Reprod Sci. 2010 Nov;17(11):987-94. Epub 2010 Aug 18.

Estrogen induces distinct patterns of microRNA expression within the mouse uterus.

Nothnick WB, Healy C.

Department of Obstetrics and Gynecology, University of Kansas Medical Center, Kansas City, KS, USA.

Control of estrogenic activity within the uterus is evident as unopposed estrogen action is associated with endometrial pathologies such as endometriosis and endometrial carcinoma. MicroRNAs (miRNAs) have emerged as important posttranscriptional regulators, which are postulated to fine-tune the actions of steroids in many systems including the uterus. The objective of the current study was to examine uterine expression of miRNAs in response to estrogen treatment within the mouse uterus using an ovariectomized, steroid-reconstituted mouse model. MicroRNA microarray analysis and subsequent quantitative real-time reverse transcriptase polymerase chain reaction (qRT-PCR) verification revealed that expression of mirn155, mirn429, and mirn451 was significantly increased by estrogen administration whereas mirn181b and mirn204 expression was significantly reduced. Pretreatment with the estrogen receptor (ER) antagonist ICI 182,780 confirmed that estrogen regulation was mediated via the classical ER pathway. This study demonstrates that estrogen regulates specific miRNAs within the murine uterus, which may participate in posttranscriptional regulation of estrogen-regulated genes.

Hum Reprod. 2010 Oct;25(10):2475-9. Epub 2010 Aug 18.

Decreased pregnancy rate is linked to abnormal uterine peristalsis caused by intramural fibroids.

Yoshino O, Hayashi T, Osuga Y, Orisaka M, Asada H, Okuda S, Hori M, Furuya M, Onuki H, Sadoshima Y, Hiroi H, Fujiwara T, Kotsuji F, Yoshimura Y, Nishii O, Taketani Y.

Department of Obstetrics and Gynecology, University of Tokyo, Tokyo 113-8655, Japan.

BACKGROUND: The relationship between fibroids and infertility remains an unsolved question, and management of intramural fibroids is controversial. During the implantation phase, uterine peristalsis is dramatically reduced, which is thought to facilitate embryo implantation. Our aims were to evaluate (i) the occurrence and frequency of uterine peristalsis in infertile women with intramural fibroids and (ii) whether the presence of uterine peristalsis decreases the pregnancy rate.

METHODS: Ninety-five infertile patients with uterine fibroids were examined using magnetic resonance imaging (MRI). Inclusion criteria were as follows: (i) presence of intramural fibroids, excluding submucosal type; (ii) no other significant infertility factors (excluding endometriosis); and (iii) regular menstrual cycles, and MRI performed at the time of implantation (luteal phase day 5-9). The frequency of junctional zone movement was evaluated using cine-mode-display MRI. After MRI, patients underwent infertility treatment for up to 4 months, and the pregnancy rate was evaluated prospectively.

RESULTS: Fifty-one patients fulfilled the inclusion criteria, and 29 (57%) and 22 (43%) patients were assigned to the low (0 or 1 time/3 min) or high frequency (≥ 2 times/3 min) uterine peristalsis group, respectively. Endometriosis incidence was the same in both groups. Ten out of the 29 patients (34%) in the low-frequency group achieved pregnancy, compared with none of the 22 patients (0%) in the high-frequency group (P< 0.005). Comparing pregnant and non-pregnant cases, 4 of 10 patients (40%) and 9 of 41 patients (22%), respectively, had endometriosis (not significant).

CONCLUSIONS: A higher frequency of uterine peristalsis during the mid-luteal phase might be one of the causes of infertility associated with intramural-type fibroids.

Fertil Steril. 2010 Aug 16. [Epub ahead of print]

Progesterone receptor gene polymorphisms and risk of endometriosis: results from an international collaborative effort.

Near AM, Wu AH, Templeman C, Van Den Berg DJ, Doherty JA, Rossing MA, Goode EL, Cunningham JM, Vierkant RA, Fridley BL, Chenevix-Trench G, Webb PM; the Australian Cancer Study (Ovarian Cancer) (ACS).,; the Australian Ovarian Cancer Study Group (AOCS).,, Kjær SK, Hogdall E, Gayther SA, Ramus SJ, Menon U, Gentry-Maharaj A, Schildkraut JM, Moorman PG, Palmieri RT, Ness RB, Moysich K, Cramer DW, Terry KL, Vitonis AF, Pike MC, Berchuck A, Pearce CL; on behalf of the Ovarian Cancer Association Consortium.

