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The two carbons entering from acetyl-CoA do not leave as CO2 on the first cycle. Carbons 2 and 3 of succinate are equivalent. Carbons 1 and 4 of succinate are equivalent. To actually understand how labeled carbons travel through the TCA cycle, you have to draw out the chemical structures of the cycle members, put a tiny little asterisk by the labeled carbon, and follow it around and around. There are two concepts, however, that you have to know in order to do this. First, the two carbons entering the cycle as acetyl-CoA are not lost as CO2 during the first turn of the TCA cycle.
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unpleasant nasality; often, if the defect is severe, there is an audible escape of air through the nose. The aforementioned developmental abnormalities of speech are sometimes associated with disturbances of higher-order language processing. Rapin and Allen have described a number of such disturbances. In one, which they call the semantic pragmatic syndrome, a failure to comprehend complex phrases and sentences is combined with uent speech and well-formed sentences that are, however, lacking in content. The syndrome resembles Wernicke or transcortical sensory aphasia (Chap. 23). In another, semantic retrieval-organization syndrome, a severe anomia blocks word nding in spontaneous speech. A mixed expressive-receptive disorder may also be seen as a developmental abnormality; it contains many of the elements of acquired Broca s aphasia (page 417). Developmental Dyslexia (Congenital Word Blindness) This condition, rst described by Hinshelwood in 1896, becomes manifest in an older child who lacks the aptitude for one or more of the speci c skills necessary to derive meaning from the printed word. Also de ned as a signi cant discrepancy between measured intelligence and reading achievement (Hynd et al), it has been found in 3 to 6 percent of all schoolchildren. There are several excellent writings on the subject, to which the interested reader is referred for a detailed account (Orton; Critchley and Critchley; Rutter and Martin; Kinsbourne; Shaywitz; Rosenberger). The main problem is an inability to read words and also to spell and to write them, despite the ability to see and recognize letters. There is no loss of the ability to recognize the meaning of objects, pictures, and diagrams. According to Shaywitz, these children lack an awareness that words can be broken down into individual units of sound and that each segment of sound is represented by a letter or letters. This has been summarized as a problem in phonologic processing, referring to the smallest unit of spoken language, the phoneme, and the inability of dyslexic individuals to appreciate a correspondence between phonemes and their written representation (graphemes). A defect in the decoding of acoustic signals is one postulated mechanism. In addition to the essential visuoperceptual defect, some individuals also manifest a failure of sequencing ability, lack of phonemic segmentation, and altered cognitive processing of langauge. De Renzi and Luchelli have also noted a de cit of verbal and visual memory. Much of what has been learned about dyslexia applies to native speakers of English more so than to those who speak Romance languages. English is more complex phonologically than most other languages for example, using 1120 graphemes to represent 40 phonemes, in contrast to Italian, which uses 33 graphemes to represent 22 phonemes (see Paulesu). Children with native orthographic languages, such as Chinese and Japanese, apparently have a far lower incidence of dyslexia. Often, before the child enters school, reading failure can be anticipated by a delay in attending to spoken words, dif culty with rhyming games, and speech characterized by frequent mispronunciations, hesitations, and dys uency; or there may be a delay in learning to speak or in attaining clear articulation. In the early school years there are dif culties in copying, color naming, and formation of number concepts as well as the persistent reversal of letters. Writing appears to be defective because of faulty perception of form and a kind of constructional and directional apraxia. Not infrequently, there is an associated vagueness about the serial order of letters in the alphabet and months in the year, as well as dif culty with numbers (acalculia) and an inability to spell and to read music.
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The control/display assembly is housed in a standard 7 5 3 aluminum electronics instrument case with a removable cover. Drill the holes in the front panel of the case for power ON switch S1, FILTER IN switch S2, RANGE switch S3 and (if used) optional recorder switch S4. Also drill the holes for SENSITIVITY, ALARM ADJUST, and RATE potentiometers (R18, R19, and R11 respectively). Cut out the hole for mounting meter M1. Note: If you want to use the monitor strictly as a security monitoring system the meter can be omitted. Drill the holes in the back panel for jacks J2 and J3, and PULSE SHAPE potentiometer R17. Drill a series of holes in a circular pattern for the speaker SPKR1. Drill holes in the bottom of the case for mounting the control/display circuit board and two quad C cell holders. Remember the circuit uses both a plus (+) 6 volt supply and a minus ( ) 6 volt supply. We chose to power the circuit from batteries, but you could use a dual 6 volt power supply to power the control/ display unit. Assemble the panel-mounted switches, jacks, potentiometers, meter and speaker to the front and back panels of the case as shown in Figure 20-2. (You might prefer to bond the face of the speaker to the inside of the back panel with RTV adhesive rather than bolts and nuts.) Determine the length of speaker wires needed to permit assembly of the circuit board in the instrument case, cut the wires to length and solder them to the board. Cut and solder all leads from panel-mounted components to the circuit board, allowing sufficient lengths to permit unimpeded circuit board assembly, yet not allowing too much slack. Cut about a 6 length of RG-174/U coaxial cable to connect INPUT jack J2 and the FILTER IN Switch S2 and two other lengths about 6 long to connect S2 to the FILTER-IN and FILTER-OUT pads on the control/display board. Strip all cable ends and solder and trim all connections. Assemble the control/display board to the base of the case with screws and 1 2 insulating standoffs, lock washers and nuts. Bolt the two quad AA cell holders to the base of the case. Position the ICs in their sockets on the control-display board, making sure that all pin 1 s are in their correct positions. Insert the eight AA cells in the spring-loaded holders, observing the correct polarity.
