DreamPharm Products:
Lutein-20||Herbs for headache, fever, and migraine ||
Milk thistle||Saw palmetto||
Triple B Super Vision||Garlic, Ginger, and Grapeseed Extract||
Ginseng and Ginkgo||Hair Million||
DHEA||Coenzyme Q10||
Sleep Aid herbal formula - natural sleep aid||Herbal Breath - herbs for bad breath problems.||
Weight loss herbal formula for menopause and pms||Ginkgo biloba||
Colon cleansing, Laxative||ViaVita, Lecithin for healthy liver
Fatty acids resources:
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
Mol Endocrinol. 2003 Sep;17(9):1805-14. Epub 2003 Jun 20.
Tudor and nuclease-like domains containing protein p100 function as coactivators for signal transducer and activator of transcription 5.
Paukku K, Yang J, Silvennoinen O.
Department of Virology, University of Helsinki, Helsinki, Finland.
Signal transducer and activator of transcription 5 (Stat5) plays a critical role in prolactin (PRL)-induced transcription of several milk protein genes. Stat5-mediated gene regulation is modulated by cooperation of Stat5 with cell type- and promoter-specific transcription factors as well as by interaction with transcriptional coregulators. Recently, the expression of a tudor and staphylococcal nuclease-like domains containing protein p100 was found to be increased in mammary epithelial cells during lactation in response to lactogenic hormones. p100 was initially identified as a transcriptional coactivator of the Epstein-Barr virus nuclear antigen 2. In this study we investigated the potential role of p100 in PRL-induced Stat5-mediated transcriptional activation. PRL stimulation increased the p100 protein levels in HC11 mouse mammary epithelial cells. p100 did not affect the early activation events of Stat5, but p100 enhanced the Stat5-dependent transcriptional activation in HC11 cells. p100 associated with Stat5 both in vivo and in vitro, and the interaction was mediated by both the tudor and staphylococcal nuclease-like domains of p100. Together these results suggest that p100 functions as a transcriptional coactivator for Stat5-dependent gene regulation and the existence of a positive regulatory loop in PRL-induced transcription, in which PRL stabilizes p100 protein, which in turn can cooperate with Stat5 in transcriptional activation.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12819296&dopt=Abstract [PubMed - in process]
Mol Endocrinol. 2003 Sep;17(9):1792-804. Epub 2003 Jun 20.
Regulation of cyclic adenosine 3',5'-monophosphate signaling and pulsatile neurosecretion by Gi-coupled plasma membrane estrogen receptors in immortalized gonadotropin-releasing hormone neurons.
Navarro CE, Abdul Saeed S, Murdock C, Martinez-Fuentes AJ, Arora KK, Krsmanovic LZ, Catt KJ.
Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892, USA.
Immortalized GnRH neurons (GT1-7) express receptors for estrogen [estrogen receptor-alpha and -beta(ERalpha and ERbeta)] and progesterone (progesterone receptor A) and exhibit positive immunostaining for both intracellular and plasma membrane ERs. Exposure of GT1-7 cells to picomolar estradiol concentrations for 5-60 min caused rapid, sustained, and dose-dependent inhibition of cAMP production. In contrast, treatment with nanomolar estradiol concentrations for 60 min increased cAMP production. The inhibitory and stimulatory actions of estradiol on cAMP formation were abolished by the ER antagonist, ICI 182,780. The estradiol-induced inhibition of cAMP production was prevented by treatment with pertussis toxin, consistent with coupling of the plasma membrane ER to an inhibitory G protein. Coimmunoprecipitation studies demonstrated an estradiol-regulated stimulatory interaction between ERalpha and Galphai3 that was prevented by the ER antagonist, ICI 182,780. Exposure of perifused GT1-7 cells and hypothalamic neurons to picomolar estradiol levels increased the GnRH peak interval, shortened peak duration, and increased peak amplitude. These findings indicate that occupancy of the plasma membrane-associated ERs expressed in GT1-7 neurons by physiological estradiol levels causes activation of a Gi protein and modulates cAMP signaling and neuropeptide secretion.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12819297&dopt=Abstract [PubMed - in process]
Mol Endocrinol. 2003 Sep;17(9):1767-76. Epub 2003 Jun 20.
Dominant inhibition of thyroid hormone action selectively in the pituitary of thyroid hormone receptor-beta null mice abolishes the regulation of thyrotropin by thyroid hormone.
Abel ED, Moura EG, Ahima RS, Campos-Barros A, Pazos-Moura CC, Boers ME, Kaulbach HC, Forrest D, Wondisford FE.
Division of Endocrinology, University of Utah School of Medicine, 15 North 2030 East, Building 533, Room 3410B, Salt Lake City, Utah 84112, USA. dale.abembg.utah.edu.
