Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0729233 (Thoracic)
 6,478 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In developing an avian model for 13-cis-retinoic acid (13cisRA) embryopathy, we found 13cisRA induced cardiovascular defects, especially Type I ventricular septal defects (VSDs) (Hart et al.: Teratology 41:463-472, '90). As the first step of investigating possible mechanisms, we have examined the light microscopic morphology of RA-induced cardiovascular defects in chick embryos. Fertilized eggs were injected via yolk sac with 150 micrograms 13cisRA in dimethylsulfoxide (DMSO), DMSO or mock injection on embryonic day 5 (E5). On E6, E7, or E8, surviving embryos were sacrificed and fixed in 10% formalin. Thoracic blocks were exised, embedded in paraffin and serially sectioned through the heart, base to apex. Slides were stained, screened for tissue orientation, then coded and evaluated without knowledge of treatment group. Examination of serial sections permitted qualitative evaluation of conotruncal ridge volume, mesenchymal organization, necrosis and extent of fusion. Extent of fusion was the only parameter influenced by 13cisRA treatment. On E6, ridge fusion was incomplete in all groups at comparable levels. On E7, ridge fusion in 13cisRA-treated embryos had not progressed as far proximally as in controls. By E8, there was a significant difference in the extent of fusion between 13cisRA-treated and non-RA-treated groups. We conclude 13cisRA-induced VSDs resulted from defective conotruncal ridge fusion and that the fusion defects did not result from decreased tissue volume, altered mesenchymal organization or increased necrosis.
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PMID:Avian model for 13-cis-retinoic acid embryopathy: morphological characterization of ventricular septal defects. 129 Jan 53

Influence of various hormones on the induction of cellular retinoic acid binding protein (CRABP) was investigated in the mouse mammary gland organ cultures. Thoracic pairs of mammary glands from the BALB/c mice were cultured for seven days in the presence of various hormones in CMRL medium at 37 degrees C under 50% O2, 5% CO2 and 45% N2 atmosphere. There was a modest increase of mammary CRABP by insulin (I) + prolactin (P), however, addition of progesterone (Pg) or estrogen (E) + Pg to the medium resulted in a dramatic increase in the CRABP. Aldosterone (A) + hydrocortisone (F), in addition to I + P, which promotes differentiation to an extent similar to that of I + P + E + Pg did not have any influence on the induction of CRABP. These results indicate that prolactin and/or Pg in the medium can increase the concentration of CRABP in the mammary gland in vitro. From the results presented in this report, as well as previous work by other investigators, it is concluded that the biological response to retinoids in the mammary tissues cannot be correlated with the absolute concentration of CRABP in the cells. However, the biological response may be dependent upon both the ability of the target organ cells to metabolize the retinoid and to have minimal concentration of CRABP for binding to the active metabolite. The functional significance of hormone-induced CRABP is presently unknown.
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PMID:Role of hormones on the induction of retinoic acid binding protein in mouse mammary gland organ culture. 299 Jul 55

Mouse mammary gland organ culture technique was utilized to determine the effects of retinoids on the prolactin-induced structural differentiation of the mammary gland. Thoracic glands from BALB/c mice pretreated with steroids differentiate in 6 days into alveolar structures in presence of insulin and prolactin. All-trans-retinoic acid and N-(-4-hydroxyphenyl)retinamide inhibit prolactin-induced structural changes in the glands. Retinyl acetate, which is effective against mammary carcinogenesis in the rat, but is ineffective against mouse mammary carcinogenesis, failed to inhibit such proliferation. These results were correlated with inhibition of [3H]thymidine incorporation into DNA in a dose related manner by retinoids effective in inhibiting mammary development.
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PMID:Retinoids inhibit prolactin-induced development of the mammary gland in vitro. 682 85