Design and Implementation of a Signal Conditioning Operational Amplifier for a Reflective Object Sensor

Industrial systems often require the acquisition of real-world analog signals for several applications. Various physical phenomena such as displacement, pressure, temperature, light intensity, etc. are measured by sensors, which is a type of transducer, and then converted into a corresponding electrical signal. The electrical signal obtained from the sensor, usually a few tens mV in magnitude, is subsequently conditioned by means of amplification, filtering, range matching, isolation etc., so that the signal can be rendered for further processing and data extraction. This thesis presents the design and implementation of a general purpose op amp used to condition a reflective object sensor’s output. The op amp is used in a non-inverting configuration, as a current-to-voltage converter to transform a phototransistor current into a usable voltage. The op amp has been implemented using CMOS architecture and fabricated in AMI 0.5-µm CMOS process available through MOSIS. The thesis begins with an overview of the various circuits involving op amps used in signal conditioning circuits. Owing to the vast number of applications for sensor signal conditioning circuits, a brief discussion of an industrial sensor circuit is also illustrated. This is followed by the complete design of the op amp and its implementation in the data acquisition circuit. The op amp is then characterized using simulation results. Finally, the test setup and the measurement results are presented. The thesis concludes with an overview of some possible future work on the sensor-op amp data acquisition circuit

Characterizing a neurodegenerative syndrome: primary progressive apraxia of speech

Apraxia of speech is a disorder of speech motor planning and/or programming that is distinguishable from aphasia and dysarthria. It most commonly results from vascular insults but can occur in degenerative diseases where it has typically been subsumed under aphasia, or it occurs in the context of more widespread neurodegeneration. The aim of this study was to determine whether apraxia of speech can present as an isolated sign of neurodegenerative disease. Between July 2010 and July 2011, 37 subjects with a neurodegenerative speech and language disorder were prospectively recruited and underwent detailed speech and language, neurological, neuropsychological and neuroimaging testing. The neuroimaging battery included 3.0 tesla volumetric head magnetic resonance imaging, [18F]-fluorodeoxyglucose and [11C] Pittsburg compound B positron emission tomography scanning. Twelve subjects were identified as having apraxia of speech without any signs of aphasia based on a comprehensive battery of language tests; hence, none met criteria for primary progressive aphasia. These subjects with primary progressive apraxia of speech included eight females and four males, with a mean age of onset of 73 years (range: 49–82). There were no specific additional shared patterns of neurological or neuropsychological impairment in the subjects with primary progressive apraxia of speech, but there was individual variability. Some subjects, for example, had mild features of behavioural change, executive dysfunction, limb apraxia or Parkinsonism. Voxel-based morphometry of grey matter revealed focal atrophy of superior lateral premotor cortex and supplementary motor area. Voxel-based morphometry of white matter showed volume loss in these same regions but with extension of loss involving the inferior premotor cortex and body of the corpus callosum. These same areas of white matter loss were observed with diffusion tensor imaging analysis, which also demonstrated reduced fractional anisotropy and increased mean diffusivity of the superior longitudinal fasciculus, particularly the premotor components. Statistical parametric mapping of the [18F]-fluorodeoxyglucose positron emission tomography scans revealed focal hypometabolism of superior lateral premotor cortex and supplementary motor area, although there was some variability across subjects noted with CortexID analysis. [11C]-Pittsburg compound B positron emission tomography binding was increased in only one of the 12 subjects, although it was unclear whether the increase was actually related to the primary progressive apraxia of speech. A syndrome characterized by progressive pure apraxia of speech clearly exists, with a neuroanatomic correlate of superior lateral premotor and supplementary motor atrophy, making this syndrome distinct from primary progressive aphasia