Characterization of the Ileal Lipid Binding Protein (FABP6) in Tissues Involved in Bile Acid and Steroid Metabolism in Poultry

Total Page:16

File Type:pdf, Size:1020Kb

Characterization of the Ileal Lipid Binding Protein (FABP6) in Tissues Involved in Bile Acid and Steroid Metabolism in Poultry Characterization of the Ileal Lipid Binding Protein (FABP6) in Tissues Involved in Bile Acid and Steroid Metabolism in Poultry Rosanne Mcquaid Department of Animal Science McGill University, Montreal 21111 Lakeshore Rd., Ste Anne De Bellevue, QC, H9X 3V9 December 2011 A thesis submitted to McGill University in partial fulfillment of the requirements of the degree of Master of Science ©Rosanne McQuaid 2011 I Table of Contents Table of Contents Characterization of the Ileal Lipid Binding Protein (FABP6) in Tissues Involved in Bile Acid and Steroid Metabolism in Poultry ..............................I Table of Contents ....................................................................................................... II List of Tables............................................................................................................... IV List of Figures ............................................................................................................. IV Abstract ..........................................................................................................................V Résumé .........................................................................................................................VI Introduction..................................................................................................................1 Fatty Acid Binding Proteins Literature Review ................................................3 Fatty Acid Binding Proteins.............................................................................................3 FABP6......................................................................................................................................5 Evidence of Bile Acid Binding Proteins in Poultry................................................ 10 Cholesterol Homeostasis............................................................................................... 12 Cholesterol Homeostasis in Poultry..................................................................................... 13 FABP6 and Cholesterol .............................................................................................................. 15 Cytochrome P450 Enzymes .......................................................................................... 17 Bile Acids............................................................................................................................. 18 Bile Acid Biosynthesis ................................................................................................................ 18 Enterohepatic Circulation......................................................................................................... 19 Steroid Hormones............................................................................................................ 22 FABP6 in Steroid Producing Tissues ......................................................................... 23 Conclusion .......................................................................................................................... 25 Materials and Methods........................................................................................... 26 Animals................................................................................................................................ 26 Tissue Collection: ............................................................................................................. 26 RNA Isolation:.................................................................................................................... 26 cDNA Synthesis: ................................................................................................................ 27 Polymerase Chain Reaction:......................................................................................... 28 PCR Cloning:....................................................................................................................... 29 Sequencing: ........................................................................................................................ 29 Relative mRNA Quantitation by Quantitative Real­ Time PCR: ....................... 29 Protein Extraction: .......................................................................................................... 31 Antibodies. ......................................................................................................................... 32 Immunoblot: ...................................................................................................................... 32 Immunohistochemistry: ................................................................................................ 32 Statistical Analysis........................................................................................................... 34 Results ......................................................................................................................... 35 Validation of Primers...................................................................................................... 35 II Sequence Alignment........................................................................................................ 36 Broilers:............................................................................................................................... 41 mRNA................................................................................................................................................. 41 Protein............................................................................................................................................... 