Formation Of Follicular Cysts Research Articles

Association of Metabolic and Endocrine Disorders with Bovine Ovarian Follicular Cysts.

After estrus, when mature follicles fail to ovulate, they may further develop to form follicular cysts, affecting the normal function of ovaries, reducing the reproductive efficiency of dairy cows and causing economic losses to cattle farms. However, the key points of ovarian follicular cysts pathogenesis remain largely unclear. The purpose of the current research was to analyze the formation mechanism of ovarian follicular cysts from hormone and gene expression profiles. The concentrations of progesterone (P4), estradiol (E2), insulin, insulin-like growth factor 1 (IGF1), leptin, adrenocorticotropic hormone (ACTH) and ghrelin in follicle fluid from bovine follicular cysts and normal follicles were examined using enzyme-linked immunosorbent assay (ELISA) or 125I-labeled radioimmunoassay (RIA); the corresponding receptors' expression of theca interna cells was tested via quantitative reverse transcription polymerase chain reaction (RT-qPCR), and the mRNA expression profiling was analyzed via RNA sequencing (RNA-seq). The results showed that the follicular cysts were characterized by significant lower E2, insulin, IGF1 and leptin levels but elevated ACTH and ghrelin levels compared with normal follicles (p < 0.05). The mRNA expressions of corresponding receptors, PGR, ESR1, ESR2, IGF1R, LEPR, IGFBP6 and GHSR, were similarly altered significantly (p < 0.05). RNA-seq identified 2514 differential expressed genes between normal follicles and follicular cysts. The Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis linked the ovarian steroidogenesis pathway, especially the STAR, 3β-HSD, CYP11A1 and CYP17A1 genes, to the formation of follicular cysts (p < 0.01). These results indicated that hormone metabolic disorders and abnormal expression levels of hormone synthesis pathway genes are associated with the formation of bovine ovarian follicular cysts.

The Use of hCG for Inducing Ovulation in Sheep Estrus Synchronization Impairs Ovulatory Follicle Growth and Fertility.

Simple SummaryThe present study, in view of the importance of finding an alternative hormone to eCG, aims to determine the response of sheep to hCG-based treatments. The findings indicate that the low fertility rates reported for protocols based on the administration of hCG for inducing ovulation during estrus synchronization in sheep may be related to a high occurrence of abnormal follicular growth patterns, disturbances, and retardments of ovulation and concomitant formation of follicular cysts in the treated females. These results preclude their practical application to induce ovulation concomitantly to estrous synchronization treatments.Currently, there is an intense effort to find an alternative hormone to eCG to induce ovulation after estrus synchronization treatments in sheep. One of the proposed alternatives is based on the use of hCG, but the results are controversial since fertility rates are commonly affected. The present study aims to evaluate, therefore, the adequacy of hCG in protocols for the synchronization of estrus and ovulation. Ovarian follicle dynamics, occurrence of estrus behavior and subsequent ovulation, quality of corpora lutea, and pregnancy rate after controlled natural mating were assessed in two consecutive trials. The findings indicate that the low fertility rates reported for the protocols based on the administration of hCG for inducing ovulation during estrus synchronization in sheep may be related to a high occurrence of abnormal follicular growth patterns, disturbances, and retardments of ovulation and concomitant formation of follicular cysts in the treated females. These results preclude their practical application to induce ovulation concomitantly to estrous synchronization treatments.

Association of RBP-4 gene polymorphisms with follicular cysts in large white sows.

