Relevant bibliographies by topics / Polycystic ovarian syndrome

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Academic literature on the topic 'Polycystic ovarian syndrome'

Author: Grafiati
Published: 4 June 2021
Last updated: 28 January 2023

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Journal articles on the topic "Polycystic ovarian syndrome"

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Gursu, Turkan, Halime Cevik, Güldeniz Aksan Desteli, Birnur Yilmaz, Tevfik Berk Bildaci, and Alper Eraslan. "Diagnostic value of shear wave velocity in polycystic ovarian syndrome." Journal of Ultrasonography 21, no. 87 (November 29, 2021): 277–81. http://dx.doi.org/10.15557/jou.2021.0047.

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Aim: In polycystic ovarian syndrome, the ovaries become stiffer due to chronic anovulation. We aimed to compare tissue elasticity in terms of shear wave velocities measured using acoustic radiation force impulse imaging technique between the ovaries of polycystic ovarian syndrome women and non-polycystic ovarian syndrome women. Material and methods: The study was designed as a retrospective data analysis of women who underwent transvaginal ultrasound and acoustic radiation force impulse imaging in a university hospital between July 2014 and March 2015, for various reasons. There were 32 polycystic ovarian syndrome patients and 32 patients without a diagnosis of polycystic ovarian syndrome. Age, body mass index, fasting glucose levels, cycle day 3 follicle stimulating hormone, luteinizing hormone, thyroid stimulating hormone, prolactin, antimullerian hormone levels, and menstrual patterns with clinical hyperandrogenism were evaluated. On the menstrual cycle days 2–4, by performing a transvaginal ultrasound scan, the ovarian volumes and antral follicle counts in both ovaries were recorded for each woman. The ultrasound system was converted into the elastography mode, and acoustic radiation force impulse imaging was performed. Shear wave velocity (m/sec) was measured at least 5 times for each ovary, and the mean value was calculated for each polycystic ovarian syndrome and non-polycystic ovarian syndrome woman. Results: Age, body mass index, fasting glucose levels, cycle day 3 follicle stimulating hormone, luteinizing hormone, thyroid stimulating hormone, and prolactin levels were similar between the groups (p >0,05). Antimullerian hormone levels, antral follicle counts, and mean ovarian volumes were statistically different between the groups (p <0,05). Mean shear wave velocity values for both ovaries were 2.12 ± 0.82 (0.78–4.9) m/sec in the polycystic ovarian syndrome group, and 1.18 ± 0.41 (0.77–2.0) m/sec in the non-polycystic ovarian syndrome group, which was statistically significantly different (p = 0.016). Conclusion: In our study, we found significantly higher shear wave velocity levels in polycystic ovarian syndrome women than non-polycystic ovarian syndrome women, which indicates an impact of the condition on shear wave velocity. The increased acoustic frequencies cause a decreased response in time to transition, and motion becomes out of phase; in other words, scattered waves are faster in stiffer ovaries. Our results are thus compatible with the pathophysiology of the disease. Shear wave velocity is a beneficial tool for evaluating ovarian elasticity in polycystic ovarian syndrome patients in whom the levels are found to be significantly higher than non-polycystic ovarian syndrome women. In light of these findings, shear wave velocity is expected to be slower than polycystic ovarian syndrome levels in ovulatory women.
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Jeengar, Pooja, and Madhubala Chauhan. "Association of metabolic syndrome in polycystic ovarian syndrome." New Indian Journal of OBGYN 3, no. 2 (January 2017): 90–94. http://dx.doi.org/10.21276/obgyn.2017.3.2.5.

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Alcalay, M., D. Bider, S. Lipitz, S. Mashiach, D. Levran, and J. Dor. "Polycystic ovarian syndrome." Gynecological Endocrinology 9, no. 2 (January 1995): 119–23. http://dx.doi.org/10.3109/09513599509160200.

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Madnani, Nina, Kaleem Khan, Phulrenu Chauhan, and Girish Parmar. "Polycystic ovarian syndrome." Indian Journal of Dermatology, Venereology, and Leprology 79, no. 3 (2013): 310. http://dx.doi.org/10.4103/0378-6323.110759.

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SHUKAR-UD-DIN, SHAZIA, SADAF AHMED ASIM, SYEDA RABIA, Rumina Tabassum, and Aisha Razzaque. "POLYCYSTIC OVARIAN SYNDROME;." Professional Medical Journal 20, no. 05 (October 15, 2013): 719–25. http://dx.doi.org/10.29309/tpmj/2013.20.05.1208.

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Background: Polycystic ovarian syndrome is a common disease among the women in reproductive age group and morecommon in South Asian women. Clinical presentations include menstrual disorders, subfertility, obesity,hirsutism, acne vulgaris andacanthosis. Objectives: The objective of study was to investigate co relation between acne and polycystic ovaries and its relation tomenstrual irregularity. Methodology: A total of 56women were enrolled in the study from Outpatient Department of Obs&Gynae andDermatology, Dow University Hosptial, Ojha campus by convenient sampling. It was cross sectional study, conducted from July 2012 toNovember 2012.Verbal consent was taken. Sociodemographic information,Anthropometric measurement (height, weight, BMI) andacne severity with affected area, menstrual irregularities were administered on pre designed questionnaire.Pelvic ultrasound forpolycystic ovaries and serum LH, FSH in follicular phase of menstrual cycle (2nd day) advised from Dow Radiology and Dow Labrespectively. Results: A total of56 patients of PCOS were enrolled during five month period. The mean age of patient was 21.1+_SD0.994. Frequency of acne was 32 (57.1%).The mean BMI was 19.66 +_SD 4.54. Face was the commonest area involved in 24 (42.9%).menstrual irregularity was found in 50 (89.4%) women. There was no statistically significant relation seen between acne andoligomenorrhea. (X2 = 0.55 , P = 0.45). It was also determined that there was no co relation seen between the acne and serumtestosterone level calculated by independent sample t test.(P = 0.17) but statistically significant association seen between severity ofacne and serum LH/FSH ratio. (t test =3.28, p= 0.004) Conclusion: Acne was found in 32 (57.1%) women with PCOS. The study resultsrevealed a significant association seen between severity of acne and serum LH/FSH ratio. Relation between acne and serum testosteronelevel was statistically insignificant.
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BUTT, KIRAN, FARAH DEEBA, and HAVAIDA ATTIQUE. "POLYCYSTIC OVARIAN SYNDROME;." Professional Medical Journal 19, no. 06 (November 5, 2012): 786–88. http://dx.doi.org/10.29309/tpmj/2012.19.06.2483.

