Blast lung injury (BLI) poses great challenges for early diagnosis and precise treatment. This review systematically summarizes the evolution of relevant biomarkers from conventional inflammatory indicators to newly identified molecular markers related to cell injury, inflammation, oxidative stress, and epigenetic regulation. It also discusses imaging combination strategies, multi-omics applications, current translational obstacles, and future research trends. This work provides valuable theoretical references for improving diagnostic accuracy, optimizing prognostic evaluation, and developing targeted therapies for BLI.

Octahydro-1,3,5,7-tetranitro-1,3,5,7-tetrazocine (HMX) is a nitramine explosive widely used in military and industrial fields. While emerging evidence suggests the neurotoxicity of HMX, the mechanisms underlying central nervous system (CNS) damage remain largely unknown. In the present study, we established a mouse model of 28-day subacute HMX exposure to explore HMX-induced neurotoxicity and underlying mechanisms in vivo. Behavioral assessments revealed that HMX increased spontaneous locomotor activity and central exploration in the open field test, and reduced immobility time in the forced swimming test, indicating abnormal emotional regulation. The Morris water maze further demonstrated impaired hippocampus-dependent spatial learning and memory in HMX-treated mice, as evidenced by prolonged platform latency. Histopathological analysis showed hippocampal demyelination in HMX-treated mice, accompanied by downregulation of myelin structural proteins (MBP, PLP1) and oligodendrocyte lineage proteins (OLIG2, CNPase). Additionally, proteomic analysis identified 173 differentially expressed proteins in the HMX-exposed hippocampus, which were enriched in myelination, synaptic transmission and neuroactive ligand-receptor interaction pathways. Collectively, our findings demonstrate that subacute HMX exposure induces behavioral deficits and demyelination in mice hippocampus, providing a novel mechanistic insight into HMX neurotoxicity and a theoretical basis for occupational health protection against HMX exposure.

Blast lung injury (BLI) is characterized by pulmonary inflammatory response and tissue injury. A rat BLI model was established using a biomedical shock tube, and the animals were divided into three groups: control, BLI model, and IL-17 A inhibitor groups. We assessed pulmonary function parameters, observed lung hemorrhage and pleural effusion, measured white cell counts in bronchoalveolar lavage fluid (BALF), quantified histopathological scores using hematoxylin and eosin (HE) staining, and analyzed the protein expression levels of IL-17 A, phospho-NF-κB p65, and inhibitor of κB kinase β (IKK-β) by Western blotting. Compared with the control group, the model group exhibited significantly increased respiratory frequency and airway resistance index. In contrast, the IL-17 A inhibitor group demonstrated significantly improved minute ventilation and peak inspiratory and expiratory flow rates. The inhibitor group also demonstrated reduced pulmonary hemorrhage and pleural effusion, lower BALF white cell counts, and reduced histopathological scores. Western blot analysis revealed that the expression levels of IL-17 A, p-p65, and IKK-β were upregulated in the model group, but were robustly suppressed by IL-17 A inhibition. In conclusion, IL-17 A inhibition effectively attenuated blast-induced pulmonary inflammatory injury, improved pulmonary function, and mitigated histopathological injury, potentially through modulation of the IL-17 A/NF-κB signaling pathway.

Exposure to volatile organic compounds (VOCs) is associated with an increased risk of lung function impairment and inflammation, particularly in infants and children. However, there is still lack of effective protective methods. Thus, this study investigates the protective effects of taurine against lung injury in young rats induced by inhalation of typical VOCs (benzene, toluene, xylene and formaldehyde). The young rats were exposed to different groups (Control, VOCs model, VOCs+0.5 % taurine and VOCs+1 % taurine) via nose-only inhalation for 4 weeks. The results showed that VOCs inhalation exposure resulted in slower weight gain, reduced food intake, alterations of lung function indices, including decrease of tidal volume (TV), minute ventilation (MV), peak inspiratory flow (PIF), peak expiratory flow (PEF), and expiratory flow at 50 % ventilation (EF50), and increase of respiratory depression (Rinx) in young rats. Moreover, VOCs inhalation exposure induced decreased serum glutathione (GSH) activity was, and increased MDA activity, 8-OHDG levels, and concentrations of IL-2, IL-1 beta and NF-kappa B. Histopathological analysis revealed sloughing of tracheal epithelial cells, inflammatory cell infiltration under the tracheal epithelium, inflammatory cell infiltration in alveoli and widening of the alveolar septa in young rats treated by VOCs. While, 1 % taurine treatment dramatically improved the tracheal and lung tissue damage, oxidative stress and inflammation marker levels. This demonstrated that 1 % taurine significantly improves lung function and prevents the progression of lung injury, which is due to the effective prevention of oxidative stress and inflammation. This study demonstrates a novel effective protection method against VOCs inhalation exposure.

