Intestinal malrotation is a congenital anomaly caused by incomplete rotation and fixation of the midgut during embryological development. Although it is usually diagnosed in infancy, rare adult cases may present with acute intestinal obstruction or perforation. Cecal volvulus is an uncommon but potentially life-threatening complication of malrotation. We report a 35-year-old woman who presented with severe abdominal pain, progressive distension, and absolute constipation for two days. Clinical examination revealed generalized peritonitis with absent bowel sounds, and an erect radiograph demonstrated free gas beneath both hemidiaphragms, indicating hollow-viscus perforation. Because of generalised peritonitis mandating urgent operation, she proceeded directly to emergency laparotomy without cross-sectional imaging. Intraoperatively, a cecal volvulus was identified in association with intestinal malrotation and Ladd's bands, together with a single perforation on the anterior wall of the ascending colon. The involved cecum and ascending colon were markedly distended and venously congested from the closed-loop obstruction but showed no frank ischemia or gangrene, and bowel color improved after detorsion. Ladd's bands were divided, the volvulus detorsed, the perforation repaired primarily in two layers, and a defunctioning loop ileostomy fashioned. The patient had an otherwise uncomplicated postoperative recovery and was discharged on postoperative day seven. The loop ileostomy was reversed at three months, and at six months the patient was well, asymptomatic, and passing normal stool without evidence of recurrence. This report highlights the importance of considering congenital malrotation in adults presenting with an acute abdomen and discusses the rationale for bowel-preserving surgery when viability is retained.

Acute type A aortic dissection (ATAAD) complicated by mesenteric malperfusion is among the most lethal cardiovascular emergencies, combining the immediate threat of aortic rupture with rapidly progressive visceral ischaemia. The optimal sequence of intervention remains controversial. Although current guidelines recommend immediate central aortic repair, this strategy may carry particularly high perioperative risk when advanced mesenteric ischaemia is already present.

Intestinal ischemia/reperfusion (I/R) injury is a life-threatening clinical condition associated with high mortality and limited therapeutic options. Ferroptosis, an iron-dependent form of regulated cell death driven by excessive lipid peroxidation, has emerged as a critical contributor to intestinal I/R injury. Nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy promotes ferroptosis by increasing intracellular iron availability; however, the upstream mechanisms governing this process remain poorly understood. Beclin-1 is a key initiator of autophagy, whereas ubiquitin-specific protease 11 (USP11) regulates protein stability through deubiquitination. Whether USP11 modulates NCOA4-mediated ferritinophagy via Beclin-1 during intestinal I/R injury remains unknown. Here, we investigated the role of the USP11/Beclin-1/NCOA4 signaling axis using a murine intestinal I/R model and an oxygen-glucose deprivation/reoxygenation (OGD/R)-induced IEC-6 cell injury model. Bioinformatic analysis, co-immunoprecipitation (CO-IP), gene knockdown, and rescue experiments were performed to characterize ferritinophagy and ferroptosis. Intestinal I/R injury and OGD/R treatment markedly induced NCOA4-mediated ferritinophagy, accompanied by enhanced lipid peroxidation and characteristic mitochondrial damage, whereas these alterations were reversed by the autophagy inhibitor 3-methyladenine (3-MA) and ferroptosis-specific inhibitor Ferrostatin-1 (Fer-1). Beclin-1 was identified as a critical interacting partner of NCOA4, and its knockdown suppressed ferritinophagy, ferroptosis, and intestinal injury. Mechanistically, USP11 expression was significantly upregulated following intestinal I/R injury and stabilized Beclin-1 through deubiquitination. Conversely, USP11 knockdown enhanced Beclin-1 ubiquitination, reduced its stability, and consequently inhibited NCOA4-mediated ferritinophagy and ferroptosis. Consistently, inhibition of USP11 markedly alleviated intestinal injury both in vivo and in vitro. Collectively, our findings reveal a previously unrecognized USP11/Beclin-1/NCOA4 signaling axis that drives ferritinophagy-dependent ferroptosis during intestinal I/R injury. By promoting Beclin-1 deubiquitination and stabilization, USP11 facilitates NCOA4-mediated ferritinophagy and subsequent ferroptotic cell death, highlighting USP11 as a promising therapeutic target for intestinal I/R injury.

Ischemia-reperfusion injury (IRI) is a clinically important consequence of blood-flow restoration after ischemia and contributes to tissue damage across multiple organ systems. This critical review evaluates the preclinical evidence for BPC 157 in rodent IRI and related reperfusion-associated vascular injury models, with particular attention to oxidative stress, endothelial and nitric oxide (NO)-related responses, inflammation, apoptosis, angiogenic signaling, and tissue injury. Searches were performed up to 24 June 2026 across PubMed/MEDLINE, Web of Science Core Collection, Scopus, PMC, publisher/DOI metadata, ClinicalTrials.gov, FDA materials, and WADA materials. Peer-reviewed rodent studies involving conventional organ-specific IRI or reperfusion-associated systemic injury were evaluated as the core IRI/reperfusion evidence according to the experimental model, BPC 157 dose, route and timing, measured outcomes, and methodological limitations, while selected major-vessel occlusion models were considered separately as related in vivo vascular evidence. Endothelial, vascular-ring, human ex vivo, and regulatory/clinical sources were used as contextual evidence rather than as evidence of IRI efficacy. Meta-analysis was not performed because of substantial heterogeneity in organ systems, injury paradigms, doses, routes, treatment timing, and outcome measures. Across the available rodent literature, BPC 157 administration has been associated with attenuation of oxidative injury, modulation of NO-related vascular responses, reductions in inflammatory and apoptotic markers, and changes in VEGF/VEGFR2-Akt-eNOS-related signaling. Organ-specific findings include biochemical, molecular, and histological protection in lower-extremity skeletal-muscle IRI; attenuation of distant-organ injury following limb IRI; neuronal and functional effects in hippocampal IRI; vascular and tissue-protective responses in intestinal/colonic IRI; and hemodynamic and histological effects in hepatic Pringle-maneuver IRI. However, the evidence base remains heterogeneous and frequently relies on short observation periods, single-dose paradigms, and incompletely characterized risk-of-bias domains. Reperfusion-like systemic and major-vessel occlusion models provide additional mechanistic context but should not be considered equivalent to conventional organ-specific IRI. Current evidence therefore supports BPC 157 as a hypothesis-generating investigational candidate for further preclinical IRI research rather than as an established therapy. Independent blinded replication, dose-response and therapeutic-window studies, pharmacokinetic/pharmacodynamic characterization, rigorous toxicology, and ultimately controlled human studies would be required before clinical translation could be considered.