Cancer Control Program, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, D.C.

OBJECTIVE: To investigate the association between self-reported endometriosis and the putative functional promoter +331C/T single nucleotide polymorphism and the PROGINS allele.

DESIGN: Control subjects from ovarian cancer case-control studies participating in the international Ovarian Cancer Association Consortium. The majority of controls are drawn from population-based studies.

SETTING: An international ovarian cancer consortium including studies from Australia, Europe, and the United States.

PATIENT(S): Five thousand eight hundred twelve white female controls, of whom 348 had endometriosis, from eight ovarian cancer case-control studies.


MAIN OUTCOME MEASURE(S): Genotypes for the +331C/T single nucleotide polymorphism and PROGINS allele and a history of endometriosis.

RESULT(S): The occurrence of endometriosis was reduced in women carrying one or more copies of the +331 T allele (odds ratio = 0.65; 95% confidence interval: 0.43-0.98), whereas there was no association between the PROGINS allele and endometriosis (odds ratio = 0.94, 95% confidence interval 0.76-1.16).

CONCLUSION(S): Additional studies of the +331C/T variant are warranted given the current finding and the equivocal results of previous studies. The +331 T allele has been shown to result in a reduced progesterone (P) receptor A to P receptor B ratio, and if the observed association with endometriosis is confirmed it would suggest that this ratio is important for this disease.

Copyright © 2010 American Society for Reproductive Medicine. Published by Elsevier Inc. All rights reserved.

Placenta. 2010 Oct;31(10):839-47. Epub 2010 Aug 15.

Wnt signalling in implantation, decidualisation and placental differentiation–review.

Sonderegger S, Pollheimer J, Knöfler M.

Prince Henry’s Institute of Medical Research, Clayton, Victoria, Australia.

The family of secreted Wingless ligands plays major roles in embryonic development, stem cell maintenance, differentiation and tissue homeostasis. Accumulating evidence suggests that the canonical Wnt pathway involving nuclear recruitment of β-catenin and activation of Wnt-dependent transcription factors is also critically involved in development and differentiation of the diverse reproductive tissues. Here, we summarise our present knowledge about expression, regulation and function of Wnt ligands and their frizzled receptors in murine and human endometrial and placental cell types. In mice, Wnt signalling promotes early trophoblast lineage development, blastocyst activation, implantation and chorion-allantois fusion. Moreover, different Wnt ligands play essential roles in the development of the murine uterine tract, in cycling endometrial cells and during decidualisation. In humans, estrogen-dependent endometrial cell proliferation, decidualisation, trophoblast attachment and invasion were shown to be controlled by the particular signalling pathway. Failures in Wnt signalling are associated with infertility, endometriosis, endometrial cancer and gestational diseases such as complete mole placentae and choriocarcinomas. However, our present knowledge is still scarce due to the complexity of the Wnt network involving numerous ligands, receptors and non-canonical pathways. Hence, much remains to be learned about the role of different Wnt signalling cascades in reproductive cell types and their changes under pathological conditions.

Copyright © 2010 Elsevier Ltd. All rights reserved.

Hum Reprod. 2010 Oct;25(10):2480-8. Epub 2010 Aug 16.

Silencing of cofilin-1 gene attenuates biological behaviours of stromal cells derived from eutopic endometria of women with endometriosis.

Xu YL, Wang DB, Liu QF, Chen YH, Yang Z.

Department of Obstetrics and Gynaecology, Shengjing Hospital, China Medical University, 36 Sanhao Street, Shenyang 110004, China.

BACKGROUND: Eutopic endometria with endometriosis (EMs) differ dramatically from normal endometria, physiologically and biochemically, yet the pathogenesis of EMs remains unclear. Cofilin-1 (CFL1), a critical modulator of the actin cystoskeleton, is associated with tumour progression, cell motility, cell adhesion, cell invasion and angiogenesis. Although eutopic endometria with EMs exhibit many malignant-like behaviours and a higher expression of CFL1 than normal endometria, the effects of CFL1 on the pathogenesis of EMs are unknown. The aim of this study was to explore the role of CFL1 expression in proliferation, apoptosis, adhesion, invasion, angiogenesis and ultrastructure of endometrial cells.

