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Find video protocols related to scientific articles indexed in Pubmed.
High C4 gene copy numbers protects against Vogt-Koyanagi-Harada syndrome in Chinese Han.
Br J Ophthalmol
PUBLISHED: 09-02-2014
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Considering the phenotypical consequences and association of C4 copy number variation (CNV) with various autoimmune diseases, we aimed to examine C4 CNVs for 1027 patients with Vogt-Koyanagi-Harada (VKH) syndrome and 2083 controls.
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Genome-wide association analysis of Vogt-Koyanagi-Harada syndrome identifies two new susceptibility loci at 1p31.2 and 10q21.3.
Nat. Genet.
PUBLISHED: 08-10-2014
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To identify new genetic risk factors for Vogt-Koyanagi-Harada (VKH) syndrome, we conducted a genome-wide association study of 2,208,258 SNPs in 774 cases and 2,009 controls with follow-up in a collection of 415 cases and 2,006 controls and a further collection of 349 cases and 1,588 controls from a Han Chinese population. We identified three loci associated with VKH syndrome susceptibility (IL23R-C1orf141, rs117633859, P(combined) = 3.42 × 10(-21), odds ratio (OR) = 1.82; ADO-ZNF365-EGR2, rs442309, P(combined) = 2.97 × 10(-11), OR = 1.37; and HLA-DRB1/DQA1, rs3021304, P(combined) = 1.26 × 10(-118), OR = 2.97). The five non-HLA genes were all expressed in human iris tissue. IL23R was also expressed in the ciliary body, and EGR2 was expressed in the ciliary body and choroid. The risk G allele of rs117633859 in the promoter region of IL23R exhibited low transcriptional activation in a cell-based reporter assay and was associated with diminished IL23R mRNA expression in human peripheral blood mononuclear cells.
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Paradoxical role of CBX8 in proliferation and metastasis of colorectal cancer.
Oncotarget
PUBLISHED: 07-23-2014
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The effect of polycomb chromobox (Cbx) proteins in cancer is context-dependent. The Chromobox homolog 8 (CBX8) was originally characterized as a transcriptional repressor, which inhibits cell proliferation in Ink4a-Arf-dependent and -independent manner. However, the role of CBX8 in colorectal cancer remains unknown. Here, we found that high CBX8 expression was associated with a low rate of distant metastasis and good prognosis in CRC patients, even though CBX8 was up-regulated in CRC cell lines and clinical samples. Knockdown of CBX8 inhibited CRC proliferation in vitro and in vivo, mostly by increasing p53 and its downstream effectors. However, knockdown of CBX8 enhanced CRC migration, invasion and metastasis in vitro and in vivo, in part through direct up-regulation of integrin ?4 (ITGB4) that in turn decreased RhoA activity. Collectively, the knockdown of CBX8 inhibited CRC proliferation, while promoting its metastasis, thus exerting paradoxical effects in CRC progression.
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A Meta-Analysis on the Relations between EGFR R521K Polymorphism and Risk of Cancer.
Int J Genomics
PUBLISHED: 06-07-2014
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The EGFR R521K polymorphism has been shown to reduce the activity of EGFR; however, the association between EGFR R521K polymorphism and the risk of cancer remains inconclusive; therefore we performed a meta-analysis to evaluate the relationship between EGFR R521K polymorphism and susceptibility to cancer. Our results suggest that the EGFR R521K polymorphism is not associated with risk of cancer, but the different chemosensitivity to anticancer drugs may need further investigation.
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Targeting the anaphase-promoting complex/cyclosome (APC/C)- bromodomain containing 7 (BRD7) pathway for human osteosarcoma.
