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Neuroinflammation Triggered by Β-Glucan/Dectin-1 Signaling Enables CNS Axon Regeneration
Neuroinflammation triggered by β-glucan/dectin-1 signaling enables CNS axon regeneration Katherine T. Baldwina,b,1, Kevin S. Carbajalc,d,1, Benjamin M. Segalc,d,2, and Roman J. Gigera,b,c,d,2 aDepartment of Cell and Developmental Biology, bCellular and Molecular Biology Graduate Program, cNeuroscience Graduate Program, and dHoltom-Garrett Program in Neuroimmunology, Department of Neurology, University of Michigan School of Medicine, Ann Arbor, MI 48109 Edited by Ben A. Barres, Stanford University School of Medicine, Stanford, CA, and approved January 22, 2015 (received for review December 22, 2014) Innate immunity can facilitate nervous system regeneration, yet growth can be undermined by concurrent toxicity (9). A deeper the underlying cellular and molecular mechanisms are not well understanding of these opposing effects will be important for understood. Here we show that intraocular injection of lipopoly- exploiting immunomodulatory pathways to promote neural re- saccharide (LPS), a bacterial cell wall component, or the fungal cell pair while minimizing bystander damage. wall extract zymosan both lead to rapid and comparable intravi- In the present study, we investigated the pathways that drive treal accumulation of blood-derived myeloid cells. However, when innate immune-mediated axon regeneration after ONC. We in- combined with retro-orbital optic nerve crush injury, lengthy duced sterile inflammation in the vitreous on the day of injury by growth of severed retinal ganglion cell (RGC) axons occurs only i.o. administration of zymosan or constituents of zymosan clas- in zymosan-injected mice, and not in LPS-injected mice. In mice sified as pathogen-associated molecular patterns (PAMPs). PAMPs dectin-1 deficient for the pattern recognition receptor but not are highly conserved microbial structures that serve as ligands for TLR2 , Toll-like receptor-2 ( ) zymosan-mediated RGC regeneration pattern recognition receptors (PRRs). -
03 November 2019 Palm Wings Ephesus Hotel Congress Center, Kus¸Adası, Aydın (Turkey)
www.actaphysiol.org December 2019 • Volume 227 • Supplement 722 OFFICIAL JOURNAL OF THE FEDERATION OF EUROPEAN PHYSIOLOGICAL SOCIETIES Turkish Society of Physiological Sciences 45th National Physiology Congress 31 October – 03 November 2019 Palm Wings Ephesus Hotel Congress Center, Kus¸adası, Aydın (Turkey) PUBLICATION HISTORY Acta Physiologica 2006– Acta Physiologica Scandinavica 1940–2005 Skandinavisches Archiv für Physiologie 1889–1939 AAPHA_v227_is722_issue-info.inddPHA_v227_is722_issue-info.indd 1 229-Nov-199-Nov-19 12:00:2112:00:21 PMPM Chief Editor INFORMATION FOR SUBSCRIBERS Pontus B. Persson, Berlin Acta Physiologica is published in 12 issues per year. Subscription prices for 2020 € Editors are: Institutional: 1112 (Europe), $1662 (The Americas), $1942 (Rest of World). Cardiovascular Physiology – Frantisek Kolar, Prague; Holger Nilsson, Gothenburg Prices are exclusive of tax. Australian GST, Canadian GST/HST and European and William E. Louch, Oslo VAT will be applied at the appropriate rates. For more information on current tax Cell Biology – Sari Lauri, Helsinki rates, please go to www.wileyonlinelibrary.com/tax-vat. The price includes online Chronobiology and Endocrinology – Charna Dibner, Geneva access to the current and all online back fi les to January 1st 2016, where available. Exercise Physiology – Jan Henriksson, Stockholm For other pricing options, including access information and terms and conditions, Gastrointestinal Physiology – Markus Sjöblom, Uppsala please visit www.wileyonlinelibrary.com/access Infl ammation – Joakim Ek, Gothenburg Metabolism and Nutritional Physiology – Karl-Heinz Herzig, Oulu DELIVERY TERMS AND LEGAL TITLE Muscle Physiology – Gabriele Pfi tzer, Cologne Where the subscription price includes print issues and delivery is to the recipients Nervous System – Alexej Verkhratsky, Manchester address, delivery terms are Delivered at Place (DAP); the recipient is responsible Renal Physiology – Peter Bie, Odense; Boye L. -
