INTRODUCTION:Thallium poisoning is a rare but highly toxic heavy metal intoxication associated with peripheral neuropathy. However, longitudinal data integrating toxicokinetic profiles with electrophysiological outcomes remain limited. METHODS:Five patients with confirmed acute thallium poisoning were evaluated. Clinical symptoms, laboratory results, dynamic serum and urinary thallium concentrations, and electrophysiological results were recorded. All patients underwent electrophysiological follow-up one year later. Thallium elimination kinetics were analyzed using nonlinear regression. RESULTS:All patients developed peripheral neuropathy. Sensory symptoms generally preceded the onset of alopecia. During treatment, dynamic monitoring showed a progressive decrease in thallium concentrations. Toxicokinetic analysis suggested an approximate first-order elimination pattern, with an estimated serum half-life ranging from 3.8 to 5.7 days. Electrophysiological studies revealed distal axonal neuropathy characterized by reduced compound muscle action potential amplitudes. At one-year follow-up, residual axonal involvement persisted in some patients. DISCUSSION:Peripheral neuropathic symptoms may serve as an early clinical indicator of thallium poisoning. Persistent electrophysiological abnormalities despite declining thallium levels suggest incomplete neurological recovery. CONCLUSIONS:Dynamic monitoring of thallium levels can help evaluate elimination kinetics during detoxification therapy. Persistent axonal injury suggests that thallium-induced neuropathy may result in long-term neurological sequelae, highlighting the importance of early diagnosis and long-term electrophysiological monitoring.

Methotrexate (MTX) has long been a first-line anti-rheumatic agent due to its efficacy and cost-effectiveness. While generally safe at the recommended weekly dosage of 5-25 mg for rheumatoid arthritis, medication errors can lead to acute toxicity, severe adverse effects, and potentially fatal outcomes. We report a case of a 51-year-old male who experienced fatal pancytopenia following an MTX medication error during treatment for rheumatoid arthritis. His blood MTX concentration measured 0.04 μmol/L 11 days after discontinuation. Postmortem examination revealed MTX-related toxicity in multiple organs, including the liver and intestines. The spleen showed a prominent increase in plasma cells, including numerous Mott cells. Forensic analysis established the cause of death as acute MTX intoxication, directly stemming from a chain of medical negligence involving prescribing, verification, and administration failures. This case underscores the necessity of rigorous therapeutic drug monitoring, individualized dosing, and robust systemic safeguards to prevent iatrogenic fatalities, highlighting its critical medicolegal and educational implications for forensic and clinical practice.

Snakebites constitute a significant global public health concern. Based on various toxic components and action mechanisms, snake venoms are typically classified into hemotoxic, neurotoxic, and histotoxic types. The pathological changes caused by different toxicities vary, which is often one of the key points in the forensic identification of snake bites. However, relying solely on this aspect often has certain limitations in the identification of snake bite cases, with poor qualitative and quantitative results. This article presents a case of identifying death caused by an Agkistrodon halys bite through the combined application of ELISA and immunohistochemistry (IHC) methods. The concentration of snake venom in the subcutaneous tissue at the fang marks was precisely measured at 6.58 ng/mL. In addition, we summarized the forensic characteristics of such snake venom poisoning by a retrospective analysis of the literature, aiming to provide reference for the forensic identification. A rare death caused by an Agkistrodon halys bite was identified and presented; A method for snake venom detection by a combination of ELISA and IHC was proposed. The forensic characteristics of Agkistrodon halys venom poisoning were summarized..

Insulin is an important protein hormone that participates in multiple metabolic pathways. Biosynthetic insulin has been widely used in the treatment of type 1 and type 2 diabetes. Currently, the number of reported cases of insulin overdose both at home and abroad is gradually increasing, and insulin homicide is no longer a means of “committing murder without leaving a trace”. At present, there are no systematic protocols for the identification of insulin overdose in the field of forensic medicine in China. This article introduces the causes, toxicological characteristics, forensic examination, laboratory testing methods and indicator reference of insulin overdose. Based on the identification practice and research results and referring to relevant studies on insulin overdose at home and abroad, this paper aims to provide recommendations and references for the formulation of forensic identification guidelines for insulin overdose cases.

