Objective Emergency response to public health emergencies constitutes a vital component of the modernization of national governance systems and capacities, directly impacting national security, social stability, and public health. This study aims to analyze the key issues and research hotspots in the field of emergency response to public health emergencies, providing theoretical foundations and practical guidance for formulating scientific and effective emergency strategies and policies. Ultimately, it seeks to enhance the nation’s capability to respond to public health emergencies and safeguard public health. Methods Using core journals indexed in the China National Knowledge Infrastructure (CNKI) database as the data source, 1094 journal articles in the field of emergency response to public health emergencies in China from 2003 to September 2024 were selected as the research sample. Citespace visualization software was employed to organize and analyze the research process in the field of emergency response to public health emergencies. Results The current research in this field predominantly involves small-scale cooperation, and the research process can be divided into four stages. The research in the emerging stage mainly focuses on the themes of emergency mechanism and emergency management, the development stage mainly centers on the themes of emergency capacity improvement and system exploration, the outbreak stage emphasizes the themes of COVID-19 and epidemic prevention and control, and the sustainable development stage highlights collaborative governance and informatization. Conclusion The COVID-19 pandemic has accelerated the development of research in this field. Currently, the field shows a continuous growth, with an increasing volume of publications. The focus of current research has shifted towards collaborative governance and the study of assessment tools, aiming to enhance the efficiency and effectiveness in responding to public health emergencies. Moreover, the field is advancing toward more systematic and comprehensive research. However, there is still a need to strengthen scientific communication and collaboration.

This paper explored the specific mechanism of ginsenoside Rg_1 in regulating mitochondrial fusion through the neurogenic gene Notch homologous protein 1(Notch1) pathway to alleviate hypoxia/reoxygenation(H/R) injury in HL-1 cells. The relative viability of HL-1 cells after six hours of hypoxia and two hours of reoxygenation was detected by cell counting kit-8(CCK-8). The lactate dehydrogenase(LDH) activity in the cell supernatant was detected by the lactate substrate method. The content of adenosine triphosphate(ATP) was detected by the luciferin method. Fluorescence probes were used to detect intracellular reactive oxygen species(Cyto-ROS) levels and mitochondrial membrane potential(ΔΨ_m). Mito-Tracker and Actin were co-imaged to detect the number of mitochondria in cells. Fluorescence quantitative polymerase chain reaction and Western blot were used to detect the mRNA and protein expression levels of Notch1, mitochondrial fusion protein 2(Mfn2), and mitochondrial fusion protein 1(Mfn1). The results showed that compared with that of the control group, the cell activity of the model group decreased, and the LDH released into the cell culture supernatant increased. The level of Cyto-ROS increased, and the content of ATP decreased. Compared with that of the model group, the cell activity of the ginsenoside Rg_1 group increased, and the LDH released into the cell culture supernatant decreased. The level of Cyto-ROS decreased, and the ATP content increased. Ginsenoside Rg_1 elevated ΔΨ_m and increased mitochondrial quantity in HL-1 cells with H/R injury and had good protection for mitochondria. After H/R injury, the mRNA and protein expression levels of Notch1 and Mfn1 decreased, while the mRNA and protein expression levels of Mfn2 increased. Ginsenoside Rg_1 increased the mRNA and protein levels of Notch1 and Mfn1, and decreased the mRNA and protein levels of Mfn2. Silencing Notch1 inhibited the action of ginsenoside Rg_1, decreased the mRNA and protein levels of Notch1 and Mfn1, and increased the mRNA and protein levels of Mfn2. In summary, ginsenoside Rg_1 regulated mitochondrial fusion through the Notch1 pathway to alleviate H/R injury in HL-1 cells.
Ginsenosides/pharmacology* ; Receptor, Notch1/genetics* ; Signal Transduction/drug effects* ; Mice ; Animals ; Mitochondrial Dynamics/drug effects* ; Mitochondria/metabolism* ; Cell Line ; Reactive Oxygen Species/metabolism* ; Oxygen/metabolism* ; Cell Hypoxia/drug effects* ; Cell Survival/drug effects* ; Membrane Potential, Mitochondrial/drug effects* ; Humans

