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Evista (Raloxifene)

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Generic Evista is the most effective preparation in struggle against female osteoporosis symptoms (bones weakness) after period of menopause. Generic Evista acts as up-to-date anti-osteoporosis remedy which provides bones strengths and health. Generic Evista acts improving bones states, their strength.

Other names for this medication:

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Also known as:  Raloxifene.


Generic Evista is created using perfect medical formula which is a magnificent weapon against women problem such as osteoporosis symptoms (bones weakness) after period of menopause. Target of Generic Evista is to make bones stronger.

Generic Evista acts as up-to-date anti-osteoporosis remedy which provides bones strengths and health. Generic Evista acts improving bones states, their strength.

Evista is also known as Raloxifene, Ralista.

Generic Evista is estrogen (woman hormone).

Generic Evista can't lead to vaginal bleeding, uterine or breast cancer, breast tenderness.

Generic name of Generic Evista is Estrogen.

Brand name of Generic Evista is Evista.


Generic Evista can be taken in form of tablets which should be taken by mouth with water.

Take Generic Evista every day at the same time and remember that its dosage depends on patient's health state.

If you want to achieve most effective results do not stop taking Generic Evista suddenly.


If you overdose Generic Evista and you don't feel good you should visit your doctor or health care provider immediately.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Throw away any unused medicine after the expiration date. Keep out of the reach of children in a container that small children cannot open.

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Generic Evista if you are allergic to Generic Evista components.

Do not take Generic Evista if you're pregnant or you plan to have a baby, or you are a nursing mother.

Be careful with Generic Evista in case of using diazoxide such as Proglycem, diazepam such as Zetran,Valium, Valrelease, cholestyramine such as Questran, colestipol such as Colestid, estrogen or hormone replacement therapy such as ERT or HRT, warfarin such as Coumadin.

Be careful with Generic Evista in case of having of cancer, stroke, liver or heart disease, breast lumps, high blood cholesterol, blood clots, triglycerides, phlebitis in the leg.

Use Generic Evista with great care in case you want to undergo an operation (dental or any other).

Generic Evista can't lead to vaginal bleeding, uterine or breast cancer, breast tenderness.

If you take Generic Evista it is dangerous to smoke cigarettes.

Generic Evista can be dangerous for children.

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evista medicine

The osteoblast-derived paracrine factor osteoprotegerin (OPG) is considered to play a key role in inhibition of osteoclast formation and activity. Recently, raloxifene, a nonsteroidal benzothiophene, was found to exert anti-resorptive effects via modulating OPG expression in osteoblasts. To explore whether raloxifene regulates bone metabolism via an OPG-dependant pathway in vivo, we investigated the effects of raloxifene on bone loss in Opg-deficient mice. The results show that bone mineral density and bone strength are increased in mice deficient for Opg after treatment with raloxifene for 30 days. Histomorphometric analysis shows that raloxifene can increase bone trabecular area and decrease the number of osteoclasts in Opg (-/-) mice. Moreover, raloxifene reduces Rankl transcription and serum level of Rankl, which is dramatically increased in Opg knockout mice. These results suggest that raloxifene-induced inhibition of bone resorption may be independent of Opg pathway in mice.

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Raloxifene, a selective estrogen receptor modulator, is estrogen-like in the skeleton and cardiovascular system and antiestrogenic in reproductive tissues. In contrast to estrogens, raloxifene is not indicated for the treatment of hot flashes. This study was designed to examine the characteristics of hot flashes among healthy postmenopausal women participating in osteoporosis prevention trials who were receiving raloxifene or placebo.

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Liposomes were prepared by thin film hydration method using 1:1 molar ratio of DSPC:Cholesterol and characterized for vesicle size, zeta potential, %entrapment efficiency, loading, drug release and transmission electron microscopy. Radiolabeling of RLH was performed with reduced technetium-99m ((99m)Tc). Binding affinity of (99m)Tc-labeled complexes was assessed by diethylene triamine penta acetic acid (DTPA) challenge test. Biodistribution study was done in New Zealand white female rabbits by administering the formulation intravaginally.