Follicular cysts, which is a common infertility disease, can cause financial losses in pig breeding programmes. The pathogenesis and mechanisms of the formation of follicular cysts are not understood clearly. In our previous study, the concentration of retinol-binding protein 4 (RBP-4) in the follicular fluid (FF) of the ovary with follicular cysts was found to be significantly higher than that of normal ovary, thereby suggesting that RBP-4 may be a candidate biomarker for porcine follicular cysts. To study the association of RBP-4 and follicular cysts further, we detected the polymorphisms of the RBP-4 gene and the presence of follicular cysts by PCR-Restriction fragment length polymorphism (RFLP) assay. In this study, we screened the mutations of RBP-4 gene in 79 sows with follicular cysts and 100 normal sows without cysts. Results showed that +249-63G>C polymorphisms were significantly associated with follicular cysts, and sows with CC genotype in RBP-4 gene had a high risk of developing follicular cysts. Hence, our findings further proved that RBP-4 may be a novel biomarker for follicular cysts, which may be valuable for the diagnosis of follicular cysts and molecular breeding of pigs.

Association of gene polymorphisms of estrogen receptor, follicle-stimulating hormone β and leptin with follicular cysts in Large White sows

Ovarian follicular cysts are one of leading causes of infertility and financial loss in pig breeding program. This study was carried out to investigate the association between polymorphisms of estrogen receptor (ESR), follicle-stimulating hormone (FSH) β, and leptin genes and follicular cysts in sows. A total of 47 and 120 sows with follicular cysts and normal follicles, respectively, were selected to evaluate whether these candidate loci affect the formation of follicular cysts in sows. The polymorphisms of ESR, FSHβ, FSHβ/HaeIII and leptin genes were tested by PCR and PCR-RFLP methods. Cyst–normal case data analysis showed that ESR/PvuII polymorphisms are highly associated with follicular cysts and that sows ESR/PvuII genotype have lower rate of suffering from cysts (P = 0.021). Unfortunately, FSHβ, FSHβ/HaeIII, and leptin C3469T polymorphisms were found no significant difference in follicular cysts sows and normal sows. These results suggest that FSHβ, FSHβ/HaeIII, and leptin C3469T genotypes are not able to effect the presence of follicular cysts (P > 0.05). In addition, the haplotype EBCM and EBTM within four loci of genes had significant dominance effect on follicular cysts (P < 0.05). The detection of ESR/PvuII polymorphisms and haplotype EBCM and EBTM can positively improve the development of biological biomarkers, which is thereby beneficial in breeding and ovary-protective therapy of reproductive disease in pigs.

Modeling of functional ovarian cysts by introducing a follicle-stimulating hormone

Aim. To study the morphofunctional state of ovaries after the introduction of recombinant FSH. Materials and methods. Two groups of mature female Wistar rats were used in the study. The experimental group consisted of 35 rats with a model of follicular ovarian cysts, while 25 rats were in the control group. Rats were taken out of the experiment on days 3, 7, 15, 30 and 60. Paraffin slides of ovaries were stained with hematoxylin and eosin by Van Gieson. Histological and morphometric investigations were performed. Results. On day 7 of FSH administration, the maximum increase in the size of the ovaries was observed due to the formation of single-cell follicular cysts. Rats in the experimental group showed a marked decrease in the number of growing follicles on day 7 and 15. The increase in atretic bodies and follicles in comparison with the control group was observed on day 7 and lasted until the end of the experiment. Additionally, on day 7 of the experiment, hyperemia and vasoconstriction were noted. The number of yellow bodies decreased during the experiment, and an increase in collagen formation occurred starting from day 15 of the experiment. Conclusion. The introduction of follicle-stimulating hormone for 7 days leads to disruption of folliculogenesis, strengthening of atresia in the ovaries, and the formation of functional cysts.

Factors of angiogenesis in the development of physiological and pathological processes of the female gonads

