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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

Cancer Epidemiol Biomarkers Prev. 2002 Aug;11(8):758-66.
Plasma concentrations of insulin-like growth factors among healthy adult men and postmenopausal women: associations with body composition, lifestyle, and reproductive factors.

Chang S, Wu X, Yu H, Spitz MR.

Department of Epidemiology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030-4009, USA. ChangSail.nih.gov

As evidence builds for cancer risk associated with insulin-like growth factors (IGFs) and their binding proteins (BPs), capitalizing on such associations for cancer prevention requires identifying the determinants of IGF levels. We measured plasma IGF-I, IGF-II, and IGF BP-3 in a cross-section of 210 men and 171 postmenopausal women enrolled in research as healthy controls. Using linear regression adjusted for age and ethnicity, we evaluated associations between IGF and IGF BP levels and gender, height, body mass index (BMI), smoking, caloric intake, physical activity, and reproductive factors. As expected, women using hormone replacement therapy (HRT) recently had significantly lower IGF-I levels than nonusers. Overall, IGF-I and IGF BP-3 levels did not differ by gender, although men had significantly higher molar ratios of IGF-I to IGF BP-3 and lower plasma IGF-II than women without recent HRT use. For men, BMI was a better predictor of IGF-I levels than height, whereas for women, height was more important. Lower IGF-II levels for both genders were associated with higher BMI and lower physical activity. Lower physical activity was associated with lower IGF BP-3 levels among men. Miscarriage number and menopausal age were positively associated with IGF BP-3 levels. HRT use strongly depressed IGF-I levels among smokers, and additional analysis revealed no remarkable associations. Caloric intake was negatively associated with IGF-I levels among men. Results for ratios of IGF-I and IGF-II to IGF BP-3 generally reflected those for IGF-I and IGF-II levels, respectively. In conclusion, whereas some traditional cancer risk factors were associated with IGF levels, altogether, they accounted for <15% of the total variability in plasma levels for each IGF, suggesting that other factors influence IGF levels.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12163330&dopt=Abstract

Cancer Epidemiol Biomarkers Prev. 2002 Aug;11(8):785-9.
Reproducibility studies and interlaboratory concordance for androgen assays of male plasma hormone levels.

Fears TR, Ziegler RG, Donaldson JL, Falk RT, Hoover RN, Stanczyk FZ, Vaught JB, Gail MH.

Biostatistics Branch, National Cancer Institute, Bethesda, Maryland 20892, USA.

To help us identify appropriate techniques and laboratories for measuring hormones, we studied the variability and reproducibility of assay measurements of androstanediol glucuronide, androstenedione, dehydroepiandrosterone (DHEA), DHEA sulfate, dihydrotestosterone, testosterone, androstanediol, androsterone glucuronide, and androsterone sulfate for five men. Four sets of two aliquots from each sample were sent to participating laboratories, and one set was used for analyses monthly for four consecutive months. For each assay, estimates of components of variance were then used to estimate the coefficient of variation, the intraclass correlation between measurements on different days from a given individual, and the minimum detectable relative difference for a standard design. These data indicate that for at least one of the laboratories a single sample with two laboratory replicates per sample of androstanediol glucuronide, androstenedrone, DHEA, DHEA sulfate, and dihydrotestosterone yields an intraclass correlation coefficient exceeding 0.80 and can be used to discriminate reliably among men. The results for testosterone, androstanediol, androsterone, glucuronide, and androsterone sulfate do not meet this test. These data do not allow us to estimate the component of variation that corresponds to repeated blood samples taken over time from the same man. This reliability study design is, however, entirely appropriate for the typical case-control study which utilizes only one sample per subject.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12163335&dopt=Abstract

