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Find video protocols related to scientific articles indexed in Pubmed.
Optimizing cultivation strategies for robust algal growth and consequent removal of inorganic nutrients in pretreated livestock effluent.
Appl. Biochem. Biotechnol.
PUBLISHED: 08-20-2014
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Dilution was employed as a pretreatment strategy to increase light transmittance and decrease ammonia toxicity in piggery effluent prior to the cultivation of microalgae. The dilution effect was quantitatively determined based on both the maximum specific nutrient consumption rate and the maximum growth coefficient to minimize the usage of diluent. The biomass productivity of microalgae was also evaluated to select the best species among the five different candidates examined. A 20-fold dilution of piggery wastewater resulted in decreased chromaticity (584 mg Pt-Co L(-1)) and total nitrogen (76 mg L(-1)), on which the microalgae cultivation was more effective for an algal growth compared to the other dilution factors. If the initial cell concentration of Scenedesmus quadricauda increased, the production of biomass tended to improve. Robust growth and harvesting of S. quadricauda were achieved, and the associated consistent removal of inorganic nutrients was accomplished during the semi-continuous cultivation of the best species.
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AN ALTERNATIVE METHOD FOR LATERAL SINUS APPROACH WITH TREPHINE DESIGN BUR: A CLINICAL REPORT.
J Oral Implantol
PUBLISHED: 06-27-2014
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Abstract Lateral bone planning antrostomy with trephine design bur has a relatively high risk of membrane perforation although it has benefites including reduced surgical time, simple procedures and relatively brief required equipment. In this case, lateral sinus approach with trephine bur can be performed with the least risk of membrane perforation by the supplemental use of the dome shaped drill originally designed for the crestal sinus approach. This technique has additional benefits to antrostomy of thick sinus wall and the sinus wall difficult to secure sight.
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STA-21, a promising STAT-3 inhibitor that reciprocally regulates Th17 and Treg cells, inhibits osteoclastogenesis in mice and humans and alleviates autoimmune inflammation in an experimental model of rheumatoid arthritis.
PUBLISHED: 04-24-2014
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To investigate the impact of STA-21, a promising STAT-3 inhibitor, on the development and progression of inflammatory arthritis and to determine the possible mechanisms by which STA-21 has antiarthritic effects in interleukin-1 receptor antagonist-knockout (IL-1Ra-KO) mice, an animal model of rheumatoid arthritis (RA).
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RhoGDI2 promotes epithelial-mesenchymal transition via induction of Snail in gastric cancer cells.
Oncotarget
PUBLISHED: 04-12-2014
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Rho GDP dissociation inhibitor 2 (RhoGDI2) expression correlates with tumor growth, metastasis, and chemoresistance in gastric cancer. Here, we show that RhoGDI2 functions in the epithelial-mesenchymal transition (EMT), which is responsible for invasiveness during tumor progression. This tumorigenic activity is associated with repression of E-cadherin by RhoGDI2 via upregulation of Snail. Overexpression of RhoGDI2 induced phenotypic changes consistent with EMT in gastric cancer cells, including abnormal epithelial cell morphology, fibroblast-like properties, and reduced intercellular adhesion. RhoGDI2 overexpression also resulted in decreased expression of the epithelial markers E-cadherin and ?-catenin and increased expression of the mesenchymal markers vimentin and fibronectin. Importantly, RhoGDI2 overexpression also stimulated the expression of Snail, a repressor of E-cadherin and inducer of EMT, but not other family members such as Slug or Twist. RNA interference-mediated knockdown of Snail expression suppressed RhoGDI2-induced EMT and invasion, confirming that the effect was Snail-specific. These results indicate that RhoGDI2 plays a critical role in tumor progression in gastric cancer through induction of EMT. Targeting RhoGDI2 may thus be a useful strategy to inhibit gastric cancer cell invasion and metastasis.
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Natural polyamines inhibit the migration of preosteoclasts by attenuating Ca(2+)-PYK2-Src-NFATc1 signaling pathways.
Amino Acids
PUBLISHED: 04-09-2014
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Natural polyamines have numerous biological activities. Several studies have reported their beneficial role in bone metabolism, but their mode of action is not fully understood. Bone diseases such as osteoporosis, which is characterized by impaired bone structure and low bone mass, are caused by an increased number of osteoclasts and/or overactivation of osteoclastogenesis. Osteoclast differentiation is a multi-complex procedure involving the following sequential steps: differentiation-migration-fusion-resorption. In this study, we found that putrescine, spermidine or spermine inhibited the RANKL-mediated migration of preosteoclasts. Furthermore, the RANKL-mediated activation of the Src-PYK2 signaling axis and of transcription factors such as NF-?B and NFATc1 was prevented by each polyamine. Anti-osteoclastogenic and anti-migration activities of polyamines were confirmed by evaluating their potential to downregulate the mRNA expression levels of osteoclastogenesis-related genes such as OSCAR, TRAP, cathepsin K and c-Src, and genes related to fusion and/or migration of preosteoclasts. Moreover, ATP-mediated elevation of cytosolic free Ca(2+) concentration ([Ca(2+)]i) was strongly inhibited by each polyamine, indicating the involvement of [Ca(2+)]i in the anti-fusion activities of polyamines. In conclusion, polyamines could exhibit anti-osteoclastogenic activity by inhibiting the migration of preosteoclasts via the Ca(2+)-PYK2-Src-NFATc1 signaling axis.
