OBJECTIVES: To investigate the role of activating transcription factor 3 (ATF3) in atherosclerotic plaques for regulating inflammatory responses during atherosclerosis (AS) progression. METHODS: Human coronary artery specimens from autopsy cases were examined for ATF3 protein expression and localization using immunofluorescence staining and Western blotting. Apolipoprotein E-deficient (ApoE^-/-) mouse models of AS induced by high-fat diet (HFD) feeding for 12 weeks were subjected to tail vein injection of adeno-associated virus serotype 9 (AAV9) to knock down ATF3 expression. After an additional 5 weeks of HFD feeding, the mice were euthanized for analyzing structural changes of the aortic plaques, and the expression levels of ATF3, inflammatory factors (CD45, CD68, IL-1β, and TNF-α), and NF-κB pathway proteins (P-IKKα/β and P-NF-κB p65) were detected. In the cell experiment, THP-1-derived foam cells were transfected with an ATF3-overexpressing plasmid or an ATF3-specific siRNA to validate the relationship between ATF3 and NF‑κB signaling. RESULTS: In human atherosclerotic plaques, ATF3 expression was significantly elevated and partially co-localized with CD68. ATF3 knockout in ApoE^-/- mice significantly increased aortic plaque volume, upregulated the inflammatory factors, enhanced phosphorylation of the NF‑κB pathway proteins, and increased the expressions of VCAM1, MMP9, and MMP2 in the plaques. In THP-1-derived foam cells, ATF3 silencing caused activation of the NF‑κB pathway, while ATF3 overexpression suppressed the activity of the NF-κB pathway. CONCLUSIONS AS promotes ATF3 expression, and ATF3 deficiency exacerbates AS progression by enhancing plaque inflammation via activating the NF-κB pathway, suggesting the potential of ATF3 as a therapeutic target for AS.
Animals ; Activating Transcription Factor 3/metabolism* ; Signal Transduction ; NF-kappa B/metabolism* ; Humans ; Mice ; Plaque, Atherosclerotic/metabolism* ; Inflammation/metabolism* ; Apolipoproteins E ; Atherosclerosis/metabolism* ; Diet, High-Fat

The construction of a medical safety system based on the medical core quality and safty systems is the foundation of the hospital. Multi-campus operation coordinated development is key to the high-quality development of public hospitals and the balanced distribution of high-quality medical resources. Building a medical safety system that comfoms to the specialized layout and operation of branch districts is very important the construction of multi-campus hospitals. In January 2023, Xidan Campus of Peking Union Medical College Hospital established a medical safety system that was compatible with its development, based on the construction of the medical core quality and safty system. The system covered four dimensions: early identification, early assessment, early intervention, and fast response. It included high-risk surgical evaluation and filing, early warning of nursing rooms, periodic medical safety rounds, and rapid response teams and cross hospital transportation of critical care rapid response teams. As of June 2024, the hospital had recorded 570 high-risk surgeries with no unplanned secondary surgeries or unplanned readmissions; Reported nursing warnings 68 times, initiated 93 emergency treatments and cross hospital transfers. All emergency patients received early warning assessments and completed graded and classified transfers and management, effectively ensuring patient safety. This practice could provide references for other multi-campus hospitals to promote the construction and development of medical safety systems.

Alzheimer′s disease (AD) is one of the most common neurodegenerative diseases. As the global population ages, incidence, morbidity and mortality of AD have increased significantly. The core pathological features of AD include β-amyloid (Aβ) deposition and phosphorylated tau aggregation, resulting in neuronal damage, abnormal mental behavior, and cognitive decline. In recent years, research breakthroughs have not only deepened the Aβ cascade hypothesis and the pathological theory of tau protein, but also made important progress in the fields of neuroimmune regulation, "microbiota-gut-brain" axis, genetic factors, especially the ApoEε4 allele. At the same time, AD has been continuously enriched in blood, cerebrospinal fluid and imaging markers, and sensitivity of markers has been improved and detection tends to be non-invasive. Therapeutic strategies for AD include traditional drugs, novel drugs targeting Aβ/tau protein, and non-pharmacological interventions such as cognitive training, non-invasive brain stimulation and exercise. This review systematically expounds the pathological mechanism, biomarkers, and treatment strategies of AD, aiming to provide a scientific basis for the establishment of a biomarker-based precision diagnosis and treatment paradigm.

