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Find video protocols related to scientific articles indexed in Pubmed.
A ratiometric fluorescent probe for sensing HOCl based on a coumarin-rhodamine dyad.
Chem. Commun. (Camb.)
PUBLISHED: 10-07-2014
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We developed a ratiometric fluorescent probe for sensing HOCl based on coumarin and rhodamine acid that is directly used as a detection moiety. The probe shows high selectivity and sensitivity toward HOCl under best working conditions of myeloperoxidase by which HOCl can be generated from hydrogen peroxide and chloride.
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Identification of dysregulated pathways associated with pancreatic cancer by survival analysis.
Mol Med Rep
PUBLISHED: 05-28-2014
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In order to identify the dysregulated pathways associated with pancreatic cancer, the fourth leading cause of cancer mortality in the United States, tumor and non?tumor samples were systematically analyzed in the present study. Initially, dysregulated genes in pancreatic cancer were identified using paired t?test. Subsequently, dysregulated biological pathways involved in the development of pancreatic cancer were identified by enrichment analysis. Finally, individual survival analysis of the significantly dysregulated functions was conducted at the pathway level. Our results indicated that the pathway named ?Pathways in cancer? was significantly correlated with survival time. In addition, the mean survival time of individual and genetic variation demonstrated a significantly negative correlation, that is, the lower the genetic variation, the longer the survival time. Furthermore, detailed analysis of genes on the pathway named ?Pathways in cancer? denoted that this pathway involved multiple cancer hallmark signals and several dysregulated cancer genes, including tumor protein p53, myelocytomatosis, Kirsten rat sarcoma, phosphatidylinositol 3?kinase, v-raf murine sarcoma viral oncogene homolog B1 and cyclin?dependent kinase inhibitor 2A. According to the DrugBank database, certain oncogenes have been validated to be the targets of drugs, including Sorafenib, Trastuzumab, Imatinib and Paclitaxel or were under investigation. An improved understanding of the pathophysiology of pancreatic cancer has been achieved based on our results and the present study aimed to provide guidance for the development of drugs to treat pancreatic cancer.
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MicroRNA-26a regulates glucose metabolism by direct targeting PDHX in colorectal cancer cells.
BMC Cancer
PUBLISHED: 04-16-2014
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Reprogramming energy metabolism has been an emerging hallmark of cancer cells. MicroRNAs play important roles in glucose metabolism.
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Regulation of endothelial progenitor cell differentiation and function by dimethylarginine dimethylaminohydrolase 2 in an asymmetric dimethylarginine-independent manner.
Cell Biol. Int.
PUBLISHED: 03-20-2014
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Endothelial progenitor cells (EPCs) are involved in the repair of vessels and angiogenesis and are useful in the treatment of ischemic diseases. The dimethylarginine dimethylaminohydrolase (DDAH)/asymmetric dimethylarginine (ADMA) pathway is regulated by silent information regulator 1 (SIRT1), leading to the senescence of endothelial cells (ECs). Here, we demonstrated that peripheral blood EPCs predominantly expressed DDAH2 that increased with EPC differentiation. EPC senescence and dysfunction were induced on interruption of DDAH2 expression, whereas the mRNA expression of vascular endothelial growth factor (VEGF) and kinase-domain insert containing receptor (KDR) were downregulated. Moreover, SIRT1 expression increased with EPC differentiation. Interruption of SIRT1 inhibited DDAH2, VEGF, and KDR expression, but had no effect on the level of ADMA. From our data, we concluded that DDAH2 is involved in the differentiation of EPCs and regulates the senescence and function of EPCs through the VEGF/KDR pathway by activation of SIRT1.
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Fluorofenidone inhibits nicotinamide adeninedinucleotide phosphate oxidase via PI3K/Akt pathway in the pathogenesis of renal interstitial fibrosis.
Nephrology (Carlton)
PUBLISHED: 07-04-2013
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Oxidative stress plays an important role in the progression of renal interstitial fibrosis. The nicotinamide adeninedinucleotide phosphate (NADPH) oxidase (Nox) family is considered one of the major sources of reactive oxygen species (ROS). In the present study, we investigated the inhibitory effects of a novel anti-fibrotic agent, Fluorofenidone (AKF-PD), upon Nox-mediated oxidative stress and deposition of extracellular matrix (ECM) in the development of renalinterstitial fibrosis.
