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/Aims: This study aimed to evaluate the performance of the Model for End-Stage Liver Disease (MELD) 3.0 for predicting mortality and liver-related complications compared with the Child-Pugh classification, albumin-bilirubin (ALBI) grade, the MELD, and the MELD sodium (MELDNa) score. Methods: We evaluated a multicenter retrospective cohort of incorporated patients with cirrhosis between 2013 and 2019. We conducted comparisons of the area under the receiver operating characteristic curve (AUROC) of the MELD3.0 and other models for predicting 3-month mortality. Additionally, we assessed the risk of cirrhosis-related complications according to the MELD3.0 score. Results: A total of 3,314 patients were included. The mean age was 55.9±11.3 years, and 70.2% of the patients were male. Within the initial 3 months, 220 patients (6.6%) died, and the MELD3.0had the best predictive performance among the tested models, with an AUROC of 0.851, outperforming the Child-Pugh classification, ALBI grade, MELD, and MELDNa. A high MELD3.0score was associated with an increased risk of mortality. Compared with that of the group with a MELD3.0 score <10 points, the adjusted hazard ratio of the group with a score of 10–20 pointswas 2.176, and that for the group with a score of ≥20 points was 4.892. Each 1-point increase inthe MELD3.0 score increased the risk of cirrhosis-related complications by 1.033-fold. The risk of hepatorenal syndrome showed the highest increase, with an adjusted hazard ratio of 1.149, followed by hepatic encephalopathy and ascites. Conclusions The MELD3.0 demonstrated robust prognostic performance in predicting mortality in patients with cirrhosis. Moreover, the MELD3.0 score was linked to cirrhosis-related complications, particularly those involving kidney function, such as hepatorenal syndrome and ascites.

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/Aims: This study aimed to evaluate the performance of the Model for End-Stage Liver Disease (MELD) 3.0 for predicting mortality and liver-related complications compared with the Child-Pugh classification, albumin-bilirubin (ALBI) grade, the MELD, and the MELD sodium (MELDNa) score. Methods: We evaluated a multicenter retrospective cohort of incorporated patients with cirrhosis between 2013 and 2019. We conducted comparisons of the area under the receiver operating characteristic curve (AUROC) of the MELD3.0 and other models for predicting 3-month mortality. Additionally, we assessed the risk of cirrhosis-related complications according to the MELD3.0 score. Results: A total of 3,314 patients were included. The mean age was 55.9±11.3 years, and 70.2% of the patients were male. Within the initial 3 months, 220 patients (6.6%) died, and the MELD3.0had the best predictive performance among the tested models, with an AUROC of 0.851, outperforming the Child-Pugh classification, ALBI grade, MELD, and MELDNa. A high MELD3.0score was associated with an increased risk of mortality. Compared with that of the group with a MELD3.0 score <10 points, the adjusted hazard ratio of the group with a score of 10–20 pointswas 2.176, and that for the group with a score of ≥20 points was 4.892. Each 1-point increase inthe MELD3.0 score increased the risk of cirrhosis-related complications by 1.033-fold. The risk of hepatorenal syndrome showed the highest increase, with an adjusted hazard ratio of 1.149, followed by hepatic encephalopathy and ascites. Conclusions The MELD3.0 demonstrated robust prognostic performance in predicting mortality in patients with cirrhosis. Moreover, the MELD3.0 score was linked to cirrhosis-related complications, particularly those involving kidney function, such as hepatorenal syndrome and ascites.

Background/Aims: This study aimed to evaluate the performance of the Model for End-Stage Liver Disease (MELD) 3.0 for predicting mortality and liver-related complications compared with the Child-Pugh classification, albumin-bilirubin (ALBI) grade, the MELD, and the MELD sodium (MELDNa) score. Methods: We evaluated a multicenter retrospective cohort of incorporated patients with cirrhosis between 2013 and 2019. We conducted comparisons of the area under the receiver operating characteristic curve (AUROC) of the MELD3.0 and other models for predicting 3-month mortality. Additionally, we assessed the risk of cirrhosis-related complications according to the MELD3.0 score. Results: A total of 3,314 patients were included. The mean age was 55.9±11.3 years, and 70.2% of the patients were male. Within the initial 3 months, 220 patients (6.6%) died, and the MELD3.0had the best predictive performance among the tested models, with an AUROC of 0.851, outperforming the Child-Pugh classification, ALBI grade, MELD, and MELDNa. A high MELD3.0score was associated with an increased risk of mortality. Compared with that of the group with a MELD3.0 score <10 points, the adjusted hazard ratio of the group with a score of 10–20 pointswas 2.176, and that for the group with a score of ≥20 points was 4.892. Each 1-point increase inthe MELD3.0 score increased the risk of cirrhosis-related complications by 1.033-fold. The risk of hepatorenal syndrome showed the highest increase, with an adjusted hazard ratio of 1.149, followed by hepatic encephalopathy and ascites. Conclusions The MELD3.0 demonstrated robust prognostic performance in predicting mortality in patients with cirrhosis. Moreover, the MELD3.0 score was linked to cirrhosis-related complications, particularly those involving kidney function, such as hepatorenal syndrome and ascites.

