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What Are Transfer Factors?
WHAT ARE TRANSFER FACTORS? More Next Blog» WHAT ARE TRANSFER FACTORS? Not a Vitamin, Mineral, Herb or Hormone. A NEW Nutritionparadigm & inHealthcare. Over 40 years in research,3000 studies in nations70 and hundreds of professionals are recommending thissupplement. product These are tiny molecules that transfer immunity informationentity from to oneanother, such as between a mother and her infant whobreastfeeds. she It does not interact with drug has It zerois alltoxity. natural,safe and effective for all people and all ages. About Me NAME: KYWONG LOCATION: KUALA LUMPUR, MALAYSIA View my complete profile SATURDAY, OCTOBER 21, 2006 WHAT ARE TRANSFER FACTORS? In a World WHAT ARE TRANSFER FACTORS? In a World Where Stres... Where Stress, Pollution, Poor Diet and New “Super Transfer Factor CARDIO bugs” Are Constantly Undermining People’s strengthened your heart wit... IMMUNE SYSTEM HERBS GINSENG & DONG QUAI - BREAST CANCER LINK? What are HOW TO BOAST UP & Transfer MODULATE YOUR IMMUNE SYSTEM AGA... Factors? In a New Trends - Fewer world where Breast Cancer Patients to stress, Get C... pollution, Acai berries in Transfer poor diet and Factor RioVida drinks new strains of What are Transfer Factors? In a world where “superbugs” str... are constantly undermining people’simmune systems, 4Life recognizes the importance of innovation in nutrition. We know that in order to January 2006 successfully battle these everyday challenges and to achieve overall well- February 2006 being, continual advancements need to be made to help support March 2006 immune strength and promote better health for you and your family. April 2006 May 2006 One of the strongest forces in nature for transferring and ensuring good October 2006 health, transfer factors has taken their place in the forefront of nutritional science. -
Characterization and Safety Profile of Transfer Factors Peptides, A
biomolecules Article Characterization and Safety Profile of Transfer Factors Peptides, a Nutritional Supplement for Immune System Regulation Hudson Polonini 1,* , Any Elisa de Souza Schmidt Gonçalves 2, Eli Dijkers 1 and Anderson de Oliveira Ferreira 1 1 Fagron B.V., Lichtenauerlaan 182, 3062 ME, Rotterdam, The Netherlands; [email protected] (E.D.); [email protected] (A.d.O.F.) 2 Infinity Pharma Brasil, Av. Pierre Simon de Laplace, 751 Techno Park, Campinas, SP 13069-320, Brazil; any.goncalves@infinitypharma.com.br * Correspondence: [email protected] Abstract: Imuno TF® is a nutritional supplement composed of isolated transfer factors (TF) from porcine spleen. It is composed of a specific mixture of molecules that impact functions of the biological systems and historically is linked to the immune system regulation. In this study, we demonstrate for the first time its proteomic analysis, nutritional composition, and safety profile in terms of mutagenic potential and acute oral dose (LD50). The obtained analysis indicated the product is a complex set of oligo- and polypeptides constituted of 163 different peptides which can potentially act on multiple mechanisms on the immune system pathways. The chemical composition showed low fat and low sugar content, saturated fatty acids-free, and the presence of 10 vitamins and 11 minerals. −1 No mutagenic effect was observed, and the LD50 was 5000 mg kg body weight. This accounts for a safe product to be used by the oral route, with potential benefits for the immune system. Citation: Polonini, H.; Gonçalves, Keywords: transfer factor; Imuno TF; safety profile; characterization; peptides; proteomics A.E.d.S.S.; Dijkers, E.; Ferreira, A.d.O. -
Structural Nature and Functions of Transfer Factors.Pdf
