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A/H1N1 antibodies and TRIB2 autoantibodies in narcolepsy patients diagnosed in conjunction with the Pandemrix vaccination campaign in Sweden 2009-2010.

https://arctichealth.org/en/permalink/ahliterature259020
Source
J Autoimmun. 2014 May;50:99-106
Publication Type
Article
Date
May-2014
Author
Alexander Lind
Anita Ramelius
Tomas Olsson
Lisen Arnheim-Dahlström
Favelle Lamb
Mohsen Khademi
Aditya Ambati
Markus Maeurer
Anna-Lena Nilsson
Izaura Lima Bomfim
Katharina Fink
Åke Lernmark
Source
J Autoimmun. 2014 May;50:99-106
Date
May-2014
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Antibodies, Viral - blood
Autoantibodies - blood
Child
Child, Preschool
Female
Gene Expression
Glutamate Decarboxylase - antagonists & inhibitors - genetics - immunology
HLA-DQ beta-Chains - genetics - immunology
Humans
Influenza A Virus, H1N1 Subtype - immunology
Influenza Vaccines - adverse effects - immunology
Influenza, Human - immunology - prevention & control
Intracellular Signaling Peptides and Proteins - antagonists & inhibitors - genetics - immunology
Male
Middle Aged
Narcolepsy - chemically induced - diagnosis - genetics - immunology
Pandemics - prevention & control
Sweden
Vaccination - adverse effects
Abstract
Narcolepsy is a lifelong sleep disorder related to hypocretin deficiency resulting from a specific loss of hypocretin-producing neurons in the lateral hypothalamic area. The disease is thought to be autoimmune due to a strong association with HLA-DQB1*06:02. In 2009 the World Health Organization (WHO) declared the H1N1 2009 flu pandemic (A/H1N1PDM09). In response to this, the Swedish vaccination campaign began in October of the same year, using the influenza vaccine Pandemrix(?). A few months later an excess of narcolepsy cases was observed. It is still unclear to what extent the vaccination campaign affected humoral autoimmunity associated with narcolepsy. We studied 47 patients with narcolepsy (6-69 years of age) and 80 healthy controls (3-61 years of age) selected after the Pandemrix vaccination campaign. The first aim was to determine antibodies against A/H1N1 and autoantibodies to Tribbles homolog 2 (TRIB2), a narcolepsy autoantigen candidate as well as to GAD65 and IA-2 as disease specificity controls. The second aim was to test if levels and frequencies of these antibodies and autoantibodies were associated with HLA-DQB1*06:02. In?vitro transcribed and translated [(35)S]-methionine and -cysteine-labeled influenza A virus (A/California/04/2009/(H1N1)) segment 4 hemagglutinin was used to detect antibodies in a radiobinding assay. Autoantibodies to TRIB2, GAD65 and IA-2 were similarly detected in standard radiobinding assays. The narcolepsy patients had higher median levels of A/H1N1 antibodies than the controls (p?=?0.006). A/H1N1 antibody levels were higher among the
PubMed ID
24485154 View in PubMed
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Alpha v beta 6 integrin down-regulates the MMP-13 expression in oral squamous cell carcinoma cells.

https://arctichealth.org/en/permalink/ahliterature16883
Source
Exp Cell Res. 2005 Oct 1;309(2):273-83
Publication Type
Article
Date
Oct-1-2005
Author
M. Ylipalosaari
G J Thomas
M. Nystrom
S. Salhimi
J F Marshall
V. Huotari
T. Tervahartiala
T. Sorsa
T. Salo
Author Affiliation
Department of Diagnostics and Oral Medicine, Institute of Dentistry, University of Oulu and Oulu University Hospital, PO Box 5281, FIN-90014 Oulu, Finland.
