ObjectiveTo analyze the research hotspots and development trends in the field of spinal cord stimulation (SCS) for spinal cord injury (SCI). MethodsLiterature about SCS for SCI was retrieve from the Web of Science (WOS) Core Collection database, with a time range from January, 1999 to July, 2025. VOSviewer 1.6.20 and CiteSpace 6.4.R2 were used to analyze the annual publication volume, countries, authors, institutions, journals and keywords. ResultsA total of 636 literatures were included. From 1999 to 2025, the overall publication trend in this field showed an upward trajectory, with recent years fluctuating but tending to stabilize. The country with the most publications was the United States (429 papers), followed by Russia (98 papers) and China (70 papers). The institution with the highest number of publications was the University of California, Los Angeles (76 papers), the author with the most publications was V. Reggie Edgerton (70 papers), and the journal with the most publications was Journal of Clinical Medicine (31 papers). The most frequently cited study focused on exploring the combination of epidural spinal cord stimulation with task-specific training to restore motor function in patients with complete SCI. Keyword analysis showed that the research hotspots in this field were mainly focused on neuroregulation mechanisms, recovery of motor and autonomic nervous dysfunction, artificial intelligence, closed-loop stimulation and brain-computer interface technology innovations. In recent years, the research focus gradually shifted from basic mechanisms to personalized and precise multifunctional rehabilitation strategies. ConclusionThe field of SCS for SCI has undergone phases of basic mechanism exploration and clinical application expansion. Current research hotspots and future trends focus primarily on the development of new stimulation paradigms and combined innovative technologies.

Objective To elucidate the molecular mechanism of sirtuin-3 (SIRT3) in regulating mitochondrial biogenesis in human renal tubular epithelial cells. Methods Cells were stimulated with different concentrations of H₂O₂ and divided into four groups: control (NC), 50 μmol/L H₂O₂, 110 μmol/L H₂O₂ and 150 μmol/L H₂O₂. SIRT3 protein expression was then measured. SIRT3 was knocked down with siRNA, and cells were further assigned to five groups: control (NC), negative-control siRNA (NCsi), SIRT3-siRNA (siSIRT3), NCsi+H₂O₂, and siSIRT3+H₂O₂. After 24 h, cellular adenosine triphosphate (ATP) and mitochondrial superoxide anion (O₂•⁻) levels were determined, together with mitochondrial expression of SIRT3, peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), nuclear respiratory factor 1 (NRF1), mitochondrial transcription factor A (TFAM), superoxide dismutase 2 (SOD2), acetylated-SOD2 and adenosine monophosphate activated protein kinase α1 (AMPKα1). Results The 110 and 150 μmol/L H₂O₂ decreased SIRT3 protein (both P<0.05). ATP and mitochondrial O₂•⁻ did not differ between NC and NCsi groups (both P>0.05). Compared to the NCsi group, the siSIRT3 group exhibited elevated O₂•⁻ level, decreased SIRT3 protein and increased expression levels of SOD2 and acetylated SOD2 protein (all P<0.05). Compared to the NCsi group, the NCsi+H₂O₂ group exhibited decreased cellular ATP levels, elevated mitochondrial O₂•⁻ levels, and reduced protein expression levels of SIRT3, SOD2, TFAM, AMPKα1, PGC-1α and NRF1 (all P<0.05). Compared with the siSIRT3 group, the siSIRT3+H₂O₂ group showed a decrease in cellular ATP levels, an increase in mitochondrial O₂•⁻ levels, a decrease in SIRT3, SOD2, TFAM, AMPKα1, PGC-1α and NRF1 protein expression levels and a decrease in acetylated SOD2 protein expression levels (all P<0.05). Compared with the NCsi+H₂O₂ group, the siSIRT3+H₂O₂ group showed a decrease in cellular ATP levels, an increase in mitochondrial O₂•⁻ levels, a decrease in SIRT3, AMPKα1, PGC-1α and NRF1, TFAM protein expression levels, and an increase in SOD2 and acetylated SOD2 protein expression levels (all P<0.05). Conclusions SIRT3 promotes mitochondrial biogenesis in tubular epithelial cells via the AMPK/PGC-1α/NRF1/TFAM axis, representing a key mechanism through which SIRT3 ameliorates oxidative stress-induced mitochondrial dysfunction.

