Earticle

Tumor cells express altered metabolic activities often linked to mitochondrial dysfunction. Such mitochondrial defects can inhibit oxidative phosphorylation, change the cellular redox status (NAD+/NADH), increase production of reactive oxygen species (ROS), and cause DNA damage that further supports tumorigenesis and a metastatic phenotype1,2. Mitochondrial Complex I (NADH dehydrogenase) is a major site of ROS production in mitochondria and regulator of the NAD+/NADH ratio. This study is focused on mitochondrial complex I as a possible modulator of tumorigenesis and progression in breast cancer. We used NADH dehydrogenase from yeast, called NDI1, to augment complexI activity in metastatic human breast cancer cells. We followed NDI1 functionality and impact on tumor cell behavior in vitro and tumor progression in vivo. Augmentation of NADH dehydrogenase activity through NDI1 resulted in an enhanced NAD+/NADH ratio and slight inhibition of ROS production. Importantly, NDI1 expression inhibited metastasis and tumor growth in the mammary fad pad of immune deficient mice, as seen by non-invasive bioluminescence imaging and histology. The mechanisms involve NDI1-induced inhibition of the AKT/mTOR survival pathway and autophagy stimulation. Knock-down of ATG5 partially reversed the anti-metastatic effect of NDI1, demonstrating that enhancement of autophagy is responsible for NDI1-mediated inhibition of breast cancer spreading. The results indicate that mitochondrial complex I activity can drastically impact tumorigenesis and metastasis in breast cancer, and that augmentation of complex I function through NDI1 can inhibit tumor formation and cancer progression through NAD+/NADH ratio modulation.

The resistance of tumour cells against cytotoxic drug is significant limitation in successful chemotherapeutic treatment of cancer. To date, no crystal structure is available for human P-gp. We developed homology model for human P-gp NBD2 by using coordinates of transporter associated protein (TAP1). Docking study was performed for 8-geranyl-chrysin (Flavonoids) inhibitor in the NBD2 model. Ligand-protein interactions were determined which indicates that the 8-geranyl chrysin shares two overlapping sites in the cytosolic domains of P-gp, the ATP site and a hydrophobic steroid-binding site.

본 논문에서는 카르테시안 벡터 모듈레이터 전치왜곡기의 선형성 개선을 극대화하기 위해서 전치왜곡기 설계시 고려해야할 파라미터들을 제시하였으며 비선형시작점 조정회로를 사용한 개선된 카르테시안 벡터 모듈레이터 진처왜곡기를 제안하였다. 전치왜곡기의 성능을 확인하기 위해서 2.5 GHz 대역 모바일 WiMax 1FA 신호를 입력으로 하는 15 W 전력증폭기에 제안한 전치왜곡기를 적용하였다. 측정결과, -45.3 dBc의 ACLR을 얻었으며 기존의 다이오드를 사용한 전치왜곡기에 비해서 선형성 개선 구간이 넓어졌을 뿐만 아니라 기존의 전치왜곡기에 비해 약 4 dB 개선된 결과를 얻었다.

In this paper, we represent considering parameters for design of a Cartesian vector modulator predistorter to maximize linearity improvement of the predistorter and propose an advanced Cartesian vector modulator predistrotrer with nonlinear starting point control circuit. In order to confirm the performance of the proposed predistorter, the predistorter is applied to power amplifier with 15 W output power for 2.5 GHz band mobile WiMax 1-FA signal. From the measured results, ACLR of -45.3 dBc with 4 dB improvement of ALCR compared with the previous predistorter is obtained and linearity improvement range is also extended.

This study presents the design and FPGA implementation of a low-power, high-throughput digital modem for Medical Implant Communication System (MICS) applications. The proposed system applies a π /4-D8PSSK modulation technique to achieve high data efficiency while maintaining low power consumption. Implemented on a Xilinx Spartan-7 FPGA, the modem achieves a data rate of 16.4 ± 0.3 Mbps, with a power consumption of 0.6 ± 0.02 W/h, demonstrating a 40% improvement in energy efficiency compared to conventional 4FSK systems. The system satisfies IEEE 802.15.6 and ITU-R RS.1346 standards, with verified waveforms through MATLAB–Simulink and Chipscope. This work contributes to localization of medical implant communication technologies and provides a foundation for ASIC-based integration for next-generation biomedical and industrial wireless systems.

Sigma-delta ACD has two main parts: analog modulator and digital filter, the performance of modulator determines the performance of sigma-delta ADC, so the design of modulator is very important. The paper introduces the principle of sigma-delta AD modulator with high accuracy and the applied over sampling technique, noise shaping technique and multi-bit quantizer technique. Determining the design scheme of modulator—three bits three orders CIFF(Cascade of integrators, feed forward form) structure, and it makes the behavior level verification for this scheme by Simulink tool in MATLAB. The simulation result shows that multi-bit quantizer modulator can get very high SNR, and based on this result it designs every part of the modulator circuit.

A 4th-Order Wideband Sigma Delta modulator structure is proposed in this paper, which uses linear system theory technique. There are many implementation techniques to improve the performance of Sigma Delta ADCs, such as noise coupling, differential sampling and dynamic elements matching. An extra loop delay is needed to be added in the system. This paper explains how to make the modulator stable with the addition of feed-forward and feed-back branches which are used to compensate the extra loop delay. Next, we restore the signal and noise transfer functions. A 4th-Order Wideband delta-sigma modulator have been designed and simulated to verify the method.

Galectin-3, a member of carbohydrate recognition protein, is often over-expressed in cancerous regions, compared to normal counterparts. Moreover, this altered galectin-3 expression correlates with the aggressiveness of the tumor and the acquisition of the metastatic phenotype, indicating that galectin-3 might modulate tumor progression and influence disease outcome. It is important to note that a change in the subcellular localization of galectin-3 occurs during the transition from normal cells to cancer cells. In this study, it deals with the underlying mechanism that galectin-3 enhances gastric cancer cell survival and motility. Therefore, we suggest that galectin-3 can serve as potential target molecule in the prevention and/or therapy of gastric cancer.