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Find video protocols related to scientific articles indexed in Pubmed.
[Analysis of serum vancomycin concentration after administration of different doses in children with Staphylococcus aureus pneumonia].
Zhongguo Dang Dai Er Ke Za Zhi
PUBLISHED: 10-26-2014
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ObBJECTIVE: To analyze serum vancomycin concentration after administration of different therapeutic doses in children with Staphylococcus aureus pneumonia (SAP) in order to determine the appropriate dose of vancomycin in clinical administration.
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[Clinical features of inhaled and blood-borne Staphylococcus aureus pneumonia and analysis of antibiotic resistance of the pathogen in children].
Zhongguo Dang Dai Er Ke Za Zhi
PUBLISHED: 10-26-2014
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To compare the clinical manifestations between inhaled and blood-borne Staphylococcus aureus pneumonia (SAP) and the antibiotic resistance between the isolates of inhaled and blood-borne Staphylococcus aureus.
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Dysfunctional endothelial progenitor cells in cardiovascular diseases: role of NADPH oxidase.
J. Cardiovasc. Pharmacol.
PUBLISHED: 09-30-2014
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Endothelial progenitor cells (EPCs) play a critical role in maintenance of the endothelial integrity and vascular homeostasis, as well as in neovascularization. Dysfunctional EPCs are believed to contribute to the endothelial dysfunction and are closely related to the development of various cardiovascular diseases, such as hypertension, hyperlipidemia and stroke. However, the underlying mechanisms of EPCs dysfunction are complicated and remain largely elusive. Recent studies have demonstrated that reactive oxygen species (ROS) are key factors that involve in modulation of stem and progenitor cell function under various physiologic and pathologic conditions. It has been shown that NADPH oxidase (NOX)-derived ROS are the major sources of ROS in cardiovascular system. Accumulating evidence suggest that NOX-mediated oxidative stress can modulate EPCs bioactivities, such as mobilization, migration and neovascularization, and that inhibition of NOX has been shown to improve EPCs functions. This review summarized recent progress in the studies on the correlation between NOX-mediated EPCs dysfunction and cardiovascular diseases.
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Long-term follow-up results of the pacing to avoid cardiac enlargement (PACE) trial.
Eur. J. Heart Fail.
PUBLISHED: 09-01-2014
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We report the results of long-term follow-up of the Pacing to Avoid Cardiac Enlargement (PACE) trial, a prospective, double-blinded, randomized, multicentre study that confirmed the superiority of biventricular (BiV) pacing compared with right ventricular apical (RVA) pacing in prevention of LV adverse remodelling and deterioration of systolic function at 1 and 2 years.
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Alda-1 reduces cerebral ischemia/reperfusion injury in rat through clearance of reactive aldehydes.
Naunyn Schmiedebergs Arch. Pharmacol.
PUBLISHED: 08-26-2014
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Many studies demonstrate that accumulation of reactive aldehydes plays an important role in cellular oxidative injury and aldehyde dehydrogenase 2 (ALDH2)-mediated detoxification of reactive aldehydes is thought as an endogenous protective mechanism against cell injury. This study was performed to explore whether Alda-1, a newly identified ALDH2 activator, was able to protect brain against ischemia/reperfusion injury through clearance of reactive aldehydes. In a rat model of focal cerebral ischemia/reperfusion injury, neurological function, infarct volume, cellular apoptosis, mortality, ALDH2 activity and protein expression, contents of 4-hydroxy-2-nonenal (4-HNE), and malondialdehyde (MDA) were determined. The results showed that ischemia/reperfusion treatment led to increase in neurological deficit score, infarct volume, cellular apoptosis, and mortality accompanied by the elevated levels of reactive aldehydes (4-HNE and MDA). There was no significant change in ALDH2 activity and protein expression. Alda-1 treatment at both dosages (15 mg/kg?×?2 or 50 mg/kg?×?2, i.g.) was able to increase the activity of ALDH2 and decrease the accumulation of reactive aldehydes concomitantly with the improvement of brain injury (decrease in infarct volume, cellular apoptosis, and mortality) and neurological function (decrease in neurological deficit score). However, Alda-1 treatment did not affect ALDH2 protein expression. Our results suggest that the protective effect of Alda-1 on cerebral ischemia/reperfusion injury is related to ALDH2 activation and clearance of reactive aldehydes.
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Mitochondrial aldehyde dehydrogenase, a potential drug target for protection of heart and brain from ischemia/reperfusion injury.
Curr Drug Targets
PUBLISHED: 08-21-2014
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Mitochondrial aldehyde dehydrogenase (ALDH2) is an isoenzyme of aldehyde dehydrogenases (ALDH), a group of enzymes that are responsible for clearance of aldehydes in the body. In animal myocardial or cerebral ischemia/ reperfusion (I/R) models, accumulation of toxic aldehydes, such as 4-hydroxy-2-nonenal and malondialdehyde, is thought to be an important mechanism for myocardial and cerebral I/R injury. Among the isoenzymes of ALDH, ALDH2 is believed to play a major role in clearance of toxic aldehydes. Thus, ALDH2 might be a potential drug target for protection of the heart or brain from I/R injury. Indeed, some of the newly identified ALDH2 activators (such as Alda-1) have demonstrated beneficial effects on heart and brain I/R injury. In addition, ALDH activity is present at high levels in some stem or progenitor cells, known as ALDH bright (ALDH(br)) cells, which possess potential value in treating patients with myocardial ischemia. The main purpose of this review is 1) to summarize recent findings regarding the role of ALDH2 in protection of heart or brain from I/R injury, 2) to list the available ALDH2 activators with their potency, selectivity and clinical potentials, and 3) to provide a rationale for ALDH(br) cells in clinical therapeutic value.
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Changes of ventricular and peripheral performance in patients with heart failure and normal ejection fraction: insights from ergometry stress echocardiography.
Eur. J. Heart Fail.
