Developmental deficits

Environmental exposures to PCBs are significantly lower than those reported in the workplace and are therefore unlikely to cause adverse human health effects in adults. However, it is apparent from the results of several recent studies on children that there was a correlation between in utero exposure to PCBs, eg, cord blood levels, and developmental deficits (65—68) including reduced bkth weight, neonatal behavior anomaUes, and poorer recognition memories. At four years of age, there was stiU a correlation between prenatal PCB exposure levels and short-term memory function (verbal and quantitative). In these studies the children were all exposed to relatively low environmental levels of PCBs. Although these effects may be related to other contaminants, it is clear that this is an area of concern regarding the potential adverse human health impacts of PCBs. 

Emhart CB, Landa B, Schell NB. 1981. Subclinical levels of lead and developmental deficit—a multivariate follow-up reassessment. Pediatrics 67 911 -919. 

Inactivating G a variants lead to Albright s hereditary osteodystrophy (AHO) in the heterozygote, snggesting that G a haploinsnfficiency canses the disorder. AHO is characterized by short statnre, obesity, brachydactyly (shortening of metacarpal and metatarsal bones), snbcntaneous ossifications, and mental or developmental deficits (86,87). The severity of the phenotype is variable. Some patients with G a mutations have few or no symptoms. 

This chapter is concerned with the neurochemical basis of developmental disability which is considered here in two forms the globally delayed or halted development seen in mental retardation, and the more circumscribed pattern of disordered development of autism. A range of deficits of important key aspects of consciousness are apparent in both conditions. Of particular relevance to consciousness are the cognitive and behavioural impairments in attention, concentration, memory, information processing and social behaviour which are commonly present. Consideration of aberrant neurotransmitter activities in these developmental deficits may provide insights into the role of neurotransmitters in consciousness. 

Gs, alpha (GNAS) 20ql3.2 Insertions/deletions and SNPs, 20 % in exon 7 Haploinsufficiency Albright s hereditary osteodystrophy (AHO), short stature, obesity, brachydactyly, subcutaneous ossifications, developmental deficits Inactivating Gas variants lead to variable phenotype related to insufficient parathyroid hormone receptor (PTHR1) in chondrocytes [96-99]... 

This boy has no history of any major medical illness that might have influenced his neurological development. He has a hypomelanotic skin condition (oculocutaneous albinism), but no vision or hearing impairments and no motor abnormalities. His developmental deficits are apparently restricted to communication, cognition, and social interactions. 

During the past years, much attention has been given to the effect of endocrine disruptors, such as PCBs and dioxins, on TH and their involvement in brain and neural development. Disruption in TH homeostasis leads to developmental deficits and nemological abnormalities (McNabb and... 

Wells PG, McCallum GP, Chen CS, Henderson JT, Lee CJJ, Perstin J, Preston TJ, Wiley Ml, Wong AW (2009) Oxidative stress in developmental origins of disease teratogenesis, neuro-developmental deficits and cancer. Toxieol Sei 108 4-18... 

Previous observations have shown that most patients who develop aseptic meningitis or encephalitis due to LCMV recover completely. No chronic infection has been described in humans, and after the acute phase the virus is cleared. However, as in all infections of the central nervous system, particularly encephalitLs, temporary or permanent neurological damage is possible. Nerve deafness and arthritis have been reported. Infection of the human fetus during the early states of pregnancy may lead to developmental deficits that are permanent. 

Ratcliffe, J. M. and Taylor, J. F. (1977). Lead in human blood and in the environment near a battery factory. Br, J, Prevent. Social. Med., 31, 154 Ernhart, C. B., Landa, B. and Schell, N. B. (1981). Subclinical levels of lead and developmental deficit - a multivariate follow-up reassessment. Pediatrics, 67,911 Ewers, U. and Erbe, R. (1980). Effects of lead, cadmium and mercury on brain adenylate cyclase. Toxicology, 16, 227... 

Erickson JT, Conover JC, Borday V, Champagnat J, Barbacid M, Yancopoulos G, Katz DM. Mice lacking brain-derived neurotrophic factor exhibit visceral sensory neuron losses distinct from mice lacking NT4 and display a severe developmental deficit in control of breathing. J Neurosci 1996 16 5361-5371. 

Ernhardt, C., Landa, B. and Schell, E. (1981) Subclinical levels of lead and developmental deficit a multivariate followup reassessment. Pediatrics, 67, 911-919 Ewers, U., Brockhaus, A., Winneke, G., Freier, I., Jermann, E. and Kramer, U. (1982) Lead in deciduous teeth of children living in a non-ferrous smelter area and a rural area of the FRG. Int. Arch. Occup. Environ. Health, 50, 139-151... 

Are the developmental deficits associated with prenatal lead exposure still mediated through foetal growth and maturational factors ... 

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