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Prenatal

D. Neubert, H.-J. Merker, and T. E. Kwasigroch, eds.. Methods in Prenatal Toxicology, Georg Thieme PubUshers, Stutgart, Germany, 1977. [Pg.240]

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. [Pg.66]

Prenatal and postnatal development, including maternal function... [Pg.106]

All three forms of spinal muscular atrophy are inherited as autosomal recessive disorders, linked to chromosome 5q. Prenatal diagnosis using closely linked markers is now available. A rare, autosomal dominant form of juvenile SMA is similar in expression to the recessive forms, but 5q is not involved. [Pg.323]

Poly-Vitamin-Saar (Chephasaar)-comb. wfm Prenatal (Cyanamid)-comb. wfm... [Pg.1241]

Roozen HG, Kerhof AJ, van den Brink W Experiences with an outpatient relapse program (community reinforcement approach) combined with naltrexone in the treatment of opioid-dependence effect on addictive behaviors and the predictive value of psychiatric comorbidity. Eur Addict Res 9 53—58, 2003 Rosen TS, Johnson HL Long-term effects of prenatal methadone maintenance. NIDA Res Monogr 59 73-83, 1985... [Pg.106]

FroschI. 1990. Prenatal toxicology of Wofatox 80 in rats. Teratology 42(2) 26A. [Pg.208]

Fuchs VS, Golbs S, Kuhnert M, et al. 1976. [Studies into the prenatal toxic action of parathion methyl on Wistar rats and comparison with prenatal toxicity cyclophosphamide and trypan blue]. Arch Exp Vet Med 30 343-350. (German)... [Pg.208]

Hansen E, Meyer O. 1980. Neurobehavioral effects of prenatal exposure to parathion-methyl on rats. Acta Morphol Acad Sci Hung 28 210. [Pg.212]

Schmidt RR. 1984. Altered development of immunocompetence following prenatal or combined prenatal-postnatal insult A timely review. J Am College Toxicol 3 57-72. [Pg.229]

Developmental Toxicity—The occurrence of adverse effects on the developing organism that may result from exposure to a chemical prior to conception (either parent), during prenatal development, or postnatally to the time of sexual maturation. Adverse developmental effects may be detected at any point in the life span of the organism. [Pg.242]

Embryotoxicity and Fetotoxicity—Any toxic effect on the conceptus as a result of prenatal exposure to a chemical the distinguishing feature between the two terms is the stage of development during which the insult occurs. The terms, as used here, include malformations and variations, altered growth, and in utero death. [Pg.242]

No information was located concerning whether the developmental process is altered in humans exposed to endosulfan either prenatally or postnatally. Studies in animals have provided inconclusive evidence (FMC 1980b, 1981 Gupta et al. 1978 Hoechst 1982, 1984a), and further well-conducted research would be helpful to clarify this issue. [Pg.200]

Female Wistar rats treated orally with 0.125-16 jug/kg/day of 2,3,7,8-tetrachlorodibenzo-p-dioxin (8-D), 50-800 jug/kg/day of 1,2,3,4-tetra-chlorodibenzo-p-dioxin (4-D , and 250-2000 /xg/kg/day of 2,7-dichloro-dibenzo-p-dioxin (2-D) and 1,000-2,000 /xg/kg/day of 2,3-dichlorodi-benzo-p-dioxin or 2-chlorodibenzo-p-dioxin during 6—15 days of gestation (first morning of a positive vaginal smear was designated as day 1) were assessed for prenatal effects of the compounds on their progeny. [Pg.71]

Tetrachlorodibenzo-p-Dioxin (8-D). Prenatal Effects. Data from 2 experiments conducted with 0.125-16 / g/kg/day doses of... [Pg.72]

Chlorodibenzo- -Dioxm. Prenatal parameters at dose levels of... [Pg.79]