The potential health and environmental risks posed by 2,4,6,8,10,12-hexanitro-2,4,6,8,10,12-hexaazaisowurtzitane (CL-20), a high-energy-density compound, have spurred research into microbial degradation strategies. While several CL-20-degrading bacterial strains have been isolated, their degradation efficiency remains suboptimal, underscoring the need for enhanced biodegradation methods to address CL-20 contamination. In this study, morphological characterization identified a novel bacterial strain, designated CzL-01, which exhibited CL-20 biodegradation capability when the compound was provided as the sole nitrogen source. This investigation employs a multi-faceted approach including 16S rRNA gene sequencing for phylogenetic analysis, quantitative assessment of CL-20 degradation efficiency, and complete genome sequencing of the isolate. This work marks the first documented investigation of the Sphingobium genus’s role in high-energy-density material catabolism. Further characterization of this strain is anticipated to elucidate the microbial metabolic pathways involved in CL-20 degradation, thereby facilitating the development of advanced bioremediation protocols for wastewater treatment applications.

Citrullination, the deimination of peptidylarginine residues into peptidylcitrulline catalyzed by the peptidylarginine deiminase (PADs), has been confirmed as a unique form of posttranslational modification of proteins. Among the five isoforms of PADs, PAD2 is a main PAD enzyme expressed in central nervous system (CNS). Previous studies reported that citrullinated proteins catalyzed by PAD2 was increasingly associated with neurological disorders such as Alzheimer’s disease, prion disease and Multiple Sclerosis. However, the physiological role of PAD2 in the CNS are still poorly elucidated. Here we reported that Pad2 knockout (KO) mice exhibited significantly increased anxiety level and impaired memory capacity. Furthermore, Western Blot analysis, immunohistochemistry and proteomics revealed alterations in synaptic-related proteins and dendritic spines in hippocampus of Pad2 KO animals. These findings indicated that Pad2 plays an important function in the CNS, which is implicated in the regulation of emotion and cognitive capacity.

Non-small cell lung cancer (NSCLC) remains the leading cause of cancer deaths worldwide. Unfortunately, effective treatment is still lacking. The p53 tumor-suppressor protein is a critical mediator of cellular growth arrest and apoptosis, and is closely related to NSCLC. Importantly, microRNAs (miRs) have been shown to influence tumor progression by targeting p53. Therefore, we screened p53-associated miRs that were differentially expressed in NSCLC and benign tissues by bioinformatic analysis. Among them miR-7 was implicated in multiple tumorigenesis related pathways. Then the novel hybrid tRNA scaffold was used to produce bio-engineered miR-7 and its inhibition to NSCLC as well as the interaction with p53 was investigated. We found that overexpression of miR-7 in NSCLC significantly inhibited the proliferation, migration, invasion, and induced apoptosis of NSCLC cells. And in vivo study exhibited dramatic inhibition of tumor growth by bio-engineered miR-7 in orthotopic NSCLC xenograft tumor mouse model. In addition, we identified Akt3 as a novel target of miR-7, the suppression of tumor growth and sensitization of chemotherapy drugs by miR-7 was related to the repression of Akt which activated MDM2-mediated ubiquitination and degradation of p53. Our results reported for the first time that miR-7 could target Akt3 and interact with genes in the p53 pathway to suppress the development of NSCLC, which also implied the therapeutic potential of bio-engineered miR-7 for NSCLC.