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JAK2-STAT3 blockade by AG490 suppresses autoimmune arthritis in mice via reciprocal regulation of regulatory T Cells and Th17 cells.
J. Immunol.
PUBLISHED: 03-31-2014
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IL-6-mediated STAT3 signaling is essential for Th17 differentiation and plays a central role in the pathogenesis of rheumatoid arthritis. To investigate the molecular mechanism underlying the antirheumatic effects and T cell regulatory effects of STAT3 inhibition, we studied the effects of the JAK 2 inhibitor AG490 on Th17 cell/regulatory T cell (Treg) balance and osteoclastogenesis. AG490 was administered to mice with collagen-induced arthritis (CIA) via i.p. injection, and its in vivo effects were determined. Differential expression of proinflammatory cytokines, including IL-17A, IL-1?, and IL-6, was analyzed by immunohistochemistry. Levels of phosphorylated STAT3 and STAT5 and differentiation of Th17 cells and Tregs after AG490 treatment in our CIA model were analyzed by immunostaining. In vitro development of Th17 cells and Tregs was analyzed by flow cytometry and real-time PCR. AG490 ameliorated the arthritic phenotype in CIA and increased the proportion of Foxp3(+) Tregs. In contrast, the proportion of IL-17A-producing T cells and levels of inflammatory markers were reduced in AG490-treated mice. Numbers of p-STAT3(+) CD4(+) T cells and p-STAT5(+) CD4(+) T cells were reduced and elevated, respectively, after treatment with AG490. Furthermore, AG490 markedly increased the expression of molecules associated with Treg development (ICOS, programmed cell death protein 1, ICAM-1, and CD103). The development and function of osteoclasts were suppressed by AG490 treatment. Our results suggest that AG490, specifically regulating the JAK2/STAT3 pathway, may be a promising treatment for rheumatoid arthritis.
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Discovery and the structural basis of a novel p21-activated kinase 4 inhibitor.
Cancer Lett.
PUBLISHED: 03-19-2014
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Functional versatility and elevated expression in cancers have endowed p21-activated kinase 4 (PAK4) as one of the first-in-class anti-cancer drug target. In this study, a novel PAK4 inhibitor, KY-04031 (N(2)-(2-(1H-indol-3-yl)ethyl)-N(4)-(1H-indazol-5-yl)-6-methoxy-1,3,5-triazine-2,4-diamine), was discovered using a high-throughput screening. Analysis of the complex crystal structure illustrated that both indole and indazole of KY-04031 are responsible for PAK4 hinge interaction. Moreover, the molecule's triazine core was found to mimic the ribose of the natural ATP substrate. The cell-based anti-cancer potency of KY-04031 was less effective than the pyrroloaminopyrazoles; however, the unique molecular feature of KY-04031 can be exploited in designing new PAK4 inhibitors.
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The effect of a desensitizer and CO2 laser irradiation on bond performance between eroded dentin and resin composite.
J Adv Prosthodont
PUBLISHED: 03-12-2014
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This study was aimed to evaluate effect of the desensitizing pretreatments on the micro-tensile bond strengths (µTBS) to eroded dentin and sound dentin.
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Intravenous immunoglobulin attenuates experimental autoimmune arthritis by inducing reciprocal regulation of Th17 and Treg cells in an interleukin-10-dependent manner.
PUBLISHED: 03-11-2014
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Intravenous immunoglobulin (IVIG) is used as a therapeutic agent in various autoimmune diseases. The aims of this study were to investigate the therapeutic effects of IVIG on collagen-induced arthritis (CIA) and identify the mechanism responsible for any therapeutic effects.
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Gene associated with retinoid-interferon-induced mortality 19 attenuates murine autoimmune arthritis by regulation of th17 and treg cells.
PUBLISHED: 02-28-2014
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STAT-3 is a key transcriptional factor in the interleukin-6 (IL-6)-mediated differentiation of Th17 cells. Because Th17 is believed to be a central player in rheumatoid arthritis (RA), we sought to evaluate whether an endogenous inhibitor of the STAT3 gene, GRIM-19 (gene associated with retinoid-interferon-induced mortality 19), could attenuate the progression and severity of murine collagen-induced arthritis (CIA) through suppression of Th17 cells and, reciprocally, could increase expression of Treg cells.
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VEGF-C mediates RhoGDI2-induced gastric cancer cell metastasis and cisplatin resistance.
Int. J. Cancer
PUBLISHED: 02-10-2014
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Rho GDP dissociation inhibitor 2 (RhoGDI2) expression is correlated with tumor growth, metastasis and chemoresistance in gastric cancer. However, the mechanisms by which RhoGDI2 promotes tumor cell survival and metastasis remain unclear. In this study, we clearly demonstrate that RhoGDI2 upregulates VEGF-C expression and RhoGDI2 expression is positively correlated with VEGF-C expression in human gastric tumor tissues as well as parental gastric cancer cell lines. VEGF-C depletion suppressed RhoGDI2-induced gastric cancer metastasis and sensitized RhoGDI2-overexpressing cells to cisplatin-induced apoptosis in vitro and in vivo. Secreted VEGF-C enhanced gastric cancer cell invasion and conferred cisplatin resistance to RhoGDI2-overexpressing cells. We also show that RhoGDI2 positively regulates Rac1 activity in gastric cancer cells. Inhibition of Rac1 expression suppressed RhoGDI2-induced VEGF-C expression, and this inhibition was associated with decreased invasiveness and increased sensitivity to cisplatin in RhoGDI2-overexpressing cells. Our results indicate that RhoGDI2 might be a potential therapeutic target for simultaneously reducing metastasis risk and enhancing chemotherapy efficacy in gastric cancer.