Oncotarget
PUBLISHED: 05-21-2014
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Osteosarcoma is the most common primary malignant bone tumor in childhood and adolescence and has a propensity for local invasion and early lung metastasis. However, the current therapies often result in chemoresistance, and a therapeutic target is not available in the clinic for osteosarcoma. Here, we report that BRD7 forms a complex with the anaphase-promoting complex/cyclosome (APC/C) and is degraded by APC/C(cdh1) and APC/C(cdc20) during the cell cycle. Moreover, BRD7 is a tumor suppressor in osteosarcoma, and the BRD7 mutant resistant to degradation by APC/C is more efficient than the wild-type protein at suppressing proliferation, colony formation, and tumor growth of osteosarcoma in vitro and in vivo. The combination of proTAME, an inhibitor of APC/C, with chemotherapeutic drugs efficiently targets osteosarcoma in vitro. Furthermore, there is a strong inverse correlation of protein levels between BRD7 and Cdh1 or Cdc20, and lower BRD7 expression is an indicator for poor prognosis in patients with osteosarcoma. Collectively, our results indicate that targeting the APC/C-BRD7 pathway may be a novel strategy for treating osteosarcoma.
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Chemerin C9 peptide induces receptor internalization through a clathrin-independent pathway.
Acta Pharmacol. Sin.
PUBLISHED: 03-24-2014
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The chemerin receptor CMKLR1 is one type of G protein-coupled receptors abundant in monocyte-derived dendritic cells and macrophages, which plays a key role in the entry of a subset of immunodeficiency viruses including HIV/SIV into lymphocytes and macrophages. The aim of this work was to investigate how CMKLR1 was internalized and whether its internalization affected cell signaling in vitro.
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Individual patterns of alcohol use.
Addict Behav
PUBLISHED: 02-27-2014
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We present methodology to identify statistically distinct patterns of daily alcohol use and classify them into categories that could be further used in monitoring of transitions between patterns such as transitions from regular to problem use.
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Cyclin D1 G870A Polymorphism and Risk of Nasopharyngeal Carcinoma: A Case-Control Study and Meta-Analysis.
PLoS ONE
PUBLISHED: 01-01-2014
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Cyclin D1 (CCND1) plays a key role in cell cycle regulation. It is a well-established human oncogene which is frequently amplified or overexpressed in cancers. The association between CCND1 G870A polymorphism and cancer risk has been widely assessed. However, a definitive conclusion between CCND1 G870A polymorphism and risk of nasopharyngeal carcinoma (NPC) remains elusive.
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A functional variant of PTPN22 confers risk for Vogt-Koyanagi-Harada syndrome but not for ankylosing spondylitis.
PLoS ONE
PUBLISHED: 01-01-2014
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Protein tyrosine phosphatase non-receptor 22 (PTPN22) is a key negative regulator of T lymphocytes and has emerged as an important candidate susceptibility factor for a number of immune-related diseases. This study aimed to examine the predisposition of PTPN22 SNPs to Vogt-Koyanagi-Harada (VKH) syndrome and acute anterior uveitis (AAU) associated with ankylosing spondylitis (AS).
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The Role of Superoxide Dismutase in the Survival of Mycobacterium tuberculosis in Macrophages.
Jpn. J. Infect. Dis.
PUBLISHED: 11-26-2013
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There is a large amount of information available regarding the chemical structure and biological activity of superoxide dismutase (SOD), which is abundantly generated by Mycobacterium tuberculosis in the early stages of growth. SOD is a strong superoxide radical scavenger, which plays a significant role in resisting oxidative stress. On the other hand, SOD mutant strains have been constructed to define the role of this molecule in the immune response to M. tuberculosis infection. These studies have suggested that the absence or attenuation of SOD can motivate innate immunity and SOD avoid destruction or growth inhibition of M. tuberculosis. For detailed investigation of how SOD proteins aid M. tuberculosis survival within macrophages, we cloned 2 SOD genes (SODA and SODC) from the M. tuberculosis H37Rv genome, overexpressed, identified, and purified the proteins, and then exposed macrophages to the proteins. Following this, we assessed NO production, the secretion of cytokine interferon-? (IFN-?) and intercellular adhesion molecule-1, the expression of IFN-? receptor and Toll-like receptor 2 on the surface of macrophages, and caspase-3 enzyme activity as well as macrophage apoptosis. Our results showed that both SODA and SODC proteins considerably reduced the production of NO and oxygen radicals and impaired cell immunologic function in early infection.