The literature review focuses on the role of various growth factors in the developing vasculature of the ovary. Vascularization plays an important role in physiological processes such as development and atresia of a follicle, the formation of the yellow body and the pathological: ovarian hyperstimulation syndrome, the formation of follicular cysts, the development of cystic ovaries, endometriosis, dysfunctional uterine bleeding. The main angiogenic factor identified vascular endothelial growth factor, participates independently and through the mediating factors in baryogenesis, which plays an important role in endothelial cell differentiation and development of vascular pattern, stimulating endothelial proliferation, migration and survival of extravascular cells of the ovary. Angiogenic activity in the ovary is also under the control of other growth factors: fibroblast growth factor, epidermal growth factor, platelet growth factor, insulin-like growth factor-1 and cytokines such as tumor necrotic factor, interleukins, components of the extracellular matrix (laminin, fibronectin) and their receptors (integrins), matrix metalloproteinases and their tissue inhibitors and regulators, proteases (plasminogen, activators urokinase and urokinase tissue type), as well as hypoxia, hypoglycemia and stress. Presents different points of view on the problem of vasculogenesis in the female gonad, as well as directions for future fundamental and practical research.

ACTH administration during formation of preovulatory follicles impairs steroidogenesis and angiogenesis in association with ovulation failure in lactating cows

Ovulation failure, follicular persistence, and formation of follicular cysts are known to impair dairy cow fertility. Although the underlying mechanism is not entirely clear, stress-induced alteration in adrenal hormone secretion can cause these ovarian pathologies. Six synchronized lactating cows were scanned daily by ultrasound, and plasma samples were taken throughout the estrous cycle. Treatment cows (n = 3) were administered with ACTH analog every 12 h from day 15 to day 21 of the cycle to induce formation of follicular cysts. Ovaries were collected at the slaughterhouse on day 23 of the cycle before appearance of follicular pathologies. Control cows (n = 3) were administered placebo, resynchronized, and administered PGF2α on day 6 of the new cycle to induce development of a preovulatory follicle. Follicular fluid was aspirated from the preovulatory follicles of each group to determine their steroid milieu. Slices were taken from the follicular wall for total messenger (m) RNA isolation and semiquantitative reverse transcription polymerase chain reaction (RT-PCR). Administration of ACTH increased (P < 0.02) plasma cortisol concentration and reduced (P < 0.01) milk production. Androstenedione and estradiol concentrations in the follicular fluids were lower (P < 0.05) in ACTH-treated follicles than those in controls. The mRNA expression of luteinizing hormone receptor, 3β-hydroxysteroid dehydrogenase, cytochrome P450 aromatase (P450arom), and cytochrome P450 17α-hydroxylase (P450c17) were lower (P < 0.02) in the ACTH-treated vs control cows. On the other hand, the expression of steroidogenic acute regulatory protein and cytochrome P450 side-chain cleavage did not differ between groups. In addition, mRNA expression of vascular endothelial growth factor (VEGF)120 and VEGF164 was higher (P < 0.01) in control than in ACTH-treated follicles, but that for angiopoietin-1 and 2 did not differ between groups. Findings indicated that ACTH administration throughout preovulatory follicle development alters follicular steroidogenesis in association with impaired angiogenesis. Such alterations might explain, in part, the mechanism underlying ovulation failure and the formation of persistent or cystic follicles under stress.

Prevalence, etiology, diagnosis, treatment and complications of supernumerary teeth.

The aim of this article was to review the literature on supernumerary teeth, analyzing their prevalence, etiology, diagnosis, treatment and possible complications. An electronic search was made in the Pubmed-Medline database up to January 2014 using the key search terms “multiple supernumerary teeth” (n=279), “prevalence supernumerary teeth” (n=361), and “supernumerary teeth” (n=2412). In addition to the articles initially identified, others were included in the review proceeding from a manual search and from any references considered of relevance. Supernumerary teeth are those that exceed the normal dental formula. They are more common in men, more common in the upper maxilla, and more prevalent in permanent dentition. Complications associated with supernumerary teeth include dental impaction, delayed eruption, ectopic eruption, overcrowding, spacing anomalies and the formation of follicular cysts. The treatment of supernumerary teeth depends on their type, position, and possible complications, detected clinically and radiographically. No clear consensus exists as to the best time to extract unerupted supernumerary teeth. Key words:Hyperdoncia, supernumerary teeth, impacted teeth, treatment, permanent teeth, deciduous teeth.