PUBLISHED: 05-17-2014
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We assessed the left ventricular (LV) and peripheral performance at rest and during exercise in healthy and heart failure subjects with normal ejection fraction (HFNEF) or with reduced ejection fraction (HFREF).
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Left anterior descending coronary artery flow impaired by right ventricular apical pacing: the role of systolic dyssynchrony.
Int. J. Cardiol.
PUBLISHED: 02-18-2014
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Right ventricular (RV) pacing may affect myocardial perfusion and coronary blood flow; however, it remains unknown whether this is related to systolic dyssynchrony induced by RV pacing. This prospective study was aimed to assess the relationship between dyssynchrony and the changes of coronary blood flow.
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Prognostic significance of Tet methylcytosine dioxygenase 2 (TET2) gene mutations in adult patients with acute myeloid leukemia: a meta-analysis.
Leuk. Lymphoma
PUBLISHED: 02-15-2014
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Tet methylcytosine dioxygenase 2 (TET2) gene mutations have recently been recognized in acute myeloid leukemia (AML). We performed a meta-analysis to evaluate the controversial prognostic significance of TET2 mutations in AML. Eight studies, covering 2552 patients with AML, were included in this analysis. Pooled hazard ratios (HRs) indicated that TET2 mutations had a poor prognostic impact on the survival of patients with AML. The combined HR for overall survival (OS) was 1.53 and the summary HR for event-free survival (EFS) was 1.64. Additionally, TET2 mutations appeared to be an adverse prognostic indicator in both patients with cytogenetically normal (CN)-AML (HR for OS: 1.43 and HR for EFS: 1.76) and subgroups of patients with favorable-risk genotypes (HR for EFS: 2.35) and intermediate-I-risk genotypes (HR for EFS: 1.57). These findings indicate that TET2 mutations have an adverse impact on prognosis and may help to justify risk-adapted therapeutic strategies for patients with AML.
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Inhibition of NOX/VPO1 pathway and inflammatory reaction by trimethoxystilbene in prevention of cardiovascular remodeling in hypoxia-induced pulmonary hypertensive rats.
J. Cardiovasc. Pharmacol.
PUBLISHED: 02-05-2014
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Recent studies show that resveratrol exerts beneficial effects on prevention of pulmonary hypertension. This study is performed to explore the effects of trimethoxystilbene, a novel resveratrol analog, on rat pulmonary vascular remodeling and right ventricular hypertrophy in hypoxia-induced pulmonary arterial hypertension (PAH) and the underlying mechanisms. Sprague-Dawley rats were placed in a chamber and exposed to 10% O(2) continuously for 4 weeks to induce PAH. The effects of trimethoxystilbene (5 or 10 mg/kg per day, intragastric [i.g.]) and resveratrol (as a positive control, 25 mg/kg per day, i.g.) on hypoxia-induced PAH vascular remodeling and right ventricle hypertrophy were evaluated. At the end of experiments, the index for pulmonary vascular remodeling and right ventricle hypertrophy, inflammatory cell infiltration in lung tissue, the plasma levels and lung tissue contents of hydrogen peroxide (H(2)O(2)), the mRNA and protein levels for NADPH oxidases (NOX2, NOX4) and vascular peroxidase 1 (VPO1) in pulmonary artery or right ventricle were measured. The results showed that trimethoxystilbene treatment significantly attenuated hypoxia-induced pulmonary vascular remodeling (such as decrease in the ratio of wall thickness to vessel external diameter) and right ventricle hypertrophy (such as decrease in the ratio of right ventricle weight to the length of the tibia), accompanied by downregulation of NOX2, NOX4, and VPO1 expression in pulmonary artery or right ventricle, decrease in H(2)O(2) production and inflammatory cell infiltration in lung tissue. Trimethoxystilbene is able to prevent pulmonary vascular remodeling and right ventricle hypertrophy in hypoxia-induced rat model of PAH, which is related to inhibition of the NOX/VPO1 pathway-mediated oxidative stress and the inflammatory reaction.
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What can three-dimensional speckle-tracking echocardiography contribute to evaluate global left ventricular systolic performance in patients with heart failure?
Int. J. Cardiol.
PUBLISHED: 01-22-2014
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Three-dimensional speckle-tracking echocardiography (3D-STE) is a newly developed technique to evaluate left ventricular (LV) deformation by measuring the area strain (AS) of endocardial surface that combines information from both longitudinal (LS) and circumferential strain (CS). We performed a study to examine myocardial deformation in patients with heart failure (HF) using 3D-STE.
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Protective effect of vitexin compound B-1 against hypoxia/reoxygenation-induced injury in differentiated PC12 cells via NADPH oxidase inhibition.
Naunyn Schmiedebergs Arch. Pharmacol.
PUBLISHED: 01-10-2014
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Vitexin compound B-1 (VB-1) is a novel member of the vitexins family isolated from the seeds of the Chinese herb Vitex negundo. This study aims to investigate whether VB-1 is able to protect nerve cells against oxidative injury and whether the antioxidative effects of VB-1 occur through a mechanism involving the inhibition of NADPH oxidase (NOX) in a manner of hypoxia-inducible factor 1? (HIF-1?)-dependent. To establish a neuronal in vitro model of oxidative stress, the differentiated PC12 cells were subjected to 5 h of hypoxia followed by 20 h of reoxygenation (H/R). Three dosages of VB-1 (10(-8), 10(-7), and 10(-6) M) were chosen to evaluate the effect of VB-1 on H/R-induced injury and the underlying mechanisms. At the end of the experiments, culture mediums and cells were collected for analysis of cellular apoptosis, lactate dehydrogenase (LDH) and caspase 3/7-like activities, reactive oxygen species (ROS) levels, 4-hydroxynonenal (4-HNE) and malondialdehye (MDA) contents, and HIF-1? and NOX expression, respectively. Our results showed that cell injury (indicated by apoptosis ratio, caspase 3/7-like activity, and LDH release), oxidative stress (indicated by ROS production, 4-HNE, and MDA contents), NOX activity, and NOX expression (NOX2 and NOX4 isoforms) were dramatically increased in PC12 cells following H/R, which were attenuated in the presence of VB-1 at dosage of 10(-7) or 10(-6) M. There was no significant change in HIF-1? expression in all experimental groups. These results provide evidence that VB-1 is able to protect the PC12 cells against H/R-induced injury through a mechanism involving the suppression of NOX expression and subsequent reduction of ROS production. The effect of VB-1 on H/R-induced NOX expression is independent on HIF-1? inhibition.