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Anti-osteoclastogenic activity of matairesinol via suppression of p38/ERK-NFATc1 signaling axis.
BMC Complement Altern Med
PUBLISHED: 01-21-2014
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Matairesinol is a plant lignan present in a wide variety of foodstuffs such as seeds, vegetables and fruits. It has various biological functions including anti-angiogenic, anti-cancer and anti-fungal activities, but its anti-osteoporotic activity, if any, is unknown.
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Anti-osteoclastogenic activity of praeruptorin A via inhibition of p38/Akt-c-Fos-NFATc1 signaling and PLC?-independent Ca2+ oscillation.
PLoS ONE
PUBLISHED: 01-01-2014
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A decrease of bone mass is a major risk factor for fracture. Several natural products have traditionally been used as herbal medicines to prevent and/or treat bone disorders including osteoporosis. Praeruptorin A is isolated from the dry root extract of Peucedanum praeruptorum Dunn and has several biological activities, but its anti-osteoporotic activity has not been studied yet.
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The role of two different collagen membranes for dehiscence defect around implants in humans.
J Oral Implantol
PUBLISHED: 12-31-2013
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Abstract The aim of this study was to elucidate the role of two types of collagen membranes (cross-linked versus non cross-linked) used in conjunction with autogenous or allogenic bone followed by xenogrenic bone particles for dehiscence defect around implants in humans. Experimental groups were divided into two groups: Group CL (Cross-linked, Ossix-plus, n =24 implants, 16 patients) and Group NCL (Non cross-linked, Bio-gide, n =25 implants, 18 patients). At the time of implant insertion and uncover surgery, measurements of the dehiscence bony height, width and surface area was made. Before applying the membrane to defects, guided bone regeneration was performed. Because it is difficult to measure the degrees of exposure, early exposure cases were excluded from the result analysis. The mean percentage gain of the dehiscence defect and the mean marginal bone reduction value of follow-up radiograph respectively did not show statistically significant differences between two groups. Both membranes exhibited satisfactory results on dehiscence defects. As a result, our authors concluded that the success of guided bone regeneration was performed simultaneously for dehiscence defects around implant, was regardless whether collagen membranes were cross-linked or non cross-linked.
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14-3-3? attenuates RhoGDI2-induced cisplatin resistance through activation of Erk and p38 in gastric cancer cells.
Oncotarget
PUBLISHED: 11-05-2013
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Rho GDP dissociation inhibitor 2 (RhoGDI2) promotes tumor growth and malignant progression and enhances chemoresistance of gastric cancer. Recently, we noted an inverse correlation between RhoGDI2 and 14-3-3? expression, which suggests that 14-3-3? is a target of gastric cancer metastasis and the chemoresistance-promoting effect of RhoGDI2. Herein, we evaluated whether 14-3-3? is regulated by RhoGDI2 and is functionally important for the RhoGDI2-induced cisplatin resistance of gastric cancer cells. We used highly metastatic and cisplatin-resistant RhoGDI2-overexpressing SNU-484 cells and observed decreased 14-3-3? mRNA and protein expression. Depletion of 14-3-3? in SNU-484 control cells enhanced cisplatin resistance, whereas restoration of 14-3-3? in RhoGDI2-overexpressing SNU-484 cells impaired cisplatin resistance in vitro and in vivo. We also found that the phosphorylation levels of Erk and p38 kinases significantly decreased in RhoGDI2-overexpressing SNU-484 cells and recovered after 14-3-3? expression, and that decreased activities of these kinases were critical for RhoGDI2-induced cisplatin resistance. In conclusion, 14-3-3? is a RhoGDI2-regulated gene that appears to be important for suppressing the chemoresistance of gastric cancer cells.
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Effects of anodized titanium with Arg-Gly-Asp (RGD) peptide immobilized via chemical grafting or physical adsorption on bone cell adhesion and differentiation.
Int J Oral Maxillofac Implants
PUBLISHED: 07-23-2013
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This study examined the effects of the immobilization of Arg-Gly-Asp (RGD) peptide (CAAALLLKERGDSK) on anodized titanium (Ti) via chemical grafting or physical adsorption methods on cell adhesion and osteoblast differentiation.
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In vivo measurements of human gingival translucency parameters.
Int J Periodontics Restorative Dent
PUBLISHED: 07-04-2013
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The aim of this study was to evaluate the relationship between gingival translucency and peri-implant mucosa. A total of 22 peri-implant sites in 16 patients who required tooth replacement in the esthetic zone were included. Color measurements were obtained using a spectrophotometer and customized colored abutments. Mucosal thickness measurements were taken incrementally 0.5 mm from the facial gingival margin on sectioned casts. A statistically significant difference in gingival translucency was observed beginning at 1.5 mm. A negative correlation was observed between the thickness and translucency parameter (TP) (r = -0.64), with TP values decreasing as the gingival thickness increased. The gingival translucency was correlated with the thickness of the peri-implant mucosa and distance from the facial gingival margin.
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In vivo action of IL-27: reciprocal regulation of Th17 and Treg cells in collagen-induced arthritis.
Exp. Mol. Med.