Source
Exp Cell Res. 2005 Oct 1;309(2):273-83
Date
Oct-1-2005
Language
English
Publication Type
Article
Keywords
Antigens, Neoplasm - physiology
Carcinoma, Squamous Cell - enzymology
Cell Line, Tumor
Collagen Type I - antagonists & inhibitors - metabolism
Collagenases - antagonists & inhibitors - biosynthesis - genetics
Down-Regulation - physiology
Gene Expression Regulation, Neoplastic - physiology
Humans
Integrins - physiology
Interstitial Collagenase - antagonists & inhibitors - biosynthesis - genetics
Membrane Proteins - antagonists & inhibitors - biosynthesis - genetics
Mouth Neoplasms - enzymology - metabolism
Neutrophil Collagenase - antagonists & inhibitors - biosynthesis - genetics
RNA, Messenger - antagonists & inhibitors - metabolism
Research Support, Non-U.S. Gov't
Abstract
The integrin alphavbeta6, a receptor for fibronectin, vitronectin, tenascin and TGF-beta latency-associated peptide (LAP), is not detectable on normal oral epithelium but is neo-expressed in oral squamous cell carcinomas (OSCC) and epithelial dysplasia. Previously it has been shown that alphavbeta6 integrin can up-regulate MMP-3 and -9 expression in OSCC cells. Using beta6-transfected and control OSCC cells we demonstrate that alphavbeta6 integrin down-regulates MMP-13 expression at both mRNA and protein level. Although expressing less MMP-13, beta6-transfected cells were found to have similar collagenolytic activity as control cells and invade at similar levels through type I collagen. Growth of the tumour cells in organotypic culture and confocal microscopy confirmed low levels of MMP-13 in cells with high alphavbeta6 expression. Furthermore, human squamous cell carcinomas of the tongue with high expression of alphavbeta6 showed lower MMP-13 levels than carcinomas with low levels of alphavbeta6. Our results suggest that alphavbeta6 down-regulates MMP-13 expression in OSCC cells and that MMP-13 is not essential for the degradation of type I collagen by OSCC cells.
PubMed ID
16024014 View in PubMed
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BRCA1 and BRCA2 bind Stat5a and suppress its transcriptional activity.

https://arctichealth.org/en/permalink/ahliterature18760
Source
FEBS Lett. 2002 Dec 4;532(1-2):247-52
Publication Type
Article
Date
Dec-4-2002
Author
H. Vidarsson
E K Mikaelsdottir
T. Rafnar
D. Bertwistle
A. Ashworth
J E Eyfjord
S. Valgeirsdottir
Author Affiliation
Molecular and Cell Biology Research Laboratory, Icelandic Cancer Society, Reykjavik, Iceland.
Source
FEBS Lett. 2002 Dec 4;532(1-2):247-52
Date
Dec-4-2002
Language
English
Publication Type
Article
Keywords
Animals
BRCA1 Protein - metabolism
BRCA2 Protein - metabolism
Breast - cytology - metabolism
Breast Neoplasms - metabolism
COS Cells
Cell Line
DNA-Binding Proteins - antagonists & inhibitors - metabolism
Epithelial Cells - metabolism
Female
Milk Proteins
Precipitin Tests
Research Support, Non-U.S. Gov't
STAT5 Transcription Factor
Trans-Activation (Genetics)
Trans-Activators - antagonists & inhibitors - metabolism
Abstract
Germline mutations in the breast cancer susceptibility genes, BRCA1 and BRCA2, are thought to account for a large portion of familial breast cancer. The increased risk of breast cancer in women carrying such mutations suggests that these proteins play a critical role in the growth regulation of mammary epithelial cells. Another protein, Stat5a, is known to be essential for growth and terminal differentiation of breast epithelial cells. Here we show that Stat5a forms a complex with both BRCA1 and BRCA2 in breast epithelial cells upon stimulation with prolactin. In addition, we show that the activity of Stat5a on the beta-casein promoter is modulated by both BRCA1 and BRCA2. This interaction may be important during the expansion and terminal differentiation of breast epithelial cells, as happens during pregnancy and lactation.
PubMed ID
12459499 View in PubMed
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Characterization of azurocidin as a permeability factor in the retina: involvement in VEGF-induced and early diabetic blood-retinal barrier breakdown.