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The prognostic role of the class III ?-tubulin in non-small cell lung cancer (NSCLC) patients receiving the taxane/vinorebine-based chemotherapy: a meta-analysis.
PLoS ONE
PUBLISHED: 01-01-2014
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A number of studies have examined the relationship between the expression of the class III ?-tubulin (TUBB3) and the treatment responses to the taxane/vinorebine-based chemotherapy in patients with non-small cell lung cancer (NSCLC). However, the results of these studies were inconsistent and inconclusive. Therefore, we conducted an up-to-date meta-analysis to evaluate the prognostic role of TUBB3 in the taxane/vinorebine-based chemotherapy.
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[Clinical analysis of 28 cases of bronchiolitis obliterans].
Zhongguo Dang Dai Er Ke Za Zhi
PUBLISHED: 10-18-2013
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To study the clinical features of bronchiolitis obliterans (BO) in children.
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Comparing CT perfusion with oxygen partial pressure in a rabbit VX2 soft-tissue tumor model.
J. Radiat. Res.
PUBLISHED: 09-26-2013
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The aim of this study was to evaluate the oxygen partial pressure of the rabbit model of the VX2 tumor using a 64-slice perfusion CT and to compare the results with that obtained using the oxygen microelectrode method. Perfusion CT was performed for 45 successfully constructed rabbit models of a VX2 brain tumor. The perfusion values of the brain tumor region of interest, the blood volume (BV), the time to peak (TTP) and the peak enhancement intensity (PEI) were measured. The results were compared with the partial pressure of oxygen (PO2) of that region of interest obtained using the oxygen microelectrode method. The perfusion values of the brain tumor region of interest in 45 successfully constructed rabbit models of a VX2 brain tumor ranged from 1.3-127.0 (average, 21.1 ± 26.7 ml/min/ml); BV ranged from 1.2-53.5 ml/100g (average, 22.2 ± 13.7 ml/100g); PEI ranged from 8.7-124.6 HU (average, 43.5 ± 28.7 HU); and TTP ranged from 8.2-62.3 s (average, 38.8 ± 14.8 s). The PO2 in the corresponding region ranged from 0.14-47 mmHg (average, 16 ± 14.8 mmHg). The perfusion CT positively correlated with the tumor PO2, which can be used for evaluating the tumor hypoxia in clinical practice.
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[Analysis of soil respiration and influence factors in wheat farmland under conservation tillage in southwest hilly region].
Huan Jing Ke Xue
PUBLISHED: 09-14-2013
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In order to investigate the effect of conservation tillage on soil respiration in dry cropping farmland in southwest purple hilly region, the LI6400-09 respiratory chamber was adopted in the experiment conducted in the experimental field in Southwest University in Beibei, Chongqing. The respiration and the hydrothermal and biotic factors of soil were measured and analyzed during the growth period of wheat in the triple intercropping system of wheat/maize/soybean. There were four treatments including T (traditional tillage), R (ridge tillage), TS (traditional tillage + straw mulching) and RS (ridge tillage + straw mulching), which were all in triplicates. The results indicated that the soil respiration rate changed in the range of 1.100-2.508 micromol x (m2 x s)(-1) during the reproductive growth stage of wheat. There were significant differences in soil respiration rate among different treatments, which could be ranked as RS > R > TS > T. The soil temperature in the 10cm layer was ranked as T > R > TS > RS. The relationship between soil respiration and soil temperature fitted well with an exponential function, in which the Q10 values were 1.25, 1.20, 1.31 and 1.26, respectively. The soil moisture in the 5cm layer was ranked as TS > RS > T > R. The best fitting model between soil moisture and soil respiration was a parabolic curve, indicating the presence of soil moisture with the strongest soil respiration. The response threshold of wheat to soil moisture was 14.80%-17.47% during the reproductive stage. The dominant groups of soil animals were Collembola and Acarina, which were correlated with soil respiration to some extent. The correlation was high in the treatments T and R, ranged from 0.669-0.921, whereas there was no remarkable correlation in the other treatments.
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Quantification of left ventricular performance in different heart failure phenotypes by comprehensive ergometry stress echocardiography.
Int. J. Cardiol.
PUBLISHED: 05-03-2013
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We evaluated the left ventricular (LV) performance in patients with heart failure and preserved ejection fraction (HFPEF) during exercise as compared to those with heart failure and reduced ejection fraction (HFREF) and healthy subjects.
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Liraglutide protects pancreatic beta cells during an early intervention in Gato-Kakizaki rats.
J Diabetes
PUBLISHED: 03-11-2013
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Glucagon-like peptide-1 (GLP-1) analogues have emerged as insulin secretagogues and are widely used in type 2 diabetic patients. GLP-1 analogues also demonstrate a promotion of beta cell proliferation and reduction of apoptosis in rodents. In the present study, we investigated the protection of pancreatic beta cells by early use (at the age of 2 weeks) of GLP-1 analogue, liraglutide in Gato-Kakizaki (GK) rats and explored the underlying mechanisms.
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Expression of apoptosis-associated microRNAs in ethanol-induced acute gastric mucosal injury via JNK pathway.
