arXiv subjects

Fred Chang

Publications and source records attributed to Fred Chang.

3 recordsLinked to original sources

arXiv2026

Design and Quantitative Evaluation of an Embedded EEG Instrumentation Platform for Real-Time SSVEP Decoding

This paper presents an embedded EEG instrumentation platform for real-time steady-state visually evoked potential (SSVEP) decoding based on an ESP32-S3 microcontroller and an ADS1299 analog front end. The system performs $8$-channel EEG acquisition, zero-phase bandpass filtering, and canonical correlation analysis entirely on-device, while supporting wireless communication and closed-loop operation without external computation. A central contribution is the quantitative characterization of the platform's measurement integrity. Reported results demonstrate a stable shorted-input noise floor ($\approx 0.08~\mu\text{V}_{\text{RMS}}$), tightly bounded sampling jitter ($0.56~\mu\text{s}$ standard deviation), and negligible long-term drift ($< 1~\text{ppm}$). Numerical fidelity analysis shows $100\%$ decision agreement between the mixed-precision embedded pipeline and a $64$-bit double-precision reference. Effective common-mode attenuation exceeded $112~\text{dB}$ under balanced conditions, with a localized $26.9~\text{dB}$ degradation observed under source-impedance mismatch. Closed-loop validation achieved $99.17\%$ online accuracy and an information transfer rate of $27.66~\text{bits/min}$. These results position the proposed system as a quantitatively characterized embedded EEG measurement and processing platform for real-time SSVEP decoding.

cs.HC↗

arXiv2024

BELT-2: Bootstrapping EEG-to-Language representation alignment for multi-task brain decoding

The remarkable success of large language models (LLMs) across various multi-modality applications is well established. However, integrating large language models with humans, or brain dynamics, remains relatively unexplored. In this paper, we introduce BELT-2, a pioneering multi-task model designed to enhance both encoding and decoding performance from EEG signals. To bolster the quality of the EEG encoder, BELT-2 is the first work to innovatively 1) adopt byte-pair encoding (BPE)-level EEG-language alignment and 2) integrate multi-task training and decoding in the EEG domain. Inspired by the idea of \textbf{\textit{Bridging the Brain with GPT}}, we further connect the multi-task EEG encoder with LLMs by utilizing prefix-tuning on intermediary output from the EEG encoder. These innovative efforts make BELT-2 a pioneering breakthrough, making it the first work in the field capable of decoding coherent and readable sentences from non-invasive brain signals. Our experiments highlight significant advancements over prior techniques in both quantitative and qualitative measures, achieving a decoding performance with a BLEU-1 score of 52.2\% on the ZuCo dataset. Furthermore, BELT-2 shows a remarkable improvement ranging from 31\% to 162\% on other translation benchmarks. Codes can be accessed via the provided anonymous link~\footnote{https://anonymous.4open.science/r/BELT-2-0048}.

eess.SP↗

arXiv2019

Reassessment of the basis of cell size control based on analysis of cell-to-cell variability

Fundamental mechanisms governing cell size control and homeostasis are still poorly understood. The relationship between sizes at division and birth in single cells is used as a metric to categorize the basis of size homeostasis [1-3]. Cells dividing at a fixed size regardless of birth size (sizer) are expected to show a division-birth slope of 0, whereas cells dividing after growing for a fixed size increment (adder) have an expected slope of +1 [4]. These two theoretical values are, however, rarely experimentally observed. For example, rod-shaped fission yeast $\it{Schizosaccharomyces}$ $\it{pombe}$ cells, which divide at a fixed surface area [5, 6], exhibit a division-birth slope for cell lengths of 0.25$\pm$0.02, significantly different from the expected sizer value of zero. Here we investigate possible reasons for this discrepancy by developing a mathematical model of sizer control including the relevant sources of variation. Our results support $\it{pure}$ sizer control and show that deviation from zero slope is exaggerated by measurement of an inappropriate geometrical quantity (e.g., length instead of area), combined with cell-to-cell radius variability. The model predicts that mutants with greater errors in size sensing or septum positioning paradoxically appear to behave as better sizers. Furthermore, accounting for cell width variability, we show that pure sizer control can in some circumstances reproduce the apparent adder behaviour observed in $\it{E. coli}$. These findings demonstrate that analysis of geometric variation can lead to new insights into cell size control.

q-bio.CB↗