; 44(9): 601-606]
A 3-Gb/s Equalizer with an Adaptive Swing Controller for TFT-LCD Interfaces
Miao-Shan Li,Yen-Chen Lin,Chai-Chi Liu,Ching-Rong Chang,Jyun-Yi Li,You-Sheng Lin,Ching-Yuan Yang 대한전자공학회 2019 Journal of semiconductor technology and science Vol.19 No.1
A 0.18-μm CMOS 3-Gb/s equalizer with an adaptive swing controller is presented for 4K2K large display panels to compensate a 24-dB channel loss. Employing the output-swing control technique, we propose the adaptive loop for the equalizer to improve adaptation accuracy without degrading the boost tuning and input swing ranges. Besides, cascading two bandpass filters (BPF) measured energy in a narrow range is much more accuracy than conventional highpass filters (HPF). The measured jitter of 3-Gb/s and 1.5-Gb/s data are 0.23-UI and 0.356-UI for 1.23-m FR4 board, respectively. The core area occupies 0.12-㎟ and the power consumption is 27-mW at 3 Gb/s from a 1.8-V supply.