Dissertations / Theses on the topic 'Fibroblast growth factor binding protein 1'
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Baker, Tabari M. "Regulation of microRNAs targeting the angiogenic switch molecule Fibroblast Growth Factor Binding Protein 1 by retinoic acid receptor activation." Thesis, Georgetown University, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=3618988.
Full textThis dissertation examines the role of retinoic acid receptor activation in the post-transcriptional regulation of a fibroblast growth factor binding protein. Previous work showed that all-trans retinoic acid (ATRA) reduces mRNA expression of the angiogenic switch molecule, Fibroblast Growth Factor Binding Protein 1 (FGFBP1 or FGF-BP), independent of an effect on transcription of the FGFBP1 mRNA. I hypothesized that a retinoid-induced microRNA was involved in FGFBP1 mRNA loss. MicroRNAs (miRs) are 19-22 nucleotide (nt) single stranded non-coding RNAs that post-transcriptionally repress mature mRNA function, thereby reducing expression of their target proteins. The current dogma suggests that miRs canonically bind to the 3' untranslated region (UTR) of mRNA through a 7-nt seed-matched site. However, recent data indicate that miRs may also bind the open reading frame (ORF) of mRNAs. In this dissertation, I show that miR-27b-3p and miR-125a-5p are induced by ATRA and target FGFBP1. Overexpression of miR-27b-3p and miR-125a-5p rapidly reduced FGFBP1 mRNA levels through a target site in the open reading frame of the FGFBP1 mRNA. Both microRNAs showed specificity for regions within the ORF of FGFBP1, suggesting that these microRNAs may also be involved in inhibiting translation of the FGFBP1 protein. Next generation sequencing data from The Cancer Genome Atlas shows that loss of these microRNAs is characteristic of several epithelial cancers, including head and neck, lung, and cervical squamous cell carcinomas, suggesting a tumor suppressor role for miRs 27a-3p and 125a-5p. In total, these data suggest an important regulatory role for miRs 27b-3p and 125a-5p in the oncogenesis of squamous cell carcinomas, through modulation of FGFBP1 expression.
Yateman, Martin Edward. "Regulation of human fibroblast insulin-like growth factor (IGF)-binding proteins by IGF-1 and cytokines, mechanisms of action and effects upon IGF bioactivity." Thesis, Queen Mary, University of London, 1995. http://qmro.qmul.ac.uk/xmlui/handle/123456789/1742.
Full textGillies, Peter John. "Modulation of dermal microvascular endithelial cell responses to growth factors and haemostatic factors in the presence of vitronectin." Thesis, Queensland University of Technology, 2008. https://eprints.qut.edu.au/37176/1/Peter_Gillies_Thesis.pdf.
Full textMontenegro, Luciana Ribeiro. "Estudo in vitro da sensibilidade ao IGF-1 de fibroblastos de crianças nascidas pequenas para a idade gestacional sem recuperação estatural pós-natal." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/5/5135/tde-08092009-132008/.
