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Find video protocols related to scientific articles indexed in Pubmed.
Fisetin Up-regulates the Expression of Adiponectin in 3T3-L1 Adipocytes via the Activation of Silent Mating Type Information Regulation 2 Homologue 1 (SIRT1)-Deacetylase and Peroxisome Proliferator-Activated Receptors (PPARs).
J. Agric. Food Chem.
PUBLISHED: 10-15-2014
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Adiponectin, an adipokine, has been described as showing physiological benefits against obesity-related malfunctions and vascular dysfunction. Several natural compounds that promote the expression and secretion of adipokines in adipocytes could be useful for treating metabolic disorders. This study investigated the effect of fisetin, a dietary flavonoid, on the regulation of adiponectin in adipocytes using 3T3-L1 preadipocytes. The expression and secretion of adiponectin increased in 3T3-L1 cells upon treatment with fisetin in a dose-dependent manner. Fisetin-induced adiponectin secretion was inhibited by peroxisome proliferator-activated receptor (PPAR) antagonists. It was also revealed that fisetin increased the activities of PPARs and silent mating type information regulation 2 homologue 1 (SIRT1) in a dose-dependent manner. Furthermore, the up-regulation of adiponectin and the activation of PPARs induced by fisetin were prevented by a SIRT1 inhibitor. Fisetin also promoted deacetylation of PPAR ? coactivator 1 (PGC-1) and its interaction with PPARs. SIRT knockdown by siRNA significantly decreased both adiponectin production and PPARs-PGC-1 interaction. These results provide evidence that fisetin promotes the gene expression of adiponectin through the activation of SIRT1 and PPARs in adipocytes.
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Effect of FGF-2 on Collagen Tissue Regeneration by Human Vertebral Bone Marrow Stem Cells.
Stem Cells Dev.
PUBLISHED: 10-14-2014
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The effects of fibroblast growth factor-2 (FGF-2) on collagen tissue regeneration by human bone marrow stem cells (hBMSCs) were investigated. hBMSCs were isolated from human vertebral body bone marrow during vertebral surgery and a population of hBMSCs with the characteristics of mesenchymal stem cells was observed. The FGF-2 treatment (5?ng/mL) affected on the colony-forming efficiency, proliferation, and in vitro differentiation of hBMSCs. Insoluble/soluble collagen and hydroxyproline synthesis was significantly enhanced in hBMSCs expanded with FGF-2 and the treatment of FGF-2 caused a reduction in the mRNA expression of collagen type I, but an increase of collagen types II and III along with lysyl oxidase family genes. Collagen formation was also examined using an in vivo assay model by transplanting hBMSCs into immunocompromised mice (n=4) and the histologic and immunohistochemical results revealed that significantly more collagen with a well-organized structure was formed by FGF-2-treated hBMSCs at 8 weeks posttransplantation (P<0.05). The DNA microarray assay demonstrated that genes related to extracellular matrix formation were significantly upregulated. To elucidate the underlying mechanism, chemical inhibitors against extracellular-signal-regulated kinase (ERK) and phosphoinositide 3-kinase (PI3K) were treated and following downstream expression was observed. Collectively, FGF-2 facilitated the collagen-producing potency of hBMSCs both in vitro and in vivo, rendering them more suitable for use in collagen regeneration in the clinical field.
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A Functional Screen Identifies miRs that Induce Radioresistance in Glioblastomas.
Mol. Cancer Res.
PUBLISHED: 09-27-2014
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The efficacy of radiotherapy in many tumor types is limited by normal tissue toxicity and by intrinsic or acquired radioresistance. Therefore, it is essential to understand the molecular network responsible for regulating radiosensitivity/resistance. Here, an unbiased functional screen identified four microRNAs (miR-1, miR-125a, miR-150, and miR-425) that induce radioresistance. Considering the clinical importance of radiotherapy for glioblastoma (GBM) patients, the impact of these miRNAs on GBM radioresistance was investigated. Overexpression of miR-1, miR-125a, miR-150 and/or miR-425 in GBM promotes radioresistance through upregulation of the cell cycle checkpoint response. Conversely, antagonizing with antagomiRs sensitizes GBM cells to irradiation, suggesting their potential as targets for inhibiting therapeutic resistance. Analysis of GBM datasets from TCGA revealed that these miRNAs are expressed in GBM patient specimens and correlate with Transforming Growth Factor Beta (TGF-beta) signaling. Finally, it is demonstrated that expression of miR-1 and miR-125a can be induced by TGF-beta and antagonized by a TGF-beta receptor inhibitor. Together, these results identify and characterize a new role for miR-425, miR-1, miR-125, and miR-150 in promoting radioresistance in GBMs and provide insight into the therapeutic application of TGF-beta inhibitors in radiotherapy. Implications: Systematic identification of miRs that cause radioresistance in gliomas is important for uncovering predictive markers for radiotherapy or targets for overcoming radioresistance.
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Heme-binding-mediated negative regulation of the tryptophan metabolic enzyme indoleamine 2,3-dioxygenase 1 (IDO1) by IDO2.
Exp. Mol. Med.
PUBLISHED: 09-03-2014
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Indoleamine 2,3-dioxygenases (IDOs) are tryptophan-catabolizing enzymes with immunomodulatory functions. However, the biological role of IDO2 and its relationship with IDO1 are unknown. To assess the relationship between IDO2 and IDO1, we investigated the effects of co-expression of human (h) IDO2 on hIDO1 activity. Cells co-expressing hIDO1 and hIDO2 showed reduced tryptophan metabolic activity compared with those expressing hIDO1 only. In a proteomic analysis, hIDO1-expressing cells exhibited enhanced expression of proteins related to the cell cycle and amino acid metabolism, and decreased expression of proteins related to cell survival. However, cells co-expressing hIDO1 and hIDO2 showed enhanced expression of negative regulators of cell apoptosis compared with those expressing hIDO1 only. Co-expression of hIDO1 and hIDO2 rescued the cell death induced by tryptophan-depletion through hIDO1 activity. Cells expressing only hIDO2 exhibited no marked differences in proteome profiles or cell growth compared with mock-transfectants. Cellular tryptophan metabolic activity and cell death were restored by co-expressing the hIDO2 mutant substituting the histidine 360 residue for alanine. These results demonstrate that hIDO2 plays a novel role as a negative regulator of hIDO1 by competing for heme-binding with hIDO1, and provide information useful for development of therapeutic strategies to control cancer and immunological disorders that target IDO molecules.
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Regulating charge injection in ambipolar organic field-effect transistors by mixed self-assembled monolayers.
ACS Appl Mater Interfaces
PUBLISHED: 08-13-2014
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We report on a technique using mixed self-assembled monolayers (SAMs) to finely regulate ambipolar charge injection in polymer organic field-effect transistors. Differing from the other works that employ single SAM specifically for efficient charge injection in p-type and n-type transistors, we blend two different SAMs of alkyl- and perfluoroalkyl thiols at different ratios and apply them to ambipolar OFETs and inverter. Thanks to the utilization of ambipolar semiconductor and one SAM mixture, the device and circuit fabrications are facile with only one step for semiconductor deposition and another for SAM treatment. This is much simpler with respect to the conventional scheme for the unipolar-device-based complementary circuitry that demands separate deposition and processing for individual p-channel and n-channel transistors. Our results show that the mixed-SAM treatments not only improve ambipolar charge injection manifesting as higher hole- and electron-mobility and smaller threshold voltage but also gradually tune the device characteristics to reach a desired condition for circuit application. Therefore, this simple but useful approach is promising for ambipolar electronics.
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Calorie Intake of Enteral Nutrition and Clinical Outcomes in Acutely Critically Ill Patients: A Meta-Analysis of Randomized Controlled Trials.
JPEN J Parenter Enteral Nutr
PUBLISHED: 07-30-2014
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Background: The appropriate calorie intake to be provided to critically ill patients via enteral nutrition (EN) remains unclear. We performed a meta-analysis of randomized controlled trials to compare the effect of initial underfeeding and full feeding in acutely critically ill patients. Materials and Methods: We searched the Medline, EMBASE, and Cochrane Central Register of Controlled Trials databases to identify randomized controlled trials that compared underfeeding with full feeding in critically ill patients. The primary outcome was overall mortality. The secondary outcomes included length of hospital stay, length of intensive care unit (ICU) stay, duration of mechanical ventilation, incidence of pneumonia, Clostridium difficile colitis, other infectious complications, and gastrointestinal intolerance. Results: In total, 4 studies were included in this meta-analysis. There was no significant difference in overall mortality between the underfeeding and full-feeding groups (odds ratio [OR], 0.94; 95% confidence interval [CI], 0.74-1.19; I(2) = 26.6%; P = .61). Subgroup analysis of the underfeeding subgroup that was fed ?33.3% of the standard caloric requirement indicated that overall mortality was significantly lower in this underfeeding subgroup than in the full-feeding group (OR, 0.63; 95% CI, 0.40-1.00; I(2) = 0%; P = .05). In contrast, no difference in overall mortality was noted between the underfeeding subgroup that was fed <33.3% of the standard caloric requirement and the full-feeding group. The length of hospital stay and length of ICU stay did not differ between the 2 groups. Moreover, no differences in other secondary clinical outcomes were noted. Conclusions: None of the analyzed clinical outcomes for the acutely critically ill patients were significantly influenced by the calorie intake of the initial EN.
