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Abstract The influence of body fat on arterial stiffness remains controversial. This study was performed to investigate the associations between four different types of body fat parameters and brachial-ankle pulse wave velocity (baPWV). A total of 3758 subjects (mean age, 53.4 ± 8.8 years; females, 36.3%) who underwent health check-up were retrospectively analyzed. Anthropometric parameters including body mass index (BMI), waist circumference (WC) and waist–hip ratio (WHR) were assessed, and visceral fat area (VFA) was calculated by bioelectrical impedance analysis. In simple linear correlation analyses, baPWV was associated with WC, WHR and VFA (P 0.05 for each). Even after controlling for potential confounders, higher baPWV was significantly associated not only with higher WHR [for > 0.90 in men and > 0.85 in women: odds ratio (OR), 1.23; 95% confidence interval (CI), 1.06–1.42; P = 0.005; for the highest tertile compared to the lowest tertile: OR, 1.38; 95% CI, 1.15–1.66; P

Background/Aims: Ulcerative colitis (UC) is an inflammatory bowel disease for which new serological markers are required. The purpose of this study was to assess the role of the mucosa-associated epithelial chemokine CCL28 in UC. Methods: The study included 50 patients; of these, 25 were patients with UC, and 25 were healthy controls. The levels of serum CCL28 were analyzed using enzyme-linked immunosorbent assay. CCL28 expression was analyzed by immunohistochemistry (IHC) in 15 representative colon tissues biopsied based on disease activity (UC patients with severe activity, five samples; UC patients with mild activity, five samples; healthy controls, five samples). Results: The serum CCL28 levels were remarkably higher (p

Abstracts Background Lymph node (LN) metastasis is negligible in early gastric cancer (EGC) within expanded criteria for endoscopic submucosal dissection (ESD). However, regional lymph nodes in abdominal CT scans are sometimes enlarged in patients with EGC within the expanded criteria for endoscopic submucosal dissection (ESD). In this study, we investigated the clinical significance of regional lymph node enlargement on abdominal CT scan in patients with EGC within the expanded criteria for ESD. Methods From December 2010 to April 2015, among 301 patients with EGC within the ESD expanded criteria, 47 patients with regional lymph node enlargement shown by abdominal CT scan were prospectively enrolled. We performed surgical resection or periodic follow-up with abdominal CT scans and upper endoscopy every 6 months to evaluate whether the enlarged lymph nodes are due to metastasis or a reactive change. Results The mean age of the 47 patients (38 males, 9 female) was 64.8 years. The enlarged lymph nodes were usually single (26/47, 44.6%) and sized as follows: 11 nodes were ≤ 5 mm, 19 were 6–10 mm, and 17 were ≥ 10 mm. Four of the 47 patients initially underwent surgical resection, and 8 patients underwent surgical resection after ESD. However, there was no lymph node metastasis in surgical specimens. Thirty-five patients received ESD and periodically followed up at a median duration of 56 months (IQR: 44–59 month). The enlarged lymph node disappeared in 12 of 35 patients, decreased in 9 patients and remained the same size in 13 patients, and increased in 1 patient. Conclusion Regional lymph node enlargement on abdominal CT scan in patients within expanded criteria for ESD of ECG may be not due to metastasis but a reactive change.

Background/Aims: Public hospitals were established to provide high quality medical services to low socioeconomic status patients. This study examined the effects of public hospitals on the treatment and prognosis of patients with five-major gastrointestinal (GI) cancers (stomach cancer, colon cancer, liver cancer, bile duct cancer, and pancreatic cancer). Methods: Among the 1,268 patients treated at Seoul National University Boramae Medical Center from January 2010 to December 2017, 164 (13%) were in the medicare group. The data were analyzed to identify and compare the clinical manifestations, treatment modality, and clinical outcomes between the groups. Results: No statistically significant differences in the clinical data (age, sex), treatment method, and five-year survival rate were observed between the health insurance group and medicare group in the five major GI cancer patients. On the other hand, some medicare group patients tended more comorbidities and fewer treatment options than health insurance patients. Conclusions: Public hospitals have a positive effect on the treatment and prognosis in medicare group patients with the five-major GI cancers.

