Influence of Race and Ethnicity on Meeting Intention to Exclusively Breast Milk Feed at Postpartum Hospital Discharge.

Costello S, Santillan D, Awelewa T, Bowdler N.

Breastfeed Med. 2025 Mar 26. doi: 10.1089/bfm.2024.0392. Epub ahead of print. PMID: 40135281.

Background: Racial/Ethnic disparities in breastfeeding practices exist despite strong evidence for significant health benefits of breastfeeding for the mother-newborn dyad. Breastfeeding intentions are known to predict breastfeeding practices at hospital discharge and breastfeeding retention in the long term. Interventions during postpartum hospitalization can help mothers achieve breastfeeding intentions and reduce racial/ethnic gaps in breastfeeding on discharge. This study aims to identify racial/ethnic disparities in meeting intentions to exclusively breast milk feed (EBMF) on hospital discharge. 

Methods: This was a retrospective cohort study of mothers who intended to EBMF and their newborns delivered at term at a single academic medical center during 2022. The primary outcome was EBMF at discharge. 

Results: Participants included non-Hispanic Black (NHB) (n = 96), Hispanic (n = 97), and non-Hispanic White (NHW) (n = 955) mothers who intended to EBMF. Mothers who identified as NHB (40.6%) or Hispanic (64.9%) were significantly less likely to EBMF compared with NHW (87.5%) mothers (odds ratio [OR] = 0.14, 95%CI [0.08, 0.23] and OR = 0.37, 95%CI [0.22, 0.61], respectively) at newborn hospital discharge. Rurality, insurance type, gravidity, parity, gestational diabetes, and birth weight were not associated with breast feeding choice/practices at discharge, but increasing age was associated with an increased likelihood of EBMF (OR = 1.07, 95%CI [1.03, 1.11]), as was neonatal intensive care unit admission (OR = 2.93, 95%CI [1.18, 7.31]). Cesarean birth was associated with decreased likelihood of EBMF (OR = 0.57, 95%CI [0.38, 0.85]). 

Conclusion: Significant racial/ethnic disparities in EBMF at hospital discharge exist among those who intended to EBMF, which are not explained by differences in other examined covariates.

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Umbilical Morcellation and Postoperative Pain in Patients Undergoing Benign Hysterectomy.

Gnade C, Kasper K

JSLS. 2025 Jan-Mar;29(1):e2024.00052. doi: 10.4293/JSLS.2024.00052. Epub 2025 Apr 3. PMID: 40182836; PMCID: PMC11967719.

Background: Morcellation has allowed patients with enlarged uteri to obtain a minimally invasive hysterectomy with improved outcomes; however, there is little information regarding postoperative pain. Our study aims to compare pain scores and opioid requirements in patients undergoing umbilical morcellation during benign minimally invasive hysterectomy versus those who do not require morcellation.

Methods: A retrospective cohort study was performed at a tertiary care center including patients who underwent total laparoscopic or supracervical hysterectomy by one high volume surgeon from 2019 to 2022. Baseline characteristics, postoperative pain scores, and morphine milligram equivalents in the acute and late setting were recorded. Two-sample t test for continuous variables and χ2 or Fisher's exact test for categorical variables were used to compare differences. A multiple regression model evaluated the effect of groups with the adjustment of confounders.

Results: A total of 232 patients underwent hysterectomy in which 57 underwent umbilical manual morcellation and 175 did not. There was no difference in postoperative complications, readmissions, or blood products required (P > 0.05). Individuals that underwent umbilical morcellation had longer operative times (226.6 vs 120.1 minutes, P < 0.01), more blood loss (311.1 vs 82.0 mL, P < 0.01), longer length of stay (0.60 vs 0.44 days, P < 0.01), increased uterine weight (1,293.2 vs 151.6 g, P < 0.01), and fibroid pathology (93.0% vs 46.3%, P < 0.01). There were no differences in postoperative pain scores, immediate and later opioid use between groups on multivariate analysis.

Conclusions: Patients who undergo umbilical morcellation, typically for large fibroid uteri, have similar postoperative pain scores, opioid use, and postoperative complications to those who undergo hysterectomy for other indications.

For a full text of the article, click here: https://pmc.ncbi.nlm.nih.gov/articles/PMC11967719/

ECPPF stratification identifies occult high-risk subgroups in stage I, grade 1 or 2, ≤50 % invasive endometrial cancer: Candidates for adjuvant therapy.

Gonzalez-Bosquet J, Shahi M, Yadav S, Kanwar N, Alvand S, Sosa C, Dowdy SC, Halling KC, Weroha SJ, Bakkum-Gamez JN, Podratz KC.

Gynecol Oncol. 2025 Apr 7;196:113-120. doi: 10.1016/j.ygyno.2025.03.030. Epub ahead of print. PMID: 40199195.

Objective: To determine whether stratification with ECPPF (E2F1 + CCNA2 log2 expression and POLE, PPP2R1A, and FBXW7 variants) could identify occult cases of high-risk endometrial cancer (EC) in a traditionally low-risk cohort.