OBJECTIVE: Gastric cancer (GC) is one of the most common malignancies seen in clinic and requires novel treatment options. Morin is a natural flavonoid extracted from the flower stalk of a highly valuable medicinal plant Prunella vulgaris L., which exhibits an anti-cancer effect in multiple types of tumors. However, the therapeutic effect and underlying mechanism of morin in treating GC remains elusive. The study aims to explore the therapeutic effect and underlying molecular mechanisms of morin in GC. METHODS: For in vitro experiments, the proliferation inhibition of morin was measured by cell counting kit-8 assay and colony formation assay in human GC cell line MKN45, human gastric adenocarcinoma cell line AGS, and human gastric epithelial cell line GES-1; for apoptosis analysis, microscopic photography, Western blotting, ubiquitination analysis, quantitative polymerase chain reaction analysis, flow cytometry, and RNA interference technology were employed. For in vivo studies, immunohistochemistry, biomedical analysis, and Western blotting were used to assess the efficacy and safety of morin in a xenograft mouse model of GC. RESULTS: Morin significantly inhibited the proliferation of GC cells MKN45 and AGS in a dose- and time-dependent manner, but did not inhibit human gastric epithelial cells GES-1. Only the caspase inhibitor Z-VAD-FMK was able to significantly reverse the inhibition of proliferation by morin in both GC cells, suggesting that apoptosis was the main type of cell death during the treatment. Morin induced intrinsic apoptosis in a dose-dependent manner in GC cells, which mainly relied on B cell leukemia/lymphoma 2 (BCL-2) associated agonist of cell death (BAD) but not phorbol-12-myristate-13-acetate-induced protein 1. The upregulation of BAD by morin was due to blocking the ubiquitination degradation of BAD, rather than the transcription regulation and the phosphorylation of BAD. Furthermore, the combination of morin and BCL-2 inhibitor navitoclax (also known as ABT-737) produced a synergistic inhibitory effect in GC cells through amplifying apoptotic signals. In addition, morin treatment significantly suppressed the growth of GC in vivo by upregulating BAD and the subsequent activation of its downstream apoptosis pathway. CONCLUSION Morin suppressed GC by inducing apoptosis, which was mainly due to blocking the ubiquitination-based degradation of the pro-apoptotic protein BAD. The combination of morin and the BCL-2 inhibitor ABT-737 synergistically amplified apoptotic signals in GC cells, which may overcome the drug resistance of the BCL-2 inhibitor. These findings indicated that morin was a potent and promising agent for GC treatment. Please cite this article as: Wang Y, Sun XY, Ma FQ, Ren MM, Zhao RH, Qin MM, Zhu XH, Xu Y, Cao ND, Chen YY, Dong TG, Pan YF, Zhao AG. Morin inhibits ubiquitination degradation of BCL-2 associated agonist of cell death and synergizes with BCL-2 inhibitor in gastric cancer cells. J Integr Med. 2025; 23(3): 320-332.
Humans ; Flavonoids/therapeutic use* ; Stomach Neoplasms/pathology* ; Animals ; Proto-Oncogene Proteins c-bcl-2/metabolism* ; Cell Line, Tumor ; Apoptosis/drug effects* ; Cell Proliferation/drug effects* ; Ubiquitination/drug effects* ; Mice ; Drug Synergism ; Mice, Inbred BALB C ; Mice, Nude ; Xenograft Model Antitumor Assays ; Flavones

OBJECTIVE: Observational studies have found associations between inflammatory bowel disease (IBD) and the risk of dementia, including Alzheimer's dementia (AD) and vascular dementia (VD); however, these findings are inconsistent. It remains unclear whether these associations are causal. METHODS: We conducted a meta-analysis by systematically searching for observational studies on the association between IBD and dementia. Mendelian randomization (MR) analysis based on summary genome-wide association studies (GWASs) was performed. Genetic correlation and Bayesian co-localization analyses were used to provide robust genetic evidence. RESULTS: Ten observational studies involving 80,565,688 participants were included in this meta-analysis. IBD was significantly associated with dementia (risk ratio [ RR] =1.36, 95% CI = 1.04-1.78; I ² = 84.8%) and VD ( RR = 2.60, 95% CI = 1.18-5.70; only one study), but not with AD ( RR = 2.00, 95% CI = 0.96-4.13; I ² = 99.8%). MR analyses did not supported significant causal associations of IBD with dementia (dementia: odds ratio [ OR] = 1.01, 95% CI = 0.98-1.03; AD: OR = 0.98, 95% CI = 0.95-1.01; VD: OR = 1.02, 95% CI = 0.97-1.07). In addition, genetic correlation and co-localization analyses did not reveal any genetic associations between IBD and dementia. CONCLUSION Our study did not provide genetic evidence for a causal association between IBD and dementia risk. The increased risk of dementia observed in observational studies may be attributed to unobserved confounding factors or detection bias.
Humans ; Mendelian Randomization Analysis ; Inflammatory Bowel Diseases/complications* ; Dementia/etiology* ; Observational Studies as Topic ; Genome-Wide Association Study

