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Pathogen research abs 1 || Pathogen research abs 2 || Pathogen research abs 3 || Pathogen research abs 4 || Pathogen research abs 5 || Hormone and endocrine research abs 1 || Hormone and endocrine research abs 2 || Hormone and endocrine research abs 3 || Hormone and endocrine research abs 4 || Hormone and endocrine research abs 5

Eur J Pharmacol. 2002 Aug 2;449(1-2):191-6.
Comparison of incadronate and alfacalcidol on increased bone turnover caused by ovariectomy in rats.

Teramura K, Fukushima S, Nozaki K, Kokubo S, Takahashi K.

Clinical Pharmacology Research Laboratories, Pharmacology Department, Institute for Drug Discovery Research, Yamanouchi Pharmaceutical Co., Ltd., 1-8, Azusawa 1-chome, Itabashi, Tokyo 174-8511, Japan. teramuramanouchi.co.jp

Mineral density of trabecular bone at the metaphyses of right tibiae was measured by peripheral quantitative computed tomography (pQCT) in ovariectomized rats. Bone mineral density (BMD) decreased dramatically in the 4 weeks following ovariectomy, suggesting that the method is sensitive enough to detect decreased bone mineral density within a short period. Orally administered incadronate dose dependently inhibited the decrease in trabecular bone mineral density induced by ovariectomy, as assessed 4 weeks after surgery. Significant inhibition was observed at doses of more than 0.3 mg/kg/day. Moreover, incadronate at doses of 1 mg/kg or more inhibited the increase in urinary deoxypyridinoline levels induced by ovariectomy, and although slightly increased serum intact parathyroid hormone (PTH) levels were observed, no significant alteration in serum calcium ion levels or urinary calcium excretion occurred. In contrast, while alfacalcidol inhibited the decrease in bone mineral density and the increase in urinary deoxypyridinoline levels at a dose of 300 ng/kg, it significantly lowered serum intact PTH levels and elevated serum free calcium levels as well as urinary calcium excretion. These results suggest that incadronate exerts its pharmacological effect (inhibition of bone resorption and increase in bone mass) by a mechanism different from that of alfacacidol.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12163124&dopt=Abstract

J Steroid Biochem Mol Biol. 2002 Jul;81(3):237-47.
Effect of tibolone (Org OD14) and its metabolites on aromatase and estrone sulfatase activity in human breast adipose stromal cells and in MCF-7 and T47D breast cancer cells.

van de Ven J, Donker GH, Sprong M, Blankenstein MA, Thijssen JH.

Department of Endocrinology, University Medical Center Utrecht, HP KE03-139.2, P.O. Box 85090, NL-3508 AB Utrecht, The Netherlands.

Tibolone (Org OD14) is a synthetic steroid used for post-menopausal hormone replacement therapy (HRT). Since HRT might increase breast cancer risk, it is important to determine the possible effects of tibolone on breast tissues. Tibolone and its metabolites Org 4094, Org 30126 and Org OM38 have been reported to inhibit estrone sulfatase activity in MCF-7 and T47D breast cancer cell lines, which suggest beneficial effects on hormone dependent breast cancer by reducing local production of free estrogens. Breast adipose stromal cells (ASCs) contain aromatase activity-an obligatory step in the biosynthesis of estrogens-and possibly contain sulfatase activity. We investigated the effects of tibolone, its metabolites and the pure progestin Org 2058 on PGE(2)-stimulated aromatase activity and on sulfatase activity in human ASC primary cultures and on sulfatase activity in MCF-7 and T47D cell lines. In MCF-7, tibolone and metabolites, but not Org 2058, were found to inhibit sulfatase activity. In T47D, tibolone inhibited sulfatase only at 10(-6)M, although weakly. ASC had high sulfatase activity, which was inhibited by 10(-6)M of tibolone, Org 4094 and Org 30126, but not by Org OM38 or Org 2058. Surprisingly, aromatase activity in ASC was increased by both tibolone and Org 2058 at 10(-6)M. As ligand binding assay results and immunohistochemistry indicated the absence of progesterone and estrogen receptors in ASC, these effects on aromatase and sulfatase activity in ASC likely take place by other routes. Because tibolone and its metabolites inhibit sulfatase activity, and because tibolone only increases aromatase activity at a high concentration, we conclude that effects of tibolone on the breast are probably safe.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12163135&dopt=Abstract

J Steroid Biochem Mol Biol. 2002 Jul;81(3):249-53.
Accumulation of 4- and 5-ene steroid sulfates in human breast cyst fluids.

Maeda Y, Tanaka E, Fujiwara M, Watanabe R, Furusawa H, Matsu T, Nakahara H, Nanba K, Higashi S, Setoguchi T.

