Quantifying Hand Strength and Isometric Pinch Individuation Using a Flexible Pressure Sensor Grid.

Modulating force between the thumb and another digit, or isometric pinch individuation, is critical for daily tasks and can be impaired due to central or peripheral nervous system injury. Because surgical and rehabilitative efforts often focus on regaining this dexterous ability, we need to be able to consistently quantify pinch individuation across time and facilities. Currently, a standardized metric for such an assessment does not exist.

Quantitative assessments of finger individuation with an instrumented glove.

Background: In clinical and research settings, hand dexterity is often assessed as finger individuation, or the ability to move one finger at a time. Despite its clinical importance, there is currently no standardized, sufficiently sensitive, or fully objective platform for these evaluations.

Methods: Here we developed two novel individuation scores and tested them against a previously developed score using a commercially available instrumented glove and data collected from 20 healthy adults.

Synchronization of kinetic and kinematic hand tasks with electrocorticography and cortical stimulation during awake craniotomies.

Awake craniotomies provide unique and invaluable scientific opportunities for neurophysiological experimentation in consenting human subjects. While such experimentation carries a long history, rigorous reporting of methodologies focusing on synchronizing data across multiple platforms is not universally reported and often not translatable to across operating rooms, facilities, or behavioral tasks. Therefore, here we detail an intraoperative data synchronization methodology designed to work across multiple commercially available platforms to collect behavioral and surgical field videos, electrocorticography, brain stimulation timing, continuous finger joint angles, and continuous finger force production.

Mechanisms and therapeutic implications of hypermutation in gliomas.

A high tumour mutational burden (hypermutation) is observed in some gliomas; however, the mechanisms by which hypermutation develops and whether it predicts the response to immunotherapy are poorly understood. Here we comprehensively analyse the molecular determinants of mutational burden and signatures in 10,294 gliomas. We delineate two main pathways to hypermutation: a de novo pathway associated with constitutional defects in DNA polymerase and mismatch repair (MMR) genes, and a more common post-treatment pathway, associated with acquired resistance driven by MMR defects in chemotherapy-sensitive gliomas that recur after treatment with the chemotherapy drug temozolomide.