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Find video protocols related to scientific articles indexed in Pubmed.
A Propensity Score-Matched Case-Control Comparative Study of Laparoscopic and Open Liver Resection for Hepatocellular Carcinoma.
J Laparoendosc Adv Surg Tech A
PUBLISHED: 11-14-2014
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Abstract Background: The aim of this study was to compare the perioperative and long-term oncologic outcomes of laparoscopic liver resection (LLR) and open liver resection (OLR) for single hepatocellular carcinoma (HCC) in case-controlled patient groups using the propensity score. Patients and Methods: Between January 2005 and February 2013, 292 patients underwent surgical resection for HCC. Of these, 202 patients who underwent surgical resection for initial treatment for a single mass were enrolled. These patients were divided into two groups according to the method of operation: the Lap group (patients who underwent LLR) and the Open group (patients who underwent OLR). To correct different demographic and clinical factors in the two groups, propensity score matching was used at a 1:1 ratio, and, finally, 102 patients were enrolled in this study, 51 patients in each group. Preoperative characteristics, perioperative results, and long-term results were retrospectively analyzed based on the prospectively recorded database. Results: Preoperative baseline variables were well balanced in both groups. There were no differences of extent of surgery and rate of anatomical resection between the two groups. With the exception of a shorter postoperative hospital stay in the Lap group than that of the Open group (8.2 days versus 12.3 days; P=.004), there were no significant differences in perioperative, pathological, and long-term outcomes. The 5-year overall survival rates were 80.1% in the Lap group and 85.7% in the Open group, respectively (P=.173). The 5-year disease-free survival rates were 67.8% in the Lap group and 54.8% in the Open group, respectively (P=.519). Conclusions: LLR for HCC is safe, and long-term oncologic outcomes in selected patients were comparable to those who underwent OLR.
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Atomistic mechanisms of codoping-induced p- to n-type conversion in nitrogen-doped graphene.
Nanoscale
PUBLISHED: 11-03-2014
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It was recently shown that nitrogen-doped graphene (NG) can exhibit both p- and n-type characters depending on the C-N bonding nature, which represents a significant bottleneck for the development of graphene-based electronics. Based on first-principles calculations, we herein scrutinize the correlations between the atomic and electronic structures of NG and particularly explore the feasibility of converting p-type NG with pyridinic, pyrrolic, and nitrilic N atoms into n- or bipolar type by introducing an additional dopant atom. Of the nine candidates B, C, O, F, Al, Si, P, S, and Cl, we find that B-, Al-, and P-codoping can anneal even relatively large vacancy defects in p-type NG. It will be also shown that, while the NG with pyridinic N can be converted into the n-type via codoping, only a bipolar type conversion can be achieved for the NG with nitrilic or pyrrolic N. The amount of work function reduction was up to 0.64 eV for the pyridinic N next to a monovacancy. The atomistic origin of such diverse type changes is analyzed based on Mulliken and crystal orbital Hamiltonian populations, which provide us with a framework to connect the local bonding chemistry with the macroscopic electronic structure in doped and/or defective graphene. Moreover, we demonstrate that the proposed codoping scheme can recover the excellent charge transport properties of pristine graphene. Both the electronic type conversion and conductance recovery in codoped NG should have significant implications for the electronic and energy device applications.
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Inhibition of adenylyl cyclase type 5 prevents L-DOPA-induced dyskinesia in an animal model of Parkinson's disease.
J. Neurosci.
PUBLISHED: 08-29-2014
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The dopamine precursor L-3,4-dihydroxyphenylalanine (L-DOPA) is widely used as a therapeutic choice for the treatment of patients with Parkinson's disease. However, the long-term use of L-DOPA leads to the development of debilitating involuntary movements, called L-DOPA-induced dyskinesia (LID). The cAMP/protein kinase A (PKA) signaling in the striatum is known to play a role in LID. However, from among the nine known adenylyl cyclases (ACs) present in the striatum, the AC that mediates LID remains unknown. To address this issue, we prepared an animal model with unilateral 6-hydroxydopamine lesions in the substantia nigra in wild-type and AC5-knock-out (KO) mice, and examined behavioral responses to short-term or long-term treatment with L-DOPA. Compared with the behavioral responses of wild-type mice, LID was profoundly reduced in AC5-KO mice. The behavioral protection of long-term treatment with L-DOPA in AC5-KO mice was preceded by a decrease in the phosphorylation levels of PKA substrates ERK (extracellular signal-regulated kinase) 1/2, MSK1 (mitogen- and stress-activated protein kinase 1), and histone H3, levels of which were all increased in the lesioned striatum of wild-type mice. Consistently, FosB/?FosB expression, which was induced by long-term L-DOPA treatment in the lesioned striatum, was also decreased in AC5-KO mice. Moreover, suppression of AC5 in the dorsal striatum with lentivirus-shRNA-AC5 was sufficient to attenuate LID, suggesting that the AC5-regulated signaling cascade in the striatum mediates LID. These results identify the AC5/cAMP system in the dorsal striatum as a therapeutic target for the treatment of LID in patients with Parkinson's disease.
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A facile synthesis of multi metal-doped rectangular ZnO nanocrystals using a nanocrystalline metal-organic framework template.
Nanoscale
PUBLISHED: 08-16-2014
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A multi metal (M: Fe, Co, and Ni)-doped rectangular ZnO nanocrystal (r-ZnO:M) was synthesised using nanocrystalline metal-organic framework-5 (n-MOF-5). After calcination in air, M-inserted n-MOF-5 led to r-ZnO:M of the wurtzite crystal structure with a small amount (<1%) of spinel ZnM2O4 phase. The inserted metal atoms of r-ZnO:M, replacing the Zn atoms of the wurtzite ZnO structure, were well-dispersed throughout the nanocrystal. Density functional theory calculations not only confirm the structural stability of wurtzite r-ZnO:M and negligible contribution of spinel ZnM2O4 but also elucidate the experimentally observed increase of visible light absorbance and appearance of ferromagnetism upon metal atom doping.
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The protective role of NAD(P)H:quinone oxidoreductase 1 on acetaminophen-induced liver injury is associated with prevention of adenosine triphosphate depletion and improvement of mitochondrial dysfunction.
Arch. Toxicol.
PUBLISHED: 07-17-2014
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An overdose of acetaminophen (APAP) causes hepatotoxicity due to its metabolite, N-acetyl-p-benzoquinone imine. NAD(P)H:quinone oxidoreductase 1 (NQO1) is an important enzyme for detoxification, because it catabolizes endogenous/exogenous quinone to hydroquinone. Although various studies have suggested the possible involvement of NQO1 in APAP-induced hepatotoxicity, its precise role in this remains unclear. We investigated the role of NQO1 against APAP-induced hepatotoxicity using a genetically modified rodent model. NQO1 wild-type (WT) and knockout (KO) mice were treated with different doses of APAP, and we evaluated the mortality and toxicity markers for cell death caused by APAP. NQO1 KO mice showed high sensitivity to APAP-mediated hepatotoxicity (as indicated by a large necrotic region) as well as increased levels of nitrotyrosine adducts and reactive oxygen species. APAP-induced cell death in the livers and primary hepatocytes of NQO1 KO mice, which was accompanied by an extensive reduction in adenosine triphosphate (ATP) levels. In accordance with this ATP depletion, cytosolic increases in mitochondrial proteins such as apoptosis-inducing factor, second mitochondria-derived activator of caspases/DIABLO, endonuclease G, and cytochrome c, which indicate severe mitochondrial dysfunction, were observed in NQO1 KO mice but not in WT mice after APAP exposure. Severe mitochondrial depolarization was also greater in hepatocytes isolated from NQO1 KO mice. Collectively, our data suggest that NQO1 plays a critical role in protection against energy depletion caused by APAP, and NQO1 may be useful in the development of therapeutic approaches to effectively diminish the hepatotoxicity caused by an APAP overdose.
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Small heterodimer partner blocks cardiac hypertrophy by interfering with GATA6 signaling.
Circ. Res.
PUBLISHED: 07-11-2014
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Small heterodimer partner (SHP; NR0B2) is an atypical orphan nuclear receptor that lacks a conventional DNA-binding domain. Through interactions with other transcription factors, SHP regulates diverse biological events, including glucose metabolism in liver. However, the role of SHP in adult heart diseases has not yet been demonstrated.
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NAD(P)H:Quinone Oxidoreductase 1 Activation Reduces Blood Pressure Through Regulation of Endothelial Nitric Oxide Synthase Acetylation in Spontaneously Hypertensive Rats.
Am. J. Hypertens.
PUBLISHED: 06-22-2014
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Endothelial nitric oxide synthase (eNOS) is involved in blood pressure (BP) regulation through the production of nitric oxide. Sirtuin I (SIRT1), an NAD-dependent protein deacetylase, promotes vascular relaxation through deacetylation and activation of eNOS. ?-Lapachone (?L) increases the cellular NAD(+)/NADH ratio by activating NAD(P)H:quinone oxidoreductase 1 (NQO1). In this study, we verified whether activation of NQO1 by ?L modulates BP through regulation of eNOS acetylation in a hypertensive animal model.
