There is no consensus about how stresses such as low water availability and temperature limit tree growth. Sink limitation to growth and survival is often inferred if a given stress does not cause non-structural carbohydrate (NSC) concentrations or levels to decline along with growth. However, trees may actively maintain or increase NSC levels under moderate carbon stress, making the pattern of reduced growth and increased NSCs compatible with carbon limitation. To test this possibility, we used full and half defoliation to impose severe and moderate carbon limitation on 2-year-old Quercus velutina Lam. saplings grown in a common garden. Saplings were harvested at either 3 weeks or 4 months after treatments were applied, representing short- and longer-term effects on woody growth and NSC levels. Both defoliation treatments maintained a lower total leaf area than controls throughout the experiment with no evidence of photosynthetic up-regulation, and resulted in a similar total biomass reduction. While fully defoliated saplings had lower starch levels than controls in the short term, half defoliated saplings maintained control starch levels in both the short and longer term. In the longer term, fully defoliated saplings had the greatest starch concentration increment, allowing them to recover to near-control starch levels. Furthermore, between the two harvest dates, fully and half defoliated saplings allocated a greater proportion of new biomass to starch than did controls. The maintenance of control starch levels in half defoliated saplings indicates that these trees actively store a substantial amount of carbon before growth is carbon saturated. In addition, the allocation shift favouring storage in defoliated saplings is consistent with the hypothesis that, as an adaptation to increasing carbon stress, trees can prioritize carbon reserve formation at the expense of growth. Our results suggest that as carbon limitation increases, reduced growth is not necessarily accompanied by a decline in NSC concentrations. Therefore, a lack of NSC decline may not be evidence that reduced tree growth under cold or water stress is caused by sink limitation.

A technology-based weight loss intervention is feasible in women with Type I endometrial cancer/hyperplasia. Both interventions produced weight loss, although more person-to-person contact produced more significant outcomes. Reductions in expression of IL-2 were related to weight loss.

To determine how obstetricians and gynecologists (OB/GYNs) perceive the gynecologic health effects of obesity and to identify perceived obstacles to counseling. OB/GYNs with 3 St. Louis health systems were emailed a 46-question survey regarding physicians' role in counseling women on the health risks of obesity and barriers faced in achieving this counseling. Differences between respondents' gender, age, practice type, years in practice, and body mass index were assessed using Chi-square or Fisher's exact tests as appropriate. Of 318 OB/GYNs emailed, 134 completed surveys, including 82 generalists and 52 subspecialists. 93% of respondents believed it was necessary to educate patients on health risks of obesity. 90% and 75%, respectively, cited diagnoses of endometrial hyperplasia and cancer as teachable moments for counseling. The most frequently cited barriers to successful counseling were lack of time, referral services, and patient tools/information. Most did not believe they had adequate reimbursement (65%), training (53%) or educational resources (50%) to counsel patients. Survey answers differed by practice setting, gender, and provider age. Although most OB/GYN providers consider obesity counseling important, execution is hindered by perceived barriers that differ by provider gender, age, and practice type. For OB/GYNs, more effective weight management counseling will require better training and practice-specific strategies. Based on survey responses, better reimbursement combined with increased resources for appropriate referrals and cancer prevention counseling are needed in order to improve weight management implementation in OB/GYN.

BACKGROUND:Patients with ovarian cancer often present with late-stage disease and nonspecific symptoms, but little is known about factors affecting the time to diagnosis (TTD) in the United States. METHODS: A retrospective, population-based study of the Surveillance, Epidemiology, and End Results-Medicare database was conducted. It included women 66 years old or older with stage II to IV epithelial ovarian cancer with at least 1 code for abdominal/pelvic pain, bloating, difficulty eating, or urinary symptoms within 1 year of the cancer diagnosis. TTD was defined from the first claim with a prespecified symptom to the ovarian cancer diagnosis. Kruskal-Wallis tests were used to assess for differences in TTD by group medians. Univariate and generalized linear models with a log-link function evaluated TTD by covariables. RESULTS: For the 13,872 women analyzed, the mean and median times to diagnosis were 2.9 and 1.1 months, respectively. The median TTD differed significantly by first symptom (P < .001), number of symptoms (P < .001), and first physician specialty seen (P < .001). In a multivariable analysis, TTD differed significantly according to race/ethnicity (P < .001), geographic region (P = .001), urban-rural location (P = .031), emergency room presentation (P < .001), and number of specialties seen (P < .001). A shorter TTD was associated with a diagnosis in 2006-2010 (relative risk [RR], 0.92; 95% confidence interval [CI], 0.87-0.98) or 2011-2015 (RR, 0.87; 95% CI, 0.81-0.93) in comparison with 1992-1999. CONCLUSIONS: The time from a symptomatic presentation to care to a diagnosis of ovarian cancer is influenced by clinical and demographic variables. This study's findings reinforce the importance of educating all physicians on ovarian cancer symptoms to aid in diagnosis. Cancer 2021;127:4151-4160.

BackgroundMayer-Rokitansky-Küster-Hauser syndrome is a rare entity with proposed genetic underpinnings. Ovarian carcinoma has well-described genetic associations and syndromes, although much of the etiology of the disease remains unknown.CasesTwo sisters present in the 1970s with primary amenorrhea, 46, XX karyotypes, and absent uteri consistent with MRKH syndrome. In the 2010s, both sisters again present for care. Case 1 presents one sister with stage IIIC serous ovarian adenocarcinoma and negative BRCA panel. Case No 2 presents the other sister with stage IIIC serous ovarian adenocarcinoma and a negative panel for 32 genetic variants associated with ovarian carcinoma.ConclusionThe familial association of two rare diseases and negative genetic workup could point to a new genetic understanding of reproductive structure development and ovarian carcinogenesis.