Objective Magnetoreception, the remarkable ability of diverse animals to sense and utilize the geomagnetic field for orientation and navigation, remains a molecularly unresolved mystery in sensory biology. The putative magnetoreceptor (MagR, previously known as IscA1) is a highly conserved iron-sulfur protein implicated in both magnetoreception and iron metabolism; however, the functional diversity among its cross-species homologs remains poorly understood. Cellular morphology is a key genetically determined trait that can be altered through genetic or environmental modifications—a process known as cell morphology engineering. Constructing engineered cells with specific morphological features and magnetic sensitivity to achieve remote, non-invasive magnetic modulation represents a crucial goal in this field with significant application potential. Therefore, this study aims to systematically investigate the effects of MagR heterologous expression on bacterial morphology and magnetic sensing capabilities, screen for MagR-based magnetically sensitive morphology engineering pathways, and reveal the underlying molecular mechanisms. Methods We systematically screened 28 MagR homologous genes from diverse prokaryotic and animal taxa to evaluate their expression and corresponding phenotypic effects in Escherichia coli (E. coli). To compare the differential magnetic responses among bacteria expressing various recombinant MagR proteins, we utilized high-throughput automated bright-field microscopic imaging and scanning electron microscopy (SEM). Furthermore, comprehensive biochemical and biophysical characterizations of iron and iron-sulfur cluster binding were performed using Ferrozine colorimetric assays, electron paramagnetic resonance (EPR) spectroscopy, ultraviolet-visible (UV-Vis) absorption, and circular dichroism (CD) spectroscopy. Additionally, 100 mT static magnetic field (SMF) exposure experiments were conducted to assess magnetically tunable phenotypes, while the intrinsic magnetic properties of purified MagR proteins were directly measured using a superconducting quantum interference device (SQUID) magnetometer. Results Our results demonstrated that the heterologous expression of MagR homologs induced varying degrees of bacterial filamentation. From this comprehensive screen, two distinct morphological patterns were identified: hydra (Hydra vulgaris) MagR (hyMagR) promoted uniform cell elongation and filamentation, exhibiting robust magnetic sensitivity manifested as significantly enhanced filamentation under the 100 mT SMF. In contrast, pigeon (Columba livia) MagR (clMagR) induced only low-frequency, extreme filamentation (sporadically exceeding 80 μm) with a relatively weaker magnetic morphological response. Mechanistically, our data unambiguously proved that these phenotypic differences are primarily driven by distinct iron redox preferences rather than total cellular iron accumulation. Specifically, hyMagR preferentially binds ferrous iron (Fe²⁺), whereas clMagR favors ferric iron (Fe³⁺) and forms more stable iron-sulfur clusters. Intriguingly, although SQUID magnetometry showed that purified clMagR exhibited approximately five-fold higher mass magnetic susceptibility than hyMagR, its cellular magnetic response was weaker. We hypothesize that the Fe²⁺-preferred intracellular environment associated with hyMagR overexpression primes the cell for enhanced generation of reactive oxygen species (ROS) via the Fenton reaction. Exposure to an SMF synergizes with this primed redox state, triggering the bacterial SOS response and upregulating cell division inhibitors to efficiently induce uniform filamentation. Conclusion Our findings identify the Fe²⁺/Fe³⁺ redox state as a critical determinant of MagR-mediated morphological remodeling and magnetic responsiveness. This discovery suggests a potential strategy for engineering magnetically responsive cellular systems for synthetic biology applications, and provides a plausible framework, which potentially combines intrinsic protein magnetism with redox-state modulation, for further investigating the evolutionary mechanisms of MagR-mediated magnetoreception.