METHODS: We isolated and cultured stromal cells derived from the eutopic endometria of 30 patients with advanced ovarian EMs (ESCs, Stromal Cells of eutopic endometria in Endometriosis patients) and 30 control patients without EMs (NSCs, Stromal Cells of eutopic endometria in Non-endometriosis patients), and evaluated their proliferation, apoptosis, adhesion, invasion and expression of markers of adhesion, invasion and angiogenesis in vitro. In addition, these functions were examined after short hairpin RNA (shRNA) was used to silence the CFL1 gene in ESCs, and pEGFP-N1-CFL recombinant plasmid was transiently transfected into NSCs to up-regulate CFL1 expression.

RESULTS: Under basal conditions, CFL1 mRNA and protein were overexpressed in ESCs. Proliferation, adhesion, invasion and markers of adhesion, invasion and angiogenesis were enhanced in ESCs compared with NSCs; in contrast, the apoptosis rate was lower in ESCs than in NSCs. Silencing the CFL1 gene in ESCs markedly attenuated proliferation, adhesion, invasion and expression of the markers, but enhanced apoptosis. Conversely, up-regulation of CFL1 in NSCs increased proliferation, adhesion, invasion and expression of the markers but reduced apoptosis.

CONCLUSIONS: The overexpression of CFL1 in ESCs is associated with enhanced proliferation, adhesion, invasion and angiogenesis and reduced apoptosis in EMs. These malignant-like behaviours of ESCs in EMs can be attenuated by inducing CFL1 gene silencing with shRNA interference.

Pathol Int. 2010 Sep;60(9):636-41.

Endometrioid adenocarcinoma of the vagina with a microglandular pattern arising from endometriosis after hysterectomy.

Nomoto K, Hori T, Kiya C, Fukuoka J, Nakashima A, Hidaka T, Saito S, Mikami Y, Tsuneyama K, Takano Y.

Department of Diagnostic Pathology, Graduate School of Medicine and Pharmaceutical Science, Toyama, University of Toyama, Toyama City, Toyama 930-0194, Japan.

Primary endometrioid adenocarcinoma rarely occurs in the vagina. Occasionally, endometrioid adenocarcinoma has a microglandular pattern. Herein, a case of primary endometrioid adenocarcinoma of the vagina with a microglandular pattern arising from pre-existing endometriosis long after a hysterectomy, is described. A 57-year-old postmenopausal woman developed a vaginal discharge over one decade after undergoing a hysterectomy. Microscopic examination of the vaginal smear and a biopsy specimen demonstrated an atypical glandular proliferation composed of columnar cells with occasional intracytoplasmic mucin and bland nuclear morphology, showing microcysts and numerous neutrophils within and around cysts. Immunohistochemically, the neoplastic cells were diffusely positive for CK7, MUC1, ER, and PR, and focally positive for vimentin, CEA, CK5/6, p63, p16(INK4a), and p53. A portion of residual endometrioid adenocarcinoma was identified adjacent to foci of endometriosis in the vaginectomy specimen. The patient has done well without evidence of recurrent disease for 1 year after surgery. Pathologists are encouraged to be aware of the occurrence of endometrioid adenocarcinoma associated with endometriosis in the vaginal stump after hysterectomy, and microglandular morphology which might be a source of misinterpretation.

Gynecol Endocrinol. 2010 Aug 16. [Epub ahead of print]

New insights into the pathophysiology of endometriosis: from chronic inflammation to danger signal.

Kajihara H, Yamada Y, Kanayama S, Furukawa N, Noguchi T, Haruta S, Yoshida S, Sado T, Oi H, Kobayashi H.

Department of Obstetrics and Gynecology, Nara Medical University, Nara, Japan.

Background. Various theories try to explain the development and progression of endometriosis, however, no single theory can explain all aspects of this disorder. Gene expression profiling studies might reveal factors that explain variability in disease development and progression, which can serve as specific biomarkers for endometriosis and novel drug development. We have recently showed that the upregulated genes were predominantly clustered in stress and detoxification, providing a mechanistic explanation for the oxidative stress and chronic inflammatory response in endometriosis. Objective. This review aims: (1) to analyse the published data, with the aim of identifying pathways consistently regulated by the endometriosis genotype and (2) to summarise the findings of specific genes, which are involved in the process of oxidative stress and inflammation. Methods. We identified gene array and proteomics studies whose data were accessible in PubMed. Results. A major finding is the increased expressions of several markers including heat shock protein, S100, fibronectin, and neutrophil elastase, which might be involved in the process of Toll-like receptor (TLR)-dependent sterile inflammation. The study reviews a convergence in the main pathogenic process, where the TLR-mediated inflammation occurs possibly through the endogenous ligands. Conclusions. In conclusion, a circulus vitiosus of both the oxidative stress pathway and the TLR pathways is generated when the process becomes chronic (danger signal spiral).

