Finding My Feet: A Dance/Movement Therapy Intern\u27s Heuristic Inquiry of Clinician Self-Care

This study is a heuristic exploration of the internship experience of one dance/movement therapy intern and the search for effective self-care methods to assist in maintaining a sense of calm and stability, as well as a sense of focus during the final academic year of a dance/movement therapy master’s program. Themes of personal and emotional stressors such as premenstrual dysphoric disorder, balancing personal and a newly emerging professional life, fitting personal religion into a secular field, trying to find self-confidence in a new creative and therapeutic role, and determining how much self-care is too much are all discussed. Previous research on clinician self-care, the effects of movement therapy on depression and stress, and the effects of intern and new clinician burnout are also touched upon to provide the reader with a clear lens through which to view this information

Cosmological constraints from the convergence 1-point probability distribution

We examine the cosmological information available from the 1-point probability distribution (PDF) of the weak-lensing convergence field, utilizing fast L-PICOLA simulations and a Fisher analysis. We find competitive constraints in the $\Omega_m$-$\sigma_8$ plane from the convergence PDF with $188\ arcmin^2$ pixels compared to the cosmic shear power spectrum with an equivalent number of modes ($\ell < 886$). The convergence PDF also partially breaks the degeneracy cosmic shear exhibits in that parameter space. A joint analysis of the convergence PDF and shear 2-point function also reduces the impact of shape measurement systematics, to which the PDF is less susceptible, and improves the total figure of merit by a factor of $2-3$, depending on the level of systematics. Finally, we present a correction factor necessary for calculating the unbiased Fisher information from finite differences using a limited number of cosmological simulations.Comment: 10 pages, 5 figure

Prolactin delays hair regrowth in mice

Mammalian hair growth is cyclic, with hair-producing follicles alternating between active (anagen) and quiescent (telogen) phases. The timing of hair cycles is advanced in prolactin receptor (PRLR) knockout mice, suggesting that prolactin has a role in regulating follicle cycling. In this study, the relationship between profiles of circulating prolactin and the first post-natal hair growth cycle was examined in female Balb/c mice. Prolactin was found to increase at 3 weeks of age, prior to the onset of anagen 1 week later. Expression of PRLR mRNA in skin increased fourfold during early anagen. This was followed by upregulation of prolactin mRNA, also expressed in the skin. Pharmacological suppression of pituitary prolactin advanced dorsal hair growth by 3.5 days. Normal hair cycling was restored by replacement with exogenous prolactin for 3 days. Increasing the duration of prolactin treatment further retarded entry into anagen. However, prolactin treatments, which began after follicles had entered anagen at 26 days of age, did not alter the subsequent progression of the hair cycle. Skin from PRLR-deficient mice grafted onto endocrine-normal hosts underwent more rapid hair cycling than comparable wild-type grafts, with reduced duration of the telogen phase. These experiments demonstrate that prolactin regulates the timing of hair growth cycles in mice via a direct effect on the skin, rather than solely via the modulation of other endocrine factors

MOLECULAR MECHANISMS ALTERING SKELETAL DEVELOPMENT AND HOMEOSTASIS IN TS65NDN DOWN SYNDROME MICE

poster abstractDown syndrome (DS) is caused by three copies of human chromosome 21 (HSA21) and results in abnormal craniofacial and appendicular bone phe-notypes. The Ts65Dn mouse model of DS contains three copies of nearly half of the genes found on HSA21, and exhibits craniofacial skeletal phenotypes similar to those observed in humans with DS. We recently demonstrated ab-normalities in the development and homeostasis of the appendicular skele-ton of Ts65Dn mice. Femurs from trisomic mice exhibit alterations in trabec-ular bone architecture and overall bone strength. Furthermore, bone for-mation rates were found to be significantly reduced, suggesting trisomy im-pacts bone development and maintenance in Ts65Dn mice, and by extension humans with DS. DYRK1A is triplicated in both humans with DS and Ts65Dn mice and its protein acts as a kinase critical during development. Dyrk1A negatively regulates the nuclear localization and activation of Nfatc, a tran-scription factor critical to signaling pathways associated with cell proliferation and bone development, and is overexpressed in the E9.5 Ts65Dn mandible precursor. We hypothesize that the previously documented Ts65Dn bone phenotype originates during embryonic development, and the presence of an extra copy of Dyrk1a contributes to the abnormal bone phenotype observed in Ts65Dn mice and humans with DS. To test our first hypothesis, analysis of the cartilage template and early bone precursor is being conducted on the femurs from embryonic day 17.5 trisomic and euploid embryos. To implicate the involvement of Dyrk1a in the DS bone phenotype, Ts65Dn mice are be-ing treated with a known Dyrk1a inhibitor, EGCG, to determine if correcting the functional expression of Dyrk1a impacts the development of the Ts65Dn postnatal bone phenotype. Understanding the molecular mechanisms under-lying DS bone phenotypes may help improve the quality of life for individuals with DS and provide viable options for the treatment of osteoporosis

EMBRYONIC BONE DEVELOPMENT AND NFAT EXPRESSION IN THE TS65DN MOUSE MODEL FOR DOWN SYNDROME

poster abstractDown syndrome (DS) is a common genetic disorder that occurs in ap-proximately 1 out of every 750 live births. DS phenotypes include cognitive deficits, altered craniofacial features, muscle hypotonia, heart defects, and abnormal bone structure. The Ts65Dn mouse model is the most common or-ganismal model used to study DS phenotypes. This model exhibits a number of phenotypic traits comparable to those of humans with DS, including bone anomalies. Past studies have shown that Ts65Dn mice exhibit weaker tra-becular bone due to less trabeculae. They have also been shown to have less bone mineral density and bone mineral content at 6 weeks of age when compared to their euploid counterparts, with the severity of these defects lessening by 16 weeks. No studies of bone development have yet decisively identified the origin of these defects. We hypothesized that abnormal endochondral ossification is responsible for the presence of these deficien-cies in bone mineral content and bone mineral density. Aberrant expression of Nfat has been implicated as the molecular cause of many DS-related phe-notypes, and activity of Nfat can be determined based upon its localization. Specifically, Nfat has been shown to control many aspects of bone develop-ment, which makes it of special interest to this research. To test our hypoth-esis of a bone deficit present during embryonic development of Ts65Dn em-bryos, we are comparing cartilaginous template characteristics, progression of the mineralization front, osteoclast activity, percent bone volume, and Nfat localization in euploid and trisomic mouse femurs at embryonic day 17.5. Our preliminary data show lower percent bone volumes in trisomic fe-murs, suggesting that endochondral ossification in Ts65Dn mice lags behind that of their euploid counterparts. These results indicate that DS bone phe-notypes do indeed originate during embryonic development and create a foundation for future work on their treatment. Supported by: National Science Foundation GK-12 Fellowship; Jerome Lejeune Foundatio