42 Layers................................................................................................................................... 44 mRNA................................................................................................................................................. 44 Protein............................................................................................................................................... 46 Turkey Embryo................................................................................................................. 51 Discussion: ................................................................................................................. 54 Tissue­Specific Distribution ......................................................................................... 56 Intestine ........................................................................................................................................... 56 Kidney ............................................................................................................................................... 58 Liver ................................................................................................................................................... 58 Testis.................................................................................................................................................. 59 Ovarian Follicles ........................................................................................................................... 59 Embryos ........................................................................................................................................... 62 Conclusion .................................................................................................................. 65 III List of Tables Table 1. Primers for Standard PCR Table 2. Quantitative PCR primers List of Figures Figure 1. FABP tertiary structure of the Beta‐Clam Figure 2. FABPs in the Small Intestine Figure 3. Regulation of FABP6 expression by sensing intracellular cholesterol and cholesterol derivatives Figure 4. Enterohepatic circulation Figure 5. Cholesterol metabolism into steroid hormones Figure 6. Location of FABP6 primers in the ORF of Gallus gallus FABP6 mRNA Figure 7. Location of FABP6 primers in the ORF of the Meleagris gallopavo FABP6 mRNA Figure 8. Chicken and Mouse FABP6 mRNA Sequence Alignment Figure 9. Chicken and Mouse FABP6 Protein Amino Acid Sequence Alignment Figure 10. Chicken and Turkey FABP6 mRNA Sequence Alignment Figure 11. Chicken and Turkey FABP6 Amino Acid Sequence Alignment Figure 12. Chicken and Turkey ASBT mRNA Sequence Alignment Figure 13. Chicken and Turkey ASBT Amino Acid Sequence Alignment Figure 14. Chicken and Turkey LXR Amino Acid Sequence Alignment Figure 15. Chicken and Turkey FXR Amino Acid Sequence Alignment Figure 16. FABP6 mRNA Abundance in Broilers Figure 17. ASBT Abundance in Broiler Tissues Figure 18. Immunoblot of FABP6 in Broilers Figure 19. FABP6 Female Intestine and Ovarian Follicles Figure 20. ASBT Female Intestine and Ovarian Follicles Figure 21. FABP6 and ASBT in the F1 Follicle Tissues Figure 22. FABP6 Immunoblot Analysis Figure 23. Immunoreactivity of the Duodenum Figure 24. Immunoreactivity of the Ileum Figure 25. Immunoreactivity of Follicles Figure 26. FABP6 in 24ED Turkey Embryo Tissues Figure 27. FABP6 in 28ED Turkey Embryo Tissues Figure 28. ASBT in 28ED Turkey Embryo Tissues IV Abstract The Characterization of Ileal Lipid Binding Protein (FABP6) in Tissues Involved in Bile Acid and Steroid Metabolism in Poultry Fatty acid binding proteins (FABPs) are a family of proteins involved in the transport of a wide variety of hydrophobic molecules within the cytosol of cells. Tissues with high levels
Recommended publications
  • Deficiency in Class III PI3-Kinase Confers Postnatal Lethality with IBD
    ARTICLE DOI: 10.1038/s41467-018-05105-8 OPEN Deficiency in class III PI3-kinase confers postnatal lethality with IBD-like features in zebrafish Shaoyang Zhao1,2,3, Jianhong Xia2,3, Xiuhua Wu2,3, Leilei Zhang2,3, Pengtao Wang2,3, Haiyun Wang2,3, Heying Li2, Xiaoshan Wang 2, Yan Chen 2, Jean Agnetti2, Yinxiong Li 2, Duanqing Pei2,3 & Xiaodong Shu2,3 The class III PI3-kinase (PIK3C3) is an enzyme responsible for the generation of phospha- tidylinositol 3-phosphate (PI3P), a critical component of vesicular membrane. Here, we report 1234567890():,; that PIK3C3 deficiency in zebrafish results in intestinal injury and inflammation. In pik3c3 mutants, gut tube forms but fails to be maintained. Gene expression analysis reveals that barrier-function-related inflammatory bowel disease (IBD) susceptibility genes (e-cadherin, hnf4a, ttc7a) are suppressed, while inflammatory response genes are stimulated in the mutants. Histological analysis shows neutrophil infiltration into mutant intestinal epithelium and the clearance of gut microbiota. Yet, gut microorganisms appear dispensable as mutants cultured under germ-free condition have similar intestinal defects. Mechanistically, we show that PIK3C3 deficiency suppresses the formation of PI3P and disrupts the polarized dis- tribution of cell-junction proteins in intestinal epithelial cells. These results not only reveal a role of PIK3C3 in gut homeostasis, but also provide a zebrafish IBD model. 1 School of Life Sciences, University of Science and Technology of China, 230027 Hefei, Anhui, China. 2 CAS Key Laboratory of Regenerative Biology, Guangzhou Institute of Biomedicine and Health-Guangzhou Medical University Joint School of Biological Sciences, South China Institute for Stem Cell Biology and Regenerative Medicine, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, 510530 Guangzhou, China.
    [Show full text]
  • A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
    Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated.