PDFlib PLOP: PDF Linearization, Optimization, Protection Page inserted by evaluation version www.pdflib.com – [email protected] Structural Nature and Functions of Transfer Factors CHARLES H. KIRKPATRICK Conrad D. Stephnzsmt Luburatmy for &starch in Immunology NationalJewish ckttcr for Immumhgy and Respimtmy Mdkine Denver, colorado80206 INTRODUCTION Successful transfer of cell-mediated immune responses from immune donors to nonimmune recipients was first described by Landsteiner and Chase in the early 1940~.~JGuinea pigs were sensitized to express contact allergy to picryl chloride or delayed hypersensitivity to tuberculin. After washed peritoneal exudate cells from the sensitized donors were given to unsensitized recipients, the recipients acquired the ability to express the cell-mediated immune responses of the donors. Further studies indicated that long-lasting and regularly successfid transfers were observed when there were syngeneic relationships between the donors and recipients, and only when intact, living donor cells were used. Attempts to transfer these reactivities with serum or dead cells were unsuccessful. Later experiments by Crepea and Cooke3 and Jeter and associates4 disclosed that under certain conditions it was possible to transfer contact hypersensitivity to simple chemicals such as poison ivy antigens and chlorodinitrobenzene (CDNB) from sensi- tized guinea pigs to unsensitized recipients with unliving lymphoid cells, allogeneic cells, and even cell extracts. The disparate results between these reports and the work of Chase have never been completely explained. The active component of the cell extracts was called “transfer factor,” and transfer of delayed-type hypersensitivity in humans with transfer factors was studied extensively by Lawrence and associates5in the 1950s. Their experiments involved lysates of blood leukocytes from donors who had positive delayed-hypersensitivity to antigens such as tuberculin (PPD), diphtheria toxoid, streptococcal M protein, or coccidioidin. -
Genomic Analyses of PMBL Reveal New Drivers and Mechanisms of Sensitivity to PD-1 Blockade
Regular Article LYMPHOID NEOPLASIA Genomic analyses of PMBL reveal new drivers and mechanisms of sensitivity to PD-1 blockade Bjoern Chapuy,1,2,* Chip Stewart,3,* Andrew J. Dunford,3,* Jaegil Kim,3 Kirsty Wienand,1 Atanas Kamburov,3 Gabriel K. Griffin,4 Pei-Hsuan Chen,4 Ana Lako,4 Robert A. Redd,5 Claire M. Cote,1 Matthew D. Ducar,6 Aaron R. Thorner,6 Scott J. Rodig,4 Gad Getz,3,7,8,† Downloaded from https://ashpublications.org/blood/article-pdf/134/26/2369/1549702/bloodbld2019002067.pdf by Margaret Shipp on 30 December 2019 and Margaret A. Shipp1,† 1Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA; 2Department of Hematology and Oncology, University Medical Center Gottingen,¨ Gottingen,¨ Germany; 3Broad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, MA; 4Department of Pathology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA; 5Department of Data Sciences and 6Center for Cancer Genome Discovery, Dana-Farber Cancer Institute, Boston, MA; and 7Department of Pathology and 8Center for Cancer Research, Massachusetts General Hospital, Harvard Medical School, Boston, MA KEY POINTS Primary mediastinal large B-cell lymphomas (PMBLs) are aggressive tumors that typically present as large mediastinal masses in young women. PMBLs share clinical, transcriptional, l Comprehensive genomic analyses of and molecular features with classical Hodgkin lymphoma (cHL), including constitutive PMBL reveal new activation of nuclear factor kB (NF-kB), JAK/STAT signaling, and programmed cell death genetic drivers such protein 1 (PD-1)–mediated immune evasion. The demonstrated efficacy of PD-1 blockade in as ZNF217. relapsed/refractory PMBLs led to recent approval by the US Food and Drug Administration l High mutational and underscored the importance of characterizing targetable genetic vulnerabilities in this burden, MSI, and disease. -