W W W .Bio Visio N .Co M New Products Added in 2020
New products added in 2020 Please find below a list of all the products added to our portfolio in the year 2020. Assay Kits Product Name Cat. No. Size Product Name Cat. No. Size N-Acetylcysteine Assay Kit (F) K2044 100 assays Human GAPDH Activity Assay Kit II K2047 100 assays Adeno-Associated Virus qPCR Quantification Kit K1473 100 Rxns Human GAPDH Inhibitor Screening Kit (C) K2043 100 assays 20 Preps, Adenovirus Purification Kit K1459 Hydroxyurea Colorimetric Assay Kit K2046 100 assays 100 Preps Iodide Colorimetric Assay Kit K2037 100 assays Aldehyde Dehydrogenase 2 Inhibitor Screening Kit (F) K2011 100 assays Laccase Activity Assay Kit (C) K2038 100 assays Aldehyde Dehydrogenase 3A1 Inhibitor Screening Kit (F) K2060 100 assays 20 Preps, Lentivirus and Retrovirus Purification Kit K1458 Alkaline Phosphatase Staining Kit K2035 50 assays 100 Preps Alpha-Mannosidase Activity Assay Kit (F) K2041 100 assays Instant Lentivirus Detection Card K1470 10 tests, 20 tests Beta-Mannosidase Activity Assay Kit (F) K2045 100 assays Lentivirus qPCR Quantification Kit K1471 100 Rxns 50 Preps, Buccal Swab DNA Purification Kit K1466 Maleimide Activated KLH-Peptide Conjugation Kit K2039 5 columns 250 Preps Methionine Adenosyltransferase Activity Assay Kit (C) K2033 100 assays CD38 Activity Assay Kit (F) K2042 100 assays miRNA Extraction Kit K1456 50 Preps EZCell™ CFDA SE Cell Tracer Kit K2057 200 assays MMP-13 Inhibitor Screening Kit (F) K2067 100 assays Choline Oxidase Activity Assay Kit (F) K2052 100 assays Mycoplasma PCR Detection Kit K1476 100 Rxns Coronavirus -
Follicle-Stimulating Hormone (FSH)
Hormone Structure (1) Principal Source Link to diagram showing locations of the main endocrine glands Thyroid-stimulating hormone (TSH) protein (201) Follicle-stimulating hormone (FSH) protein (204) Luteinizing hormone (LH) protein (204) Anterior lobe of pituitary Prolactin (PRL) protein (198) Growth hormone (GH) protein (191) Adrenocorticotropic hormone (ACTH) peptide (39) Vasopressin peptide (9) Posterior lobe of pituitary Oxytocin peptide (9) Thyrotropin-releasing hormone (TRH) peptide (3) Gonadotropin-releasing hormone (GnRH) peptide (10) Growth hormone-releasing hormone (GHRH) peptides (40, 44) Hypothalamus Corticotropin-releasing hormone (CRH) peptide (41) Somatostatin peptides (14, 28) Dopamine tyrosine derivative Melatonin tryptophan derivative Pineal gland Thyroxine (T4) tyrosine derivative Thyroid Gland Calcitonin peptide (32) Parathyroid hormone (PTH) protein (84) Parathyroid glands FGF-23 (phosphatonin) protein (251) Osteocalcin peptide (49) Bone Lipocalin 2 protein (198) Erythropoietin (EPO) protein (166) Glucocorticoids (e.g., cortisol) steroids Mineralocorticoids (e.g., aldosterone) steroids Adrenal cortex Androgens (e.g., testosterone) steroids Adrenaline (epinephrine) tyrosine derivative Adrenal medulla Noradrenaline (norepinephrine) tyrosine derivative Estrogens (e.g., estradiol) steroid Ovarian follicle Progesterone steroid Corpus luteum and placenta Human chorionic gonadotropin (HCG) protein (237) Trophoblast and placenta Androgens (e.g., testosterone) steroid Testes Insulin protein (51) Glucagon peptide (29) Pancreas -
US 2017/0020926 A1 Mata-Fink Et Al