Curr Opin Obstet Gynecol. 2010 Oct;22(5):375-80.

Female sexual dysfunction and adolescents.

Greydanus DE, Matytsina L.

Pediatrics & Human Development, Michigan State University College of Human Medicine, MSU/Kalamazoo Center for Medical Studies, 1000 Oakland Drive, Kalamazoo, MI 49008-1284, USA.

PURPOSE OF REVIEW: To review recent publications in the area of sexual dysfunction in females including the adolescent age group.

RECENT FINDINGS: Though as many as 40% of adult females have a sexual dysfunction, the incidence among adolescent females is unknown. Though over half of adolescents are sexually active, sexual dysfunction is not a term universally accepted among the general public as well as researchers. Research on sexual dysfunction in females typically starts with age 18 years or over. Causes of sexual dysfunction include medical disorders, gynecological problems, which started from the adolescent age, psychiatric disorders, and complications of medications such as selective serotonin reuptake inhibitors (SSRIs), antipsychotics, and others. Management includes identification of the specific sexual dysfunction and treatment of the underlying condition, including surgical treatment in such cases as absent vagina or obstetrics fistula. Psychological therapy is helpful when psychological factors are contributory to the dysfunction. Pharmacologic principles of management cases can, for example, include treatment of gynecological problems such as pelvic inflammatory disease (PID) or endometriosis as a cause of sexual dysfunction or include removal of the offending drug, use of glutamatergic strategies or trazodone in SSRI-association dysfunction, and addition of bupropion or other medications in select cases. No medication is FDA-approved for sexual dysfunction in females.

SUMMARY: Sexual dysfunction in females includes lack of sexual desire, sexual pain disorders (as dyspareunia), anorgasmia, and sexual arousal dysfunction. Acceptance of the high incidence of sexual dysfunction in all female populations is necessary to appreciate this phenomenon in the adolescent cohort, because some gynecological disease can arise from the adolescent age and can cause sexual dysfunction. Some sexual dysfunctions require immediate treatment, including surgical in the case of congenital anomaly, ovarian cyst, or tumor. Current understanding is based on extrapolation of research in the adult population. Management principles include removal of offending drugs and treatment of underlying disorders. Research in the adolescent population is recommended for more understanding and acceptance of this phenomenon in this age group.

Clin Nucl Med. 2010 Sep;35(9):722-3.

Inflammatory pseudotumor of the lung with high FDG uptake.

Huellner MW, Schwizer B, Burger I, Fengels I, Schläpfer R, Bussmann C, Strobel K.

Department of Nuclear Medicine and Radiology, Cantonal Hospital Lucerne, Lucerne, Switzerland.

We present the case of a 23-year-old woman with 2 episodes of hemoptysis. Computed tomography showed a small mass lesion with an adjacent cyst in the left lower lobe. On whole-body fluorodeoxyglucose positron emission tomography/computed tomography, the lesion had a high focal fluorodeoxyglucose-uptake (SUVmax 21.0). Differential diagnosis included tuberculosis, fungal infection, and tumors such as bronchial carcinoma, sarcoma, or rare entities like endometriosis. Bronchoscopy with transbronchial biopsies failed to deliver a conclusive diagnosis. Lobectomy was performed, and histopathology presented an inflammatory myofibroblastic pseudotumor.

J Clin Endocrinol Metab. 2010 Aug 11. [Epub ahead of print]

Altered Retinoid Uptake and Action Contributes to Cell Survival in Endometriosis.

Pavone ME, Reierstad S, Sun H, Milad M, Bulun SE, Cheng YH.

Divisions of Reproductive Biology Research (M.E.P., S.R., S.E.B., Y.-H.C.) and Reproductive Endocrinology and Infertility (M.E.P., M.M., S.E.B.), Department of Obstetrics and Gynecology, Feinberg School of Medicine at Northwestern University, Chicago, Illinois 60611; Department of Physiology (H.S.) and Jules Stein Eye Institute (H.S.), David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, California 90095; and Brain Research Institute (H.S.), University of California Los Angeles, Los Angeles, California 90095.

