Objective: This study was to evaluate the effectiveness of an individually tailored program based on self-measurement of blood glucose on health behavior and HbA1c in diabetes and pre-diabetes patients. Methods: The program consisted of seven sessions for 12 weeks which were carried out every two weeks. Almost all sessions were progressed on untact method except for the first and last session. The 71 subjects were assessed for their knowledge of diabetes, health behavior, the experience of self-measurement of blood glucose, body mass Index (BMI) and hemoglobin A1c (HbA1c) at before and after the program. They were also evaluated on their degree of utilization of blood glucose measurements after the program. Results: Each mean score on their knowledge of diabetes, health behavior and the experience of self-measurement of blood glucose was significantly increased from 14.77, 25.50, and 2.70 to 15.41, 28.40, and 4.81, respectively. Each mean score on both BMI and HbA1c (n=53) was significantly decreased from 24.47kg/m2 and 7.27% to 24.01kg/m2 and 6.67%, respectively. The post-HbA1c had a significant negative correlation(r=-0.415) with the degree of utilization of blood glucose measurements. The degree of utilization of blood glucose measurements had a significant positive correlation(r=0.581) with post-health behavior. Conclusions The program shows effectiveness in improving HbA1c in Type 2 diabetes and pre-diabetes patients. The post-HbA1c might be related to the degree of utilization of blood glucose measurements which might be related to the health behavior.

Background: Psoriasis is a chronic inflammatory skin disease. The etiology of psoriasis is not fully understood, but the genetic background is considered to be the most important factor. To date, many psoriasis-related genes have been discovered, but the role of many important genes has not been well understood. Objective: The purpose of this study is to uncover possible roles of MDA5 in psoriasis. Methods: Expression of MDA5 was investigated using immunohistochemistry. Then, MDA5 was overexpressed in keratinocytes using a recombinant adenovirus. Results: As a result of immunohistochemical staining, the expression of MDA5 was significantly increased in the epidermis of psoriasis compared to normal skin. Similarly, the expression of MDA5 was increased in imiquimod-induced psoriasiform dermatitis model. In cultured keratinocytes, toll-like receptor 3 agonist poly(I:C) induced expression of MDA5 at both mRNA and protein levels. When MDA5 was overexpressed using a recombinant adenovirus, poly(I:C)-induced cytokine expression was significantly increased. Finally, MDA5 overexpression significantly inhibited calcium-induced differentiation of keratinocytes. Conclusion These results suggest that MDA5 increases in psoriasis and negatively regulates keratinocyte differentiation.

Background: Psoriasis is a chronic inflammatory skin disease. The etiology of psoriasis is not fully understood, but the genetic background is considered to be the most important factor. To date, many psoriasis-related genes have been discovered, but the role of many important genes has not been well understood. Objective: The purpose of this study is to uncover possible roles of MDA5 in psoriasis. Methods: Expression of MDA5 was investigated using immunohistochemistry. Then, MDA5 was overexpressed in keratinocytes using a recombinant adenovirus. Results: As a result of immunohistochemical staining, the expression of MDA5 was significantly increased in the epidermis of psoriasis compared to normal skin. Similarly, the expression of MDA5 was increased in imiquimod-induced psoriasiform dermatitis model. In cultured keratinocytes, toll-like receptor 3 agonist poly(I:C) induced expression of MDA5 at both mRNA and protein levels. When MDA5 was overexpressed using a recombinant adenovirus, poly(I:C)-induced cytokine expression was significantly increased. Finally, MDA5 overexpression significantly inhibited calcium-induced differentiation of keratinocytes. Conclusion These results suggest that MDA5 increases in psoriasis and negatively regulates keratinocyte differentiation.

