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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

J Biol Chem. 2002 Oct 25;277(43):41259-67. Epub 2002 Aug 16.
Repression of DAX-1 and induction of SF-1 expression. Two mechanisms contributing to the activation of aldosterone biosynthesis in adrenal glomerulosa cells.

Osman H, Murigande C, Nadakal A, Capponi AM.

Division of Endocrinology and Diabetology, University Hospital, 24 rue Micheli-du-Crest, CH-111 Geneva 14, Switzerland.

Angiotensin II (Ang II) and adrenocorticotropic hormone stimulate aldosterone biosynthesis in the zona glomerulosa of the adrenal cortex through induction of the expression of the steroidogenic acute regulatory (StAR) protein, which promotes intramitochondrial cholesterol transfer. To understand the mechanism of this induction of the StAR protein, we have examined the effect of Ang II and forskolin, a mimicker of adrenocorticotropic hormone action, on two transcription factors known to modulate StAR gene expression in opposite ways, DAX-1 and SF-1, in bovine adrenal glomerulosa cells in primary culture. Ang II markedly inhibited DAX-1 protein expression in a time- and concentration-dependent manner (to 38.7 +/- 12.9% of controls at 3 nm after 6 h, p < 0.01), an effect that required de novo protein synthesis and ERK2/1 activation. This effect was associated with a concomitant decrease in DAX-1 mRNA and an increase in mitochondrial StAR protein levels. Similarly, forskolin dramatically repressed DAX-1 protein and mRNA expression (to 19.6 +/- 1.8 and 50.3 +/- 4.7% of controls, respectively, p < 0.01). Neither Ang II nor forskolin affected DAX-1 protein and mRNA stability. The aldosterone response to Ang II was markedly reduced (to 59 +/- 4% of controls, p < 0.01) in transiently transfected cells overexpressing DAX-1. Whereas Ang II was without effect on SF-1 expression, forskolin significantly increased SF-1 protein and mRNA levels in a cycloheximide-sensitive manner (to 167.4 +/- 16.6 and 173.1 +/- 25.1% of controls after 6 h, respectively, p < 0.01). These results demonstrate that the balance between repressor and inducer function of DAX-1 and SF-1 are of critical importance in the regulation of adrenal aldosterone biosynthesis.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12186872&dopt=Abstract

Proc Natl Acad Sci U S A. 2002 Sep 3;99(18):11866-71. Epub 2002 Aug 19.
The expression of growth hormone-releasing hormone (GHRH) and splice variants of its receptor in human gastroenteropancreatic carcinomas.

Busto R, Schally AV, Varga JL, Garcia-Fernandez MO, Groot K, Armatis P, Szepeshazi K.

Endocrine, Polypeptide, and Cancer Institute, Veterans Affairs Medical Center, and Section of Experimental Medicine, Department of Medicine, Tulane University School of Medicine, New Orleans, LA 70112, USA.

Splice variants (SVs) of receptors for growth hormone-releasing hormone (GHRH) have been found in primary human prostate cancers and diverse human cancer cell lines. GHRH antagonists inhibit growth of various experimental human cancers, including pancreatic and colorectal, xenografted into nude mice or cultured in vitro, and their antiproliferative action could be mediated in part through SVs of GHRH receptors. In this study we examined the expression of mRNA for GHRH and for SVs of its receptors in tumors of human pancreatic, colorectal, and gastric cancer cell lines grown in nude mice. mRNA for both GHRH and SV(1) isoform of GHRH receptors was expressed in tumors of pancreatic (SW1990, PANC-1, MIA PaCa-2, Capan-1, Capan-2, and CFPAC1), colonic (COLO 320DM and HT-29), and gastric (NCI-N87, HS746T, and AGS) cancer cell lines; mRNA for SV(2) was also present in Capan-1, Capan-2, CFPAC1, HT-29, and NCI-N87 tumors. In proliferation studies in vitro, the growth of pancreatic, colonic, and gastric cancer cells was stimulated by GHRH(1-29)NH(2) and inhibited by GHRH antagonist JV-1-38. The stimulation of some gastroenteropancreatic cancer cells by GHRH was followed by an increase in cAMP production, and GHRH antagonist JV-1-38 competitively inhibited this effect. Our study indicates the presence of an autocrine/paracrine stimulatory loop based on GHRH and SV(1) of GHRH receptors in human pancreatic, colorectal, and gastric cancers. The finding of SV(1) receptor in human cancers provides an approach to an antitumor therapy based on the blockade of this receptor by specific GHRH antagonists.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12186980&dopt=Abstract

Gynecol Obstet Invest. 2002;53(4):224-30.
The expression of apoptosis-related proteins Bcl-2 and Ki67 in endometrium of ovulatory menstrual cycles.

