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Primary aldosteronism is the most common secondary endocrine form of hypertension and causes many cardiovascular injuries. KCNJ5 somatic mutations have recently been identified in aldosterone-producing adenoma. However, their impacts on left ventricular remodeling precluding the interference of age, sex, and blood pressure are still uncertain. We enrolled 184 aldosterone-producing adenoma patients who received adrenalectomy. Clinical, biochemical, and echocardiographic data were analyzed preoperatively and 1 year postoperatively. KCNJ5 gene sequencing of aldosterone-producing adenoma was performed. After propensity score matching for age, sex, body mass index, blood pressure, hypertension duration, and number of hypertensive medications, there were 60 patients in each group with and without KCNJ5 mutations. The mutation carriers had higher left ventricular mass index (LVMI) and inappropriately excessive LVMI (ieLVMI) and lower e′ than the noncarriers. After adrenalectomy, the mutation carriers had greater decreases in LVMI and ieLVMI than the noncarriers. In addition, only mutation carriers had a significant decrease in E/e′ after surgery. In multivariate analysis, baseline LVMI correlated with KCNJ5 mutations, the number of hypertensive medications, and systolic blood pressure. Baseline ieLVMI correlated with KCNJ5 mutations and the number of hypertensive medications. The regression of both LVMI and ieLVMI after surgery was mainly correlated with KCNJ5 mutations and changes in systolic blood pressure. Aldosterone-producing adenoma patients with KCNJ5 mutations had higher LVMI and ieLVMI and a greater regression of LVMI and ieLVMI after adrenalectomy than those without mutations. The patients with KCNJ5 mutations also benefited from adrenalectomy with regard to left ventricular diastolic function, whereas noncarriers did not.

Background/purpose: Genetic variant of HSD3B1 1245 is known to augment androgen production at peripheral tissue as skin. This study aimed to investigate whether women with polycystic ovary syndrome inheriting this variant exhibit specific androgenic phenotypes. Methods: A cross-sectional study of Taiwanese women with polycystic ovary syndrome, defined by Rotterdam criteria, at the reproductive endocrinology outpatient clinic in a university affiliated hospital. Results: The presence of female pattern hair loss in women with polycystic ovary syndrome was significantly associated with an increased body mass index, decreased sex hormone binding globulin and high density lipoprotein cholesterol levels, elevated triglyceride levels, and increased prevalence of hypertension. Using stepwise multivariate logistic regression analysis, body mass index, triglyceride and HSD3B1 1245 AC or CC genotype were significantly related to female pattern hair loss in women with polycystic ovary syndrome after considering other variables. Overweight women with polycystic ovary syndrome had significantly higher risk of female pattern hair loss than normal-weight women with polycystic ovary syndrome. The presence of female pattern hair loss was higher in overweight women with polycystic ovary syndrome who comprised HSD3B1 AC or CC genotype compared with wild type. Conclusion: Carrying the HSD3B1 1245C allele and overweight are associated with the presence of female pattern hair loss in women with polycystic ovary syndrome. Keywords: Androgenetic alopecia, Female pattern hair loss, HSD3B1, Obesity, Polycystic ovary syndrome

Simple Summary Primary aldosteronism (PA) is the most common form of secondary hypertension and induces various cardiovascular injuries. Aldosterone-producing adenoma (APA) is one of the major forms of PA. The occurrence of APA is closely correlated with somatic mutations, including KCNJ5. We described here the impact of KCNJ5 somatic mutations on arterial stiffness excluding the influence of age, sex, and blood pressure status. We found KCNJ5 mutation carriers had similar arterial stiffness before surgery, but greater improvement of arterial stiffness after adrenalectomy compared with non-carriers. Hence, APA patients with KCNJ5 mutations had a greater improvement in arterial stiffness after adrenalectomy than those without mutations. Abstract Primary aldosteronism is the most common form of secondary hypertension and induces various cardiovascular injuries. In aldosterone-producing adenoma (APA), the impact of KCNJ5 somatic mutations on arterial stiffness excluding the influence of confounding factors is uncertain. We enrolled 213 APA patients who were scheduled to undergo adrenalectomy. KCNJ5 gene sequencing of APA was performed. After propensity score matching (PSM) for age, sex, body mass index, blood pressure, number of hypertensive medications, and hypertension duration, there were 66 patients in each group with and without KCNJ5 mutations. The mutation carriers had a higher aldosterone level and lower log transformed brachial–ankle pulse wave velocity (baPWV) than the non-carriers before PSM, but no difference in log baPWV after PSM. One year after adrenalectomy, the mutation carriers had greater decreases in log plasma aldosterone concentration, log aldosterone–renin activity ratio, and log baPWV than the non-carriers after PSM. Only the mutation carriers had a significant decrease in log baPWV after surgery both before and after PSM. KCNJ5 mutations were not correlated with baseline baPWV after PSM but were significantly correlated with ∆baPWV after surgery both before and after PSM. Conclusively, APA patients with KCNJ5 mutations had a greater regression in arterial stiffness after adrenalectomy than those without mutations.