Purpose: Chronic rhinosinusitis with nasal polyps (CRSwNP) is a complex inflammatory disease of the nasal and paranasal sinus mucosa. The disease is associated with mitochondrial dysfunction, structural changes in the mitochondria, and reactive oxygen species (ROS) generation. This study investigated whether there are functional and morphological changes in the mitochondria in the epithelial cells of nasal polyps (NPs) and Staphylococcus aureus enterotoxin B (SEB)-stimulated nasal epithelial cells. Methods: In all, 30 patients with CRSwNP and 15 healthy subjects were enrolled. Mitochondrial ROS (mtROS) and changes in mitochondrial functions and structures were investigated in the uncinate tissue (UT) of healthy controls, the UT or NPs of CRSwNP patients, and human nasal epithelial cells with or without SEB stimulation. Results: Oxidative phosphorylation complexes showed various responses following SEB stimulation in the nasal epithelial cells, and their expressions were significantly higher in the NPs of patients with CRSwNP than in the UT of controls. Generation of mtROS was increased following SEB exposure in nasal epithelial cells and was reduced by pretreatment with MitoTEMPO, which is used as an mtROS scavenger. In the tissues, mtROS was significantly increased in the NPs of CRSwNP patients compared to the UT of controls or CRSwNP patients. The expressions of fusion- and fission-related molecules were also significantly higher in SEB-exposed nasal epithelial cells than in non-exposed cells. In tissues, the expression of fission (fission mediator protein 1)- and fusion (membrane and mitofusin-1, and optic atrophy protein 1)-related molecules was significantly higher in the NPs of CRSwNP patients than in UT of controls or CRSwNP patients. Transmission electron microscopy revealed elongated mitochondria in SEB-exposed nasal epithelial cells and epithelial cells of NPs. Conclusions Production of mtROS, disrupted mitochondrial function, and structural changes in nasal epithelial cells might be involved in the pathogenesis of CRSwNP.

Purpose: Chronic rhinosinusitis with nasal polyps (CRSwNP) is a complex inflammatory disease of the nasal and paranasal sinus mucosa. The disease is associated with mitochondrial dysfunction, structural changes in the mitochondria, and reactive oxygen species (ROS) generation. This study investigated whether there are functional and morphological changes in the mitochondria in the epithelial cells of nasal polyps (NPs) and Staphylococcus aureus enterotoxin B (SEB)-stimulated nasal epithelial cells. Methods: In all, 30 patients with CRSwNP and 15 healthy subjects were enrolled. Mitochondrial ROS (mtROS) and changes in mitochondrial functions and structures were investigated in the uncinate tissue (UT) of healthy controls, the UT or NPs of CRSwNP patients, and human nasal epithelial cells with or without SEB stimulation. Results: Oxidative phosphorylation complexes showed various responses following SEB stimulation in the nasal epithelial cells, and their expressions were significantly higher in the NPs of patients with CRSwNP than in the UT of controls. Generation of mtROS was increased following SEB exposure in nasal epithelial cells and was reduced by pretreatment with MitoTEMPO, which is used as an mtROS scavenger. In the tissues, mtROS was significantly increased in the NPs of CRSwNP patients compared to the UT of controls or CRSwNP patients. The expressions of fusion- and fission-related molecules were also significantly higher in SEB-exposed nasal epithelial cells than in non-exposed cells. In tissues, the expression of fission (fission mediator protein 1)- and fusion (membrane and mitofusin-1, and optic atrophy protein 1)-related molecules was significantly higher in the NPs of CRSwNP patients than in UT of controls or CRSwNP patients. Transmission electron microscopy revealed elongated mitochondria in SEB-exposed nasal epithelial cells and epithelial cells of NPs. Conclusions Production of mtROS, disrupted mitochondrial function, and structural changes in nasal epithelial cells might be involved in the pathogenesis of CRSwNP.

Background: Psoriasis is a common chronic inflammatory skin disease. The development of psoriasis is dependent on many intercellular events such as innate immunity and T cell-mediated inflammation. Furthermore, genetic factors are strongly implicated in the pathophysiology of psoriasis. Although a variety of susceptible genes are identified, it is likely that many important genes remain undisclosed. Objective: The aim of this study is to investigate the possible role of lysine demethylase 2A (KDM2A) in the pathophysiology of psoriasis. Methods: We examined the expression of KDM2A using a well established imiquimod-induced psoriasiform dermatitis model. Results: Immunohistochemistry analysis showed that expression of KDM2A was increased in imiquimod-induced psoriasiform dermatitis. Consistent with this result, KDM2A level was markedly increased in the epidermis of psoriatic patient. When keratinocytes were stimulated with TLR3 agonist poly(I:C), KDM2A was increased at both the mRNA and protein levels. Poly(I:C) increased the expression of psoriasis-related cytokines including tumor necrosis factor-α, interleukin-8, and CCL20, and KDM2A inhibitor daminozide enhanced the poly(I:C)-induced cytokine expression. Finally, topical co-application of imiquimod and daminozide exacerbated the imiquimod-induced psoriasiform dermatitis. Conclusion Together, these results suggest that KDM2A is increased to negatively regulate the inflammatory reaction of epidermal keratinocytes in psoriasis.