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Limitations include the lack of a control group, the possibility of the changes being due to the natural disease course, and potential selection bias.

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Only bisphosphonates are cost-effective for fracture prevention in osteoporotic women aged 65 or older and this economic advantage is also maintained in subsets who have a lower relative risk of future fracture.

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Little information is available on the comparative effectiveness of osteoporosis pharmacotherapies.

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Two types of mammary tumors were studied: tumors transplanted in BALB/c mice that are medroxyprogesterone acetate (MPA)-dependent for growth, and tumors induced in Sprague-Dawley rats by intraperitoneal injection of N-nitroso-N-methylurea (NMU). Tumors from mice treated with MPA, E(2), Tam or Ral and NMU-treated rats were analyzed and compared to that of control.

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The percentage of Ki-67-stained nuclei per 500 cells in the mammary epithelium was 42.33 ± 6.18 and 15.51 ± 3.71 [mean ± standard error of the mean (SEM)] in the control and experimental groups, respectively (p < 0.001).

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A review of all published reports was facilitated by the use of Medline computer searches.

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Tamoxifen had an oestrogen receptor dependent, direct, inhibitory effect on human osteoclast differentiation and bone resorption, whereas ospemifene and raloxifene required osteoblastic cells to achieve a similar inhibition. The effects of ospemifene and raloxifene were mediated by oestrogen receptors by a mechanism involving paracrine induction of osteoprotegerin in cultures with osteoblast derived osteosarcoma cells.

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A set of now-completed, randomised clinical trials form the basis of our clinical understanding of the effects of raloxifen on the bones and are discussed in the paper.

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This study examined patients' risk profiles and adherence to treatment in relation to the effect of risedronate and raloxifene on hip fracture incidence. Administrative billing data were used to follow two cohorts of women aged 65 and older after starting therapy with either risedronate (n = 86,735) or raloxifene (n = 37,726). The fracture risk profile was described using a 6-month history period before starting therapy. Effectiveness of each therapy was evaluated by comparing the incidence of hip fractures during the first 3 months with the subsequent 12 months among women adherent (medication possession ratio >80%) compared with those non-adherent to treatment. At the start of therapy, the raloxifene cohort was younger than the risedronate cohort (median age 73 vs. 76 years) and had fewer prior fractures (p < 0.01 for both). In the first 3 months of therapy, hip fracture incidence was lower in the raloxifene group (0.51 per 100 person-years) compared with the risedronate group (0.94 per 100 person-years). In the subsequent 12 months, the incidence of hip fractures decreased among patients adherent to the risedronate regimen [relative risk (RR) 0.70, 95% CI 0.59-0.84, p < 0.01] and did not change significantly among patients adherent to the raloxifene regimen (RR 1.02, 95% CI 0.73-1.44). In poorly adherent patients, neither drug decreased hip fracture risk. Risedronate treatment in adherent patients rapidly decreased the risk of hip fractures, whereas raloxifene treatment did not.

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Postmenopausal hormone therapy (HT) is associated with an increased risk for arterial and venous thrombosis.

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Raloxifene is a selective oestrogen receptor modulator with effects on bone and breast cancer and cardiovascular disease risk. The aim of this study was to examine the influence of raloxifene treatment on surrogate markers of atherosclerosis and the correlation of these markers with raloxifene serum concentrations.

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Most domains in the Osteoporosis Assessment Questionnaire 2.0 demonstrated robust psychometric properties; however, several domains not showing these criteria may need to be reassessed and removed for a potentially shorter and validated version of the Osteoporosis Assessment Questionnaire.

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The treatment that is proposed in this study can constitute a temporary alternative during the period of transition from HT to raloxifene.