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PKB/Akt phosphorylation of ERR? contributes to insulin-mediated inhibition of hepatic gluconeogenesis.
Diabetologia
PUBLISHED: 06-05-2014
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Insulin resistance, a major contributor to the pathogenesis of type 2 diabetes, leads to increased hepatic glucose production (HGP) owing to an impaired ability of insulin to suppress hepatic gluconeogenesis. Nuclear receptor oestrogen-related receptor ? (ERR?) is a major transcriptional regulator of hepatic gluconeogenesis. In this study, we investigated insulin-dependent post-translational modifications (PTMs) altering the transcriptional activity of ERR? for the regulation of hepatic gluconeogenesis.
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SIK2 Is Critical in the Regulation of Lipid Homeostasis and Adipogenesis In Vivo.
Diabetes
PUBLISHED: 06-04-2014
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Cyclic AMP promotes chronic expression of target genes mainly by protein kinase A-dependent activation of CREB transcription factor machineries in the metabolic tissues. Here, we wanted to elaborate whether CREB-regulated transcription factor (CRTC)2 and its negative regulator salt-inducible kinase (SIK)2 are involved in the transcriptional control of the metabolic pathway in adipocytes. SIK2 knockout (SIK2 KO) mice exhibited higher blood glucose levels that were associated with impaired glucose and insulin tolerance. Hypertriglyceridemia was apparent in SIK2 KO mice, mainly due to the increased lipolysis from white adipocytes and the decreased fatty acid uptake in the peripheral tissues. Investigation of white adipocytes revealed the increases in fat cell size and macrophage infiltration, which could be linked to the metabolic anomaly that is associated in these mice. Interestingly, SIK2 KO promoted the enhancement in the CRTC2-CREB transcriptional pathway in white adipocytes. SIK2 KO mice displayed increased expression of activating transcription factor (ATF)3 and subsequent downregulation of GLUT4 expression and reduction in high-molecular weight adiponectin levels in the plasma, leading to the reduced glucose uptake in the muscle and white adipocytes. The effect of SIK2-dependent regulation of adipocyte metabolism was further confirmed by in vitro cell cultures of 3T3 L1 adipocytes and the differentiated preadipocytes from the SIK2 or CRTC2 KO mice. Collectively, these data suggest that SIK2 is critical in regulating whole-body glucose metabolism primarily by controlling the CRTC2-CREB function of the white adipocytes.
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Large-scale organic single-crystal thin films and transistor arrays via the evaporation-controlled fluidic channel method.
ACS Appl Mater Interfaces
PUBLISHED: 05-07-2014
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We report a facile and versatile approach for fabricating large-area organic thin film transistor (OTFTs) arrays via a fluidic channel method. Evaporation-controlled fluidic channel-containing organic semiconductors easily produce large-area organic single-crystalline thin films in a quite uniform manner. The unidirectional movement of the meniscus and the subsequent film growth via solvent evaporation inside the fluidic channel correspond to the simulation based on the finite element method. Utilizing this fluidic channel method, we fabricated high-performance 6,13-bis(triisopropylsilylethynyl)pentacene OTFT arrays with average and maximal mobilities of 0.71 and 2.18 cm(2) V(-1) s(-1), respectively, while exhibiting current on:off ratios of >1 × 10(6). We claim that this scalable fluidic channel method offers a competitive way to fabricate high-performance and large-area organic semiconductor devices for a variety of applications.
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Endoscopic treatment of pancreatic calculi.
Clin Endosc
PUBLISHED: 04-11-2014
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Chronic pancreatitis is a progressive inflammatory disease that destroys pancreatic parenchyma and alters ductal stricture, leading to ductal destruction and abdominal pain. Pancreatic duct stones (PDSs) are a common complication of chronic pancreatitis that requires treatment to relieve abdominal pain and improve pancreas function. Endoscopic therapy, extracorporeal shock wave lithotripsy (ESWL), and surgery are treatment modalities of PDSs, although lingering controversies have hindered a consensus recommendation. Many comparative studies have reported that surgery is the superior treatment because of reduced duration and frequency of hospitalization, cost, pain relief, and reintervention, while endoscopic therapy is effective and less invasive but cannot be used in all patients. Surgery is the treatment of choice when endoscopic therapy has failed, malignancy is suspected, or duodenal stricture is present. However, in patients with the appropriate indications or at high-risk for surgery, endoscopic therapy in combination with ESWL can be considered a first-line treatment. We expect that the development of advanced endoscopic techniques and equipment will expand the role of endoscopic treatment in PDS removal.
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Home blood pressure is the predictor of subclinical target organ damage like ambulatory blood pressure monitoring in untreated hypertensive patients.
Anadolu Kardiyol Derg
PUBLISHED: 04-08-2014
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Home blood pressure (HBP) measurements are known as an important adjunct to office blood pressure (OBP) measurements in clinical practice. But little is known about the relationship between HBP and subclinical target organ damage (TOD) other than left ventricular hypertrophy (LVH). So we investigated the relationship of HBP measurements with subclinical TOD in untreated hypertensive patients.
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Differences in ward-to-cath lab systolic blood pressure predicts long-term adverse outcomes after drug-eluting stent implantation.
Heart Vessels
PUBLISHED: 04-04-2014
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We sought to investigate the effect of ward-to-cath lab blood pressure (BP) differences on long-term clinical outcomes in patients undergoing percutaneous coronary intervention (PCI) with drug-eluting stent (DES). There are limited data available on the association between PCI with DES and BP differences on long-term clinical outcomes. This study enrolled 994 patients who underwent PCI with DES from March 2003 to August 2007. Resting BP was measured in a ward environment before transfer to the cardiac catheterization lab (cath lab), and again when the patient was laid down on the cath lab table. Patients were divided into two groups according to the difference in ward-to-cath lab systolic BP. Large difference group (n = 383) was defined as the absolute systolic difference of >20 mmHg and small difference group (n = 424) as the absolute systolic difference of ?20 mmHg. The primary endpoints were all-cause mortality, cardiac death, nonfatal myocardial infarction and stroke. A total of 807 patients (mean age 60 ± 10 years, 522 males) received follow-up for 5.1 ± 2.4 years. The rate of all-cause mortality was significantly higher in the large difference group compared to the small difference group (6.6 vs. 2.8 %; adjusted hazard ratio (HR) 2.43; 95 % confidence interval (CI) 1.22-4.83; p = 0.012). There were higher cardiac deaths seen in the large difference group compared to the small difference group (3.9 vs. 1.4 %; adjusted HR 2.84; 95 % CI 1.1-7.31; p = 0.031). Stroke (2.4 vs. 1.2 %, p = 0.125) and TVR (3.7 vs. 1.7 %, p = 0.051) had higher trends in the large difference group compared to the small difference group. The composite of primary endpoints (all-cause mortality, cardiac death, nonfatal MI and stroke) occurred more frequently in the large difference group compared to the small difference group (10.0 vs. 6.4 %; adjusted HR 1.71; 95 % CI 1.04-2.81; p = 0.033). A difference in ward-to-cath lab systolic BP of >20 mmHg may contribute to increased adverse outcomes in the form of all-cause mortality and cardiac deaths in patients undergoing PCI with DES.
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Improved severe hepatopulmonary syndrome after liver transplantation in an adolescent with end-stage liver disease secondary to biliary atresia.
Clin Mol Hepatol
PUBLISHED: 03-26-2014
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Hepatopulmonary syndrome (HPS) is a serious complication of end-stage liver disease, which is characterized by hypoxia, intrapulmonary vascular dilatation, and liver cirrhosis. Liver transplantation (LT) is the only curative treatment modality for patients with HPS. However, morbidity and mortality after LT, especially in cases of severe HPS, remain high. This case report describes a patient with typical findings of an extracardiac pulmonary arteriovenous shunt on contrast-enhanced transesophageal echocardiography (TEE), and clubbing fingers, who had complete correction of HPS by deceased donor LT. The patient was a 16-year-old female who was born with biliary atresia and underwent porto-enterostomy on the 55th day after birth. She had been suffered from progressive liver failure with dyspnea, clubbing fingers, and cyanosis. Preoperative arterial blood gas analysis revealed severe hypoxia (arterial O2 tension of 54.5 mmHg and O2 saturation of 84.2%). Contrast-enhanced TEE revealed an extracardiac right-to-left shunt, which suggested an intrapulmonary arteriovenous shunt. The patient recovered successfully after LT, not only with respect to physical parameters but also for pychosocial activity, including school performance, during the 30-month follow-up period.
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ADAM33 gene polymorphisms are associated with the risk of idiopathic pulmonary fibrosis.
Lung
PUBLISHED: 03-21-2014
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Idiopathic pulmonary fibrosis (IPF) is characterized by progressive dyspnea and worsening lung function due to remodeling of the lung, including epithelial mesenchymal transition. ADAM33 is a disintegrin and metalloprotease domain-containing protein, which may be related to lung fibrosis by exerting angiogenesis and remodeling of the lung. Thus, we evaluated the association of single-nucleotide polymorphisms (SNPs) of ADAM33 with the risk of IPF.
