(1) Background: Irritable bowel syndrome (IBS) is a global public health problem, the pathogenesis of which has not been fully explored. Limiting fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAP) can relieve symptoms in some patients with IBS. Studies have shown that normal microcirculation perfusion is necessary to maintain the primary function of the gastrointestinal system. Here, we hypothesized that IBS pathogenesis might be related to abnormalities in colonic microcirculation. A low-FODMAP diet could alleviate visceral hypersensitivity (VH) by improving colonic microcirculation; (2) Methods: C57BL/6 mice were raised to establish an IBS-like rodent model using water avoidance (WA) stress or SHAM-WA as a control, one hour per day for ten days. The mice in the WA group were administered different levels of the FODMAP diet: 2.1% regular FODMAP (WA-RF), 10% high FODMAP diet (WA-HF), 5% medium FODMAP diet (WA-MF), and 0% low FODMAP diet (WA-LF) for the following 14 days. The body weight and food consumption of the mice were recorded. Visceral sensitivity was measured as colorectal distention (CRD) using the abdominal withdrawal reflex (AWR) score. Colonic microcirculation was assessed using laser speckle contrast imaging (LCSI). Vascular endothelial-derived growth factor (VEGF) was detected using immunofluorescence staining; (3) Results: The threshold values of CRD pressure in the WA-RF, WA-HF, and WA-MF groups were significantly lower than those in the SHAM-WA group. Moreover, we observed that colonic microcirculation perfusion decreased, and the expression of VEGF protein increased in these three groups of mice. Interestingly, a low-FODMAP dietary intervention could reverse this situation. Specifically, a low-FODMAP diet increased colonic microcirculation perfusion, reduced VEGF protein expression in mice, and increased the threshold of VH. There was a significant positive correlation between colonic microcirculation and threshold for VH; (4) Conclusions: These results demonstrate that a low-FODMAP diet can alter VH by affecting colonic microcirculation. Changes in intestinal microcirculation may be related to VEGF expression.

The aim of this study is to explore the association between umbilical cord blood (UCB) vitamin A levels and late preterm infants morbidities. We conducted a prospective cohort study of 208 late-preterm infants(from 34 ⁰/₇ to 36 ⁶/₇ weeks gestational age) between January 1, 2014 and June 30, 2015. UCB specimens were collected shortly after birth, and vitamin A levels were determined by enzyme-linked immunosorbent assay. Prevalence of low UCB vitamin A level < 0.7 μmol/L was 37.5% in late preterm infants. In comparison to vaginal delivery, cesarean section was associated with UCB vitamin A level < 0.7 μmol/L (P < 0.001). Nevertheless, UCB vitamin A levels did not correlate with gestational age, birth weight, and gender. UCB vitamin A level < 0.7 μmol/L was not an independent risk factor for hospitalization, oxygen supplementation, hyperbilirubinemia, sepsis, and respiratory distress syndrome. Conclusions: Low umbilical cord blood vitamin A levels are common among late-preterm infants. Cesarean section delivery is associated with low umbilical cord blood vitamin A level. Low umbilical cord blood vitamin A levels at birth do not increase morbidity of late-preterm infants, including hyperbilirubinemia, sepsis, and respiratory distress syndrome. What is Known: • Late preterm infants have a higher morbidity and mortality rates when compared to term infants. • Low plasma vitamin A levels increase the risk of preterm infants’ morbidity. What is New: • Late preterm infants commonly have low level of umbilical cord blood vitamin A. • Low umbilical cord blood vitamin A level at birth appears to be not associated with the morbidity of late-preterm infants. • Cesarean section is associated with low umbilical cord blood vitamin A level < 0.7 μmol/L compared with vaginal delivery.