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The association of adipose-derived dimethylarginine dimethylaminohydrolase-2 with insulin sensitivity in experimental type 2 diabetes mellitus.
Acta Biochim. Biophys. Sin. (Shanghai)
PUBLISHED: 05-23-2013
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Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthase (NOS), which can be hydrolyzed by dimethylarginine-dimethylaminohydrolase (DDAH). It has been reported that adipocytes can produce DDAH/ADMA, but its role remains unknown. In the present study, we examined the effects of adipocyte-derived DDAH/ADMA on insulin sensitivity using animal and cell models. Results showed that in adipose tissue of high fat diet-fed diabetic rats, as well as in high glucose (25 mM) plus insulin (100 nM)-treated 3T3-L1 adipocytes, expression levels of insulin receptor substance-1 (IRS-1), glucose transporter-4 (GLUT-4), and DDAH isoform-2 (DDAH-2) were down-regulated compared with control, although DDAH-1 expression showed no significant changes. We also observed that nitric oxide bioavailability, DDAH and NOS activities were subsequently decreased, while the local ADMA content was elevated in diabetic adipose tissue. Transfection of human DDAH-2 gene into high glucose- and insulin-treated 3T3-L1 adipocytes significantly ameliorated DDAH activity, reduced ADMA contents, and up-regulated the mRNA expression levels of IRS-1 and GLUT-4. These findings suggested that in the development of type 2 diabetes mellitus, local DDAH-2 in adipocytes might play an important role in regulating insulin sensitivity.
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The expression and regulation of DFNA5 in human hepatocellular carcinoma DFNA5 in hepatocellular carcinoma.
Mol. Biol. Rep.
PUBLISHED: 04-29-2013
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Hepatocellular carcinoma is a primary malignancy of hepatocytes which accounts for 80 % of all primary liver cancers. DFNA5 has been identified as a tumor suppressor gene with an important role in several frequent forms of cancers, while little is known about its role in hepatocellular carcinoma. Through comparison of the DFNA5 protein expression in hepatocellular carcinoma cells (HepG2) with human fetal lung fibroblast cells (MRC5), we found that the DFNA5 protein expression in hepatocellular carcinoma cells was significantly lower than that in normal cells. The transfection of DFNA5 gene into HepG2 cells could increase DFNA5 protein expression, which subsequently led to inhibition of cell proliferation. Underlying mechanism study revealed that decreased proliferation was due to increased apoptosis and cell cycle arrest. In view of the important role of DFNA5 gene in carcinogenesis, these findings are expected to provide new understanding on development and treatment of human hepatocellular carcinoma.
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Bioinformatics method to analyze the mechanism of pancreatic cancer disorder.
J. Comput. Biol.
PUBLISHED: 04-24-2013
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Pancreatic cancer is an aggressive malignancy with a five-year mortality of 97-98% due to widespread metastatic disease. A better understanding of the molecular mechanism of pancreatic cancer is beneficial for the development of novel approaches for early detection and monitoring of pancreatic cancer. We aim to comprehensively identify the gene expression profile in pancreatic cancer and explore the molecular pathway of pancreatic cancer disorder. Using GSE15471 datasets downloaded from Gene Expression Omnibus data, we first screened the differentially expressed genes in pancreatic cancer using packages in R language. The key pathways of differentially expressed genes were investigated with the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis and synergetic network construction based on weighted Jaccard index. A total of 13,211 differentially expressed genes were identified, and they were enriched in several pathways, such as mitogen-activated protein kinase (MAPK) signaling pathway, transforming growth factor (TGF)-beta signaling pathway, Janus kinase-signal transducers and activators of transcription (JAK-STAT) signaling pathway, and calcium signaling pathway, as well as cell cycle, focal adhesion, complement and coagulation cascades, and leukocyte transendothelial migration. Synergetic pathway network analysis revealed that cytokine-cytokine receptor interaction pathway, calcium signaling pathway, and focal adhesion pathway were three important pathways in the development of pancreatic cancer. The method introduced here is helpful to screen the key pathways for controlling pancreatic cancer progression and provide potential therapeutic targets in the treatment of pancreatic cancer.
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Transplantation of neural stem cells overexpressing glial cell line-derived neurotrophic factor enhances Akt and Erk1/2 signaling and neurogenesis in rats after stroke.
Chin. Med. J.
