Fat embolism syndrome is a rare but potentially fatal complication that can occur after major trauma, long-bone fracture, or orthopedic surgery. Symptoms typically manifest 24–72 hours after the initial injury. However, in patients with severe underlying disease, the disease course can be aggressive and occasionally fatal within hours. This report presents an autopsy-confirmed case of rapidly progressive fat embolism syndrome after a femoral fracture in a patient with severe idiopathic pulmonary fibrosis. The patient experienced progressive respiratory distress within two hours of the fracture and died five hours post-injury. Postmortem examination revealed advanced pulmonary fibrosis and clear evidence of a systemic fat embolism.

Fecal impaction (FI) is a potentially fatal condition characterized by the accumulation of large, hardened fecal masses in the large intestine, resulting in mechanical obstruction. This condition is commonly observed in older adults but can also affect younger populations, particularly patients with psychiatric conditions who face increased risk due to medication side effects, autonomic dysfunction, and inadequate bowel management. This report describes two forensic autopsy cases of fatal FI in patients with neuropsychiatric disorders. The first case involved a 52-year-old man with mild intellectual disability who had received long-term psychiatric treatment. Autopsy findings included marked colonic dilation (maximum diameter >10 cm), ischemic mucosal changes, and a large fecal mass (~2,200 g) obstructing the sigmoid and descending colon. The second case involved a 25-year-old man with severe intellectual disability. Autopsy revealed severe colonic dilation (maximum diameter of 12 cm), extensive FI along rectum and descending colon, and no evidence of alternative causes of death. In both cases, death was attributed to mechanical intestinal obstruction secondary to FI. These cases highlight the forensic significance of FI as a cause of sudden death in patients with neuropsychiatric disorders. Symptoms such as paradoxical diarrhea may be misinterpreted, and the inadvertent use of contraindicated medications (e.g., antidiarrheals) can worsen the condition, contributing to fatal outcomes. Furthermore, forensic evaluation must assess whether inadequate medical intervention or neglect played a role in the progression of FI. Early recognition, proactive bowel management, and interdisciplinary collaboration are critical to preventing fatal events in high-risk patients with neuropsychiatric disorders.

Oxidative stress due to hyperglycemia damages the functions of retinal pigment epithelial (RPE) cells and is a major risk factor for diabetic retinopathy (DR). Paeoniflorin is a monoterpenoid glycoside found in the roots of Paeonia lactiflora Pall and has been reported to have a variety of health benefits. However, the mechanisms underlying its therapeutic effects on high glucose (HG)-induced oxidative damage in RPE cells are not fully understood. In this study, we investigated the protective effect of paeoniflorin against HG-induced oxidative damage in cultured human RPE ARPE-19 cells, an in vitro model of hyperglycemia. Pretreatment with paeoniflorin markedly reduced HG-induced cytotoxicity and DNA damage. Paeoniflorin inhibited HG-induced apoptosis by suppressing activation of the caspase cascade, and this suppression was associated with the blockade of cytochrome c release to cytoplasm by maintaining mitochondrial membrane stability. In addition, paeoniflorin suppressed the HG-induced production of reactive oxygen species (ROS), increased the phosphorylation of nuclear factor erythroid 2-related factor 2 (Nrf2), a key redox regulator, and the expression of its downstream factor heme oxygenase-1 (HO-1). On the other hand, zinc protoporphyrin (ZnPP), an inhibitor of HO-1, abolished the protective effect of paeoniflorin against ROS production in HG-treated cells. Furthermore, ZnPP reversed the protective effects of paeoniflorin against HG-induced cellular damage and induced mitochondrial damage, DNA injury, and apoptosis in paeoniflorin-treated cells. These results suggest that paeoniflorin protects RPE cells from HG-mediated oxidative stress-induced cytotoxicity by activating Nrf2/HO-1 signaling and highlight the potential therapeutic use of paeoniflorin to improve the symptoms of DR.

Oxidative stress due to hyperglycemia damages the functions of retinal pigment epithelial (RPE) cells and is a major risk factor for diabetic retinopathy (DR). Paeoniflorin is a monoterpenoid glycoside found in the roots of Paeonia lactiflora Pall and has been reported to have a variety of health benefits. However, the mechanisms underlying its therapeutic effects on high glucose (HG)-induced oxidative damage in RPE cells are not fully understood. In this study, we investigated the protective effect of paeoniflorin against HG-induced oxidative damage in cultured human RPE ARPE-19 cells, an in vitro model of hyperglycemia. Pretreatment with paeoniflorin markedly reduced HG-induced cytotoxicity and DNA damage. Paeoniflorin inhibited HG-induced apoptosis by suppressing activation of the caspase cascade, and this suppression was associated with the blockade of cytochrome c release to cytoplasm by maintaining mitochondrial membrane stability. In addition, paeoniflorin suppressed the HG-induced production of reactive oxygen species (ROS), increased the phosphorylation of nuclear factor erythroid 2-related factor 2 (Nrf2), a key redox regulator, and the expression of its downstream factor heme oxygenase-1 (HO-1). On the other hand, zinc protoporphyrin (ZnPP), an inhibitor of HO-1, abolished the protective effect of paeoniflorin against ROS production in HG-treated cells. Furthermore, ZnPP reversed the protective effects of paeoniflorin against HG-induced cellular damage and induced mitochondrial damage, DNA injury, and apoptosis in paeoniflorin-treated cells. These results suggest that paeoniflorin protects RPE cells from HG-mediated oxidative stress-induced cytotoxicity by activating Nrf2/HO-1 signaling and highlight the potential therapeutic use of paeoniflorin to improve the symptoms of DR.

