S. B. Moodbidri
Indian Council of Medical Research
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Featured researches published by S. B. Moodbidri.
Archives of Andrology | 1980
S. Vijayalakshmi; S. B. Moodbidri; A. H. Bandivdekar; A. R. Sheth
Both testicular and ovarian inhibin preparations caused a dose-related inhibition of binding of 125I-hFSH to rat testicular receptors. Testicular inhibin also suppressed the FSH-induced production of cAMP by rats testis in vitro. These data demonstrate a direct action of inhibin at the testicular level by interfering with FSH action.
Cellular and Molecular Life Sciences | 1981
S. B. Moodbidri; S. Vijayalakshmi; A. H. Bandivdekar; A. R. Sheth
Both testicular and ovarian inhibin preparations blocked GnRH synthesis by the hypothalamus and consequently reduced the circulating level of FSH. The serum level of LH was unaffected.
Cellular and Molecular Life Sciences | 1984
A. H. Bandivdekar; S. B. Moodbidri; A. R. Sheth
Low molecular weight inhibin (1500 daltons) was obtained from sheep, human, rat and chicken testes by sequential chromatography on Sephadex G-100 and G-25. In addition to its ability to suppress circulating FSH levels in adult castrated male rats, it also exhibits binding inhibition of I125hFSH to rat testicular receptors.
Journal of Immunoassay | 1992
Sophy M. Jose; S. B. Moodbidri; A. R. Sheth
A simple and sensitive enzyme-linked immunosorbent assay (ELISA) is described for the measurement of inhibin in urine and seminal plasma. Standards used cover a range from 50 ng to 0.05 ng/0.1 ml with a detection limit of 0.098 ng/0.1 ml. Coefficients of variation for intra-assay precision and for inter-assay precision were obtained and compared favourably with RIA. Given the ease of application, this technique is an useful alternative to existing radioimmuno-assays for this peptide.
Archives of Andrology | 1992
S. B. Moodbidri; Seema V. Garde; A. R. Sheth
Historically, inhibin was thought to be a testicular hormone involved in the regulation of pituitary FSH by a negative feedback control. The ability of inhibin to preferentially suppress FSH without affecting LH triggered extensive research for its possible use as a male contraceptive, suggesting a plurality of molecular forms and a multiplicity of biological actions of this putative hormone. It also became evident that inhibin is not unique to the testis, as presumed earlier, and can even be obtained from the ovary. This has necessitated a fundamental revision of the original concept of inhibin. Unfortunately, not many perceive inhibin as a loose conglomerate of structurally dissimilar, FSH-suppressing proteins and insist on singling out a 32-kDa protein derived from ovarian follicular fluid to be designated as inhibin. This article highlights features common to two distinctly different types of inhibin: seminal inhibin and ovarian inhibin. Evidence is also provided to indicate that the term inhibin need not be specific to the ovarian protein, but encompasses proteins hitherto dismissed as inhibin-like or inhibin-related proteins.
Archive | 1988
A. R. Sheth; S. B. Moodbidri; Nandita J. Arbatti
Follicle-stimulating hormone (FSH) has a vital role to play in various reproductive processes. In the male, FSH is necessary for the quantitative maintenance of normal spermatogenesis. The neutralization of endogenous FSH by the administration of FSH antibodies to nonhuman primates severely affects spermatogenesis (68,83). In the female, FSH is involved in the growth and maturation of follicles as well as in the selection of the dominant follicle (27). Therefore, the selective suppression of FSH synthesis, release, and action by any agent will offer new approaches to the regulation of fertility in both men and women, Inhibin is one such substance that fits the bill. Inhibin is a putative gonadal hormone that, in recent years, has established itself as a factor responsible for the control of FSH. Besides, certain dimmers of the β-subunit of inhibin are known to activate the release of FSH (44,77). It is tempting to speculate, therefore, that the native inhibin and the β-dimer may account for the differential control of FSH and LH, which could not be explained by the prevailing concept of the regulation of gonadotropins by a single decapeptide-gonadotropin-releasing hormone (GH) (Fig. 11.1).
Journal of Andrology | 1982
Atmaram H. Bandivdekar; S. Vijayalakshmi; S. B. Moodbidri; A. R. Sheth
International Journal of Andrology | 1981
S. Vijayalakshmi; Parul R. Sheth; S. P. Dandekar; A. Y. Vaze; S. B. Moodbidri; A. R. Sheth
International Journal of Andrology | 1986
U. Natraj; G. Vanage; A. Didolkar; S. B. Moodbidri; A. R. Sheth
Archive | 1982
A. R. Sheth; S. Vijayalakshmi; Parul R. Sheth; Atmaram H. Bandivdekar; S. B. Moodbidri