https://arctichealth.org/en/permalink/ahliterature93705
Source
Invest Ophthalmol Vis Sci. 2008 Feb;49(2):726-31
Publication Type
Article
Date
Feb-2008
Author
Skondra Dimitra
Noda Kousuke
Almulki Lama
Tayyari Faryan
Frimmel Sonja
Nakazawa Toru
Kim Ivana K
Zandi Souska
Thomas Kennard L
Miller Joan W
Gragoudas Evangelos S
Hafezi-Moghadam Ali
Author Affiliation
Angiogenesis Laboratory, Massachusetts Eye & Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, MA 02114, USA.
Source
Invest Ophthalmol Vis Sci. 2008 Feb;49(2):726-31
Date
Feb-2008
Language
English
Publication Type
Article
Keywords
Animals
Antimicrobial Cationic Peptides - antagonists & inhibitors - pharmacology
Aprotinin - pharmacology
Blood Proteins - antagonists & inhibitors - pharmacology
Blood-Retinal Barrier - drug effects
Capillary Permeability - drug effects
Carrier Proteins - antagonists & inhibitors - pharmacology
Diabetes Mellitus, Experimental - complications
Diabetic Retinopathy - etiology - metabolism - prevention & control
Evans Blue - metabolism
Male
Monocyte Chemoattractant Proteins - pharmacology
Rats
Rats, Inbred BN
Rats, Long-Evans
Retinal Vessels - drug effects
Serine Proteinase Inhibitors - pharmacology
Vascular Endothelial Growth Factor A - pharmacology
Abstract
PURPOSE: Azurocidin, released by neutrophils during leukocyte-endothelial interaction, is a main cause of neutrophil-evoked vascular leakage. Its role in the retina, however, is unknown. METHODS: Brown Norway rats received intravitreal injections of azurocidin and vehicle control. Blood-retinal barrier (BRB) breakdown was quantified using the Evans blue (EB) dye technique 1, 3, and 24 hours after intravitreal injection. To block azurocidin, aprotinin was injected intravenously before the intravitreal injections. To investigate whether azurocidin plays a role in vascular endothelial growth factor (VEGF)-induced BRB breakdown, rats were treated intravenously with aprotinin, followed by intravitreal injection of VEGF(164). BRB breakdown was quantified 24 hours later. To investigate whether azurocidin may mediate BRB breakdown in early diabetes, aprotinin or vehicle was injected intravenously each day for 2 weeks to streptozotocin-induced diabetic rats, and BRB breakdown was quantified. RESULTS: Intravitreal injection of azurocidin (20 microg) induced a 6.8-fold increase in vascular permeability compared with control at 1-3 hours (P
PubMed ID
18235021 View in PubMed
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Cholesterol ester transfer protein inhibition by TA-8995 in patients with mild dyslipidaemia (TULIP): a randomised, double-blind, placebo-controlled phase 2 trial.

https://arctichealth.org/en/permalink/ahliterature265749
Source
Lancet. 2015 Aug 1;386(9992):452-60
Publication Type
Article
Date
Aug-1-2015
Author
G Kees Hovingh
John J P Kastelein
Sander J H van Deventer
Patrick Round
John Ford
Danish Saleheen
Daniel J Rader
H Bryan Brewer
Philip J Barter
Source
Lancet. 2015 Aug 1;386(9992):452-60
Date
Aug-1-2015
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Cholesterol Ester Transfer Proteins - antagonists & inhibitors
Cholesterol, HDL - blood - drug effects
Cholesterol, LDL - blood - drug effects
Denmark
Double-Blind Method
Dyslipidemias - drug therapy
Female
Fluorobenzenes - administration & dosage
Heptanoic Acids - administration & dosage
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors - administration & dosage
Male
Middle Aged
Netherlands
Pyrimidines - administration & dosage
Pyrroles - administration & dosage
Quinolines - administration & dosage - pharmacology
Sulfonamides - administration & dosage
Treatment Outcome
Young Adult
Abstract
Dyslipidaemia remains a significant risk factor for cardiovascular disease and additional lipid-modifying treatments are warranted to further decrease the cardiovascular disease burden. We assessed the safety, tolerability and efficacy of a novel cholesterol esterase transfer protein (CETP) inhibitor TA-8995 in patients with mild dyslipidaemia.