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Anti-human protein S antibody induces tissue factor expression through a direct interaction with platelet phosphofructokinase.
Thromb. Res.
PUBLISHED: 08-28-2013
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Autoantibodies including anti-human protein S antibody (anti-hPS Ab) and anti-human protein C antibody (anti-hPC Ab) can be detected in patients with autoimmune diseases with hypercoagulability. The objective of the present study was to determine the effects and molecular pathways of these autoantibodies on tissue factor (TF) expression in human coronary artery endothelial cells (HCAECs).
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Copy number variations of complement component C4 are associated with Behçets disease but not with ankylosing spondylitis associated with acute anterior uveitis.
Arthritis Rheum.
PUBLISHED: 05-30-2013
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Complement component C4 copy number variations are associated with various inflammatory diseases. This study was undertaken to investigate whether copy number variations of C4 are also involved in the pathogenesis of Behçets disease (BD).
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Chromobox homolog 4 is correlated with prognosis and tumor cell growth in hepatocellular carcinoma.
Ann. Surg. Oncol.
PUBLISHED: 04-17-2013
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Chromobox homolog 4 (CBX4) is a member of the chromobox family of Polycomb group proteins involved in the chromatin remodeling and transcriptional regulation. However, its clinical relevance in hepatocellular carcinoma (HCC) has not yet been explored.
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A functional variant of pre-miRNA-196a2 confers risk for Behcets disease but not for Vogt-Koyanagi-Harada syndrome or AAU in ankylosing spondylitis.
Hum. Genet.
PUBLISHED: 04-05-2013
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This study aimed to investigate the predisposition of common pre-miRNA SNPs with Behcets disease (BD), Vogt-Koyanagi-Harada (VKH) syndrome and acute anterior uveitis (AAU) associated with ankylosing spondylitis (AS). A two-stage association study was carried out in 859 BD, 400 VKH syndrome, 209 AAU(+)AS(+) patients and 1,685 controls all belonging to a Chinese Han population. Genotyping, the expression of miR-196a and Bach1 (the target gene of miR-196a), cell proliferation, cytokine production were examined by PCR-RFLP, real-time PCR, CCK8 and ELISA. In the first stage study, the results showed significantly increased frequencies of the miR-196a2/rs11614913 TT genotype and T allele in BD patients (adjusted P(c) = 0.024, OR = 1.63; adjusted P(c) = 5.4 × 10(-3), OR = 1.45, respectively). However, no significant association of the tested SNPs with VKH and AAU(+)AS(+) patients was observed. The second stage and combined studies confirmed the association of rs11614913 with BD (TT genotype: adjusted P(c) = 6×10(-5), OR = 1.53; T allele: adjusted P(c) = 8×10(-6), OR = 1.35; CC genotype: adjusted P(c) = 0.024, OR = 0.68). A stratified analysis showed an association of the rs11614913 TT genotype and T allele with the arthritis subgroup of BD (P(c) = 5.3 × 10(-3), OR = 1.89; P(c) = 0.015, OR = 1.56, respectively). Functional experiments showed a decreased miR-196a expression, an increased Bach1 expression and an increased production of IL-1? and MCP-1 in TT cases compared to CC cases (P = 0.023, P = 0.0073, P = 0.012, P = 0.002, respectively). This study shows that a functional variant of miR-196a2 confers risk for BD but not for VKH syndrome or AAU(+)AS(+) by modulating the miR-196a gene expression and by regulating pro-inflammatory IL-1? and MCP-1 production.
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Genetic variants in the JAK1 gene confer higher risk of Behcets disease with ocular involvement in Han Chinese.
Hum. Genet.
