ObjectiveTranscranial magneto-acoustic stimulation (TMAS) is an emerging non-invasive neuromodulation technique that may provide a novel non-pharmacological intervention strategy for Parkinson's disease (PD). PD is characterized by the progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNc), leading to motor impairments such as bradykinesia, tremor, and rigidity. Increasing evidence indicates that mitochondrial dysfunction and impaired mitochondrial quality control are central mechanisms underlying dopaminergic neuronal loss. In particular, abnormalities in mitophagy and mitochondrial fission-fusion balance contribute substantially to oxidative stress, energy metabolic failure, and neuronal injury. At present, most clinical treatments for PD mainly alleviate symptoms but do not effectively halt disease progression. Therefore, exploring new interventions targeting the core pathological mechanisms is of considerable significance. This study aims to investigate whether TMAS can improve neural damage and motor dysfunction in PD mice by regulating mitophagy and the fission/fusion dynamic balance, thereby providing theoretical and experimental support for its application in PD treatment. MethodsMale C57BL/6 mice were used in this study. A PD model was established by intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) for 7 consecutive days. After model induction, mice in the intervention group received TMAS once daily for 14 consecutive days, whereas the corresponding control group received sham stimulation. The stimulation target was positioned over the primary motor cortex (M1). Motor performance was evaluated using the pole test and the open-field test. To verify the activation effect of TMAS on the target cortical region, c-Fos immunohistochemistry was performed in the M1. To assess nigral dopaminergic neuronal injury, tyrosine hydroxylase (TH) immunohistochemistry was used to quantify TH-positive neurons in the SNc. Mitochondrial function was evaluated by measuring reactive oxygen species (ROS) levels and adenosine triphosphate (ATP) content in the SNc. Western blot was further performed to determine the expression of mitophagy-related proteins, including PINK1, Parkin, LC3-II, and p62, as well as mitochondrial dynamics-related proteins, including Drp1 and Opa1. ResultsTMAS significantly increased the number of c-Fos-positive cells in M1 (P<0.000 1), indicating effective activation of neurons in the targeted cortical region. Compared with the control group, MPTP-treated mice exhibited marked motor dysfunction, including a significant reduction in total distance traveled in the open-field test (P<0.000 1) and mean speed (P=0.000 1), as well as significant prolongation of turn time and total climbing time in the pole test (P<0.000 1). These behavioral impairments were accompanied by a substantial loss of TH-positive dopaminergic neurons in the SNc, whereas TMAS significantly increased TH-positive neuron survival (P<0.000 1). In parallel, MPTP induced a pronounced increase in ROS levels and a significant reduction in ATP content, indicating severe mitochondrial dysfunction and energy metabolism impairment (P<0.01). TMAS treatment significantly improved motor performance, as reflected by the reversal of MPTP-induced impairment in the open-field and pole tests, and significantly reduced ROS accumulation (P<0.01) while restoring ATP production (P<0.001). At the molecular level, MPTP markedly downregulated PINK1 and Parkin, decreased p62 expression, increased LC3-II accumulation, elevated Drp1 expression, and reduced Opa1 expression, whereas TMAS significantly reversed these abnormalities, suggesting restoration of mitophagy-related mitochondrial quality control and re-establishment of mitochondrial fission-fusion balance. Collectively, these findings indicate that TMAS ameliorates MPTP-induced neurotoxicity and restores mitochondrial homeostasis and energy metabolism. ConclusionTMAS effectively attenuates neural damage and improves motor dysfunction in MPTP-induced PD mice. Its neuroprotective effects are closely associated with multidimensional regulation of the mitochondrial quality control system, including restoration of PINK1/Parkin-mediated mitophagy and rebalancing of Drp1/Opa1-related mitochondrial dynamics. Rather than acting only as a symptomatic neuromodulatory intervention, TMAS may influence a key pathological axis of PD by improving mitochondrial homeostasis in SNc and protecting nigral dopaminergic neurons. These findings provide experimental evidence supporting TMAS as a promising non-invasive physical intervention for PD.