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Relationship between EGFR mutations and clinicopathological features of lung adenocarcinomas diagnosed via small biopsies.
Anticancer Res.
PUBLISHED: 06-13-2014
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We performed this study to evaluate the frequency of epidermal growth factor receptor (EGFR) mutations and their association with the histological subtype of lung adenocarcinoma diagnosed via small biopsy specimens.
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Effects of three-dimensional polymer networks in vertical alignment liquid crystal display controlled by in-plane field.
Opt Express
PUBLISHED: 06-13-2014
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Polymer network in vertical alignment liquid crystal cell driven by in-plane field (VA-IPS) is formed in three dimensions to achieve fast response time and to keep the liquid crystal alignment even when an external pressure is applied to the cell. The network formed by UV irradiation to vertically aligned liquid crystal cell with reactive mesogen does not disturb a dark state while exhibiting very fast decaying response time less than 2ms in all grey scales and almost zero pooling mura. The proposed device has a strong potential to be applicable to field sequential display owing to super-fast response time and flexible display owing to polymer network in bulk which supports a gap between two substrates.
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Inhibition of indoleamine 2,3-dioxygenase (IDO) by stereoisomers of 1-methyl tryptophan in an experimental graft-versus-tumor model.
Exp. Hematol.
PUBLISHED: 06-07-2014
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Indoleamine 2,3-dioxygenase (IDO) is a rate-limiting enzyme in tryptophan catabolism that plays an important role in the induction of immune tolerance. Its role in graft-versus-tumor effect after allogeneic stem cell transplantation (allo-SCT) remains unclear. Using a murine graft-versus-tumor model of reduced-intensity allo-HSCT followed by donor leukocyte infusion (DLI), we examined the role of IDO inhibition. Two stereoisomers of 1-methyl tryptophan (1-MT), a small-molecule inhibitor of IDO, reduced the growth of inoculated tumor in the mice that received DLI and had higher expression of IDO1 and IFN?. However, L-1MT, but not D-1MT, mitigated tumor growth in mice that did not receive DLI and did not express IDO1 and IFN?. Accordingly, both stereoisomers reduced plasma kynurenine concentrations early after DLI and enhanced in vitro cytotoxic lymphocyte function after allogeneic mixed lymphocyte reaction. Furthermore, L-1MT was more efficient in causing direct cytotoxic effects than D-1MT. Our results suggest that IDO inhibition can benefit anti-tumor therapy in the setting of reduced-intensity allo-SCT using DLI.
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MicroRNAs down-regulate homologous recombination in the G1 phase of cycling cells to maintain genomic stability.
Elife
PUBLISHED: 05-21-2014
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Homologous recombination (HR)-mediated repair of DNA double-strand break (DSB)s is restricted to the post-replicative phases of the cell cycle. Initiation of HR in the G1 phase blocks non-homologous end joining (NHEJ) impairing DSB repair. Completion of HR in G1 cells can lead to the loss-of-heterozygosity (LOH), which is potentially carcinogenic. We conducted a gain-of-function screen to identify miRNAs that regulate HR-mediated DSB repair, and of these miRNAs, miR-1255b, miR-148b*, and miR-193b* specifically suppress the HR-pathway in the G1 phase. These miRNAs target the transcripts of HR factors, BRCA1, BRCA2, and RAD51, and inhibiting miR-1255b, miR-148b*, and miR-193b* increases expression of BRCA1/BRCA2/RAD51 specifically in the G1-phase leading to impaired DSB repair. Depletion of CtIP, a BRCA1-associated DNA end resection protein, rescues this phenotype. Furthermore, deletion of miR-1255b, miR-148b*, and miR-193b* in independent cohorts of ovarian tumors correlates with significant increase in LOH events/chromosomal aberrations and BRCA1 expression.DOI: http://dx.doi.org/10.7554/eLife.02445.001.
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Sublethal concentrations of 17-AAG suppress homologous recombination DNA repair and enhance sensitivity to carboplatin and olaparib in HR proficient ovarian cancer cells.
Oncotarget
PUBLISHED: 05-07-2014
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The promise of PARP-inhibitors(PARPis) in the management of epithelial ovarian cancer(EOC) is tempered by the fact that approximately 50% of patients with homologous recombination (HR)-proficient tumors do not respond well to these agents. Combination of PARPis with agents that inhibit HR may represent an effective strategy to enhance their activity in HR-proficient tumors. Using a bioinformatics approach, we identified that heat shock protein 90 inhibitors(HSP90i) may suppress HR and thus revert HR-proficient to HR-deficient tumors. Analysis of publicly available gene expression data showed that exposure of HR-proficient breast cancer cell lines to HSP90i 17-AAG(17-allylamino-17-demethoxygeldanamycin) downregulated HR, ATM and Fanconi Anemia pathways. In HR-proficient EOC cells, 17-AAG suppressed HR as assessed using the RAD51 foci formation assay and this was further confirmed using the Direct Repeat-GFP reporter assay. Furthermore, 17-AAG downregulated BRCA1 and/or RAD51 protein levels, and induced significantly more ?H2AX activation in combination with olaparib compared to olaparib alone. Finally, sublethal concentrations of 17-AAG sensitized HR-proficient EOC lines to olaparib and carboplatin but did not affect sensitivity of the HR-deficient OVCAR8 line arguing that the 17-AAG mediated sensitization is dependent on suppression of HR. These results provide a preclinical rationale for using a combination of olaparib/17-AAG in HR-proficient EOC.
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A case of nonthrombotic pulmonary embolism after facial injection of hyaluronic Acid in an illegal cosmetic procedure.
Tuberc Respir Dis (Seoul)
PUBLISHED: 04-17-2014
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Hyaluronic acid is widely used in medical procedures, particularly in cosmetic procedures administered by physicians or nonmedical personnel. The materials used for cosmetic procedures by physicians as well as illegally by non-medical personnel can cause nonthrombotic pulmonary embolism (NTPE). We report the case of a woman with acute respiratory failure, neurologic symptoms and petechiae after an illegal procedure of hyaluronic acid dermal filler performed by an unlicensed medical practitioner 3 days before symptom onset. Although a few cases of NTPE after injection of hyaluronic acid have been reported yet, this is the first typical case showing a NTPE manifestation after the facial injection of hyaluronic acid.
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A paradoxical pattern of indoleamine 2,3-dioxygenase expression in the colon tissues of patients with acute graft-versus-host disease.
Exp. Hematol.
PUBLISHED: 03-31-2014
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Indoleamine 2,3-dioxygenase (IDO) is a rate-limiting enzyme for tryptophan catabolism that plays an important role in the induction of immune tolerance. It is induced in the colon and exerts its effects there, regulating T-cell proliferation and survival. To address the role of IDO in acute graft-versus-host disease (AGVHD) after human allogeneic hematopoietic stem cell transplantation, we analyzed the relationship between IDO expression in colon tissues and clinical outcomes among 41 AGVHD patients who were diagnosed as gut AGVHD by a colon mucosal biopsy within 100 days posttransplantation. By in situ immunohistochemical analyses, IDO expression was measured in colon mucosal mononuclear cells (MNCs) and endothelial cells (ECs) in GVHD areas. High IDO expression in MNCs and low IDO expression in ECs had a trend toward a lower nonrelapse mortality (p = 0.157 and p = 0.062, respectively). Multivariate analysis showed that high MNC combined with low EC IDO expression (p = 0.046), as well as low disease risk (p = 0.012), are associated with lower nonrelapse mortality. Paradoxical upregulation of IDO expression in colon MNCs and ECs may represent a new predictive factor for prognosis in gut AGVHD after human allogeneic hematopoietic stem cell transplantation.
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Development and comparative evaluation of new shapes of pillows.
J Phys Ther Sci
PUBLISHED: 03-25-2014
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The purpose of this study was to determine pillow designs suitable for supine and side-lying positions. [Subjects] Twenty female and twenty male subjects with a mean age of 22.7?years (SD = 1.3) participated in the study. [Methods] First, a three-dimensional motion analysis system was used to analyze the movements of the head and the shoulder joints during changes from supine positions to side-lying positions. Second, the height from the face to the shoulder and the height from the floor to the middle of the neck in a side-lying position were measured. Third, the weight distribution ratios of the head and the trunk were compared using general pillows (polyester sponge), memory foam, and prototype pillows. [Results] During position changes from supine positions to side-lying positions, the head moved in a fan shape, and the shoulder joint moved an average of 4.4 cm upward. The height from the face to the shoulder was 9?cm on average. The height from the floor to the middle of the neck was 11?cm on average. The weight distribution ratios between the head and the trunk were compared among general pillows (polyester sponge), memory foam, and prototype pillows. The results showed significant differences in the side-lying position. [Conclusion] Pillows with uniform heights are not suitable for a supine or side-lying position. In the case of both positions, users should be allowed to select pillows in shapes that can support the neck.
