Defect prevalent

Araneta, M., Destiche, D., Schlangen, K., Merz, R., Forrester, M., Gray, G. (2000). Birth defects prevalence among infants of Persian Gulf War veterans born in Hawaii, 1989-1993. Teratology, 62(4), 195-204. 

G.C., Birth defects prevalence among infants of Gulf War veterans bom in Hawaii, 1989-1993, presented at the Research Working Group Persian Gulf Veterans Coordinating Board Conference on Federally Sponsored Gulf War Veterans Research, June 23 -25, 1999. 

Michigan Department of Community Health.(2008). Birth defects prevalence and mortality tables, http //www.mdch.state.mi.us/pha/ osr/BirthDefects/summary.asp... 

Properties of a nanocrystal can be influenced markedly by encasing it in a sheath of another material [531]. The material of the shell in such a core-shell structure can be a metal, semiconductor, or an oxide. The shell material helps to impart novel, desired properties on the nanocrystals. For example, defects prevalent in the surface states of semiconductor nanocrystals can be transferred to a buffer layer of the shell material to obtain better emission from the nanocrystals. We use the notation, core-shell to denote core-shell structures. We employ the following classification to describe the nature of the core and the shell semiconductor-semiconductor, metal-metal and metal-oxide, semiconductor-oxide and oxide-oxide. The classification is artificial in that the nanocrystals result from similar synthetic strategies. The motivation for carrying out the modification of the shell material, however, differs in each case. 

Above 570°C, a distinct break occurs in the Arrhenius plot for iron, corresponding to the appearance of FeO in the scale. The Arrhenius plot is then non-linear at higher temperatures. This curvature is due to the wide stoichiometry limits of FeO limits which diverge progressively with increasing temperature. Diffraction studies have shown that complex clusters of vacancies exist in Fe, , 0 Such defect clustering is more prevalent in oxides... 

Additional studies of the Woburn population have been completed (MDPH 1994). The final report indicated that there was an increased prevalence in choanal atresia, a rare respiratory effect, and hypospadias/congenital chordee. A small increase in eye defects was observed, but there was no association between TCE exposure and heart defects. There was no statistically significant associations between exposure concentrations and birth defects, although analyses was limited by the small number of cases observed. Based on four cases in the Woburn population, a rate of 0.88 was observed in the exposed population, compared to rates of 0.11 and 0.13 in the Atlanta and California comparison populations, respectively. In a prospective study completed after well closure, the rate of choanal atresia was 0.88 (based on 1 case) in Woburn, 0.11 in the surrounding communities, and 0.2 and 0.13 in Atlanta and California, respectively. The study authors cautioned that their study did not rule out moderate increases in rates of the less common adverse reproductive outcomes. For these outcomes only large increases would have been detected. 

Figure 8.6 summarizes our current knowledge of the appearance of point defects in STM images. The most prevalent point defects on sputtered/annealed Ti02(l 1 0) lxl surfaces have been identified as Ob-vacs, OHb, and OHb pairs and these are shown in a ball model together with an STM image decorated with a number of all three types of defects. 

Carnitine palmitoyltransferase deficiency is an autosomal recessive myopathy caused by a genetic defect of the mitochondrial enzyme CPT (Fig. 42-2). The disease is prevalent in men (male female ratio, 5.5 1) and appears to be the most common cause of recurrent myoglobinuria in adults [4]. 

Phenylalanine hydroxylase (PH) which requires tetrahydrobiopterin (BH4) as a cofactor, is defective in cases of phenylketonuria (PKU). This is a rare (prevalence 1 / 15 000 in the United Kingdom) genetic condition characterized by fair complexion, learning difficulties and mental impairment. If PH is either not present in the hepatocytes or is unable to bind BH4 and is therefore non functional, phenylalanine accumulates within the cells. Enzymes in minor pathways which are normally not very active metabolize phenylalanine ultimately to phenylpyruvate (i.e. a phenylketone). To use the traffic flow analogy introduced in Chapter 1, the main road is blocked so vehicles are forced along side roads. Phenylpyruvate is excreted in the urine (phenyl-ketone-uria), where it may be detected but a confirmatory blood test is required for a reliable diagnosis of PKU to be made. 

The gas plant that was destroyed had been initially commissioned in 1969. It had not undergone a mechanical inspection for six years. Shutdowns were initially scheduled at three-year intervals, but this interval was extended to five years. The plant had not been retrofitted with modern instrumentation. Pen recorders were prevalent in the control room and operating problems had been encountered with several control valves. Three months before the incident, ice plugging in lines caused several process upsets that were not fully investigated. A defective bypass valve had leaked gas to the atmosphere and had been awaiting maintenance up until one day before the accident. 

Defects in the domain of apo B-100 that binds to the LDL receptor impair the endocytosis of LDL, leading to hypercholesterolemia of moderate severity. Tendon xanthomas may occur. These disorders are as prevalent as familial hypercholesterolemia. Response to reductase inhibitors is variable. Up-regulation of LDL receptors in liver increases endocytosis of LDL precursors but does not increase uptake of ligand-defective LDL particles. Niacin often has beneficial effects by reducing VLDL production. 

Familial hypercholesterolemia (FH) is one of the most common genetic disorders in lipoprotein metabolism, and causes elevated cholesterol levels. This autosomal dominant disorder with a prevalence of about 1/500 in Western countries is caused by mutations in the LDLR gene. The LDLR defect impairs the catabolism of LDL and results in elevation of plasma LDL-cholesterol. Untreated heterozygous FH patients have 2-3 times elevated cholesterol levels and have a 100-fold increased risk to die... 

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