hermes.cam.ac.uk

1 The potential vasodilator function of the peptide ghrelin, recently identified as the endogenous ligand of the growth hormone secretagogue orphan receptor (GHS-R), was investigated in human endothelium-denuded internal mammary artery. The peptide endothelin-1 (ET-1) is a potent and long-lasting vasoconstrictor. Comparisons were made with established and putative endogenous vasodilators to determine if any could reverse ET-1-induced vasoconstriction in this vessel. 2 Ghrelin (0.1-300 nM) potently dilated 10 nM ET-1-induced constrictions (pD(2) 8.39+/-0.29; E(MAX) 63+/-5.6%; n=9/14, responders/total). 3 ANP (pD(2) 7.75+/-0.14; E(MAX) 106+/-2.0; n=5/5) and CGRP (pD(2) 8.08+/-0.17; E(MAX) 76+/-15% n=5/6) both produced complete reversal of the constrictor response to ET-1 (E(MAX) not significantly different from 100%, P>0.05 one-sample t-test). 4 The following caused partial reversal of the ET-1 response: Adrenomedullin (n=9/9) and two peptides derived from proadrenomedullin, PAMP-12 (n=6/7) and PAMP-20 (n=9/9) (pD(2) values 7.63+/-0.28, 7.97+/-0.23 and 8.51+/-0.29; E(MAX) 58+/-7.3, 54+/-10 and 51+/-7.8% respectively). Unexpectedly, amylin was only 2 fold less potent than CGRP, although there was less than 50% reversal of the ET-1 constriction (pD(2) 7.86+/-0.30; E(MAX) 41+/-5.4%; n=7/9). CNP (n=6/6) also partially reversed constrictions to ET-1 (E(MAX) 53+/-6.3; pD(2) 8.07+/-0.38). 5 BNP (n=4/5) and PGI(2) (n=6/8) were weak vasodilators, since concentration-response curves failed to reach a maximum within the range tested. PGE(2) caused a small dilatation in some vessels (E(MAX) 17+/-2.1%; pD(2) 8.63+/-0.36; n=4/8). 6 We have demonstrated ghrelin to be an effective, endothelium-independent vasodilator of the long-lasting constrictor ET-1 in human arteries producing responses similar to those of adrenomedullin (P>0.05, ANOVA). British Journal of Pharmacology (2002) 136, 1146-1152

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12163347&dopt=Abstract

Am J Pathol. 2002 Aug;161(2):665-72.
Molecular characterization of human meningiomas by gene expression profiling using high-density oligonucleotide microarrays.

Watson MA, Gutmann DH, Peterson K, Chicoine MR, Kleinschmidt-DeMasters BK, Brown HG, Perry A.

Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri 63110-1093, USA.

Meningiomas are common central nervous system neoplasms that exhibit remarkably diverse histopathology and biological behavior. Compared to astrocytomas, the most common central nervous system tumor, little is known about the molecular pathways critical for meningioma tumor formation and malignant progression. As an initial step toward characterizing the genetic basis of meningioma pathogenesis, we assessed cancer-related gene expression profiles of nonneoplastic leptomeningeal specimens and human meningiomas of varying World Health Organization (WHO) grade using high-density oligonucleotide microarrays. Although expression profile differences between nonneoplastic and meningioma specimens were readily discernible, the expression profile of a subset of genes could also distinguish WHO grade I from WHO grades II and III tumors. Altered expression levels of several genes identified in this study have been previously noted in meningiomas (eg, growth hormone receptor, IGFBP-7, endothelin receptor A, IGF2). However, we also identified a number of novel genes whose expression was associated with WHO grade and was confirmed by reverse transcriptase-polymerase chain reaction in a larger, independent set of meningeal tumors (n = 47). This report represents the first gene expression profiling studies of meningiomas and identifies some initial candidate genes that may provide further insights into the genetic basis for meningioma pathogenesis.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12163391&dopt=Abstract

J Exp Med. 2002 Aug 5;196(3):311-21.
Functional inactivation of CXC chemokine receptor 4-mediated responses through SOCS3 up-regulation.

Soriano SF, Hernanz-Falcon P, Rodriguez-Frade JM, De Ana AM, Garzon R, Carvalho-Pinto C, Vila-Coro AJ, Zaballos A, Balomenos D, Martinez-A C, Mellado M.

Department of Immunology and Oncology, Centro Nacional de Biotecnologia/Consejo Superior de Investigaciones Cientificas, Universidad Autonoma de Madrid, Campus de Cantoblanco, Spain.

Hematopoietic cell growth, differentiation, and chemotactic responses require coordinated action between cytokines and chemokines. Cytokines promote receptor oligomerization, followed by Janus kinase (JAK) kinase activation, signal transducers and transactivators of transcription (STAT) nuclear translocation, and transcription of cytokine-responsive genes. These include genes that encode a family of negative regulators of cytokine signaling, the suppressors of cytokine signaling (SOCS) proteins. After binding their specific receptors, chemokines trigger receptor dimerization and activate the JAK/STAT pathway. We show that SOCS3 overexpression or up-regulation, stimulated by a cytokine such as growth hormone, impairs the response to CXCL12, measured by Ca(2+) flux and chemotaxis in vitro and in vivo. This effect is mediated by SOCS3 binding to the CXC chemokine receptor 4 receptor, blocking JAK/STAT and Galpha(i) pathways, without interfering with cell surface chemokine receptor expression. The data provide clear evidence for signaling cross-talk between cytokine and chemokine responses in building a functional immune system.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12163560&dopt=Abstract

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