PURPOSE: Visceral fat (VF) is closely associated with many metabolic risk factors and is also known to be a strong predictive factor for severe metabolic complications in adults. But there are only a few studies concerning the association of VF and risk factors for metabolic syndrome (MS) in children and adolescents. In our study, we emphasized the association of VF [measured by VF computed tomography (VFCT)] and risk factors for metabolic syndrome in children and adolescents. MATERIALS AND METHODS: The subjects were outpatients aged 6 to 18 years who underwent VFCT in the family medicine of The Catholic University of Korea from January 2005 to August 2009. There were 82 patients in total (42 children, 40 adolescents). Height, weight, blood pressure (BP), blood tests, body composition analysis and VF were measured. The three groups were also classified by metabolic score. RESULTS: In children, only high density lipoprotein cholesterol (HDL-C) showed a statistically significant difference, while in adolescents, triglyceride, HDL-C, BP, body mass index (BMI), waist circumference (WC) and VFA showed statistically significant differences. In terms of VFA, fasting glucose, BP, BMI, basal metabolic rate (BMR) and WC showed statistically significant differences. BMI showed a statistically significant difference in terms of BP, BMR, WC, VFA and HDL-C. CONCLUSION: There is a need to acknowledge the statistically significant associations of VF and risk factors for MS in children and adolescents. Screening tests for BP, cholesterol, fasting glucose and WC should be given in clinics for children and adolescents so that MS can be detected and its risk factors treated early.
Adolescent ; Body Mass Index ; Child ; Female ; Humans ; Intra-Abdominal Fat/*physiology ; Male ; Metabolic Syndrome X/*epidemiology/metabolism/physiopathology ; Risk Factors ; Waist Circumference/physiology

Papular elastolytic giant cell granuloma is an unusual variant of annular elastolytic giant cell granuloma, characterized by the development of asymptomatic, multiple, small erythematous papules on both sun-exposed and non-sun-exposed area. Histopathologically, it shows a granulomatous infiltration, accompanied by the absence of the elastic tissue and phagocytosis of elastic fibers by multinucleated giant cell. An 83-year-old man was presented with a 1 year history of multiple erythematous papules on his abdomen and lower legs. Histopathologic finding showed a non-palisading granulomatous infiltration with multinucleated giant cells and engulfing elastic fibers. We, herein, report an unusual case of papular elastolytic giant cell granuloma, which occurred on non-sun-exposed skin.
Abdomen ; Aged, 80 and over ; Elastic Tissue ; Giant Cells ; Granuloma, Giant Cell ; Humans ; Leg ; Phagocytosis ; Skin

15-deoxy-delta12,14-PGJ2(15d-PGJ2) is a natural ligand that activates the peroxisome proliferators-activated receptor (PPAR) gamma, a member of nuclear receptor family implicated in regulation of lipid metabolism and adipocyte differentiation. Recent studies have shown that 15d-PGJ2 is the potent anti-inflammatory agent functioning via PPARgamma-dependent and -independent mechanisms. Most postulated mechanisms for anti-inflammatory action of PPARgamma agonists are involved in inhibiting NF-kappaB signaling pathway. We examined the possibility that IL-6 signaling via the Jak-Stat pathway is modulated by 15d-PGJ2 in lymphocytes and also examined whether the inhibition of IL-6 signaling is dependent of PPARgamma. 15d-PGJ2 blocked IL-6 induced Stat1 and Stat3 activation in primary human lymphocytes, Jurkat cells and immortalized rheumatoid arthritis B cells. Inhibition of IL-6 signaling was induced rapidly within 15 min after treatment of 15d-PGJ2. Other PPARgamma-agonists, such as troglitazone and ciglitazone, did not inhibit IL-6 signaling, indicating that 15d-PGJ2 affect the IL-6-induced Jak-Stat signaling pathway via PPARgamma-independent mechanism. Although cycloheximide reversed 15d-PGJ2-mediated inhibition of Stat3 activation, actinomycin D had no effect on 15d-PGJ2-mediated inhibition of IL-6 signaling, indicating that inhibition of IL-6 signaling occur independent of de novo gene expression. These results show that 15d-PGJ2 specifically inhibit Jak-Stat signaling pathway in lymphocytes, and suggest that 15d-PGJ2 may regulate inflammatory reactions through the modulation of different signaling pathway other than NF-kappaB in lymphocytes.
Arthritis, Rheumatoid/metabolism/pathology ; Chromans/pharmacology ; Cycloheximide/pharmacology ; DNA-Binding Proteins/*metabolism ; Dactinomycin/pharmacology ; Gene Expression Regulation ; Humans ; Hypoglycemic Agents/pharmacology ; Interleukin-6/*pharmacology ; Jurkat Cells/metabolism/pathology ; Lymphocytes/cytology/*drug effects/*metabolism ; NF-kappa B/metabolism ; PPAR gamma/metabolism ; Phosphorylation ; Prostaglandin D2/*analogs & derivatives/pharmacology ; Protein Synthesis Inhibitors/pharmacology ; Research Support, Non-U.S. Gov't ; *Signal Transduction ; Thiazolidinediones/pharmacology ; Trans-Activators/*metabolism