Alcohol
PUBLISHED: 02-23-2013
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MicroRNAs (miRNAs) have been shown to be closely associated with cellular apoptosis, but their involvement in response to ethanol-induced gastric mucosal epithelial cell apoptosis remains largely unknown. The purpose of this study was to investigate the expression profile of apoptosis-associated miRNAs in ethanol-induced acute gastric mucosal injury and the mechanisms underlying injury. Gastric mucosal injury was induced in rats by oral administration of ethanol, and gastric tissues were collected for analysis of gastric ulcer index, apoptosis ratio, caspase-3 activity, and miRNAs expression. Cell cultures of human gastric mucosal epithelial cells (GES-1) were incubated with ethanol to induce apoptosis. Mimics or inhibitors of miRNAs or c-Jun N-terminal kinase (JNK) inhibitor were added to the cell culture medium. GES-1 cells were collected for analysis of apoptosis ratio, caspase-3 activity, miRNAs expression, and protein phosphorylation levels of JNK, p38 mitogen-activated protein kinase (p38MAPK), or extracellular signal-regulated kinase (ERK). In the animal experiments, gastric ulcer index, cellular apoptosis, and caspase-3 activity were significantly increased, accompanied by up-regulation of miR-145 and down-regulation of the microRNAs miR-17, miR-19a, miR-21, miR-181a, and miR-200c. In the human cell culture experiments, the anti-apoptotic effects of miR-19a and miR-21 or pro-apoptotic effect of miR-145 were confirmed by their corresponding mimics or inhibitor; the ethanol-induced GES-1 apoptosis as well as the changes in miRNAs expression were significantly attenuated in the presence of JNK inhibitor. These results demonstrated that miR-145, miR-19a, and miR-21 were the apoptosis-associated miRNAs in gastric mucosal epithelial cells. The regulation of expression of these 3 miRNAs in ethanol-induced GES-1 apoptosis involved the JNK pathway.
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Identification and field evaluation of non-host volatiles disturbing host location by the tea geometrid, Ectropis obliqua.
J. Chem. Ecol.
PUBLISHED: 02-21-2013
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Volatile organic compounds derived from non-host plants, Ocimum basilicum, Rosmarinus officinalis, Corymbia citriodora, and Ruta graveolens, can be used to mask host plant odors, and are repellent to the tea geometrid, Ectropis obliqua. Volatile compounds were collected by headspace absorption, and the components were identified and quantified by using gas chromatography/mass spectrometry. The responses of antennae of female E. obliqua to the compounds were evaluated with gas chromatography/electroantennography detection. Qualitative and quantitative differences were found among the four odor profiles. Consistent electroantennographic activity was obtained for eight of the volatiles from the four plants: ?-myrcene, ?-terpinene, ?-terpinene, linalool, cis-verbenol, camphor, ?-terpineol, and verbenone. In a Y-tube bioassay, six chemicals, ?-myrcene, ?-terpinene, (R)-(-)-linalool, (S)-(-)-cis-verbenol, (R)-(+)-camphor, and (S)-(-)-verbenone, were the main compounds responsible for repelling E. obliqua. An eight-component mixture including all of the bioactive compounds (in a ratio of 13:2:13:8:1:24:6:17) from R. officinalis was significantly more effective at repelling the moths than any single compound or a mixture of equal amounts of the eight compounds. Field results demonstrated that intercropping tea plants with R. officinalis effectively suppressed E. obliqua infestations in a tea plantation. Our findings suggests that odor blends of R. officinalis play a role in disturbing host orientation behavior, and in repelling E. obliqua adults, and that R. officinalis should be considered when developing "push-pull" strategies aimed at optimizing the control of E. obliqua with semiochemicals.
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Lyoniresinol 3?-O-?-D-Glucopyranoside-Mediated Hypoglycaemia and Its Influence on Apoptosis-Regulatory Protein Expression in the Injured Kidneys of Streptozotocin-Induced Mice.
PLoS ONE
PUBLISHED: 01-01-2013
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Averrhoa carambola L. (Oxalidaceae) root (ACLR) has a long history of use in traditional Chinese medicine for treating diabetes and diabetic nephropathy (DN). (±)-Lyoniresinol 3?-O-?-D-glucopyranoside (LGP1, LGP2) were two chiral lignan glucosides that were isolated from the ACLR. The purpose of this study was to investigate the effect of LGP1 and LGP2-mediated hypoglycaemia on renal injury in streptozotocin (STZ)-induced diabetic mice. STZ-induced diabetic mice were administrated LGP1 and LGP2 orally (20, 40, 80 mg/kg body weight/d) for 14 days. Hyperglycaemia and the expression of related proteins such as nuclear factor-?B (NF-?B), caspase-3, -8, -9, and Bcl-associated X protein (Bax) were markedly decreased by LGP1 treatment. However, LGP2 treatment had no hypoglycaemic activity. Diabetes-dependent alterations in the kidney such as glomerular hypertrophy, excessive extracellular matrix amassing, and glomerular and tubular basement membrane thickening were improved after 14 days of LGP1 treatment. B cell lymphoma Leukaemia-2 (Bcl-2) expression was reduced in the STZ-induced diabetic mouse kidneys but was enhanced by LGP1 treatment. These findings suggest that LGP1 treatment may inhibit diabetic nephropathy progression and may regulate several pharmacological targets for treating or preventing diabetic nephropathy.
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Beneficial effects of capsiate on ethanol-induced mucosal injury in rats are related to stimulation of calcitonin gene-related Peptide release.
Planta Med.
PUBLISHED: 09-16-2011
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Capsiate is a non-pungent analogue of capsaicin from CH-19 Sweet peppers. Capsaicin is reported to trigger calcitonin gene-related peptide (CGRP) release through activation of transient receptor potential vanilloid subfamily member 1 (TRPV1) and produces beneficial effects on gastric mucosa. This study aimed to investigate whether capsiate is able to produce beneficial effects on gastric mucosa and whether the protective effects of capsipate occur through a mechanism involving the activation of TRPV1 and CGRP release. A rat model of gastric mucosal injury was established by the oral administration of acidified ethanol. Gastric tissues were collected for analysis of the gastric ulcer index, cellular apoptosis, activities of caspase-3, catalase and superoxide dismutase (SOD), and levels of CGRP, TNF-?, and malondialdehyde (MDA). Our results show that the acute administration of ethanol significantly increased the gastric ulcer index concomitantly with an increase in cellular apoptosis, caspase-3 activity, and TNF-? and MDA levels, as well as a decrease in the activities of catalase and SOD. Pretreatment with 1 mg/kg capsiate attenuated ethanol-induced gastric mucosal injury and cellular apoptosis accompanied by an increase in CGRP level, catalase, and SOD activities, and a decrease in caspase-3 activity, and TNF-? and MDA levels. The effects of capsiate were inhibited by capsazepine, an antagonist of TRPV1. These results suggest that capsiate is able to produce beneficial effects on ethanol-induced gastric mucosal injury. These effects are related to the stimulation of CGRP release through the activation of TRPV1.