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Follow-up outcomes of endoscopic resection for early gastric cancer with undifferentiated histology.
Surg Endosc
PUBLISHED: 03-11-2014
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The application of endoscopic resection (ER) for undifferentiated-type early gastric cancer (UD-EGC) remains controversial. The aim was to examine long-term outcomes of ER for UD-EGC. Furthermore, we investigated whether long-term outcomes of ER differed between poorly differentiated adenocarcinoma (PD) and signet ring cell carcinoma (SRC).
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Polymorphisms of ATF6B Are Potentially Associated With FEV1 Decline by Aspirin Provocation in Asthmatics.
Allergy Asthma Immunol Res
PUBLISHED: 03-04-2014
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Endoplasmic reticulum (ER) stress has recently been observed to activate NF-kappaB and induce inflammatory responses such as asthma. Activating transcription factor 6? (ATF6B) is known to regulate ATF?-mediated ER stress response. The aim of this study is to investigate the associations of ATF6B genetic variants with aspirin-exacerbated respiratory disease (AERD) and its major phenotype, % decline of FEV1 by aspirin provocation.
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Efficacy of two different self-expanding nitinol stents for atherosclerotic femoropopliteal arterial disease (SENS-FP trial): study protocol for a randomized controlled trial.
Trials
PUBLISHED: 03-01-2014
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There have been few randomized control trials comparing the incidence of stent fracture and primary patency among different self-expanding nitinol stents to date. The SMART™ CONTROL stent (Cordis Corp, Miami Lakes, Florida, United States) has a peak-to-valley bridge and inline interconnection, whereas the COMPLETE™-SE stent (Medtronic Vascular, Santa Rosa, California, United States) crowns have been configured to minimize crown-to-crown interaction, increasing the stent's flexibility without compromising radial strength. Further, the 2011 ESC (European society of cardiology) guidelines recommend that dual antiplatelet therapy with aspirin and a thienopyridine such as clopidogrel should be administered for at least one month after infrainguinal bare metal stent implantation. Cilostazol has been reported to reduce intimal hyperplasia and subsequent repeat revascularization. To date, there has been no randomized study comparing the safety and efficacy of two different antiplatelet regimens, clopidogrel and cilostazol, following successful femoropopliteal stenting.
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Genome-wide association study identifies ALLC polymorphisms correlated with FEV? change by corticosteroid.
Clin. Chim. Acta
PUBLISHED: 01-04-2014
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Asthma can be suppressed by inhaled corticosteroids (ICS). However, response to ICS shows marked inter-individual variability. This study is aimed to identify the genetic variants associated with the change in the percentage of forced expiratory volume in 1second (%?FEV1) following ICS treatment.
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Effects of annealing conditions on the dielectric properties of solution-processed Al2O3 layers for indium-zinc-tin-oxide thin-film transistors.
J Nanosci Nanotechnol
PUBLISHED: 11-20-2013
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In this paper, the effects of annealing conditions on the dielectric properties of solution-processed aluminum oxide (Al2O3) layers for indium-zinc-tin-oxide (IZTO) thin-film transistors (TFTs) have been investigated. The dielectric properties of Al2O3 layers such as leakage current density and dielectric strength were largely affected by their annealing conditions. In particular, oxygen partial pressure in rapid thermal annealing, and the temperature profile of hot plate annealing had profound effects on the dielectric properties. From a refractive index analysis, the enhanced dielectric properties of Al2O3 gate dielectrics can be attributed to higher film density depending on the annealing conditions. With the low-temperature-annealed Al2O3 gate dielectric at 350 degrees C, solution-processed IZTO TFTs with a field-effect mobility of approximately 2.2 cm2/Vs were successfully fabricated.
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Recanalization of refractory benign biliary stricture using magnetic compression anastomosis.
Endoscopy
PUBLISHED: 11-19-2013
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Background and study aims: Endoscopic or percutaneous treatments are preferentially attempted for benign biliary stricture (BBS). However, these methods are not feasible if a guide wire cannot be passed through the stricture. This study evaluated the usefulness and technical requirements of magnetic compression anastomosis (MCA) in refractory BBS.? Patients and methods: MCA was performed in patients with BBS that had not been resolved with conventional treatments. One magnet was delivered through the percutaneous transhepatic biliary drainage tract and the other magnet was advanced through three different routes. After magnet approximation and recanalization, an internal drainage catheter was placed for 6 months and then removed. Results: Seven patients underwent MCA, and recanalization was successfully achieved in five. MCA failure in two cases was attributed to long stenotic segments and parallel alignment of the axes of the magnets. The mean follow-up period after recanalization was 485.2 days. Five patients with successful recanalization showed no MCA-related complications or restenosis. Conclusions: MCA represents an alternative nonsurgical method of BBS recanalization that cannot be treated with conventional methods.
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Retinoic acid receptor alpha: One of plasma biomarkers associated with exacerbation of chronic obstructive pulmonary disease.
COPD
PUBLISHED: 10-10-2013
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Abstract Background: Exacerbation of COPD is a major risk factor for bad prognosis of COPD. A few plasma proteins have been discovered to associate with hospital admission due to exacerbation up to date. We tried to find new plasma biomarkers to predict the exacerbation of COPD. Methods: We examined the plasma of normal control (n = 8) and COPD stable (n = 8) and exacerbation (n = 8) using 2-Dimentional Electrophoresis. The differentially expressed protein spots were identified by MALDI-TOF. ELISA were performed for quantitative measurement of RAR? in plasma from normal control (n = 37) and COPD (n = 35). Results: 17 proteins were differentially expressed in plasma between stable and exacerbation state in the subjects with COPD. Identification using MALDI-TOF showed that retinoic acid receptor alpha, ninein, isoform CRA_a, alpha-1 antitrypsin, fibrinogen gamma, tyrosyl-DNA phosphodiesterase 2, and T cell receptor delta chain were increased in exacerbation of COPD, while fibrin beta, Crystal Structure Of An Autoimmune Complex Between A Human Igm RF* And Igg1 Fc, transferrin, serpin peptidase inhibitor member 6, complement factor B preproprotein, Chain B, Crig Bound To C3c, and WD repeat-containing protein 1 isoform 1 were decreased. Quantitative measurement showed that RAR? plasma levels significantly increased in exacerbation state compared to stable state of COPD (n = 14). In the plasma of stable state, the COPD subjects (n = 14) having more than 0.4 time/yr of admission had very high levels of RAR alpha protein and those (n = 11) having less than 0.4 times/yr of admission had the intermediate levels compared to those having no exacerbation (n = 10). ROC analysis of RAR alpha levels to frequency of admission showed an area under the curve of 0.844. A cut-off of 0.154 ng/ml of RAR alpha predicted hospital admission with a sensitivity of 71.4% and a specificity of 92.8%. Conclusion: The proteomic analysis of plasma indicates that alteration of several proteins may be associated with admission of COPD. Among them, plasma RAR alpha level may predict hospital admission with a sensitivity of 71.4% and a specificity of 92.8%.
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Protection of NAD(P)H:quinone oxidoreductase 1 against renal ischemia/reperfusion injury in mice.
Free Radic. Biol. Med.
PUBLISHED: 08-28-2013
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Ischemia/reperfusion (I/R) is the most common cause of acute renal injury. I/R-induced reactive oxygen species (ROS) are thought to be a major factor in the development of acute renal injury by promoting the initial tubular damage. NAD(P)H:quinone oxidoreductase 1 (NQO1) is a well-known antioxidant protein that regulates ROS generation. The purpose of this study was to investigate whether NQO1 modulates the renal I/R injury (IRI) associated with NADPH oxidase (NOX)-derived ROS production in an animal model. We analyzed renal function, oxidative stress, and tubular apoptosis after IRI. NQO1(-/-) mice showed increased blood urea nitrogen and creatinine levels, tubular damage, oxidative stress, and apoptosis. In the kidneys of NQO1(-/-) mice, the cellular NADPH/NADP(+) ratio was significantly higher and NOX activity was markedly higher than in those of NQO1(+/+) mice. The activation of NQO1 by ?-lapachone (?L) significantly improved renal dysfunction and reduced tubular cell damage, oxidative stress, and apoptosis by renal I/R. Moreover, the ?L treatment significantly lowered the cellular NADPH/NADP(+) ratio and dramatically reduced NOX activity in the kidneys after IRI. From these results, it was concluded that NQO1 has a protective role against renal injury induced by I/R and that this effect appears to be mediated by decreased NOX activity via cellular NADPH/NADP(+) modulation. These results provide convincing evidence that NQO1 activation might be beneficial for ameliorating renal injury induced by I/R.
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Neurolymphomatosis of Brachial Plexus in Patients with Non-Hodgkins Lymphoma.
