558 research outputs found
The Tyranny of the Majority: A Case Study of the McCarthy Era
Alexis de Tocqueville observed in his travels through the United States in the 1830s that the system of majoritarian representation could become subject to a ‘tyranny of the majority’. This concept exists on the political and the social axis. The tyranny of the majority of the social axis, where majorities impose their viewpoints on minorities and subjugate minorities to their opinion is most extensively analyzed in this chapter. In this, minorities tend to conform to majority opinion out of fear of repercussions. This chapter thus provides a link between the tyranny of the majority and the conformity theory. It researches whether American society has become subject to the tyranny of the majority during the McCarthy era. The main claim derived from this research problem is that American society was indeed subject to the tyranny of the majority during the McCarthy era. Nevertheless, a tension was apparent in society. Although minorities indeed conformed to majority opinion and there was a climate of political intolerance, some minorities were in fact able to turn the conformity theory upside down and influenced the majority in such a way that minority opinion prevailed. This phenomenon was noticeable in the Civil Rights Movement, where African Americans persuaded predominantly white Americans that African Americans should be granted equal rights. In short, American society is highly in flux. Although the tyranny of the majority became a social reality during the McCarthy era, at the same time a minority was able to persuade the majority of its viewpoints
Regulation of ovarian function: the role of anti-Mullerian hormone
Anti-Mullerian hormone (AMH), also known as Mullerian inhibiting
substance, is a member of the transforming growth factor beta superfamily
of growth and differentiation factors. In contrast to other members of the
family, which exert a broad range of functions in multiple tissues, the
principal function of AMH is to induce regression of the Mullerian ducts
during male sex differentiation. However, the patterns of expression of
AMH and its type II receptor in the postnatal ovary indicate that AMH may
play an important role in ovarian folliculogenesis. This review describes
several in vivo and in vitro studies showing that AMH participates in two
critical selection points of follicle development: it inhibits the
recruitment of primordial follicles into the pool of growing follicles and
also decreases the responsiveness of growing follicles to FSH
Ovarian follicle growth and development: role of anti-Müllerian hormone
The central reproductive organ of the female is the ovary. In mammalian species, the
females have two ovaries, which are located in the abdomen near the kidneys. The ovary
has two lnajor functions. First of all, it produces the female gametes or oocytes, which can
develop inside the ovary until they reach the developmental stage at which they can be
fertilised by the male gametes. Second, the ovary produces steroid hormones, whicll are
important for the development of female characteristics and behaviour.
In the ovary the gametes are found in special structures, the so-called ovarian follicles.
Normal developnlent of the ovary and the ovarian follicles is very iInportant for female
fertility. This cl,apter starts with a description of gonad formation in the mammalian
female, on basis of observations on the development in female nlice, and focuses on the
most iInportant factors involved in gonad formation. Fl1l1hernlore, the process of ovarian
follicle development is described, again on basis of data generated mainly from studies
in the mouse, and also rat. Ovarian follicle developnlent is under tight control by luan)
hormones and growth factors, and therefore the action of only the most important regulatory
factors will be mentioned. This thesis focuses on the role of anti-Mullerian hormone
(AM H), one of the ovarian growth factors, in ovarian follicle development
Control of ovarian primordial follicle activation
The ovarian follicles develop initially from primordial follicles. The majority of ovarian primordial follicles are maintained quiescently as a reserve for the reproductive life span. Only a few of them are activated and develop to an advanced follicular stage. The maintenance of dormancy and activation of primordial follicles are controlled by coordinated actions of a suppressor/activator with close communications with somatic cells and intra-oocyte signaling pathways. Many growth factors and signaling pathways have been identified and the transforming growth factor-beta superfamily plays important roles in early folliculogenesis. However, the mechanism of maintaining the dormancy and survival of primordial follicles has remained unknown for decades. Recently, since the first finding that all primordial follicles are activated prematurely in mice deficient forkhead box O3a, phosphatidylinositol 3 kinase/phosphatase and tensin homolog (PTEN) signaling pathway was reported to be important in the regulation of dormancy and initial follicular activation. With these informations on early folliculogenesis, clinical application can be expected such as in vitro maturation of immature oocytes or in vitro activation of follicles by PTEN inhibitor in cryopreserved ovarian cortical tissues for fertility preservation
Control of primordial follicle recruitment by anti-Mullerian hormone in the mouse ovary
The dimeric glycoprotein anti-Mullerian hormone (AMH) is a member of the
transforming growth factor-beta superfamily of growth and differentiation
factors. During male fetal sex differentiation, AMH is produced by Sertoli
cells and induces degeneration of the Mullerian ducts, which form the
anlagen of part of the internal female genital system. In females, AMH is
produced by the ovary, but only postnatally. The function of AMH in the
ovary is, however, still unknown. Female AMH null mice were reported to be
fertile, with normal litter size, but this does not exclude a more subtle
function for ovarian AMH. To investigate the function of AMH in the ovary,
the complete follicle population was determined in AMH null mice, in mice
heterozygous for the AMH null mutation, and in wild-type mice of different
ages: 25 days, 4 months, and 13 months. In the present study we found that
ovaries of 25-day- and 4-month-old AMH null females, compared to those of
wild-type females, contain more preantral and small antral follicles. In
addition, in 4- and 13-month-old AMH null females, smaller numbers of
primordial follicles were found. Actually, in 13-month-old AMH null
females, almost no primordial follicles could be detected, coinciding with
a reduced number of preantral and small antral follicles in these females.