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Prevalence and determinants of incomplete right atrial reverse remodeling after device closure of atrial septal defects.
Am. J. Cardiol.
PUBLISHED: 01-27-2011
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Whether the relief of chronic right atrial (RA) volume load by device closure of an atrial septal defect (ASD) normalizes RA size is unknown. The present study evaluated the prevalence and determinants of incomplete RA reverse remodeling (RAR) after ASD closure in adults. Transthoracic echocardiography was performed in 44 consecutive patients with secundum ASD (age 43 ± 17 years, 10 men) without a history of atrial arrhythmia shortly before and at 3 months after device closure of ASD. The pulmonary/systemic flow ratio was derived using invasive oximetry. The RA size had significantly decreased at 3 months of follow-up (RA volume index [RAVI] 52 ± 29 to 27 ± 17 ml/m(2), p <0.001). Incomplete RAR (defined as a RAVI of ?21 ml/m(2)) was detected in 25 patients (57%) after closure. They were older, had a larger pulmonary/systemic flow ratio, a higher pulmonary arterial systolic pressure, more tricuspid regurgitation, and larger RA, left atrial, and right ventricular sizes before closure than those with a normalized right atrium. Before closure, RAVI was the only independent determinant for incomplete RAR (odds ratio 1.115, 95% confidence interval 1.019 to 1.220; p = 0.018). A cutoff value of RAVI of ?40 ml/m(2) has a sensitivity of 84% and specificity of 72% in the receiver operating characteristic curve. The preclosure RAVI correlated moderately with the shunt-duration index, calculated by multiplying the age to pulmonary/systemic flow ratio (r = 0.64, p <0.01). In conclusion, incomplete RAR occurred in >1/2 of the adult patients at 3 months after ASD device closure and was related to excessive preclosure RA dilation.
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Vanillyl nonanoate protects rat gastric mucosa from ethanol-induced injury through a mechanism involving calcitonin gene-related peptide.
Eur. J. Pharmacol.
PUBLISHED: 01-25-2011
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Previous studies have demonstrated that capsaicin-sensitive sensory nerves are involved in the protection of gastric mucosa against damage by various stimuli and calcitoin gene-related peptide (CGRP) is a potential mediator in this process. This study was performed to explore the effect of vanillyl nonanoate, a capsaicin analog, on ethanol-induced gastric mucosal injury and the possible underlying mechanisms. A rat model of gastric mucosal injury was induced by oral administration of acidified ethanol and gastric tissues were collected for analysis of gastric ulcer index, cellular apoptosis, the activities of caspase-3, catalase and superoxide dismutase (SOD), levels of CGRP, TNF-? and malondialdehyde (MDA). The results showed that acute administration of ethanol significantly increased gastric ulcer index concomitantly with increased cellular apoptosis, caspase-3 activity, TNF-? and MDA levels as well as decreased activities of catalase and SOD. Pretreatment with 1mg/kg vanillyl nonanoate significantly attenuated ethanol-induced gastric mucosal injury and cellular apoptosis accompanied by increase of CGRP expression, and SOD activity and decrease of caspase-3 activity, TNF-? and MDA levels. The effects of vanillyl nonanoate were inhibited by capsazepine, an antagonist of capsaicin receptor. Our results suggested that vanillyl nonanoate was able to protect the gastric mucosa against ethanol-induced gastric mucosal injury. The underlying mechanism is related to stimulation of CGRP release and subsequent suppression of ethanol-induced inflammatory reaction, cellular apoptosis and oxidative stress.
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[Effect observed on hepatic egg granuloma inhibitted in mice after using rsj26GST vaccine from Schistosoma japonicum].
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
PUBLISHED: 11-09-2010
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To study the anti-schistosomiasis effect in mouse immunized with rSj26GST vaccine.
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[Proportion of incidence of etiological agents in children with non-specific chronic cough in Chongqing: a follow-up study].
Zhonghua Er Ke Za Zhi
PUBLISHED: 11-09-2010
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To investigate the proportion of incidence of children with non-specific chronic cough in Chongqing and analyze the characteristics of etiology during the follow-up.
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Phloroglucinol protects gastric mucosa against ethanol-induced injury through regulating myeloperoxidase and catalase activities.
Fundam Clin Pharmacol
PUBLISHED: 09-30-2010
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It has been shown that oxidative stress plays an important role in the pathogenesis of ethanol-induced acute gastric mucosal injury, and phloroglucinol, a smooth muscle relaxant, has been reported to possess anti-oxidative properties. In this study, we explored the effect of phloroglucinol on ethanol-induced gastric mucosal injury and the possible underlying mechanisms. The rat model of gastric mucosal injury was induced by oral administration of acidified ethanol, and the gastric tissues were collected for analysis of gastric ulcer index (UI), cellular apoptosis, anti-O(2) ? or OH? formation activity, malondialdehyde (MDA) content, and the activities of myeloperoxidase (MPO), catalase and glutathione peroxidase. The results showed that acute administration of ethanol significantly increased gastric UI concomitantly with the increased cellular apoptosis, MDA contents, MPO activity as well as the decreased activities of catalase and anti-O(2) ? or OH? formation, which was reversed by pretreatment with phloroglucinol. Although ethanol treatment significantly decreased the activity of glutathione peroxidase, pretreatment with phloroglucinol did not significantly affect the activity of the same. The results suggest that phloroglucinol could protect the gastric mucosa against ethanol-induced injury, which is related to inhibiting the MPO activity and increasing the catalase activity in the gastric tissues.
