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- All Subjects: Imaging
- All Subjects: TBI
- Creators: Stabenfeldt, Sarah
ing systems. Performance of ROICs affect the quality of images obtained from IR
imaging systems. Contemporary infrared imaging applications demand ROICs that
can support large dynamic range, high frame rate, high output data rate, at low
cost, size and power. Some of these applications are military surveillance, remote
sensing in space and earth science missions and medical diagnosis. This work focuses
on developing a ROIC unit cell prototype for National Aeronautics and Space Ad
ministration(NASA), Jet Propulsion Laboratory’s(JPL’s) space applications. These
space applications also demand high sensitivity, longer integration times(large well
capacity), wide operating temperature range, wide input current range and immunity
to radiation events such as Single Event Latchup(SEL).
This work proposes a digital ROIC(DROIC) unit cell prototype of 30ux30u size,
to be used mainly with NASA JPL’s High Operating Temperature Barrier Infrared
Detectors(HOT BIRDs). Current state of the art DROICs achieve a dynamic range
of 16 bits using advanced 65-90nm CMOS processes which adds a lot of cost overhead.
The DROIC pixel proposed in this work uses a low cost 180nm CMOS process and
supports a dynamic range of 20 bits operating at a low frame rate of 100 frames per
second(fps), and a dynamic range of 12 bits operating at a high frame rate of 5kfps.
The total electron well capacity of this DROIC pixel is 1.27 billion electrons, enabling
integration times as long as 10ms, to achieve better dynamic range. The DROIC unit
cell uses an in-pixel 12-bit coarse ADC and an external 8-bit DAC based fine ADC.
The proposed DROIC uses layout techniques that make it immune to radiation up to
300krad(Si) of total ionizing dose(TID) and single event latch-up(SEL). It also has a
wide input current range from 10pA to 1uA and supports detectors operating from
Short-wave infrared (SWIR) to longwave infrared (LWIR) regions.
Time-Lapse Visualization of Microglia Cell Processes using Fluorescent Miniature (Miniscope) Imaging
Traumatic brain injury (TBI) is defined as an injury to the head that disrupts normal brain function. TBI has been described as a disease process that can lead to an increased risk for developing chronic neurodegenerative diseases, like frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS). A pathological hallmark of FTLD and a hallmark of ALS is the nuclear mislocalization of TAR DNA Binding Protein 43 (TDP-43). This project aims to explore neurodegenerative effects of TBI on cortical lesion area using immunohistochemical markers of TDP-43 proteinopathies. We analyzed the total percent of NEUN positive cells displaying TDP-43 nuclear mislocalization. We found that the percent of NEUN positive cells displaying TDP-43 nuclear mislocalization was significantly higher in cortical tissue following TBI when compared to the age-matched control brains. The cortical lesion area was analyzed for each injured brain sample, with respect to days post-injury (DPI), and it was found that there were no statistically significant differences between cortical lesion areas across time points. The percent of NEUN positive cells displaying TDP-43 nuclear mislocalization was analyzed for each cortical tissue sample, with respect to cortical lesion area, and it was found that there were no statistically significant differences between the percent of NEUN positive cells displaying TDP-43 nuclear mislocalization, with respect to cortical lesion area. In conclusion, we found no correlation between the percent of cortical NEUN positive cells displaying TDP-43 nuclear mislocalization with respect to the size of the cortical lesion area.
Annually approximately 1.5 million Americans suffer from a traumatic brain injury (TBI) increasing the risk of developing a further neurological complication later in life [1-3]. The molecular drivers of the subsequent ensuing pathologies after the initial injury event are vast and include signaling processes that may contribute to neurodegenerative diseases such as Alzheimer’s Disease (AD). One such molecular signaling pathway that may link TBI to AD is necroptosis. Necroptosis is an atypical mode of cell death compared with traditional apoptosis, both of which have been demonstrated to be present post-TBI [4-6]. Necroptosis is initiated by tissue necrosis factor (TNF) signaling through the RIPK1/RIPK3/MLKL pathway, leading to cell failure and subsequent death. Prior studies in rodent TBI models report necroptotic activity acutely after injury, within 48 hours. Here, the study objective was to recapitulate prior data and characterize MLKL and RIPK1 cortical expression post-TBI with our lab’s controlled cortical impact mouse model. Using standard immunohistochemistry approaches, it was determined that the tissue sections acquired by prior lab members were of poor quality to conduct robust MLKL and RIPK1 immunostaining assessment. Therefore, the thesis focused on presenting the staining method completed. The discussion also expanded on expected results from these studies regarding the spatial distribution necroptotic signaling in this TBI model.