Dissertations / Theses on the topic 'Uterine myometrium'

The objective of this study is to remove or, at least, reduce the noise in uterine EMG recordings, which at their present noise level render the data unusable. Predicting when true labor will start and recognizing when labor actually starts are important for both normal and complex pregnancies. For normal pregnancy, the prognosis of labor is important for reducing unnecessary hospital costs. About 10% of the four million babies born each year in the United States are born prematurely. At $1,500 a day for neonatal intensive care, this comprises national health care expenses of well over $5 billion. Spectral analysis, filter design, and 1/3 octave analysis were applied to analyze the uterine EMG recordings. Signal-to-noise ratio was increased with IIR Butterworth bandstop filter. The spectral band between 0.25 and 0.4 Hz shows matching of the Toco belt via spectral analysis. Nevertheless, 1/3 octave analysis gives the highest correct detection percentage compare with frequency analysis and filter design.

Although prostaglandins (PG) and oxytocin are crucial mediators of uterine contractility, their receptor-mediated effects during the menstrual cycle, pregnancy and labour are not fully understood. The aim of this thesis was to elucidate the functional expression of EP, FP, TP and oxytocin receptors in isolated human myometrium relative to myocyte mRNA and signal transduction pathways. Myometrial samples were obtained from consenting non-pregnant and pregnant donors. Functional techniques were used to determine isometric muscle contractions. Primary uterine myocytes and fibroblasts were cultured at term to identify stimulated changes in calcium (Ca2+), cyclic adenosine monophosphate (cAMP) and mRNA. Myometrial strips exhibited spontaneous contractions, which were most active midcycle under oestrogenic conditions. At this time intrinsic contractility and responsiveness to uterotonins decreased towards the fundus. PGE2 produced bellshaped responses with predominant utero-relaxant effects mediated via the EP2 subtype. Although activity was partially restored by PGE2 through EP3/1 receptors, tissue excitation was more pronounced at FP, TP and oxytocin receptors. Despite high FP mRNA expression, the lower segment uterus was particularly responsive to U46619 and oxytocin at term pregnancy. Even so, Ca2+ mobilisation by oxytocin was greater via principal release from intracellular stores. Incubations with atosiban, progesterone and a rho-kinase inhibitor reduced oxytocin-stimulated Ca2+ transients. EP2 also attenuated oxytocic effects but this appeared to be mediated through cAMP rather than Ca2+ signalling pathways. With advancing labour, intrinsic myogenic activity declined in parallel with oxytocin desensitisation. However, TP-induced contractions were continued in the lower parturient uterus. These findings demonstrate that PG and oxytocin receptor expression are regulated in a hormone-dependent temporal and spatial manner. EP2-mediated cAMP formation appears to promote uterine quiescence, whilst TP receptors may control muscle tonus during parturition. These receptors and their messenger systems represent effective tocolytic targets for uterine hypercontractile disorders, such as dysmenorrhoea and preterm labour.
Allergan Inc.

Although prostaglandins (PG) and oxytocin are crucial mediators of uterine contractility, their receptor-mediated effects during the menstrual cycle, pregnancy and labour are not fully understood. The aim of this thesis was to elucidate the functional expression of EP, FP, TP and oxytocin receptors in isolated human myometrium relative to myocyte mRNA and signal transduction pathways. Myometrial samples were obtained from consenting non-pregnant and pregnant donors. Functional techniques were used to determine isometric muscle contractions. Primary uterine myocytes and fibroblasts were cultured at term to identify stimulated changes in calcium (Ca2+), cyclic adenosine monophosphate (cAMP) and mRNA. Myometrial strips exhibited spontaneous contractions, which were most active midcycle under oestrogenic conditions. At this time intrinsic contractility and responsiveness to uterotonins decreased towards the fundus. PGE2 produced bellshaped responses with predominant utero-relaxant effects mediated via the EP2 subtype. Although activity was partially restored by PGE2 through EP3/1 receptors, tissue excitation was more pronounced at FP, TP and oxytocin receptors. Despite high FP mRNA expression, the lower segment uterus was particularly responsive to U46619 and oxytocin at term pregnancy. Even so, Ca2+ mobilisation by oxytocin was greater via principal release from intracellular stores. Incubations with atosiban, progesterone and a rho-kinase inhibitor reduced oxytocin-stimulated Ca2+ transients. EP2 also attenuated oxytocic effects but this appeared to be mediated through cAMP rather than Ca2+ signalling pathways. With advancing labour, intrinsic myogenic activity declined in parallel with oxytocin desensitisation. However, TP-induced contractions were continued in the lower parturient uterus. These findings demonstrate that PG and oxytocin receptor expression are regulated in a hormone-dependent temporal and spatial manner. EP2-mediated cAMP formation appears to promote uterine quiescence, whilst TP receptors may control muscle tonus during parturition. These receptors and their messenger systems represent effective tocolytic targets for uterine hypercontractile disorders, such as dysmenorrhoea and preterm labour.

