Background: The exposome encompasses all factors people encounter through life, with the skin constantly exposed. While particulate matter (PM) and sleep deprivation are known to contribute to barrier dysfunction, their combined effects remain unclear. Objective: To evaluate the independent and combined effects of PM exposure and short-term sleep deprivation on skin barrier function. Methods: Forty healthy Korean women (aged 24–58 years) were enrolled in this study. Forearms were divided into 4 sites: control, PM exposure, sleep deprivation, and PM plus sleep deprivation. Parameters such as trans-epidermal water loss (TEWL), hydration, elasticity, roughness, and redness were measured at baseline and post-exposure. RNA sequencing and reverse transcription-polymerase chain reaction were conducted on tape-stripped skin samples. Results: PM exposure significantly increased TEWL (+25.59%, p<0.01), roughness (+21.9%, p<0.01), and redness (+13.7%, p<0.0001) while reducing elasticity (−3.98%, p<0.01). Sleep deprivation modestly reduced elasticity (−1.39%, p<0.05) without affecting other parameters.Combined PM and sleep deprivation did not further exacerbate barrier dysfunction compared to PM alone. RNA sequencing revealed reduced FLG and LORICRIN expression and upregulated endoplasmic reticulum (ER) stress markers (HSP90B1, CANX) in both PM and sleep deprivation conditions. Conclusion PM exposure impaired skin barrier function, while short-term sleep deprivation alone did not significantly affect the barrier, either independently or in combination with PM.However, it was observed that the sleep deprivation-only, while not directly causing barrier damage, induced changes in ER stress-related gene expression in tape-stripped skin samples, like the PM exposure-only. This suggests that such signaling pathways could potentially exacerbate skin barrier deterioration.

Objectives: This study aimed to evaluate the correlation between mast cell (MC) density in rosacea-affected skin and the expression of key inflammatory mediators, including IL-6, TNF-α, and cathelicidin LL-37. By comparing lesions rich in MCs with those having fewer MCs, we sought to elucidate the role of MCs in the inflammatory mechanisms underlying rosacea pathogenesis.

Methods: Specimens were collected from 20 patients diagnosed with rosacea who attended the outpatient clinic between 2008 and 2013. Each specimen underwent staining using hematoxylin/eosin, Giemsa, IL-6, LL-37, and TNF-α for both histopathological and immunohistochemical analyses. The number of stained cells was counted across 10 randomly selected dermal layers at a magnification of ×400 using light microscopy. The results were categorized based on the number of MCs counted: more than 10 MCs were classified as MC-rich, and 10 or fewer MCs as MC-poor.

Results: Among the 20 patients (10 MC-rich and 10 MC-poor), the MC-rich group demonstrated significantly higher MC counts than the MC-poor group (P<0.001). However, there were no significant differences in the expression levels of IL-6, LL-37, or TNF-α between the two groups. Additionally, MC density did not show any significant associations with patient demographics, clinical characteristics, or systemic comorbidities.

Conclusion: Increased MC density was not associated with differences in IL-6, TNF-α, or LL-37 expression in rosacea lesions. These findings suggest that MC infiltration may not directly influence the inflammatory mediator profile in rosacea. Further research is required to identify distinctive pathological features or markers that can elucidate the mechanisms of rosacea.

Objectives: This study aimed to evaluate the correlation between mast cell (MC) density in rosacea-affected skin and the expression of key inflammatory mediators, including IL-6, TNF-α, and cathelicidin LL-37. By comparing lesions rich in MCs with those having fewer MCs, we sought to elucidate the role of MCs in the inflammatory mechanisms underlying rosacea pathogenesis.

Methods: Specimens were collected from 20 patients diagnosed with rosacea who attended the outpatient clinic between 2008 and 2013. Each specimen underwent staining using hematoxylin/eosin, Giemsa, IL-6, LL-37, and TNF-α for both histopathological and immunohistochemical analyses. The number of stained cells was counted across 10 randomly selected dermal layers at a magnification of ×400 using light microscopy. The results were categorized based on the number of MCs counted: more than 10 MCs were classified as MC-rich, and 10 or fewer MCs as MC-poor.

Results: Among the 20 patients (10 MC-rich and 10 MC-poor), the MC-rich group demonstrated significantly higher MC counts than the MC-poor group (P<0.001). However, there were no significant differences in the expression levels of IL-6, LL-37, or TNF-α between the two groups. Additionally, MC density did not show any significant associations with patient demographics, clinical characteristics, or systemic comorbidities.

Conclusion: Increased MC density was not associated with differences in IL-6, TNF-α, or LL-37 expression in rosacea lesions. These findings suggest that MC infiltration may not directly influence the inflammatory mediator profile in rosacea. Further research is required to identify distinctive pathological features or markers that can elucidate the mechanisms of rosacea.

