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22 results on '"Babus, Janice K"'

1. NPRL3 loss alters neuronal morphology, mTOR localization, cortical lamination and seizure threshold

Author

Iffland, Philip H, primary, Everett, Mariah E, additional, Cobb-Pitstick, Katherine M, additional, Bowser, Lauren E, additional, Barnes, Allan E, additional, Babus, Janice K, additional, Romanowski, Andrea J, additional, Baybis, Marianna, additional, Elziny, Soad, additional, Puffenberger, Erik G, additional, Gonzaga-Jauregui, Claudia, additional, Poulopoulos, Alexandros, additional, Carson, Vincent J, additional, and Crino, Peter B, additional

Published
2022
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5. NPRL3: Direct Effects on Human Phenotypic Variability, mTOR Signaling, Subcellular mTOR Localization, Cortical Lamination, and Seizure Susceptibility

Author

Iffland, Philip H., primary, Everett, Mariah E., additional, Cobb-Pitstick, Katherine M., additional, Bowser, Lauren E., additional, Barnes, Allan E., additional, Babus, Janice K., additional, Romanowski, Andrea, additional, Baybis, Marianna, additional, Puffenberger, Erik G., additional, Gonzaga-Jauregui, Claudia, additional, Poulopoulos, Alexandros, additional, Carson, Vincent J., additional, and Crino, Peter B., additional

Published
2020
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9. Role of endotoxin in the response to experimentally induced bacteremia in chronically prepared rats

Author

Carlson, Drew E., Babus, Janice K., Nguyuza, Nkhensani, Melhen-Stancofski, Hiba, and Eastridge, Brian J.

Subjects
Endotoxins -- Physiological aspects, Bacteremia -- Physiological aspects, Bacterial infections -- Physiological aspects, Biological sciences
Abstract

The physiological responses to endotoxin during experimental bacteremia were analyzed in rats administered with nonfatal, nonhypotensive doses of Escherichia coli suspended in saline. Infusions of Escherichia coli induced submaximal elevations in plasma adrenocorticotropin (ACTH) which was partly mediated by free endotoxin. However, the effects of fatal doses of Escherichia coli in rats were not mediated by endotoxin.

Published
1997

22. BAX is involved in regulating follicular growth, but is dispensable for follicle atresia in adult mouse ovaries.

Author

Greenfield, Chuck R., Babus, Janice K., Furth, Priscilla A., Marion, Sam, Hoyer, Patricia B., and Flaws, Jodi A.

Subjects
MAMMALS, ANIMAL populations, CELLS, HISTOLOGY, OVARIES
Abstract

Mammalian females are endowed with a finite number of primordial follicles at birth or shortly thereafter. Immediately following the formation of the primordial follicle pool, cohorts of these follicles are recruited to begin growth, and this recruitment continues until the primordial follicle population is depleted. Once recruited, a follicle will either grow and ovulate or undergo atresia. Follicle atresia results from the apoptotic death of follicular cells. Members of the BCL-2 family of proteins are important regulators of apoptosis in most cells including in the ovary. Here, we tested the hypothesis that the proapoptotic BAX is an important regulator of follicle survival. We used a variety of histological and biochemical techniques to investigate the impact of Bax deletion on follicle growth and death. We observed that the Bax deletion results in delayed vaginal opening and altered follicular growth. Young adult Bax-deficient ovaries contained increased numbers of primordial follicles and a trend towards reduced numbers of growing follicles. Bax deficiency led to a reduction in average litter size, and also a reduction in the number of oocytes ovulated in response to exogenous gonadotropins. In contrast, Bax deficiency did not alter follicle atresia. In conclusion, BAX appears to be an important regulator of follicle growth, but is dispensable for follicle atresia in mice. [ABSTRACT FROM AUTHOR]

Published
2007
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