Objective To analyze and explore the health response capability construction in the long-term recovery phase of nuclear or radiological emergencies. Methods By evaluating China’s participation in an international nuclear emergency exercise organized by Organization for Economic Co-operation and Development’s Nuclear Energy Agency, and considering the relevant guidelines published by international organizations such as the International Atomic Energy Agency, the sections that need to be strengthened in the health response during the long-term recovery phase of nuclear or radiological emergencies were analyzed. The related issues such as health monitoring and medical follow-up were explored. Results The tasks in the long-term recovery phase mainly include monitoring the affected population and information management, medical follow-up, and psychological assistance. In response to potential nuclear or radiological emergencies, 22 nuclear emergency medical rescue bases have been established in China, with a geographical distribution that includes key regions. Relevant institutions have basic capabilities of health response to nuclear or radiological emergencies. However, the exercise shows that strategy and capacity construction in long-term recovery phase are weak points in health response to nuclear or radiological emergencies. China should further strengthen strategies in major public protection actions and information management of affected populations in nuclear or radiological emergencies. Conclusion It is recommended to develop standard operating procedures for major public protection actions, long-term health monitoring and evaluation of affected populations, medical follow-up, and psychological assistance in the future. A unified health registration system for affected populations in nuclear or radiological emergencies should be established to further enhance China’s health response capabilities during the long-term recovery phase of nuclear or radiological emergencies.

Objective To explore the efficacy of Krackow locking loop technique combined with the modified Kessler suture technique in the treatment of acute closed Achilles tendon rupture.Methods From January 2020 to January 2022,162 cases of acute closed Achilles tendon rupture were treated with Krackow locking loop technique combined with the modified Kessler suture technique.The patients were treated with the same postoperative rehabilitation plans.The American Orthopaedic Foot and Ankle Society(AOFAS)hindfoot score and Achilles Tendon Total Rupture Score(ATRS)were collected to evaluate the functions.Results The operation time was 24-40 min(mean,31.9±4.6 min).All incisions healed in one stage without infection or sural nerve injury.Complications occurred in 2 patients,including 1 case of deep venous thrombosis and 1 case of trauma-related re-rupture.The recovery time of ankle flexion and extension motion was4-12 weeks(mean,7.6±1.9 weeks),the recovery time of single-legged heel rise height on the affected side was 10-18 weeks(mean,13.3±1.8 weeks),and the recovery time of fast walking or jogging was 14-26 weeks(mean,19.1±1.8 weeks).The 162 patients was followed up for 14-25 months(mean,19.0 months).The AOFAS hindfoot score increased from(54.4±4.4)points preoperatively to(98.0±4.0)points at the last follow-up(t =-104.402,P =0.000).The ATRS score increased from(52.0±8.3)points preoperatively to(91.2±2.4)points at the last follow-up(t =-62.823,P = 0.000).Conclusions For young and middle-aged patients with acute closed Achilles tendon rupture,Krackow locking loop technique combined with the modified Kessler suture technique can achieve good clinical outcomes.Early functional exercise is required to return to work and life.

Objective To analyze and explore the health response capability construction in the long-term recovery phase of nuclear or radiological emergencies. Methods By evaluating China’s participation in an international nuclear emergency exercise organized by Organization for Economic Co-operation and Development’s Nuclear Energy Agency, and considering the relevant guidelines published by international organizations such as the International Atomic Energy Agency, the sections that need to be strengthened in the health response during the long-term recovery phase of nuclear or radiological emergencies were analyzed. The related issues such as health monitoring and medical follow-up were explored. Results The tasks in the long-term recovery phase mainly include monitoring the affected population and information management, medical follow-up, and psychological assistance. In response to potential nuclear or radiological emergencies, 22 nuclear emergency medical rescue bases have been established in China, with a geographical distribution that includes key regions. Relevant institutions have basic capabilities of health response to nuclear or radiological emergencies. However, the exercise shows that strategy and capacity construction in long-term recovery phase are weak points in health response to nuclear or radiological emergencies. China should further strengthen strategies in major public protection actions and information management of affected populations in nuclear or radiological emergencies. Conclusion It is recommended to develop standard operating procedures for major public protection actions, long-term health monitoring and evaluation of affected populations, medical follow-up, and psychological assistance in the future. A unified health registration system for affected populations in nuclear or radiological emergencies should be established to further enhance China’s health response capabilities during the long-term recovery phase of nuclear or radiological emergencies.

