As China accelerates its efforts in deep space exploration and long-duration space missions, including the operationalization of the Tiangong Space Station and the development of manned lunar missions, safeguarding astronauts’ physiological and cognitive functions under extreme space conditions becomes a pressing scientific imperative. Among the multifactorial stressors of spaceflight, microgravity emerges as a particularly potent disruptor of neurobehavioral homeostasis. Dopamine (DA) plays a central role in regulating behavior under space microgravity by influencing reward processing, motivation, executive function and sensorimotor integration. Changes in gravity disrupt dopaminergic signaling at multiple levels, leading to impairments in motor coordination, cognitive flexibility, and emotional stability. Microgravity exposure induces a cascade of neurobiological changes that challenge dopaminergic stability at multiple levels: from the transcriptional regulation of DA synthesis enzymes and the excitability of DA neurons, to receptor distribution dynamics and the efficiency of downstream signaling pathways. These changes involve downregulation of tyrosine hydroxylase in the substantia nigra, reduced phosphorylation of DA receptors, and alterations in vesicular monoamine transporter expression, all of which compromise synaptic DA availability. Experimental findings from space analog studies and simulated microgravity models suggest that gravitational unloading alters striatal and mesocorticolimbic DA circuitry, resulting in diminished motor coordination, impaired vestibular compensation, and decreased cognitive flexibility. These alterations not only compromise astronauts’ operational performance but also elevate the risk of mood disturbances and motivational deficits during prolonged missions. The review systematically synthesizes current findings across multiple domains: molecular neurobiology, behavioral neuroscience, and gravitational physiology. It highlights that maintaining DA homeostasis is pivotal in preserving neuroplasticity, particularly within brain regions critical to adaptation, such as the basal ganglia, prefrontal cortex, and cerebellum. The paper also discusses the dual-edged nature of DA plasticity: while adaptive remodeling of synapses and receptor sensitivity can serve as compensatory mechanisms under stress, chronic dopaminergic imbalance may lead to maladaptive outcomes, such as cognitive rigidity and motor dysregulation. Furthermore, we propose a conceptual framework that integrates homeostatic neuroregulation with the demands of space environmental adaptation. By drawing from interdisciplinary research, the review underscores the potential of multiple intervention strategies including pharmacological treatment, nutritional support, neural stimulation techniques, and most importantly, structured physical exercise. Recent rodent studies demonstrate that treadmill exercise upregulates DA transporter expression in the dorsal striatum, enhances tyrosine hydroxylase activity, and increases DA release during cognitive tasks, indicating both protective and restorative effects on dopaminergic networks. Thus, exercise is highlighted as a key approach because of its sustained effects on DA production, receptor function, and brain plasticity, making it a strong candidate for developing effective measures to support astronauts in maintaining cognitive and emotional stability during space missions. In conclusion, the paper not only underscores the centrality of DA homeostasis in space neuroscience but also reflects the authors’ broader academic viewpoint: understanding the neurochemical substrates of behavior under microgravity is fundamental to both space health and terrestrial neuroscience. By bridging basic neurobiology with applied space medicine, this work contributes to the emerging field of gravitational neurobiology and provides a foundation for future research into individualized performance optimization in extreme environments.

The innate immune system serves as the body’s first line of defense against pathogens and plays a central role in inflammation regulation, immune homeostasis, and tumor immunosurveillance. In recent years, with the growing recognition of the concept “exercise is medicine”, increasing attention has been paid to the immunoregulatory effects of physical activity. Accumulating evidence suggests that regular, moderate-intensity exercise significantly enhances innate immunity by strengthening the skin-mucosal barrier, increasing levels of secretory immunoglobulin A (sIgA), and improving the functional capacity of key immune cells such as natural killer (NK) cells, neutrophils, macrophages, and dendritic cells. It also modulates the complement system and various inflammatory mediators. This review comprehensively summarizes the effects of exercise on each component of the innate immune system and highlights the underlying molecular mechanisms, including activation of AMP-activated protein kinase (AMPK), inhibition of nuclear factor-kappa B (NF-κB), enhancement of mitochondrial function via the PGC-1α/TFAM axis, and initiation of autophagy through the ULK1/mTOR pathway. Emerging mechanisms are also discussed, such as exercise-induced epigenetic modifications (e.g., histone acetylation and miRNA regulation), modulation of the gut microbiota, and metabolite-mediated immune programming (e.g., short-chain fatty acids (SCFAs), β‑hydroxybutyrate). The effects of exercise on innate immunity vary considerably among individuals, depending on factors such as age, sex, and comorbidities. For example, adolescents exhibit enhanced NK cell mobilization, whereas older adults benefit from reduced chronic inflammation and immune aging. Sex hormones and metabolic conditions (e.g., obesity, diabetes, chronic obstructive pulmonary disease, cancer) further modulate the immune response to exercise. Based on these insights, we propose a personalized approach to exercise prescription guided by the FITT (frequency, intensity, time, and type) principle, aiming to optimize immune outcomes across diverse populations. Importantly, given the dual role of exercise in immune activation and regulation, caution is warranted: while moderate exercise enhances immune defense, excessive or high-intensity activity may induce transient immunosuppression. In pathological contexts such as infection, autoimmune diseases, or tissue injury, exercise intensity and timing must be carefully adjusted. This review provides practical guidelines for exercise-based immune modulation and underscores the need for dose-response studies and advancements in precision exercise medicine. In conclusion, exercise represents a safe and effective strategy for enhancing innate immune function and mitigating chronic inflammatory diseases.