Динаміка морфогенезу і функціонального розвитку алотрансплантата оваріальної тканини щурів

We examined the dynamics of folliculogenesis in ovarian tissue allograft and its endocrine function in an organism of castrated recipient rats during 100 days. Growth and development of ovarian tissue and its steroidogenic function in heterotopic transplantation were determined by its initial morphological organization. Allotransplantation of mature ovarian tissue was found to cause preservation of its morphological structure, whereas the transplantation of neonatal ovarian tissue caused formation of follicular cysts. At 100th day of observation, we observed a recovery of the levels of sex hormones to the physiological norm after transplantation of both mature ovarian tissue and neonatal tissue of 10-days of postnatal development.

Alteration in localization of steroid hormone receptors and coregulatory proteins in follicles from cows with induced ovarian follicular cysts

Cystic ovarian disease (COD) is an important cause of infertility in cattle. The altered follicular dynamics and cellular differentiation observed in COD may be mediated through a disruption of the expression of steroid receptors and their associated transcriptional cofactors. The aim of this study was to determine the protein expression profiles of ESR1, ESR2, PGR, AR, NCOA3, NCOR2, and PHB2 (REA) in ovarian follicles in an experimental model of COD induced by the administration of ACTH. Ovaries were collected and follicles were dissected from heifers during the follicular phase (control) or from heifers treated with ACTH to induce the formation of ovarian follicular cysts. Ovaries were fixed, sectioned, and stained immunohistochemically for steroid receptors and the associated transcription factors. The relative expression of ESR1 was similar in follicular cysts and in tertiary follicles from both control and cystic cows and was significantly higher than in secondary follicles. The expression of ESR2 in the granulosa was higher in cystic follicles. No differences were seen for PGR. The expression of androgen receptor was significantly increased in tertiary follicles with lower immunostaining in cysts. The expression of NCOA3 was observed in the granulosa and theca with a significantly increased expression in the theca interna of cystic follicles. The highest levels of NCOR2 expression in granulosa, theca interna, and theca externa were observed in cysts. In granulosa cells, NCOR2 levels increase progressively as follicles mature and the treatment had no effect. In summary, ovaries from animals with induced COD exhibited altered steroid receptor expression compared with normal animals, as well as changes in the expression of their regulators. It is reasonable to suggest that in conditions characterized by altered ovulation and follicular persistence, such as COD, changes in the intra-ovarian expression of these proteins could play a role in their pathogenesis.

Systemic inflammation, cellular influx and up-regulation of ovarian VCAM-1 expression in a mouse model of polycystic ovary syndrome (PCOS)

PCOS, a major cause of anovulatory sterility, is associated with obesity, insulin resistance and chronic inflammation. New evidence suggests that the immune system aggravates the clinical features of PCOS. Our aim was to study the immune, metabolic and endocrine features of a mouse model of PCOS elicited by androgenisation using dehydroepiandrosterone (DHEA). We observed a significant weight gain and insulin resistance in DHEA-androgenised mice, coupled with the formation of ovarian follicular cysts. DHEA up-regulated the expression of vascular cell adhesion molecule (VCAM)-1 and intercellular adhesion molecule (ICAM)-1 in the granulosa cell layer of the majority of cysts, and VCAM-1 expression in the theca cell layer of all follicles and cysts. The expression of these markers was low in control tissue. Peritoneal cells from PCOS-mice showed enhanced production of inflammatory cytokines, suggesting an association between chronic inflammation and PCOS. In addition, DHEA-androgenisation induced the activation of CD4(+) cells both in vivo and in vitro, and their expression of the respective ligands for VCAM-1 and ICAM-1, VLA-4 and LFA-1, as assessed in vitro. CD4(+) cells were present in androgenised ovaries, especially in the granulosa cell layer of cysts with high VCAM-1 expression. Herein, we present novel evidence that the immune system is activated systemically and locally in a mouse model for PCOS. We propose that VCAM-1 is involved in aggravating PCOS symptoms by promoting leukocyte recruitment to the ovaries and perpetuating local inflammation. These findings offer novel therapeutic opportunities for PCOS, such as blockage of VCAM-1 expression.

