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.

Epstein-Barr virus (EBV) and human papillomavirus (HPV) play an important role in the occurrence and development of various malignant neoplasms, such as cervical neoplasms, oral cavity neoplasms, and nasopharyngeal neoplasms. This review primarily discusses the co-infection of EBV and HPV in cervical neoplasms, oral cavity neoplasms, and nasopharyngeal neoplasms. Many in-depth discussions have focused on the role of EBV and HPV co-infection in related neoplasms. Most studies believed that they are complementary to each other, but a few argued that the infection between these two viruses is mutually exclusive. Clarifying the mechanisms and roles of EBV and HPV co-infection in cervical neoplasms, oral cavity neoplasms, and nasopharyngeal neoplasms will provide important breakthroughs for the treatment and prevention of virus-related neoplasms.

Fibrosis, the pathological scarring of vital organs, is a severe and often irreversible condition that leads to progressive organ dysfunction. It is particularly pronounced in organs like the liver, kidneys, lungs, and heart. Despite its clinical significance, the full understanding of its etiology and complex pathogenesis remains incomplete, posing substantial challenges to diagnosing, treating, and preventing the progression of fibrosis. Among the various molecular players involved, platelet-derived growth factor-C (PDGF-C) has emerged as a crucial factor in fibrotic diseases, contributing to the pathological transformation of tissues in several key organs. PDGF-C is a member of the PDGFs family of growth factors and is synthesized and secreted by various cell types, including fibroblasts, smooth muscle cells, and endothelial cells. It acts through both autocrine and paracrine mechanisms, exerting its biological effects by binding to and activating the PDGF receptors (PDGFRs), specifically PDGFRα and PDGFRβ. This binding triggers multiple intracellular signaling pathways, such as JAK/STAT, PI3K/AKT and Ras-MAPK pathways. which are integral to the regulation of cell proliferation, survival, migration, and fibrosis. Notably, PDGF-C has been shown to promote the proliferation and migration of fibroblasts, key effector cells in the fibrotic process, thus accelerating the accumulation of extracellular matrix components and the formation of fibrotic tissue. Numerous studies have documented an upregulation of PDGF-C expression in various fibrotic diseases, suggesting its significant role in the initiation and progression of fibrosis. For instance, in liver fibrosis, PDGF-C stimulates hepatic stellate cell activation, contributing to the excessive deposition of collagen and other extracellular matrix proteins. Similarly, in pulmonary fibrosis, PDGF-C enhances the migration of fibroblasts into the damaged areas of lungs, thereby worsening the pathological process. Such findings highlight the pivotal role of PDGF-C in fibrotic diseases and underscore its potential as a therapeutic target for these conditions. Given its central role in the pathogenesis of fibrosis, PDGF-C has become an attractive target for therapeutic intervention. Several studies have focused on developing inhibitors that block the PDGF-C/PDGFR signaling pathway. These inhibitors aim to reduce fibroblast activation, prevent the excessive accumulation of extracellular matrix components, and halt the progression of fibrosis. Preclinical studies have demonstrated the efficacy of such inhibitors in animal models of liver, kidney, and lung fibrosis, with promising results in reducing fibrotic lesions and improving organ function. Furthermore, several clinical inhibitors, such as Olaratumab and Seralutinib, are ongoing to assess the safety and efficacy of these inhibitors in human patients, offering hope for novel therapeutic options in the treatment of fibrotic diseases. In conclusion, PDGF-C plays a critical role in the development and progression of fibrosis in vital organs. Its ability to regulate fibroblast activity and influence key signaling pathways makes it a promising target for therapeutic strategies aiming at combating fibrosis. Ongoing research into the regulation of PDGF-C expression and the development of PDGF-C/PDGFR inhibitors holds the potential to offer new insights and approaches for the diagnosis, treatment, and prevention of fibrotic diseases. Ultimately, these efforts may lead to the development of more effective and targeted therapies that can mitigate the impact of fibrosis and improve patient outcomes.

