Prolonged skin inflammation is caused by disrupted skin barrier resulting in chronic inflammatory diseases such as atopic dermatitis. As a potent natural product with anti-inflammatory property, Aster glehni (A. glehni) is a traditional edible herb and has been used to treat diabetes or colitis-associated colon cancer. In present study, we figured out an additional effect of A. glehni ethanol extract (AGE) in pro-inflammatory cytokines-stimulated human keratinocytes. Mixture of tumor necrosis factor-alpha (TNF-α) and interferongamma (IFN-γ) was used to induce inflammatory responses in the HaCaT keratinocytes. AGE suppressed activation of ERK mitogen-activated protein kinase, nuclear factor (NF)-κB, and signal transducer and activator of transcription 1 and 3 (STAT1 and STAT3). The treatment of AGE inhibited mRNA expressions of proinflammatory cytokines in TNF-α and IFN-γ-stimulated HaCaT cells. Also, AGE induced up-regulated expressions of skin barrier molecules like filaggrin, loricrin, or ZO-1. We evaluated the effects of AGE on protein or mRNA expression levels using western blot or qRT-PCR, respectively. Taken together, these results suggest that the treatment of AGE exerts anti-inflammatory effect on keratinocytes through suppressing inflammatory signaling pathways and up-regulating skin molecules in HaCaT keratinocytes.

Prolonged skin inflammation is caused by disrupted skin barrier resulting in chronic inflammatory diseases such as atopic dermatitis. As a potent natural product with anti-inflammatory property, Aster glehni (A. glehni) is a traditional edible herb and has been used to treat diabetes or colitis-associated colon cancer. In present study, we figured out an additional effect of A. glehni ethanol extract (AGE) in pro-inflammatory cytokines-stimulated human keratinocytes. Mixture of tumor necrosis factor-alpha (TNF-α) and interferongamma (IFN-γ) was used to induce inflammatory responses in the HaCaT keratinocytes. AGE suppressed activation of ERK mitogen-activated protein kinase, nuclear factor (NF)-κB, and signal transducer and activator of transcription 1 and 3 (STAT1 and STAT3). The treatment of AGE inhibited mRNA expressions of proinflammatory cytokines in TNF-α and IFN-γ-stimulated HaCaT cells. Also, AGE induced up-regulated expressions of skin barrier molecules like filaggrin, loricrin, or ZO-1. We evaluated the effects of AGE on protein or mRNA expression levels using western blot or qRT-PCR, respectively. Taken together, these results suggest that the treatment of AGE exerts anti-inflammatory effect on keratinocytes through suppressing inflammatory signaling pathways and up-regulating skin molecules in HaCaT keratinocytes.

Prolonged skin inflammation is caused by disrupted skin barrier resulting in chronic inflammatory diseases such as atopic dermatitis. As a potent natural product with anti-inflammatory property, Aster glehni (A. glehni) is a traditional edible herb and has been used to treat diabetes or colitis-associated colon cancer. In present study, we figured out an additional effect of A. glehni ethanol extract (AGE) in pro-inflammatory cytokines-stimulated human keratinocytes. Mixture of tumor necrosis factor-alpha (TNF-α) and interferongamma (IFN-γ) was used to induce inflammatory responses in the HaCaT keratinocytes. AGE suppressed activation of ERK mitogen-activated protein kinase, nuclear factor (NF)-κB, and signal transducer and activator of transcription 1 and 3 (STAT1 and STAT3). The treatment of AGE inhibited mRNA expressions of proinflammatory cytokines in TNF-α and IFN-γ-stimulated HaCaT cells. Also, AGE induced up-regulated expressions of skin barrier molecules like filaggrin, loricrin, or ZO-1. We evaluated the effects of AGE on protein or mRNA expression levels using western blot or qRT-PCR, respectively. Taken together, these results suggest that the treatment of AGE exerts anti-inflammatory effect on keratinocytes through suppressing inflammatory signaling pathways and up-regulating skin molecules in HaCaT keratinocytes.