US 20170020926A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2017/0020926 A1 Mata-Fink et al. (43) Pub. Date: Jan. 26, 2017 (54) METHODS AND COMPOSITIONS FOR 62/006,825, filed on Jun. 2, 2014, provisional appli MMUNOMODULATION cation No. 62/006,829, filed on Jun. 2, 2014, provi sional application No. 62/006,832, filed on Jun. 2, (71) Applicant: RUBIUS THERAPEUTICS, INC., 2014, provisional application No. 61/991.319, filed Cambridge, MA (US) on May 9, 2014, provisional application No. 61/973, 764, filed on Apr. 1, 2014, provisional application No. (72) Inventors: Jordi Mata-Fink, Somerville, MA 61/973,763, filed on Apr. 1, 2014. (US); John Round, Cambridge, MA (US); Noubar B. Afeyan, Lexington, (30) Foreign Application Priority Data MA (US); Avak Kahvejian, Arlington, MA (US) Nov. 12, 2014 (US) ................. PCT/US2O14/0653O4 (21) Appl. No.: 15/301,046 Publication Classification (22) PCT Fed: Mar. 13, 2015 (51) Int. Cl. A6II 35/28 (2006.01) (86) PCT No.: PCT/US2O15/02O614 CI2N 5/078 (2006.01) (52) U.S. Cl. S 371 (c)(1), CPC ............. A61K 35/28 (2013.01); C12N5/0641 (2) Date: Sep. 30, 2016 (2013.01): CI2N 5/0644 (2013.01); A61 K Related U.S. Application Data 2035/122 (2013.01) (60) Provisional application No. 62/059,100, filed on Oct. (57) ABSTRACT 2, 2014, provisional application No. 62/025,367, filed on Jul. 16, 2014, provisional application No. 62/006, Provided are cells containing exogenous antigen and uses 828, filed on Jun. 2, 2014, provisional application No. -
The Impaired Response of Circulating Asprosin Concentrations to Glucose Levels Fluctuation May Be One of the Causes of Type 2 Diabetes – a Narrative Review
Trojanowska Paulina, Trojanowska Alina, Szydełko Joanna, Tywanek Ewa, Łuczyk Robert Jan. The impaired response of circulating asprosin concentrations to glucose levels fluctuation may be one of the causes of type 2 diabetes – a narrative review. Journal of Education, Health and Sport. 2020;10(9):846-854. eISSN 2391-8306. DOI http://dx.doi.org/10.12775/JEHS.2020.10.09.10 2 https://apcz.umk.pl/czasopisma/index.php/JEHS/article/view/JEHS.2020.10.09. 10 2 https://zenodo.org/record/4054287 The journal has had 5 points in Ministry of Science and Higher Education parametric evaluation. § 8. 2) and § 12. 1. 2) 22.02.2019. © The Authors 2020; This article is published with open access at Licensee Open Journal Systems of Nicolaus Copernicus University in Torun, Poland Open Access. This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author (s) and source are credited. This is an open access article licensed under the terms of the Creative Commons Attribution Non commercial license Share alike. (http://creativecommons.org/licenses/by-nc-sa/4.0/) which permits unrestricted, non commercial use, distribution and reproduction in any medium, provided the work is properly cited. The authors declare that there is no conflict of interests regarding the publication of this paper. Received: 21.09.2020. Revised: 27.09.2020. Accepted: 28.09.2020. The impaired response of circulating asprosin concentrations -
Oncomodulin and Macrophages Derived Factors in Pancreas Injury and Development Paradigms
Vol.2, No.1, 1-8 (2013) Modern Research in Inflammation http://dx.doi.org/10.4236/mri.2013.21001 Oncomodulin and macrophages derived factors in pancreas injury and development paradigms Joël Fleury Djoba Siawaya1,2*, Carmen Capito1, Raphael Scharfmann1 1Centre de Recherche “Croissance et Signalisation”, Inserm Unité-845, Faculté de Médecine Paris 5, Paris, France; *Corresponding Author: [email protected], [email protected] 2Laboratoire National de Santé Publique, Unité de Recherche, Libreville, Gabon Received 6 December 2012; revised 14 January 2013; accepted 5 February 2013 ABSTRACT against beta cells appears to be the