Thyroid hormones, T4 and T3, regulate their own production by feedback inhibition of TSH and TRH synthesis in the pituitary and hypothalamus when T3 binds to thyroid hormone receptors (TRs) that interact with the promoters of the genes for the TSH subunit and TRH. All TR isoforms are believed to be involved in the regulation of this endocrine axis, as evidenced by the massive dysregulation of TSH production in mice lacking all TR isoforms. However, the relative contributions of TR isoforms in the pituitary vs. the hypothalamus remain to be completely elucidated. Thus, to determine the relative contribution of pituitary expression of TR-alpha in the regulation of the hypothalamic-pituitary-thyroid axis, we selectively impaired TR-alpha function in TR-beta null mice (TR-beta-/-) by pituitary restricted expression of a dominant negative TR-beta transgene harboring a delta337T mutation. These animals exhibited 10-fold and 32-fold increase in T4 and TSH concentrations, respectively. Moreover, the negative regulation of TSH by exogenous T3 was completely absent and a paradoxical increase in TSH concentrations and TSH-beta mRNA was observed. In contrast, prepro-TRH expression levels in T3-treated TR-beta-/- were similar to levels observed in the delta337/TR-beta-/- mice, and ligand-independent activation of TSH in hypothyroid mice was equivalently impaired. Thus, isolated TR-beta deficiency in TRH paraventricular hypothalamic nucleus neurons and impaired function of all TRs in the pituitary recapitulate the baseline hormonal disturbances that characterize mice with complete absence of all TRs.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12819298&dopt=Abstract [PubMed - in process]
Mol Endocrinol. 2003 Sep;17(9):1880-92. Epub 2003 Jun 20.
Heterozygous Men1 mutant mice develop a range of endocrine tumors mimicking multiple endocrine neoplasia type 1.
Bertolino P, Tong WM, Galendo D, Wang ZQ, Zhang CX.
Laboratory of Genetics, Centre National de la Recherche Scientifique, Faculty of Medicine, University of Lyon, Lyon, France.
Multiple endocrine neoplasia type 1 (MEN1) is a hereditary syndrome characterized by the occurrence of multiple endocrine tumors of the parathyroid, pancreas, and anterior pituitary in patients. To study tumorigenesis related to the MEN1 syndrome, we have generated Men1 knockout mice using the gene targeting approach. Heterozygous Men1 mutant mice developed the same range of major endocrine tumors as is seen in MEN1 patients, affecting the parathyroid, pancreatic islets, pituitary and adrenal glands, as well as the thyroid, and exhibiting multistage tumor progression with metastatic potential. In particular, extrapancreatic gastrinoma, pancreatic glucagonoma, and mixed hormone-producing tumors in islets were observed. In addition, there was a high incidence of gonadal tumors of endocrine origin, i.e. Leydig cell tumors, and ovary sex-cord stromal cell tumors in heterozygous Men1 mutant mice. Hormonal disturbance, such as abnormal PTH and insulin levels, was also observed in these mice. These tumors were associated with loss of heterozygosity of the wild-type Men1 allele, suggesting that menin is involved in suppressing the development of these endocrine tumors. All of these features are reminiscent of MEN1 symptoms in humans and establish heterozygous Men1 mutant mice as a suitable model for this disease.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12819299&dopt=Abstract [PubMed - in process]
Theriogenology. 2003 Apr 15;59(8):1741-9.
FSH priming improves oocyte maturation, but priming with FSH or hCG has no effect on subsequent embryonic development in an in vitro maturation program.
Junk SM, Dharmarajan A, Yovich JL.
PIVET Medical Center, 166-168 Cambridge Street, Leederville, Perth 6007, Australia. pivetminet.net.au
AIM: To determine whether maturation and subsequent blastocyst development of in vitro matured oocytes can be improved by in vivo follicle stimulating hormone (FSH) or human chorionic gonadotrophin (hCG) priming, using a mouse model. EXPERIMENTAL DESIGN: Five groups of oocytes were used: in vivo control, in vitro matured (IVM) control, IVM after 24 h in vivo priming with FSH, IVM after 48 h in vivo priming with FSH and IVM after 16 h in vivo priming with hCG. In vitro fertilization (IVF) was performed on all groups.Oocyte maturation, fertilization, blastocyst development rates and blastocyst cell numbers were assessed for all groups. RESULTS: Significant improvement in oocyte maturation was observed in the two FSH priming groups compared with the IVM control group (P<0.005 and P<0.001, respectively). There were no significant differences in fertilization between all five groups. Blastocyst development was significantly higher in the in vivo control compared to the IVM groups (P<0.001). No significant differences were observed in blastocyst cell numbers among all five groups. CONCLUSIONS: While FSH priming improves the maturation rate of IVM oocytes, FSH or hCG priming does not improve development to the blastocyst stage.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12566148&dopt=Abstract
The most ostensive feature that distinguishes us human from chimps and other primates is the lack of bodily hair. During evolutionary process, we have lost the majority of hair. Hair is no longer an essential part of our body, just like appendix. What little hair we still have on our scalp and a few other bodily parts is still regarded as significant for reasons other than biological necessity. Hair loss is naturally accompanied by aging process, although the extent of hair loss and the timing of onset vary widely among individuals. Thus, loss of hair and baldness is considered as a symbol of maturity or old age. Like winkles and other signs of aging, hair loss is not welcome by most people, because we don't welcome aging, and being perceived as an aging person. However, it is alopecia, or premature hair loss that especially concerns certain people.
Hair Million is a blend of Asian herbs that wards off hair loss and promotes hair growth. Of various approaches to hair restoration, Hair Million offers advantages including low cost compared with other methods or drugs, and safety, because it is made of safe and healthy herbs.
DreamPharm Online Healthy Supplements ||
Constipation relief, laxative, colon cleansing ||
Lutein ||
Progesterone Cream ||
Natural herbal formula for hair loss problems ||