Craniocerebral and pulmonary injuries are primary blast-induced damages, assessed via numerical simulations, animal models, and postmortem human surrogates (PMHS). Recent years, the successful development of shock wave cell models and organoid models has provided new research directions for evaluation of blast injuries. Particularly human-derived organoids that can highly simulating the structure and function of human organs, significantly enhancing the physiological relevance of the models. Additionally, AI-based models (machine/deep learning) show promise in blast injury prediction and assessment. This review systematically summarizes the biological effects of explosive shock waves, the application of conventional assessment models and their limitations, and emerging technologies-cell/organoid models and AI applications. The utilization of cell models, human-derived organoid models, and AI models for the assessment of blast-induced biological injuries and subsequent research holds significant importance for understanding the cellular mechanisms of injury, protective research, and injury warning systems.

Octahydro-1,3,5,7-tetranitro-1,3,5,7-tetrazocine (HMX) is a globally recognized energetic material that widely used in industrial, mining, and military fields. Like hexahydro-1,3,5-trinitro-1,3,5-triazine (RDX) and other nitramine compounds, HMX has also been reported to exhibit neurotoxicity. However, the molecular mechanisms underlying the toxic effects of HMX remain poorly understood. Therefore, this study aims to investigate the neurotoxicity induced by HMX by adopting PC12 cells. The results show that HMX treatment decreased cell viability and upregulated the intracellular free calcium ions (Ca2+) in PC12 cells. Furthermore, HMX caused aggravated oxidative stress in PC12 cells, as evidenced by the upregulations of reactive oxygen species (ROS) and malondialdehyde (MDA). Intracellular biochemical assays demonstrated that HMX induced loss of mitochondrial membrane potential in PC12 cells. Notably, altered expression of brain-derived neurotrophic factor (BDNF) and ionotropic glutamate receptors (iGluRs), as well as an abnormal transcription profile, were also observed in PC12 cells treated by HMX. These findings suggest that HMX exerts toxic effects on PC12 cells, involved in oxidative stress, and disturbances in Ca2+ and BDNF, accompanied by aberrant iGluRs. Overall, the present study helps us better understand the health hazards associated with HMX and provides valuable insights for developing the health protection standards related to HMX exposure.

Background: Blast traumatic brain injury (bTBI) can result in depression-like behaviors in the acute and chronic phases. SSRIs have been shown to significantly alleviate depression-like behaviors in animal models of traumatic brain injury (TBI) by increasing serotonin (5-HT) and brain-derived neurotrophic factor (BDNF) in the hippocampus. However, the therapeutic effects of SSRIs on depression caused by bTBI remain unclear. Objective: Therefore, this study was aimed at investigating the therapeutic effects of SSRIs on depression-like behaviors in bTBI models. Methods: We created a rat model to study mild TBI by subjecting rats to increased blast overpressures (BOP) and injecting fluoxetine and escitalopram SSRIs intraperitoneally for 28 days. Results: On day 14 post-BOP exposure, rats treated with SSRIs showed decreased depression-like behaviors. This finding was accompanied by higher 5-HT levels in the hippocampus and increased numbers of Nestin-positive cells in the dentate gyrus. Furthermore, rats treated with SSRIs exhibited increased pCREB and BDNF protein expression in the hippocampus on days 7, 14, and 28 after bTBI. Conclusions: Overall, our findings indicate that SSRI-induced recovery from depression-like behaviors after mild bTBI is associated with the upregulation of 5-HT levels, pCREB and BDNF expression, and neurogenesis in the hippocampus.

To investigate the dynamic response characteristics of personnel injuries caused by blast shock waves under actual working conditions, experimental studies on blast-induced injuries in rats, behavioral experiments post-injury, and pathological examinations were conducted, followed by injury assessments. The results showed that all rats died when the peak overpressure was 0.427 MPa. At a peak overpressure of 0.192 MPa, the rats were assessed as moderately injured. Behavioral tests at 7 and 28 days revealed reduced motor ability and decreased autonomous exploration, with statistically significant results (P < 0.05). Pathological examinations indicated gradual recovery of brain and lung tissues, with only minor residual damage by day 28. At a peak overpressure of 0.125 MPa, the rats were classified as mildly injured. Statistically significant behavioral differences were observed only on day 7 (P < 0.05), and pathological results demonstrated complete recovery of brain and lung tissues by day 28. These findings provide valuable references for future personnel injury assessments and engineering applications.