Dear Editor, Crimean-Congo hemorrhagic fever(CCHF),caused by the CCHF virus(CCHFV),is a severe tick-borne illness with a wide geographical distri-bution,posing a significant threat with case fatality rates ranging from 5％to 70％(Hawman and Feldmann,2023).Due to the lack of approved vaccines and therapeutics,the World Health Organization(WHO)has listed CCHF as one of the priority diseases(Semper et al.,2024).

Antipsychotics are a category of psychotropic medications that often require long-term or even lifelong administration, and they are also routinely screened in forensic examinations. Clinically, the use of antipsychotics can usually cause observed signs, such as QT interval prolongation, supraventricular tachycardia and conduction block. A relatively high proportion of deaths among individuals taking these medications present as negative autopsies, making cause of death determination in cases involving antipsychotics particularly unique and challenging. At present, due to the lack of effective detection indicators and standardized forensic protocols for such negative autopsy cases, forensic scientists often can only provide exclusionary or presumptive cause of death determinations. This situation frequently calls into question the scientific rigor and professional credibility of forensic opinions. To address this issue, this consensus integrates opinions from domestic forensic and related field experts, summarizes the latest evidence from forensic toxicology and molecular identification relevant to such difficult cases, and provides recommendations for case investigation, sampling and laboratory testing of such cases. It aims to offer scientific evidence for cause of death determination in antipsychotics-related deaths with negative autopsy findings, to better integrate evidence from forensic pathology, forensic toxicology, and forensic genetics, and to serve as a reference for conducting related forensic identifications.

Cardiac rupture in blunt cardiac injuries, though uncommon, can be fatal. A particularly rare occurrence is blunt cardiac rupture of the left ventricle without external chest injury. Herein, we report a case of cardiac rupture without external chest injuries in a 21-year-old man who died after a physical altercation. The cause of death was attributed to cardiac rupture caused by blunt force. We analysed the differential diagnoses of cardiac rupture with intact pericardium, including cardiac diseases, blunt chest injury, cardiopulmonary resuscitation, and Takotsubo cardiomyopathy. Additionally, we discussed the relevant factors for cardiac rupture in this case, including sudden enormous force, cardiac cycle, chest wall compliance, and alcohol consumption. Furthermore, we highlighted that no explicable cause other than cardiac rupture accounted for the death.

Xylazine, an α 2 ‐adrenergic receptor agonist commonly used as a veterinary sedative, has gained notoriety for its increasing misuse in combination with opioids, such as fentanyl, to potentiate its effects. This trend has led to a rise in cases of xylazine poisoning. Although timely diagnosis and intervention have reduced fatalities, the postmortem pathological manifestations and lethal blood concentration of xylazine alone remain poorly characterized due to its common co‐occurrence in toxicology with fentanyl. This study presented a case of homicide involving fatal intoxication solely from xylazine overdose without coadministration of other central nervous system drugs, detailing the multi‐organ pathological changes observed and quantifying the decedent's blood xylazine concentration at 13.34 μg/mL using liquid chromatography‐tandem mass spectrometry (LC–MS/MS). The findings aimed to provide forensic practitioners with valuable insights for the identification and investigation of fatal xylazine poisoning cases.