In this randomised, double-blind, placebo-controlled, parallel-group phase 2 trial, we recruited patients (aged 18-75 years) from 17 sites (hospitals and independent clinical research organisations) in the Netherlands and Denmark with fasting LDL cholesterol levels between 2·5 mmol/L and 4·5 mmol/L, HDL cholesterol levels between 0·8 and 1·8 mmol/L and triglyceride levels below 4·5 mmol/L after washout of lipid-lowering treatments. Patients were randomly allocated (1:1) by a computer-generated randomisation schedule to receive one of the following nine treatments: a once a day dose of 1 mg, 2·5 mg, 5 mg, or 10 mg TA-8995 or matching placebo; 10 mg TA-8995 plus 20 mg atorvastatin; 10 mg TA-8995 plus 10 mg rosuvastatin or 20 mg atorvastatin or 10 mg rosuvastatin alone. We overencapsulated statins to achieve masking. The primary outcome was percentage change in LDL cholesterol and HDL cholesterol from baseline at week 12, analysed by intention to treat. This study is registered with ClinicalTrials.gov, number NCT01970215.
Between Aug 15, 2013, and Jan 10, 2014, 364 patients were enrolled. At week 12, LDL cholesterol levels were reduced by 27·4% in patients assigned to the 1 mg dose, 32·7% in patients given the 2·5 mg dose, 45·3% in those given the 5 mg dose, and 45·3% in those given the 10 mg dose (p
Notes
Comment In: Lancet. 2015 Aug 1;386(9992):412-426047976
PubMed ID
26047975 View in PubMed
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Effective stimulation of growth in MCF-7 human breast cancer cells by inhibition of syntaxin18 by external guide sequence and ribonuclease P.

https://arctichealth.org/en/permalink/ahliterature92355
Source
Cancer Lett. 2008 Dec 8;272(1):167-75
Publication Type
Article
Date
Dec-8-2008
Author
Bassett Tyler
Harpur Brock
Poon Ho Y
Kuo Kuo-Hsing
Lee Chow H
Author Affiliation
Chemistry Program, University of Northern British Columbia, 3333 University Way, Prince George, BC, Canada V2N 4Z9.
Source
Cancer Lett. 2008 Dec 8;272(1):167-75
Date
Dec-8-2008
Language
English
Publication Type
Article
Keywords
Breast Neoplasms - pathology
Cell Division
Cell Line, Tumor
Cell Survival
DNA Primers
Down-Regulation
Female
Genes, myc
Humans
Plasmids
Polymerase Chain Reaction
Promoter Regions, Genetic
Qa-SNARE Proteins - antagonists & inhibitors - genetics - physiology
RNA, Messenger - genetics
RNA, Neoplasm - genetics - isolation & purification
Ribonuclease P - metabolism
Abstract
Syntaxin18 (Stx18) is an endoplasmic reticulum (ER)-membrane bound SNARE protein involved in membrane trafficking between the ER and Golgi as well as in phagocytosis. Stx18 has also been shown to physically interact with proteins involved in the cell cycle and apoptosis. These findings suggest the possible role of Stx18 in regulating cell growth. In this study, we used theoretically designed external guide sequence molecule which utilizes RNase P to cleave Stx18 mRNA and down-regulate Stx18 levels in MCF-7 human breast cancer cells. We showed that down-regulation of Stx18 leads to significant enhancement of growth in MCF-7 cells. Consistent with this finding was the observation that over-expression of Stx18 using the CMV promoter led to suppression of cell growth. Over-expressing Stx18 had no effect on c-myc mRNA expression and half-life, suggesting that the mechanism does not involve control at the transcriptional and post-transcriptional level of the c-myc gene. Finally, we showed that Stx18 is over-expressed in clinical human breast cancer. Overall, this study showed that Stx18 plays a role in the growth of human breast cancer cells and provided the basis for further investigation in determining whether it can be used as a prognostic marker and as a molecular target in the treatment of breast cancer.