Prolonged skin inflammation is caused by disrupted skin barrier resulting in chronic inflammatory diseases such as atopic dermatitis. As a potent natural product with anti-inflammatory property, Aster glehni (A. glehni) is a traditional edible herb and has been used to treat diabetes or colitis-associated colon cancer. In present study, we figured out an additional effect of A. glehni ethanol extract (AGE) in pro-inflammatory cytokines-stimulated human keratinocytes. Mixture of tumor necrosis factor-alpha (TNF-α) and interferongamma (IFN-γ) was used to induce inflammatory responses in the HaCaT keratinocytes. AGE suppressed activation of ERK mitogen-activated protein kinase, nuclear factor (NF)-κB, and signal transducer and activator of transcription 1 and 3 (STAT1 and STAT3). The treatment of AGE inhibited mRNA expressions of proinflammatory cytokines in TNF-α and IFN-γ-stimulated HaCaT cells. Also, AGE induced up-regulated expressions of skin barrier molecules like filaggrin, loricrin, or ZO-1. We evaluated the effects of AGE on protein or mRNA expression levels using western blot or qRT-PCR, respectively. Taken together, these results suggest that the treatment of AGE exerts anti-inflammatory effect on keratinocytes through suppressing inflammatory signaling pathways and up-regulating skin molecules in HaCaT keratinocytes.

Prolonged skin inflammation is caused by disrupted skin barrier resulting in chronic inflammatory diseases such as atopic dermatitis. As a potent natural product with anti-inflammatory property, Aster glehni (A. glehni) is a traditional edible herb and has been used to treat diabetes or colitis-associated colon cancer. In present study, we figured out an additional effect of A. glehni ethanol extract (AGE) in pro-inflammatory cytokines-stimulated human keratinocytes. Mixture of tumor necrosis factor-alpha (TNF-α) and interferongamma (IFN-γ) was used to induce inflammatory responses in the HaCaT keratinocytes. AGE suppressed activation of ERK mitogen-activated protein kinase, nuclear factor (NF)-κB, and signal transducer and activator of transcription 1 and 3 (STAT1 and STAT3). The treatment of AGE inhibited mRNA expressions of proinflammatory cytokines in TNF-α and IFN-γ-stimulated HaCaT cells. Also, AGE induced up-regulated expressions of skin barrier molecules like filaggrin, loricrin, or ZO-1. We evaluated the effects of AGE on protein or mRNA expression levels using western blot or qRT-PCR, respectively. Taken together, these results suggest that the treatment of AGE exerts anti-inflammatory effect on keratinocytes through suppressing inflammatory signaling pathways and up-regulating skin molecules in HaCaT keratinocytes.

Purpose: This study aimed to evaluate the long-term prognosis of patients with gastric mucosa-associated lymphoid tissue (MALT) lymphoma, including overall survival (OS), remission, and factors associated with an aggressive disease course. Materials and Methods: Medical records of 153 patients diagnosed with gastric MALT lymphoma between 2013 and 2020 were retrospectively reviewed. Patients experiencing relapse, progression, high-grade transformation, or residual diseasewere included in the aggressive group and were compared with those in the indolent group. Additionally, the endoscopic findings of Helicobacter pylori-negative patients were reviewed. Results: Patient characteristics were as follows: mean age (56.9±11.2 years), sex (male, 51.0%), H. pylori infection (positive, 79.7%), endoscopic location (distal, 89.5%), endoscopic feature (superficial, 89.5%), clinical stage (stage I, 92.8%), invasion depth by endoscopic ultrasound (mucosa, n=115, 75.7%), and bone marrow result (no involvement, n=77, 100.0%). The median follow-up period was 59 months (mean, 61; range, 36–124) and the continuous remission period (n=149) was 51 months (mean, 50; range, 3–112). The 5-year survival rate was 97.7% while the 5-year continuous remission was 88.3%. Factors associated with the patients in the aggressive group were old age, sex(male), and clinical stage II or higher. H. pylori-negative patients’ endoscopy revealed a high incidence of atrophic gastritis in the antrum. Conclusions The long-term prognosis of gastric MALT lymphoma appears indolent and is indicated by the 5-year OS and continuous remission rates. Aggressive disease courses are associated with old age, sex (male), and clinical stage II or higher, but are not related to OS.