Chronic cerebral hypoperfusion (CCH) is an important contributor to vascular cognitive impairment and neurodegenerative disorders, characterized by neuronal injury, blood-brain barrier (BBB) disruption, neuroinflammation, mitochondrial dysfunction, and synaptic impairment. Increasing evidence suggests that the microbiota-gut-brain axis plays a crucial role in ischemic brain injury. CCH is associated with gut microbiota dysbiosis, intestinal barrier dysfunction, and reduced production of microbiota-derived short-chain fatty acids (SCFAs), which may be linked to cognitive decline through bidirectional gut-brain communication. This review summarizes the mechanisms potentially involved in CCH-related neurological damage and highlights the potential neuroprotective effects of SCFAs, including regulation of neuroinflammation, BBB integrity, mitochondrial homeostasis, neuronal apoptosis, and synaptic plasticity. Furthermore, potential microbiota-targeted therapeutic strategies, such as fecal microbiota transplantation, probiotics/prebiotics, and SCFA supplementation, are discussed. Targeting gut microbiota-derived SCFAs may represents a promising approach for improving CCH-associated cognitive impairment, although further clinical validation is required.

Bochdalek diaphragmatic hernias are congenital diaphragmatic defects through which abdominal viscera herniate into the thoracic cavity and are typically diagnosed in newborns and infants. Adult presentations are uncommon and may present with heterogeneous manifestations, ranging from asymptomatic to life-threatening complications. A 72-year-old male with a history of urinary retention presented with acute lower abdominal pain and vomiting. Initial physical examination and laboratory studies suggested a urinary tract infection. Despite adequate treatment, the patient's condition deteriorated, and progressive hemodynamic instability led to the diagnosis of septic shock secondary to intestinal obstruction. Chest X-ray incidentally revealed intrathoracic bowel loops, raising suspicion for a diaphragmatic hernia, while computed tomography confirmed the Bochdalek hernia with strangulated bowel. Emergency laparoscopic exploration identified a 3 x 3 cm diaphragmatic defect with herniated small bowel. Due to irreducible herniation and dense adhesions, the procedure was converted to laparotomy. The defect was enlarged to facilitate reduction, followed by resection of 1.2 m of necrotic small bowel, primary diaphragmatic repair, and bowel anastomosis. The patient recovered and remained recurrence-free after four years. This case underscores that adult diaphragmatic hernias may initially present with nonspecific symptoms in patients with comorbidities that suggest more common diagnoses, sometimes leading to premature diagnostic closure. Prompt reassessment and broad differential diagnosis for patients with clinical deterioration and unclear etiology are key to timely recognition of complicated adult diaphragmatic hernias. Early surgical management can then ensure favorable outcomes even in severe, life-threatening complications.

Acute organophosphorus pesticide poisoning (AOPP) may cause intestinal infarction via intra-abdominal hypertension (IAH) and non-occlusive mesenteric ischemia (NOMI). Although this complication carries high mortality, early laparotomy, resection of necrotic bowel, and comprehensive therapy can improve survival, as supported by our successfully treated case.

. Indications and management of nasogastric tube. The review by Alverdy et al examines current evidence on the indications, placement, and management of nasogastric tubes (NGTs) used for gastric decompression. Historically employed since the 17th century, modern NGTs - particularly the Salem sump - enable effective aspiration while minimizing mucosal injury. The primary indication remains small bowel obstruction, most often caused by adhesions. In uncomplicated cases without ischemia or peritonitis, NGT based conservative management resolves approximately 75% of obstructions. Water soluble contrast agents retain diagnostic value but do not reduce surgical rates.Routine postoperative NGT use after elective abdominal surgery is not supported by evidence. Multiple meta analyses show earlier return of bowel function, fewer pulmonary complications, and shorter hospital stays when NGTs are avoided. Recent trials in pancreatic surgery confirm no benefit from routine decompression and suggest a possible increase in mortality. ERAS protocols across colorectal, gastric, pancreatic, esophageal, hepatobiliary, and gynecologic surgery consistently recommend selective rather than routine use, reserving NGTs for severe distension, refractory vomiting, delayed gastric emptying, or high aspiration risk.Contraindications include facial trauma, caustic ingestion, esophageal perforation, and fixed obstructions; relative contraindications involve coagulopathy, varices, recent upper GI anastomosis, and severe nasal pathology. Proper insertion technique, radiographic confirmation when needed, secure fixation, and daily reassessment are essential. Complications range from nasal trauma and misplacement into the airway to electrolyte disturbances, aspiration, and pressure injuries.Overall, NGTs remain valuable for targeted decompression, but evidence strongly supports selective, time limited use with vigilant monitoring and prompt removal when no longer indicated.