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Inamdar, S.

Publications and source records attributed to Inamdar, S..

2 recordsLinked to original sources

Highly Adaptive Conductive Polymer Electronics Enhance Neural Data and Learning Accuracy

Human skin, the bodys largest organ, plays a vital role in sensing and transmitting neuronal, mechanical, and biochemical signals, making it an essential non-invasive interface for health monitoring, rehabilitation, and human-machine interaction. However, aging-related changes, including thinning, increased wrinkling, dryness, and altered collagen structure, significantly impact electrical impedance, conductance, and contact stability, challenging the fidelity and consistency of bioelectronic signal acquisition. Here, we address this gap by developing "AdapSkin," an age-adaptive, skin-mimicking, bio-adhesive, and stretchable polymeric electronic skin interface that seamlessly conforms to diverse skin properties, enabling high-fidelity and high-density electrophysiological recording. The soft electrodes of AdapSkin are composed of an aqueously processed, homogeneously mixed organic nanocomposite with a conductive polymer percolation network, forming a gel-like interface that reduces modulus and enhances skin-electrode contact. The materials platform achieves extraordinary softness and electrical stretchability of up to 1200% through a double-network composite structure. AdapSkin significantly minimizes age-induced variations in interfacial impedance and signal-to-noise ratio (SNR), improving signal consistency for neuromuscular assessment, prosthetic control, and rehabilitation applications. Scalable fabrication enables the creation of large-area electrode arrays, which reduces motion artifacts, improves sEMG mapping reliability, and ensures long-term signal stability across various age groups. Machine learning analysis further demonstrates AdapSkins superior accuracy in gesture classification for elderly users, highlighting its potential to enhance prosthetic control, assistive robotics, and rehabilitation for individuals with sarcopenia and neuromuscular decline. By improving signal quality and adaptability in aging populations, AdapSkin advances fair bioelectronic interfaces, fostering more equitable and effective healthcare technologies for age-related conditions.

bioengineering↗

RORyt+CD4+ T cells promote IL-23R-mediated neuronal cell apoptosis in the central nervous system

Transcription factors T-bet and ROR{psi}t play a crucial role in neuronal autoimmunity, and mice deficient in these two factors do not develop experimental autoimmune encephalomyelitis (EAE). The independent role of T-bet and ROR{psi}t in the pathogenesis of EAE and how they help induce apoptosis of neurons in the central nervous system (CNS) during neuronal autoimmunity is unclear. In the present study, we showed that myelin oligodendrocyte glycoprotein (MOG35-55) peptide-specific Th1 cells deficient in ROR{psi}t could cross BBB but fail to induce apoptosis of neurons and EAE. Pathogenic Th17 cell-derived cytokines GM-CSF, TNF-, IL-17A, and IL-21 significantly increase the surface expression of IL-23R on neuronal cells. Furthermore, we showed that, in EAE, neurons in the brain and spinal cord express IL-23R. IL-23-IL-23R signaling in neuronal cells caused phosphorylation of STAT3 (Ser727 and Tyr705) and induced cleaved caspase 3 and cleaved poly (ADP-ribose) polymerase-1 (PARP-1) molecules in an IL-23R-dependent manner and caused apoptosis. Thus, we provided a mechanism where we showed that T-bet is required to recruit pathogenic Th17 cells and ROR{psi}t expression to drive the apoptosis of IL-23R+ neurons in the CNS and cause EAE. Understanding detailed molecular mechanisms will help to design better strategies to control neuroinflammation and autoimmunity. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=136 SRC="FIGDIR/small/537133v1_ufig1.gif" ALT="Figure 1"> View larger version (39K): org.highwire.dtl.DTLVardef@2586b0org.highwire.dtl.DTLVardef@1adb3deorg.highwire.dtl.DTLVardef@fbce53org.highwire.dtl.DTLVardef@1a6d4ae_HPS_FORMAT_FIGEXP M_FIG C_FIG One Sentence SummaryIL-23-IL-23R signaling promotes apoptosis of CNS neurons.

immunology↗