This paper explains the mechanism of the mutual switching between physiological sleep and wakefulness from the aspects of the sleep circadian system and the sleep homeostasis system. In the circadian rhythm system, with the suprachiasmatic nucleus as the core, the anatomical connections between the suprachiasmatic nucleusand various systems that affect sleep are summarized, starting from the suprachiasmatic nucleus, passing through the four pathways of the melatonin system, namely, subventricular area of the hypothalamus, the ventrolateral nucleus of the preoptic area, orexin neurons, and melatonin, then the related mechanisms of their regulation of sleep and wakefulness are expounded. In the sleep homeostasis system, with adenosine and prostaglandin D2 as targets, the role of hypnogen in sleep arousal mechanisms in regulation is also expounded.

Glucagon-like peptide-1 ( GLP-1 ) is secreted by gut enteroendocrine cells. GLP-1 receptor agonists ( GLP-1 RAs) control glucose-related augmentation of insulin and suppress glu-cagon secretion. GLP-lRAs also inhibit gastric emptying, food intake and limit weight gain. In the past decade, significant progresses have been made in the investigation on the effects of GLP-1 RAs on cardiovascular system. The potential advantages of oral small-molecule GLP-1 RAs could improve the application of this class of drugs. This review highlights the multiple cardiovascular profiles of GLP-1 RAs in the treatment of cardiovascular diseases to provide new insights into cardiovascular benefits of GLP-1 RAs.

Objective To investigate the effect and mechanism of transplantation of neuregulin1(NRG1)gene-modified bone marrow mesenchymal stem cells(BMSCs)on the repair of hemi-transected spinal cord injury(SCI)in rats.Methods Isolated and cultured rat BMSCs,followed by transfection with the NRG1 gene.The levels of NRG1 in BMSCs lysate and culture supernatant was deected by ELISA method,and the proliferation activity of the BMSCs was detected by cell counting method.Forty-three healthy 8-week-old SD rats were randomly divided into control group(n=10),SCI model group(n=10),BMSCs group(n=10),and NRG1-BMSCs group(n=13).After establishing the spinal cord hemisection model,animals received in-situ transplantation of BMSCs or NRG1-BMSCs.On the 1,7,14,21,and 28 days after transplantation,the hind limb motor function was evaluated using BBB score and inclined plate test;on the 7th day after transplantation,the migration and distribution of transplanted cells was monitored using a fluorescence microscope;on the 28th day after transplantation,the pathological changes of rat spinal cord tissues was examined using HE staining and Nissl staining;cell apoptosis using TUNEL staining,and levels of endoplasmic reticulum stress-related proteins[X-box binding protein 1(XBP1),C/EBP homologous protein(CHOP),activating transcription factor 4(ATF4),ATF6,glucose-regulated protein 78(GRP78)]and apoptosis-related proteins[B-cell lymphoma-2(Bcl-2)and Bcl-2-associated protein X(Bax)]in rat spinal cord tissues using Western blotting.Results BMSCs were successfully isolated,cultured,and transfected with the NRG1 gene.ELISA method results showed that the NRG1 contents in the NRG1-BMSCs lysate and culture supernatant were significantly higher than that of BMSCs in a time-dependent manner(P<0.05).The proliferation activity of NRG1-BMSCs was significantly higher than that of BMSCs(P<0.05).On the 21 and 28 days after transplantation,the BBB score and the slope angle of the inclined plate in NRG1-BMSCs group were higher than those in SCI model group or BMSCs group(P<0.05).However,it did not reverse to the level in control group(P<0.05).On the 28th day after transplantation,compared with the SCI model group and BMSCs group,neuronal pyknosis reduced,the Nissl body density increased,the expression levels of XBP1,CHOP,ATF4,ATF6,GRP78,and Bax,and the rate of TUNEL-positive cells significantly reduced in NRG1-BMSCs group(P<0.05),and the expression level of Bcl-2 significantly increased(P<0.05).Conclusion Transplantation of NRG1 gene-modified BMSCs can alleviate SCI and improve the recovery of motor function in rats.The mechanism may be related to promoting the proliferation activity of BMSCs,inhibiting cell apoptosis,and mitigating endoplasmic reticulum stress.