PUBLISHED: 04-06-2013
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Our previous studies have indicated that the beneficial effects of grafting neural stem cells (NSCs) overexpressing glial cell line-derived neurotrophic factor (GDNF) in rats after stroke. However, the underlying mechanisms are highly debatable. In this study, we investigated whether neurogenesis, Akt, and extracellular signal-regulated kinase 1/2 (Erk1/2) signaling were involved in this process.
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Involvement of DDAH/ADMA pathway in the pathogenesis of rheumatoid arthritis in rats.
Int. Immunopharmacol.
PUBLISHED: 02-22-2013
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Endothelial dysfunction is the early stage of atherosclerosis, which is typically associated with rheumatoid arthritis (RA), a chronic inflammatory autoimmune disorder. Asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase inhibitor, is not only an independent predictor for endothelial dysfunction but also a proinflammatory mediator. It has been shown that the level of ADMA was elevated in patients with RA. In the present study, we investigated the potential effect of ADMA on inflammation process in collagen-induced arthritis (CIA) animal model and primary cultured fibroblast-like synoviocytes (FLS) exposed to tumor necrosis factor-? (TNF-?). In CIA rats, the plasma levels of inflammatory cytokines TNF-?, interleukin-1? (IL-1?) and IL-6 were markedly increased, while the plasma levels of ADMA did not increase. The expression of dimethylarginine dimethylohydrolase2 (DDAH2), the key enzyme for ADMA degradation, was markedly reduced in inflamed joint synovium of CIA rats. Moreover, the expression of anti-inflammatory factor cortistatin (CST) was markedly decreased in joint synovium of CIA rats. Treatment of cultured FLS with TNF-? significantly increased the levels of ADMA, and decreased the expression of DDAH2 mRNA and protein accompany with an increase in the levels of IL-1? and IL-6 and a reduction in the expression of CST mRNA and protein, and the effects of TNF-? were abolished by DDAH2 overexpression. Treatment of FLS with ADMA also significantly increased the levels of IL-1? and IL-6, and reduced the expression of CST. These findings suggest that DDAH/ADMA participates in the pathogenesis of RA, and that the effect of DDAH/ADMA may be mediated by CST.
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Effect of resveratrol derivative BTM-0512 on high glucose-induced dysfunction of endothelial cells: role of SIRT1.
Can. J. Physiol. Pharmacol.
PUBLISHED: 09-09-2011
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Hyperglycemia impairs the function of endothelial cells. Sirtuin 1 (SIRT1) is involved in regulating the function of endothelial cells. Resveratrol, a polyphenol found in many plant species, exerts protective effects on endothelial cells through activation of SIRT1. The aims of this work were to explore whether BTM-0512, a novel derivative of resveratrol, is able to exert beneficial effects on high glucose-induced dysfunction of endothelial cells through regulation of SIRT1. We found that high glucose significantly impaired the function of endothelial cells as shown by reduced tube formation, cell migration, and cell adhesion concomitantly with downregulation of mRNA expression of SIRT1 and vascular endothelial growth factor as well as increased tumor necrosis factor-? release and reactive oxygen species production. These effects of high glucose were inhibited by pretreatment with BTM-0512. The beneficial effects of BTM-0512 on high glucose-induced cell dysfunction were abolished by splitomicin, a specific inhibitor of SIRT1. The regulatory effects of BTM-0512 on high glucose-induced changes in vascular endothelial growth factor mRNA expression and tumor necrosis factor-? release were also abolished by splitomicin. The results suggest that BTM-0512 exerts beneficial effects on high glucose-induced endothelial cell dysfunction through regulation of the SIRT1 - reactive oxygen species - vascular endothelial growth factor - tumor necrosis factor-? pathway.
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Role of VPO1, a newly identified heme-containing peroxidase, in ox-LDL induced endothelial cell apoptosis.
Free Radic. Biol. Med.
