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Sridhar, K.

Publications and source records attributed to Sridhar, K..

2 recordsLinked to original sources

Changes in peripheral sensory afference do not alter predictive motor planning: evidence from carpal tunnel syndrome

Anticipatory control organises motor output prior to predictable perturbations and is expressed in multi-digit tasks as anticipatory synergy adjustments (ASAs), which coordinate digit forces before movement onset. Whether such feedforward coordination depends on peripheral sensory input remains unclear. Carpal tunnel syndrome provides a model of altered median nerve afference with within-subject restoration following surgical decompression. We quantified ASA onset and amplitude in eleven individuals with carpal tunnel syndrome performing a multi-finger grasp-and-release task before and three weeks after decompression surgery. Postoperatively, sensory function improved, and total grip force decreased significantly across task phases, indicating more efficient force regulation. In contrast, ASA onset timing and amplitude were unchanged. Equivalence testing confirmed that pre- and post-operative ASA measures fell within predefined bounds of practical equivalence. These findings demonstrate a central-peripheral dissociation: feedback-mediated grip force scaling is sensory-dependent and rapidly recalibrates following afferent restoration, whereas feedforward synergy coordination remains stable despite months of degraded peripheral input. The preserved ASA suggests that central motor planning circuits maintain anticipatory coordination through efferent copy or cerebellar-mediated internal models that do not require continuous peripheral recalibration. This resilience may reflect the brains ability to maintain predictive motor planning despite chronic sensory degradation, with implications for understanding compensatory mechanisms in peripheral neuropathies and the limits of sensory-dependent motor adaptation.

neuroscience↗

Leptospira surface protein LigA plays a multifaceted role in modulating the host innate immune response

Leptospira, a zoonotic pathogen, is known to infect various hosts and can establish persistent infection. This remarkable ability of bacteria is attributed to its potential to modulate the host immune response by exploiting its surface proteins. We have identified and characterized the domain of the variable region of Leptospira immunoglobulin-like protein A (LAV) involved in immune modulation. The 11th domain (A11) of the variable region of LigA (LAV) induces a strong TLR4 dependent innate response leading to subsequent induction of humoral and cellular immune responses in mice. A11 is also involved in acquiring complement regulator FH and binds to host protease Plasminogen (PLG), there by mediating functional activity to escape from complement-mediated killing. The deletion of A11 domain significantly impaired TLR4 signaling and subsequent reduction in the innate and adaptive immune response. It also inhibited the binding of FH and PLG thereby mediating killing of bacteria. Our study discovered an unprecedented role of LAV as a nuclease capable of degrading Neutrophil Extracellular Traps (NETs). This nuclease activity was primarily mediated by A11. These results highlighted the moonlighting function of LigA and demonstrated that a single domain of a surface protein is involved in evading a myriad of host innate immune defenses, which might allow the persistence of Leptospira in different hosts for a long term without clearance.

immunology↗