main cause for the loss of the insulin-producing beta cells leading to insulin Prior studies in the optic nerve injury paradigm deficiency whereas, in type 2 diabetes obesity related showed conflicting data regarding production pro-inflammatory response is involved in the develop- and significance of the Ca2+-binding protein on- ment of insulin resistance. comodulin (OCM). Some have shown its potent Although treatment options for the type 1 diabetes re- axon-regenerative or-growth attribute, where other main principally limited to insulin replacement therapy, showed little to no effect. We show here that today new avenues such as islet cell regeneration, re- pancreas inflammation lead to macrophages in- growth of host own islet cells or islet transplantation are filtration that produce OCM and inflamed tissues being explored. The principal roadblock to the wide- that express OCM receptors in vivo. In culture spread application of these new therapeutic approaches OCM has a cytostatic effect on embryonic pan- creas explants. Secretory products of zymosan- are the molecular mechanisms and relevant growth fac- activated macrophages are cytotoxic and fac- tors implicated in endocrine pancreas development which tors derived from non-activated macrophages are yet to be fully elucidated and which are required seem to promote pancreas development. -
Asprosin-Neutralizing Antibodies As a Treatment for Metabolic Syndrome
RESEARCH ARTICLE Asprosin-neutralizing antibodies as a treatment for metabolic syndrome Ila Mishra1†, Clemens Duerrschmid1†, Zhiqiang Ku2, Yang He3, Wei Xie1, Elizabeth Sabath Silva1, Jennifer Hoffman1, Wei Xin4, Ningyan Zhang2, Yong Xu3, Zhiqiang An2, Atul R Chopra1,5,6* 1Harrington Discovery Institute, University Hospitals, Cleveland, United States; 2Texas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, United States; 3Baylor College of Medicine, Houston, United States; 4Department of Pathology, Case Western Reserve University, Cleveland, United States; 5Department of Medicine, Case Western Reserve University, Cleveland, United States; 6Department of Genetics and Genome Sciences, Case Western Reserve University, Cleveland, United States Abstract Background: Recently, we discovered a new glucogenic and centrally acting orexigenic hormone – asprosin. Asprosin is elevated in metabolic syndrome (MS) patients, and its genetic loss results in reduced appetite, leanness, and blood glucose burden, leading to protection from MS. Methods: We generated three independent monoclonal antibodies (mAbs) that recognize unique asprosin epitopes and investigated their preclinical efficacy and tolerability in the treatment of MS. Results: Anti-asprosin mAbs from three distinct species lowered appetite and body weight, and reduced blood glucose in a dose-dependent and epitope-agnostic fashion in three independent MS mouse models, with an IC50 of ~1.5 mg/kg. The mAbs displayed a half-life of over 3days in vivo, *For correspondence: with equilibrium dissociation-constants in picomolar to low nanomolar range. [email protected] Conclusions: We demonstrate that anti-asprosin mAbs are dual-effect pharmacologic therapy that †These authors contributed targets two key pillars of MS – over-nutrition and hyperglycemia. -
Effect of Swimming Training on Levels of Asprosin, Lipid Profile, Glucose and Insulin Resistance in Rats with Metabolic Syndrome
