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G Cai

Publications and source records attributed to G Cai.

93 records · Page 6Linked to original sources
PubMed1990

[Isolation and detection of murine transplantable breast tumor antigen by McAb F36/22].

A transplantable murine breast tumor antigen (called JC tumor) has been recognized by the detection of McAb F36/22 with the method of immunoblotting. JC tumor antigen was isolated by Sepharose-CL-4B, then was purified by McAb F36/22 affinity chromatography. Solid phase RIA detection demonstrated that the specific activity of the antigen which was purified by 188.4 times was 148,000 cpm/mg protein. SDS-PAGE and immunoblot analysis revealed that the tumor antigen possessed a molecular weight of 60kd. Competitive binding RIA indicated that JC tumor antigen inhibited the combining of ductal carcinoma antigen with McAb F36/22. It implied that some groups (antigen determinant) on JC tumor antigen were the same as or similar to those on ductal cancer antigen.

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PubMedDate not supplied

Attenuation of cocaine-induced genomic and functional responses in prenatal cocaine-exposed rabbits.

The effects of in utero cocaine exposure on cocaine-induced genomic and functional responses in postnatal life were examined. Pregnant Dutch Belted rabbits were injected intravenously, twice daily, with cocaine hydrochloride (4 mg/kg) or saline from day 8 through day 29 of pregnancy. Prenatally exposed kits were challenged with cocaine on postnatal day 20. In prenatal saline-exposed kits, cocaine induced time- and dose-dependent c-fos gene expression in both frontal cortex and striatum. Prenatal cocaine exposure reduced cocaine-induced c-fos responses by 35-58% in the frontal cortex and 37-41% in the striatum. Cocaine-induced functional responses that included head bobbing, seizure, and locomotor activity were also attenuated in prenatal cocaine-exposed kits. Cocaine-induced c-fos expression and functional responses were blocked by the D(1) dopamine receptor antagonist, SCH23390, or by the serotonin receptor antagonist, methysergide, but not by the D(2) dopamine receptor antagonist, L-sulpride. The results indicate that in utero cocaine exposure leads to diminished responses to cocaine challenge in the offspring, which may be mediated by prenatal cocaine-induced alterations in one or more components of the D(1) dopamine and/or serotonin receptor signaling systems during early postnatal life.

Animals↗