Hu Zhao

Accurate determination of cause of death and estimation of postmortem interval (PMI) are critical yet challenging tasks in forensic science, particularly i

Objective: Accurate estimation of post-mortem submersion interval (PMSI) is a critical challenge in forensic science. The current research has largely focused on the microbial communities in the skin and gut, which are susceptible to environmental contamination, while the potential of internal tissues remains underexplored. This study aimed to investigate whether the microbiome of skeletal muscle, a relatively closed ecosystem, undergoes a predictable succession following submersion in water PMSI and to evaluate its potential for building a high-precision PMSI prediction model, which is independent of the cause of death (drowning vs. post-mortem submersion). Methods: Using 72 male Sprague–Dawley rats, we established drowning (D group) and post-mortem submersion (PS group) models. After submersion in natural aquatic environment for 14 days, skeletal muscle samples were collected at six time. The microbial communities were profiled by high-throughput sequencing of the V3–V4 region of the 16S rRNA gene, followed by analyses of alpha and beta diversity. Based on the observed successional patterns, a two-stage prediction model combining classification and regression algorithms (e.g., random forest, RF) was developed. Results: The skeletal muscle microbiome exhibited a significant and predictable successional pattern, clearly partitioning into an early-phase (0–3 days) and a late-phase (5–14 days) (PERMANOVA, p < 0.001). This succession was characterized by a shift from the dominant community of Proteobacteria to the dominant community of Firmicutes. Importantly, the cause of death did not significantly impact either the alpha or beta diversity of the microbial communities (PERMANOVA, p = 0.251). The resulting two-stage prediction model demonstrated excellent performance: the classification model distinguished the early and late phases with an accuracy of 90.9% (AUC = 0.9504), and the mean absolute errors (MAE) of regression models was 0.303 days in the early phase and 1.293 days in the late phase. Conclusion: The rat skeletal muscle microbiome undergoes a regular and predictable post-mortem succession unrelated to the cause of death. The stable “microbial clock” within the internal tissue allows the construction of a high-precision two-stage machine learning model for PMSI estimation. Our results establish skeletal muscle as a highly promising new target for forensic microbiology, offering a robust theoretical basis and technical approach to resolving challenges in long-term PMSI estimation.

Traumatic brain injury (TBI) is one of the leading causes of death and disability. Animal and clinical studies of TBI have greatly changed the clinical practice of TBI with the development and application of new technologies. However, with the development of forensic science, legal issues related to TBI continue to emerge, and it is still far from satisfactory that the practical application of relevant research findings as legal evidence in court practice. This review discusses an overview of the latest progress of TBI through neuropathological changes, secondary injury mechanisms, postmortem neuroimaging, cognitive, emotional, and behavioral impairments, biomarkers, and the effects of toxins and drugs on brain injury from a forensic perspective. Meanwhile, we highlight the interpretability and limitations of findings on TBI in legal proceedings are ongoing challenges.

Methamphetamine, a commonly abused drug, is known for its high relapse rate. The persistence of addictive memories associated with methamphetamine poses a significant challenge in preventing relapse. Memory retrieval and subsequent reconsolidation provide an opportunity to disrupt addictive memories. However, the key node in the brain network involved in methamphetamine-associated memory retrieval has not been clearly defined. In this study, using the conditioned place preference in male mice, whole brain c-FOS mapping and functional connectivity analysis, together with chemogenetic manipulations of neural circuits, we identified the medial prefrontal cortex (mPFC) as a critical hub that integrates inputs from the retrosplenial cortex and the ventral tegmental area to support both the expression and reconsolidation of methamphetamine-associated memory during its retrieval. Surprisingly, with further cell-type specific analysis and manipulation, we also observed that methamphetamine-associated memory retrieval activated inhibitory neurons in the mPFC to facilitate memory reconsolidation, while suppressing excitatory neurons to aid memory expression. These findings provide novel insights into the neural circuits and cellular mechanisms involved in the retrieval process of addictive memories. They suggest that targeting the balance between excitation and inhibition in the mPFC during memory retrieval could be a promising treatment strategy to prevent relapse in methamphetamine addiction.

Editorial: Traumatic stress disorders

Introduction: Fear memory generalization is regarded as the core characteristic of posttraumatic stress disorder (PTSD) development. However, the mechanism that contributes to the generalization of conditioned fear memory is still unclear. The generalization is generally considered to be a mismatch that occurs during memory consolidation.Methods: Foot shocks and tones were given as unconditioned stress and conditioned stress, respectively for fear conditioning training. Immunofluorescence staining, western blotting and qPCR were performed to determine the expression of different genes in amygdala of mice after fear conditioning training. Cycloheximide was used as a protein synthesis inhibitor and 2-methyl-6-phenylethynyl-pyridine was injected for mGluR5 inhibition.Results: Fear conditioning using caused incremental generalization, which was clearly observed during training. The density of c-Fos⁺ cells or the synaptic p-NMDAR expression did not differ with stress intensities. Strong-shock fear conditioning could induce significant mGluR5 de novo synthesis in the amygdala, which was not observed in the weak-shock group. Inhibition of mGluR5 impaired fear memory generalization induced by strong-shock fear conditioning, but the generalization level induced by weak-shock training was enhanced.Discussion: These results indicated that mGluR5 in the amygdala is critical to the function of inappropriate fear memory generalization and suggested that this may be a potential target for the treatment of PTSD.