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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

Med Sci Sports Exerc. 2003 Feb;35(2):263-9.
Evaluation of stress responses to interval training at low and moderate altitudes.

Niess AM, Fehrenbach E, Strobel G, Roecker K, Schneider EM, Buergler J, Fuss S, Lehmann R, Northoff H, Dickhuth HH.

Center of Internal Medicine, Department of Rehabilitative and Preventive Sports Medicine, University of Freiburg, Freiburg, Germany. niessml.ukl.uni-freiburg.de

PURPOSE: The purpose of the present field study was to explore whether extensive interval training (IT) performed with a similar behavior of blood lactate (LA) at an altitude of 1800 m (ALT) and near sea level (SL) goes along with a comparable hormonal, metabolic, and acute phase response in highly trained endurance athletes. METHODS: Twelve distance runners (VO2 64.6 +/- 6.9 mL.kg(-1) ) performed IT (10 x 1000 m, 2-min rest) at SL with a running velocity (V) corresponding to 112% of the individual anaerobic threshold (IAT). After an acclimatization period of 7 d, IT was repeated with a lower V (107% IAT) at ALT. Blood samples were drawn at rest, 0, 0.3, 3, and 24 h after IT. LA during IT was similar at SL and ALT (5.4 +/- 1.3/5.3 +/- 1.2 mmol.L(-1)), whereas HR tended to be higher at SL. RESULTS: Postexercise rises in plasma noradrenaline (NA), NA sulfate, adrenaline, glucose, interleukin-6 (IL-6), and neutrophils were significantly more pronounced at ALT. The increase of cortisol and human growth hormone showed an insignificant trend toward higher values at ALT. A slight but significant increase of plasma erythropoietin was only apparent after IT at ALT. No differences between either condition were observed for exercise-related changes in free fatty acids, IL-8, lympho-, or monocyte counts. CONCLUSIONS: In spite of a matched accumulation pattern of LA between ALT and N, stress responses, such as sympathetic activation and hepatic glucose release, still appear to be greater at ALT. This additional impact of moderate ALT on the stress response to IT should be taken into account if repeated training sessions are performed within a short period of time.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12569215&dopt=Abstract

FEBS Lett. 1999 Feb 12;444(2-3):239-44.
The structure of human parathyroid hormone-related protein(1-34) in near-physiological solution.

Weidler M, Marx UC, Seidel G, Schafer W, Hoffmann E, Esswein A, Rosch P.

Lehrstuhl fur Biopolymere, Universitat Bayreuth, Germany.

Parathyroid hormone-related protein plays a major role in the pathogenesis of humoral hypercalcemia of malignancy. Under normal physiological conditions, parathyroid hormone-related protein is produced in a wide variety of tissues and acts in an autocrine or paracrine fashion. Parathyroid hormone-related protein and parathyroid hormone bind to and activate the same G-protein-coupled receptor. Here we present the structure of the biologically active NH2-terminal domain of human parathyroid hormone-related protein(1-34) in near-physiological solution in the absence of crowding reagents as determined by two-dimensional proton magnetic resonance spectroscopy. An improved strategy for structure calculation revealed the presence of two helices, His-5-Leu-8 and Gln-16-Leu-27, connected by a flexible linker. The parathyroid hormone-related protein(1-34) structure and the structure of human parathyroid hormone(1-37) as well as human parathyroid hormone(1-34) are highly similar, except for the well defined turn, His-14-Ser-17, present in parathyroid hormone. Thus, the similarity of the binding affinities of parathyroid hormone and parathyroid hormone-related protein to their common receptor may be based on their structural similarity.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10050767&dopt=Abstract

Eur J Endocrinol. 1999 Feb;140(2):174-9.
Apo E phenotype and changes in serum lipids in adult patients during growth hormone replacement.

Leese GP, Wallymahmed M, Wieringa G, VanHeyningen C, MacFarlane IA.

Department of Endocrinology, Ninewells Hospital, Dundee, UK.

OBJECTIVE: To determine whether apo E phenotype influences changes in lipid profiles induced by growth hormone replacement in growth hormone (GH)-deficient adults. DESIGNS: Patients were treated for 6 months with recombinant human GH (hGH), given in a dose of 0.125 U/kg per week for 4 weeks followed by 0.25 U/kg per week thereafter. The effects on serum lipids and the influence of apo E phenotype were examined. METHODS: Thirty patients (aged 35.1+/-11.8 years: mean +/- S.D.) with adult growth hormone deficiency with included in the study. Fasting serum samples were analysed for apo E phenotype total cholesterol, high-density lipoprotein (HDL)-cholesterol, triglycerides, lipoprotein (a) (Lp(a)) and IGF-I. Low-density lipoprotein (LDL)-cholesterol was calculated using the Friedwald formula. RESULTS: Six months of replacement treatment with hGH resulted in a reduction in HDL-cholesterol from 0.90+/-0.10 to 0.68+/-0.08 mmol/l (P<0.01), and a small, non-significant reduction in total cholesterol from 6.14+/-0.40 to 5.99+/-0.35 mmol/l (P = 0.06). There was no significant change in the other lipid parameters. The decrease in HDL-cholesterol concentration was greater in patients carrying the apo E2 allele (0.40+/-0.07 mmol/l, P<0.05) than in patients homozygous for the apo E3 allele (0.23+/-0.04 mmol/l) and patients carrying the apo E4 allele (0.15+/-0.36 mmol/l). Patients with the apo E4 allele had lower baseline cholesterol concentrations than patients lacking the apo E4 allele, and this persisted after treatment with hGH (P<0.05). CONCLUSIONS: Apo E phenotype may be a determining factor in the response of HDL-cholesterol to hGH in GH-deficient adults.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10069664&dopt=Abstract

Biochemistry. 1999 Mar 2;38(9):2654-60.
Identification of 1 alpha,25-dihydroxyvitamin D3 response elements in the human transforming growth factor beta 2 gene.

