Cats: The domestic cat, Felis catus, of the carnivore family FELIDAE, comprising over 30 different breeds. The domestic cat is descended primarily from the wild cat of Africa and extreme southwestern Asia. Though probably present in towns in Palestine as long ago as 7000 years, actual domestication occurred in Egypt about 4000 years ago. (From Walker's Mammals of the World, 6th ed, p801)Search Engine: Software used to locate data or information stored in machine-readable form locally or at a distance such as an INTERNET site.Databases, Genetic: Databases devoted to knowledge about specific genes and gene products.Catalase: An oxidoreductase that catalyzes the conversion of HYDROGEN PEROXIDE to water and oxygen. It is present in many animal cells. A deficiency of this enzyme results in ACATALASIA.Chloramphenicol O-Acetyltransferase: An enzyme that catalyzes the acetylation of chloramphenicol to yield chloramphenicol 3-acetate. Since chloramphenicol 3-acetate does not bind to bacterial ribosomes and is not an inhibitor of peptidyltransferase, the enzyme is responsible for the naturally occurring chloramphenicol resistance in bacteria. The enzyme, for which variants are known, is found in both gram-negative and gram-positive bacteria. EC 2.3.1.28.Genome, Human: The complete genetic complement contained in the DNA of a set of CHROMOSOMES in a HUMAN. The length of the human genome is about 3 billion base pairs.Cat Diseases: Diseases of the domestic cat (Felis catus or F. domesticus). This term does not include diseases of the so-called big cats such as CHEETAHS; LIONS; tigers, cougars, panthers, leopards, and other Felidae for which the heading CARNIVORA is used.Antibodies: Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the ANTIGEN (or a very similar shape) that induced their synthesis in cells of the lymphoid series (especially PLASMA CELLS).Internet: A loose confederation of computer communication networks around the world. The networks that make up the Internet are connected through several backbone networks. The Internet grew out of the US Government ARPAnet project and was designed to facilitate information exchange.Genes: A category of nucleic acid sequences that function as units of heredity and which code for the basic instructions for the development, reproduction, and maintenance of organisms.International Classification of Diseases: A system of categories to which morbid entries are assigned according to established criteria. Included is the entire range of conditions in a manageable number of categories, grouped to facilitate mortality reporting. It is produced by the World Health Organization (From ICD-10, p1). The Clinical Modifications, produced by the UNITED STATES DEPT. OF HEALTH AND HUMAN SERVICES, are larger extensions used for morbidity and general epidemiological purposes, primarily in the U.S.Databases, Factual: Extensive collections, reputedly complete, of facts and data garnered from material of a specialized subject area and made available for analysis and application. The collection can be automated by various contemporary methods for retrieval. The concept should be differentiated from DATABASES, BIBLIOGRAPHIC which is restricted to collections of bibliographic references.Clinical Coding: Process of substituting a symbol or code for a term such as a diagnosis or procedure. (from Slee's Health Care Terms, 3d ed.)Insurance Claim Review: Review of claims by insurance companies to determine liability and amount of payment for various services. The review may also include determination of eligibility of the claimant or beneficiary or of the provider of the benefit; determination that the benefit is covered or not payable under another policy; or determination that the service was necessary and of reasonable cost and quality.United StatesInsurance Claim Reporting: The design, completion, and filing of forms with the insurer.Retrospective Studies: Studies used to test etiologic hypotheses in which inferences about an exposure to putative causal factors are derived from data relating to characteristics of persons under study or to events or experiences in their past. The essential feature is that some of the persons under study have the disease or outcome of interest and their characteristics are compared with those of unaffected persons.Medical Records: Recording of pertinent information concerning patient's illness or illnesses.Patient Discharge: The administrative process of discharging the patient, alive or dead, from hospitals or other health facilities.Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing HEMOGLOBIN whose function is to transport OXYGEN.Luminol: 5-Amino-2,3-dihydro-1,4-phthalazinedione. Substance that emits light on oxidation. It is used in chemical determinations.Erythrocyte Membrane: The semi-permeable outer structure of a red blood cell. It is known as a red cell 'ghost' after HEMOLYSIS.Sodium Hypochlorite: It is used as an oxidizing and bleaching agent and as a disinfectant. (From Grant & Hackh's Chemical Dictionary, 5th ed)Erythrocyte Aging: The senescence of RED BLOOD CELLS. Lacking the organelles that make protein synthesis possible, the mature erythrocyte is incapable of self-repair, reproduction, and carrying out certain functions performed by other cells. This limits the average life span of an erythrocyte to 120 days.Designer Drugs: Drugs designed and synthesized, often for illegal street use, by modification of existing drug structures (e.g., amphetamines). Of special interest are MPTP (a reverse ester of meperidine), MDA (3,4-methylenedioxyamphetamine), and MDMA (3,4-methylenedioxymethamphetamine). Many drugs act on the aminergic system, the physiologically active biogenic amines.Hemolysis: The destruction of ERYTHROCYTES by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity.Hemoglobins, Abnormal: Hemoglobins characterized by structural alterations within the molecule. The alteration can be either absence, addition or substitution of one or more amino acids in the globin part of the molecule at selected positions in the polypeptide chains.Glutathione: A tripeptide with many roles in cells. It conjugates to drugs to make them more soluble for excretion, is a cofactor for some