Acute aerobic exercise alters neurotrophic and growth factor concentrations, increases neural activity and improves cognitive and motor function. Additionally, acute exercise increases excitation and reduces inhibition in the motor cortex as assessed via transcranial magnetic stimulation (TMS). The propensity for exercise-induced neuroplasticity may be greater in females, as females show greater neuroplasticity induction following non-invasive brain stimulation (NIBS) compared to males. In females, NIBS yields greater neuroplasticity during ovulation, when estradiol levels are higher, compared to menstruation, suggesting that ovarian hormones may also impact exercise-induced neuroplasticity. To date, it is unknown whether biological sex and ovarian hormones impact neuroplasticity induced by acute aerobic exercise. The present thesis investigated the effects of biological sex and ovarian hormones on the magnitude and direction of neuroplasticity induced by acute aerobic exercise. Fourteen females and fourteen age- and fitness-matched males participated in two sessions in which dependent measures were acquired before and following a single bout of aerobic exercise. Females were tested in the follicular (~day 7) and luteal (~day 21) phases of the menstrual cycle and males were also tested on two occasions separated by ~14 days. The exercise intervention consisted of 5 minutes of warm up, 20 minutes of moderate intensity continuous cycling at 65-70% maximal heart rate, and 5 minutes cool down. TMS was used to obtain motor evoked potential (MEP) recruitment curves and short interval intracortical inhibition (SICI) from the right first dorsal interosseous muscle. Blood measures of estradiol, progesterone, testosterone, and brain-derived neurotrophic factor were assessed before exercise on both testing sessions. Results indicated that only females showed increases in MEP recruitment curve following exercise, and this occurred regardless of menstrual cycle phase. SICI did not change following exercise for males or females on either testing session. The estrogen to progesterone ratio in females was greater in the follicular phase compared to the luteal phase. There was a trend towards greater serum BDNF levels in females in the luteal phase compared to the follicular phase. Sex hormones and BDNF levels did not vary across sessions in males. These findings indicate biological sex, but not ovarian hormones, is an important factor to consider when inducing neuroplasticity using acute exercise. / Thesis / Master of Science (MSc)

Congestive heart failure represents one of the leading causes of death in industrialized countries. A subset of heart failure situations are linked to genetic mutations, many of which reside in sarcomeric proteins. With the prevalence of mutations as approximately 1:500, the location of a mutation plays a direct role in the severity and lethality of the resulting disease state. The point mutation Arg403Glu (R403Q) located on the myosin heavy chain molecule is no exception with a resulting development of left ventricular hypertrophy, myocyte disarray, and increased cellular fibrosis. Given the severity of this mutation in humans, a mouse model was developed to recapitulate these phenotypic characteristics. An additional confounding factor often overlooked when studying the effects of cardiac disease is the role of biological sex. We, therefore, tested the hypothesis that R403Q mice will display altered crossbridge kinetics, specifically an increase in functioning at the expense of energy efficiency, and that biological sex will impact the cardiac response to the R403Q mutation in terms of both crossbridge functioning and post-translational modifications. To do this, we used both male and female R403Q transgenic mice and quantified myofilament mechanical properties including Ca²⁺ sensitivity, crossbridge cycling kinetics, and tension cost of contraction. In addition, phosphorylation patterning was quantified for one of the central, sarcomeric regulatory proteins, cardiac troponin I. We used 2 month animals which do not display overt pathology in the form of hypertrophy in order to minimize downstream, confounding effects. We were able to find that disease and biological sex played an important role in defining these parameters and suggests females are able to better compensate to the presence of altered sarcomeric interactions. Future investigations should focus on altered kinase activity, possibly driven by interactions with estrogen, in order to better define how females can retain cardiac functioning given a disease condition.

