An Assessment of Business of Medicine Knowledge in Obstetrics and Gynecology Fellows: A Pilot Study.

STUDY OBJECTIVE: To identify knowledge gaps in business education among obstetrics and gynecology fellows METHODS: An online anonymous survey was distributed to obstetrics and gynecology subspecialty fellows, including pediatric and adolescent gynecology, minimally invasive gynecologic surgery, and reproductive endocrinology and infertility fellows. RESULTS: Of the 483 fellows who received the questionnaire, 159 completed the surveys, resulting in a response rate of 32.9%. A total of 80 reproductive endocrinology and infertility fellows (50.3%), 47 minimally invasive gynecologic surgery fellows (29.6%), and 32 pediatric and adolescent gynecology (20.1%) fellows completed the survey. Over half reported debt from either undergraduate or medical school (52.2%). Over half (58.5%) reported 0 hours of finance education in their residency or fellowship training. In general, fellows reported relatively higher levels of confidence in nonmedical aspects of business, such as purchasing a home (63.9%), life and disability insurance (57.2%), and making financial plans for the future (57.9%). Conversely, a large portion of fellows reported feeling "not at all confident" in business topics related to the field of medicine, including contract negotiation (24.7%), non-competes (27.1%), relative value units system-based pay (32.0%), general office practice management (58.2%), legal aspects of business (71.8%), accounting and billing (54.4%), and marketing (55.7%). CONCLUSION: Our survey demonstrates an unmet demand among obstetrics and gynecology fellows to learn topics related to the business of medicine. Knowledge of these topics is critical for those pursuing private practice or academic medicine. Future initiatives should evaluate other subspecialties and prioritize creating a standardized education tool to better prepare trainees entering medical practice.

Uterine myomas: effect of prior myomectomy on pregnancy outcomes.

OBJECTIVE: Reproductive aged women with fibroids must weigh the risks and benefits of preconception myomectomy. Women with fibroids may have higher rates of fetal growth restriction (FGR) and stillbirth; however, there is a paucity of data on the impact of myomectomy on pregnancy outcomes. We compared perinatal outcomes in women with prior myomectomy versus those with no prior myomectomy and at least one fibroid ≥ 5 cm. METHODS: Retrospective cohort study of women at a single center who delivered between 2008 and 2017 with a viable intrauterine pregnancy at initial ultrasound scan and either prior myomectomy, or, in the no-myomectomy cohort, at least one fibroid ≥ 5 cm on a prenatal scan performed at < 21 weeks' gestation (wga). Pregnancies complicated by major congenital anomalies were excluded. Primary outcome was preterm birth (PTB) < 37wga. Secondary outcomes included rates of spontaneous loss, cesarean delivery (CD), abnormal placentation, malpresentation, FGR, birthweight, birthweight percentile, estimated blood loss (EBL), blood transfusion, and neonatal survival to discharge. RESULTS: A total of 290 women met inclusion criteria: 70 had a prior myomectomy, 220 women had ≥1 fibroid ≥5cm. Women with prior myomectomy were older, more likely to have private insurance, and more likely used artificial reproductive technology to conceive; 20% with prior myomectomy still had at least one ≥ 5 cm myoma on their obstetric scan. Rates of spontaneous loss were lower in the prior myomectomy group (1.4% vs 7.3%; p = .08). Of the 273 pregnancies continuing beyond 20 weeks, women with prior myomectomy had significantly more PTBs (35% vs. 21%, p = .02) and significantly different primary birth indications (p < .0001). However, after controlling for late preterm, prelabor cesareans recommended by providers in the myomectomy cohort, the difference in PTB rates was not significant (p = .13). The myomectomy group had more CDs (88% vs. 53%, p < .0001), higher EBL (1250 mL vs. 811 mL, p = .04), and a trend toward more blood transfusions (16% vs 8%, p = .05). Other selected outcomes were similar, including rates of FGR. CONCLUSIONS: Women with prior myomectomy had significantly more PTBs, due in part to more preterm, prelabor cesareans in the late preterm period. Otherwise, prior myomectomy did not confer appreciable obstetric or perinatal benefits, as patients had more CDs, and higher EBL. Recommendations to perform preterm prelabor cesareans in this population may explain some of the PTB disparity. The effect of prior myomectomy on early pregnancy loss and infertility requires further study.