PUBLISHED: 07-03-2013
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Interleukin (IL)-27 is a novel cytokine of the IL-6/IL-12 family that has been reported to be involved in the pathogenesis of autoimmune diseases and has a pivotal role as both a pro- and anti-inflammatory cytokine. We investigated the in vivo effects of IL-27 on arthritis severity in a murine collagen-induced arthritis (CIA) model and its mechanism of action regarding control of regulatory T (Tregs) and IL-17-producing T helper 17 (Th17) cells. IL-27-Fc-treated CIA mice showed a lower severity of arthritis. IL-17 expression in the spleens was significantly decreased in IL-27-Fc-treated CIA mice compared with that in the CIA model. The Th17 population was decreased in the spleens of IL-27-Fc-treated CIA mice, whereas the CD4(+)CD25(+)Foxp3(+) Treg population increased. In vitro studies revealed that IL-27 inhibited IL-17 production in murine CD4(+) T cells, and the effect was associated with retinoic acid-related orphan receptor ?T and signal transducer and activator of transcription 3 inhibition. In contrast, fluorescein isothiocyanate-labeled forkhead box P3 (Foxp3) and IL-10 were profoundly augmented by IL-27 treatment. Regarding the suppressive capacity of Treg cells, the proportions of CTLA-4(+) (cytotoxic T-lymphocyte antigen 4), PD-1(+) (programmed cell death protein 1) and GITR(+) (glucocorticoid-induced tumor necrosis factor receptor) Tregs increased in the spleens of IL-27-Fc-treated CIA mice. Furthermore, in vitro differentiated Treg cells with IL-27 exerted a more suppressive capacity on T-cell proliferation. We found that IL-27 acts as a reciprocal regulator of the Th17 and Treg populations in CD4(+) cells isolated from healthy human peripheral blood mononuclear cells (PBMCs), as well as from humans with rheumatoid arthritis (RA) PBMCs. Our study suggests that IL-27 has the potential to ameliorate overwhelming inflammation in patients with RA through a reciprocal regulation of Th17 and Treg cells.
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PF-3758309, p21-activated kinase 4 inhibitor, suppresses migration and invasion of A549 human lung cancer cells via regulation of CREB, NF-?B, and ?-catenin signalings.
Mol. Cell. Biochem.
PUBLISHED: 06-12-2013
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Migration and invasion comprise key steps in cancer metastasis. Through the migration and invasion into and out of lymphatic and/or blood vessels, cancer cells can be spread out into the tissues in remote site from the origin. Degradation of extracellular matrix (ECM) must be preceded prior to the metastasis of cancer cells. Matrix metalloproteinases (MMP) can degrade ECM, thus allow cells to migrate from the original site. Among MMPs, two gelatinase MMP-2 and MMP-9 play particularly important roles in ECM degradation. Here, we report that recently developed p21-activated kinase 4 inhibitor PF-3758309 shows anti-metastatic effect in A549 human lung cancer cell. PF-3758309 suppresses CREB, NF-?B, and ?-catenin pathways, which are well known to be closely related with cell migration. This leads to the downregulation of MMP-2/MMP-9 expressions and the inhibition of A549 lung cancer metastasis.
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Physical stability of arginine-glycine-aspartic acid peptide coated on anodized implants after installation.
J Adv Prosthodont
PUBLISHED: 04-25-2013
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The aim of this study was to evaluate the stability of arginine-glycine-aspartic acid (RGD) peptide coatings on implants by measuring the amount of peptide remaining after installation.
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Proteomic analysis of the biological response of MG63 osteoblast-like cells to titanium implants.
Odontology
PUBLISHED: 04-14-2013
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Understanding of the interaction between human MG63 osteoblast-like cells and surfaces is necessary in the field of tissue engineering and biomaterials. Various titanium surfaces are widely used as not only implant materials, but also as miniscrews in orthodontics. Our goal was to assess the proteomic response of MG63 osteoblast-like cells to different titanium surfaces. MG63 osteoblast-like cells were cultured on three different titanium surfaces: a smooth surface (S), a sandblasted with large grit and acid-etched surface (SLA), and a surface coated with a thin layer of hydroxyapatite (HA). Cells grown on the rougher surfaces (SLA and HA) exhibited downregulated cell proliferation and morphological changes. In the proteomic analysis, cells grown on the SLA surface showed upregulated expression of protocadherin-?3 precursor, kinase insert domain receptor, fibroblast growth factor receptor-3, and insulin-like growth factor I, while the expression levels of cell adhesion kinase, collagen ?-1(I) chain precursor, collagen type XI ?2, and cadherin-11 were upregulated in cells grown on the HA surface. These proteins are known to be involved in osteoblast adhesion, growth, and differentiation. Thus, the surface properties of dental materials can influence the expression of proteins involved in osseointegration-related processes. Proteomic analysis may reveal changes in novel proteins that explain why osseointegration varies depending on surface properties.
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CK2 inhibitor CX4945 induces sequential inactivation of proteins in the signaling pathways related with cell migration and suppresses metastasis of A549 human lung cancer cells.
Bioorg. Med. Chem. Lett.