Adenomyosis is a uterine disease where ectopic, non-neoplastic endometrium is histologically observed within the myometrium. The research presented herein examines the hypothesis that uterine adenomyosis is caused by abnormal behaviour of the cells at the endometrial-myometrial interface (EMI) through the actions of nerve growth factors (NGF), their receptors, the caveolin proteins and wnt signalling pathways during estradiol (E2) or tamoxifen (TMX) stimulation. In a 3-dimensional coculture model, the invasion depth of endometrial stromal cells from affected uteri was greater than that of unaffected uteri. Furthermore, invasion depth of unaffected and affected stromal cells increased by an average of 41.3% and 64.6%, respectively in the presence of E2 and 73.3% and 73.5%, respectively in the presence of TMX, indicating an inherent predisposition of the stromal cell for myometrial invasion and the enhancing effects of both E2 and TMX. Immunohistochemical analysis of NGF expression indicated a significant 2-4 fold increase in adenomyosis with the transcript level (measured by qRT-PCR) showing decreased expression in normal myocytes (0.72 fold) in response to E2 and increased expression in both normal (1.08 fold) and adenomyotic myocytes (1.20 fold) in response to TMX. Similarly, caveolin 1 protein expression was increased in the adenomyotic group, whilst transcripts for the caveolin 1a (0.70 fold) and caveolin 1b (0.82 fold) isoforms were reduced by E2 in normal myocytes. Conversely, TMX increased caveolin 1a (1.4 fold) and caveolin 1b (1.32 fold) expression in the adenomyotic myocytes. The data for the caveolin 2 data mirrored that of caveolin 1 in that caveolin 2a and 2b protein expression showed increased expression in the adenomyotic group, whilst the transcript levels of the caveolin isoforms 2a (0.65 fold) and 2b (0.79 fold) were reduced by E2 in normal myocytes, while upregulated by TMX in adenomyosis group (1.57 and 2.00 fold, respectively). Wnt5a expression at both the transcript and protein level was decreased in adenomyosis implicating the loss of wnt5a in adenomyosis progression. Furthermore, decidualisation experiments of isolated stromal cells from normal and adenomyotic uteri suggested no difference in the timing to decidualisation, with no significant difference in cell morphology, IGFBP-1 or prolactin expression, which strongly suggests that disordered stromal differentiation is not the main causal event in the pathogenesis of adenomyosis. Overall, the results from this research supported the key hypothesis of disordered cellular function and gene expression at the uterine endometrial-myometrial interface in adenomyosis.

Etude réalisée pendant la gestation chez la rate rendue diabétique par injection de streptozotocine, dans le but d'identifier quelques facteurs impliqués dans le développement de l'hypotrophie foetale: sont évalués le rôle des perturbations hémodynamiques utéroplacentaires, et l'hypertonie du myomètre, avec les facteurs neuro-endocriniens impliqués dans ces modifications

