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201. The international collaborative study of maternal phenylketonuria: status report 1998

Author

Koch, Richard, primary, Friedman, Eva, additional, Azen, Colleen, additional, Hanley, William, additional, Levy, Harvey, additional, Matalon, Reuben, additional, Rouse, Bobbye, additional, Trefz, Fritz, additional, Waisbren, Susan, additional, Michals-Matalon, Kimberley, additional, Acosta, Phyllis, additional, Güttler, Fleming, additional, Ullrich, Kurt, additional, Platt, Lawrence, additional, and de la Cruz, Felix, additional

Published
2000
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204. Outcome at Age 4 Years in Offspring of Women With Maternal Phenylketonuria: The Maternal PKU Collaborative Study

Author

Waisbren, Susan E., primary, Hanley, William, additional, Levy, Harvey L., additional, Shifrin, Harvey, additional, Allred, Elizabeth, additional, Azen, Colleen, additional, Chang, Pi-Nian, additional, Cipcic-Schmidt, Sanja, additional, Cruz, Felix de la, additional, Hall, Ramona, additional, Matalon, Reuben, additional, Nanson, Jo, additional, Rouse, Bobbye, additional, Trefz, Fritz, additional, and Koch, Richard, additional

Published
2000
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211. How GAMA expands the market

Author

Levy, Harvey

Subjects
Arts and entertainment industries, Business
Abstract

ON BEHALF OF GAMA I would like to thank you for your informative article 'How School Guitar Is Expanding The Market' in your October 2010 issue. One of the challenges [...]

Published
2010

213. A missense mutation (Q279R) in the Fumarylacetoacetate Hydrolase gene, responsible for hereditary tyrosinemia, acts as a splicing mutation

Author

Baklouti Faouzi, Levy Harvey L, Bergeron Anne, Poudrier Jacques A, Dreumont Natacha, and Tanguay Robert M

Subjects
lcsh:QH426-470, Hydrolases, Tyrosinemias, RNA Splicing, DNA Mutational Analysis, Mutation, Missense, Infant, Fibroblasts, lcsh:Genetics, Liver, Mutation, Humans, Female, Genetic Predisposition to Disease, RNA, Messenger, Research Article
Abstract

Background Tyrosinemia type I, the most severe disease of the tyrosine catabolic pathway is caused by a deficiency in fumarylacetoacetate hydrolase (FAH). A patient showing few of the symptoms associated with the disease, was found to be a compound heterozygote for a splice mutation, IVS6-1g->t, and a putative missense mutation, Q279R. Analysis of FAH expression in liver sections obtained after resection for hepatocellular carcinoma revealed a mosaic pattern of expression. No FAH was found in tumor regions while a healthy region contained enzyme-expressing nodules. Results Analysis of DNA from a FAH expressing region showed that the expression of the protein was due to correction of the Q279R mutation. RT-PCR was used to assess if Q279R RNA was produced in the liver cells and in fibroblasts from the patient. Normal mRNA was found in the liver region where the mutation had reverted while splicing intermediates were found in non-expressing regions suggesting that the Q279R mutation acted as a splicing mutation in vivo. Sequence of transcripts showed skipping of exon 8 alone or together with exon 9. Using minigenes in transfection assays, the Q279R mutation was shown to induce skipping of exon 9 when placed in a constitutive splicing environment. Conclusion These data suggest that the putative missense mutation Q279R in the FAH gene acts as a splicing mutation in vivo. Moreover FAH expression can be partially restored in certain liver cells as a result of a reversion of the Q279R mutation and expansion of the corrected cells.

