Relevant bibliographies by topics / Oestrogen deficiency

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  2. Dissertations / Theses
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  4. Book chapters

Academic literature on the topic 'Oestrogen deficiency'

Author: Grafiati
Published: 4 June 2021
Last updated: 13 February 2022

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Journal articles on the topic "Oestrogen deficiency"

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Robinson, Dudley, and Linda Cardozo. "The pathophysiology and management of postmenopausal urogenital oestrogen deficiency." British Menopause Society Journal 7, no. 2 (June 1, 2001): 67–73. http://dx.doi.org/10.1258/136218001100321263.

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Increasing life expectancy has led to an increasingly elderly population and it is now common for women to spend a third of their lives in the oestrogen-deficient postmenopausal state. Oestrogen is known to have an important physiological impact on the female lower urinary tract and the loss of endogenous oestrogen is associated with the development of urogenital atrophy and lower urinary tract dysfunction, offering a rationale for prevention and treatment. Whilst the role of systemic hormone replacement therapy and the use of topical oestrogens in the management of urogenital atrophy has been firmly established, the use of oestrogens in urinary incontinence remains more controversial. Oestrogen therapy alone has been shown to have little effect in management of genuine stress incontinence, although it may have a synergistic role when used with an α-adrenergic agonist. When considering the irritative urinary symptoms associated with urinary urgency and urge incontinence, oestrogen may be beneficialalthough this may simply reflect a reversal of urogenital atrophy rather than a direct effect on the lower urinary tract. Finally, oestrogens would appear to be efficacious in the management of recurrent lower urinary tract infections, with the most convincing evidence being in support of local vaginal administration.
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2

Laron, Z., R. Kauli, and A. Pertzelan. "Clinical evidence on the role of oestrogens in the development of the breasts." Proceedings of the Royal Society of Edinburgh. Section B. Biological Sciences 95 (1989): 13–22. http://dx.doi.org/10.1017/s0269727000010514.

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SynopsisGirls start their puberty including breast development around age 8. Though the best correlation found is that with oestradiol, most girls still have at the onset of breast development oestrogen levels in the normal range for adult males. Therefore, it seems that oestrogen receptor sensitivity plays an important role in breast development. An important insight into the hormonal interplay in breast development was obtained when comparing the effect of exogenous oestrogens in forty-five girls with four different aetiologies of oestrogen deficiency: gonadal dysgenesis (GD). 17-alpha hydroxylase deficiency (17-OHase def), isolated gonadotrophin deficiency (IGnD) and multiple pituitary hormone deficiencies (MPHD). None of the girls had any breast development in the absence of oestrogens. Treatment with oestrogen was given in an identical manner to all. In GD, in whom the hypothalamic-pituitary functions were normal, treatment led to full development of breasts in a relatively short period. In IGnD and MPHD, breast development was incomplete even after years of oestrogen treatment. The conspicuous difference of the hormonal status between GD and IGnD and MPHD is that the latter two groups lack gonadotrophins, while in GD and 17-OHase def. these hormones are pathologically elevated. Thus the gonadotrophins seem to play an important role in mammary gland development. In the girl with 17-OHase def., it was also found that cortisol is necessary for normal breast development. A girl with hyperprolactinaemia due to a microadenoma had delayed puberty including slow breast development. Upon bromocriptine treatment the prolactin fell, the oestrogens rose and puberty including breast development occurred. Patients with Laron-type dwarfism (isolated IGF-I deficiency) have been found to have normal breast development.
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Sturdee, D. W. "Clinical symptoms of oestrogen deficiency." Current Obstetrics & Gynaecology 7, no. 4 (December 1997): 190–96. http://dx.doi.org/10.1016/s0957-5847(97)80032-7.

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Cattanach, John. "OESTROGEN DEFICIENCY AFTER TUBAL LIGATION." Lancet 325, no. 8433 (April 1985): 847–49. http://dx.doi.org/10.1016/s0140-6736(85)92209-3.