enzymes, is involved in protein disulfide bond rearrangement and reduces peroxides.Hajdu-Cheney Syndrome: Rare, autosomal dominant syndrome characterized by ACRO-OSTEOLYSIS, generalized OSTEOPOROSIS, and skull deformations.Adrenal Hyperplasia, Congenital: A group of inherited disorders of the ADRENAL GLANDS, caused by enzyme defects in the synthesis of cortisol (HYDROCORTISONE) and/or ALDOSTERONE leading to accumulation of precursors for ANDROGENS. Depending on the hormone imbalance, congenital adrenal hyperplasia can be classified as salt-wasting, hypertensive, virilizing, or feminizing. Defects in STEROID 21-HYDROXYLASE; STEROID 11-BETA-HYDROXYLASE; STEROID 17-ALPHA-HYDROXYLASE; 3-beta-hydroxysteroid dehydrogenase (3-HYDROXYSTEROID DEHYDROGENASES); TESTOSTERONE 5-ALPHA-REDUCTASE; or steroidogenic acute regulatory protein; among others, underlie these disorders.Exfoliation Syndrome: The deposition of flaky, translucent fibrillar material most conspicuous on the anterior lens capsule and pupillary margin but also in both surfaces of the iris, the zonules, trabecular meshwork, ciliary body, corneal endothelium, and orbital blood vessels. It sometimes forms a membrane on the anterior iris surface. Exfoliation refers to the shedding of pigment by the iris. (Newell, Ophthalmology, 7th ed, p380)Tooth Exfoliation: Physiologic loss of the primary dentition. (Zwemer, Boucher's Clinical Dental Terminology, 4th ed)Hypophosphatasia: A genetic metabolic disorder resulting from serum and bone alkaline phosphatase deficiency leading to hypercalcemia, ethanolamine phosphatemia, and ethanolamine phosphaturia. Clinical manifestations include severe skeletal defects resembling vitamin D-resistant rickets, failure of the calvarium to calcify, dyspnea, cyanosis, vomiting, constipation, renal calcinosis, failure to thrive, disorders of movement, beading of the costochondral junction, and rachitic bone changes. (From Dorland, 27th ed)Cherubism: A fibro-osseous hereditary disease of the jaws. The swollen jaws and raised eyes give a cherubic appearance; multiple radiolucencies are evident upon radiographic examination.Leukocyte-Adhesion Deficiency Syndrome: Rare, autosomal recessive disorder caused by deficiency of the beta 2 integrin receptors (RECEPTORS, LEUKOCYTE-ADHESION) comprising the CD11/CD18 family of glycoproteins. The syndrome is characterized by abnormal adhesion-dependent functions, especially defective tissue emigration of neutrophils, leading to recurrent infection.Bone Resorption: Bone loss due to osteoclastic activity.Ehlers-Danlos Syndrome: A heterogeneous group of autosomally inherited COLLAGEN DISEASES caused by defects in the synthesis or structure of FIBRILLAR COLLAGEN. There are numerous subtypes: classical, hypermobility, vascular, and others. Common clinical features include hyperextensible skin and joints, skin fragility and reduced wound healing capability.Steroid 21-Hydroxylase: An adrenal microsomal cytochrome P450 enzyme that catalyzes the 21-hydroxylation of steroids in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP21 gene, converts progesterones to precursors of adrenal steroid hormones (CORTICOSTERONE; HYDROCORTISONE). Defects in CYP21 cause congenital adrenal hyperplasia (ADRENAL HYPERPLASIA, CONGENITAL).alpha 1-Antitrypsin Deficiency: Deficiency of the protease inhibitor ALPHA 1-ANTITRYPSIN that manifests primarily as PULMONARY EMPHYSEMA and LIVER CIRRHOSIS.alpha 1-Antitrypsin: Plasma glycoprotein member of the serpin superfamily which inhibits TRYPSIN; NEUTROPHIL ELASTASE; and other PROTEOLYTIC ENZYMES.Reference Standards: A basis of value established for the measure of quantity, weight, extent or quality, e.g. weight standards, standard solutions, methods, techniques, and procedures used in diagnosis and therapy.Pulmonary Emphysema: Enlargement of air spaces distal to the TERMINAL BRONCHIOLES where gas-exchange normally takes place. This is usually due to destruction of the alveolar wall. Pulmonary emphysema can be classified by the location and distribution of the lesions.Gene Expression Profiling: The determination of the pattern of genes expressed at the level of GENETIC TRANSCRIPTION, under specific circumstances or in a specific cell.Emphysema: A pathological accumulation of air in tissues or organs.Phenotype: The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.alpha 1-Antichymotrypsin: Glycoprotein found in alpha(1)-globulin region in human serum. It inhibits chymotrypsin-like proteinases in vivo and has cytotoxic killer-cell activity in vitro. The protein also has a role as an acute-phase protein and is active in the control of immunologic and inflammatory processes, and as a tumor marker. It is a member of the serpin superfamily.Trypsin Inhibitors: Serine proteinase inhibitors which inhibit trypsin. They may be endogenous or exogenous compounds.Pancreatic Elastase: A protease of broad specificity, obtained from dried pancreas. Molecular weight is approximately 25,000. The enzyme breaks down elastin, the specific protein of elastic fibers, and digests other proteins such as fibrin, hemoglobin, and albumin. EC 3.4.21.36.Pragmatic Clinical Trials as Topic: Works about randomized clinical trials that compare interventions in clinical settings and which look at a range of effectiveness outcomes and impacts.Genome: The genetic complement of an organism, including all of its GENES, as represented in its DNA, or in some cases, its RNA.Genome, Bacterial: The genetic complement of a BACTERIA as represented in its DNA.Genome, Viral: The complete genetic complement contained in a DNA or RNA molecule in a virus.Genome, Plant: The genetic complement of a plant (PLANTS) as represented in its DNA.Sequence Analysis, DNA: A multistage process that includes cloning, physical mapping, subcloning, determination of the DNA SEQUENCE, and information analysis.Phylogeny: The relationships of groups of organisms as reflected by their genetic makeup.Genomics: The systematic study of the complete DNA sequences (GENOME) of organisms.Genome, Mitochondrial: The genetic complement of MITOCHONDRIA as represented in their DNA.
(1/34) Hydrogen peroxide and coffee induce G:C-->T:A transversions in the lacI gene of catalase-defective Escherichia coli.