Transcriptome Analysis of Human Diabetic Kidney Disease
ORIGINAL ARTICLE Transcriptome Analysis of Human Diabetic Kidney Disease Karolina I. Woroniecka,1 Ae Seo Deok Park,1 Davoud Mohtat,2 David B. Thomas,3 James M. Pullman,4 and Katalin Susztak1,5 OBJECTIVE—Diabetic kidney disease (DKD) is the single cases, mild and then moderate mesangial expansion can be leading cause of kidney failure in the U.S., for which a cure has observed. In general, diabetic kidney disease (DKD) is not yet been found. The aim of our study was to provide an considered a nonimmune-mediated degenerative disease unbiased catalog of gene-expression changes in human diabetic of the glomerulus; however, it has long been noted that kidney biopsy samples. complement and immunoglobulins sometimes can be de- — tected in diseased glomeruli, although their role and sig- RESEARCH DESIGN AND METHODS Affymetrix expression fi arrays were used to identify differentially regulated transcripts in ni cance is not clear (4). 44 microdissected human kidney samples. The DKD samples were The understanding of DKD has been challenged by multi- significant for their racial diversity and decreased glomerular ple issues. First, the diagnosis of DKD usually is made using filtration rate (~20–30 mL/min). Stringent statistical analysis, using clinical criteria, and kidney biopsy often is not performed. the Benjamini-Hochberg corrected two-tailed t test, was used to According to current clinical practice, the development of identify differentially expressed transcripts in control and diseased albuminuria in patients with diabetes is sufficient to make the glomeruli and tubuli. Two different Web-based algorithms were fi diagnosis of DKD (5). We do not understand the correlation used to de ne differentially regulated pathways. -
Genome-Wide Identification of Genes Regulating DNA Methylation Using Genetic Anchors for Causal Inference
bioRxiv preprint doi: https://doi.org/10.1101/823807; this version posted October 30, 2019. 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 4.0 International license. Genome-wide identification of genes regulating DNA methylation using genetic anchors for causal inference Paul J. Hop1,2, René Luijk1, Lucia Daxinger3, Maarten van Iterson1, Koen F. Dekkers1, Rick Jansen4, BIOS Consortium5, Joyce B.J. van Meurs6, Peter A.C. ’t Hoen 7, M. Arfan Ikram8, Marleen M.J. van Greevenbroek9,10, Dorret I. Boomsma11, P. Eline Slagboom1, Jan H. Veldink2, Erik W. van Zwet12, Bastiaan T. Heijmans1* 1 Molecular Epidemiology, Department of Biomedical Data Sciences, Leiden University Medical Center, Leiden, 2333 ZC, The Netherlands 2 Department of Neurology, UMC Utrecht Brain Center, University Medical Centre Utrecht, Utrecht University, Utrecht 3584 CG, Netherlands 3 Department of Human Genetics, Leiden University Medical Center, Leiden, 2333 ZC, The Netherlands 4 Department of Psychiatry, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam, 1081 HV, The Netherlands 5 Biobank-based Integrated Omics Study Consortium. For a complete list of authors, see the acknowledgements. 6 Department of Internal Medicine, Erasmus Medical Centre, Rotterdam, The Netherlands. 7 Centre for Molecular and Biomolecular Informatics, Radboud Institute for Molecular Life Sciences, Radboud University -
Chemokine Profiles of Interstitial Pneumonia in Patients With