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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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Recent advances in the study on capsaicinoids and capsinoids.
Eur. J. Pharmacol.
PUBLISHED: 06-12-2010
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Chili peppers are the major source of nature capsaicinoids, which consist of capsaicin, dihydrocapsaicin, nordihydrocapsaicin, homodihydrocapsaicin, and homocapsaicin, etc. Capsaicinoids are found to exert multiple pharmacological and physiological effects including the activities of analgesia, anticancer, anti-inflammation, antioxidant and anti-obesity. Therefore, capsaicinoids may have the potential value in clinic for pain relief, cancer prevention and weight loss. In addition, capsaicinoids also display the benefits on cardiovascular and gastrointestinal system. It has been shown that capsaicinoids are potential agonists of capsaicin receptor or transient receptor potential vanilloid subfamily member 1 (TRPV1). They could exert the effects not only through the receptor-dependent pathway but also through the receptor-independent one. CH-19 Sweet peppers are the source of nature capsinoids, which share similar structure with capsaicinoids and consist of capsiate, dihydrocapsiate, and nordihydrocapsiate, etc, Comparing with capsaicinoids, capsinoids are less pungent and easily broken down in the normal aqueous conditions. So far, it has been found that capsinoids possess the biological properties of antitumor, antioxidant and anti-obesity. Since capsinoids are less toxic than capsaicinoids, therefore, capsinoids may have the advantages over capsaicinoids in clinical applications such as cancer prevention and weight loss.
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Iron content of ferritin modulates its uptake by intestinal epithelium: implications for co-transport of prions.
Mol Brain
PUBLISHED: 04-01-2010
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The spread of Chronic Wasting Disease (CWD) in the deer and elk population has caused serious public health concerns due to its potential to infect farm animals and humans. Like other prion disorders such a sporadic Creutzfeldt-Jakob-disease of humans and Mad Cow Disease of cattle, CWD is caused by PrP-scrapie (PrPSc), a beta-sheet rich isoform of a normal cell surface glycoprotein, the prion protein (PrPC). Since PrPSc is sufficient to cause infection and neurotoxicity if ingested by a susceptible host, it is important to understand the mechanism by which it crosses the stringent epithelial cell barrier of the small intestine. Possible mechanisms include co-transport with ferritin in ingested food and uptake by dendritic cells. Since ferritin is ubiquitously expressed and shares considerable homology among species, co-transport of PrPSc with ferritin can result in cross-species spread with deleterious consequences. We have used a combination of in vitro and in vivo models of intestinal epithelial cell barrier to understand the role of ferritin in mediating PrPSc uptake and transport. In this report, we demonstrate that PrPSc and ferritin from CWD affected deer and elk brains and scrapie from sheep resist degradation by digestive enzymes, and are transcytosed across a tight monolayer of human epithelial cells with significant efficiency. Likewise, ferritin from hamster brains is taken up by mouse intestinal epithelial cells in vivo, indicating that uptake of ferritin is not limited by species differences as described for prions. More importantly, the iron content of ferritin determines its efficiency of uptake and transport by Caco-2 cells and mouse models, providing insight into the mechanism(s) of ferritin and PrPSc uptake by intestinal epithelial cells.
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Paradoxical role of prion protein aggregates in redox-iron induced toxicity.
PLoS ONE
PUBLISHED: 03-29-2010
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Imbalance of iron homeostasis has been reported in sporadic Creutzfeldt-Jakob-disease (sCJD) affected human and scrapie infected animal brains, but the contribution of this phenotype to disease associated neurotoxicity is unclear.
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[Construction and identification of yeast expression plasmids containing mouse signal transducers and activators of transcription-4/6].
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
PUBLISHED: 03-17-2010
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To construct yeast expression plasmids containing mouse STAT4/6 gene for further study of their interaction with other proteins in yeast two-hybrid system.
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Vitamin A deficiency and wheezing.
World J Pediatr
PUBLISHED: 02-09-2010
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Vitamin A deficiency may increase the responsiveness of the respiratory tract and increase the risk of respiratory tract infection, resulting in airway obstruction and wheezing. This study aimed to investigate the relation between vitamin A deficiency and infant wheezing.
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Abnormal brain iron homeostasis in human and animal prion disorders.
PLoS Pathog.
PUBLISHED: 02-12-2009
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Neurotoxicity in all prion disorders is believed to result from the accumulation of PrP-scrapie (PrP(Sc)), a beta-sheet rich isoform of a normal cell-surface glycoprotein, the prion protein (PrP(C)). Limited reports suggest imbalance of brain iron homeostasis as a significant associated cause of neurotoxicity in prion-infected cell and mouse models. However, systematic studies on the generality of this phenomenon and the underlying mechanism(s) leading to iron dyshomeostasis in diseased brains are lacking. In this report, we demonstrate that prion disease-affected human, hamster, and mouse brains show increased total and redox-active Fe (II) iron, and a paradoxical increase in major iron uptake proteins transferrin (Tf) and transferrin receptor (TfR) at the end stage of disease. Furthermore, examination of scrapie-inoculated hamster brains at different timepoints following infection shows increased levels of Tf with time, suggesting increasing iron deficiency with disease progression. Sporadic Creutzfeldt-Jakob disease (sCJD)-affected human brains show a similar increase in total iron and a direct correlation between PrP and Tf levels, implicating PrP(Sc) as the underlying cause of iron deficiency. Increased binding of Tf to the cerebellar Purkinje cell neurons of sCJD brains further indicates upregulation of TfR and a phenotype of neuronal iron deficiency in diseased brains despite increased iron levels. The likely cause of this phenotype is sequestration of iron in brain ferritin that becomes detergent-insoluble in PrP(Sc)-infected cell lines and sCJD brain homogenates. These results suggest that sequestration of iron in PrP(Sc)-ferritin complexes induces a state of iron bio-insufficiency in prion disease-affected brains, resulting in increased uptake and a state of iron dyshomeostasis. An additional unexpected observation is the resistance of Tf to digestion by proteinase-K, providing a reliable marker for iron levels in postmortem human brains. These data implicate redox-iron in prion disease-associated neurotoxicity, a novel observation with significant implications for prion disease pathogenesis.
