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.

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.

Purpose: Alzheimer’s disease (AD) dementia may not be a single disease entity. Early-onset AD (EOAD) and late-onset AD (LOAD) have been united under the same eponym of AD until now, but disentangling the heterogeneity according to the age of sonset has been a major tenet in the field of AD research. Materials and Methods: Ninety-nine patients with AD (EOAD, n=54; LOAD, n=45) and 66 cognitively normal controls completed both [18F]THK5351 and [18F]flutemetamol (FLUTE) positron emission tomography scans along with structural magnetic resonance imaging and detailed neuropsychological tests. Results: EOAD patients had higher THK retention in the precuneus, parietal, and frontal lobe, while LOAD patients had higher THK retention in the medial temporal lobe. Intravoxel correlation analyses revealed that EOAD presented narrower territory of local FLUTE-THK correlation, while LOAD presented broader territory of correlation extending to overall parieto-occipito-temporal regions. EOAD patients had broader brain areas which showed significant negative correlations between cortical thickness and THK retention, whereas in LOAD, only limited brain areas showed significant correlation with THK retention. In EOAD, most of the cognitive test results were correlated with THK retention. However, a few cognitive test results were correlated with THK retention in LOAD. Conclusion LOAD seemed to show gradual increase in tau and amyloid, and those two pathologies have association to each other. On the other hand, in EOAD, tau and amyloid may develop more abruptly and independently. These findings suggest LOAD and EOAD may have different courses of pathomechanism.