A novel approach for bi-directional motion estimation and compensation

2004 ◽  
Author(s):  
F. Ahmadianpour ◽  
M.O. Ahmad
Keyword(s):  
Motion Estimation ◽  
Novel Approach ◽  
Directional Motion

An Advanced Parallel FPGA Architecture for Bi-Directional Motion Estimation

2015 ◽  
Vol 8 (9) ◽  
pp. 235-244
Author(s):  
Yangfan Huang ◽  
Minjun Deng ◽  
Donglian Li ◽  
Zhenzhen Li ◽  
Mingyan Yu ◽  
...  
Keyword(s):  
Motion Estimation ◽  
Fpga Architecture ◽  
Directional Motion

New frame rate up-conversion using bi-directional motion estimation

2000 ◽  
Vol 46 (3) ◽  
pp. 603-609 ◽  
Author(s):  
Byung-Tae Choi ◽  
Sung-Hee Lee ◽  
Sung-Jea Ko
Keyword(s):  
Motion Estimation ◽  
Frame Rate ◽  
Directional Motion ◽  
Frame Rate Up Conversion

Copper-dependent ATP7B up-regulation drives the resistance of TMEM16A-overexpressing head-and-neck cancer models to platinum toxicity

2019 ◽  
Vol 476 (24) ◽  
pp. 3705-3719 ◽  
Author(s):  
Avani Vyas ◽  
Umamaheswar Duvvuri ◽  
Kirill Kiselyov
Keyword(s):  
Oxidative Stress ◽  
Head And Neck ◽  
Transcriptional Activation ◽  
Platinum Resistance ◽  
Mrna Levels ◽  
Strong Positive Correlation ◽  
Platinum Compounds ◽  
Copper Chelation ◽  
Novel Approach ◽  
Cancer Models

Platinum-containing drugs such as cisplatin and carboplatin are routinely used for the treatment of many solid tumors including squamous cell carcinoma of the head and neck (SCCHN). However, SCCHN resistance to platinum compounds is well documented. The resistance to platinum has been linked to the activity of divalent transporter ATP7B, which pumps platinum from the cytoplasm into lysosomes, decreasing its concentration in the cytoplasm. Several cancer models show increased expression of ATP7B; however, the reason for such an increase is not known. Here we show a strong positive correlation between mRNA levels of TMEM16A and ATP7B in human SCCHN tumors. TMEM16A overexpression and depletion in SCCHN cell lines caused parallel changes in the ATP7B mRNA levels. The ATP7B increase in TMEM16A-overexpressing cells was reversed by suppression of NADPH oxidase 2 (NOX2), by the antioxidant N-Acetyl-Cysteine (NAC) and by copper chelation using cuprizone and bathocuproine sulphonate (BCS). Pretreatment with either chelator significantly increased cisplatin's sensitivity, particularly in the context of TMEM16A overexpression. We propose that increased oxidative stress in TMEM16A-overexpressing cells liberates the chelated copper in the cytoplasm, leading to the transcriptional activation of ATP7B expression. This, in turn, decreases the efficacy of platinum compounds by promoting their vesicular sequestration. We think that such a new explanation of the mechanism of SCCHN tumors’ platinum resistance identifies novel approach to treating these tumors.

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