Mertens HJ, Heineman MJ, Evers JL.

Department of Obstetrics and Gynecology, Research Institute Growth and Development, GROW, University Hospital Maastricht, The Netherlands. hmertenrbisconcern.nl

BACKGROUND: During the menstrual cycle, a rapid sequence of proliferation, differentiation and cell death occurs in the human endometrium. Mechanisms involved in cell proliferation have been studied extensively. Apoptosis has recently been recognized to be a physiologic phenomenon. The aim of this study was to investigate the mechanisms involved in hormone-dependent tissue remodeling by measuring Bcl-2, an apoptosis inhibitor, and Ki67, a proliferation marker, as expressed in normal human endometrium. METHODS: Paraffin-embedded endometrial sections of 30 uteri were immunostained for Bcl-2 and Ki67; expression was scored in cavitary epithelium, functional and basal glandular epithelial and stromal cells of the endometrium. RESULTS: Bcl-2 expression increased in the proliferative phases and decreased significantly in the secretory phases, especially in glandular epithelial cells (131 +/- 45 for functional laminal cells and 227 +/- 68 for basal laminal cells to 0). Ki67 expression showed the same cyclic pattern with a later onset (145 +/- 63 for functional laminal cells and 13 +/- 8 for basal laminal cells to 0). CONCLUSION: Bcl-2 promotes cell survival by preventing apoptosis. Proliferation is the result of increasing estradiol concentration, high estrogen receptor expression and growth hormones and high Bcl-2 and Ki67 expression. After the onset of progesterone production, Bcl-2 levels decrease and Ki67 levels and androgen receptor expression in stromal cells disappear resulting in cell disintegration and menstruation. Persistent Bcl-2 expression, like we saw in basal laminal stromal and epithelial cells, accounts for the privilege of escaping from apoptosis-inducing signals. This allows reconstruction of the functional endometrium from its preserved basal layer after menstruation. 2002 S. Karger AG, Basel

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12186988&dopt=Abstract

J Urol. 2002 Sep;168(3):995-1000.
Prognostic significance of the nadir prostate specific antigen level after hormone therapy for prostate cancer.

Kwak C, Jeong SJ, Park MS, Lee E, Lee SE.

Department of Urology, Seoul National University College of Medicine and Clinical Research Institute, Seoul National University Hospital, Seoul, Korea.

PURPOSE: We determine whether the nadir prostate specific antigen (PSA) level after hormone therapy can be used to predict the progression to hormone refractory prostate cancer. MATERIALS AND METHODS: We reviewed the progressive status and survival of 177 patients with stage C or D prostate cancer who had received hormone therapy at our institution. The overall survival rate, incidence of progression to hormone refractory prostate cancer and interval until progression were analyzed with reference to the nadir PSA level. Multiple regression analysis was used to analyze the predictive factors for progression to hormone refractory prostate cancer, and the relative efficacy of the nadir PSA level in predicting progression was evaluated by receiver operating characteristics analysis. RESULTS: Median followup was 39 months (range 3 to 89) and 85.4% of patients (151) responded to treatment, of whom 77.5% (117) had progression to hormone refractory prostate cancer. Median time until nadir PSA levels were reached after hormone therapy was 8.1 months and median time until hormone refractory prostate cancer was 24.0 months. Nadir PSA levels were less than 0.2 ng./ml. in 31% of respondents, 0.2 to 1.0 ng./ml. in 23%, 1.1 to 10 ng./ml. in 42% and greater than 10 ng./ml. in 5%. These groups had similar clinicopathological characteristics. Nadir PSA levels correlated significantly with pretreatment PSA levels, Gleason scores and progression to hormone refractory prostate cancer (p = 0.01, p <0.01 and p <0.001, respectively), and inversely correlated with the interval to the establishment of hormone refractory prostate cancer (r = -0.465, p <0.05). By univariate analysis bone metastasis, nadir PSA, PSA at 6 months after treatment and pretreatment PSA were significantly associated with progression to hormone refractory prostate cancer. Only the nadir PSA was calculated to be an independent factor by multivariate analysis. Receiver operating characteristics analysis indicated that nadir PSA predicted progression to hormone refractory prostate cancer after 2 years with an accuracy of 86.2%. With the lower limit of the nadir PSA level set to 1.1 ng./ml., sensitivity was 80.3% and specificity was 83.8%, and these levels were deemed the most appropriate. Furthermore, nadir PSA after hormone therapy was an independent prognosticator for survival, as were initial levels of hemoglobin and alkaline phosphatase. CONCLUSIONS: The nadir PSA level after hormone therapy may be the most accurate factor predicting the progression to hormone refractory prostate cancer and is an independent prognostic factor for survival. Furthermore, a lower limit for the nadir PSA level of 1.1 ng./ml. gives optimal sensitivity and specificity.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12187207&dopt=Abstract