PUBLISHED: 07-07-2011
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Myeloperoxidase (MPO) is an important enzyme involved in the genesis and development of atherosclerosis. Vascular peroxidase 1 (VPO1) is a newly discovered member of the peroxidase family that is mainly expressed in vascular endothelial cells and smooth muscle cells and has structural characteristics and biological activity similar to those of MPO. Our specific aims were to explore the effects of VPO1 on endothelial cell apoptosis induced by oxidized low-density lipoprotein (ox-LDL) and the underlying mechanisms. The results showed that ox-LDL induced endothelial cell apoptosis and the expression of VPO1 in endothelial cells in a concentration- and time-dependent manner concomitant with increased intracellular reactive oxygen species (ROS) and hypochlorous acid (HOCl) generation, and up-regulated protein expression of the NADPH oxidase gp91(phox) subunit and phosphorylation of p38 MAPK. All these effects of ox-LDL were inhibited by VPO1 gene silencing and NADPH oxidase gp91(phox) subunit gene silencing or by pretreatment with the NADPH oxidase inhibitor apocynin or diphenyliodonium. The p38 MAPK inhibitor SB203580 or the caspase-3 inhibitor DEVD-CHO significantly inhibited ox-LDL-induced endothelial cell apoptosis, but had no effect on intracellular ROS and HOCl generation or the expression of NADPH oxidase gp91(phox) subunit or VPO1. Collectively, these findings suggest for the first time that VPO1 plays a critical role in ox-LDL-induced endothelial cell apoptosis and that there is a positive feedback loop between VPO1/HOCl and the now-accepted dogma that the NADPH oxidase/ROS/p38 MAPK/caspase-3 pathway is involved in ox-LDL-induced endothelial cell apoptosis.
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Laryngeal aerodynamic analysis in assisting with the diagnosis of muscle tension dysphonia.
J Voice
PUBLISHED: 05-07-2011
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To estimate the aerodynamic multiparameters for patients with muscular tension dysphonia (MTD) and evaluate voice aerodynamic analysis for assisting the diagnosis of this disorder.
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Fluorofenidone attenuates renal interstitial fibrosis in the rat model of obstructive nephropathy.
Mol. Cell. Biochem.
PUBLISHED: 04-15-2011
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Fluorofenidone (FD) is a novel pyridone agent with significant antifibrotic effects in vitro. The purpose of this study is to investigate the effects of FD on renal interstitial fibrosis in rats with obstructive nephropathy caused by unilateral ureteral obstruction (UUO). With pirfenidone (PD, 500 mg/kg/day) and enalapril (10 mg/kg/day) as the positive treatment controls, the rats in different experimental groups were administered with FD (500 mg/kg/day) from day 4 to day 14 after UUO. The tubulointerstitial injury, interstitial collagen deposition, and expression of type I and type III collagen, transforming growth factor-?(1) (TGF-?(1)), connective tissue growth factor (CTGF), platelet-derived growth factor (PDGF), ?-smooth muscle actin (?-SMA), and tissue inhibitor of metalloproteinase-1 (TIMP-1) were assessed. FD treatment significantly attenuated the prominently increased scores of tubulointerstitial injury, interstitial collagen deposition, and protein expression of type I and type III collagen in ureter-obstructed kidneys, respectively. As compared with untreated rats, FD also significantly reduced the expression of ?-SMA, TGF-?(1), CTGF, PDGF, and inhibitor of TIMP-1 in the obstructed kidneys. Fluorofenidone attenuates renal interstitial fibrosis in the rat model of obstructive nephropathy through its regulation on fibrogenic growth factors, tubular cell transdifferentiation, and extracellular matrix.
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Fluorofenidone attenuates diabetic nephropathy and kidney fibrosis in db/db mice.
Pharmacology
PUBLISHED: 02-25-2011
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Fluorofenidone [1-(3-fluorophenyl)-5-methyl-2-(1H)-pyridone, AKF-PD], a novel pyridone agent, showed potent antifibrotic properties. The aim of the present study was to investigate the effects of AKF-PD on diabetic nephropathy and kidney fibrosis, and to obtain an insight into its mechanisms of action.
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Involvement of vascular peroxidase 1 in angiotensin II-induced vascular smooth muscle cell proliferation.
Cardiovasc. Res.
PUBLISHED: 02-03-2011
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Vascular peroxidase 1 (VPO1) is a newly identified haem-containing peroxidase that catalyses the oxidation of a variety of substrates by hydrogen peroxide (H(2)O(2)). Considering the well-defined effects of H(2)O(2) on the vascular remodelling during hypertension, and that VPO1 can utilize H(2)O(2) generated from co-expressed NADPH oxidases to catalyse peroxidative reactions, the aims of this study were to determine the potential role of VPO1 in vascular remodelling during hypertension.