The mutagenicity of hydrogen peroxide (H2O2) was compared with that of coffee, a complex mixture which generates H2O2. An Escherichia coli strain defective in catalase activity (katG katE double mutant) and carrying a single copy mucAB (pRW144) plasmid was constructed to enhance the mutagenic response to oxidants. The ability of the mucAB genes to influence the type, frequency and distribution of H2O2-induced mutations was also investigated in isogenic bacteria lacking pRW144. Induced mutational spectra were characterized and compared with that of spontaneous mutagenesis. A total of 444 independent forward mutations affecting the first 210 bp of the lacI gene were identified by DNA sequence analysis. The spontaneous mutation spectrum showed no bias (P = 0.52) for substitutions at G:C base pairs. In contrast, in the H2O2-induced spectrum substitutions occurred preferentially at G:C base pairs (P < 0.0001) with a preponderance of G:C-->T:A transversions (43.4% of H2O2-induced mutants versus 17.3% of spontaneous mutants). These data support the view that 7,8-dihydro-8-oxoguanine is the main premutagenic lesion induced by H2O2 and that catalase-defective bacteria have elevated levels of 8-oxoguanine in chromosome DNA after H2O2 exposure. Coffee produced a similar distribution of mutational events as H2O2 (P > 0.05), suggesting that this compound may be the main cause of the coffee-induced mutagenesis. The presence of plasmid pRW144 did not affect the frequency of H2O2-induced G:C-->T:A transversions, but caused an increase in A:T-->T:A transversions and a decrease in -1 base frameshifts. Although the frequencies of G:C-->T:A transversions were similar in all three induced spectra (H2O2 and coffee +/- pRW144), differences were observed in location of mutations throughout the target gene.  (+info)

