The c-Jun N-terminal kinase （JNK） signaling pathway， a key member of the mitogen-activated protein kinase （MAPK） family， plays a central role in the pathogenesis and progression of central nervous system （CNS） diseases by regulating core biological processes such as apoptosis， inflammatory responses， synaptic plasticity， and autophagy. This article sorts out and analyzes relevant literature published domestically and internationally in recent years， summarizing the mechanisms of action of the JNK signaling pathway in common CNS diseases and the research progress in traditional Chinese medicine （TCM） interventions in CNS diseases through the regulation of the JNK signaling pathway. Studies have shown that active components of TCM， such as berberine， paeoniflorin， and astragaloside Ⅳ， as well as compound formulations like Heixiaoyao san， Ditan tang， and Buyang huanwu tang， can exert neuroprotective effects in various CNS disorders， including Alzheimer’s disease， Parkinson’s disease， cerebral ischemia-reperfusion injury， and epilepsy， by inhibiting the aberrant activation of the JNK signaling pathway， thereby alleviating neuroinflammation， oxidative stress， and neuronal apoptosis， while improving synaptic function and cognitive behavioral deficits， regulating autophagy， and maintaining blood-brain barrier integrity.

Alzheimer’s disease （AD） is an age-related neurodegenerative disorder. Marrow-sea insufficiency serves as the fundamental basis for the onset of AD. Early syndrome differentiation-based intervention helps to delay disease progression， and improve patients’ cognitive function. Qifu yin is a representative specialized prescription for AD with marrow-sea insufficiency syndrome. Studies demonstrate that Qifu yin exerts neuroprotective effects through multiple pathways， including inhibiting the abnormal deposition of amyloid β -protein and hyperphosphorylation of tau protein， alleviating neuroinflammation， regulating oxidative stress and mitochondrial dysfunction， modulating the cholinergic system， and improving synaptic plasticity. Qifu yin combined with Western medicine such as donepezil， memantine， and butylphthalide， or combined with external therapies such as acupuncture， can effectively improve cognitive function and activities of daily living in AD patients with favorable safety. Future research should focus on the core pathogenesis and key targets of AD with marrow-sea insufficiency syndrome， provide in-depth elucidation of the scientific connotation of Qifu yin’s “tonifying the kidney to produce marrow”， and further conduct high-quality clinical studies to provide scientific evidence for the prevention and treatment of AD with marrow-sea insufficiency syndrome.

Objective To investigate the relationship between platelet distribution width(PDW)and coronary artery calcification(CAC)in overweight and obese populations.Methods Clinical and chest CT data of 10 838 subjects with overweight or obesity(body mass index[BMI]≥24 kg/m2)were retrospectively analyzed.The subjects were divided into CAC group(n=4 237)and non-CAC group(n=6 601)based on CAC scores obtained from chest CT.The relationship between PDW and CAC in overweight and obese populations was analyzed after controlling confounding variables.A threshold effect analysis was conducted using a two-stage logistic model to find the non-linear inflection point.Subgroup analyses and interaction tests were conducted to validate the stability of the relationship between PDW and CAC.Results Non-linear relationship was observed between PDW and CAC risk in overweight and obese populations.The risk of CAC decreased with the increase of PDW which ≤17.80％(OR=0.82),but increased with the increase of PDW(OR=1.04)which＞17.80％.Subgroup analysis showed that the relationship between PDW and CAC remained stable in subgroups of different genders,BMI(＜28 kg/m2,≥28 kg/m2)and hypertension(all P＞0.05).Compared with aged＜40 years or ≥60 years subgroups,under the same PDW,aged≥40 and＜60 years subgroups had higher risk of CAC(interaction P=0.015).Conclusion Nonlinear relationship existed between PDW and CAC in overweight and obese populations.Both excessively high and low PDW were risk factors of CAC.

Adverse drug reactions (ADRs) significantly impact clinical medication safety. The timely identification and prediction of ADRs rely on the efficient analysis of real-world data, such as electronic health records, social media, and spontaneous reporting databases. In recent years, the rapid advancement of artificial intelligence, particularly large language models, in natural language processing, causal reasoning, and complex data mining has provided new technological means for real-time ADRs monitoring and individualized prediction. This paper summarizes the latest research achievements in AI-driven ADRs monitoring. Focusing on diverse data sources, including structured databases and electronic health records, it elaborates on the advantages andchallenges of AI in ADRs event extraction, relationship identification, causal analysis, and risk prediction. The aim is to provide a theoretical reference for constructing more intelligent and efficient ADRs monitoring systems.