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Objective: The objective of the present study was to determine the changes in the glucose level and lipid profile in patients withpolycystic ovarian syndrome (PCOS). Study Design: Descriptive study. Place and Duration of the study: This study was conducted atInstitute of Molecular Biology and Biotechnology, The University of Lahore from June 2009 to June 2010. Patients and Methods: Total 50patients with PCOS were included and 50 age-matched control subjects were also selected for comparison. Their glucose levels and lipidprofile were assessed using commercial kits. The data thus obtained was subjected to statistical analysis. Results: Significant differences(P<0.05) in fasting blood glucose level and individual parameters of lipid profile were observed in women with PCOS. A higher prevalence ofhypertriglyceridemia, hypercholesterolemia, higher LDL, lower HDL and higher fasting blood glucose levels was explored in PCOS womenthan controls. Conclusions: Abnormal glucose level and lipid profile in PCOS women showed that these women are at an increased risk ofdeveloping diabetes and subsequently cardiovascular diseases.
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Yasin, Misbah, and Fouzia Yasmeen. "POLYCYSTIC OVARIAN SYNDROME." Professional Medical Journal 21, no. 01 (December 5, 2018): 179–84. http://dx.doi.org/10.29309/tpmj/2014.21.01.1918.

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Objectives: The objective of this study is to: describe the pattern of disease inpatients with polycystic ovarian syndrome. Data Source: Medline Data Base. Design Of Study:Descriptive case series study. Settings: Gynaecological Outpatient Department of Ghurki trustteaching hospital Lahore. Duration: 6months period, from 8th October 2012 to 7th April 2013.Materials & Methods: Sixty cases of polycystic ovarian syndrome as diagnosed on ultrasoundwere selected. These cases were examined for height, weight, body mass index, hirsutism, acne,acnthosis nigricans, breast examination (galactorrhoea). These cases were investigated forblood sugar (random), Fasting Insulin, pelvic ultrasound, LH, FSH and serum prolactin. Results:The mean age of the patients were 24.93±5.67 years. There were 28 (47%) patients of menstrualdisturbance, 18 (30%) patients of subfertility, 9 (13%) of obesity. There were 13 (21.7%) patients2of BMI level of equal to or less than 25 kg/m and 47 (78.3%) patients of BMI level more than 252kg/m . There were 25 (41.7%) patients of hirsuitim, 14 (23.3%) patients of acne and 17 (28.3%)patients of acanthoris nigricans on physical examination. There were 28 (46.7%) patients of LHlevel of more than 10 IU/L (raised) and 1 (1.7%) patient of more than 350 mU/L prolactin (raised).The mean right ovary volume of the patients was 12.08±3.04 and mean left ovarian volume of thepatients was 11.86±4.83. Conclusions: Hirsutism and cycle disturbances are the major clinicalfeatures of polycystic ovarian syndrome patients. Obesity seems to be more prevalent inpolycystic ovarian syndrome patients. The ratio between LH and FSH as a diagnostic tool waslow in our patients.
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Saleem, Shemaila, Fauzia Hanif, and Amanat Ali. "POLYCYSTIC OVARIAN SYNDROME;." Professional Medical Journal 24, no. 06 (June 5, 2017): 834–38. http://dx.doi.org/10.29309/tpmj/2017.24.06.1196.

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Background: Numerous ailments encompassing endometriosis, infertility andpolycystic ovarian syndrome (PCOS) are associated with Vitamin D deficiency. It is due to theexpression of vitamin D receptors in various tissues other than skeleton. Objectives: The currentstudy was conducted to compare the levels of vitamin D with body mass index in women withPCOS and healthy females of Rawalpindi. Study Design: Descriptive cross-sectional study.Period: 6 months. Setting: Research work was done at Railway Hospital (Gynecology andObstetrics Department), Rawalpindi in alliance with Islamic International Medical College,Rawalpindi. Materials and methods: A sample of 50 apparently healthy women and 100cases of polycystic ovarian syndrome in their reproductive age (15-45 years) were selectedafter diagnosis by the clinician. Data was assembled by using a pre-structured questionnaire.Data analysis was carried out using SPSS version 21. Results: Our results show that the bodymass index in patients with polycystic ovarian syndrome (27.094+4.369) was considerably(p-value < 0.05) more in contrast to the healthy controls (20.739+3.452) but no significant(p-value >0.05) difference was observed between vitamin D levels across a range of Bodymass indices among the controls and cases. Conclusion: No significant association betweenBMI and vitamin D status was found in healthy as well as PCO women.
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Harding, Emma. "Polycystic Ovarian Syndrome." InnovAiT: Education and inspiration for general practice 3, no. 2 (January 16, 2010): 71–75. http://dx.doi.org/10.1093/innovait/inp124.

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Abell, Sue, and John L. Ey. "Polycystic Ovarian Syndrome." Clinical Pediatrics 47, no. 9 (July 14, 2008): 969–70. http://dx.doi.org/10.1177/0009922807303932.