Induction of secretory leukocyte protease inhibitor (SLPI) in estradiol valerate (EV) induced polycystic ovary

The excessive administration of estradiol valerate induces polycystic ovary syndrome by formation of follicular cysts. Secretory leukocyte protease inhibitor (SLPI) promotes wound healing by decreasing the excessive inflammatory response, stimulating keratinocyte proliferation and increasing collagen deposition through the inhibition of protease activity. In this study, SLPI expression was high in the ovarian stroma, corpus luteum, unilaminar primary follicle, multilaminar primary follicle and granulose layer of the antral follicle in polycystic ovary (PCO) compared to the normal ovary. SLPI was expressed strongly in the theca around the cyst in PCO compared to the mature follicle in the normal ovary. The levels of SLPI mRNA and protein expression were higher in PCO than in the normal ovary, and the level of MMP-2 expression was lower in PCO. These results showed that the formation of a cyst was initiated from a multilaminar primary follicle and SLPI expression was increased depending on the morphological changes in the follicle and ovarian stroma. Therefore, an increase in SLPI may be related to the suppression of tissue disruption, and act as a protease inhibitor in PCO, suggesting that SLPI increases independently of the estrogen concentration in pathological tissues.

Biochemical and hormonal composition of follicular cysts in water buffalo ( Bubalus bubalis)

The objective of this study was to examine the follicular fluid biochemical and hormonal changes associated with ovarian follicular cysts in buffalo. Follicular fluid was aspirated from eight cysts and eight preovulatory follicles, and subjected to biochemical and hormonal analyses. Cysts were characterized by a greater ( P < 0.01) concentration of nitric oxide and lesser concentrations of ascorbic acid and glucose than that of preovulatory follicles ( P < 0.01 and P < 0.05, respectively). Furthermore, follicular cysts had greater concentrations of progesterone ( P < 0.001), triiodothyronine (T 3) and cortisol ( P < 0.05) and lesser concentrations of insulin ( P < 0.001) than preovulatory follicles. The results indicate follicular cysts in buffalo have an altered biochemical and hormonal composition. The alterations include increases in nitric oxide, progesterone, cortisol and T 3 concentrations with a concurrent reduction in ascorbic acid, insulin and glucose concentrations. The study suggests that greater progesterone concentrations possibly inhibit the onset of LH surge resulting in formation of follicular cysts in buffalo. In addition, it implies the plausible role of intra-ovarian regulators such as nitric oxide, ascorbic acid and insulin in development of the condition.

Clinical management of supernumerary teeth: A report of two cases

Supernumerary tooth may closely resemble the teeth of the group to which it belongs, i.e. molars, premolars or anterior teeth, or it may bear little resemblance in size or shape to which it is associated. Many complications can be associated with supernumeraries, like impaction, delayed eruption or ectopic eruption of adjacent teeth, crowding, development of median diastema and eruption into floor of the nasal cavity. This may also cause the formation of follicular cysts with significant bone destruction. Early intervention to remove it is usually required to obtain reasonable alignment and occlusal relationship. This article will present the clinical management of an (i) impacted supernumerary tooth impeding the eruption of maxillary central incisor and (ii) erupted supernumerary tooth with midline diastema.

Exogenous androstenedione induces formation of follicular cysts and premature luteinization of granulosa cells in the ovary