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Involvement of profilin-1 in angiotensin II-induced vascular smooth muscle cell proliferation.
Vascul. Pharmacol.
PUBLISHED: 01-05-2011
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Profilin-1, a regulator of actin polymerization, has recently been linked to vascular hypertrophy and remodeling. Whether profilin-1 is involved in angiotensin (Ang) II-induced proliferation of vascular smooth muscle cells leading to vascular remodeling in hypertension remains unclear. The present study was designed to analyze the correlation of profilin-1 and vascular remodeling during hypertension and to evaluate the role of profilin-1 in proliferation of vascular smooth muscle cells and the underlying mechanisms. The vascular morphology and the expression of profilin-1 in arterial tissues of spontaneously hypertensive rats and Wistar-Kyoto rats were assessed. The profilin-1 expression was significantly increased concomitantly with definite vascular remodeling by evaluating the media thickness, lumen diameter, media thickness-to-lumen diameter ratio and mean nuclear area in artery media in spontaneously hypertensive rats, which was inhibited by treatment with losartan. In cultured rat aortic smooth muscle cells (RASMCs), Ang II induced profilin-1 expression in a dose- and time-dependent manner. Knockdown of profilin-1 using small hairpin RNA inhibited Ang II-induced proliferation of RASMCs. Moreover, blockade of JAK2/STAT3 signaling pathway also inhibited Ang II-induced proliferation of RASMCs and profilin-1 expression. These results suggest that profilin-1 mediates the proliferation of RASMCs induced by Ang II via activation of Ang II type 1 receptor/JAK2/STAT3 signaling pathway, which may contribute to vascular remodeling in hypertension.
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Ginsenoside Rb1 regulates the expressions of brain-derived neurotrophic factor and caspase-3 and induces neurogenesis in rats with experimental cerebral ischemia.
J Ethnopharmacol
PUBLISHED: 06-23-2010
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Recent studies have revealed that ginsenoside Rb1 (GRb1) is neuroprotective for cerebral ischemia. However, the mechanism underlying of this function is unclear. We assessed whether this neuroprotective effect of GRb1 was mediated by the levels of brain-derived neurotrophic factor (BDNF), by the levels of caspase-3 proteins and by induced neurogenesis in rats following transient cerebral ischemia or not.
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The role of the DDAH-ADMA pathway in the protective effect of resveratrol analog BTM-0512 on gastric mucosal injury.
Can. J. Physiol. Pharmacol.
PUBLISHED: 06-18-2010
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A recent study showed that resveratrol, a polyphenol found in many plant species, exerts dual effects on gastric mucosal injury. By using the model of ethanol-induced gastric mucosal injury in the present study, we explored the effect of trans-3,5,4-trimethoxystilbene (BTM-0512), a novel analog of resveratrol, on gastric mucosal injury and the possible underlying mechanisms. Gastric mucosal injury in the rat was induced by oral administration of acidified ethanol. The gastric tissues were collected for determination of the gastric ulcer index, asymmetric dimethylarginine (ADMA) and nitric oxide (NO) contents, the activity of dimethylarginine dimethylaminohydrolase (DDAH) and superoxide anion (O2(-)) or hydroxyl radical (OH*) formation. The results showed that acute administration of ethanol significantly increased the gastric ulcer index concomitantly with the decrease in DDAH activity and NO content as well as the increase in ADMA content, effects that were reversed by pretreatment with BTM-0512 (100 mg/kg) or L-arginine (300 mg/kg). Administration of BTM-0512 did not show a significant effect on O2(-) or OH. formation. The results suggest that BTM-0512 could protect the gastric mucosa against ethanol-induced injury, which is mainly related to an increase in DDAH activity and subsequent decrease in ADMA content.
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Electromagnetic scattering for a uniaxial anisotropic sphere in an off-axis obliquely incident Gaussian beam.
J Opt Soc Am A Opt Image Sci Vis
PUBLISHED: 05-29-2010
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An analytical solution to the scattering of an off-axis Gaussian beam obliquely incident on a uniaxial anisotropic sphere is obtained in the particle-centered system. Based on the local approximation to the off-axis beam shape coefficients and the coordinate rotation theory, the off-axis obliquely incident Gaussian beam is expanded with the spherical vector wave functions in the primary coordinate of the uniaxial anisotropic sphere. The internal fields of the uniaxial anisotropic sphere are proposed in the integrating form of the spherical vector wave functions by introducing the Fourier transform. By matching the fields on the boundary and solving matrix equations, the expansion coefficients are analytically derived. The influences of the beam waist center positioning and the obliquely incident angles, as well as the permittivity tensors on the far scattered field distributions, are numerically presented. The correctness of the theory is verified by comparing our numerical results in special cases with results from the references and with calculations by other algorithms.