Context: Retinoic acid (RA) controls multiple biological processes via exerting opposing effects on cell survival. Retinol uptake into cells is controlled by stimulated by RA 6 (STRA6). RA is then produced from retinol in the cytosol. Partitioning of RA between the nuclear receptors RA receptor alpha and peroxisome-proliferator-activated receptor beta/delta is regulated by cytosol-to-nuclear shuttling proteins cellular RA binding protein 2 (CRABP2) and fatty acid binding protein 5 (FABP5), which induce apoptosis or enhance survival, respectively. The roles of these mechanisms in endometrium or endometriosis remain unknown. Objective: The aim was to determine the regulation of retinoid uptake and RA action in primary stromal cells from endometrium (n = 10) or endometriosis (n = 10). Results: Progesterone receptor was necessary for high STRA6 and CRABP2 expression in endometrial stromal cells. STRA6, which was responsible for labeled retinoid uptake, was strikingly lower in endometriotic cells compared to endometrial cells. CRABP2 knockdown in endometrial cells increased survival, and FABP5 knockdown in endometriotic cells decreased survival without altering the expression of downstream nuclear retinoic acid receptor alpha and peroxisome-proliferator-activated receptor beta/delta. Conclusions: In endometrial stromal cells, progesterone receptor up-regulates expression of STRA6 and CRABP2, which control retinol uptake and growth-suppressor actions of RA. In endometriotic stromal cells, decreased expression of these genes leads to decreased retinol uptake and dominant FABP5-mediated prosurvival activity.

J Obstet Gynaecol. 2010;30(6):642.

An unusual case of post-traumatic endometriosis involving the sciatic nerve in the right greater sciatic notch.

Shetty A, Fishwick KT, Rambani R, Acharya S.

Department of Gynaecology, Dewsbury District Hospital, Dewsbury, West Yorkshire, UK.

Reprod Sci. 2010 Nov;17(11):995-1005. Epub 2010 Aug 9.

Promoter hypermethylation of progesterone receptor isoform B (PR-B) in adenomyosis and its rectification by a histone deacetylase inhibitor and a demethylation agent.

Jichan Nie, Xishi Liu, Guo SW.

Shanghai OB/GYN Hospital, Shanghai Medical College, Fudan University, Shanghai, China.

Adenomyosis is a fairly common gynecologic disease with unknown pathogenesis. We sought to investigate as to whether the promoter of progesterone receptor isoform B (PR-B) is hypermethylated in adenomyosis and to investigate the treatment of ectopic endometrial stromal cells with trichostatin A (TSA), a histone deacetylase inhibitor (HDI), and 5-aza-2-deoxycytidine (ADC), a demethylation agent, on PR-B gene and protein expression, and on cell viability. Ectopic endometrial tissue specimens were obtained from 9 women with adenomyosis whereas control endometrial tissue samples were obtained from 8 women with surgically diagnosed benign ovarian cysts but without any clinical history of endometriosis/adenomyosis/ myoma. Endometrial stromal cells were isolated, purified, cultured, and analyzed by methylation-specific polymerase chain reaction (PCR), real-time reverse transcriptase PCR (RT-PCR), and Western blot analysis, cell viability assays, and fluorescence-activated cell sorting. We found that none of the normal endometrial stromal cells had PR-B promoter methylation. In contrast, 2 out of 3 ectopic endometrial stromall cells had PR-B hypermethylation (P < .05). The treatment with both TSA and ADC elevated PR-B gene and protein expression in ectopic, but not in normal, endometrial stromal cells. Both TSA and ADC treatment dose-dependently reduced cell viability of ectopic endometrial stromal cells. Trichostatin A and ADC treatment also suppressed the cell cycle progression in ectopic endometrial stromal cells. Thus, this study provides the first piece of evidence that adenomyosis has epigenetic aberration and may also be an epigenetic disease amenable to rectification by pharmacological means. This perspective may shed new light onto the pathogenesis of adenomyosis and lead to novel ways to treat the disease.

Ginekol Pol. 2010 Jun;81(6):414-21.

HOXA11 gene expression in women with and without impaired infertility.

[Article in Polish]

Szczepańska M, Wirstlein P, Skrzypczak J.

Katedra Ginekologii, Połoznictwa i Onkologii Ginekologicznej, Klinika Rozrodczości, Uniwersytet Medyczny im. K. Marcinkowskiego w Poznaniu.

