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In a group of 48 inherited aminoacidopathies tabulated by Rosenberg and Scriver, at least one-half were associated with recognizable neurologic abnormalities Twenty other aminoacidopathies result in a defect in the renal transport of amino acids, some of which secondarily damage the nervous system Usually, when the nervous system is involved, the only clinical manifestation is simply a lag in psychomotor development, which, if mild, does not become apparent until the second and third years or later Like other inherited metabolic disorders, the aminoacidurias do not impair growth, development, or maturation in utero or interfere with parturition (This is the result of the maternal blood supply, which de nes the amino acid balance in utero) No physical sign betrays their presence in the early months of life The only possible means of detection is by the screening of all newborns The relative frequency of these diseases is indicated in Table 37-1, and the practical tests for their identi cation are summarized in Table 37-2 Three aminoacidopathies of the late infantile and early childhood period phenylketonuria (PKU), tyrosinemia, and Hartnup disease are described here because of their clinical importance and because they exemplify different types of biochemical defect Reference is also made to certain other aminoacidurias, described in the rst part of this chapter, which, like Hartnup disease, are associated with intermittent ataxia Only passing comments are made about the other aminoacidurias, which are exceedingly rare or have only an uncertain effect on the nervous system A detailed and relatively current account of these disorders can be found in the monograph of Scriver and coworkers The Phenylketonurias (PKU, Phenylalanine Hydroxylase De ciency) Apart from being the most frequent of the aminoacidurias, this entity has a special historical signi cance Since its discovery by F lling in 1934, it has remained the classic example of an aminoaciduria and illustrates three principles of medical genetics: rst, it is inherited as an autosomal recessive trait; second, it exempli es Garrod s cardinal principle of gene action, in which genetic factors specify chemical reactions as well as biochemical individuality; third, PKU is expressed only in an environment that contains an abundance of L-phenylalanine Thus, as predicted by Galton, the ultimate phenotype is a product of nature and nurture (Scriver and Clow) One must refer to the phenylketonurias in the plural, for there are (1) the usual type and several mild and severe variants thereof,. asp.net mvc pdf library asp . net - How to display PDF in div for a particular id using MVC ...
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Free source code and tutorials for Software developers and Architects.; Updated: 6 Jul 2018. in all of which mental retardation is invariable if the disease is not treated early in life, (2) other types, presumably allelic mutations, in which there is hyperphenylalaninemia without PKU and without effect on the nervous system, and (3) a rare adult type with a progressive spastic paraparesis or without neurologic manifestations Also there are a small number of patients (3 percent in our series) in whom a lowering of the hyperphenylalaninemia does not prevent the progression of the neurologic lesion At birth, the typical PKU infant is believed to have a normal nervous system The disease appears later, only after long exposure of the nervous system to phenylalanine (PA), because the homozygous infant lacks the means of protecting the nervous system However, if the mother is homozygous with high PA levels in the blood during pregnancy, the CNS is damaged in utero and the heterozygous infant is mentally defective from birth In the classic form of PKU, the impairment of psychomotor development can usually be recognized in the latter part of the rst year, when expected performance lags By 5 to 6 years in an untreated child, when the IQ can be estimated, it is usually less than 20, occasionally 20 to 50, and exceptionally above 50 Hyperactivity, aggressivity, self-injurious behavior including severe injury to the eyes, clumsy gait, ne tremor of the hands, poor coordination, odd posturings, repetitious digital mannerisms and other so-called rhythmias, and slight corticospinal tract signs stand out as the main clinical manifestations Athetosis, dystonia, and frank cerebellar ataxia have been described but must be exceedingly rare Also, seizures are said to occur in 25 percent of severely retarded patients, taking the form at rst of exor spasms and later of absence and grand mal attacks However, of more than 30 of PKU patients at the Fernald School, a number of which we have followed clinically, none had seizures or extrapyramidal signs The majority are blue-eyed and fair in skin and hair color, and their skin is rough and dry and subject to eczema A musty body odor (due to phenylacetic acid excretion) can often be detected Twothirds are slightly microcephalic The fundi are normal, and there is no visceral enlargement or skeletal abnormality There are individuals living in the community with asymptomatic PKU and normal intelligence Instances of PKU in which the symptoms are of adult onset are rare but of interest because of the entirely unexpected diagnosis The few such cases reported and summarized by Kassim and colleagues, with a case of their own, have developed a progressive spastic paraparesis, some with mild dementia The phenylalanine levels have been at values that re ect total or partial enzyme de ciency The nding of high levels of serum phenylalanine (above 15 mg/dL) and of phenylpyruvic acid in the blood, CSF, and urine are diagnostic of PKU The level is normal at birth and rises only after the rst few days But screening by the Guthrie (ferric chloride) test will reliably identify the patient at risk The addition of 3 to 5 drops of 10% ferric chloride to 1 mL of urine is a simple and informative test It yields an emerald-green color that reaches a peak intensity in 3 to 4 min and fades in 20 to 40 min In contrast, the green-brown color in the urine of patients with histidinemia is permanent In maple syrup urine disease, the ferric chloride test gives a navy-blue color; propionic and methylmalonic acidemia and either ketones or salicylates in the urine yield a purple color The fundamental biochemical abnormality is a de ciency of the hepatic enzyme PA hydroxylase; the failure of conversion of PA to tyrosine results in the excretion of phenylpyruvic acid by affected individuals The precise step that is faulty in the complex phenylalanine hydroxylating reaction is still unknown. convert byte array to pdf mvc Add MVC PDF Viewer - Feedback and Feature Requests - Telerik
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