This article explored the specific mechanism by which ginsenoside Rg_1 regulates cellular autophagy to attenuate hypoxia/reoxygenation(H/R) injury in HL-1 cardiomyocytes through the microRNA155(miR-155)/neurogenic gene Notch homologous protein 1(Notch1)/hairy and enhancer of split 1(Hes1) pathway. An HL-1 cell model with H/R injury was constructed, and ginsenoside Rg_1 and/or Notch1 inhibitor DAPT and miR-155 mimics were used to treat cells. Cell counting kit(CCK)-8 was used to detect the relative viability of HL-1 cells with H/R injury. The lactate dehydrogenase(LDH) content in cell culture medium supernatant was detected by using an LDH assay kit, and autophagosome in cells was observed by transmission electron microscopy. The level of autophagy in cells was detected through the mono-dansyl-cadaverine(MDC) detection method. Fluorescence quantitative polymerase chain reaction was used to detect the mRNA levels of miR-155, Notch1, Hes1, and microtubule-associated protein1 light chain 3(LC3), and Western blot was used to detect the protein expression levels of Notch1, Hes1, LC3Ⅰ, and LC3Ⅱ. The results show that after H/R injury, the activity of HL-1 cells decreases, and LDH leakage increases. Besides, the number of intracellular autophagosomes increases, and the mRNA level of LC3 and the LC3Ⅱ/LC3Ⅰ ratio are elevated. In addition, ginsenoside Rg_1 can increase cell activity, decrease LDH leakage and the number of intracellular autophagosomes, and reduce the mRNA level of LC3 and the LC3Ⅱ/LC3Ⅰ ratio. Therefore, it plays a cardioprotective role by inhibiting autophagy, and Notch1 inhibitor or miR-155 overexpression can inhibit the effect of ginsenoside Rg_1, promote autophagy, and aggravate H/R injury in HL-1 cells. Ginsenoside Rg_1 can inhibit the reduction of Notch1 and Hes1 mRNA levels and protein expressions and the increase in miR-155 mRNA levels caused by H/R injury, while Notch1 inhibitors or miR-155 overexpression show the opposite effect. In summary, ginsenoside Rg_1 can regulate autophagy through the miR-155/Notch1/Hes1 pathway to alleviate H/R injury in HL-1 cardiomyocytes.
Ginsenosides/pharmacology* ; MicroRNAs/metabolism* ; Autophagy/drug effects* ; Receptor, Notch1/genetics* ; Transcription Factor HES-1/genetics* ; Mice ; Animals ; Cell Line ; Signal Transduction/drug effects* ; Myocytes, Cardiac/cytology* ; Cell Hypoxia/drug effects*

OBJECTIVE: To observe the protective effect and mechanism of hydroxyl safflower yellow A (HSYA) from myocardial ischemia-reperfusion injury on human umbilical vein endothelial cells (HUVECs). METHODS: HUVECs were treated with oxygen-glucose deprivation reperfusion (OGD/R) to simulate the ischemia reperfusion model, and cell counting kit-8 was used to detect the protective effect of different concentrations (1.25-160 µ mol/L) of HSYA on HUVECs after OGD/R. HSYA 80 µ mol/L was used for follow-up experiments. The contents of inflammatory cytokines interleukin (IL)-18, IL-1 β, monocyte chemotactic protein 1 (MCP-1), tumor necrosis factor α (TNF-α) and IL-6 before and after administration were measured by enzyme-linked immunosorbent assay. The protein expressions of toll-like receptor, NOD-like receptor containing pyrin domain 3 (NLRP3), gasdermin D (GSDMD) and GSDMD-N-terminal domain (GSDMD-N) before and after administration were detected by Western blot. NLRP3 inflammasome inhibitor cytokine release inhibitory drug 3 sodium salt (CRID3 sodium salt, also known as MCC950) and agonist were added, and the changes of NLRP3, cysteine-aspartic acid protease 1 (Caspase-1), GSDMD and GSDMD-N protein expressions were detected by Western blot. RESULTS: HSYA inhibited OGD/R-induced inflammation and significantly decreased the contents of inflammatory cytokines IL-18, IL-1 β, MCP-1, TNF-α and IL-6 (P<0.01 or P<0.05). At the same time, by inhibiting NLRP3/Caspase-1/GSDMD pathway, HSYA can reduce the occurrence of pyroptosis after OGD/R and reduce the expression of NLRP3, Caspase-1, GSDMD and GSDMD-N proteins (P<0.01). CONCLUSIONS The protective effect of HSYA on HUVECs after OGD/R is related to down-regulating the expression of NLRP3 inflammasome and inhibiting pyroptosis.
NLR Family, Pyrin Domain-Containing 3 Protein/metabolism* ; Human Umbilical Vein Endothelial Cells/metabolism* ; Humans ; Chalcone/analogs & derivatives* ; Quinones/pharmacology* ; Pyroptosis/drug effects* ; Caspase 1/metabolism* ; Glucose ; Phosphate-Binding Proteins/metabolism* ; Signal Transduction/drug effects* ; Intracellular Signaling Peptides and Proteins/metabolism* ; Oxygen/metabolism* ; Cytokines/metabolism* ; Gasdermins