Objectives: This study aimed to evaluate the correlation between mast cell (MC) density in rosacea-affected skin and the expression of key inflammatory mediators, including IL-6, TNF-α, and cathelicidin LL-37. By comparing lesions rich in MCs with those having fewer MCs, we sought to elucidate the role of MCs in the inflammatory mechanisms underlying rosacea pathogenesis.

Methods: Specimens were collected from 20 patients diagnosed with rosacea who attended the outpatient clinic between 2008 and 2013. Each specimen underwent staining using hematoxylin/eosin, Giemsa, IL-6, LL-37, and TNF-α for both histopathological and immunohistochemical analyses. The number of stained cells was counted across 10 randomly selected dermal layers at a magnification of ×400 using light microscopy. The results were categorized based on the number of MCs counted: more than 10 MCs were classified as MC-rich, and 10 or fewer MCs as MC-poor.

Results: Among the 20 patients (10 MC-rich and 10 MC-poor), the MC-rich group demonstrated significantly higher MC counts than the MC-poor group (P<0.001). However, there were no significant differences in the expression levels of IL-6, LL-37, or TNF-α between the two groups. Additionally, MC density did not show any significant associations with patient demographics, clinical characteristics, or systemic comorbidities.

Conclusion: Increased MC density was not associated with differences in IL-6, TNF-α, or LL-37 expression in rosacea lesions. These findings suggest that MC infiltration may not directly influence the inflammatory mediator profile in rosacea. Further research is required to identify distinctive pathological features or markers that can elucidate the mechanisms of rosacea.

Objectives: This study aimed to evaluate the correlation between mast cell (MC) density in rosacea-affected skin and the expression of key inflammatory mediators, including IL-6, TNF-α, and cathelicidin LL-37. By comparing lesions rich in MCs with those having fewer MCs, we sought to elucidate the role of MCs in the inflammatory mechanisms underlying rosacea pathogenesis.

Methods: Specimens were collected from 20 patients diagnosed with rosacea who attended the outpatient clinic between 2008 and 2013. Each specimen underwent staining using hematoxylin/eosin, Giemsa, IL-6, LL-37, and TNF-α for both histopathological and immunohistochemical analyses. The number of stained cells was counted across 10 randomly selected dermal layers at a magnification of ×400 using light microscopy. The results were categorized based on the number of MCs counted: more than 10 MCs were classified as MC-rich, and 10 or fewer MCs as MC-poor.

Results: Among the 20 patients (10 MC-rich and 10 MC-poor), the MC-rich group demonstrated significantly higher MC counts than the MC-poor group (P<0.001). However, there were no significant differences in the expression levels of IL-6, LL-37, or TNF-α between the two groups. Additionally, MC density did not show any significant associations with patient demographics, clinical characteristics, or systemic comorbidities.

Conclusion: Increased MC density was not associated with differences in IL-6, TNF-α, or LL-37 expression in rosacea lesions. These findings suggest that MC infiltration may not directly influence the inflammatory mediator profile in rosacea. Further research is required to identify distinctive pathological features or markers that can elucidate the mechanisms of rosacea.

Objectives: This study aimed to evaluate the correlation between mast cell (MC) density in rosacea-affected skin and the expression of key inflammatory mediators, including IL-6, TNF-α, and cathelicidin LL-37. By comparing lesions rich in MCs with those having fewer MCs, we sought to elucidate the role of MCs in the inflammatory mechanisms underlying rosacea pathogenesis.

Methods: Specimens were collected from 20 patients diagnosed with rosacea who attended the outpatient clinic between 2008 and 2013. Each specimen underwent staining using hematoxylin/eosin, Giemsa, IL-6, LL-37, and TNF-α for both histopathological and immunohistochemical analyses. The number of stained cells was counted across 10 randomly selected dermal layers at a magnification of ×400 using light microscopy. The results were categorized based on the number of MCs counted: more than 10 MCs were classified as MC-rich, and 10 or fewer MCs as MC-poor.

Results: Among the 20 patients (10 MC-rich and 10 MC-poor), the MC-rich group demonstrated significantly higher MC counts than the MC-poor group (P<0.001). However, there were no significant differences in the expression levels of IL-6, LL-37, or TNF-α between the two groups. Additionally, MC density did not show any significant associations with patient demographics, clinical characteristics, or systemic comorbidities.

Conclusion: Increased MC density was not associated with differences in IL-6, TNF-α, or LL-37 expression in rosacea lesions. These findings suggest that MC infiltration may not directly influence the inflammatory mediator profile in rosacea. Further research is required to identify distinctive pathological features or markers that can elucidate the mechanisms of rosacea.

