Suboptimal management of severe menopausal symptoms by Nigerian Gynaecologists: a call for mandatory continuing medical education for physicians

<p>Abstract</p> <p>Background</p> <p>Effective management of menopause is an important way to improve the quality of life of the increasing number of older women. The study sought to find out if Nigerian Gynaecologists offer effective treatment for severe menopausal symptoms.</p> <p>Methods</p> <p>126 Nigerian Gynaecologists representing the six health zones of Nigeria were interviewed to determine the menopausal symptoms they had ever encountered in their practices, frequency of the symptoms, treatments ever offered for severe symptoms including their attitude to, and practice of hormone replacement therapy.</p> <p>Results</p> <p>A Nigerian Gynaecologist encountered an average of one patient with menopausal symptoms every three months (range: 0-3 patients per month). The commoner symptoms they encountered were hot flushes (88%), insomnia (75.4%), depression (58.0%), irritability (56.3%), night sweats (55.6%) and muscle pains (54.8%) while urinary symptoms (16.7%) and fracture (1.6%) were less common. Treatments ever offered for severe symptoms were reassurance (90.5%), anxiolytics (68.3%), analgesics (14.3), HRT (7.9%), Vitamins (4%), Beta-blockers (3.2%) and Danazol (2.4%). These treatments were offered as a matter of institutional traditions rather than being based on any evidence of their efficacy.</p> <p>Conclusion</p> <p>The result revealed that most Nigerian Gynaecologists prefer reassurance and anxiolytics for managing severe menopausal symptoms instead of evidence-based effective therapies. A policy of mandatory continuing medical education for Nigerian physicians is recommended to ensure evidence-based management of gynaecological problems, including menopause.</p

Tamoxifen and Flaxseed Alter Angiogenesis Regulators in Normal Human Breast Tissue In Vivo

The incidence of breast cancer is increasing in the Western world and there is an urgent need for studies of the mechanisms of sex steroids in order to develop novel preventive strategies. Diet modifications may be among the means for breast cancer prevention. Angiogenesis, key in tumor progression, is regulated by the balance between pro- and anti-angiogenic factors, which are controlled in the extracellular space. Sampling of these molecules at their bioactive compartment is therefore needed. The aims of this study were to explore if tamoxifen, one of the most used anti-estrogen treatments for breast cancer affected some of the most important endogenous angiogenesis regulators, vascular endothelial growth factor (VEGF), angiogenin, and endostatin in normal breast tissue in vivo and if a diet supplementation with flaxseed had similar effects as tamoxifen in the breast. Microdialysis was used for in situ sampling of extracellular proteins in normal breast tissue of women before and after six weeks of tamoxifen treatment or before and after addition of 25 g/day of ground flaxseed to the diet or in control women. We show significant correlations between estradiol and levels of VEGF, angiogenin, and endostatin in vivo, which was verified in ex vivo breast tissue culture. Moreover, tamoxifen decreased the levels of VEGF and angiogenin in the breast whereas endostatin increased significantly. Flaxseed did not alter VEGF or angiogenin levels but similar to tamoxifen the levels of endostatin increased significantly. We conclude that one of the mechanisms of tamoxifen in normal breast tissue include tipping of the angiogenic balance into an anti-angiogenic state and that flaxseed has limited effects on the pro-angiogenic factors whereas the anti-angiogenic endostatin may be modified by diet. Further studies of diet modifications for breast cancer prevention are warranted

Comparison of static friction with self-ligating, modified slot design and conventional brackets

OBJECTIVE: To compare the static frictional forces generated at the bracket/wire interface of stainless steel brackets with different geometries and angulations, combined with orthodontic wires of different diameters. MATERIAL AND METHODS: The frictional forces were evaluated with three different types of metal brackets: a passive self-ligating (SmartClip(TM), 3M/Unitek, Monrovia, USA), with a modified slot design (Mini Uni Twin(TM), 3M/Unitek, Monrovia, USA) and conventional (Kirium, Abzil, São José do Rio Preto, Brazil). The samples were mounted in a testing device with three different angulations and tested with 0.014" and 0.018" stainless steel wires (American Orthodontics, Sheboygan, USA). The static frictional force was measured using a universal testing machine (DL 500, EMIC(®), São José dos Pinhais, Brazil) with a crosshead speed of 1 mm/min. Statistical analysis was performed by two-way ANOVA followed by Bonferroni's post hoc test. RESULTS: There was a significant difference (p<0.05) in static friction when the three types of brackets were tested with the same wire size. The wire diameter influenced friction only when the brackets had a 10º angulation (p<0.05). The angulation influenced friction (p<0.05) when the brackets were associated with a 0.018" wire. CONCLUSION: Brackets with a modified slot design showed intermediate static frictional force values between the conventional and self-ligating brackets tested

Estrogen regulation of apoptosis: how can one hormone stimulate and inhibit?

The link between estrogen and the development and proliferation of breast cancer is well documented. Estrogen stimulates growth and inhibits apoptosis through estrogen receptor-mediated mechanisms in many cell types. Interestingly, there is strong evidence that estrogen induces apoptosis in breast cancer and other cell types. Forty years ago, before the development of tamoxifen, high-dose estrogen was used to induce tumor regression of hormone-dependent breast cancer in post-menopausal women. While the mechanisms by which estrogen induces apoptosis were not completely known, recent evidence from our laboratory and others demonstrates the involvement of the extrinsic (Fas/FasL) and the intrinsic (mitochondria) pathways in this process. We discuss the different apoptotic signaling pathways involved in E2 (17β-estradiol)-induced apoptosis, including the intrinsic and extrinsic apoptosis pathways, the NF-κB (nuclear factor-kappa-B)-mediated survival pathway as well as the PI3K (phosphoinositide 3-kinase)/Akt signaling pathway. Breast cancer cells can also be sensitized to estrogen-induced apoptosis through suppression of glutathione by BSO (L-buthionine sulfoximine). This finding has implications for the control of breast cancer with low-dose estrogen and other targeted therapeutic drugs