Objective Magnetoreception, the remarkable ability of diverse animals to sense and utilize the geomagnetic field for orientation and navigation, remains a molecularly unresolved mystery in sensory biology. The putative magnetoreceptor (MagR, previously known as IscA1) is a highly conserved iron-sulfur protein implicated in both magnetoreception and iron metabolism; however, the functional diversity among its cross-species homologs remains poorly understood. Cellular morphology is a key genetically determined trait that can be altered through genetic or environmental modifications—a process known as cell morphology engineering. Constructing engineered cells with specific morphological features and magnetic sensitivity to achieve remote, non-invasive magnetic modulation represents a crucial goal in this field with significant application potential. Therefore, this study aims to systematically investigate the effects of MagR heterologous expression on bacterial morphology and magnetic sensing capabilities, screen for MagR-based magnetically sensitive morphology engineering pathways, and reveal the underlying molecular mechanisms. Methods We systematically screened 28 MagR homologous genes from diverse prokaryotic and animal taxa to evaluate their expression and corresponding phenotypic effects in Escherichia coli (E. coli). To compare the differential magnetic responses among bacteria expressing various recombinant MagR proteins, we utilized high-throughput automated bright-field microscopic imaging and scanning electron microscopy (SEM). Furthermore, comprehensive biochemical and biophysical characterizations of iron and iron-sulfur cluster binding were performed using Ferrozine colorimetric assays, electron paramagnetic resonance (EPR) spectroscopy, ultraviolet-visible (UV-Vis) absorption, and circular dichroism (CD) spectroscopy. Additionally, 100 mT static magnetic field (SMF) exposure experiments were conducted to assess magnetically tunable phenotypes, while the intrinsic magnetic properties of purified MagR proteins were directly measured using a superconducting quantum interference device (SQUID) magnetometer. Results Our results demonstrated that the heterologous expression of MagR homologs induced varying degrees of bacterial filamentation. From this comprehensive screen, two distinct morphological patterns were identified: hydra (Hydra vulgaris) MagR (hyMagR) promoted uniform cell elongation and filamentation, exhibiting robust magnetic sensitivity manifested as significantly enhanced filamentation under the 100 mT SMF. In contrast, pigeon (Columba livia) MagR (clMagR) induced only low-frequency, extreme filamentation (sporadically exceeding 80 μm) with a relatively weaker magnetic morphological response. Mechanistically, our data unambiguously proved that these phenotypic differences are primarily driven by distinct iron redox preferences rather than total cellular iron accumulation. Specifically, hyMagR preferentially binds ferrous iron (Fe²⁺), whereas clMagR favors ferric iron (Fe³⁺) and forms more stable iron-sulfur clusters. Intriguingly, although SQUID magnetometry showed that purified clMagR exhibited approximately five-fold higher mass magnetic susceptibility than hyMagR, its cellular magnetic response was weaker. We hypothesize that the Fe²⁺-preferred intracellular environment associated with hyMagR overexpression primes the cell for enhanced generation of reactive oxygen species (ROS) via the Fenton reaction. Exposure to an SMF synergizes with this primed redox state, triggering the bacterial SOS response and upregulating cell division inhibitors to efficiently induce uniform filamentation. Conclusion Our findings identify the Fe²⁺/Fe³⁺ redox state as a critical determinant of MagR-mediated morphological remodeling and magnetic responsiveness. This discovery suggests a potential strategy for engineering magnetically responsive cellular systems for synthetic biology applications, and provides a plausible framework, which potentially combines intrinsic protein magnetism with redox-state modulation, for further investigating the evolutionary mechanisms of MagR-mediated magnetoreception.

Objective:To investigate the clinical manifestation, therapy, and prognosis of Susac syndrome and enhance the understanding of this disease.Methods:A case summary was made.The clinical data of two siblings with Susac syndrome treated at Children′s Medical Center, Peking University First Hospital in January 2024 were summarized.Reported cases of pediatric Susac syndrome were reviewed.Results:The onset of the disease in the two siblings was at the age of 3.00 and 6.75 years, with recurrent headaches, tinnitus, hearing loss and encephalopathy symptoms.Cranial magnetic resonance imaging showed multiple cerebral microbleeding and microinfarction lesions, " snowball like" in the corpus callosum and diffuse white matter edema in the brain.Audiometry revealed sensorineural hearing loss.In one case, ophthalmic fluorescein angiography revealed ischemic changes due to branch retinal artery occlusions.No pathogenic variants were detected in gene testing.This child was diagnosed with Susac syndrome, and the symptoms were improved after treatment with Corticosteroids and Rituximab.No relapse was observed during the 9-month follow-up.A total of 20 pediatric cases of Susac syndrome were retrieved, including 18 reported previously and 2 cases from this study.There were 2 boys and 18 girls, with the age of onset ranging from 2.5 to 17.0 years.The common initial symptoms included headache (19 cases), vertigo and tinnitus or hearing loss (9 cases), and vision impairment or visual field defect (4 cases). The symptoms were improved after immunotherapy.Conclusions:With a low incidence, Susac syndrome is rare in children and difficult to diagnose.There may be a genetic predisposition in such disease.Early diagnosis and immunotherapy can low the relapse and improve the prognosis.