Hyponatremia in patients with central nervous system disorders is suggestive of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), and volume restriction is recommended for its correction. However, if volume depletion is present in a situation otherwise compatible with SIADH, cerebral salt wasting syndrome (CSWS) should be considered as the cause of the hyponatremia to avoid hypovolemic shock that may be induced by the standard management of SIADH, i.e. volume restriction. We present a case of a 17-year-old male patient with CSWS associated with tuberculous meningitis. The clinical feature of the patient comprised hyponatremia, excessive natriuresis, polyuria, and hypovolemia. Following the administration of saline and fludrocortisone, natriuresis and polyuria were decreased, and the hyponatremia improved
Adolescent ; Central Nervous System Diseases ; Fludrocortisone ; Humans ; Hyponatremia ; Hypovolemia ; Inappropriate ADH Syndrome ; Male ; Natriuresis ; Polyuria ; Shock ; Tuberculosis, Meningeal* ; Wasting Syndrome*

BACKGROUND AND OBJECTIVES: It has been demonstrated that the concentration of plasma nerve growth factor (NGF) effects nerve sprouting. In addition, the relationship between plasma NGF concentration and the occurrence of ventricular tachyarrhythmia (VT) has been reported in animal models of myocardial infarction (MI). However, the causal relationship between NGF and VT remains unclear in humans. The aim of the current study was to determine whether NGF is increased in patients with MI. In addition, the relationship between the concentration of plasma NGF and the inducibility of VT was evaluated. SUBJECTS AND METHODS: We studied 15 patients with stable angina pectoris (SA) and 30 patients with an acute MI (AMI). The patients in the AMI group were divided into VT occurrence (n=14) and non-VT occurrence groups (n=16). Thirty-four patients suspected to have VT underwent programmed electrical stimulation (PES) and were divided into an idiopathic VT group (n=24) and an induced VT with PES {healthy control (C) group; n=10}. Plasma NGF concentrations were measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: The plasma concentrations of the AMI group were significantly increased compared to the C group {median (interquartile range), 18.9 (8.7) vs. 10.3 (12.5) pg/mL, p<0.05} and the patients with SA {18.9 (8.7) vs. 15.1 (6.7) pg/mL, p<0.05}, but not significantly different from those in the idiopathic VT group {median (interquartile range), 18.9 (8.7) vs. 18.7 (8.5) pg/mL, p=0.89}. There was no significant difference in the plasma NGF concentrations between the C and SA groups {10.3 (12.5) vs. 15.1 (6.7) pg/mL, p=0.18}. In the AMI patients, there was no significant difference in the plasma NGF concentrations between patients with VT and those without VT {18.5 (6.7) vs. 21.2 (10.2) pg/mL, p=0.25}. CONCLUSION: The plasma NGF concentrations were increased in patients with an AMI compared to patients with SA and Cs.
Angina, Stable ; Electric Stimulation ; Enzyme-Linked Immunosorbent Assay ; Humans ; Models, Animal ; Myocardial Infarction ; Nerve Growth Factor ; Plasma ; Tachycardia