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Dissertations / Theses on the topic "Polycystic ovarian syndrome"

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Alzanati, Nadia. "Polycystic ovarian syndrome and adipose tissue : contribution of peripheral androgen synthesis to hyperandrogenism in polycystic ovarian syndrome." Thesis, University of Nottingham, 2017. http://eprints.nottingham.ac.uk/39390/.

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Background: Polycystic ovarian syndrome (PCOS) is the most common endocrine, reproductive, metabolic and psychological disorder in women of childbearing age, affecting 6-10% of premenopausal women. Hyperandrogenism is the most important biochemical feature of the syndrome, which is responsible for the clinical features of PCOS, and is frequently associated with metabolic disturbance, such as insulin resistance, dyslipidaemia, glucose intolerance and hypertension, regardless of the presence of obesity. In several studies, attention has focused on androgen as the main factor for development of metabolic disturbance, which observed in women with PCOS. The relationship between adipose tissue and the pathophysiology of PCOS, in terms of development of hyperandrogenism and its relation to development of insulin resistance with compensatory hyperinsulinemia still not fully understood. Based on epidemiological studies, the association between circulating androgen levels and insulin resistance, as well as central obesity is a direct correlation. Although ovaries and adrenal glands are the main sources of androgens, adipose tissue is also one of the most important peripheral tissues involved in the production of androgens. Adipose tissue is not just an organ with energy storage; it also has endocrine, paracrine and autocrine functions, due to secretion of active peptides, known as adipokines, and hormones, such as androgens. In order to understand the role of adipose tissue in the development of hyperandrogenism, we hypothesised that “Androgen metabolic pathways leading to testosterone production in subcutaneous adipose tissue are altered in women with PCOS.” The excess adipose tissue androgen synthesis plays an important role in PCOS pathogenesis. Aims: The main aim of this study was to analyse and compare the expression level of the two key enzymes in androgens synthesis, 17-α-hydroxylase/17.20-lyase (CYP17A1) and 17-β-hydroxysteroid dehydrogenase type 5 (AKR1C3) in adipose tissue of women with and without PCOS. These are responsible for locally synthesised sex steroid hormones, mainly androgens; CYP17A1 is responsible in the production of the precursors of androgens and AKR1C3 is responsible in the conversion of inactive androgen (androstenedione) to its active form, testosterone. In addition, to understand the mechanism of androgen production this study employed isolated pre-adipocytes cultures and in vitro differentiated to mature adipocytes with close regulation of the impact of insulin and LH as the most two hormones which have effect in sex steroid synthesis. In doing so, we investigated androgen synthesis by activation and expression of the main steroidogenic enzymes CYP17A1 and AKR1C3 in adipocytes of non-PCOS and PCOS women. This enabled us to study the difference in the CYP17A1 mRNA and AKR1C3 mRNA expression levels, as well as the concentration of testosterone secretion across non-PCOS and PCOS cultures. This also indicated the probability of a pathway leading to localised synthesis of adipocytes and to investigate if there is a role for PI3-K signaling pathway in insulin regulation of testosterone synthesis in peripheral adipose tissue of women with and without PCOS. Methods: In order to achieve these aims, subcutaneous adipose tissue samples (SC) were surgically obtained during gynecological surgery from women with and without PCOS. All participants were of reproductive age (20-45) with a BMI of 20-35kg/m2. Total RNA was isolated from frozen adipose tissue samples of non-PCOS (n=8) and PCOS (n=8) after matching, using Trizol reagent method, followed by reverse transcription. Quantitative RT-PCR was performed to determine the expression of a panel of reference genes (GAPDH, ACTB, and LPR10), and target genes (CYP17A1 and AKR1C3). Data were analysed with GenEx and compared using ΔΔCt method. AKR1C3 protein expression in non-PCOS (n=3) and PCOS (n=3) was measured and compared by using western blot (WB) technique. Pre-adipocytes were isolated from fresh adipose tissue samples by enzyme digestion (collagenase) method and in vitro differentiated to mature adipocytes, which were cultured in FCS-free medium, Recombinant insulin +/-LH+/-PI3-k inhibitor (LY294002) was added to the cell culture at different concentrations, in preparation for investigating any change in the expression of steroidogenic enzymes (CYP17A1, AKR1C3) by RT-PCR, after extraction of total RNA The supernatant was collected for testosterone measurement before and after treatment using enzyme-linked immunosorbent assay (ELISA). Results: Of the reference genes testes, GABDH, ACTB, and LRP10 were shown to be consistently expressed across the PCOS and non-PCOS women. The mean± SEM relative expression level of AKR1C3 mRNA in PCOS adipose tissue was 15.1± 2.0, which was significantly (P=0.0003) greater than that (3.3±1.1) of non-PCOS women. However, the expression level of CYP17A1 mRNA was not significantly (p=0.56) different between the two groups. AKR1C3 protein expression level was less expressed in PCOS and there was no significant (P > 0.05) difference in the protein expression between two groups. CYP17A1, AKR1C3 and testosterone were significantly higher in PCOS (n=5) versus the non-PCOS (n=5) in treated and un-treated cultures. Insulin did not alter CYP17A1 or AKR1C3 mRNA expression in PCOS group. In the non-PCOS, AKR1C3 significantly increased with gradual increase in insulin concentrations, 1nM/l (P=0.001), 10 nM/l (P=0.004), and 100 nM/l (P=0.0003). Insulin up regulates AKR1C3 mRNA expression (no treatment (0), 1, 10,100) (0.96±0.21) (1.59±0.84) (2.39±1.23) and (7.42±0.85) respectively. LH± insulin did not alter the expression of either of the enzymes in PCOS Insulin increased testosterone concentration in non-PCOS but not in the PCOS, testosterone concentration in the supernatant of untreated cultured PCOS (n=5) adipocytes (mean± SEM, 129.3±2.5 pg /ml) was significantly higher (P < 0.0001) than that (33.7±4.6 pg /ml) of non-PCOS (n=5) adipocytes. Insulin addition in different concentrations (1nM/l, 10nM/l, 100nM/l) resulted in a significant increase in testosterone concentrations (94.1±7.1; 118.2±18.2, 200.0±7.3 pg/ml, respectively) in the supernatant of cultured non-PCOS adipocytes, but not in the PCOS adipocytes (118.1±1.8, 90.5±6.4, 89.3±7.6 pg/ml, respectively). The increase of testosterone levels in the non-PCOS adipocyte culture supernatant followed a dose dependent fashion. The magnitude of increase in testosterone concentrations in non-PCOS adipocyte culture supernatant was markedly increased when LH was added to insulin. Adding PI3-K inhibitor (LY294002, 10ng/ml) to insulin did not change the magnitude of insulin effects on testosterone concentrations in non-PCOS adipocyte culture supernatant. Conclusion: The data obtained suggests that adipose tissue has the ability to produce its own steroid hormone after detection of the main key enzymes of androgen biosynthesis, and it revealed a 5-fold increase in the expression level of AKR1C3 mRNA in subcutaneous adipose tissue of PCOS women. It is therefore possible to postulate that peripheral adipose tissue plays an important role as a source of excess androgen production in women with PCOS. This could potentially pave the way for the development of innovative therapeutic targets for the management of this very common syndrome. In addition, we show a markedly higher CYP17A1, AKR1C3 and testosterone in peripheral adipose tissue of PCOS vs. non-PCOS women. This supports the hypothesis that peripheral adipose tissue plays an important role in the pathogenesis of hyperandrogenaemia and PCOS. Insulin and LH seem to play a role in the increased androgen synthesis in adipose tissue of PCOS women, but not through the PI3-K signaling pathway. PI3-K signaling pathway does not seem to be involved in insulin regulation of testosterone synthesis in peripheral adipose tissue of women with or without PCOS.
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Hudecova, Miriam. "Reproductive and Metabolic Consequences of the Polycystic Ovarian Syndrome." Doctoral thesis, Uppsala universitet, Institutionen för kvinnors och barns hälsa, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-123248.