The HMG-CoA reductase inhibitor, simvastatin, exhibits anti-metastatic and anti-tumorigenic effects in ovarian cancer.

Ovarian cancer is the 5th leading cause of cancer death among women in the United States. The mevalonate pathway is thought to be a potential oncogenic pathway in the pathogenesis of ovarian cancer. Simvastatin, a 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMGCR) inhibitor, is a widely used drug for inhibiting the synthesis of cholesterol and may also have anti-tumorigenic activity. Our goal was to evaluate the effects of simvastatin on ovarian cancer cell lines, primary cultures of ovarian cancer cells and in an orthotopic ovarian cancer mouse model. Simvastatin significantly inhibited cellular proliferation, induced cell cycle G1 arrest and apoptosis, and caused cellular stress via reduction in the enzymatic activity of HMGCR and inhibition of the MAPK and mTOR pathways in ovarian cancer cells. Furthermore, simvastatin induced DNA damage and reduced cell adhesion and invasion. Simvastatin also exerted anti-proliferative effects on primary cell cultures of ovarian cancer. Treatment with simvastatin in an orthotopic mouse model reduced ovarian tumor growth, coincident with decreased Ki-67, HMGCR, phosphorylated-Akt and phosphorylated-p42/44 protein expression. Our findings demonstrate that simvastatin may have therapeutic benefit for ovarian cancer treatment and be worthy of further exploration in clinical trials.

Evaluation of the anti-tumor effects of lactate dehydrogenase inhibitor galloflavin in endometrial cancer cells.

High rates of aerobic glycolysis represent a key mechanism by which endometrial cancer cells consume glucose as its primary energy source. The up-regulated glycolytic pathway is a common therapeutic target whose inhibition has implications for anti-tumor activity in cancer cells. The present study was aimed at evaluating the potential of a novel lactate dehydrogenase (LDH) inhibitor, Galloflavin, as a therapeutic agent for endometrial cancer. Our results revealed that Galloflavin effectively inhibited cell growth in endometrial cancer cell lines and primary cultures of human endometrial cancer through its involvement in multiple signaling pathways that regulate metabolism, cell cycle, apoptosis, cell stress and metastasis.

Simvastatin, an HMG-CoA reductase inhibitor, exhibits anti-metastatic and anti-tumorigenic effects in endometrial cancer.

OBJECTIVE: Our goal was to evaluate the effects of simvastatin on endometrial cancer cell lines and primary cultures of endometrial cancer cells. METHODS: Cell proliferation in the ECC-1 and Ishikawa endometrial cancer cell lines and primary cultures of endometrial cancer cells was assessed by MTT assay. Apoptosis and cell cycle were detected by Annexin V assay and propidium iodide staining, respectively. Reactive oxygen species and cell adhesion were assessed using ELISA assays. Invasion was analyzed using a transwell invasion assay. Mitochondrial DNA damage was confirmed using qPCR. The effects of simvastatin on the AKT/mTOR and MAPK pathways were determined by Western blotting. RESULTS: Simvastatin inhibited cell proliferation in a dose-dependent manner in both endometrial cancer cell lines and 5/8 primary cultures of endometrial cancer cells. Simvastatin treatment resulted in G1 cell cycle arrest, a reduction in the enzymatic activity of HMG-CoA, induction of apoptosis as well as DNA damage and cellular stress. Treatment with simvastatin resulted in inhibition of the MAPK pathway and exhibited differential effects on the AKT/mTOR pathway in the ECC-1 and Ishikawa cells. Minimal change in AKT phosphorylation was seen in both cell lines. An increase in phosphorylated S6 was seen in ECC-1 and a decrease was seen in Ishikawa. Treatment with simvastatin reduced cell adhesion and invasion (p<0.01) in both cell lines. CONCLUSION: Simvastatin had significant anti-proliferative and anti-metastatic effects in endometrial cancer cells, possibly through modulation of the MAPK and AKT/mTOR pathways, suggesting that statins may be a promising treatment strategy for endometrial cancer.