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Mi-Eun Kim,* Myoung-Lyun Heo* Department of Nursing, Jeonju University, Jeonju-si, Korea*These authors contributed equally to this workCorrespondence: Myoung-Lyun Heo, Department of Nursing, Jeonju University, Jeonju-si, 55069, South Korea, Tel +82-63-2209, Fax +82-63-220-2054, Email prayerhj23@jj.ac.krPurpose: This study aimed to translate the Pandemic-Related Pregnancy Stress Scale into Korean and validate the translated instrument.Patients and Methods: After translating the instrument, seven items of two factors (preparedness and perinatal infection stress) were selected for content validity testing. Validity and reliability were evaluated using SPSS 25.0 and AMOS 26.0. An online survey, via Google Forms, was conducted from January 20 to January 26, 2022. Participants were 283 pregnant women in Korea who consented to participate in the study.Results: Exploratory factor analysis revealed factor loadings on two factors of 0.64– 0.87 with a total variance explained of 69.77%. Confirmatory factor analysis indicated good model fit (RMR = 0.03, RMSEA = 0.06, GFI = 0.98, SRMR = 0.03), and convergent and discriminant validity were established. Concurrent validity was established based on the correlation with the Revised Prenatal Distress Questionnaire (r = 0.45), and the reliability of the final instrument was indicated by Cronbach’s α = 0.87.Conclusion: The Pandemic-Related Pregnancy Stress Scale was validated for use in the Korean population. The Korean version of the Pandemic-Related Pregnancy Stress Scale can be utilized to measure pandemic-related stress in pregnant women.Keywords: Pandemic-Related Pregnancy Stress Scale, PREPS, Korean women, COVID-19, pregnancy stress

BACKGROUND In order to successfully treat scabies and to prevent its spread, it is important to identify the factors that can influence the outcome of scabies treatment. OBJECTIVES This study was designed to evaluate the risk factors associated with treatment resistance scabies during use of an effective topical medication. METHODS A retrospective cohort study was performed in patients with scabies infestations confirmed by potassium hydroxide (KOH) examinations. Patient characteristics, clinical features and treatment history were collected. The treatment resistance group included patients with persistent scabies infestations for more than 28 days after initiation of antiscabies treatment with 5% permethrin cream. RESULTS In total, 138 patients with scabies infestations treated between January 2017 and December 2020 were included in this study. Of these, 100 (72.5%) patients were treated successfully, while 38 (27.5%) patients experienced treatment resistance. In the univariable analysis, risk factors for treatment resistance scabies included impaired cognitive function (OR = 2.66, 95% CI, 1.15-6.14), limited mobility (OR = 2.97, 95% CI, 1.30-6.83), inpatient status (vs. outpatient, OR = 3.3, 95% CI, 1.28-8.54), topical steroid use before diagnosis (OR = 3.52, 95% CI, 1.61-7.81), systemic steroid use before diagnosis (OR = 3.57, 95% CI, 1.26-10.34) and a positive KOH exam after the first treatment (OR = 7.25, 95% CI, 3.24-17.11). In the multivariable analysis, limited mobility (OR = 3.46, 95% CI, 1.02-12.11) and topical steroid use before diagnosis (OR = 3.65, 95% CI, 1.41-9.75) were significant predictive factors for treatment resistance scabies. CONCLUSIONS Scabies patients with limited mobility and topical steroid use before diagnosis are at high risk of treatment resistance. Dermatologists should take these findings into consideration when treating patients with scabies infestations.

Betaine is the major water-soluble component of Lycium chinensis. Although there are reports of a protective effect of betaine on fatty liver disease, the underlying mechanisms are unclear. We investigated the effects of betaine on forkhead box O6 (FoxO6) and peroxisome proliferator-activated receptor gamma (PPARγ) expression, which are associated with hepatic lipid accumulation. In this study, we attempted to elucidate the molecular regulation of betaine on hyperglycemia-induced lipid accumulation via FoxO6 activation. HepG2 cells and liver tissue isolated from db/db mice treated with betaine at a dose of 50 mg/kg/day for 3 weeks were used. In the present study, we investigated whether betaine ameliorates hepatic steatosis by inhibiting FoxO6/PPARγ signaling in liver cells. Interestingly, betaine notably decreased lipid accumulation in FoxO6-induced mRNA expression of lipogenesis-related genes. In addition, hepatic insulin signaling was decreased; and activation of FoxO6, which is negatively regulated by Akt, was reduced by betaine treatment. Furthermore, betaine inhibited the FoxO6 interaction with PPARγ and cellular triglycerides in high-glucose- or FoxO6-overexpression-treated liver cells. In addition, we confirmed that betaine administration via oral gavage significantly ameliorated hepatic steatosis in db/db mice. The protein level of PPARγ, a lipogenic transcription factor, was decreased in the livers of db/db mice. Therefore, it has previously been shown to induce hepatic steatosis. We conclude that betaine ameliorates hepatic steatosis, at least in part, by inhibiting the interaction between FoxO6 and PPARγ, thereby suppressing lipogenic gene transcription.

Previously, we reported that Sargassum horneri (Turner) C. Agardh (S. horneri) is a brown algae species that exerts anti-inflammatory activity toward murine macrophages. However, the anti-neuroinflammatory effects and the mechanism of S. horneri on microglia cells are still unknown. We investigated the anti-neuroinflammatory effects of S. horneri extract on microglia in vitro and in vivo. In the present study, we found that S. horneri was not cytotoxic to BV-2 microglia cells and it significantly decreased lipopolysaccharide (LPS)-induced NO production. Moreover, S. horneri also diminished the protein expression of iNOS, COX-2, and cytokine production, including IL-1β, TNF-α, and IL-6, on LPS-stimulated microglia activation. S. horneri elicited anti-neuroinflammatory effects by inhibiting phosphorylation of p38 MAPK and NF-κB. In addition, S. horneri inhibited astrocytes and microglia activation in LPS-challenged mice brain. Therefore, these results suggested that S. horneri exerted anti-neuroinflammatory effects on LPS-stimulated microglia cell activation by inhibiting neuroinflammatory factors and NF-κB signaling.