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Prion protein modulates cellular iron uptake: a novel function with implications for prion disease pathogenesis.
PLoS ONE
PUBLISHED: 02-12-2009
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Converging evidence leaves little doubt that a change in the conformation of prion protein (PrP(C)) from a mainly alpha-helical to a beta-sheet rich PrP-scrapie (PrP(Sc)) form is the main event responsible for prion disease associated neurotoxicity. However, neither the mechanism of toxicity by PrP(Sc), nor the normal function of PrP(C) is entirely clear. Recent reports suggest that imbalance of iron homeostasis is a common feature of prion infected cells and mouse models, implicating redox-iron in prion disease pathogenesis. In this report, we provide evidence that PrP(C) mediates cellular iron uptake and transport, and mutant PrP forms alter cellular iron levels differentially. Using human neuroblastoma cells as models, we demonstrate that over-expression of PrP(C) increases intra-cellular iron relative to non-transfected controls as indicated by an increase in total cellular iron, the cellular labile iron pool (LIP), and iron content of ferritin. As a result, the levels of iron uptake proteins transferrin (Tf) and transferrin receptor (TfR) are decreased, and expression of iron storage protein ferritin is increased. The positive effect of PrP(C) on ferritin iron content is enhanced by stimulating PrP(C) endocytosis, and reversed by cross-linking PrP(C) on the plasma membrane. Expression of mutant PrP forms lacking the octapeptide-repeats, the membrane anchor, or carrying the pathogenic mutation PrP(102L) decreases ferritin iron content significantly relative to PrP(C) expressing cells, but the effect on cellular LIP and levels of Tf, TfR, and ferritin is complex, varying with the mutation. Neither PrP(C) nor the mutant PrP forms influence the rate or amount of iron released into the medium, suggesting a functional role for PrP(C) in cellular iron uptake and transport to ferritin, and dysfunction of PrP(C) as a significant contributing factor of brain iron imbalance in prion disorders.
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Prion protein (PrP) knock-out mice show altered iron metabolism: a functional role for PrP in iron uptake and transport.
PLoS ONE
PUBLISHED: 02-04-2009
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Despite overwhelming evidence implicating the prion protein (PrP) in prion disease pathogenesis, the normal function of this cell surface glycoprotein remains unclear. In previous reports we demonstrated that PrP mediates cellular iron uptake and transport, and aggregation of PrP to the disease causing PrP-scrapie (PrP(Sc)) form results in imbalance of iron homeostasis in prion disease affected human and animal brains. Here, we show that selective deletion of PrP in transgenic mice (PrP(KO)) alters systemic iron homeostasis as reflected in hematological parameters and levels of total iron and iron regulatory proteins in the plasma, liver, spleen, and brain of PrP(KO) mice relative to matched wild type controls. Introduction of radiolabeled iron ((59)FeCl(3)) to Wt and PrP(KO) mice by gastric gavage reveals inefficient transport of (59)Fe from the duodenum to the blood stream, an early abortive spike of erythropoiesis in the long bones and spleen, and eventual decreased (59)Fe content in red blood cells and all major organs of PrP(KO) mice relative to Wt controls. The iron deficient phenotype of PrP(KO) mice is reversed by expressing Wt PrP in the PrP(KO) background, demonstrating a functional role for PrP in iron uptake and transport. Since iron is required for essential metabolic processes and is also potentially toxic if mismanaged, these results suggest that loss of normal function of PrP due to aggregation to the PrP(Sc) form induces imbalance of brain iron homeostasis, resulting in disease associated neurotoxicity.
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[NADPH oxidase inhibitor apocynin attenuates ischemia/reperfusion induced myocardial injury in rats].
Zhonghua Xin Xue Guan Bing Za Zhi
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To explore the role of NADPH oxidase inhibitor apocynin on ischemia/reperfusion (I/R)-induced myocardial injury.
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Characterization of mid-term atrial geometrical and electrical remodeling following device closure of atrial septal defects in adults.
Int. J. Cardiol.
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Late-onset atrial arrhythmia after successful closure of atrial septal defect (ASD) is not uncommon. Right atrial (RA) enlargement and increased electrocardiographic P-wave dispersion (Pd) independently predict the development of atrial arrhythmia. Data on the degree of right atrial (RA) geometrical and electrical remodeling following device closure of ASD are limited.
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Stimulation of calcitonin gene-related peptide release through targeting capsaicin receptor: a potential strategy for gastric mucosal protection.
Dig. Dis. Sci.
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Calcitonin gene-related peptide (CGRP) is a predominant neurotransmitter from capsaicin-sensitive sensory nerves, which are widely distributed in the gastrointestinal system. These sensory nerves are reported to be involved in the protection of gastric mucosa against damage by various stimuli, and CGRP is a potential mediator in this process. In addition to increase in gastric mucosal blood flow, the beneficial effects of CGRP on gastric mucosa include inhibition of gastric acid secretion, prevention of cellular apoptosis and oxidative injury. The synthesis and release of CGRP is regulated by the capsaicin receptor which is known as transient receptor potential vanilloid subfamily member 1 (TRPV1) and the agonists of TRPV1 have the potential for gastric mucosal protection. So far, multiple TRPV1 agonists, including capsaicin, capsiate, anandamide and rutaecarpine are reported to exert beneficial effects on gastric mucosal injury induced by various stimuli. Therefore, the TRPV1/CGRP pathway represents a novel target for therapeutic intervention in human gastric mucosal injury.
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[Etiology of nonspecific chronic cough in children and relationship between TRPV1 gene polymorphisms and nonspecific chronic cough].
Zhongguo Dang Dai Er Ke Za Zhi
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To explore the causes of nonspecific chronic cough in children and relationship between transient receptor potential vanilloid 1 (TRPV1) gene polymorphisms and nonspecific chronic cough.
