61. DIETARY HYPERSENITIVITIES: GI AND SKIN dermatoses (dog and cat) Atopy; Other allergic dermatoses; Fatdeficiency seborrhea; galt.Breakdown of natural defense systems predisposes to food hypersensitivity http://education.vetmed.vt.edu/Curriculum/VM8264/11/

DIETARY HYPERSENITIVITIES: GI AND SKIN Learning Objectives By the end of this session, the student should be able to: List nutrients of concern related to skin and GI sensitivities in the cat and dog. Describe common food allergens and clinical signs associated with diet hypersensitivities. Outline feeding strategies to manage diet-associated enteritis. Participate in oral case review. INTRODUCTION Estimated that 15 % of the canine population suffers from allergic disease. Flea Allergy Dermatitis Atopy Food Hypersensitivity Nutrition plays an import role as an adjunct in the medical management of many dermatological and gastrointestinal problems. Key tools in the nutritional management of allergic disease are limited antigen diets and limited ingredient diets. CLINICAL IMPORTANCE OF SKIN DISORDERS Most common reason for dogs and cats to visit the veterinarian. Problems include: bacterial infections, ectoparasites, allergies (food intolerance), fungal infections, inappropriate nutrition, and neoplasia. In certain cases of nutrient-responsive skin disorders, the animal may have a genetic or acquired inability to absorb, utilize, or metabolize the nutrient as compared to a true deficiency.

62. Locus-Specific Mutation Databases galt, galt analysis database, Emory University, Atlanta, USA. GCH1, GTP cyclohydrolaseI deficiency, University Children's Hospital, Zurich, Switzerland. http://www.uwcm.ac.uk/uwcm/mg/docs/oth_mut.html

Locus-Specific Mutation Databases A considerable number of locus-specific mutation databases have been constructed and made publically available via the internet. Many of the lesions present in these databases are included in the Human Gene Mutation Database . However, the locus-specific databases may contain additional unpublished material. An article reviewing current locus-specific databases recently appeared in Genome Res Please note that these sites listed below are not maintained in Cardiff, and that all queries regarding them should be addressed to the curators of the site in question. It should also be noted that inclusion of a site here does not automatically imply that the curators of HGMD have approved either the quality of the site or its contents. Gene(s) Database Host Institution ATP-binding cassette transporter retina Retina International Multidrug resistance-associated protein 6 Retina International Sulphonylurea receptor X-linked adrenoleukodystrophy Academic Medical Center, Amsterdam, Holland and Kennedy Krieger Institute, Baltimore MD, USA ABO Blood group antigen mutation database Albert Einstein College of Medicine, New York, USA

63. Chronic Latent Tetany Of Magnesium Deficiency: CFS, FM, Migraine Hass GM, Laing GH, galt RM et al. Recent advances Immunopathology of magnesium deficiencyin rats Induction of tumors; incidence, transmission and prevention http://www.mgwater.com/clmd.shtml

THE MAGNESIUM WEB SITE REVIEW Review and Hypothesis: Might Patients with the Chronic Fatigue Syndrome Have Latent Tetany of Magnesium Deficiency Mildred Seelig, MD, MPH Mildred Seelig is Adjunct Professor of Nutrition, School of Public Health, University of North Carolina School of Medicine, Chapel Hill, NC and Adjunct Professor, Family and Preventive Medicine, Emory University School of Medicine, Atlanta, GA. Address correspondence to: Dr. Mildred Seelig, 1075-F North Jamestown Road, Decatur, GA 30033-3679. Appreciation is expressed to Harry Preuss for suggesting that the author consider the possibility that magnesium deficiency might be a contributory factor in the pathogenesis of chronic fatigue syndrome for a joint session of the ACN and the AACFS, October, 1996, and to Kay Franz for undertaking a literature search for her on CFS and related disorders. Journal of Chronic Fatigue Syndrome, Vol. 4(2) 1998 ABSTRACT. . [Article copies available for a fee from The Haworth Document Delivery Service: 1-800-342-9678. E-mail address: getinfo@haworthpressinc.com] KEYWORDS.

