• ETRI Journal
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• 제38권2호
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• pp.235-243
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• 2016

A low-noise readout integrated circuit (ROIC) for a microelectromechanical systems (MEMS) microphone is presented in this paper. A positive feedback signal amplification technique is applied at the front-end of the ROIC to minimize the effect of the output buffer noise. A feedback scheme in the source follower prevents degradation of the noise performance caused by both the noise of the input reference current and the noise of the power supply. A voltage booster adopts noise filters to cut out the noise of the sensor bias voltage. The prototype ROIC achieves an input referred noise (A-weighted) of -114.2 dBV over an audio bandwidth of 20 Hz to 20 kHz with a $136{\mu}A$ current consumption. The chip is occupied with an active area of $0.35mm^2$ and a chip area of $0.54mm^2$.

• Molecules and Cells
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• 제37권9호
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• pp.672-684
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• 2014

The exact causes of cell death in Parkinson's disease (PD) remain unknown despite extensive studies on PD.The identification of signaling and metabolic pathways involved in PD might provide insight into the molecular mechanisms underlying PD. The neurotoxin 1-methyl-4-phenylpyridinium ($MPP^+$) induces cellular changes characteristic of PD, and $MPP^+$-based models have been extensively used for PD studies. In this study, pathways that were significantly perturbed in $MPP^+$-treated human neuroblastoma SH-EP cells were identified from genome-wide gene expression data for five time points (1.5, 3, 9, 12, and 24 h) after treatment. The mitogen-activated protein kinase (MAPK) signaling pathway and endoplasmic reticulum (ER) protein processing pathway showed significant perturbation at all time points. Perturbation of each of these pathways resulted in the common outcome of upregulation of DNA-damage-inducible transcript 3 (DDIT3). Genes involved in ER protein processing pathway included ubiquitin ligase complex genes and ER-associated degradation (ERAD)-related genes. Additionally, overexpression of DDIT3 might induce oxidative stress via glutathione depletion as a result of overexpression of CHAC1. This study suggests that upregulation of DDIT3 caused by perturbation of the MAPK signaling pathway and ER protein processing pathway might play a key role in $MPP^+$-induced neuronal cell death. Moreover, the toxicity signal of $MPP^+$ resulting from mitochondrial dysfunction through inhibition of complex I of the electron transport chain might feed back to the mitochondria via ER stress. This positive feedback could contribute to amplification of the death signal induced by $MPP^+$.