Insulin, a pivotal hormone synthesized by the pancreas and regulated through hepatic first-pass metabolism, plays an essential role in the management of diabetes. However, non-therapeutic exposure to insulin can lead to life-threatening hypoglycemia. The postmortem diagnosis of fatalities resulting from exogenous insulin presents numerous forensic challenges, including the disruption of pharmacokinetic evidence due to the rapid degradation of insulin after death and the lack of pathognomonic histopathological markers. These factors create significant obstacles in establishing medicolegal causality. Furthermore, the mechanisms underlying insulin overdose-induced injury to the pancreas and liver are poorly understood. This study aims to address these gaps by integrating standardized histopathology, precision laser microdissection, and advanced proteomics to systematically profile the global proteome and phosphoproteome of the liver and pancreas. Furthermore, it includes spatially resolved proteomic mapping of pancreatic microcompartments (islets versus acini) in models of insulin overdose. Comparative analysis with controls revealed dysregulated proteins and phosphorylation sites, along with perturbations in metabolic pathways, primarily affecting pancreatic exocrine and hepatic function. Cross-organ comparative analysis elucidated organ-specific alterations in proteins and phosphorylation sites, uncovering core functional perturbations in these vital organs. In conclusion, this study presents a multi-level proteomic resource that profiles insulin-overdosed rat models and provides insights into the core pathological and molecular signatures.

Insulin, a peptide hormone essential for blood glucose regulation, is typically quantified in clinical practice using immunoassays. While sensitive, these assays lack specificity and are often inadequate for the precise qualification and quantification in forensic practices. To address this limitation, we developed and validated an LC-Orbitrap-HRMS method for the quantification of intact insulin and its analogues in four postmortem matrices: plasma, liver, kidney, and adipose tissue. Method validation demonstrated linearity for human insulin in plasma from 0.1 to 100 ng/mL, with accuracy between 90.1 % and 106.9 %. Notably, in challenging matrices such as adipose tissue, the LLOQ was 1 ng/mL, with accuracy range from 94.1 % to 100.2 %, confirming robust analytical performance. The validated method was applied on two forensic cases involving suspected insulin overdose. Insulin concentrations in subcutaneous adipose tissue from the injection sites were significantly elevated, measuring 743.1 ng/mL and 53.2 ng/mL, respectively. These results demonstrate the utility of the method in providing reliable evidence for the investigation of suspected fatal insulin intoxication.

Insulin overdose severely disrupts hepatic glucose metabolism, leading to toxic changes in the liver that may play an important role in the diagnosis and identification of insulin overdose. A rat model of insulin overdose was established in this study. ALT and AST levels were measured to assess liver function. Hematoxylin and eosin, oil red O, and periodic acid-Schiff staining were used to evaluate pathological liver injury. Ultrastructural changes in hepatocyte organelles were observed under a transmission electron microscope. The expression levels of liver gluconeogenesis-related proteins, including forkhead box protein O1 (FOXO1) and phosphorylated FOXO1 (p-FOXO1), phosphoenolpyruvate carboxykinase (PEPCK), glucose-6-phosphatase catalytic subunit (G6PC), chromosome region maintenance 1 (CRM1), and tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein (14-3-3), were detected in the rat model and human autopsy liver tissues using immunohistochemistry and immunofluorescence. The insulin overdose group showed elevated ALT/AST, hepatocyte fatty degeneration, glycogen depletion, mitochondrial swelling, and cristae loss. The recovery group exhibited milder fatty changes, glycogen accumulation, and restored mitochondria. Insulin overdose increased hepatic p-FOXO1, CRM1, and 14-3-3 expression but decreased PEPCK and G6PC. FOXO1 shifted from nuclear to cytoplasmic localization in overdose groups, with partial nuclear recovery post-recovery. Insulin overdose leads to hypoglycemia, which in turn causes hepatocyte damage. Insulin overdose promotes the nuclear translocation of FOXO1 protein in hepatocytes, and this process shows high reproducibility in human cases of fatal insulin overdose. The coordinated changes in these indicators have significant value in detecting and diagnosing fatal cases of insulin overdose.