64. Corporate Counsel Center the fourth floor and the entire third floor at 11128 John galt Boulevard, Omaha inthe Building, and Landlord shall not be personally liable for any deficiency. http://contracts.corporate.findlaw.com/agreements/paypal/omaha.lease.2000.04.25.

Search FindLaw Corp Counsel Articles Contracts Litigation Watch News Commentaries Research Tools: Business Contracts Litigation Watch Article Database SEC Edgar Industry Centers: Automobiles Construction Consumer Products Energy ... Wholesale Practice Area Centers: ADR Antitrust Bankruptcy Class Action Defense ... White Collar Crime FindLaw Links: Legal Software Message Boards Newsletters Online CLE Email: Password: Register Help Feedback LEASE THIS LEASE AGREEMENT (this "Lease") is entered into as of this day of April, 2000, between Metro-Omaha Associates, L.L.C., a Nebraska limited liability company ("Landlord"), and X.Com Corporation, a California Corporation ("Tenant"). Lease Grant. Subject to the terms of this Lease, Landlord leases to Tenant, and Tenant leases from Landlord premises comprised of approximately 24,359 rentable square feet as depicted in the plan attached as Exhibit A (the " Premises ") in the office building known as The Metropolitan Business Center located on the majority of the south wing of the fourth floor and the entire third floor at 11128 John Galt Boulevard, Omaha, Nebraska (collectively, the " Building "). As hereinafter used, the term "the Premises" shall refer to the combination of the Initial Premises and the Secondary Premises, as those terms are hereafter defined. Provided such determination is made on or before May 15, 2000, the actual rentable area of the Premises shall be determined in accordance with the Standard Method for Measuring "Floor Area in Office Buildings, Approved June 7, 1996 ("

65. Interstate Mainline Deficiencies Submit a mainline deficiency. Credits. dse Darren Stuart Embry; hbeHB Elkins; jjk Jeff Kitsko; jdg John David galt; je Jon Enslin; http://www.ajfroggie.com/roads/deficiency/i-mainline.htm

Interstate Mainline Deficiencies Submit a mainline deficiency U.S.: [ AR DC FL GA ... WI United States of America Arkansas Highway Location Deficiency type Comments Credit I-40 North Little Rock single lane Westbound only. jl I-55 West Memphis, at merge onto I-40 single lane Northbound only. ajf District of Columbia Highway Location Deficiency type Comments Credit I-395 exit from Southwest-Southeast Freeway single lane Northbound only. ov Florida Highway Location Deficiency type Comments Credit I-95 Jacksonville, junction with I-10 single lane Temporary: due to construction of new Fuller Warren Bridge. bb Georgia Highway Location Deficiency type Comments Credit I-75 Macon, junction with I-16 single lane Southbound only. smc Illinois Highway Location Deficiency type Comments Credit I-94 north of Chicago, east end of Edens Spur single lane Eastbound only. bb, mgk I-39 Cherry Valley, at I-90 (Northwest Tollway) merge single lane pmj, mgk I-39 Rockford, at west US 20 split single lane mgk I-74 Moline, at I-80 single lane mc, mgk I-74 and I-80 "bump" in Colona single lane mc, mgk

66. IGADEF 50% of these patients show reversal of their IgA deficiency. A. Primary role ofIgA is in defense of the Mucosal Immune System which includes galt or Gut http://www.allergy-asthma.org/IGADEF.htm