    [Show full text]
  • Fatty Acid Binding Proteins Have the Potential to Channel Dietary Fatty Acids Into Enterocyte Nuclei
    Supplemental Material can be found at: http://www.jlr.org/content/suppl/2015/12/11/jlr.M062232.DC1 .html Fatty acid binding proteins have the potential to channel dietary fatty acids into enterocyte nuclei Adriana Esteves , 1, * Anja Knoll-Gellida , 1,†,§ Lucia Canclini , * Maria Cecilia Silvarrey , * Michèle André , †,§ and Patrick J. Babin 2,†,§ Facultad de Ciencias,* Universidad de la República , 11400 Montevideo, Uruguay ; University Bordeaux, † Maladies Rares: Génétique et Métabolisme (MRGM), F-33615 Pessac, France ; and INSERM, § U1211, F-33076, Bordeaux, France Abstract Intracellular lipid binding proteins, including Together with cellular retinol and retinoic acid binding fatty acid binding proteins (FABPs) 1 and 2, are highly ex- proteins, these abundant chaperone proteins are mem- pressed in tissues involved in the active lipid metabolism. A bers of an ancient conserved multigene family of intra- zebrafi sh model was used to demonstrate differential ex- cellular lipid binding proteins ( 4–6 ). The evolutionary pression levels of fabp1b.1 , fabp1b.2 , and fabp2 transcripts relationships of vertebrate FABPs were clarifi ed using phy- Downloaded from in liver, anterior intestine, and brain. Transcription levels of fabp1b.1 and fabp2 in the anterior intestine were up- logenetic and conserved synteny analyses ( 7, 8 ). They bind regulated after feeding and modulated according to diet long-chain FAs (LCFAs) and other lipophilic compounds formulation. Immunofl uorescence and electron microscopy ( 9–12 ) and are believed to be implicated in FA intracellu- immunodetection with gold particles localized these FABPs lar uptake and transport, lipid metabolism regulation, in the microvilli, cytosol, and nuclei of most enterocytes protection from the harmful effects of nonesterifi ed in the anterior intestinal mucosa.
    [Show full text]
  • Expression of Selected Genes Involved in Steroidogenesis in the Course of Enucleation-Induced Rat Adrenal Regeneration
    INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE 33: 613-623, 2014 Expression of selected genes involved in steroidogenesis in the course of enucleation-induced rat adrenal regeneration MARIANNA TYCZEWSKA, MARCIN RUCINSKI, AGNIESZKA ZIOLKOWSKA, MARCIN TREJTER, MARTA SZYSZKA and LUDWIK K. MALENDOWICZ Department of Histology and Embryology, Poznan University of Medical Sciences, Poznan, Poland Received October 28, 2013; Accepted December 6, 2013 DOI: 10.3892/ijmm.2013.1599 Abstract. The enucleation-induced (EI) rapid proliferation however, throughout the entire experimental period, there were of adrenocortical cells is followed by their differentiation, no statistically significant differences observed. After the initial the degree of which may be characterized by the expression decrease in steroidogenic factor 1 (Sf-1) mRNA levels observed of genes directly and indirectly involved in steroid hormone on the 1st day of the experiment, a marked upregulation in its biosynthesis. In this study, out of 30,000 transcripts of genes expression was observed from there on. Data from the current identified by means of Affymetrix Rat Gene 1.1 ST Array, we study strongly suggest the role of Fabp6, Lipe and Soat1 in aimed to select genes (either up- or downregulated) involved supplying substrates of regenerating adrenocortical cells for in steroidogenesis in the course of enucleation-induced adrenal steroid synthesis. Our results indicate that during the first days regeneration. On day 1, we found 32 genes with altered of adrenal regeneration, intense synthesis of cholesterol may expression levels, 15 were upregulated and 17 were down- occur, which is then followed by its conversion into cholesteryl regulated [i.e., 3β-hydroxysteroid dehydrogenase (Hsd3β), esters.
