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- All Subjects: Biology
- Creators: Kuang, Yang
- Creators: Department of Psychology
- Resource Type: Text
The bull shark, Carcharhinus leucas, is a large species that it is commonly distributed worldwide in tropical and subtropical waters. Despite the bull sharks global distribution, little is known about its life history. In particular, the limited reproductive information suggests the bull shark is placental viviparous, assumed to have a biennial cycle, and that newborn pup nurseries are near the coast. In order to conserve and protect any species, an understanding of the habitats where reproductive events occur is needed. In order to better understand the habitat use in Biscayne bay, Fla, and whether certain areas are critical during the reproductive cycle of bull sharks, I will evaluate circulating levels of the hormones progesterone, estradiol, and testosterone using radioimmunoassay. These samples were collected by the University of Miami opportunistically between 2012-2020 shipped to Arizona State University, where they were analyzed. For my study a total of 73 mature samples, 27 females and 46 males, were collected over the sampling period. The results indicated that Biscayne bay is an important gestation area for bull sharks. The hormonal trends for males and females demonstrated an interesting reproductive cycle, which were further supported through other placental viviparous reproductive patterns. Females had a low level of estradiol throughout most of the year, besides in the summer where there were no sharks in the bay due to movement to estuaries. During their return to the bay, there was a peak in progesterone indicating early pregnancy. Male testosterone levels indicated that there was a production in sperm right before females speculated peak in estradiol.
receptor (RAR) and vitamin D receptor (VDR). The RXR/RAR dimer is activated by ligand all
trans retinoic acid (ATRA), which culminates in gut-specific effector T cell migration. Similarly,
the VDR/RXR dimer binds 1,25(OH)2D3 to cause skin-specific effector T cell migration.
Targeted migration is a potent addition to current vaccines, as it would induce activated T cell
trafficking to appropriate areas of the immune system and ensure optimal stimulation (40).
ATRA, while in use clinically, is limited by toxicity and chemical instability. Rexinoids
are stable, synthetically developed ligands specific for the RXR. We have previously shown that
select rexinoids can enhance upregulation of gut tropic CCR9 receptors on effector T cells.
However, it is important to establish whether these cells can actually migrate, to show the
potential of rexinoids as vaccine adjuvants that can cause gut specific T cell migration.
Additionally, since the RXR is a major contributor to VDR-mediated transcription and
epidermotropism (15), it is worth investigating whether these compounds can also function as
adjuvants that promote migration by increasing expression of skin tropic CCR10 receptors on T
cells.
Prior experiments have demonstrated that select rexinoids can induce gut tropic migration
of CD8+ T cells in an in vitro assay and are comparable in effectiveness to ATRA (7). The effect
of rexinoids on CD4+ T cells is unknown however, so the aim of this project was to determine if
rexinoids can cause gut tropic migration in CD4+ T cells to a similar extent. A secondary aim
was to investigate whether varying concentrations in 1,25-Dihydroxyvitamin D3 can be linked to
increasing CCR10 upregulation on Jurkat CD4+ T cells, with the future aim to combine 1,25
Dihydroxyvitamin D3 with rexinoids.
These hypotheses were tested using murine splenocytes for the migration experiment, and
human Jurkat CD4+ T cells for the vitamin D experiment. Migration was assessed using a
Transwell chemotaxis assay. Our findings support the potential of rexinoids as compounds
capable of causing gut-tropic migration in murine CD4+ T cells in vitro, like ATRA. We did not
observe conclusive evidence that vitamin D3 causes upregulated CCR10 expression, but this
experiment must be repeated with a human primary T cell line.
Sleep is imperative for health and wellness with direct impacts on brain function, physiology, emotional well-being, performance and safety when compromised. Adolescents and young adults are increasingly affected by factors affecting the maintenance of regular sleep schedules. College and university students are a potentially vulnerable population to sleep deprivation and sleep insufficiency. Possible factors that could contribute to poor sleep hygiene include, but are not limited to, academic pressures, social activities, and increased screen time. Arguably, students are still experiencing bone mineralization, until the age of 30 or even 40 years old, which makes it more important to understand the effects that altered sleep patterns could have on continued development of bone health. It is our understanding that to date, studies assessing the risk of sleep insufficiency on bone mineral density in college students have not been conducted. We hypothesized that college-aged students, between the ages of 18-25 years, with shorter sleep durations, greater sleep schedule variability, and poorer sleep environments will have significantly lower bone mineral density. ActiGraph monitoring, via a wrist ActiWatch was used to quantitatively measure sleep habits for up to 7 consecutive days. During the week-long study participants also captured their self-reported sleep data through the use of a sleep diary. Participants were measured one time within the study for bone mineral density of the lumbar spine and total hip through a dual energy x-ray absorptiometry. This was a preliminary analysis of a larger cross-sectional analysis looked at 17 participants, of which there were 14 females and 3 males, (n=5, 1 and 11 Hispanic, Black and White, respectively). The mean age of participants was 20.8±1.7 y with an average BMI of 22.9±3.2 kg/m2. ActiWatch measurement data showed a mean daily sleep duration of participants to be 437.5 ± 43.1 (372.5 – 509.4) minutes. Mean sleep efficiency (minutes of sleep divided by minutes of time in bed) and mean number of awakenings were 87.4±4.3 (75.4-93.4) minutes and 32.1±6.4 (22.3-42.7) awakenings, respectively. The median time for wake after sleep onset (WASO) was 34.5±10.5 (18.3-67.4) minutes. The mean bone mineral density (BMD) for the hips was 1.06±0.14 (0.81-1.28) g/cm2 with a mean BMD of the lumbar spine being 1.24±0.12 (0.92-1.43) g/cm2. Age-matched Z-scores of the hips was 0.31±0.96 (-1.6-2.1) and lumbar spine was 0.53 (IQR: 0.13, 0.98; -2.25-1.55). Neither sleep duration nor sleep efficiency was significantly correlated to BMD of either locations. While WASO was positively associated with hip and spine BMD, this value was not statistically significant in this population. Overall, associations between sleep and BMD of the femur and spine were not seen in this cohort. Further work utilizing a larger cohort will allow for control of covariates while looking for potential associations between bone health, sleep duration and efficiency.