Michelle M. Klinek, M.D. March 23, 1995 IMMUNOGLOBULIN A DEFICIENCY I. EPIDEMIOLOGY * Recently a subgroup has been identified with Partial Deficiency. Believed to be a separate disease than complete IgA deficiency 50% of these patients show reversal of their IgA deficiency all have normal T cell proliferation Cause ascribed to environmental factors in some cases 1. Drugs - phenytoin, sulfasalazine, penicillamine 2. Viral induced ie. Rubella, EBV * Prevalence in Caucasians is approximately 1:660, Japanese 1:18,500 and among blacks is undefined. II. CLINICAL FEATURES A. Primary role of IgA is in defense of the Mucosal Immune System which includes GALT or Gut associated lymphoid tissue and BALT bronchus associated lymphoid tissue. 1. IgA can be actively and efficiently secreted through epithelial cells to mucosal sites - a 70kg adult secretes about 3gm/day accounting for 60-70% of total antibody output - in humans IgA is encoded by 2 genes Figure 1 1 IgA1 which is primary constituent of circulating IgA 2 IgA2 which is a constituent of secretory IgA Figure 2 2. IgA has the ability to join J chains which are produced by B cells which confers the ability to polymerize and then be connected to the secretory component produced by epithelial cells. This protects the IgA from proteolytic digestion and mediates transport of IgA into muscosal lumens. (GI tract, salivary glands, bronchial mucosa, lactating mammary glands and uterine mucosa)

67. BioMed Central | Full Text | The Clinical And Molecular Spectrum Of Galactosemia galactose1-phosphate uridyltransferase (galt; EC2.7.7.10) and uridine-diphosphategalactose-4' epimerase (GALE; EC 5.1.3.2). The most common deficiency in all http://www.biomedcentral.com/1471-2431/2/7/

Welcome guest user home journals A-Z journals by subject advanced search ... Volume 2 Viewing options Abstract Full text PDF Pre-publication history Other links: E-mail to a friend Download references Post a comment PubMed record ... Related articles in PubMed Search PubMed For Henderson H Leisegang F Brown R Eley B Key E-mail Corresponding author Research article The clinical and molecular spectrum of galactosemia in patients from the Cape Town region of South Africa Howard Henderson Felicity Leisegang Ruth Brown and Brian Eley Department of Chemical Pathology and School of Child and Adolescent Health, Red Cross Children's Hospital, University of Cape Town, Cape Town, South Africa Dept of Pediatrics, and School of Child and Adolescent Health, Red Cross Children's Hospital, University of Cape Town, Cape Town, South Africa BMC Pediatrics The electronic version of this article is the complete one and can be found online at: http://www.biomedcentral.com/1471-2431/2/7 Received Accepted Published Outline Abstract Abstract Background Methods Results ... Pre-publication history Background The objective of this study was to document the clinical, laboratory and genetic features of galactosemia in patients from the Cape Town metropolitan region.

68. Wisconsin Phenylketonuria (PKU); Biotinidase deficiency (BD); Congenital Adrenal Hyperplasia(CAH); Cystic Fibrosis (CF); Galactosemia (galt); Congenital Hypothyroidism (CH http://www.krabbes.com/demographic_study/united_states/wisconsin.htm

Krabbe Demographic Study Wisconsin New Born Screening Information To submit demographic information about your child please click here If you would like to help gather information in your area please e-mail us Wisconsin Established criteria for screening purposes. Criteria 1 Prevalence: Prevalence of the disorder must warrant screening. Criteria 2 Morbidity and Mortality: Early detection benefits outweigh adverse consequence of false positives, costs to screen , etc. Criteria 3 Potential for successful treatment: Effective management can be implemented to benefit infants. Criteria 4 Laboratory Feasibility: Methodology must be adaptable to mass screening. Criteria 5 Costs: Cost of the test must be comparable to that of other established tests./ If you would like to know what you can do to help get Krabbe's Disease on the Wisconsin new born screening list please click here Wisconsin currently screens for 7 disorders and has 15 optional disorders that they will screen for: Mandated Selected Population Only Pilot Program Phenylketonuria (PKU) Biotinidase Deficiency (BD) Congenital Adrenal Hyperplasia (CAH) Cystic Fibrosis (CF) Galactosemia (Galt) Congenital Hypothyroidism (CH) Maple Syrup Urine Disease (MSUD) Hydroxy 3-Methylglutary-CoA Lyase Deficiency (HMG) 3Ketothiolase Deficiency (3Keto) 3-Methylcrotonyl-CoA Carboxylase Deficiency (3MCC) Glutaryl-CoA Dehydrogenase Deficiency Type 1 (GA-1) Isovaleryl-CoA Dehydrogenase Deficiency (IVA) Methylmalonic Acidemia (MMA)