PubMed ID
18722709 View in PubMed
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Effect of antiallergic drugs on interleukin 5-induced eosinophil infiltration of rat airways.

https://arctichealth.org/en/permalink/ahliterature15396
Source
Biol Pharm Bull. 2002 Mar;25(3):318-22
Publication Type
Article
Date
Mar-2002
Author
Toshiaki Takizawa
Naoki Kawada
Hiroyuki Tanaka
Hiroichi Nagai
Author Affiliation
Department of Pharmacology, Gifu Pharmaceutical University, Japan. ttakizaw@kowa.co.jp
Source
Biol Pharm Bull. 2002 Mar;25(3):318-22
Date
Mar-2002
Language
English
Publication Type
Article
Keywords
Animals
Anti-Allergic Agents - pharmacology
Benzimidazoles - pharmacology
Bronchi - pathology
Bronchoalveolar Lavage Fluid - cytology
Eosinophils - cytology - drug effects - metabolism
Interleukin-5 - antagonists & inhibitors - pharmacology
Male
Prednisolone - pharmacology
Rats
Rats, Inbred F344
Recombinant Proteins - antagonists & inhibitors - pharmacology
Abstract
Interleukin (IL)-5 is thought to play important roles in asthma and to be a potential therapeutic target. An intratracheal injection of murine recombinant IL-5 (3-30 microg/animal) induced a dose-dependent increase in the number of eosinophils in the bronchoalveolar lavage fluid of Brown Norway (BN) rats 24 h after administration. Bovine serum albumin (30pg/animal), used as reference material, did not cause any change. The reaction was not observed in F344 rats. The increase in the number of eosinophils did not accompany bronchial hyperreactivity in BN or F344 rats. Prednisolone (3-10 mg/kg, i.p.) and emedastine (30 mg/kg, p.o.) reduced the increased number of eosinophils induced by the IL-5 challenge. These results suggest that IL-5 is a potent inducer of eosinophils in the airway of BN rats. Prednisolone and emedastine are effective against IL-5-induced eosinophilia.
PubMed ID
11913525 View in PubMed
Less detail

[Effect of UCP2 activity inhibitor genipin on heart function of aging rats]

https://arctichealth.org/en/permalink/ahliterature98282
Source
Fiziol Zh. 2009;55(5):28-34
Publication Type
Article
Date
2009
Author
Iu V Hoshovs'ka
T V Shymans'ka
V F Sahach
Source
Fiziol Zh. 2009;55(5):28-34
Date
2009
Language
Ukrainian
Publication Type
Article
Keywords
Aging - metabolism - physiology
Animals
Calcium Chloride - pharmacology
Dose-Response Relationship, Drug
Heart Function Tests
Ion Channels - antagonists & inhibitors
Iridoids - pharmacology
Male
Mitochondrial Proteins - antagonists & inhibitors
Myocardial Contraction - drug effects - physiology
Myocardial Reperfusion
Myocardial Reperfusion Injury - metabolism - physiopathology
Myocardium - metabolism
Oxygen Consumption - physiology
Rats
Rats, Wistar
Abstract
To estimate the role of uncoupling proteins in aging rat heart recovery from prolonged ischemia we used genipin application during Langendorfpreparation. It was shown that genipin in dose-depended manner depressed coronary flow, heart rate and cardiac diastolic function. Such effect was similar to that observed during myocardial Ca2+ overload by gradually elevated CaCl2, in perfusion solution. Moreover, postischemic disturbances of cardiodynamic parameters, oxygen cost of myocardial work were much increased in genipin pretreated hearts that in control ones. Thus, genipin inhibition of UCP2 activity has cardiodepressive effects that imply UCPs in cardiac calcium regulation.
PubMed ID
20095381 View in PubMed
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Effects of a 5-lipoxygenase-activating protein inhibitor on biomarkers associated with risk of myocardial infarction: a randomized trial.