Objective To investigate the relationship between platelet distribution width(PDW)and coronary artery calcification(CAC)in overweight and obese populations.Methods Clinical and chest CT data of 10 838 subjects with overweight or obesity(body mass index[BMI]≥24 kg/m2)were retrospectively analyzed.The subjects were divided into CAC group(n=4 237)and non-CAC group(n=6 601)based on CAC scores obtained from chest CT.The relationship between PDW and CAC in overweight and obese populations was analyzed after controlling confounding variables.A threshold effect analysis was conducted using a two-stage logistic model to find the non-linear inflection point.Subgroup analyses and interaction tests were conducted to validate the stability of the relationship between PDW and CAC.Results Non-linear relationship was observed between PDW and CAC risk in overweight and obese populations.The risk of CAC decreased with the increase of PDW which ≤17.80％(OR=0.82),but increased with the increase of PDW(OR=1.04)which＞17.80％.Subgroup analysis showed that the relationship between PDW and CAC remained stable in subgroups of different genders,BMI(＜28 kg/m2,≥28 kg/m2)and hypertension(all P＞0.05).Compared with aged＜40 years or ≥60 years subgroups,under the same PDW,aged≥40 and＜60 years subgroups had higher risk of CAC(interaction P=0.015).Conclusion Nonlinear relationship existed between PDW and CAC in overweight and obese populations.Both excessively high and low PDW were risk factors of CAC.

Objective To evaluate the molecular mechanisms by which dendritic cells(DCs)detect variations in the extracellular mechanical microenvironment and dynamically adjust their migration behavior.Methods Hydrogel substrates with varied stiffness were constructed to investigate the influence of the mechanical microenvironment on the DC migration behavior.A fibrotic rat liver model was established in combination with immunohistochemistry experiments to investigate the effect of liver fibrosis on the DC migration capability.Furthermore,potential key molecules involved in the mechanical sensing cascade during DC migration were analyzed using single-cell sequencing data from human/mouse fibrotic livers.Moreover,RT-qPCR was used to examine the expression levels of these key molecules in mouse DCs on substrates of different stiffness.Results The migration capability of DCs on stiff substrates was significantly lower than that on soft substrates.The DC infiltration in fibrotic rat livers increased,and 682 differentially expressed genes(DEGs)were observed between liver-infiltrating DCs from cirrhosis patients and normal individuals.Furthermore,focusing on genes relevant to cytoskeleton regulation and migration based on KEGG and GO pathway enrichment analysis,12 potential key molecules mediating stiffness detection during DC migration were identified.Among these,the expression levels of AIF1,GPR65,MYL12B,RAC1,and RHOG were upregulated in patients with liver cirrhosis,whereas those of ACTB,ACTG1,ARF6,CDC42,COTL1,PFN1,and TMSB10 were downregulated.Subsequently,the expression levels of ACTB and CDC42 were downregulated in mouse DCs grown on stiff substrates.This was consistent with the circumstance of liver-infiltrating DC in human cirrhotic patients.Conclusions Liver fibrosis potentially impairs DC migration and thereby,results in increased DC infiltration.ACTB and CDC42 are potential regulators of DC stiffness during migration.This study has provided a theoretical basis and an inspiring novel strategy for optimizing DC-mediated antitumor immune functions.

Objective:To investigate the efficacy and safety of tirofiban versus argatroban in the treatment of acute ischemic stroke. Methods:This study was a retrospective cohort study. Sixty-eight patients with acute ischemic stroke who were continuously admitted to Department of Neurology of The Third People's Hospital of Hubei Province from August 2022 to September 2023 were divided into tirofiban group ( n = 33) and argatroban group ( n = 35) according to the treatment regimen. Both groups were treated according to their respective treatment protocols for 7 days. Clinical outcomes were assessed based on the modified Rankin Scale (mRS) scores. The excellent clinical outcome (mRS score 0-1 points), good clinical outcome (mRS score 0-2 points), symptomatic intracranial hemorrhage, and mortality rates were compared between the two groups at 90 days post-treatment. Results:In the tirofiban group, the proportion of excellent clinical outcomes was 30.3% (10/33), which was significantly lower than the 65.7% (23/35) in the argatroban group (χ2 = 8.53, P = 0.003). However, the difference in the proportion of good clinical outcomes between the two groups was not statistically significant [54.5% (18/33) vs. 74.3% (26/35), χ2 = 2.90, P = 0.089]. There were no statistically significant differences between the two groups regarding symptomatic intracranial hemorrhage and mortality rates (both P > 0.05). Conclusion:For patients with acute ischemic stroke, the use of tirofiban or argatroban is effective and safe. Patients treated with argatroban are more likely to achieve excellent clinical outcomes; however, larger randomized controlled trials are needed for further confirmation.

