Scalable Approach to Consumer Wearable Postmarket Surveillance: Development and Validation Study.

Background: With the capability to render prediagnoses, consumer wearables have the potential to affect subsequent diagnoses and the level of care in the health care delivery setting. Despite this, postmarket surveillance of consumer wearables has been hindered by the lack of codified terms in electronic health records (EHRs) to capture wearable use.

Objective: We sought to develop a weak supervision-based approach to demonstrate the feasibility and efficacy of EHR-based postmarket surveillance on consumer wearables that render atrial fibrillation (AF) prediagnoses.

Investigating real-world consequences of biases in commonly used clinical calculators.

Objectives: To evaluate whether one summary metric of calculator performance sufficiently conveys equity across different demographic subgroups, as well as to evaluate how calculator predictive performance affects downstream health outcomes.

Study Design: We evaluate 3 commonly used clinical calculators-Model for End-Stage Liver Disease (MELD), CHA2DS2-VASc, and simplified Pulmonary Embolism Severity Index (sPESI)-on the cohort extracted from the Stanford Medicine Research Data Repository, following the cohort selection process as described in respective calculator derivation papers.

Methods: We quantified the predictive performance of the 3 clinical calculators across sex and race.

GABAA receptor-binding protein promotes sensitivity to apoptosis induced by chemotherapeutic agents.

In the present study, the expression of human γ-aminobutyrate type A (GABAA) receptor-binding protein (GABARBP) is downregulated in ovarian cancer cell lines and tissues. We also found that the specific function of GABAPBP was that of a novel pro-apoptotic protein. Both GABARBP and cisplatin suppressed cancer cell proliferation in a concentration-dependent manner.

sMEK1 enhances gemcitabine anti-cancer activity through inhibition of phosphorylation of Akt/mTOR.

Recently, we reported that sMEK1 is down-regulated in cancer cells and tissues, and that it enhances the pro-proliferative effect as a novel pro-apoptotic protein. However, the biological mechanism of the sMEK1 tumor suppressor in the cellular signal pathway has not been well understood. In our current work, we examined whether sMEK1 could promote the cytotoxic activity of gemcitabine in the human ovarian carcinoma system.

Obesity and sex steroid changes across puberty: evidence for marked hyperandrogenemia in pre- and early pubertal obese girls.

Context: Peripubertal obesity is associated with abnormal sex steroid concentrations, but the timing of onset and degree of these abnormalities remain unclear.

Objective: The objective of the study was to assess the degree of hyperandrogenemia across puberty in obese girls and assess overnight sex steroid changes in Tanner stage 1-3 girls.

Design: This was a cross-sectional analysis.

Increased luteinizing hormone pulse frequency in obese oligomenorrheic girls with no evidence of hyperandrogenism.

Objective: To determine whether obese, nonhirsute adolescents with oligomenorrhea exhibit similar increased LH pulse secretion patterns compared with obese girls with polycystic ovary syndrome (PCOS).

Design: Prospective, observational study.

Setting: Tertiary university hospital.

The association of obesity and hyperandrogenemia during the pubertal transition in girls: obesity as a potential factor in the genesis of postpubertal hyperandrogenism.

Context: Adolescent hyperandrogenemia is considered a forerunner of adult polycystic ovary syndrome, but its etiology remains uncertain.

Objective: Our objective was to explore the hypothesis that peripubertal obesity is associated with hyperandrogenemia.

Design And Setting: We performed a cross-sectional analysis of data obtained at General Clinical Research Centers.

Ovarian imaging by magnetic resonance in obese adolescent girls with polycystic ovary syndrome: a pilot study.

Objective: To determine whether magnetic resonance (MR) imaging can serve as a useful investigational tool in the assessment of the polycystic ovary as compared with transabdominal ultrasound (US) for obese adolescents with polycystic ovary syndrome (PCOS).

Design: Prospective observational study.

Setting: Tertiary university hospital.

Progesterone inhibition of the hypothalamic gonadotropin-releasing hormone pulse generator: evidence for varied effects in hyperandrogenemic adolescent girls.

Compared with normal women, adults with polycystic ovarian syndrome (PCOS) require higher progesterone (P) concentrations to inhibit GnRH (LH) pulse frequency, which contributes to persistently rapid GnRH pulses and elevated LH levels in PCOS. To explore the origin of this abnormality, we assessed hypothalamic sensitivity to P feedback in nine normal controls and 11 hyperandrogenemic (HA) adolescents. Subjects first underwent frequent blood sampling for 11 h to assess baseline LH pulse frequency.

Luteinizing hormone secretion is not influenced by insulin infusion in women with polycystic ovary syndrome despite improved insulin sensitivity during pioglitazone treatment.

It has been reported in women with polycystic ovary syndrome (PCOS) that LH secretion is not altered by insulin infusion. To determine whether insulin resistance may have precluded an effect of insulin, pulsatile LH secretion and gonadotropin responses to GnRH were examined in PCOS women (n = 9) before and after pioglitazone treatment (45 mg/d) for 20 wk in the presence and absence of a hyperinsulinemic euglycemic clamp (80 mU/m2.min).

Enhanced granulosa cell responsiveness to follicle-stimulating hormone during insulin infusion in women with polycystic ovary syndrome treated with pioglitazone.

Women with polycystic ovary syndrome (PCOS) are known to exhibit insulin resistance with compensatory hyperinsulinemia. To determine the role of hyperinsulinemia on follicle function in PCOS, we examined 24-h estradiol (E(2)) responses to recombinant human FSH (r-hFSH), 75 IU, before and during insulin infusion both before and after administration of pioglitazone (30 mg/d) in seven PCOS women. Each subject underwent two 10-h hyperinsulinemic-euglycemic clamps at rates of 30 (low dose) and 200 (high dose) mU/m(2).

Increased luteinizing hormone secretion in women with polycystic ovary syndrome is unaltered by prolonged insulin infusion.

In PCOS women with insulin resistance, hyperinsulinemia may contribute to inappropriate gonadotropin secretion. To determine whether insulin influences gonadotropin release in PCOS, pulsatile LH secretion and gonadotropin responses to GnRH were evaluated before (phase 1) and during (phase 2) insulin infusion. In phase 1, 11 PCOS and 9 normal women on separate days underwent 1) frequent blood sampling (q 10 min) for 12 h and 2) gonadotropin stimulation by successive doses of GnRH, 2 microg, 10 microg, and 20 microg, administered i.