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Synthesis, characterization and vasculoprotective effects of nitric oxide-donating derivatives of chrysin.
Bioorg. Med. Chem.
PUBLISHED: 02-06-2010
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Vascular complications are major causes of disability and death in patients with diabetes mellitus. It is often characterized by endothelial dysfunction. Studies have shown that either the loss of nitric oxide bioactivity or the decreased biosynthesis of NO is a central mechanism in endothelial dysfunction. As such, the delivery of exogenous NO is an attractive therapeutic option that has been used to slow the progress of diabetic vascular complications. In this paper, a novel group of hybrid nitric oxide-releasing chrysin derivatives was synthesized. The results indicated that all these chrysin derivatives exhibited in vitro inhibitory activities against aldose reductase and advanced glycation end-products formation. And some of them were even found to increase the glucose consumption of HepG2 cells. Furthermore, all compounds released NO upon incubation with phosphate buffer at pH 7.4. These hybrid ester NO donor prodrugs offer a potential drug design concept for the development of therapeutic or preventive agents for vascular complications due to diabetes.
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Inhibitory effect of resveratrol derivative BTM-0512 on high glucose-induced cell senescence involves dimethylaminohydrolase/asymmetric dimethylarginine pathway.
Clin. Exp. Pharmacol. Physiol.
PUBLISHED: 02-04-2010
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1. It has been reported that resveratrol exerts the inhibitory effects on aging through activation of sirtuin 1 (SIRT1) and dimethylarginine dimethylaminohydrolase (DDAH)/asymmetric dimethylarginine (ADMA) pathway involved in the high glucose-induced endothelial cell senescence. 2. The aims of this work were to explore whether BTM-0512, a novel derivative of resveratrol, was able to exert the beneficial effect on high glucose-induced cellular senescence through regulating the DDAH/ADMA pathway and to explore whether the regulatory effect of BTM-0512 on DDAH/ADMA pathway was related to the activation of SIRT1. 3. The senescence model of endothelial cells was induced by high glucose and the cells were collected for the determination of beta-galactosidase and DDAH activity, ADMA level, DDAH and SIRT1 mRNA expression. 4. The results showed that high glucose significantly increased the ratio of senescent cells concomitantly with the decreased DDAH activity, the downregulated DDAH2 and SIRT1 mRNA expressions and the increased ADMA levels, which were attenuated by pretreatment with BTM-0512. 5. The beneficial effects of BTM-0512 on high glucose-induced senescence were blocked by splimtomicin, the specific inhibitor of SIRT1, or by silencing DDAH2 expression. 6. The results suggest that BTM-0512 was able to exert the beneficial effects on high glucose-induced cellular senescence through regulating the DDAH/ADMA pathway, and its regulatory effect on DDAH/ADMA pathway was related to the activation of SIRT1.
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[Quantitative analysis of the concentration of Br-doping in micro-shell coating with XRF].
Guang Pu Xue Yu Guang Pu Fen Xi
PUBLISHED: 10-09-2009
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In inertial confinement fusion (ICF) physics experiment, the micro-shell that contains Br-doped CH coating must be characterized for doping Br concentration level. X-ray fluorescence (XRF), with its unique capability to quantitatively determine concentrations of most elements simultaneously and non-destructively, is generally the method of choice for total dopant (Z > 11) concentration. In the present paper, a method to determine the dopant concentration in ICF micro-shell coating with X-ray fluorescence spectrometry is described, and the calibration model is founded by the calculation of fluorescence intensity of film and micro-shell sample. Based on the calibration model, the fluorescence intensity vs concentration of Br-doped CH coating of micro-shell was obtained. The experiment result shows that X-ray fluorescence spectrometry is a nondestructive and accurate method of measurement of coating dopant in the inertial confinement fusion micro-shell sample, and the measuring error is about 5% for Br doped CH coating of micro-shells with 10 micron thickness coating.