AIM:To explore the mechanism of doxorubicin/copper(DOX/Cu)complex induced copper death in hepatocellular carcinoma cells.METHODS:Human hepatocellular carcinoma cell line Huh7 was treated with DOX/Cu 0,2.5,4,7.5,10 and 12.5 μmol/L.The cell viability was detected by CCK-8 method.The cell proliferation level was observed by laser microscopy and proliferation kit.The cell invasion ability was determined by cell scratch assay.The flow cytometry was used to de-tect intracellular reactive oxygen species(ROS)and copper ion levels.And the western blot was used to detect intracellular iron-sulfur cluster proteins expression levels.RESULTS:With the increase of DOX/Cu concentration,cell viability,cell prolifera-tion and invasion ability decreased gradually.The copper ion chelating agent(TTM)can significantly restore the effects of DOX/Cu on cell viability.After DOX/Cu treatment,intracellular copper ion and ROS levels related to coproptosis were significantly increased,accompanied by the loss of iron-sulfur cluster proteins.CONCLUSION:DOX/Cu can inhibit hepatocellular carcinoma cells through cuproptosis.

Objective:To investigate the association between dietary diversity and the risk of major adverse cardiovascular events (MACE) after percutaneous coronary intervention (PCI) in patients with coronary heart disease (CHD) .Methods:A total of 553 patients diagnosed with CHD and undergoing PCI in the Department of Cardiology at the Second Affiliated Hospital of Harbin Medical University between May and November 2023 were enrolled using a convenience sampling method. A Semi-Quantitative Food Frequency Questionnaire was used to assess patients' dietary intake after PCI, and the Dietary Diversity Score (DDS) was calculated. Patients were followed up for one year to determine the incidence of MACE.Results:History of hypertension, history of hyperlipidemia, body mass index, use of antiplatelet agents, use of diuretics, triglycerides, smoking index and DDS were identified as factors influencing the occurrence of MACE after PCI ( P<0.05) . Among these, higher dietary diversity had a protective effect against MACE. Conclusions:After PCI, patients with lower DDS experienced MACE more frequently than those with higher scores. Increased dietary diversity can effectively help prevent MACE in patients after PCI.

AIM:To explore the mechanism of doxorubicin/copper(DOX/Cu)complex induced copper death in hepatocellular carcinoma cells.METHODS:Human hepatocellular carcinoma cell line Huh7 was treated with DOX/Cu 0,2.5,4,7.5,10 and 12.5 μmol/L.The cell viability was detected by CCK-8 method.The cell proliferation level was observed by laser microscopy and proliferation kit.The cell invasion ability was determined by cell scratch assay.The flow cytometry was used to de-tect intracellular reactive oxygen species(ROS)and copper ion levels.And the western blot was used to detect intracellular iron-sulfur cluster proteins expression levels.RESULTS:With the increase of DOX/Cu concentration,cell viability,cell prolifera-tion and invasion ability decreased gradually.The copper ion chelating agent(TTM)can significantly restore the effects of DOX/Cu on cell viability.After DOX/Cu treatment,intracellular copper ion and ROS levels related to coproptosis were significantly increased,accompanied by the loss of iron-sulfur cluster proteins.CONCLUSION:DOX/Cu can inhibit hepatocellular carcinoma cells through cuproptosis.

Objective:To investigate the association between dietary diversity and the risk of major adverse cardiovascular events (MACE) after percutaneous coronary intervention (PCI) in patients with coronary heart disease (CHD) .Methods:A total of 553 patients diagnosed with CHD and undergoing PCI in the Department of Cardiology at the Second Affiliated Hospital of Harbin Medical University between May and November 2023 were enrolled using a convenience sampling method. A Semi-Quantitative Food Frequency Questionnaire was used to assess patients' dietary intake after PCI, and the Dietary Diversity Score (DDS) was calculated. Patients were followed up for one year to determine the incidence of MACE.Results:History of hypertension, history of hyperlipidemia, body mass index, use of antiplatelet agents, use of diuretics, triglycerides, smoking index and DDS were identified as factors influencing the occurrence of MACE after PCI ( P<0.05) . Among these, higher dietary diversity had a protective effect against MACE. Conclusions:After PCI, patients with lower DDS experienced MACE more frequently than those with higher scores. Increased dietary diversity can effectively help prevent MACE in patients after PCI.

