Anti-Mouse CD105 (Endoglin) PE 100 ug
- Known as:
- Antibody toMouse CD105 (Endoglin) PE 100 ug
- Catalog number:
- 12-1051-82
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Mouse CD105 (Endoglin) 100
Related genes to: Anti-Mouse CD105 (Endoglin) PE 100 ug
- Gene:
- ENG NIH gene
- Name:
- endoglin
- Previous symbol:
- ORW1, ORW
- Synonyms:
- END, HHT1, CD105
- Chromosome:
- 9q34.11
- Locus Type:
- gene with protein product
- Date approved:
- 1993-03-03
- Date modifiied:
- 2019-04-23
Related products to: Anti-Mouse CD105 (Endoglin) PE 100 ug
Related articles to: Anti-Mouse CD105 (Endoglin) PE 100 ug
- Integrating frequency-tuned, adaptive brain stimulation with brain-computer interfaces (BCIs) allows direct tests of the causal role of brain oscillations and advances BCIs toward bi-directional operation. A central challenge is that stimulation-induced artifacts overlap with endogenous brain rhythms, undermining robust real-time signal decoding and contingent BCI feedback. Here, we overcome this limitation by introducing an artifact-suppression approach that enables robust motor-imagery BCI control during frequency-tuned amplitude-modulated transcranial alternating current stimulation (AM-tACS). We developed a real-time spatial filtering pipeline that combines spatio-spectral decomposition (SSD) with beamforming and evaluated its performance against a standard Laplacian filter in 14 healthy participants. BCI control was assessed both in the absence of stimulation and during stimulation. We hypothesized that only the SSD-beamforming approach would preserve robust BCI control under stimulation. In the absence of stimulation, both pipelines supported robust BCI control (SSD-beamforming: 73 ± 9%; Laplacian: 72 ± 8%; p = .849). During AM-tACS, Laplacian filtering showed a marked performance decline to near chance level (58 ± 9%; p < .001). However, with SSD-beamforming, robust BCI control was preserved (76 ± 9%). These results demonstrate that robust BCI control during frequency-tuned AM-tACS is achievable. By enabling simultaneous stimulation and decoding, this approach establishes a new paradigm for testing the causal contributions of brain rhythms during ongoing BCI control and for advancing stimulation-informed, bi-directional BCI interventions. Future work will determine how AM-tACS can be leveraged to enhance BCI performance but also promote neuroplasticity during restorative BCI applications. - Source: PubMed
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Vermehren MareikePeekhaus NielsColucci AnnalisaWiskow MarianHaslacher DavidCurio GabrielSoekadar Surjo R - Age-related mobility decline is frequently accompanied by a redistribution of joint kinetics, where older adults compensate for reduced ankle function by increasing demand on the hip. Paradoxically, this compensatory shift typically coincides with age-related reductions in maximal hip power. Although robotic exoskeletons can provide immediate energetic benefits, conventional control strategies have limited previous studies in this population to specific tasks such as steady-state walking, which do not fully reflect mobility demands in the home and community. Here, we implement a task-agnostic hip exoskeleton controller that is inherently sensitive to joint power and validate its efficacy in eight older adults. Across a battery of hip-intensive activities that included level walking, ramp ascent, stair climbing, and sit-to-stand transitions, the exoskeleton matched biological power profiles with high accuracy (mean cosine similarity 0.89). Assistance significantly reduced sagittal plane biological positive work by 24.7% at the hip and by 9.3% for the lower limb, while simultaneously augmenting peak total (biological + exoskeleton) hip power and reducing peak biological hip power and torque. These results suggest that hip exoskeletons can potentially enhance endurance through biological work reduction, and increase functional reserve through total power augmentation, serving as a promising biomechanical intervention to support elderly mobility. - Source: PubMed
Publication date: 2026/09/10
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Publication date: 2026/09/11
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