Full textIntroduction: Children born small for gestational age (SGA) have a higher risk of staying with short stature in adulthood. The insulin-like growth factors (IGF-1 and IGF-2) are the main endocrine factor determining fetal growth. Most of the known actions of IGFs are mediated by IGF-1R, a tyrosine kinase receptor. Recently, the IGF-1 insensitivity was identified causing growth retardation in children born SGA who who did not present spontaneous catch-up growth in postnatal life. Affected children had elevated IGF-1 and IGFBP-3 levels in addition to microcephaly. The role of post receptor defects in IGF-1 signaling on the deficit of growth is still unclear. Objective: To assess IGF-1 action and signaling in vitro in fibroblasts from SGA children. Methods: Fibroblasts cell cultures were developed from 2 controls (C1 and C2) and 4 patients with pre- and post-natal growth retardation (SGA1, SGA2, SGA3 and SGA4). IGF-1 insensitivity was demonstrated by severe pre and postnatal growth impairment without any evident cause, IGF1 SDS > 0 and poor growth response during high doses of hGH treatment. Three SGA patients presented microcephaly. Defects in the gene of the IGF1 and IGF1R were excluded by direct sequencing. One patient (SGA1) presents the Silver- Russell syndrome (SRS) with loss of methylation of the paternal allele in the ICR1 (imprinting center region 1) chromosome 11p15, important for IGF-2 expression. IGF-1 action was assessed by cell proliferation by colorimetric assay. IGF-1 signaling was assessed by AKT and ERK phosphorylation after IGF-1 stimulation through SDS-PAGE of intracellular extract followed by immunoblotting with specific antibodies. The expression of IGF1R and IGFBP3 gene was determined by Real-time quantitative PCR and the levels of the IGF-1R and IGBP-3 protein by direct immunoblotting. Results: The SGA1, SGA2 and SGA3 cell lines proliferated 31%, 60% and 78% less under IGF-1 stimulation in comparison of controls fibroblasts, respectively. The expression of IGF1R mRNA and the level of total amount of IGF-1R protein were similar in all SGA and control cell lines. Despite normal IGF-1R structure and quantity, the same 3 SGA cell lines that presented low proliferation response also had 50 to 85% lower ERK phosphorylation after IGF-1 treatment (p <0.001), although the similar total content of ERK1/2. In relation to PI3K pathway activation, all SGA cell cultures presented normal AKT phosphorilation. Fibroblasts from the SGA1 patient presented a 14x increase in IGFBP3 mRNA and 2x more IGFBP-3 secretion to culture serum medium. Treatment with desIGF-1, an IGF-1 analogue with low affinity for IGFBPs although retains its ability to activate the IGF-1R, did not recover cell proliferation or ERK phosphorylation. All cell lines presented similar amount of GRB10 protein Conclusion: Three of 4 SGA patients showed evidence of post-receptor IGF-1 insensitivity. The cell line SGA1, obtained from a SRS patient with ICR1 hypomethylation, showed increased expression and secretion of IGFBP-3, which was not directly responsible for inhibition in IGF- 1 action. Further studies should be developed to identify the molecular cause of IGF-1 post-receptor insensitivity observed in our patients.
Marshall, Nicholas John. "The influence of insulin-like growth factor 1 and its analogues on fibroblasts and dermal wound healing." Title page, table of contents and synopsis only, 1998. http://web4.library.adelaide.edu.au/theses/09MD/09mdm3685.pdf.
Full textMartin, Christopher School of Biomedical Engineering UNSW. "Investigation of exogenous growth factors; platelet derived growth factor, insulin-like growth factor binding protein and fibroblast growth factor, and their influence on in vivo bone repair." Awarded by:University of New South Wales. School of Biomedical Engineering, 2006. http://handle.unsw.edu.au/1959.4/30405.
Full textParipelly, Rammohan. "Molecular Level Interaction of Human Fibroblast Growth Factor-1 (hFGF-1) With Phloridzin." TopSCHOLAR®, 2013. http://digitalcommons.wku.edu/theses/1314.
Full textHamilton, Fairley. "Regulation of sex hormone binding globulin and insulin-like growth factor binding protein-1." Thesis, University College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.243549.
Full textGeitgey, Delaney Kate. "Evaluating the role of fibroblast activation protein and fibroblast growth factor 21 in growth hormone-induced adipose tissue fibrosis." Ohio University Honors Tutorial College / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=ouhonors1587596581428154.
Full textÖklü, Rahmi. "Expression of latent transforming growth factor-β1 binding protein-1 in atherosclerosis." Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621723.
Full textRajwani, Dr Adil. "Mechanisms by which Insulin-like Growth Factor Binding Protein-1 modulates Endothelial Function." Thesis, University of Leeds, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.521475.
Full textBabajko, Sylvie. "Regulation transcriptionnelle de l'expression hepatique de l'insulin-like growth factor binding protein-1 (igfbp-1)." Paris 6, 1993. http://www.theses.fr/1993PA066505.
Full textWilson, Heather-Marie Porterfield. "The role of insulin-like growth factor binding protein-related protein-1 in human breast cancer /." Thesis, Connect to this title online; UW restricted, 2002. http://hdl.handle.net/1773/6352.
Full textLindgren, Björn. "Regulation of insulin-like growth factor binding protein-1 (IGFBP-1) and implications in catabolic conditions /." Stockholm, 1997. http://diss.kib.ki.se/1997/91-628-2411-2/.