Background/Purpose: Abnormal folliculogenesis is one of the cardinal presentations of polycystic ovarian syndrome (PCOS) and permeability of follicular wall has been proposed to be involved in the normal follicular growth. However, whether or not there is a change in intrafollicular permeability underlies PCOS is unknown. Methods: This was a tertiary center-based case–control study. From 2014 to 2015, thirteen patients with PCOS who underwent in vitro fertilization-embryo transfer (IVF-ET) were enrolled. Eleven normo-ovulatory patients who underwent IVF-ET due to male factor and/or tubal factor infertility were enrolled as the control group. The influence of ovarian follicular fluid (FF) on endothelial cell permeability was evaluated using a human umbilical vein endothelial cell monolayer permeability assay. The intrafollicular expression profiles of angiogenesis-related proteins were analyzed using a Human Angiogenesis Protein Array Kit. Results: The FF from PCOS patients caused significantly poorer endothelial cell permeability comparing with the effect of FF from the control group (46% ± 12% vs. 58% ± 9%, P = 0.023). Among the 55 angiogenesis-related proteins tested, there was a significantly higher level of intrafollicular platelet factor 4 (PF4) and PF4/IL-8 complex in the PCOS group (p = 0.004). The anti-permeability effect of PF4 was related to the decrease in the intercellular gaps and antagonistic binding with IL-8. Conclusion: Our study provides the first evidence of the pathophysiologic contribution of the well-known angiostatic protein, PF4, on human reproductive biology. The increase of the intrafollicular PF4 and its anti-permeability effect might affect the formation of FF and folliculogenesis in PCOS. Keywords: Angiogenesis, Folliculogenesis, Permeability, Platelet factor 4, Polycystic ovarian syndrome

// Ruey-Jien Chen 1 , Chia-Tung Shun 2 , Men-Luh Yen 1 , Chia-Hung Chou 1 and Ming-Chieh Lin 2 1 Department of Obstetrics and Gynecology, National Taiwan University, Taipei 100, Taiwan 2 Department of Pathology, National Taiwan University, Taipei 100, Taiwan Correspondence to: Ruey-Jien Chen, email: rjchen@ntuh.gov.tw Keywords: G9a, angiogenesis, cancer cell proliferation, xenograft, patient survival Received: April 09, 2016 Accepted: May 12, 2017 Published: July 07, 2017 ABSTRACT Research suggests that the epigenetic regulator G9a, a H3K9 histone methyltransferase, is involved in cancer invasion and metastasis. Here we show that G9a is linked to cancer angiogenesis and poor patient survival. Invasive cervical cancer has a higher G9a expression than cancer precursors or normal epithelium. Pharmacological inhibition and genetic silencing of G9a suppresses H3K9 methylation, cancer cell proliferation, angiogenesis, and cancer cell invasion/migration, but not apoptosis. Microarray and quantitative reverse transcription polymerase chain reaction analyses reveal that G9a induces a cohort of angiogenic factors that include angiogenin, interleukin-8, and C-X-C motif chemokine ligand 16. Depressing G9a by either pharmacological inhibitor or gene knock down significantly reduces angiogenic factor expression. Moreover, promoting G9a gene expression augments transcription and angiogenic function. A luciferase reporter assay suggests that knockdown of G9a inhibits transcriptional activation of interleukin-8. G9a depletion suppresses xenograft tumor growth in mouse model, which is linked to a decrease in microvessel density and proliferating cell nuclear antigen expression. Clinically, higher G9a expression correlates with poorer survival for cancer patients. For patients’ primary tumors a positive correlation between G9a expression and microvessel density also exists. In addition to increasing tumor cell proliferation, G9a promotes tumor angiogenesis and reduces the patient survival rate. G9a may possess great value for targeted therapies.