PUBLISHED: 02-14-2013
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Recent surveys have identified SLC22A4, SLC22A5, RUNX1, JAK1 as susceptibility genes for various immune-related diseases. An association study was performed in 738 Behcets patients with ocular involvement and 1,873 controls using the iPLEX system method. The first-stage study for 30 SNPs showed that SNPs rs2780815, rs310241, rs3790532 in JAK1 were associated with Behcets disease in Han Chinese (Pc(Bonferroni correction) = 0.022-7.7 × 10(-3)). The G allele and AA genotype of SNP rs2834643 in RUNX1 (Pc = 0.041-1.75 × 10(-3)), but none of the other SNPs, were associated with Behcets disease. Haplotype analysis for the SLC22A4, SLC22A5 genes showed an increased tendency for AGTCTGCCGC frequency in patients compared with controls; however, the significance was lost after Bonferroni correction (P = 0.004, Pc > 0.05). Subsequently, we further replicated the significantly associated SNPs using another independent cohort. Replication and combining studies showed that three SNPs rs2780815, rs310241, rs3790532 in JAK1, but not SNP rs2834643 in RUNX1, were consistently associated with Behcets disease (replication: Pc = 0.012-9.60 × 10(-4); combining: Pc = 0.030-1.90 × 10(-4)). SNPs rs2780815, rs310241, rs3790532 were estimated to confer a population attributable risk of 35.0, 28.0, 27.0 %, respectively. We found a strong association between HLA-B51 with Behcets disease in Chinese Han population (P = 1.35 × 10(-73); OR = 5.15; 95 % CI 4.28-6.19). GMDR analysis showed that no gene-gene interaction was detectable between JAK1 and HLA-B51. Logistic analysis indicated that the JAK1 gene was an independent risk factor for Behcets disease (P > 0.05). Real-time PCR analysis showed that no difference on the expression of JAK1 in PBMCs or LPS-stimulated PBMCs between individuals with the different rs1762780815 genotypes studied (P > 0.05). In conclusion, this study suggests that JAK1, but not SLC22A4, SLC22A5 and RUNX1, contributes to the genetic susceptibility to Behcets disease with ocular involvement.
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Green tea polyphenols reduced fat deposits in high fat-fed rats via erk1/2-PPAR?-adiponectin pathway.
PLoS ONE
PUBLISHED: 01-15-2013
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Hypoadiponectinemia contributes to the development of obesity and related disorders such as diabetes, hyperlipidemia, and cardiovascular diseases. In this study we investigated the effects of green tea polyphenols (GTPs) on adiponectin levels and fat deposits in high fat (HF) fed rats, the mechanism of signaling pathway was explored as well.
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The use of covariates to identify records with implausible gestational ages using the birthweight distribution.
Paediatr Perinat Epidemiol
PUBLISHED: 07-31-2010
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The objective of this study was to evaluate the usefulness of covariates in identifying birth records with implausible values of gestational age. Birthweight distributions for births with early reported gestational ages are markedly bimodal, suggesting a mixture of two distributions. Most births form a normal-shaped left-hand (primary) distribution and a smaller number form the right-hand (secondary) distribution. The births in the secondary distribution are thought to have gestational age mistakenly reported. Prior work has found that births in the secondary distribution are at higher risk of poor outcomes than those in the primary distribution. Using 2002 US Natality data for gestational ages 26-35 weeks, we fit normal mixture models to birthweight with and without covariates (maternal race, education, parity, age, region of the country, prenatal care initiation) by reported gestational age. Additional models were stratified by infant sex. This approach allowed for the relationship between the covariates and birthweight to differ between the components. Mixture models fit reasonably well for reported gestational ages <33 weeks, but not for later weeks. Counter to the hypothesis, results were similar for models with and without covariates or stratification or both, although stratified models without covariates predicted slightly more girls and slightly fewer boys in the secondary distribution than did the corresponding unstratified models. For reported gestational ages <33 weeks, predictions from the four sets of models were highly correlated and predictions were similar for subgroups defined by the clinical estimates of gestational age and other covariates. For births with reported gestational ages of 29 or more weeks, the proportion in the secondary distribution exceeded 30%, although this varied by maternal characteristics. The use of covariates and stratification complicated model fitting without materially improving identification of implausible gestational age values, supporting inferences from prior studies using data cleaned without consideration of maternal or infant characteristics.