Full textNi, Weimin. "The brain development retardation in insulin-like growth factor binding protein-1 transgenic mice." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq23442.pdf.
Full textButler, Georgina Susan. "A novel approach to study interactions of insulin-like growth factor binding protein-1." Thesis, University of Leicester, 1996. http://hdl.handle.net/2381/35189.
Full textVijayan, Aneesh. "A comparative study of insulin like growth factor binding protein-5 and transforming growth factor-beta 1 on epithelial-mesenchymal transition." Thesis, University of Strathclyde, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.502281.
Full textHills, Frank Adrian. "Levels of insulin-like growth factor-I (IGF-1) and IGF binding protein-1 in disorders of human fetal growth." Thesis, University of London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.417595.
Full textFoster, Ernest Byron Pascoe David D. "Acute regulation of IGF-1 by differential growth-factor-binding-protein expression, inhibition, and proteolysis." Auburn, Ala, 2008. http://repo.lib.auburn.edu/EtdRoot/2008/SUMMER/Health_and_Human_Performance/Dissertation/Foster_Ernest_45.pdf.
Full textBoraie, Anwar Abdullah. "Insulin-like growth factor binding protein 1 (IGFBP-1) : a potential marker of insulin resistance and cardiovascular risk." Thesis, University of Surrey, 2010. http://epubs.surrey.ac.uk/843496/.
Full textNoble, Anthony M. "In vitro examination of vitronectin, insulin-like growth factor, insulin-like growth factor binding protein complexes as treatments to accelerate the healing of diabetic ulcers." Thesis, Queensland University of Technology, 2008. https://eprints.qut.edu.au/16670/1/Anthony_Michael_Noble_Thesis.pdf.
Full textNanayakkara, Sachith N. "The role of IGF-1 and hormone binding proteins in understanding insulin-associated equine laminitis." Thesis, Queensland University of Technology, 2018. https://eprints.qut.edu.au/118300/1/Sachith_Nanayakkara_Thesis.pdf.
Full textMarsh, Andrew. "Characterisation of the type I IGF receptor binding surfaces of insulin-like growth factor 1 using protein engineering." Thesis, University of Newcastle Upon Tyne, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.245705.
Full textBatra, Sumit. "Innovative Purification Protocol for Heparin Binding Proteins: Relevance in Biopharmaceutical and Biomedical Applications." TopSCHOLAR®, 2011. http://digitalcommons.wku.edu/theses/1062.
Full textDunaiski, Vera. "Effects of IGF-1 or LR3IGF-1 infusion on components of the GH/IGF-1 axis in pigs /." Title page, contents and abstract only, 1997. http://web4.library.adelaide.edu.au/theses/09PH/09phd897.pdf.
Full textHarrela, Maija. "Twin and epidemiological studies on insulin-like growth factor binding protein-1 : relationships to insulin sensitivity and cardiovascular risk." Helsinki : University of Helsinki, 2002. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/harrela/.
Full textAziz, Amir. "Enhancing vascular endothelial repair in the setting of insulin resistance : effects of insulin-like growth factor binding protein-1." Thesis, University of Leeds, 2014. http://etheses.whiterose.ac.uk/8010/.
Full textHack, Nicole L. "The Insulin-Like Growth Factor-1 (IGF1) System as a Potential Biomarker for Nutritional Status and Growth Rate in Pacific Rockfish (SEBASTES SPP.)." DigitalCommons@CalPoly, 2017. https://digitalcommons.calpoly.edu/theses/1824.
Full textKachra, Zarin. "Regulation of insulin-like growth factor-I (IGF-I) and IGF-binding protein-1 (IGFBP-1) mRNA levels in cultured rat hepatocytes." Thesis, McGill University, 1993. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=41300.
Full textIGF-I mRNA levels were stimulated 2.0 to 2.5 fold by bovine growth hormone (bGH) and 1.8 to 2.0 fold by glucagon but on combining bGH and glucagon, a synergistic effect was observed and IGF-I mRNA level was augmented 10 to 12 fold. Octreotide blocked the hGH induced stimulation of IGF-I production in serum and hepatic IGF-I mRNA levels in hypophysectomized rats. This effect could have been partly due to the low levels of glucagon in serum when hypophysectomized rats were treated with hGH and octreotide. Octreotide was also found to inhibit GH stimulated IGF-I mRNA levels in rat hepatocytes.