Mushroom poisoning incidents happen infrequently, yet owing to the non-lethal nature of most toxins and the efficacy of timely treatment, fatalities from mushroom poisoning are uncommon, leading to a scarcity of pertinent clinical and pathological data. Here, we reported a case of death caused by the consumption of raw mushrooms, alongside detailed clinical data and multi-organs pathological alterations, which underscored its potential significant reference value in forensic practice. Futhermore, ibotenic acid, a type of mushroom toxin, was detected both in the patient’s blood and gastric lavage fluid about 19 h after the consumption of mushrooms, and was successfully quantified at concentrations of 0.381 µg/mL and 0.202 µg/mL, respectively, indicating a relatively significant finding.

This study aimed to synthesize and analyze toxicological characteristics from reported cases of human anticoagulant rodenticide poisoning, providing reference data for clinical diagnosis and forensic practices. We systematically identified English-language case reports (published since 2000) of human anticoagulant rodenticide poisoning via PubMed and Web of Science. A retrospective analysis was performed on various characteristics, including year, age, gender, manner of poisoning, latency period, clinical symptoms and examination results, primary treatment methods, pathological changes in fatal cases, types and concentrations of rodenticides, and toxicological analysis methods. A total of 88 poisoning cases were identified, comprising 52 cases of accidental poisoning, 31 cases of suicidal poisoning, 3 cases of unknown poisoning and 2 cases of homicide. The median latency period was 4 days (range: 1 ∼ 30). Multi-organ hemorrhage was the predominant clinical manifestation, with hematuria being the most frequently reported symptom (n = 39). Coagulation function tests revealed average values of aPTT, PT, and INR of aPTT: 110 (3.71 ∼ 212) s, PT: 100 (11.6 ∼ 300) s and INR: 9 (0.98 ∼ 38.2), respectively, all significantly exceeding normal ranges. Vitamin K1 administration (intravenous or oral) was the primary treatment. Six fatalities occurred and autopsy findings in three cases primarily indicated multi-organ hemorrhage and necrosis. About the types of rodenticides, a total of 38 cases reported 7 distinct types, with brodifacoum and bromadiolone being the most common, presenting median concentrations of 0.15 μg/mL (0.05 ∼ 10) and 0.1215 μg/mL (0.00032 ∼ 1.665), respectively, which may be significant for clinical diagnosis and forensic identification. In Conclusion, this retrospective analysis characterized key features of 88 cases of anticoagulant rodenticide poisoning and may provide valuable reference to support clinical management and forensic investigation in suspected poisoning events.

In forensic identification, there are many cases of hair poisoning detection and analysis to assist forensic identification, with fewer reported cases using morphological features to assist forensic identification. Herein, we report the case of a 13-year-old girl who had been raped and killed. The body was abandoned in a snowy wilderness and was discovered 5 months later. After an on-site investigation and forensic examination, the case conformed to the characteristics of a homicide, and a strand of hair left on the deceased's scarf became key evidence. Through morphological methods such as stereomicroscopy, optical microscopy, and scanning electron microscopy, we believe that the hair conformed to the morphological and histological characteristics of pubic hair, which helped clarify the case. Based on this case, we believe that the morphological characteristics of hair are of great significance for forensic identification and that rich morphological observation methods can enhance the evidential value of hair in forensic cases.

Nitrous oxide (N2O) abuse is becoming increasingly popular worldwide. Moreover, the use of N2O combined with other substances, such as alcohol, is also common. Accidental deaths associated with N2O abuse are rare in forensic practice, with most fatal cases involving continuous inhalation equipment or exposure in a confined space. In contrast, the inhalation of N2O using balloons is traditionally regarded as a relatively safe method. In this report, we present an unusual fatal case of a 16-year-old girl who died after drinking alcohol and inhaling N2O from balloons. The decedent was found in a prone position with the nose and mouth compressed against the bed. Cyanosis of nails, pulmonary and cerebral edema, and the positive expression of HIF-1α in lung, myocardium and brain, were indicative of asphyxiation. Toxicological analysis revealed a peripheral blood ethanol concentration of 140 mg/dL and cardiac blood N2O concentration of 74.5 μL/mL. N2O was also positively detected in the lungs, stomach contents, gastric air, and the brain. In conclusion, we determined that the decedent died from accidental asphyxia related to N2O inhalation, prone positioning, and alcohol consumption. We also investigated chronic N2O abuse from a forensic perspective. This report aims to help forensic pathologists manage similar cases. It also reminds N2O abusers of potential dangers.