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Figure 7.3 Specifying the type of recipients for the new address list.
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KEMPER TL, BAUMAN M: Neuropathology of autism. J Neuropathol Exp Neurol 57:645, 1998. KINSBOURNE M: Myoclonic encephalopathy of infants. J Neurol Neurosurg Psychiatry 25:271, 1962. KLINE MW, SHEARER WT: Impact of human immunode ciency virus infection on women and infants. Infect Dis Clin North Am 6:1, 1992. KNIGHT SJ, REGAN R, NICOD A, et al: Subtle chromosomal rearrangements in children with unexplained mental retardation. Lancet 354:1676, 1999. KRISHNAMOORTHY KS, KUEHNLE KJ, TODRES ID, DELONG GR: Neurodevelopmental outcome of survivors with posthemorrhagic hydrocephalus following grade II neonatal intraventricular hemorrhage. Ann Neurol 15:201, 1984. LANDRIEU P: Approches de la pathologic cerebelleuse chronique chez l enfant. Rev Neurol (Paris) 149:776, 1993. LECOUTEUR A, BAILEY A, GOODE S, et al: A broader phenotype of autism: The clinical spectrum in twins. J Child Psychol Psychiatry 37:785, 1996. LEMIEUX BG: Chromosome-linked disorders, in Swaiman K (ed): Pediatric Neurology: Principles and Practice, 2nd ed. St. Louis, Mosby, 1994, pp 357 419. LEVENE MI, GRINDULIS H, SANDS C, MOORE JR: Comparison of two methods of predicting outcome in perinatal asphyxia. Lancet 1:67, 1986. LEVINE DN, FISHER MA, CAVINESS VS JR: Porencephaly with microgyria: A pathologic study. Acta Neuropathol (Berl) 29:99, 1974. LEWIS EO: Types of mental de ciency and their social signi cance. J Ment Sci 79:298, 1933. LICHTENSTEIN BW: Neuro bromatosis (Von Recklinghausen s disease of the nervous system). Arch Neurol Psychiatry 62:822, 1949. LORBER J: Spina bi da cystica: Results of treatment of 270 cases with criteria for selection in the future. Arch Dis Child 47:854, 1972. LORBER J, PRIESTLEY BL: Children with large heads: A practical approach to diagnosis in 557 children with special reference to 109 children with megalencephaly. Dev Med Child Neurol 23:494, 1981. LOSNER RR, GLENN GM, WALTHER M, et al: von Hippel-Lindau disease. Lancet 361:2059, 2003. LUBS HA: A marker X chromosome. Am J Hum Genet 21:231, 1969. LYNN RB, BUCHANAN DC, FENICHEL GM, FREEMAN FR: Agenesis of the corpus callosum. Arch Neurol 37:444, 1980. LYON G, EVRARD PH: Neuropediatrie. Paris, Masson, 1987. MARSHALL PC, BRETT EM, WILSON J: Myoclonic encephalopathy of childhood (the dancing eye syndrome): A long-term follow-up study. Neurology 28:348, 1978. MARTIN JP, BELL JA: A pedigree of mental defect showing sex linkage. J Neurol Neurosurg Psychiatry 6:154, 1943. MARTUZA RL, ELDRIDGE R: Neuro bromatosis 2 (bilateral acoustic neuro bromatosis). N Engl J Med 318:684, 1988. MEDICAL TASK FORCE ON ANENCEPHALY: The infant with anencephaly. N Engl J Med 322:669, 1990. MILUNSKY A: Prenatal detection of neural tube defects: VI. Experience with 20,000 pregnancies. JAMA 244:2731, 1980. MOCHIDA GH, WALSH CA: Genetic basis of developmental malformations of the cerebral cortex. Arch Neurol 61:637, 2004. MOLONEY DM, WALL SA, ASHWORTH GJ, et al: Prevalence of Pro250Arg mutation of broblast growth factor receptor in coronal craniosynostosis. Lancet 349:1059, 1997. MUHLE R, TRENTACOSTE SV, RAPIN I: The genetics of autism. Pediatrics 113:472, 2004. MYERS RE: Experimental models of perinatal brain damage: Relevance to human pathology, in Glueck L (ed): Intrauterine Asphyxia and the Developing Fetal Brain. Bethesda, MD, Year Book, 1977, pp 37 97. NAIDU S: Rett syndrome: A disorder affecting early brain growth. Ann Neurol 42:3, 1997. NELLHAUS G: Head circumference from birth to 18 years. Pediatrics 41: 106, 1968. NELSON KB, ELLENBERG JH: Antecedents of cerebral palsy. N Engl J Med 315:81, 1986.
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This section has presented only half of the security requirements: the web catalog content definition as well as the data presented through that content must be protected. The next section focuses completely on securing the data presented through Oracle BI.
The signal crosses the membrane and activates gene transcription. Signals for soluble receptors include steroid hormones, retinoic acid, thyroid hormone, and vitamin D.
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