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Ginsberg, J., and P. Hardiman. "Oestrogen deficiency and estradiol implants." BMJ 300, no. 6716 (January 6, 1990): 44–45. http://dx.doi.org/10.1136/bmj.300.6716.44-a.

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Gangar, K., D. Fraser, M. Whitehead, and M. Cust. "Oestrogen deficiency and oestradiol implants." BMJ 300, no. 6716 (January 6, 1990): 44–45. http://dx.doi.org/10.1136/bmj.300.6716.44-b.

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Ginsburg, J., and P. Hardiman. "Oestrogen deficiency and oestradiol implants." BMJ 299, no. 6706 (October 21, 1989): 1031. http://dx.doi.org/10.1136/bmj.299.6706.1031-a.

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Gangar, K. F., M. P. Cust, and M. I. Whitehead. "Oestrogen deficiency and oestradiol implants." BMJ 299, no. 6710 (November 18, 1989): 1279–80. http://dx.doi.org/10.1136/bmj.299.6710.1279-c.

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Cattanach, John F. "Oestrogen deficiency following pelvic inflammatory disease." Medical Journal of Australia 153, no. 7 (October 1990): 433–34. http://dx.doi.org/10.5694/j.1326-5377.1990.tb125522.x.

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10

Rozenberg, S., C. Antoine, B. Carly, and F. Liebens. "MANAGING OESTROGEN DEFICIENCY AFTER BREAST CANCER." Maturitas 63 (May 2009): S6—S7. http://dx.doi.org/10.1016/s0378-5122(09)70024-6.

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Dissertations / Theses on the topic "Oestrogen deficiency"

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Rajaratnam, Rema Antonette Prince of Wales Clinical School UNSW. "The effects of polyethylene wear debris and oestrogen deficiency on fracture healing in a rodent model." Awarded by:University of New South Wales. Prince of Wales Clinical School, 2005. http://handle.unsw.edu.au/1959.4/23351.

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Patients who suffer from severe joint destruction caused by arthritis often undergo total joint arthroplasty (TJA). A major limitation of this treatment and common long-term complication is the development of aseptic loosening of the prosthesis in as many as 20% of patients. The current paradigm to explain aseptic loosening proposes that wear debris generated from the prosthesis initiates a macrophage-mediated inflammatory response by resident macrophages, leading to osteoclast activation and bone resorption at the implant interface. This can then lead to the development of a peri-prosthetic fracture. The principal aim of fracture healing is to restore the bone to its original form and strength. However, this ultimate goal can be altered if the healing is impaired. This impairment may be due to bone disease (osteoporosis) or even the introduction of a foreign material such as PE wear debris that could have migrated from the articulating surface to the fracture site. A standard closed unilateral fracture of the right femur was performed in both normal and oestrogen deficient rats following fixation with a k-wire. Ceridust (PE wear debris) was combined with hyaluronic acid and saline and injected directly into the fracture site. Femurs were assessed using radiographs, histology and immunohistochemistry. Histological analysis revealed that complete remodelling was achieved in all control groups by 6 weeks post-fracture with mechanical strength returning to normal values. The mechanical properties of the fractures were not influenced by the presence of PE wear debris in the dose and timing examined. Histology and immunohistochemistry however, did reveal a local effect of the presence of PE wear debris. The histology adjacent to the PE particles was inferior to the controls but did not manifest itself in a reduction in the mechanical properties except in the oestrogen deficient bone at 6 weeks post-fracture. The levels of MMP-1 and TNF-?? correlated to the presence of PE particles. In this thesis, I have shown the mechanism by which bone remodelling in fracture healing could be retarded due to the presence of PE wear debris, by increased matrix degradation in both normal and oestrogen deficient animals.
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Low, Adrian Kah Wai Clinical School Prince of Wales Hospital Faculty of Medicine UNSW. "The molecular biology of cancellous bone defects and oestrogen deficiency fractures, in rodents; and the in vivo effects of acid on bone healing." Publisher:University of New South Wales. Clinical School - Prince of Wales Hospital, 2008. http://handle.unsw.edu.au/1959.4/42884.

