Search Results
You are looking at 1 - 9 of 9 items for
- Author: R. M. DAS x
- Refine by access: All content x
Search for other papers by R. M. DAS in
Google Scholar
PubMed
SUMMARY
The duration of stages of the cell cycle in the uterine epithelial and stromal tissues of ovariectomized mice was estimated by the labelled mitosis method. In untreated animals the mean duration of the S phase (DNA synthesis) was 10·5 h in the glandular and luminal epithelium. Oestrogen treatment shortened it to 6 h in both tissues. In the endometrial stroma of progesterone-treated mice the duration of S was 8 h; when oestrogen was given it increased slightly. The generation times estimated under steady-state conditions were 270,156 and 383 h respectively in the lumen, glands and stroma of untreated mice. After oestrogen stimulation the responses became highly synchronized.
Search for other papers by R. M. DAS in
Google Scholar
PubMed
The number of cells that synthesize DNA in the uterine luminal epithelium of ovariectomized mice and in the uterine connective tissue stroma of progesterone-treated mice reaches a maximum approximately 15 h after oestrogen is given (Martin, Finn & Trinder, 1973a, b). Martin & Finn (1968) maintained that the time-course of the mitotic response was similar in both tissues, but DNA synthesis has been shown to be of 3 h shorter duration in the oestrogen-stimulated epithelium than in the stroma (Das, 1972), and on this basis the time-courses of the mitotic responses might be expected to differ.
Albino mice were ovariectomized under tribromoethanol (Avertin) anaesthesia. Five days later they were primed with 100 ng oestradiol s.c. for 3 days. Starting 2 days after priming, groups of five mice received daily injections of 1 mg progesterone s.c. for 4 days, and 50 ng oestradiol were given with the last injection. Other
Search for other papers by R. M. DAS in
Google Scholar
PubMed
Search for other papers by L. MARTIN in
Google Scholar
PubMed
Oestradiol stimulates uterine luminal epithelial cells of ovariectomized mice to pass through two rounds of cell division in quick succession (Das, 1972; Martin, Finn & Trinder, 1973). Progesterone injected with the oestrogen blocks entry of some cells into the first round of proliferation without affecting G1, S or G2 in the remainder, but blocks entry of these cells into the second round. This suggested that cells were only sensitive to progesterone in early G1 (Martin, Das & Finn, 1973). In the present experiment we attempted to delineate the sensitive period in greater detail.
Randomly bred albino mice were ovariectomized and primed as described previously (Das, 1972). Five days after priming they were separated into ten groups of three. All were given 50 ng oestradiol subcutaneously in 0·1 ml arachis oil at 0 h and 25 μCi [3H]thymidine ([3H]Thd; sp. act. 5 Ci/mm, Amersham) intraperitoneally
Search for other papers by R. M. DAS in
Google Scholar
PubMed
Search for other papers by G. K. BENSON in
Google Scholar
PubMed
SUMMARY
Adult virgin, regularly cyclic female guinea-pigs were treated with different doses of luteinizing hormone (LH) and follicle-stimulating hormone during the late luteal phase of the oestrous cycle. The onset of the next oestrus was delayed and the length of the dioestrous stage was prolonged beyond the normal range in all the treated groups, but for a maximum period in the animals receiving LH alone.
The results indicate a dual role of LH on the normal cycle of the guineapig. It has been suggested that either luteotrophin release from the pituitary or an intrinsic luteotrophic action is probably a part of the function of LH in addition to its ovulation-inducing function in the guinea-pig.
Search for other papers by R. M. DAS in
Google Scholar
PubMed
Search for other papers by G. K. BENSON in
Google Scholar
PubMed
SUMMARY
Pituitaries from adult or young guinea-pigs were implanted under the kidney capsule of intact adult female guinea-pigs between the 3rd and 5th days of the oestrous cycle.
The oestrous cycles in the recipients of adult pituitaries were mostly normal in length. Seven out of nine animals engrafted with pituitaries from their own litters had a prolonged dioestrus, ranging from 8 to 16 days longer than normal, at the end of which oestrus and ovulation occurred. When the grafts contained pituitaries from one male and one female pup the cycle extension was more pronounced than when they were composed of pituitaries from two or three female pups.
The occurrence of prolonged dioestrus accompanied by a delayed ovulation in the graft-bearing animals is suggested to be associated with the production of luteotrophic hormone by the graft tissue, possibly deriving from basophil cells.