The unique synergy observed with glucagon and bGH on IGF-I mRNA levels in hepatocytes was not reproduced by T$ sb3$, oPRL, dexamethasone, EGF or insulin when each was added in combination with bGH or glucagon. Like glucagon, the addition of IBMX or (Bu)$ sb2$cAMP stimulated IGF-I mRNA levels 1.8 to 2.0 fold, but in the presence of bGH, IGF-I mRNA levels were stimulated 10 to 12 fold. PMA stimulated IGF-I mRNA levels 1.2 to 1.4 fold but displayed no synergism when added with bGH. The stimulatory effect of bGH plus glucagon on IGF-I mRNA levels was inhibited in PKC depleted cells, in the presence of inhibitors of PKC and in the presence of cycloheximide. bGH had no posttranscriptional effect on IGF-I mRNA stability whereas glucagon or (Bu)$ sb2$cAMP stabilized IGF-I mRNA at a posttranscriptional level.
In summary, the major hormonal regulators of hepatic IGF-I mRNA levels appear to be GH and glucagon. Hepatic IGF-I mRNA levels are regulated by pathways involving protein kinase C and, protein kinase A as well as by synthesis of one or more protein(s).
Glucagon and dexamethasone each stimulated IGFBP-1 mRNA levels 3 to 4 fold whereas bGH and T$ sb3$ each inhibited IGFBP-1 mRNA levels 45 to 70%. Insulin, which inhibited IGFBP-1 mRNA levels 95%, was the most powerful inhibitor and was also found to inhibit IGFBP-1 mRNA levels in the presence of dexamethasone. IBMX and (Bu)$ sb2$cAMP stimulated IGFBP-1 mRNA levels 6 to 8 fold whereas PMA inhibited IGFBP-1 mRNA levels 40 to 50%. The inhibitory effect of bGH on IGFBP-1 mRNA levels was abolished in PKC depleted cells and also in the presence of inhibitors of PKC. In the presence of cycloheximide, IGFBP-1 mRNA was superinduced by bGH. bGH had no posttranscriptional effect on IGFBP-1 mRNA whereas glucagon and (Bu)$ sb2$cAMP stabilized IGFBP-1 mRNA at a postranscriptional level.
In summary, bGH, T$ sb3$ and insulin inhibited whereas dexamethasone and glucagon stimulated IGFBP-1 mRNA levels in hepatocytes. Effect of glucagon may be via elevation of cAMP levels, whereas the effect of bGH may be via activation of PKC levels. The inhibitory effect of bGH appears to require synthesis of one or more protein(s) besides stimulation of PKC levels.
Lemos, Nadiane Albuquerque. "Avaliação de IGF-1 (Insulin-like growth factor-1), IGFBP-1 e IGFBP-3 (Insulin-like to growth binding protein-1 e 3) no fluído folicular de pacientes infertéis com endometriose." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2002. http://hdl.handle.net/10183/2958.
Full textTippana, Mangapathiraju. "Development of a novel tissue targeted nerve growth factor: Fibronectin chimeric protein as a potential therapeutic for peripheral nerve regeneration." Thesis, Queensland University of Technology, 2018. https://eprints.qut.edu.au/120280/1/Mangapathiraju_Tippana_Thesis.pdf.
Full textArmbrust, Moritz [Verfasser]. "Der Zusammenhang zwischen den Blutplasmakonzentrationen des zirkulierenden Insulin-like-Growth-Factor-1 sowie des Insulin-like-Growth-Factor-Binding-Protein-3 und dem funktionell-neurologischen Outcome nach ischämischem Schlaganfall / Moritz Armbrust." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2016. http://d-nb.info/1100387617/34.