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evista buy 2017-02-17

Estrogens have cell-specific effects on a variety of physiological endpoints including regulation of mitochondrial biogenesis and activity. Estrogens regulate gene transcription by the classical genomic mechanism of binding to estrogen receptors alpha and beta (ERalpha and ERbeta) as well as the more recently described nongenomic pathways involving plasma membrane-associated ERs that activate intracellular protein kinase-mediated phosphorylation signaling cascades. Here I evista buy will review the rapid and longer-term effects of estrogen on mitochondrial function. The identification of ERalpha and ERbeta within mitochondria of various cells and tissues is discussed with a model of estrogen regulation of the transcription of nuclear respiratory factor-1 (NRF-1, NRF1). NRF-1 subsequently promotes transcription of mitochondrial transcription factor Tfam (mtDNA maintenance factor, also called mtTFA) and then Tfam targets mtDNA-encoded genes. The nuclear effects of estrogens on gene expression directly controlling mitochondrial biogenesis, oxygen consumption, mtDNA transcription, and apoptosis are reviewed. Overall, we are just beginning to evaluate the many direct and indirect effects of estrogens on mitochondrial activities.

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We previously demonstrated that 1 or 5 mg per day of tamoxifen (T) given for four weeks before surgery reduces Ki-67 in breast cancer (BC) patients to the same extent as the standard 20 mg/d. Given the long half-life of T, evista buy a weekly dose (10 mg per week (w)) may be worth testing. Also, raloxifene (R) has shown Ki-67 reduction in postmenopausal patients in a preoperative setting, but data in premenopausal women are limited. We conducted a randomized trial testing T 10 mg/w vs. R 60 mg/d vs. placebo in a presurgical model.

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Women with the highest IR-HOMA scores were associated with a significantly Stromectol Online higher weight, body mass index, waist and waist-to-hip ratio (p < 0.05). Raloxifene significantly reduced the IR-HOMA scores from 5.76 ± 2.91 to 1.93 ± 0.96 (p = 0.02) and modified the lipid profile in insulin-resistant patients when compared with the placebo group and those patients receiving raloxifene in the insulin-sensitive group.

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Hormone replacement therapy has been implicated in the increased incidence of breast cancer, although selective estrogen receptor modulators have been shown to be effective in the prevention of breast cancer. Breast cancers are associated with increased mammary blood flow compared to benign breast lesions. However, few studies have examined the hemodynamic effects of hormonal agents on the mammary circulation that promote or reduce the risk of breast cancers. Although estradiol-17beta has been shown to increase mammary blood flow, the effect of selective estrogen receptor modulators remains undetermined. We therefore compared the vascular effects of selective Vasotec Drug Card estrogen receptor modulators and estrogens on mammary blood flow.

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University of Pennsylvania Health System. Zofran 50 Mg

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In the 1960s, compounds known as nonsteroidal antiestrogens were identified as potential contraceptives, but the drugs caused the induction of ovulation in subfertile women. Tamoxifen and clomiphene were marketed for this indication. However, tamoxifen was advanced for the treatment of breast cancer in the 1970s through a close cooperation between the laboratory and the clinical trials community. The extensive use of long-term adjuvant tamoxifen has resulted in saving the lives of 400,000 women with breast cancer. Tamoxifen is a selective estrogen receptor modulator (SERM) that produces antiestrogenic actions in the breast but estrogen-like actions in bone and lowers serum cholesterol. These properties not only allowed the application of tamoxifen as the first chemopreventive in high-risk pre- and postmenopausal women but also the development of raloxifene to prevent osteoporosis with the potential to prevent breast cancer in postmenopausal women. The future development of Nexium Reviews 2014 SERMs holds the promise of preventing osteoporosis and coronary heart disease as well as breast and endometrial cancer.