Monolithic perovskite/Si tandem solar cells have attracted particular interest because of the potential to achieve high power conversion efficiencies. However, tandem cells require the use of textured Si substrates for efficient light harvesting, and conformal deposition of the perovskite absorption layer on textured Si substrates remains challenging. Here, we introduce a process to prepare a conformal methylammonium lead iodide (MAPbI3) film on the various substrates regardless of their morphologies via the electrodeposition followed by vapor reaction. First, PbO2 films were electrodeposited on the planar indium tin oxide/NiO substrates in aqueous electrolyte, with their thickness and grain size controlled by adjusting the potential and reaction time. XPS and XRD analyses confirmed that the PbO2 film was fully reduced to PbO by annealing under a reducing atmosphere. Finally, the PbO films were converted into conformal MAPbI3 via MAI vapor reaction for 25 min at 180 °C. We also demonstrated that the PbO2 films could be evenly deposited on textured Si/ITO substrates using pulsed electrodeposition and were then converted into conformal MAPbI3 using the same vapor reaction process. The proposed approach thus provides a novel route for the preparation of high-quality perovskite films on both planar and textured substrates. Keywords: Electrochemical deposition, Thermal vapor reaction, Kinetics, Perovskite

AimLiver cirrhosis and features of muscle or adipose tissues may affect the severity of acute pancreatitis (AP). We aimed to evaluate the impact of body composition parameters and liver cirrhosis on the severity of AP in patients with alcohol-induced AP (AAP).MethodsPatients with presumed AAP who underwent CT within one week after admission were retrospectively enrolled. L3 sectional areas of abdominal fat and muscle, and mean muscle attenuations (MMAs) were quantified. The presence of liver cirrhosis was determined using clinical and CT findings. Factors potentially associated with moderately severe or severe AP were included in the multivariable logistic regression analysis.ResultsA total of 242 patients (47.0 ± 12.6 years, 215 males) with presumed AAP were included. The mild and moderately severe/severe (MSS) groups included 137 (56.6%) and 105 patients (43.4%), respectively. Patients in the MSS group had higher rates of liver cirrhosis, organ failure, and local complications. Among body composition parameters, mean MMA (33.4 vs 36.8 HU, PConclusionThe results of this study suggest that liver cirrhosis has a significant impact on the severity of AAP. Of the body composition parameters examined, MMA and abdominal muscle mass showed potential as promising predictors.

AimsMetabolic syndrome (MS) is a global health problem associated with an increased risk of diabetes mellitus (DM), cardiovascular disease (CVD), and cancer. Body composition parameters, including obesity, visceral adiposity, and sarcopenia contribute to the development of MS and CVD. Previous studies have investigated the association of individual body composition parameters with MS. Studies analyzing the association between multiple body composition parameters and MS have been rare. We aimed to investigate the association between MS and multiple body composition parameters, including obesity, visceral adiposity, and sarcopenia.MethodsA total of 13,620 subjects who underwent voluntary routine checkups at the Health Care Center of our institution between October 2014 and December 2019 were enrolled. Only data from the first examination of subjects who underwent repeated checkups were included. Clinical and laboratory data were collected. Skeletal muscle mass and visceral fat area (VFA) were measured using bioelectrical impedance analysis. Appendicular skeletal muscle mass (ASM) was divided by body weight (in kg) and expressed as a percentage (calculated as, ASM% = ASM × 100/Weight). Data were compared between the groups based on obesity, VFA, and ASM%. Logistic regression analysis was performed to determine the risk of MS in each group.ResultsBody mass index and VFA were significantly higher in subjects with MS than in those without MS. ASM% was significantly lower in subjects with MS than in those without MS. Subjects with obesity, visceral adiposity, or sarcopenia had a higher prevalence of MS than those without. As the number of metabolic components increased from 0 to 5, we identified a decreasing trend of ASM% and an increasing trend of VFA and BMI (P for trend < 0.001 for all). In the paired analyses, all the three body composition parameters showed additive effects in predicting MS. In the logistic regression analysis, the three parameters were associated with an increased risk of MS after adjustment for age, sex, hypertension, DM, dyslipidemia, smoking, alcohol intake, and C-reactive protein.ConclusionsObesity, visceral adiposity, and sarcopenia showed additive effects on MS prediction. Subjects with obesity, visceral adiposity, or sarcopenia were significantly associated with the increased risk of MS after adjustment for multiple confounders. Increasing skeletal muscle and reducing visceral fat may be strategies for the prevention or treatment of MS.

