An Op-Ed Writing Curriculum for Medical Students to Engage in Advocacy Through Public Writing.

BACKGROUND: Op-ed writing can be a powerful and accessible advocacy tool for physicians, but training is lacking in undergraduate medical education. AIM: To train and engage first-year medical students in op-ed writing. SETTING: Midwestern research-intensive medical school. PARTICIPANTS: All students in a required first-year health policy course in 2021 and 2022. PROGRAM DESCRIPTION: For their health policy course's final assignment, students could opt to write an op-ed on a healthcare issue of their choice. All students received written instruction on op-ed writing. Additionally, they could access a seminar, coaching and editing by peers and faculty, and publication guidance. PROGRAM EVALUATION: Of 179 students over 2 years, 105 chose to write op-eds. Fifty-one attended the seminar, 35 attended peer coaching sessions, 33 accessed structured peer editing, and 23 received faculty assistance. Thirty-eight students submitted a total of 42 op-eds for publication. Twenty-two pieces were published in major outlets and 17 in the university's health policy review. Of the 22 in major outlets, 21 received editing from either peers or faculty. DISCUSSION: An op-ed writing curriculum can be integrated into an existing medical school health policy course, resulting in a high level of engagement and in published op-eds by medical students.

The use of adjunctive mechanical dilation at the time of induction termination and adverse health outcomes: a systematic review.

OBJECTIVE: This study aimed to assess if the use of mechanical dilation at the time of induction termination is associated with changes in the time from initiation of labor to expulsion of the fetus (induction-to-expulsion interval) and with the frequency of health complications when compared with medication management alone. DATA SOURCES: PubMed, CINAHAL, Scopus, and the Cochrane Central Register of Controlled Trials were queried from January 2000 to May 2023. STUDY ELIGIBILITY CRITERIA: We included randomized controlled trials of individuals who were assigned to undergo mechanical dilation (ie, laminaria, Dilapan-S, and intracervical Foley balloon catheter) in combination with the use of medication and compared it with the outcomes of medication use (eg, prostaglandins, antiprogestins, oxytocin) alone. METHODS: The primary outcome was the induction-to-expulsion interval. The secondary outcomes were the incidence of clinical chorioamnionitis, sepsis, hemorrhage, the need for blood transfusion and uterotonics, cervical laceration, the need for adjunctive procedures (eg, dilation and curettage), failed induction termination, uterine rupture, intensive care unit admission, or death. Assessment of bias was performed using the Cochrane Risk of Bias tool. A subgroup analysis was performed among studies deemed to be at low risk of bias. RESULTS: Of 864 abstracts identified, 11 met the inclusion criteria. Five studies demonstrated a shorter induction-to-expulsion interval among those randomized to mechanical dilation, whereas 6 studies demonstrated a similar or longer induction-to-expulsion interval. There were no significant differences reported in the frequency of any adverse outcomes between the trial arms. In addition, most studies (8/11) exhibited moderate to high levels of bias. In an analysis of the 3 studies deemed to have a low risk of bias, 1 (n=60) demonstrated a longer induction-to-expulsion interval with adjunctive laminaria, 1 (n=60) demonstrated a shorter induction-to-expulsion interval with adjunctive intracervical Foley balloon catheter use, and 1 demonstrated no difference in the induction-to-expulsion interval with adjunctive Dilapan-S use (n=180). CONCLUSION: Only a small number of studies, most of which were of low quality, assessed mechanical dilation for induction termination. The results of these studies were inconsistent in terms of the induction-to-expulsion interval of adjunctive mechanical methods in comparison with medication management alone. Studies did not reveal significant differences between the groups in adverse outcomes. Further research should investigate the use of mechanical dilation at the time of induction termination using high-quality methods.

Site-1 protease inhibits mitochondrial respiration by controlling the TGF-ß target gene Mss51.