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Polycystic ovary syndrome (PCOS) is a complex clinical condition characterized by hyperandrogenism and chronic oligo/anovulation. Infrequent ovulation and metabolic alterations in women with PCOS are associated with subfertility and probably increased miscarriage rates compared with normal fertile women. The overall risk of developing type 2 diabetes and impaired glucose tolerance (IGT) is three- to sevenfold higher in PCOS women, and the onset of glucose intolerance seems to occur at an earlier age than in healthy controls. Women with PCOS also have several risk factors for cardiovascular disease, although it is unclear whether they actually experience more cardiovascular events than other women. Very few studies assessing the long-term reproductive and metabolic consequences in older women with previously confirmed PCOS have been conducted. In this long-term follow-up of women with PCOS, 84 women with a diagnosis of PCOS between 1987 and 1995 and age at the follow-up > 35 years and an age-matched population-based group of control women participated. Data on reproductive outcome, ovarian reserve, endothelial function, insulin sensitivity and beta-cell function were collected. According to our results most women with PCOS had given birth and the rate of spontaneous pregnancies was relatively high. The rate of miscarriages was not increased in PCOS patients and the ultrasound findings together with increased levels of anti-müllerian hormone suggested that their ovarian reserve is superior to women of similar age. PCOS women displayed signs of endothelial dysfunction, but this was largely due to the increased prevalence of independent risk factors for cardiovascular disease such as increased BMI, triglycerides and blood pressures. IGT and type 2 diabetes occurred more often in PCOS women. Free androgen levels and beta-cell function decreased over time whereas insulin sensitivity remained unchanged. Obesity at young age and progressive weight-gain rendered them more prone to be insulin resistant at the follow-up. Beta-cell function was increased in PCOS women in comparison with control subjects but declined over time. Independent of PCOS phenotype at the index assessment and persistence of PCOS symptoms at the follow-up investigation, premenopausal women with PCOS had lower insulin sensitivity and increased beta cell function in comparison with control subjects. Conclusion: The long-term reproductive outcomes of PCOS are similar compared to women with normal ovaries. Although symptoms and androgen levels are normalized over time, women with PCOS continue to display reduced insulin sensitivity and increased beta-cell function and they also have an increased risk of IGT and type 2 diabetes.
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Marsden, Philippa Jane. "Insulin action and ovarian function in polycystic ovary syndrome." Thesis, University of Newcastle Upon Tyne, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.313272.

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Kilpatrick, Kaylon Ann. "Starvation induces Polycystic Ovarian Syndrome (PCOS) like symptoms in Drosophila melanogaster." Thesis, Mississippi College, 2016. http://pqdtopen.proquest.com/#viewpdf?dispub=10128977.

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Polycystic Ovarian Syndrome (PCOS) is a metabolic and endocrine disorder that is the most common cause of infertility. PCOS can manifest itself as a long and short term disability and is characterized by insulin resistance (IR), hyperandrogenism, anovulation, hyperinsulinaemia and polycystic ovaries. Our lack of understanding of this disorder and its long term effects has complicated the treatment of the disorder; yet, it is clear that PCOS involves the intricate interaction between genetics, environments and behaviors. To study this disease, scientists have used various animal models. Since the Drosophila model for PCOS has only been postulated,in this work, we determined whether starvation along with the addition of steroid hormones would induce a PCOS-like disorder in D. melanogaster after 24 hour exposure.

