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003 1-3998/85/1904-44 lA$02.00 Vol. 19, No. 4, 1985 PEDIATRIC RESEARCH Printed in U.S.A. Copyright O 1985 International Pediatric Research Foundation,Inc. SUBJECT INDEX TO ABSTRACTS 1,25 (OH)2 D 1200 ADENOSINE DEAMINASE 909, 962, ALCOHOLISM 514 1,25 DIHYDROXYVITAMIN D3 973 967 ALDOSTERONE 333, 334, 808, 1,251 DIHYDROXYVITAMIN D 1223, ADENOSINE TRIPHOSPHATASE 323, 1591, 1605 1681 1571 ALKALINE PHOSPHATASE 728, 1200 14C DEOXYGLUCOSE 1316 ADENOSINE TRIPHOSPHATE 90, 98, ALKALOSIS 796 17 HYDROXYPROGESTERONE 436 860, 1600 ALKALOSIS, RESPIRATORY 1409 21 HYDROXYLASE DEFICIENCY 861 ADENOTONSILLECTOMY 1725 ALLERGY 652 21 HYDROXYLASE DEFICIENCY, ADENOVIRUS INFECTIONS 950 ALLOGENEIC 1018 NONCLASSICAL 861 ADENOVIRUSES, HUMAN 585 ALLOGRAFT REJECTION 1647 24 HOUR 440 ADENYL CYCLASE 277, 439, 1592 ALLOGRAFTS 1593, 1593 24 HYDROXYLASE RESPONSE 1200 ADHERENCE 880 ALMITRINE 837 25 (OH) D 1200 ADHESION 309 ALOPECIA 973 25 HYDROXYVITAMIN D 1 HYDROXYLASE ADHESIVE GLYCOPROTEINS 880 ALPHA 1-ANTITRYPSIN 1822 1223 ADIPOCYTE 713 ALPHA 1-ANTITRYPSIN DEFICIENCY 2H (OH) D 1200 ADIPOSE TISSUE 1187 813 3 BETAHYDROXYSTEROID ADIPOSITY 713 ALPHA FETOPROTEINS 1296, 1305 DEHYDROGENASE 431 ADOLESCENT BEHAVIOR 10, 19 ALPHA MANNOSIDASE 1241 3 METHYLGLUTACONIC ACID 823 ADOLESCENT PREGNANCY 20 ALPHA TOCOPHEROL 1466 3 METHYLGLUTACONIC ACIDURIA 823 ADRENAL 275, 334 ALTERNATE DAY STEROIDS 1726 3 METHYLGLUTARIC ACID 823 ADRENAL ANDROGEN SECRETION 480 ALTITUDE 273 4 CHANNEL PNEUMOGRAM 1523 ADRENAL CORTICOSTEROIDS 454 ALUMINUM 1595 5' NUCLEOTIDASE 881 ADRENAL HYPERPLASIA 431, 467 ALUMINUM EXCRETION 1582 51 CR SODIUM CHROMATE 1034 ADRENAL HYPERPLASIA, CONGENITAL ALUMINUM HYDROXIDE 1582 437, 461, 502, 839, 872 ALVEOLAR EPITHELIAL CELLS 1754 A23187 880, 952 ADRENAL MEDULLA 284 ALVEOLAR LIQUID ABSORPTION AAPO2 1443, 1552 ADRENAL STEROIDOGENESIS 454 1730 ABDOMEN 678, 722, 1797 ADRENALECTOMY 325, 669, 705 ALVEOLAR PHOTEINOSIS 296 ABDOMINAL PALPATION 1320 ADRENERGIC ALPHA RECEPTOR ALVEOLI 1344, 1371 ABNORMALITIES 287, 568, 840, AGONISTS 380 AMBIGUOUS GENITALIA 1280 1053, 1209, 1298 ADRENERGIC ALPHA RECEPTOR AMBULATORY 541 ABNORMALITIES, DRUG INDUCED 514 BLOCKADERS 96 AMEBIASIS 951 ABNORMALITIES, MULTIPLE 802 ADRENERGIC BETA RECEPTOR AMIKACIN 368 ABORTION 867 AGONISTS 405, 1757 AMILORIDE 78, 341, 992, 1570 ABORTION, ' HABITUAL 825 ADRENERGIC BETA RECEPTOR AMINO ACTD METABOLISM 1188 ABSCESS 593, 1173 BLOCKADERS 291 AMINO ACID TRANSPORT 719 ABSORPTIOMETRY 594 ADRENOCORTICAL NODULAR AMINO ACIDS 248, 260, 699, ABSORPTION 372, 680, 681, 691, DYSPLASIA 450 755, 869, 1186, 1710 ACCIDENT PRONENESS 513 ADRENOLEUKODYSTROPHY, NEONATAL AMINO ACIDS DIAMINO 869 ACCIDENTS 513 ONSET 811 AMINO ACIDS, INTRACELLULAR 676 ACETAMINOPHEN 358, 416, 636, AEROMONAS HYDROPHILA 591 AMINO ACIDS, PLASMA 702 1138 AEROSOL INHALATION 1787 AMINO ACIDS, SULFUR 1584 