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Human podoplanin-positive monocytes and platelets enhance lymphangiogenesis through the activation of the podoplanin/CLEC-2 axis.
Mol. Ther.
PUBLISHED: 03-18-2014
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Emerging studies suggested that murine podoplanin-positive monocytes (PPMs) are involved in lymphangiogenesis. The goal of this study was to demonstrate the therapeutic lymphangiogenesis of human PPMs by the interaction with platelets. Aggregation culture of human peripheral blood mononuclear cells (PBMCs) resulted in cellular aggregates termed hematospheres. During 5-day culture, PPMs expanded exponentially and expressed several lymphatic endothelial cell-specific markers including vascular endothelial growth factor receptor (VEGFR)-3 and well-established lymphangiogenic transcription factors. Next, we investigated the potential interaction of PPMs with platelets that had C-type lectin-like receptor-2 (CLEC-2), a receptor of podoplanin. In vitro coculture of PPMs and platelets stimulated PPMs to strongly express lymphatic endothelial markers and upregulate lymphangiogenic cytokines. Recombinant human CLEC-2 also stimulated PPMs through Akt and Erk signaling. Likewise, platelets in coculture with PPMs augmented secretion of a lymphangiogenic cytokine, interleukin (IL)-1-?, via podoplanin/CLEC-2 axis. The supernatant obtained from coculture was able to enhance the migration, viability, and proliferation of lymphatic endothelial cell. Local injection of hematospheres with platelets significantly increased lymphatic neovascularization and facilitated wound healing in the full-thickness skin wounds of nude mice. Cotreatment with PPMs and platelets augments lymphangiogenesis through podoplanin/CLEC-2 axis, which thus would be a promising novel strategy of cell therapy to treat human lymphatic vessel disease.
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Kinetics of IFN-? and IL-17 Production by CD4 and CD8 T Cells during Acute Graft-versus-Host Disease.
Immune Netw
PUBLISHED: 03-16-2014
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Graft-versus-host disease (GVHD) is a fatal complication that occurs after allogeneic hematopoietic stem cell transplantation. To understand the dynamics of CD4 and CD8 T cell production of IFN-? and IL-17 during GVHD progression, we established a GVHD model by transplanting T cell-depleted bone marrow (TCD-BM) and purified T cells from B6 mice into irradiated BALB.B, creating an MHC-matched but minor histocompatibility (H) antigen-mismatched transplantation (B6 ? BALB.B GVHD). Transplantation-induced GVHD was confirmed by the presence of the appropriate compositional changes in the T cell compartments and innate immune cells in the blood and the systemic secretion of inflammatory cytokines. Using this B6 ? BALB.B GVHD model, we showed that the production of IFN-? and IL-17 by CD4 T cells preceded that by CD8 T cells in the spleen, mesenteric lymph node, liver, and lung in the BALB.B GVHD host, and Th1 differentiation predated Th17 differentiation in all organs during GVHD progression. Such changes in cytokine production were based on changes in cytokine gene expression by the T cells at different time points during GVHD development. These results demonstrate that both IFN-? and IL-17 are produced by CD4 and CD8 T cells but with different kinetics during GVHD progression.
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CIC-DUX sarcomas demonstrate frequent MYC amplification and ETS-family transcription factor expression.
Mod. Pathol.
PUBLISHED: 03-11-2014
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Recent molecular advances have identified a novel, clinically aggressive subgroup of undifferentiated round cell sarcomas defined molecularly by oncogenic fusion of the gene, CIC, and either DUX4 or its paralog, DUX4L, herein termed CIC-DUX sarcomas. Morphologically, CIC-DUX sarcomas are round cell sarcomas with high-grade nuclear features, including vesicular chromatin and nucleoli, patchy clear cell foci, myxoid change, and necrosis. Here, we studied a cohort of 10 cases, including 6 newly identified cases, 2 with paired metastases. Given our prior observation of trisomy 8 in these tumors, we assayed for amplification and expression of MYC (c-Myc) and representative downstream targets. Trisomy 8 was detected in 5/7 testable cases, with further amplification of MYC locus in 6/7 testable cases and immunohistochemical expression of MYC in 10/10. The canonical MYC transcriptional target, p21, but not MTDH, was differentially expressed compared with Ewing sarcomas. Given prior observation of induction of ETS-family transcription factors by the fusion oncoprotein, we assayed and identified highly prevalent positivity for ERG (9/10) and FLI1 (8/8). These findings are cautionary regarding use of these immunostains in prospective case workup, whereas the prevalent MYC amplification may represent a therapeutically targetable oncogenic pathway in CIC-DUX sarcomas.Modern Pathology advance online publication, 20 June 2014; doi:10.1038/modpathol.2014.83.
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IL-1?-stimulated urokinase plasminogen activator expression through NF-?B in gastric cancer after HGF treatment.
Oncol. Rep.
PUBLISHED: 02-19-2014
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The potential of hepatocyte growth factor (HGF) to regulate the expression of urokinase plasminogen activator (uPA) in a gastric cancer cell is not widely acknowledged. To identify the genes associated with the plasminogen activator proteolytic axis by HGF, we used cDNA microarray technology and selected genes upregulated or downregulated in two gastric cell lines (NUGC-3 and MKN-28). First, IL-1? RNA and protein were confirmed to be upregulated. Then, we investigated the effect of IL-1? induced by HGF on the uPA system, facilitating the migration and invasion of cancer cells in the metastatic process. The role for IL-1? in HGF-induced upregulation of uPA was determined by knockdown of IL-1? with IL-1? shRNA and a chromatin immune precipitation assay. The levels of IL-1? and uPA were upregulated in cells treated with HGF in a dose-dependent manner. HGF-induced upregulation of uPA was suppressed by IL-1? knockdown. HGF enhanced the binding activity of NF-?B to the uPA promoter in control cells, but not in the IL-1? shRNA cells. We confirmed the functional role of HGF inactivation of the uPA promoter by a reporter gene assay. Downregulation of IL-1? using IL-1? shRNA also decreased cell proliferation and in vitro cell invasion. IL-1? stimulated uPA expression through ERK and NF-?B in gastric cancer, which may therefore be promising targets for gastric cancer therapy.
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The Human Ortholog of Acid-Sensing Ion Channel Gene ASIC1a Is Associated with Panic Disorder and Amygdala Structure and Function.
Biol. Psychiatry
PUBLISHED: 02-18-2014
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Individuals with panic disorder (PD) exhibit a hypersensitivity to inhaled carbon dioxide, possibly reflecting a lowered threshold for sensing signals of suffocation. Animal studies have shown that carbon dioxide-mediated fear behavior depends on chemosensing of acidosis in the amygdala via the acid-sensing ion channel ASIC1a. We examined whether the human ortholog of the ASIC1a gene, ACCN2, is associated with the presence of PD and with amygdala structure and function.
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Hepatobiliary risk factors for clinical outcome of Kawasaki disease in children.
BMC Pediatr
PUBLISHED: 02-13-2014
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Kawasaki disease (KD) is an acute febrile vasculitis that causes coronary artery abnormality (CAA) as a complication. In some patients, an association has been noted between elevated liver enzymes or an abnormal gallbladder (GB) and hepatobiliary involvement in KD. In this study, we aimed to evaluate clinical, laboratory, and ultrasonographic (USG) risk factors of hepatobiliary involvement for the intravenous immunoglobulin (IVIG) resistance and the development of CAA in children with KD.
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Deficiency of developmental endothelial locus-1 (Del-1) aggravates bleomycin-induced pulmonary fibrosis in mice.
Biochem. Biophys. Res. Commun.
PUBLISHED: 01-30-2014
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Pulmonary fibrosis is a lung disease wherein lung parenchyma is gradually and irreversibly replaced with collagen. The molecular pathogenesis of pulmonary fibrosis is not fully understood and the only effective treatment available is lung transplantation. To test if Del-1, an endogenous anti-inflammatory molecule, may be implicated in the development of pulmonary fibrosis, we induced pulmonary fibrosis in wild type (WT) and Del-1(-/-) mice by intratracheal administration of bleomycin. Del-1 expression in the lung was decreased in the WT mice treated with bleomycin compared to control mice. In addition, bleomycin-induced pulmonary fibrosis increased collagen deposition and TGF-? production in the lung of Del-1(-/-) mice. Finally, Del-1(-/-) mice treated with bleomycin displayed higher weight loss and greater mortality than did WT mice identically treated. These findings suggest that Del-1 may negatively regulate development of pulmonary fibrosis. Further delineation of a role for Del-1 in the development of pulmonary fibrosis will broaden our understanding of the molecular pathogenesis of this disease and hopefully help develop potential therapeutics.
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Effect of azithromycin on Prevotella intermedia lipopolysaccharide-induced production of interleukin-6 in murine macrophages.
Eur. J. Pharmacol.