Objective:To investigate the prevalence and risk factors of stroke in residents of Hanzhong community, Wuhan city, Hubei province, and develop subsequent prevention and treatment measures.Methods:A questionnaire survey, physical examination, and laboratory tests were conducted from May 1 to July 31, 2023, among a population of 801 residents aged 40 years and older in Hanzhong community, Wuhan city, Hubei province, using multi-stage whole cluster random sampling.Results:Among the 801 residents surveyed, 28 were found to have suffered from stroke, yielding a prevalence rate of 3.5%. Additionally, there were 255 individuals identified as high-risk, accounting for 31.8% of the population. The risk factors for stroke, ranked from highest to lowest in prevalence, were as follows: hypertension (24.3%), dyslipidemia (23.6%), lack of exercise (17.6%), smoking (13.1%), diabetes (12.0%), family history of stroke (9.0%), obesity or overweight (8.6%), and atrial fibrillation or valvular heart disease (3.0%). The prevalence of stroke is higher in men than in women, and it continues to increase with advancing age (χ 2 = 33.95, P < 0.001). Homocysteine is likely to contribute to the occurrence of stroke through its association with hypertension (χ2 = 42.63, P < 0.001). Additionally, homocysteine levels have emerged as another significant risk factor for stroke among individuals who are at high risk (χ2 = 5.74, P < 0.05). Conclusion:In Hanzhong community, Wuhan city, Hubei province, smoking, hypertension, overweight, and obesity are the major risk factors for stroke among residents aged 40 years and older. Homocysteinemia is closely related to these high-risk factors for stroke. Therefore, screening and prevention of elevated homocysteine levels will be one of the critical indicators for the subsequent screening and prevention of stroke.

Objective To evaluate the molecular mechanisms by which dendritic cells(DCs)detect variations in the extracellular mechanical microenvironment and dynamically adjust their migration behavior.Methods Hydrogel substrates with varied stiffness were constructed to investigate the influence of the mechanical microenvironment on the DC migration behavior.A fibrotic rat liver model was established in combination with immunohistochemistry experiments to investigate the effect of liver fibrosis on the DC migration capability.Furthermore,potential key molecules involved in the mechanical sensing cascade during DC migration were analyzed using single-cell sequencing data from human/mouse fibrotic livers.Moreover,RT-qPCR was used to examine the expression levels of these key molecules in mouse DCs on substrates of different stiffness.Results The migration capability of DCs on stiff substrates was significantly lower than that on soft substrates.The DC infiltration in fibrotic rat livers increased,and 682 differentially expressed genes(DEGs)were observed between liver-infiltrating DCs from cirrhosis patients and normal individuals.Furthermore,focusing on genes relevant to cytoskeleton regulation and migration based on KEGG and GO pathway enrichment analysis,12 potential key molecules mediating stiffness detection during DC migration were identified.Among these,the expression levels of AIF1,GPR65,MYL12B,RAC1,and RHOG were upregulated in patients with liver cirrhosis,whereas those of ACTB,ACTG1,ARF6,CDC42,COTL1,PFN1,and TMSB10 were downregulated.Subsequently,the expression levels of ACTB and CDC42 were downregulated in mouse DCs grown on stiff substrates.This was consistent with the circumstance of liver-infiltrating DC in human cirrhotic patients.Conclusions Liver fibrosis potentially impairs DC migration and thereby,results in increased DC infiltration.ACTB and CDC42 are potential regulators of DC stiffness during migration.This study has provided a theoretical basis and an inspiring novel strategy for optimizing DC-mediated antitumor immune functions.

Quality management and control of single disease is a means to continuously improve medical quality and safety by building a set of quality control indicators and evaluation systems based on the whole process of disease diagnosis and treatment. In the actual single disease management process, the reporting of each disease involved data from various systems such as electronic medical records, and the data integration was difficult. While the traditional manual reporting method took a lot of time and the data accuracy could not be guaranteed. In the development process of hospital informatization, a hospital has designed a set of intelligent full-closed loop single disease management platform based on the hospital information system, by integrating the existing human and information data resources of the hospital. This platform integrated functions of single disease intranet reporting, in-depth capture of reporting elements, single-disease quality index management, and single-disease real-time intelligent control, in order to promote more refined and intelligent disease management and thus steadily improve medical quality and safety.