Objective To propose a dynamic early warning model based on machine learning methods and validate its predi-ctive efficacy so as to achieve precise assessment and early warning of mortality risk in patients with traumatic hypothermia.Methods Firstly,a total of 480 patients who met inclusion criteria were retrospectively selected from the eICU database and randomly divided into training and test sets at an 8∶2 ratio.Secondly,physiological parameters were extracted from these patients,and five machine learning algorithms including XGBoost,AdaBoost,LightGBM,logistic regression(LR)and random forest(RF)were employed respectively to develop dynamic mortality risk warning models for traumatic hypothermia patients,utilizing a 1-hour observation window.Thirdly,receiver operating characteristic curves(ROC)were plotted using the test set data and the effects of different warning windows on the model performance were analyzed by calculating the AUC.Finally,the interpretability of the models was analyzed using the SHapley Additive exPlanations(SHAP)algorithm to elucidate the contribution of each feature to predictive performance.Results The optimal warning window for the dynamic warning model constructed using the eICU database was 12 hours,and in case of 12-hour warning window the logistic regression model achieved the highest AUC of 0.935 and showed optimal predictive performance.The results of the interpretability analysis by the SHAP algorithm showed that body temperature was the feature that had the greatest impact on the model results,and its reduction was positively correlated with the increased risk of death.Conclusion The machine learning-based dynamic warning model for mortality risk in traumatic hypothermia patients enables real-time dynamic risk assessment,providing robust support for clinicians to identify the patient's condition changes at an early stage and references for the adjustment of clinical treatment programs.[Chinese Medical Equipment Journal,2025,46(3):9-14]

Under the current situation of "low prevalence and low infection" of schistosomiasis in China, and to provide a basis for achieving the goal of eliminating schistosomiasis by 2030 proposed by the Healthy China Action (2019 - 2030) as scheduled, the Hunan Provincial Corps Hospital of the Chinese People's Armed Police Force established a schistosomiasis monitoring and early warning index system based on the previous studies on schistosomiasis early warning index system and the recent literature analysis, combined with the current potential risk factors affecting the transmission and prevalence of schistosomiasis, and organized two rounds of expert consultation and carried out project promotion meetings. The experts reached a consensus on the comprehensiveness and practicability of the index system, aiming to lay a solid foundation for construction of China's schistosomiasis prevention and control early warning system.

Objective To investigate the effects of estrogen signaling on T-cell recruitment and polarization in acutely injured skeletal muscle.Methods One hundred C57BL/6 male mice,one hundred and eighty C57BL/6 female mice were selected.Twenty-five female mice were ovariectomized(OVX)and 10 male mice were taken as the sham-operated(sham).Then,cardiotoxin(CTX)induced tibialis anterior(TA)injury for preparing mice myoinjury model.Subcutaneous injection of 17β-estradiol(E2)or estrogen receptor antagonist 4-hydroxytamoxifen(4-OHT)was performed.A total of 140 mice(70 males and 70 females)were divided into four group including:PBS-male,CTX-male,PBS-female,and CTX-female.Serum estradiol(E2)levels were measured by ELISA,and muscle injury models were validated via HE staining.Subsequently,20 male and 20 female mice were selected for immunofluorescence(IF)and Real-time PCR to assess estrogen receptors(ER)expression in injured muscle tissue.Further,10 male and 40 female mice were allocated into five experimental groups,including CTX,CTX+E2,CTX+4-OHT,CTX+OVX,CTX+sham.HE staining and IF were performed to evaluate inflammatory infiltration in the injured muscle.Additionally,50 female mice were divided into CTX and CTX+OVX groups,and IF combined with flow cytometry were used to analyze T-cell phenotypes and muscle fiber regeneration in the injured muscle.Results In vivo,serum E2 and myofiber ERβ increased post-injury in mice of both sexes,significantly higher in females.Compared to the control group,E2 alleviated inflammation,OVX exacerbated inflammation,increased CD4+T-cell infiltration,elevated T helper 1 cell(Th1)response,decreased regulatory T cells(Tregs),impaired regeneration.In vitro,IFN-γ/LPS significantly upregulated ERβ in myotubes.Conclusion Estrogen signaling critically regulates muscle inflammation.Estrogen deficiency(OVX)delays repair of skeletal muscle by promoting Th1 response and suppressing Tregs function.