Eosinophilic granulomatosis with polyangiitis (EGPA, also known as the Churg-Strauss syndrome) is a disorder characterized by asthma, peripheral eosinophilia and systemic vasculitis. It rarely occurs in children, so that physicians may frequently mistake it for a simple uncontrolled asthma. Since a subsequent cardiac involvement is critical for the prognosis, it is important to suspect EGPA in children with severe, uncontrolled asthma. The cardiac manifestations in EGPA are variable from asymptomatic electrocardiogram abnormalities to pericarditis with pericardial effusion, myocarditis with cardiomyopathy, heart failure, and sudden cardiac death. Although delayed treatment may lead to fatal cardiac complications in EGPA, adequate immune suppression can reverse cardiac impairment. We report a 14-year-old girl with persistent asthma refractory to steroids who was eventually diagnosed with an anti-neutrophil cytoplasmic antibody-negative EGPA.
Adolescent ; Asthma ; Cardiomyopathies ; Child ; Churg-Strauss Syndrome ; Cytoplasm ; Death, Sudden, Cardiac ; Electrocardiography ; Eosinophilia ; Eosinophils ; Female ; Granulomatosis with Polyangiitis ; Heart Failure ; Heart ; Humans ; Myocarditis ; Pericardial Effusion ; Pericarditis ; Prognosis ; Steroids ; Systemic Vasculitis

PURPOSE: This study was a systematic review and meta-analysis to explore the factors related to quality of life in heart transplant recipients. METHODS: To identify studies that suggested the factors related to the quality of life in heart transplant recipients, we searched the articles published from 1974 to November 2018 using Six databases, PubMed, CINAHL, EMBASE, Cochrane, KMBASE and RISS. A total of 22 studies were selected out of 5,234 for the systematic review and meta-analysis on the basis of the PRISMA flow. The quality of study was assessed by assessment tool form the NIH and meta-analysis was performed using the ‘R 3.5.2’ version to analyze the correlated effect sizes. RESULTS: Factors related to quality of life in heart transplant recipients were categorized into six domains based on the health-related quality of life model introduced by Ferrans: individual, environmental, biological function, symptoms, functional status, and general health perception. In the meta-analysis, 34 factors were used and 17 factors having significant effect sizes were as follows: self-efficacy, demoralization, perceived control, current occupational status, age, marital status, health promotion life style in the individual characteristics; stress in environmental characteristics; physical function status, creatinine level, left ventricular ejection fraction (LVEF) in biological function; anxiety, depression, symptom frequency and distress in symptoms domain; coping, self-care compliance in functional status. CONCLUSION The findings indicate that the multi-dimensional factors influencing the quality of life in heart transplant recipients and provide the evidence for developing effective interventions for improving the quality of life of recipients.

BACKGROUND: Skin hydration is a common problem both in elderly and young people as dry skin may cause irritation, dermatological disorders, and wrinkles. While both genetic and environmental factors seem to influence skin hydration, thorough genetic studies on skin hydration have not yet been conducted. OBJECTIVE: We used a genome-wide association study (GWAS) to explore the genetic elements underlying skin hydration by regulating epidermal differentiation and skin barrier function. METHODS: A GWAS was conducted to investigate the genetic factors influencing skin hydration in 100 Korean females along with molecular studies of genes in human epidermal keratinocytes for functional study in vitro. RESULTS: Among several single nucleotide polymorphisms identified in GWAS, we focused on Single Stranded DNA Binding Protein 3 (SSBP3) which is associated with DNA replication and DNA damage repair. To better understand the role of SSBP3 in skin cells, we introduced a calcium-induced differentiation keratinocyte culture system model and found that SSBP3 was upregulated in keratinocytes in a differentiation dependent manner. When SSBP3 was overexpressed using a recombinant adenovirus, the expression of differentiation-related genes such as loricrin and involucrin was markedly increased. CONCLUSION: Taken together, our results suggest that genetic variants in the intronic region of SSBP3 could be determinants in skin hydration of Korean females. SSBP3 represents a new candidate gene to evaluate the molecular basis of the hydration ability in individuals.
Adenoviridae ; Aged ; Cell Differentiation ; DNA Damage ; DNA Replication ; DNA, Single-Stranded* ; DNA-Binding Proteins* ; Female ; Genome-Wide Association Study ; Humans ; In Vitro Techniques ; Introns ; Keratinocytes ; Polymorphism, Single Nucleotide ; Skin*