Methods: We identified 97 cases of clinicopathologic low-risk endometrioid EC (defined as stage I, grade 1 or 2, limited [≤50 %] myometrial invasion) from The Cancer Genome Atlas (TCGA). Twelve cases had POLE mutations (mu) and 15 had PPP2R1Amu or FBXW7mu. Log2 CCNA2 + E2F1 expression was low (<4.75) for 56 cases and high (>4.75) for 19 (termed CCNA2 + E2F1 low or high, respectively). CCNA2 + E2F1 high and PPP2R1Amu/FBXW7mu were simultaneously present for 5 cases. Survival comparisons were based on log-rank tests.

Results: Five-year progression-free survival (PFS) curves for POLEmu and CCNA2 + E2F1 low differed substantially from CCNA2 + E2F1 high and PPP2R1mu/FBXW7mu cases (P < .001). The latter 2 subgroups, combined (n = 29) and designated as molecular high risk (MHR), had an estimated 5-year PFS <50 %. Adverse outcomes were associated with MHR for cases harboring CTNNB1mu (P < .001), ARID1Amu (P = .03), and PTENmu (P = .002). TCGA classification was not prognostically significant for this cohort (P = .10), but ECPPF MHR identified compromised subgroups within major TCGA subclasses (P = .004). CCNA2 + E2F1 high and expression of its downstream targets were positively correlated (P < .001) with expression of genes involved in chemoresistance (ie, homologous recombination, cell cycle regulation, antiapoptotic processes).

Conclusions: ECPPF supports a taxonomy in which occult, high-risk disease is identified among cases traditionally considered low risk. With high-risk cases unlikely to respond to current first-line chemotherapy, case identification should prompt proactive therapeutic intervention with alternative molecular-based treatment targets.

For a full text of the article, click here: https://www.sciencedirect.com/science/article/pii/S0090825825001076?via%3Dihub

Disrupted fetal carbohydrate metabolism in children with autism spectrum disorder.

Gumusoglu SB, Schickling BM, Santillan DA, Teesch LM, Santillan MK.

J Neurodev Disord. 2025 Mar 29;17(1):16. doi: 10.1186/s11689-025-09601-z. PMID: 40158086; PMCID: PMC11954230.

Background: Despite the power and promise of early detection and treatment in autism spectrum disorder (ASD), early-life biomarkers are limited. An early-life risk biosignature would advance the field's understanding of ASD pathogenies and targets for early diagnosis and intervention. We therefore sought to add to the growing ASD biomarker literature and evaluate whether fetal metabolomics are altered in idiopathic ASD.

Methods: Banked cord blood plasma samples (N = 36 control, 16 ASD) were analyzed via gas chromatography and mass spectrometry (GC-MS). Samples were from babies later diagnosed with idiopathic ASD (non-familial, non-syndromic) or matched, neurotypical controls. Metabolite set enrichment analysis (MSEA) and biomarker prediction were performed (MetaboAnalyst).

Results: We detected 76 metabolites in all samples. Of these, 20 metabolites differed significantly between groups: 10 increased and 10 decreased in ASD samples relative to neurotypical controls (p < 0.05). MSEA revealed significant changes in metabolic pathways related to carbohydrate metabolism and glycemic control. Untargeted principle components analysis of all metabolites did not reveal group differences, while targeted biomarker assessment (using only Fructose 6-phosphate, D-Mannose, and D-Fructose) by a Random Forest algorithm generated an area under the curve (AUC) = 0.766 (95% CI: 0.612-0.896) for ASD prediction.

Conclusions: Despite a high and increasing prevalence, ASD has no definitive biomarkers or available treatments for its core symptoms. ASD's earliest developmental antecedents remain unclear. We find that fetal plasma metabolomics differ with child ASD status, in particular invoking altered carbohydrate metabolism. While prior clinical and preclinical work has linked carbohydrate metabolism to ASD, no prior fetal studies have reported these disruptions in neonates or fetuses who go on to be diagnosed with ASD. Future work will investigate concordance with maternal metabolomics to determine maternal-fetal mechanisms.

For a full text of the article, click here: https://jneurodevdisorders.biomedcentral.com/articles/10.1186/s11689-025-09601-z

Alternative Splicing of CADM1 in Preeclampsia: Implications for Endothelial Dysfunction and Offspring Cardiovascular Risk.

Schickling B, Santillan MK, Santillan DA.

Physiol Genomics. 2025 Apr 4. doi: 10.1152/physiolgenomics.00047.2025. Epub ahead of print. PMID: 40183784.

For a full text of the article, click here: https://journals.physiology.org/doi/pdf/10.1152/physiolgenomics.00047.2025

Periods of susceptibility for associations between phthalate exposure and preterm birth: Results from a pooled analysis of 16 US cohorts.