Objective Obesity has been reported to have a modulatory effect on the ovulatory functions of patients with polycystic ovary syndrome. The role of adipokines in this obesity-associated ovulatory disturbance has not been extensively explored. In this study, the relationships between obesity, adipokine production from visceral fat, and ovarian folliculogenesis were explored in a mice model of induced obesity. Methods Obesity was induced in female C57BL/6 mice fed ad libitum with high-fat feed and fructose water for 4 weeks. Follicular developments in the ovaries were assessed by histopathology in these diet-induced obese mice. Changes in adipokine expression in the peri-ovarian adipose tissues were screened with an adipokine array. The adipokine with the most significant increase over time was identified. The functions of the adipokine in angiogenic processes were evaluated in a cell model of endothelial proliferation. The in vivo effects of neutralizing this adipokine using specific antibodies were assessed in the same obesity model. Results A high-fat and fructose diet induced an accumulation of early ovarian follicles and a reduction in mature follicles and corpus lutea. The number of microvessels in the early follicles also decreased. The adipokine protein array of the peri-ovarian adipose tissues identified a progressive increase in IL-10 expression with the duration of the obesogenic diet. In vitro experiments in the endothelial cell model confirmed IL-10 as a disrupter of VEGF-induced angiogenesis. Administration of anti-IL-10 antibodies prevented the histopathological changes induced by the obesogenic diet and further highlighted the role of IL-10 in disrupting folliculogenesis. Conclusions Obesity may disrupt normal folliculogenesis through increased production of IL-10 in visceral fats. This relationship may help clarify the reported association between obesity and ovulatory dysfunction, which has been found in patients with polycystic ovary syndrome. However, the duration of this study was short, which limited conclusions on the long-term reproductive outcomes., Highlights • Obesity increases IL-10 expression in visceral adipose. • IL-10 disrupts VEGF-induced angiogenesis in an endothelial cell model. • Disrupted angiogenesis is associated with disturbed folliculogenesis. • Anti-IL-10 antibody prevents the altered folliculogenesis induced by obesity. • Abnormal production of IL-10 may be a cause of dysovulation in obese individuals.

Solution processing enables organic devices to be fabricated cost-effectively, while deep-red emitters enable displays with high color saturation and lighting with high light quality. However, limited deep-red emitters were reported with solution-process feasibility and high efficiency. We demonstrate here a high-efficiency, solution-process-feasible deep-red emitter by coupling the highly efficient phosphorescent complex with a highly thermally stable fluorescent compound. The device exhibits a maximum external quantum efficiency of 11.2% at 10 cd m–2 and 8.4% at 100 cd m–2. The latter is coupled with an ultradeep red emission (0.70, 0.27) and a potential color saturation of 108%. Besides the intrinsically high-efficiency nature of the phosphorescent complex, the record high efficiency may be attributable to the spirally configured fluorene moiety in the fluorescent compound to prevent concentration-quenching effect, a proper host to enable an effective host-to-guest energy transfer, and the employed coh...

The effect of aldosterone on vascular smooth muscle cell function is still unclear. One method to measure vascular smooth muscle cell function is endothelial-independent vascular dilation, for which the key factor is sarcoplasmic reticulum calcium adenosine triphosphatase (SERCA).Our objective was to investigate the effect of aldosterone on vascular smooth muscle cell function and SERCA regulation.We prospectively analyzed 35 patients with primary aldosteronism (PA; 32 patients with aldosterone-producing adenoma and three patients with idiopathic hyperaldosteronism) and 30 patients with essential hypertension (EH) who were enrolled as the control group. Flow and nitrate-mediated dilation were performed in both groups and 1 year after adrenalectomy in the patients with aldosterone-producing adenoma. In addition, we investigated the effect of aldosterone on SERCA regulation in human aortic smooth muscle cells.This study took place in an academic clinical research center.Participants included 35 patients with PA and 30 patients with EH.Adrenalectomy was undertaken in patients with aldosterone-producing adenoma.The PA patients had significantly lower flow-mediated dilation (FMD) and nitrate-mediated dilation (NMD) values than the patients with EH (FMD: 13 ± 6 vs 16 ± 4; NMD: 16 ± 6 vs 19 ± 5; both P.05). FMD/NMD were significantly correlated with log 24 hour-urine aldosterone (FMD: r = -0.287, P = .048; NMD: r = -0.402, P = .005) but not blood pressure. The impaired FMD and NMD values were significantly restored 1 year after adrenalectomy (FMD: 11 ± 4 to 19 ± 7; NMD: 15 ± 6 to 21 ± 6; both P.01). Under confocal microscopy, aldosterone was shown to suppress the expression of SERCA2a of human aortic smooth muscle cells. Aldosterone significantly suppressed the expression of SERCA2a from 10(-8) M in mRNA and protein levels. This suppression was through down-regulation of mineralocorticoid receptor dependent mitochondrial transcription factors A and B2.Aldosterone impairs vascular smooth muscle cell function and suppresses SERCA 2a expression.