BACKGROUND AND OBJECTIVES: While pulmonary vein isolation (PVI) is an effective curative procedure for patients with atrial fibrillation (AF), pulmonary vein (PV) stenosis is a potential complication which may lead to symptoms that are often unrecognized. The aim of this study was to compare differences between ablation sites in pulmonary venous flow (PVF) measured by transthoracic Doppler echocardiography (TTE) before and after PVI. SUBJECTS AND METHODS: One hundred five patients (M : F=64 : 41; mean age 56+/-10 years) with paroxysmal AF (n=78) or chronic, persistent AF (n=27) were enrolled. PVI strategies consisted of ostial ablation (n=75; OA group) and antral ablation using an electroanatomic mapping system (n=30; AA group). The ostial diameter was estimated by magnetic resonance imaging (MRI) in patients with PVF > or =110 cm/sec by TTE after PVI. RESULTS: No patient complained of PV stenosis-related symptoms. Changes in mean peak right PV systolic (-6.7+/-28.1 vs. 10.9+/-25.9 cm/sec, p=0.038) and diastolic (-4.1+/-17.0 vs. 9.9+/-25.9 cm/sec, p=0.021) flow velocities were lower in the AA group than in the OA group. Although the change in mean peak systolic flow velocity of the left PV before and after PVI in the AA group was significantly lower than the change in the OA group (-13.4+/-25.1 vs. 9.2+/-22.3 cm/sec, p=0.016), there was no difference in peak diastolic flow velocity. Two patients in the OA group had high PVF velocities (118 cm/sec and 133 cm/sec) on TTE, and their maximum PV stenoses measured by MRI were 62.5% and 50.0%, respectively. CONCLUSION: PV stenosis after PVI could be detected by TTE, and PVI by antral ablation using an electroanatomic mapping system might be safer and more useful for the prevention of PV stenosis.
Atrial Fibrillation ; Carbamates ; Catheter Ablation ; Catheters ; Constriction, Pathologic ; Echocardiography ; Echocardiography, Doppler ; Follow-Up Studies ; Humans ; Magnetic Resonance Imaging ; Organometallic Compounds ; Pulmonary Veins

Advanced or metastatic breast cancer affects multiple organs and is a leading cause of cancer-related death. Cancer metastasis is associated with epithelial-mesenchymal metastasis (EMT). However, the specific signals that induce and regulate EMT in carcinoma cells remain unclear. PRR16/Largen is a cell size regulator that is independent of mTOR and Hippo signalling pathways. However, little is known about the role PRR16 plays in the EMT process. We found that the expression of PRR16 was increased in mesenchymal breast cancer cell lines. PRR16 overexpression induced EMT in MCF7 breast cancer cells and enhances migration and invasion. To determine how PRR16 induces EMT, the binding proteins for PRR16 were screened, revealing that PRR16 binds to Abl interactor 2 (ABI2). We then investigated whether ABI2 is involved in EMT. Gene silencing of ABI2 induces EMT, leading to enhanced migration and invasion. ABI2 is a gene that codes for a protein that interacts with ABL proto-oncogene 1 (ABL1) kinase. Therefore, we investigated whether the change in ABI2 expression affected the activation of ABL1 kinase. The knockdown of ABI2 and PRR16 overexpression increased the phosphorylation of Y412 in ABL1 kinase. Our results suggest that PRR16 may be involved in EMT by binding to ABI2 and interfering with its inhibition of ABL1 kinase. This indicates that ABL1 kinase inhibitors may be potential therapeutic agents for the treatment of PRR16-related breast cancer.