Friedman A, Welch BM, Keil AP, Bloom MS, Braun JM, Buckley JP, Dabelea D, Factor-Litvak P, Meeker JD, Michels KB, Padmanabhan V, Starling AP, Weinberg CR, Aalborg J, Alshawabkeh AN, Barrett ES, Binder AM, Bradman A, Bush NR, Calafat AM, Cantonwine DE, Christenbury KE, Cordero JF, Engel SM, Eskenazi B, Harley KG, Hauser R, Herbstman JB, Holland N, James-Todd T, Jukic AMZ, Lanphear BP, McElrath TF, Messerlian C, Newman RB, Nguyen RHN, O'Brien KM, Rauh VA, Redmon JB, Rich DQ, Rosen EM, Sathyanarayana S, Schmidt RJ, Sparks AE, Swan SH, Wang C, Watkins DJ, Weinberger B, Wenzel AG, Wilcox AJ, Yolton K, Zhang Y, Zota AR, Ferguson KK

Environ Int. 2025 Mar 20;198:109392. doi: 10.1016/j.envint.2025.109392. Epub ahead of print. PMID: 40132438.

Background: Phthalate exposure during pregnancy has been associated with preterm birth, but mechanisms of action may depend on the timing of exposure.

Objective: Investigate critical periods of susceptibility during pregnancy for associations between urinary phthalate metabolite concentrations and preterm birth.

Methods: Individual-level data were pooled from 16 US cohorts (N = 6045, n = 539 preterm births). We examined trimester-averaged urinary phthalate metabolite concentrations. Most phthalate metabolites had 2248, 3703, and 3172 observations in the first, second, and third trimesters, respectively. Our primary analysis used logistic regression models with generalized estimating equations (GEE) under a multiple informant approach to estimate trimester-specific odds ratios (ORs) of preterm birth and significant (p < 0.20) heterogeneity in effect estimates by trimester. Adjusted models included interactions between each covariate and trimester.

Results: Differences in trimester-specific associations between phthalate metabolites and preterm birth were most evident for di-2-ethylhexyl phthalate (DEHP) metabolites. For example, an interquartile range increase in mono (2-ethylhexyl) phthalate (MEHP) during the first and second trimesters was associated with ORs of 1.15 (95 % confidence interval [CI]: 0.99, 1.33) and 1.11 (95 % CI: 0.97, 1.28) for preterm birth, respectively, but this association was null in the third trimester (OR = 0.91 [95 % CI: 0.76, 1.09]) (p-heterogeneity = 0.03).

Conclusion: The association of preterm birth with gestational biomarkers of DEHP exposure, but not other phthalate metabolites, differed by the timing of exposure. First and second trimester exposures demonstrated the greatest associations. Our study also highlights methodological considerations for critical periods of susceptibility analyses in pooled studies.

For a full text of the article, click here: https://www.sciencedirect.com/science/article/pii/S0160412025001436?via%3Dihub

Circulating extracellular vesicles protein expression for early prediction of platinum-resistance in high-grade serous ovarian cancer.

Wagner V, Morton M, Dorayappan KDP, Gonzalez A, Yu L, Sakaue T, Conrads T, Maxwell GL, Cosgrove C, Backes F, Wang QE, Cohn DE, O'Malley DM, Selvendiran K.

Oncogene. 2025 Apr 10. doi: 10.1038/s41388-025-03382-4. Epub ahead of print. PMID: 40210758.

Platinum resistance in high-grade serous ovarian carcinoma (HGSOC) portends a poor prognosis. Although initial platinum-based chemotherapy response rates are high, 15-20% of patients demonstrate primary resistance to platinum therapy and almost all patients will develop platinum resistance in the recurrent setting. No predictive or diagnostic biomarkers have been utilized specific to platinum resistance. This study aimed to identify candidate biomarkers for platinum resistance in HGSOC using an extracellular vesicle (EV) based approach. We found differentially expressed and distinct EV proteins, namely TMEM205 and CFH, in patients with platinum-resistant (PR) HGSOC compared to those of platinum-sensitive (PS) patients, utilizing liquid chromatography-tandem mass spectrometry (LC-MS/MS). Expression of these EV proteins were validated in patient-derived PR cell lines as well as in clinically relevant mouse models of HGSOC post-platinum therapy. We corroborated these findings using serum samples from patients with PS and PR-HGSOC. Both EV CFH and EV TMEM205 exhibited excellent diagnostic capability for PR as noted by receiver operating characteristic curves with area under the curve values of 0.95 and 0.84, respectively. The high diagnostic performance of TMEM205 and CFH within EVs compared to the relatively poor performance of conventional serum proteins such as Ca125 suggests their robust potential as non-invasive biomarkers for detecting platinum resistance in HGSOC. Furthermore, the ROC curve for the combined biomarker demonstrated excellent diagnostic performance, with an AUC of 0.973, a true positive rate (TPR) of 0.938, and a false positive rate (FPR) of 0.062. Incorporating this multi-protein biomarker panel alongside established biomarkers further enhances diagnostic accuracy. Serum EV CFH and TMEM205 are promising biomarkers for early detection of platinum resistance in HGSOC and may highlight underlying chemoresistance mechanisms, offering potential future therapeutic targets.

For a full text of the article, click here: https://www.nature.com/articles/s41388-025-03382-4