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This prospective randomized single-blind placebo-controlled clinical trial was carried out to evaluate the effects of raloxifene administration on uterine and leiomyoma sizes in premenopausal women. Ninety healthy premenopausal women affected by asymptomatic uterine leiomyomas were enrolled and treated with raloxifene at the doses of 60 mg/d (group A), 180 mg/d (group B), or placebo (group C). The duration of the treatment was 6 cycles of 28 d each. At entry and after three and six cycles, uterine and leiomyoma sizes were measured by transvaginal ultrasonography. The difference between uterine and leiomyoma volumes (Delta size) was calculated in all subjects. The characteristics of the menstrual cycles and the side effects of the treatments were recorded using a daily diary. The severity of the uterine bleedings was assessed using a rank scale. Throughout the study, no significant changes were observed in uterine Strattera Cost Canada and leiomyoma size or in Delta size among the three groups and within each group of treatment. The length and severity of uterine bleedings was not significantly different between the three groups and within each group. In conclusion, raloxifene has no significant effect on uterine and leiomyoma size or on menstrual cycle in premenopausal women.

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In postmenopausal women with osteoporosis, 3 years of treatment with raloxifene had no effect Plavix Tablet Usage on urinary incontinence.

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Raloxifene treatment was useful for the prevention Zyloprim Overdose of BMD deterioration in postmenopausal dialysis patients with controlled iPTH levels.

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One of two oral treatments: 5 days of 100 mg/day Moduretic Dose of CC or R.

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To explore decision making and the use of probabilities for decision making from the perspective of women who were risk-eligible Valtrex Generic Name to enroll in the Study of Tamoxifen and Raloxifene (STAR).

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Loss of bone mineral density occurs after discontinuation of teriparatide, if no subsequent treatment is given. Sequential raloxifene prevented rapid bone loss at lumbar spine and further increased bone mineral density (BMD) at femoral neck, whether raloxifene was started immediately or Flagyl Alcohol Interaction after a one-year delay following teriparatide treatment.

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No significant differences existed between groups for baseline measurements prior to phase I. In phase I, for all subjects combined, total cholesterol and low-density lipoprotein cholesterol both showed a significant increase (median increase of 0.2 mmol/l, p = 0.008 and 0.4 mmol/l, p< 0.001, respectively), while triglycerides decreased significantly (median decrease of 0.2 mmol/l, p< Detrol Generic Medication 0.001). For the primary analysis (phase II to phase IV), the mean change from baseline observations showed no significant differences between the therapy groups for serum lipids, fibrinogen, vital signs or weight. In the comparison phase (phase II), changes in serum lipids, fibrinogen, vital signs and weight were not significantly different between groups.

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Several agents have been advocated for breast cancer primary prevention. However, few of Famvir 1000 Mg them appear effective, the associated severe adverse effects limiting their uptake.

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To determine whether women taking raloxifene have a lower Retrovir Generic Name risk of invasive breast cancer.

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We aimed to analyze the effects of raloxifene and estrogen on thyroid gland morphology of ovariectomized rats. Raloxifene treatment led to effects similar to those of estrogen on thyroid glands from ovariectomized rats, so that both were able to normalize the changes detected after ovariectomy.

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There were no obvious additional safety concerns for women aged 75 years or older who were treated with raloxifene. The findings in this post hoc evaluation suggest no differences in adverse events in the age groups evaluated.

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In men, the stimulation of GH and inhibition of LH secretion by testosterone requires aromatization to estradiol. Tamoxifen, a selective estrogen receptor modulator (SERM), possesses central estrogen antagonistic effect but peripheral hepatic agonist effect, lowering IGF-I. Thus, tamoxifen is likely to perturb the neuroendocrine regulation of GH and gonadal axes. Raloxifene, a SERM, is used for therapy of osteoporosis in both sexes. Its neuroendocrine effects in men are poorly understood.

