Search

Due to a limited number of informative articles available on collegiate rodeo and its athletes, the purpose of this work was to examine the relationship between anthropometric measurements and physical fitness of rodeo athletes; to add to the limited literature focused on a physical profile of rodeo athletes. Within the protocol of university IRB guidelines, 14 (20.86 ± 1.17 years; 178.2 ± 7.85 cm; 86.48 ± 21.39 Kg) male rodeo athletes at a division I school located in the Southwest United States participated in two consecutive six-week resistance training programs. Anthropometric data and fitness performance data from each participating athlete were gathered. The following data were collected: body fat percentage, lean body mass (LBM), vertical jump height, T-test, 300-yard shuttle times, barbell back squat, bench press, trap bar deadlift one repetition maximums (1RMs), single- hand reaction time, and multi-hand reaction time. Research methods included exploratory analysis - including means and standard deviations - to enable a correlational analysis. Descriptive data analysis revealed that the trap bar deadlift 1RM had a significant relationship with the bench press 1RM (r=0.874, p=0.005) and back squat 1RM (r=0.938, p=0.002). Likely due to limited experience performing resistance training, 1RM performances were possibly based on increased neuromuscular efficiencies – i.e., a ‘learning effect’. This study offers new and unique information upon the modern rodeo athlete which can help exercise science practitioners design more efficient training programs.

The adoption of the term grievance-fuelled violence reflects the fact that similarities exist between those committing violent acts in the context of grievance in different settings, so potentially allowing the application of insights gained in the study of one group to be applied to others. Given the low base rate of violence against public figures, studies in the field of violence against those in the public eye have tended to use, as a proxy for violence, attempts by the individuals concerned to achieve unwarranted and unwanted proximity to the subject of their attention, given that approach is a necessary prerequisite for most forms of attack. In such studies, one factor that has frequently been considered is whether the making of threats is associated with a subsequent approach. The results have been varied, with no correlation found in some, a negative correlation in others, and a positive correlation in at least one. Such studies have been retrospective, using case files prepared for other purposes, and samples of cases have been selected according to their victims’ sector of employment – for instance, politicians, celebrities, judiciary, and the corporate world. This study of a sample of 126 threat assessment cases, using a prospective methodology, looks at the associations between the making of threats and subsequent approach from a different angle – that of a standardised and validated classification of underlying motivation. It finds that particular types and forms of threat are significantly associated with subsequent approach in cases that are fuelled by grievance, but not in those with the motivation of seeking a relationship. Furthermore, when a sample with a mixture of motivational categories was examined in the manner of previous studies, such associations with threat were not apparent. These results refine the existing understanding of the significance of threats in public-facing cases. Future research projects in this area might usefully incorporate the consideration of underlying motivation, in particular grievance.

The kisspeptin receptor, crucial for hypothalamic control of puberty and reproduction, is also present in the pituitary gland. Its role in the pituitary gland is not defined. Kisspeptin signaling via the Kiss1r could potentially regulate reproductive function at the level of pituitary gonadotrope. Using Cre/Lox technology, we deleted the Kiss1r gene in pituitary gonadotropes (PKiRKO). PKiRKO males have normal genital development (anogenital distance WT: 19.1 ± 0.4 vs. PKiRKO: 18.5 ± 0.4 mm), puberty onset, testes cell structure on gross histology, normal testes size, and fertility. PKiRKO males showed significantly decreased serum FSH levels compared to WT males (5.6 ± 1.9 vs. 10.2 ± 1.8 ng/ml) with comparable LH (1.1 ± 0.2 vs. 1.8 ± 0.4 ng/ml) and testosterone levels (351.8 ± 213.0 vs. 342.2 ± 183.0 ng/dl). PKiRKO females have normal puberty onset, cyclicity, LH and FSH levels and fertility. Overall, these findings indicate that absence of pituitary Kiss1r reduces FSH levels in male mice without affecting testis function. PKiRKO mice have normal reproductive function in both males and females.

Understanding the mechanisms governing metabolic reprogramming that underlie potential vulnerabilities in cancer cells is key to developing novel therapeutic strategies. The catalytic enzyme UDP-glucose pyrophosphorylase 2 (UGP2) drives the production of UDP-glucose. Our recent work demonstrated the crucial role of UGP2 in cancer growth and its regulation of cellular metabolic processes.