Published
2001

227. Maternal Mild Hyperphenylalaninaemia

Author

Levy, Harvey L., primary, Waisbren, Susan E., additional, Lobbregt, Deborah, additional, Allred, Elizabeth, additional, Schuler, Agnes, additional, Trefz, Friedrich K., additional, Schweitzer, Susanne M., additional, Sardharwalla, I. B., additional, Walter, J. H., additional, Barwell, B. E., additional, Berlin, Chester M., additional, and Leviton, Alan, additional

Published
1995
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229. Dietary amino acid intakes associated with a low-phenylalanine diet combined with amino acid medical foods and glycomacropeptide medical foods and neuropsychological outcomes in subjects with phenylketonuria

Author

Stroup, Bridget M., Murali, Sangita G., Nair, Nivedita, Sawin, Emily A., Rohr, Fran, Levy, Harvey L., and Ney, Denise M.

Subjects
Tyrosine, Leucine, Arginine, Executive function, Delis-Kaplan Executive Function System, Cambridge Neuropsychological Test Automated Battery
Abstract

This article provides original data on median dietary intake of 18 amino acids from amino acid medical foods, glycomacropeptide medical foods, and natural foods based on 3-day food records obtained from subjects with phenylketonuria who consumed low-phenylalanine diets in combination with amino acid medical foods and glycomacropeptide medical foods for 3 weeks each in a crossover design. The sample size of 30 subjects included 20 subjects with classical phenylketonuria and 10 with a milder or variant form of phenylketonuria. Results are presented for the Delis-Kaplan Executive Function System and the Cambridge Neuropsychological Test Automated Battery; the tests were administered at the end of each 3-week dietary treatment with amino acid medical foods and glycomacropeptide medical foods. The data are supplemental to our clinical trial, entitled “Glycomacropetide for nutritional management of phenylketonuria: a randomized, controlled, crossover trial, 2016 (1) and “Metabolomic changes demonstrate reduced bioavailability of tyrosine and altered metabolism of tryptophan via the kynurenine pathway with ingestion of medical foods in phenylketonuria, 2017 (2). This data has been made public and has utility to clinicians and researchers due to the following: 1) This provides the first comprehensive report of typical intakes of 18 amino acids from natural foods, as well as amino acid and glycomacropeptide medical foods in adolescents and adults with phenylketonuria; and 2) This is the first evidence of similar standardized neuropsychological testing data in adolescents and adults with early-treated phenylketonuria who consumed amino acid and glycomacropeptide medical foods.

Published
2017
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237. The Effect of Nutrient Intake on Pregnancy Outcome in Maternal Phenylketonuriaa

Author

KOCH, RICHARD, primary, WENZ, ELIZABETH, additional, AZEN, COLLEEN, additional, FRIEDMAN, EVA G., additional, LEVY, HARVEY, additional, ROHR, FRANCES, additional, ROUSE, BOBBYE, additional, CASTIGLIONI, LOIS, additional, MATALON, REUBEN, additional, MICHALS‐MATALON, KIMBERLEE, additional, HANLEY, WILLIAM, additional, AUSTIN, VALERIE, additional, de LA CRUZ, FELIX, additional, and ACOSTA, PHYLLIS B., additional

Published
1993
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245. Contributors