    [Show full text]
  • Characterization of the Ileal Lipid Binding Protein (FABP6) in Tissues Involved in Bile Acid and Steroid Metabolism in Poultry
    Characterization of the Ileal Lipid Binding Protein (FABP6) in Tissues Involved in Bile Acid and Steroid Metabolism in Poultry Rosanne Mcquaid Department of Animal Science McGill University, Montreal 21111 Lakeshore Rd., Ste Anne De Bellevue, QC, H9X 3V9 December 2011 A thesis submitted to McGill University in partial fulfillment of the requirements of the degree of Master of Science ©Rosanne McQuaid 2011 I Table of Contents Table of Contents Characterization of the Ileal Lipid Binding Protein (FABP6) in Tissues Involved in Bile Acid and Steroid Metabolism in Poultry ..............................I Table of Contents ....................................................................................................... II List of Tables............................................................................................................... IV List of Figures ............................................................................................................. IV Abstract ..........................................................................................................................V Résumé .........................................................................................................................VI Introduction..................................................................................................................1 Fatty Acid Binding Proteins Literature Review ................................................3 Fatty Acid Binding Proteins.............................................................................................3
    [Show full text]
  • Pathways & Key Molecular Targets
    PATHWAYS & KEY MOLECULAR TARGETS NF-κB Signaling Bi-directional Cross-talk Between HIF1-alpha and NF kappa B Antigen TNFa, LPS, IL-1 BCR Growth CANONICAL Factor Growth NON-CANONICAL SENPs Hypoxia Ca2+ IKB NF-κB Upregulates HIFs Factor LTα1β2 Degradation TNF-α Receptor α/β α/β mlg mlg HIF-1α CD40L HIF-1α Inhibits LTBR IKK-γ NF-κB Signaling TAK1 HIF-1β HIF-2α IL1 PI3K IKK-α IKK-β LYN P Under Inflammatory TRAF2 HIF1α ? p50 RelA/p65 SYK BCAP TRAF3 CD40 P P TNFR1 Conditions XIAP P IL1R RIP cIAPs NIK TRAF2 IkB TRADD PHD1 cIAPs Ubc13 ? p50 TRAF2 NIK BAFF PHD3 p50 RelA/p65 Nuclear Translocation & LPS TRAF3 FIH RelA/p65 Target Gene TRIF Upregulation IRAK cIAPs PDK1 BAFFR TLRs TRIF TAB2/3 TAK1 MHC-Antigen TRAF3 NIK IRAK Degradation TRAF3 MYD88 MALT1 Select NF-κB Target Genes NF-κB Signaling Inhibitors TCR Small NIK Functions Gene Names Activity in NF-κB Signaling TRAF6 IKK-γ AKT LCK Molecules NIK ZAP70 NIK IKK-α IKK-β Cytokines/Chemokines & Their BAFF/TNFSF13B, BLIMP1/PRDM1, CCL1, CCL11, CCL15, CCL17, CCL19, CCL2/MCP1, CCL20, CCL22, SP 100030 NF-κB and AP-1 dual inhibitor P P NIK Modulators CCL23, CCL28, CCL3, CCL4, CCL5/RANTES, CINC-1, CX3CL1/Fractalkine, CXCL1, CXCL2, CXCL3, CXCL5, IT 901 NF-κB c-Rel subunit inhibitor Accumulation CXCL9, IFNB1, IL10, IL11, IL12A(p35), IL12B(p40), IL13, IL17, IL1A, IL1B, IL1RN/IL1RA, IL2, IL23A(p19), GSK3 IL27(p28), IL27B, IL6, IL8, IL9, INFA5, KC, LTA/TNFβ, LTB/TNFSF3, TNF/TNFα, TNFSF10/TRAIL, VEGI Bay 11-7085 Irreversible inhibitor of TNF-α-induced IκBα phosphorylation Ro 106-9920 Inhibitor of NF-κB activation