(2/34) Tissue and organ expression of catalase in acatalasemic beagle dogs.

Acatalasemic Beagle dogs which were maintained in our laboratories showed no sign of catalase activity at all in the erythrocytes, and glutathione peroxidase and superoxide dismutase were at normal levels. Immunoblotting analysis demonstrated that no catalase protein is detectable in their erythrocytes. On the other hand, catalase activity was detected in other tissues and organs, albeit at varying, lower levels than in normal dogs. Quantitative immunoblotting analysis consistently demonstrated that the catalase protein is expressed in the liver and kidneys of acatalasemic dogs in proportion to the activity in these organs. The catalase mRNA expressions in the blood, liver and kidneys in acatalasemic dogs were almost the same as those in normal dogs. These results suggested that catalytically normal catalase protein is translated from mRNA in the tissues and organs including erythrocytes, but in erythrocytes this enzyme protein is disposed of by an unknown mechanism.  (+info)

(3/34) cDNA cloning and expression of mutant catalase from the hypocatalasemic mouse: comparison with the acatalasemic mutant.

Mutant catalase cDNAs from the hypocatalasemic and acatalasemic mice were cloned and expressed in bacteria. A novel missense mutation, Asp (AAT) to Ser (AGT), was identified at amino acid position 439 of the hypocatalasemic catalase. Analysis of recombinant catalase mutants revealed that the mutation is responsible for the reduced activity of hypocatalasemic catalase and the unstable tetrameric structure of acatalasemic catalase was also suggested.  (+info)

(4/34) Characterization of hydrogen peroxide removal reaction by hemoglobin in the presence of reduced pyridine nucleotides.

Hydrogen peroxide removal rates by hemoglobin were enhanced in the presence of reduced pyridine nucleotides. The species which had the activity to oxidize pyridine nucleotides was purified from human blood and identified as hemoglobin A. Hydrogen peroxide removal rates by hemoglobin A without reduced pyridine nucleotides at 0.2 mM hydrogen peroxide were 0.87+/-0.11 micromol/s/g hemoglobin, and the removal rates using 0.2 mM NADH and NADPH were 2.02+/-0.20 and 1.96+/-0.31 micromol/s/g hemoglobin, respectively. We deduced that the removal reaction by hemoglobin included formations of methemoglobin and the ferryl radical and reduction of the latter with pyridine nucleotides. The hydrogen peroxide removal ability by hemoglobin was less than that by catalase but was larger than that by glutathione peroxidase-glutathione reductase system at 0.2 mM hydrogen peroxide. Under acatalasemic conditions, it was suggested that NAD(P)H were important factors to prevent the oxidative degradation of hemoglobin.  (+info)

(5/34) Properties of acatalasic cells growing in vitro.