ACHONDROPLASIA 818, 863 AEROSOLS 1724 AMINO TRANSFERASES 1226 ACID SECRETION 721 AFFERENT ARTERIOLE 1601 AMINOGLYCOSIDES 368, 378, ACIDOSIS 143, 1274, 1684 AFFINITY CHROMATOGRAPHY 1259 1462, 1569 ACNE 14, 1132 AFTERLOAD 139 AMINOTRANSFERASES 869 ACOUSTIC OTOSCOPE 772 AFTERLOAD REDUCTION 127 AMIODARONE 158 ACQUIRED IMMUNE DEFICIENCY AGAMMAGLOBULINEMIA 1246 AMMONIA 817, 1193, 1245 SYNDROME 592, 633, 957, 958, AGENT ORANGE 842 AMNIOCENTESIS 1504 959, 1005, 1016, 1018, 1031, AGGREGATION 987 AMNION 255 1119, 1708, 1742 1791 AGRANULOCYTOSIS 891, 915 AMNIOTIC FLUID 320, 1292, ACRODERMATITIS ENTEROPATHICA AIR POLLUTANTS 546 1504, 1746 1261 AIRWAY HYPERREACTIVITY 1864 AMNIOTIC MEMBRANE DRESSING 843 ACTH 480 AIRWAY RESISTANCE 1461 AMNIOTIC MEMBRANE IMPLANTATION ACTIN 955 AIRWAYS 345, 546 843 ACTIVATION 1004 ALANINE 1260 AMOXICILLIN 1059, 1608 ACTIVATOR PROTEINS 1715 ALASKA 544 AMPICILLIN 762, 1154 ACTIVITY 439 ALBUMIN 1322 AMYGDALOID BODY 1692 ACYCLOVIR 1065, 1066, 1133 ALBUMINS 1359 AMYLASE 703 ADENOSINE 388, 1749 ALBUTEROL AEROSOL 1785 ANAL SPHINCTER 694 ALCOHOL 79 ANALGESIA 415 ADENOSINE CYCLIC MONOPHOSPHATE ALCOHOL ABUSE 1316 ANATOMIC CORRECTION 77 329, 343, 357, 1223, 1633 ALCOHOL DRINKING 19 ANDROGEN EXCESS 446 441A SUBJECT INDEX TO ABSTRACTS ANDROGEN RESISTANCE 481 ANTIGEN ANTIBODY REACTIONS ASPIRIN 636, 775, 925, 948, 994, ANDROGENS 275, 276, 321, 435, 1153 1172 461, 467, 481, 502, 505 ANTIGENS 883 ASSAY 886 ANEMIA 887, 893, 911, 917, 1385, ANTIGENS, VIRAL 1091 ASTHMA 375, 827, 1731, 1752, 1454, 1455, 1537 ANTIHISTAMINE 928 1757, 1761, 1770, 1773, 1786, ANEMIA, AUTOI- HEMOLYTIC ANTINUCLEAR FACTORS 1013 1864 1003 ANTIOXIDANT ACTIVITY 384 ASTHMA, BRONCHIAL 1785, 1787 ANEMIA, CONGENITAL ANTIOXIDANT ENZYMES 315, 1837, ASTHMA THERAPY 789 DYSERYTHROPOIETIC 887 1838 ASYMMETRIES 1658 ANEMIA, CONGENITAL HEMOLYTIC ANTIOXIDANTS 278 ATAXIA TELENGIECTASIA 1002, 1028 933 ANTIPYRINE 15, 1441, 1442 ATELECTAS IS 1447 ANEMIA, CONGENITAL HYPOPLASTIC ANTIPYRINE CLEARANCE 15 ATHEROSCLEROSIS 537 909 ANTITHYROGLOBULIN 24 ATRIAL MYXOMA 450 ANEMIA, MEGALOBLASTIC 852 ANTITOXINS 1141 ATRIAL NATRIURETIC FACTOR 1587 ANEMIA, APLASTIC 891 ANTIVIRAL AGENTS 1107, 1130, ATRIOPEPTINS 1587 ANESTHESIA 401, 415, 1725 1140, 1156 ATRIOVENTRICULAR BLOCK 160, ANEUPLOIDY 836 ANUS, DISEASES 723 161, 162 ANEURYSMS 590 ANXIETY 47 ATRIOVENTRICULAR NODE 161, 162 ANGIOGRAPHY 77, 126 AORTA 95, 151, 1370, 1511, ATROPINE 1353 ANG IOTENS IN 1585 1547 ATTENTION DEFICIT DISORDER WITH ANGIOTENSIN I1 333, 1601 AORTA, THORACIC 152 HYPERACTIVITY 28, 59, 64, ANOGENITAL INDEX 1280 AORTIC COARCTATION 83, 95 1682, 1703 ANORECTAL MANOMETRY, BALLOON AORTIC ROOT 151 AUDIOGRAMS 37 694 AORTIC STENOSIS 138 AUDITORY TUBE 975 ANOREXIA 1193, 1213 AORTIC VALVE 138 AUTISM 1680, 1692 ANOREXIA NERVOSA 2, 34, 483 AORTIC VALVOTOMY 138 AUTOIMMUNE DISEASE 894 ANOXEMIA 82, 319, 1415 APGAR SCORE 787, 1360 AUTONOMIC