    [Show full text]
  • Mouse Samples
    AssayGate, Inc. 9607 Dr. Perry Road Suite 103. Ijamsville, MD 21754. Tel: (301)874-0988. Fax: (301)560-8288. ELISA Services for Mouse Samples ID Mouse Analyte 1 1, 25-Dihydroxyvitamin D3 (DHVD3) 2 17-Hydroxyprogesterone (17-OHP) 3 2',5'-Oligoadenylate Synthetase 1 (OAS1) 4 25-Hydroxyvitamin D3 (HVD3) 5 5-Hydroxytryptamine (5-HT) 6 8-Hydroxydeoxyguanosine (8-OHdG) 7 A Disintegrin And Metalloprotease 8 (ADAM8) 8 A Disintegrin And Metalloprotease 9 (ADAM9) 9 Acetyl Coenzyme A Carboxylase Alpha (ACACa) 10 Acetylcholine (ACH) 11 Acid Phosphatase 1 (ACP1) 12 Acid Phosphatase 2, Lysosomal (ACP2) 13 Acid Phosphatase 3, Prostatic (ACP3) 14 Acid Phosphatase 5, Tartrate Resistant (ACP5) 15 Actin Alpha 2, Smooth Muscle (ACTa2) 16 Actin Related Protein 2/3 Complex Subunit 4 (ARPC4) 17 Actinin Alpha 2 (ACTN2) 18 Activated Leukocyte Cell Adhesion Molecule (ALCAM) 19 Activated Protein C (APC) 20 Activating Transcription Factor 5 (ATF5) 21 Activin A (ACVA) 22 Activin AB (ACVAB) 23 Activity Regulated Cytoskeleton Associated Protein (ARC) 24 Adenylate Cyclase Activating Polypeptide 1, Pituitary (ADCYAP1) 25 Adiponectin (ADP) 26 Adiponectin Receptor 1 (ADIPOR1) 27 Adrenergic Receptor, Alpha 1A (ADRa1A) 28 Adrenocorticotropic Hormone (ACTH) 29 Adrenomedullin (ADM) 30 Advanced Glycosylation End Product Specific Receptor (AGER) 31 Afamin (AFM) 32 Aggrecan (AGC) 33 Alanine Aminotransferase (ALT) 1 34 Albumin (ALB) 35 Alcohol Dehydrogenase 1 (ADH1) 36 Alcohol Dehydrogenase 7 (ADH7) 37 Aldehyde Dehydrogenase, Mitochondrial (ALDM) 38 Aldosterone (ALD) 39 Alkaline
    [Show full text]
  • Adipose Gene Expression Profiles Reveal Novel Insights Into the Adaptation of Northern Eurasian Semi-Domestic Reindeer (Rangifer
    bioRxiv preprint doi: https://doi.org/10.1101/2021.04.17.440269; this version posted April 19, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. 1 Adipose gene expression profiles reveal novel insights into the 2 adaptation of northern Eurasian semi-domestic reindeer 3 (Rangifer tarandus) 4 Short title: Reindeer adipose transcriptome 5 6 Melak Weldenegodguad1, 2, Kisun Pokharel1¶, Laura Niiranen3¶, Päivi Soppela4, 7 Innokentyi Ammosov5, Mervi Honkatukia6, Heli Lindeberg1, Jaana Peippo1, 6, Tiina 8 Reilas1, Nuccio Mazzullo4, Kari A. Mäkelä3, Tommi Nyman7, Arja Tervahauta2, 9 Karl-Heinz Herzig8, 9, 10, Florian Stammler4, Juha Kantanen1* 10 11 1 Natural Resources Institute Finland (Luke), Jokioinen, Finland 12 2 Department of Environmental and Biological Sciences, University of Eastern 13 Finland, Kuopio, Finland 14 3 Research Unit of Biomedicine, Faculty of Medicine, University of Oulu, Oulu, 15 Finland 16 4 Arctic Centre, University of Lapland, Rovaniemi, Finland 17 5 Board of Agricultural Office of Eveno-Bytantaj Region, Batagay-Alyta, The Sakha 18 Republic (Yakutia), Russia 19 6 NordGen—Nordic Genetic Resource Center, Ås, Norway 20 7 Department of Ecosystems in the Barents Region, Norwegian Institute of 21 Bioeconomy Research, Svanvik, Norway 22 8 Research Unit of Biomedicine, Medical Research Center, Faculty of Medicine, 23 University of Oulu bioRxiv preprint doi: https://doi.org/10.1101/2021.04.17.440269; this version posted April 19, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity.