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[Technical optimization for extracting hypotensive active peptides from Agrocybe aegerita].
Nan Fang Yi Ke Da Xue Xue Bao
PUBLISHED: 06-30-2010
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To optimize the techniques for extracting hypotensive active peptides from Agrocybe aegerita.
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The anti-nociceptive effect and the possible mechanism of acupoint stimulation caused by chemical irritants in the bee venom pain model.
Brain Res.
PUBLISHED: 06-08-2010
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Many studies have demonstrated the anti-nociceptive and anti-inflammatory effects of injecting bee venom (BV) into the Zusanli (ZSL) acupoint in rats. The present study was designed to determine whether the injection of other chemical irritants, such as formalin and complete Freunds adjuvant (CFA), into the ZSL acupoint can produce anti-nociceptive and anti-inflammatory effects in the BV pain model and to determine the possible mechanisms underlying these effects. First, the effects of injecting BV, formalin, CFA, or saline into the ZSL acupoint on intraplantar BV-induced persistent spontaneous pain, mechanical hyperalgesia, and inflammatory swelling of the injected paw were observed. BV, formalin, CFA, and saline injection into the ZSL acupoint significantly inhibited intraplantar BV-induced persistent spontaneous nociception (PSN) and mechanical hyperalgesia but had no effect on intraplantar BV-induced inflammatory swelling. Next, the effects of pretreatment with naloxone (5mg/kg, ip) or injection of 0.15% capsaicin into the ZSL acupoint on the anti-nociceptive effect of BV acupuncture (BVA) were observed. Pretreatment with naloxone had no effect on the BVA-induced anti-nociceptive effect, intraplantar BV-induced PSN, and mechanical hyperalgesia. Pretreatment with capsaicin produced partial blockage of the BVA-induced anti-nociceptive effect on PSN, but it had no effect on BVA-induced anti-nociception of mechanical hyperalgesia. These results suggest that (1) chemical irritant acupuncture produces the anti-nociceptive effect but not the anti-inflammatory effect in the BV pain model, and (2) chemical irritant acupuncture-induced analgesia is a common mechanism that is not specific to BV acupuncture. Our results also suggest that the BVA-induced anti-nociceptive mechanism is partially mediated by capsaicin-sensitive primary afferent fibers but not by endogenous mu opioid receptors in the BV pain model.
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Cloning and characterization of Rv0621 gene related to surfactant stress tolerance in Mycobacterium tuberculosis.
Mol. Biol. Rep.
PUBLISHED: 10-02-2009
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To understand how Mycobacterium tuberculosis (M. tuberculosis) could survive in human lung, Genomic expression library of M. tuberculosis in Escherichia coli (E. coli) had been prepared. Taking advantage of the genetic simplicity of E. coli and the functional conservation of some prokaryote proteins, a surfactant stress resistant gene Rv0621 was identified, which encodes a 37 kDa putative membrane protein. The E. coli colony with the partial Rv0621 gene insert, named S1, was able to grow in medium containing 0.4% sodium dodecyl sulfate, while the strain carried empty vector was unable to grow. The full length of the Rv0621 gene was then cloned into plasmid pET32a (+) expressed in E. coli BL21 (DE3). Using gas chromatographic-mass spectrometric (GC-MS), the fatty acid composition of the E. coli BL21 (DE3) carrying Rv0621-pET32a (+) and the E. coli BL21 (DE3) carrying empty vector pET32a (+) were compared. E. coli BL21 (DE3) carrying Rv0621-pET32a (+) contained more oleic acid. This suggests the gene may be involved in regulation of fatty acid synthesis and M. tuberculosis resistance to the surfactant defense of its host.
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Highly active antiretroviral therapy drugs inhibit in vitro cholesterol efflux from human macrophage-derived foam cells.
Lab. Invest.