Objective To propose a dynamic early warning model based on machine learning methods and validate its predi-ctive efficacy so as to achieve precise assessment and early warning of mortality risk in patients with traumatic hypothermia.Methods Firstly,a total of 480 patients who met inclusion criteria were retrospectively selected from the eICU database and randomly divided into training and test sets at an 8∶2 ratio.Secondly,physiological parameters were extracted from these patients,and five machine learning algorithms including XGBoost,AdaBoost,LightGBM,logistic regression(LR)and random forest(RF)were employed respectively to develop dynamic mortality risk warning models for traumatic hypothermia patients,utilizing a 1-hour observation window.Thirdly,receiver operating characteristic curves(ROC)were plotted using the test set data and the effects of different warning windows on the model performance were analyzed by calculating the AUC.Finally,the interpretability of the models was analyzed using the SHapley Additive exPlanations(SHAP)algorithm to elucidate the contribution of each feature to predictive performance.Results The optimal warning window for the dynamic warning model constructed using the eICU database was 12 hours,and in case of 12-hour warning window the logistic regression model achieved the highest AUC of 0.935 and showed optimal predictive performance.The results of the interpretability analysis by the SHAP algorithm showed that body temperature was the feature that had the greatest impact on the model results,and its reduction was positively correlated with the increased risk of death.Conclusion The machine learning-based dynamic warning model for mortality risk in traumatic hypothermia patients enables real-time dynamic risk assessment,providing robust support for clinicians to identify the patient's condition changes at an early stage and references for the adjustment of clinical treatment programs.[Chinese Medical Equipment Journal,2025,46(3):9-14]

Objective To investigate the therapeutic potential and prophylactic value of concomitant administration of nonsteroidal anti-inflammatory drug(NSAID)and antimicrobial agents in mitigating the incidence and severity of trauma-induced sepsis.Methods A retrospective cohort study encompassed the collection of clinical records from trauma patients managed in the department of intensive care unit(ICU)of Daping Hospital,Army Medical University(Third Military Medical University)from June 2008 to June 2024.Based on administered therapeutic protocols,patients were stratified into a control group(receiving antibiotic monotherapy)and a experimental group(undergoing adjunctive therapy with NSAID in conjunction with antimicrobial agents).Intergroup comparisons were performed to elucidate differences in baseline clinical characteristics and laboratory indices pertinent to therapeutic outcomes.Results A total of 268 trauma patients were included,with 72 patients in the control group and 196 patients in the experimental group.The majority of cases involved open trauma(67.5%)and injuries sustained from traffic accidents(44.0%),reflecting the principal mechanisms of injury.The respiratory tract was the most common site of infection(67.5%),with Acinetobacter baumannii(A.baumannii)emerging as the leading causative microorganism(18.0%).Among therapeutic agents,ibuprofen represented the most frequently employed NSAID(59.8%),whereas cephalosporins constituted the predominant class of antimicrobials(30.5%).Following intervention,the lymphocyte percentage(LYM%)was markedly elevated in the experimental group relative to control group[0.14(0.09,0.20)vs.0.12(0.09,0.15),P<0.01].In contrast,the levels of white blood cell count(WBC),neutrophil percentage(NEU%),D-dimer,glucose(Glu),and lactic acid(Lac)were significantly reduced[WBC(×109/L):8.82(6.36,12.96)vs.12.10(7.78,15.54);NEU%:0.76(0.67,0.81)vs.0.78(0.72,0.83);D-dimer(μg/L):2208.0(889.5,3301.5)vs.2943.9(1735.4,4997.6);Glu(mmol/L):6.8(6.2,7.9)vs.7.7(6.6,9.2);Lac(mmol/L):0.9(0.6,1.2)vs.1.1(0.8,1.5),all P<0.05].The experimental group demonstrated a significantly reduced incidence of traumatic sepsis compared with the control group[15.8%(31/196)vs.26.4%(19/72),P<0.05].Conclusion The combination of NSAID and antimicrobial agents exerts its protective effect by attenuating inflammatory and stress responses,reestablishing immune homeostasis,correcting coagulopathy,and enhancing tissue perfusion,thereby significantly decreasing the incidence of traumatic sepsis and contributing to improved prognostic outcomes in injured patients.