Background We showed that the activation of the nucleotide-binding oligomerization domain-like receptor pyrin domain-containing-3 (NLRP3) inflammasome by the forkhead box O6 (FoxO6) transcription factor through binding of the thioredoxin-interacting protein (TXNIP) under inflammatory conditions might lead to hepatic steatosis. Although the role of the FoxO6 in mediating lipid accumulation and the chronic inflammatory process underlying the pathophysiology of hepatic steatosis are well explored, the precise mechanisms of the involvement of FoxO6 have not fully been delineated to date. Methods NLRP3 inflammasome and lipogenesis were monitored in mice overexpressed with constitutively active (CA)-FoxO6 allele, and FoxO6-null mice. In vitro study, liver cells overexpressing CA-FoxO6 were treated with palmitate, and then alterations in lipid metabolism were measured. Results The focus of our investigation was to apply palmitate treatment to elucidate the mechanisms underlying the role of FoxO6 in the activation of the cytokine IL-1β through the NLRP3 inflammasome. Initial experiments revealed that palmitate-induced FoxO6 activity was caused by its dephosphorylation, which induced its transcriptional activity. Further palmitate experiments showed increased expression of IL-1β and the hepatic NLRP3 inflammasome complex, including adapter protein ASC, and pro-caspase-1. Furthermore, TXNIP, a key regulator of cellular redox state in the upstream NLRP3 inflammasome, was induced by FoxO6 in liver and HepG2 cells. Conclusion The main contribution of the current study is the identification of FoxO6 as a key signaling element upstream of TXNIP in the regulation of the hepatic NLRP3 inflammasome of the molecular mechanisms involved in hepatic lipogenesis.

Inflammation exacerbates systemic pathophysiological conditions and chronic inflammation is a sustained and systemic phenomenon that aggravates aging that can lead to chronic age-related diseases. These inflammatory phenomena have recently been redefined and delineated at the molecular, cellular, and systemic levels. Many transcription factors that are activated in response to tumor metabolic state have been reported to be regulated by a class of histone deacetylase called sirtuins (SIRTs). Sirtuins play a pivotal role in the regulation of tumor cell metabolism, proliferation, and angiogenesis, including oxidative stress and inflammation. The SIRT1-mediated signaling pathway in diabetes and cancer is the SIRT1/forkhead-box class O (FoxO)/nuclear factor-kappa B (NF-κB) pathway. In this review, we describe the accumulation of SIRT1-, NF-κB-, and FoxO-mediated inflammatory processes and cellular proinflammatory signaling pathways. We also describe the proinflammatory mechanisms underlying metabolic molecular pathways in various diseases such as liver cancer and diabetes. Finally, the regulation of cancer and diabetes through the anti-inflammatory effects of natural compounds is highlighted. Evidence from inflammation studies strongly suggests that cells may be a major source of cytokines secreted during various diseases. A better understanding of the mechanisms that underpin the inflammatory response and palliative role of natural compounds will provide insights into the molecular mechanisms of inflammation and various diseases for potential intervention.

Forkhead box O transcription factors (FoxOs) play an important role in maintaining normal cell physiology by regulating survival, apoptosis, autophagy, oxidative stress, the development and maturation of T and B lymphocytes, and the secretion of inflammatory cytokines. Cell types whose functions are regulated by FoxOs include keratinocytes, mucosal dermis, neutrophils, macrophages, dendritic cells, tumor-infiltrating activated regulatory T (Tregs) cells, B cells, and natural killer (NK) cells. FoxOs plays a crucial role in physiological and pathological immune responses. FoxOs control the development and function of Foxp3+ Tregs. Treg cells and Th17 cells are subsets of CD4+ T cells, which play an essential role in immune homeostasis and infection. Dysregulation of the Th17/Treg cell balance has been implicated in the development and progression of several disorders, such as autoimmune diseases, inflammatory diseases, and cancer. In addition, FoxOs are stimulated by the mitogen-activated protein (MAP) kinase pathway and inhibited by the PI3 kinase/AKT pathway. Downstream target genes of FoxOs include pro-inflammatory signaling molecules (toll-like receptor (TLR) 2, TLR4, interleukin (IL)-1β, and tumor necrosis factor (TNF)-α), chemokine receptors (CCR7 and CXCR2), B-cell regulators (APRIL and BLYS), T-regulatory modulators (Foxp3 and CTLA-4), and DNA repair enzymes (GADD45α). Here, we review the recent progress in our understanding of FoxOs as the key molecules involved in immune cell differentiation and its role in the initiation of autoimmune diseases caused by dysregulation of immune cell balance. Additionally, in various diseases, FoxOs act as a cancer repressor, and reviving the activity of FoxOs forces Tregs to egress from various tissues. However, FoxOs regulate the cytotoxicity of both CD8+ T and NK cells against tumor cells, aiding in the restoration of redox and inflammatory homeostasis, repair of the damaged tissue, and activation of immune cells. A better understanding of FoxOs regulation may help develop novel potential therapeutics for treating immune/oxidative stress-related diseases.