PUBLISHED: 03-30-2013
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Casein kinase 2 (CK2) is known to be involved in various cellular processes such as cell cycle, apoptosis and proliferation. It has been reported that the inhibition of CK2 induced by recently developed small molecule CX4945 shows anti-cancer effects including anti-proliferation and anti-angiogenesis in several different cancers including prostate cancer. Here we report that migration and invasion of A549 human lung cancer cells are suppressed by the inhibition of CK2 induced by CX4945. We found that CX4945 sequentially attenuates the proteins in PI3K/Akt and MAPK pathways, two signaling pathways related with cell migration. This sequential control of signal pathways inhibits the expression of membrane type 1-matrix metalloproteinase and this leads to the selective attenuation of one of the gelatinases, MMP-2, which can degrade components of extracellular matrix, and metastasis of A549 human lung cancer cell.
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Discovery of non-LBD inhibitor for androgen receptor by structure-guide design.
Bioorg. Med. Chem. Lett.
PUBLISHED: 03-06-2013
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In this study, we synthesized the BF-3 binding small molecules, a series of pyridazinone-based compounds, as a novel class of non-LBP antiandrogens for treating prostate cancer by inhibiting androgen receptor. The new class compound was discovered to inhibitor the viability of AR-dependent human prostate LNCap cells and AR activity combining with the computational method. It showed a good physicochemical and PK property.
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Midazolam induces cellular apoptosis in human cancer cells and inhibits tumor growth in xenograft mice.
Mol. Cells
PUBLISHED: 02-11-2013
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Midazolam is a widely used anesthetic of the benzodiazepine class that has shown cytotoxicity and apoptosisinducing activity in neuronal cells and lymphocytes. This study aims to evaluate the effect of midazolam on growth of K562 human leukemia cells and HT29 colon cancer cells. The in vivo effect of midazolam was investigated in BALB/c-nu mice bearing K562 and HT29 cells human tumor xenografts. The results show that midazolam decreased the viability of K562 and HT29 cells by inducing apoptosis and S phase cell-cycle arrest in a concentration-dependent manner. Midazolam activated caspase-9, capspase-3 and PARP indicating induction of the mitochondrial intrinsic pathway of apoptosis. Midazolam lowered mitochondrial membrane potential and increased apoptotic DNA fragmentation. Midazolam showed reactive oxygen species (ROS) scavenging activity through inhibition of NADPH oxidase 2 (Nox2) enzyme activity in K562 cells. Midazolam caused inhibition of pERK1/2 signaling which led to inhibition of the anti-apoptotic proteins Bcl-XL and XIAP and phosphorylation activation of the pro-apoptotic protein Bid. Midazolam inhibited growth of HT29 tumors in xenograft mice. Collectively our results demonstrate that midazolam caused growth inhibition of cancer cells via activation of the mitochondrial intrinsic pathway of apoptosis and inhibited HT29 tumor growth in xenograft mice. The mechanism underlying these effects of midazolam might be suppression of ROS production leading to modulation of apoptosis and growth regulatory proteins. These findings present possible clinical implications of midazolam as an anesthetic to relieve pain during in vivo anticancer drug delivery and to enhance anticancer efficacy through its ROS-scavenging and pro-apoptotic properties.
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IL-17-mediated Bcl-2 expression regulates survival of fibroblast-like synoviocytes in rheumatoid arthritis through STAT3 activation.
Arthritis Res. Ther.
PUBLISHED: 01-29-2013
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INTRODUCTION: Fibroblast-like synoviocytes (FLSs) are a major cell population of the pannus that invades adjacent cartilage and bone in rheumatoid arthritis (RA). The study was undertaken to determine the effect of interleukin-17 (IL-17) on the survival and/or proliferation of FLSs from RA patients and to investigate whether signal tranducer and activator of transcription 3 (STAT3) is implicated in this process. METHODS: Bcl-2 and Bax expression in FLSs was determined using the real-time PCR and western blot analysis. The expression of Bcl-2 and phosphoSTAT3 in synovial tissues was investigated by confocal microscope. Apoptosis of FLSs was detected by Annexin V/propidium iodide staining and/or phase contrast microscopy. The proliferation of FLSs was determined by CCK-8 ELISA assay. RESULTS: The pro-apoptotic Bax is decreased and anti-apoptotic Bcl-2 is increased in FLSs from RA patients compared with those from patients with osteoarthritis (OA). IL-17 upregulated the expression of Bcl-2 in FLSs from RA patients, but not in FLSs from OA patients. STAT3 was found to mediate IL-17-induced Bcl-2 upregulation in FLSs from RA patients. Additionally, IL-17 promoted the survival and proliferation of FLSs from RA patients. Most importantly, treatment with STAT3 inhibitor reversed the protective effect of IL-17 on FLSs apoptosis induced by sodium nitroprusside (SNP). CONCLUSIONS: Our data demonstrate that STAT3 is critical in IL-17-induced survival of FLS from RA patients. Therefore, therapeutic strategies that target the IL-17/STAT3 pathway might be strong candidates for RA treatment modalities.
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Fracture load of monolithic CAD/CAM lithium disilicate ceramic crowns and veneered zirconia crowns as a posterior implant restoration.
Implant Dent
PUBLISHED: 01-09-2013
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To compare the fracture load and failure mode of the monolithic lithium disilicate crown (e.max group) and 2 types of veneered zirconia crowns, hand layer (ZV group) and heat pressed (ZP group), as a posterior implant-supported restoration.
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p53 controls autoimmune arthritis via STAT-mediated regulation of the Th17 cell/Treg cell balance in mice.
Arthritis Rheum.
