Military Medical Research军事医学研究
Military Medical Research(英文缩写 MILITARY MED RES),ISSN 2095-7467,eISSN 2054-9369,中文译名:军事医学研究 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-27 至 2026-09-27，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 34.915 | Q1 |
| 2022 | 21.100 | Q1 |
| 2023 | 16.700 | Q1 |
| 2024 | 22.900 | Q1 |
| 2025 | 29.000 | Q1 |
Military Medical Research 最新收录文献
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1. Post-traumatic stress disorder: pathogenesis, epidemiological characteristics, animal models, and potential therapeutic strategies.
1. 创伤后应激障碍：发病机制、流行病学特征、动物模型和潜在的治疗策略PMID:日期:2026-12-01Post-traumatic stress disorder (PTSD) is a complex neurobehavioral disorder that disproportionately affects military service members. The clinical presentation of PTSD is heterogeneous and may overlap with other psychiatric conditions. According to the Fifth Edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), common symptoms include memory loss, mood and personality changes, impulsiveness, aggression, anxiety, and depression. The pathophysiological mechanisms underlying PTSD remain incompletely understood, although research implicates pathways involving the hypothalamic-pituitary-adrenal (HPA) axis, dysfunctional neural circuitry, neurochemical imbalances, neuroinflammatory processes, and genetic and epigenetic factors. Approximately 7% of the U.S. adult population has met the diagnostic criteria for PTSD in their lifetime, with a substantially higher prevalence of 12%-30% among military personnel. Multiple animal models, including single-stressor, intermediate complexity, social interaction, predator stress, and blast exposure paradigms, have been employed to investigate PTSD mechanisms. Current treatment strategies typically integrate pharmacotherapy and psychotherapy. Military service members are at increased risk for blast injuries, which frequently result in traumatic brain injury (TBI). Although some symptoms of TBI may resolve, approximately 20% of affected individuals develop new symptoms, including PTSD. Evidence suggests that exposure to blast shock waves (BSWs) serves as a critical trigger for the clinical manifestations of both TBI and PTSD. Recent studies have identified several mechanisms contributing to BSW-induced brain dysfunction, including intraneuronal accumulation of phosphorylated Tau (p-Tau), activation of the dynorphin/kappa opioid receptor, and activation of metabotropic glutamate receptor 2/3 signaling pathways. This review provides an overview of the clinical features, treatments, pathophysiology, and epidemiology of PTSD, as well as animal models and their limitations in replicating PTSD-like symptoms. It further examines the relationship between BSW exposure, brain injury, and PTSD, discusses animal models that simulate blast trauma and PTSD-like symptoms, and evaluates potential therapies to mitigate BSW-induced PTSD. Finally, the review addresses the limitations of current models and proposes future directions for elucidating the mechanisms linking brain trauma to PTSD.
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2. USP18 exacerbates myocardial I/R injury by inhibiting Parkin mitophagy through the deubiquitinase PTEN-L.