博士
高雄醫學院
醫學研究所
84
Considering smooth muscle contraction or relaxation, adenosine plays very important role. It has beenreported in animal experiments, adenosine couldinduceuterine myometrium contraction and uterine arteryrelaxation. To investigate the effect of adenosine inhuman uterine myometrium and uterine artery, adenosine and adenosine analogues have been applied to human non-pregnant myometrium strips and segments of uterineartery in vitro. The contraction or relaxation effectwas recorded by polygraph. The pharmacologicclassification of receptors for adenosine was determinedby the potency order of adenosine and adenosineanalogues. For single myocyte study, the effect of adenosine onintracellular freecalcium has been studied. Intracellular free calcium was coupled with Fluo-3 andscanned by laser cytometer. The changes of intracellular free calcium was declared after addition of adenosine. Adenosine induced human uterine artery relaxation, the potency of analogue was NECA > R-PIA > adenosine inorder, indicating the A2 receptor effect. Adenosine inconcentrations of 10-6M and 2 × 10-5M could decrease intracellular calcium produced by phenylephrine (10-6M). The effect of adenosine in uterine artery was similar tothat in endothelium intact or denuded preparation. Therefore, adenosine induced relaxation of human uterine artery was thought via A2 receptor, decreasing intracellular calcium and independent of endothelium. On the other hand, adenosine could produce human uterine muscle contraction. The potency was R-PIA = NECA> adenosien in order. The effect could be blocked byselective A1 receptor antagonist such as DPCPX, which indicated A1 receptor effect. Adenosine elicited rapid, biphasic increase in intracellular calcium levels, whichinvolved release from intracellular calcium stores andcalcium entry in uterine myocyte. The intracellular calciumlevel at the plateau phase induced by adenosinemust associate with the presence of extracellular calcium. Adenosine induced intracellular calcium response was significantly inhibited by DPCPX. The non- selectiveadenosine receptor antagonist, XAC, revealed less potent. The calcium response to adenosine was completely prevented by pretreatment of the cellswith pertussis toxin, implicating the involvement of Gi in the receptor- mediated response. The results have demonstrated the modulation effectof adenosine on humanuterine myometrium and uterine artery. In human uterus, adenosine A1 receptor was notedin uterine myometrium. While adenosine A2 receptor was determined in uterine artery. According to the effect of different receptors, adenosine caused increase inintracellular calcium on uterine myometrium. However, adenosine produced decrease in intracellular calcium on uterine artery. Finally, We will reveal the hypothesis of modulation in the smooth muscle cells by andenosine.

by Lai-pang Law.
Thesis (M.Phil.)--Chinese University of Hong Kong, 1997.
Includes bibliographical references (leaves 148-182).
ABSTRACT
LIST OF ILLUSTRATIONS
LIST OF TABLES
ACKNOWLEDGEMENTS
ABBREVIATIONS
Chapter CHAPTER I --- INTRODUCTION --- p.1
Chapter CHAPTER II --- LITERATURE REVIEW --- p.4
Chapter 2.1 --- The uterus and its changes in the normal menstrual cycle
Chapter 2.2 --- Anatomy and physiology of normal myometrium
Chapter 2.3 --- Clinical features and management of uterine leiomyoma
Chapter 2.4 --- Pathology of human uterine leiomyoma
Chapter 2.5 --- The relationship between growth fractions and ER in breast carcinoma
Chapter 2.6 --- Steroid receptors and epidermal growth factor receptor
Chapter 2.6.1 --- Steroid receptors
Chapter 2.6.2 --- Epidermal growth factor receptor
Chapter 2.7 --- "Structures of oestrogen receptor, progesterone receptor, Ki-67 and epidermal growth factor receptor"
Chapter 2.7.1 --- The structure of oestrogen receptor
Chapter 2.7.2 --- The structure of progesterone receptor
Chapter 2.7.3 --- The structure of Ki-67
Chapter 2.7.4 --- The structure of epidermal growth factor receptor
Chapter 2.8 --- "Antibodies to steroid receptors, monoclonal Ki-67 and epidermal growth factor receptor"
Chapter 2.8.1 --- Steroid receptors
Chapter 2.8.2 --- Monoclonal Ki-67
Chapter 2.8.3 --- Epidermal growth factor receptor
Chapter 2.9 --- "Functions of steroid receptors, Ki-67 and epidermal growth factor receptor"
Chapter 2.9.1 --- The functions of steroid receptors
Chapter 2.9.2 --- The functions of Ki-67
Chapter 2.9.3 --- The functions of epidermal growth factor receptor
Chapter 2.10 --- Cell cycle
Chapter 2.11 --- Immunohistochemistry
Chapter 2.11.1 --- Introduction
Chapter 2.11.2 --- Methodology of immunostaining
Chapter 2.11.3 --- Avidin-biotin-peroxidase complex technique
Chapter 2.11.4 --- Chromogens
Chapter 2.11.5 --- Enhancement methods
Chapter 2.11.6 --- Fixation for immunohistochemistry
Chapter CHAPTER III --- MATERIALS AND METHODS --- p.63
Chapter 3.1 --- Reagents and chemicals
Chapter 3.1.1 --- Primary monoclonal antibodies
Chapter 3.1.2 --- Secondary antibodies
Chapter 3.1.3 --- Avidin-biotin complex
Chapter 3.1.4 --- DAB solution
Chapter 3.1.5 --- Buffers
Chapter 3.1.6 --- Miscellaneous
Chapter 3.2 --- Patients and specimens
Chapter 3.2.1 --- Specimen collection
Chapter 3.2.2 --- Preparation of specimens
Chapter 3.3 --- Immunohistochemical staining
Chapter 3.3.1 --- Slide preparation
Chapter 3.3.2 --- Antigen retrieval
Chapter 3.3.3 --- Procedures of immunohistochemical staining
Chapter 3.3.4 --- Interpretation of immunostaining
Chapter CHAPTER IV --- RESULTS --- p.80
Chapter 4.1 --- Clinical information
Chapter 4.2 --- Oestrogen receptor
Chapter 4.3 --- Progesterone receptor
Chapter 4.4 --- Epidermal growth factor receptor
Chapter 4.5 --- Ki-67
Chapter CHAPTER V --- DISCUSSION --- p.120
Chapter 5.1 --- Methods and interpretation of the results
Chapter 5.1.1 --- The advantages of the immunohistochemical staining technique
Chapter 5.1.2 --- Interpretation and reporting of immunohistochemical results
Chapter 5.1.3 --- Interpretation of the results by semi- quantitative assessment and statistical analysis
Chapter 5.2 --- The status of steroid receptors in uterine leiomyoma
Chapter 5.2.1 --- ER status in uterine leiomyoma and normal myometrium
Chapter 5.2.2 --- PR status in uterine leiomyoma and normal myometrium
Chapter 5.3 --- EGF-R status in uterine leiomyoma
Chapter 5.4 --- Ki-67 status in uterine leiomyoma and normal myometrium
Chapter 5.5 --- "The relationship between steroid receptors, Ki-67, EGF-R and uterine leiomyoma growth"
Chapter 5.6 --- Biological indices in the assessment of tumor
Chapter 5.7 --- Microwave technology in immunohistology for surgical pathology
Chapter CHAPTER VI --- CONCLUSIONS --- p.144
REFERENCES --- p.148