Objective To investigate the diagnostic value of contrast-enhanced ultrasound(CEUS)combined with serum Smad ubiquitin regulatory factor 1(SMURF1)detection for thyroid cancer.Methods A total of 144 suspected thyroid cancer patients admitted to Lishui branch of Zhongda Hospital Affiliated to Southeast University from February 2019 to February 2020 were selected as the study subjects.Based on the histopathological results,they were divided into the thyroid cancer group(76 cases)and the benign group(68 cases).All patients underwent contrast-enhanced ultrasound examination and serum SMURF1 level detection;the diagnostic value of contrast-enhanced ultrasound parameters,serum SMURF1 detection alone,and the combination of the two methods for thyroid cancer were analyzed.Results Contrast-enhanced ultrasound parameters peak intensity(PI),mean perfusion intensity(SImean)and maximum perfusion intensity(SImax)in the thyroid cancer group were lower than those in the benign group,and the level of SMURF1 mRNA was higher than that in the benign group(P<0.05).The sensitivity of contrast-enhanced ultrasound parameter SImax in the diagnosis of thyroid cancer was 82.89%,the specificity was 72.06%,the accuracy was 77.78%,and the Kappa value was 0.552.The sensitivity of serum SMURF1 in the diagnosis of thyroid cancer was 65.79%,the specificity was 94.12%,the accuracy was 79.17%,and the Kappa value was 0.589.The sensitivity,specificity,accuracy and Kappa value of SImax combined with serum SMURF1 in the diagnosis of thyroid cancer were 97.37%,85.29%,91.67%and 0.832,respectively,which were higher than those of SImax and SMURF1 alone(P<0.05),the AUC of the combination of the two methods was 0.927,which was significantly higher than that of the two methods alone(Zcombined vs.SImax=3.999,P<0.001;Zcombined vs.SMURF1=3.270,P=0.001).Conclusion Contrast-enhanced ultrasound combined with serum SMURF1 detection can improve the diagnostic efficiency of thyroid cancer,which may avoid the over-diagnosis on the premise of ensuring the effective diagnosis of thyroid cancer patients.

Objective To investigate whether Angelica Sinensis and Astragalus capsules(AAC)regulates myocardial autophagy in heart failure rats via the phosphatidylinositol 3 kinase(PI3K)/protein kinase(Akt)/mammalian target of sirolimus(mTOR)signaling pathway.Methods A rat model of heart failure was constructed by intraperitoneal 2.5 mg·kg-1 doxorubicin,and another 8 rats served as the control group.The modeling rats were randomly divided into model group,control group and experimental-L,-M,-H groups.Control group was given 30 mg·kg-1 3-methyladenine by intraperitoneal injection;experimental-L,-M,-H groups were given 150,300 and 450 mg·kg-1 AAC by gavage,respectively;blank and model groups were given the same quantity of sterile distilled water.Six groups were administered once daily for 6 weeks.The cardiac function was measured by ultrasound,and the expression levels of PI3K,Akt,mTOR,sequestosome 1(P62)and microtubule-associated light chain protein 3-Ⅱ/Ⅰ(LC3 Ⅱ/Ⅰ)in myocardial tissue were measured by Western blot.Results In the blank,model,control and experimental-H groups,the left ventricular ejection fraction values were(85.00±3.63)％,(56.75±4.83)％,(75.63±3.70)％and(72.75±4.23)％;the relative expression levels of PI3K were 1.00±0,0.28±0.05,0.64±0.08 and 0.74±0.16;phosphorylated Akt/Akt were 1.00±0,0.49±0.06,0.90±0.16 and 0.95±0.10;phosphorylated mTOR/mTOR values were 1.00±0,0.42±0.09,0.73±0.13 and 0.83±0.08;the relative expression levels of P62 proteins were 1.00±0,0.24±0.12,0.57±0.09 and 0.96±0.10;the relative expression levels of LC3 Ⅱ/Ⅰ proteins were 1.00±0,4.31±0.75,2.20±0.76 and 1.59±0.24,respectively.Compared to the model group,statistical significant were identified in the experimental-H and control groups(all P＜0.05).Conclusion AAC can regulate PI3K/Akt/mTOR pathway,inhibit myocardial autophagy and improve cardiac function in rats with heart failure.