PUBLISHED: 09-21-2009
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We previously reported that HIV protease inhibitor, ritonavir, could inhibit cholesterol efflux and induce endothelial dysfunction. In this study, we further determined the effects and molecular mechanisms of a clinically relevant combination of highly active antiretroviral therapy (HAART) drugs on in vitro cholesterol efflux from human macrophage-derived foam cells. Foam cells derived from human monocyte cell line (THP-1) and periphery blood mononuclear cells (PBMCs) treated with HAART drugs including stavudine, didanosine and indinavir individually or in combination of three drugs (3-plex), followed by the initiation of cholesterol efflux with apolipoprotein A-I (apoA-I). Clinically relevant concentrations of HAART 3-plex significantly reduced cholesterol efflux in foam cells derived from THP-1 and PBMCs. HAART 3-plex significantly reduced the intracellular cholesterol transport molecule caveolin-1, whereas it increased superoxide anion production in THP-1 foam cells as compared with controls. Furthermore, mitochondrial membrane potential was significantly reduced, whereas the expression of NADPH oxidase subunit p67(phox) was increased in HAART 3-plex-treated macrophages. Consequently, antioxidants including ginsenosides Rb1 and Rg1, S-allyl cysteine sulphoxide (SACS), simvastatin (SVT) and vitamin E significantly abolished HAART 3-plex-induced inhibition of cholesterol efflux. Therefore, HAART drugs significantly inhibit cholesterol efflux from human macrophage-derived foam cells through downregulation of caveolin-1 and increase of oxidative stress.
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Differential roles of peripheral metabotropic glutamate receptors in bee venom-induced nociception and inflammation in conscious rats.
J Pain
PUBLISHED: 06-03-2009
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Intraplantar injection of bee venom (BV) produces persistent spontaneous nociception (PSN), hyperalgesia, and inflammatory swelling of the injected paw. The present study was designed to determine the roles of peripheral metabotropic glutamate receptors (mGluRs) in BV-induced nociception and inflammation. We determined the effects of the group I mGluR antagonist AIDA, the group II mGluR agonist ADPC, and the group III mGluR agonist L-AP4 on BV-induced PSN, mechanical hyperalgesia, and inflammatory swelling. Pretreatment with intraplantar injections of AIDA, ADPC or L-AP4 at different doses significantly inhibited BV-induced PSN over the 1-hour observational period. The inhibitory effects of ADPC and L-AP4 were completely abolished by pretreatment with the group II mGluR antagonist LY341495 and the group III mGluR antagonist MSOP, respectively. Pretreatment with ADPC prevented the BV-induced decrease in paw-withdrawal mechanical threshold (PWMT) in a dose-dependent manner, while pretreatment with AIDA or L-AP4 had no effect. The antihyperalgesic effect of ADPC was completely abolished by pretreatment with LY341495. Pretreatment with AIDA, ADPC or L-AP4 at different doses had no effect on the BV-induced increase in the paw volume (PV), a measurement of inflammatory swelling. All contralateral drug treatments at the highest doses had no effect on BV-induced PSN, decreases in PWMT or increases in PV, eliminating the possibility of drug-induced systemic effects. These data suggest that the activation of mGluRs in the periphery may play a differential role in BV-induced nociception and inflammation.
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Differential roles of peripheral mitogen-activated protein kinase signal transduction pathways in bee venom-induced nociception and inflammation in conscious rats.