Aims An excess of aldosterone results in cardiac remodelling and fibrosis. Interleukin-6 (IL-6) is a key mediator in the fibrotic process; however, the effect of aldosterone on the expression of IL-6 remains unclear. We investigated whether aldosterone induces the expression of IL-6 and thereby contributes to the fibrotic process. Methods and results In this clinical study, we prospectively enrolled 25 patients with primary aldosteronism (PA) and 26 patients with essential hypertension (EH). The PA patients had higher plasma IL-6 levels, left ventricular mass index, degree of myocardial fibrosis, and more impaired diastolic function than the EH patients. In addition, plasma IL-6 levels were positively correlated with 24-h urinary aldosterone and echocardiographic parameters. In cell studies, we investigated the possible molecular mechanism how aldosterone-induced IL-6 secretion and the further effects of collagen production. Aldosterone significantly induced IL-6 protein and mRNA production in human umbilical vein endothelial cells. Intracellular signalling occurred through the mineralocorticoid receptor/PI3K/Akt/NF-kB pathway. In cardiac fibroblasts, IL-6 trans-signalling played a critical role in aldosterone-induced IL-6-enhanced fibrosis-related factor expression. To further investigate the role of IL-6 trans-signalling in aldosterone-induced cardiac fibrosis, we measured the severity of myocardial fibrosis in aldosterone infusion mice models including an IL-6 chemical inhibitor and Sgp130 Knockin Transgenic Mice. Mice receiving recombinant soluble gp130 and Sgp130 Knockin Transgenic Mice prevented myocardial fibrosis and cardiac hypertrophy by aldosterone infusion. Conclusions IL-6 trans-signalling contributes to aldosterone-induced cardiac fibrosis.

Background Ventricular remodeling following myocardial infarction (MI) is closely associated with cyclooxygenase-2 (COX-2) expression. 5-methoxytryptophan (5-MTP) was reported to control COX-2 expression. Objectives To investigeate the association between 5-MTP and post-MI left ventricular remodeling. Methods This prospective study enrolled 26 non-diabetic patients with first-time ST segment elevation myocardial infarction (STEMI), and 58 controls. Levels of 5-MTP, N-terminal of pro-brain natriuretic peptide (NT-proBNP), aminoterminal propeptide of type III procollagen, matrix metalloproteinase-9, and tissue inhibitor of metalloproteinase-1 were measured at day 1, day 3, 3months, 6months, and 1year post-MI. Echocardiography was performed during the acute stage (within 72h) and 3months, 6months, and 1year post-MI. Results The STEMI patients had a significantly lower plasma 5-MTP level at day 1 which reached a nadir at 3months post-MI. The level of 5-MTP at day 3 post-MI was significantly correlated with the level of NT-proBNP 1year post-MI, suggesting that the level of plasma 5-MTP in the early phase after MI may predict subsequent cardiac stress and failure. Receiver operating characteristic curve analysis revealed that plasma 5-MTP had the best area under the curve value to predict plasma NT-proBNP 1year post-MI. Further analysis using net reclassification improvement and integrated discrimination improvement models confirmed that plasma 5-MTP at day 3 post-MI significantly improved the predictive power of each of the parameters. Conclusion In non-diabetic STEMI patients, plasma 5-MTP levels were associated with biomarkers of post-MI left ventricular remodeling and damage.

The benefit of ω-3 fatty acids in fat emulsion remains controversial. This study evaluated the effect of ω-3 fatty acids on immune and inflammatory modulation in surgical intensive care unit (SICU) patients.Thirty-eight patients admitted to the SICU after major surgery were enrolled in this prospective controlled study and randomized to receive parenteral nutrition (PN) with equal volume and calories from glucose, nitrogen, and fat but different lipid components for 7 postoperative days. Group A (n = 12) received a mixture of soybean and medium-chain triglyceride oils; group B (n = 18) received a fat emulsion with part of the lipid replaced by fish oil. Blood tests, including lipid profile, routine biochemistry, inflammatory cytokines, and lymphocyte subpopulations, were evaluated preoperatively and on postoperative days 4 and 7.Both lipid regimens were well tolerated. There was a trend toward reduced serum inflammatory cytokines in group B vs group A with significant differences regarding interleukin (IL)-1, IL-8, and interferon (IFN)-γ on postoperative day 4 (P.05) and IL-1, IL-8, IFN-γ, IL-6, and tumor necrosis factor-α on postoperative day 7 (P.05). There was a reduction in postoperative liver dysfunction (A vs B: 50% vs 33.3%) and infection rate (A vs B: 41.7% vs 27.8%) in group B, although this was not statistically significant. There was no mortality in either group.This study suggests that supplementation of parenteral ω-3 fatty acids in PN is safe and may improve immune and hyperinflammatory response for SICU patients after major surgery.

