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: Few meta-analyses of head-to-head comparisons between subcutaneous immunotherapy (SCIT) and sublingual immunotherapy (SLIT) for perennial allergic rhinitis (AR) have been performed so far. This study aimed to compare the efficacy, safety, and adherence of SCIT and SLIT in patients with house dust mite (HDM)-sensitized AR through a meta-analysis of head-to-head comparative studies. Methods: A meta-analysis based on direct comparisons of SCIT and SLIT in HDM-sensitized AR was performed, using randomized controlled trials (RCTs) and nonrandomized studies (NRSs), on efficacy, safety, and adherence, which had been published until April 30, 2021. Treatment efficacy was calculated as the standardized mean difference in symptoms and medication scores after treatment between SCIT and SLIT. Safety and adherence to treatment were compared with the relative risk (RR) of SCIT and SLIT. Results: Six RCTs and 3 NRS scores were analyzed. No statistically significant difference was noticed in improvement in symptoms and medication scores between SCIT and SLIT groups. Systemic adverse events occurred more frequently in SCIT than in SLIT in both RCT (RR, 3.97; 95% confidence interval [CI], 0.50–31.57) and NRS (RR, 5.48; 95% CI, 1.94–15.50). SCIT showed significantly higher adherence than did SLIT (RR, 1.16; 95% CI, 0.92–1.47). Conclusion No significant difference in efficacy was noticed between the 2 modalities for HDM-sensitized AR. However, SLIT had significantly lower number of systemic adverse reactions, and SCIT had more preferable adherence.

Background: Epinephrine (EPI) or norepinephrine (NOR) is widely used to treat cardiovascular collapse during lipid emulsion (LE) resuscitation for drug toxicity. However, the effect of LE on the vasoconstriction caused by EPI or NOR remains unknown. The purpose of this study was to examine the effect of an LE (Intralipid) on the vasoconstriction caused by EPI and NOR in isolated rat aorta. Methods: The effect of LE on the vasoconstriction caused by EPI or NOR in isolated rat aorta was examined. Additionally, the effect of LE on the calcium increase caused by EPI or NOR was investigated. The distribution constant (KD: lipid to aqueous phase) of EPI or NOR between a LE (1%) and an aqueous phase was determined. Results: LE (1 and 2%) did not significantly alter vasoconstriction caused by EPI or NOR in isolated endothelium-intact aorta. Moreover, the LE did not significantly alter the increased calcium level caused by EPI or NOR. The log KD of EPI in the LE (1%) was −0.71, −0.99, and −1.00 at 20, 50, and 100 mM ionic strength, respectively. The log KD of NOR in the LE (1%) was −1.22, −1.25, and −0.96 at 20, 50, and 100 mM ionic strength, respectively. Conclusions Taken together, the Intralipid emulsion did not alter vasoconstriction induced by EPI or NOR that seems to be due to the hydrophilicity of EPI or NOR, leading to sustained hemodynamic support produced by EPI or NOR used during LE resuscitation.

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.

Background: Pediatric alopecia areata (AA) can affect the quality of life (QoL) of patients and their family members. Research on the QoL and burden on family members in pediatric AA is limited. Objective: This nationwide multicenter questionnaire study described the QoL and burden of the family members of patients with pediatric AA. Methods: This nationwide multicenter questionnaire study enrolled AA patients between the ages of 5 and 18 years from March 1, 2017 to February 28, 2018. Enrolled patients and their parents completed the modified Children’s Dermatology Life Quality Index (CDLQI) and the modified Dermatitis Family Impact (mDFI). The disease severity was measured using the Severity of Alopecia Tool (SALT) survey scores. Results: A total of 268 patients with AA from 22 hospitals participated in this study. Our study found that the efficacy and satisfaction of previous treatments of AA decreased as the severity of the disease increased. The use of home-based therapies and traditional medicines increased with the increasing severity of the disease, but the efficacy felt by patients was limited. CDLQI and mDFI scores were higher in patients with extensive AA than those with mild to moderate AA. The economic and time burden of the family members also increased as the severity of the disease increased. Conclusion The severity of the AA is indirectly proportional to the QoL of patients and their family members and directly proportional to the burden. Physicians need to understand these characteristics of pediatric AA and provide appropriate intervention to patients and their family members.

Background: and Purpose A multifactorial antiepileptic mechanism underlies the ketogenic diet (KD), and one of the proposed mechanisms of action is that the KD inhibits the mammalian target of rapamycin (mTOR) pathway. To test this clinically, this study aimed to determine the efficacy of the KD in patients with pathologically confirmed focal cortical dysplasia (FCD) due to genetically identifiable mTOR pathway dysregulation. Methods: A cohort of patients with pathologically confirmed FCD after epilepsy surgery and who were screened for the presence of germline and somatic mutations related to the mTOR pathway in peripheral blood and resected brain tissue was constructed prospectively. A retrospective review of the efficacy of the prior KD in these patients was performed. Results: Twenty-five patients with pathologically confirmed FCD and who were screened for the presence of detectable somatic mTOR pathway mutations had received a sufficient KD. Twelve of these patients (48.0%) had germline or somatic detectable mTOR pathway mutations. A response was defined as a ≥50% reduction in seizure frequency. The efficacy of the KD after 3 months of dietary therapy was superior in patients with detectable mTOR pathway mutations than in patients without detectable mTOR pathway mutations, although the difference was not statistically significant (responder rates of 58.3% vs. 38.5%, p=0.434). Conclusions A greater proportion of patients with mTOR pathway responded to the KD, but there was no statistically significant difference in efficacy of the KD between patients with and without detectable mTOR pathway mutations. Further study is warranted due to the smallness of the sample and the limited number of mTOR pathway genes tested in this study.