Appendicitis combined with Meckel's diverticulum obstruction, perforation, and inflammation in children: Three case reports.

BACKGROUND: Meckel's diverticulum is a common congenital malformation of the small intestine, with the three most common complications being obstruction, perforation, and inflammation. To date, only a few cases have been reported worldwide. In children, the clinical symptoms are similar to appendicitis. As most of the imaging features are nonspecific, the preoperative diagnosis is not precise. In addition, the clinical characteristics are highly similar to pediatric acute appendicitis, thus special attention is necessary to distinguish Meckel's diverticulum from pediatric appendicitis. Patients with poor disease control should undergo laparoscopic exploration to avoid serious complications, including intestinal necrosis, intestinal perforation and gastrointestinal bleeding. CASE SUMMARY: This report presents three cases of appendicitis in children combined with intestinal obstruction, which was caused by fibrous bands (ligaments) arising from the top part of Meckel's diverticulum, diverticular perforation, and diverticular inflammation. All three patients, aged 11-12 years, had acute appendicitis as their initial clinical presentation. All were treated by laparoscopic surgery with a favorable outcome. A complete dataset including clinical presentation, diagnostic imaging, surgical information, and histopathologic findings was also provided. CONCLUSION: Preoperative diagnosis of Meckel's diverticulum and its complications is challenging because its clinical signs and complications are similar to those of appendicitis in children. Laparoscopy combined with laparotomy is useful for diagnosis and treatment.

Retention and the Intersection of Structural Inequities in a Breastfeeding Intervention Study.

Introduction: Women below the poverty threshold have lower representation and retention in breastfeeding studies. Methods: A secondary analysis of a longitudinal randomized controlled self-management for breast and nipple pain during breastfeeding study. Participants completed online surveys at discharge, weeks 1, 2, 3, 6, 9, 12, 18, and 24, with face-to-face interviews at 6 and 24 weeks. Text messages were sent to participants when modules and surveys were due. Retention was assessed in R with descriptive statistics, Mann-Whitney, Pearson's chi-square, and Cox Proportional Hazard Regression. Results: Two hundred and forty-four women (89 ≤$50,000 and 155 >$50,000) were recruited. Retention rates at 1 (93%), 2 (87%), 6 (82%), 9 (77%) and 24 (72%) weeks. For women of low income compared to those of high income there was a hazard ratio (HR) of 2.5 (p=0.0001) for retention. For non-Hispanic Black and Hispanic women compared to the combined non-Hispanic White and Other group, HRs for retention were 3.3 and 2.6 respectively (p=0.0001). Adjustment for age in the final hazard regression model of income, age, race and ethnicity decreased the HR for women of low income to 1.6 and HRs for non-Hispanic Black and Hispanic women to 2.1 and 1.9, respectively (p=.0001). However, none of the individual factors in the model achieved statistical significance. Discussion: Retention in breastfeeding studies impacts breastfeeding duration, a key lifelong preventative health behavior. Despite accessible study design, retention of women desiring to breastfeed was adversely affected by the intersection of income, race and ethnicity, and age.

Reassessing endothelial-to-mesenchymal transition in mouse bone marrow: insights from lineage tracing models.

Endothelial cells (ECs) and bone marrow stromal cells (BMSCs) play crucial roles in supporting hematopoiesis and hematopoietic regeneration. However, whether ECs are a source of BMSCs remains unclear. Here, we evaluate the contribution of endothelial-to-mesenchymal transition to BMSC generation in postnatal mice. Single-cell RNA sequencing identifies ECs expressing BMSC markers Prrx1 and Lepr; however, this could not be validated using Prrx1-Cre and Lepr-Cre transgenic mice. Additionally, only a minority of BMSCs are marked by EC lineage tracing models using Cdh5-rtTA-tetO-Cre or Tek-CreERT2. Moreover, Cdh5+ BMSCs and Tek+ BMSCs show distinct spatial distributions and characteristic mesenchymal markers, suggestive of their origination from different progenitors rather than CDH5+ TEK+ ECs. Furthermore, myeloablation induced by 5-fluorouracil treatment does not increase Cdh5+ BMSCs. Our findings indicate that ECs hardly convert to BMSCs during homeostasis and myeloablation-induced hematopoietic regeneration, highlighting the importance of using appropriate genetic models and conducting careful data interpretation in studies concerning endothelial-to-mesenchymal transition.