Purpose Hepatitis B virus (HBV) reactivation can occur after radiotherapy (RT) for hepatobiliary malignancies. Our previous in vitro culture study identified interleukin-6 (IL-6) as the main bystander mediator of RT-induced HBV replication. We attempted to examine the molecular mechanism in HBV-transgenic mice. Methods and materials HBV transgenic mice were treated with whole liver RT (4 Gy daily for 5 days) with or without administration of IL-6 (400 ng twice daily for 15 days). The serum level of HBV DNA was measured using real-time polymerase chain reaction, and the IL-6 concentration was measured using enzyme-linked immunosorbent assay. The intensity of immunostaining with antibodies to HBV core protein and phosphorylated signal transducer and activator of transcription (STAT)3 in the mouse liver was qualitatively analyzed. HepG2.2.15 cells (a human hepatoblastoma cell line that persistently produces HBV DNA) were used to investigate the molecular role of IL-6 plus RT in HBV reactivation. Results HBV reactivation was induced in vivo with IL-6 plus RT (5.58-fold) compared with RT alone (1.31-fold, p = .005), IL-6 alone (1.31-fold, p = .005), or sham treatment (1.22-fold, p = .004). HBV core protein staining confirmed augmentation of intrahepatic HBV replication. IL-6 plus RT-induced HBV DNA replication in HepG2.2.15 cells was suppressed by the STAT3 inhibitor AG490 and by transfection with dominant-negative STAT3 plasmid. Phosphorylated STAT3 staining was strongest in liver tissue from mice treated with IL-6 plus RT. The mobility shift assay demonstrated that reactivation was mediated through the interaction of phosphorylated STAT3/hepatocyte nuclear factor-3 complex with HBV enhancer 1. Conclusion RT to the liver and longer sustained IL-6 induced HBV reactivation through the STAT3 signal transduction pathway.

Since both the parents need to work and look after their babies/infants simultaneously, the families bear more workload. Thus, this paper presents an innovative infant monitoring system consisting of an embedded system platform with a Linux kernel embedded operation system using the TCP/IP protocol, a CMOS image sensor, and peripheral control systems. The key feature of the system is that it can be used to monitor the living environment and the activities of the babies and/or infants through a web browser at any time from any place in the world. In order to increase the accuracy of the temperature sensor, the measured values from the digital temperature sensor were calibrated using regression analysis methods, resulting in an accuracy of ± 0.1°C, a correlation coefficient of 0.996, and a standard deviation of 0.124. The experimental results show that the proposed concept and the resulting system are feasible.

Through in situ reduction of a gold precursor, we have tethered gold nanoparticles (Au NPs) to the side chains of poly{2,7-(9,9' -dioctylfluorene)-co-4-diphenylamino-4' -bipenylmethylsulfide) (PF-DBMS) through its ArSCH 3 anchor groups. The presence of 1 wt % of the tethered Au NPs led to a reduction in the degree of aggregation of the polymer chains, resulting in a 50 % increase in its quantum yield. The electroluminescence of a 1 wt % Au/PF-DBMS device was almost four times higher in terms of its maximum brightness and its full-width-at-half-maximum emission peak was much narrower than that of a pure PF-DBMS device; the presence of a small amount of Au NPs significantly enhances the electron injection and transport and suppresses the photo-oxidation of PF-DBMS.

Objectives To study the role of selected cytokines and growth factors involved in the pathogenesis of fetal chylous pleural effusion. Methods Seventeen fetuses with prenatal chylothorax at gestational age (GA) 17–29 weeks were enrolled as the study group during the period 2003–2005. Their pleural effusion (n = 17) and amniotic fluid (n = 17) were drawn when disease set in. Eleven fetuses received cordocentesis because of suspected fetal anemia. Forty-one normal fetuses without adverse perinatal outcome at GA 17-29 weeks received amniocentesis and were enrolled in the reference group. Levels of hepatocyte growth factor (HGF), stromal-derived factor-1(SDF-1), vascular endothelial growth factor (VEGF), interleukin-8 (IL-8), macrophage migratory inhibition factor (MIF), and interleukin-6 (IL-6) were determined in the samples from both groups (amniotic fluid, pleural fluid, and cord blood from the study group and amniotic fluid from the reference group) by enzyme-linked immunoassay (EIA). Results No significant differences were observed in the amniotic fluids between the study group and the reference group regarding levels of IL-6, IL-8, MIF, SDF-1, HGF and VEGF. In the study group, levels of IL-8, VEGF and SDF-1 (all pro-angiogenic) showed no significant differences between the amniotic fluid, cord blood and pleural effusion. The level of HGF (proangiogenic) was significantly higher in the amniotic fluid than in the cord blood or the pleural effusion, but there were no significant differences between the levels in the pleural fluid and in the cord blood. Interestingly, the levels of MIF and IL-6 (both are proinflammatory) in the amniotic fluid and in the pleural effusion were much higher than the levels in the cord blood. Conclusion Our study demonstrated that the levels of pro-inflammatory proteins (MIF and IL-6) that we tested were higher in the fetal pleural effusion than in the fetal circulation, a phenomenon not observed in the levels of proangiogenic proteins (HGF, SDF-1, VEGF, IL-8). This result implies that inflammation-related proteins may be more relevant than the angiogenesis-related proteins in the local environment of accumulating pleural effusion, a prominent feature of prenatal chylothorax. Copyright © 2007 John Wiley & Sons, Ltd.