69. HUGO MDI/title> Storage Disease Type II,GSDII, Pompe Disease Lysosomal aglucosidase deficiency,http//www.eur galt 230400 No 1. Galactosaemia, http//www.ich.bris.ac.uk/galtdb http://www.genomic.unimelb.edu.au/mdi/dblist/glsdbg.html

Locus Specific Mutation Databases Last Updated 18 February 2003 A to F G H I ... Q to Z GENE DESIGNATION/ OMIM No. DATABASE NAME INTERNET ADDRESS CURATOR/S G6PD Mutations http://www.bioinf.org.uk/g6pd/ Colin Kwok Veronica Lam Dept. Biochem. -Faculty of Medicine The University of Hong Kong Andrew Martin Reading,UK Glucose-6-Phosphate -dehydrogenase http://rialto.com/favism/mutat.htm E. Beutler -Scripps California T. Vulliamy -RPMS, London L. Luzzato -Dep Hum, Gen. NY,NY GAA Glycogen Storage Disease Type II,GSDII, Pompe Disease Lysosomal a-glucosidase Deficiency http://www.eur.nl/FGG/CH1/pompe/ A.J. J. Reuser Erasmus University Rotterdam, The Netherlands GALB Mutations in the a-N-Acetylgalactosaminidase gene causing Schindler disease http://www.mssm.edu/crc/mutations/schindler.html ENCOURAGED BY HUGO/MDI Kenneth H. Astrin

70. F2 Translate this page Cependant les taux de galt sont normaux en cas d'altération hépatique. recessive,inborn error of galactose metabolism due to the deficiency of galactose-I http://autisme.france.free.fr/docs/f2.htm

Retour Base Documentaire GALACTOSEMIE Définition Le terme de galactosémie désigne deux erreurs innées du métabolisme du galactose.. On en reconnaît deux types. La galactosémie "classique" est due à un déficit en galactose 1-phosphatase uridyl transférase (GALT), elle est typiquement associée à une cataracte, un retard mental et une cirrhose. Le deuxième type, déficit en galactokinase, entraîne principalement une cataracte. Pathogénie Le lactose, principal sucre du lait, est un disaccharide contenant du galactose et du glucose ; il est hydrolysé après ingestion par la lactase intestinale. Normalement, le galactose absorbé est transformé en glucose au niveau du foie. La première réaction de cette voie concerne la phosphorylation du galactose en galactose-1-phosphatase par la galactokinase (codée par un gène situé sur le chromosome 17). Puis le galactose-1-phosphatase en glucose-1-phosphatase par la GALT, dont le gène est situé sur le chromosome 9. Cette réaction est réversible grâce à une épimérase. Le galactose peut aussi entrer dans plusieurs voies métaboliques. Il peut être transformé (par réduction) en présence de NADPH (ou NADH) en galactitol (dulcitol) par une aldose réductase. Le galactose peut être oxydé de façon limitée par une galactose oxydase aboutissant à la formation d'acide galactosique, de xylulose et de CO2. Une ou plusieurs de ces voies peut être à la base d'une anomalie métabolique du galactose chez les galactosiques.