PUBLISHED: 01-27-2014
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Interleukin-6 (IL-6) is a key proinflammatory cytokine which plays a central role in the pathogenesis of periodontal disease. Host modulatory agents targeting at inhibiting IL-6, therefore, appear to be beneficial in slowing the progression of periodontal disease and potentially reducing destructive aspects of the host response. The present study was designed to investigate the effect of the macrolide antibiotic azithromycin on IL-6 generation in murine macrophages treated with lipopolysaccharide (LPS) from Prevotella intermedia, a pathogen implicated in inflammatory periodontal disease, and its mechanisms of action. Azithromycin significantly suppressed IL-6 production as well as its mRNA expression in P. intermedia LPS-activated RAW264.7 cells. LPS-induced activation of JNK and p38 was not affected by azithromycin treatment. Azithromycin failed to prevent P. intermedia LPS from degrading I?B-?. Instead, azithromycin significantly diminished nuclear translocation and DNA binding activity of NF-?B p50 subunit induced with LPS. Azithromycin inhibited P. intermedia LPS-induced STAT1 and STAT3 phosphorylation. In addition, azithromycin up-regulated the mRNA level of SOCS1 in cells treated with LPS. In conclusion, azithromycin significantly attenuated P. intermedia LPS-induced production of IL-6 in murine macrophages via inhibition of NF-?B, STAT1 and STAT3 activation, which is possibly related to the activation of SOCS1 signaling. Further in vivo studies are required to better evaluate the potential of azithromycin in the treatment of periodontal disease.
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Health-promotion and disease-prevention behaviors of primary-care practitioners.
Korean J Fam Med
PUBLISHED: 01-23-2014
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In the 1990s the primary focus of medicine was shifted to disease prevention. Accordingly, it became the responsibility of primary-care physicians to educate and counsel the general population not only on disease prevention specifically but health promotion generally as well. Moreover, it was, and is still today, considered important that physicians provide positive examples of health-promotion behaviors to patients. The purpose of this study was to investigate physicians' health-promotion behaviors and to identify the factors that influence them.
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Developmental endothelial locus-1 inhibits MIF production through suppression of NF-?B in macrophages.
Int. J. Mol. Med.
PUBLISHED: 01-22-2014
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Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine that regulates leukocyte recruitment, thereby playing a pivotal role in the regulation of innate and adaptive immunity and tumor progression. Elevated levels of MIF are associated with numerous inflammatory disorders and cancers. To determine whether developmental endothelial locus-1 (Del-1) regulated MIF, RAW264.7 macrophages were treated with Del-1 and assessed using ELISA. The results showed that MIF was downregulated in macrophages by Del-1, an endogenous anti-inflammatory protein that was previously shown to limit leukocyte adhesion and migration. Treatment of RAW264.7 macrophages with Del-1 inhibited constitutive and lipopolysaccharide (LPS)-induced MIF secretion. Recombinant Del-1 protein attenuated the phosphorylation of I?B? induced by a relatively low concentration of LPS in THP-1 monocytes, but did not inhibit I?B? phosphorylation in response to a relatively high concentration of LPS. Concomitantly, translocation of NF-?B to the nucleus was inhibited by Del-1 in LPS-activated macrophages. In addition, conditioned medium harvested from cells transfected with a Del-1 expression plasmid suppressed NF-?B activation in response to relatively low concentrations of TNF-?, albeit not the activation that was induced by a relatively high concentration of TNF-?. On the other hand, although Del-1 enhanced the macrophage expression of p53, a known negative regulator of MIF production, MIF production was not significantly affected by the level of p53 in mouse bone marrow-derived macrophages. These findings suggested that Del-1 controls NF-?B-activated MIF production in macrophages, and the potential application of Del-1 to therapeutic modalities for chronic inflammation-associated cancers.
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Impact of apigenin and kaempferol on human head and neck squamous cell carcinoma.
Oral Surg Oral Med Oral Pathol Oral Radiol
PUBLISHED: 01-21-2014
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Apigenin and kaempferol are plant flavonoids with reported chemopreventive activities. This study aimed to determine the effect of apigenin and kaempferol on cell viability in cultured cells derived from the pharynx (FaDu cell line), an oral cavity carcinoma (PCI-13 cell line), and a metastatic lymph node (PCI-15B cell line) and in explanted FaDu cells.
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Comparative analysis of rosacea and cutaneous lupus erythematosus: histopathologic features, T-cell subsets, and plasmacytoid dendritic cells.
J. Am. Acad. Dermatol.
PUBLISHED: 01-17-2014
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Distinction of rosacea and cutaneous lupus erythematosus (LE) can be challenging because of significant clinical and histologic overlap. A controlled study comparing these conditions is lacking.
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Biochemical and clinical correlation of intraplaque neovascularization using contrast-enhanced ultrasound of the carotid artery.
Atherosclerosis
PUBLISHED: 01-15-2014
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Several biomarkers reflecting inflammatory or proteolytic activity have been known to represent plaque vulnerability. Moreover, a recent study confirmed that contrast-enhanced ultrasound (CEUS) can visualize intraplaque neovascularization (IPN) and demonstrate plaque vulnerability. In this study, we tried to demonstrate that IPN detected by CEUS was correlated with several well-known biomarkers and clinical outcome in patients with coronary artery disease (CAD).
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Association of microRNAs and pathologic response to preoperative chemotherapy in triple negative breast cancer: preliminary report.
Mol. Biol. Rep.
PUBLISHED: 01-11-2014
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Triple negative breast cancer (TNBC) has caught the attention of oncologists worldwide because of poor prognosis and paucity of targeted therapies. Gene pathways have been widely studied, but less is known about epigenetic factors such as microRNAs (miRNAs) and their role in tailoring an individual systemic and surgical approach for breast cancer patients. The aim of the study was to examine selected miRNAs in TNBC core biopsies sampled before preoperative chemotherapy and the subsequent pathologic response in mastectomy or breast conservation specimens. Prior to treatment, core needle biopsies were collected from 11 female patients with inoperable locally advanced TNBC or large resectable tumors suitable for down-staging. In all 11 TNBC core biopsies we analyzed 19 miRNAs per sample: 512, 190, 200, 346, 148, 449, 203, 577, 93, 126, 423, 129, 193, 182, 136, 135, 191, 122 and 222 (miRCURY LNA™ Universal RT microRNA polymerase chain reaction Custom Pick & Mixpanels). The Wilcoxon signed-rank test was used to compare related samples. Ingenuity pathway analysis was used to evaluate potential functional significance of differentially expressed miRNAs. Statistical analysis showed that 3 of 19 miRNAs differed in relation to pathologic response i.e. good versus poor. These differences failed to reach statistical significance, although a trend was observed (p=0.06). Among these miRNAs, we identified-miR-200b-3p, miR-190a and miR-512-5p. In summary, our results indicate that higher miR-200b-3p, higher miR-190a and lower miR-512-5p expression levels in core biopsies sampled from TNBC patients may be associated with better pathologic response to chemotherapy and the increased feasibility of breast conserving surgery in these patients. Although these results were from a small cohort, they provide an important basis for larger, prospective, multicenter studies to investigate the potential role of miRNAs in neoadjuvant setting.
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The influence of different durations of aerobic exercise on fuel utilization, lactate level and antioxidant defense system in trained rats.
Nutr Res Pract
PUBLISHED: 01-06-2014
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This study investigated the influence of different durations of aerobic exercise on fuel utilization, lactate levels and antioxidative status in trained rats. Forty rats underwent physical training (T, n = 20) or non- training (NT, n = 20) for 6 weeks. For physical training, animals exercised on a treadmill for 30 min 5 days per week. At the end of week 6, the animals in each group were subdivided into BE, DE-0.5, DE-1 and DE-2, which were sacrificed at the end of week 6 without having performed exercise or after exercise on a treadmill for 0.5h, 1h and 2h, respectively, immediately before being sacrificed. The plasma glucose level in DE-2 of the NT group was significantly lower than in the other groups. Muscle and liver glycogen levels were significantly lower in DE-1 and DE-2, but there were no significant differences between DE-1 and DE-2 in the T group. Liver protein in DE-2 of the NT group was significantly lower. Muscle TG levels were decreased in DE-0.5 of the T group, while those of the NT group were decreased in DE-1. FFA levels were increased in DE-0.5 of the T group and in DE-1 of the NT group. Lactate levels were increased in DE-0.5 of the NT group, while they were increased in DE-1 of the T group. Catalase activity of the T group was lower in BE but higher in DE-0.5, DE-1 and DE-2. SOD activities were higher in trained rats, while the GSH/GSSG ratios were higher in BE, DE-0.5 and DE-1 in the T group, and there was no difference in that of DE-2. There were no differences in MDA levels in BE and DE-0.5, but they were significantly lower in DE-1 and DE-2 of the T group. Overall, the results of this study, suggest that training may improve exercise performance by facilitating the mobilization and oxidation of fat and conserving limited carbohydrate storage, and that it may delay the onset of fatigue and enhance the antioxidative defense system, but cannot support two hours of vigorous exercise.
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Ewing sarcoma.
Semin Diagn Pathol
PUBLISHED: 01-05-2014
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Classification of small round cell tumors of bone is often challenging due to overlapping clinicopathologic features. The purpose of this article is to review the clinical, radiological, histologic, and molecular features of Ewing sarcoma and to provide a discussion of the differential diagnosis of small round cell tumors of bone.