An adjustable output power ratio branch line coupler design is proposed. The mixed transmission line and shunted capacitor T-type equivalent circuit replaced the arms of the general branch line forms the tuning mechanism. By changing the shunted capacitors values, the power at output ports could shift to the desired ratio. A prototype circuit designed at 925MHz has been simulated and fabricated on FR4 substrate. The simulated experimental results show that the output power ratio changing is in a good agreement at the design frequency.

OBJECTIVE To test if collagen markers are associated with aldosterone-induced diastolic dysfunction. BACKGROUND Although primary aldosteronism is associated with more prominent cardiac remodeling and diastolic dysfunction, the reversibility of diastolic function is unclear. In addition, there is no known biomarker associated with aldosterone-induced diastolic dysfunction. METHODS We enrolled 27 patients with aldosterone-producing adenoma (APA) preparing for adrenalectomy, and 27 patients with essential hypertension prospectively from October 2006 to March 2010 at a tertiary referral center. Plasma matrix metalloproteinase-2 (MMP-2) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) were measured, and echocardiography including tissue Doppler images was performed in both groups and 1 year after receiving adrenalectomy in the APA group. RESULTS The baseline plasma TIMP-1 level (88.4 ± 38.7 vs. 63.6 ± 32.5 ng/ml; P = 0.014), left ventricular mass index (LVMI), and E/E' ratio (11.5 ± 2.9 vs. 9.0 ± 2.1; P

We demonstrated that in a nanocrystalline TiO2/poly(2-methoxy-5-(2 0 -ethylhexyloxy)-1,4-phenylene vinylene) (MEHPPV) composite, electroluminescence of this composite is enhanced via addition of TiO2 nanoneedles. The TiO2 nanoneedles enhance the partial crystallization of MEH-PPV around TiO2, which in turn causes a decrease in the hole barrier height and an increase in hole mobility. The IYV measurement was established on an indium tin oxide/MEHPPV:TiO2/Al device to identify the electrical properties of the composites.

Context Patients with primary aldosteronism are associated with increased myocardial fibrosis. Galectin-3 is one of the most important mediators between macrophage activation and myocardial fibrosis. Objective To investigate whether aldosterone induces galectin-3 secretion in vitro and in vivo. Methods and Results We investigated the possible molecular mechanism of aldosterone-induced galectin-3 secretion in macrophage cell lines (THP-1 and RAW 264.7 cells). Aldosterone induced galectin-3 secretion through mineralocorticoid receptors via the PI3K/Akt and NF-κB transcription signaling pathways. In addition, aldosterone-induced galectin-3 expression enhanced fibrosis-related factor expression in fibroblasts. We observed that galectin-3 mRNA from peripheral blood mononuclear cells and serum galectin-3 levels were both significantly increased in mice implanted with aldosterone pellets on days 7 and 14. We then conducted a prospective preliminary clinical study to investigate the association between aldosterone and galectin-3. Patients with aldosterone-producing adenoma had a significantly higher plasma galectin-3 level than patients with essential hypertension. One year after adrenalectomy, the plasma galectin-3 level had decreased significantly in the patients with aldosterone-producing adenoma. Conclusion This study demonstrated that aldosterone could induce galectin-3 secretion in vitro and in vivo.

Recently, there are many researches on the design of RF probes. Usually the materials of RF probe are tungsten and copper beryllium. They employed fabrication process of soldering and drawing of metal wire, which are not compatible with MEMS or IC fabrication process. Precise and high skill assembly is needed to finish the final probe module therefore results in high cost. This paper presents a novel RF probe module design which can be fabricated by Micro Electro Mechanical (MEM) fabrication process to reduce the cost. We use microwave simulation software, such as IE3D, Microwave Office, and Fidelity for design and analysis, and to know what kind of probe can reach the optimal impedance match and S-parameter. The design flow chart is coaxial cable to transform square coaxial cable, finally, in order to match up CPW standard pitches, therefore, design rectangular coaxial transition and success suitable ratio. Probe can match 50?.