Adult-onset Still’s disease (AOSD) is a rare systemic inflammatory disease characterized by spiking fever, arthralgia, skin rashes, and hyperferritinemia. The rash is usually salmon-colored, non-itchy, accompanied by fever, and disappears with an improvement of fever. However, in some cases, the rash persisted regardless of fever. Here, we present a case of AOSD with an atypical persistent rash that showed histological findings resembling those of neutrophilic urticarial dermatosis. The patient was a 60-year-old woman with high fever, arthralgia, and a persistent flagellated skin rash. Despite systemic steroid treatment, the patient developed a serious complication: macrophage activation syndrome. Since this case presented with an atypical persistent rash with histological resemblance to neutrophilic urticarial dermatosis, we report its contribution to the further study of AOSD.

Background/Aims: A relationship between fatty liver and lung function impairment has been identified, and both are independently associated with metabolic dysfunction. However, the temporal relationship between changes in fatty liver status and lung function and their genome-wide association remain unclear. Methods: This longitudinal cohort consisted of subjects who received serial health check-ups, including liver ultrasonography and spirometry, for ≥3 years between 2003 and 2015. Lung func-tion decline rates were classified as “slow” and “accelerated” and compared among four different sonographic changes in steatosis status: “normal,” “improved,” “worsened,” and “persistent.” A genome-wide association study was conducted between the two groups: normal/improved steatosis with a slow decline in lung function versus worsened/persistent steatosis with an accelerated decline in lung function. Results: Among 6,149 individuals, the annual rates of decline in forced vital capacity (FVC) and forced expiratory volume measured in the first second of exhalation (FEV 1 ) were higher in the worsened/persistent steatosis group than in the normal/improved steatosis group. In multivariable analysis, persistent or worsened status of fatty liver was significantly associated with accelerated declines in FVC (persistent status, odds ratio [OR]=1.22, 95% confidence interval [CI]=1.04–1.44; worsened status, OR=1.30, 95% CI=1.12–1.50), while improved status of fatty liver was significantly associated with slow declines in FEV 1 (OR=0.77, 95% CI=0.64–0.92). The PNPLA3 risk gene was most strongly associated with steatosis status change and accelerated declines in FVC (rs12483959, p=2.61×10 -7 ) and FEV 1(rs2294433, p=3.69×10 -8 ). Conclusions Regression of fatty liver is related to lung function decline. Continuing efforts to improve fatty liver may preserve lung function, especially for subjects with a high genetic risk.

Background: Lipid emulsion (LE) is effective in treating intractable cardiac depression induced by the toxicity of highly lipid-soluble drugs including local anesthetics. However, the effect of LE on chloroquine (CQ)-evoked cardiac toxicity remains unclear. This study aimed to examine the effect of Lipofundin MCT/LCT, an LE, on the cardiotoxicity caused by CQ in H9c2 rat cardiomyoblasts and elucidate the underlying cellular mechanism. Methods: The effects of CQ (1 × 10-4 M), LE, and the reactive oxygen species (ROS) scavengers mitotempo and N-acetyl-L-cysteine (NAC), alone or combined, on cell viability and migration, apoptosis, ROS production, calcium levels, mitochondrial membrane potential, and adenosine triphosphate (ATP) were examined. Additionally, the effects of LE on the activities of catalase (CAT), malondialdehyde (MDA), and superoxide dismutase (SOD) induced by CQ were assessed. Results: Pretreatment with LE, mitotempo, or NAC reversed the reduction in cell migration and viability, mitochondrial membrane potential, and ATP levels evoked by CQ, and inhibited the increase in cleaved caspase-3, ROS, and calcium concentration induced by CQ. LE inhibited the increase in Bax expression, terminal deoxynucleotidyl transferase dUTP nick end labeling-positive cells, MDA activity, and late apoptosis, and reversed the reduction in SOD and CAT activity induced by CQ. CQ did not significantly affect cleaved caspase-8 expression, and LE did not significantly affect CQ concentration. Conclusions Collectively, these results suggest that LE (Lipofundin MCT/LCT) inhibits the cardiotoxicity and late apoptosis induced by CQ toxicity via the intrinsic mitochondrial apoptotic pathway that is associated with direct inhibition of ROS production.