AN INVESTIGATION OF CUTTING MECHANISMS AND STRAIN FIELDS DURING ORTHOGONAL CUTTING IN CFRPs

Fiber-reinforced plastics (FRPs) are typically difficult to machine due to their highly heterogeneous and anisotropic nature and the presence of two phases (fiber and matrix) with vastly different strengths and stiffnesses. Typical machining damage mechanisms in FRPs include series of brittle fractures (especially for thermosets) due to shearing and cracking of matrix material, fiber pull-outs, burring, fuzzing, fiber-matrix debonding, etc. With the aim of understanding the influence of the pronounced heterogeneity and anisotropy observed in FRPs, ``Idealized'' Carbon FRP (I-CFRP) plates were prepared using epoxy resin with embedded equispaced tows of carbon fibers. Orthogonal cutting of these I-CFRPs was carried out, and the chip formation characteristics, cutting force signals and strain distributions obtained during machining were analyzed using the Digital Image Correlation (DIC) technique. In addition, the same procedure was repeated on Uni-Directional CFRPs (UD-CFRPs). Chip formation mechanisms in FRPs were found to depend on the depth of cut and fiber orientation with pure epoxy showing a pronounced ``size effect.'' Experimental results indicate that in-situ full field strain measurements from DIC coupled with force measurements using dynamometry provide an adequate measure of anisotropy and heterogeneity during orthogonal cutting.

SYNGAP1: Mind the Gap

A cardinal feature of early stages of human brain development centers on the sensory, cognitive, and emotional experiences that shape neuronal-circuit formation and refinement. Consequently, alterations in these processes account for many psychiatric and neurodevelopmental disorders. Neurodevelopment disorders affect 3-4% of the world population. The impact of these disorders presents a major challenge to clinicians, geneticists, and neuroscientists. Mutations that cause neurodevelopmental disorders are commonly found in genes encoding proteins that regulate synaptic function. Investigation of the underlying mechanisms using gain or loss of function approaches has revealed alterations in dendritic spine structure, function, and plasticity, consequently modulating the neuronal circuit formation and thereby raising the possibility of neurodevelopmental disorders resulting from synaptopathies. One such gene, SYNGAP1 (Synaptic Ras-GTPase-activating protein) has been shown to cause Intellectual Disability (ID) with comorbid Autism Spectrum Disorder (ASD) and epilepsy in children. SYNGAP1 is a negative regulator of Ras, Rap and of AMPA receptor trafficking to the postsynaptic membrane, thereby regulating not only synaptic plasticity, but also neuronal homeostasis. Recent studies on the neurophysiology of SYNGAP1, using Syngapl mouse models, have provided deeper insights into how downstream signaling proteins and synaptic plasticity are regulated by SYNGAP1. This knowledge has led to a better understanding of the function of SYNGAP1 and suggests a potential target during critical period of development when the brain is more susceptible to therapeutic intervention.

SYNGAP1: Mind the Gap

A cardinal feature of early stages of human brain development centers on the sensory, cognitive, and emotional experiences that shape neuronal-circuit formation and refinement. Consequently, alterations in these processes account for many psychiatric and neurodevelopmental disorders. Neurodevelopment disorders affect 3-4% of the world population. The impact of these disorders presents a major challenge to clinicians, geneticists, and neuroscientists. Mutations that cause neurodevelopmental disorders are commonly found in genes encoding proteins that regulate synaptic function. Investigation of the underlying mechanisms using gain or loss of function approaches has revealed alterations in dendritic spine structure, function, and plasticity, consequently modulating the neuronal circuit formation and thereby raising the possibility of neurodevelopmental disorders resulting from synaptopathies. One such gene, SYNGAP1 (Synaptic Ras-GTPase-activating protein) has been shown to cause Intellectual Disability (ID) with comorbid Autism Spectrum Disorder (ASD) and epilepsy in children. SYNGAP1 is a negative regulator of Ras, Rap and of AMPA receptor trafficking to the postsynaptic membrane, thereby regulating not only synaptic plasticity, but also neuronal homeostasis. Recent studies on the neurophysiology of SYNGAP1, using Syngapl mouse models, have provided deeper insights into how downstream signaling proteins and synaptic plasticity are regulated by SYNGAP1. This knowledge has led to a better understanding of the function of SYNGAP1 and suggests a potential target during critical period of development when the brain is more susceptible to therapeutic intervention.

Thermo-optic Degradation of Single-Modedness in Active LMA fibers and Simple Compensation Mechanisms

We demonstrate significant thermo-optic degradation of single-modedness in active large mode area fibers due to heat generation in the fiber. We propose and demonstrate through simulations, simple compensation mechanisms using custom length dependent fiber coiling.

Effect of strain rate response and pin diameter on mechanically mixed layer formation and wear mechanisms in a Ti6Al4V-SS316L pair

Three mechanisms operate during wear of materials. These mechanisms include the Strain Rate Response (SRR - effect of strain rate on plastic deformation), Tribo-Chemical Reactions (TCR) and formation of Mechanically Mixed Layers (MML). The present work investigates the effect of these three in context of the formation of MML. For this wear experiments are done on a pin-on-disc machine using Ti64 as the pin and SS316L as the disc. It is seen that apart from the speed and load, which control the SRR and TCR, the diameter of the pin controls the formation of MML, especially at higher speeds.