Acatalasia, a disease due to homozygosity for a Mendelian gene, is characterized by the absence of the enzyme catalase from the tissues of the human body. Red cells from heterozygotes have enzyme activities about one-half normal. In this paper, the development of cell lines from skin biopsies on an affected homozygote, a heterozygote, and eight control patients is described. The cell type is the euploid "fibroblast." It was found that acatalasic cells lacked the enzyme, even after growing for many months in a medium rich in catalase. The control lines all had mean catalase activities double or more that of the heterozygous line. Selection experiments, in which the growth of cells exposed for 20 minutes to varying concentrations of hydrogen peroxide was measured, did not provide a system for preferentially eliminating acatalasic cells. Certain other experiments bearing on the enzymatic defect in this disease were performed.  (+info)

(6/34) Acatalasemia sensitizes renal tubular epithelial cells to apoptosis and exacerbates renal fibrosis after unilateral ureteral obstruction.

Tissue homeostasis is determined by the balance between oxidants and antioxidants. Catalase is an important antioxidant enzyme regulating the level of intracellular hydrogen peroxide and hydroxyl radicals. The effect of catalase deficiency on renal tubulointerstitial injury induced by unilateral ureteral obstruction (UUO) has been studied in homozygous acatalasemic mutant mice (C3H/AnLCs(b)Cs(b)) compared with wild-type mice (C3H/AnLCs(a)Cs(a)). Complete UUO caused interstitial cell infiltration, tubular dilation and atrophy, and interstitial fibrosis with accumulation of type IV collagen in obstructed kidneys (OBK) of both mouse groups. However, the degree of injury showed a significant increase in OBK of acatalasemic mice compared with that of wild-type mice until day 7. The deposition of lipid peroxidation products including 4-hydroxy-2-hexenal, malondialdehyde, and 4-hydroxy-2-nonenal was severer in dilated tubules of acatalasemic OBK. Apoptosis in tubular epithelial cells significantly increased in acatalasemic OBK at day 4. Expression of caspase-9, a marker of mitochondrial pathway-derived apoptosis, increased in dilated tubules of acatalasemic mice. The level of catalase activity remained low in acatalasemic OBK until day 7 without compensatory upregulation of glutathione peroxidase activity. The data indicate that acatalasemia exacerbated oxidation of renal tissue and sensitized tubular epithelial cells to apoptosis in OBK of UUO. This study demonstrates that catalase deficiency enhanced tubulointerstitial injury and fibrosis in a murine model of UUO and thus supports the protective role of catalase in this model.  (+info)

(7/34) Inhibitory effects of prior low-dose X-ray irradiation on carbon tetrachloride-induced hepatopathy in acatalasemic mice.

The catalase activities in blood and organs of the acatalasemic (C3H/AnLCs(b)Cs(b)) mouse of C3H strain are lower than those of the normal (C3H/AnLCs (a)Cs(a)) mouse. We examined the effects of prior low-dose (0.5 Gy) X-ray irradiation, which reduced the oxidative damage under carbon tetrachloride-induced hepatopathy in the acatalasemic or normal mice. The acatalasemic mice showed a significantly lower catalase activity and a significantly higher glutathione peroxidase activity compared with those in the normal mice. Moreover, low-dose irradiation increased the catalase activity in the acatalasemic mouse liver to a level similar to that of the normal mouse liver. Pathological examinations and analyses of blood glutamic oxaloacetic and glutamic pyruvic transaminase activity and lipid peroxide levels showed that carbon tetrachloride induced hepatopathy was inhibited by low-dose irradiation. These findings may indicate that the free radical reaction induced by the lack of catalase and the administration of carbon tetrachloride is more properly neutralized by high glutathione peroxidase activity and low-dose irradiation in the acatalasemic mouse liver.  (+info)

(8/34) Telmisartan inhibits both oxidative stress and renal fibrosis after unilateral ureteral obstruction in acatalasemic mice.

