NOVA SOUTHEASTERN UNIVERSITY MATL Action Research Project VERIFICATION COVER SHEET MATL Student Name and NSU ID ARP School Site Where Project was Implemented: ___________________ Elementary School Dates of Implementation: AUGUST 2008 – JANUARY 2009 School Site Address and Phone: ARP One-sentence Problem Statement: By incorporating cooperative learning‚ guided reading and Reader’s Theatre‚ this research educator improved nineteen second grade at risk students reading comprehension levels by increasing
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Vol. 21 Summer 2005 Newborn Screening in the 21st Century From the Editors and Authors: Since our last Update on Newborn Screening in 1998‚ there has been significant expansion of newborn screening programs in various regions of the country‚ mostly to include metabolic disorders identifiable by tandem mass spectrometry. States in our region are just now starting to expand their programs. The Summer 2005 Genetic Drift provides an update on newborn dried blood spot screening (NBS). Specifically
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MDP10508 ENDOCRINE AND NUTRITION BIOCHEMISTRY ASSIGNMENT ANSWER ALL OF THE QUESTIONS BELOW. (70 marks) 1. Comment on the statement below: ‘Glycolysis and Gluconeogenesis are reciprocally regulated’ Reciprocally regulated means when one process takes place in a cell‚ the other process will essentially inactivated. This regulation ensures that either glycolysis or gluconeogenesis predominate as to prevent concurrent activity in two closely parallel pathways‚ where if both Glycolysis and Gluconeogenesis
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a clinically significant block in a metabolic pathway resulting either in accumulation of substrate behind the block or deficiency of the product. All IEMs are all genetically transmitted typically in an autosomal recessive or X-linked recessive fashion. The major categories are: Organic acidemias (e.g.‚ methylmalonic or propionic acidemia‚ multiple carboxylase deficiency) are caused by abnormal metabolism of proteins‚ fats or carbohydrates and are characterized by marked metabolic acidosis
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acids(KIC)‚ alpha-keto- beta methyl valeric acid(KMV) and alpha-ket oo isovaleric acid(KIV). The next step is oxidative decarboxylation of the BCKAs catalyzed by an also single enzyme complex‚ i.e.‚ the mitochondrial branched- chain alpha-ketoacid dehydrogenase complex (BCKDC). The metabolic block happens in this reaction. Through further enzymatic reaction‚ the end products are acetoacetate‚ succinyl- CoA and.
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colon malignancy‚ stomach malignancy‚ hepatoma and cervical tumor. It can bring about symptoms‚ for example‚ neutropenia ‚Thrombocytopenia‚ cardiotoxicity ‚ the runs and mucositis. The reason for these unfavorable responses is Dihydropyrimidine Dehydrogenase (DPD) lack. Looseness of the bowels is extreme and dosage constraining and is declined by co-treatment with calcium folinate. Neutropenia tops 9 to14 days in the wake of starting the treatment. Thrombocytopenia tends to top for around 7 to17
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hypothesize‚ for example‚ that if malate dehydrogenase will cease to do its job in Krebs cycle‚ two major problems will occur‚ as a result. First‚ malate dehydrogenase is the one of the enzymes that facilitates electron transport to NAD+ and creating NADH. Therefore‚ the final output of electron carrier NADH will be reduced to eight from ten per molecule of glucose‚ rendering the whole process less efficient. Second‚ the product of malate dehydrogenase is oxaloacetate‚ the same molecule that is
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responsible. Overproduction of lactate also occurs with cyanide poisoning or certain malignancies. Underutilization involves removal of lactic acid by oxidation or conversion to glucose. Liver disease‚ inhibition of gluconeogenesis‚ pyruvate dehydrogenase (thiamine) deficiency‚ and uncoupling of oxidative phosphorylation are the most common causes. The kidneys also contribute to lactate removal. Concerns have been raised regarding the role of metformin in the production of lactic acidosis‚ on the basis of
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fructose. The individuals liver and kidneys attempt to use this sugar for energy and due to the incomplete breakdown of fructose‚ toxic byproducts are produced which eventually leads to serious illness. The genetic condition causes an enzyme deficiency (fructose-1-phosphate aldolase) which in turn causes the build-up of fructose-1-phosphate . The overabundance of fructose-1-phosphate prevents glycogen breakdown and ultimately the
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are codes for certain function that are found in DNA. The combination of genes is what makes each individual unique. MCADD is a genetic disorder‚ caused by a mutation or damage to the gene‚ ACADM‚ that codes for the enzyme‚ medium chain acyl CoA dehydrogenase. This results in the enzyme being absent or existing in minimal quantities. An enzyme increases the rate of a chemical reaction. Our body needs many enzymes in order to make the materials needed for our bodies to function and be healthy. The mutation
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