Case Rep Oncol Med
PUBLISHED: 08-27-2013
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Neurolymphomatosis (NL) is a rare clinical disease where neoplastic cells invade the cranial nerves and peripheral nerve roots, plexus, or other nerves in patients with hematologic malignancy. Most NL cases are caused by B-cell non-Hodgkins lymphoma (NHL). Diagnosis can be made by imaging with positron emission tomography (PET) and magnetic resonance imaging (MRI). We experienced two cases of NL involving the brachial plexus in patients with NHL. One patient, who had NHL with central nervous system (CNS) involvement, experienced complete remission after 8 cycles of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) chemotherapy but relapsed into NL of the brachial plexus 5 months later. The other patient, who suffered from primary central nervous system lymphoma (PCNSL), had been undergoing chemoradiotherapy but progressed to NL of the brachial plexus.
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Extraction of quantitative parameters for describing the microstructure of solid oxide fuel cells.
Microsc. Microanal.
PUBLISHED: 08-08-2013
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Digital quantification of a two-dimensional structure was applied to a GDC(Gd?O?-doped CeO?)/LSM(La?.??Sr?.??MnO?) composite cathode employed for solid oxide fuel cells. With the aid of high-resolution imaging capability based on secondary and backscattered electron images, two-dimensional electron micrographs were converted to digital binary files using an image processing tool combined with the line intercept method. Statistical analysis combined with a metallurgical tool was employed to determine microstructural factors, i.e., volume fraction, size distribution, and interconnectivity. The current work reports the quantification of the two-dimensional structural images of GDC/LSM composites applicable to solid oxide fuel cells, with the aim of obtaining the volume fraction, size distribution, and interconnectivity as functions of composite composition. The volume fractions of the solid constituent phases exhibit compositional dependence in cathodes; however, LSM interconnectivity increases gradually as a function of LSM composition, whereas that of GDC decreases significantly at 50 wt% LSM.
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Histopathologic validation of optical coherence tomography findings of non-apposed side-branch struts in porcine arteries.
J Invasive Cardiol
PUBLISHED: 07-02-2013
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The presence of uncovered struts overlying side branch is considered to be a potential risk of stent thrombosis. The accuracy in detection of neointimal strut coverage at branch point by optical coherence tomography (OCT) has not been validated in comparison with histology.
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Nonalcoholic fatty liver disease is associated with coronary artery disease in Koreans.
World J. Gastroenterol.
PUBLISHED: 06-20-2013
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To investigate whether nonalcoholic fatty liver disease (NAFLD) affects coronary artery disease (CAD) and identify candidate mediators.
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Inverse agonist of nuclear receptor ERR? mediates antidiabetic effect through inhibition of hepatic gluconeogenesis.
Diabetes
PUBLISHED: 06-17-2013
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Type 2 diabetes mellitus (T2DM) is a progressive metabolic disorder with diverse pathological manifestations and is often associated with abnormal regulation of hepatic glucose production. Many nuclear receptors known to control the hepatic gluconeogenic program are potential targets for the treatment of T2DM and its complications. Nevertheless, the therapeutic potential of the estrogen-related receptor ? (ERR?) in T2DM remains unknown. In this study, we show that the nuclear receptor ERR? is a major contributor to hyperglycemia under diabetic conditions by controlling hepatic glucose production. Hepatic ERR? expression induced by fasting and diabetic conditions resulted in elevated levels of gluconeogenic gene expression and blood glucose in wild-type mice. Conversely, ablation of hepatic ERR? gene expression reduced the expression of gluconeogenic genes and normalized blood glucose levels in mouse models of T2DM: db/db and diet-induced obesity (DIO) mice. In addition, a hyperinsulinemic-euglycemic clamp study and long-term studies of the antidiabetic effects of GSK5182, the ERR?-specific inverse agonist, in db/db and DIO mice demonstrated that GSK5182 normalizes hyperglycemia mainly through inhibition of hepatic glucose production. Our findings suggest that the ability of GSK5182 to control hepatic glucose production can be used as a novel therapeutic approach for the treatment of T2DM.
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NQO1 activation regulates angiotensin-converting enzyme shedding in spontaneously hypertensive rats.
Cardiovasc. Res.
PUBLISHED: 06-06-2013
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Angiotensin-converting enzyme (ACE) plays a key role in blood pressure (BP) homeostasis via regulation of angiotensin II. Active ACE ectodomain is enzymatically cleaved and released into body fluids, including plasma, and elevated plasma ACE levels are associated with increased BP. ?-lapachone (?L) has been shown to increase cellular NAD(+)/NADH ratio via activation of NAD(P)H:quinone oxidoreductase 1 (NQO1). In this study, we evaluated whether NQO1 activation by ?L modulates BP through regulation of ACE shedding in an animal model of hypertension.
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Endovascular stent-graft repair for abdominal aortic aneurysm in a patient with a short and severely angulated proximal aortic neck.
Cardiovasc J Afr
PUBLISHED: 05-11-2013
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Serious anatomical limitations to endovascular aortic aneurysm repair (EVAR) are mostly related to the anatomical characteristics of the proximal neck of the aneurysm. A 75-year-old male was referred for management of an incidentally found large asymptomatic infra-renal saccular abdominal aortic aneurysm. Its proximal aortic neck was short and severely angulated. We performed successful EVAR in this patient without surgical intervention.
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Relationship between aspirin/clopidogrel resistance and intra-stent thrombi assessed by follow-up optical coherence tomography after drug-eluting stent implantation.
Eur Heart J Cardiovasc Imaging
PUBLISHED: 05-08-2013
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No data exist regarding the relationship between aspirin/clopidogrel resistance and intra-stent thrombi on follow-up optical coherence tomography (OCT) after drug-eluting stent (DES) implantation. The purpose of this study was to evaluate the relationship between aspirin/clopidogrel resistance and intra-stent thrombi on the follow-up OCT in DES-treated patients.
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Protective role of NAD(P)H:quinone oxidoreductase 1 (NQO1) in cisplatin-induced nephrotoxicity.
Toxicol. Lett.
PUBLISHED: 04-26-2013
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Although cisplatin is widely used as an anti-cancer agent, its use is significantly limited because of its tendency to induce nephrotoxicity through poorly understood mechanisms. NAD(P)H:quinone oxidoreductase 1 (NQO1) is well known to regulate ROS generation. The purpose of this study was to investigate whether NQO1 modulates cisplatin-induced renal failure associated with NADPH oxidase (NOX)-derived ROS production in an animal model. NQO1-/- mice were treated with cisplatin (18 mg/kg) and renal function, oxidative stress, and tubular apoptosis were assessed. NQO1-/- mice showed increased blood urea nitrogen and creatinine levels, tubular damage, oxidative stress, and apoptosis. In accordance with these results, the cellular NADPH/NADP ratio and NOX activity were markedly increased in the kidneys of NQO1-/- mice compared to NQO1+/+ mice. In addition, activation of NQO1 by ?L treatment significantly improved renal dysfunction and reduced tubular cell damage, oxidative stress, and apoptosis. This study demonstrates that NQO1 protects cells against renal failure induced by cisplatin, and that this effect is mediated by decreased NOX activity via cellular NADPH/NADP modulation. These results provide convincing evidence that NQO1 might be beneficial for ameliorating renal failure induced by cisplatin.
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Distinct Mechanisms of DNA Sensing Based on N-Doped Carbon Nanotubes with Enhanced Conductance and Chemical Selectivity.
Small
PUBLISHED: 04-22-2013
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N-doped capped carbon nanotube (CNT) electrodes applied to DNA sequencing are studied by first-principles calculations. For the face-on nucleobase junction configurations, a conventional conductance ordering is obtained where the largest signal results from guanine according to its high highest occupied molecular orbital (HOMO) level, whereas for the edge-on counterparts a distinct conductance ordering is observed where the low-HOMO thymine provides the largest signal. The edge-on mode is shown to operate based on a novel molecular sensing mechanism that reflects the chemical connectivity between N-doped CNT caps that can act both as electron donors and electron acceptors and DNA functional groups that include the hyperconjugated thymine methyl group.
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Scoparone inhibits adipocyte differentiation through down-regulation of peroxisome proliferators-activated receptor ? in 3T3-L1 preadipocytes.
Food Chem
PUBLISHED: 04-07-2013
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This study was performed to investigate the effect of scoparone on the differentiation of 3T3-L1 preadipocytes. Scoparone inhibited triglyceride (TG) accumulation in the mature adipocytes, evidenced by Oil-red O staining and intracellular quantification. Real time-PCR analysis showed that scoparone significantly down-regulated the mRNA expression of key adipogenic transcription factors, PPAR?, C/EBP?, compared with mature adipocytes. Scoparone appeared to reduce mRNA expression of SREBP1c and FAS being related to the late stage of adipogenesis. Furthermore, aP2 and CD36/FAT, as adipocyte-specific genes, were decreased in mature adipocytes by scoparone treatment. Moreover, scoparone inhibited the up-regulated expression of PPAR? target genes by rosiglitazone to near that observed in cells treated with GW9662. The luciferase assay revealed that scoparone negatively regulates the transcriptional activity of PPAR?. Chromatin immunoprecipitation assay also showed that participation of scoparone in the regulation of PPAR?. Collectively, scoparone has a PPAR? antagonic effect and suppresses differentiation through down-regulation of adipogenic genes by PPAR? inhibition in 3T3-L1 preadipocytes.