In women with PCOS, testosterone levels and the expression of the androgen receptor are elevated. In fruit flies, ecdysone (E) and its “active” form, 20-hydroxyecdysone (20E), are homologous to the human testosterone and 20-hydroxytestosterone, respectively. This hormone is required for circadian cycles, molting, and maturation in insects. More specifically, this hormone is also located in ovarian tissue and aids in follicular development. The receptor for ecdysone is the ecdysone receptor (EcR). In this work, we examined the expression of the ecdysone receptor (EcR) upon starvation for up to 24 hours by immunofluorescence microcopy. Using qRT-PCR, we determined the levels of expression of genes usually associated with inflammation. Ovarian dysfunction was examined by measuring the fecundity of the females. Starvation increases the expression of the EcR and pro-inflammatory gene expression and decreases fecundity, suggesting that Drosophila melanogaster is a potentially useful model organism in the study of PCOS.

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Desjardins, G. Clarissa (Gina Clarissa). "Role of the hypothalamic opioid system in estradiol-induced polycystic ovarian syndrome." Thesis, McGill University, 1992. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=41015.

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The intrahypothalamic distribution of mu, delta and kappa opioid receptor types was examined by in vitro radioautography using the opioid ligands $ sp{125}$I-FK-33 824, $ sp{125}$I-DTLET and $ sp{125}$I-DPDYN, respectively as selective markers. The density and distribution of these receptors in the hypothalamus of normal rats was then compared to that of rats injected with estradiol valerate in order to verify the location of the described increase in $ sp3$H-naloxone binding and to identify the specific opioid receptor type involved. Analysis of opioid receptor changes following long-term exposure to estradiol revealed that mu opioid binding densities were significantly increased in the medial preoptic area of EV-treated animals. Delta and kappa opioid binding densities were unchanged in the medial preoptic area although a slight decrease in delta sites was observed in the suprachiasmatic nucleus. Hypothalamic $ beta$-endorphin concentrations were concomitantly decreased in EV-treated animals, suggesting that observed increases in mu opioid binding were due to a compensatory up-regulation of receptors secondary to loss of $ beta$-endorphin input from the arcuate nucleus. To confirm this interpretation, mu opioid receptor binding was measured in the MPOA of animals treated with monosodium glutamate, which destroys the arcuate nucleus. Results indicated that mu opioid receptor binding densities were inversely proportional to hypothalamic $ beta$-endorphin concentrations in the same animals supporting the existence of a causal relationship between chronic reductions in hypothalamic $ beta$-endorphin concentrations and mu opioid receptor upregulation in the medial preoptic area.
To further document the decreased concentrations of $ beta$-endorphin in the hypothalamus of EV-treated animals, light microscopic immunocytochemistry for $ beta$-endorphin was performed in colchicine treated control and EV-injected rats. Eight weeks following EV treatment, a 60% decrease in the total number of $ beta$-endorphin-immunoreactive neurons was detected in the arcuate nucleus, while neuron numbers for nearby neuronal populations were unchanged. These results were confirmed in biochemical experiments demonstrating reduced hypothalamic $ beta$-endorphin concentrations in the absence of changes in neuropeptide-Y and met-enkephalin in EV-treated rats as compared to controls. Cell counts performed in Nissl-stained material using unbiased stereological methods revealed a reduction in the total number of neurons in the EV-treated group as compared to controls. Furthermore, the estimated number of neurons lost ($ sim$3500) corresponded precisely with the total number of $ beta$-endorphin neurons lost ($ sim$3600) as estimated using quantitative immunocytochemistry. Together, these findings strongly suggest that $ beta$-endorphin neurons are selectively destroyed following long-term exposure to estradiol. Results demonstrated that EV-treated animals co-treated with vitamin E displayed hypothalamic $ beta$-endorphin concentrations similar to controls. In addition, these animals maintained regular estrous cycles and displayed normal ovarian morphology. These findings suggest that estradiol-induced neurotoxicity of $ beta$-endorphin neurons involves the production of free radicals and further supports the notion that the loss of these neurons is important to the induction of chronic anovulation and polycystic ovaries resulting after EV treatment. (Abstract shortened by UMI.)
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Wang, Qi. "Chemerin and Prohibitin in the Regulation of Ovarian Follicular Development and their Potential Involvement in Polycystic Ovarian Syndrome." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/24098.

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Follicular growth and maturation are tightly regulated processes, which involve the participation of endocrine, autocrineparacrine factors and intracellular molecules. Due to the numerous research efforts, a large number of regulators and their mechanisms of regulation of follicular growth and differentiation have been established. Although the abnormal expression and activities of some of these regulators are believed to be associated with ovarian dysfunction diseases, such as polycystic ovarian syndrome (PCOS), the etiology and pathogenesis of this syndrome are not completely understood. In this thesis, we have identified two novel regulators of follicular growth and differentiation and examined the cellular and molecular mechanisms that contribute to the folliculogenesis. We present here that chemerin reduces FSH-induced steroidogenic enzyme expression and steroid hormone production in follicles and granulosa cells. Prohibitin expression is upregulated by chemerin and knockdown of prohibitin attenuates the suppressive role of chemerin on steroidogenesis, an action regulated by Akt. Using an androgenized rodent model, we also present the dysregulation of chemerin and prohibitin and their association with dysregulated follicular steroidogenesis. Our data and preliminary clinical studies demonstrate the potential involvement of chemerin and prohibitin in the etiology of PCOS. These studies significantly improve the knowledge of ovarian functions and the pathophysiology of PCOS, and provide important clues for the development of novel diagnosis biomarkers and new treatment strategies for this complex syndrome.
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Sprung, Victoria Spencer. "The impact of obesity and fitness on endothelial function in polycystic ovarian syndrome." Thesis, Liverpool John Moores University, 2012. http://researchonline.ljmu.ac.uk/6119/.