Objective To evaluate the predictive value of global longitudinal strain(GLS)measured by cardiac magnetic resonance(CMR)feature-tracking technique for left ventricular remodeling(LVR)after percutaneous coronary intervention(PCI)in patients with acute ST-segment elevation myocardial infarction(STEMI).Methods A total of 403 patients undergoing PCI for acute STEMI were prospectively recruited from multiple centers in China.CMR examinations were performed one week(7±2 days)and 6 months after myocardial infarction to obtain GLS,global radial strain(GRS),global circumferential strain(GCS),ejection fraction(LVEF)and infarct size(IS).The primary endpoint was LVR,defined as an increase of left ventricle end-diastolic volume by≥20%or an increase of left ventricle end-systolic volume by≥15%from the baseline determined by CMR at 6 months.Logistic regression analysis was performed to evaluate the predictive value of CMR parameters for LVR.Results LVR occurred in 101 of the patients at 6 months after myocardial infarction.Compared with those without LVR(n=302),the patients in LVR group exhibited significantly higher GLS and GCS(P<0.001)and lower GRS and LVEF(P<0.001).Logistic regression analysis indicated that both GLS(OR=1.387,95%CI:1.223-1.573;P<0.001)and LVEF(OR=0.951,95%CI:0.914-0.990;P=0.015)were independent predictors of LVR.ROC curve analysis showed that at the optimal cutoff value of-10.6%,GLS had a sensitivity of 74.3%and a specificity of 71.9%for predicting LVR.The AUC of GLS was similar to that of LVEF for predicting LVR(P=0.146),but was significantly greater than those of other parameters such as GCS,GRS and IS(P<0.05);the AUC of LVEF did not differ significantly from those of the other parameters(P>0.05).Conclusion In patients receiving PCI for STEMI,GLS measured by CMR is a significant predictor of LVR occurrence with better performance than GRS,GCS,IS and LVEF.

Objective To elucidate the clinical significance of high expression levels of endonuclease meiosis 1(EME1)in the prognosis of hepatocellular carcinoma(HCC).Methods The Cancer Genome Atlas(TCGA)and Gene Expression Omnibus(GEO)databases were used to screen and analyze differential gene expression between HCC and non-tumor tissues.A retrospective collection of liver tissue samples from 80 HCC patients who underwent hepatectomy in the Fifth Medical Center of Chinese PLA General Hospital between January 2010 and December 2014 was performed.Immunohistochemistry analysis was employed to detect the EME1 expression levels.Survival analysis was then conducted to assess the impact of EME1 expression on 5-year postoperative survival rate of HCC patients.Additionally,gene enrichment analysis was applied to predict the function of EME1 in HCC.Results A total of 371 HCC tissue samples and 50 non-tumor liver tissue samples from TCGA database were analyzed,revealing significantly higher EME1 expression in HCC tissues.Microarray analysis of 107 samples within the GEO database(70 HCC tissues and 37 non-tumor tissues)confirmed that EME1 mRNA expression was markedly elevated in HCC tissues compared with non-tumor tissues(P<0.05).The 5-year overall survival(OS)rate was notably lower in high EME1 expression group than that in low expression group(44.1%vs.53.0%,P<0.05).Semi-quantitative immunohistochemistry analysis demonstrated that patients with high EME1 expression had a significantly lower OS rate than those with low EME1 expression(32.8%vs.45.0%,P<0.05).Multivariate COX regression analysis identified that high EME1 expression(HR=2.234,95%CI 1.073-4.649,P=0.032)and advanced China liver caner(CNLC)staging(HR=4.317,95%CI 1.799-10.359,P=0.001)were independent risk factors for the 5-year OS of post-operation patients with HCC.Conclusion Elevated EME1 expression in HCC tissues correlates with an adverse prognosis of HCC and suggests that EME1 could serve as a potential therapeutic target for HCC.

Patients with severe trauma require an extremely timely treatment and transfusion plays an irreplaceable role in the emergency treatment of such patients. An increasing number of evidence-based medicinal evidences and clinical practices suggest that patients with severe traumatic bleeding benefit from early transfusion of low-titer group O whole blood or hemostatic resuscitation with red blood cells, plasma and platelet of a balanced ratio. However, the current domestic mode of blood supply cannot fully meet the requirements of timely and effective blood transfusion for emergency treatment of patients with severe trauma in clinical practice. In order to solve the key problems in blood supply and blood transfusion strategies for emergency treatment of severe trauma, Branch of Clinical Transfusion Medicine of Chinese Medical Association, Group for Trauma Emergency Care and Multiple Injuries of Trauma Branch of Chinese Medical Association, Young Scholar Group of Disaster Medicine Branch of Chinese Medical Association organized domestic experts of blood transfusion medicine and trauma treatment to jointly formulate Chinese expert consensus on blood support mode and blood transfusion strategies for emergency treatment of severe trauma patients ( version 2024). Based on the evidence-based medical evidence and Delphi method of expert consultation and voting, 10 recommendations were put forward from two aspects of blood support mode and transfusion strategies, aiming to provide a reference for transfusion resuscitation in the emergency treatment of severe trauma and further improve the success rate of treatment of patients with severe trauma.