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Guidelines for managing children with type 1 diabetes (TIDM) at summer camp (ADA, 2007) has been clearly outlined by the American Diabetes Association (ADA) and is similar to day care or school guidelines except for the acknowledgement of increased physical activity. Diabetes camp allows opportunities for school-aged children and adolescents to interact with peers who also have diabetes but also provides an opportunity for them to live and learn more about their chronic condition in a safe environment. Self-management is promoted in a relaxed setting. Camp provides parents a respite from the pressures of day-to-day diabetes management. Recent empirical studies suggest improved short term (after 7 months) glycemic control for adolescents, especially girls with T1DM after attending summer camp (Wang, Stewart, Tuli, & White, 2008). Typically, there is an experienced medical director at the camp who oversees the daily diabetes care of the children in partnership with the nursing staff educators, nutritionists, and in some instances, nursing, medical and pharmacy students (Condren, 2003). Camp counselors are also a critical group to the functioning of the camp and the day-to-day management of each child’s diabetes as they have 24/7 contact with the children. They should be very familiar and comfortable with the identification and management of hypo-/hyperglycemia including administering glucagon(ADA, 2007). For the Joslin and Barton Diabetes camps, diabetes education for the camp staff occurs prior to start of camp. The camp staff have had varying exposure with diabetes, some have T1DM and have attended camp themselves, others have no personal experience with T1DM. Training includes overall review of pathophysiology, signs and symptoms of hypoglycemia and hyperglycemia with associated treatment (including emergency treatment), glucose monitoring, insulin injections, pump therapy, nutrition, insulin use and exercise, and psychological issues (ADA, 2007). Human Patient Simulation (HPS) has been used in medical education (Alinier, Hunt, Gordon, & Harwood, 2006) for almost four decades, but only in the past ten years has nursing employed this educational strategy to enhance student nurse education (Dunn, 2004). In particular, the ability to improve critical thinking, decision making and clinical skills makes it potentially a viable teaching strategy to help teach caregivers of children with special health care needs (and in this case, T1DM). These life-sized computerized manikins can provide real time diabetes management experiences for parents in a controlled health care setting. Using this teaching strategy may help caregivers more quickly learn and become confident in managing the chronic condition. No reports could be found where this teaching technology has been used to educate camp staff. We were especially interested in those counselors who had not been exposed to T1DM and its management and to see if HPS would augment their learning experiences at the beginning of the camp orientation. Therefore, the purpose of this study was to pilot test the use of HPS with young adult camp staff. The aims included: To test the feasibility of teaching camp counselors with a learning vignette on hypoglycemia using the HPS compared to the standard education experience To measure differences between the experimental and control group on their diabetes knowledge and self-efficacy To explore differences controlling for baseline exposure of caring for individuals with T1DM.

Müllerian Inhibiting Substance (MIS), a secreted glycoprotein in the Transforming Growth Factor-beta (TGF-beta) family of growth factors, mediates regression of the Müllerian ducts during embryonic sex differentiation in males. In Persistent Müllerian Duct Syndrome (PMDS), rather than undergoing involution, the Müllerian ducts persist in males, giving rise to the uterus, Fallopian tubes, and upper vagina. Genetic defects in MIS or its receptor (MISRII) have been identified in patients with PMDS. The phenotype in the canine model of PMDS derived from the miniature schnauzer breed is strikingly similar to that of human patients. In this model, PMDS is inherited as a sex-limited autosomal recessive trait. Previous studies indicated that a defect in the MIS receptor or its downstream signaling pathway was likely to be causative of the canine syndrome. In this study the canine PMDS phenotype and clinical sequelae are described in detail. Affected and unaffected members of this pedigree are genotyped, identifying a single base pair substitution in MISRII that introduces a stop codon in exon 3. The homozygous mutation terminates translation at 80 amino acids, eliminating much of the extracellular domain and the entire transmembrane and intracellular signaling domains. Findings in this model may enable insights to be garnered from correlation of detailed clinical descriptions with molecular defects, which are not otherwise possible in the human syndrome.

The primary function of testicular Leydig cells is the production of androgens to promote sexual differentiation in the fetus, secondary sexual maturation at puberty, and spermatogenesis in the adult. The fetal and postnatal (adult) populations of Leydig cells differ morphologically and have distinct profiles of gene expression. As postnatal Leydig cells differentiate, they transition through three discrete maturational stages characterized by decreasing proliferative rate and increasing testosterone biosynthetic capacity. In this review, we discuss the development of both fetal and postnatal Leydig cells and review the regulation of this process by some of the key hormones and growth factors.

Individuals with Down syndrome (DS) are at an increased risk of developing thyroid disease, primarily autoimmune, with a lifetime prevalence ranging from 13% to 63% [Mattheis, 1997]. Fort et al. [1984] also found congenital hypothyroidism to be about 28 times more common among infants with DS than in the general population with an incidence of 1% (0.7% permanent and 0.3% transient congenital hypothyroidism) detected by newborn screening. Beyond the newborn period, the incidence of elevated TSH values in DS increases and has been reported to be as high as 85% of infants under the age of 12 months [Sharav et al., 1988]. This is a treatable cause of mental retardation, thus early detection and treatment are essential in order to maximize cognitive abilities in this already impaired population. Unfortunately, there are few studies systematically examining the frequency of thyroid disease in very young children. Current health supervision guidelines for children with DS suggest reviewing results of the newborn thyroid function screen, then repeating thyroid function tests at the age of 6 months and 12 months, and then annually [Cunniff et al., 2001].