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Abstract The Milestones were initiated by the Accreditation Council for Graduate Medical Education (ACGME) to provide a framework for monitoring a trainee’s progression throughout residency/fellowship. The Milestones describe stepwise skill progression through six core domains of clinical competency: Patient Care, Medical Knowledge, Interpersonal and Communication Skills, Practice-based Learning and Improvement, Professionalism, and Systems-based Practice. Since their introduction in 2013, several barriers to implementation have emerged. Thus, the ACGME launched the Milestones 2.0 project to develop updated specialty-specific milestones. The Pediatric Endocrinology Milestones 2.0 project aimed to improve upon Milestones 1.0 by addressing common limitations, providing resources for faculty to easily incorporate milestones into their assessment of trainees, and adding sub-competencies in health disparities, patient safety, and physician well-being. This paper reviews the development of the Pediatric Endocrinology Milestones 2.0 including the major changes from Milestones 1.0, development of the Supplemental Guide, and how Milestones 2.0 can be applied at the program level. Although use of the Milestones are required only for ACGME programs, the tools provided in Milestones 2.0 are applicable to fellowship programs worldwide.

The factors controlling linear growth and weight gain in the human fetus and newborn infant are poorly understood. We review here the changes in linear growth, weight gain, lean body mass, and fat mass during mid- and late gestation and the early postnatal period in the context of changes in the secretion and action of maternal, placental, fetal, and neonatal hormones, growth factors, and adipocytokines. We assess the effects of hormonal determinants on placental nutrient delivery and the impact of preterm delivery on hormone expression and postnatal growth and metabolic function. We then discuss the effects of various maternal disorders and nutritional and pharmacologic interventions on fetal and perinatal hormone and growth factor production, growth, and fat deposition and consider important unresolved questions in the field.

Background . Faculty factors not inherently related to teaching effectiveness can influence teaching ratings. No studies have focused on pediatric faculty who possess unique differences from general medical faculty. Methods . We designed a retrospective observational study to compare faculty teaching ratings with measured factors across 3 academic pediatric institutions. Results . Our study included 196 faculty members. The majority (76%) of variation in teaching effectiveness ratings was not accounted for by any measured variable, but 24% was attributed to measurable factors. Increased resident exposure (sequential r 2 = .10, P < .0001) significantly affected teaching effectiveness. Variation between resident ratings of pediatric faculty teaching can be partially explained by measured factors not necessarily related to teaching effectiveness. Conclusions . The identification of faculty factors that significantly contribute to rating variation can enhance interpretation of these rating.

We present a data-based perspective concerning the recent Maclean’s magazine rankings of Canadian universities, including cluster and other analyses of the 2007 and 2008 data. Canadian universities empirically resemble and relate to each other in a manner different from their formal classification and final rank ordering in the Maclean’s system. Several pitfalls in ranking procedures, related to invalid and unreliable relationships among indices underlying the final ranks, are outlined, along with relevant findings from previous studies. In their present format, although they have become increasingly publicized and promoted, data based on the Maclean’s system are of limited practical use to students. Perhaps more important, ranking exercises have unintended though potentially serious consequences in terms of the intellectual and personal well-being of students.

Abstract A consequence of over 400 years of human exploitation of Galápagos tortoises (Chelonoidis niger ssp.) is the extinction of several subspecies and the decimation of others. As humans captured, killed, and/or removed tortoises for food, oil, museums, and zoos, they also colonized the archipelago resulting in the introduction of invasive plants, animals, and manipulated landscapes for farming, ranching, and infrastructure. Given current conservation and revitalization efforts for tortoises and their habitats, here we investigate nineteenth and twentieth century Galápagos tortoise dietary ecology using museum and archaeological specimens coupled with analysis of carbon (δ13Ccollagen and δ13Capatite), nitrogen (δ15N), hydrogen (δD) and oxygen (δ18Oapatite) stable isotopes and radiocarbon dating. We identify that Galápagos tortoise diets vary between and within islands over time, and that long-term anthropogenic impacts influenced change in tortoise stable isotope ecology by using 57 individual tortoises from 10 different subspecies collected between 1833 and 1967—a 134-year period. On lower elevation islands, which are often hotter and drier, tortoises tend to consume more C4 vegetation (cacti and grasses). Our research suggests human exploitation of tortoises and anthropogenic impacts on vegetation contributed to the extinction of the Floreana Island tortoise (C. n. niger) in the 1850s.

Despite the potential for the chemokine class as therapeutic targets in immune mediated disease, success has been limited. Many chemokines can bind to multiple receptors and many receptors have multiple ligands, with few exceptions. One of those exceptions is CCL20, which exclusively pairs to CCR6 and is associated with several immunologic conditions, thus providing a promising therapeutic target. Following successful evaluation in a single dose, first time in human clinical study, GSK3050002-a humanized IgG1 monoclonal antibody against human CCL20-was evaluated in a 26-week cynomolgus monkey toxicology study. A high incidence of unexpected vascular and organ inflammation was observed microscopically, leading to the decision to halt clinical development. Here we report a dose-responsive increase in the incidence and severity of inflammation in multiple organs from monkeys receiving 30 and 300 mg/kg/week by either subcutaneous or intravenous injection. Histomorphological changes resembled an immune complex-mediated pathology, which is often due to formation of anti-drug antibodies in monkeys receiving a human protein therapeutic and thus not predictive of clinical outcome. However, the presentation was atypical in that there was a clear dose response with a very high incidence of inflammation with a low incidence of ADA that did not correlate well individually. Additionally, the immunohistologic presentation was atypical in that the severity and distribution of tissue inflammation was greater than the numbers of associated immune complexes (i.e., granular deposits). An extensive ex vivo analysis of large molecular weight protein complexes in monkey serum from this study and in human serum samples demonstrated a time-dependent aggregation of GSK3050002, that was not predicted by in vitro assays. The aggregates also contained complement components. These findings support the hypothesis that immune complexes of drug aggregates, not necessarily including anti-drug antibodies, can fix complement, accumulate over time, and trigger immune complex disease. A situation which may have increased clinical relevance than typical anti-drug antibody-associated immune complex disease in monkeys administered human antibody proteins.

Historical and archaeological evidence documents the importation of sea turtles from the eastern Pacific Ocean (Baja California) to California during the Gold Rush (1848–1855) and through the end of 19th century, but it is unknown whether these 19th century sea turtles foraged in similar ways to their modern counterparts. To identify the species of two Gold Rush-era sea turtle specimens recovered from archaeological deposits in San Francisco, California, we first analyze ancient DNA (aDNA). We then analyze carbon (d13Ccol), nitrogen (d15N), and hydrogen (dD) stable isotopes of bone collagen and carbon (d13Cap) and oxygen (d18Oap) stable isotopes of bone apatite to test if eastern Pacific sea turtle diets have changed over the past 160 years. Ancient DNA confirms that both archaeological specimens are green sea turtles (Chelonia mydas). The stable isotope values from the 19th-century specimens are statistically indistinguishable from the modern comparatives in both d13Ccoland d15N, suggesting that green sea turtle dietary intake has remained relatively unchanged since the 1850s. However, the values are unclear for dD and d18Oapand require additional research. Social Media: Ancient DNA and isotopic analysis of 1850s sea turtles suggest stability in sea turtle foraging through time despite environmental changes.