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Over time, tumor treatment resistance inadvertently develops when androgen de-privation therapy (ADT) is applied to metastasized prostate cancer (PCa). To combat tumor resistance, while reducing the harsh side effects of hormone therapy, the clinician may opt to cyclically alternates the patient’s treatment on and off. This method,known as intermittent ADT, is an alternative to continuous ADT that improves the patient’s quality of life while testosterone levels recover between cycles. In this paper,we explore the response of intermittent ADT to metastasized prostate cancer by employing a previously clinical data validated mathematical model to new clinical data from patients undergoing Abiraterone therapy. This cell quota model, a system of ordinary differential equations constructed using Droop’s nutrient limiting theory, assumes the tumor comprises of castration-sensitive (CS) and castration-resistant (CR)cancer sub-populations. The two sub-populations rely on varying levels of intracellular androgen for growth, death and transformation. Due to the complexity of the model,we carry out sensitivity analyses to study the effect of certain parameters on their outputs, and to increase the identifiability of each patient’s unique parameter set. The model’s forecasting results show consistent accuracy for patients with sufficient data,which means the model could give useful information in practice, especially to decide whether an additional round of treatment would be effective.
Pelvic Circumferential Compression Devices (PCCDs), an important medical device when caring for patients with pelvic fractures, play a crucial role in the stabilization and reduction of the fracture. During pelvic fracture cases, control of internal bleeding through access to the femoral artery is of utmost importance. Current designs of PCCDs do not allow vital access to this artery and in attempts to gain access, medical professionals and emergency care providers choose to cut into the PCCDs or place them in suboptimal positions with unknown downstream effects. We researched the effects on surface pressure and the overall pressure distribution created by the PCCDs when they are modified or placed incorrectly on the patient. In addition, we investigated the effects of those misuses on pelvic fracture reduction, a key parameter in stabilizing the patient during critical care. We hypothesized that incorrectly placing or modifying the PCCD will result in increased surface pressure and decreased fracture reduction. Our mannequin studies show that for SAM Sling and T-POD, surface pressure increases if a PCCD is incorrectly placed or modified, in support of our hypothesis. However, opposite results occurred for the Pelvic Binder, where the correctly placed PCCD had higher surface pressure when compared to the incorrectly placed or modified PCCD. Additionally, pressure distribution was significantly affected by the modification of the PCCDs. The cadaver lab measurements show that modifying or incorrectly placing the PCCDs significantly limits their ability to reduce the pelvic fracture. These results suggest that while modifying or incorrectly placing PCCDs allows access to the femoral artery, there are potentially dangerous effects to the patient including increased surface pressures and limited fracture reduction.
Pelvic Circumferential Compression Devices (PCCDs), an important medical device when caring for patients with pelvic fractures, play a crucial role in the stabilization and reduction of the fracture. During pelvic fracture cases, control of internal bleeding through access to the femoral artery is of utmost importance. Current designs of PCCDs do not allow vital access to this artery and in attempts to gain access, medical professionals and emergency care providers choose to cut into the PCCDs or place them in suboptimal positions with unknown downstream effects. We researched the effects on surface pressure and the overall pressure distribution created by the PCCDs when they are modified or placed incorrectly on the patient. In addition, we investigated the effects of those misuses on pelvic fracture reduction, a key parameter in stabilizing the patient during critical care. We hypothesized that incorrectly placing or modifying the PCCD will result in increased surface pressure and decreased fracture reduction. Our mannequin studies show that for SAM Sling and T-POD, surface pressure increases if a PCCD is incorrectly placed or modified, in support of our hypothesis. However, opposite results occurred for the Pelvic Binder, where the correctly placed PCCD had higher surface pressure when compared to the incorrectly placed or modified PCCD. Additionally, pressure distribution was significantly affected by the modification of the PCCDs. The cadaver lab measurements show that modifying or incorrectly placing the PCCDs significantly limits their ability to reduce the pelvic fracture. These results suggest that while modifying or incorrectly placing PCCDs allows access to the femoral artery, there are potentially dangerous effects to the patient including increased surface pressures and limited fracture reduction.
Cancer rates vary between people, between cultures, and between tissue types, driven by clinically relevant distinctions in the risk factors that lead to different cancer types. Despite the importance of cancer location in human health, little is known about tissue-specific cancers in non-human animals. We can gain significant insight into how evolutionary history has shaped mechanisms of cancer suppression by examining how life history traits impact cancer susceptibility across species. Here, we perform multi-level analysis to test how species-level life history strategies are associated with differences in neoplasia prevalence, and apply this to mammary neoplasia within mammals. We propose that the same patterns of cancer prevalence that have been reported across species will be maintained at the tissue-specific level. We used a combination of factor analysis and phylogenetic regression on 13 life history traits across 90 mammalian species to determine the correlation between a life history trait and how it relates to mammary neoplasia prevalence. The factor analysis presented ways to calculate quantifiable underlying factors that contribute to covariance of entangled life history variables. A greater risk of mammary neoplasia was found to be correlated most significantly with shorter gestation length. With this analysis, a framework is provided for how different life history modalities can influence cancer vulnerability. Additionally, statistical methods developed for this project present a framework for future comparative oncology studies and have the potential for many diverse applications.