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We have isolated a highly expressed splice variant mRNA of murine estrogen receptor-beta (ERbeta), mERbeta2, containing an in-frame 54 nucleotide insertion between exons 5 and 6 of wild-type mERbeta1. The predicted ERbeta2 protein contains 18 amino acids inserted in the ligand binding domain of mERbeta1. Recombinant protein generated by in vitro transcription/translation showed that mERbeta2 had markedly reduced ligand binding (K(D)=17.7+/-4.7 nM, mean+/-s.e.m., n=3) compared with mERbeta1-bound (3)H-estradiol (K(D)=0.56+/- 0.19 nM, mean+/-s.e.m., n=3). Both receptors bound similarly to palindromic estrogen responsive elements (EREs) in vitro and in vivo, and similarly bent DNA. Transcriptional activity was assessed using transient transfection analysis into a homologous murine cell line, NIH 3T3 cells. mERbeta1 transactivated ERE-tk-CAT reporter genes similarly to mERalpha, whereas mERbeta2 had little activity except at high ligand concentrations. However, under conditions in which mERbeta2 is unlikely to be ligand saturated, co-transfected mERbeta2 inhibited activity of mERalpha and possibly mERbeta1 on ERE-tk-CAT genes. Using a 'novel raloxifene responsive' gene reporter system (TGF-beta3-CAT), we found the ability of estradiol and LY117018 to activate both mERalpha and mERbeta1 on this promoter was identical, and mERbeta2 activity in the presence of either estradiol or LY117018 was only slightly less than that observed with either mERbeta1 or mERalpha. Both mERbeta1 and mERbeta2 when liganded with LY117018 inhibited transcription at a classical ERE-regulated promoter under these transfection conditions, which was in marked contrast to their stimulatory effect at the transforming growth factor-beta3 promoter. These data suggest that responsiveness of gene expression to a relatively highly expressed variant murine ERbeta isoform, mERbeta2, is both ligand and promoter specific. Determination of the relative level of expression of mERbeta1 mRNA and mERbeta2 mRNA in mouse tissues indicated predominance of mERbeta2 mRNA in some but not all tissues. These data suggest that the mERbeta2 may have some tissue-specific and promoter-specific modulatory effects.

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A MEDLINE search was performed for January 1980 through September 1998 using the key terms raloxifene, estrogen, CVD, lipoproteins, and osteoporosis.

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Covalent binding of reactive metabolites to cytochrome P450s (P450s) often causes their mechanism-based inactivation (MBI), resulting in drug-drug interactions or toxicity. The detection and identification of the P450 sites to which reactive metabolites bind would elucidate MBI mechanisms. We describe a proteomic approach using nano-LC/linear ion trap-Fourier transform ion cyclotron resonance (FTICR) mass spectrometry to characterize the binding of a reactive metabolite of raloxifene, which is a known P450 3A4 inhibitor, to the P450 3A4 isozyme. LTQ-FT analyses revealed that the metabolic reaction of raloxifene in a reconstituted P450 3A4 system formed a reactive metabolite adduct to P450 3A4 apoprotein, accompanied by a mass shift of 471 Da relative to intact P450 3A4 apoprotein. The reaction mixtures were digested with trypsin, and then the tryptic digests were analyzed by nano-LC-MS/MS. This technique revealed that VWGFYDGQQPVLAITDPDMIK (position 71-91) was a tryptic peptide modified by the reactive metabolite derived from raloxifene. The site of adduction with the reactive metabolite was further postulated to be the nucleophilic OH group of Tyr-75 of P450 3A4. A proteomic approach using LTQ-FT can yield direct information on the P450 3A4 modification site without radiolabeled compounds. In addition, this information can elucidate mechanisms involved in the covalent binding of reactive metabolites and the inactivation of P450 3A4.

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We tested the safety and tolerability of combination exemestane and raloxifene in 11 postmenopausal women with a history of hormone receptor-negative breast cancer. Patients were randomized to either raloxifene (60 mg PO daily) or exemestane (25 mg PO daily) for 2 weeks. Patients then initiated combination therapy at the same dose levels for a minimum of 1 year. Pharmacokinetic and pharmacodynamic data for plasma estrogens, raloxifene, exemestane, and their metabolites were collected at the end of single-agent therapy and during combination therapy.