ObjectiveTranscranial magneto-acoustic stimulation (TMAS) is an emerging non-invasive neuromodulation technique that may provide a novel non-pharmacological intervention strategy for Parkinson's disease (PD). PD is characterized by the progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNc), leading to motor impairments such as bradykinesia, tremor, and rigidity. Increasing evidence indicates that mitochondrial dysfunction and impaired mitochondrial quality control are central mechanisms underlying dopaminergic neuronal loss. In particular, abnormalities in mitophagy and mitochondrial fission-fusion balance contribute substantially to oxidative stress, energy metabolic failure, and neuronal injury. At present, most clinical treatments for PD mainly alleviate symptoms but do not effectively halt disease progression. Therefore, exploring new interventions targeting the core pathological mechanisms is of considerable significance. This study aims to investigate whether TMAS can improve neural damage and motor dysfunction in PD mice by regulating mitophagy and the fission/fusion dynamic balance, thereby providing theoretical and experimental support for its application in PD treatment. MethodsMale C57BL/6 mice were used in this study. A PD model was established by intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) for 7 consecutive days. After model induction, mice in the intervention group received TMAS once daily for 14 consecutive days, whereas the corresponding control group received sham stimulation. The stimulation target was positioned over the primary motor cortex (M1). Motor performance was evaluated using the pole test and the open-field test. To verify the activation effect of TMAS on the target cortical region, c-Fos immunohistochemistry was performed in the M1. To assess nigral dopaminergic neuronal injury, tyrosine hydroxylase (TH) immunohistochemistry was used to quantify TH-positive neurons in the SNc. Mitochondrial function was evaluated by measuring reactive oxygen species (ROS) levels and adenosine triphosphate (ATP) content in the SNc. Western blot was further performed to determine the expression of mitophagy-related proteins, including PINK1, Parkin, LC3-II, and p62, as well as mitochondrial dynamics-related proteins, including Drp1 and Opa1. ResultsTMAS significantly increased the number of c-Fos-positive cells in M1 (P<0.000 1), indicating effective activation of neurons in the targeted cortical region. Compared with the control group, MPTP-treated mice exhibited marked motor dysfunction, including a significant reduction in total distance traveled in the open-field test (P<0.000 1) and mean speed (P=0.000 1), as well as significant prolongation of turn time and total climbing time in the pole test (P<0.000 1). These behavioral impairments were accompanied by a substantial loss of TH-positive dopaminergic neurons in the SNc, whereas TMAS significantly increased TH-positive neuron survival (P<0.000 1). In parallel, MPTP induced a pronounced increase in ROS levels and a significant reduction in ATP content, indicating severe mitochondrial dysfunction and energy metabolism impairment (P<0.01). TMAS treatment significantly improved motor performance, as reflected by the reversal of MPTP-induced impairment in the open-field and pole tests, and significantly reduced ROS accumulation (P<0.01) while restoring ATP production (P<0.001). At the molecular level, MPTP markedly downregulated PINK1 and Parkin, decreased p62 expression, increased LC3-II accumulation, elevated Drp1 expression, and reduced Opa1 expression, whereas TMAS significantly reversed these abnormalities, suggesting restoration of mitophagy-related mitochondrial quality control and re-establishment of mitochondrial fission-fusion balance. Collectively, these findings indicate that TMAS ameliorates MPTP-induced neurotoxicity and restores mitochondrial homeostasis and energy metabolism. ConclusionTMAS effectively attenuates neural damage and improves motor dysfunction in MPTP-induced PD mice. Its neuroprotective effects are closely associated with multidimensional regulation of the mitochondrial quality control system, including restoration of PINK1/Parkin-mediated mitophagy and rebalancing of Drp1/Opa1-related mitochondrial dynamics. Rather than acting only as a symptomatic neuromodulatory intervention, TMAS may influence a key pathological axis of PD by improving mitochondrial homeostasis in SNc and protecting nigral dopaminergic neurons. These findings provide experimental evidence supporting TMAS as a promising non-invasive physical intervention for PD.