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The management of significant bone defects, delayed and non-union of fractures can be extremely challenging. Development of specific treatment is hindered by an absence of information regarding the molecular events which regulate these processes. In this thesis, a bilateral cancellous bone defect model of the femur and tibia was developed in a rodent and the spatiotemporal profile of TGF-β, BMP 2 and 7, Smads 1, 4 and 5 characterised. Next, the capability of acid solution to augment healing was tested in both a bone defect and in a closed femoral fracture model. Finally, a long term oestrogen deficiency (OVX) rat model of postmenopausal osteoporosis was characterised and the spatiotemporal profiles of IGF-1, IGFR-1, MMP-1, MMP-3, MMP-9, MMP-13, TIMP-1, TIMP-2, BMP-2, BMP-4, BMP-7, TGF-β, Smad4, Smad7, VEGF, Flt-1, Ihh and FGF-2 were compared in femoral osteotomies between OVX and Sham groups. The bilateral cancellous defect model was successfully created with a number of advantages with which to recommend its use in future studies. TGF-β, BMP 2 and 7, Smads 1, 4 and 5 had characteristic spatiotemporal profiles during cancellous bone defect healing suggesting that they have a regulatory role. The results of the acid study were inconclusive and problems with substance delivery and maintenance at the desired site need to be addressed in the future to fully test this hypothesis. No significant differences were detected on histology or three-point mechanical testing between the fracture calluses of acid and control groups. In the final study, OVX rats after six months had significantly increased weight and decreased bone mineral density compared to their sham counterparts. A histological delay in osteotomy healing was observed in the OVX group but no significant differences on tensile testing were seen between OVX and Sham groups up to six weeks. Immunohistochemistry revealed that delayed healing may be due to the down-regulation of IGF-1, BMP-2, 4, and 7 and the up-regulation of MMP-3 in OVX compared to Sham groups. In conclusion, the results of this thesis give some insight into the molecular biology of bone defects and osteoporotic fractures. This information may also be useful in the development of specific treatments aimed at augmenting healing in bone defects and osteoporotic fractures.
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Books on the topic "Oestrogen deficiency"

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W, Shaw Robert, ed. Oestrogen deficiency: Causes and consequences. Lancs, UK: Parthenon Pub. Group, 1996.

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2

Bonne, Eriksen Peter, and Samsioe Göran, eds. The urogenital, oestrogen deficiency syndrome. Bagsvaerd, Denmark: Novo industri, 1987.

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3

Shaw, R. W. Oestrogen Deficiency: Causes and Consequences (Advances in Reproductive Endocrinology, 8). Informa Healthcare, 1996.

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4

Hodgkiss, Andrew. Psychiatric consequences of cancer treatments: surgery and radiotherapy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198759911.003.0005.

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Surgery and radiotherapy for cancers can disrupt mental health through direct biological mechanisms in addition to the well-described psychological distress associated with the physical consequences of treatment. Upper bowel surgery and bilateral oophorectomy both frequently provoke psychopathology. Total gastrectomy, or ileal resection, causes an inevitable vitamin B12 deficiency. The molecular mechanisms by which these surgical treatments provoke depressive symptoms, or even a dementia, are considered. Raised homocysteine levels and reduced SAM availability are involved. Chronic gonadal oestrogen deprivation increases the risk of anxiety, depression, and dementia in later life. The likely molecular basis for this is discussed. Hypothyroidism, with its associated psychopathology, complicates radiotherapy for head & neck cancers in 40 per cent of patients. The chapter closes with a review of the effects of whole-brain radiotherapy on cognitive function, and the psychopathology arising from radiation-induced hypopituitarism.
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Sprague, Stuart M., and James M. Pullman. Spectrum of bone pathologies in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0122.