Author

Abman, Steven H., Ahmed, Amina, Allen, Marilee C., Askenazi, David, Back, Stephen A., Baldwin, H. Scott, Ballard, Roberta A., Bancalari, Eduardo, Bates, Carlton M., Batisky, Donald L., Baumgart, Stephen, Benedetti, Thomas J., Berry, Gerard T., Bianchi, Diana W., Binenbaum, Gil, Bollepalli, Sureka, Bonifacio, Sonia L., Cairo, Mitchell S., Campbell, Katherine H., Caplan, Michael, Cederbaum, Stephen, Chandra, Sudhish, Chen, Ming, Claure, Nelson, Clyman, Ronald I., Cohen, Bernard A., Cole, F. Sessions, Copelovitch, Lawrence, Cunningham, Michael, de Alba Campomanes, Alejandra G., Dees, Ellen, Denne, Scott C., Devaskar, Sherin U., DiBlasi, Robert M., Dimmitt, Reed A., Eichenwald, Eric C., Eisenstein, Eli M., Evans, Jacquelyn R., Evans, Kelly, Farmer, Diana L., Ferrieri, Patricia, Ferriero, Donna M., Finer, Neil N., Fraga, Maria Victoria, Furman, Lydia, Furth, Susan, Gauda, Estelle B., Glader, Bertil, Gleason, Christine A., Goldberg, Michael J., Gonzalez, Fernando, Gopalani, Sameer, Grant, P. Ellen, Greene, Carol L., Guevara-Gallardo, Salvador, Guignard, Jean-Pierre, Guttentag, Susan, Haldeman-Englert, Chad R., Hansen, Thomas, Hing, Anne V., Hohimer, A. Roger, Hostetter, Margaret K., Hull, Andrew D., Jackson, J. Craig, Jain, Lucky, Jain, Vandana, Janjua, Halima Saadia, Juul, Sandra E., Kalkunte, Satyan, Kaplan, Bernard S., Keller, Roberta L., Kelly, Thomas F., Kern, Steven E., Kerkar, Nanda, Kinsella, John P., Kirsch, Roxanne, Kleinman, Monica E., Klitzner, Thomas S., Lambert, Sarah M., Lantos, John D., Leone, Tina A., Leppert, Mary, Levy, Harvey L., Lewin, Mark, Lin-Su, Karen, L. Loh, Mignon, Lorch, Scott A., Lugo, Ralph A., Mai, Volker, Marino, Bradley S., Markovitz, Barry, Marquard, Kerri, Martin, Camilia R., Martin, Richard J., Matthay, Katherine K., Matthews, Dana C., Mayock, Dennis E., Meadow, William L., Menon, Ram K., Mercuri, Eugenio, Mohan, Sowmya S., Moley, Kelle, Mollen, Thomas J., Moore, Jeremy P., Moore, Thomas R., Munson, David A., Murray, Jeffrey C., Neu, Josef, New, Maria I., Nguyen-Vermillion, Annie, Niklas, Victoria, Nimkarn, Saroj, Padbury, James F., Pane, Marika, Paneth, Nigel, Parker, Thomas A., Patterson, Janna C., Pettker, Christian M., Plawner, Lauren L., Poenaru, Dan, Poindexter, Brenda B., Posencheg, Michael A., Prabhu, Sanjay P., Püttgen, Katherine B., Quinn, Graham E., Raju, Tonse N.K., Ramos, Gladys A., Reinking, Benjamin E., Richardson, C. Peter, Rimoin, David L., Robbins, Elizabeth, Robertson, Richard L., Rollins, Mark D., Rose, Susan R., Rosen, Mark A., Rubin, Lewis P., Sahai, Inderneel, Saitta, Sulagna C., Sánchez, Pablo J., Satou, Gary M., Schanler, Richard J., Scher, Mark S., Schleiss, Mark R., Scholz, Thomas D., Schwaderer, Andrew L., Seri, Istvan, Sharma, Surendra, Shereck, Evan B., Sibley, Eric, Signore, Caroline, Simmons, Rebecca, Smith, Jeffrey B., Smith, Lorie B., Song, Clara, Steinhorn, Robin H., Suchy, Frederick J., Sulyok, Endre, Tarczy-Hornoch, Peter, Taylor, George A., Taylor, James A., Thomas, Janet A., Tiller, George E., Tran, Mark M., Trautman, Michael Stone, Upperman, Jeffrey S., van de Ven, Carmella, Vernon, Margaret M., Allan Walker, W., Wallen, Linda D., Waller, Sarah A., Warady, Bradley A., Ward, Robert M., Watchko, Jon F., Wernovsky, Gil, White, Klane K., Williams, Calvin B., Woodrum, David, Woodward, George A., Wright, Dakara Rucker, Wright, Jeffrey A., Wright, Linda L., Young, Christopher M., Young, Guy, Zackai, Elaine H., and Zderic, Stephen A.