Fecal impaction (FI) is a potentially fatal condition characterized by the accumulation of large, hardened fecal masses in the large intestine, resulting in mechanical obstruction. This condition is commonly observed in older adults but can also affect younger populations, particularly patients with psychiatric conditions who face increased risk due to medication side effects, autonomic dysfunction, and inadequate bowel management. This report describes two forensic autopsy cases of fatal FI in patients with neuropsychiatric disorders. The first case involved a 52-year-old man with mild intellectual disability who had received long-term psychiatric treatment. Autopsy findings included marked colonic dilation (maximum diameter >10 cm), ischemic mucosal changes, and a large fecal mass (~2,200 g) obstructing the sigmoid and descending colon. The second case involved a 25-year-old man with severe intellectual disability. Autopsy revealed severe colonic dilation (maximum diameter of 12 cm), extensive FI along rectum and descending colon, and no evidence of alternative causes of death. In both cases, death was attributed to mechanical intestinal obstruction secondary to FI. These cases highlight the forensic significance of FI as a cause of sudden death in patients with neuropsychiatric disorders. Symptoms such as paradoxical diarrhea may be misinterpreted, and the inadvertent use of contraindicated medications (e.g., antidiarrheals) can worsen the condition, contributing to fatal outcomes. Furthermore, forensic evaluation must assess whether inadequate medical intervention or neglect played a role in the progression of FI. Early recognition, proactive bowel management, and interdisciplinary collaboration are critical to preventing fatal events in high-risk patients with neuropsychiatric disorders.

Oxidative stress due to hyperglycemia damages the functions of retinal pigment epithelial (RPE) cells and is a major risk factor for diabetic retinopathy (DR). Paeoniflorin is a monoterpenoid glycoside found in the roots of Paeonia lactiflora Pall and has been reported to have a variety of health benefits. However, the mechanisms underlying its therapeutic effects on high glucose (HG)-induced oxidative damage in RPE cells are not fully understood. In this study, we investigated the protective effect of paeoniflorin against HG-induced oxidative damage in cultured human RPE ARPE-19 cells, an in vitro model of hyperglycemia. Pretreatment with paeoniflorin markedly reduced HG-induced cytotoxicity and DNA damage. Paeoniflorin inhibited HG-induced apoptosis by suppressing activation of the caspase cascade, and this suppression was associated with the blockade of cytochrome c release to cytoplasm by maintaining mitochondrial membrane stability. In addition, paeoniflorin suppressed the HG-induced production of reactive oxygen species (ROS), increased the phosphorylation of nuclear factor erythroid 2-related factor 2 (Nrf2), a key redox regulator, and the expression of its downstream factor heme oxygenase-1 (HO-1). On the other hand, zinc protoporphyrin (ZnPP), an inhibitor of HO-1, abolished the protective effect of paeoniflorin against ROS production in HG-treated cells. Furthermore, ZnPP reversed the protective effects of paeoniflorin against HG-induced cellular damage and induced mitochondrial damage, DNA injury, and apoptosis in paeoniflorin-treated cells. These results suggest that paeoniflorin protects RPE cells from HG-mediated oxidative stress-induced cytotoxicity by activating Nrf2/HO-1 signaling and highlight the potential therapeutic use of paeoniflorin to improve the symptoms of DR.

Fecal impaction (FI) is a potentially fatal condition characterized by the accumulation of large, hardened fecal masses in the large intestine, resulting in mechanical obstruction. This condition is commonly observed in older adults but can also affect younger populations, particularly patients with psychiatric conditions who face increased risk due to medication side effects, autonomic dysfunction, and inadequate bowel management. This report describes two forensic autopsy cases of fatal FI in patients with neuropsychiatric disorders. The first case involved a 52-year-old man with mild intellectual disability who had received long-term psychiatric treatment. Autopsy findings included marked colonic dilation (maximum diameter >10 cm), ischemic mucosal changes, and a large fecal mass (~2,200 g) obstructing the sigmoid and descending colon. The second case involved a 25-year-old man with severe intellectual disability. Autopsy revealed severe colonic dilation (maximum diameter of 12 cm), extensive FI along rectum and descending colon, and no evidence of alternative causes of death. In both cases, death was attributed to mechanical intestinal obstruction secondary to FI. These cases highlight the forensic significance of FI as a cause of sudden death in patients with neuropsychiatric disorders. Symptoms such as paradoxical diarrhea may be misinterpreted, and the inadvertent use of contraindicated medications (e.g., antidiarrheals) can worsen the condition, contributing to fatal outcomes. Furthermore, forensic evaluation must assess whether inadequate medical intervention or neglect played a role in the progression of FI. Early recognition, proactive bowel management, and interdisciplinary collaboration are critical to preventing fatal events in high-risk patients with neuropsychiatric disorders.