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Internal and external electromagnetic fields for on-axis Gaussian beam scattering from a uniaxial anisotropic sphere.
J Opt Soc Am A Opt Image Sci Vis
PUBLISHED: 08-04-2009
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Scattering of an on-axis Gaussian beam by a uniaxial anisotropic sphere is studied. The incident on-axis Gaussian beam is expanded in terms of spherical vector wave functions, and the beam shape coefficients are obtained by applying the local approximation. The internal fields of a uniaxial anisotropic sphere are proposed in the integrating form of the spherical vector wave functions by introducing the Fourier transform. Utilizing the continuous tangential boundary conditions, both the scattered and the internal field coefficients are derived analytically. Numerical calculations are presented. The effects of the beam width, beam waist center positioning, and anisotropy on scattering properties are analyzed. The internal and near-surface field distributions are also discussed, and the two eigenmodes are characterized. The continuity on the surface of a uniaxial anisotropic sphere is well confirmed.
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Role of anandamide transporter in regulating calcitonin gene-related peptide production and blood pressure in hypertension.
J. Hypertens.
PUBLISHED: 05-23-2009
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To explore the role of anandamide (AEA) transporter in regulating calcitonin gene-related peptide (CGRP) production and blood pressure.
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Involvement of dimethylarginine dimethylaminohydrolase-2 in visfatin-enhanced angiogenic function of endothelial cells.
Diabetes Metab. Res. Rev.
PUBLISHED: 02-21-2009
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Visfatin, a new adipocytokine, was reported to promote angiogenesis. Dimethylarginine dimethylaminohydrolase (DDAH), which could regulate vascular endothelial growth factor (VEGF) expression in endothelial cells, is thought as a novel modulator of angiogenesis. The aim of the study was to investigate the role of DDAH2 in visfatin-induced angiogenesis in human umbilical vein endothelial cells (HUVECs).
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All-trans retinoic acid inhibits cobalt chloride-induced apoptosis in PC12 cells: role of the dimethylarginine dimethylaminohydrolase/asymmetric dimethylarginine pathway.
J. Neurosci. Res.
PUBLISHED: 01-22-2009
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Previous studies have shown that the endogenous nitric oxide synthase inhibitor asymmetric dimethylarginine (ADMA) and its specific hydrolase dimethylarginine dimethylaminohydrolase (DDAH) are involved in the regulation of apoptosis in different cell types. In the present study, we investigated the role of the DDAH/ADMA pathway in cobalt chloride (CoCl(2))-induced apoptosis and the antiapoptotic effect of all-trans retinoic acid (atRA) in undifferentiated pheochromocytoma (PC12) cells. Treatment of CoCl(2) (125 microM) for 48 hr significantly induced the apoptosis of PC12 cells, concomitantly with increased intracellular reactive oxygen species (ROS) production and caspase-3 activity. CoCl(2) treatment also decreased the activity of DDAH and the expression of DDAH2 (mRNA and protein), resulting in an increased level of ADMA. All these alterations induced by CoCl(2) were attenuated by atRA (0.1, 1, or 10 microM). Interestingly, the antiapoptotic effects of atRA were inhibited by DDAH2 small RNA interference. In contrast, DDAH2 overexpression inhibited the proapoptotic effects of CoCl(2). We also found that treatment of exogenous ADMA (3, 10, or 30 microM) induced the apoptosis of PC12 cells in a concentration- and time-dependent manner, which was inhibited by the antioxidant or the caspase-3 inhibitor. These findings suggest that the modulation of the DDAH/ADMA/ROS pathway plays an important role in CoCl(2)-induced apoptosis and the antiapoptotic effects of atRA in undifferentiated PC12 cells.
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Evaluation of in vivo antioxidant and immunity enhancing activities of sodium aescinate injection liquid.
