Visual stimuli design plays an important role in brain-computer interfaces (BCIs) based on visual evoked potentials (VEPs). Variations in stimulus parameters have been shown to affect both decoding accuracy and subjective perception experience, implying the need for a trade-off in design. In this study, we comprehensively and systematically compared various combinations of amplitude contrast and spectral content parameters in the stimulus design to quantify their impact on decoding performance and subject comfort. Specifically, three parameters were investigated: 1) contrast level, 2) temporal pattern (periodic steady-state or pseudo-random code-modulated), and 3) frequency range. We collected electroencephalogram (EEG) data and subjective perception ratings from ten subjects and evaluated the decoding accuracy and subject comfort rating for different combinations of the stimulus parameters. Our results indicate that while high-frequency steady-state VEP (SSVEP) stimuli were rated the most comfortable, they also had the lowest decoding accuracy. Conversely, low-frequency SSVEP stimuli were rated the least comfortable but had the highest decoding accuracy. Standard and high-frequency M-sequence code-modulated VEPs (c-VEPs) produced intermediates between the two. We observed a consistent trade-off relationship between decoding accuracy and subjective comfort level across all parameters. Based on our findings, we offer c-VEP as a preferable stimulus for achieving reliable decoding accuracy while maintaining a reasonable level of comfortability.

Pulmonary arterial hypertension (PAH) is marked by vascular remodeling, yet the role of adventitial fibrosis—and its modulation by sex and hormonal status—remains unclear. We examined stage-specific adventitial remodeling and pulmonary artery adventitial fibroblast (PAAF) mechanosensitivity in male, ovary-intact female, and ovariectomized (OVX) female Sprague–Dawley rats with SuHx-induced PAH. Hemodynamics, pulmonary artery histology, and adventitia-specific transcriptional profiling were integrated with in vitro assays of PAAFs exposed to defined substrate stiffness and stretch. All groups developed comparable increases in mean pulmonary arterial pressure, but vascular resistance shift and adventitial fibrosis diverged by sex: intact females showed attenuated increase in pulmonary vascular resistance and transient collagen accumulation, whereas OVX females mirrored the sustained, male-like progression. Extracellular matrix (ECM) gene activation occurred without smooth muscle actin induction, suggesting noncanonical fibrotic pathways. In vitro, intact female PAAFs required higher substrate stiffness to induce profibrotic gene expression, indicating a hormone-modulated stiffness threshold. OVX PAAFs showed persistent transcriptional reprogramming, while stretch-induced ECM upregulation occurred predominantly in male-derived PAAFs. These findings demonstrate that adventitial fibrosis in PAH is shaped by both hormonal and chromosomal sex, independent of hemodynamic severity, and highlight fibroblast mechanosensitivity as a potential target for stage- and sex-specific interventions.

Pulmonary arterial hypertension (PAH) alters pulmonary vascular mechanics, increasing arterial stiffness and pulsatile right ventricular afterload, yet mechanical differences across disease stages in the proximal pulmonary arteries remain poorly defined. Here, we quantified temporal alterations in pulmonary arterial mechanics in the sugen–hypoxia (SuHx) rat model of PAH. In vivo hemodynamics were combined with ex vivo tubular biaxial testing of left and right pulmonary arteries to quantify characteristic impedance, wall thickness, stiffness, and viscoelastic behavior. Constitutive modeling was used to estimate circumferential Young’s modulus and relaxation time constants. SuHx animals exhibited significant increases in mean pulmonary arterial pressure and characteristic impedance relative to controls. Both pulmonary arteries exhibited increased stiffness at both disease stages, whereas significant wall thickening was observed only at the later stage. Viscoelastic relaxation time constants exhibited decreasing trends but did not differ significantly across groups. These findings demonstrate stage-dependent differences in proximal pulmonary artery mechanics and highlight arterial stiffening as a key contributor to altered pulmonary hemodynamics in PAH.