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Novel self-expandable, stent-based transcatheter pulmonic valve: a preclinical animal study.
Int. J. Cardiol.
PUBLISHED: 01-04-2014
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Because transcatheter implantation of pulmonary valve is indicated for limited-size dysfunctional right ventricular outflow tract only as a balloon-expandable stent, we investigated the feasibility of a large-diameter self-expandable valved stent and the durability of the valve after >6 months.
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C-reactive protein inhibits survivin expression via Akt/mTOR pathway downregulation by PTEN expression in cardiac myocytes.
PLoS ONE
PUBLISHED: 01-01-2014
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C-reactive protein (CRP) is one of the most important biomarkers for arteriosclerosis and cardiovascular disease. Recent studies have shown that CRP affects cell cycle and inflammatory process in cardiac myocytes. Survivin is also involved in cardiac myocytes replication and apoptosis. Reduction of survivin expression is associated with less favorable cardiac remodeling in animal models. However, the effect of CRP on survivin expression and its cellular mechanism has not yet been studied. We demonstrated that treatment of CRP resulted in a significant decrease of survivin protein expression in a concentration-dependent manner in cardiac myocytes. The upstream signaling proteins of survivin, such as Akt, mTOR and p70S6K, were also downregulated by CRP treatment. In addition, CRP increased the protein and mRNA levels of PTEN. The siRNA transfection or specific inhibitor treatment for PTEN restored the CRP-induced downregulation of Akt/mTOR/p70S6K pathway and survivin protein expression. Moreover, pretreatment with a specific p53 inhibitor decreased the CRP-induced PTEN expression. ERK-specific inhibitor also blocked the p53 phosphorylation and PTEN expression induced by CRP. Our study provides a novel insight into CRP-induced downregulation of survivin protein expression in cardiac myocytes through mechanisms that involved in downregulation of Akt/mTOR/p70S6K pathway by expression of PTEN.
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High glucose-induced jagged 1 in endothelial cells disturbs notch signaling for angiogenesis: A novel mechanism of diabetic vasculopathy.
J. Mol. Cell. Cardiol.
PUBLISHED: 11-19-2013
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Angiogenesis is a multistep process which is orchestrated by intercellular signaling. We developed an in vitro model of human angiogenesis to identify a pathologic angiogenesis and intercellular signaling in high glucose condition. We co-cultivated human endothelial cells (ECs) and smooth muscle cells (SMCs) in a spheroid on an SMC monolayer for 7days either in high glucose or in control condition. We analyzed vascular growth and expression of notch or its ligands with confocal microscopy. Abnormal angiogenesis by high glucose condition was characterized by (1) increased sprouting and branching (high glucose vs. normal: number of sprouts 20.3±1.5 vs. 13.7±2.9, p=0.024; number of branching points 7.6±2.5 vs. 2.3±2.1, p=0.047), (2) decreased vascular diameter (diameter of the tubes 13.4±6.1?m vs. 19.1±8.8?m, p=0.012) and (3) destabilization of the tubes. We identified that high glucose induced jagged 1 and suppressed notch1 in ECs whereas it did not affect Dll4. Constitutive jagged 1 overexpression or inhibition of notch1 in ECs induced abnormal angiogenesis as the high glucose condition did. Endothelial-specific shRNA targeting jagged 1 rescued the aberrant angiogenesis in high glucose condition. High glucose condition induced an abnormal endothelial intercellular signaling leading to aberrant angiogenesis. It is a novel mechanism of diabetic microvasculopathy which can be a therapeutic target beyond glucose control.
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DHA suppresses Prevotella intermedia lipopolysaccharide-induced production of proinflammatory mediators in murine macrophages.
Br. J. Nutr.
PUBLISHED: 11-19-2013
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Several reports have indicated that dietary intake of DHA is associated with lower prevalence of periodontitis. In the present study, we investigated the effect of DHA on the production of proinflammatory mediators in murine macrophage-like RAW264.7 cells stimulated with lipopolysaccharide (LPS) isolated from Prevotella intermedia, a pathogen implicated in inflammatory periodontal disease, and its mechanisms of action. LPS was isolated from lyophilised P. intermedia ATCC 25 611 cells using the standard hot-phenol-water protocol. Culture supernatants were collected and assayed for NO, IL-1? and IL-6. Real-time PCR analysis was carried out to detect the expression of inducible NO synthase (iNOS), IL-1?, IL-6 and haeme oxygenase-1 (HO-1) mRNA. Immunoblot analysis was carried out to quantify the expression of iNOS and HO-1 protein and concentrations of signalling proteins. DNA-binding activities of NF-?B subunits were determined using an ELISA-based assay kit. DHA significantly attenuated the production of NO, IL-1? and IL-6 at both gene transcription and translation levels in P. intermedia LPS-activated RAW264.7 cells. DHA induced the expression of HO-1 in cells treated with P. intermedia LPS. Selective inhibition of HO-1 activity by tin protoporphyrin IX significantly mitigated the inhibitory effects of DHA on LPS-induced NO production. DHA significantly attenuated the phosphorylation of c-Jun N-terminal kinase induced by LPS. In addition, DHA suppressed the transcriptional activity of NF-?B by regulating the nuclear translocation and DNA-binding activity of NF-?B p50 subunit and inhibited the phosphorylation of signal transducer and activator of transcription 1. Further in vivo studies are needed to better evaluate the potential of DHA in humans as a therapeutic agent to treat periodontal disease.
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p53 regulates the transcription of the anti-inflammatory molecule developmental endothelial locus-1 (Del-1).
Oncotarget
PUBLISHED: 11-07-2013
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Developmental endothelial locus-1 (Del-1) is an endothelium-derived anti-inflammatory molecule that is downregulated by inflammatory stimuli. Little is known about the molecular mechanisms by which Del-1 transcription is regulated. In the present study, a DNA sequence upstream of the Del-1 gene was analyzed and putative p53 response elements (p53REs) were identified. An approximately 2 kb fragment upstream of the translation start site displayed the highest Del-1 transcriptional activity, and the transcriptional activity of this fragment was enhanced by overexpression of p53. Chemical activation of endogenous p53 elevated the levels of Del-1 mRNA. Site-directed mutagenesis of CATG in the consensus sequences of the 2 kb fragment to TATA significantly reduced the transcription of Del-1. Chromatin immunoprecipitation revealed recruitment of p53 to the p53REs of the Del-1 promoter, resulting in increased Del-1 transcription. Finally, primary endothelial cells isolated from mice with reduced levels of p53 showed a decrease in Del-1 mRNA compared to wild-type endothelial cells. Moreover, Del-1 reciprocally enhanced p53 expression in primary endothelial cells. Thus, these findings suggest that Del-1 is a novel transcriptional target gene of p53.
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Interaction of CD99 with its paralog CD99L2 positively regulates CD99L2 trafficking to cell surfaces.
J. Immunol.
PUBLISHED: 10-16-2013
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Mouse CD99 and its paralog CD99-like 2 (CD99L2) are surface proteins implicated in cellular adhesion and migration. Although their distributions overlap in a wide variety of cells, their physical/functional relationship is currently unknown. In this study, we show the interaction between the two molecules and its consequence for membrane trafficking of mouse (m)CD99L2. The interaction was analyzed by bimolecular fluorescence complementation, immunoprecipitation, and fluorescence resonance energy transfer assays. When coexpressed, mCD99 formed heterodimers with mCD99L2, as well as homodimers, and the heterodimers were localized more efficiently at the plasma membrane than were the homodimers. Their interaction was cytoplasmic domain-dependent and enhanced mCD99L2 trafficking to the plasma membrane regardless of whether it was transiently overexpressed or endogenously expressed. Surface levels of endogenous mCD99L2 were markedly low on thymocytes, splenic leukocytes, and CTL lines derived from CD99-deficient mice. Importantly, the surface levels of mCD99L2 on mCD99-deficient cells recovered significantly when wild-type mCD99 was exogenously introduced, but they remained low when a cytoplasmic domain mutant of mCD99 was introduced. Our results demonstrate a novel role for mCD99 in membrane trafficking of mCD99L2, providing useful insights into controlling transendothelial migration of leukocytes.
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Effects of maternal exposure to di(2-ethylhexyl)phthalate (DEHP) during pregnancy on susceptibility to neonatal asthma.
Toxicol. Appl. Pharmacol.
PUBLISHED: 10-01-2013
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Di(2-ethylhexyl) phthalate (DEHP) is used as a plasticizer and is widely dispersed in the environment. In this study, we investigated the effects of maternal exposure to DEHP during pregnancy on neonatal asthma susceptibility using a murine model of asthma induced by ovalbumin (OVA). Pregnant BALB/c mice received DEHP from gestation day 13 to lactation day 21. Their offspring were sensitized on postnatal days (PNDs) 9 and 15 by intraperitoneal injection of 0.5?g OVA with 200?g aluminum hydroxide. On PNDs 22, 23 and 24, live pups received an airway challenge of OVA for 30min. Offspring from pregnant mice that received DEHP showed reductions in inflammatory cell count, interleukin (IL)-4, IL-13, and eotaxin in their bronchoalveolar lavage fluid and in total immunoglobulin E and OVA-specific IgE in their plasma compared with offspring from pregnant mice that did not receive DEHP treatment. These results were consistent with histological analysis and immunoblotting. Maternal exposure to DEHP reduces airway inflammation and mucus production in offspring, with a decrease in inducible nitric oxide synthase (iNOS) in the lung tissue. This study suggests that maternal exposure to DEHP during pregnancy reduces asthmatic responses induced by OVA challenge in offspring. These effects were considered to be closely related to the suppression of Th2 immune responses and iNOS expression.