Fecal impaction (FI) is a potentially fatal condition characterized by the accumulation of large, hardened fecal masses in the large intestine, resulting in mechanical obstruction. This condition is commonly observed in older adults but can also affect younger populations, particularly patients with psychiatric conditions who face increased risk due to medication side effects, autonomic dysfunction, and inadequate bowel management. This report describes two forensic autopsy cases of fatal FI in patients with neuropsychiatric disorders. The first case involved a 52-year-old man with mild intellectual disability who had received long-term psychiatric treatment. Autopsy findings included marked colonic dilation (maximum diameter >10 cm), ischemic mucosal changes, and a large fecal mass (~2,200 g) obstructing the sigmoid and descending colon. The second case involved a 25-year-old man with severe intellectual disability. Autopsy revealed severe colonic dilation (maximum diameter of 12 cm), extensive FI along rectum and descending colon, and no evidence of alternative causes of death. In both cases, death was attributed to mechanical intestinal obstruction secondary to FI. These cases highlight the forensic significance of FI as a cause of sudden death in patients with neuropsychiatric disorders. Symptoms such as paradoxical diarrhea may be misinterpreted, and the inadvertent use of contraindicated medications (e.g., antidiarrheals) can worsen the condition, contributing to fatal outcomes. Furthermore, forensic evaluation must assess whether inadequate medical intervention or neglect played a role in the progression of FI. Early recognition, proactive bowel management, and interdisciplinary collaboration are critical to preventing fatal events in high-risk patients with neuropsychiatric disorders.

Purpose: Esophagojejunostomy leakage (EJL) remains one of the most critical complications following total gastrectomy for gastric cancer. This study aimed to evaluate the evolving therapeutic approaches and clinical outcomes of EJL using data from a large-scale multicenter retrospective cohort. Methods: Among 6,577 patients who underwent total gastrectomy or proximal gastrectomy with double tract reconstruction at nine institutions from 2003 to 2024, 196 (3.0%) developed EJL. Of these, 162 patients with comprehensive clinical data were included in the final analysis. The study examined treatment modalities, changes in management over time, patient characteristics, surgical variables, and clinical outcomes. Four groups were defined according to treatment approach: conservative, endoscopic, reoperation, and multimodal (combined) therapy. Results: Endoscopic therapy was first introduced in 2011 and has progressively supplanted reoperation, now comprising 32.5% of cases. The average time to EJL diagnosis was 8.4 days after surgery. Overall in-hospital mortality was 6.1% (10/162). When conservative management was excluded, endoscopic treatment demonstrated the highest rate of therapeutic success (94.3%, p = 0.004). Both the duration until diet resumption and length of hospital stay were notably reduced in the endoscopic and conservative groups compared with reoperation and multimodal therapy (p < 0.001). Moreover, although the highest post-leakage hospitalization costs were observed with multimodal treatment (p < 0.001), overall hospitalization expenses were significantly lower for patients managed conservatively or with endoscopic intervention (p < 0.001). Conclusion Over the past two decades, management of EJL has shifted toward endoscopic approaches. Endoscopic therapies yield superior clinical outcomes and should be considered a primary option for appropriate candidates.

BACKGROUND: Current tendon and ligament reconstruction surgeries rely on scar tissue healing which differs from native bone-to-tendon interface (BTI) tissue. We aimed to engineer Synovium-derived mesenchymal stem cells (Sy-MSCs) based scaffold-free fibrocartilage constructs and investigate in vivo bone–tendon interface (BTI) healing efficacy in a rat anterior cruciate ligament (ACL) reconstruction model. METHODS: Sy-MSCs were isolated from knee joint of rats. Scaffold-free sy-MSC constructs were fabricated and cultured in differentiation media including TGF-b-only, CTGF-only, and TGF-b + CTGF. Collagenase treatment on tendon grafts was optimized to improve cell-to-graft integration. The effects of fibrocartilage differentiation and collagenase treatment on BTI integration was assessed by conducting histological staining, cell adhesion assay, and tensile testing. Finally, histological and biomechanical analyses were used to evaluate in vivo efficacy of fibrocartilage construct in a rat ACL reconstruction model. RESULTS: Fibrocartilage-like features were observed with in the scaffold-free sy-MSC constructs when applying TGF-band CTGF concurrently. Fifteen minutes collagenase treatment increased cellular attachment 1.9-fold compared to the Control group without affecting tensile strength. The failure stress was highest in the Col + D + group (22.494 ± 13.74 Kpa) compared to other groups at integration analysis in vitro. The ACL Recon + FC group exhibited a significant 88% increase in estimated stiffness (p = 0.0102) compared to the ACL Recon group at the 4-week postoperative period. CONCLUSION Scaffold-free, fibrocartilage engineering together with tendon collagenase treatment enhanced fibrocartilaginous BTI healing in ACL reconstruction.