Objective:To investigate the feasibility, safety and reasonable operation of nasointestinal canal indwelling guided by miniature system in severe neurosurgery patients, and compare its advantages and disadvantages with traditional blind insertion.Methods:A prospective randomized controlled trial design was used to select 128 critically ill patients in need of enteral nutrition support at the Department of Neurosurgery, the First Affiliated Hospital of Nanjing Medical University from March 2022 to October 2023 by convenient sampling method. They were divided into blind insertion group and visualization group by random number table method, with 64 cases in each group. Nasointestinal canal indwelling was performed in the blind insertion group by traditional blind insertion method, and in the visualization group, nasointestinal canal indwelling was performed by indentations guided by the miniature visualization system. The success rate of initial catheterization, the time of catheterization, complications, changes of vital signs during catheterization and changes of nutritional indexes after catheterization were evaluated in 2 groups.Results:In the blind insertion group, there were 35 males and 29 females, aged (59.44 ± 13.84) years old. In the visualization group, there were 41 males and 23 females, aged (58.28 ± 12.08) years old. The success rate of the first catheter placement in the visual group was 96.8% (62/64), higher than that in the blind group 82.8% (53/64), and the difference was statistically significant ( χ2=6.94, P<0.05). The catheter placement time of the visualization group was (20.08 ± 2.69) min, which was shorter than that of the blind insertion group (38.19 ± 3.79) min, and the difference between the two groups was statistically significant ( t=29.99, P<0.05). There was no significant difference in the incidence of complications, changes of vital signs during catheterization and the changes of nutritional indexes after catheterization between two groups (all P>0.05). Conclusions:Compared with traditional blind nasointestinal canal indwelling, nasointestinal canal indwelling guided by the miniature visualization system can improve the success rate of the first catheterization and shorten the catheterization time. Although there is no difference in the complication rate, changes in vital signs during catheterization and changes in nutritional indexes after catheterization, it is believed that with the continuous development and upgrading of this technology, it will further reflect the advantages of this technology, which is worthy of further clinical trials and application.

Objective:This study aimed to explore the status of radiological Kashin-Beck disease (KBD) among school-aged children in Chamdo City, Tibet, through a 3-year monitoring survey, providing epidemiological evidence for prevention and control strategies.Methods:The target areas for this study were Luolong, Bianba, and Basu counties in Chamdo City, Tibet Autonomous Region, identified as having the most severe historical cases of KBD. Children aged 7-12 years attending school were enrolled as study subjects. Anteroposterior X-ray films of the right-hand were taken, and radiological diagnoses were made based on the "Diagnosis of Kashin-Beck Disease" criteria (WS/T 207-2010). Two experienced researchers independently reviewed the X-rays, and intra- and inter-group consistency were assessed using weighted Kappa values and percentage agreement. Cross-sectional surveys were conducted in 2017 and 2020 to describe the X-ray detection rates of KBD, and logistic regression analysis was employed to construct a predictive model of risk factors for radiological KBD cases.Results:In 2017, a total of 5,711 children aged 7-12 years in Chamdo City, Tibet, participated in the baseline cross-sectional survey (average age 9.2 years, 48.0% female), with 28 cases of radiological KBD. The age- and gender-standardized prevalence rate was 0.527%. In 2020, 6,771 participants (average age 9.3 years, 49.5% female) underwent a second cross-sectional survey, with 9 cases of radiological KBD and a standardized prevalence rate of 0.134%. Logistic regression analysis indicated that older age [ OR=2.439, 95% CI(1.299, 4.580), P=0.006] and female gender [ OR=8.157, 95% CI(1.016, 65.528), P=0.048] were independent risk factors for radiological KBD cases. Conversely, higher residential altitude, under the premise of Tibet's high altitude, was a protective factor [ OR=0.995, 95% CI(0.990, 0.999), P=0.032). Conclusion:The radiographically positive detection rate of KBD among school-aged children in Chamdo City, Tibet Autonomous Region, is at an extremely low level and showing a declining trend, reaching the historical standard in 2020. Considering the absence of positive signs in affected children, it suggests that local KBD has been effectively eliminated.