www.nature.com/scientificreports OPEN Chemokine profiles of interstitial pneumonia in patients with dermatomyositis: a case control Received: 16 November 2016 Accepted: 30 March 2017 study Published: xx xx xxxx Katsuhiro Oda1, Takuya Kotani1, Tohru Takeuchi1, Takaaki Ishida1, Takeshi Shoda1, Kentaro Isoda1, Shuzo Yoshida1, Yasuichiro Nishimura2 & Shigeki Makino1 Chemokines play an important role in the pathophysiology of dermatomyositis (DM) with interstitial pneumonia (IP). However, the relation between chemokines and the disease activity or prognosis of DM-IP has not been elucidated. We evaluated the serum C-C motif chemokine ligand (CCL) 2, Th1 chemokines (C-X-C motif chemokine ligand [CXCL] 9, CXCL10, CXCL11), and Th2 chemokine (CCL17) profiles of 30 patients, and examined the relation between these chemokines and the disease activity or prognosis of DM-IP. Initial serum CCL2 level was higher in the death group (P = 0.007). To determine the cut-off points effective as poor prognostic factors of DM-IP, ROC curve analysis was carried out on initial serum CCL2 level. The value that maximized the area under the ROC curve was 894 pg/mL (sensitivity: 100%, specificity: 70.8%). Serum CCL2, CXCL9, CXCL10, and CXCL11 levels were lower at 2 weeks after treatment initiation than before treatment. Serum CCL2, CXCL10, and CXCL11 levels at 2 weeks after treatment initiation were higher in the death group. Serum levels of chemokines such as CCL2, CXCL10, and CXCL11 may be possible biomarkers of disease activity and prognosis in DM-IP, and serum CCL2 level may be useful when deciding initial treatment. Dermatomyositis (DM) is one of the idiopathic inflammatory myopathies characterized by inflammation of skin and muscle1, 2. -
The Role of the NFAT Signalling Pathway in Diffuse Large B-Cell Lymphoma
The role of the NFAT signalling pathway in Diffuse Large B-cell Lymphoma Holly White Doctor of Philosophy Thesis September 2015 Supervisors: Dr Chris Bacon, Professor Neil Perkins & Dr Vikki Rand Northern Institute for Cancer Research Word count: 66,024 1 Abstract Diffuse Large B-Cell Lymphomas (DLBCL) are common, aggressive malignancies of mature B-lymphocytes that represent ~40% of lymphomas. Despite the widespread use of combined immunochemotherapy, approximately 50% of patients with DLBCL die from their disease. The two main DLBCL subgroups resemble activated B cells (ABC) or germinal centre B cells (GCB), where patients with ABC-DLBCL have significantly worse outcome. There is urgent need for novel therapeutic strategies in the treatment of DLBCL, which requires a better understanding of the molecular pathways upon which tumours depend. Accumulating evidence suggests that the signalling networks promoting and sustaining DLBCL derive from dysregulation of the normal pathways controlling B-lymphocyte activation and differentiation. There is increasing evidence indicating important roles for the NFAT family of transcription factors in DLBCL. Constitutively-active nuclear NFAT2 has been demonstrated in approximately 40% of primary DLBCL samples and NFAT has been shown to regulate a small number of genes associated with DLBCL growth/survival. This project investigated the role of NFAT in DLBCL. Nuclear localisation and activation of NFAT family members were characterised in a panel of DLBCL cell lines and chemical inhibition of calcineurin/NFAT, using Cyclosporin A (CsA), indicated dependency on the calcineurin/NFAT pathway for survival. Gene expression microarray analysis performed in DLBCL cell lines treated with CsA revealed potential NFAT target genes involved in the tumour microenvironment and anergy. -
Recurrent Genetic Mutations in Lymphoid Malignancies
