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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Descriptions of endocrine disruption have largely been associated with wildlife and driven by observations documenting estrogenic, androgenic, antiandrogenic, and antithyroid actions. These actions, in response to exposure to ecologically relevant concentrations of various environmental contaminants, have now been established in numerous vertebrate species. However, many potential mechanisms and endocrine actions have not been studied. For example, the DDT [1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane] metabolite, p,p -DDE [1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene] is known to disrupt prostaglandin synthesis in the uterus of birds, providing part of the explanation for DDT-induced egg shell thinning. Few studies have examined prostaglandin synthesis as a target for endocrine disruption, yet these hormones are active in reproduction, immune responses, and cardiovascular physiology. Future studies must broaden the basic science approach to endocrine disruption, thereby expanding the mechanisms and endocrine end points examined. This goal should be accomplished even if the primary influence and funding continue to emphasize a narrower approach based on regulatory needs. Without this broader approach, research into endocrine disruption will become dominated by a narrow dogma, focusing on a few end points and mechanisms.
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PMID:Endocrine disrupting contaminants--beyond the dogma. 1681 40

To clarify breeding failure in avian species caused by the estrogenicity of chemicals, alterations in the reproductive systems of Japanese quail exposed in ovo to a xenoestrogen were investigated. An injection of diethylstilbestrol (DES) into the yolk before incubation decreased, after sexual maturation, egg-laying performance of female quails, which accompanied inducing abnormal development of the oviducts. All females treated with 50 ng DES/g of egg did not lay eggs, while 0.5-5 ng DES/g reduced egg weight and eggshell strength and thickness. In the uterus (shell gland), the mRNAs for calcium regulating factors, osteopontin and calbindin D28 K, were reduced dose-dependently by DES. Scanning electron microscopy showed that shell thinning was pronounced in the mammillary and cuticular layers of the eggshell, regions where osteopontin proteins are reportedly located. These indicate that transovarian exposure to xenoestrogens causes malformation and dysfunction of the oviducts, where calcium regulating molecules could play key roles in eggshell thinning.
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PMID:Mechanisms of estrogen-induced effects in avian reproduction caused by transovarian application of a xenoestrogen, diethylstilbestrol. 1859 71

A 42-year-old pregnant (22 weeks) woman with a history of peptic ulcer 20 years earlier, was presented to our gynaecological clinic with acute abdominal pain in 2005. She was para-1, had delivered a healthy child two years earlier and now she had an uncomplicated pregnancy. Upon admittance she was pale, hyperventilating and complained of epigastric pain and nausea. There was no vaginal bleeding and no uterine contractions. Ultrasound examination revealed a single fetus with normal cardiac activity. During the examination blood pressure suddenly dropped and the patient was considered to be in a state of pre-shock. Intraabdominal hemorrhage was suspected and she underwent immediate exploratory laparotomy. Uterine rupture with an intact gestational sac extruding through the laceration in the middle of the fundal region of the uterus was found. A sub-total hysterectomy was performed. The physio-pathology leading to the uterine rupture is discussed. An interstitial pregnancy close to the ostium internum (cornual pregnancy) may have lead to the thinning and rupture of the uterine wall in the fundal part. Alternatively, the placenta's location in the upper uterine cavity (possibly caused by a 3 cm myoma that seemed to divide the uterine cavity into two compartments) may have caused thinning and rupture of the uterine wall in the fundal part. The literature describing uterine rupture in the second trimester is reviewed.
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PMID:[A woman in the second trimester of pregnancy with acute abdominal pain]. 1892 2

