Supplementary Material for: Incarcerated small bowel herniation in a stoma mimicking sigmoid end colostomy prolapse

Introduction: A stoma prolapse is easy to diagnose by visual examination, and it rarely incarcerates. Therefore, manual reduction is usually performed as soon as the diagnosis is made. In this report, we describe a case of stoma prolapse that could not be reduced manually and ruptured because an incarcerated parastomal hernia occurred in the stoma, mimicking stoma prolapse. Case presentation: A 66-year-old woman underwent total hysterectomy, bilateral salpingo-oophorectomy, pelvic and para-aortic lymphadenectomy, omentectomy, resection of dissemination, and low anterior resection with formation of a sigmoid end colostomy for endometrial cancer with infiltration of the rectum. Fourteen months after the initial operation, she presented with stoma prolapse and multiple episodes of vomiting. The prolapsed stoma was 20 cm in length, appeared swollen and edematous, and was somewhat firm. Although it looked viable, some of the mucosa was darkish red, indicating congestion. Therefore, the diagnosis was sigmoid end colostomy prolapse with an ischemic component. An attempt at manual reduction resulted in rupture, so an emergency laparotomy was performed. Intraoperatively, we found that the ileum was incarcerated in the aperture created where the colostomy had been formed. When the incarcerated ileum was released, the stoma prolapse could be reduced easily. The end colostomy was refashioned in the left upper quadrant of the abdomen. Conclusion: An incarcerated parastomal hernia can mimic stoma prolapse. If the findings differ from those of typical stoma prolapse, imaging should be performed to confirm whether another clinical entity is involved in the stoma prolapse

Supplementary Material for: Characterization of Kidney and Skeleton Phenotypes of Mice Double Heterozygous for Foxc1 and Foxc2

Foxc1 and Foxc2 play key roles in mouse development. Foxc1 mutant mice develop duplex kidneys with double ureters, and lack calvarial and sternal bones. Foxc2 null mice have been reported to have glomerular abnormalities in the kidney and axial skeletal anomalies. Expression patterns of Foxc1 and Foxc2 overlap extensively and are believed to have interactive roles. However, cooperative roles of these factors in glomerular and skeletal development are unknown. Therefore, we examined the kidneys and skeleton of mice that were double heterozygous for Foxc1 and Foxc2. Double heterozygotes were generated by mating single heterozygotes for Foxc1 and Foxc2. Newborn double heterozygous mice showed many anomalies in the kidney and urinary tract resembling Foxc1 phenotypes, including duplex kidneys, double ureters, hydronephrosis and mega-ureter. Some mice had hydronephrosis alone. In addition to these macroscopic anomalies, some mice had abnormal glomeruli and disorganized glomerular capillaries observed in Foxc2 phenotypes. Interestingly, these mice also showed glomerular cysts not observed in the single-gene knockout of either Foxc1 or Foxc2 but observed in conditional knockout of Foxc2 in the kidney. Serial section analysis revealed that all cystic glomeruli were connected to proximal tubules, precluding the possibility of atubular glomeruli resulting in cyst formation. Dorsally opened vertebral arches and malformations of sternal bones in the double heterozygotes were phenotypes similar to Foxc1 null mice. Absent or split vertebral bodies in the double heterozygotes were phenotypes similar to Foxc2 null mice, whilst hydrocephalus noted in the Foxc1 phenotype was not observed. Thus, Foxc1 and Foxc2 have a role in kidney and axial skeleton development. These transcription factors might interact in the regulation of the embryogenesis of these organs

Supplementary Material for: Natural History of Small Gastric Subepithelial Lesions Less than 20 mm: A Multicenter Retrospective Observational Study (NUTSHELL20 Study)

Background and Aim: Small gastric subepithelial lesions (SELs) are sometimes encountered in daily esophagogastroduodenoscopy (EGD) practice, but whether once-annual or twice-annual endoscopy can provide sufficient follow-up remains unclear. Because follow-up based on small-SEL characteristics is important, this study clarified the natural history of gastric SELs less than 20 mm. Methods: This retrospective multicenter observation study conducted at 24 Japanese hospitals during April 2000 to March 2020 examined small gastric SELs of ≤20 mm diameter. The primary outcome was the rate of size increase of those SELs detected using EGD, with growth times assessed irrespective of SEL pathological diagnoses. Results: We examined 824 cases with tumors of 1–5 mm diameter in 298 (36.2%) cases, 6–10 mm in 344 (41.7%) cases, 11–15 mm in 112 (13.6%) cases, and 16–20 mm in 70 (8.50%) cases. An increase of small gastric SELs was observed in 70/824 patients (8.5%). The SELs larger than 6 mm increased, even after 10 years. No-change and increasing groups had no significantly different malignant findings at diagnosis. In cases of gastrointestinal stromal tumors (GISTs), internal cystic change in endoscopic ultrasound (EUS) is a risk factor for an increased tumor size. The predictive tumor growth cutoff size at initial diagnosis was 13.5 mm. Conclusions: Small gastric SELs less than 20 mm have an approximately 8.5% chance of increase. Predictive markers for GIST growth are tumor size ≥13.5 mm and internal cystic change in EUS