Molecules
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Oxidative stress is involved in the development and progression of disease. Because sodium aescinate has been reported to have immunity enhancing and antioxidative effects, we investigated its activity by employing a hepatocellular carcinoma (HCC) mouse model. Sixty BALB/c mice were randomly divided into four groups, including a 1.4 mg/kg treated group (n = 15), a 2.8 mg/kg treated group (n = 15), an untreated hepatocellular carcinoma control group (n = 15) and a normal control group (n = 15). After H22 cells were cultured for one week, we collected 2 × 10? cells and injected them subcutaneously as 0.2 mL cell suspensions in sterile saline into the right shoulder region of every mouse. The animals were monitored for changes in activity, physical condition and body weight during the experiment. The next day after injection of H22 cells, animals in these test groups received one intraperitoneal injection of drug or physiological saline for 13 days. Results showed that in the sodium aescinate injection liquid (SAIL)-treated HCC mice, serum interleukin-1 beta (IL-1?), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-?), interferon-gamma (IFN-?), Gamma-glutamyltransferase (?-GT), alanine transaminase (ALT), aspartate transaminase (AST) and alkaline phosphatase (ALP) levels were significantly decreased compared with normal control mice. In addition, treatment with sodium aescinate injection liquid significantly decreased blood and liver malondialdehyde (MDA) levels, increased glutathione (GSH) levels, and antioxidant enzyme [superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px)] activities in a dose-dependent manner. We conclude that sodium aescinate injection liquid can decrease oxidative injury and enhance immunity functions in HCC mice.
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Dimethylarginine dimethylaminohydrolase 1 regulates nerve growth factor-promoted differentiation of PC12 cells in a nitric oxide-dependent but asymmetric dimethylargenine-independent manner.
J. Neurosci. Res.
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There are significant morphological and biochemical alterations during nerve growth factor (NGF)-promoted neuronal differentiation, and the process is regulated by molecules, including nitric oxide (NO). Dimethylarginine dimethylaminohydrolase (DDAH) is thought to play a critical role in regulating NO production via hydrolyzing the endogenous NO synthase (NOS) inhibitor asymmetric dimethylarginine (ADMA). Thus, we tested the role of DDAH in NGF-promoted differentiation of PC12 (pheochromocytoma) cells. The present results show that both mRNA and protein levels of DDAH1 were increased, whereas those of DDAH2 were decreased, during NGF-promoted cell differentiation. Both the DDAH activity and the ADMA level in cultured medium were unchanged in this process. NGF promoted neurite formation and induced the expression of microtubule-associated protein 2 (MAP2), a neuronal marker, which were both significantly repressed by DDAH1 silence with small interfering RNA but not by DDAH2 silence. The expressions of three isoforms of NOS were markedly upregulated after NGF stimulation with a time course similar to that of DDAH1, which were attenuated by DDAH1 silence. Conversely, overexpression of DDAH1 accelerated neurite formation in PC12 cells, concomitantly with upregulating the expression of three NOS isoforms. In summary, our data reveal the critical regulatory effect of DDAH1 on NGF-promoted differentiation of PC12 cells in an NOS/NO-dependent but ADMA-independent manner.
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Advanced glycation end-products impair Na(+) /K(+) - ATPase activity in diabetic cardiomyopathy: role of the AMPK/ SIRT1 pathway.
Clin. Exp. Pharmacol. Physiol.
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Decreased Na(+) /K(+) -ATPase activity and both sirtuin 1 (SIRT1) and AMPK have been reported to be involved in the development of diabetic cardiomyopathy (DCM). This work aimed to investigate the advanced glycation end products (AGEs) that impair Na(+) /K(+) -ATPase stability by regulating the AMPK/SIRT1 pathway during progression of DCM. To study type 1 diabetic mellitus (T1DM), a disease model in rats was established by a single intraperitoneal injection of streptozotocin (STZ, 65 mg/kg), and neonatal rat cardiomyocytes were also cultured. Heart function was detected by Doppler, and SIRT1 and AMPK protein expression were detected by immunohistochemistry and Western blotting. Na(+) /K(+) -ATPase activity was also monitored. Using in vivo rat models of DCM, we showed that Na(+) /K(+) -ATPase activity decreased when both AMPK and SIRT1 expression were downregulated. In vitro, AGEs impaired Na(+) /K(+) -ATPase activity and decreased the AMPK and SIRT1 expression. SIRT1 overexpression increased Na(+) /K(+) -ATPase activity. 5-aminoimidazole-4-carboxamide-3-ribonucleoside (AICAR) upregulated SIRT1 expression and increased Na(+) /K(+) -ATPase activity, which could be partially abolished by splitomicin. Our results suggest that the dysfunction of DCM is related with AGEs-induced Na(+) /K(+) -ATPase activity impairment through a mechanism involving the AMPK/SIRT1 pathway. This article is protected by copyright. All rights reserved.
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