Psychometric properties of the simplified Chinese version of the observer OPTION5 scale.

BACKGROUND: OPTION5 is a scale used to evaluate shared decision making (SDM) in health care from an observer's perspective; however, to date, there is no simplified Chinese version of this scale. OBJECTIVES: This study aims to produce a simplified Chinese version of the OPTION5 scale and to test its psychometric properties. METHODS: One rater observed and audio-recorded consultations between general practitioners (GPs) and chronically ill patients in a Beijing community health service center (CHSC) from May to June 2019. Meanwhile, demographic data of the patients and GPs were collected via information forms. Two raters assessed inter- and intra-rater reliability by calculating the intraclass correlation coefficient (ICC) and weighted Cohen's Kappa values. Internal consistency was assessed using Cronbach's α value. Concurrent was calculated by Spearman's rank correlation coefficient. RESULTS: A total of 209 consultations were recorded and evaluated. As concerns inter-rater reliability, the ICC of the OPTION5 was 0.859 on the total score level, with Cohen's weighted k ranging from 0.376 (item 5) to 0.649 (item 2) on the single item level. With regard to intra-rater reliability, the ICC was 0.945 on the total score level, with Cohen's weighted k ranging from 0.469 (item 5) to 0.883 (item1) on the single item level. Cronbach's α value of all 5 items amounted to 0.746. Spearman's rank correlation coefficient between OPTION5 and OPTION12 for Chinese versions was 0.660. CONCLUSIONS: The simplified Chinese version of the OPTION5 scale, developed using stringent translation procedures, demonstrated satisfactory psychometric characteristics. Specifically, inter- and intra-rater reliabilities were excellent, while criterion validity was moderate. The simplified Chinese version of the OPTION5 scale can be implemented in clinical settings to evaluate SDM of treatment during consultations between GPs and chronically ill patients.

Aberrant H19 Expression Disrupts Ovarian Cyp17 and Testosterone Production and Is Associated with Polycystic Ovary Syndrome in Women.

As one of the most common endocrine disorders affecting women, polycystic ovary syndrome (PCOS) is associated with serious conditions including anovulation, endometrial cancer, infertility, hyperandrogenemia, and an increased risk for obesity and metabolic derangements. One contributing etiology to the pathophysiology of hyperandrogenemia associated with PCOS is an intrinsic alteration in ovarian steroidogenesis, leading to enhanced synthesis of androgens including testosterone. Studies have suggested that the increased testosterone synthesis seen in PCOS is driven in part by increased activity of CYP17A1, the rate-limiting enzyme for the formation of androgens in the gonads and adrenal cortex, which represents a critical factor driving enhanced testosterone secretion in PCOS. In this work, we evaluated the hypothesis that dysregulation of the noncoding RNA H19 results in aberrant CYP17 and testosterone production. To achieve this, we measured Cyp17 in ovarian tissues of H19 knockout mice, and quantified serum testosterone levels, in comparison with wild-type controls. We also evaluated circulating and ovarian H19 expression and correlated results with the presence or absence of PCOS in a group of women undergoing evaluation and treatment for infertility. We found that the loss of H19 in a mouse model results in decreased ovarian Cyp17, along with decreased serum testosterone in female mice. Moreover, utilizing serum samples and cumulus cells from women with PCOS, we showed that circulating and ovarian levels of H19 are increased in women with PCOS compared to controls. Findings from our multimodal experimental strategy, involving both a mouse model of dysregulated H19 expression and clinical serum and ovarian cellular samples from women with PCOS, suggest that the loss of H19 may disrupt androgen production via a Cyp17-mediated mechanism. Conversely, excess H19 may play a role in the pathogenesis of PCOS-associated hyperandrogenemia.

Emerging roles for noncoding RNAs in female sex steroids and reproductive disease.

The "central dogma" of molecular biology, that is, that DNA blueprints encode messenger RNAs which are destined for translation into protein, has been challenged in recent decades. In actuality, a significant portion of the genome encodes transcripts that are transcribed into functional RNA. These noncoding RNAs (ncRNAs), which are not transcribed into protein, play critical roles in a wide variety of biological processes. A growing body of evidence derived from mouse models and human data demonstrates that ncRNAs are dysregulated in various reproductive pathologies, and that their expression is essential for female gametogenesis and fertility. Yet in many instances it is unclear how dysregulation of ncRNA expression leads to a disease process. In this review, we highlight new observations regarding the roles of ncRNAs in the pathogenesis of disordered female steroid hormone production and disease, with an emphasis on long noncoding RNAs (lncRNAs) and microRNAs (miRNAs). We will focus our discussion in the context of three ovarian disorders which are characterized in part by altered steroid hormone biology - diminished ovarian reserve, premature ovarian insufficiency, and polycystic ovary syndrome. We will also discuss the limitations and challenges faced in studying noncoding RNAs and sex steroid hormone production. An enhanced understanding of the role of ncRNAs in sex hormone regulatory networks is essential in order to advance the development of potential diagnostic markers and therapeutic targets for diseases, including those in reproductive health. Our deepened understanding of ncRNAs has the potential to uncover new applications and therapies; however, in many cases, the next steps will involve distinguishing critical ncRNAs from those which are merely changing in response to a particular disease state, or which are altogether unrelated to disease pathophysiology.