2. USP18通过去泛素酶PTEN-L抑制Parkin自噬，加重心肌I/R损伤PMID:日期:2026-12-01Mitochondrial quality control is essential for limiting myocardial injury induced by ischemia/reperfusion (I/R), a major contributor to adverse outcomes after reperfusion therapy. This study aimed to determine whether the deubiquitinase ubiquitin-specific protease 18 (USP18) regulates mitophagy during cardiac I/R injury and thereby represents a potential therapeutic target to attenuate myocardial I/R injury. Cardiac-specific knockout mice were subjected to cardiac I/R injury. To elucidate the role of USP18 in mitophagy regulation and cardiac I/R injury, we performed RNA sequencing, proteomic mass spectrometry, transmission electron microscopy, and mitophagy assays. In parallel, adeno-associated virus serotype 9 (AAV9)-mediated overexpression of USP18, knockdown of and phosphatase and tensin homolog-long (), and administration of an anti-PTEN-L neutralizing antibody were used to elucidate the underlying mechanisms. Additionally, serum samples from patients with ST-segment elevation myocardial infarction (STEMI) were collected to assess clinical relevance. USP18 expression was upregulated in mouse hearts following I/R injury and in ischemic human heart tissue. Cardiac-specific deficiency mitigated I/R-induced acute myocardial injury, mitochondrial dysfunction, and adverse cardiac remodeling, whereas USP18 overexpression exacerbated these pathological changes. Mechanistically, USP18 interacted with PTEN-L, which in turn bound to and inhibited the phosphorylation and translocation of Parkin to mitochondria, thereby suppressing mitophagy. knockdown abolished the cardioprotective effects conferred by deficiency, whereas knockdown reversed the detrimental effect of USP18 overexpression. Moreover, PTEN-L also exerted pathogenic effects a paracrine mechanism, as neutralizing PTEN-L with an antibody attenuated cardiac I/R injury. Serum PTEN-L levels were elevated in STEMI patients, particularly postintervention. USP18 impairs mitophagy and exacerbates cardiac I/R injury through a PTEN-L-Parkin axis, involving both intracellular and paracrine mechanisms. Targeting the USP18-PTEN-L pathway may represent a novel therapeutic strategy to alleviate myocardial I/R injury.
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3. tDCS improves early Alzheimer's disease by synaptic vesicle fusion and release.
3. tDCS通过突触小泡融合和释放改善早期阿尔茨海默病PMID:日期:2026-12-01Working memory deficits, one of the earliest hallmarks of Alzheimer's disease (AD), are closely linked to abnormal neural activity in the dorsolateral prefrontal cortex (DLPFC). Transcranial direct current stimulation (tDCS), a non-invasive neuromodulation therapy, has been shown to ameliorate early AD working memory deficits by modulating excitatory activity in the DLPFC, yet the underlying mechanisms remain incompletely understood. This investigation was structured around 3 experimental phases. We initially applied tDCS to stimulate the left prefrontal cortex (PFC) of transgenic mice with 5 familial AD (5×FAD) 5 d per week for 4 weeks. Subsequently, we employed optogenetic (Opt) techniques to modulate left PFC glutamatergic neurons. Finally, we inhibited soluble N-ethylmaleimide-sensitive factor attachment receptor (SNARE) expression in the left PFC to elucidate the essential function of SNARE complex assembly with chaperone molecules in orchestrating synaptic vesicle release. tDCS treatment improved working memory deficits in early-stage AD mice. This was accompanied by increased cerebral blood flow, enhanced neuronal excitability, amelioration of neurochemical metabolic disorders, and reduced amyloid β-protein (Aβ) deposition in the left PFC. Opt stimulation of PFC glutamatergic neurons similarly improved working memory, indicating the association between tDCS's therapeutic effects and synaptic plasticity of excitatory neurons. Crucially, tDCS facilitated synaptic vesicle fusion and release, evidenced by increased vesicle numbers, enhanced release probability, improved synaptic transmission efficacy, and upregulation of the SNARE complex, Snap25, and Syt1. Inhibiting SNARE expression in the left PFC attenuated the tDCS-induced improvements in synaptic vesicle release and working memory. These findings collectively demonstrate that left PFC-targeted tDCS modulates interactions between the SNARE complex and chaperone molecules, thereby promoting synaptic vesicle fusion and release. This mechanism underlies the amelioration of early AD-like working memory impairment by tDCS.
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4. 3D bioprinting of tissues and organs for systemic diseases and localized injuries.