NERVOUS SYSTEM 284, ANOXIA 99, 175, 199, 265, 366, APNEA 1413 388, 707, 1433, 1697 BS: 56 AUTOPSY 522, 552, 595, 1542, ANTENATAL SCORING 977 DB: 259, 283 1678 ANTERIOR CEREBRAL ARTERY 310 DP: 345, 359, 388, 393 AUTOREGULATION 1457, 1717 ANTERIOR FONTANELLE 1426 EP: 577 AZOTHIOPRIN 1644 ANTHRACYCLINE 136 GI: 701 ANTHROPOMETRIC VARIABLES 1382 GP: 776 B CELLS 965 ANTHROPOMETRICS 713 NN: 1396, 1397, 1400, 1412, B LYMPHOCYTES 883, 1027, 1130 ANTHROPOMETRY 619 1413, 1438, 1453, 1467, BABOON 303, 317, 340, 1327, ANTIAMOEBIC PROPERTIES 951 1477, 1497, 1523, 1521, 1443, 1552 ANTIARRHYTHMIA AGENTS 376 1532, 1554 BACTEREMIA 508, 557, 593, 761, ANTIBIOTICS 418, 732, 784, PU: 1729, 1745, 1759, 1799, 1054, 1125, 1146 1069, 1081, 1160, 1561 1801, 1821, 1827, 1841 BACTERIA 541, 553, 745, 1082, ANTIBODIES 972, 979, 1066, APNEA OF PREMATURITY 361, 1414 1096, 1180, 1602 1073, 1102, 1115, 1149, 1155, APOPROTEINS 253, 1365, 1775 BACTERIA, AEROBIC 202 1410 APPENDICITIS 1058 BACTERIAL CULTURES 798 ANTIBODIES TO EBSTEIN BARR A!!'CHIDONIC ACID 1286 BACTERIAL INFECTIONS 1159, VIRUS 1118 ARACHIDONIC ACIDS 1832, 1833, 1163, 1332, 1333 ANTIBODIES, ANTIHISTONES 953 1834 BACTERIAL VACCINES 1100, 1102, ANTIBODIES, ANTIMICROSOMAL 24 ARGININE 274, 817 1103, 1149 ANTIBODIES, ANTINUCLEOLAR 953 ARGIPRESSIN 144, 185, 1549, BACTERICIDAL 1371, 1835 ANTIBODIES, BACTERIAL 1007, 1590, 1717 BACTERIOLOGICAL TECHNICS 1125, 1086, 1103, 1122 ARNOLD CHIARI MALFORMATION 1361 AN'*lBODIES,BASEMENT MEMBRANE 1719 BACTERIOPHAGE 958 1619 AROUSAL 1821 BARBITURATES 1369, 1390 ANTIBODIES, GLIADIN 692 AROUSAL RESPONSES 1821 BARE LYMPHOCYTE SYNDROME 1042 ANTIBODIES, MONOCLONAL 804, ARRHYTHMIA 89, 147, 157, 168, BAYLEY SCALES OF INFANT 896, 903, 914, 955, 963, 963, 168 DEVELOPMENT 46, 65, 381, 986, 1035, 1105, 1162, 1758 ARTERIAL OXYGENATION 156 1297, 1341 ANTIBODIES, PLATELET 945 ARTERIES 182, 196, 1433 BEHAVIOR 11, 1446, 1472 ANTIBODIES, SERUM 1062, 1102, ARTERITIS 775 BEHAVIORAL MEDICINE 42 1103 ARTHRITIS, INFECTIOUS 1129 BEHAVIORAL THERAPY 74 ANTIBODIES, VIRAL 1091 ARTHRITIS, JUVENILE RHEUMATOID BENZOATE 1244 ANTIBODY ASSAYS 1434 989, 1019 BETA 2 MICROGLOBULIN 1603 ANTIBODY BINDING 1619 ARTHROGRWOSIS 826 BETA GLUCURONIDASE DEFICIENCY ANTIBODY CONTAINING CELLS 996 ' ARTHROPATHY 1301, 1019 1232 ANTIBODY DEPENDENT CELLULAR ARYLSULFATASE A 1715 BETA-LACTAMASES 1057, 1163 CYTOTOXICITY 1000, 1011 ASCITES 213, 214, 565 BETAMETHASONE 1094, 1364, 1504 ANTIBODY DETERMINATION 1092 ASCORBIC ACID 913 BETHANECHOL COMPOUNDS 731 ANTIBODY FORMATION 1000 ASPHYXIA 113, 143, 232, 1457, BICARBONATE 1645 ANTICONVULSANTS 394, 417 1459, 1520, 1660, 1675, 1685, BICU 1712 ANTIDEPRESSANTS, TRICYCLIC 1713, 1716 BIFIDOBACTERIA 643 168, 168 ASPHYXIA NEONATORUM 52, 306, BILE ACID UPTAKE 616 ANTIDIURETIC HORMONE 1816 787, 1372, 1487, 1678 BILE ACIDS AND SALTS 639, 653, ANTIGEN ANTIBODY COMPLEX 982 ASPIRATION SYNDROME 285 