Publications by authors named "Teresa Henderson"

Objectives: Concerns about the cognitive adverse effects of electroconvulsive therapy (ECT) are common among recipients of the treatment despite its relatively small adverse effects on cognitive functioning. Interventions aimed at remediating or improving coping with cognitive adverse effects of ECT have not been developed. The Enhancing Cognitive Domains after ECT (ENCODE) program is a new group intervention aimed at teaching self-management strategies to cope with the cognitive challenges and associated anxiety that often accompanies ECT.

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Objective: The purpose of this study was to test whether a quantitative high-throughput molecular screen can be used to probe human endometrium and initiate the development of molecular diagnostic tools with potential for identification of therapeutic targets in women with menstrual complaints.

Study Design: Endometrium was collected from 10 patients with complaint of heavy bleeding, classified into mid or late secretory phase of the menstrual cycle by histologic dating and serum progesterone concentration. Total RNA was extracted and gene activity assessed using high-density oligonucleotide arrays.

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Key reproductive events, such as menstruation and implantation, are considered to be inflammatory processes and glucocorticoids act as anti-inflammatory agents. The balance of expression of types 1 and 2 11beta-hydroxysteroid dehydrogenases (11betaHSD) controls the availability of cortisol to bind to the glucocorticoid receptor (GR) and mineralocorticoid receptor (MR). Expression profiles of glucocorticoid-metabolising enzymes and their cognate receptors have been characterized in the reproductive tract.

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The menstrual cycle is a complex interaction of sex steroids, prostanoids, and cytokines that lead to coordinated tissue degradation, regeneration and repair. The transcription factor hypoxia-inducible factor (HIF-1) plays critical roles in cellular responses to hypoxia, the generation of an inflammatory response and vasculogenesis through transcriptional activation of angiogenic genes. We hypothesize that HIF-1 is expressed in human endometrium and that locally synthesized prostaglandins (PGE2 and PGF(2alpha)) regulate HIF-1 activity.

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Context: Progesterone acting via its cognate receptor is critical to maintaining a viable endometrial environment for implantation and pregnancy. During medical termination of pregnancy, the biological effect of progesterone is pharmacologically withdrawn and prostaglandins administered exogenously. Leukocytes within the uterus are the effector cells of an inflammatory response and play important roles in both tissue breakdown and remodeling.

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Background: The levonorgestrel-releasing intrauterine system (LNG-IUS) is a highly effective contraceptive. However, unscheduled breakthrough bleeding (BTB), leads to discontinuation in a proportion of users. The LNG-IUS down-regulates endometrial progesterone and estrogen receptors and this may play a role in the mechanism responsible for BTB.

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The endometrium contains a unique subset of uterine-specific natural killer (uNK) cells, the proposed functions of which include a role in decidualization, menstruation, and implantation. These cells increase in number during the mid-late secretory phase of the menstrual cycle and are also present in large numbers in early pregnancy. The cyclical nature of uNK cell appearance suggests hormonal regulation of these cells.

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Estrogen action is mediated via two subtypes of the estrogen receptor (ER), usually referred to as ERalpha and ERbeta. We have previously compared the spatial and temporal expressions of ERalpha and ERbeta proteins in human endometrium and reported that endothelial cells exclusively express ERbeta. In the present study we have extended our investigations to compare the pattern of expression of wild-type (ERbeta1) and a newly identified ERbeta variant isoform (ERbetacx/beta2) that lacks the ability to bind steroids.

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The mechanism of mifepristone-induced vaginal bleeding and endometrial shedding was investigated in 13 women who took 200 mg mifepristone in the midluteal phase on d 8 after the onset of the urinary LH surge (LH+8). Endometrial biopsies were collected, 6-24 h after mifepristone (group 1, n = 7) or 36-48 h after mifepristone (group 2, n = 6), and compared with those from a control group in the midluteal phase (n = 7). All women reported vaginal bleeding commencing 36-48 h after taking mifepristone.

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