Objectives: Numerous studies have explored the causes and spread of outbreaks, yet there is a lack of research on post-coronavirus disease 2019 condition (PCC) in Korea. The goal of this study was to identify the various types of PCC and associated factors in discharged patients and to provide directions for the ongoing health management of confirmed patients. Methods: A telephone survey was conducted among 680 coronavirus disease 2019 (COVID-19) patients diagnosed between July 7, 2021 and August 26, 2021, in Dangjin, Chungnam, Korea. A descriptive analysis of characteristics, univariate analysis, and regression were performed using data from basic epidemiological surveys conducted at the time of diagnosis and post-discharge questionnaires. Results: Of the 585 patients who responded, 159 (27.2%) developed PCC. Of the 211 patients with no initial symptoms, 27 (12.8%) developed PCC, versus 132 (35.3%) of the 374 patients with initial symptoms. Among the initial symptoms, fever or chills, cough or sputum, loss of smell, and sore throat were associated with PCC. Compared to patients with less than 10 days of hospitalization, those with a hospitalization period of 21 days to 30 days (odds ratio [OR], 2.3; 95% confidence interval [CI], 1.0 to 5.2) and 31 days or more (OR, 5.8; 95% CI, 1.9 to 18.1) had a higher risk of PCC. Conclusions More than a quarter of COVID-19 patients, including those who had no initial symptoms, experienced PCC in Korea. People with the initial symptoms of fever, chills, and respiratory symptoms and those who had prolonged hospital stays had a high risk of PCC.

Lipocalin-2 (LCN2) is a key mediator of various cellular processes. Recent studies have indicated that LCN2 also plays an important role in central nervous system (CNS) injuries and neurological diseases, such as spinal cord injury, stroke, experimental autoimmune encephalomyelitis, and neurodegenerative diseases. Here, we investigated the role of LCN2 in a rodent model of lipopolysaccharide (LPS)-induced neuroinflammation. At 24 hours after intraperitoneal injection of LPS, LCN2 expression was strongly induced in the brain; LCN2 was mainly expressed in endothelial cells, astrocytes, and microglia. Next, we used LCN2-deficient mice to further investigate the role of LCN2 in neuroinflammation. LCN2 deficiency attenuated LPS-induced glial activation in the brain. In a mechanistic study employing glia/neuron co-cultures, LCN2 deficiency reduced glial neurotoxicity. Our results indicate that LCN2 plays a central role in the neuroinflammatory responses following LPS administration, and that LCN2 might contribute to the uncontrolled neurotoxic glial activation under excessive and chronic inflammatory conditions.
Animals ; Astrocytes ; Brain ; Central Nervous System ; Coculture Techniques ; Encephalomyelitis, Autoimmune, Experimental ; Endothelial Cells ; Injections, Intraperitoneal ; Mice* ; Microglia ; Neurodegenerative Diseases ; Neurons ; Rodentia ; Spinal Cord Injuries ; Stroke