The experimental model of cortical dysplasia (CD) obtained by administering carmustine (1-3-bis-chloroethyl-nitrosurea [BCNU]) in pregnant rat uterus mimics the histopathological abnormalities observed in human CD patients: altered cortical layering, and presence of heterotopia and dysmorphic/heterotopic neurons. To investigate further the cortical layering disruption and the neuronal composition of heterotopia in BCNU-exposed cortex, we analyzed the expression pattern of the transcription factors Nurr1, Er81, Ror-beta, and Cux2 (respectively specific markers of layers VI, V, IV and superficial layers) in the cortical areas of BCNU-treated rats by means of in situ hybridization, and compared the findings with those observed in adult control rats. Combining in situ hybridization and immunohistochemistry we also investigated the origin of dysmorphic or heterotopic neurons. The main results of the present study are (i) the analysis of cortical layer thickness revealed that the cortical thinning in the BCNU model was prevalently restricted to the superficial layers; (ii) in cortical and periventricular heterotopia, the prevalent presence of superficial layer neurons in the internal areas, and deeper layer neurons in a more peripheral region, demonstrated a rudimentary pattern of laminar organization in nodule formation; and (iii) the Er81 signal in the dysmorphic and heterotopic pyramidal neurons located in layers I/II showed that they belong to layer V. These results shed light on the disorganization of the laminar architecture of the BCNU model by providing correlations with normal cortical layering and revealing the ontogenesis of heterotopia and heterotopic/dysmorphic neurons. They also provide strong evidence of the usefulness of layer-specific markers in investigating the neuropathology of CD, thus opening up the possibility of expanding their application to human neuropathology.
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PMID:Expression of layer-specific markers in the adult neocortex of BCNU-Treated rat, a model of cortical dysplasia. 1917 81

In this study, a female pubertal assay on the effects of parabens, including methyl-, ethyl-, propyl-, isopropyl-, butyl-, and isobutylparaben, was performed in a female Sprague-Dawley rat model during the juvenile-peripubertal period. The rats were orally treated with these parabens from postnatal day 21-40 in a dose-dependent manner (62.5, 250 and 1000 mg/kg body weight [BW]/day). 17alpha-Ethinylestradiol (1mg/kg BW/day) was used as a positive control and corn oil as a vehicle. A high dose of methyl- and isopropylparaben (1000 mg/kg BW/day) resulted in a significant delay in the date of vaginal opening and a decrease in length of the estrous cycle. In measurements of organ weight and body weight, we observed significant weight changes in ovaries, adrenal glands, thyroid glands, liver, and kidneys; conversely, body weight was not altered following paraben treatment. The potential effects of parabens on estrogenicity were shown in histopathological abnormities in the reproductive organs. Histological analysis of the ovaries from the peripubertal rats revealed a decrease of corpora lutea, increase in the number of cystic follicles, and thinning of the follicular epithelium. In addition, morphological studies of the uterus revealed the myometrial hypertrophy by a high dose of propyl- and isopropylparaben (1000 mg/kg-day), and in all dose groups of butyl- and isobutylparabens. However, no significant histopathological changes were observed in the other organs (i.e. adrenal and thyroid glands). We also observed a significant decrease in serum estradiol and thyroxine concentrations in methyl-, ethyl-, propyl-, isopropyl-, and isobutylparaben-treated groups. A receptor-binding assay indicated that the relative binding affinities of parabens to estrogen receptors occurred in the order: isobutylparaben>butylparaben>isopropylparaben=propylparaben>ethylparaben. These values were much lower than the binding affinity for 17beta-estradiol. Taken together, long-term exposure to parabens, which show less estrogenic activity than estradiol, can produce suppressive effects on hormonal responsiveness and can disrupt the morphology of reproductive target tissues. In addition, the relation between thyroid weight and thyroid hormone may influence circulating levels of parabens, suggesting the effects of parabens as thyrotoxic during this critical stage of development in female rats.
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PMID:Potential estrogenic effect(s) of parabens at the prepubertal stage of a postnatal female rat model. 2013 80