Search for other papers by R. P. DAS in
Google Scholar
PubMed
Search for other papers by M. J. PERRAULT in
Google Scholar
PubMed
SUMMARY
The role of the thyroid in cold-induced atrophy of the genital accessory organs and the protection by treatment with testosterone against such atrophy have been evaluated in intact and castrated male rats.
Treatment with thyroxine or exposure to cold reduced the weight and some of the activities of the genital accessory organs in intact but not in castrated rats.
Testosterone propionate implants not only protected these organs from the cold-induced atrophy but also stimulated them beyond the level of intact controls kept at room temperature.
The weight and some functions of the genital accessory organs of testosterone-treated castrated rats were decreased after cold exposure. These changes were more pronounced when thyroxine was administered simultaneously.
The results suggest that the cold-induced atrophy of the accessory organs is due to the release of excess thyroid hormone and that implants of testosterone propionate can prevent this atrophy.
Search for other papers by T. K. Das in
Google Scholar
PubMed
Search for other papers by R. Mazumder in
Google Scholar
PubMed
Search for other papers by N. M. Biswas in
Google Scholar
PubMed
ABSTRACT
Quantitative evaluation of spermatogenesis at stage VII of the cycle of the seminiferous epithelium and radioimmunoassay of plasma testosterone were performed in adult Wistar rats after intraventricular injection of 5,6-dihydroxytryptamine (5,6-DHT). The rats were killed 2, 10 and 21 days after injection. Brain 5-hydroxytryptamine (5-HT) and plasma testosterone levels were found to be significantly lower in all rats treated with 5,6-DHT. A significant reduction in step 7 spermatid count was also observed after 10 and 21 days. Supplementation with human chorionic gonadotrophin for 21 days in rats injected with 5,6-DHT partially prevented the step 7 spermatid degeneration and increased testosterone levels without producing any effect on brain concentrations of 5-HT. These results suggest that changes in testicular steroidogenesis and spermatogenesis are secondary to pituitary gonadotrophin release which, in turn, is under the influence of brain 5-HT neurones.
J. Endocr. (1985) 106, 395–400
Search for other papers by L. MARTIN in
Google Scholar
PubMed
Search for other papers by R. M. DAS in
Google Scholar
PubMed
Search for other papers by C. A. FINN in
Google Scholar
PubMed
SUMMARY
Progesterone given at the same time as oestradiol-17β prevented approximately 40% of uterine luminal epithelial cells from entering DNA synthesis, but did not prolong the G1, S or G2 phases in the remainder. However, it blocked the entry of these cells into a second round of DNA synthesis. It is suggested that uterine luminal epithelial cells are only sensitive to progesterone for a limited period in G1.
Search for other papers by M. Zaidi in
Google Scholar
PubMed
Search for other papers by T. J. Chambers in
Google Scholar
PubMed
Search for other papers by R. E. Gaines Das in
Google Scholar
PubMed
Search for other papers by H. R. Morris in
Google Scholar
PubMed
Search for other papers by I. MacIntyre in
Google Scholar
PubMed
ABSTRACT
The calcitonin gene encodes a small family of peptides: calcitonin, calcitonin gene-related peptide (CGRP) and katacalcin. Whereas calcitonin is concerned with skeletal maintenance, the function, if any, of katacalcin is still unknown. In the present study we have assessed resorption of human cortical bone substrate by isolated rat osteoclasts and have shown that CGRP acts directly on the osteoclast to inhibit bone resorption. The three CGRP peptides (rat, human(a) and human(β)) caused an almost equivalent decrease in osteoclastic bone resorption and were approximately 1000-fold less potent than human calcitonin in this respect. The responses of human calcitonin and human CGRP(α) were additive. Furthermore, prior treatment with trypsin to destroy receptors abolished the responsiveness of osteoclasts to CGRP and calcitonin. The carboxyl- and amino-terminal fragments of CGRP were found not to inhibit bone resorption, suggesting that the whole molecule of CGRP is necessary for biological activity. We have therefore suggested that the calcitonin-like effects of CGRP, seen both in vivo in the rat bioassay and in vitro in organ cultures, are due to the direct action of CGRP on the osteoclast, probably mediated through the calcitonin receptor. Though it is unlikely that CGRP is involved in the regulation of plasma calcium, the peptide may be an important local regulator of bone cell function.
J. Endocr. (1987) 115,511–518