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Cardiac tamponade complicated by acupuncture: hemopericardium due to shredded coronary artery injury.
Yonsei Med. J.
PUBLISHED: 04-04-2013
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We report a case of 62-year-old man with cardiac tamponade due to coronary artery injury after acupuncture into the substernum. After resuscitation of cardiac arrest, we performed emergent pericardiocentesis. Nevertheless, the cardiac arrest recurred, and the emergent operation on cardiopulmonary bypass was performed. We identified hemopericardium due to shredded acute marginal branch of right coronary artery, and it was ligated leading to termination of bleeding. The patient was discharged without any other complications.
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The orphan nuclear receptor small heterodimer partner negatively regulates pancreatic beta cell survival and hyperglycemia in multiple low-dose streptozotocin-induced type 1 diabetic mice.
Int. J. Biochem. Cell Biol.
PUBLISHED: 03-27-2013
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The small heterodimer partner (SHP; NR0B2) regulates the transcription of a variety of target genes and controls a variety of physiological functions in various tissues. However, the role of SHP in beta cell has not been fully determined yet. We used SHP knockout (SHP KO) mice to investigate the role of SHP in multiple low-dose streptozotocin (MLDS)-induced diabetes. Blood glucose and insulin levels were measured until 20 days, and intraperitoneal glucose tolerance and glucose-stimulated insulin secretion tests were performed. The expression of apoptotic genes and beta cell markers were detected by quantitative realtime-polymerase chain reaction, immunostaining and western blot analysis. SHP KO mice showed significantly lower blood glucose, higher insulin levels, and enhanced glucose tolerance compared with wild type (WT) mice after MLDS treatment. Moreover, beta cell mass and pancreatic insulin content were remarkably increased in SHP KO mice. In the response to glucose stimulation, islets of SHP KO showed increased insulin secretion via up-regulation of beta cell enriched transcription factors compared to WT mice after streptozotocin (STZ) treatment. In quantification for beta cell apoptosis at day 1 post STZ treatment, the SHP KO mice showed significantly increased anti-apoptotic gene expression and decreased release of apoptotic markers cytochrome c, smac/diablo, and only a few apoptotic beta cells were found in SHP KO pancreas through inactivation of caspase-3, compared to those of WT. These data demonstrate that SHP deficiency ameliorates hyperglycemia and preserves islet function by inhibiting apoptosis of pancreatic beta cells and up-regulating of their enriched transcriptional factors.
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In vivo imaging of islet transplantation using PLGA nanoparticles containing iron oxide and indocyanine green.
Magn Reson Med
PUBLISHED: 03-22-2013
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PURPOSE: We determined whether poly(lactic-co-glycolic acid) nanoparticles would be a useful reagent for the successful monitoring of isolated islets by magnetic resonance imaging and optical imaging systems, without clinically relevant toxicity in vitro or in vivo. METHODS: We used iron oxide for MR imaging and a cyanide dye approved by the Food and Drug Administration (indocyanine green) for optical imaging and estimated the in vivo detection of transplanted pancreatic islets. RESULTS: The poly(lactic-co-glycolic acid) nanoparticles were associated with the islets in vitro and were successfully detected by 4.7 T (MR) and optical imaging, without other toxic effects. When labeled islets were transplanted under the mouse kidney capsule, in vivo T2 / T2*-weighted scans with 4.7 T MR detected as few as 300 labeled islets by 4 weeks. Optical in vivo imaging revealed indocyanine green fluorescence by 2 and 4 days after transplantation of islets containing 250 and 500 µg/mL poly(lactic-co-glycolic acid) nanoparticles, respectively. These results were further supported by the immunohistochemical results for insulin and iron in the recipient mouse kidney and pancreas. CONCLUSIONS: Taken together, these data indicate that poly(lactic-co-glycolic acid) nanoparticles may be used to label transplanted islets and may be imaged with in vivo MR and optical imaging systems. Magn Reson Med, 2013. © 2013 Wiley Periodicals, Inc.
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Davallialactone protects against acetaminophen overdose-induced liver injuries in mice.
Food Chem. Toxicol.
PUBLISHED: 03-14-2013
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Oxidative stress is closely associated with acetaminophen (APAP)-induced toxicity. Davallialactone (DAVA), a hispidin analog derived from the mushroom Inonotus xeranticus, has antioxidant properties. This study evaluated whether DAVA plays protective roles against APAP hepatotoxicity in mice. Pretreatments with DAVA (10 mg/kg) prior to exposures of mice to a hepatotoxic dose of 600 mg/kg APAP significantly increased survival rate compared to APAP alone. To verify this effect, mice were treated with 400 mg/kg APAP 30 min after DAVA administration and were then sacrificed after 0.5, 1, 3, and 6 h. APAP alone caused severe liver injuries as characterized by increased plasma GOT and GPT levels, ATP and GSH depletion, and peroxynitrite and 4-HNE formations. These liver damages induced by APAP were significantly attenuated by DAVA pretreatments. The GSH/GSSG ratio nearly recovered to the levels observed in non-APAP-treated mice at 6h after APAP treatment in DAVA-pretreated mice. Furthermore, while hepatic ROS levels were increased by APAP exposures, pretreatments with DAVA completely blocked ROS formation. In addition, APAP-induced sustained activations of JNK and ERK were remarkably reduced by DAVA pretreatment. In conclusion, these results suggest that DAVA plays protective roles against APAP-mediated hepatotoxicity through function as ROS scavenger.
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Benefit of systematic segmentectomy of the hepatocellular carcinoma: revisiting the dye injection method for various portal vein branches.
Ann. Surg.
PUBLISHED: 03-13-2013
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Systematic segmentectomy is useful in treating small hepatocellular carcinoma in the cirrhotic liver. However, accomplishment of an exact systematic segmentectomy still remains a challenging procedure because of the variable anatomy of portal branches. We evaluated the usefulness of the dye injection method for systematic segmentectomy, which focuses on the various patterns of portal vein (PV) branches feeding the tumor.
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Risk factors influencing rebleeding after bronchial artery embolization on the management of hemoptysis associated with pulmonary tuberculosis.
Tuberc Respir Dis (Seoul)
PUBLISHED: 02-26-2013
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Hemoptysis due to pulmonary tuberculosis (TB) frequently develops in Korea where the prevalence of TB is intermediate. The effect of bronchial artery embolization (BAE) on the control of massive hemoptysis has been well known. This study is designed to identify the risk factors contributing to rebleeding after BAE in patients with TB.
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Characteristic analysis of aspheric quasi-optical lens antenna in millimeter-wave radiometer imaging system.
Appl Opt
PUBLISHED: 02-26-2013
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Quasi-optical imaging systems require low blurring effect and large depth of focus (DOF) to get an acceptable sharpness of the image. To reduce aberration-limited blurring, the aspheric convex plano lenses with an aperture diameter of 350 mm are designed in W-band. We analyzed theoretically and experimentally the millimeter-wave band lens characteristics, such as beam spot size, spatial resolution (SR), and DOF, via f-number. It is first used to verify the DOF through f-number in the system-level test with the developed W-band radiometer imaging system. We have confirmed that the larger f-number of quasi-optical lens leads to a larger DOF but a lower SR.
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Increased vulnerability to ?-cell destruction and diabetes in mice lacking NAD(P)H:quinone oxidoreductase 1.
Toxicol. Lett.
PUBLISHED: 02-19-2013
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NAD(P)H:quinone oxidoreductase 1 (NQO1) has been known to protect cells against stressors, including the diabetogenic reagent streptozotocin (STZ). The present study demonstrated that NQO1 deficiency resulted in increased pancreatic ?-cell death induced by multiple low dose of STZ (MLDS) injections. NQO1 knockout (KO) mice showed hyperglycemia, body weight loss, impaired glucose clearance rate and a lower plasma insulin level after MLDS treatment. Moreover, ?-cell mass and pancreatic insulin content were significantly lower in KO mice than in wild-type (WT) mice after MLDS treatment. Five days after the first STZ treatment, the islets of KO mice had substantially more TUNEL-positive ?-cells than those of WT mice, but there was no difference in the regeneration of ?-cells between KO mice and WT mice. At the same time, MLDS-treated KO mice showed significantly increased apoptotic markers in ?-cells, including cleaved caspase 3, Smac/DIABLO and AIF (apoptosis inducing factor) in the cytoplasm. These results suggest that mice deficient in NQO1 are vulnerable to MLDS-induced ?-cell destruction and diabetes, caused by increase of ?-cell apoptosis in pancreas.
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Relationship between hospital volume and risk-adjusted mortality rate following percutaneous coronary intervention in Korea, 2003 to 2004.
Anadolu Kardiyol Derg
PUBLISHED: 02-06-2013
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There have been a large number of studies that have investigated the relationship between outcomes and provider volume for a wide variety of medical conditions and surgical conditions. The objective of this study was to explore the relation between hospital volume and risk-adjusted mortality following percutaneous coronary intervention between 2003 and 2004 in Korea.