Dendritic cells (DCs) are play critical roles in the priming and regulation of immune responses. DCs rapidly process and convey these antigens to prime antigen-specific T cells. Therefore, regulation of DCs functions is important for immunity and immunotherapies. Immune adjuvants for DCs activation are needed to improve the efficacy of vaccines against tumors and many infectious diseases. Therefore, we demonstrate that H. fusiformis extract can regulate DCs maturation and activation. H. fusiformis extract induced costimulatory molecules (CD 80 and CD86), antigen-presenting molecules (major histocompatibility complex (MHC) I and II), CCR7 expression, and interleukin (IL)-12 production in DCs. These effects are associated with upregulation of mitogen-activated protein kinase (MAPK) signaling pathway. In addition, H. fusiformis extract induces costimulatory molecules on splenic DCs and activated CD8+ T cells in vivo. Taken together, these findings suggest that H. fusiformis extract may be a potential efficient immune therapeutic compound in DCs-mediated immunotherapies. Abbreviations CTL: cytotoxic T lymphocytes; DCs: dendritic cells; ERK: extracellular signal-regulated kinases; IL: interleukini; JNK: c-Jun N-terminal kinase; MAPK: mitogen-activated protein kinase; MHC: major histocompatibility complex

Osteoarthritis (OA), which is caused by joint damage, is the most common form of arthritis, affecting millions of people worldwide. This damage can accumulate over time, which is why aging is one of the main contributors to joint damage associated with OA. The OA-related proteins that have been reported to date have been identified by the comparative analysis of OA patients with normal controls, following surgical or pharmacological treatment. For the first time, the present study analyzed OA-related proteins in patients with OA according to the International Cartilage Repair Society (ICRS) scale. Changes in protein expression can be observed during the OA process. The present study demonstrated differential protein expression patterns in articular cartilage from ICRS1- and ICRS3-graded OA patients. ICRS grade-matched OA knee samples from 12 OA patients, 6 ICRS grade 1 patients and 6 ICRS3 patients were subjected to proteomic analysis using the LTQ-Orbitrap mass spectrometry system. A total of 231 unique proteins were identified as expressed across the ICRS1 and ICRS3 OA patient groups. Relative differences in protein expression associated with the following classifications were observed: Biological adhesion, cell killing, cellular process, development process and molecular function. Although some of these proteins have been previously reported to be associated with rheumatoid arthritis, including cartilage oligomeric matrix protein, collagen types, angiogenin, complement C5 and CD59 glycoprotein, numerous additional proteins were newly identified, which may further help our understanding of disease pathogenesis. These findings suggested that these proteins may be used to develop novel therapeutic targets for OA.

Neuroinflammation is a specific or nonspecific immunological reaction in the central nervous system that is induced by microglia activation. Appropriate regulation of activated microglial cells is therefore important for inhibiting neuroinflammation. Hesperetin is a natural flavanone and an aglycone of hesperidin that is found in citrus fruits. Hesperetin reportedly possesses anti-inflammatory, anti-cancer, and antioxidant effects. However, the anti-neuroinflammatory effects of hesperetin on microglia are still unknown. Here, we investigated the anti-neuroinflammatory effects of hesperetin on lipopolysaccharide (LPS)-stimulated BV-2 microglial cells. We found that hesperetin strongly inhibited nitric oxide production and expression of inducible nitric oxide synthase in LPS-stimulated BV-2 microglial cells. Hesperetin also significantly reduced secretion of inflammatory cytokines including interleukin (IL)-1β and IL-6. Furthermore, hesperetin down-regulated the phosphorylation of extracellular signal-regulated kinase (ERK)1/2 and p38 mitogen-activated protein kinase, exerting anti-inflammatory effects. Hesperetin suppressed astrocyte and microglia activation in the LPS-challenged mouse brain. Collectively, our findings indicate that hesperetin inhibits microglia-mediated neuroinflammation and could be a prophylactic treatment for neurodegenerative diseases.

Previously we reported that Sargassum horneri (Turner) C. Agardh (S. horneri) is a brown algae species that exerts anti-inflammatory activity toward murine macrophages. However, the anti-neuroinflammatory effects and the mechanism of S. horneri on microglia cells are still unknown. We investigated the anti-neuroinflammatory effects of S. horneri extract on microglia in vitro and in vivo. In present study, we found that S. horneri was not cytotoxic to BV-2 microglia cells, and it significantly decreased lipopolysaccharide (LPS)-induced NO production. Moreover, S. horneri also diminished the protein expression of iNOS, COX-2, and cytokines production including IL-1b, TNF-a, and IL-6 on LPS-stimulated microglia activation. S. horneri elicited anti-neuroinflammatory effects by inhibiting phosphorylation of p38 MAPK and NF-kB. In addition, S. horneri inhibited astrocytes and microglia activation in LPS-challenged mice brain. Therefore, these results suggested that S. horneri exerted anti-neuroinflammatory effects on LPS-stimulated microglia cells activation by inhibiting MAPK phosphorylation and NF-kB signaling.

Background Team-based learning in nursing education has shown higher rates of students that meet the learning outcomes in problem-solving. But students claim team-based learning has its drawbacks, and that the readiness assurance test takes too much time. Therefore, it is necessary to examine how the group readiness assurance test in team-based learning effects student's educational outcomes. Objectives This study was conducted to investigate the effects of the group readiness assurance tests on nursing students' problem solving, learning satisfaction, and team efficacy. Design & method This study used a crossover study design. The researchers conducted their study in team-based learning classes at a Korean university. The classes were conducted for eight weeks with nursing majors. In total, 194 students in their third year participated. Students received two different treatments: with and without a team test. The washout period was four weeks. Results There was no statistically significant difference in nursing students' problem solving (t = 0.41, p = .679), learning satisfaction (t = 0.80, p = .420), or team efficacy (t = 1.20, p = .228) depending on the presence or absence of a team test. Conclusions When using team-based learning with nursing students, instructors should consider whether to conduct group readiness assurance tests are an efficient educational intervention and if they achieve the expected educational goals.