PUBLISHED: 01-03-2013
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To investigate the connection between p53 and interleukin-17-producing Th17 cell/Treg cell balance in rheumatoid arthritis (RA).
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PLC? is required for RhoGDI2-mediated cisplatin resistance in gastric cancer.
Biochem. Biophys. Res. Commun.
PUBLISHED: 09-22-2011
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Rho GDP dissociation inhibitor 2 (RhoGDI2) is a regulator of the Rho family GTPases. Recent work from our laboratory suggests that RhoGDI2 expression potentially enhances resistance to cisplatin as well as promotes tumor growth and malignant progression in gastric cancer. In this study, we demonstrate that phospholipase C-gamma (PLC?) is required for RhoGDI2-mediated cisplatin resistance and cancer cell invasion in gastric cancer. The levels of phosphorylated PLC? are markedly enhanced in RhoGDI2-overexpressing SNU-484 cells and, by contrast, repressed in RhoGDI2-depleted MKN-28 cells. Depletion of PLC? expression or inhibition of its activity not only significantly increases cisplatin-induced apoptosis but also suppresses the invasive ability of RhoGDI2-overexpressing SNU-484 cells. Taken together, our results suggest that PLC? plays a key role in RhoGDI2-mediated cisplatin resistance and cell invasion in gastric cancer cells.
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Isolated double-chambered right ventricle in a young adult.
Korean Circ J
PUBLISHED: 05-31-2011
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Double-chambered right ventricle (DCRV) is a rare congenital heart disorder in which the right ventricle is divided by an anomalous muscle bundle into a high pressure inlet portion and a low pressure outlet portion. We report a case of isolated DCRV without symptoms in adulthood, diagnosed through echocardiography, cardiac catheterization and cardiac magnetic resonance imaging.
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Regulation of the female rat estrous cycle by a neural cell-specific epidermal growth factor-like repeat domain containing protein, NELL2.
Mol. Cells
PUBLISHED: 04-25-2011
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NELL2, a protein containing epidermal growth factor-like repeat domains, is predominantly expressed in the nervous system. In the mammalian brain, NELL2 expression is mostly neuronal. Previously we found that NELL2 is involved in the onset of female puberty by regulating the release of gonadotropin-releasing hormone (GnRH), and in normal male sexual behavior by controlling the development of the sexually dimorphic nucleus of the preoptic area (POA). In this study we investigated the effect of NELL2 on the female rat estrous cycle. NELL2 expression in the POA was highest during the proestrous phase. NELL2 mRNA levels in the POA were increased by estrogen treatment in ovariectomized female rats. Blocking NELL2 synthesis in the female rat hypothalamus decreased the expression of kisspeptin 1, an important regulator of the GnRH neuronal apparatus, and resulted in disruption of the estrous cycle at the diestrous phase. These results indicate that NELL2 is involved in the maintenance of the normal female reproductive cycle in mammals.
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Clinical implications of mandible and neck measurements in non-obese asian snorers: ansan city general population-based study.
Clin Exp Otorhinolaryngol
PUBLISHED: 03-17-2011
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Anthropometric abnormalities of the mandible and neck may contribute to snoring in non-obese Asians. The study evaluated the clinical implications of mandible and neck measurements in non-obese Asian snorers.
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A Survey on Ubiquitous Healthcare Service Demand among Diabetic Patients.
Diabetes Metab J
PUBLISHED: 02-28-2011
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Advanced information technology can be used when developing diagnostic and treatment strategies to provide better care for diabetic patients. However, the levels of need and demand for the use of technological advances have not been investigated in diabetic patients. We proposed and developed an individualized, ubiquitous (U)-healthcare service using advanced information technology for more effective glucose control. Prior to our service initiation, we surveyed patient needs and other pertinent information.
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Risk assessment for clinical attachment loss of periodontal tissue in Korean adults.
J Adv Prosthodont
PUBLISHED: 02-08-2011
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The purpose of this study was to assess the prevalence and extent of clinical attachment loss of periodontal tissue and to find out variables related to clinical attachment loss (CAL) in Korean adults older than 40 years of age.
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Improvement in left ventricular systolic dyssynchrony in hypertensive patients after treatment of hypertension.
Korean Circ J
PUBLISHED: 01-31-2011
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Left ventricular (LV) dyssynchrony has been commonly detected among hypertensive patients with normal LV systolic function and no evidence of congestive heart failure. The purpose of our study was to assess the changes in LV systolic dyssynchrony (SDS(LV)) among hypertensive patients after antihypertensive treatment, and to determine the relationship between SDS(LV) and other conventional echocardiographic parameters.
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Improved glycemic control without hypoglycemia in elderly diabetic patients using the ubiquitous healthcare service, a new medical information system.
Diabetes Care
PUBLISHED: 01-29-2011
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To improve quality and efficiency of care for elderly patients with type 2 diabetes, we introduced elderly-friendly strategies to the clinical decision support system (CDSS)-based ubiquitous healthcare (u-healthcare) service, which is an individualized health management system using advanced medical information technology.
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Relationship between tooth loss and carotid intima-media thickness in Korean adults.
J Adv Prosthodont
PUBLISHED: 09-08-2010
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The aim of this study was to examine the relationship between tooth loss and sub-clinical atherosclerosis in Korean adults.
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Effect of two-phase fabrication method for the optimum fit of light-polymerized record bases.