Objective To investigate the current status of family resilience of children with cancer and analyze its influencing factors,to provide a basis for medical staff to formulate intervention plans.Methods Using a convenient sampling method,children with cancer who were hospitalized in 2 tertiary hospitals in Henan Province from January to April 2024 were selected for the survey.A general information questionnaire,family resilience assessment scale,quality of life family version,ZBI caregiver burden interview,and social support rating scale were used to understand the current status of family resilience of children with cancer and to explore the related influencing factors by univariate analysis and multiple stepwise linear regression analysis.Results A total of 280 questionnaires were distributed and 265 valid questionnaires were recovered,with a valid questionnaire recovery rate of 94.64％.The total score of family resilience for primary caregivers of children with cancer was(185.63±30.66).The multiple stepwise linear regression analysis results showed that the children's self-care ability,caregiver's work status,family care burden,and social support level were the influencing factors for family resilience of children with cancer(P＜0.05),and the explanatory variance was 51.3％.Conclusion The family resilience of children with cancer is at a medium level.The worse the children's self-care ability and the heavier the family care burden,the worse the family resilience;the caregiver's work status and good social support are helpful for the family resilience of children with cancer.Healthcare workers should develop intervention programs to address these factors to enhance the family resilience of children with cancer.

OBJECTIVE To develop a nomogram model for prediction of the risk of sepsis in the patients with acute liver failure(ALF)and validate its clinical value.METHODS Totally 228 patients with ALF who were treated in the Fifth Medical Center of Chinese PLA General Hospital from Jan.2009 to Mar.2023 were recruited as the re-search subjects and were grouped according to the occurrence of sepsis,the clinical characteristics and results of laboratory tests were collected from the patients.The subjects were brought into multivariate logistic regression a-nalysis after the primary screening with univariate regression analysis,the independent predictive factors were screened out,and the nomogram model was established.The accuracy,calibration accuracy and clinical practica-bility of the model were assessed by means of receiver operating characteristic(ROC)curves,calibration curves and decision curve analysis(DCA).RESULTS Among the 228 patients with ALF,159(69.74％)were diagnosed with sepsis.Totally 6 independent predictive factors were screened out by the multivariate analysis,including age[odd ratio(OR)=1.098,95％CI:1.030 to 1.220],aspartate transaminase(OR=0.998,95％CI:0.996 to 0.999),white blood cells counts(OR=1.037,95％CI:1.020 to 1.064),hemoglobulin(OR=0.981,95％CI:0.962 to 0.998),lactic acid(OR=1.187,95％CI:1.022 to 1.426)and mechanical ventilation(OR=3.463,95％CI:2.340 to 5.125).The area under the curve(AUC)of the nomogram model was 0.864(95％CI:0.807 to 0.921)in the training set,0.817(95％CI:0.717 to 0.918)in the validation set,remarkably better than that of sequential organ failure assessment(SOFA)scores[0.710(95％CI:0.625 to 0.795)and 0.647(95％CI:0.515 to 0.779)].Hosmer-Lemeshow test(P=0.512)and the calibrated curves showed that the predication probability of the model was highly consistent with the actual risk,and DC A indicated that the net clinical benefit was brought more from the model than from SOFA score.CONCLUSION The age,hemoglobulin,aspartate transaminase,white blood cells counts,lactic acid and mechanical ventilation are the independent predictive factors for the sepsis in the ALF patients.The nomogram model established based on the factors has high predictive efficiency and clini-cal application value.