Currently, there is a great clinical demand for biocompatible and robust tissue-engineered tubular scaffolds for use as artificial vascular graft materials. Despite considerable research on vascular scaffolds, there has still been only limited development of scaffold materials possessing both sufficient mechanical strengths and biological effects for vascular application. In this work, we designed a mechanically robust, bilayered scaffold and manufactured it by combining electrospinning (ELSP) and three-dimensional (3D) printing techniques. This material was coated with polydopamine (PDA) and vascular endothelial growth factor (VEGF) was grafted directly on the scaffold surface to induce potent angiogenic activity. We confirmed that the coated-PDA layer was evenly deposited on the bare polycaprolactone (PCL) scaffold and could enable abundant VEGF immobilization with enhanced hydrophilicity. The VEGF immobilized porous tubular scaffold was well prepared without mechanical weakness induced by surface modification steps. During in vitro and in vivo testing, VEGF immobilized scaffolds elicited markedly enhanced vascular cell proliferation and angiogenic differentiation, as compared to non-treated groups. These results demonstrate that the developed scaffolds may represent an innovative paradigm in vascular tissue engineering by inducing angiogenesis as a means of remodeling and healing vascular defects for use in restorative procedures.

Preparing for the impacts of climate change, especially extreme rainfall events, is not a “one size fits all” process. Exhaustive case studies must be reported to understand the impact of c...

The purpose of this study was to identify and localize mucosal epithelial progenitor cells (EPCs) in the rat vagina. Rat vagina was obtained from f77emale Sprague-Dawley rats (12 weeks old, n = 20). To identify EPCs in vagina, we followed a single-cell isolation protocol and analyzed the number of cells staining positive for EPC markers by flow cytometry. The expression of EPC-specific markers (CD44, ERα, PR) was evaluated by immunofluorescence. As shown by confocal immunofluorescence, CD44/ERα double-labeled cells were mainly expressed in the basal cell and suprabasal cell layers. Immunofluorescent staining of CD44 was expressed in the plasma membrane of the vaginal epithelium, and ERα was expressed in the cytoplasm of the vaginal epithelium. The CD44/ERα double-positive cells were noted in the rat vagina by flow cytometric analysis. PR-labeled cells were localized in the intermediate layer of the epithelial space of the vagina. The results revealed the existence of EPCs in the vagina. These findings imply that resident EPCs may have a role in the regeneration of vaginal mucosa.

Microglia, resident macrophages of the central nervous system (CNS), is responsible for immune responses and homeostasis of the CNS. Microglia plays a complex role in neuroinflammation, which has been implicated in neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. Therefore, therapeutic agents that suppress the microglia-mediated inflammatory response could potentially be used in the prevention or treatment of neurodegenerative diseases. Vanillin, a primary component of vanilla bean extract, has anti-inflammatory, anticancer, and antitumor properties. However, the effects of vanillin on the anti-neuroinflammatory responses of microglial cells are still poorly understood. In this study, we investigated the mechanism by which vanillin induces anti-neuroinflammatory responses in lipopolysaccharide (LPS)-stimulated BV-2 microglial cells. We found that vanillin significantly decreased the production of nitric oxide and pro-inflammatory cytokines, including interleukin (IL)-1β, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6). Vanillin also reduced the protein levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), as well as the mRNA expression levels of IL-1β, TNF-α, and IL-6. Moreover, vanillin inhibited the phosphorylation of mitogen-activated protein kinases (MAPKs) and nuclear factor (NF)-κB. Collectively, these results suggest that vanillin has anti-neuroinflammatory properties and may act as a natural therapeutic agent for neuroinflammatory diseases.

Neuroinflammation resulting from microglial activation is involved in the pathogenesis of neurodegenerative diseases, including Parkinson's diseases. Microglial activation plays an important role in neuroinflammation and contributes to several neurological disorders. Hence, inhibition of both microglial activation and the generation of pro-inflammatory cytokines may lead to an effective treatment for neurodegenerative diseases. In the present study, the anti-neuroinflammatory effects of galangin were investigated in lipopolysaccharide (LPS)-stimulated BV-2 microglial cells. Galangin significantly decreased the generation of nitric oxide, interleukin-1β, and inducible nitric oxide synthase in LPS-stimulated BV-2 microglial cells. In addition, galangin inhibited the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase 1/2. Furthermore, it was observed that activation of both IκB-α and nuclear factor kappa B (NF-κB) was significantly increased following LPS stimulation, and this effect was suppressed by galangin treatment. In conclusion, galangin displayed an anti-neuroinflammatory activity in LPS-stimulated BV-2 microglial cells. Galangin inhibited LPS-induced neuroinflammation via the MAPK and NF-κB signaling pathways and might act as a natural therapeutic agent for the treatment of various neuroinflammatory conditions.