The construction of a medical safety system based on the medical core quality and safty systems is the foundation of the hospital. Multi-campus operation coordinated development is key to the high-quality development of public hospitals and the balanced distribution of high-quality medical resources. Building a medical safety system that comfoms to the specialized layout and operation of branch districts is very important the construction of multi-campus hospitals. In January 2023, Xidan Campus of Peking Union Medical College Hospital established a medical safety system that was compatible with its development, based on the construction of the medical core quality and safty system. The system covered four dimensions: early identification, early assessment, early intervention, and fast response. It included high-risk surgical evaluation and filing, early warning of nursing rooms, periodic medical safety rounds, and rapid response teams and cross hospital transportation of critical care rapid response teams. As of June 2024, the hospital had recorded 570 high-risk surgeries with no unplanned secondary surgeries or unplanned readmissions; Reported nursing warnings 68 times, initiated 93 emergency treatments and cross hospital transfers. All emergency patients received early warning assessments and completed graded and classified transfers and management, effectively ensuring patient safety. This practice could provide references for other multi-campus hospitals to promote the construction and development of medical safety systems.

Alzheimer′s disease (AD) is one of the most common neurodegenerative diseases. As the global population ages, incidence, morbidity and mortality of AD have increased significantly. The core pathological features of AD include β-amyloid (Aβ) deposition and phosphorylated tau aggregation, resulting in neuronal damage, abnormal mental behavior, and cognitive decline. In recent years, research breakthroughs have not only deepened the Aβ cascade hypothesis and the pathological theory of tau protein, but also made important progress in the fields of neuroimmune regulation, "microbiota-gut-brain" axis, genetic factors, especially the ApoEε4 allele. At the same time, AD has been continuously enriched in blood, cerebrospinal fluid and imaging markers, and sensitivity of markers has been improved and detection tends to be non-invasive. Therapeutic strategies for AD include traditional drugs, novel drugs targeting Aβ/tau protein, and non-pharmacological interventions such as cognitive training, non-invasive brain stimulation and exercise. This review systematically expounds the pathological mechanism, biomarkers, and treatment strategies of AD, aiming to provide a scientific basis for the establishment of a biomarker-based precision diagnosis and treatment paradigm.

ObjectiveTo assess the microstructural involvement of gray matter in recovered COVID-19 patients using Synthetic MRI. MethodsThis study was conducted in 29 recovered COVID-19 patients， including severe group （SG， n=11） and ordinary group （OG， n=18）. Healthy volunteers matched by age， sex， BMI and years of education were selected as a healthy control group （HC=23 cases）. Each subject underwent synthetic MRI to generate quantitative T₁ and T₂ maps， and the T₁ and T₂ maps were segmented into 90 regions of interest （ROIs） using automatic anatomical labeling （AAL） mapping. T₁ and T₂ values for each ROI were obtained by averaging all voxels within the ROIs. The T₁ and T₂ values of the 90 brain regions between the three groups were compared. ResultsRelative to HC， the SG had significantly higher T2 values in bilateral orbital superior frontal gyrus， bilateral parahippocampal gyrus， bilateral putamen， bilateral middle temporal gyrus， bilateral Inferior temporal gyrus， left orbital superior frontal gyrus， left orbital inferior frontal gyrus， left gyrus rectus， left anterior cingulate and paracingulate gyri， right median cingulate and paracingulate gyri， left posterior cingulate gyrus， and left supramarginal gyrus （P＜0.05）； Relative to OG， SG showed significantly increased T₂ values in the left rectus gyrus， left parahippocampal gyrus， bilateral middle temporal gyrus， and bilateral inferior temporal gyrus （P＜0.05）. Relative to HC， the T₁ values of SG were significantly increased in bilateral orbital superior frontal gyrus， left rectus gyrus， left anterior cingulate and paracingulate gyri， right posterior cingulate gyrus， left parahippocampal gyrus， left lingual gyrus， left putamen， left thalamus（P＜0.05）； Relative to OG， the T₁ values of SG were significantly higher in the right posterior cingulate gyrus， right calcarine fissure and surrounding cortex， and left putamen （P＜0.05）. ConclusionsEven after recovering from COVID-19， patients may still have persistent or delayed damage to their brain gray matter structure， which is correlated with the severity of the condition. SyMRI can serve as a sensitive tool to assess the extent of microstructural damage to the central nervous system， aiding in early diagnosis of the disease.