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Polycystic ovarian syndrome (PCOS) is a highly prevalent heterogeneous syndrome associated with abdominal obesity, insulin resistance and the metabolic syndrome. This clustering of risk factors could translate into an adverse cardiovascular disease (CVD) risk profile. Endothelial dysfunction, an early barometer of CVD, has been exhibited by women with PCOS; however, it remains unclear whether endothelial dysfunction is independent of CVD risk factors in this population. Exercise training has been found to enhance conduit artery and cutaneous microvessel endothelial function in various populations. Nevertheless, limited research exists regarding the cardiovascular effects of exercise in PCOS, and its impact on endothelial function in conduit arteries and cutaneous microvessels, has not been explored. The primary aim of this thesis was to examine nitric oxide (NO)-mediated endothelial function at different levels of the vascular tree in women with PCOS and to establish whether supervised exercise training induces a therapeutic effect on endothelial function. A systematic review of published studies comparing FMD in PCOS and control women was conducted. Twenty-one published studies were identified for inclusion (pCOS n=908; controls n=566). Differences in FMD between PCOS and controls were synthesised and meta-regressed against BMI and age. The pooled mean FMD was 3.5% lower (95% CI=3.4, 3.7%; P < 0.001) in women with PCOS compared with controls; and the PCOS-mediated reduction in FMD was most evident in studies involving less obese women. PCOS [n=35, 28y (95% CI=26, 30), 31kg/m2 (95% CI=27, 35)] and control women [n=16, 32y (95% CI=30, 35), 30kg/m2 (95% CI=25, 32)] were recruited. Brachial artery endothelial function was assessed using flow-mediated dilation (FMD). Internal adipose tissue (lAT), subcutaneous (SAT), visceral (VAT) and abdominal SAT was quantified using whole body magnetic resonance imaging and IH magnetic resonance spectroscopy quantified liver and skeletal muscle fat. Cardiorespiratory fitness, glycaemic control, reproductive hormone and lipid profiles were also assessed. FMD was impaired in PCOS when compared with control women [-4.5% (95% CI=-6.3, -2.8), P < O.OOl]. When FMD was adjusted for individual differences in IAT [-4.3% (95% CI=-6.l, -2.4), P < O.OOl], VAT [-4.4% (95% CI=-6.3, -2.5), P < O.OOl] and insulin resistance [-3.9% (95% CI=-5.6, -2.1), P < O.OO 1], the difference in FMD between groups remained. Ten women with PCOS [27y (95% CI=23, 32), 31 kg/rrr' (95% CI=28, 34)] completed a 16-week supervised exercise programme while 7 women with PCOS [29y (95% CI=24, 35), 35kg/m2 (95%CI=31, 40)] opted for conventional care and followed simple lifestyle advice. Exercise training improved FMD to a greater degree than conventional care [3.4% (95% CI=1.8, 5.1), P > 0.0005] and in parallel greater improvements in cardiorespiratory fitness were observed with exercise [4.7ml/kg/min (95% CI=1.4, 7.9), P=0.005]. These changes with exercise occurred independently of changes in VAT, SAT or insulin resistance. NO-mediated vasodilation in the cutaneous microvessels was examined in 11 PCOS [29y (95% CI=25, 34), 34kg/m2 (95% CI=30, 38)] and 6 control women [29y (95% CI=21, 37), 34kg/m2 (95% CI=28, 39)] using laser Doppler flowmetry combined with intra-dermal microdialysis of L-NG-monomethyl arginine to assay the NO dilator system in response to incremental local heating of the forearm. Six women with PCOS [30y (95% CI=22, 37), 31kg/m2 (95% CI=25, 37)] then undertook a 16-week exercise-training programme. Nitric oxide contribution was attenuated in women with PCOS at peak heating [-16.0CVCmax (95% CI=-32.5, 0.6), P=0.05] and during prolonged maximal heating [-15.4CVCmax (95% CI=- 29.6, -1.3), P=0.04], compared with control women. Cardiorespiratory fitness improved by 5.0ml/kg/min (95% CI=0.9, 9.2) following exercise training (P=0.03). This was accompanied by increased NO contribution to cutaneous blood flow between 36.5-42°C (P < 0.05), at peak heating [19.6CVCmax (95% CI=4.3, 34.9), P=0.02] and during prolonged maximal heating [17.1CVCmax (95% CI=2.2, 32.2), P=0.03]. The findings from this thesis suggest that endothelial dysfunction is an intrinsic characteristic of PCOS and that supervised exercise training enhances endothelial function in both conduit vessels and cutaneous microvessels, independent of adiposity or traditional CVD risk factors. The direct impact of exercise training on the vasculature of women with PCOS may decrease the risk of CVD morbidities, such as hypertension, and consequently reduce cardiovascular mortality in post-menopausal years.
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El, Mahdi E. "Studies to investigate a possible association between Polycystic Ovary Syndrome and Epithelial Ovarian Cancer." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1397057/.