71. SECTION 2: deficiency. 5.3. Galactosylceramide lipidosis. 5.3. galt. 1.11. Gammacystathionasedeficiency. 6.4. Ganglioside sialidase deficiency. 3.4. http://www.sun.ac.za/healthsciences/schools/basic_appl_health/chempat/dept/imdsc

SECTION 2 ALPHABETICAL INDEX OF INHERITED METABOLIC DEFECTS Click on letter of alphabet to jump to disease starting with that letter. A B C D ... Z A Abetalipoproteinaemia Acetyl galactosaminidase deficiency Acetyl neuraminidase deficiency Acid-alpha-1,4-glucosidase deficiency Acid-alpha-N-acetyl neuraminidase deficiency Acid esterase deficiency Acid lipase deficiency Acid phosphatase deficiency Adenosine deaminase deficiency Adenylosuccinate deficiency Adrenoleukodystrophy (ALD) Alpha 1-antitrypsin deficiency Alpha-fucosidase deficiency Alpha-galactosidase A deficiency Alpha-galactosidase B deficiency Alpha-glucosidase deficiency Alpha-L-iduronidase deficience Alpha-mannosidase deficiency Alpha-methylaceto-acetyl-CoA-beta-ketothiolase deficiency Alpha-N-acetyl galactosaminidase deficiency Alpha-N-acetyl neuraminidase deficiency Alpha-thalassaemia Amino acid metabolism Amino adipic aciduria Amylo-1,6-glucosidase deficiency Amylopectinosis Andersen disease Anderson-Fabry disease Antitrypsin deficiency (alpha-1) Apolipoprotein CII deficiency Arginase deficiency Argininosuccinate lyase deficiency Argininosuccinate synthetase deficiency Argininosuccinic aciduria Arylsulphatase A deficiency Arylsulphatase B deficiency Aspartyl-beta-glucosaminidase deficiency Aspartylglucosaminuria Ataxia telangiectasia B Beta-galactosidase deficiency Beta-glucosaminidase deficiency Beta-glucosidase deficiency Beta-glucuronidase deficiency Beta-ketothiolase deficiency Beta-lipoproteinaemia Beta-mannosidase deficiency Beta-methylcrotonyl-CoA-carboxylase deficiency

72. Untitled 1.11, Galactosaemia Galactose1-P-uridyl transferase deficiency (galt). http://www.sun.ac.za/healthsciences/schools/basic_appl_health/chempat/dept/isc3c

1.0 CARBOHYDRATE METABOLISM NAME OF DISORDER LABORATORY Glycogenosis Type I (Von Gierke disease) Glucose-6-phosphatase deficiency (liver) Hum Genet SAIMR Glycogenosis Type II (Pompe disease) Acid-alpha-1,4-glucosidase deficiency Hum Genet SAIMR Glycogenosis Type III (Cori disease) Debranching amylo-1,6-glucosidase deficiency Glycogenosis Type IV (Amylopectinosis; Andersen disease) Brancher enzyme deficiency Glycogenosis Type V (McArdle disease) Phosphorylase deficiency (muscle) Chem Path UCT Chem Path UOFS Glycogenosis Type VI (Hers disease) Phosphorylase deficiency (liver) Hum Genet SAIMR Glycogenosis Type VII Phosphofructokinase deficiency Glycogenosis Type VIII Phosphorylase kinase deficiency (liver) Glycogenosis IXa and IXb Autosomal recessive and X-linked forms Hum Genet SAIMR Hyperoxaluria Biochem Potch U Chem Path Red X Galactosaemia Galactokinase deficiency Biochem Potch U Chem Path Red X Hum Genet SAIMR Galactosaemia Galactose-1-P-uridyl transferase deficiency (GALT) Biochem Potch U Chem Path Red X Hum Genet SAIMR Pyruvate dehydrogenase deficiency Biochem Potch U Chem Path UCT Pyruvate kinase deficiency Chem Path UCT Chem Path U Stell

73. Forskning - Ämnets Namn - Institutionens Namn Aims and Methods We characterize the basic elements of adaptive immune systemof seahorse to understand more of the galtdeficiency in this fish. http://www.umu.se/climi/immuno/forskning/forskprj.html