OBJECTIVES Inflammation is a primary response of the innate immune system against various infections. Macrophages are a type of immune cell that have a critical role in the inflammation. Recent studies reported that various natural compounds could regulate immune responses such as inflammation. Trans-cinnamaldehyde (TCA) is a natural compound from cinnamon, especially abundant in cinnamon bark. Previous studies reported that TCA has anti-biofilm, anti-microbial, and anti-cancer activities. However, the anti-inflammatory effects and the mechanism of TCA on macrophages are still unknown. MATERIALS AND METHODS Raw 264.7 murine macrophage cells were used in this study. Major assays were MTT, Griess assay, Western blot, enzyme-linked immunosorbent assay (ELISA) and reverse transcription (RT)-PCR analysis. RESULTS In this study, we investigated the anti-inflammatory effects of TCA on the RAW 264.7 murine macrophage cell line. TCA significantly decreased lipopolysaccharide (LPS)-induced nitric oxide (NO) production in a dose-dependent manner. Moreover, TCA treatment significantly reduced mRNA expression and protein expression of inducible NO synthase (iNOS) in LPS-stimulated macrophages in a dose-dependent manner. TCA treatment also diminished the mRNA expression level and secretion of IL-1β, IL-6 and TNF-α in LPS-activated macrophages. TCA elicited the anti-inflammatory effects by inhibiting ERK, JNK and p38 MPAKs phosphorylation in the cells. DISCUSSION AND CONCLUSION TCA elicits the anti-inflammatory effects on LPS-stimulated macrophage activation via suppression of MAPKs phosphorylation, and pro-inflammatory gene expression. Therefore, this study provides important information regarding the use of TCA as a candidate therapeutic agent against inflammation.

Thyroid cancer is the most common endocrine malignancy and can range in severity from relatively slow-growing occult differentiated thyroid cancer to uniformly aggressive and fatal anaplastic thyroid cancer. A subset of patients with papillary thyroid cancer present with aggressive disease that is refractory to conventional treatment. Myricetin is a flavonol compound found in a variety of berries as well as walnuts and herbs. Previous studies have demonstrated that myricetin exhibits anti-cancer activity against several tumor types. However, an anti-cancer effect of myricetin against human papillary thyroid cancer (HPTC) cells has not been established. The present investigation was undertaken to gain insights into the molecular mechanism of the anti-cancer activity of myricetin against HPTC cells. We examined the cytotoxicity, DNA damaging, and cell cycle arresting activities of myricetin using SNU-790 HPTC cells. We found that myricetin exhibited cytotoxicity and induced DNA condensation in SNU-790 HPTC cells in a dose-dependent manner. Moreover, myricetin up-regulated the activation of caspase cascades and the Bax:Bcl-2 expression ratio. In addition, myricetin induced the release of apoptosis-inducing factor (AIF) and altered the mitochondrial membrane potential. Our results suggest that myricetin induces the death of SNU-790 HPTC cells and thus may prove useful in the development of therapeutic agents for human thyroid cancers.

Introduction Stress can lead to poor sleep and compromise immune function and it is important to identify approaches that can address such problems and improve quality of life. The aim of this randomized controlled trial was to examine whether aromatherapy via inhalation of essential oils could relieve perceived stress, depression, and improve sleep quality, and immune function. Methods Subjects aged 20–60 years responding to a recruitment advertisement posted in a general hospital were randomly assigned into either an aromatherapy group (n = 30) or a waiting list control group (n = 30). The subjects in the experimental treatment were asked to inhale an essential oil blend of lemon, eucalyptus, tea tree, and peppermint in a ratio of 4:2:2:1. The essential oil blend was inhaled by wearing a pendant during the day and sleeping near an aromatherapy stone at night for four weeks. Perceived stress, stress index, autonomic nervous system (ANS) activation, and glycated hemoglobin (HbA1c) levels were measured to examine stress. In addition, depression was measured using the Center for Epidemiologic Studies Depression Scale (CES-D). Sleep quality and immune state were also measured. Results The aromatherapy group had significantly lower perceived stress levels (p Conclusions In conclusion, inhalation of essential oils as per aromatherapy, resulted in lower perceived stress and depression, as well as better sleep quality, but did not influence physiological parameters, such as the stress index or immune state.

Aim Thyroid cancer is the most common endocrine malignancy, with an increasing incidence worldwide. Most thyroid cancers are well differentiated and have a favorable outcome. However, undifferentiated thyroid cancers are one of the most lethal human malignancies. Anaplastic thyroid cancer (ATC) accounts for 2% of all thyroid cancers, and its median survival rate is low. ATC is responsible for more than one-third of thyroid cancer-related deaths. Myricetin is a flavonol compound found in walnuts, herbs, and various berries and is known to induce apoptotic death of various types of cancer cells. However, an anticancer effect of myricetin against human anaplastic thyroid cancer (HATCs) cells has not been demonstrated. Materials and methods In the present study, the anticancer effects and mechanism of action of myricetin were examined using SNU-80 HATC cells. SNU-80 HATC cells were treated with various concentrations of myricetin and compared with untreated controls. Results Myricetin significantly reduced HATC cell proliferation, by approximately 70%. A substantial proportion of dead cells exhibited arrest in the sub-G1 phase. Myricetin also exhibited cytotoxicity and induced DNA condensation in SNU-80 HATC cells in a dose-dependent manner. The mechanism of myricetin-induced cell death involved an increase in the activation of caspase cascades and the Bax:Bcl-2 ratio at a concentration of 100 μM. Myricetin also induced the release of apoptosis-inducing factor (AIF) from mitochondria into the cytosol and altered the mitochondrial membrane potential. Conclusion Our results indicate that myricetin is a potent inducer of HATC cell death and may thus prove useful in the development of therapeutic agents for HATC.

