LU|ZONE|UL Collection: Masters Theses of Laurentian UniversityMasters Theses of Laurentian Universityhttps://zone.biblio.laurentian.ca/handle/10219/4792024-03-29T02:14:03Z2024-03-29T02:14:03ZMuscle temperature influences oxygen uptake and blood flow during single leg isokinetic exercise.McCue, Alexushttps://zone.biblio.laurentian.ca/handle/10219/37992022-01-20T03:49:12Z2020-12-02T00:00:00ZTitle: Muscle temperature influences oxygen uptake and blood flow during single leg isokinetic exercise.
Authors: McCue, Alexus
Abstract: Thermal changes in muscle tissues (i.e: cooling and heating) modulate local oxygen
transport from the muscle and into the cell. Whether a change in skeletal muscle oxygen
transport subsequently regulate oxygen consumption (V̇ O2m) and tissue oxygenation
(%TSI) during exercise is unclear. The purpose of this study was to assess the effects of
skeletal muscle cooling and heating on muscle blood flow (Q̇ mus), V̇ O2m, and %TSI during
single-leg isokinetic exercise. Eleven men exercised during 3-min intervals under
thermoneutral (TN) condition, and localized muscle heating (HT) and cooling (CO), at
10%, 30%, and 50% of their maximal voluntary contraction (MVC). An occlusion
technique combined to near-infrared spectroscopy was used to estimate V̇ O2m and Q̇ mus
before and after exercise bouts.
The results of this study showed that Q̇ mus was significantly increased in HT, while
V̇ O2m was instead decreased in CO. Muscle temperature did not significantly change %TSI
during exercise. Moreover, the relationship between Q̇ mus and V̇ O2m (TN: 0.173 0.101,
CO: 0.187 0.0655, and HT:0.107 0.0413) was steeper in CO compared to HT (p =
0.009). In conclusion, this study demonstrated that muscle temperature regulates the blood
flow/O2 consumption relationship during incremental isokinetic exercise.2020-12-02T00:00:00ZThe effects of YAP activity on retinoic acid signaling in the embryonic epicardiumBongfeldt, Danika P.https://zone.biblio.laurentian.ca/handle/10219/37972024-03-27T07:35:54Z2020-12-17T00:00:00ZTitle: The effects of YAP activity on retinoic acid signaling in the embryonic epicardium
Authors: Bongfeldt, Danika P.
Abstract: Retinoic acid (RA), a metabolite of vitamin A, is primarily produced by epicardial cells
and is required for the proper differentiation of epicardial cells into cardiac fibroblasts and VSMCs
during heart development. Recent literature has suggested that both mechanotransduction, which
is mechanical stimuli eliciting chemical responses within the cell, and the Hippo signaling pathway
could potentially regulate RA-signaling. The transcriptional co-activator YAP is regulated by the
Hippo-pathway and mechanotransduction and elicits changes in gene transcription through the
TEAD transcription factor. Recently it was found that there were TEAD motifs in the Dhrs3 gene
and YAP showed specific binding to the Dhrs3 enhancer via chromatin immunoprecipitation
combined with qPCR (ChIP-PCR) in the mouse epicardial cell line MEC1. However, beyond its
effects on the expression of Dhrs3 it is not clear if YAP actually affects RA-signaling. We
hypothesized that YAP regulates retinoic acid signaling in embryonic epicardial cells. The first
aim was to assess if YAP regulates the transcription of enzymes and receptors involved in RA
metabolism or signaling in MEC1 cells. Using RT-qPCR we investigated the effect of
constitutively active YAP, or conversely suppressed YAP activity on Dhrs3, Raldh2, RAR𝛽,
Cyp26A1, and Cyp26B1 expression. To suppress YAP activity, a YAP small interfering RNA
(siRNA), or the YAP-TEAD chemical inhibitor, Verteporfin, were utilized but these manipulations
did not show significant effects on YAP targets, or retinoid receptors and enzymes in MEC1 cells.
To overexpress YAP, a constitutively active form of YAP, YAP25SA, was transfected into MEC1
cells. We were able to confirm a direct relationship between Cyp26a1 expression and YAP activity
as YAP25SA increased Cyp26a1 mRNA expression by 37.8-fold within 6 hours of transfection.
As well, we were able to determine that YAP25SA affected Cyp26a1 expression through a TEAD
mechanism; as co-transfection of YAP25SA with YTIP-GFP, a plasmid expressing a peptide that interferes with YAP-TEAD interaction significantly diminished the effects of YAP25SA on
Cyp26a1 expression. The second aim investigated if YAP regulates the metabolism of retinol into
RA by utilizing the two-hybrid Gal4-RAR;UAS-tk-Gaussia luciferase reporter system that
estimate the amount of RA produced by monitoring the activation of the Gal4RAR reporter.
Transfection of MEC1 cells with YAP25SA allowed more retinol to be converted to RA and for a
longer period of time when compared to the control. Since the activity of YAP influences the
expression of Cyp26a1 and metabolism of retinol, it was concluded that YAP activity plays a role
in RA-signaling.2020-12-17T00:00:00ZFreedom in play, as opposed to control in gamesSoderman, S. Lowellhttps://zone.biblio.laurentian.ca/handle/10219/37952022-01-20T03:48:18Z2021-05-14T00:00:00ZTitle: Freedom in play, as opposed to control in games
Authors: Soderman, S. Lowell
Abstract: In this thesis I identify an important distinction: play per se is essentially free, whereas games per
se are to the contrary essentially controlled. While free play and controlled games are regularly
complimentary, I argue there can be rather substantive dangers when this distinction is variously
confused, such that being free is wrongly understood as being controlled, or vice versa where
being controlled is wrongly understood as being free.2021-05-14T00:00:00ZHigh-fat diet-induced loss of muramyl dipeptide sensitivityWilliams, Laura Mariehttps://zone.biblio.laurentian.ca/handle/10219/37942024-03-27T07:33:38Z2020-08-24T00:00:00ZTitle: High-fat diet-induced loss of muramyl dipeptide sensitivity
Authors: Williams, Laura Marie
Abstract: Glucagon-like peptide-1 (GLP-1) is an insulin-stimulating hormone released from
enteroendocrine cells. Muramyl dipeptide (MDP) is a peptidoglycan motif which has insulin-
sensitizing effects in obesogenic mice by acting through the nucleotide oligomerization domain 2
(NOD2) receptor. We hypothesized that MDP enhances glucose tolerance by inducing intestinal
GLP-1 secretion through NOD2 activation. We observed a significant increase in GLP-1
secretion when L-cells were treated with a fatty acid MDP derivative (L18-MDP). Additionally,
we demonstrated NOD2 expression in mouse intestine and in L-cells. Two intraperitoneal
injections of MDP (5mg/kg) significantly increased fasting total GLP-1 in chow-fed mice; an
effect that was lost during the onset of hyperglycemia during a high-fat diet. No improvement in
oral glucose tolerance was observed in MDP-treated mice. Finally, we demonstrated in L-cells
that hyperglycemic conditions reduce NOD2 and GLP-1 mRNA expression. Together these
findings suggest MDP may play a role in enhancing GLP-1 during euglycemia but loses its
ability to do so in hyperglycemia.2020-08-24T00:00:00Z