Immunologi Forskningsprojekt / Research Projects Projects are sorted in alphabetic order by the family name of the main researcher ON THE ROLE OF HUMAN INTESTINAL EPITHELIAL CELLS IN INNATE IMMUNITY Project group Supported by the Medical Research Council, the Swedish Cancer Society. 2000-10-09 : Secretion of antimicrobial peptides and proteins into the mucous appears to be an important component in the immune protection of the gut from infectious insult. Effects of inflammation on this innate antimicrobial defense in human intestine were studied. Intestinal epithelial cells were analysed for expression of the antimicrobial a -defensins HD5 and HD6, b -defensins HBD1 and HBD2, hCAP18 and lysozyme. Methods : Samples were obtained from jejunum, ileum and colon of patients suffering from inflammatory bowel disease (IBD), ulcerative colitis (UC) or Crohn's disease, and from controls with no history of intestinal inflammation. Four colon carcinoma cell lines were also analysed. All six antimicrobial agents were analysed at the mRNA level. Real-time quantitative RT-PCR assays were constructed for HD5, HBD1, HBD2, and lysozyme. HD5, hCAP18 and lysozyme were analysed at the protein level by immunohistochemistry of intestinal tissue.

74. Istituto Giannina Gaslini - Cell Bank FUCOSIDOSIS, 230000. GALACTOKINASE deficiency, 230200. GALACTOSE EPIMERASE deficiency,230350. GALACTOSEMIA (galt ), 230400. GANGLIOSIDOSIS GM 1 TYPE 1, 230500. http://www.gaslini.org/DPPM/diaglist.htm

Gaslini Cell Line and DNA Bank DIAGNOSIS LIST DIAGNOSIS OMIM Number ACYL-CoA DEHYDROGENASE, LONG CHAIN, DEF. ADENOSINE DEAMINASE ADRENAL HYPERPLASIA III ADRENOLEUKODYSTROPHY ... ZELLWEGER Site by Dr. Mirella Filocamo Weekly update by Lucia Obino. Last update: 27/01/2003 10.17.58 Telethon grants have made this catalogue possible Best view 800x600 with Internet Explorer Last update:27/01/2003 10.17.58

75. Newborn Screening Biotinidase deficiency Congenital Adrenal Hyperplasia (CAH) Congenital Hypothyroidism(CH) Congenital Toxoplasmosis Cystic Fibrosis (CF) Galactosemia (galt), http://trose.20m.com/NBS/nbs.html

NEWBORN SCREENING The newborn screening test (NBS) is often is referred to as the "PKU" test, but the NBS test screens for more than just PKU. It tests babies for between 3 and 8 hereditary disorders. The test is done to find out if your baby has inherited a disorder for which early treatment can prevent death or mental retardation. It is very important that your baby is tested as soon as possible. Even parents who have no family history of these disorders, or who have already had healthy children can still have children with these disorders. In fact, most children with these disorders come from families with no previous history of the condition. The NBS blood test is performed by pricking your baby's heel and putting a few drops of blood on a special filter paper. The paper is sent to the laboratory where several tests are performed. The results are then sent to your hospital and doctor. If the test shows abnormal results, you will be notified and given directions on what to do. Follow the directions carefully. Usually additional tests will be necessary to determine if your child has the disorder. Each state has different laws surrounding newborn screening in their state, and all babies are screened within the guidelines of these individual state laws. This means that your state could screen for as few as 3 disorders. To find out which of the disorders your state screens for in the NBS

76. CFS - A Nurtitional Approach sperm count, hair loss, skin conditions, diarrhoea, immune deficiency, behaviouraland the gastrointestinal tract the Gut Associated Lymphoid Tissue (galt). http://www.acnem.org/journal/17-1_june_1998/cfs-a_nutritional_approach.htm