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Stabilization of mutant BRCA1 protein confers PARP inhibitor and platinum resistance.
Proc. Natl. Acad. Sci. U.S.A.
PUBLISHED: 10-01-2013
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Breast Cancer Type 1 Susceptibility Protein (BRCA1)-deficient cells have compromised DNA repair and are sensitive to poly(ADP-ribose) polymerase (PARP) inhibitors. Despite initial responses, the development of resistance limits clinical efficacy. Mutations in the BRCA C-terminal (BRCT) domain of BRCA1 frequently create protein products unable to fold that are subject to protease-mediated degradation. Here, we show HSP90-mediated stabilization of a BRCT domain mutant BRCA1 protein under PARP inhibitor selection pressure. The stabilized mutant BRCA1 protein interacted with PALB2-BRCA2-RAD51, was essential for RAD51 focus formation, and conferred PARP inhibitor as well as cisplatin resistance. Treatment of resistant cells with the HSP90 inhibitor 17-dimethylaminoethylamino-17-demethoxygeldanamycin reduced mutant BRCA1 protein levels and restored their sensitivity to PARP inhibition. Resistant cells also acquired a TP53BP1 mutation that facilitated DNA end resection in the absence of a BRCA1 protein capable of binding CtIP. Finally, concomitant increased mutant BRCA1 and decreased 53BP1 protein expression occur in clinical samples of BRCA1-mutated recurrent ovarian carcinomas that have developed resistance to platinum. These results provide evidence for a two-event mechanism by which BRCA1-mutant tumors acquire anticancer therapy resistance.
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Device size for transcatheter closure of ovoid interatrial septal defect.
Heart Surg Forum
PUBLISHED: 08-21-2013
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For successful transcatheter closure of an atrial septal defect with the Amplatzer septal occluder, the shape of the defect should be considered before selecting the device size. The purpose of this study was to evaluate the results of transcatheter closure of an ovoid atrial septal defect.
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Outcome of transcatheter closure of oval shaped atrial septal defect with amplatzer septal occluder.
Yonsei Med. J.
PUBLISHED: 08-07-2013
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For the successful completion of transcatheter closure of atrial septal defects with the Amplatzer septal occluder, shape of the defects should be considered prior to selecting the device. The purpose of this study is to evaluate the results of a transcatheter closure of oval shaped atrial septal defect.
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Vertical alignment of liquid crystals with zinc oxide nanorods.
Nanotechnology
PUBLISHED: 07-30-2013
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The alignment of liquid crystals (LCs) on zinc oxide (ZnO) nanorods grown vertically on an indium tin oxide (ITO) layer has been investigated as an alternative alignment layer for the vertical alignment of LCs. We found that the degree of vertical alignment strongly depends on the length and density of the vertically aligned ZnO nanorods on the ITO layer and also that a uniform vertical alignment using the proposed structure can be achieved. Finally, vertically aligned LC cells with ZnO nanorods were fabricated and their electro-optical properties were evaluated and compared with those of a conventional vertically aligned LC cell with a polymer alignment layer.
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Undifferentiated small round cell sarcoma with t(4;19)(q35;q13.1) CIC-DUX4 fusion: a novel highly aggressive soft tissue tumor with distinctive histopathology.
Am. J. Surg. Pathol.
PUBLISHED: 07-27-2013
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A subset of small round cell sarcomas remains difficult to classify. Among these, a rare tumor harboring a t(4;19)(q35;q13.1) with CIC-DUX4 fusion has been described. The aim of this study is to better understand its clinicopathologic features. Four cases of CIC-DUX4 sarcoma, all arising in adults (3 women, 1 man, aged 20 to 43 y), were identified using conventional cytogenetic, reverse transcription polymerase chain reaction (RT-PCR) and fluorescence in situ hybridization (FISH) methods. All 4 tumors demonstrated CIC-DUX4 fusion transcript by both RT-PCR and FISH and CIC rearrangement by FISH. Cytogenetic results from 2 tumors showed t(4;19)(q35;q13.1) occurring as part of a simple karyotype in 1 tumor and as part of a complex karyotype in the other, the latter from a postchemotherapy specimen. Both tumors harbored trisomy 8 and lacked any other known sarcoma-associated translocation. No EWS or SYT rearrangements were detected by RT-PCR or FISH. The tumors had small round cell morphology with a distinctive constellation of histologic features including extensive geographic necrosis, mild nuclear pleomorphism with coarse chromatin and prominent nucleoli, clear cell areas, and focal myxoid matrix. Only focal staining for CD99 was present in each tumor. Two had very focal cytokeratin staining. All tumors were negative for desmin, myogenin, TLE-1, and S100 protein, whereas nuclear INI-1 staining was retained. The tumors were highly aggressive, and all patients died of disseminated disease within 16.8 months. CIC-DUX4 sarcoma represents a novel translocation-associated sarcoma with distinctive histopathologic features and rapid disease progression.
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Radiofrequency catheter ablation for supraventricular tachycardia: a comparison study of children aged 0-4 and 5-9 years.
Pacing Clin Electrophysiol
PUBLISHED: 07-10-2013
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The safety and effectiveness of radiofrequency catheter ablation (RFCA) for supraventricular tachycardia (SVT) in young children was investigated.
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Transcatheter closure of small ductus arteriosus with amplatzer vascular plug.
Korean J Pediatr
PUBLISHED: 06-26-2013
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The purpose of this study was to share our experience of transcatheter closure of small patent ductus arteriosus (PDA) by using an Amplatzer vascular plug (AVP).
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Airway compression in children with congenital heart disease evaluated using computed tomography.
Ann. Thorac. Surg.
PUBLISHED: 06-26-2013
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Extrinsic airway compression often complicates the course of congenital heart disease (CHD) repair. This study investigated the risk factors and outcome of airway compression evaluated using computed tomography (CT) in CHD patients.
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A case of progressive ductal constriction in a fetus.
Korean Circ J
PUBLISHED: 05-19-2013
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The ductus arteriosus is a normal and essential structure in fetal circulation. Since the introduction of fetal echocardiography, there have been reports of ductal constriction, many of which were related to maternal use of some medications. However, there have been some reports of idiopathic ductal constriction, which usually present in later gestation. Recently we experienced a case, which initially showed an S-shaped ductus with mild narrowing at 23 weeks and 27 weeks gestation and developed severe ductal constriction at 33 weeks. Soon after birth, ductus was searched for but no ductus was found in 2-D and color images. The neonate required mechanical ventilation with supplemental oxygen for 3 days. All echocardiographic abnormalities were normalized in 7 months. We report progressive ductal constriction in an S-shaped ductus and emphasize the importance of continuous follow up extending to the third trimester and even immediately after birth.
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Solvent-free fluidic organic dye lasers.
Opt Express
PUBLISHED: 05-15-2013
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We report on the demonstration of liquid organic dye lasers based on 9-(2-ethylhexyl)carbazole (EHCz), so-called liquid carbazole, doped with green- and red-emitting laser dyes. Both waveguide and Fabry-Perot type microcavity fluidic organic dye lasers were prepared by capillary action under solvent-free conditions. Cascade Förster-type energy transfer processes from liquid carbazole to laser dyes were employed to achieve color-variable amplified spontaneous emission and lasing. Overall, this study provides the first step towards the development of solvent-free fluidic organic semiconducting lasers and demonstrates a new kind of optoelectronic applications for liquid organic semiconductors.
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Implantable cardioverter defibrillator therapy in pediatric and congenital heart disease patients: a single tertiary center experience in Korea.
Korean J Pediatr
PUBLISHED: 03-18-2013
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The use of implantable cardioverter defibrillators (ICDs) to prevent sudden cardiac death is increasing in children and adolescents. This study investigated the use of ICDs in children with congenital heart disease.
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Interaction of physical trainings and coffee intakes in fuel utilization during exercise in rats.
