Abstract
Gallium nitride high-electron-mobility transistors (GaN-HEMTs) suffer from trapping effects that increases device on-state resistance ( $R_\mathrm{DS(on)}$ ) above its theoretical value. This increase is a function of the applied dc bias when the device is in its off state, and the time which the device is biased for. Thus, dynamic $R_\mathrm{DS(on)}$ of different commercial GaN-HEMTs are characterised at different bias voltages in the paper by a proposed new measurement circuit. The time-constants associated with trapping and detrapping effects in the device are extracted using the proposed circuit and it is shown that variations in $R_\mathrm{DS(on)}$ can be predicted using a series of RC circuit networks. A new methodology for integrating these $R_\mathrm{DS(on)}$ predictions into existing gallium nitride-high-electron-mobility transistors models in standard SPICE simulators to improve model accuracy is then presented. Finally, device dynamic $R_\mathrm{DS(on)}$ values of the model is compared and validated with the measurement when it switches in a power converter with different duty cycles and switching voltages.
Highlights
Parkinson’s disease (PD) is a neurodegenerative motor disorder that primarily affects the elderly
Rodents within the PD model groups spent a significantly increased time in the beam and pole tests compared to controls, whereas rodents that received BCP both orally and i.p., or RSV, displayed significantly decreased beam and pole test times [51,52,54,57]
One study monitored mitochondrial complex-I (MC-1) activity, which was decreased in the PD model group but significantly increased by RSV treatment [50]
Summary
Parkinson’s disease (PD) is a neurodegenerative motor disorder that primarily affects the elderly. Patients with PD may display non-motor symptomology and overlap of signs and symptoms with atypical Parkinsonian syndromes such as multiple system atrophy (MSA) and dementia with Lewy bodies, which renders absolute diagnosis challenging [2]. PD is characterized histopathologically by the loss of dopaminergic neurons within the substantia nigra pars compacta (SNpc) and accumulation of protein aggregates including α-synuclein within Lewy-bodies (LBs) [6,7,8,9]. The oligomeric and aggregated forms of α-synuclein can be neurotoxic and can promote loss of dopaminergic neurons [6,7,8,9]. PD is primarily an idiopathic disease, for which age is the major risk factor [10]. Genetic vulnerability to PD has been observed in a minority of PD cases (10–15%) via rare familial mutants, including those in α-synuclein that trigger early onset
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