BACKGROUND: Reactive oxygen species are involved in many of the angiotensin II signalling pathways. We have thus investigated whether the angiotensin II type 1 (AT1) receptor antagonist, telmisartan, can inhibit the accelerated renal fibrosis and excess oxidative stress, which occurs after unilateral ureteral obstruction (UUO) in acatalasemic mice. METHODS: The effect of daily intraperitoneal injection of telmisartan (0.1-0.3 mg/kg body weight) on the renal tubulointerstitial injury induced by UUO has been studied in homozygous acatalasemic mutant mice (C3H/AnLCs b Cs b) and wild-type mice (C3H/AnLCs a Cs a). We evaluated the systemic blood pressure of the mice on the seventh day. In addition, the tubulointerstitial expression of collagens type I and type IV, the p22-, p47- and p67-phox subunits of NADPH oxidase, 4-hydroxy-2-nonenal, and 4-hydroxy-2-hexenal lipid peroxidation products were assessed by immunohistochemistry. The level of apoptosis was determined by terminal deoxynucleotidyl transferase nick end-labelling analysis, while the mRNA level of the p22-, p47- and p67-phox subunits was quantified by real-time PCR. The renal content of each of the antioxidant enzymes catalase, glutathione peroxidase and superoxide dismutase was determined by specific assay. RESULTS: Obstructed kidneys from acatalasemic mice exhibited increased tubulointerstitial deposition in dilated tubules of collagens type I and IV, lipid peroxidation products, and the p22/p47/p67-phox subunits of NADPH oxidase. The level of the p22/p47/p67-phox subunit mRNA, and of apoptosis in tubular epithelial cells, was also increased compared with those from wild-type kidneys. Treatment with telmisartan attenuated all of the changes and prevented renal fibrosis in a dose-dependent manner; despite the low dose (0.1 mg/kg). The treatment did not lower the systemic blood pressure. The catalase activity remained low in acatalasemic obstructed kidneys without compensatory upregulation of glutathione peroxidase or superoxide dismutase activity; the level of neither anti-oxidant enzymes in obstructed kidneys was affected by telmisartan. CONCLUSIONS: The AT1 receptor antagonist telmisartan ameliorated renal fibrosis after UUO by inhibition of oxidative stress, even under acatalasemic conditions.  (+info)