To investigate the effects of androstenedione on ovarian follicle development. Experimental study. University research laboratory. Female Wistar-Imamichi rats and BDF1 mice. Rats were injected with androstenedione. Ovarian follicles of mice were cultured in the presence of androstenedione. Ovarian morphology; ovarian cell types undergoing apoptosis; ovarian expression of cytochrome P450 aromatase (P450arom), cytochrome P450 side-chain cleavage (P450scc), and cyclin-dependent kinase inhibitor p27(kip1); serum levels of T, E(2), and P in rats; and ultrastructure of granulosa cells from cultured follicles of mice. In androstenedione-treated rat ovaries, follicular cysts were formed, and apoptotic cells were found in the inner part of granulosa cell layers of antral follicles. Androstenedione administration down-regulated expression of P450arom but up-regulated expression of P450scc and p27(Kip1) in the granulosa cells of antral follicles. Serum T levels were significantly increased in androstenedione-treated rats. In mouse follicles exposed to androstenedione, the granulosa cells contained abundant lipid droplets and mitochondria with complex tubular cristae. Excess androgen enhances apoptosis in the inner part of granulosa cell layers of antral follicles, resulting in the formation of follicular cysts. It is also demonstrated that androgen stimulates premature luteinization of granulosa cells.

Locus Coeruleus Mediates Cold Stress-Induced Polycystic Ovary in Rats

Previous reports about the rat ovary have shown that cold stress promotes ovarian morphological alterations related to a polycystic ovary (PCO) condition through activation of the ovarian sympathetic nerves. Because the noradrenergic nucleus locus coeruleus (LC) is activated by cold stress and synaptically connected to the preganglionic cell bodies of the ovarian sympathetic pathway, this study aimed to evaluate the LC's role in cold stress-induced PCO in rats. Ovarian morphology and endocrine and sympathetic functions were evaluated after 8 wk of chronic intermittent cold stress (4 C, 3 h/d) in rats with or without LC lesion. The effect of acute and chronic cold stress upon the LC neuron activity was confirmed by Fos protein expression in tyrosine hydroxylase-immunoreactive neurons. Cold stress induced the formation of follicular cysts, type III follicles, and follicles with hyperthecosis alongside increased plasma estradiol and testosterone levels, irregular estrous cyclicity, and reduced ovulation. Considering estradiol release in vitro, cold stress potentiated the ovarian response to human chorionic gonadotropin. Ovarian norepinephrine (NE) was not altered after 8 wk of stress. However, LC lesion reduced NE activity in the ovary of cold-stressed rats, but not in controls, and prevented all the cold stress effects evaluated. Cold stress increased the number of Fos/tyrosine hydroxylase-immunoreactive neurons in the LC, but this effect was more pronounced for acute stress as compared with chronic stress. These results show that cold stress promotes PCO in rats, which apparently depends on ovarian NE activity that, under this condition, is regulated by the noradrenergic nucleus LC.

Toxic Mother's Milk

Wan et al . created tissue-specific knockout mice deficient in peroxisome proliferator-activated receptor γ (PPARγ), which is a transcription factor regulated by fatty acids, some prostaglandins, and components of oxidized low-density lipoprotein particles and which regulates lipid biosynthesis. The mice were deficient in PPARγ in the hematopoietic and endothelial tissues. Pups nursed from mothers deficient in PPARγ exhibited growth retardation and hair loss that was completely reversed after the pups were weaned. Furthermore, pups deficient in PPARγ fostered by a wild-type mother did not exhibit these abnormalities, and wild-type pups fostered with the PPARγ-deficient mothers exhibited hair loss and low weight until weaning, confirming that the problem was maternal. Investigation of the skin of the pups nursed by the PPARγ-deficient mothers showed the formation of follicular cysts, which appeared to result from an inflammatory response that was characterized by leukocyte infiltration, elevated expression, and abundance of inflammatory cytokines and cyclooxygenase (COX-1 and COX-2). Hair loss was partially prevented if the pups were treated with aspirin, a COX inhibitor. Inflammation was also noted in the livers of the pups nursed by the PPARγ-deficient mothers. Histological analysis of the mammary tissue of the PPARγ-deficient mice showed increased lipid accumulation. Transcription analysis revealed that the PPARγ-deficient mammary glands exhibited decreased expression of homeobox genes and matrix metalloproteinases involved in mammary gland development. The expression of genes encoding two lipid oxidation enzymes that are involved in the production of inflammatory lipids was elevated in the mutant mice. When a mouse macrophage cell line was exposed to milk from the PPARγ-deficient mice in the presence of lipoprotein lipase, which is involved in lipid digestion, the cells increased production of inflammatory mediators. Furthermore, the skin from the mouse pups fed by the PPARγ-deficient mice exhibited an altered lipid profile compared with pups fed by wild-type mice, and mass analysis suggested that one group of lipids present in the skin of pups fed by the PPARγ-deficient mice was oxidized free fatty acids. Investigation of the gene expression of the macrophages from the mutant mice, which do not express PPARγ in the macrophages but do in the epithelial cells and adipocytes in the mammary gland, revealed that the macrophages had elevated expression of genes encoding enzymes that produce PPAΡγ ligands. The authors propose that these ligands activated PPARγ in the epithelial and adipocyte tissue of the mammary gland, leading to excessive production of inflammatory lipids. Y. Wan, A. Saghatelian, L.-W. Chong, C.-L. Zhang, B. F. Cravatt, R. M. Evans, Maternal PPARγ protects nursing neonates by suppressing the production of inflammatory milk. Genes Dev. 21 , 1895-1908 (2007). [Abstract] [Full Text]