Traumatic brain injury (TBI) is a complex neurological disease caused by external forces impacting the head and is one of the leading causes of mortality and disability worldwide, exerting a significant impact on public health and socioeconomic conditions. Current research on TBI has focused primarily on assessing injury severity, determining clinical treatment, and improving patient prognosis. The timely and accurate diagnosis of TBI in clinical settings and the implementation of effective therapeutic strategies remain challenging. However, a deeper understanding of changes in gene expression and underlying molecular regulatory processes may alleviate this pressing issue. MicroRNAs (miRNAs), a class of short noncoding RNA molecules, play crucial roles in cellular physiology and pathology by regulating gene expression. With advancements in research, miRNAs have garnered increasing attention in TBI studies. This review summarizes the progress of miRNA research in TBI and explores the potential of miRNAs as diagnostic and prognostic markers and therapeutic targets for TBI.

Hexanitrohexaazaisowurtzitane (CL-20) is a high-energy-density material known for its exceptional explosive performance, but it suffers from significant safety concerns due to its high sensitivity. To mitigate this issue, researchers have explored the synthesis of CL-20-based cocrystals with other energetic materials to achieve a balance between energy output and safety. Recent advancements in CL-20 cocrystals have focused on developing novel synthesis methods and leveraging computational design techniques to predict and optimize their physicochemical properties. However, the toxicity of CL-20 cocrystals, along with their environmental and health risks, remains a critical concern. This review systematically examines recent progress in CL-20 cocrystal energetic materials, emphasizing toxicity profiles and mechanistic insights into their components. The findings serve as a foundation for the development of safer energetic materials, thereby facilitating sustainable advancements in manufacturing technologies and industrial applications of CL-20.

Cisplatin resistance coupled with adverse effects presents substantial hurdles in the treatment of ovarian cancer. Both cold atmospheric plasma and plasma-activated liquid (PAL) hold the ability to induce DNA damage, which is a primary target of cisplatin. In this study, we investigate the potential of PAL in augmenting cisplatin sensitivity or diminishing the necessary drug dosage by impairing the DNA of cisplatin-resistant cancer cells. We found that plasma irradiated medium exceeding 40 s could decrease the viability, induce DNA damage, trigger cell cycle arrest, and augment apoptosis and autophagy in two types of cisplatin-resistant ovarian cancer cells (A2780/DDP and SKOV3/DDP) after a 24 h incubation period. Notably, pre-treatment with 40 s plasma-activated medium (PAM) for 2 h significantly enhanced the anti-cancer effect of cisplatin administered at lower doses on these cell types. RNA-seq, quantitative real-time PCR and Western blotting analysis revealed that PAM treatment could downregulate the expression of several pivotal proteins involved in nucleotide excision repair (NER) and homologous recombination repair (HRR). The mouse xenograft tumor model demonstrated that plasma-activated saline and cisplatin synergistically inhibited tumor growth and significantly suppressed the expression of proteins related to HRR and NER pathways. We identified plasma-derived peroxide generation in PAM as crucial in these processes. These results pave the way for considering PAM as an adjuvant treatment for cisplatin-resistant ovarian cancer and other abdominal cancers. Additionally, the findings indicate the feasibility of reducing cisplatin dosage to alleviate side effects through sensitization.

Depleted uranium (DU), as a heavy metal material extensively utilized in the industrial sector, poses potential health risks to humans through various exposure pathways, including inhalation, ingestion, and dermal contact. To comprehensively understand the toxicological hazards of DU, this study conducted a literature search in the Web of Science Core Collection database using "DU" and "toxicity" as keywords, covering the period from January 2000 to December 2023. A total of 65 papers related to human, animal, or cellular studies on DU were included. This review delves into the latest research advancements on the origin and toxicokinetics of DU, as well as its pulmonary toxicity, neurotoxicity, nephrotoxicity, immunotoxicity, hepatotoxicity, reproductive toxicity, cancer, bone toxicity, and hematological toxicity. The aim of this review is to gain a deeper understanding of the health hazards posed by DU, which is of significant importance for formulating corresponding protection strategies and measures.