J Urol. 2002 Sep;168(3):1188-92.
No association of serum gonadal or pituitary hormones with prognostic parameters in stages T1 to T3 PN0M0 prostate cancer.

Fodstad P, Bjoro T, Torlakovic G, Fossa SD.

Department of Clinical Research, Norwegian Radium Hospital, University of Oslo, Oslo, Norway.

PURPOSE: Recent reports suggest a possible association of the clinical aggressiveness of prostate cancer with low serum testosterone, and high serum levels of lutenizing hormone (LH) and/or follicle-stimulating hormone (FSH). This hypothesis was tested in the current study. MATERIALS AND METHODS: Serum levels of testosterone, LH, FSH, estradiol and sex hormone-binding globulin were determined as well as the calculated ratio of testosterone-to-sex hormonebinding globulin in 370 patients with newly diagnosed, stages T1 to T3 pN0M0 prostate cancer. The results were related to T category, Gleason score and serum prostate specific antigen (PSA). RESULTS: No statistically significant association was found for the serum levels of testosterone, LH, FSH, estradiol, sex hormone-binding globulin or the testosterone-to-sex hormone-binding globulin ratio with T category, Gleason score or PSA. In contrast to expectations, serum testosterone values within the lowest quartile were not associated with elevated LH. Of the 370 patients 17 (5%) had serum testosterone below the normal range (8 nmol./l. or less) and only 3 of these 17 showed elevated LH levels. CONCLUSIONS: Serum levels reflecting the pituitary-gonadal axis at diagnosis are not associated with clinically used measures of tumor aggressiveness (T category, Gleason score or PSA) in patients with newly diagnosed T1 to T3 pN0M0 prostate cancer.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12187265&dopt=Abstract

The average human scalp is covered by approximatey 100,000 hair follicles. Each hair undergoes hair cycle and normally 50-100 hairs randomly fall out a day, which is unnoticeable because lost hair is replaced by as many new hairs springing up daily. Hair loss results from the fall out of hair from the hair follicle. Alopecia or excessive, premature hair loss is the condition caused by many factors. Loss of hair itself does not pose critical health problems because biological role of human hair is relatively marginal. Hair on our scalp protects the head from mechanical shock, heat loss, and exposure to UV-light. The eyelashes and eyebrowes protect the eyes, and hair in the ear canal or the nasal passages help filter out particles and pathogens, thus protecting our internal organs. However, hair does play important social role: it is one of the major determinants of our appearance and identity in daily life. Fullness of hair also implicates or manifests physical integrity and youthfulness of the person. Losing hair could have more than just emotional impacts on individuals. The hair is a unique organ that goes through a characteristic cycle consisting of an immature phase, a growing phase called anagen, a transitional phase between the growing phase and the resting phase called catagen, and finally a resting phase called telogen in which the hair stops growing, waiting to fall out. 85-90% of hairs on our body are in anagen phase or growing phase, which lasts anywhere from two to five years. This phase is followed by a short regression phase, or catagen, which lasts 2-3 weeks. Approximately 1% of hair follicles are in catagen. Approximately 10-15% of hair follicles are in the resting phase, the telogen, which lasts about 3-5 months. Hair follicles typically goes through 10-20 asynchronous cycles during the lifetime. Persistent loss of more than 150 hairs would consist a state of hair loss, or alopecia, albeit it could be temporary.

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