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These data demonstrate that raloxifene has vascular relaxing properties. The surprising finding is that the receptor-dependent effects via the endothelium are observed in coronary arteries from both male and female animals.

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Athymic mice were transplanted with an endometrial tumor model (ECC-1 E2) that is responsive to estrogen and has never been exposed to antiestrogen. In addition, we used three breast tumor models: a tamoxifen-naïve tumor (T47D-E2) and two tamoxifen-stimulated tumors (MT2 TAM and MCF-7 TAM LT). The antiestrogen GW5638 (1.5 mg daily), tamoxifen (0.5 mg or 1.5 mg daily), and raloxifene (1.5 mg daily) were given p.o. The pure antiestrogen ICI182,780 (5 mg once a week) was given s.c. Western blots from MCF-7 TAM breast tumors were performed to demonstrate the regulation of estrogen receptor alpha expression by different ligands.

evista buy 2015-11-02

Raloxifene, a selective estrogen receptor modulator, is estrogen-like in the skeleton and cardiovascular system and antiestrogenic in reproductive tissues. In contrast to estrogens, raloxifene is not indicated for the treatment of hot flashes. This study was designed to examine the characteristics of hot flashes among healthy postmenopausal women participating in osteoporosis prevention trials who were receiving raloxifene or placebo.

evista buy 2017-05-25

To examine raloxifene use among women with a history of breast cancer.

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Estrogen down-regulated alpha1A-adrenergic receptor expression in the urethral smooth muscle of female rats, while raloxifene and levormeloxifene had no significant effect. These findings represent a possible molecular mechanism through which estrogen, raloxifene and levormeloxifene differentially affect urinary continence.

evista buy 2017-07-20

We evaluated bone mass, bone microarchitecture, and bone strength in adult OVX, osteopenic rats, during different sequences of vehicle (Veh), parathyroid hormone (PTH), Aln, or raloxifene (Ral) in three 90-day treatment periods, over 9 months. Differences among groups were evaluated. The interrelationships of bone mass and microarchitecture endpoints and their relationship to bone strength were studied.

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Estradiol and some selective estrogen receptor modulators (SERMs) are neuroprotective in a variety of experimental models of neurodegeneration, reduce the inflammatory response of glial cells, reduce anxiety and depression, promote cognition and modulate synaptic plasticity in the hippocampus of rodents. In this study we have assessed whether estradiol and two SERMs currently used in clinics, tamoxifen and raloxifene, affect medial prefrontal cortex function and morphology. Rats were ovariectomized and six days later some animals received a subcutaneous injection of the estrogenic compounds. In a first experiment animals were treated with estradiol benzoate or sesame oil vehicle. In a second experiment animals received raloxifene, tamoxifen or dimethyl sulfoxide as vehicle. Twenty four hours after the pharmacological treatment, animals were challenged to solve an allocentric working memory paradigm in a "Y" maze. Twenty trials consisting of a study phase and a test phase were conducted according to a delayed match-to-sample procedure in a single one-day session. Animals that were not submitted to behavioral test were used for Golgi analysis of the prefrontal cortex. Rats treated with estradiol benzoate, tamoxifen or raloxifene performed better in the Y maze and showed a significant increase in the numerical density of dendritic spines in secondary apical dendrites of layer III pyramidal neurons from the prelimbic/infralimbic prefrontal cortex, compared to their respective control groups. These findings suggest that estradiol, tamoxifen and raloxifene improve prefrontal cortex-related cognitive performance and modulate prefrontal cortex morphology in ovariectomized rats.

evista buy 2015-08-25

The anti-osteoporotic drug raloxifene reduces the risk of vertebral fractures by increasing bone mass density. We investigated whether raloxifene offers any benefits in augmenting early fixation of orthopedic implants in the setting of impaction bone grafting.