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine 1312 Recurrent Genetic Mutations in Lymphoid Malignancies EMMA YOUNG ACTA UNIVERSITATIS UPSALIENSIS ISSN 1651-6206 ISBN 978-91-554-9850-4 UPPSALA urn:nbn:se:uu:diva-314956 2017 Dissertation presented at Uppsala University to be publicly examined in Rudbecksalen, Dag Hammarskjölds Väg 20, Uppsala, Friday, 5 May 2017 at 13:15 for the degree of Doctor of Philosophy (Faculty of Medicine). The examination will be conducted in English. Faculty examiner: Professor Dimitar Efremov (Molecular Hematology Group of the International Centre for Genetic Engineering and Biotechnology (ICGEB) in Trieste, Italy). Abstract Young, E. 2017. Recurrent Genetic Mutations in Lymphoid Malignancies. Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine 1312. 82 pp. Uppsala: Acta Universitatis Upsaliensis. ISBN 978-91-554-9850-4. In recent years, the genetic landscape of B-cell derived lymphoid malignancies, including chronic lymphocytic leukemia (CLL), has been rapidly unraveled, identifying recurrent genetic mutations with potential clinical impact. Interestingly, ~30% of all CLL patients can be assigned to more homogeneous subsets based on the expression of a similar or “stereotyped” B-cell receptor (BcR). Considering that biased distribution of genetic mutations was recently indicated in specific stereotyped subsets, in paper I, we screened 565 subset cases, preferentially assigned to clinically aggressive subsets, and confirm the SF3B1 mutational bias in subset #2 (45%), but also report on similarly marked enrichment in subset #3 (46%). In contrast, NOTCH1 mutations were predominantly detected in subsets #1, #8, #59 and #99 (22-34%). This data further highlights a subset-biased acquisition of genetic mutations in the pathogenesis of at least certain subsets. -
Supplemental Materials
SUPPLEMENTARY DATA shRNA-containing lentiviral vectors. The shRNAs for each target genes were designed with the aid of web-based Invitrogen Block-It program. The oligonucleotides containing Fra-1, c-Jun or slug shRNA sequences were inserted into pLV-shRNA vector (Biosettia, San Diego, CA) according to manufacturer’s protocol. The Fra-1 mRNA target sequences are 5’- GGAGACTGACAAACTGGAAGA-3’ and 5’-GGATGGTACAGCCTCATTTCC-3’. The c-Jun mRNA target sequences are 5’-GGAACAGGTGGCACAGCTTAA-3’ and 5’- GGCACAGCTTAAACAGAAAGT-3’. The slug mRNA target sequences are 5’- GCATTTGCAGACAGGTCAAAT-3’ and 5’-GCTCATCTGCAGACCCATTCT-3’. Slug promoter construction. The slug promoter (GeneBank Accession number AB300659) was synthesized by PCR using genomic DNA isolated from MDA-MB-231 cells. The synthesized fragment was subcloned into pGL4-luciferase reporter gene plasmid (Promega, Madison, WI) and sequence confirmed by automated DNA sequencing. To generate AP1 mutant, the AP1 consensus sequence in the slug promoter was destroyed by introducing mutation at nucleotide 1009-1011 (GAC AGA). To determine the promoter activity, wild-type or mutant slug promoter reporter gene construct was transfected into MCF-7, MDA-MB-231, MDA-MB-436 or ZR-75-1 cells for 36 hrs and cell lysates collected to measure luciferase activity using Lipofectamine (Invitrogen, Carlsbad, CA). To determine the effect of Fra-1/c-Jun expression on slug promoter activity, the promoter reporter gene construct was co-transfected with expression vectors encoding Fra-1 and c-Jun into MCF-7 and ZR-75-1 cells for 48 hrs followed by the analysis of luciferase activity. Plasmid containing Renilla Luciferase gene was included during transfection to serve as an internal control and Dual Luciferase Assay System (Promega, Madison, WI) was used for measuring luciferase activity. -
Technical Paper