This study evaluated the involvement of hypophyseal-gonadal and hypophyseal-adrenal axes as a possible mechanism of sodium arsenite toxicity in ovary and uterus by the coadministration of hCG. Subchronic treatment of 0.4 ppm of sodium arsenite/(100 g body weight day) via drinking water for seven estrous cycles significantly suppressed the plasma levels of leutinizing hormone, follicle-stimulating hormone, and estradiol along with sluggish ovarian activities of Delta(5),3beta-hydroxysteroid dehydrogenase and 17beta-hydroxysteroid dehydrogenase followed by a reduction in gonadal tissue peroxidase activities in mature female rats at diestrous phase. Noticeable weight loss of the ovary and uterus along with prolonged diestrous phase and increased deposition of arsenic in the plasma and in these reproductive organs were also demonstrated following the ingestion of arsenic. Follicular atresia and thinning of the uterine luminal diameter were evident after sodium arsenite treatment. Effective protection of gonadal weight loss, suppressed ovarian steroidogenesis, and altered ovarian and uterine peroxidase activities were noticed when 1.0 IU hCG/(100 g body weight day) is given in arsenic-intoxicated rats. Normal estrous cyclicity was restored toward the control level after hCG coadministration, though the elimination of elementary arsenic from the plasma and gonadal tissues was impossible. A significant recovery in the restoration of ovarian and uterine histoarchitecture was prominent after hCG treatment. Adrenal hypertrophy and steroidogenic arrest of the adrenal gland along with altered level of brain monoamines in the midbrain and diencephalons following arsenic intoxication were also ameliorated after hCG coadministration.
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PMID:The involvement of hypophyseal-gonadal and hypophyseal-adrenal axes in arsenic-mediated ovarian and uterine toxicity: modulation by hCG. 2014 81

We previously demonstrated that in the CD-1 mouse, which exhibits a high incidence of age-related adenomyosis, neonatal exposure to tamoxifen induced premature uterine adenomyosis and was associated with abnormal development particularly of the inner myometrium. In the present study, we examined the effect of neonatal tamoxifen administration upon uterine development in the C57/BL6J mouse strain that is not known to develop uterine adenomyosis. Female C57/BL6J pups (n=20) were treated with oral tamoxifen (1 mg/kg) from age 1 to 5 days. Uteri from control and treated mice were obtained on days 5, 10, 15 and 42 of age. We examined sections histologically using image analysis and immunohistochemistry for alpha-smooth muscle actin (ACTA2, alpha-SMA), desmin, vimentin, laminin, fibronectin and oestrogen receptor-alpha (ESR1). Following tamoxifen exposure, all uteri showed inner myometrium thinning, lack of continuity, disorganisation and bundling. However, adenomyosis was not seen in any uterus. ACTA2 immunostaining was less in the circular muscle layer of treated mice. The temporal pattern of desmin immunostaining found in control mice was absent in tamoxifen-treated mice. There was no difference in the localisation of laminin or fibronectin between control and tamoxifen-treated groups. However, laminin immunostaining was reduced in the circular muscle layer of treated mice. Vimentin could not be detected in either group. In conclusion, our results demonstrate that the development of the inner myometrium is particularly sensitive to oestrogen antagonism, and is affected by steroid receptor modulation. Although tamoxifen induces inner myometrial changes including that of ACTA2, desmin, ESR1 and laminin expression in C57/BL6J neonatal mice similar to those induced in CD-1 mice, C57/BL6J mice did not develop premature adenomyosis. Thus, disruption of the development and differentiation of the inner myometrium cannot alone explain the development of tamoxifen-associated adenomyosis, and this must be dependent upon its interaction with strain-dependent factors.
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PMID:Neonatal administration of tamoxifen causes disruption of myometrial development but not adenomyosis in the C57/BL6J mouse. 2036 91

