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Modelling the control of ovulation and polycystic ovary syndrome (1997)

Chávez-Ross, A. ; Franks, S. ; Mason, H. D. ; [et al.]

Springer

Journal of mathematical biology 36 (1997), S. 95-118

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ISSN: 1432-1416

Keywords: Key words: Ovulation ; Lacker models ; Polycystic ovary syndrome ; PCOS

Source: Springer Online Journal Archives 1860-2000

Topics: Biology , Mathematics

Notes: Abstract. The control of ovulation in mammalian species appears to be a highly robust process. The primary mechanism is believed to be competition amongst a group of developing follicles, mediated by a hormonal feedback loop involving in the first instance the pituitary. Successful follicles reach maturity and ovulate, the remainder atrophy and die. A model of this control process has been derived by Lacker and his group. Based on simple qualitative assumptions about the hormonal feedback loop, this is able to reflect many of the basic physiological features of ovulation in mammals. However, a fundamental hypothesis of Lacker’s work is that all follicles are identical and respond to hormonal signals in precisely the same way. Not only is this improbable, but it also leads to several aspects of the model which are qualitatively unrealistic, most notable of these is its inability to accurately model the condition known as Polycystic Ovary Syndrome. This common malfunction of the ovulatory control mechanism accounts for up to three-quarters of cases of anovulatory infertility in humans and its understanding is therefore of considerable medical significance. In this paper we extend the analysis of Lacker’s model to the case of non-identical follicles; this allows us to obtain behaviour much closer to that observed in PCOS patients and to draw some tentative conclusions about the mechanisms underlying this condition.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1007/s002850050092

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In utero exposure to microwave radiation and rat brain development (1984)

Merritt, J. H. ; Hardy, K. A. ; Chamness, A. F.

New York, NY [u.a.] : Wiley-Blackwell

Bioelectromagnetics 5 (1984), S. 315-322

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ISSN: 0197-8462

Keywords: brain ; rat ; development ; microwaves ; Life and Medical Sciences ; Occupational Health and Environmental Toxicology

Source: Wiley InterScience Backfile Collection 1832-2000

Topics: Biology , Physics

Notes: Timed-pregnancy rats were exposed in a circular waveguide system starting on day 2 of gestation. The system operated at 2,450 MHz (pulsed waves; 8 μs PW; 830 pps). Specific absorption rate (SAR) was maintained at 0.4 W/kg by increasing the input power as the animals grew in size. On day 18 of gestation the dams were removed from the waveguide cages and euthanized; the fetuses were removed and weighed. Fetal brains were excised and weighed, and brain RNA, DNA and protein were determined. Values for measured parameters of the radiated fetuses did not differ significantly from those of sham-exposed fetuses. A regression of brain weight on body weight showed no micrencephalous fetuses in the radiation group when using as a criterion a regression line based on two standard errors of the estimate of the sham-exposed group. In addition, metrics derived from brain DNA (ie, cell number and cell size) showed no significant differences when radiation was compared to sham exposure. We conclude that 2,450-MHz microwave radiation, at an SAR of 0.4 W/kg, did not produce significant alterations in brain organogenesis.

Additional Material: 3 Ill.