Abstract Impaired estrogens action is associated with features of the metabolic syndrome in animal models and humans. We sought to determine whether disruption of hepatic estrogens action in adult male mice could recapitulate aspects of the metabolic syndrome to understand the mechanistic basis for the phenotype. We found 17β-estradiol (E2) inhibited hepatic gluconeogenic genes such as phosphoenolpyruvate carboxykinase 1 (Pck-1) and glucose 6-phosphatase (G6Pase) and this effect was absent in mice lacking liver estrogen receptor α (Esr1) (LERKO mice). Male LERKO mice displayed elevated hepatic gluconeogenic activity and fasting hyperglycemia. We also observed increased liver lipid deposits and triglyceride levels in male LERKO mice, resulting from increased hepatic lipogenesis as reflected by increased mRNA levels of fatty acid synthase (Fas) and acetyl-CoA carboxylase (Acc1). ChIP assay demonstrated estradiol (E2) induced ESR1 binding to Pck-1, G6Pase, Fas and Acc1 promoters. Metabolic phenotyping demonstrated both basal metabolic rate and feeding were lower for the LERKO mice as compared to Controls. Furthermore, the respiratory exchange rate was significantly lower in LERKO mice than in Controls, suggesting an increase in lipid oxidation. Our data indicate that hepatic E2/ESR1 signaling plays a key role in the maintenance of gluconeogenesis and lipid metabolism in males.

Kisspeptin was initially identified as a metastasis suppressor. Shortly after the initial discovery, a key physiologic role for kisspeptin emerged in the regulation of fertility, with kisspeptin acting as a neurotransmitter via the kisspeptin receptor, its cognate receptor, to regulate hypothalamic GnRH neurons, thereby affecting pituitary–gonadal function. Recent work has demonstrated a more expansive role for kisspeptin signaling in a variety of organ systems. Kisspeptin has been revealed as a significant player in regulating glucose homeostasis, feeding behavior, body composition as well as cardiac function. The direct impact of kisspeptin on peripheral metabolic tissues has only recently been recognized. Here, we review the emerging endocrine role of kisspeptin in regulating metabolic function. Controversies and current limitations in the field as well as areas of future studies toward kisspeptin’s diverse array of functions will be highlighted.

Ovarian steroids, estradiol and progesterone, play central roles in regulating female reproduction by acting as both positive and negative regulators of gonadotropin-releasing hormone (GnRH) secretion in the hypothalamus. Recent studies have identified kisspeptin neurons of the hypothalamus as the target of estrogenic regulation of GnRH secretion. In this study, we aimed to determine the significance of progesterone receptor (PGR) expression in the kisspeptin neurons. To this end, the Pgr gene was selectively ablated in mouse kisspeptin neurons and the reproductive consequence assessed. The hypothalamus of the Pgr deficient female mouse expressed kisspeptin, the pituitary released LH in response to GnRH stimulation, and the ovary ovulated when stimulated with gonadotropins. However, the mutant mouse gradually lost cyclicity, was unable to generate a LH surge in response to rising estradiol, and eventually became infertile. Taken together, these results indicate that the loss of PGR impairs kisspeptin secretory machinery and therefore that PGR plays a critical role in regulating kisspeptin secretion.

Infertility associated with obesity is characterized by abnormal hormone release from reproductive tissues in the hypothalamus, pituitary, and ovary. These tissues maintain insulin sensitivity upon peripheral insulin resistance. Insulin receptor signaling may play a role in the dysregulation of gonadotropin-releasing hormone (GnRH) secretion in obesity, but the interdependence of hormone secretion in the reproductive axis and the multi-hormone and tissue dysfunction in obesity hinders investigations of putative contributing factors to the disrupted GnRH secretion. To determine the role of GnRH insulin receptor signaling in the dysregulation of GnRH secretion in obesity, we created murine models of diet-induced obesity (DIO) with and without intact insulin signaling in the GnRH neuron. Obese control female mice were infertile with higher luteinizing hormone levels and higher GnRH pulse amplitude and total pulsatile secretion compared to lean control mice. In contrast, DIO mice with a GnRH specific knockout of insulin receptor had improved fertility, luteinizing hormone levels approaching lean mice, and GnRH pulse amplitude and total secretion similar to lean mice. Pituitary responsiveness was similar between genotypes. These results suggest that in the obese state, insulin receptor signaling in GnRH neurons increases GnRH pulsatile secretion and consequent LH secretion, contributing to reproductive dysfunction.

Abstract Mucin protein glycosylation is important in determining biological properties of mucus gels, which form protective barriers at mucosal surfaces of the body such as the intestine. Ecological factors including: age, sex, and diet can change mucus barrier properties by modulating mucin glycosylation. However, as our understanding stems from controlled laboratory studies in house mice, the combined influence of ecological factors on mucin glycosylation in real-world contexts remains limited. In this study, we used histological staining with ‘Alcian Blue, Periodic Acid, Schiff’s’ and ‘High-Iron diamine’ to assess the acidic nature of mucins stored within goblet cells of the intestine, in a wild mouse population (Mus musculus). Using statistical models, we identified sex as among the most influential ecological factors determining the acidity of intestinal mucin glycans in wild mice. Our data from wild mice and experiments using laboratory mice suggest estrogen signalling associates with an increase in the relative abundance of sialylated mucins. Thus, estrogen signalling may underpin sex differences observed in the colonic mucus of wild and laboratory mice. These findings highlight the significant influence of ecological parameters on mucosal barrier sites and the complementary role of wild populations in augmenting standard laboratory studies in the advancement of mucus biology.