675, 708, 714, 734, 737, 743 SUBJECT INDEX TO ABSTRACTS 443A BILE DUCT 635 BONE AND BONES 3, 438, 594, 1439, 1722, 1723, 1801 BILIARY OBSTRUCTION 1254 627, 1238, 1681 CALCIFEDIOL 671 BILIARY TRACT 635, 739 BONE CELLS 1249 CALCIFEDIOL METABOLISM 488 BILIRUBIN 646, 647, 660, 1322, BONE DENSITY 432, 1201 CALCIFEROL 1264 1349, 1359, 1380, 1465, 1469, BONE DISEASES, DEVELOPMENTAL CALCITONIN 1550 1474, 1486, 1510, 1518, 1546, 812 CALCITRIOL 1604 1679, 1695 BONE MARROW 871, 886, 891, CALCIUM BINDING 1025 903, 904, 931, 950, 960, 969, AM: 3 BINDING ASSAY 925 985, 1008, 1275 CV: 112 BINDING CAPACITY 1200 BONE MARROW TRANSPLANTATION DB: 260 BINDING PROTEINS 1793 950, 967, 993 EN: 500 BIOENERGETICS 90 BONE MINERALIZATION 3, 626 EP: 556 BIOFEEDBACK 31 BONE NEOPLASMS 840 GI: 626, 672, 708, 718, 733, BIOGENIC AMINES 943 BOHDETELLA PERTUSSIS 1089 736, 756 BIOLOGICAL RESPONSE MODIFIERS BOTTLE FEEDING 10 IM: 956 896, 963 BRADYCARDIA 1453, 1523 ME: 1253, 1272 BIOLOGICAL TRANSPORT 669, 739, BRAIN NP: 1581, 1604,
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    © Michael Ash BSc DO ND F.DipION 2010 4/29/2010 'The role of Nutritional Therapy in the care of individuals with cardiovascular related problems' Michael Ash BSc (Hons) DO ND F DipION mBANT NTCC Osteopath Naturopath Nutritional Therapist Researcher Author Nutritional Therapy • A Functional Medicine approach to optimise outcomes, ease of engagement and compliance. • 8 Practical strategies & how to avoid common pitfalls. • Interaction of the immune system with the heart. • GastroCentric Perspective. • How food selection can provide a multi faceted benefit. • Supplements of benefit. 1 © Michael Ash BSc DO ND F.DipION 2010 4/29/2010 Client Overview Goals Determine their aims and outcomes – the purpose of the plan is to support the patients goals with evidence based strategies Identify realistic goals, obtain agreement that these are achievable and describe plan ASSESMENT ANTECEDENTS TRIGGERS Medical history review and systems analysis assess the: MEDIATORS Antecedents: Sex, Age, Genetics, Lifestyle, Experiences, Trauma, Childhood, Stress, etc. Triggers: Events that initiate illness or symptoms – stress, infection, environmental toxins, food. etc. – look to see if they can be removed or controlled Mediators: Cytokines, prostaglandins, free radicals, neurotransmitters, fear, personal value, behavioural conditioning, poverty, etc. Evolutionary Nutritional Therapy • In physiology, foetal nutritional stress appears to flip an evolved switch that sets the body into a state that protects against starvation. • When these individuals encounter modern diets, they respond with the deadly metabolic syndrome of obesity, hypertension, and diabetes. • Barker DJ, Eriksson JG, Forsén T, Osmond C.Fetal origins of adult disease: strength of effects and biological basis. Int J Epidemiol. 2002 Dec;31(6):1235-9.