J Pain
PUBLISHED: 04-18-2009
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Intraplantar injection of bee venom (BV) produces persistent spontaneous nociception (PSN) and hyperalgesia, as well as obvious inflammatory swelling, in the paws of injected rats. The present study was designed to determine the peripheral roles of mitogen-activated protein kinase (MAPK) signal transduction pathways in BV-induced nociception and inflammation. We examined the effect of intraplantar injection of an ERK1/2 inhibitor, PD98059, and a p38 inhibitor, SB202190, on BV-induced PSN, mechanical hyperalgesia, and inflammatory swelling. We found that (1) pretreatment with SB202190 (0.1 to 10 microg) had no effect on BV-induced PSN, whereas pretreatment with PD98059 (0.1 to 100 microg) produced a significant and dose-dependent inhibition of BV-induced PSN; (2) pretreatment with PD98059 (0.1 to 100 microg) had no effect on BV-induced decreases in paw withdrawal mechanical threshold (PWMT), while pretreatment with SB202190 (0.1 to 10 microg) produced an obvious prevention of the BV-induced decrease in PWMT; and (3) pretreatment with PD98059 (0.1 to 100 microg) had no effect on BV-induced increase in paw volume (PV), whereas pretreatment with SB202190 (0.1 to 10 microg) produced a dose-related inhibition of BV-induced increases in PV. No contralateral drug treatments, even at the highest dose, had any effect on BV-induced PSN, PWMT or PV, ruling out the systemic effect of these drugs. These results suggest that peripheral MAPK signal transduction pathways may play differential roles in bee venom-induced nociception and inflammation. Targeting specific peripheral MAPKs might prove effective in the treatment of persistent pain and inflammation.
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Covalent linkage of heparin provides a stable anti-coagulation surface of decellularized porcine arteries.
J. Cell. Mol. Med.
PUBLISHED: 04-15-2009
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Establishing thrombosis-resistant surface is crucial to develop tissue-engineered small diameter vascular grafts for arterial reconstructive procedures. The objective of this study was to evaluate the stability and anti-coagulation properties of heparin covalently linked to decellularized porcine carotid arteries. Cellular components of porcine carotid arteries were completely removed with chemical and physical means. Heparin was covalently linked to the decellularized vessels by a chemical reaction of the carboxyl end of amino acids with hydroxylamine sulphate salt and heparin-EDC. Bound heparin contents were measured by quantitative colorimetric assay of toluidine blue staining. The average content of heparin in treated vessels was 35.6 +/- 11.6 mg/cm(2) tissue, which represented 6.21 +/- 2.03 UPS heparin/cm(2) tissue. The stability of heparin linkage was tested by incubating the heparin-linked vessels either in PBS at 37 degrees C or in 70% alcohol at room temperature up to 21 days, showing no significant reduction of heparin content. Anti-coagulation property of bound heparin was determined with a clotting time assay using fresh dog blood. Standardized small pieces of non-heparin-bound vessels were clotted in fresh dog blood within 10 min., whereas all heparin-bound vessels did not form clot during 1-hr observation. In vivo platelet deposition of the vessel was determined with a baboon model of the femoral arteriovenous external shunt and (111)Indium labelling of platelets. There were 1.38 +/- 0.07 x 10(9) and 0.64 +/- 0.11 x 10(9) baboon platelets deposited on the control and heparin-linked vessels, respectively, at 60 min. These data demonstrate that covalent linkage of heparin provides an effective and stable anti-coagulation surface of decellularized porcine carotid arteries. This study may suggest a new strategy to develop tissue-engineered biological vascular grafts, which could be used for human coronary or low extremity artery bypasses.
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8-Chloro-4-cyclo-hexyl-2H-1,4-benzoxazin-3(4H)-one.
Acta Crystallogr Sect E Struct Rep Online
PUBLISHED: 03-05-2009
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In the crystal structure of title compound, C(14)H(16)ClNO(2), the cyclo-hexyl ring is in a chair conformation. The molecules are connected into centrosymmetric dimers via weak C-H?O hydrogen bonds.
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Human protein S inhibits the uptake of AcLDL and expression of SR-A through Mer receptor tyrosine kinase in human macrophages.
