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In this work a review of the technology surrounding high deflection strain sensing with an emphasis on that of a recently developed nickel nano-composite strain sensor is presented. A new base silicone material was identified for the nickel nano-composite strain sensor that improves its mechanical stiffness and conductive properties. A previously identified cyclic creep concern was mitigated through preconditioning and the use of adhered backing materials. Through a block design experiment the strain/resistance curves for the strain sensors were characterized over a wide range of nano-filler material compositions. An analytical model was developed based on observation that the resistance of the sensors follows a log-normal response with respect to applied strain. The model demonstrated high fidelity in representing the resistance-strain relationship of the sensors yielding an average R2 value of .93. A standard least squares statistical analysis confirmed strong relationships between curve fit parameters of the modified log-normal model and additive volume fractions with significance at the .05 level for each case. A suitable strain gauge composition was selected for a specific application: a fetal monitoring device. A prototype belt was developed that is worn over the abdomen to detect deflections cause by labor contractions and other fetal movements. Simulation testing on the device was performed and the device was found to be a feasible option for fetal monitoring.

Sickle cell disease (SCD) is one of the most common hemoglobinopathies worldwide. It is caused by a homozygous mutation in codon 6 of the beta globin gene (HBB), which leads to polymerization of the variant hemoglobin and sickled red blood cells that obstruct blood vessels and reduce oxygen delivery to tissues. Patients with SCD have multiple clinical problems, including pain crises, anemia and organ damage. However, not all patients with SCD display all these clinical manifestations. One major factor for reduced occurrences of symptoms is fetal hemoglobin (HbF). HbF is the main hemoglobin in the fetus, and declines one year after birth to less than one percent of total hemoglobin. Nevertheless, there are individuals who continue to have high levels of HbF into adulthood, which is beneficial for an individual with SCD because HbF reduces the amount of sickle polymer in red blood cells. There are three major quantitative trait loci (QTL) associated with high HbF. However, these QTL account for 20-45% of HbF variance. Therefore, further investigation is required to fully understand how HbF is regulated. The HBS1L-MYB intergenic polymorphism (HMIP) on chromosome 6q23 is one of the major QTL associated with high HbF. This region is also known to regulate other erythroid-specific traits due to an enhancer element that promotes the expression of the downstream gene, MYB, which controls hemoglobin expression and erythroid proliferation and maturation. The presence of RNA polymerase II binding and a 50-bp transcript suggested that a long noncoding RNA (lncRNA) is transcribed from this region. LncRNAs are non-protein-coding transcripts greater than 200 nucleotides and are involved in gene regulation. Therefore, it was hypothesized that a lncRNA is transcribed from the enhancer of MYB and regulates hemoglobin expression. I characterized a novel lncRNA, 1283 bp in length that was differentially expressed among various tissue types, among erythroid progenitor cells with different hemoglobin makeup, and also during erythroid differentiation. Furthermore, knockdown of this lncRNA, named the HBS1L-MYB intergenic long noncoding RNA (HMI-LNCRNA), significantly increased HbF. Taken together, these observations suggest that HMI-LNCRNA can be a possible therapeutic target to increase HbF expression in patients with SCD and β-thalassemia. / 2018-05-01T00:00:00Z

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<p> Fetal exposure to cigarette smoke is associated with an increased risk of adult-onset metabolic abnormalities. In Canada, nicotine replacement therapy (NRT) is recommended as a safe smoking cessation aid for pregnant women. However, our laboratory has demonstrated that fetal and neonatal nicotine exposure results in glucose intolerance in adult rats. The goal of this thesis was to determine the mechanism(s) underlying the observed dysglycemia following fetal and neonatal nicotine exposure, with a specific focus on the effects of nicotine on pancreatic development and postnatal beta cell function.</p> <p> Nulliparous female Wistar rats received daily subcutaneous injections of either saline or nicotine bitartrate (1 mg/kg/d) for 2 weeks prior to mating until weaning (postnatal day 21 - PND21 ). Pancreatic tissue was collected from male offspring at birth (PND1), 3, 7, 15 and 26 weeks of age. For the critical windows study, dams received nicotine or saline during different stages of pancreatic development, including: A) pre-mating only, B) pre-mating + pregnancy only, C) pre-mating, pregnancy and lactation, or D) pre-mating + lactation only. For the intervention study, nicotine-exposed dams received either normal chow or diet containing antioxidants (1000 IU/kg vitamin E, 0.25% w/w coenzyme Q10 and 0.05% w/w α-lipoic acid) during mating, pregnancy and lactation.</p> <p> Results from this thesis demonstrate that exposure to nicotine during both fetal and neonatal development (but neither stage alone) causes a permenant loss of beta cell mass beginning at birth, and adult-onset dysglycemia in rodents. Furthermore, nicotine exposure induces pancreatic oxidative stress and mitochondrial-mediated beta cell apoptosis in neonates, followed by a progressive decline in mitochondrial structure and function. Maternal treatment with a dietary antioxidant cocktail during pregnancy and lactation protected the developing beta cells from nicotine-induced apoptosis and mitochondrial swelling. These data indicate that the safety of NRT use during pregnancy should be re-evaluated.</p> / Thesis / Doctor of Philosophy (PhD)

The objective of the present study was to evaluate the effects of low input development protocols on Southeastern replacement beef females and their offspring. Fall and spring calving crossbred beef heifers managed through one of two heifer development programs (low input, LOW or conventionally developed, CON) were evaluated for metrics of uterine artery hemodynamics, patterns of heifer and offspring growth, postpartum reproductive performance, and economic efficiency. There were significant treatment × season (P = 0.0001) and season × day (P = 0.003) interactions on heifer body weight (BW) during gestation. There was a season × day interaction on total blood flow (TBF; P = 0.05) whereby TBF increased as gestation progressed and spring calving heifers displayed increased TBF. When adjusted for BW, an additional main effect of treatment was observed (P = 0.0007) in which LOW heifers had increased TBF compared to CON heifers. There were no significant main effects of treatment or season or interactions thereof on the proportion of females cycling at the start of the breeding season (P > 0.05). Additionally, there were main effects of treatment (P = 0.0095; P = 0.02) and season (P = 0.012; P = 0.007) on calf ADG and weaning weights, respectively whereby calves born to CON females grew faster than calves born to LOW heifers, and SPRING calves gained more rapidly than FALL calves. Partial budgeting demonstrated that LOW bred heifers were $250/hd less expensive to purchase than CON heifers due to lighter BW. Calves born to LOW females yielded $6.38 less per calf compared to CON calves. The discrepancy in reproductive efficiency coupled with the failure of LOW females to achieve BW similar to CON females resulted in a difference of $403/hd in average cull value between LOW and CON females in which CON females were worth more. Thus, CON females were $159.18 more profitable than LOW females when purchased as bred heifers and sold at the weaning of their first calf. In conclusion, though uterine artery BF was not negatively affected, low input heifer development resulted in sub-optimal heifer growth, poor first calf performance, and inadequate reproductive efficiency.

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