Nutr Res Pract
PUBLISHED: 02-25-2013
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This study investigates the impact of exercises, coffee intakes, and physical trainings on fuel utilization in rats. Ninety-six rats were fed a control diet with either water (C) or coffee (CF; 0.12 g freeze-dried instant coffee/100 g body weight/d). Additionally, the animals go through physical training (TC and TCF) or no training (NTC and NTCF) for 4 weeks. For physical training, animals have to exercise on treadmills for 30 minutes (5 d per week, 15° incline, 0.5-0.8 km/h). At the end of week 4, the animals in each group were subdivided into three exercise groups: before exercise (BE), during exercise (DE), and after exercise (AE). The DE rats exercised on treadmills for 1 hour immediately before being sacrificed. Hemoglobin, hematocrit, glucose, glycogen, protein, triglyceride (TG), and free fatty acid (FFA) levels in the plasma, liver, and skeletal muscle of the rats were compared accordingly. Organ weights were also measured. Coffee-training interaction had a significant impact on heart weight, visceral fat, hemoglobin, hematocrit, liver glycogen in DE and AE, and liver triglyceride in DE and AE. Exercise (meaning exercised on a treadmill for 1 hour immediately before being sacrificed) training interaction was significant in liver glycogen, muscle glycogen in control diet and control diet with coffee, FFA and muscle TG levels at control diet with coffee group. Exercise-coffee interactions significantly influenced the FFA with no training groups. Exercise-coffee-training interaction significantly effects on FFA, Liver TG and Muscle TG. Coffee intakes can increase lipolysis during exercising but coffee consumptions delay the recovery of liver glycogen levels in trained rats after exercising. Coffee intakes can increase lipolysis during exercising but coffee consumptions delay the recovery of liver glycogen levels in trained rats after exercising. Coffee can be an effective ergogenic aid during exercise for physically trained rats.
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Low-tidal volume mechanical ventilation in patients with acute respiratory distress syndrome caused by pandemic influenza A/H1N1 infection.
J Crit Care
PUBLISHED: 02-22-2013
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Low-tidal volume (TV) mechanical ventilation is an important manipulation in managing patients with acute respiratory distress syndrome (ARDS). However, there is no definite evidence to support the use of this intervention in patients with viral etiologies.
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Charity begins at home: non-coding RNA functions in DNA repair.
Nat. Rev. Mol. Cell Biol.
PUBLISHED: 02-06-2013
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During the past decade, evolutionarily conserved microRNAs (miRNAs) have been characterized as regulators of almost every cellular process and signalling pathway. There is now emerging evidence that this new class of regulators also impinges on the DNA damage response (DDR). Both miRNAs and other small non-coding RNAs (ncRNAs) are induced at DNA breaks and mediate the repair process. These intriguing observations raise the possibility that crosstalk between ncRNAs and the DDR might provide a means of efficient and accurate DNA repair and facilitate the maintenance of genomic stability.
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Protective effect of survivin in Doxorubicin-induced cell death in h9c2 cardiac myocytes.
Korean Circ J
PUBLISHED: 02-05-2013
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Apoptosis has been known to be an important mechanism of doxorubicin-induced cardiotoxicity. Survivin, which belongs to the inhibitor of apoptosis protein family, is associated with apoptosis and alteration of the cardiac myocyte molecular pathways. Therefore, we investigated the anti-apoptotic effect and cellular mechanisms of survivin using a protein delivery system in a doxorubicin-induced cardiac myocyte injury model.
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Comparison of Metabolic Characteristics of Metabolically Healthy but Obese (MHO) Middle-Aged Men According to Different Criteria.
Korean J Fam Med
PUBLISHED: 01-28-2013
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To compare the prevalence and metabolic characteristics of metabolically healthy but obese (MHO) individuals according to different criteria.
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Sudden cardiac arrest during anesthesia in a 30-month-old boy with syndactyly: a case of genetically proven Timothy syndrome.
J. Korean Med. Sci.
PUBLISHED: 01-25-2013
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Timothy syndrome, long QT syndrome type 8, is highly malignant with ventricular tachyarrhythmia. A 30-month-old boy had sudden cardiac arrest during anesthesia induction before plastic surgery for bilateral cutaneous syndactyly. After successful resuscitation, prolonged QT interval (QTc, 0.58-0.60 sec) and T-wave alternans were found in his electrocardiogram. Starting ?-blocker to prevent further tachycardia and collapse event, then there were no more arrhythmic events. The genes KCNQ1, KCNH2, KCNE1 and 2, and SCN5A were negative for long QT syndrome. The mutation p.Gly406Arg was confirmed in CACNA1C, which maintains L-type calcium channel depolarization in the heart and other systems.
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Solution processed small molecule-based green phosphorescent organic light-emitting diodes using polymer binder.
J Nanosci Nanotechnol
PUBLISHED: 12-26-2011
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The authors have demonstrated efficient green organic light-emitting diodes (OLEDs) by using polymer binder. We fabricated small molecular green OLEDs and mixed polymer as a binder such as polystyrene (PS) or poly(N-vinylcarbazole) (PVK). The 4,4-N,N-dicarbazole-biphenyl (CBP) is a small molecular material with excellent electrical properties however it become crystalline at high temperature. Polymer binder prevents crystallization of CBP and lead to high efficiency. Therefore, we added PS or PVK into CBP as a polymer binder. As a result, we obtained maximum luminous efficiency, power efficiency and quantum efficiency of 22.8 cd/A, 11.6 Im/W and 6.61% at 23% PS added device.
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Duplication of intrachromosomal insertion segments 4q32?q35 confirmed by comparative genomic hybridization and fluorescent in situ hybridization.
Clin Exp Reprod Med
PUBLISHED: 12-12-2011
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A 35-year-old man with infertility was referred for chromosomal analysis. In routine cytogenetic analysis, the patient was seen to have additional material of unknown origin on the terminal region of the short arm of chromosome 4. To determine the origin of the unknown material, we carried out high-resolution banding, comparative genomic hybridization (CGH), and FISH. CGH showed a gain of signal on the region of 4q32?q35. FISH using whole chromosome painting and subtelomeric region probes for chromosome 4 confirmed the aberrant chromosome as an intrachromosomal insertion duplication of 4q32?q35. Duplication often leads to some phenotypic abnormalities; however, our patient showed an almost normal phenotype except for congenital dysfunction in spermatogenesis.
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Partial anomalous pulmonary venous connection to the superior vena cava: the outcome after the Warden procedure.
Eur J Cardiothorac Surg
PUBLISHED: 12-12-2011
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Partial anomalous pulmonary venous connection (PAPVC) draining into the superior vena cava (SVC) has been repaired with various techniques. We investigated the outcome of the Warden procedure for repair of this anomaly.
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PTEN modulates miR-21 processing via RNA-regulatory protein RNH1.
PLoS ONE
PUBLISHED: 10-13-2011
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Aberrant miR-21 expression is closely associated with cell proliferation, anti-apoptosis, migration, invasion, and metastasis in various cancers. However, the regulatory mechanism of miR-21 biogenesis is largely unknown. Here, we demonstrated that the tumor suppressor PTEN negatively regulates the expression of oncogenic miR-21 at the post-transcriptional level. Moreover, our results suggest that PTEN plays such a role through the indirect interaction with the Drosha complex. To elucidate how PTEN regulates pri- to pre-miR-21 processing, we attempted to find PTEN-interacting proteins and identified an RNA-regulatory protein, RNH1. Using the sensor to monitor pri-miR-21 processing, we demonstrated that RNH1 is necessary and sufficient for pri-miR-21 processing. Moreover, our results propose that the nuclear localization of RNH1 is important for this function. Further analysis showed that RNH1 directly interacts with the Drosha complex and that PTEN blocks this interaction. Taken together, these results suggest that the PTEN-mediated miR-21 regulation is achieved by inhibiting the interaction between the Drosha complex and RNH1, revealing previously unidentified role of PTEN in the oncogenic miR-21 biogenesis.
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Residents expectation of family medicine-specific training program and its current state.
Korean J Fam Med
PUBLISHED: 10-07-2011
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The family medicine residency program consists mainly of clinical rotations in other specialties and the family medicine-specific training. We conducted this study to investigate how family medicine residents evaluated their training program that include family-oriented medicine, clinical preventive medicine, behavioral science and research in primary care.
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Development of novel CH223191-based antagonists of the aryl hydrocarbon receptor.
Mol. Pharmacol.
PUBLISHED: 10-03-2011
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Aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that regulates genes involved in drug/xenobiotic metabolism, cell cycle progression, cell fate determination, immune function, and inflammatory response. Increasing evidence that AHR plays a role in the pathophysiology of a number of human disease states is driving the need for improved pharmacological tools to be used for understanding the in vivo impact of AHR modulation. In this study, we have characterized and used structure-activity relationship analyses of a newly synthesized library of derivatives of the potent AHR antagonist 2-methyl-2H-pyrazole-3-carboxylic acid (2-methyl-4-o-tolylazo-phenyl)-amide (CH223191). Initial screening of these compounds revealed that those bearing groups with strong electronegativity at the R1 position (i.e., CHD-5, CHD-11, and CHD-12) versus those that are more electron-poor at this position (i.e., CHD-7 and CHD-8) elicited the most potent AHR antagonistic properties. The ability of these derivatives to inhibit agonist (2,3,7,8-tetrachlorodibenzo-p-dioxin) binding, nuclear translocation of AHR, and agonist-induced enzyme activity also were determined and support the initial findings. Furthermore, CH223191, but not CHD-5, CHD-11, or CHD-12, was found to exhibit AHR-independent proproliferative properties. These results contribute to our understanding of the structural requirements of potent AHR antagonists and the development of effective pharmacological tools to be used for studying the pathophysiological role of AHR.
