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- All Subjects: Chemistry
- Creators: School of Molecular Sciences
Though schizophrenia was categorized as a mental illness over 100 years ago, there is a plethora of knowledge that continues to perplex the scientific and medical community alike. This tragic mental disorder affects approximately 1% of the general population, and many of these individuals are homeless if left untreated. Each schizophrenia patient has a different set of symptoms, so all of these patients experience a variety of positive and negative symptoms. Negative symptoms are called so as they are in absence, and some examples include apathy, anhedonia, lack of motivation, reduced social drive, and reduced cognitive functioning. Positive behavior, on the other hand, is a change in behavior or thoughts such as visual or auditory hallucinations, delusions, confused thoughts, disorganized speech, and trouble concentrating. Because schizophrenia patients do not share the exact same set of symptoms, research in schizophrenia requires a tremendous amount of medical resources. Over the last few years, new studies have started in the field of schizophrenia involving proteomics, or the study of proteins and their function. This new frontier gives doctors and scientists alike a new opportunity to improve the quality of life of schizophrenia patients by providing a potential method through which patients would receive individualized treatment based on their specific symptoms.
In order to further compare porcine and human-derived enzymes, a determination of the enzyme effectiveness was done via digestion simulation. The digestion for both the human and porcine-derived enzymes consisted of three steps: oral, gastric, and intestinal. After the digestion, the absorbance for each enzyme class as well as a dilution curve of the formula used was read and recorded. Using the standard dilution curve and the absorbance values for each unknown, the formula and thus enzyme concentration that was lost through the reaction was able to be calculated.
The effectiveness of both the human and porcine enzymes, determined by the percent of formula lost, was 18.2% and 19.7%, respectively, with an error of 0.6% from the spectrophotometer, and an error of about 10% from the scale used for measuring the enzymes. This error was likely due to the small mass required of the enzymes and can be prevented in the future by performing the experiment at a larger scale.
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.