Home CFS: A nutritional approach Hilton Lowe MB,BS, FACNEM Introduction Chronic fatigue syndrome is the end result of multi-system dysfunction. There are probably multiple aetiologies. The nutritional approach to correct physiological function is aimed at the digestive tract, liver function, inflammatory control and adrenal dysfunction. Assessment and optimisation of physiological function at these integral areas show a predictable benefit using nutritional supplements combined with minimal use of synthetic pharmaceuticals. The approach is wholistic. Blood tests are used to exclude recognised diseases and to assess liver status, vitamin status, immune function, allergic inflammatory status and intestinal absorption; three-day faecal fats to reflect digestive ability; urinary indican for intestinal dysbiosis; hair mineral analysis to reveal mineral imbalances and reflect on adrenal function. The interpretation of these test is critical. Definition The chronic fatigue syndrome, as defined by Fukuda et al., 1994, comprises clinically evaluated, unexplained, persistent or relapsing fatigue, which is persistent for six months or more. It has definite onset. It is not the result of ongoing exertion and is not substantially relieved by rest. CFS results in substantial reduction in previous levels of occupational, educational, social or personal activities. Also, four or more of the following symptoms are concurrent, persistent for six months or more, and did not predate the fatigue: sore throat; impaired short term memory and concentration; tender cervical or axillary lymph nodes; muscle pain; multi-joint pain without arthritis; headache of a new type, pattern or severity; unrefreshing sleep; post-exertional malaise lasting more than twenty-four hours.

77. Gene-DIsease Set For Chromosome 9 fbp deficiency (fbpd) is inherited as an autosomal recessive disorder mainlyin the liver and causes lifethreatening episodes of galt, galt, galt, 9p13, http://www.ebi.ac.uk/proteome/HUMAN/chromosomes/disease_set/9.html

Gene-Disease set for chromosome , according to SPTr. [Alternative view: Complete gene set Gene GDB GeneCards Location MIM Acc Nr Description Disease PubMed Ensembl InterPro CluSTr STRING ATP-binding cassette, sub-family A, member 1 (ATP-binding cassette transporter 1) (ATP-binding cassette 1) (ABC-1) (Cholesterol efflux regulatory protein). defects in abca1 are a cause of high density lipoprotein deficiency type 1 (hdld1) [mim:205400], also known as tangier disease (td). hdld1 is a recessive disorder characterized by absence of high density lipoprotein (hdl) cholesterol from plasma, hepatosplenomegaly, peripheral neuropathy, and frequently premature coronary artery disease (cad) defects in abca1 are a cause of high density lipoprotein deficiency type 2 (hdld2) [mim:604091], also known as familial hypoalphalipoproteinemia (fha). hdld2 is inherited as autosomal dominant trait and shows a reduction in cellular cholesterol efflux Proto-oncogene tyrosine-protein kinase ABL1 (EC 2.7.1.112) (p150) (c-ABL). participates in a t(9;22)(q34;q11) chromosomal translocation that produces a bcr-abl oncogene responsible for chronic myeloid leukemia (cml), acute myeloid leukemia (aml), and acute lymphoblastic leukemia (all) Adenylate kinase isoenzyme 1 (EC 2.7.4.3) (ATP-AMP transphosphorylase) (AK1) (Myokinase).

78. CompletePlanet - Directory Glaucoma G Keywords diseases, syndrome, disease, gastrointestinal, gallstones, galactosemia,health, conditions_and_diseases, dmoz, galt, deficiency, gastric, cancer http://www.completeplanet.com/Health_Medicine/Diseases_Conditions/Specific_Condi

Search Databases for: Search All Within Glaucoma Top Specific Conditions No further results below this node. NODE RESULTS 11-20 of 20 INFO Keywords: product, disease, prostate, disorders, competitor, pressure, blood, below, shop, name, city, state, zip, telephone, refund, learning, currently, development, check, hair, impotence, halitosis, smoking, tooth, bleaching, acne, wrinkles, arthritis, items, days http://www.duplipharmresearch.com/info-page.htm Categories... Relevance Popular Links Open Directory - Health: Conditions and Diseases: G Keywords: diseases, syndrome, disease, gastrointestinal, gallstones, galactosemia, health, conditions_and_diseases, dmoz, galt, deficiency, gastric, cancer, url, edit, disorders, disorder, gaucher, reflux, genital, warts, gerstmann, directory, glaucoma, glomerular, glomerulonephritis, glutaricaciduria, goiter, gonorrhea, pt http://dmoz.org/Health/Conditions_and_Diseases/G/ Categories... Relevance Popular Links In DQM Welcome to The Schepens Eye Research Institute Keywords: map, vision, schepens, people, information, opportunities, employment, advanced, text, research, training, eyes, publications, news, future, events, street, boston, telephone, geninfo, staniford, eri, harvard, edu, updated, brian, anderson

