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Neuronal Nitric Oxide Synthase (nNOS,NOS1) rs693534 and rs7977109 Variants and Risk for Migraine
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94.
Krisztina Takács Eva Guillamon Mercedes Martin Pedrosa Carmen Cuadrado Carmen Burbano Mercedes Muzquiz 《Food and Agricultural Immunology》2014,25(2):173-185
Détente Instantanée Contrôlée (DIC) technology was used to reduce immunoglobulin E (IgE) reactivity of legume proteins. Soybean, roasted peanut, chickpea and lentil seeds were treated at three or six bars for 60 or 180s. The effect of this treatment on the IgE-binding pattern of the legume proteins – separated by sodium-dodecyl-sulphate polyacrylamide gel electrophoresis – was monitored by five individual paediatric legume allergic and – two individual negative control human sera. A highly cross-reactive legume positive serum was selected for the two-dimensional electrophoreses immunoblots to compare the IgE reactive protein patterns, before and after the DIC treatment. The number of the identified IgE reactive spots was highly reduced for soybean (0/7) and chickpea (2/7), and moderately reduced for lentil (4/7) when the seeds were treated at a higher pressure (6 bar) and for a longer time (180 s), but this treatment was not effective for roasted peanut (6/8) where the intensity of the IgE reactive resistant spots were even stronger. 相似文献
95.
Marta Lishnevsky Lena C. Young Steven J. Woods Steven D. Groshong Randall J. Basaraba John M. Gilchrist David M. Higgins Mercedes Gonzalez-Juarrero Todd A. Bass William A. Muller Alan R. Schenkel 《Experimental and molecular pathology》2014
Platelet Endothelial Cell Adhesion Molecule 1 (PECAM-1) deficient mice in the FVB/n strain exhibit fatal chronic pulmonary fibrotic disease. The illness occurs in the absence of a detectable pro-inflammatory event. PECAM-1 is vital to the stability of vascular permeability, leukocyte extravasation, clotting of platelets, and clearance of apoptotic cells. We show here that the spontaneous development of fibrotic disease in PECAM-1 deficient FVB/n mice is characterized by early loss of vascular integrity in pulmonary capillaries, resulting in spontaneous microbleeds. Hemosiderin-positive macrophages were found in interstitial spaces and bronchoalveolar lavage (BAL) fluid in relatively healthy animals. We also observed a gradually increasing presence of hemosiderin-positive macrophages and fibrin deposition in the advanced stages of disease, corresponding to the accumulation of collagen, IL-10 expression, and myofibroblasts expressing alpha smooth muscle actin (SMA). Together with the growing evidence that pulmonary microbleeds and coagulation play an active part in human pulmonary fibrosis, this data further supports our hypothesis that PECAM-1 expression is necessary for vascular barrier function control and regulation of homeostasis specifically, in the pulmonary environment. 相似文献
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Yong-Jie Zhang Karen Jansen-West Ya-Fei Xu Tania F. Gendron Kevin F. Bieniek Wen-Lang Lin Hiroki Sasaguri Thomas Caulfield Jaime Hubbard Lillian Daughrity Jeannie Chew Veronique V. Belzil Mercedes Prudencio Jeannette N. Stankowski Monica Castanedes-Casey Ena Whitelaw Peter E. A. Ash Michael DeTure Rosa Rademakers Kevin B. Boylan Dennis W. Dickson Leonard Petrucelli 《Acta neuropathologica》2014,128(4):505-524
The occurrence of repeat-associated non-ATG (RAN) translation, an atypical form of translation of expanded repeats that results in the synthesis of homopolymeric expansion proteins, is becoming more widely appreciated among microsatellite expansion disorders. Such disorders include amyotrophic lateral sclerosis and frontotemporal dementia caused by a hexanucleotide repeat expansion in the C9ORF72 gene (c9FTD/ALS). We and others have recently shown that this bidirectionally transcribed repeat is RAN translated, and the “c9RAN proteins” thusly produced form neuronal inclusions throughout the central nervous system of c9FTD/ALS patients. Nonetheless, the potential contribution of c9RAN proteins to disease pathogenesis remains poorly understood. In the present study, we demonstrate that poly(GA) c9RAN proteins are neurotoxic and may be implicated in the neurodegenerative processes of c9FTD/ALS. Specifically, we show that expression of poly(GA) proteins in cultured cells and primary neurons leads to the formation of soluble and insoluble high molecular weight species, as well as inclusions composed of filaments similar to those observed in c9FTD/ALS brain tissues. The expression of poly(GA) proteins is accompanied by caspase-3 activation, impaired neurite outgrowth, inhibition of proteasome activity, and evidence of endoplasmic reticulum (ER) stress. Of importance, ER stress inhibitors, salubrinal and TUDCA, provide protection against poly(GA)-induced toxicity. Taken together, our data provide compelling evidence towards establishing RAN translation as a pathogenic mechanism of c9FTD/ALS, and suggest that targeting the ER using small molecules may be a promising therapeutic approach for these devastating diseases. 相似文献
98.