PMID:日期:2026-12-01Three-dimensional (3D) bioprinting integrates engineering, materials science, and biology to fabricate living tissues with precise spatial control. By enabling the layer-by-layer deposition of cells and biomaterials, it overcomes many limitations of traditional scaffold-based tissue engineering and offers new opportunities for regenerative and personalized medicine. This review presents a comprehensive overview of recent advances in 3D bioprinting. It introduces a systematic, ASTM-aligned classification of key bioprinting modalities, extrusion, jetting, and vat photopolymerization, along with their respective material and biological design requirements. It also summarizes recent progress in bio-ink development and crosslinking strategies that improve print fidelity and functional tissue maturation. In addition, the review highlights applications in both systemic disease modelling and treatment (such as cardiovascular, endocrine/metabolic, and neurodegenerative disorders) and localized tissue repair (including skin, musculoskeletal, cartilage, and bone), emphasizing their relevance to civilian healthcare and military medicine. By combining technological innovation, biological insights, and regulatory considerations, this review outlines how advances in multi-modal bioprinting and intelligent process control can accelerate the translation of laboratory research into clinically viable, patient-specific therapies, driving the next generation of regenerative medicine.
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5. Pathophysiology-guided biomarkers and therapeutics for precision trauma medicine in polytrauma with musculoskeletal injuries.
PMID:日期:2026-12-01Polytrauma with predominant musculoskeletal (MSK) injury, resulting from blast, blunt, and crush mechanisms, remains a leading and complex challenge in both military and civilian medicine. These injuries not only disrupt tissues structurally but also trigger systemic cascades involving immune imbalance, endothelial dysfunction, mitochondrial stress, and premature cellular senescence. Such pathological processes contribute to both immediate clinical instability and long-term complications such as fibrosis, aberrant bone formation, neuroinflammation, and chronic disability. Conventional injury assessments, which rely heavily on anatomical scoring and nonspecific blood markers, fail to capture the dynamic molecular landscape underlying these conditions. To address this critical gap, we performed a comprehensive scoping review integrating evidence from basic science, translational studies, and clinical research published between January 2000 to June 2025, with particular emphasis on recent advances. The review highlights the discovery and validation of emerging blood-based and molecular biomarkers, including fatty acid-binding protein 3, syndecan-1, galectin-3, and trauma-associated microRNAs, as well as innovative diagnostic paradigms such as wearable biosensors, minimally invasive liquid biopsy platforms, and artificial intelligence (AI)-driven analytics. Unlike prior reviews, our analysis uniquely integrates findings across both military and civilian trauma contexts, providing actionable frameworks for clinical application. Building on these insights, we outline a practical roadmap: 1) deploy integrated multi-marker panels for early risk stratification, 2) expand inclusive trauma biobanking to capture diverse injury phenotypes, and 3) use adaptive, data-driven tools for real-time triage and personalized intervention. This approach links acute systemic responses to downstream recovery and rehabilitation, offering actionable guidance for both military and civilian trauma systems.
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7. Frostbite: diagnosis, treatment, prognosis, and future directions.
PMID:日期:2026-12-01From cold-weather training to deployments in high altitude and arctic conditions, frostbite injury and its sequelae remain a serious concern in military operations. Frostbite harms tissue in two distinct ways. The first involves ice crystal formation within tissue, resulting in mechanical damage and ischemia. The second occurs secondary to the inflammatory and prothrombotic state caused by reperfusion from rewarming frozen tissue. Frostbite injuries can be classified in a number of ways, but no perfect system exists. Initial work-up and diagnosis are primarily clinical. However, in equipped treatment facilities, advanced imaging modalities such as technetium-m (mTc) bone scintigraphy, magnetic resonance angiography, single-photon emission computed tomography/computed tomography (SPECT/CT), and more can play a role in diagnosis and treatment. In resource-constrained environments, such as the deployed setting, management should involve an algorithmic approach. After concurrent hypothermia and/or trauma have been evaluated for and treated, active rewarming should take place so long as there is no risk of refreezing. During re-warming, surgical consultation and evacuation considerations should be considered. Once evacuated to a definitive treatment facility, thrombolytic as well as other therapies may be indicated. Unless there is evidence of severe damage or infection, surgical management is typically delayed until injury margins are fully demarcated. Longer-term prognosis is dependent on severity, with deeper injuries often resulting in longer hospital stays, more amputations, and chronic disability. Looking forward, future frostbite research should aim to bridge field and hospital care with the goal of minimizing tissue loss and accelerating functional recovery.