Alzheimer's disease (AD) is a neurodegenerative disease associated with the accumulation of amyloid-beta oligomers (AßO). Recent studies have demonstrated that mitochondria-specific autophagy (mitophagy) contributes to mitochondrial quality control by selectively eliminating the dysfunctional mitochondria. Mitochondria motility, which is regulated by Miro1, is also associated with neuronal cell functions. However, the role played by Miro1 in the mitophagy mechanism, especially relative to AßO and neurodegenerative disorders, remains unknown. In this study, AßO induced mitochondrial dysfunction, enhanced Parkin-mediated mitophagy, and reduced mitochondrial quantities in hippocampal neuronal cells (HT-22 cells). We demonstrated that AßO-induced mitochondrial fragmentation could be rescued to the elongated mitochondrial form and that mitophagy could be mitigated by the stable overexpression of Miro1 or by pretreatment with N-acetylcysteine (NAC)-a reactive oxygen species (ROS) scavenger-as assessed by immunocytochemistry. Moreover, using time-lapse imaging, under live cell-conditions, we verified that mitochondrial motility was rescued by the Miro1 overexpression. Finally, in hippocampus from amyloid precursor protein (APP)/presenilin 1 (PS1)/Tau triple-transgenic mice, we noted that the co-localization between mitochondria and LC3B puncta was increased. Taken together, these results indicated that up-regulated ROS, induced by AßO, increased the degree of mitophagy and decreased the Miro1 expression levels. In contrast, the Miro1 overexpression ameliorated AßO-mediated mitophagy and increased the mitochondrial motility. In AD model mice, AßO induced mitophagy in the hippocampus. Thus, our results would improve our understanding of the role of mitophagy in AD toward facilitating the development of novel therapeutic agents for the treatment of AßO-mediated diseases. [ABSTRACT FROM AUTHOR]

Purpose The aim of this study was to determine the prevalence of antibiotic susceptibility and resistance of Escherichia coli in urinary tract infections (UTIs) in children. Methods We retrospectively reviewed the clinical records of 212 inpatients aged 18 years or younger with UTIs treated at the Pediatric Department of Dongguk University Gyeongju Hospital between January 2008 and December 2016. For comparison, patients were divided into three groups according to age as follows: group 1, ≤1 month; group 2, >1 month to ≤12 months; and group 3, ≥13 months. The antibiotic resistance rates from January 2008 to December 2012 (study period 1) and from January 2013 to December 2016 (study period 2) were analyzed statistically by group. Results As the patient age increased, the antibiotic resistance rate to ampicillin (P=0.013), levofloxacin (P=0.050), piperacillin/tazobactam (TZP) (P

Stroke is a serious, adverse neurological event and the third leading cause of death and disability worldwide. Most strokes are caused by a block in cerebral blood flow, resulting in neurological deficits through the death of brain tissue. Recombinant tissue plasminogen activator (rt-PA) is currently the only immediate treatment medication for stroke. The goal of rt-PA administration is to reduce the thrombus and/or embolism via thrombolysis; however, the administration of rt-PA must occur within a very short therapeutic timeframe (3 h to 6 h) after symptom onset. Components of the pathological mechanisms involved in ischemic stroke can be used as potential biomarkers in current treatment. However, none are currently under investigation in clinical trials; thus, further studies investigating biomarkers are needed. After ischemic stroke, microglial cells can be activated and release inflammatory cytokines. These cytokines lead to severe neurotoxicity via the overactivation of microglia in prolonged and lasting insults such as stroke. Thus, the balanced regulation of microglial activation may be necessary for therapy. Stem cell therapy is a promising clinical treatment strategy for ischemic stroke. Stem cells can increase the functional recovery of damaged tissue after post-ischemic stroke through various mechanisms including the secretion of neurotrophic factors, immunomodulation, the stimulation of endogenous neurogenesis, and neovascularization. To investigate the use of stem cell therapy for neurological diseases in preclinical studies, however, it is important to develop imaging technologies that are able to evaluate disease progression and to “chase” (i.e., track or monitor) transplanted stem cells in recipients. Imaging technology development is rapidly advancing, and more sensitive techniques, such as the invasive and non-invasive multimodal techniques, are under development. Here, we summarize the potential risk factors and biomarker treatment strategies, stem cell-based therapy and emerging multimodal imaging techniques in the context of stroke. This current review provides a conceptual framework for considering the therapeutic targets and directions for the treatment of brain dysfunctions, with a particular focus on ischemic stroke.