  • Megalencephaly and Macrocephaly

    Megalencephaly and Macrocephaly

    277 Megalencephaly and Macrocephaly KellenD.Winden,MD,PhD1 Christopher J. Yuskaitis, MD, PhD1 Annapurna Poduri, MD, MPH2 1 Department of Neurology, Boston Children’s Hospital, Boston, Address for correspondence Annapurna Poduri, Epilepsy Genetics Massachusetts Program, Division of Epilepsy and Clinical Electrophysiology, 2 Epilepsy Genetics Program, Division of Epilepsy and Clinical Department of Neurology, Fegan 9, Boston Children’s Hospital, 300 Electrophysiology, Department of Neurology, Boston Children’s Longwood Avenue, Boston, MA 02115 Hospital, Boston, Massachusetts (e-mail: [email protected]). Semin Neurol 2015;35:277–287. Abstract Megalencephaly is a developmental disorder characterized by brain overgrowth secondary to increased size and/or numbers of neurons and glia. These disorders can be divided into metabolic and developmental categories based on their molecular etiologies. Metabolic megalencephalies are mostly caused by genetic defects in cellular metabolism, whereas developmental megalencephalies have recently been shown to be caused by alterations in signaling pathways that regulate neuronal replication, growth, and migration. These disorders often lead to epilepsy, developmental disabilities, and Keywords behavioral problems; specific disorders have associations with overgrowth or abnor- ► megalencephaly malities in other tissues. The molecular underpinnings of many of these disorders are ► hemimegalencephaly now understood, providing insight into how dysregulation of critical pathways leads to ►
  • The Effect of Vitamin Supplementation on Subclinical

    The Effect of Vitamin Supplementation on Subclinical

    molecules Review The Effect of Vitamin Supplementation on Subclinical Atherosclerosis in Patients without Manifest Cardiovascular Diseases: Never-ending Hope or Underestimated Effect? Ovidiu Mitu 1,2,* , Ioana Alexandra Cirneala 1,*, Andrada Ioana Lupsan 3, Mircea Iurciuc 4 , 5 5 2, Ivona Mitu , Daniela Cristina Dimitriu , Alexandru Dan Costache y , Antoniu Octavian Petris 1,2 and Irina Iuliana Costache 1,2 1 Department of Cardiology, Clinical Emergency Hospital “Sf. Spiridon”, 700111 Iasi, Romania 2 1st Medical Department, University of Medicine and Pharmacy “Grigore T. Popa”, 700115 Iasi, Romania 3 Department of Cardiology, University of Medicine, Pharmacy, Science and Technology, 540139 Targu Mures, Romania 4 Department of Cardiology, University of Medicine and Pharmacy “Victor Babes”, 300041 Timisoara, Romania 5 2nd Morpho-Functional Department, University of Medicine and Pharmacy “Grigore T. Popa”, 700115 Iasi, Romania * Correspondence: [email protected] (O.M.); [email protected] (I.A.C.); Tel.: +40-745-279-714 (O.M.) Medical Student, University of Medicine and Pharmacy “Grigore T. Popa”, 700115 Iasi, Romania. y Academic Editors: Raluca Maria Pop, Ada Popolo and Stefan Cristian Vesa Received: 25 March 2020; Accepted: 7 April 2020; Published: 9 April 2020 Abstract: Micronutrients, especially vitamins, play an important role in the evolution of cardiovascular diseases (CVD). It has been speculated that additional intake of vitamins may reduce the CVD burden by acting on the inflammatory and oxidative response starting from early stages of atherosclerosis, when the vascular impairment might still be reversible or, at least, slowed down. The current review assesses the role of major vitamins on subclinical atherosclerosis process and the potential clinical implications in patients without CVD.