ObjectiveTo investigate the effect of Shugan Quyu Jiedu prescription （SGQYJDF） on inducing ferroptosis in hepatocellular carcinoma cells based on the tumor protein 53 （p53）/solute carrier family 7 member 11 （SLC7A11）/glutathione peroxidase 4 （GPX4） pathway. MethodMHCC97H cells were divided into the blank serum group （10% blank serum medium）， SGQYJDF-containing serum low concentration group （5% SGQYJDF-containing serum and 5% blank serum medium）， SGQYJDF-containing serum medium concentration group （7.5% SGQYJDF-containing serum and 2.5% blank serum medium）， SGQYJDF-containing serum high concentration group （10% SGQYJDF-containing serum medium） and sorafenib group （sorafenib concentration of 10 μmol·L^-1 in 10% blank serum medium）. After 24 hours of intervention， the cell survival rate was detected by cell counting kit-8 （CCK-8） assay. The cell proliferation ability was detected by 5-ethynyl-2′-deoxyuridine （EdU） staining. The intracellular ferrous ion （Fe²⁺） level was detected by ferrous ion fluorescent probe （FerroOrange） staining. The intracellular malondialdehyde （MDA） and glutathione （GSH） levels were detected by colorimetric assays. The ultrastructure of mitochondria was observed by transmission electron microscopy. The expression levels of ferroptosis-related proteins p53， SLC7A11 and GPX4 were detected by Western blot. ResultIn terms of cell viability， compared with the blank serum group， the SGQYJDF group showed a dose-dependent decrease in the survival rate of MHCC97H cells. Effect of the medium and high concentrations of SGQYJDF on the survival rate of MHCC97H cells were significantly decreased （P<0.01）. Additionally， the results of the EdU assay showed that both the medium and high concentrations of SGQYJDF were able to inhibit the proliferation ability of MHCC97H cells （P<0.05， P<0.01）. Regarding the biochemical indicators of ferroptosis， compared to the blank serum group， the medium and high concentrations of SGQYJDF were able to dose-dependently increase the intracellular Fe²⁺ level （P<0.01）. The low， medium， and high concentrations of SGQYJDF were able to dose-dependently decrease the level of GSH in MHCC97H cells （P<0.01） and increase the level of MDA in the cells （P<0.05， P<0.01）. In terms of pathway-related protein expression， compared to the blank serum group， the medium and high concentrations of SGQYJDF could significantly increase the expression of p53 （P<0.01）. The low， medium， and high concentrations of SGQYJDF could significantly decrease the expression of GPX4 （P<0.01）. The high concentration of SGQYJDF could decrease the expression of SLC7A11 （P<0.01）. In terms of the cell morphology of ferroptosis， compared with the blank serum group， transmission electron microscopy revealed that the low concentration of SGQYJDF caused mitochondrial deformation， while the medium and high concentrations of SGQYJDF resulted in reduced mitochondrial volume， increased double-layer membrane density， and decreased mitochondrial cristae. These features were similar to those of sorafenib-induced ferroptosis. Furthermore， compared with the sorafenib group， the high concentration of SGQYJDF showed no statistically significant differences in cell survival rate， proliferation ability， Fe²⁺ level， MDA level， and GSH level. ConclusionThe results suggest that SGQYJDF may induce ferroptosis and inhibit proliferation in hepatocellular carcinoma MHCC97H cells by upregulating the expression of p53， suppressing the expressions of GPX4 and SLC7A11， downregulating the level of GSH， and leading to the accumulation of intracellular Fe²⁺ and MDA.