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Polycystic ovarian syndrome (PCOS) is one of the most common endocrine disorders, affecting 5 % to 10 % of women of reproductive age. The Syndrome is associated with Type II diabetes and endometrial carcinoma but an association with epithelial ovarian cancer has also been suggested. The studies described in this thesis were designed to investigate this association at population, cellular and molecular levels. In the first study, a cross sectional questionnaire survey was conducted of 121 women aged between the ages of 20 and 40, with or without PCOS. Analysis of the replies from 52 women with PCOS and 82 controls, showed that women with PCOS were significantly more likely to give a positive family history of breast cancer and myocardial infarction (20% vs 5%, p<0.05 and 35% vs 15%, p, 0.05, respectively). The second study was performed on 102 formalin fixed, paraffin embedded ovarian biopsies. In this study the surface epithelium of PCOS ovaries was compared with controls. The results showed significant epithelial changes in the PCOS group, with a higher prevalence of Psammoma bodies and mitoses (p< 0.01 and p < 0.02, respectively). Expression of cell cycle and apoptotic (p53, Cyclin D, Ki67 and bcl2) proteins in the ovarian surface epithelium was assessed using immunohistochemistry in 15 PCOS subjects and 15 controls. P53 expression was significantly (p= 0.003) increased in the PCOS women compared with controls. The third project was performed to identify gene expression in ovaries from women with PCOS, ovarian cancer and healthy controls (three ovaries from each group were utilized). 34(2%) genes consistently varied in abundance between normal and PCOS samples, 12 genes were over expressed in PCOS and 22 under expressed. One of the over expressed genes identified is human alpha 2 smooth muscle actin. It was 15 fold higher in PCOS ovary, than in normal ovary p< 0.001. Conclusions: the results of these studies do not provide convincing evidence of a correlation between PCOS and ovarian cancer.
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Al-Mizyen, Ebtisam S. S. "Unilateral versus bilateral laparoscopic ovarian diathermy in the management of infertile women with clomiphene citrate resistant polycystic ovarian syndrome." Thesis, Queen Mary, University of London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.538365.

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Konecki, Angela. "A Retrospective Analysis of the Effect Weight Loss and Metformin use in Polycystic Ovarian Syndrome." The University of Arizona, 2006. http://hdl.handle.net/10150/624469.

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Class of 2006 Abstract
Objectives: To determine if Polycystic Ovarian Syndrome (PCOS) patients treated with lifestyle changes and metformin resulted in ovulation after six months of treatment. Methods: A retrospective chart review of initial patient visits at an infertility clinic were obtained. Patients that were given a diagnosis of PCOS were further reviewed for age at initial diagnosis, weight, height, ovarian cysts, lifestyle recommendations (diet, exercise, and vitamin use), metformin recommendations and usage, and if ovulation occurred after six months of treatment. Results: A total of 1011 charts were reviewed. At the initial office visit, 206 (20.38%) of these patients were classified as having PCOS. Of PCOS patients, 113 (54.85%) patients ovulated after six months of treatment. In the average initial weight, ovulators averaged slightly less weight than did non-ovulators (171.77 pounds ± 44.26 vs. 188.65 pounds ± 51.37, p=0.0121). This also follows true for the initial BMI of ovulators vs. non-ovulators (29.53 kg/m2 ± 10.14 vs. 32.69 kg/m2 ± 13.03, p=0.0521). There was a significant difference in metformin use between ovulators and non-ovulators (90.27% vs. 73.12%, p=0.0024). More ovulators were found to continue metformin treatment as compared to non-ovulators. Conclusions: In this specific infertility clinic setting, 20.3% of patients were diagnosed with PCOS at the initial office visit. Of these PCOS patients, treatment with lifestyle changes and metformin use resulted in 55% of patients achieving ovulation at six months. This study shows that weight loss, through lifestyle modification and metformin treatment, increases this population’s chances of ovulation within six months of therapy.
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Books on the topic "Polycystic ovarian syndrome"

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Polycystic ovarian syndrome: An enigmatic endrocrinological disorder. New York: Nova Biomedical Books, 2011.

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Diamanti-Kandarakis, Evanthia, John E. Nestler, Dimitrios Panidis, and Renato Pasquali, eds. Insulin Resistance and Polycystic Ovarian Syndrome. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-310-3.

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Evanthia, Diamanti-Kandarkis, ed. Insulin resistance and polycystic ovarian syndrome: Pathogenesis, evaluation, and treatment. Totowa, N.J: Humana Press, 2007.

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Samra, J. S. Endocrine and metabolic studies in patients with polycystic ovarian syndrome. Birmingham: University of Birmingham, 1992.

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Futterweit, Walter. A patient's guide to PCOS: Understanding and reversing polycystic ovarian syndrome. Edited by Ryan George. New York: Henry Holt, 2006.

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Parker, James N., and Philip M. Parker. Polycystic ovarian syndrome: A medical dictionary, bibliography, and annotated research guide to Internet references. San Diego, CA: ICON Health, 2004.

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Humphrey, Katie. Freedom from PCOS: 3 proven steps to naturally overcome polycystic ovarian syndrome and insulin resistance. [S.l.]: K. Humphrey, 2010.

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FRACOG, Kovacs Gabor MRCOG, and Norman Robert, eds. Polycystic ovary syndrome. 2nd ed. Cambridge: Cambridge University Press, 2007.

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Y, Boutaleb, and Gzouli A, eds. The treatment of endometriosis--and other disorders and infections. Carnforth, Lancs, UK: Parthenon Pub. Group, 1991.

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Elsheikh, Mohgah. Polycystic ovary syndrome. Oxford: Oxford University Press, 2008.

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Book chapters on the topic "Polycystic ovarian syndrome"

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Annamalai, Aniyizhai. "Polycystic Ovarian Syndrome." In Medical Management of Psychotropic Side Effects, 287–88. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-51026-2_46.

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Hernandez, M. Isabel, and Verónica Mericq. "Polycystic Ovarian Syndrome." In Brook's Clinical Pediatric Endocrinology, 559–70. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444316728.ch21.

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De Nicola, Ana Luisa Alencar, and Harley De Nicola. "Polycystic Ovarian Syndrome." In Atlas of Imaging in Infertility, 11–18. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-13893-0_2.

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Pal, Lubna, and Shefali Pathy. "Polycystic ovarian syndrome." In Evidence-based Obstetrics and Gynecology, 117–29. Chichester, UK: John Wiley & Sons, Ltd, 2018. http://dx.doi.org/10.1002/9781119072980.ch12.

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Al-Salem, Ahmed H. "Polycystic Ovarian Syndrome." In Pediatric Gynecology, 253–74. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-49984-6_14.

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Shoupe, Donna. "Polycystic Ovarian Syndrome." In Management of Common Problems in Obstetrics and Gynecology, 411–15. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444323030.ch93.