    [Show full text]
  • Investigations of 12Α-Hydroxylated Bile Acid Signaling in Intestinal Organoids
    INVESTIGATIONS OF 12α-HYDROXYLATED BILE ACID SIGNALING IN INTESTINAL ORGANOIDS Tiara Rinjani Ahmad Submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Graduate School of Arts and Sciences COLUMBIA UNIVERSITY 2019 © 2019 Tiara R. Ahmad All rights reserved ABSTRACT Investigations of 12α-Hydroxylated Bile Acid Signaling in Intestinal Organoids Tiara R. Ahmad Bile acids (BAs) comprise a diverse group of cholesterol metabolites with multiple modes of action. Much of the role of BAs and their receptors in energy homeostasis has been discerned from studies on genetic and/or pharmacologic manipulations. Additionally, changes in BA metabolism and transport have been reported in settings of insulin resistance, obesity, and liver dysfunction. Thus, BA-based interventions have been proposed for treatment of metabolic diseases. However, the heterogeneity of endogenous BAs lends to different affinities for and potencies in activating the various BA receptors, and the effects of altering BA composition per se are incompletely understood. In this dissertation, we aimed to characterize the effects of altering BA composition by stimulating intestinal organoids with distinct BA pools modeled after those in humans and mice. Unexpectedly, we found that BA composition regulated expression of the manganese transporter encoded by Slc30a10 and manganese efflux from cells, suggesting a role for BAs in metal homeostasis. We also identified genes that were similarly and differentially regulated by the distinct mouse and human BA pools. Overall, our studies reveal a pathway by which BAs could modulate micronutrient metabolism, which might also mediate known effects of BAs on macronutrient metabolism. Table of Contents List of Figures ……………………………………………………………………………………..
    [Show full text]
  • IMMUNICONCEPT INDIA PVT. LTD. F-242A, Street No
    IMMUNICONCEPT INDIA PVT. LTD. F-242A, Street No. 7, Pandav Nagar, Mayur Vihar Phase-I, New Delhi-110091 Tel.: +91 11 22753711, 43063564 [email protected] Fax.: +91 11 22753710 [email protected] IMMUNICONCEPT INDIA PVT. LTD. www.immunoconceptindia.com Product Catalog-Diagnostics (Elisa Kits & Rapid Tests) INDEX STREPTAVIDIN - COATED WELLS ELISA KITS Pack Size Kit sensitivity/ Product Name Incubation Standard Range SL.NO DESCRIPTION SHEET (Wells) components specificity TSH Elisa Kit (Serum/Plasma) 60'/15' at RT 96/192/480 7 cal(0-40ng/ml),with control RTU/CE,IVD 0.037ng/ml 1 STREPTAVIDIN - COATED WELLS ELISA KITS 1 T3 Elisa Kit (Serum/Plasma) 60'/15' at RT 96/192 6 cal(0-8ng/ml),with control RTU/CE,IVD 0.037ng/ml T4 Elisa Kit (Serum/Plasma) 60'/15' at RT 96/192 6 cal(0-25µg/dl),with control RTU/CE,IVD 0.16µg/dl 2 REPRODUCTION (Fertility & Steroidal Hormone) 2 6 cal(0-100mIU/ml),with FSH Elisa Kit (Serum/Plasma) 60'/15' at RT 96 RTU/CE,IVD 0.002mIU/ml control 3 TUMER MARKER (CANCER MARKER) 4 6 cal(0-200mIU/ml),with LH Elisa Kit (Serum/Plasma) 45'/15'at RT 96 RTU/CE,IVD 0.012 mIU/ml control 4 VITAMINS DETECTION KITS 5 6 cal(0-250mIU/ml),with HCG Elisa Kit (Serum/Plasma) 60'/15'at RT 96 RTU/CE,IVD 0.082mIU/ml control Prolactin Elisa Kit (Serum/ 5 PRENATAL SCREENING 6 60'/15'at RT 96 6 cal(0-100ng/ml),with control RTU/CE,IVD 0.002 mIU/ml Plasma) 6 AUTOIMMUNITY 7 FT3 Elisa Kit (Serum/Plasma) 45'/15'at RT 96 6 cal(0-16pg/ml),with control RTU/CE,IVD 0.037pg/ml FT4 Elisa Kit (Serum/Plasma) 45'/15'at RT 96 6 cal(0-8ng/ml),with
    [Show full text]
  • Free PDF Download