Viral myocarditis, an inflammatory heart disorder caused by viral infections, often leads to poor outcomes due to the lack of effective prevention and treatment strategies. Despite the characteristic feature of cardiomyocyte death in this condition, the underlying mechanisms and potential therapeutic approaches remain poorly understood. Traditional Chinese medicine (TCM), despite its extensive history in treating various diseases, has not yet been approved for the treatment of viral myocarditis. Here, we screened six TCM patent injections recommended by clinical practice guidelines for treating cardiovascular diseases and discovered that Danhong Injection (DHI) markedly reduced cardiomyocyte death induced by Coxsackievirus B3 (CVB3). Additionally, in a CVB3-infected mouse model of viral myocarditis, DHI treatment notably alleviated cardiomyocyte death (including apoptosis, necroptosis and pyroptosis), as well as inflammation, cardiac dysfunction, and mortality. Mechanistically, DHI exerted its protective effects by inhibiting CaMKII through its active monomer Dihydrotanshinone I (Dih-I), identified as a CaMKII inhibitor. In viral myocarditis patients, CaMKII phosphorylation was upregulated in the hearts. The anti-inflammatory properties and CaMKII inhibition effects of DHI were further validated in primary human peripheral blood mononuclear cells. Our findings not only demonstrate the central role of CaMKII-mediated cardiomyocyte death in the progression of viral myocarditis, but also highlight DHI as a promising therapeutic intervention for managing viral myocarditis-induced cardiac injury and related pathological response.

Insulin overdose may cause hypoglycemic encephalopathy. In this study, Mendelian randomization was employed to analyze changes in the serum metabolites of patients with hypoglycemic encephalopathy, and metabolomics analysis was conducted to detect differential metabolites in the serum of a rat model of hypoglycemic encephalopathy induced by insulin overdose. The results indicated an overall upward trend in the tryptophan metabolism pathway in patients with hypoglycemic encephalopathy and rats with hypoglycemic encephalopathy caused by insulin overdose, while serum glutamate levels declined. The metabolic changes in the tryptophan pathway provide new insights into the impact of hypoglycemia on brain function. The related products of the tryptophan metabolism pathway have a certain diagnostic value for hypoglycemic encephalopathy and forensic identification of insulin overdose-induced hypoglycemic encephalopathy death.

Starvation-related deaths are not uncommon worldwide particularly in economically underdeveloped regions. However, the forensic characterization of such cases remains limited due to underdeveloped local forensic systems. Here we presented a case of a neonate who died of starvation after being abandoned in the wild for 14 days, and 9 additional reported cases were identified by a systematic search of PubMed and MEDLINE databases. Based on these findings, the key forensic characteristics were summarized. Significant reductions in body or organ weight were consistently documented across all ten cases; PAS staining of the liver revealed markedly depleted glycogen stores in four cases. Of the four cases involving children under ten years of age, three demonstrated severe thymic atrophy. In our case, we observed pronounced calcification of thymic corpuscles. These findings suggest that thymic pathological changes may play a potential role in the forensic assessment of starvation deaths in children. In the absence of forensic standards for diagnosing starvation deaths, our case report and consolidated review provide valuable reference points for the forensic evaluation of similar incidents.

Infective endocarditis (IE) and myocardial abscesses caused by Rhodococcus erythropolis are rare clinical manifestations in healthy individuals. We report the autopsy of a 43-year-old male who suffered from IE caused by R. erythropolis infection and died of an atrioventricular node abscess, arrhythmia, and heart failure. This case indicates that the possibility of infection affecting the cardiac conduction system should be considered in arrhythmia-related IE cases. Our findings suggest that clinicians should consider the possibility of R. erythropolis infection in arrhythmia cases associated with IE.