Tetrachlorodibenzo-p-dioxin elicited no apparent prenatal or postnatal effects when doses of up to 800 /xg/kg/day were given orally for 10 days of gestation. Treatment with 250-2000 /xg/kg/day of 2,7-di-chlorodibenzo-p-dioxin (99% purity) had no significant effect on prenatal and postnatal measures of toxicity but caused a low incidence of cardiac lesions. 2,3-Dichlorodibenzo-p-dioxin and 2-chlorodibenzo-p-dioxin up to 2000 /xg/kg/day had no adverse effect on survival, average weight, and skeleton of term fetuses. [Pg.82]

KHERA AND RUDDiCK Polychlowdihenzo-p-dioxins and 2-Chlorodibenzo- -Dioxin Prenatal Data... [Pg.83]

The detection of restriction fi agment length polymorphisms (RFLPs) facilitates prenatal detection of hereditary disorders such as sickle cell trait, beta-thalassemia, infant phenylketonuria, and Huntington s disease. Detection of RFLPs involves cleavage of double-stranded DNA by restriction endonucleases, which can detect subtle alterations in DNA that affect their recognized sites. Chapter 40 provides further details concerning the use of PCR and restriction enzymes for diagnosis. [Pg.57]

In general, the porphyrias described are inherited in an autosomal dominant manner, with the exception of congenital erythropoietic porphyria, which is inherited in a recessive mode. The precise abnormalities in the genes directing synthesis of the enzymes involved in heme biosynthesis have been determined in some instances. Thus, the use of appropriate gene probes has made possible the prenatal diagnosis of some of the porphyrias. [Pg.274]

DNA sequences as short as 50-100 bp and as long as 10 kb can be amplified. Twenty cycles provide an amplification of 10 and 30 cycles of 10. The PCR allows the DNA in a single cell, hair follicle, or spermatozoon to be amplified and analyzed. Thus, the applications of PCR to forensic medicine are obvious. The PCR is also used (1) to detect Infectious agents, especially latent viruses (2) to make prenatal genetic diagnoses (3) to detect allelic polymorphisms (4) to establish precise tissue types for transplants and (5) to study... [Pg.405]


See other pages where Prenatal is mentioned: [Pg.245]    [Pg.58]    [Pg.93]    [Pg.94]    [Pg.107]    [Pg.332]    [Pg.495]    [Pg.696]    [Pg.1119]    [Pg.1106]    [Pg.286]    [Pg.299]    [Pg.26]    [Pg.71]    [Pg.74]    [Pg.107]    [Pg.154]    [Pg.172]    [Pg.71]    [Pg.73]    [Pg.78]    [Pg.79]    [Pg.81]    [Pg.81]    [Pg.249]    [Pg.255]   
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See also in sourсe #XX -- [ Pg.39 , Pg.42 , Pg.66 , Pg.74 ]

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Mercury prenatal

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Nerve prenatal function

Ottawa Prenatal Prospective Study

Polycyclic aromatic hydrocarbons prenatal exposure

Prenatal Diagnosis and Treatment

Prenatal brain

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Prenatal damage/disruptions

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Prenatal development studies

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Prenatal diagnosis

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Prenatal drug exposure

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Prenatal environment

Prenatal environmental impacts/effects

Prenatal exposure

Prenatal exposure abilities

Prenatal exposure effect

Prenatal exposure to PCBs

Prenatal exposure to alcohol

Prenatal exposure to lead

Prenatal exposure, biomarkers

Prenatal genetic testing

Prenatal growth

Prenatal hairs

Prenatal impacts

Prenatal lead exposure

Prenatal lead exposure animal studies

Prenatal lead exposure measures

Prenatal mortality

Prenatal olfaction

Prenatal stress

Prenatal studies

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Prenatal toxicology

Prenatal ultrasound

Prenatal vitamins

Prenatal vulnerabilities

Prenate - Folic acid

Reproductive toxicity prenatal exposure

Reproductive/developmental toxicity studies prenatal/postnatal development

Screening and prenatal diagnosis

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