    Eur opean Rev iew for Med ical and Pharmacol ogical Sci ences 2014; 18: 1033-1040 Identified differently expressed genes in renal cell carcinoma by using multiple microarray datasets running head: differently expressed genes in renal cell carcinoma Y. CHENG, M. HONG 1, B. CHENG Department of Urinary Surgery, Affiliated Hospital of Luzhou Medical College in Sichuan Province, Luzhou, China 1Department of Operating Room, Affiliated Hospital of Luzhou Medical College in Sichuan Province, Luzhou, China Abstract. – OBJECTIVE : The purpose of this tases 1,2 . It was the most common form of kidney study was to identify differentially expressed cancer, accounted for approximately 3% of adult genes and analysis biological processes related malignancy 3,4 . The incidence of RCC was in - to renal cell carcinoma. 5 METHODS: A meta-analysis was performed creasing in the past few years . The risk factors using the Rank Product package of Gene Ex - for its development are still under intense investi - pression Omnibus datasets of renal cell carcino - gation 6. ma. Then Gene Ontology enrichment analyses RCC is a complex disease that many genes and pathway analysis were performed based on and signaling pathways are involved in its devel - Gene Ontology website and Kyoto Encyclopedia opment 7. Analysis of gene regulation mechanism of Genes and Genomes. Protein-protein interac - tion network was constructed used Cytoscape can help us understand RCC. Gene regulation software. analysis used high-throughput experiment RESULTS: We identified a total of 1992 differ - method such as microarray has increased in re - entially expressed genes Rank Product package cently years. Many differential expression genes of renal cell carcinoma, 840 of them were not in - (DEGs) were identified by microarray.
    [Show full text]
  • Method for the Development of Gene Panels For
    (19) & (11) EP 1 364 069 B1 (12) EUROPEAN PATENT SPECIFICATION (45) Date of publication and mention (51) Int Cl.: of the grant of the patent: C12Q 1/68 (2006.01) 22.04.2009 Bulletin 2009/17 (86) International application number: (21) Application number: 02724190.0 PCT/EP2002/002255 (22) Date of filing: 01.03.2002 (87) International publication number: WO 2002/070742 (12.09.2002 Gazette 2002/37) (54) METHOD FOR THE DEVELOPMENT OF GENE PANELS FOR DIAGNOSTIC AND THERAPEUTIC PURPOSES BASED ON THE EXPRESSION AND METHYLATOIN STATUS OF THE GENES VERFAHREN ZUR ENTWICKLUNG VON GENSÄTZEN ZU DIAGNOSTISCHEN UND THERAPEUTISCHEN ZWECKEN AUF GRUNDLAGE DES EXPRESSIONS- UND METHYLIERUNGSSTATUS DER GENE PROCEDE DE MISE AU POINT DE GROUPES D’ECHANTILLONS DE GENES A DES FINS DE DIAGNOSTIC ET DE THERAPIE QUI SONT BASES SUR L’EXPRESSION ET L’ETAT DE METHYLATION DES GENES (84) Designated Contracting States: (56) References cited: AT BE CH CY DE DK ES FI FR GB GR IE IT LI LU WO-A-00/39347 WO-A-00/44934 MC NL PT SE TR WO-A-00/70090 WO-A-01/18241 (30) Priority: 01.03.2001 US 272549 P • HERMAN J G ET AL: "INCIDENCE AND FUNCTIONAL CONSEQUENCES OF HMLH1 (43) Date of publication of application: PROMOTOR HYPERMETHYLATION IN 26.11.2003 Bulletin 2003/48 COLORECTAL CARCINOMA" PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF (73) Proprietor: Epigenomics AG USA, NATIONAL ACADEMY OF SCIENCE. 10178 Berlin (DE) WASHINGTON, US, vol. 95, June 1998 (1998-06), pages 6870-6875, XP002944676 ISSN: 0027-8424 (72) Inventors: • GUO YONGJING ET AL: "DNA methylation status • OLEK, Alexander of uPA promoter directly affects the expression 10115 Berlin (DE) of uPA in human breast cancer cells to alter their • BERLIN, Kurt invasive potential" PROCEEDINGS OF THE 14532 Stahndorf (DE) ANNUAL MEETING OF THE AMERICAN ASSOCIATION FOR CANCER RESEARCH, NEW (74) Representative: Krauss, Jan et al YORK, NY, US, vol.
    [Show full text]