Wu Y, Craig TA, Lutz WH, Kumar R.

Nephrology Research Unit, Mayo Clinic/Foundation, Rochester, Minnesota 55905, USA.

Transforming growth factor-beta (TGF-beta) is one of the most abundant growth factors secreted by bone cells, and regulation of TGF-beta expression is crucial for bone development and growth. Previous studies from our laboratory demonstrated that 1 alpha, 25-dihydroxyvitamin D3 (1 alpha,25(OH)2D3) inhibits human osteoblast and keratinocyte growth by increasing TGF-beta2 secretion and synthesis. To examine the mechanism by which 1 alpha,25(OH)2D3 regulates TGF-beta 2 transcription in osteoblasts, we ligated segments of the human TGF-beta 2 promoter 5' of a growth hormone reporter gene in a growth hormone reporter plasmid and examined the effects of 1 alpha,25(OH)2D3 administration on the expression of growth hormone in cells transfected with such chimeric promoter-reporter plasmids. The promoter region extending from -973 to +68 bp of the transcription start site elicited a 7-fold increase in reporter gene activity in transiently transfected osteoblasts after 1 alpha,25(OH)2D3 treatment, whereas the region from -553 to +68 bp of the transcription start site showed no response following 1 alpha,25(OH)2D3 treatment. Transfection of osteoblasts with reporter plasmids containing TGF-beta 2 promoter DNA from -869 to -658 bp revealed a 3.8-fold increase in reporter gene activity. DNA fragments from this region (-743 to -676 bp and -786 to -728 bp) ligated into reporter plasmids also showed increases in reporter activity. Gel retardation assay experiments showed that DNA fragments from -774 to -735 bp and -714 to -675 bp both formed a DNA-protein complex with bacterially expressed human retinoic acid X receptor alpha (RXR alpha) and vitamin D receptor (VDR) and with nuclear extracts from human bone cells. Addition of a vitamin D receptor antibody to reactions containing the aforesaid DNA fragments and bone cell nuclear extract resulted in further retardation of the mobility of the DNA-protein complex (super-shifting). Removal of two putative direct repeat DNA fragments in this region abolished VDR-RXR alpha-vitamin D response element complex formation. The TGF-beta 2 promoter contains two imperfect direct repeat DNA sequences: TGTAGAACAAGTAGA and AATGAAGTTGGTGGA that mediate the effect of 1 alpha,25(OH)2D3.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10052935&dopt=Abstract

Fertil Steril. 1999 Mar;71(3):431-5.
Polymorphism T-->C (-34 bp) of gene CYP17 promoter in Greek patients with polycystic ovary syndrome.

Diamanti-Kandarakis E, Bartzis MI, Zapanti ED, Spina GG, Filandra FA, Tsianateli TC, Bergiele AT, Kouli CR.

First Department of Internal Medicine, Athens University School of Medicine, Laiko General Hospital, Greece.

OBJECTIVE: To investigate the frequency of T-->C substitution (-34 bp) of gene CYP17 promoter in Greek patients with polycystic ovary syndrome (PCOS) and to elucidate its role in the pathogenesis of the syndrome. DESIGN: Follow-up study. SETTING: Academic research setting. PATIENT(S): Fifty patients with PCOS and 50 healthy women. INTERVENTION(S): Body mass index and the waist-hip ratio were determined for each woman. Blood samples were obtained for DNA analysis and hormone estimates. MAIN OUTCOME MEASURE(S): Serum total T levels. RESULT(S): Seventeen patients (34%) did not carry the base pair substitution (genotype A1A1) and their mean (+/- SD) total T level was 75.7+/-32.2 ngl/dL, 29 patients (58%) were heterozygous carriers of the A2 allele (genotype A1A2) and their mean total T level was 77.8+/-29.9 ng/dL, and 4 patients (8%) carried the A2 allele in homozygosity (genotype A2A2) and their mean total T level was 87.0+/-2.8 ngl/dL. Twenty-two controls had the genotype A1A1 (44%) and their mean total T level was 39.1+/-15.5 ng/dL, whereas 28 (56%) had the genotype A1A2 and their mean total T level was 44.9+/-22.1 ng/dL. Homozygosity of the polymorphic A2 allele was not observed in controls, and this difference (8% versus 0%) was statistically significant. CONCLUSION(S): Although this base pair substitution is not the primary genetic defect in PCOS, it may aggravate the clinical picture of hyperandrogenemia, particularly when homozygosity exists.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10065777&dopt=Abstract

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