*  ICD-10 Chapter IV: Endocrine, nutritional and metabolic diseases
Defects of catalase and peroxidase Acatalasia (Takahara) (E80.4) Gilbert's syndrome (E80.5) Crigler-Najjar syndrome (E80.6) ...
*  Acatalasia
Occurrence of acatalasia is often the result of mutation in the CAT gene which codes for the enzyme catalase. Researchers ... Acatalasia (also called acatalasemia, or Takahara's disease) is an autosomal recessive peroxisomal disorder caused by low ...
*  Catalase
Some humans have very low levels of catalase (acatalasia), yet show few ill effects. Catalase is usually located in a cellular ...
*  Oxidative stress
Reductive stress Acatalasia Antioxidant Bruce Ames Denham Harman Malondialdehyde, an oxidative stress marker Mitochondrial free ...
*  Kawasaki Medical School
Takahara Shigeo - One‐time Professor who discovered Acatalasia Official site Official site (in Japanese) Medical Museum ...
*  List of MeSH codes (C18)
... acatalasia MeSH C18.452.648.556.750.112 --- adrenoleukodystrophy MeSH C18.452.648.556.750.200 --- chondrodysplasia punctata, ...
*  List of MeSH codes (C16)
... acatalasia MeSH C16.320.565.556.750.112 --- adrenoleukodystrophy MeSH C16.320.565.556.750.200 --- chondrodysplasia punctata, ...
*  List of cutaneous conditions
Acatalasia (acatalasemia, Takahara's disease) Acquired dyskeratotic leukoplakia Actinic cheilitis (actinic cheilosis) Acute ...
Acatalasia | Article about acatalasia by The Free Dictionary  Acatalasia | Article about acatalasia by The Free Dictionary
Find out information about acatalasia. Congenital absence of the enzyme catalase Explanation of acatalasia ... acatalasia. Also found in: Medical, Wikipedia. acatalasia. [¦ā·ka·tə′lā·zhē·ə or zhə] (medicine) Congenital absence of the ... Acatalasia , Article about acatalasia by The Free Dictionary https://encyclopedia2.thefreedictionary.com/acatalasia ... The absence of CAT in the blood and other tissues in the human body leads to the occurrence of acatalasia, which is manifested ...
more infohttps://encyclopedia2.thefreedictionary.com/acatalasia
Acatalasia - Wikipedia  Acatalasia - Wikipedia
Occurrence of acatalasia is often the result of mutation in the CAT gene which codes for the enzyme catalase. Researchers ... Acatalasia (also called acatalasemia, or Takahara's disease) is an autosomal recessive peroxisomal disorder caused by low ...
more infohttps://en.wikipedia.org/wiki/Acatalasia
LABOKLIN (UK)| Genetic Diseases | Dogs| Catalase Deficiency ( CAT ) / Hypocatalasemia / Acatalasia  LABOKLIN (UK)| Genetic Diseases | Dogs| Catalase Deficiency ( CAT ) / Hypocatalasemia / Acatalasia
... hypocatalasemia or acatalasia) is a rare inherited disorder that is caused by recessive mutation in the CAT gene which is ... The dog is likely to develop Catalase Deficiency ( CAT ) / Hypocatalasemia / Acatalasia and will pass the mutant gene to its ... Catalase Deficiency (hypocatalasemia or acatalasia) is a rare inherited disorder that is caused by recessive mutation in the ... It is very unlikely that the dog will develop Catalase Deficiency ( CAT ) / Hypocatalasemia / Acatalasia. The dog will never ...
more infohttp://www.laboklin.co.uk/laboklin/showGeneticTest.jsp?testID=8552
Acatalasia  Acatalasia
... (also called acatalasemia, or Takahara's disease) is a deficiency of the enzyme catalase, is a relatively benign ... Factors of Acatalasia:. *Many patients with acatalasia are asymptomatic, while some develop mouth sores. Acatalasia ( ... Acatalasia. Definition: Acatalasia (also called acatalasemia, or Takahara's disease) is a deficiency of the enzyme catalase, is ... Acatalasia is often the result of mutations in both copies of the CAT gene which codes for the enzyme catalase. There are ...
more infohttp://www.assignmentpoint.com/science/medical/acatalasia.html
ACATALASIA | Kamus Kedokteran, Keperawatan, Kebidanan, Kefarmasian, Kesehatan Online Lengkap | KAMUS.FARMASI-ID.COM  ACATALASIA | Kamus Kedokteran, Keperawatan, Kebidanan, Kefarmasian, Kesehatan Online Lengkap | KAMUS.FARMASI-ID.COM
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more infohttps://kamus.farmasi-id.com/glossary/acatalasia/
CAT Gene - GeneCards | CATA Protein | CATA Antibody  CAT Gene - GeneCards | CATA Protein | CATA Antibody
acatalasia Relevant External Links for CAT. Genetic Association Database (GAD) CAT Human Genome Epidemiology (HuGE) Navigator ...