Purpose Radiotherapy is integrated into the multimodal treatment of localized hepatocellular carcinoma (HCC) refractory to conventional treatment. Tumor control remains unsatisfactory and the sublethal effect associates with secondary spread. The use of an effective molecularly targeted agent in combination with radiotherapy is a potential therapeutic approach. Our aim was to assess the effect of combining a phenylbutyrate-derived histone deacetylase (HDAC) inhibitor, AR-42, with radiotherapy in in vitro and in vivo models of human HCC. Methods and Materials Human HCC cell lines (Huh-7 and PLC-5) were used to evaluate the in vitro synergism of combining AR-42 with irradiation. Flow cytometry analyzed the cell cycle changes, whereas Western blot investigated the protein expressions after the combined treatment. Severe combined immunodeficient (SCID) mice bearing ectopic and orthotopic HCC xenografts were treated with AR-42 and/or radiotherapy for the in vivo response. Results AR-42 significantly enhanced radiation-induced cell death by the inhibition of the DNA end-binding activity of Ku70, a highly versatile regulatory protein for DNA repair, telomere maintenance, and apoptosis. In ectopic xenografts of Huh-7 and PLC-5, pretreatment with AR-42 significantly enhanced the tumor-suppressive effect of radiotherapy by 48% and 66%, respectively. A similar combinatorial effect of AR-42 (10 and 25 mg/kg) and radiotherapy was observed in Huh-7 orthotopic model of tumor growth by 52% and 82%, respectively. This tumor suppression was associated with inhibition of intratumoral Ku70 activity as well as reductions in markers of HDAC activity and proliferation, and increased apoptosis. Conclusion AR-42 is a potent, orally bioavailable inhibitor of HDAC with therapeutic value as a radiosensitizer of HCC.

In this study, we evaluated the effectiveness of using swept-source optical coherence tomography (SS-OCT) to monitor the enhancement of hepatocellular carcinoma (HCC) cell invasiveness by radiation. SS-OCT images were acquired and recorded to obtain three-dimensional datasets at discrete time points of 12, 24 and 48 h after irradiating HepG2 cells with 7.5 Gy. The cell migration distance in three-dimensional tissue models was quantified from images of radiation-induced and sham-irradiated cells, and this method was compared with the conventional Boyden chamber assay conducted at the same time points. SS-OCT measurements show that most cells were found near the gel surface, but a few were much deeper. Among those HCC cells with a high degree of migration capability, the mean migration distances at 24 h and 48 h were significantly greater for irradiated cells than for sham-irradiated cells (0.7 +/- 0.23 mm versus 0.65 +/- 0.26 mm at 24 h, P = 0.019 and 0.84 +/- 0.30 mm versus 0.65 +/- 0.524 mm at 48 h, P = 0.009). The results of radiation-enhanced invasion in HCC cells obtained by the non-invasive, quantitative SS-OCT method were consistent with those obtained using the traditional assay for measuring biological invasion.

Printed electronics have attracted increasing attention in recent years due to its flexible format, easy process and potentially low cost features. Achieving good performance organic Schottky diode as the key component of a rectifier for printed RFID applications became a critical task. The electrical performances of an organic Schottky diode can be improved by inserting an intermediate layer between the semiconductor and electrode surfaces. This interface plays an important role in improving rectification ratio and lifetime of a polymer diode. In this work, a 13.56 MHz rectifier based on a polymer Schottky diode will be demonstrated and a wireless energy transmission built on flexible substrates will be proposed.

Printed electronics have attracted increasing attentions in recent years due to its flexible format, easy process and potentially low cost features. Achieving good performance organic Schottky diode as the key component of a rectifier for printed RFID applications became a critical task. The electrical performances of an organic Schottky diode electrical can be improved by inserting an intermediate layer between the semiconductor and electrode surfaces. This interface plays an important role in improving rectification ratio and lifetime of a polymer diode. In this work, a 13.56MHz rectifier based on a polymer Schottky diode will be demonstrated and a wireless energy transmission built on flexible substrates will be proposed.

Background/aim: Primary aldosteronism (PA) patients are correlated to higher cardiovascular events, endothelial function, and altered cardiac structure. Macrophage-mediated low grade inflammation plays important role of aldosterone-induced myocardial and vascular fibrosis. However, theeffect of aldosterone on macrophage movementis still unclear. Methods: We investigated the effect of aldosterone on macrophage movement and its mechanism. We used THP-1 as cell model of macrophage, and transwell assay to evaluate the migration and infiltration of cell. Two periods (16 hour and 48 hour) wereused to evaluate the migration and infiltration of macrophage. Results: Aldosterone increased THP-1 migration and infiltrationsince 10−8 M at 48 hours but not 16 hours. Aldosterone induced both galectin-3 and IL-6 production in THP-1 cell. In contrast, aldosterone does not affect the production of matrix metalloproteinase-2 and tissue inhibitor of metalloproteinase-1in THP-1. The increased migration and infiltrationby aldosterone was inhibited partially by IL-6 siRNA but not galectin-3 siRNA. Aldosterone also induced Rho-ROCK up-regulation but also partially inhibited by IL-6 siRNA. The aldosterone induced cell migration and infiltration was blocked by Y27632 (Rho-ROCK inhibitor). Conclusions: Aldosterone increased microphage migration and infiltration. The process was partially involved IL-6/Rho-ROCK pathway.