Um caso de tumor adenomatoide é apresentado. A paciente, uma mulher de 49 anos, foi submetida à uma histerectomia vaginal por dor pélvica severa renitente à terapia médica. O diagnóstico de tumor adenomatoide foi feito com base na histologia e imunohistoquímica. O tumor adenomatoide deve ser considerado como diagnóstico diferencial de leiomiomas em casos de pacientes com dores pélvicas severas e útero volumoso à palpação.
The adenomatoid tumour (AT) is a rare benign mesothelial proliferation (1). In the genital tract it occurs predominantly in the myometrium or fallopian tubes, rarely in the broad ligament, the ovary, and the extra genital peritoneum of females and the epididymis, spermatic cord, tunica vaginalis and tunica albuginea of males (2). Most AT of the uterus present as solitary asymptomatic lesions diagnosed as incidental findings in hysterectomy specimens, and multiple AT (mAT) are rare (3). We describe a clinical case of a patient with symptomatic mAT.

碩士
國立陽明大學
解剖暨細胞生物學研究所
97
Extensive uterine surgery may cause significant myometrial defects that may lead to severe sequelae, including placenta accreta and uterine rupture during subsequent pregnancy. Recent evidences have suggested that mesenchymal stem cells (MSCs) derived from bone marrow are capable of self renewal and differentiation into three germ layers, including smooth muscle cells of mesodermal origin. Therefore, it is likely that MSCs may be used to strengthen the repair of myometrial defects and prevent severe sequalae following major uterine operations. However, to date there has been no study on the application of MSCs to uterine repair. In this study, we developed an effective therapeutic alternative, utilizing the unique features of MSCs, to treat uterine defects. We investigated whether transforming growth factor-beta1 (TGF-beta1), fibronectin and ascorbic acid could synergistically induce MSCs to acquire the phenotypical characteristics of smooth muscle cells (SMCs), followed by transplantation to repair uterine defects in an animal model. In vitro, MSCs were found to differentiate to SMC-like cells in response to TGF-beta1, fibronectin and ascorbic acid, as revealed by the up-regulated expression of calponin. Furthermore, we demonstrated synergistic effects of TGF-beta1, fibronectin and ascorbic acid on MSC differentiation into SMC-like cells. Furthermore, the ability of these MSC-derived SMC-like cells to resist trophoblast invasion was examined using a co-culture model, thereby investigating their potential application to prevent placenta accreta. As compared with undifferentiated MSCs, MSC-derived SMC-like cells more efficiently resisted trophoblast invasion, though not as effectively as freshly isolated myometrial cells. Finally, we established an animal model of uterine defect repair. Injection of MSCs into the myometrial defects was shown to accelerate the repair of defects and MSCs were detected in the uterine tissue sections at the end of the repair process. Our results demonstrated that MSCs could be differentiated into SMC-like cells and utilized to repair myometrial defects, thereby benefitting women undergoing uterine surgery with extensive myometrial resection.