Obesity Medicine 15 (2019) 100111 Contents lists available at ScienceDirect Obesity Medicine journal homepage: www.elsevier.com/locate/obmed Original research Effect of swimming training on levels of asprosin, lipid profile, glucose and insulin resistance in rats with metabolic syndrome T ∗ Hossein Nakhaeia, Mehdi Mogharnasia, Hamed Fanaeib,c, a Department of Sport Sciences, Faculty of Sport Sciences, University of Birjand, Birjand, Iran b Pregnancy Health Research Center, Zahedan University of Medical Sciences, Zahedan, Iran c Department of Physiology, School of Medicine, Zahedan University of Medical Sciences, Zahedan, Iran ARTICLE INFO ABSTRACT Keywords: Background: Asprosin is a novel biomarker that associated with type 2 diabetes mellitus. The aim of this study Continuous training was to investigate the effects of continuous and interval swimming training on the asprosin, lipid profile, glucose Interval training concentration and insulin resistance serum levels of rats with metabolic syndrome. Asprosin Methods: Forty-eight male Wistar rats were randomly divided into two groups, standard diet (SD) and high-fat Lipid profile diet (HD), and received their respective diets for a period of 12 weeks without exercise stimuli. After this period, Metabolic syndrome the animals were randomly divided into four groups (n = 8); normal control standard diet (NC), control (Ctr), continuous training (load 0–3% body mass, 5 d/wk, for 8 weeks, CT) and interval training (load 5–16% body mass, 5 d/wk, for 8 weeks, IT). The continuous and interval training consisted of a swimming exercise performed over eight weeks. Result: The NC and trained groups showed lower values of total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDL-C) and glucose concentration compared to Ctr group. -
Serum Concentration of Asprosin in New-Onset Type 2 Diabetes
Naiemian et al. Diabetol Metab Syndr (2020) 12:65 https://doi.org/10.1186/s13098-020-00564-w Diabetology & Metabolic Syndrome RESEARCH Open Access Serum concentration of asprosin in new-onset type 2 diabetes Shakiba Naiemian1, Mohsen Naeemipour2, Mehdi Zarei3, Moslem Lari Najaf4, Ali Gohari2, Mohammad Reza Behroozikhah2, Hafez Heydari2* and Mohammad Miri5* Abstract Background: Asprosin, a newly identifed adipokine, is pathologically increased in individuals with insulin resist- ance. However, the available evidence on the association of asprosin and type 2 diabetes mellitus (T2DM) status is still scarce. Therefore, this study aimed to determine the relationship between serum concentrations of asprosin and T2DM status. Methods: This observational study was performed based on 194 adults (97 newly diagnosed T2DM and 97 healthy individuals). Anthropometric and biochemical variables were determined in all participants. Serum concentrations of asprosin were measured using enzyme-linked immunosorbent assay (ELISA). Results: In patients with T2DM, the serum concentrations of asprosin were signifcantly higher than the healthy con- trols (4.18 [IQR: 4.4] vs. 3.5 [IQR: 1.85], P < 0.001). The concentrations of asprosin were signifcantly correlated with body mass index (BMI) and fasting blood glucose (FBG) in healthy subjects and with BMI, FBG, hemoglobin A1c (HbA1c), homeostatic model assessment of insulin resistance (HOMA-IR), and quantitative insulin check index (QUICKI), triacyl- glycerol (TAG) and total cholesterol/high-density lipoprotein cholesterol (TC/HDL-C) ratio in the T2DM group. In fully adjusted model, the odds ratio (OR) of T2DM with serum concentrations of asprosin was approximately 1.547 (95% CI 1.293–1.850, P < 0.001) compared to the control group. -
An Investigation of the Relationship Between New Fasting Hormone Asprosin, Obesity and Acute–Chronic Exercise: Current Systematic Review
