Patients with liver cirrhosis are more susceptible to various bacterial or viral infections due to immune dysfunction. Recent studies have shown that compared with the general population， individuals with liver cirrhosis show a significant increase in the incidence rate of adverse outcomes after severe acute respiratory syndrome coronavirus 2 infection， including the progression of liver injury and the increase in mortality rate. Vaccination can reduce the incidence rates of breakthrough infections and severe coronavirus disease 2019 （COVID-19） in patients with liver cirrhosis， but such patients have low immune response and thus require booster doses to enhance immunity. This article reviews the clinical features of cirrhotic patients with COVID-19 and related management strategies， in order to provide evidence-based guidance for the clinical diagnosis and treatment of such patients.

Objective: To explore the impact of adverse childhood experiences (ACEs) on health risk behaviors (HRBs) among college students and the mediating role of psychological symptoms, so as to provide a basis for developing intervention strategies. Methods: From March to April 2023, a convenience cluster sample of 1 801 students from 12 universities in Nanning, Liuzhou, Guilin, Wuzhou of Guangxi completed an online survey. A self designed questionnaire, Adverse Childhood Experiences-International Questionnaire (ACE-IQ) and Symptom Checklist-90 (SCL-90) were used for evaluation tools. Binary Logistic regression, structural equation modeling (SEM) and Bootstrap methods were used to analyze the associations and mediating effects. Results: Overall, 71.2% of college students experienced at least one type of ACE, with emotional neglect (40.3%) and emotional abuse ( 25.2 %) having the highest detection rates. The top three HRBs were unhealthy diet (77.8%), physical inactivity (54.1%), and smoking/alcohol use (18.5%). Logistic regression showed that poor family functioning, abuse, and extra familial violence were each associated with an increased risk of smoking/alcohol use ( OR =1.14, 1.11, 1.18) and deliberate self harm ( OR =1.26, 1.19,1.30) (all P <0.05). Experience of abuse increased the risk of high risk sexual behavior and family dysfunction increaded the risk of physical inactivity, respectively ( OR = 1.07 , 1.04, both P <0.05). Mediation analysis revealed that anxiety ( β =0.20) and depression ( β = 0.09 ) partially mediated the pathway from poor family functioning to deliberate self harm; paranoia ( β =0.02) partially mediated the pathway from abuse to high risk sexual behavior; and obsessive-compulsive symptoms ( β =0.26) and depression ( β =0.10) partially mediated the pathway from extra familial violence to deliberate self harm (all P <0.05). Conclusion Psychological symptoms play a mediating role in the association between ACEs and HRBs, and mental health interventions may reduce the risk of HRBs among college students.

Rheumatoid arthritis （RA） is an autoimmune disease characterized by chronic synovial inflammation and joint destruction， with a complex pathogenesis. Macrophage polarization plays a pivotal role in disease progression. Recent studies demonstrate that microRNA （miRNA）， as critical post-transcriptional regulators， can participate in the inflammatory response process by regulating the polarization state of macrophages， thereby aggravating RA joint damage. This review summarizes the mechanism of action of various miRNA in regulating macrophage polarization， and emphasizes their potential therapeutic value in RA.

Objective To explore the safety and feasibility of 5G remote robot-assisted thoracoscopic anatomic lobectomy and segmentectomy. Methods A retrospective analysis was conducted on patients who underwent 5G remote robot-assisted thoracoscopic anatomic lobectomy or segmentectomy between July and September 2024. The surgeries were performed collaboratively by Shanghai Chest Hospital, Affiliated Hospital of Yangzhou University, and The First Affiliated Hospital of Nanchang University. Perioperative outcomes were recorded and analyzed. Results Ten patients were included, comprising 4 anatomic lobectomies and 6 segmentectomies. The median age was 61.0 (56.0, 72.0) years. The median intraoperative bi-directional network latency was 52.5 (39.0, 54.0) ms. There were no instances of network interruption, robot-related adverse events, or conversions to open thoracotomy. The median postoperative chest tube drainage volume was 500.0 (375.0, 600.0) mL, and the median hospital stay was 5.5 (4.0, 6.0) days. No complications of Clavien-Dindo grade Ⅱor higher occurred. All patients were recurrence-free and alive during the 6-month postoperative follow-up period. Conclusion 5G remote robot-assisted thoracoscopic surgery demonstrates high safety and operational stability. This technology shows promising potential for clinical application and is worthy of further development and utilization.