Objective To explore the feasibility and short-term clinical efficacy of single segment thora-columbar tuberculosis treated with one-stage posterior approach lamina-sparing decompression.Methods A total of 11 patients with single segment thoracolumbar tuberculosis who underwent one-stage posterior ap-proach preservation of vertebral plate lesion removal,bone graft fusion,and internal fixation treatment in this hospital from September 2021 to June 2022 were selected.C-reactive protein(CRP)and erythrocyte sedimen-tation rate(ESR)were monitored to evaluate tuberculosis bacteremia and activity control,visual analogue scale(VAS)score and Oswestry disability index(ODI)were followed up to evaluate the improvement of clin-ical function,and the American Spinal Injury Association(ASIA)injury scale was used to evaluate neurologi-cal function,and the correction of kyphosis was followed up.Results All 11 patients were fully followed up.The average surgical duration is(270.91±45.98)minutes,and the average surgical bleeding is(522.72± 194.11)mL.During the follow-up period,none of the 11 patients experienced tuberculosis recurrence,and all 11 patients achieved bone graft fusion.The fusion time was 6-9 months after surgery with an average of(7.36±1.12)months.Two patients with preoperative nerve damage recovered after surgery.During the fol-low-up period,11 patients did not experience any complications related to surgery.The average CRP,ESR,ODI score,and VAS score of postoperative patients decreased compared to preoperative levels,and further de-creased at 12 months after surgery;The patient's kyphosis caused by thoracolumbar tuberculosis was correc-ted,and no obvious angle loss was found at the last follow-up(P＞0.05).Conclusion One-stage posterior ap-proach lamina-sparing decompression is a safe and effective method for treating single segment thoracolumbar tuberculosis.

Objective: To investigate epidemiological characteristics of notifiable infectious diseases in Zhejiang Province in 2023, so as to provide the evidence for strengthening prevention and control of infectious diseases. Methods: Data pertaining to notifiable infectious diseases reported in Zhejiang Province in 2023 were retrieved from the Infectious Disease Surveillance System of Chinese Disease Prevention and Control Information System. The incidence and mortality were analyzed according to the classification of notifiable infectious diseases and transmission routes, and epidemiological characteristics of infectious diseases were descriptively analyzed. Results: Thirty types of notifiable infectious diseases with 2 955 699 cases and 427 deaths were reported in Zhejiang Province in 2023, with a reported incidence rate of 4 493.93/105 and a reported mortality rate of 0.649 2/105. A total of 679 notifiable infectious disease emergencies were reported, with 26 514 cases and 1 case death (rabies). The emergencies mainly occurred in schools and preschool institutions, with 621 cases accounting for 91.46%. There were 1 case of cholera reported in class A notifiable infectious diseases and no death, 22 types of class B notifiable infectious diseases, with a reported incidence rate of 552.46/105 and a reported mortality rate of 0.644 7/105, and 8 types of class C notifiable infectious diseases, with a reported incidence rate of 3 941.48/105 and a reported mortality rate of 0.004 6/105. The incidence rates of respiratory, intestinal, blood-borne and sexually transmitted, natural and insect-borne infectious diseases were 4 028.67/105, 381.59/105, 81.15/105 and 1.35/105, respectively, according to transmission routes. Influenza (3 561.78/105) and COVID-19 (423.77/105) reported the highest incidence, and AIDS (0.477 4/105) and tuberculosis (0.130 8/105) reported the highest mortality. Conclusion The incidence rates of respiratory and intestinal infectious diseases were high in Zhejiang Province in 2023, and schools and preschool institutions were the main places of diseases occurred.