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Histologic bone abnormalities begin very early in the course of chronic kidney disease. The KDIGO guidelines recommend that bone disease in patients with chronic kidney disease should be diagnosed on the basis of bone biopsy examination, with bone histomorphometry. They have also proposed a new classification system (TMV), using three key features of bone histology—turnover, mineralization, and volume—to describe bone disease in these patients. However, bone biopsy is still rarely performed today, as it involves an invasive procedure and highly specialized laboratory techniques. High-turnover bone disease (osteitis fibrosa cystica) is mainly related to secondary hyperparathyroidism and is characterized by increased rates of both bone formation and resorption, with extensive osteoclast and osteoblast activity, and a progressive increase in peritrabecular marrow space fibrosis. On the other hand, low-turnover (adynamic) bone disease involves a decline in osteoblast and osteoclast activities, reduced new bone formation and mineralization, and endosteal fibrosis. The pathophysiological mechanisms of adynamic bone include vitamin D deficiency, hyperphosphataemia, metabolic acidosis, inflammation, low oestrogen and testosterone levels, bone resistance to parathyroid hormone, and high serum fibroblast growth factor 23. Mixed uraemic osteodystrophy describes a combination of osteitis fibrosa and mineralization defect. In the past few decades, an increase in the prevalence of mixed uraemic osteodystrophy and adynamic bone disease has been observed.
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Book chapters on the topic "Oestrogen deficiency"

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Brincat, M., C. Moniz, M. Savvas, and J. W. W. Studd. "Oestrogen Deficiency and Connective Tissues." In HRT and Osteoporosis, 47–55. London: Springer London, 1990. http://dx.doi.org/10.1007/978-1-4471-1799-5_5.

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Cardozo, L. D. "Oestrogen Deficiency and the Bladder." In HRT and Osteoporosis, 57–71. London: Springer London, 1990. http://dx.doi.org/10.1007/978-1-4471-1799-5_6.

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Sarrel, Philip M. "Role Of Oestrogen Deficiency In Women With Syndrome X." In Developments in Cardiovascular Medicine, 249–65. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2596-7_16.

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4

Oliver, Rema, G. Yee, Y. Yu, J. B. Matthews, E. Ingham, and W. R. Walsh. "Fracture Healing in the Presence of Polyethylene Wear Debris and Oestrogen Deficiency." In Key Engineering Materials, 831–34. Stafa: Trans Tech Publications Ltd., 2007. http://dx.doi.org/10.4028/0-87849-456-1.831.

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Burger, Henry G., and Helena J. Teede. "Endocrinology of the menopause and hormone replacement therapy." In Oxford Textbook of Endocrinology and Diabetes, 1492–503. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.0116.

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A major endocrine function of the human ovary is the production of oestradiol, a hormone essential for the development of the secondary sex characteristics, for normal reproduction, and for the integrity of the cardiovascular, skeletal, and central nervous systems in particular. Oestradiol is a product of the granulosa cells, and hence its secretion is dependent largely on the presence of ovarian follicles. The number of those follicles falls steeply in the last 10 years or so of reproductive life (1), to approach zero at around the time of final menses (Fig. 10.1.2.1). This results in a profound decline in oestradiol production, to levels less than 10% of those observed during reproductive life. The question of whether the consequences of this decline are to be regarded as ‘natural,’ or as giving rise to a pathological state of oestrogen deficiency, is a controversial one. This chapter describes the endocrine changes which take place from the mid-reproductive years through to the postmenopausal years, and addresses the consequences of these changes and their possible prevention.
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Gooren, Louis J. G. "Gynaecomastia." In Oxford Textbook of Endocrinology and Diabetes, 1459–62. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.9131.