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Heat stress (HS) is a substantial economic burden for the livestock industry, and the problem is expected to increase because of unprecedented warming temperatures caused by climate change. Skeletal muscle, which is the main source of income for the meat industry, is particularly sensitive to HS. Lean tissue accretion declines during HS, in part because of inefficient metabolism and altered metabolic flexibility. The first study examined whether thyroid hormone (TH) administration during HS could maintain metabolic flexibility in HS skeletal and cardiac muscle. Gilts (n=39) were placed in one of five treatment groups: Thermoneutral control (TNC), HS for 1 day (HS1C), HS1 with TH supplementation (HS1TH), HS for 7 days (HS7C), HS7 with TH supplementation (HS7TH). Semitendinosus red skeletal muscle (STR) and right ventricle cardiac muscle (RV) were dissected and snap-frozen for subsequent analysis. Metabolic flexibility (MF; P=0.08) tended to differ between HS1C, HS7C, with HS7TH being the lowest (P < 0.05) in STR. Pyruvate oxidation significantly differed with the lowest in HS1TH and highest in HS7TH in RV muscles (P < 0.05) but metabolic flexibility did not differ. However, citrate synthase (CS) and cytochrome C oxidase (COX) activity did not differ between treatments. The second experiment investigated the difference in skeletal muscle metabolism between gilts and barrows. Pigs (n=8/sex) were exposed to TNC, HS1, or HS7 environments. Skeletal muscle samples were used to analyze in vivo metabolism. Barrows tended (P=0.09) to be more MF than gilts even though no changes in mitochondrial enzyme activity were observed. However, gilts differed between environmental treatments regarding CS activity (P=0.03). Blood serum from the treated pigs was placed on skeletal muscle cell cultures. Metabolic flexibility between the in vivo muscle samples and the cell cultures was similar. In vitro culture at 37°C recapitulated the in vivo metabolic flexibility pattern. When the cell culture temperature was maintained at 41°C, MF was the lowest in cultures that received HS7 blood serum. In vitro males incubated at 41°C displayed an increase in CS and COX activity (P<0.01) but females increased 3-hydroxyacyl-CoA dehydrogenase (BHAD) activity at the same incubation temperature (P=0.02). This data indicates that in vivo systemic factor(s) can alter skeletal muscle metabolism in vitro. / Master of Science / Heat stress (HS) presents a significant economic challenge to the livestock industry, particularly affecting the growth of skeletal muscle, which is vital for meat production. This problem is expected to worsen with climate change. In this study, we explored the potential of thyroid hormone (TH) supplementation to maintain metabolic flexibility in skeletal and cardiac muscles during HS. We exposed gilts to varying HS conditions and administered TH to determine its impact on metabolic processes in muscle tissues. Results showed that HS reduced metabolic flexibility, with TH supplementation having a beneficial effect on pyruvate oxidation in cardiac muscle under chronic HS conditions but no significant impact on skeletal muscle. Additionally, we compared the metabolic responses of male and female pigs under different environmental conditions and found that males tended to maintain better metabolic flexibility in vivo. In vitro experiments using muscle cell cultures confirmed that the systemic effects from HS pigs could alter muscle metabolism. These findings suggest that biological sex may impact some of the metabolic disruptions caused by HS, though further research is needed to fully understand the mechanisms involved.

Genetic sex -the apparent fundamental biological cause of the two male and female human varieties- is a 20th century construct. Looking down the microscope, the stained chromosomes are concrete countable entities and lend themselves easily to genetic determinism. As the chromosome composition of a person is generally fixed at the time of conception, when a Y- or X-bearing sperm is united with the X-bearing egg, a person’s genetic sex is taken as permanent and unchanging throughout their life. Drawing upon gender theory as well as science and technology studies this thesis explores how our particular construction of the concept of ‘genetic sex’ relies on four features of biological sex (binary, fixed, spanning nature, and found throughout the body) and in addition proposes one unique feature, inheritance. The empirical research is based on an analysis of popular science books as well as two case studies of how genes relate to sex determination and development. The analysis of the metaphors used in these books and journal articles reveals how now, with genomic efforts to explore gene expression profiles, there is a shift away from seeing genes as having ‘responsibilities’ for determining phenotypes towards seeing them play a role along with other genes in genetic cascades where other factors such as timing can be incorporated. The analysis of genomic features such as imprinting and X-chromosome inactivation also provide evidence that such a change should be recognised. Rather than seeing sex in terms of fixed and static differences and similarities, current research offers new ways of conceptualising similarities and differences as dynamic and responsive to environment. This supports wider understandings of ‘biology’ as relying on the interactions between genetic processes, cellular environment, and tissue environment – in which the social physicality of bodies is important in forming and maintaining a person’s biology and genetic processes. Yet as the historical analysis of the shift between the one sex to two sex model indicates, it remains to be seen whether the social sphere will respond by incorporating this new evidence into the tacit, everyday understandings of sex or seek to maintain the binary and fixed relationship(s) between men and women by governing them as males and females.

