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Studies on bovine congenital defectsRwuaan, Joseph S. January 1979 (has links)
Call number: LD2668 .T4 1979 R92 / Master of Science
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Body weights and selected organ measurements from pigs stillborn or dying neonatallyHerren, Charles Edward January 2011 (has links)
Typescript. / Digitized by Kansas Correctional Industries
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Pathogenesis of inherited eyelid closure failure in the mouse.Harris, Muriel Joyce. January 1965 (has links)
The mouse is normally born with its eyelids fused. This fusion occurs during day 16 of gestation (full term 19-20 days) and the eyes do not normally open again until approximately fourteen days after birth (Gruneberg, 1952). Thus "open eye at birth" constitutes a congenital defect in the mouse. This may be followed by abnormalities of structure and function in the eye, such as corneal opacity, probably resulting from postnatal exposure to injury and infection. [...]
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Pathogenesis of inherited eyelid closure failure in the mouse.Harris, Muriel Joyce. January 1965 (has links)
No description available.
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Teratogenicity of coniine, a nicotinic alkaloid from Conium maculatum (poison hemlock)Forsyth, Carol S. 20 August 1993 (has links)
Graduation date: 1994
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The genetics of microphthalmia in mice.Coté, Gilbert Bernard. January 1972 (has links)
No description available.
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Studies on a cytoplasmically transmitted strain difference in response to the teratogen 6-aminonicotinamidePollard, D. Russell (Donald Russell) January 1969 (has links)
No description available.
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The genetics of microphthalmia in mice.Coté, Gilbert Bernard. January 1972 (has links)
No description available.
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Studies on a cytoplasmically transmitted strain difference in response to the teratogen 6-aminonicotinamidePollard, D. Russell (Donald Russell) January 1969 (has links)
No description available.
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Quantification of the potentiating effects of caffeine on the teratogenicity of acetazolamide in C57BL/6J miceKelich, Stephanie L. January 1988 (has links)
The study was designed to determine what type of potentiation,.if any, occurred between caffeine and acetazolamide. Caffeine (75 mg/kg) and/or acetazolamide (200, 1000, or 1500 mg/kg) were administered to pregnant C57BL/6J dams on day 9 of gestation. Fetuses were removed on the eighteenth day of gestation via cesarean section and examined for gross morphological malformations using a Bausch & Lomb SKV1070P dissecting microscope. Treatment with HD-ACZM and HD+CAFF resulted in a reduction of fetal weight. Maternal exposure to MD-ACZM and HD-ACZM caused a statistically significant (P < .001) and dose-dependent increase in the percent of C57BL/6J fetuses with ectrodactyly along with increased severity of the defects displayed (relative to controls). An increase in the number of ectrodactylous fetuses and the severity of defects was also observed in all groups administered caffeine and acetazolamide, reaching statistical significance in the MD+CAFF and HD+CAFF groups (P < .001). Because potentiation of the teratogenic effects of acetazolamide was exhibited only in the MD+CAFF vs. MD-ACZM groups, the type of potentiation occurring between caffeine and acetazolamide can not be determined. / Department of Physiology and Health Science
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