J Adv Prosthodont
PUBLISHED: 08-06-2010
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The aims of this study were to suggest a method of fabrication of the record base using a light-polymerized resin by applying the two-phase fabrication method for the improvement of the fit of the record base and to compare the degree of fit according to the separation site.
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The effect of external beam radiotherapy volume on locoregional control in patients with locoregionally advanced or recurrent nonanaplastic thyroid cancer.
Radiat Oncol
PUBLISHED: 05-25-2010
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We evaluated outcomes of patients treated with external beam radiotherapy (EBRT) for locoregionally advanced or recurrent nonanaplastic thyroid cancer and analyzed the effect of EBRT volume on locoregional control.
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Outcomes of postoperative simultaneous modulated accelerated radiotherapy for head-and-neck squamous cell carcinoma.
Int. J. Radiat. Oncol. Biol. Phys.
PUBLISHED: 01-29-2010
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To evaluate the treatment efficacy and toxicity of postoperative simultaneous modulated accelerated radiotherapy (SMART) for patients with head-and-neck squamous cell carcinoma (HNSCC).
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A comparison of the implant stability among various implant systems: clinical study.
J Adv Prosthodont
PUBLISHED: 01-19-2009
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To determine the change in stability of single-stage, three different design of implant systems in humans utilizing resonance frequency analysis for early healing period (24 weeks), without loading.
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Interleukin-2/anti-interleukin-2 monoclonal antibody immune complex suppresses collagen-induced arthritis in mice by fortifying interleukin-2/STAT5 signalling pathways.
Immunology
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In this study, we investigated the effects of administration of interleukin-2 (IL-2)/JES6-1 (anti-IL-2 monoclonal antibody) immune complexes on the expansion and activation of regulatory T (Treg) cells, the down-regulation of T helper type 17 (Th17) cells, and the control of the severity of collagen-induced arthritis (CIA). Wild-type and CIA-induced wild-type mice were injected intraperitoneally (i.p.) with IL-2 or IL-2/JES6-1 complex three times at 2-day intervals. Treg cell surface markers were analysed by flow cytometry. After injecting IL-2 or IL-2/JES6-1, the time kinetics of IL-2 signalling molecules was examined by FACS and Western blotting. Concentrations of IL-17 and IL-10 were measured by ELISA. Injection of IL-2/JES6-1 increased the proportion of Foxp3+ Treg cells among splenic CD4+ T cells, which reached the highest level on day 4 after injection. Up-regulation of CTLA4, GITR and glycoprotein-A repetitions predominant (GARP) was observed. Activation of p-signal transducer and activator of transcription 5 (STAT5) was apparent within 3 hr after injection of IL-2/JES6-1 complexes. Expression of IL-2 signalling molecules, including p-AKT and p-p38/mitogen-activated protein kinase, was also higher in splenocytes treated with IL-2/JES6-1 complexes. Injection of IL-2/JES6-1 complexes suppressed the induction of CIA and the production of IL-17 and inflammatory responses while increasing the level of IL-10 in the spleen. The expansion of Treg cells (via STAT5) and the concomitant increase in IL-2 signalling pathways by IL-2/JES6-1 complexes suggests their potential use as a novel therapeutic agent for the treatment of autoimmune arthritis.
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Preoperative serum thyroglobulin as a useful predictive marker to differentiate follicular thyroid cancer from benign nodules in indeterminate nodules.
J. Korean Med. Sci.
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Indeterminate cytology results increase the number of repetitive procedure and unnecessary surgery. This study was designed to find useful and simple predictive tools to differentiate malignant thyroid nodules from indeterminate nodules. We retrospectively enrolled 164 patients who had undergone thyroid surgery as a result of indeterminate cytology in the National Cancer Center. We reviewed patients age at diagnosis, sex, preoperative biochemical markers such as thyroglobulin (Tg), anti-Tg antibody, free T4 and TSH level, and sonographical and pathological findings, which were subjected to statistical analysis. We found several clinical and sonographical predictive factors that showed significant differences. Young age, male, preoperative high Tg level, and hypoechoic nodule on sonography all increased cancer probability significantly in multivariate analysis. With a cut-off value of 187.5 ng/mL Tg, sensitivity and specificity were 54.8% and 90.1%, respectively (AUC 0.748, P < 0.001). In the case of nodule size > 1.7 cm, elevated serum Tg predicts the risk of malignancy; especially Tg > 70 ng/mL (odds ratio 3.245, 95% confidence interval 1.115-9.450, P = 0.038). Preoperative Tg levels had very high specificity in predicting thyroid cancer in case of suspicious follicular neoplasm. Therefore, Tg levels may be a useful marker for differentiating thyroid cancer from benign thyroid nodules in the cytological diagnosis of indeterminate nodules.
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Wear evaluation of the human enamel opposing different Y-TZP dental ceramics and other porcelains.
J Dent
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This study examined the wear resistance of human enamel and feldspathic porcelain after simulated mastication against 3 zirconia ceramics, heat-pressed ceramic and conventional feldspathic porcelain.
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Palatal bone thickness compared with cone-beam computed tomography in adolescents and adults for mini-implant placement.
Am J Orthod Dentofacial Orthop
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The purpose of this study was to compare the bone thickness of the palatal areas in early and late mixed and early permanent dentitions according to dental age.
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Anti-androgen receptor activity of apoptotic CK2 inhibitor CX4945 in human prostate cancer LNCap cells.
Bioorg. Med. Chem. Lett.