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Shukla, Alpana, and Lindsay Mandel. "Polycystic Ovarian Syndrome." In Obesity Management, 31–40. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-030-01039-3_4.

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Wierman, Margaret E. "Polycystic Ovarian Syndrome." In 2016 Meet-The-Professor: Endocrine Case Management, 306–9. 2055 L Street, NW, Suite 600, Washington, DC 20036: The Endocrine Society, 2016. http://dx.doi.org/10.1210/mtp5.9781943550043.ch57.

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Mason, Helen D., Nafi Dilaver, and Suman Rice. "Ovarian Dysfunction in Polycystic Ovary Syndrome." In Polycystic Ovary Syndrome, 53–70. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8394-6_4.

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Fauser, Bart C. J. M., Frank J. Broekmans, Joop S. E. Laven, Nick S. Macklon, and Basil Tarlatzis. "Polycystic Ovary Syndrome." In Insulin Resistance and Polycystic Ovarian Syndrome, 287–96. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-310-3_21.

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Conference papers on the topic "Polycystic ovarian syndrome"

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Madhumitha, J., M. Kalaiyarasi, and S. Sakthiya Ram. "Automated Polycystic Ovarian Syndrome Identification with Follicle Recognition." In 2021 3rd International Conference on Signal Processing and Communication (ICPSC). IEEE, 2021. http://dx.doi.org/10.1109/icspc51351.2021.9451720.

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Tanwar, Akanksha, Anima Jain, and Anamika Chauhan. "Accessible Polycystic Ovarian Syndrome Diagnosis Using Machine Learning." In 2022 3rd International Conference for Emerging Technology (INCET). IEEE, 2022. http://dx.doi.org/10.1109/incet54531.2022.9824049.

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Mehrotra, Palak, Chandan Chakraborty, Biswanath Ghoshdastidar, Sudarshan Ghoshdastidar, and Kakoli Ghoshdastidar. "Automated ovarian follicle recognition for Polycystic Ovary Syndrome." In 2011 IEEE International Conference on Image Information Processing (ICIIP). IEEE, 2011. http://dx.doi.org/10.1109/iciip.2011.6108968.

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Nandalike, Kiran, CHHAVI Agarwal, SUSAN Coupey, Sanghun Sin, and Raanan Arens. "Polysomnographic Findings In Adolescent Girls With Polycystic Ovarian Syndrome." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2430.

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Deshpande, Sharvari S., and Asmita Wakankar. "Automated detection of Polycystic Ovarian Syndrome using follicle recognition." In 2014 International Conference on Advanced Communication, Control and Computing Technologies (ICACCCT). IEEE, 2014. http://dx.doi.org/10.1109/icaccct.2014.7019318.

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Rathod, Yash, Aryan Komare, Ruchita Ajgaonkar, Shruti Chindarkar, Gajanan Nagare, Neelam Punjabi, and Yogesh Karpate. "Predictive Analysis of Polycystic Ovarian Syndrome using CatBoost Algorithm." In 2022 IEEE Region 10 Symposium (TENSYMP). IEEE, 2022. http://dx.doi.org/10.1109/tensymp54529.2022.9864439.

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Soni, Palvi, and Sheveta Vashisht. "Exploration on Polycystic Ovarian Syndrome and Data Mining Techniques." In 2018 3rd International Conference on Communication and Electronics Systems (ICCES). IEEE, 2018. http://dx.doi.org/10.1109/cesys.2018.8724087.

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Soomro, Mehak, and Ather Akhlaq. "Impact of Cyberchondriasis on Polycystic Ovarian Syndrome Patients Searching Health Information Online." In DH'18: International Digital Health Conference. New York, NY, USA: ACM, 2018. http://dx.doi.org/10.1145/3194658.3194685.

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Harris, Holly R., Kara L. Cushing-Haugen, Sara Lindström, and Kathryn L. Terry. "Abstract DP-007: POLYCYSTIC OVARY SYNDROME AND OVARIAN CANCER RISK: A MENDELIAN RANDOMIZATION ANALYSIS." In Abstracts: 12th Biennial Ovarian Cancer Research Symposium; September 13-15, 2018; Seattle, Washington. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1557-3265.ovcasymp18-dp-007.

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Alotaibi, M., and A. Alsinan. "A mobile Polycystic ovarian syndrome management and awareness system for Gulf countries: System architecture." In 2016 SAI Computing Conference (SAI). IEEE, 2016. http://dx.doi.org/10.1109/sai.2016.7556124.

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Reports on the topic "Polycystic ovarian syndrome"

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Liang, Xingyan, Yu Su, Chunli Lu, and Hongxia Ma. Chinese herbal medicine combined with acupuncture for women with polycystic ovarian syndrome. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2021. http://dx.doi.org/10.37766/inplasy2021.8.0048.

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Glintborg, Dorte, Naja Due Kolster, Pernille Ravn, and Marianne Skovsager Andersen. Prospective risk of type 2 diabetes in normal weight women with polycystic ovary syndrome. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2022. http://dx.doi.org/10.37766/inplasy2022.6.0070.

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Review question / Objective: To investigate the risk for type 2 diabetes (T2D) in normal weight women with PCOS. The following PECOs (Population, Exposure, Comparator and Outcome) were included: Population: Pre- and postmenopausal women. Exposure: PCOS Comparator: Healthy control or background population. Outcome: T2D. Condition being studied: Polycystic ovary syndrome (PCOS) is a common endocrine disorder of reproductive-aged women with a prevalence of 15–20%. Polycystic ovary syndrome (PCOS) is most often defined according to the Rotterdam criteria, which include irregular ovulation, biochemical/clinical hyperandrogenism, and/or polycystic ovaries when other causes are excluded.
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