Published
2012
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246. Efficacy of sapropterin dihydrochloride (tetrahydrobiopterin, 6R-BH4) for reduction of phenylalanine concentration in patients with phenylketonuria: a phase III randomised placebo-controlled study.

Author

Levy, Harvey L., Milanowski, Andrzej, Chakrapani, Anupam, Cleary, Maureen, Lee, Philip, Trefz, Friedrich K., Whitley, Chester B., Feillet, François, Feigenbaum, Annette S., Bebchuk, Judith D., Christ-Schmidt, Heidi, and Dorenbaum, Alex

Subjects
*PHENYLKETONURIA, *PHENYLALANINE, *AMINO acid metabolism disorders, *ANALYSIS of covariance, *LOW-phenylalanine diet, *PATIENTS, *TETRAHYDROBIOPTERIN, *OXIDATION
Abstract

The article focuses on a study examining the use of sapropterin for the reduction of phenylalanine levels in blood for patients suffering from phenylketonuria. It states that sapropterin is a biologically active form of tetrahydrobiopterin, which in some patients with phenylketonuria can increase the oxidation of phenylalanine and could allow some patients to relax or end their low-phenylalanine diets. The study tested phenylaline levels in the patients blood for six weeks with a baseline of the levels before medication began at week 0. The article examines mean change in blood phenylalanine concentrations after six weeks with an analysis of the covariance model from the baseline to week 6.

Published
2007
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247. The clinical aspects of newborn screening: Importance of newborn screening follow-up.

Author

James, Philip M. and Levy, Harvey L.

Subjects
*MEDICAL screening, *METABOLIC disorders, *ENDOCRINE diseases, *METHODOLOGY, DIAGNOSIS of neonatal diseases
Abstract

The aim of newborn screening is to identify presymptomatic healthy infants that will develop significant metabolic or endocrine derangements if left undiagnosed and untreated. The goal of ultimately reducing or eliminating irreversible sequelae is reached by maximizing test sensitivity of the primary newborn screening that measures specific analytes by a number of methodologies. Differentiation of true from false negatives is accomplished by the test specificity. This review discusses disorders for which, in general, there are available therapies and that are detected by routine and expanded newborn screening. Recommendations are presented for evaluation by a primary care physician, with confirmation by a metabolic or endocrinology specialist. Disorders are organized in tabular format by class of pathway or analyte, with attention to typical clinical presentations, confirmatory biochemical and molecular tests, and therapies. There are numerous challenges in clinical follow-up, including diagnosis and appropriate understanding of the consequences of the disorders. The data required to meet these challenges can be acquired only by large scale longitudinal comprehensive studies of outcome in children identified by newborn screening. Only with such data can newborn screening fully serve families. © 2006 Wiley-Liss, Inc. MRDD Research Reviews 2006;12:246–254. [ABSTRACT FROM AUTHOR]

Published
2006
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248. The use of betaine in the treatment of elevated homocysteine

Author

Lawson-Yuen, Amy and Levy, Harvey L.

Subjects
*HOMOCYSTEINE, *CORONARY disease, *METHIONINE, *CEREBRAL edema
Abstract

Abstract: Elevation of homocysteine is implicated in multiple medical conditions, including classical homocystinuria, a variety of remethylation disorders, and most recently in coronary artery disease. Betaine is a methyl donor agent that is beneficial in lowering homocysteine through the remethylation of methionine. Betaine therapy alone has been shown to prevent vascular events in homocystinuria and may have clinical benefits in other hyperhomocysteinemic disorders when used as adjunctive therapy. Betaine does raise the methionine level and cerebral edema has occurred when plasma methionine exceeds 1000μmol/L. Thus the plasma methionine as well as homocysteine must be monitored in patients receiving betaine. [Copyright &y& Elsevier]

Published
2006
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