INTRODUCTION: HOXA genes are receptivity markers and their altered expression can help identify women with implantation defect.

OBJECTIVES: The purpose of this study was to examine the expression pattern of HOXA11 and expression and localization of its protein product in the endometrium of women with endometriosis, idiopathic infertility and normal fertile patients during different phases of the menstrual cycle.

MATERIAL AND METHODS: We evaluated HOXA11 mRNA level in the endometrium from endometriosis (n=36), idiopathic infertility (n=48) and fertile patients (n=30) during a menstrual cycle. The amounts of mRNA were determined by real-time quantitative PCR. Using the immunohistochemical techniques we compared the localization of HOXA11 protein in the proliferative, early secretory and midsecretory endometrium in all of the studied groups. Endometrial biopsy was performed by pipelle or during hysteroscopy.

RESULTS: We observed statistically significantly elevated HOXA11 transcripts levels in the midsecretory phase in both, the idiopathic infertility and the fertile control groups (p<0.05). Patients with endometriosis had low HOXA11 transcript level in the implantation window. Normal fertile patients showed statistically significantly decreased (p=0.003) HOXA11 mRNA level in the proliferative phase and statistically significantly increased level (p=0.018) in midsecretory phase, comparing to endometriosis patients. HOXA11 protein were localized in the nuclei of the endometrial stromal cells whereas the cytoplasm of these cells did not stain.

CONCLUSION: Our results suggest that altered HOXA11 gene expression in the endometrium during a menstrual cycle may be a common phenomenon among patients with endometriosis and may cause infertility in this group of patients. Further research should explain the mechanism of altered expression of HOXA11 gene.

Chin J Integr Med. 2010 Jun;16(3):283-8. Epub 2010 Aug 8.

Current progress of Chinese medicinal treatment of endometriosis.

Jiang H, Shen Y, Wang XG.

Zhejiang University of Traditional Chinese Medicine, Hangzhou, China.

Endometriosis (EM) is one of the common and frequently encountered gynecological diseases that seriously influences women’s health. Its morbidity reaches 10%-15% in women at reproductive ages, and shows an evident rising tendency. In recent years, the Chinese medicine treatment of EM has won favorable therapeutic effects with few adverse reactions. A brief review on this topic has been made through analyzing and summarizing recent pertinent literatures in terms of treatment depending on syndrome differentiation, cycle treatment, external treatment, integrative medicinal treatment, so as to try to know the status quo of Chinese medicine treatment on EM, and to provide some instructive views for clinical treatment and research.

Hum Reprod. 2010 Oct;25(10):2551-8. Epub 2010 Aug 6.

Size and spatial orientation of uterine tissue transplants on the peritoneum crucially determine the growth and cyst formation of endometriosis-like lesions in mice.

Körbel C, Menger MD, Laschke MW.

Institute for Clinical & Experimental Surgery, University of Saarland, 66421 Homburg/Saar, Germany.

BACKGROUND: In many studies in rodents, intraperitoneal endometriosis-like lesions are surgically induced by syngeneic or autologous transplantation of uterine tissue samples, which are sutured to the abdominal wall. However, until now the surgical techniques have not been standardized, and we address this issue here.

METHODS: Uterine tissue samples were transplanted to the peritoneum of C57BL/6 mice (four study groups, n = 7 each). Using non-invasive high-resolution ultrasound imaging over a period of 4 weeks, we analyzed growth characteristics and cyst formation of the endometriosis-like lesions which developed, in relation to mode of transplantation (syngeneic versus autologous), type of tissue fixed adjacent to the peritoneum (endometrium versus perimetrium), and size of tissue transplanted (2 versus 3 mm). Immunohistochemical analysis was also performed.

RESULTS: When the perimetrium, with underlying myometrium, was sutured next to the host peritoneum the endometriosis-like lesions which developed exhibited a higher growth rate (P< 0.05 versus endometrium), and contained more proliferating cell nuclear antigen (PCNA)-positive cells and an increased microvessel density (both P< 0.05 versus endometrium). In the group with 3 mm uterine tissue grafts, lesion growth was significantly decreased when compared with 2 mm samples (P< 0.05). However, the larger grafts developed more cysts throughout the observation period than the smaller ones. There was no difference between syngeneic and autologous endometriosis-like lesions.