Driven by the global trend of population aging， the prevalence of neurodegenerative diseases， including Alzheimer’s disease （AD）， Parkinson’s disease （PD）， Huntington’s disease （HD）， and amyotrophic lateral sclerosis （ALS）， has been rising consistently. The pathogenic mechanisms of these disorders are complex， and effective disease-modifying therapies remain an unmet clinical need. Ferroptosis， a regulated cell death modality driven by iron-dependent lipid peroxidation， has been widely implicated in the occurrence and evolution of the aforementioned conditions. Under pathological states， both perturbed iron metabolism and reactive oxygen species （ROS） accumulation can precipitate ferroptosis. Specifically， iron overload exacerbates oxidative injury via the Fenton reaction， disrupts the glutathione （GSH）-based antioxidant defense system， and induces extensive peroxidation of polyunsaturated fatty acids （PUFAs）， ultimately culminating in neuronal damage. Furthermore， ferroptosis interacts synergistically with other pathological hallmarks， such as oxidative stress， neuroinflammation， aberrant protein aggregation， and apoptosis， thereby accelerating disease progression. A synthesis of current evidence indicates that disrupted iron homeostasis， enhanced lipid peroxidation， GSH depletion， and impaired glutathione peroxidase 4 （GPX4） activity constitute the common basis for ferroptosis in these neurodegenerative diseases. Concurrently， ferroptosis also displays certain disease‑specific characteristics by engaging distinct pathogenic proteins and regulatory pathways in each disorder. In this review， we delineate the molecular regulatory framework of ferroptosis， summarize its research progress in AD， PD， HD， and ALS， and highlight both shared mechanisms and divergent regulatory pathways across these diseases， with the goal of informing future investigations into disease pathogenesis and the discovery of novel strategies.

Driven by the global trend of population aging， the prevalence of neurodegenerative diseases， including Alzheimer’s disease （AD）， Parkinson’s disease （PD）， Huntington’s disease （HD）， and amyotrophic lateral sclerosis （ALS）， has been rising consistently. The pathogenic mechanisms of these disorders are complex， and effective disease-modifying therapies remain an unmet clinical need. Ferroptosis， a regulated cell death modality driven by iron-dependent lipid peroxidation， has been widely implicated in the occurrence and evolution of the aforementioned conditions. Under pathological states， both perturbed iron metabolism and reactive oxygen species （ROS） accumulation can precipitate ferroptosis. Specifically， iron overload exacerbates oxidative injury via the Fenton reaction， disrupts the glutathione （GSH）-based antioxidant defense system， and induces extensive peroxidation of polyunsaturated fatty acids （PUFAs）， ultimately culminating in neuronal damage. Furthermore， ferroptosis interacts synergistically with other pathological hallmarks， such as oxidative stress， neuroinflammation， aberrant protein aggregation， and apoptosis， thereby accelerating disease progression. A synthesis of current evidence indicates that disrupted iron homeostasis， enhanced lipid peroxidation， GSH depletion， and impaired glutathione peroxidase 4 （GPX4） activity constitute the common basis for ferroptosis in these neurodegenerative diseases. Concurrently， ferroptosis also displays certain disease‑specific characteristics by engaging distinct pathogenic proteins and regulatory pathways in each disorder. In this review， we delineate the molecular regulatory framework of ferroptosis， summarize its research progress in AD， PD， HD， and ALS， and highlight both shared mechanisms and divergent regulatory pathways across these diseases， with the goal of informing future investigations into disease pathogenesis and the discovery of novel strategies.

OBJECTIVE To evaluate the impact of dual antiplatelet therapy （DAPT） at different durations on prognosis and safety after percutaneous coronary intervention （PCI）.METHODS PubMed，The Cochrane Library， Embase， Medline， CNKI， Wanfang data， and VIP database were searched to collect randomized controlled trials of DAPT in patients after PCI， from database inception to March 20， 2026. After literature screening， data extraction， and quality assessment， a meta-analysis was performed using RevMan 5.4 software.RESULTS A total of 19 studies were included， involving 44 072 patients. Meta-analysis results showed that there were no statistically significant differences between the two groups in incidence rate of major adverse cardiovascular events [relative risk（RR）＝0.99， 95% confidence interval（CI）（0.90， 1.08）， P ＝0.80]， all-cause mortality rate[RR＝0.93， 95%CI（0.81，1.05）， P ＝0.24]， cardiovascular-related mortality rate[RR＝0.87， 95%CI（0.73， 1.04）， P ＝0.12]， the incidence rate of myocardial infarction [RR＝1.11，95%CI（0.97，1.27）， P ＝0.14]， the incidence rate of stent thrombosis[RR＝1.50，95%CI（0.99，2.28）， P ＝0.06]， the incidence rate of revascularization[RR＝1.00， 95%CI（0.86， 1.15）， P ＝0.95]， the incidence rate of stroke[RR＝1.03， 95%CI（0.82， 1.28）， P ＝0.81]. The incidence rate of bleeding events in the short-term DAPT group was significantly lower than in the long-term DAPT group[RR＝0.61， 95%CI（0.53， 0.69）， P ＜0.000 01].CONCLUSIONS Short-term and long-term DAPT in patients after PCI were associated with comparable risks of all-cause mortality， cardiovascular-related mortality， myocardial infarction， stent thrombosis， revascularization， stroke， and major adverse cardiovascular events； however， short-term DAPT showed a more prominent advantage in reducing bleeding risk.