ARCHIVES OF PHYSIOLOGY AND BIOCHEMISTRY https://doi.org/10.1080/13813455.2020.1767652 REVIEW ARTICLE An investigation of the relationship between new fasting hormone asprosin, obesity and acute–chronic exercise: current systematic review Halil _Ibrahim Ceylana and Ozcan€ Saygınb aFaculty of Kazim Karabekir Education, Physical Education and Sports Teaching Department, Ataturk University, Erzurum, Turkey; bFaculty of Sports Sciences, Coaching Science Department, Mugla Sitki Kocman University, Mugla, Turkey ABSTRACT ARTICLE HISTORY The purpose of this study was to reveal the relationship between new fasting hormone asprosin, obes- Received 31 March 2020 ity, and acute–chronic exercise. The prisma guidelines were followed in forming the methodological Revised 5 May 2020 model of this review. The articles between 2016 and 2020 (including March) were identified by scan- Accepted 7 May 2020 ning Google Scholar, Pub Med, and Science Direct databases. Thirty-five articles were defined from Published online 18 May 188 articles. Three cross-sectional, and 1 prospective cohort design studies in adults, and 3 cross-sec- 2020 tional studies in children were found. Three randomised-control group designed studies which exam- KEYWORDS ined the effect of acute exercise on serum asprosin levels in obese individuals. Asprosin may be a new Appetite; asprosin; exercise; therapeutic biomarker to be considered in the development, but long-term and deep-rooted obesity; systematic review researches are needed, and increasing the number of studies examining the effect of exercise on asprosin in the future might help us to identify the mechanisms underlying the decrease or increase in asprosin after exercise. Introduction obesity, it is necessary to understand especially how appe- tite/nutritional behaviours are regulated in the control of Obesity is a global public health problem, and ranked 5th body weight, and this also helps to develop new strategies with 4.8% of deaths worldwide (Wilson et al. -
INFLAMMATION-DERIVED GROWTH FACTORS Optic Nerve Regeneration Is Becoming a Reality
INFLAMMATION-DERIVED GROWTH FACTORS Optic nerve regeneration is becoming a reality. BY YUQIN YIN, MD, PHD; AND LARRY I. BENOWITZ, PHD ptic nerve trauma, ischemia, and or RAGs) in a pattern similar to that seen mannose, which is abundant in the vit- certain degenerative eye diseases during peripheral nerve regeneration.3 reous and cerebrospinal fluid, stimulates can lead to permanent vision Genetic deletion of two receptors appreciable axon growth from goldfish Oloss due to the inability of retinal that are expressed by inflammatory cells, RGCs and moderate outgrowth from rat ganglion cells (RGCs) to regenerate the Toll-like receptor 2 (TLR2) and dectin-1, RGCs. These effects require elevation of axons that convey visual information eliminates the proregenerative effects of cAMP and are strongly augmented by from the eye to the brain and the sub- zymosan, despite not altering the general a protein secreted by activated macro- sequent death of RGCs. Over the past profile of infiltrative cells.4 β-glucan is a phages.2,8 Using column chromatogra- 20 years, considerable progress has been component of zymosan that stimulates phy, mass spectrometry, and bioassays, made in defining factors that promote cells of the innate immune system via we identified the 11 kDa Ca2+-binding or suppress axon regeneration and RGC dectin-1, and curdlan, a particulate form protein oncomodulin (Ocm) as a major survival after optic nerve injury. of β-glucan, mimics the effects of zymo- growth-promoting factor associated This article describes research from san on regeneration.4 with inflammation.9 our lab that has identified trophic fac- Combining intraocular inflammation Ocm is secreted by infiltrative neutro- tors derived from inflammatory cells with elevation of cAMP and PTEN dele- phils and macrophages, and it accumu- that promote appreciable levels of tion in RGCs and other cells infected lates in the neural retina 12 to 24 hours optic nerve regeneration.