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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





Clin Endocrinol (Oxf). 2003 Jul;59(1):115-28.
Characterization of the intracellular mechanisms mediating somatostatin and lanreotide inhibition of DNA synthesis and growth hormone release from dispersed human GH-secreting pituitary adenoma cells in vitro.

Florio T, Thellung S, Corsaro A, Bocca L, Arena S, Pattarozzi A, Villa V, Massa A, Diana F, Schettini D, Barbieri F, Ravetti JL, Spaziante R, Giusti M, Schettini G.

Pharmacology and Neuroscience, National Institute for Cancer Research, c/o Advanced Biotechnology Center (CBA), Genova, Italy. floriba.unige.it

OBJECTIVE: Somatostatin is an endogenous inhibitor of hormone secretion and cell proliferation. Treatment with somatostatin analogues in humans causes a reduction in size and secretory activity of endocrine tumours, including GH-secreting pituitary adenomas. This study was aimed to characterize the intracellular mechanisms mediating the in vitro antiproliferative and antisecretory effects of somatostatin and its analogue lanreotide, on primary cultures of GH-secreting pituitary adenoma cells. DESIGN: Thirteen GH-secreting pituitary adenoma postsurgical specimens were analysed for somatostatin receptor (SSTR) mRNA expression and a subset of them was analysed in vitro for the effect of somatostatin on cell proliferation, assessed by means of [3H]-thymidine uptake, and GH release, using an immunoradiometric assay. Moreover, the intracellular signalling involved in such effects has been studied. RESULTS: All the adenomas analysed expressed at least one somatostatin receptor subtype mRNA. SSTR2 mRNA was identified in 77% of the adenomas, SSTR1 and SSTR3 in 69% and SSTR5 in 60%. Somatostatin and lanreotide inhibited cell proliferation in phorbol ester (PMA)-stimulated conditions (10/13 adenomas), as well as after fetal calf serum (3/3 adenomas) or IGF-I stimulation (2/2 adenomas). Conversely, GHRH or forskolin treatments did not significantly affect DNA synthesis in adenoma cells in the presence or absence of somatostatin (2/2 and 4/4 adenomas, respectively). Vanadate pretreatment reversed somatostatin inhibition of PMA-induced DNA synthesis suggesting an involvement of tyrosine phosphatase in this effect (2/2 adenomas); this was confirmed by the direct induction of tyrosine phosphatase activity in two adenomas after somatostatin treatment. Somatostatin and also lanreotide caused significant inhibition of phorbol ester, forskolin, GHRH and KCl-dependent increase of GH secretion in the culture medium. Moreover, voltage-sensitive calcium channel activity induced by 40 mm KCl depolarization in microfluorimetric analysis, was significantly reduced (5/5 adenomas). CONCLUSIONS: These data show that somatostatin and lanreotide inhibit human GH-secreting pituitary adenoma cell proliferation and hormone release in vitro, and suggest that the activation of tyrosine phosphatases may represent intracellular signals mediating the antiproliferative effects and that the inhibition of the voltage-dependent calcium channels and adenylyl cyclase activities may control GH secretion.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12807513&dopt=Abstract [PubMed - in process]



J Pharmacol Exp Ther. 2003 Jun 13 [Epub ahead of print].
Modeling of Corticosteroid Pharmacogenomics in Rat Liver Using Gene Microarrays.

Jin JY, Almon RR, DuBois DC, Jusko WJ.

University at Buffalo.

Corticosteroid (CS) pharmacogenomics were studied using gene microarrays in rat liver. Methylprednisolone (MPL) was administered intravenously at 50 mg/kg. Rats were sacrificed and liver excised at 17 time points over 72 hours. RNAs from individual livers were used to query Affymetrix GeneChips(R) which contain sequences for 8000 genes. Cluster analysis revealed 6 temporal patterns consisting of 197 CS-responsive probes representing 143 genes. Based on our fifth-generation model of CS pharmacokinetics/pharmacodynamics (PK/PD), mechanistic models were developed to describe the time-pattern for each CS-responsive gene. Two clusters showed increased expression with different effect duration. PD models assuming CS stimulation of mRNA synthesis were applied. Another two clusters showed an initial decline followed by delayed increase, suggesting two mechanisms might be involved jointly. The initial suppression was captured by CS inhibition of mRNA synthesis or stimulation of degradation. CS may also stimulate the production of a biosignal (transcription factors or other hormones) which can cause secondary induction of the target mRNA. One cluster showed a very abrupt increase in message followed by rapid decrease. These genes were lymphocytic in origin and were modeled combining the fast gene induction effect of CS in lymphoid cells and its direct lymphocyte trafficking effect. Another cluster showed reduction persisting for 18 hr, which was described by CS inhibition of mRNA synthesis. Our results reveal the marked diversity of genes regulated by CS via a limited array of mechanisms. These PD models provide quantitation of CS pharmacogenomics and new hypotheses regarding understanding of diverse mechanisms of CS action.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12808002&dopt=Abstract [PubMed - as supplied by publisher]



J Cell Sci. 2003 Jul 15;116(Pt 14):2975-86.
Collagen-IV and laminin-1 regulate estrogen receptor alpha expression and function in mouse mammary epithelial cells.

Novaro V, Roskelley CD, Bissell MJ.

Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA.

