For those living lives devoted to taking care of others, it can be difficult to remember to take care of themselves. This thesis project is a review of quantitative and qualitative literature pertaining to self-care for the caregivers of Alzheimer's and dementia patients. Three nursing diagnoses and related nursing interventions were created using data from the evidence-based literature. With the proper knowledge and assistance, caregivers can better prepare for the future and participate in health-promoting self-care activities which may improve their quality of life.

Lossy compression is a form of compression that slightly degrades a signal in ways that are ideally not detectable to the human ear. This is opposite to lossless compression, in which the sample is not degraded at all. While lossless compression may seem like the best option, lossy compression, which is used in most audio and video, reduces transmission time and results in much smaller file sizes. However, this compression can affect quality if it goes too far. The more compression there is on a waveform, the more degradation there is, and once a file is lossy compressed, this process is not reversible. This project will observe the degradation of an audio signal after the application of Singular Value Decomposition compression, a lossy compression that eliminates singular values from a signal’s matrix.

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.