In almost all females heterozygous for the AMH null mutation the number of
follicles fell in between the numbers found in wild-type and AMH null
females. In 4-month-old AMH null females serum inhibin levels were higher
and FSH levels were lower compared to those in wild-type females. In
contrast, inhibin levels were lower in 13-month-old AMH null females, and
FSH levels were unchanged compared to those in wild-type females.
Furthermore, the weight of the ovaries was twice as high in the
4-month-old AMH null females as in age-matched wild-type females. We
conclude that AMH plays an important role in primordial follicle
recruitment, such that more primordial follicles are recruited in AMH null
mice than in wild-type mice; the mice heterozygous for the AMH null
mutation take an in-between position. Consequently, the ovaries of AMH
null females and those of females heterozygous for the AMH null mutation
will show a relatively early depletion of their stock of primordial
follicles. The female AMH null mouse may thus provide a useful model to
study regulation of primordial follicle recruitment and the relation
between follicular dynamics and ovarian aging
Temporal changes in inhibin subunit mRNAs during atresia of preovulatory follicles in the rat
This study aimed to investigate the time course of disappearance of the
mRNAs of the various subunits of inhibin in follicles which become
atretic. An animal model was used in which atresia of preovulatory
follicles could be studied in a chronological order. Injection of
gonadotrophin-releasing hormone (GnRH) antagonist (20 microg) at the
morning of pro-oestrus (P) blocked ovulation and the 10-12 preovulatory
follicles became gradually atretic. A second injection was given the next
day to prevent delayed ovulation. The rate of atresia could be delayed by
simultaneous administration of a subovulatory dose of human chorionic
gonadotrophin (hCG) (0.5 IU) and could be advanced by administration of a
fivefold larger amount of GnRH antagonist. Functional activity of
follicles becoming atretic was studied by measuring oestradiol production
after incubation of individual follicles for 4 h. Follicles isolated 24 h
after the first injection of GnRH antagonist (P+24) already secreted
significantly less oestradiol in vitro than follicles isolated at
pro-oestrus, although they were morphologically not different from
pro-oestrous follicles. Follicles isolated at P+24 from hCG-treated rats
secreted more oestradiol compared with follicles from rats not treated
with hCG. In contrast, follicles isolated at P+24 from rats that were
given a fivefold larger amount of GnRH antagonist secreted less
oestradiol. Once this model was validated, temporal changes in inhibin
subunit mRNAs in follicles undergoing atresia were measured by in situ
hybridization and RNase protection assay. In situ hybridization showed
abundant alpha- and betaA-subunit mRNA in the whole granulosa layer of
preovulatory follicles at P and P+24, while betaB-subunit mRNA was
restricted to the antral layer and cumulus. At P+48 the amount of alpha-
and betaA-subunit mRNA had declined and was restricted to the cumulus,
whereas betaB-subunit mRNA was absent. In the atretic follicles present at
P+72 and P+96, mRNAs of all three inhibin subunits were absent.
Administration of 0.5 IU hCG delayed the decline in the amount of alpha,
betaA and betaB mRNA in preovulatory follicles at P+48. RNase protection
assay of inhibin subunits in isolated follicles revealed no changes
between P and P+24. However, at P+48, the mRNAs of alpha- an
Effect of androgen treatment during foetal and/or neonatal life on ovarian function in prepubertal and adult rats
We investigated the effects of different windows of testosterone propionate (TP) treatment during foetal and neonatal life in female rats to determine whether and when excess androgen exposure would cause disruption of adult reproductive function. Animals were killed prepubertally at d25 and as adults at d90. Plasma samples were taken for hormone analysis and ovaries serial sectioned for morphometric analyses. In prepubertal animals, only foetal+postnatal and late postnatal TP resulted in increased body weights, and an increase in transitory, but reduced antral follicle numbers without affecting total follicle populations. Treatment with TP during both foetal+postnatal life resulted in the development of streak ovaries with activated follicles containing oocytes that only progressed to a small antral (smA) stage and inactive uteri. TP exposure during foetal or late postnatal life had no effect upon adult reproductive function or the total follicle population, although there was a reduction in the primordial follicle pool. In contrast, TP treatment during full postnatal life (d1-25) resulted in anovulation in adults (d90). These animals were heavier, had a greater ovarian stromal compartment, no differences in follicle thecal cell area, but reduced numbers of anti-Mullerian hormone-positive smA follicles when compared with controls. Significantly reduced uterine weights lead reduced follicle oestradiol production. These results support the concept that androgen programming of adult female reproductive function occurs only during specific time windows in foetal and neonatal life with implications for the development of polycystic ovary syndrome in women
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