Objective　By comparing the changes in public health emergency response capacity and epidemic response effect in Yangzhou before and after the outbreak of COVID-19, we can provide a reference for epidemic prevention and control work in the post-COVID-19 era. Methods　The three periods of 2018-2019, 2020-2022, and 2023 were selected to correspond to the pre-COVID-19 period, the middle period, and the post-COVID-19 period, respectively, and the epidemic period of COVID-19 was divided into two sub-dimensions: the early epidemic period of 2020 and the high-intensity epidemic period of 2021-2022. Through questionnaire surveys and descriptive epidemiology, a comprehensive comparison was conducted on all aspects of emergency response capacity and the effectiveness of epidemic management. Results　Since the outbreak of COVID-19, the Yangzhou emergency response system has set up a joint control and prevention network of cities, counties, and districts, as well as special emergency departments in all regions; optimized the personnel allocation and professional disposal teams; improved the number, mode, and coverage of emergency plans, emergency drills, and training; optimized emergency material reserve and dispatch; and standardized institutional construction. The overall incidence of influenza outbreaks decreased from 2.71% to 1.03% and 1.50%; During the different epidemic periods of COVID-19, the average duration of influenza outbreaks decreased continuously, which was 16.70, 11.34, and 9.88 days, respectively. The proportion of influenza outbreaks that met the criteria for a public health emergency controlled within an average incubation period increased from 18.75% in the pre-COVID-19 period to 75.00% in the post-COVID-19 period. Conclusion　The public health emergency response capacity of Yangzhou city has been improved after the COVID-19 epidemic, but there are still shortcomings in the emergency management mechanism, the function of emergency departments, the multi-trigger monitoring warning system, the quantity and quality of professionals, and the multi-department coordination mechanism. In particular, the capacity of county-level emergency response teams needs to be continuously strengthened, which can be achieved by gradually improving emergency management systems and monitoring warning systems, further strengthening talent training, continuously promoting the integration of medical and prevention, and focusing on practical effects.

Objective    To explore the application value of synchronous CT-guided percutaneous biopsy followed by radiofrequency ablation in the diagnosis and treatment of lung tumors. Methods    The clinical data of 21 patients with lung tumors were retrospectively analyzed. There were 8 males and 13 females aged 68 (51, 73) years. A total of 24 lesions underwent CT-guided percutaneous biopsy and concurrent radiofrequency ablation. The effectiveness and safety of this protocol were analyzed. Results    All 21 patients successfully completed the procedures. The diameter of 24 lesions was 17.0 (13.3, 19.0) mm. Biopsy specimens met the requirements of pathological diagnosis, and the effectiveness of specimens was 100.0%. The incidence of small amount of pneumothorax/pleural shrinkage after procedures was 19.0% (4/21) and the incidence of tension pneumothorax was 4.7% (1/21). There was no obvious bleeding or other complications. Conclusion    Synchronous CT-guided percutaneous biopsy followed by radiofrequency ablation combines two interventional techniques, which is safe and effective in the diagnosis and treatment of lung tumors, and it is worthy of popularization and application in clinic.

BACKGROUNDIntense exercise can cause injury and apoptosis, but few studies have reported its effect on the central nervous system (CNS). The initial reason for hippocampus injury is the excitotoxicity of glutamate and calcium overload. Intracellular free Ca(2+) ([Ca(2+)]i) overload may trigger the apoptosis pathway and neuron damage. The aim of this study was to investigate whether intense exercise could cause hippocampus apoptosis and neuron damage and then to determine which pathway was activated by this apoptosis.

METHODSWe used one bout of swimming exhaustion rats as models. Intracellular [Ca(2+)]i was measured to estimate the calcium overload by Fura-2/AM immediately after exhaustion; glial fibrillary acidic protein (GFAP) and synaptophysin (SYP) immunofluorescence were performed for estimating astrocyte activation and synapse plasticity 24 hours after exhaustion. Apoptosis cells were displayed using dUTP nick end labelling (TUNEL) stain; endoplasmic reticulum (ER) stress-induced apoptosis pathway and mitochondrial apoptosis pathway were synchronously detected by Western blotting.

RESULTSAn increasing level of intracellular [Ca(2+)]i (P < 0.01) was found in the hippocampus immediately after exhaustion. GFAP and SYP immunofluorescence showed that the astrocytes are activated, and the synapse plasticity collapsed significantly 24 hours after exhaustion. TUNEL stain showed that the number of apoptosis cells were notably raised (P < 0.01); Western blotting of the apoptosis pathway showed increasing levels of caspase-3 cleavage (P < 0.01), Bax (P < 0.01), caspase-12 cleavage (P < 0.01), C/EBP-homologous protein (CHOP) (P < 0.01), and phospho-Junaminoterminal kinases (p-JNK; P < 0.01) and decreasing level of Bcl-2 (P < 0.01). Our results proved that exhaustion can induce hippocampus injury and apoptosis by [Ca(2+)]i overload, with collapsed synaptic plasticity as the injury pattern and ER stress-induced apoptosis as the activated pathway.

CONCLUSIONIntense exercise can cause excessive apoptosis and synapse plasticity damage in the hippocampus with [Ca(2+)]i overload as the initial reason, and thus provides leads for therapeutic interventions in the brain health of athletes.

Animals ; Apoptosis ; physiology ; Blotting, Western ; Calcium ; metabolism ; Endoplasmic Reticulum Stress ; physiology ; Glial Fibrillary Acidic Protein ; metabolism ; Hippocampus ; metabolism ; In Situ Nick-End Labeling ; Male ; Physical Conditioning, Animal ; Rats ; Rats, Sprague-Dawley ; Synaptophysin ; metabolism