The expression level and functional activity of estrogen receptor alpha is an important determinant of breast physiology and breast cancer treatment. However, it has been difficult to identify the signals that regulate estrogen receptor because cultured mammary epithelial cells generally do not respond to estrogenic signals. Here, we use a combination of two- and three-dimensional culture systems to dissect the extracellular signals that control endogenous estrogen receptor alpha. Its expression was greatly reduced when primary mammary epithelial cells were placed on tissue culture plastic; however, the presence of a reconstituted basement membrane in combination with lactogenic hormones partially prevented this decrease. Estrogen receptor alpha expression in primary mammary fibroblasts was not altered by these culture conditions, indicating that its regulation is cell type specific. Moreover, estrogen receptor-dependent reporter gene expression, as well as estrogen receptor alpha levels, were increased threefold in a functionally normal mammary epithelial cell line when reconstituted basement membrane was added to the medium. This regulatory effect of reconstituted basement membrane was reproduced by two of its components, collagen-IV and laminin-1, and it was blocked by antibodies against alpha2, alpha6 and beta1 integrin subunits. Our results indicate that integrin-mediated response to specific basement membrane components, rather than cell rounding or cell growth arrest induced by reconstituted basement membrane, is critical in the regulation of estrogen receptor alpha expression and function in mammary epithelial cells.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12808020&dopt=Abstract [PubMed - in process]



Proc Natl Acad Sci U S A. 2003 Jun 24;100(13):7996-8001. Epub 2003 Jun 13.
Effect of insulin on human skeletal muscle mitochondrial ATP production, protein synthesis, and mRNA transcripts.

Stump CS, Short KR, Bigelow ML, Schimke JM, Nair KS.

Department of Endocrinology, Metabolism, and Nutrition, Mayo Clinic and Foundation, Rochester, MN 55905, USA.

Mitochondria are the primary site of skeletal muscle fuel metabolism and ATP production. Although insulin is a major regulator of fuel metabolism, its effect on mitochondrial ATP production is not known. Here we report increases in vastus lateralis muscle mitochondrial ATP production capacity (32-42%) in healthy humans (P < 0.01) i.v. infused with insulin (1.5 milliunits/kg of fat-free mass per min) while clamping glucose, amino acids, glucagon, and growth hormone. Increased ATP production occurred in association with increased mRNA levels from both mitochondrial (NADH dehydrogenase subunit IV) and nuclear [cytochrome c oxidase (COX) subunit IV] genes (164-180%) encoding mitochondrial proteins (P < 0.05). In addition, muscle mitochondrial protein synthesis, and COX and citrate synthase enzyme activities were increased by insulin (P < 0.05). Further studies demonstrated no effect of low to high insulin levels on muscle mitochondrial ATP production for people with type 2 diabetes mellitus, whereas matched nondiabetic controls increased 16-26% (P < 0.02) when four different substrate combinations were used. In conclusion, insulin stimulates mitochondrial oxidative phosphorylation in skeletal muscle along with synthesis of gene transcripts and mitochondrial protein in human subjects. Skeletal muscle of type 2 diabetic patients has a reduced capacity to increase ATP production with high insulin levels.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12808136&dopt=Abstract



Nat Biotechnol. 2003 Jul;21(7):807-12. Epub 2003 Jun 15.
Measurement of the millisecond activation switch of G protein-coupled receptors in living cells.

Vilardaga JP, Bunemann M, Krasel C, Castro M, Lohse MJ.

Institute of Pharmacology and Toxicology, University of Wurzburg, Versbacher Str. 9, D-97078 Wurzburg, Germany.

Hormones and neurotransmitters transduce signals through G protein-coupled receptors (GPCR). Despite their common signaling pathways, however, the responses they elicit have different temporal patterns. To reveal the molecular basis for these differences we have developed a generally applicable fluorescence-based technique for real-time monitoring of the activation switch of GPCRs in living cells. We used such direct measurements to investigate the activation of the alpha(2A)-adrenergic receptor (alpha(2A)AR; neurotransmitter) and the parathyroid hormone receptor (PTHR; hormone) and observed much faster kinetics than expected: approximately 40 ms for the alpha(2A)AR and approximately 1 s for the PTHR. The different switch times are in agreement with the different receptors' biological functions. Agonists and antagonists could rapidly switch the receptors on or off, whereas a partial agonist caused only a partial signal. This approach allows the comparison of agonist and partial agonist intrinsic activities at the receptor level and provides evidence for millisecond activation times of GPCRs.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12808462&dopt=Abstract [PubMed - in process]







Prescription drugs, surgical hair transplantation, topical application of various oils or creams... Also prayer and wishing...
Hair Million is an alternative approach to hair loss problems. Anecdotes and personal experiences testify that it works. Hair Million shows positive results and improvement for age-related hair thinning and hair loss for a large fraction of people who take it. How does it work? Good question. The molecular biological or clinical mechanisms of action as to how Hair Million exactly works to help stop hair loss, and promote hair growth is completely unknown. The only evidences for the effecacy of Hair Million on hair growth are only anedotal and based on personal experiences. There has been no clinical trials or placebo controlled statistical analysis on the efficacy of Hair Million on hair loss and hair growth.
That's enough for many people. Also, there are two merits in the hair restoration herbal formula:
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DHEA is a natural hormone, and it is produced in our body by the adrenal glands. DHEA has been suggested to provide numerous potential benefits. DHEA (or dehydroepiandrosterone) is converted into androgens (male hormones) or estrogens (female hormones) in the cells.





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