Y. Chen, S. L. Pan, J. C. Wang, C. H. Chou, S. H. Kuo, J. C. H. Cheng, C. M. Teng Department of Oncology, National Taiwan University Hospital, Taipei, Taiwan, Pharmacological Institute, College of Medicine, National Taiwan University, Taipei, Taiwan, Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine, Taipei, Taiwan, Department of Internal Medicine, National Taiwan University College of Medicine, Taipei, Taiwan

Purpose/Objective: Metastasis has been the lethal factor in cancer patients. YC-1, 3-(5 -hydroxymethyl-2 -furyl)-1-benzylindazole, an agent developed for circulatory disorders by inhibiting platelet aggregation and vascular contraction, was found to inhibit hypoxia inducible factor-1 (HIF-1) activity. HIF-1 is a stress protein during radiation and modulates genes associated with cancer invasion and metastasis. With HIF-1 as a molecular target of YC-1, we try to clarify the therapeutic effect and mechanism of YC-1 on radiation induced cancer metastasis.

SummaryFlt-4, a VEGF receptor, is activated by its specific ligand, VEGF-C. The resultant signaling pathway promotes angiogenesis and/or lymphangiogenesis. This report provides evidence that the VEGF-C/Flt-4 axis enhances cancer cell mobility and invasiveness and contributes to the promotion of cancer cell metastasis. VEGF-C/Flt-4-mediated invasion and metastasis of cancer cells were found to require upregulation of the neural cell adhesion molecule contactin-1 through activation of the Src-p38 MAPK-C/EBP-dependent pathway. Examination of tumor tissues from various types of cancers revealed high levels of Flt-4 and VEGF-C expression that correlated closely with clinical metastasis and patient survival. The VEGF-C/Flt-4 axis, through upregulation of contactin-1, may regulate the invasive capacity in different types of cancer cells.

Background Acute kidney injury (AKI) is common in preterm infants and is associated with high mortality and morbidity. New biomarkers for the early detection of AKI have been identified. Specifically, urinary neutrophil gelatinase-associated lipocalin (uNGAL) is a new and powerful biomarker for AKI and sepsis. Our study evaluated the reference range of uNGAL in healthy neonates in Taiwan. Methods This study examined 24 preterm and 38 term infants without clinical complications. Urine samples were collected and the uNGAL values were measured at postnatal age (PNA) 3 days, 7 days, 14 days, and 21 days in the preterm infants and at PNA 3 days in the term infants. The uNGAL values were tested using enzyme-linked immunosorbent assay. Results The median uNGAL values in the preterm infants at PNA 3 days, 7 days, 14 days, and 21 days were 41.52 ng/mL, 35.82 ng/mL, 43.79 ng/mL, and 30.85 ng/mL, respectively. The median value at PNA 3 days in the term infants was 88.1 ng/mL. No significant differences associated with gestational age, birth body weight, or PNA were observed among the preterm infants. However, the uNGAL values in the female term infants were higher than those in the male term infants ( p = 0.003). Conclusion This study presents preliminary data on uNGAL levels in neonates in Taiwan. A large-scale study investigating the correlations between uNGAL and with gestational age, birth body weight, sex, and PNA is recommended.

Objective: Obesity and insulin resistance are associated with increased iron stores, but have conflicting effects on ovarian reserve in women with polycystic ovary syndrome (PCOS). Iron-catalyzed oxidative stress might be detrimental to ovarian tissue and granulosa cell function. In this study we determined the association between body iron stores, obesity, and ovarian reserve in women with PCOS. Materials and Methods: One hundred and fifty-six women diagnosed with PCOS according to Rotterdam criteria and 30 normoweight healthy control women were enrolled in this cross-sectional study. Ovarian volume, total antral follicle count, and the anti-Müllerian hormone (AMH) level were measured as an indicator of ovarian reserve. Results: Ferritin and transferrin-bound iron levels were significantly higher in women with PCOS than normoweight controls. Obese women with PCOS had higher ferritin levels (p = 0.006), but lower AMH levels (p