The mitochondrial response to changes in cellular energy demand is necessary for cellular adaptation and organ function. Many genes are essential in orchestrating this response, including the transforming growth factor (TGF)-ß1 target gene Mss51, an inhibitor of skeletal muscle mitochondrial respiration. Although Mss51 is implicated in the pathophysiology of obesity and musculoskeletal disease, how Mss51 is regulated is not entirely understood. Site-1 protease (S1P) is a key activator of several transcription factors required for cellular adaptation. However, the role of S1P in muscle is unknown. Here, we identify S1P as a negative regulator of muscle mass and mitochondrial respiration. S1P disruption in mouse skeletal muscle reduces Mss51 expression and increases muscle mass and mitochondrial respiration. The effects of S1P deficiency on mitochondrial activity are counteracted by overexpressing Mss51, suggesting that one way S1P inhibits respiration is by regulating Mss51. These discoveries expand our understanding of TGF-ß signaling and S1P function.

Human Placenta Buffers the Fetus from Adverse Effects of Perceived Maternal Stress.

Maternal stress during pregnancy is linked to several negative birth outcomes. The placenta, a unique pregnancy-specific organ, not only nourishes and protects the fetus but is also the major source of progesterone and estrogens. As the placenta becomes the primary source of maternal progesterone (P4) and estradiol between 6-9 weeks of gestation, and these hormones are critical for maintaining pregnancy, maternal stress may modulate levels of these steroids to impact birth outcomes. The objective was to test whether maternal perceived stress crosses the placental barrier to modulate fetal steroids, including cortisol, which is a downstream indicator of maternal hypothalamic-pituitary-adrenal (HPA) axis regulation and is associated with negative fetal outcomes. Nulliparous women, 18 years or older, with no known history of adrenal or endocrine illness were recruited during their third trimester of pregnancy at the University of California San Francisco (UCSF) Mission Bay hospital obstetrics clinics. Simultaneous measurement of 10 steroid metabolites in maternal (plasma and hair) and fetal (cord blood and placenta) samples was performed using tandem mass spectrometry along with assessment of the perceived stress score and sociodemographic status. While the maternal perceived stress score (PSS) and sociodemographic status were positively associated with each other and each with the body mass index (BMI) (r = 0.73, p = 0.0008; r = 0.48, p = 0.05; r = 0.59, p = 0.014, respectively), PSS did not correlate with maternal or fetal cortisol, cortisone levels, or fetal birth weight. Regardless of maternal PSS or BMI, fetal steroid levels remained stable and unaffected. Progesterone was the only steroid analyte quantifiable in maternal hair and correlated positively with PSS (r = 0.964, p = 0.003), whereas cord estradiol was negatively associated with PSS (r = -0.94, p = 0.017). In conclusion, hair progesterone might serve as a better marker of maternal stress than cortisol or cortisone and maternal PSS negatively impacts fetal estradiol levels. Findings have implications for improved biomarkers of stress and targets for future research to identify factors that buffer the fetus from adverse effects of maternal stress.

Corticotropin-Releasing Factor Family: A Stress Hormone-Receptor System's Emerging Role in Mediating Sex-Specific Signaling.

No organ in the body is impervious to the effects of stress, and a coordinated response from all organs is essential to deal with stressors. A dysregulated stress response that fails to bring systems back to homeostasis leads to compromised function and ultimately a diseased state. The components of the corticotropin-releasing factor (CRF) family, an ancient and evolutionarily conserved stress hormone-receptor system, helps both initiate stress responses and bring systems back to homeostasis once the stressors are removed. The mammalian CRF family comprises of four known agonists, CRF and urocortins (UCN1-3), and two known G protein-coupled receptors (GPCRs), CRF1 and CRF2. Evolutionarily, precursors of CRF- and urocortin-like peptides and their receptors were involved in osmoregulation/diuretic functions, in addition to nutrient sensing. Both CRF and UCN1 peptide hormones as well as their receptors appeared after a duplication event nearly 400 million years ago. All four agonists and both CRF receptors show sex-specific changes in expression and/or function, and single nucleotide polymorphisms are associated with a plethora of human diseases. CRF receptors harbor N-terminal cleavable peptide sequences, conferring biased ligand properties. CRF receptors have the ability to heteromerize with each other as well as with other GPCRs. Taken together, CRF receptors and their agonists due to their versatile functional adaptability mediate nuanced responses and are uniquely positioned to orchestrate sex-specific signaling and function in several tissues.