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Transcatheter closure of multiple atrial septal defects with the amplatzer device.
Korean Circ J
PUBLISHED: 09-29-2011
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Percutaneous device occlusion of secundum atrial septal defect (ASD) has become an accepted alternative to surgical repair. A variety of devices have been used successfully. However, all of them have limitations. We report our experience with two devices used to close multiple ASDs.
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The Utility of HbA1c as a Diagnostic Criterion of Diabetes.
Korean J Fam Med
PUBLISHED: 09-18-2011
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Hemoglobin A1c (HbA1c) was adopted as a new standard criterion for diagnosing diabetes. We investigated the diagnostic utility of HbA1c by comparing the 2003 American Diabetes Association (ADA) diagnostic criteria of diabetes with HbA1c of 6.5%. Furthermore, the cut-off value for HbA1c was investigated using receiver operating characteristic curves.
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Peroxisome proliferator-activated receptor-? activates endothelial progenitor cells to induce angio-myogenesis through matrix metallo-proteinase-9-mediated insulin-like growth factor-1 paracrine networks.
Eur. Heart J.
PUBLISHED: 09-14-2011
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The roles of peroxisome proliferator-activated receptor (PPAR)-? in vascular biology are mainly unknown. We investigated the effects of PPAR-? activation on the paracrine networks between endothelial progenitor cells (EPCs) and endothelial cells (ECs)/skeletal muscle.
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Production of graphene by exfoliation of graphite in a volatile organic solvent.
Nanotechnology
PUBLISHED: 08-11-2011
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The production of unfunctionalized and nonoxidized graphene by exfoliation of graphite in a volatile solvent, 1-propanol, is reported. A stable homogeneous dispersion of graphene was obtained by mild sonication of graphite powder and subsequent centrifugation. The presence of a graphene monolayer was observed by atomic force microscopy and transmission electron microscopy. The solvent, 1-propanol, from the deposited dispersion was simply and quickly removed by air drying at room temperature, without the help of high temperature annealing or vacuum drying, which shortens production time and does not leave any residue of the solvent in the graphene sheets.
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Permanent epicardial pacing in pediatric patients: 12-year experience at a single center.
Ann. Thorac. Surg.
PUBLISHED: 07-29-2011
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Permanent cardiac pacing is not often done in children, and when done is usually accomplished through epicardial pacing. We reviewed a 12-year experience with the implantation of epicardial pacemakers by our clinical group.
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Ubiquitin ligase CHIP induces TRAF2 proteasomal degradation and NF-?B inactivation to regulate breast cancer cell invasion.
J. Cell. Biochem.
PUBLISHED: 07-28-2011
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Transcriptional factor nuclear factor-kappaB (NF-?B) plays a crucial role in human breast cancer cell invasion and metastasis. The carboxyl terminus of Hsc70-interacting protein (CHIP) is a U-box-type ubiquitin ligase that induces ubiquitination and proteasomal degradation of its substrate proteins. In this study, we investigated the role of CHIP in the NF-?B pathway in the invasion of MDA-MB-231 cells, a highly aggressive breast cancer cell line. We showed that overexpression of CHIP significantly inhibits the invasion of the MDA-MB-231 cells. The overexpression of CHIP suppressed expression of urokinase plasminogen activator (uPA) and matrix metalloproteinase-9 (MMP-9) in MDA-MB-231 cells. Moreover, CHIP strongly inhibited the nuclear localization and the transcriptional activity of NF-?B. The activation of the IkappaB kinase complex (IKK) was also blocked by CHIP overexpression. Importantly, CHIP overexpression resulted in a significant decrease in the level of TNF receptor-associated factor 2 (TRAF2), an upstream key player in the NF-?B pathway. However, the level of TRAF2 was restored after treatment with a proteasome inhibitor, MG-132. Moreover, CHIP overexpression promoted the ubiquitination of TRAF2. We also found cell invasion significantly decreased in cells transfected with TRAF2 small interfering RNA (siRNA). In contrast, when CHIP expression was suppressed by siRNA in poorly invasive MCF-7 cells, cell invasion significantly increased in conjunction with enhanced NF-?B activation and TRAF2 levels. Taken together, these results suggest that CHIP regulates NF-?B-mediated cell invasion via the down-regulation of TRAF2.
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Pathological findings following radical prostatectomy in patients who are candidates for active surveillance: impact of varying PSA levels.
Asian J. Androl.
PUBLISHED: 07-25-2011
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Active surveillance is an acceptable treatment option in men with a low-risk prostate cancer. In the present study, we have retrospectively reviewed the outcomes of 509 men who fit the criteria for active surveillance but selected radical prostatectomy. Then, the impact of varying prostate-specific antigen (PSA) levels on the risk of upstaging and upgrading in these patients was assessed. Pathological characteristics of patients who fulfilled the inclusion criteria under three active surveillance criteria--those of the University of California-San Francisco, the National Cancer Institute and the European Association of Urology--were examined. The proportion of men who were deemed candidates for active surveillance but were subsequently upstaged or upgraded was determined. Of 509 patients, 186 (36.5%), 132 (25.9%) and 88 (17.3%) men fulfilled the active surveillance criteria, respectively. Upgrading (Gleason scores 7-10) ranged from 32.8% to 38.6%, while upstaging (?pT3) ranged from 10.2% to 12.5%, depending on the three active surveillance criteria. After a median follow-up of 24 months, three patients developed a biochemical recurrence. When the impact of varying PSA levels was examined using a test for trend analysis in the context of PSA for each protocol, rates of upstaging were lower in men with PSA <4 ng ml(-1). However, there was no impact of varying PSA levels on upgrading. In conclusion, commonly used active surveillance protocols carry the risks of upgrading and upstaging. More reliable and accurate markers are needed to better stratify the risks of men who are appropriate candidates for active surveillance.
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Down-regulation of survivin suppresses uro-plasminogen activator through transcription factor JunB.
Exp. Mol. Med.
PUBLISHED: 07-08-2011
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Survivin, a member of the inhibitors of apoptosis protein family, is expressed during development and in various human cancers. However, the clinical relevance of survivin in cancer is still a matter of debate. Genes induced by hepatocyte growth factor (HGF) were screened using cDNA microarray technology in the stomach cancer cell lines, NUGC3 and MKN28. The levels of JunB, survivin, and uro-plasminogen activator (uPA) were up-regulated in cells treated with HGF in a dose-dependent manner. HGF-induced up regulation of JunB, survivin, and uPA was inhibited by pre-treatment with a MEK inhibitor (PD 98059). HGF-induced up-regulation of uPA was repressed by survivin knockdown. HGF enhanced the binding activity of JunB to the survivin promoter in control cells, but not in the JunB-shRNA cells. Transfection with survivin- shRNA resulted in a decrement of cell proliferation, as determined with MTT assays. In an in vitro invasion assay, significantly fewer cells transfected with survivin shRNA than control cells were able to invade across a Matrigel membrane barrier. In conclusion, survivin appeared to play an important role in the up-regulation of uPA induced by HGF via JunB and might contribute to HGF-mediated tumor invasion and metastasis, which may serve as a promising target for gastric cancer therapy.
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Peroxisome proliferator-activated receptor-gamma agonists suppress tissue factor overexpression in rat balloon injury model with paclitaxel infusion.
PLoS ONE
PUBLISHED: 07-07-2011
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The role and underlying mechanisms of rosiglitazone, a peroxisome proliferator-activated receptor-gamma (PPAR-?) agonist, on myocardial infarction are poorly understood. We investigated the effects of this PPAR-? agonist on the expression of tissue factor (TF), a primary molecule for thrombosis, and elucidated its underlying mechanisms. The PPAR-? agonist inhibited TF expression in response to TNF-? in human umbilical vein endothelial cells, human monocytic leukemia cell line, and human umbilical arterial smooth muscle cells. The overexpression of TF was mediated by increased phosphorylation of mitogen-activated protein kinase (MAPK), which was blocked by the PPAR-? agonist. The effective MAPK differed depending on each cell type. Luciferase and ChIP assays showed that transcription factor, activator protein-1 (AP-1), was a pivotal target of the PPAR-? agonist to lower TF transcription. Intriguingly, two main drugs for drug-eluting stent, paclitaxel or rapamycin, significantly exaggerated thrombin-induced TF expression, which was also effectively blocked by the PPAR-? agonist in all cell types. This PPAR-? agonist did not impair TF pathway inhibitor (TFPI) in three cell types. In rat balloon injury model (Sprague-Dawley rats, n?=?10/group) with continuous paclitaxel infusion, the PPAR-? agonist attenuated TF expression by 70±5% (n?=?4; P<0.0001) in injured vasculature. Taken together, rosiglitazone reduced TF expression in three critical cell types involved in vascular thrombus formation via MAPK and AP-1 inhibitions. Also, this PPAR-? agonist reversed the paclitaxel-induced aggravation of TF expression, which suggests a possibility that the benefits might outweigh its risks in a group of patients with paclitaxel-eluting stent implanted.
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What is Visualize?

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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We use abstracts found on PubMed and match them to JoVE videos to create a list of 10 to 30 related methods videos.

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In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.