  • The Efficacy of Pantothenic Acid As a Modifier of Body Composition in a Porcine Model of Obesity Development

    The Efficacy of Pantothenic Acid As a Modifier of Body Composition in a Porcine Model of Obesity Development

    Iowa State University Capstones, Theses and Retrospective Theses and Dissertations Dissertations 1-1-2004 The efficacy of pantothenic acid as a modifier of body composition in a porcine model of obesity development Carey Ann Baldwin Iowa State University Follow this and additional works at: https://lib.dr.iastate.edu/rtd Recommended Citation Baldwin, Carey Ann, "The efficacy of pantothenic acid as a modifier of body composition in a porcine model of obesity development" (2004). Retrospective Theses and Dissertations. 20349. https://lib.dr.iastate.edu/rtd/20349 This Thesis is brought to you for free and open access by the Iowa State University Capstones, Theses and Dissertations at Iowa State University Digital Repository. It has been accepted for inclusion in Retrospective Theses and Dissertations by an authorized administrator of Iowa State University Digital Repository. For more information, please contact [email protected]. The efficacy of pantothenic acid as a modifier of body composition in a porcine model of obesity development by Carey Ann Baldwin A thesis submitted to the graduate faculty in partial fulfillment of the requirements for the degree of MASTER OF SCIENCE Major: Animal Nutrition Program of Study Committee: Tim Stahly, Major Professor Paul Flakoll Chad Stahl Iowa State University Ames, Iowa 2004 Copyright© Carey Ann Baldwin, 2004. All rights reserved. 11 Graduate College Iowa State University This is to certify that the master's thesis of Carey Ann Baldwin has met the thesis requirements of Iowa State University Signatures have been redacted for privacy 111 TABLE OF CONTENTS ACKNOWLEDGEMENTS Vl ABSTRACT Vll CHAPTER 1. GENERAL INTRODUCTION 1 Introduction 1 Thesis Organization 2 Literature Cited 2 CHAPTER 2.
  • Genetics of Congenital Hand Anomalies

    Genetics of Congenital Hand Anomalies

    G. C. Schwabe1 S. Mundlos2 Genetics of Congenital Hand Anomalies Die Genetik angeborener Handfehlbildungen Original Article Abstract Zusammenfassung Congenital limb malformations exhibit a wide spectrum of phe- Angeborene Handfehlbildungen sind durch ein breites Spektrum notypic manifestations and may occur as an isolated malforma- an phänotypischen Manifestationen gekennzeichnet. Sie treten tion and as part of a syndrome. They are individually rare, but als isolierte Malformation oder als Teil verschiedener Syndrome due to their overall frequency and severity they are of clinical auf. Die einzelnen Formen kongenitaler Handfehlbildungen sind relevance. In recent years, increasing knowledge of the molecu- selten, besitzen aber aufgrund ihrer Häufigkeit insgesamt und lar basis of embryonic development has significantly enhanced der hohen Belastung für Betroffene erhebliche klinische Rele- our understanding of congenital limb malformations. In addi- vanz. Die fortschreitende Erkenntnis über die molekularen Me- tion, genetic studies have revealed the molecular basis of an in- chanismen der Embryonalentwicklung haben in den letzten Jah- creasing number of conditions with primary or secondary limb ren wesentlich dazu beigetragen, die genetischen Ursachen kon- involvement. The molecular findings have led to a regrouping of genitaler Malformationen besser zu verstehen. Der hohe Grad an malformations in genetic terms. However, the establishment of phänotypischer Variabilität kongenitaler Handfehlbildungen er- precise genotype-phenotype correlations for limb malforma- schwert jedoch eine Etablierung präziser Genotyp-Phänotyp- tions is difficult due to the high degree of phenotypic variability. Korrelationen. In diesem Übersichtsartikel präsentieren wir das We present an overview of congenital limb malformations based Spektrum kongenitaler Malformationen, basierend auf einer ent- 85 on an anatomic and genetic concept reflecting recent molecular wicklungsbiologischen, anatomischen und genetischen Klassifi- and developmental insights.