79. Welcome To The The CLEAR PATH TO HEALING Newsletter Is the deficiency of Aspirin the Cause of Headaches? QUESTION OF THE WEEK Whatis Gluten and Which Grains are Gluten Free? 2. Mind – Who is John galt? http://www.dreamrealityproductions.com/newsletters/Issue 2.htm

"The Life-Changing, Must Have Book for the New Millennium!" Visitors Welcome to the The CLEAR PATH TO HEALING Newsletter, Issue 2 by Dr. Barry S. Weinberg http://www.placeforhealing.com drbarry@placeforhealing.com FREE Weekly Wisdom to Live a Life you Love! Forward this issue to a Friend! A L Y V E - Always Live Your Vision...Everyday Issue #2 May June 3, 2001 IN THIS ISSUE 1. Body – Is the Deficiency of Aspirin the Cause of Headaches? QUESTION OF THE WEEK - What is Gluten and Which Grains are Gluten Free? 2. Mind – Who is John Galt? 3. Spirit – Are we the Victim or Creator of our Circumstance? 4. Relationships – CONTEST - What would you do? (SUBSCRIBER REPLIES REQUESTED! BEST ANSWER JUDGED WILL WIN A FREE TAPE - "YOU DESERVE THE GIFT OF HEALTH.") 5. Society – World Wildlife Fund 6. Prosperity – The 10%/20% Path to Abundance 7. Life Purpose – The Big Rocks This publication is sent only to subscribers. If you have received this and choose not to, please click on the UNSUBSCRIBE link at the end of this document and you will immediately be removed from our mailing list. We apologize for the inconvenience. Body – Secrets to Abundant Health Is the Deficiency of Aspirin the Cause of Disease?

80. Introduction Galactosa emia is caused by mutations of the galt gene mapped to locus 9p13. Theresulting in deficiency of galactose1-phosphate uridyl transferase results in http://www.daisynetwork.org.uk/pofintro.htm

Premature Ovarian Failure A brief background to the causes of premature ovarian failure by Dr Gerard Conway - Consultant Endocrinologist, The Middlesex Hospital, Mortimer Street, London W1N 8AA Introduction In the United Kingdom the age distribution of the menopause has a median at the age of 50 years with one percent of women menstruating after the age of 60 and one percent entering menopause before the age of 40. The age of the natural menopause is closely inherited and it is also affected by environmental factors such as smoking. A menopause before the age of 40 is most commonly taken to be the definition of 'premature ovarian failure' although this figure is arbitrary. Estimates of the prevalence of premature ovarian failure range between 0.3 and 1% and this condition account for approximately 25% of women presenting amenorrhoea. The ovary comprises four cell types, germ cells, granulosa cells, theca cells and support cells. The integrity of germ cells and granulosa cells is closely interdependent so their survival and failure occur in parallel. Some mechanisms of ovarian failure primarily result in germ cell depletion, X chromosome abnormalities for instance, while others target granulosa cells only, e.g. FSH receptor mutations. Terminology Here are some terms which are applied to differences in timing and severity of ovarian failure: Gonadal dysgenesis describes the failure of the ovary to develop but is also loosely applied to the presentation of ovarian failure with primary amenorrhoea and failure to develop secondary sexual characteristics.

A  B  C  D  E  F  G  H  I  J  K  L  M  N  O  P  Q  R  S  T  U  V  W  X  Y  Z

Page 4     61-80 of 88    Back | 1  | 2  | 3  | 4  | 5  | Next 20