Endoplasmic reticulum (ER) stress generally occurs in secretory cell types. It has been reported that Leydig cells, which produce testosterone in response to human chorionic gonadotropin (hCG), express key steroidogenic enzymes for the regulation of testosterone synthesis. In this study, we analyzed whether hCG induces ER stress via three unfolded protein response (UPR) pathways in mouse Leydig tumor (mLTC-1) cells and the testis. Treatment with hCG induced ER stress in mLTC-1 cells via the ATF6, IRE1a/XBP1, and eIF2α/GADD34/ATF4 UPR pathways, and transient expression of 50 kDa protein activating transcription factor 6 (p50ATF6) reduced the expression level of steroidogenic 3β-hydroxysteroid dehydrogenase ▵5-▵4-isomerase (3β-HSD) enzyme. In an in vivo model, high-level hCG treatment induced expression of p50ATF6 while that of steroidogenic enzymes, especially 3b-HSD, 17α-hydroxylase/C17-20 lyase (CYP17), and 17β-hydrozysteroid dehydrogenase (17β-HSD), was reduced. Expression levels of steroidogenic enzymes were restored by the ER stress inhibitor tauroursodeoxycholic acid (TUDCA). Furthermore, lentivirus-mediated transient expression of p50ATF6 reduced the expression level of 3β-HSD in the testis. Protein expression levels of phospho-JNK, CHOP, and cleaved caspases-12 and -3 as markers of ER stress-mediated apoptosis markedly increased in response to high-level hCG treatment in mLTC-1 cells and the testis. Based on transmission electron microscopy and H&E staining of the testis, it was shown that abnormal ER morphology and destruction of testicular histology induced by high-level hCG treatment were reversed by the addition of TUDCA. These findings suggest that hCG-induced ER stress plays important roles in steroidogenic enzyme expression via modulation of the ATF6 pathway as well as ER stress-mediated apoptosis in Leydig cells. [ABSTRACT FROM AUTHOR]

5-Lipoxygenase (5-LO) catalyzes the formation of two major groups of leukotrienes, leukotriene B4 and cysteinyl leukotrienes (CysLTs), and it has been implicated as a promising drug target to treat various inflammatory diseases. However, its role in osteo-clastogenesis has not been investigated. In this study, we used mouse bone marrow-derived macrophages (BMMs) to show that 5-LO inhibitor suppresses RANKL-induced osteoclast formation. Inhibition of 5-LO was associated with impaired activation of multiple signaling events downstream of RANK, including ERK and p38 phosphorylation, and IKB degradation, followed by a decrease in NFATcl expression. Ectopic overexpression of a constitutively active form of NFATcl partly rescued the antiosteoclastogenic effect of 5-LO inhibitor. The knockdown of 5-LO in BMMs also resulted in a significant reduction in RANKL-induced osteoclast formation, accompanied by decreased expression of NFATcl. Similar effects were shown with CysLT receptor (CysLTR)l/2 antagonist and small RNA for CysLTRl in BMMs, indicating the involvement of CysLT and CysLTRl in 5-LO-mediated osteo-clastogenesis. Finally, 5-LO inhibitor suppressed LPS-induced osteoclast formation and bone loss in the in vivo mouse experiments, suggesting a potential therapeutic strategy for treating diseases involving bone destruction. Taken together, the results of this study demonstrate that 5-LO is a key mediator of RANKL-induced osteoclast formation and possibly a novel therapeutic target for bone-resorption diseases. [ABSTRACT FROM AUTHOR]

Dysregulation of liver functions leads to insulin resistance causing type 2 diabetes mellitus and is often found in chronic liver diseases. However, the mechanisms of hepatic dysfunction leading to hepatic metabolic disorder are still poorly understood in chronic liver diseases. The current work investigated the role of hepatitis B virus X protein (HBx) in regulating glucose metabolism. We studied HBx-overexpressing (HBxTg) mice and HBxTg mice lacking inducible nitric oxide synthase (iNOS). Here we show that gene expressions of the key gluconeogenic enzymes were significantly increased in HepG2 cells expressing HBx (HepG2-HBx) and in non-tumor liver tissues of hepatitis B virus patients with high levels of HBx expression. In the liver of HBxTg mice, the expressions of gluconeogenic genes were also elevated, leading to hyperglycemia by increasing hepatic glucose production. However, this effect was insufficient to cause systemic insulin resistance. Importantly, the actions of HBx on hepatic glucose metabolism are thought to be mediated via iNOS signaling, as evidenced by the fact that deficiency of iNOS restored HBx-induced hyperglycemia by suppressing the gene expression of gluconeogenic enzymes. Treatment of HepG2-HBx cells with nitric oxide (NO) caused a significant increase in the expression of gluconeogenic genes, but JNK1 inhibition was completely normalized. Furthermore, hyperactivation of JNK1 in the liver of HBxTg mice was also suppressed in the absence of iNOS, indicating the critical role for JNK in the mutual regulation of HBx- and iNOS-mediated glucose metabolism. These findings establish a novel mechanism of HBx-driven hepatic metabolic disorder that is modulated by iNOS-mediated activation of JNK. [ABSTRACT FROM AUTHOR]