The Propagation of Race and Racial Differences as Biological in Preclinical Education.

Modern scientific research has demonstrated that race is a social construct rather than a biological construct. Yet, medical education research suggests that medical faculty still sometimes characterize race and racial differences as biological during lectures. To explore this dynamic, we reviewed (1) how race is presented in the preclinical curriculum of an undergraduate medical institution and (2) how preclinical faculty both define race and attribute disparate health outcomes to race.

Alterations in Glucose Effectiveness and Insulin Dynamics: Polycystic Ovary Syndrome or Body Mass Index.

Background/aims: To delineate the relationship of polycystic ovary syndrome (PCOS), obesity, and hyperandrogenism (HA) with glucose and insulin dynamics in adolescents across a broad body mass index (BMI).

Methods: Seventy-four PCOS subjects (aged 16 years) and 82 controls (aged 16 years) were evaluated by an oral glucose tolerance test. Subjects were categorized by BMI: normal weight (21 ± 0.

Polycystic Ovary Syndrome in Adolescents.

Polycystic ovary syndrome (PCOS) is a familial heterogeneous disorder affecting 6% to 10% of reproductive-age women. The use of criteria developed for adult women is problematic for the adolescent girl because the clinical features associated with PCOS are normal pubertal events. The recent consensus statement on PCOS in adolescents stated that hyperandrogenism and oligomenorrhea need to persist for at least 2 years to consider the diagnosis of PCOS.

Altered decorin and Smad expression in human fetal membranes in PPROM.

Humans with Ehlers-Danlos syndrome, a subtype of which is caused by abnormal decorin expression, are at increased risk of preterm birth due to preterm premature rupture of fetal membranes (PPROM). In the mouse model, the absence of decorin leads to fetal membrane abnormalities, preterm birth, and dysregulation of decorin's downstream pathway components, including the transcription factor p-Smad-2. However, the role of decorin and p-Smad-2 in idiopathic human PPROM is unknown.