Objective:Molecular mechanisms underlying compound heterozygous mutations in a patient with inherited antithrombin (AT) deficiency.Methods:The proband was admitted to the First Affiliated Hospital of Wenzhou Medical University in November 2018 with a one-day history of sudden syncope and limb twitching. Peripheral venous blood was collected from the proband and members of his lineages, totaling nine persons across three generations, and a family lineage survey was conducted. AT activity (AT:A) was measured using a chromogenic substrate assay, while AT antigen (AT:Ag) was detected through an immunoturbidimetric assay. Mutation sites were identified by means of Sanger sequencing of the SERPINC1 gene, and silico tools were applied to predict the mutational conservation and hydrophobicity changes. Recombinant plasmid expression vectors were constructed and transfected into HEK293T cells for in vitro overexpression studies. The recombinant AT protein was characterized using Western Blotting, ELISA, and cellular immunofluorescence assays.Results:The proband was a 21-year-old man with type Ⅰ AT deficiency. His AT:A was 33%, along with a corresponding reduction in AT:Ag. The genetic analysis revealed there was a heterozygous insertion mutation at c.318_319insT (p.Asn107*) and a heterozygous missense mutation at c.922G>T (p.Gly308Cys) in exons 2 and 5, respectively. These mutation sites were entirely conserved among the homologous species. Additionally, hydrophobicity studies showed that the p.Gly308Cys mutation will decrease the hydrophilicity of amino acid residues 307-313. The in vitro expression studies indicated a reduction of approximately 46.98%±2.94% and 41.35%±1.48% in the amount of recombinant protein AT-G308C in transfected cell lysates and culture supernatants, respectively. Treatment with the proteasome inhibitor (MG132) restored the cytoplasmic levels of AT-G308C protein to a level similar to that of wild-type protein. However, neither cell lysate nor culture supernatant demonstrated the presence of the recombinant protein AT-N107*. Conclusions:The heterozygous insertion mutation of p.Asn107* and the heterozygous missense mutation of p.Gly308Cys have been associated with reduced AT levels in proband. The p.Asn107* heterozygous insertion mutation may initiate the degradation of mRNA via nonsense mutation-mediated mechanisms, which would remove the defective transcripts, as well as the p.The Gly308Cys heterozygous missense mutation may cause the AT protein to undergo proteasome-dependent degradation by modifying the hydrophobicity of nearby residues in the cytoplasm.

Objective To analyze the prognosis and influencing factors in patients with radioiodine-refractory differentiated thyroid cancer (RAIR-DTC). Methods A retrospective analysis was conducted on 52 patients with RAIR-DTC who underwent ineffective ¹³¹I therapy at the Department of Nuclear Medicine, Cancer Hospital, Chinese Academy of Medical Sciences from October 2016 to January 2020. Patients were categorized into progression and stable groups based on disease progression within five years post-treatment. Differences between groups were analyzed using chi-square test and logistic regression. Independent prognostic risk factors were identified using a Cox proportional hazards model. The Kaplan-Meier method with log-rank test was used to evaluate the impact of treatment on the prognosis of the progression group. Results The 3-year and 5-year survival rates of the 52 patients with RAIR-DTC were 88.5% and 73.1%, respectively. In the progression group, the rates were 81.8% and 57.6%. In the stable group, the rates were 100% and 100%. There were significant differences between the two groups in terms of age, presence of extrathyroidal extension, and the initial ¹³¹I treatment dose (P < 0.05). Univariate analysis indicated that the age, pre-ablation stimulated thyroglobulin level before the first ¹³¹I treatment, the neutrophil-to-lymphocyte ratio before the first treatment, and the sites of recurrence and metastasis were significantly associated with overall survival (P < 0.05). Multivariate analysis showed that age > 55 years (HR=12.40, 95% CI= 2.09-73.57, P=0.001) and distant metastasis (HR=24.47, 95% CI=4.17-143.75, P < 0.001) were independent risk factors for poor prognosis. Kaplan-Meier curve analysis showed that local surgery and/or targeted therapy significantly prolonged progression-free survival in the progression group (P < 0.001). Conclusion The prognosis for RAIR-DTC is poor, with advanced age and distant metastasis significantly associated with unfavorable outcomes. In elderly patients and those with extrathyroidal invasion, the treatment dose during initial ¹³¹I therapy may be appropriately increased to delay disease progression. For patients with disease progression, prompt local surgical intervention and/or targeted therapy is recommended.