Hawley K Navasa N Olson CM Bates TC Garg R Hedrick MN Conze D Rincón M Anguita J 《The Journal of infectious diseases》2012,206(2):283-291
The interaction of macrophages with infectious agents leads to the activation of several signaling cascades, including mitogen-activated protein (MAP) kinases, such as p38. We now demonstrate that p38 MAP kinase-mediated responses are critical components to the immune response to Borrelia burgdorferi. The pharmacological and genetic inhibition of p38 MAP kinase activity during infection with the spirochete results in increased carditis. In transgenic mice that express a dominant negative form of p38 MAP kinase specifically in macrophages, production of the invariant natural killer T (iNKT) cell-attracting chemokine MCP-1 and of the antigen-presenting molecule CD1d are significantly reduced. The expression of the transgene therefore results in the deficient infiltration of iNKT cells, their decreased activation, and a diminished production of interferon γ (IFN-γ), leading to increased bacterial burdens and inflammation. These results show that p38 MAP kinase provides critical checkpoints for the protective immune response to the spirochete during infection of the heart. 相似文献
99.
M Camacho A Martinez-Perez A Buil L Siguero S Alcolea S López J Fontcuberta JC Souto L Vila JM Soria 《Atherosclerosis》2012,224(1):129-135
ObjectiveLeukotrienes (LT) play a role in inflammation, cardiovascular diseases, and cancer. Although some studies suggest that there are genes that determine variability of some LT-related phenotypes, the genetic influence on these phenotypes has not been evaluated.MethodsThe relative contributions of genetic and environmental influences to the 5-lipoxygenase pathway-related phenotypes (5-Lipoxygenase, five lipoxygenase activating protein (FLAP), LTA4-hydrolase and LTC4-synthase expression, and LTB4-plasma concentration and LTB4 production by stimulated whole blood) were assessed in a sample of 934 individuals in 35 extended families. Our design is based on extended families recruited through a probands with idiopathic thrombophilia. This strategy allows us the analysis of the effects of measured covariates (such as sex, age and smoking), genes, and environmental variables shared by members of a household.ResultsAll of these phenotypes showed significant genetic contributions, with heritabilities ranging from 0.33 to 0.51 for enzyme expression and from 0.25 to 0.50 for LTB4 production of the residual phenotypic variance. Significant phenotypic and genetic correlation among the LT-related traits was found. More importantly, FLAP and LTA4-hydrolase expression exhibit significant genetic correlations with arterial thrombosis, indicating that some of the genes that influence quantitative variation in these phenotypes also influence the risk of thrombosis.ConclusionThis is the first study that quantifies the genetic component of 5-Lipoxygenase pathway phenotypes. The high heritability of these traits and the significant genetic correlations between arterial thrombosis and some of these phenotypes suggest that the exploitation of correlated quantitative phenotypes will aid the search for susceptibility genes. 相似文献
100.
Champaneri S Xu X Carnethon MR Bertoni AG Seeman T Diez Roux A Golden SH 《Metabolism: clinical and experimental》2012,61(7):986-995
The objective was to examine the cross-sectional association of diurnal salivary cortisol curve components and urinary catecholamines with diabetes status. Up to 18 salivary cortisol samples over 3 days and overnight urinary catecholamines were collected from 1002 participants in the Multi-Ethnic Study of Atherosclerosis. Diabetes was defined as a fasting blood glucose of at least 126 mg/dL or medication use. Cortisol curve measures included awakening cortisol, cortisol awakening response, early decline, late decline, and cortisol area under the curve (AUC). Urinary catecholamines included epinephrine, norepinephrine, and dopamine. Participants with diabetes had significantly lower cortisol awakening response (β = -0.19; 95% confidence interval [CI], -0.34 to -0.04) than those without diabetes in multivariable models. Whereas men with diabetes had a nonsignificant trend toward lower total AUC (β = -1.56; 95% CI, -3.93 to 0.80), women with diabetes had significantly higher total AUC (β = 2.62; 95% CI, 0.72 to 4.51) (P = .02 for interaction) compared with those without diabetes. Men but not women with diabetes had significantly lower urinary catecholamines compared with those without diabetes (P < .05). Diabetes is associated with neuroendocrine dysregulation, which may differ by sex. Further studies are needed to determine the role of the neuroendocrine system in the pathophysiology of diabetes. 相似文献