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Androgen receptor (AR) is crucial for transcriptional signaling in prostate cancers. The anti-cancer activity of protein kinase CK2 (formerly called casein kinase 2)-specific small molecule inhibitors have been reported in several cancers including prostate cancers. The orally available CX4945, a potent and selective small molecule inhibitor of CK2, has advanced into human clinical trials and has exhibited strong anti-tumor activity. The inhibition of CK2 leads to a down-regulation of the AR-dependent transcription, but the functional relevance of CX4945 to AR-dependent transcription in AR-positive LNCap cells has not been studied yet. Our observation of inhibitory effects of CX4945 on the expression or phosphorylation levels of CK2?, Akt and anti-apoptotic molecules including IAP family members agreed with a previous study showing the effect of CK2 inhibition in cancer cells. This study also provides novel information on the impact of CX4945 in the inhibition of AR-dependent transcriptional activation in LNCap cells via its down-regulation. Pharmacologic inhibition experiment revealed that CX4945 could exhibit its anti-cancer activity in LNCap cells via the independent inhibitions of AR and Akt-survivin signalings.
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Thiourea compound AW00178 sensitizes human H1299 lung carcinoma cells to TRAIL-mediated apoptosis.
Bioorg. Med. Chem. Lett.
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The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) triggers apoptosis in a wide variety of cancer cells. Recently, cancer cell resistance to TRAIL-mediated apoptosis has become a challenging issue in the development of TRAIL-based anti-cancer therapies. In this study, we found that 1-(5-chloro-2-methyl-phenyl)-3-[4-(5-trifluoromethyl-pyrazol-1-yl)-phenyl]-thiourea (AW00178) was able to sensitize TRAIL-resistant human lung cancer H1299 cells to TRAIL-mediated apoptosis. Treatment with AW00178, either alone or in combination with TRAIL, induced the expression of CHOP, a protein related to TRAIL sensitivity, and reduced the expression of survivin, an anti-apoptotic protein involved in TRAIL resistance. Additionally, AW00178, alone or in combination with TRAIL, induced the activation of c-Jun and inactivation of Akt. A pharmacologic inhibition study revealed that c-Jun activation and Akt inactivation were strongly related to CHOP induction and survivin down-regulation, respectively. In summary, these results suggested that AW00178 mediated sensitization to TRAIL-mediated apoptosis in H1299 cells by increasing sensitivity and decreasing resistance to TRAIL via the induction of c-Jun-dependent CHOP expression and the reduction of Akt-dependent survivin expression, respectively.
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Proteomics-based strategy to delineate the molecular mechanisms of RhoGDI2-induced metastasis and drug resistance in gastric cancer.
J. Proteome Res.
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Rho GDP dissociation inhibitor 2 (RhoGDI2) was initially identified as a regulator of the Rho family of GTPases. Our recent works suggest that RhoGDI2 promotes tumor growth and malignant progression, as well as enhances chemoresistance in gastric cancer. Here, we delineate the mechanism by which RhoGDI2 promotes gastric cancer cell invasion and chemoresistance using two-dimensional gel electrophoresis (2-DE) on proteins derived from a RhoGDI2-overexpressing SNU-484 human gastric cancer cell line and control cells. Differentially expressed proteins were identified using matrix-assisted laser desorption ionization-time-of-flight mass spectrometry (MALDI-TOF-MS). In total, 47 differential protein spots were identified; 33 were upregulated, and 14 were downregulated by RhoGDI2 overexpression. Upregulation of SAE1, Cathepsin D, Cofilin1, CIAPIN1, and PAK2 proteins was validated by Western blot analysis. Loss-of-function analysis using small interference RNA (siRNA) directed against candidate genes reveals the need for CIAPIN1 and PAK2 in RhoGDI2-induced cancer cell invasion and Cathepsin D and PAK2 in RhoGDI2-mediated chemoresistance in gastric cancer cells. These data extend our understanding of the genes that act downstream of RhoGDI2 during the progression of gastric cancer and the acquisition of chemoresistance.
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AW00179 potentiates TRAIL-mediated death of human lung cancer H1299 cells through ROS-JNK-c-Jun-mediated up-regulation of DR5 and down-regulation of anti-apoptotic molecules.
Amino Acids
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Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) triggers apoptosis in tumor cells, but when used alone, it is not effective at treating TRAIL-resistant tumors. This resistance is challenging for TRAIL-based anti-cancer therapies. In this study, we found that 1-(4-trifluoromethoxy-phenyl)-3-[4-(5-trifluoromethyl-2,5-dihydro-pyrazol-1-yl)-phenyl]-urea (AW00179) sensitized human lung cancer H1299 cells to TRAIL-mediated apoptosis. Even in the absence of TRAIL, AW00179 strongly induced DR5 expression and decreased the expression of anti-apoptotic proteins, suggesting that the sensitizing effect of AW00179 on TRAIL-mediated apoptosis is due to increased levels of DR5 protein and decreased anti-apoptotic molecules. AW00179 also induced the activation of c-Jun and ERK; however, a pharmacologic inhibition study revealed that JNK-c-Jun signaling is involved in the induction of DR5 expression. In addition, reactive oxygen species (ROS) appear to be involved in AW00179 activity. In conclusion, AW00179 has the potential to sensitize H1299 cells to TRAIL-mediated apoptosis through two distinct mechanisms: ROS-JNK-c-Jun-mediated up-regulation of DR5, and down-regulation of anti-apoptotic molecules.
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