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Sandhu, P.

Publications and source records attributed to Sandhu, P..

2 recordsLinked to original sources

Information-theory analysis of mouse string-pulling agrees with Fitts's Law: Increasing task difficulty engages multiple sensorimotor modalities in a dual oscillator behavior

Mouse string pulling, in which a mouse reels in a string with hand-over-hand movements, can provide insights into skilled motor behavior, neurological status, and cognitive function. The task involves two oscillatory movements connected by the string. The snout tracks the pendulum movement of the string produced by hand-over-hand pulls and so guides the hands to grasp the string. The present study examines the allocation of time required to pull strings of varying diameter. Movement is also described with end-point measures, string-pulling topography with 2D markerless pose estimates based on transfer learning with deep neural networks, and Mat-lab image-segmentation and heuristic algorithms for object tracking. With reduced string diameter, mice took longer to pull 60cm long strings. They also made more pulling cycles, misses, and mouth engagements, and displayed changes in the amplitude and frequency of pull cycles. The time measures agree with Fittss law in showing that increased task difficulty slows behavior and engages multiple compensatory sensorimotor modalities. The analysis reveals that time is a valuable resource in skilled motor behavior and information-theory can serve as a measure of its effective use.

animal behavior and cognition↗

Vitexin alters Staphylococcus aureus surface hydrophobicity to interfere with biofilm formation.

Bacterial surface hydrophobicity is one of the determinant biophysical parameters of bacterial aggregation for being networked to form biofilm. Phytoconstituents like vitexin have long been in use for their antibacterial effect. The present work is aimed to characterise the effect of vitexin on S. aureus surface hydrophobicity and corresponding aggregation to form biofilm. We have found that vitexin shows minimum inhibitory concentration at 252 g/ml against S. aureus. Vitexin reduces cell surface hydrophobicity and membrane permeability at sub-MIC dose of 126 g/ml. The in silico binding analysis showed higher binding affinity of vitexin with surface proteins of S. aureus. Down regulation of dltA, icaAB and reduction in membrane potential under sub-MIC dose of vitexin, explains reduced S. aureus surface hydrophobicity. Vitexin has substantially reduced the intracellular adhesion of planktonic cells to form biofilm through interference of EPS formation, motility and subsequent execution of virulence. This was supported by the observation that vitexin down regulates the expression of icaAB and agrAC genes of S. aureus. In addition, vitexin also found to potentiate antibiofilm activity of sub-MIC dose of gentamicin and azithromycin. Furthermore, CFU count, histological examination of mouse tissue and immunomodulatory study justifies the in vivo protective effect of vitexin from S. aureus biofilm associated infection. Finally it can be inferred that, vitexin has the ability to modulate S. aureus cell surface hydrophobicity which can further interfere biofilm formation of the bacteria.\n\nImportanceThere has been substantial information known about role of bacterial surface hydrophobicity during attachment of single planktonic bacterial cells to any surface and the subsequent development of mature biofilm. This study presents the effect of flavone phytoconstituent vitexin on modulation of cell surface hydrophobicity in reducing formation of biofilm. Our findings also highlight the ability of vitexin in reducing in vivo S. aureus biofilm which will eventually outcompete the corresponding in vitro antibiofilm effect. Synergistic effect of vitexin on azithromycin and gentamicin point to a regime where development of drug tolerance may be addressed. Our findings explore one probable way of overcoming drug tolerance through application of vitexin in addressing the issue of S. aureus biofilm through modulation of cell surface hydrophobicity.

microbiology↗