Bone loss caused by long-duration spaceflight seriously affects the skeletal health of astronauts. There are many shortcomings in currently available treatments for weightlessness-induced bone loss. The aim of this study was to evaluate the preventive effect of Angelica dahuricae Radix (AR) on simulated microgravity-induced bone loss. Here, we established a hind limb unloading (HLU) mouse model and treated HLU mice with AR (2 g/kg) for 4 weeks. Results indicated that AR significantly inhibited simulated microgravity-induced bone loss. In addition, the components in AR were analyzed using UPLC-MS/MS; results showed that a total of 224 compounds were detected in AR, which mainly contained 7 classes of components. Moreover, the network pharmacological predictions suggested that active ingredients of AR might act on PTGS2 to prevent bone loss. These results elucidate the efficacy of AR in preventing microgravity-induced bone loss and its potential for use in protecting the bone health of astronauts.

ABSTRACTMilitary personnel, firefighters, and fire survivors exhibit a higher prevalence of mental health conditions such as depression and post‐traumatic stress disorder (PTSD) compared to the general population. While numerous studies have examined the neurological impacts of physical trauma and psychological stress, research on acute neurobehavioral effects of gas inhalation from explosions or fires is limited. This study investigates the early‐stage neurobehavioral and neuronal consequences of acute explosion gas inhalation in Sprague–Dawley rats. Rats were exposed to simulated explosive gas and subsequently assessed using behavioral tests and neurobiological analyses. The high‐dose exposure group demonstrated significant depression‐like behaviors, including reduced mobility and exploration. However, neuronal damage was not evident in histological analyses. Immunofluorescence revealed increased density of radial glia and oligodendrocytes in specific brain regions, suggesting hypoxia and axon damage induced by gas inhalation as a potential mechanism for the observed neurobehavioral changes. These findings underscore the acute impact of explosion gas inhalation on mental health, highlighting the habenula and dentate gyrus of hippocampus as the possible target regions. The findings are expected to support early diagnosis and treatment strategies for brain injuries caused by explosion gas, offering insights into early intervention for depression and PTSD in affected populations.

Hexafluoroisobutylene (HFIB) is an important compound widely used in semiconductor lithography materials, refrigerants, fluorine coatings, and pharmaceutical intermediates in the fluorination industry. Owing to its toxicity, the occupational exposure in the workplace, especially for pregnant woman is the concern and there is still lack of the data of HFIB toxicity on pregnancy and fetal development. Here, for the first time, we investigated the effects of HFIB on pregnant rats and fetal development. The pregnant rats were exposed to different doses of HFIB (0 ppm, 27.2 ppm, 53.5 ppm, 105.6 ppm) via whole-body inhalation for the period of organogenesis, which from implantation (gestation day 5) to the day prior to scheduled caesarean section (gestation day 19). The results showed that the pregnant rats exposed to 105.6 ppm HFIB displayed systemic toxicity, including a decrease in body weight and food consumption, as well as tracheal inflammation, pulmonary interstitial inflammation and renal tubular swelling. Moreover, reduced fetal and placental weights, delayed ossification, and a reduced number of ossification centers were observed in fetuses delivered by pregnant rats exposed to 105.6 ppm. These effects were attributed to severe maternal weight loss. In addition, it would be useful to note that no whole-body, visceral or skeletal congenital malformations were observed. However, HFIB exposure at 53.5 ppm showed no significant adverse effects on pregnant rats and fetuses. These findings demonstrate that 105.6 ppm HFIB is a toxic concentration, while 53.5 ppm HFIB is the no-observed-adverse-effect concentration (NOAEC) for both pregnancy and fetal development. This study for the first time to provide evidence for the health risk of HFIB exposure on pregnancy and fetal development.

Spider silk protein, renowned for its excellent mechanical properties, biodegradability, chemical stability, and low immune and inflammatory response activation, consists of a core domain with a repeat sequence and non-repeating sequences at the N-terminal and C-terminal. In this review, we focus on the relationship between the silk structure and its mechanical properties, exploring the potential applications of spider silk materials in the detection of energetic materials.