Department of Surgery I, Miyazaki Medical College, Japan. maedayost.miyazaki-med.ac.jp

Gross cystic disease of the breast is one of the most common diseases of adult females. Breast cyst fluid contains various steroid hormones. In order to obtain more information about the concentrations of 4- and 5-ene steroids in human breast cyst fluids, levels of pregnenolone sulfate (PREGS), pregnenolone (PREG), dehydroepiandrosterone sulfate (DHEAS) and dehydroepiandrosterone (DHEA) were determined by high-performance liquid chromatography (HPLC). A total of 35 human breast cyst fluid samples, obtained from 35 patients (28-54 years old) were analyzed. Cyst fluid electrolytes were simultaneously determined. Levels of PREGS (mean+/-S.D.) were 26.9+/-20.0 micromol/l (N=35) and of PREG were <0.1 micromol/l. Levels of DHEAS and DHEA were 89.1+/-111.7 micromol/l (N=35) and 0.3+/-0.2 micromol/l (N=35), respectively. Cyst fluids were divided into two groups (types I and II) according to their electrolyte ratio (K(+)/Na(+)). The cysts of the type I group (K(+)/Na(+) >1.5) contained significantly higher levels of PREGS (39.9+/-21.1 micromol/l) and DHEAS (133.2+/-87.9 micromol/l) than those of the type II group (K(+)/Na(+) <1.5), the mean levels of which were 19.8+/-16.2 micromol/dl for PREGS, and 36.3+/-29.0 micromol/dl for DHEAS (P<0.05). PREGS and DHEAS levels in the cysts were significantly correlated (r=0.49; P<0.01). Human breast cyst fluids contain high concentration of DHEAS and PREGS, especially in the cyst fluids containing high K(+)/Na(+) ratios.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12163136&dopt=Abstract

FEBS Lett. 2002 Aug 14;525(1-3):116-20.
Ethanol inhibits leptin-induced STAT3 activation in Huh7 cells.

Degawa-Yamauchi M, Uotani S, Yamaguchi Y, Takahashi R, Abe T, Kuwahara H, Yamasaki H, Eguchi K.

First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, 852-8501, Nagasaki, Japan.

Leptin, an adipocyte-derived hormone, regulates food intake and energy expenditure in the hypothalamus via its receptor, member of the class I cytokine receptor family. Leptin resistance has been observed in rodents and in humans. However, the mechanisms could not be explained in most cases of human obesity, except for rare cases with mutations in the leptin receptor. Recent reports demonstrated that ethanol inhibited the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway activated by some members of the class I cytokine receptor family. In this study, we examined the effects of ethanol on the leptin-induced JAK/STAT signaling pathway using human hepatoma cell lines transiently expressing long form of the leptin receptor. A 30 min pretreatment with ethanol dose-dependently inhibited the leptin-induced STAT3 phosphorylation. Furthermore, to determine the time course of ethanol inhibitory effects, the cells were incubated in 10 mM ethanol for various times. Partial inhibition of leptin-induced STAT3 activation was seen after 1 min of treatment with ethanol and completely inhibited after 30 min pretreatment. SB 202190, a p38 mitogen-activated protein kinase (MAPK) inhibitor, partly prevented this inhibition by ethanol of leptin-induced STAT3 activation. These findings suggest that ethanol time- and dose-dependently inhibits the leptin action, in part via p38 MAPK.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12163172&dopt=Abstract

Cancer Epidemiol Biomarkers Prev. 2002 Aug;11(8):686-97.
Environmental toxins and breast cancer on Long Island. II. Organochlorine compound levels in blood.

Gammon MD, Wolff MS, Neugut AI, Eng SM, Teitelbaum SL, Britton JA, Terry MB, Levin B, Stellman SD, Kabat GC, Hatch M, Senie R, Berkowitz G, Bradlow HL, Garbowski G, Maffeo C, Montalvan P, Kemeny M, Citron M, Schnabel F, Schuss A, Hajdu S, Vinceguerra V, Niguidula N, Ireland K, Santella RM.

Department of Epidemiology, University of North Carolina, School of Public Health, Chapel Hill, North Carolina 27599-7435, USA. gammomail.unc.edu

Whether environmental contaminants increase breast cancer risk among women on Long Island, NY, is unknown. The study objective is to determine whether breast cancer risk is increased in relation to organochlorines, compounds with known estrogenic characteristics that were extensively used on Long Island and other areas of the United States. Recent reports do not support a strong association, although there are concerns with high risks observed in subgroups of women. Blood samples from 646 case and 429 control women from a population-based case-control study conducted on Long Island were analyzed. No substantial elevation in breast cancer risk was observed in relation to the highest quintile of lipid-adjusted serum levels of p,p'-bis(4-chlorophenyl)-1,1-dichloroethene (DDE) [odds ratio (OR), 1.20 versus lowest quintile; 95% confidence interval (CI), 0.76-1.90], chlordane (OR, 0.98; 95% CI, 0.62-1.55), dieldrin (OR, 1.37; 95% CI, 0.69-2.72), the sum of the four most frequently occurring PCB congeners (nos. 118, 153, 138, and 180; OR, 0.83; 95% CI, 0.54-1.29), and other PCB congener groupings. No dose-response relations were apparent. Nor was risk increased in relation to organochlorines among women who had not breastfed or were overweight, postmenopausal, or long-term residents of Long Island; or with whether the case was diagnosed with invasive rather than in situ disease, or with a hormone receptor-positive tumor. These findings, based on the largest number of samples analyzed to date among primarily white women, do not support the hypothesis that organochlorines increase breast cancer risk among Long Island women.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12163320&dopt=Abstract

Like developmental biology of any part of our body, hair growth is a complicated process. Hence the homework for modern science to yet unravel the process and mechanism to a completion. There exist a number of traditional and alternative therapeutic methods that include drugs, surgery, suppelements, and even snake oils that have been developed and used for those who lose hair. No understanding, and there is no solution. Of course, none of these approaches are perfect for all hair loss problems, especially due to the heterogeneity of the causes underlying hair losses. Most of chemical drugs and hair transplantation surgeries are accompanied by undesirable side effects.

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