CONCLUSIONS: Our study demonstrates that size and spatial orientation of peritoneally fixed uterine tissue samples crucially determine growth and cyst formation of endometriotic lesions in mice. These findings should improve the standardization and reliability of future studies, performed in the frequently used mouse model of surgically induced endometriosis.

J Gynecol Obstet Biol Reprod (Paris). 2010 Aug 5. [Epub ahead of print]

An unexpected aetiology of massive haemoperitoneum during pregnancy.

[Article in French]

Tourette C, Carcopino X, Taranger-Charpin C, Boubli L.

Service de gynécologie obstétrique, hôpital Nord, chemin des Bourrely, 13915 Marseille cedex 20, France.

We report the case of a 28-year-old woman who was diagnosed with massive hémoperitoneum while being 28 weeks pregnant. This para one woman had no previous history of endometriosis. During emergency caesarean section, she was diagnosed with superficial uterine rupture due to the spontaneous tearing of a sigmoid colon endometriotic lesion that was adherent to the posterior wall of the uterus. Endometriotic lesion is an exceptional aetiology of spontaneous hemoperitoneum during pregnancy and is usually due to the rupture of uterine vessel. To our knowledge, spontaneous rupture of a colon lesion adherent to the posterior surface of the uterus has not yet been reported.

Copyright © 2010 Elsevier Masson SAS. All rights reserved.

J Proteome Res. 2010 Sep 3;9(9):4407-19.

Differential proteome profiling of eutopic endometrium from women with endometriosis to understand etiology of endometriosis.

Rai P, Kota V, Deendayal M, Shivaji S.

Centre for Cellular and Molecular Biology, Uppal Road, Hyderabad 500007, India.

The identification of molecular differences in the endometrium of women with endometriosis is an important step toward understanding the pathogenesis of this condition and for developing novel strategies for the treatment of associated infertility and pain. In this study, we investigated protein expression analysis of eutopic endometrium from women with and without endometriosis. The proteomic analysis revealed molecular dysregulation of more than 70 proteins in the proliferative phase of eutopic endometrium in stage IV and secretory phase of stage II, III and IV endometriosis. Using mass spectrometry, 48 proteins spots which were consistently differentially expressed from stage II to IV endometriosis were identified. The differentially expressed proteins include structural proteins, proteins involved in stress response, protein-folding and protein-turnover, immunity, energy production, signal transduction, RNA biogenesis, protein biosynthesis, and nuclear proteins. Immunoblot and immunohistochemical analyses confirmed the observed changes in eight representative proteins. The present study provides identification of new players that have a potential role in the initiation and progression of endometriosis and also sets a framework for further investigations on mechanisms underlying the pathogenesis of endometriosis.

Acta Chir Belg. 2010 May-Jun;110(3):303-7.

Scar endometriosis in the abdominal wall: a predictable condition for experienced surgeons.

Akbulut S, Sevinc MM, Bakir S, Cakabay B, Sezgin A.

Department of Surgery, Diyarbakir Education and Research Hospital, Diyarbakir, Turkey.

PURPOSE: Endometriosis in surgical scars develops in 0.1% of those women who undergo Caesarean section or other obstetric surgery. Herein we analyse and discuss the clinico-pathological characteristics of 15 patients with scar endometriosis in the abdominal wall.

METHODS: Fifteen cases of scar endometriosis in the abdominal wall that were treated surgically in our department between 2003 and 2009 were examined retrospectively. Age, parity, complaint, medical or surgical history, pre/postoperative hormonotherapy, size of the mass, surgical procedure, follow-up and disease recurrence were analysed.

RESULTS: This retrospective study included 15 patients presenting with 17 postoperative abdominal wall masses. The mean age of the patients was 32.1 +/- 6.0 years (range, 23-48). Eleven of the patients had a painful mass that became bigger before menstruation, two had palpable masses only, and two were hospitalised because of a mass with persistent pain. The locations of the masses were as follows: eight were close to the right side and three were close to the left side; two were in the middle of the Pfanenstiel incision and two were in trocar tracts. The patients’ surgical histories included Caesarean section in thirteen, bilateral laparoscopic ovarian cyst excision in one, and laparoscopic appendectomy in one.

CONCLUSIONS: If a patient presents with incision pain and a palpable mass after gynaecologic surgery, an incisional endometrioma should be considered. Surgical excision and hormone therapy are effective treatment approaches in these patients.


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