Bee venom (BV), also known as apitoxin, is widely used in traditional oriental medicine to treat immune-related diseases. Recent studies suggest that BV could be beneficial for the treatment of neurodegenerative diseases. Parkinson's disease (PD) is the second most common neurodegenerative disease next to Alzheimer's disease, and PD pathologies are closely associated with neuroinflammation. Previous studies have suggested the neuroprotective effects of BV in animal models of PD are due to the modulation of inflammation. However, the molecular mechanisms responsible for the anti-neuroinflammatory effect of BV have not been elucidated in astrocytes. Here, the authors investigated the neuroprotective effects of BV and pramipexole (PPX; a positive control) in a subchronic MPTP-induced murine PD model. Both BV and PPX prevented MPTP-induced impairments in motor performance and reduced dopaminergic neuron loss, and furthermore, these neuroprotective effects of BV and PPX were found to be associated with reduced astroglial activation in vivo PD model. However, in MPP(+) treated primary cultured astrocytes, BV modulated astrocyte activation, whereas PPX did not, indicating that the neuroprotective effects of PPX were not mediated by neuroinflammation. These findings suggest that BV should be considered a potential therapeutic or preventive agent for PD and other neuroinflammatory associated disorders.

// Daeui Park 1,2,3 , Byoung-Chul Kim 1,2 , Chul-Hong Kim 4 , Yeon Ja Choi 1 , Hyoung Oh Jeong 1 , Mi Eun Kim 5 , Jun Sik Lee 5 , Min Hi Park 1 , Ki Wung Chung 1 , Dae Hyun Kim 1 , Jaewon Lee 1 , Dong-Soon Im 1 , Seokjoo Yoon 2,3 , Sunghoon Lee 6 , Byung Pal Yu 7 , Jong Bhak 6 and Hae Young Chung 1 1 Molecular Inflammation Research Center for Aging Intervention, Pusan National University, Busan, Korea 2 Department of Predictive Toxicology, Korea Institute of Toxicology, Daejeon, Korea 3 Human and Environmental Toxicology, School of Engineering, University of Science and Technology, Daejeon, Korea 4 GenomicTree Inc., Yuseong-gu, Daejeon, Korea 5 Department of Biology, College of Natural Sciences, Chosun University, Gwangju, Korea 6 Personal Genomics Institute,Genome Research Foundation, Suwon, Korea 7 Department of Physiology, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA Correspondence to: Hae Young Chung, email: // Jong Bhak, email: // Keywords : aging; inflammation; RNA-Seq; differentially expressed genes; novel genes; alternative splicing, Gerotarget Received : October 05, 2015 Accepted : April 18, 2016 Published : May 03, 2016 Abstract Age-related dysregulated inflammation plays an essential role as a major risk factor underlying the pathophysiological aging process. To better understand how inflammatory processes are related to aging at the molecular level, we sequenced the transcriptome of young and aged rat kidney using RNA-Seq to detect known genes, novel genes, and alternative splicing events that are differentially expressed. By comparing young (6 months of age) and old (25 months of age) rats, we detected 722 up-regulated genes and 111 down-regulated genes. In the aged rats, we found 32 novel genes and 107 alternatively spliced genes. Notably, 6.6% of the up-regulated genes were related to inflammation ( P < 2.2 × 10 -16 , Fisher exact t-test); 15.6% were novel genes with functional protein domains ( P = 1.4 × 10 -5 ); and 6.5% were genes showing alternative splicing events ( P = 3.3 × 10 -4 ). Based on the results of pathway analysis, we detected the involvement of inflammation-related pathways such as cytokines ( P = 4.4 × 10 -16 ), which were found up-regulated in the aged rats. Furthermore, an up-regulated inflammatory gene analysis identified the involvement of transcription factors, such as STAT4, EGR1, and FOSL1, which regulate cancer as well as inflammation in aging processes. Thus, RNA changes in these pathways support their involvement in the pro-inflammatory status during aging. We propose that whole RNA-Seq is a useful tool to identify novel genes and alternative splicing events by documenting broadly implicated inflammation-related genes involved in aging processes.

PURPOSE The purpose of this study was to investigate the effects of aromatherapy on sleep quality. METHODS This is a systematic review of randomized controlled trial studies (PROSPERO registration number CRD42017064519). In this study, the PICO were adults and the elderly, aromatherapy intervention, a comparative intervention with the control and placebo oil groups, and sleep. The selected articles were in English, Korean, and Chinese. RESULTS The results of the meta-analysis showed that the effect sizes of the experimental group were 1.03 (n=763, SMD=1.03, 95% CI 0.66 to 1.39) (Z=5.47, p

Forkhead box O(FoxO) is a transcription factor which is involved in cell cycle progression, cell survival and DNA-repair. Dendritic cells(DCs) are professional antigen-presenting cells which present the antigens to T lymphocytes and regulate the adaptive immunity. Previous studies indicated that FoxO1 and 3 are plays a critical role in DC maturation and DC-T cell interaction. FoxO6, a member of FoxO family, is less attended than other FoxO families, because limited expression region of FoxO6. Also, the effect of FoxO6 is still unknown. Here, we investigated the effect of FoxO6 in dendritic cells. Phosphorylated FoxO6 is increased and acetylated FoxO6 is decreased during dendritic cell differentiation. Moreover, deficiency of Foxo6 altered antigen capacity of dendiritc cells. Therefore, we expect that FoxO6 has important role in DC differentiation and maturation, and will further investigate the functions and the mechanisms of FoxO6 on DC. And alteration of FoxO6 expression level had effect on DCs maturation.

B7H3 is a new molecule that can regulate T cells-mediated immune responses. Several studies suggested a costimulatory function for B7-H3 in murine models of cancer. In contrast, clinical association of B7-H3 expression suggested a coinhibitory role. The physiological role of B7-H3 is still unclear. To investigate the B7-H3 functions on T cell activation, we used the B7-H3 peptide, B7-H3 negative and overexpressed tumor cells. To establish the T cell inhibitory gene database by B7-H3, we performed the microarray. In the results, B7-H3 inhibited the T cell proliferation and production of cytokines including IL-2 and IFN-γ. We identified the 12 significant effective genes, and confirm the mRNA expression by real-time PCR. These results suggest that B7-H3 showed the co-inhibitory role on T cell functions. And further study is needed to identify the receptor and mechanism of B7-H3 on T cell function.