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/Aims: This study aimed to evaluate the performance of the Model for End-Stage Liver Disease (MELD) 3.0 for predicting mortality and liver-related complications compared with the Child-Pugh classification, albumin-bilirubin (ALBI) grade, the MELD, and the MELD sodium (MELDNa) score. Methods: We evaluated a multicenter retrospective cohort of incorporated patients with cirrhosis between 2013 and 2019. We conducted comparisons of the area under the receiver operating characteristic curve (AUROC) of the MELD3.0 and other models for predicting 3-month mortality. Additionally, we assessed the risk of cirrhosis-related complications according to the MELD3.0 score. Results: A total of 3,314 patients were included. The mean age was 55.9±11.3 years, and 70.2% of the patients were male. Within the initial 3 months, 220 patients (6.6%) died, and the MELD3.0had the best predictive performance among the tested models, with an AUROC of 0.851, outperforming the Child-Pugh classification, ALBI grade, MELD, and MELDNa. A high MELD3.0score was associated with an increased risk of mortality. Compared with that of the group with a MELD3.0 score <10 points, the adjusted hazard ratio of the group with a score of 10–20 pointswas 2.176, and that for the group with a score of ≥20 points was 4.892. Each 1-point increase inthe MELD3.0 score increased the risk of cirrhosis-related complications by 1.033-fold. The risk of hepatorenal syndrome showed the highest increase, with an adjusted hazard ratio of 1.149, followed by hepatic encephalopathy and ascites. Conclusions The MELD3.0 demonstrated robust prognostic performance in predicting mortality in patients with cirrhosis. Moreover, the MELD3.0 score was linked to cirrhosis-related complications, particularly those involving kidney function, such as hepatorenal syndrome and ascites.

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: Bullous pemphigoid (BP) is an autoimmune blistering disease driven by autoantibodies against BP180 and BP230. While type 2 inflammation plays a key role, the precise immune cell alterations and transcriptomic changes remain unclear. Objective: To characterize immune cell composition and transcriptomic changes in BP patients using fluorescence-activated cell sorting (FACS)-based immunophenotyping and RNA sequencing. Methods: A case-control study was conducted on 10 newly diagnosed, treatment-naive BP patients and six healthy controls. Disease activity was assessed using the Bullous Pemphigoid Disease Area Index (BPDAI). Peripheral blood mononuclear cells were isolated for FACS analysis to determine immune cell subsets. RNA sequencing was performed to identify differentially expressed genes (DEGs) and enriched pathways. Statistical analyses included t-tests, Mann-Whitney U tests, and correlation analysis. Results: FACS analysis revealed a reduction in CD4 + T cells, T helper 2 (Th2), and B cells in BP patients (p<0.05), alongside an increase in M2a-like monocytes (p<0.001). RNA sequencing identified 262 DEGs, with secretory leukocyte peptidase inhibitor (SLPI) and transmembrane protein 237 being the most significantly upregulated. Proline-serine-threonine phosphatase interacting protein 2 (PSTPIP2) and SAM domain, SH3 domain, and nuclear localization signals 1 (SAMSN1) positively correlated with BPDAI (p<0.001). Gene ontology analysis highlighted enrichment in inflammatory responses and neutrophil degranulation pathways. Conclusion BP patients show distinct immune dysregulation, including decreased CD4 + T cells, Th2, and B cells, increased M2a-like monocytes, altered gene expression profiles, and correlations between PSTPIP2, SAMSN1 and disease activity. These findings provide insights into pathogenesis and potential therapeutic targets of BP.