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Biomedical subjects

G F Chernoff

Publications and source records attributed to G F Chernoff.

28 records · Page 2Linked to original sources
PubMed1982

Possible mesodermal origin for axial dysraphic disorders.

We report four patients who provide clinical evidence supporting the hypothesis that axial dysraphic states may result from a primary disturbance in the chordoaxial mesoderm. One infant had complete craniorachischisis, an omphalocele, and ambiguous genitalia. A second infant had anencephaly and an omphalocele. The third had iniencephaly. The fourth had cervical vertebral fusion defects, an occipital menigocele, and a laterality malformation sequence. Alteration in the development of structures derived from the chordoaxial mesoderm could explain all of the structure defects observed in the four patients. This hypothesis accounts for the nature of the defects seen in association with dysraphic disorders and for the genetic relationship observed between neural tube defects and vertebral anomalies.

Abnormalities, Multiple↗
PubMed1982

Mouse fetal hydantoin syndrome: effects of maternal seizures.

To test the effect of maternal seizure disorders on prenatal structural development, the mouse neurological mutant quaking (qk) was used. Administering phenytoin in the drinking water of females homozygous for the quaking allele reduced the frequency of tonic-clonic seizures typical for this mutant from a background rate of 2.06 to 0.34 seizures per mouse day. As the seizure frequency decreased, the percentage of fetuses exhibiting abnormalities associated with the mouse fetal hydantoin syndrome increased from 0 to 77. As in previous studies with the mouse syndrome, the increase in malformations was associated with increased maternal serum phenytoin levels. The results of this study indicate that the maternal serum phenytoin level, and not the maternal seizure disorder, is the etiologic agent responsible for the malformations observed in this syndrome.

Abnormalities, Drug-Induced↗
PubMed1980

The fetal alcohol syndrome in mice: maternal variables.

CBA, C3H, and C57 female mice maintained on a diet of 20 percent ethanol-derived calories prior to and throughout gestation were mated in a diallele cross. Prenatal death, malformations, and fetal weights were directly related to maternal blood alcohol levels, indicating a maternal effect. Fetal abnormalities and maternal blood alcohol levels varied with maternal strain (CBA > C3H > C57) and were inversely related to maternal alcohol dehydrogenase activity. Microsomal ethanol oxidizing systems induction was directly associated with increased fetal abnormalities, being greatest in CBA females. These results indicate that liability for the pattern of malformation observed in this syndrome is dependent on maternal blood alcohol levels, which are determined by the rate of maternal alcohol metabolism as well as the amount of maternal alcohol consumption.

Alcohol Oxidoreductases↗
PubMed1977

The fetal alcohol syndrome in mice: an animal model.

CBA and C3H female mice were maintained on liquid diets--Metrecal plus ethanol--containing 15-35% ethanol-derived calories. These diets, which resulted in alcohol blood levels of 73-398 mg/100 ml blood in nonpregnant females, were the sole sustenance for the females for at least 30 days before and throughout gestation. Females were killed on day 18 of gestation and offspring examined for skeletal and soft tissue anomalies. Prenatal death and maldevelopment increased with the level of alcohol intake. Deficient occiput ossification, neural anomalies, and low fetal weight occurred with low ethanol diets, and cardiac and eye-lid dysmorphology with higher ethanol diets. This pattern of malformations, which exhibited both a dose-response effect and strain differences in susceptibility, indicated that chronic maternal alcoholism is embryolethal and teratogenic in mice.

Abnormalities, Drug-Induced↗
PubMedDate not supplied

First arch malformation: a new craniofacial mutant in the mouse.

The first arch malformation arising in a BALB/c strain of mice, has been shown to be inherited as a single autosomal recessive gene and is given the provisional gene symbol far. Affected newborns have extensive bony defects of the face and skull, including a cleft secondary palate, and die within 24 hours of birth. Most of the abnormalities occur in bones derived from the first branchial arch and most of the bony derivatives of the first arch are abnormal in the mutant.

Animals↗
PubMedDate not supplied

Shiverer: an autosomal recessive mutant mouse with myelin deficiency.

Shiverer is an autosomal recessive trait in the mouse characterized by early generalized tremors that become prominent in the hindquarters with age. Seizure behavior begins after weaning and increases in frequency during the animal's shortened lifespan. The most prominent pathological feature is a deficiency of myelin and myelin basic protein in the central nervous system.

Animals↗
PubMedDate not supplied

Issues in regulatory protection of reproductive health in the workplace.

Provisions of federal laws that protect reproductive health in the workplace and information on recent federal actions that seek to enhance such protection are reviewed. California's Birth Defects Prevention Act and its Proposition 65, regulatory programs that specifically address reproductive toxicity, also are described.

Abnormalities, Drug-Induced↗