evista buy 2015-10-14

10-6 M Raloxifene had no ossification-inducing effect on female MSCs, but it had an ossification-promoting effect; it had no osteogenic effect on male MSCs. Therefore, raloxifene has a sex difference with regard to its osteogenic effect on MSCs. Moreover, combined treatment with raloxifene plus OS has an effect on female MSCs. These results provide a useful insight into the possible influence of raloxifene after MSC transplantation in clinical practice.

evista buy 2016-11-24

The dose-dependent effect of a 24 h treatment with estradiol (E(2)) (1, 2, 5, 10 nM) and raloxifene (Rx) (1, 5, 10, 20 microM) on ER alpha and ER beta mRNA expression, collagen bio-synthesis, prolidase activity, MMP-2, MMP-9, insulin-like growth factor I receptor expression (IGF-1R) and beta1-integrin expressions in cultured fibroblasts obtained from postmenopausal women were examined. Both ligands increased mRNA expression of ER compared to control. Rx at 5 and 10 microM concentrations had greater stimulative effect on collagen biosynthesis, prolidase activity and IGF-1R expression compared to E(2) at 2 and 5 nM concentration. Both studied ER ligands had no effect on beta1-integrin receptor expressions. MMP-2 expression was not detected in human skin fibroblast culture. In contrast to estradiol raloxifene inhibited the expression of MMP-9. Raloxifene had stronger positive stimulative effects on collagen biosynthesis, through different biochemical mechanisms, than estradiol in human skin fibroblasts and might reverse some of the postmenopausal changes in skin or connective tissue. Increase of collagen synthesis induced by raloxifene may be activated by both estrogen receptor dependent and independent pathways such as up-regulation of estrogen receptors, up-regulation of IGF receptor, transcriptional regulation of collagen genes by estrogen receptor-raloxifene complex, increasing of prolidase activity or finally by inhibition of MMP-9 expression.

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The dropout rate was 23% (41 patients): 20 patients (31%) in the raloxifene group and 21 (18%) in the alendronate group (P = 0.0041). The main reasons for dropout were side effects and/or noncompliance, 16 and 24 patients (39% and 58.53%) respectively. The most frequent side effect was abdominal pain in 9 patients (42.8%) who discontinued alendronate use. The reasons for non-compliance were a fear of side effects and high drug price in 6 (30%) and 4 (20%) patients respectively in the raloxifene group, and inconvenience caused by medication use in 3 patients (14.3%) in the alendronate group. Logistic regression analysis of factors that may influence compliance included age, previous fractures, family history of osteoporosis, bone density T-score less than -2.5, and presence and number of concomitant diseases. Age was the only statistically significant parameter in this model: 67.8 +/- 8.8 in non-compliant versus 64.11 +/- 7.4 in compliant patients (P = 0.029).

evista buy 2015-10-17

The direct effects of keoxifene (LY 156758), a benzothiphene-derived antiestrogen, on granulosa cell differentiation were examined in vitro using primary cultures of rat granulosa cells. The effect of keoxifene on FSH-stimulated aromatase activity was biphasic in pattern, enhancing at lower concentrations (up to 10(-8) M), and inhibiting at higher concentrations (greater than 10(-6) M). Keoxifene inhibited FSH-stimulated progestin production in a dose-dependent fashion with an IC50 of 5 X 10(-8) M. FSH-induced LH receptors were also inhibited by keoxifene with an IC50 of 5 X 10(-7) M. These findings suggest that keoxifene has direct pharmacologic actions at the ovarian level. In contrast to the earlier reported estrogenic actions of triphenylethylene antiestrogens at the ovarian level, the benzothiphene-derived antiestrogens may be clinically more useful in the management of estrogen-dependent malignancies.

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One hundred eighty community settings and medical practices in 25 countries including the United States.

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While it is obvious that patients should be involved in the decision making process, questions arise as to whether it is feasible to inform them objectively.