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.

Objective: : Chiari II malformation (CM II) is still the main cause of severe morbidity and mortality in children with open neural tube defects (ONTDs). The goal of this study was to validate a CM II model in late-stage chick embryos with surgically induced ONTDs. Methods: : To make the chick embryo model of ONTD, their neural tubes were opened for a length of 5–6 somites at the thoracic level in Hamburger and Hamilton stage 18 chick embryos (n=150). They were reincubated in ovo. up to a total age of 17–21 days. A total of 19 embryos survived and were assigned to either the postoperative day (POD) 14–15 group (n=6) or the POD 17–18 group (n=13). Magnetic resonance imaging (MRI) and histopathologic findings of embryo heads with spinal ONTDs were compared with age-matched normal chick embryos. Results: : The chick embryos with ONTDs demonstrated definite and constant structural changes, such as downward displacement of the cerebellum to just above the foramen magnum and narrow and small cerebrospinal fluid spaces in the crowded small posterior fossa. These morphologic features were more prominent in the POD 17–18 group than in the POD 14–15 group. Conclusion : This is the first description of CM II with spinal ONTD in a late-stage chick embryo model with MRI and histopathological analysis. The morphological changes of the posterior fossa in this study mimic those of CM II associated with spinal ONTD in humans. This model will facilitate investigation of the pathogenesis of CM II.

Ruptured intracranial aneurysms in infants are rare and infantile fusiform anterior cerebral artery (ACA) aneurysms are much rarer. In this report, we described the case of a 7-month-old infant with a ruptured fusiform ACA aneurysm who presented with seizure and underwent endovascular treatment. The patient was initially in a coma and the neurologic condition did not improve after treatment. The clinical characteristics of the case and literature review were discussed.

Objective: Animal models of spinal cord injuries (SCIs) use rats to simulate human SCIs.Among the various techniques, clips have been used to reproduce the compression-contusion model. However, the mechanism of injury in discogenic incomplete SCI may differ from that in clip injury; however, a model has yet to be established. Previously, we issued a patent (No.10-2053770) for a rat SCI model using Merocel ® , a water-absorbing self-expanding polymer sponge. The objectives of this study were to compare the locomotor and histopathological changes between the Merocel ® -compression model (MC group) and clip compression model (clip group). Methods: This study included 4 groups of rats: MC (n=30), MC-sham (n=5), clip (n=30), and clip-sham (n=5). Locomotor function was evaluated in all groups using the Basso, Beattie, and Bresnahan (BBB) scoring system, 4 weeks after injury. Histopathological analyses included morphology, presence of inflammatory cells, microglial activation, and extent of neuronal damage, which were compared among the groups. Results: The BBB scores in the MC group were significantly higher than those in the clip group throughout the 4 weeks (p<0.01). Neuropathological changes in the MC group were significantly less severe than those in the clip group. In addition, motor neurons were well preserved in the ventral horn of the MC group but poorly preserved in the ventral horn of the clip group. Conclusion The novel MC group can help elucidate the pathophysiology of acute discogenic incomplete SCIs and may be applied in various SCI therapeutic strategies.

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.