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8. The cellular response capacity (CRC) as a novel immunomonitoring approach in sepsis.
8. 细胞反应能力（CRC）作为脓毒症的一种新型免疫监测方法PMID:日期:2026-12-01Early recognition of sepsis remains difficult in clinical practice because conventional humoral biomarkers such as C-reactive protein, procalcitonin, and interleukin-6 (IL-6) exhibit unfavorable, slow-release kinetics and rise hours after the onset of infection. Flow cytometry enables upstream, cell-based immunomonitoring, but its clinical use is restricted by poor standardization of fluorescence measurements. In this study, the neutrophil cellular response capacity (CRC) was developed and evaluated as a standardized approach for rapid assessment of systemic inflammation in bacteremia and sepsis. The CRC is based on a flow cytometry-based framework that defines a stable maximal stimulation reference point for neutrophil granulocytes. The CRC was evaluated in a human whole blood bacteremia model with graded exposure to and compared with humoral inflammatory markers. Next, the CRC was assessed in a prospective intensive care unit sepsis cohort. Moreover, preliminary validation was performed in an independent sepsis cohort and in patients undergoing cardiac surgery. In the bacteremia model, the CRC of neutrophil markers CD10, CD11b, and CD66b increased in a dose-dependent manner with increasing bacterial burden and detected inflammation at lower pathogen burdens than IL-6 and other humoral mediators, with a superior area under the receiver operating characteristic curve. In clinical sepsis, the CRC discriminated patients from age- and sex-matched healthy volunteers, with the CRC of CD11b showing the highest diagnostic performance. CRC values increased over time in patients with sepsis, consistent with immunological recovery. The maximal stimulation reference point for CD11b remained stable across inflammatory states, cohorts, and instruments. In addition, the CRC more precisely captured the onset and resolution of surgery-induced inflammation than conventional biomarkers. The CRC provides a rapid, standardized, and robust cell-based immunomonitoring tool that outperforms traditional humoral markers in experimental bacteremia and reliably identifies sepsis in clinical cohorts, strongly supporting its use as a novel biomarker for earlier, more precise sepsis diagnosis and monitoring.
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9. RNA as a genome architect: G-loops in G-quadruplex regulation.
9. RNA作为基因组建筑师：G-四链体调控中的G-环PMID:日期:2026-01-14该文献暂无摘要。
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10. The "cytokine storm" in infection and sepsis: win the battle but lose the war.
10. 感染和败血症中的“细胞因子风暴”：赢得战斗，但输掉战争PMID:日期:2026-01-12The cytokine storm, a life-threatening systemic inflammatory syndrome, is the primary driver of multiorgan failure in different clinical situations, including severe infections, autoimmune diseases, chimeric antigen receptor (CAR) T cell immunotherapy for cancer, and genetic syndromes. This review focuses primarily on cytokine storms triggered by severe infections such as viral pneumonia and bacterial sepsis, and explores the underlying mechanisms of cytokine storms and potential therapeutic interventions. Cytokine storms are characterized primarily by the excessive release of proinflammatory cytokines, which are triggered by pathogen-associated molecular patterns (PAMPs), damage-associated molecular patterns (DAMPs), and PANoptosis, all of which activate immune signaling cascades. Amplification mechanisms involve positive feedback loops and the failure of negative feedback mechanisms, leading to uncontrolled inflammation. Like a pyrrhic victory, the excessive activation of the immune system eliminated invading pathogens but caused catastrophic damage due to multiple organ dysfunction syndrome (MODS), turning the life-saving response into a life-threatening war. Therapeutic strategies, including cytokine antagonists, Janus kinase (JAK) inhibitors, caspase inhibitors, glucocorticoids, and blood purification therapies, aim to interrupt the self-amplifying cycle of inflammation that propagates organ injury, thereby reducing MODS and mortality. Challenges include optimizing the treatment timing and patient stratification. Future research should focus on combination therapies and personalized medicine based on the heterogeneity of infections and sepsis. Advances in multiomics and targeted therapies provide new hope for managing infections and sepsis.