Objective To compare the difference,agreement,and axial length measurement success rate between biometers ZW-30 and IOLMaser 700 based on swept-source optical coherence tomography for the measurement of ocular bi-ological parameters in patients with cataracts.Methods A total of 126 cataract patients(233 eyes)who were advised to undergo cataract surgery at the Department of Ophthalmology at Beijing Tongren Hospital,Capital Medical University from January to February 2024 were included in this study.Two biometers were used to measure the axial length(AL),mean keratometry(Km),anterior chamber depth(ACD),lens thickness(LT),central corneal thickness(CCT),and horizontal corneal diameter[namely,the white-to-white(WTW)distance].The axial measurement success rate of the two biometers and the difference and agreement between the parameters were calculated.Results The mean difference between ZW-30 and IOLMaster 700 was(-0.006±0.042)mm for AL,(-0.074±0.204)D for Km,(0.031±0.051)mm for ACD,(0.001±0.005)mm for CCT,and(-0.286±0.337)mm for WTW,and the differences were statistically significant(all P＜0.05).The mean difference between ZW-30 and IOLMaster 700 was(0.008±0.215)mm for LT,and the difference was not statis-tically significant(t=0.579,P=0.563).The 95％limits of agreement range was between-0.011 mm and 0.000 mm for AL,between-0.474 D and 0.326 D for Km,between-0.010 mm and 0.012 mm for CCT,between-0.068 mm and 0.131 mm for ACD,between-0.116 mm and 0.159 mm for LT,and between-0.947 mm and 0.376 mm for WTW.The intra-class correlation coefficient of all measurements ranged from 0.790 to 1.000.The AL measurement success rate of IOLMaster 700 and ZW-30 was 95.3％and 95.7％,respectively.The latter had an AL measurement success rate of 98.7％after manually marking the position of the retinal identification line.Conclusion There were statistically significant differences between ZW-30 and IOLMaster 700 in the measurement of the AL,Km,ACD,and CCT,which,however,were not clinically significant.The agreement between both was good.ZW-30 had a higher AL measurement success rate,espe-cially for the manual identification function of eyes with opacified refractive media,which can further improve the AL meas-urement success rate and provide reference for clinical work.

Aim To investigate the role of triggering receptor expressed on myeloidcells 2(TREM2)in syn-aptic plasticity induced by cocaine addiction.Methods C57BL/6J mice and Trem2 knockout mice were uti-lized in this study to evaluate the alterations in postsyn-aptic density protein 95(PSD-95)and synapsin 1(SYN1)within the cortex and hippocampus of co-caine-addicted mice by using immunological tech-niques.Results HE staining and Nissl staining showed increased neuronal damage in the hippocampus and cortex of mice after cocaine addiction.The results of immunohistochemistry and fluorescence of PSD-95 and SYN1 were consistent with the expression trend of Western blot.In the wild type mouse model,the ex-pression level of PSD-95 in the hippocampus and cortex was lower than that in the saline group,and the ex-pression of SYN1 was higher than that in the saline group.In the knockout mouse model,the expression levels of PSD-95 and SYN1 in the hippocampus and cortex were significantly higher than those in the saline group after cocaine addiction.The expression levels of PSD-95 and SYN1 in the hippocampus and cortex of cocaine knockout mice were higher than those of co-caine wild type mice.Conclusion Cocaine addiction can change the synaptic plasticity,and TREM2 plays a regulatory role in the synaptic plasticity of hippocampus and cortex in mice with cocaine injury.TREM2 is ex-pected to be a new target for studying the mechanism of cocaine addiction.

Cyclic GMP-AMP synthase(cGAS)is a congenital immune sensor that can recognize cytoplasm abnormal dsDNA.By catalyzing the second messenger cyclic GMP-AMP(cGAMP)formation,it activates stimulator of interferon genes(STING),releases type Ⅰ interferon and inflammatory cytokines,activates the host immune response,and participates in cerebral ischemia reperfusion injury(CIRI)cascade reaction.This article reviews the research progress of the mechanism of cGAS-STING signaling pathway participation in CIRI,hoping to provide ideas for its treatment.