This study examined to what extent the biological sex of the nurse-physician interactants affects the interpersonal communication satisfaction experienced by the nurse. Hypotheses One and Two predicted that communication satisfaction would differ significantly across various combinations of sex of nurse and sex of physician dyads. Hypothesis Three predicted that male nurses would experience higher levels of communication satisfaction than would female nurses. Interpersonal communication satisfaction was operationalized by two self-report instruments. The sample included 153 male and female nurses. Results indicated that same-sex interactions were more satisfying for female nurses, while mixed-sex interactions were more satisfying for male nurses. Nurses reported greater communication satisfaction when interacting with female physicians. Hypothesis three was not supported.

This thesis examines in Swedish teacher education often neglected areas to increase the understanding for the essential differences between the two sexes and furthermore: how these differences affect us from an evolutionary and biological perspective. The study investigates previous research within the area - particularly evolution, neurology, hormones and genetics that affects our behavior. It also scrutinizes theories of social construction which primarily lodged the foundation for learning within the last century and served as explanation model for how human beings turn out in life. Research is analyzed regarding how music may be perceived differently and how they may affect stereotypical choices regarding instrument and other preferences. Also, the study evaluates research regarding how the Swedish school is designed to uphold gender equality in their goals and in their national curriculum. Finally, conclusions whether the Swedish school is providing enforcement regarding scientific regulations, which the law demands from it – in this case biological factors – are being looked at. The results show that biological differences between males and females may influence human behavior to a greater degree than earlier predictions, and that the Swedish school is mostly founded on a social constructionist point of view. These results indirectly question the Swedish National Agency for Education’s definition of equality, which paradoxical may lead to equity. Or, equality by outcome. Which do not take biological sex differences, or even individual differences into account.

No description available.

Firstly, the theoretical framework of this thesis presents definitions of terms that will be needed further on in the thesis. Primarily, there are definitions of stress, teaching profession and gender. The theoretical part of the thesis also serves as an overview of existing knowledge about the occupational stress of teachers. Lastly, I will try to elucidate the problems associated with measuring and interpreting selected studies on the occupational stress of teachers. The practical part of the thesis states three research problems. The first one explores the connection between the teacher's biological sex and the degree of occupational burnout, the second research problem examines the connection between the personality type of the teacher and the degree of occupational burnout and the last one puts the teacher's workload in the context of an inclusive environment. In principle, it has been established that individual mediators have no significant influence on the perceived workload of the teacher.

Adipose tissue inflammation has an impact on liver health and it has been demonstrated that chronic alcohol consumption leads to the expression of pro-inflammatory markers in the adipose tissue. A thorough characterization of alcohol-induced adipose inflammation is lacking, and is important to understand in order to identify immune-related mechanisms that drive this phenomenon. Current therapeutic regimens for alcoholic liver disease are ineffective. It is critical to understand how other organs influence liver injury in this disease when developing novel and effective therapies in the future. Alcoholic liver disease exhibits a sexual dimorphism; women are more susceptible to liver injury than men and the same paradigm exists in rodent models. Here, I demonstrate that female mice have greater alcohol-induced adipose tissue inflammation than male mice, evidenced by greater expression of pro-inflammatory cytokines and cell markers. Further, female mice also exhibit higher expression of toll-like receptor genes in the adipose tissue, suggesting a potential role for the innate immune system in alcohol-induced adipose inflammation. Toll-like receptor 4 (TLR4) has been demonstrated to drive inflammation in both the liver and adipose tissue. I used both germline and conditional knockouts of Tlr4 to characterize alcohol-induced changes in the immune cell composition of adipose tissue. Alcohol increased the number of pro-inflammatory adipose tissue macrophages. This macrophage phenotype switching is partially dependent on TLR4; germline, but not myeloid-specific, Tlr4-deletion prevents macrophage phenotype switching. Overall, my work demonstrates that alcohol-induced adipose tissue inflammation is related to liver injury and that TLR4 contributes to adipose macrophage phenotype switching.