We previously isolated pseudane-VII from the secondary metabolites of Pseudoalteromonas sp. M2 in marine water, and demonstrated its anti-inflammatory efficacy on macrophages. However, the molecular mechanism by which pseudane-VII suppresses neuroinflammation has not yet been elucidated in brain microglia. Microglia is activated by immunological stimulation or brain injury. Activated microglia secrete proinflammatory mediators which damage neurons. Neuroinflammation appears to be associated with certain neurological diseases, including Parkinson&rsquo, s disease and Alzheimer&rsquo, s disease. Natural compounds that suppress microglial inflammatory responses could potentially be used to prevent neurodegenerative diseases or slow their progression. In the present study, we found that pseudane-VII suppresses neuroinflammation in lipopolysaccaride (LPS)-stimulated BV-2 microglial cells and brain. Pseudane-VII was shown to inhibit the LPS-stimulated NO, ROS production and the expression of iNOS and COX-2. To identify the signaling pathway targeted by pseudane-VII, we used western blot analysis to assess the LPS-induced phosphorylation state of p38, ERK1/2, JNK1/2, and nuclear factor-kappaB (NF-&kappa, B). We found that pseudane-VII attenuated LPS-induced phosphorylation of MAPK and NF-&kappa, B. Moreover, administration of pseudane-VII in mice significantly reduced LPS-induced iNOS expression and microglia activation in brain. Taken together, our findings suggest that pseudane-VII may represent a potential novel target for treatment for neurodegenerative diseases.

Skin inflammation and dermal injuries are a major clinical problem because current therapies are limited to treating established scars, and there is a poor understanding of healing mechanisms. Mussel adhesive proteins (MAPs) have great potential in many tissue engineering and biomedical applications. It has been successfully demonstrated that the redesigned hybrid type MAP (fp-151) can be utilized as a promising adhesive biomaterial. The aim of this study was to develop a novel recombinant protein using fp-151 and vitronectin (VT) and to elucidate the anti-inflammatory effects of this recombinant protein on macrophages and keratinocytes.Lipopolysaccharide (LPS) was used to stimulate macrophages and UVB was used to stimulate keratinocytes. Inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 were analyzed by Western Blot. Inflammatory cytokines and NO and ROS production were analyzed.In macrophages stimulated by LPS, expression of the inflammatory factors iNOS, COX-2, and NO production increased, while the r-fp-151-VT-treated groups had suppressed expression of iNOS, COX-2, and NO production in a dose-dependent manner. In addition, keratinocytes stimulated by UVB and treated with r-fp-151-VT had reduced expression of iNOS and COX-2. Interestingly, in UVB-irradiated keratinocytes, inflammatory cytokines, such as interleukin (IL)-1b, IL-6, and tumor necrosis factor (TNF)-a, were significantly reduced by r-fp-151-VT treatment.These results suggest that the anti-inflammatory activity of r-fp-151-VT was more effective in keratinocytes, suggesting that it can be used as a therapeutic agent to treat skin inflammation.

Objective To investigate the effects of testosterone on cavernosal endothelial progenitor cells (EPCs) in a castrated rat model. Materials and methods In all, 45 male Sprague–Dawley rats (12-weeks old) were divided into control, surgical castration, and castration with testosterone replacement groups. The rats were castrated under ketamine anaesthesia, and testosterone was administered by daily subcutaneous injection of 3 mg/kg testosterone propionate. The corpus cavernosum was obtained after perfusion with 10 mL saline via the abdominal aorta 4 weeks later. The expression of EPC-specific markers [cluster of differentiation 34 (CD34), fetal liver kinase 1 (Flk1), and vascular endothelial (VE)-cadherin] was evaluated by flow cytometry analysis and immunofluorescence staining. Results CD34+/Flk1+ and CD34+/VE-cadherin+ cells were detected in the cavernosal sinusoidal endothelial space. Flow cytometry analysis showed that CD34 and Flk1 double positive cells (EPCs) comprised ≈3.79% of the corpus cavernosum in normal rats. The percentage of EPC marker-positive cells decreased significantly in the castration group (2.8%; P < 0.05) and was restored to 3.56% after testosterone supplementation. Confocal microscopy revealed that the numbers of CD34+/Flk1+ and CD34+/VE-cadherin+ cells decreased in castrated rats compared with controls, but were similar to control levels in rats receiving testosterone replacement. Conclusions The EPC markers were expressed in the cavernosal sinusoidal endothelial space, and the numbers of resident EPCs were regulated by testosterone. These results suggest that testosterone replacement therapy may improve erectile function by modulating EPCs in patients with hypogonadism.

The inflow of nonpoint pollution sources due to sustainable development and urbanization is gradually increasing and causes a diversity of water pollution. There are lots of difficulties to find a solution as the problems related to variation of hydrological and natural phenomenon. A differentiated method to estimate the nonpoint pollution sources has been proposed using rainfall and characteristics of urbanization and observed data from sewage treatment districts in the study. The types of nonpoint pollution sources on an assumption of combined sewer system have been classified as three types which are inflow of rainfall, bypass of sewage treatments, and combined sewer overflows from a river. Three types for estimation of nonpoint pollution sources applied more accurately to generate a amount of nonpoint pollution loads. This study is expecting a wide application for effective water resource management on TMDL (total maximum delivery load) unit watershed and sewage treatment districts.

