Amanita exitialis is a lethal mushroom species found in southern China. Its amatoxins can cause acute liver injury with a high case-fatality rate. However, reports combining toxin detection in clinical specimens with autopsy pathology remain limited. We conducted a retrospective analysis of A. exitialis poisoning events treated at Chuxiong Yi Autonomous Prefecture People’s Hospital from 2019 to 2024. Toxins were measured in collected mushrooms, patient blood, and urine. Clinical data included demographics, complications, laboratory parameters, and autopsy findings. Associations between a time-weighted urinary amatoxin exposure metric and laboratory indices were assessed. Ten poisoning incidents involving 27 individuals were identified, including five deaths. We collected 10 mushroom samples, 120 urine samples, and 108 blood samples. α-amanitin, β-amanitin, phallacidin, and phallisacin were detected in mushrooms and urine. The detection rates of α-AMA, β-AMA, PCD, and PSC in urine samples were 31.67%, 5.00%, 38.33%, and 49.17%, respectively. Only three blood samples tested positive for α-AMA. The time-weighted urinary amatoxin exposure metric was positively correlated with total bilirubin (TBIL), aspartate aminotransferase (AST), alanine aminotransferase (ALT), blood urea nitrogen (BUN), creatinine (Cr), creatine kinase (CK), creatine kinase isoenzymes (CK-MB), prothrombin time (PT), activated partial thromboplastin time (APTT), and international normalized ratio (INR). Early symptoms included nausea, vomiting, diarrhea, abdominal pain, and distention; later findings involved injury to the liver, kidneys, intestines, heart, and lungs. On the fourth day following ingestion, there was a marked increase in bilirubin levels and a concurrent decrease in liver enzymes, indicating severe damage to the hepatocytes. Platelet count, white blood cell count, hemoglobin, and red blood cell count decreased over time. Autopsies demonstrated hepatic, renal, and myocardial injury, gastrointestinal mucosal exfoliation, and multiorgan hemorrhage. In summary, A. exitialis poisoning is primarily characterized by liver damage, accompanied by injuries to the kidneys, myocardium, and intestines, as well as multiorgan hemorrhaging, which may lead to blood toxicity. The detection rate of toxins in urine samples is relatively high, and early urine toxin testing can help clarify the diagnosis and guide treatment.

Background: Traumatic brain injury (TBI) poses a significant threat to human health. Ferroptosis has been reported to promote secondary brain damage, but whether ferroptosis affects injury se-verity is currently unknown. Objective: We aim to explore the relationship between ferroptosis in brain and neurological deficits in TBI models. Methods: Male Sprague-Dawley rats were randomly divided into four groups: a sham group, a mild TBI group (mTBI), a mild-moderate TBI group (mmTBI), and a severe TBI group (sTBI). Rat model of TBI was established, neurological function deficits were evaluated using modified Neurological Severity Score (mNSS). Magnetic resonance imaging (MRI), transmission electron microscopy (TEM), and Prussian blue staining were em-ployed to observe ferroptosis in the rat brains. Western blot analysis was used to detect the ex-pression of ferroptosis-related proteins, and the correlation between mNSS scores and the ex-pression of these markers was analyzed. Results: 1) MRI scans showed the TBI groups exhibited high itensity in the T2WI sequence and low intensity in the T2*WI sequence, indicating iron dep-osition. 2) TEM and Prussian blue staining showed neurons in the TBI group exhibited iron-positive cells and morphological changes of ferroptosis. 3) Western blot showed ferropto-sis-related proteins were significantly reduced in the mmTBI and sTBI groups. 4) MDA levels were significantly elevated in TBI groups, and mNSS scores increased with injury severity. Correlation analysis revealed a significant negative correlation between mNSS scores and ferroptosis inhibi-tors expression, and a positive correlation with MDA levels. Conclusion: Iron deposition and ferroptosis occur in brain tissue after TBI, and they are closely associated with the severity of neurological impairment.

Spinal cord injury (SCI) often results in severe neurological dysfunction, and myelin repair is a critical step in the recovery of neurological function. Electroacupuncture (EA), a therapeutic method that combines traditional acupuncture with electrical stimulation, has been widely applied in the field of nerve repair. However, the specific signaling pathways involved in EA have not been fully elucidated. This study aims to investigate the effects of EA on myelin regeneration in SCI rats and to verify whether the Neuregulin1 (NRG1)-ErbB4 signaling pathway plays a role in this process. SCI rats were induced by aneurysm clip injury at the T10 spinal segment. A polyethylene (PE) catheter was implanted into the vertebral canal between the L5-6 intervertebral spaces and fixed subcutaneously to establish a long-term drug delivery system. Exogenous NRG1 and its antagonist were administered through the PE catheter every other day, with a volume of 20 µL per injection. EA treatment was applied at the Dazhui (GV14) and Mingmen (GV4) acupuncture points every other day, each session lasting 30 min for 4 consecutive weeks. The results showed that EA treatment significantly promoted the expression of myelin basic protein (MBP) in spinal cord tissue and improved hind limb motor function in the rats. Furthermore, exogenous NRG1 produced similar effects to EA. In conclusion, the NRG1-ErbB4 signaling pathway plays an important role in EA-induced myelin regeneration in SCI rats.

Background: Traumatic brain injury (TBI) is a critical condition that significantly endangers hu-man health. Investigating the mechanisms underlying secondary injury in TBI can facilitate early intervention and treatment strategies. The metabolism of intracellular iron is pivotal in the sec-ondary injury process following TBI, with ferroptosis identified as a contributing factor. However, research exploring the relationship between the extent of ferroptosis and the severity of neuro-logical deficits across various TBI models is still limited. Objective: This study seeks to examine the association between ferroptosis in brain tissues and neurological impairments in TBI models with differing injury severities, thereby providing a theoretical framework for understanding the mechanisms and standardizing treatment approaches for TBI. Methods: 36 Male Sprague-Dawley rats were randomly assigned to four groups: a sham group, a mild TBI group (mTBI), a mild-moderate TBI group (mmTBI), and a severe TBI group (sTBI). A rat model of TBI with var-ying injury levels was established using the Feeney free-fall impact method. Neurological function deficits were assessed using the modified Neurological Severity Score (mNSS). Magnetic reso-nance imaging (MRI), transmission electron microscopy (TEM), and Prussian blue staining were utilized to examine iron deposition and ferroptosis in the cortical regions of the rat brains. Western blot analysis was conducted to evaluate the expression of ferroptosis-related molecular markers, and the correlation between mNSS scores and these markers was analyzed. Results: 1) MRI scans indicated that, in comparison to the sham group, the TBI groups displayed elevated signals in the T2WI and T2*WI sequences, signifying brain injury, edema, and hemorrhage. T2*WI revealed diminished signals surrounding the injured areas, indicating iron deposition. 2) TEM analysis revealed that neurons in the TBI group exhibited morphological alterations, including mitochon-drial atrophy, membrane thickening, and partial rupture of the outer membrane. 3) Prussian blue staining demonstrated a progressive increase in iron-positive cells correlating with TBI severity. 4) Western blot results indicated that the expression levels of ferroptosis-related proteins (FTH1 and GPX4) were significantly lower in the mmTBI and sTBI groups compared to the sham group. 5) MDA levels were markedly elevated in the TBI groups, and mNSS scores increased with the se-verity of injury. Correlation analysis revealed a significant negative correlation between mNSS scores and the expression of ferroptosis inhibitors FTH1 and GPX4, alongside a positive correlation with MDA levels. Conclusion: Iron deposition and ferroptosis occur in brain tissue following TBI, and they are closely linked to the severity of neurological impairment.