Journal of Yeungnam Medical Science

Original article

A study on the mental health of students at a medical school during COVID-19 outbreak: a retrospective study: Yu Ra Kim, Hye Jin Park, Bon-Hoon Koo, Ji Young Hwang, Young Hwan Lee; J Yeungnam Med Sci. 2022;39(4):314-321. Published online August 16, 2022; DOI: https://doi.org/10.12701/jyms.2022.00437

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Background
In this study, the degree of anxiety, depression, and stress caused by coronavirus disease 2019 (COVID-19) was identified, as well as the need for psychological prevention measures among medical students in the Daegu region that was designated the first special disaster area due to the spread of COVID-19.
Methods
The subjects of this study were 318 medical students in Daegu who voluntarily participated in an online test using the Hospital Anxiety and Depression Scale and Impact of Event Scale-Revised Korean version. As a result of the test, risk students received immediate telephone counseling, and the effect of this telephone counseling was analyzed.
Results
There were no differences in depression, anxiety, or stress according to gender and grade. As a result of immediate telephone counseling for risk students, significant differences were found in depression, anxiety, and stress, and the counseling was found to be effective.
Conclusion
For medical students who are easily exposed to stress, the importance of psychological prevention measures and effectiveness of non-face-to-face counseling should be recognized. In the field of medical education, we must do our best to build a system that can be used immediately at the appropriate time for these programs.

Citations

Citations to this article as recorded by

Study on the Learning Environment of Medical Students in the COVID-19
Yu Ra Kim, Hye Jin Park, Saeyoon Kim
Keimyung Medical Journal.2023; 42(2): 80. CrossRef

Original Article

The Effects of Hantaan Virus on the Expression of Platelet Activating Factor Receptor and on the Activity of Platelet Activating Factor Acetylhydrolase.: Ji Young Hwang, Jong Won Park, Sae Yong Hong, Ho Sun Park; Yeungnam Univ J Med. 2008;25(1):41-49. Published online June 30, 2008; DOI: https://doi.org/10.12701/yujm.2008.25.1.41

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Abstract PDF: BACKGROUND
The central physiological derangement of hemorrhagic fever with renal syndrome (HFRS) caused by hantaan virus (HTNV) is a vascular dysfunction, manifested by hemorrhage, impaired vascular tone and increased vascular permeability. Platelet activating factor (PAF), whose actions are mediated through a specific receptor, is a potent bioactive lipid. PAF has diverse biological functions in the vascular system, such as increasing vascular permeability, adhesion of leukocytes to the endothelium and reduction of cardiac output, which result in hypotension and shock. The goal of the present study was to investigate whether PAF is involved in the pathogenesis of HFRS. For this purpose, we evaluated the effect of HTNV on the expression of PAF receptor (PAF-R) and on the activity of PAF-acetylhydrolase (PAF-AH) instead of PAF because PAF is rapidly degraded by PAF-AH in vivo. MATERIALS AND METHODS: To evaluate the expression of PAF-R, we performed reverse-transcription PCR, western blot and FACS analyses using HTNV-infected human umbilical vein endothelial cells (HUVECs) and non-infected (control) HUVECs. In addition, we measured the activity of plasma PAF-AH in HFRS patients and normal healthy persons. RESULTS: The mRNA and protein expression of PAF-R was increased in HTNV-infected HUVECs compared with control HUVECs at 2 and 3 days post-infection (d.p.i.). FACS analysis showed that HTNV induced the surface expression of PAF-R in HUVECs from 2 d.p.i. The activity of plasma PAF-AH was 2.5-fold lower in HFRS patients than in normal healthy persons. CONCLUSION: Increased PAF-R expression by HTNV might increase the responsiveness to PAF in endothelial cells. Reduced PAF-AH activity in the blood of HFRS patients might delay PAF degradation. These results suggest that changes in PAF-R and PAF-AH by HTNV might influence to PAF activity and might be involved in the vascular dysfunction of HFRS.

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