In recent, the impacts of urbanization on hydrology and water quality can be minimized with the use of Low Impact Development (LID) practices in urban areas. But, there are no ways to verify or to show the quantitative effectiveness with LID practices. This study designed and developed to perform experiments in natural or artificial representation of hydrological cycle, which is called rainfall-runoff simulator to be able to quantify factors in hydrological system. This simulator was applied to a pervious pavement block. The study conducted analysis of effectiveness for a pervious pavement block by comparing the results with a general pavement block. The result from the pervious pavement block showed remarkably reduction effect on surface runoff with increase of rainfall intensity and more duration time. Also, the simulator was possible to control no surface runoff by a rainfall intensity at 50 mm/hr for an hour. The research indicated possibility and effectiveness for LID practices. This might be widely available to apply to LID practices verification. Therefore, the study is possible to make use of practical standards on fundamental studies.

Objective Menstrual pain is not a disease, but it is a problem that periodically makes women uncomfortable during menstrual cycles. There has been a continuing effort to alleviate menstrual cramps in the medical field. Aromatherapy, one of the alternative complementary therapies, has been used as a way to alleviate menstrual cramps, but there is still little evidence of how to use it. Therefore, in this study, we tried to find and provide the evidence of relieving effects of menstrual cramps. Design This study involved a systematic review and meta-analysis. The study was to identify the effects of aromatherapy on menstrual pain through a systematic review of the relevant literature from Korea and abroad and a meta-analysis of the data from studies meeting our inclusion criteria. Data sources We obtained articles published in English from PubMed, the Cumulative Index to Nursing and Allied Health Literature (CINAHL), and the Cochrane Central Register of Controlled Trials (CENTRAL), and we also obtained articles by searching the Korean databases Research Information Service System (RISS), DBPIA, and Korean Studies Information Service System (KISS). Review methods A systematic review was performed on all searchable articles published form inception to October 17, 2016, using the international and Korean databases noted above. The search terms used was ((aromatherapy OR aroma* OR essential oil) AND (dysmenorrhea OR menstrual pain)). Articles were selected for analysis from among the retrieved articles based on the key questions and the inclusion and exclusion criteria using a PRISMA flow diagram. The 21 articles entire texts were reviewed and qualitatively analyzed while seven articles were quantitatively analyzed using RevMan software ver. 5.3. Results In a comparison between the experimental groups, which received an aromatherapy intervention, and the control groups, which received no treatment of any kind, the dysmenorrhea score in the experimental group decreased by 2.67 points (mean difference −2.67), showing a statistically significant difference(Z = 7.79, p 2 = 0%). Compared to the placebo group, which received a placebo oil treatment, the dysmenorrhea score in the experimental group decreased by 1.71 points (mean difference, −1.71), showing a statistically significant difference (Z = 4.51, p 2 = 81%). Conclusions Aromatherapy was an effective intervention for reducing dysmenorrhea. However, because the analysis showed that the aroma intervention methods were diverse and that the basis for the intervention methods was weak, the possibility of randomization bias was high.

Inflammation is the major symptom of the innate immune response to microbial infection. Macrophages, immune response-related cells, play a role in the inflammatory response. Galangin is a member of the flavonols and is found in Alpinia officinarum, galangal root and propolis. Previous studies have demonstrated that galangin has antioxidant, anticancer, and antineoplastic activities. However, the anti-inflammatory effects of galangin are still unknown. In this study, we investigated the anti-inflammatory effects of galangin on RAW 264.7 murine macrophages. Galagin was not cytotoxic to RAW 264.7 cells, and nitric oxide (NO) production induced by lipopolysaccharide (LPS)-stimulated macrophages was significantly decreased by the addition of 50 μM galangin. Moreover, galangin treatment reduced mRNA levels of cytokines, including IL-1β and IL-6, and proinflammatory genes, such as iNOS in LPS-activated macrophages in a dose-dependent manner. Galangin treatment also decreased the protein expression levels of iNOS in activated macrophages. Galangin was found to elicit anti-inflammatory effects by inhibiting ERK and NF-κB-p65 phosphorylation. In addition, galangin-inhibited IL-1β production in LPS-activated macrophages. These results suggest that galangin elicits anti-inflammatory effects on LPS-activated macrophages via the inhibition of ERK, NF-κB-p65 and proinflammatory gene expression.

Inflammation is major symptom of the innate immune response by infection of microbes. Macrophages, one of immune response related cells, play a role in inflammatory response. Recent studies reported that various natural products can regulate the activation of immune cells such as macrophage. Sargassum horneri (Turner) C. Agardh is one of brown algae. Recently, various seaweeds including brown algae have antioxidant and anti-inflammatory effects. However, anti-inflammatory effects of Sargassum horneri (Turner) C. Agardh are still unknown. In this study, we investigated anti-inflammatory effects of ethanolic extract of Sargassum horneri (Turner) C. Agardh (ESH) on RAW 264.7 murine macrophage cell line. The ESH was extracted from dried Sargassum horneri (Turner) C. Agardh with 70% ethanol and then lyophilized at -40 °C. ESH was not cytotoxic to RAW 264.7, and nitric oxide (NO) production induced by LPS-stimulated macrophage activation was significantly decreased by the addition of 200 μg/mL of ESH. Moreover, ESH treatment reduced mRNA level of cytokines, including IL-1β, and pro-inflammatory genes such as iNOS and COX-2 in LPS-stimulated macrophage activation in a dose-dependent manner. ESH was found to elicit anti-inflammatory effects by inhibiting ERK, p-p38 and NF-κB phosphorylation. In addition, ESH inhibited the release of IL-1β in LPS-stimulated macrophages. These results suggest that ESH elicits anti-inflammatory effects on LPS-stimulated macrophage activation via the inhibition of ERK, p-p38, NF-κB, and pro-inflammatory gene expression.