Unusual case of double acute intoxication with tamoxifen complicated by miscarriage

Abstract Background: A 24-year-old female had attempted suicide twice, at the age of 20 and 24, using tamoxifen. Case report: Subsequent to the first acute intoxication a development of bilateral ovarian cysts was observed. Cysts regressed spontaneously within 8 weeks. Five weeks after the second suicidal attempt, pregnant patient (15 weeks of gestation) was admitted to the hospital with vaginal bleeding and suspicion of miscarriage. The autopsy of the fetus did not reveal any gross abnormalities, whereas the microscopic examination demonstrated numerous foci of necrosis in the placental decidua. Other fetal membranes as well as the umbilical cord were normal. Conclusions:1.Acute intoxication with tamoxifen may be connected with the formation of follicular ovarian cysts.2.During pregnancy, intoxication with tamoxifen, may result in delayed miscarriage.

Formation of Follicular Cysts in Cattle and Therapeutic Effects of Controlled Internal Drug Release

Follicular cysts in cattle result from excessive growth of the dominant follicle without ovulation and still constitute a major reproductive disorder in this species. One key hormonal characteristic of cows with follicular cysts is the lack of an LH surge, although they have increased plasma estradiol concentrations. Another is a relatively high level of pulsatile secretion of LH that promotes continued growth of the dominant follicle. These LH characteristics seem to result from a functional abnormality in the feedback regulation of LH secretion by estradiol. Treatment with controlled internal drug release devices that increase circulating progesterone levels is effective in resolving follicular cystic conditions by 1) lowering pulsatile LH secretion and 2) restoring the ability of the hypothalamo-pituitary axis to generate an LH surge in response to an increase in circulating estradiol.

Effects of tamoxifen and soluble tumor-associated antigens on ovarian structure in mammary tumor-bearing rats

Previously, we showed that the 66 and 51 kDa soluble tumor-associated antigens (sTAAs) have distinct suppressive effects on chemically induced mammary cancer in rats, both alone and in combination with the hormone-related anticancer drug tamoxifen. Here, we describe the effects of both sTAA and tamoxifen on the histological structure of ovaries in mammary tumor-bearing 30- to 34-week-old rats. Central ovary sections were pooled, the number of the healthy and degenerated follicles were counted, and the size of the corpora lutea was estimated. In follicular development primordial, primary, preantral and antral stages were recognized. Only healthy follicles with visible nuclei were counted. Follicular degeneration was estimated as the number of atretic follicles with follicular remnants. Treatment with tamoxifen alone or in combination with sTAA significantly increased the number of primordial follicles and atretic follicles in the ovaries, and promoted the formation of small follicular cysts. Total area of the corpora lutea decreased. sTAA participated in this process by increasing apoptosis in degenerated follicles.