SUMMARY: Preterm infants face a unique trajectory of gut microbiome assembly, shaped by the convergence of physiological immaturity, necessary clinical interventions, and the neonatal intensive care unit environment. This dysbiotic ecosystem—characterized by low diversity, depletion of beneficial commensals such as Bifidobacterium , and expansion of pathobionts, including Enterobacteriaceae—is increasingly recognized as a central mediator of neonatal morbidity. This review synthesizes current evidence on preterm microbiome development, its role in necrotizing enterocolitis through mechanisms involving Toll-like receptor 4 signaling, bile acid dysmetabolism, and immune dysregulation, and its systemic impact via gut-organ axes linking the intestine to the brain, lung, eye, and systemic circulation. We critically evaluate microbiome-targeted interventions across the translational spectrum, from foundational practices such as human milk feeding and antibiotic stewardship to active modulation with probiotics and prebiotics, and emerging precision strategies, including postbiotics, phage therapy, and fecal microbiota transplantation. Methodological advances in multi-omics, machine learning, and digital twin modeling are paving the way for personalized, predictive microbiome-mediated care. We also address the hidden burden of antimicrobial resistance in the preterm gut and the challenges of translating mechanistic insights into clinical practice. Looking forward, embracing the complexity of the preterm microbiome as a dynamic, multi-kingdom ecosystem is essential for developing holistic interventions that improve both short-term survival and long-term neurodevelopmental, respiratory, and metabolic outcomes.

Background: Neonatal hypothermia is common around the world; however, profound hypothermia is a very rare—but life-threatening—event. Clinical Findings: This was a very rare case involving a 15-day old preterm infant diagnosed with profound hypothermia (rectal temperature, 27°C) concomitant with severe coagulation dysfunction and leukopenia on admission. Primary Diagnosis: Profound hypothermia together with severe coagulopathy, leukopenia, late-onset sepsis, and pneumonia. Interventions: The patient was rewarmed slowly, with a rectal temperature rising at a rate of 0.5°C/h < R < 1°C/h. Vital signs were closely monitored. Coagulation factors were supplemented by intravenous infusion of fresh frozen plasma. Supportive treatment with intravenous infusion of immunoglobulin was provided, and antibiotics were used empirically. Nil per os and intravenous rehydration were also implemented. Outcomes: The condition of the preterm infant gradually improved and was successfully discharged. Practice Recommendations: Profound hypothermia is very rare in preterm infants. However, once it occurs, it may be concomitant with severe coagulopathy and leukopenia. Successful management involves slow rewarming, prompt supplementation of coagulation factors, empirical antibiotics, and supportive treatment.

Rationale: Neonatal gastrointestinal perforation (NGP) is a life-threatening condition requiring urgent intervention. While exploratory laparotomy remains the standard treatment, conservative management offers an alternative when surgery is not feasible. This case demonstrates the successful use of comprehensive conservative therapy in a high-risk infant with NGP and suspected intestinal stenosis. Patient concerns: A 6-day-old, small-for-gestational-age male infant presented with vomiting, abdominal distension, and respiratory distress. Clinical deterioration led to the diagnosis of pneumoperitoneum, sepsis, and suspected necrotizing enterocolitis. Diagnoses: NGP secondary to suspected necrotizing enterocolitis, with complications including septic shock, purulent meningitis, scrotal abscess, zinc deficiency, and malnutrition. Interventions: Following parental refusal of laparotomy, conservative management was initiated, including peritoneal drainage, gastrointestinal decompression, broad-spectrum antibiotics, inotropic support, and parenteral nutrition. Nutritional support included zinc supplementation and gradual enteral feeding. Outcomes: The infant survived after 134 days of hospitalization, despite multiple complications. Long-term follow-up at 8 months revealed neurodevelopmental delays (developmental quotient 61), though physical growth was adequate with successful transition to complementary feeding. Lessons: This case confirms that conservative management with peritoneal drainage and intensive multidisciplinary support can be a viable option for NGP, even in complex scenarios where surgery is not possible. It underscores the importance of vigilant monitoring, nutritional management, and awareness of potential long-term neurodevelopmental sequelae in such cases.