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Glyceollin improves endoplasmic reticulum stress-induced insulin resistance through CaMKK-AMPK pathway in L6 myotubes.
J. Nutr. Biochem.
PUBLISHED: 01-11-2013
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Glyceollin has been shown to have antidiabetic properties, although its molecular mechanism is not known. Here, we have investigated the metabolic effects of glyceollin in animal models of insulin resistance and in endoplasmic reticulum (ER) stress-responsive muscle cells. db/db mice were treated with glyceollin for 4weeks and triglycerides, total cholesterol, low-density lipoprotein (LDL) and high-density lipoprotein (HDL) levels were measured. Glyceollin reduced serum insulin and triglycerides and increased HDL levels in db/db mice. Furthermore, glyceollin caused a significant improvement in glucose homeostasis without altering body weight and food intake in db/db mice. In muscle cells, glyceollin increased the activity of AMP-activated protein kinase (AMPK) as well as cellular glucose uptake. Fatty acid oxidation was also increased. In parallel, phosphorylation of acetyl-CoA carboxylase (ACC) at Ser-79 was increased, consistent with decreased ACC activity. An insulin-resistant state was induced by exposing cells to 5?g/ml of tunicamycin as indicated by decreased insulin-mediated tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) and glucose uptake. Inhibition of insulin-mediated tyrosine phosphorylation of IRS-1 and glucose uptake under ER stress was prevented by glyceollin. Strikingly, glyceollin reduced ER stress-induced, c-Jun NH2-terminal kinase activation and subsequently increased insulin signaling via stimulation of AMPK activity in L6 myotubes. Pharmacologic inhibition or knockdown of Ca(2+)/calmodulin-dependent protein kinase kinase blocked glyceollin-increased AMPK phosphorylation and insulin sensitivity under ER stress conditions. Taken together, these results indicate that glyceollin-mediated enhancement of insulin sensitivity under ER stress conditions is predominantly accomplished by activating AMPK, thereby having beneficial effects on hyperglycemia and insulin resistance.
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Overexpression of apolipoprotein A1 in the lung abrogates fibrosis in experimental silicosis.
PLoS ONE
PUBLISHED: 01-02-2013
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The inhalation of silica particles induces silicosis, an inflammatory and fibrotic lung disease characterized by the early accumulation of macrophages and neutrophils in the airspace and subsequent appearance of silicotic nodules as a result of progressive fibrosis. This study evaluated whether apolipoprotein A1 (ApoA1) protects against ongoing fibrosis and promotes the resolution of established experimental lung silicosis. Crystallized silica was intratracheally administered to 6- to 8-week-old transgenic mice expressing human ApoA1 in their alveolar epithelial cells (day 0). ApoA1 was overexpressed beginning on day 7 (ApoA1_D7 group) or day 15 (ApoA1_D15 group). The mice were sacrificed on day 30 for an evaluation of lung histology; the measurement of collagen, transforming growth factor-b1 and lipoxin A4; and a TUNEL assay for apoptotic cells. The ApoA1_D7 and D15 groups showed significant reductions in the silica-induced increase in inflammatory cells, silicotic nodule area, and collagen deposition compared with the silica-treated ApoA1 non-overexpressing mice. The level of transforming growth factor-b1 decreased in the bronchoalveolar lavage fluid, whereas lipoxin A4 was increased in the ApoA1_D7 and D15 groups compared with the silica-treated ApoA1 non-overexpressing mice. The silica-induced increase in the number of apoptotic cells was significantly reduced in the lungs of mice overexpressing ApoA1. Overexpression of ApoA1 decreased silica-induced lung inflammation and fibrotic nodule formation. The restoration of lipoxin A4 may contribute to the protective effect of ApoA1 overexpression against silica-induced lung fibrosis.
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A genome-wide association study of total serum and mite-specific IgEs in asthma patients.
PLoS ONE
PUBLISHED: 01-01-2013
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Immunoglobulin E (IgE) is one of the central players in asthma and allergic diseases. Although the serum IgE level, a useful endophenotype, is generally increased in patients with asthma, genetic factors influencing IgE regulation in asthma are still not fully understood. To identify the genetic variations associated with total serum and mite-specific IgEs in asthmatics, a genome-wide association study (GWAS) of 657,366 single nucleotide polymorphisms (SNPs) was performed in 877 Korean asthmatics. This study found that several new genes might be associated with total IgE in asthmatics, such as CRIM1 (rs848512, P?=?1.18×10(-6); rs711254, P?=?6.73×10(-6)), ZNF71 (rs10404342, P?=?7.60×10(-6)), TLN1 (rs4879926, P?=?7.74×10(-6)), and SYNPO2 (rs1472066, P?=?8.36×10(-6); rs1038770, P?=?8.66×10(-6)). Regarding the association of specific IgE to house dust mites, it was observed that intergenic SNPs nearby to OPRK1 and LOC730217 might be associated with Dermatophagoides pteronyssinus (D.p.) and Dermatophagoides farinae (D.f.) in asthmatics, respectively. In further pathway analysis, the phosphatidylinositol signaling system and adherens junction pathways were estimated to play a role in the regulation of total IgE levels in asthma. Although functional evaluations and replications of these results in other populations are needed, this GWAS of serum IgE in asthmatics could facilitate improved understanding of the role of the newly identified genetic variants in asthma and its related phenotypes.
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Hepatic cannabinoid receptor type 1 mediates alcohol-induced regulation of bile acid enzyme genes expression via CREBH.
PLoS ONE
PUBLISHED: 01-01-2013
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Bile acids concentration in liver is tightly regulated to prevent cell damage. Previous studies have demonstrated that deregulation of bile acid homeostasis can lead to cholestatic liver disease. Recently, we have shown that ER-bound transcription factor Crebh is a downstream effector of hepatic Cb1r signaling pathway. In this study, we have investigated the effect of alcohol exposure on hepatic bile acid homeostasis and elucidated the mediatory roles of Cb1r and Crebh in this process. We found that alcohol exposure or Cb1r-agonist 2-AG treatment increases hepatic bile acid synthesis and serum ALT, AST levels in vivo alongwith significant increase in Crebh gene expression and activation. Alcohol exposure activated Cb1r, Crebh, and perturbed bile acid homeostasis. Overexpression of Crebh increased the expression of key bile acid synthesis enzyme genes via direct binding of Crebh to their promoters, whereas Cb1r knockout and Crebh-knockdown mice were protected against alcohol-induced perturbation of bile acid homeostasis. Interestingly, insulin treatment protected against Cb1r-mediated Crebh-induced disruption of bile acid homeostasis. Furthermore, Crebh expression and activation was found to be markedly increased in insulin resistance conditions and Crebh knockdown in diabetic mice model (db/db) significantly reversed alcohol-induced disruption of bile acid homeostasis. Overall, our study demonstrates a novel regulatory mechanism of hepatic bile acid metabolism by alcohol via Cb1r-mediated activation of Crebh, and suggests that targeting Crebh can be of therapeutic potential in ameliorating alcohol-induced perturbation of bile acid homeostasis.
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Diet-induced obesity dramatically reduces the efficacy of a 2009 pandemic H1N1 vaccine in a mouse model.
J. Infect. Dis.
PUBLISHED: 12-05-2011
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Obesity, a risk factor for increased severity of diverse diseases, is believed to have negative impact on vaccine efficacy. Recently, mortality has emerged as an outcome of pandemic influenza A virus subtype H1N1, necessitating development of effective vaccine strategies. Here we investigated effects of diet-induced obesity on vaccine-induced immune responses and protective efficacy against pandemic H1N1 influenza virus.
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Relationship between group-specific component protein and the development of asthma.
Am. J. Respir. Crit. Care Med.
PUBLISHED: 11-09-2011
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Airway inflammation and remodeling during asthma are attributed to the altered expression of biologically relevant proteins.
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Generation of human induced pluripotent stem cells from osteoarthritis patient-derived synovial cells.
Arthritis Rheum.
PUBLISHED: 09-29-2011
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This study was undertaken to generate and characterize human induced pluripotent stem cells (PSCs) from patients with osteoarthritis (OA) and to examine whether these cells can be developed into disease-relevant cell types for use in disease modeling and drug discovery.
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Controlled deposition of a high-performance small-molecule organic single-crystal transistor array by direct ink-jet printing.
Adv. Mater. Weinheim
PUBLISHED: 08-08-2011
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Ink-jet printed small-molecule organic single-crystal transistors are realized by using selective surface energy modification, precise control of volume density of ink droplets on spatially patterned areas, and a co-solvent system to control solvent evaporation properties. The single-crystal formation in bottom-contact-structured transistors via direct printing is expected to permit high-density array fabrication in large-area electronics.
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Antiatherogenic effect of antioxidant polyphenols from Phellinus baumii in apolipoprotein E-deficient mice.
Ann. Nutr. Metab.
PUBLISHED: 07-17-2011
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The present study was carried out to investigate the antiatherosclerotic effect of antioxidant polyphenols from Phellinus baumii (PBE) in apolipoprotein E-deficient (apoE-/-) mice.