Blood
PUBLISHED: 02-07-2009
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Human protein S is an anticoagulation protein. However, it is unknown whether protein S could regulate the expression and function of macrophage scavenger receptor A (SR-A) in macrophages. Human THP-1 monocytes and peripheral blood monocytes were differentiated into macrophages and then treated with physiological concentrations of human protein S. We found that protein S significantly reduced acetylated low-density lipoprotein (AcLDL) uptake and binding by macrophages and decreased the intracellular cholesteryl ester content. Protein S suppressed the expression of the SR-A at both mRNA and protein levels. Protein S reduced the SR-A promoter activity primarily through inhibition in the binding of transcription factors to the AP-1 promoter element in macrophages. Furthermore, human protein S could bind and induce phosphorylation of Mer receptor tyrosine kinase (Mer RTK). Soluble Mer protein or tyrosine kinase inhibitor herbimycin A effectively blocked the effects of protein S on AcLDL uptake. Immunohistochemical analysis revealed that the level of protein S was substantially increased in human atherosclerotic arteries. Thus, human protein S can inhibit the expression and activity of SR-A through Mer RTK in macrophages, suggesting that human protein S is a modulator for macrophage functions in uptaking of modified lipoproteins.
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Functional characterization of three mouse formyl peptide receptors.
Mol. Pharmacol.
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The evolutionary relationship and functional correlation between human formyl peptide receptors (FPRs) and their mouse counterparts remain incompletely understood. We examined three members of the mouse formyl peptide receptor subfamily (mFprs) and found that they differ in agonist preference and cellular distributions. When stably expressed in transfected rat basophilic leukemia (RBL-2H3) cells, mFpr1 was readily activated by N-formylated peptides derived from Listeria monocytogenes (fMIVTLF), Staphylococcus aureus (fMIFL), and mitochondria (fMMYALF). In contrast, the Escherichia coli-derived fMLF was 1000-fold less potent. The aforementioned peptides were much less efficacious at mFpr2, which responded better to the synthetic hexapeptide WKYMVm, the synthetic agonists Quin-C1 (a substituted quinazolinone), and compound 43 (a nitrosylated pyrazolone derivative). Saturation binding assays showed that mFpr1 and mFpr2 were expressed at similar levels on the cell surface, although their affinity for N-formyl-Met-Leu-Phe-Ile-Ile-Lys-fluorescein isothiocyanate varied by more than 1000-fold [dissociation constant (K(d)) values of 2.8 nM for mFpr1 and 4.8 ?M for mFpr2]). Contrary to these receptors, mFpr-rs1 responded poorly to all the previously mentioned peptides that were tested. Fluorescent microscopy revealed an intracellular distribution pattern of mFpr-rs1. On the basis of these results, we conclude that mFpr1 is an ortholog of human FPR1 with certain pharmacologic properties of human FPR2/ALX, whereas mFpr2 has much lower affinity for formyl peptides. The intracellular distribution of mFpr-rs1 suggests an evolutionary correlation with human FPR3.
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Identifying implausible gestational ages in preterm babies with Bayesian mixture?models.
Stat Med
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Infant birth weight and gestational age are two important variables in obstetric research. The primary measure of gestational age used in US birth data is based on a mothers recall of her last menstrual period, which has been shown to introduce random or systematic errors. To mitigate some of those errors, Oja et al., Platt et al., and Tentoni et al. estimated the probabilities of gestational ages being misreported under the assumption that the distribution of infant birth weights for a true gestational age is approximately Gaussian. From this assumption, Oja et al. fitted a three-component mixture model, and Tentoni et al. and Platt et al. fitted two-component mixture models. We build on their methods and develop a Bayesian mixture model. We then extend our methods using reversible jump Markov chain Monte Carlo to incorporate the uncertainty in the number of components in the model. We conduct simulation studies and apply our methods to singleton births with reported gestational ages of 23-32?weeks using 2001-2008 US birth data. Results show that a three-component mixture model fits the birth data better for gestational ages reported as 25?weeks or less; and a two-component mixture model fits better for the higher gestational ages. Under the assumption that our Bayesian mixture models are appropriate for US birth data, our research provides useful statistical tools to identify records with implausible gestational ages, and the techniques can be used in part of a multiple-imputation procedure for missing and implausible gestational ages.
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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.

How does it work?

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

Video X seems to be unrelated to Abstract Y...

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.