more infohttp://www.genecards.org/cgi-bin/carddisp.pl?gene=CAT&interactions=40
A - Health Conditions - Genetics Home Reference - NIH  A - Health Conditions - Genetics Home Reference - NIH
acatalasia, see Acatalasemia. *ACC, see Nonsyndromic aplasia cutis congenita. *ACCPN, see Andermann syndrome ...
more infohttps://ghr.nlm.nih.gov/condition
Science Essays, Science Research papers  Science Essays, Science Research papers
Acatalasia. 7 pages, 1846 words. Access Control Lists. 11 pages, 2959 words. ...
more infohttp://essaysbank.com/essays/science/a
Free Science essay paper  Free Science essay paper
Acatalasia. 7 pages / 1846 words. Download. Access Control Lists. 10 pages / 2959 words ...
more infohttps://manyessays.com/essays/science/a
2011 ICD-9-CM Diagnosis Code 277.89 : Other specified disorders of metabolism  2011 ICD-9-CM Diagnosis Code 277.89 : Other specified disorders of metabolism
Acatalasia 277.89. *Christian's syndrome (chronic histiocytosis X) 277.89. *Disease, diseased - see also Syndrome*. Christian's ...
more infohttp://www.icd9data.com/2011/Volume1/240-279/270-279/277/277.89.htm
Catalase | definition of catalase by Medical dictionary  Catalase | definition of catalase by Medical dictionary
Deficiency results in acatalasia. adj., adj catalat´ic.. cat·a·lase. (kat'ă-lās), [MIM*115500] A hemoprotein catalyzing the ... genetic deficiency of the enzyme results in acatalasia.catalat´ic. catalase. (kăt′l-ās′, -āz′). n.. An enzyme found in living ...
more infohttps://medical-dictionary.thefreedictionary.com/catalase
Congenital Adrenal Hyperplasia: A Case Report With Premature Teeth Exfoliation and Bone Resorption | Case Reports | Pediatrics  Congenital Adrenal Hyperplasia: A Case Report With Premature Teeth Exfoliation and Bone Resorption | Case Reports | Pediatrics
Hypophosphatasia, immunodeficiency, diabetes mellitus, hyperthyroidism, and acatalasia can be excluded with hematologic ... acatalasia, Singleton-Merten syndrome, Hajdu-Cheney syndrome, Coffin-Lowry syndrome, and Chediak-Higashi syndrome. ...
more infohttp://pediatrics.aappublications.org/content/135/6/e1524
LABOKLIN (UK)|Genetic Diseases | Dogs  LABOKLIN (UK)|Genetic Diseases | Dogs
Catalase Deficiency ( CAT ) / Hypocatalasemia / Acatalasia New Breed: Beagle. 1-2 weeks £ 40.00 + vat (£48.00 incl vat) ...
more infohttp://www.laboklin.co.uk/laboklin/GeneticDiseases.jsp?catID=DogsGD
Human Catalase ELISA Kit (ab171572) | Abcam  Human Catalase ELISA Kit (ab171572) | Abcam
Catalase is encoded by the CAT gene, defects in CAT are the cause of acatalasia (ACATLAS), also known as acatalasemia. This ... Defects in CAT are the cause of acatalasia (ACATLAS) [MIM:115500]; also known as acatalasemia. This disease is characterized by ...
more infohttps://www.abcam.com/human-catalase-elisa-kit-ab171572.html
Recombinant Human Catalase protein (ab172164) | Abcam  Recombinant Human Catalase protein (ab172164) | Abcam
Defects in CAT are the cause of acatalasia (ACATLAS) [MIM:115500]; also known as acatalasemia. This disease is characterized by ...
more infohttps://www.abcam.com/recombinant-human-catalase-protein-ab172164.html
Glycogen storage disease type V  Glycogen storage disease type V
Alpha 1-antitrypsin deficiency - Cystic fibrosis - Amyloidosis (Familial Mediterranean fever) - Acatalasia. Categories: ...
more infohttps://www.bionity.com/en/encyclopedia/Glycogen_storage_disease_type_V.html
Alpha 1-antitrypsin deficiency  Alpha 1-antitrypsin deficiency
... - Cystic fibrosis - Amyloidosis (Familial Mediterranean fever) - Acatalasia. Categories: ...
more infohttps://www.bionity.com/en/encyclopedia/Alpha_1-antitrypsin_deficiency.html
StateMaster - Encyclopedia: Pathology  StateMaster - Encyclopedia: Pathology
Acatalasia (or Takaharas disease) is a peroxisomal disorder caused by a catalase deficiency. ... For other uses, see Eye ( ...
more infohttp://www.statemaster.com/encyclopedia/Pathology
Conditions of the mucous membranes Test and Flashcards  Conditions of the mucous membranes Test and Flashcards
Acatalasia (also called acatalasemia, or Takahara's disease) is an autosomal recessive peroxisomal disorder caused by a ... Acatalasia (also called acatalasemia, or Takahara's disease) is an autosomal recessive peroxisomal disorder caused by a ... Acatalasia, Cutaneous sinus of dental origin, Oral florid papillomatosis, Desquamative gingivitis, Oral mucocele, Leukoplakia ...
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