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Cannabinoid receptor type 1 (CB1R) signaling regulates hepatic gluconeogenesis via induction of endoplasmic reticulum-bound transcription factor cAMP-responsive element-binding protein H (CREBH) in primary hepatocytes.
J. Biol. Chem.
PUBLISHED: 06-21-2011
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Activated cannabinoid 1 receptor (CB1R) signaling has been implicated in the development of phenotypes associated with fatty liver, insulin resistance, and impaired suppression of hepatic glucose output. Endoplasmic reticulum stress-associated liver-specific transcription factor CREBH is emerging as a critical player in various hepatic metabolic pathways and regulates hepatic gluconeogenesis in diet-induced obese settings. In this study, we elucidated the critical role of CREBH in mediating CB1R signaling to regulate glucose homeostasis in primary rat and human hepatocytes. mRNA and protein levels and glucose production were analyzed in primary rat and human hepatocytes. ChIP assays were performed together with various transcriptional analyses using standard techniques. CB1R activation by 2-arachidonoylglycerol (2-AG) specifically induced CREBH gene expression via phosphorylation of the JNK signaling pathway and c-Jun binding to the AP-1 binding site in the CREBH gene promoter. 2-AG treatment significantly induced hepatic gluconeogenic gene expression and glucose production in primary hepatocytes, and we demonstrated that the CREBH binding site mutant significantly attenuated 2-AG-mediated activation of the gluconeogenic gene promoter. Endogenous knockdown of CREBH led to ablation of 2-AG-induced gluconeogenic gene expression and glucose production, and the CB1R antagonist AM251 or insulin exhibited repression of CREBH gene induction and subsequently inhibited gluconeogenesis in both rat and human primary hepatocytes. These results demonstrate a novel mechanism of action of activated CB1R signaling to induce hepatic gluconeogenesis via direct activation of CREBH, thereby contributing to a better understanding of the endocannabinoid signaling mechanism involved in regulating the hepatic glucose metabolism.
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Prevention of salt-induced renal injury by activation of NAD(P)H:quinone oxidoreductase 1, associated with NADPH oxidase.
Free Radic. Biol. Med.
PUBLISHED: 05-31-2011
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NADPH oxidase (NOX) is a predominant source of reactive oxygen species (ROS), and the activity of NOX, which uses NADPH as a common rate-limiting substrate, is upregulated by prolonged dietary salt intake. ?-Lapachone (?L), a well-known substrate of NAD(P)H:quinone oxidoreductase 1 (NQO1), decreases the cellular NAD(P)H/NAD(P)(+) ratio via activation of NQO1. In this study, we evaluated whether NQO1 activation by ?L modulates salt-induced renal injury associated with NOX-derived ROS regulation in an animal model. Dahl salt-sensitive (DS) rats fed a high-salt (HS) diet were used to investigate the renoprotective effect of NQO1 activation. ?L treatment significantly lowered the cellular NAD(P)H:NAD(P)(+) ratio and dramatically reduced NOX activity in the kidneys of HS diet-fed DS rats. In accordance with this, total ROS production and expression of oxidative adducts also decreased in the ?L-treated group. Furthermore, HS diet-induced proteinuria and glomerular damage were markedly suppressed, and inflammation, fibrosis, and apoptotic cell death were significantly diminished by ?L treatment. This study is the first to demonstrate that activation of NQO1 has a renoprotective effect that is mediated by NOX activity via modulation of the cellular NAD(P)H:NAD(P)(+) ratio. These results provide strong evidence that NQO1 might be a new therapeutic target for the prevention of salt-induced renal injury.
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Association of FANCC polymorphisms with FEV1 decline in aspirin exacerbated respiratory disease.
Mol. Biol. Rep.
PUBLISHED: 05-28-2011
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Aspirin exacerbated respiratory disease (AERD) is a clinical condition characterized by severe decline in forced expiratory volume in one second (FEV1) following the ingestion of non-steroidal anti-inflammatory drugs (NSAIDs), including aspirin. The exacerbated inflammatory response in Fancc-deficient mice has been reported to be associated with hemopoietic responses that are also related to AERD pathogenesis. To investigate associations of FANCC polymorphisms with AERD and related phenotypes, this study genotyped 25 common single nucleotide polymorphisms (SNPs) in a total of 592 Korean asthmatics including 163 AERD and 429 aspirin-tolerant asthma (ATA) subjects. Logistic analysis revealed that genetic polymorphisms of the FANCC gene might not be directly related to AERD development and nasal polyposis (P > 0.05). However, the FEV1 decline by aspirin provocation showed significant associations with FANCC polymorphisms (P = 0.006-0.04) and a haplotype (unique to rs4647416G > A, P = 0.01 under co-dominant, P = 0.006 under recessive model). In silico analysis showed that the "A" allele of rs4647376C > A, which was more prevalent in AERD than in ATA, could act as a potential branch point (BP) site for alternative splicing (BP score = 4.16). Although replications in independent cohorts and further functional evaluations are still needed, our preliminary findings suggest that FANCC polymorphisms might be associated with the obstructive symptoms in allergic diseases.
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Multidetector computed tomography (MDCT) images with soft tissue and bone algorithm reconstruction in head and facial trauma.
J Clin Neurosci
PUBLISHED: 05-10-2011
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We aimed to evaluate the usefulness of multidetector CT (MDCT) scan images with soft tissue and bone algorithm reconstruction in nine patients for investigation of head and facial trauma. We compared these MDCT scans with the conventional brain CT scans and facial bone CT scans of eight patients with head and facial trauma. The overall radiation dose did not differ significantly between the two groups (Mann-Whitney test, p=0.370) but the MDCT scans with soft tissue and bone algorithm reconstruction avoided overlapping scan range radiation exposure, especially to the eye and lower half of the brain.
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Genes associated with recurrence of hepatocellular carcinoma: integrated analysis by gene expression and methylation profiling.
J. Korean Med. Sci.
PUBLISHED: 04-23-2011
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Gene expression is suppressed by DNA methylation. The goal of this study was to identify genes whose CpG site methylation and mRNA expression are associated with recurrence after surgical resection for hepatocellular carcinoma (HCC). Sixty-two HCCs were examined by both whole genome DNA methylation and transcriptome analysis. The Cox model was used to select genes associated with recurrence. A validation was performed in an independent cohort of 66 HCC patients. Among fifty-nine common genes, increased CpG site methylation and decreased mRNA expression were associated with recurrence for 12 genes (Group A), whereas decreased CpG site methylation and increased mRNA expression were associated with recurrence for 25 genes (Group B). The remaining 22 genes were defined as Group C. Complement factor H (CFH) and myosin VIIA and Rab interacting protein (MYRIP) in Group A; proline/serine-rich coiled-coil 1 (PSRC1), meiotic recombination 11 homolog A (MRE11A), and myosin IE (MYO1E) in Group B; and autophagy-related protein LC3 A (MAP1LC3A), and NADH dehydrogenase 1 alpha subcomplex assembly factor 1 (NDUFAF1) in Group C were validated. In conclusion, potential tumor suppressor (CFH, MYRIP) and oncogenes (PSRC1, MRE11A, MYO1E) in HCC are reported. The regulation of individual genes by methylation in hepatocarcinogenesis needs to be validated.
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Activation of NAD(P)H:quinone oxidoreductase ameliorates spontaneous hypertension in an animal model via modulation of eNOS activity.
Cardiovasc. Res.
PUBLISHED: 04-18-2011
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Hypertension is one of the most common human diseases worldwide, and extensive research efforts are focused upon the identification and utilizing of novel therapeutic drug targets. Nitric oxide (NO) produced by endothelial NO synthase (eNOS) is an important regulator of blood pressure (BP). ?-Lapachone (?L), a well-known substrate of NAD(P)H:quinone oxidoreductase (NQO1), increases the cellular NAD(+)/NADH ratio via the activation of NQO1. In this study, we evaluated whether ?L-induced activation of NQO1 modulates BP in an animal model of hypertension.
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Association analysis of thromboxane A synthase 1 gene polymorphisms with aspirin intolerance in asthmatic patients.
Pharmacogenomics
PUBLISHED: 04-01-2011
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Thromboxane A synthase (TBXAS1) converts prostaglandin H to thromboxane A, a potent constrictor of smooth respiratory muscle. Thus, functional alterations of the TBXAS1 gene may contribute to aspirin-intolerant asthma (AIA).
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Hepatoprotective effect of Platycodon grandiflorum against chronic ethanol-induced oxidative stress in C57BL/6 mice.
Ann. Nutr. Metab.
PUBLISHED: 03-25-2011
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This study was carried out to evaluate the hepatoprotective effect of Platycodon grandiflorum (PG) in ethanol (EtOH)-induced liver damage.
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A Phellinus baumii extract reduces obesity in high-fat diet-fed mice and absorption of triglyceride in lipid-loaded mice.