Endogenous bioactive small molecules are characterized by low molecular weight,high biological activity,low immunogenicity,and rapid synthesis and metabolism,play a pivotal role in maintaining vascular homeostasis.Vascular calcification(VC)is a abnormal deposition of calcium and phosphorus in the vessel wall.Endogenous bioactive small molecules such as cardiovascular bioactive peptides,adipokines and gaseous molecules participate in the process of VC through various mechanisms.This review summarises the advances in relationship between endogenous bioactive small molecules and the occurrence,development,and related mechanisms of VC.

Objective:To observe the efficacy of probiotics in the adjuvant treatment of bronchial asthma and to explore the relationship between their action and intestinal flora.Methods:A total of 76 newly diagnosed patients with mild-to-moderate bronchial asthma treated at Baotou Central Hospital between November 2023 and January 2025 were randomly divided into two groups:the conventional treatment group(n=38)and the combined probiotic treatment group(n=38).Post-treatment comparisons were made between the two groups regarding symptom resolution time,Asthma Control Test(ACT)scores,lung function,fractional exhaled nitric oxide(FeNO)levels,serum inflammatory cytokines,complement levels,and other indicators.Faecal samples were collected for 16S rDNA sequencing of gut microbiota.Results:Baseline characteristics showed no significant differences between the two groups(P＞0.05).Compared to the conventional treatment group,the combined probiotic group exhibited significantly shorter resolution times for asthma symptoms and lung rales(P＜0.001),significantly higher ACT scores,FEV1,and PEF(P＜0.001),and significantly lower FeNO levels(P＜0.001).Additionally,serum interleukin-6(IL-6),tumor necrosis factor-α(TNF-α),and complement C3 levels were significantly reduced(P＜0.001),while serum interleukin-6(IL-10)levels were significantly increased(P＜0.001).16S rDNA sequencing revealed no significant changes in gut microbiota richness or diversity in the conventional treatment group before and after treatment(P＞0.05),whereas intestinal flora richness and diversity were significantly increased in the combined probiotic treatment group compared to the pre-treatment group(P＜0.05).Correlation analysis between gut microbiota and inflammatory markers demonstrated that Faecalibacterium and Bifidobacterium abundance were negatively correlated with TNF-α levels(P＜0.05),while Escherichia-Shigella,and Streptococcus abundance were positively correlated with TNF-α levels(P＜0.05).Streptococcus and Klebsiella abundance were positively correlated with IL-6 levels(P＜0.05).Escherichia-Shigella and Streptococcus abundance were negatively correlated with IL-10 levels and positively correlated with complement C3 levels(P＜0.05).Conclusion:Probiotics may assist in improving bronchial asthma symptoms by influencing the gut flora to reduce the inflammatory response.

Objective To design an individually portable oral treatment device to solve the problems of oral diagnosis and treatment under field conditions in alpine regions.Methods The individually portable oral treatment device had a trolley box structure and consisted of an outer box,an inner framework and an operation panel.The outer box was made of low-density polyethylene material and formed by by one-time rotational moulding process;the inner framework integrated a plateau com-pressor,an independent negative-pressure compressor,an integrated control system for programmable logic controller(PLC),an individually portable respiratory synchronized pulsed oxygen supply module for plateau application;there were several curative devices equipped in the operation panel,including a 3-way syringe,a high-speed turbine handpiece,an electric variable-speed handpiece,a water control switch,a light curing machine and an ultrasonic dental cleaning handpiece.Trials were carried out with the test-phase prototype in alpine regions so as to verify the performance of the device.Results Trials proved that the prototype gained advantages in mobility,multifunctionality and pressure supply facilitating continuous operation of power gas source for oral diagnosis and treatment in alpine regions.Conclusion The device developed solves the problems in pressure insufficiency and instability,control system integration,portability and oxygen supply for medical staffs,improves the mobility of oral diagnosis and treatment in alpine regions and enhances the oral support service and equipment effectively.[Chinese Medical Equipment Journal,2025,46(1):108-113]