During habitation on low-Earth-orbit (LEO) space stations, astronauts are exposed to a combination of orbital microgravity, space radiation, an enclosed and artificially controlled cabin environment, altered sleep-wake rhythms, and sustained operational and psychosocial demands. These factors can modify sensorimotor inputs, body-fluid distribution, arousal state, and task-related neural processing, thereby affecting brain function and behavior. Because evidence from real spaceflight remains limited by small samples, heterogeneous mission durations, and different measurement time points, this review integrates findings from real human spaceflight with relevant ground-based analog studies while treating real orbital studies as the primary source of evidence. We focus on electroencephalography (EEG) and event-related potentials (ERPs), structural and functional neuroimaging, and sensorimotor and cognitive outcomes, with particular attention to the direction, anatomical distribution, temporal course, and possible physiological significance of the reported changes. EEG studies indicate that long-duration spaceflight is associated with increased resting-state beta activity, particularly in sensorimotor and frontotemporal regions, together with state-dependent alterations in beta-band functional connectivity. In contrast, alpha source power and functional connectivity associated with the default mode network are reduced during long-duration missions, and some of these effects may persist into the early postflight period. Task-related electrophysiological findings further suggest that sustained mental workload can weaken frontocentral theta-temporoparietal gamma phase-amplitude coupling, whereas in-flight decision-making is accompanied by reduced P300 amplitude and reorganization of feedback-related potentials. Short-duration missions, however, have shown relative preservation of posterior dominant rhythms and some ERP measures, indicating that mission duration, recording state, and task demands substantially influence the observed electrophysiological phenotype. Neuroimaging provides complementary evidence at structural and network levels. Long-duration spaceflight has been associated with upward brain displacement, ventricular and cerebrospinal fluid expansion, regional gray- and white-matter remodeling, and alterations in white-matter structural connectivity. Functional magnetic resonance imaging (fMRI) studies further indicate reorganization of vestibular-sensorimotor, visual, and default mode networks. Some network changes recover after return to Earth, whereas others may remain detectable for months. Importantly, most MRI measurements are obtained after landing rather than in orbit; therefore, postflight findings may reflect a mixture of in-flight adaptation, the rapid transition back to 1 g, and subsequent readaptation rather than a single spaceflight effect. Behavioral evidence is most consistent for sensorimotor function. Early after return, astronauts frequently show impaired postural control, gait, spatial orientation, and coordination, consistent with reweighting among vestibular, visual, and proprioceptive information. By comparison, simple cognition and some critical operational tasks are often preserved. More subtle or high-load processes-including sustained attention, feedback evaluation, temporal processing, error monitoring, and metacognitive calibration may be more sensitive than global cognitive performance. This dissociation between neural change and preserved behavior suggests that altered brain activity should not automatically be interpreted as functional deterioration. Integrating the available modalities, we propose that LEO space-station habitation is better characterized by system-specific and stage-dependent neural adaptation than by a generalized increase or decline in brain function. The most coherent cross-modal pattern involves sensorimotor reorganization: reduced gravitational reference and weight-bearing feedback under microgravity may drive reweighting of vestibular, visual, and proprioceptive inputs, accompanied by changes in beta activity and vestibular-sensorimotor networks and followed by transient postflight sensorimotor deficits. A second major process involves fluid-related structural remodeling, in which cephalad fluid shifts and altered hydrostatic gradients may contribute to changes in cerebrospinal fluid spaces, ventricular volume, and brain tissue configuration. Resting-state and cognitive electrophysiological changes likely represent additional adjustments in network regulation and resource allocation, but their functional interpretation remains more dependent on sleep, workload, recording conditions, and individual differences. Future studies should move beyond isolated pre-post comparisons and group averages toward standardized longitudinal designs spanning preflight, multiple in-flight time points, and postflight recovery. Synchronized assessment of brain function, behavior, sleep, and key environmental parameters should be used to characterize individual adaptation trajectories and determine which neural changes reflect successful compensation, which predict delayed recovery, and which have genuine value for brain-health risk prediction and individualized countermeasures.