J Med Food
PUBLISHED: 02-22-2011
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This study evaluated the anti-obesity effects of Phellinus baumii extract (PBE) in high-fat diet (HFD)-fed mice. Male 8-week-old C57BL/6 mice were randomly divided into four groups: control, normal chow diet plus vehicle; HFD-control, high-fat plus vehicle; HFD plus orlistat (Xenical(®), Roche, Basel, Switzerland) (50?mg/kg); and HFD plus PBE (500?mg/kg). PBE was administered daily by oral gavage for 12 weeks. Oral administration of PBE (500?mg/kg) significantly reduced body weight gain, hepatic lipid concentrations, and fat accumulation in epididymal adipocytes compared with mice fed HFD alone (P?
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Prevalence of electrocardiographic findings suggestive of sudden cardiac death risk in 10,867 apparently healthy young Korean men.
Pacing Clin Electrophysiol
PUBLISHED: 02-17-2011
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The objective of this study was to determine the prevalence of electrocardiographic (ECG) findings suggestive of sudden cardiac death risk in apparently healthy young Korean men.
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The association of a single-nucleotide polymorphism of the IL-2 inducible T-cell Kinase gene with asthma.
Ann. Hum. Genet.
PUBLISHED: 02-15-2011
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Asthma manifests as TH2-dominant airway inflammation regulated by inducible T-cell kinase (ITK). To investigate associations between genetic variants of the ITK gene and asthma, 31 single-nucleotide polymorphisms (SNPs) were genotyped in 303 normal controls and 498 asthmatics and the two groups were compared using logistic regression models. The functional effects of the ITK promoter SNP were assessed using pGL3 luciferase reporter systems and gel-shift assays. The minor allele-196C>T in the promoter region of the ITK gene was significantly more frequent in asthmatics than in controls. The luciferase activity of the PGL3-ITK-196T allele construct was higher than that of the -196C allele. In the gel-shift assay, -196T double-stranded oligonucleotides bound more strongly to Jurkat cell nuclear protein compared to the -196C double-stranded oligonucleotides. People with the -rare allele 196C>T may be more susceptible to asthma via transcriptional regulation of the ITK gene.
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Protective Effect of Korean Red Ginseng against Aflatoxin B1-Induced Hepatotoxicity in Rat.
J Ginseng Res
PUBLISHED: 01-19-2011
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Korean red ginseng (KRG), the steamed root of Panax ginseng Meyer, has a variety of biological properties, including anti-inflammatory, antioxidant and anticancer effects. Aflatoxin B1 (AFB1) produced by the Aspergillus spp. causes acute hepatotoxicity by lipid peroxidation and oxidative DNA damage, and induces liver carcinoma in humans and laboratory animals. This study was performed to examine the protective effects of KRG against hepatotoxicity induced by AFB1 using liver-specific serum marker analysis, histopathology, and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling. In addition, to elucidate the possible mechanism of hepatoprotective effects, superoxide dismutase, catalase, glutathione peroxidase, and malondialdehyde were analyzed. Rats were treated with 250 mg/kg of KRG (KRG group) or saline (AFB1 group) for 4 weeks and then received 150 ?g/kg of AFB1 intraperitoneally for 3 days. Rats were sacrificed at 12 h, 24 h, 48 h, 72 h, or 1 wk after AFB1 treatment. In the KRG pre-treatment group, serum alanine aminotransferase, aspartate aminotransferase, and malondialdehyde levels were low, but superoxide dismutase, catalase, and glutathione peroxidase activities were high as compared to the AFB1 alone group. Histopathologically, AFB1 treatment induced necrosis and apoptosis in hepatocytes, and led to inflammatory cells infiltration in the liver. KRG pre-treatment ameliorated these changes. These results indicate that KRG may have protective effects against hepatotoxicity induced by AFB1 that involve the antioxidant properties of KRG.
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Hepatoprotective effects of chestnut (Castanea crenata) inner shell extract against chronic ethanol-induced oxidative stress in C57BL/6 mice.
Food Chem. Toxicol.
PUBLISHED: 01-03-2011
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This study was carried out to evaluate the protective effects of chestnut inner shell extract (CISE) on chronic ethanol-induced oxidative stress in liver. Mice were fed a control liquid diet (Normal-control), liquid diet containing ethanol alone (EtOH+Vehicle), or were administered CISE and ethanol (EtOH+CISE) for 6 weeks. Administration of ethanol induced liver damage with significant increase of plasma GOT, GPT, hepatic triglyceride (TG) and thiobarbituric acid reactive substance (TBARS) levels. By contrast, co-treatment of CISE with ethanol significantly decreased the activities of GOT and GPT in the plasma, and hepatic TG and TBARS levels. Histological observations were consistent with the result obtained from hepatic lipid quantification. Moreover, CISE treatment with ethanol decreased CYP2E1 expression and increased activities of catalase and superoxide dismutase, which were significantly inhibited by treatment with ethanol alone. To determine the active compound of CISE, fractionation of CISE was conducted and scoparone and scopoletin were identified as main compounds. These compounds were also shown to inhibit the ethanol-induced reduction in antioxidant enzyme activity in an in vitro model system. These results suggest that CISE has protective effects against ethanol-induced oxidative damage, possibly by inhibition of lipid accumulation, peroxidation and increase of antioxidant defense system in the liver.
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Putative association of SMAPIL polymorphisms with risk of aspirin intolerance in asthmatics.
J Asthma
PUBLISHED: 09-14-2010
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Aspirin-intolerant asthma (AIA), as a clinical syndrome caused by aspirin, is characterized by lung inflammation and reversible bronchoconstriction. Recently, the altered trafficking and diminished airway reactivity have been implicated in allergic airway remodeling. The stromal membrane-associated protein 1-like (SMAP1L) exerts common and distinct functions in vesicle trafficking including endocytosis. The disturbance of pulmonary surfactant synthesis has been elucidated to be associated with asthma experimentally. Moreover, in alveolar type II (ATII) cells that synthesize pulmonary surfactant, alterations of clathrin-dependent endocytosis cause disturbance at the surfactant function, suggesting that SMAP1L, which directly interacts with clathrin, could be associated with asthma and related phenotypes.
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AMPK-dependent repression of hepatic gluconeogenesis via disruption of CREB.CRTC2 complex by orphan nuclear receptor small heterodimer partner.
J. Biol. Chem.
PUBLISHED: 08-05-2010
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Orphan nuclear receptor small heterodimer partner (SHP) plays a key role in transcriptional repression of gluconeogenic enzyme gene expression. Here, we show that SHP inhibited protein kinase A-mediated transcriptional activity of cAMP-response element-binding protein (CREB), a major regulator of glucose metabolism, to modulate hepatic gluconeogenic gene expression. Deletion analysis of phosphoenolpyruvate carboxykinase (PEPCK) promoter demonstrated that SHP inhibited forskolin-mediated induction of PEPCK gene transcription via inhibition of CREB transcriptional activity. In vivo imaging demonstrated that SHP inhibited CREB-regulated transcription coactivator 2 (CRTC2)-mediated cAMP-response element-driven promoter activity. Furthermore, overexpression of SHP using adenovirus SHP decreased CRTC2-dependent elevations in blood glucose levels and PEPCK or glucose-6-phosphatase (G6Pase) expression in mice. SHP and CREB physically interacted and were co-localized in vivo. Importantly, SHP inhibited both wild type CRTC2 and S171A (constitutively active form of CRTC2) coactivator activity and disrupted CRTC2 recruitment on the PEPCK gene promoter. In addition, metformin or overexpression of a constitutively active form of AMPK (Ad-CA-AMPK) inhibited S171A-mediated PEPCK and G6Pase gene expression, and hepatic glucose production and knockdown of SHP partially relieved the metformin- and Ad-CA-AMPK-mediated repression of hepatic gluconeogenic enzyme gene expression in primary rat hepatocytes. In conclusion, our results suggest that a delayed effect of metformin-mediated induction of SHP gene expression inhibits CREB-dependent hepatic gluconeogenesis.
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Inhibitory effect of glyceollin isolated from soybean against melanogenesis in B16 melanoma cells.
BMB Rep
PUBLISHED: 07-29-2010
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Natural products with non-toxic and environmentally friendly properties are good resources for skin-whitening cosmetic agents when compared to artificial synthetic chemicals. Here, we investigated the effect of glyceollin produced to induce disease resistance responses of soybean to specific races of an incompatible pathogen, phytophthora sojae, on melanogenesis and discussed their mechanisms in melanin biosynthesis. We found that glyceollin inhibits melanin synthesis and tyrosinase activity in B16 melanoma cells without cytotoxicity. To elucidate the mechanism of the effect of glyceollin on melanogenesis, we conducted western blot analysis for melanogenic enzymes such as tyrosinase, tyrosinase-related protein-1 (TRP-1), and TRP-2. Glyceollin inhibited tyrosinase and TRP-1 protein expression. Additionally, glyceollin effectively inhibited intracellular cAMP levels in B16 melanoma cells stimulated by alpha-melanocyte stimulating hormone (alpha-MSH). These results suggest that the whitening activity of glyceollin may be due to the inhibition of cAMP involved in the signal pathway of alpha-MSH in B16 melanoma cells.
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JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

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