Blog dedicated to the continuous education in Gynecology and Endocrinology

 

OESTROGEN RECEPTOR ALPHA LOCALISATION IN THE PREFRONTAL CORTEX OF THREE MAMMALIAN SPECIES.

Montague D, Weickert CS, Tomaskovic-Crook E, Rothmond DA, Kleinman JE, Rubinow DR.

J Neuroendocrinol. 2008 Apr 28.

Oestrogen modulates cognitive function and affective behaviours subserved by the prefrontal cortex (PFC). 0Identifying and localising oestrogen receptor alpha, ERalpha, in human PFC will contribute to our understanding of the molecular mechanism of oestrogen action in this region. more

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PROGESTIN RECEPTOR SUBTYPES IN THE BRAIN: THE KNOWN AND THE UNKNOWN.

Mani S.

Endocrinology. 2008 Jun;149(6):2750-6
Progesterone (P), the most biologically active progestin of ovarian origin, modulates numerous cellular functions in the central nervous system to coordinate physiology and reproduction. The neurobiological activity of P is mediated not by a single form of the progestin receptor (PR), but by two neural isoforms of PRs, PR-A and PR-B. more

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ESTROGEN RECEPTOR Α SPLICE VARIANTS IN THE HUMAN BRAIN

T.A. Ishunina and D.F. Swaab

In the present review we discuss recent findings showing that, in addition to the canonical estrogen receptor α (ERα), the level of various ERα splice variants is changed in the human brain in aging and Alzheimer’s disease (AD) at both the mRNA and protein level and that they should be considered for the understanding of estrogen effects on the brain and estrogen therapy pitfalls. Indeed, the expression pattern of certain splice forms is brain area-specific. Thus, the major isoform found in the mamillary body (MB) appeared to be del. 7 (deletion of exon 7), while in the hippocampus del. 4 (exon 4 omitted) was expressed at the highest level. Furthermore, while transcripts missing exons 7 and 2 declined with aging in the MB of patients > 60 years old, no age-related alterations were determined for a number of splice variants in the hippocampus. A novel MB1 isoform with a 168 bp deletion within the transactivation function 1 of the ERα, turned out to accumulate in the histaminergic tuberomamillary nucleus of postmenopausal women. Finally, the level of alternatively spliced ERα may also change in AD in a brain area specific manner and so the sensitivity for estrogen therapy.

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STEPPED CARE TREATMENT OF POSTPARTUM DEPRESSION A PRIMARY CARE-BASED MANAGEMENT MODEL.

Womens Health Issues. 2008 Jan-Feb;18(1):44-52.
Gjerdingen D, Katon W, Rich DE.

BACKGROUND AND PURPOSE: Postpartum depression (PPD), the most prevalent serious postpartum complication, is a devastating illness that negatively impacts not only the mother, but also her infant, other family members, and work performance. There is an extensive body of research addressing systems-based quality improvement efforts for treatment of depression in primary care populations; however, little of this research has been directed toward postpartum populations. This paper presents a health care systems-based quality improvement model for the treatment of PPD derived from research outcomes in general primary care populations. METHODS: OVID/MEDLINE and PsychINFO searches were performed using the following terms: depression, postpartum depression, mass screening, collaborative care, stepped care, psychotherapy, cognitive-behavioral therapy, interpersonal therapy, and education as keywords. MAIN FINDINGS: The PPD management model described herein includes screening and diagnosis, initiation of active treatment, and use of collaborative care, which includes primary care visits, case manager follow-up, and more intensive care, through specialty consultation or referral, for complicated or difficult cases. CONCLUSION: Stepped care, a form of collaborative depression treatment, is proposed as a practical, cost-effective method for improving PPD diagnosis and clinical outcomes.

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17 HYPOXIA-INDUCED APOPTOTIC CELL DEATH IS PREVENTED BY OESTRADIOL VIA OESTROGEN RECEPTORS IN DEVELOPING CNS.

J Neuroendocrinol. 2008 Jan
Pozo Devoto VM, Giusti S, Chavez JC, de Plazas SF.

Neuroprotective effects of oestrogens have been demonstrated against a variety of insults including excitotoxicity, oxidative stress and cerebral ischemia under certain conditions. However, the molecular mechanisms underlying oestrogen neuroprotection are still unclear. We aimed to determine if 17-beta oestradiol (E(2)) administration post-hypoxia (p-hx) was neuroprotective and if these actions were mediated through oestrogen receptors (ER). For this purpose, 12-embyonic day old chickens were subjected to acute hypoxia (8% [O(2)], 60 min), followed by different reoxygenation periods. To test the neuroprotective effect of E(2) and its mechanism, embryos were injected 30 min after the end of hypoxia with E(2) alone or with ICI 182,780, a competitive antagonist of ER. Cytochrome c (cyt c) release, an indicator of mitochondrial apoptotic pathway, was measured by western blot in optic lobe cytosolic extracts. DNA fragmentation by TUNEL fluorescence and caspase-3 fragmentation by immunofluorescence were detected on optic lobe sections. Acute hypoxia produces a significant increase in cyt c release from mitochondria at 4 h p-hx, followed by an increase in TUNEL positive cells two hours later (6 h p-hx). Administration of E(2) (0.5mg/egg) produced a significant decrease in cytosolic cyt c levels at 4 h p-hx, in casapse-3 activation and in TUNEL positive cells at 6 h p-hx when compared to vehicle treated embryos. In the E(2)-ICI 182,780 treated embryos, cyt c release, caspase-3 fragmentation and TUNEL positive cells were similar to the hypoxic embryos, thus suggesting the requirement of E(2)-ER interaction for E(2) mediated neuroprotective effects. In conclusion, E(2) prevents hypoxia induced cyt c release and posterior cell death and these effects are mediated by oestrogen receptors.

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