TECHNICAL PAPER BIOCHEMISTRY OF TRANSFER FACTOR I. INTRODUCTION Glutrasol products are comprised of three main ingredients: 1. transfer factor 2. glucans 3. lactic acid generating bacteria. Minor ingredients are adjusted for specific applications. This disclosure focuses on transfer factor. We know Glutrasol works because TEST groups repeatedly show dramatic improvement, relative to CONTROL groups. Here is information on how (biochemically) Glutrasol works. II. INDUCER/SUPPRESSOR FRACTIONS OF TRANSFER FACTOR Transfer factors are produced by T-lymphocytes and can transfer the ability to recognize a pathogen to cells that have not been in contact with the pathogen. They also heighten the immune system’s ability to react (increased reactivity or inducer function) to pathogens. Transfer factor produces a trigger for T-cell recognition of antigen. Transfer factor is a mixture of peptides, typically with a molecular weight < 10,000 Daltons. It's more appropriate to speak of "transfer factors" instead of "transfer factor." Fortunately, today's preparative methods produce consistent mixtures, which lead to repeatable responses. Fractions within the mixture serve different (and sometimes opposite) purposes. Two particularly important fractions are (1) the inducer fraction, and (2) the suppressor fraction [1][2]. Opposing functions were confirmed using the direct Leucocyte Migration Inhibition (LMI) test. These two fractions are consistent with field observations that transfer factor balances the immune system. For example, Date: 12/27/16 Author: Jack Menear, Chief Scientist and Patent Strategist, CortControl, LLC www.cortcontrol.com 1-855-982-2263 [email protected] TECHNICAL PAPER 1. The inducer fraction of transfer factor links the immune cells with an antigen-binding site, thereby increasing their reactivity to an antigenic stimulus. -
Circulating Tumor DNA Reveals Genetics, Clonal Evolution, and Residual Disease in Classical Hodgkin Lymphoma
From www.bloodjournal.org by Fredrik Schjesvold on August 4, 2018. For personal use only. Plenary Paper LYMPHOID NEOPLASIA Circulating tumor DNA reveals genetics, clonal evolution, and residual disease in classical Hodgkin lymphoma Valeria Spina,1,* Alessio Bruscaggin,1,* Annarosa Cuccaro,2 Maurizio Martini,3 Martina Di Trani,4 Gabriela Forestieri,1 Martina Manzoni,5 Adalgisa Condoluci,1,6 Alberto Arribas,1 Lodovico Terzi-Di-Bergamo,1 Silvia Laura Locatelli,4 Elisa Cupelli,2 Luca Ceriani,6 Alden A. Moccia,6 Anastasios Stathis,6 Luca Nassi,7 Clara Deambrogi,7 Fary Diop,7 Francesca Guidetti,1 Alessandra Cocomazzi,3 Salvatore Annunziata,8 Vittoria Rufini,8 Alessandro Giordano,8 Antonino Neri,5,9 Renzo Boldorini,10 Bernhard Gerber,6 Francesco Bertoni,1,6 Michele Ghielmini,6 Georg Stussi,¨ 6 Armando Santoro,4,11 Franco Cavalli,1,6 Emanuele Zucca,6 Luigi Maria Larocca,3 Gianluca Gaidano,7 Stefan Hohaus,2,† Carmelo Carlo-Stella,4,11,† and Davide Rossi1,6,† 1Institute of Oncology Research, Bellinzona, Switzerland; 2Institute of Hematology and 3Division of Pathology, Policlinico Gemelli Foundation, Catholic University of the Sacred Heart, Rome, Italy; 4Humanitas Cancer Center, Humanitas Clinical and Research Center, Milan, Italy; 5Department of Oncology and Hemato-oncology, University of Milan, Milan, Italy; 6Oncology Institute of Southern Switzerland, Bellinzona, Switzerland; 7Division of Hematology, Department of Translational Medicine, University of Eastern Piedmont, Novara, Italy; 8Institute of Nuclear Medicine, Policlinico Gemelli Foundation, Catholic University of the Sacred Heart, Rome, Italy; 9Hematology Unit, Foundation Ca’ Granda IRCCS, Ospedale Maggiore Policlinico, Milan, Italy; 10Division of Pathology, Department of Health Science, University of Eastern Piedmont, Novara, Italy; and 11Department of Biomedical Sciences, Humanitas University, Milan, Italy KEY POINTS The rarity of neoplastic cells in the biopsy imposes major technical hurdles that have so far limited genomic studies in classical Hodgkin lymphoma (cHL).