Background: Islet transplantation holds promise for treating selected type 1 diabetes mellitus patients, yet the scarcity of human donor organs impedes widespread adoption. Porcine islets, deemed a viable alternative, recently demonstrated successful longterm survival without zoonotic risks in a clinically relevant pig-to-non-human primate islet transplantation model. This success prompted the development of a clinical trial protocol for porcine islet xenotransplantation in humans. Methods: A single-center, open-label clinical trial initiated by the sponsor will assess the safety and efficacy of porcine islet transplantation for diabetes patients at Gachon Hospital. The protocol received approval from the Gachon Hospital Institutional Review Board (IRB) and the Korean Ministry of Food and Drug Safety (MFDS) under the Investigational New Drug (IND) process. Two diabetic patients, experiencing inadequate glycemic control despite intensive insulin treatment and frequent hypoglycemic unawareness, will be enrolled. Participants and their family members will engage in deliberation before xenotransplantation during the screening period. Each patient will receive islets isolated from designated pathogen-free pigs. Immunosuppressants and systemic infection prophylaxis will follow the program schedule. The primary endpoint is to confirm the safety of porcine islets in patients, and the secondary endpoint is to assess whether porcine islets can reduce insulin dose and the frequency of hypoglycemic unawareness. Conclusion A clinical trial protocol adhering to global consensus guidelines for porcine islet xenotransplantation is presented, facilitating streamlined implementation of comparable human trials worldwide.

Background: Islet transplantation holds promise for treating selected type 1 diabetes mellitus patients, yet the scarcity of human donor organs impedes widespread adoption. Porcine islets, deemed a viable alternative, recently demonstrated successful longterm survival without zoonotic risks in a clinically relevant pig-to-non-human primate islet transplantation model. This success prompted the development of a clinical trial protocol for porcine islet xenotransplantation in humans. Methods: A single-center, open-label clinical trial initiated by the sponsor will assess the safety and efficacy of porcine islet transplantation for diabetes patients at Gachon Hospital. The protocol received approval from the Gachon Hospital Institutional Review Board (IRB) and the Korean Ministry of Food and Drug Safety (MFDS) under the Investigational New Drug (IND) process. Two diabetic patients, experiencing inadequate glycemic control despite intensive insulin treatment and frequent hypoglycemic unawareness, will be enrolled. Participants and their family members will engage in deliberation before xenotransplantation during the screening period. Each patient will receive islets isolated from designated pathogen-free pigs. Immunosuppressants and systemic infection prophylaxis will follow the program schedule. The primary endpoint is to confirm the safety of porcine islets in patients, and the secondary endpoint is to assess whether porcine islets can reduce insulin dose and the frequency of hypoglycemic unawareness. Conclusion A clinical trial protocol adhering to global consensus guidelines for porcine islet xenotransplantation is presented, facilitating streamlined implementation of comparable human trials worldwide.

The Korean Society of Infectious Diseases has been regularly publishing guidelines for adult immunization since 2007. Following the release of coronavirus disease 2019 (COVID-19) vaccination recommendations in 2023, significant changes have occurred due to the emergence of new variant strains and the waning immunity from previous vaccinations. This article provides a comprehensive update as of November 2024, incorporating the latest evidence and guidelines. Focusing on the 2024–2025 season, this article reviews vaccines currently authorized in Korea and assesses their effectiveness against the predominant JN.1 lineage variants. The updated recommendations prioritize high-risk groups, including adults aged 65 and older, individuals with underlying medical conditions, residents of facilities vulnerable to infection, pregnant women, and healthcare workers, for vaccination with updated vaccines targeting the JN.1 strain. Additionally, COVID-19 vaccination is available for all individuals aged 6 months and older. For most adults, a single-dose strategy is emphasized, while tailored schedules may be recommended for immunocompromised individuals. This update aims to optimize vaccination strategies in Korea to ensure comprehensive protection for high-risk populations.

Background: Islet transplantation holds promise for treating selected type 1 diabetes mellitus patients, yet the scarcity of human donor organs impedes widespread adoption. Porcine islets, deemed a viable alternative, recently demonstrated successful longterm survival without zoonotic risks in a clinically relevant pig-to-non-human primate islet transplantation model. This success prompted the development of a clinical trial protocol for porcine islet xenotransplantation in humans. Methods: A single-center, open-label clinical trial initiated by the sponsor will assess the safety and efficacy of porcine islet transplantation for diabetes patients at Gachon Hospital. The protocol received approval from the Gachon Hospital Institutional Review Board (IRB) and the Korean Ministry of Food and Drug Safety (MFDS) under the Investigational New Drug (IND) process. Two diabetic patients, experiencing inadequate glycemic control despite intensive insulin treatment and frequent hypoglycemic unawareness, will be enrolled. Participants and their family members will engage in deliberation before xenotransplantation during the screening period. Each patient will receive islets isolated from designated pathogen-free pigs. Immunosuppressants and systemic infection prophylaxis will follow the program schedule. The primary endpoint is to confirm the safety of porcine islets in patients, and the secondary endpoint is to assess whether porcine islets can reduce insulin dose and the frequency of hypoglycemic unawareness. Conclusion A clinical trial protocol adhering to global consensus guidelines for porcine islet xenotransplantation is presented, facilitating streamlined implementation of comparable human trials worldwide.