https://arctichealth.org/en/permalink/ahliterature53159
Source
JAMA. 2005 May 11;293(18):2245-56
Publication Type
Article
Date
May-11-2005
Author
Hakon Hakonarson
Sverrir Thorvaldsson
Anna Helgadottir
Daniel Gudbjartsson
Florian Zink
Margret Andresdottir
Andrei Manolescu
David O Arnar
Karl Andersen
Axel Sigurdsson
Gestur Thorgeirsson
Asgeir Jonsson
Uggi Agnarsson
Halldora Bjornsdottir
Gizur Gottskalksson
Atli Einarsson
Hrefna Gudmundsdottir
Asdis E Adalsteinsdottir
Kolbeinn Gudmundsson
Kristleifur Kristjansson
Thordur Hardarson
Arni Kristinsson
Eric J Topol
Jeffrey Gulcher
Augustine Kong
Mark Gurney
Gudmundur Thorgeirsson
Kari Stefansson
Author Affiliation
Decode Genetics Inc, Reykjavik, Iceland. hakonh@decode.is
Source
JAMA. 2005 May 11;293(18):2245-56
Date
May-11-2005
Language
English
Publication Type
Article
Keywords
Aged
Biological Markers - metabolism
Carrier Proteins - antagonists & inhibitors - genetics
Coronary Arteriosclerosis - drug therapy - genetics - metabolism
Cross-Over Studies
Epoxide Hydrolases - genetics
Female
Humans
Leukotriene B4 - metabolism
Leukotriene E4 - metabolism
Lipoxygenase Inhibitors - therapeutic use
Male
Membrane Proteins - antagonists & inhibitors - genetics
Middle Aged
Myocardial Infarction - genetics - metabolism - prevention & control
Peroxidase - metabolism
Polymorphism, Single Nucleotide
Prospective Studies
Quinolines - therapeutic use
Research Support, Non-U.S. Gov't
Risk factors
Abstract
CONTEXT: Myocardial infarction (MI) is the leading cause of death in the world. Variants in the 5-lipoxygenase-activating protein (FLAP) gene are associated with risk of MI. OBJECTIVE: To determine the effect of an inhibitor of FLAP on levels of biomarkers associated with MI risk. DESIGN, SETTING, AND PATIENTS: A randomized, prospective, placebo-controlled, crossover trial of an inhibitor of FLAP (DG-031) in MI patients who carry at-risk variants in the FLAP gene or in the leukotriene A4 hydrolase gene. Of 268 patients screened, 191 were carriers of at-risk variants in FLAP (87%) or leukotriene A4 hydrolase (13%). Individuals were enrolled in April 2004 and were followed up by designated cardiologists from a university hospital in Iceland until September 2004. INTERVENTIONS: Patients were first randomized to receive 250 mg/d of DG-031, 500 mg/d of DG-031, 750 mg/d of DG-031, or placebo. After a 2-week washout period, patients received DG-031 if they had received placebo first or placebo if they had received DG-031 first. Treatment periods lasted for 4 weeks. MAIN OUTCOME MEASURES: Changes in levels of biomarkers associated with risk of MI. RESULTS: In response to 750 mg/d of DG-031, production of leukotriene B4 was significantly reduced by 26% (95% confidence interval [CI], 10%-39%; P = .003) and myeloperoxidase was significantly reduced by 12% (95% CI, 2%-21%; P = .02). The higher 2 doses of DG-031 produced a nonsignificant reduction in C-reactive protein (16%; 95% CI, -2% to 31%; P = .07) at 2 weeks. However, there was a more pronounced reduction (25%; 95% CI, 5%-40%; P = .02) in C-reactive protein at the end of the washout period that persisted for another 4 weeks thereafter. The FLAP inhibitor DG-031 was well tolerated and was not associated with any serious adverse events. CONCLUSION: In patients with specific at-risk variants of 2 genes in the leukotriene pathway, DG-031 led to significant and dose-dependent suppression of biomarkers that are associated with increased risk of MI events.
Notes
Comment In: JAMA. 2005 May 11;293(18):2277-915886385
PubMed ID
15886380 View in PubMed
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35 records – page 1 of 4.