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Parenchymal and stromal cells with the potential for normal breast development are equally present in prepubertal boys and girls. Men and women do not differ in sensitivity to the hormonal action of sex steroids, and therefore men have the same potential to develop breasts as women. Whether this actually occurs obviously depends on a person’s hormonal milieu. In order to understand the pathophysiology of gynaecomastia it is essential to know that breast tissue is, for its development, under control of both stimulatory hormonal action (oestrogens and progestogens) and inhibitory hormonal action of androgens. Gynaecomastia typically occurs when there is a relative dominance of oestrogenic over androgenic action; many cases of gynaecomastia are not the result of an overproduction of oestrogens per se, but rather due to the failing inhibitory action of androgens (1). In the assessment of gynaecomastia, as much attention must be paid to a potential source of feminizing hormones as to decreased androgen production or interference with the biological action of androgens. Oestrogens stimulate the proliferation and differentiation of parenchymal ductal elements while progesterone supports alveolar development. The biological actions of oestrogens and progesterone do not appear in cases of growth hormone deficiency. Prolactin stimulates the differentiated ducts to produce milk. Testosterone inhibits the growth and differentiation of breast development, probably through an antioestrogenic action (1). Whatever the cause, gynaecomastia shows the same histological developmental pattern. At first, there is florid ductal proliferation, with epithelial hyperplasia and increase in stromal and periductal connective tissue, with increased vascularity and periductal oedema. After approximately one year, there is increased stromal hyalinization, dilation of the ducts, and a marked reduction in epithelial proliferation, a ‘burnt-out’ phase of the condition. The result is inactive fibrotic tissue which no longer responds to endocrine therapy. Gynaecomastia is not an uncommon finding and most cases will not represent a serious medical condition. However, gynaecomastia may signify the presence of a malignancy producing oestrogens, aromatase (the enzyme that converts androgens to oestrogens), or human chorionic gonadotrophin (hCG). Common locations of such tumours are the testis, lungs, liver or the gastrointestinal tract. Consequently, cases of gynaecomastia must be taken seriously and the diagnostic approach must reasonably rule out a malignancy in order to avoid any undue delay in its diagnosis.
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Pollak, Eleanor S., and Katherine A. High. "Genetic disorders of coagulation." In Oxford Textbook of Medicine, edited by Chris Hatton and Deborah Hay, 5532–46. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0546.

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Haemophilia is a familial X-linked disorder due to deficiency of either factor VIII (haemophilia A) or factor IX (haemophilia B), components of the intrinsic enzymatic complex that activates factor X. Clinical features and diagnosis—the main manifestations are bleeding into joints and soft tissues, with haemophilic arthropathy and joint deformity being inevitable complications in untreated patients. Other features include pseudotumours, bleeding into the urinary system, and bleeding following clinical procedures. Laboratory diagnosis is based on a modification of the classic activated partial thromboplastin time (APTT) assay, with inhibitor screening used to exclude other causes of prolonged APTT. Treatment—involves the administration of the deficient factor VIII or factor IX, most commonly ‘on demand’ in response to bleeding, with prophylactic treatment given before surgery. Von Willebrand’s disease is a common autosomal dominant disorder of platelet function caused by a functional deficiency of von Willebrand factor (VWF). VWF, normally synthesized by megakaryocytes, prevents degradation of factor VIII; VWF, also made by endothelial cells, enhances platelet activation and recruitment at sites of tissue damage. Treatment—mild von Willebrand’s disease is treated with desmopressin 1-deamino-8-d-arginine vasopressin (DDAVP), which releases factor VIII and VWF from endothelial cells. Other treatments include ε‎-aminocaproic acid, oestrogens, and factor VIII concentrates. Other hereditary disorders of coagulation, including (1) hereditary deficiency of the plasma metalloproteinase ADAMTS13; (2) combined deficiency of coagulation factors V and VIII; (3) factor XI deficiency; (4) inherited deficiencies of factors II, V, VII, and X; and (5) deficiency of the contact activating factors, factor XIII, and fibrinogen, and hypercoagulable diseases due to deficiencies of anticoagulants or propensity to thrombosis are discussed in this chapter.
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