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Comparison of 64-slice CT perfusion imaging with contrast-enhanced CT for evaluating the target volume for three-dimensional conformal radiotherapy in the rabbit VX2 brain tumor model.
J. Radiat. Res.
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CT perfusion imaging is a promising technique for delineating the target volume for three-dimensional conformal radiotherapy, but it is difficult in humans to obtain gross pathological samples at the same level of the brain tumor to evaluate this technique. The aim of this study was to use the BV map of CT perfusion imaging to assess the target volume in the rabbit VX2 brain tumor model, which has similar characteristics to human brain tumor, and compare the results to those of CECT. New Zealand white rabbits were used for the animal model. After tumor cell implantation 21 rabbits underwent 64-slice CT scanning. The target slice was selected and the maximum major axis length and minimum minor axis length of the tumor in the target slice on BV maps and contrast-enhanced CT images were measured. Pathological specimens were obtained from the rabbit brains which were removed intact. The GTV and CTV of the imaging methods were compared. Scanning was successful in 20 rabbits. The CECT images showed the target area for the VX2 tumor in 16 rabbits. The BV maps showed the target area for the tumor in 20 rabbits. The probability was 95% that the GTV determined by pathology can be covered completely when BV maps are used. CT perfusion imaging appears to be a promising technique for delineating the GTV of brain tumors in clinical practice.
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Improved coronary artery blood flow following the correction of systolic dyssynchrony with cardiac resynchronization therapy.
Int. J. Cardiol.
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Coronary blood flow (CBF) is improved by cardiac resynchronization therapy (CRT) and impaired by right ventricular apical (RVA) pacing in patients with heart failure. However, the underlying mechanism remains unclear.
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A novel pathway of NADPH oxidase/vascular peroxidase 1 in mediating oxidative injury following ischemia-reperfusion.
Basic Res. Cardiol.
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Vascular peroxidase 1 (VPO1) can utilize reactive oxygen species (ROS) generated from NADPH oxidase (NOX) to catalyze peroxidative reactions. This study was performed to identify a novel pathway of NOX/VPO1 in mediating the oxidative injury following myocardial ischemia reperfusion (IR). In a rat model of myocardial IR, the infarct size, serum creatine kinase (CK) activity, apoptosis, NOX activity, NOX2 and VPO1 expression were measured. In a cell (rat heart-derived H9c2 cells) model of hypoxia/reoxygenation (HR), the apoptosis, NOX activity, NOX2 and VPO1 expression, and H(2)O(2) and HOCl levels were examined. In vivo, IR caused 54.8 ± 1.7 % infarct size in myocardium accompanied by elevated activities of CK, caspase-3 and NOX, up-regulated VPO1 expression and high numbers of myocardial apoptotic cells; these effects were attenuated by pretreatment with the inhibitor of NOX. In vitro, inhibition of NOX or silencing of NOX2 or VPO1 expression significantly suppressed HR-induced cellular apoptosis concomitantly with decreased HOCl production. Inhibition of NOX or silencing of NOX2 led to a decrease in H(2)O(2) production accompanied by a decrease in VPO1 expression and HOCl production. However, silencing of VPO1 expression did not affect NOX2 expression and H(2)O(2) production. H(2)O(2)-induced VPO1 expression was partially reversed by JNK or p38 MAPK inhibitor. Our results demonstrate a novel pathway of NOX2/VPO1 in myocardium, where VPO1 coordinates with NOX2 and amplifies the role of NOX-derived ROS in oxidative injury following IR.
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Outcome of in vitro fertilization following stimulation with highly purified hMG or recombinant FSH in downregulated women of advanced reproductive age: a prospective, randomized and controlled trial.
Gynecol. Endocrinol.
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To compare highly purified human menopausal gonadotropin (HP-hMG) with recombinant follicle-stimulating hormone (rFSH) on ovarian response and pregnancy outcome in downregulated women of advanced reproductive age.
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Alpha lipoic acid protects heart against myocardial ischemia-reperfusion injury through a mechanism involving aldehyde dehydrogenase 2 activation.
Eur. J. Pharmacol.
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Recent studies demonstrate that alpha lipoic acid can prevent nitroglycerin tolerance by restoring aldehyde dehydrogenase 2 (ALDH2) activity and ALDH2-mediated detoxification of aldehydes is thought as an endogenous mechanism against ischemia-reperfusion injury. This study was performed to explore whether the cardioprotective effect of alpha lipoic acid was related to activation of ALDH2 and the underlying mechanisms. In a Langendorff model of ischemia-reperfusion in rats, cardiac function, activities of creatine kinase (CK) and ALDH2, contents of 4-hydroxy-2-nonenal (4-HNE) and malondialdehyde (MDA) were measured. In a cell model of hypoxia-reoxygenation, the apoptosis, ALDH activity, reactive oxygen species level, 4-HNE and MDA contents were examined. In the isolated hearts, ischemia-reperfusion treatment led to cardiac dysfunction accompanied by an increase in 4-HNE and MDA contents. Pretreatment with lipoic acid significantly up-regulated myocardial ALDH2 activity concomitantly with an improvement of cardiac dysfunction and a decrease in 4-HNE and MDA contents, these effects were blocked by the inhibitor of ALDH2. Similarly, in the cultured cardiomyocytes, hypoxia-reoxygenation treatment induced apoptosis accompanied by an increase in the production of reactive oxygen species, 4-HNE and MDA. Administration of lipoic acid significantly up-regulated cellular ALDH2 activity concomitantly with a reduction in apoptosis, production of reactive oxygen species, 4-HNE and MDA, these effects were reversed in the presence of ALDH2 or PKC? inhibitors. Our results suggest that the cardioprotective effects of lipoic acid on ischemia-reperfusion injury are through a mechanism involving ALDH2 activation. The regulatory effect of lipoic acid on ALDH2 activity is dependent on PKC? signaling pathway.
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JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

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