The eggshell of lizards is a complex structure composed of organic and inorganic molecules secreted by the oviduct, which protects the embryo by providing a barrier to the external environment and also allows the exchange of respiratory gases and water for life support. Calcium deposited on the surface of the eggshell provides an important nutrient source for the embryo. Variation in physical conditions encountered by eggs results in a tradeoff among these functions and influences eggshell structure. Evolution of prolonged uterine egg retention results in a significant change in the incubation environment, notably reduction in efficiency of gas exchange, and selection should favor a concomitant reduction in eggshell thickness. This model is supported by studies that demonstrate an inverse correlation between eggshell thickness and length of uterine egg retention. One mechanism leading to thinning of the eggshell is reduction in size of uterine shell glands. Saiphos equalis is an Australian scincid lizard with an unusual pattern of geographic variation in reproductive mode. All populations retain eggs in the uterus beyond the embryonic stage at oviposition typical for lizards, and some are viviparous. We compared structure and histochemistry of the uterus and eggshell of two populations of S. equalis, prolonged egg retention, and viviparous to test the hypotheses: 1) eggshell thickness is inversely correlated with length of egg retention and 2) eggshell thickness is positively correlated with size of shell glands. We found support for the first hypothesis but also found that eggshells of both populations are surprisingly thick compared with other lizards. Our histochemical data support prior conclusions that uterine shell glands are the source of protein fiber matrix of the eggshell, but we did not find a correlation between size of shell glands and eggshell thickness. Eggshell thickness is likely determined by density of uterine shell glands in this species.
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PMID:Uterine and eggshell structure and histochemistry in a lizard with prolonged uterine egg retention (Lacertilia, Scincidae, Saiphos). 2071 48

Methotrexate (MTX) an antifolate drug and leucovorin its antidote, are used in the treatment of both neoplastic and non-neoplastic diseases in young women. We hypothesize that MTX treatment might comprise a deleterious effect on fast proliferating reproductive cells, an unavoidable and unwanted side effect. MTX given dose dependently to rats for 20 days prevented vaginal cyclicity and caused a reduction in serum progesterone and estradiol. External morphology of reproductive tract displayed thinning of organs and reduction in their weights. To reveal mechanism of MTX action, we examined the histology of ovary, oviduct, uterus, cervix and vagina. Results suggested that in a dose-dependent fashion MTX restrained preantral and antral follicular growth in ovary. Epithelium and stroma of oviduct, uterus, cervix and vagina were disrupted and lost their normal structures. Such alterations in ovarian function raised serum follicle stimulating hormone, luteinizing hormonal profiles. Expression of steroidogenic acute regulatory protein and P450 cholesterol side chain cleavage gene, which are both essential for steroidogenesis, markedly decreased in ovary upon MTX treatment. Total RNA, DNA and protein concentrations, glucose 6 phosphate dehydrogenase, lactate dehydrogenase and alkaline phosphatase enzyme activities in ovary were distinctly altered. Leucovorin supplementation and withdrawal of the treatment, improved MTX caused effects partially. These results for the first time indicate that the malfunction of female reproductive organs by MTX treatment in young women is not only correlated to the disrupted circulating levels of hormones and histoarchitecture of tissues but also discrepancies in steroidogenic genes and hormone regulated enzyme activities in ovary.
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PMID:Effect of methotrexate and leucovorin on female reproductive tract of albino rats. 2121 37

A 74-year-old woman was admitted to our emergency room complaining of general weakness and anorexia that started 20 days earlier. She denied other underlying diseases that might have provoked chronic renal disease. Her serum creatinine was 12.35 mg/dL. A pelvic examination and computed tomography revealed severe bilateral hydroureteronephrosis with marked cortical thinning induced by total uterine prolapse. She was started on emergency hemodialysis due to her uremic symptoms and severe metabolic acidosis. Despite Foley catheter insertion and manual reduction of uterus for 1 month, renal function was not recovered. The department of gynecology was strongly opposed to performing a procedure to reverse the hydroureteronephrosis due to the irreversibility of her renal function. She is undergoing chronic maintenance hemodialysis. This is a case report of rare end-stage renal disease (ESRD) caused by obstructive uropathy due to pelvic organ prolapse (POP). We should consider POP as a cause of ESRD.
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PMID:Obstructive uropathy by total uterine prolapse leading to end-stage renal disease. 2255 23


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