Full textLubina, Solomon Alexandra. "The role of placental alkaline phosphatase in the regulation of insulin-like growth factor binding protein-1 in pregnancy complicated by diabetes." Thesis, University of Manchester, 2011. https://www.research.manchester.ac.uk/portal/en/theses/the-role-of-placental-alkaline-phosphatase-in-the-regulation-of-insulinlike-growth-factor-binding-protein1-in-pregnancy-complicated-by-diabetes(c906fb09-38d2-4f9b-a391-e24c7e9a539e).html.
Full textEkman, Bertil. "IGF-I in growth hormone deficiency and in type 1 diabetes /." Linköping : Univ, 2002. http://www.bibl.liu.se/liupubl/disp/disp2002/med757s.pdf.
Full textBerg, Ulrika. "The IGF-IGFBP system in aerobic exercise - with focus on skeletal muscle /." Stockholm : Institutionen för kvinnors och barns hälsa, Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-379-5/.
Full textLacey, Derek. "NFκB independent pathway activation of rheumatoid arthritis FLS by macrophage migration inhibitory factor (MIF)." Monash University, Faculty of Medicine, 2003. http://arrow.monash.edu.au/hdl/1959.1/9457.
Full textKurkinen-Räty, M. (Merja). "Preterm birth and preterm infant:a clinical study on certain etiological and diagnostic factors, and the outcome of infants." Doctoral thesis, Oulun yliopisto, 2000. http://urn.fi/urn:isbn:9514258266.
Full textBayayibign, Biruhalem Assefa [Verfasser]. "Insulin-like growth factor (IGF) binding protein-2, independently of IGF-1, induces GLUT-4 translocation and glucose uptake in 3T3-L1 adipocytes / Biruhalem Assefa Bayayibign." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2018. http://d-nb.info/1172074402/34.
Full textKekki, Minnamaija. "Prediction and prevention of spontaneus preterm delivery and peripartum infections by screening for cervical insulin-like growth factor-binding protein-1 and bacterial vaginosis in pregnancy." Helsinki : University of Helsinki, 2002. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/kekki/.
Full textLubik, Amy Anne. "The role of insulin and IGF2 signalling on metabolic pathways in prostate cancer progression." Thesis, Queensland University of Technology, 2011. https://eprints.qut.edu.au/49029/1/Amy_Lubik_Thesis.pdf.
Full textPazaitis, Nikolaos [Verfasser], Stefan [Gutachter] Hüttelmaier, Jan-Henning [Gutachter] Klussmann, and Martin [Gutachter] Pichler. "In vitro und in vivo Untersuchungen zur Tumorigenität des Insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) : [kumulative Dissertation] / Nikolaos Pazaitis ; Gutachter: Stefan Hüttelmaier, Jan-Henning Klussmann, Martin Pichler." Halle (Saale) : Universitäts- und Landesbibliothek Sachsen-Anhalt, 2020. http://d-nb.info/122112997X/34.
Full textKashyap, Abhishek S. "In vitro functional characterisation of IGF-I : VN-induced breast cancer progression." Thesis, Queensland University of Technology, 2012. https://eprints.qut.edu.au/62165/1/Abhishek_Kashyap_Thesis.pdf.
Full textGebski, Bijanka L. "Investigating TNF inhibition of IGF-1 signalling via JNK in cell culture models of skeletal muscle atrophy." University of Western Australia. School of Anatomy and Human Biology, 2009. http://theses.library.uwa.edu.au/adt-WU2010.0097.
Full textHallatschek, Werner. "Die Regulation des humanen Lipopolysaccharid bindenden Proteins (hLBP)." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2005. http://dx.doi.org/10.18452/15202.
Full textLipopolysaccharide (LPS) binding protein (LBP) is an acute phase protein with the ability to bind and transfer LPS of Gram-negative bacteria. This soluble pattern recognition molecule represents an important defense principle of the host. Regulation of the hepatic acute phase response and its termination are important mechanisms for limiting systemic inflammatory activity of the host. Here were analyze the cooperation of Interleukin (IL)-1, IL-6, and Dexamethasone (Dex) at LBP expression in the hepatoma cell lines HuH-7 and Hep G2. The major inducer of LBP expression is IL-6. Within the LBP promoter numerously highly consensus binding sites such as AP-1, C/EBP-beta? and STAT3 are present, that confer transcriptional activity as shown by truncation and mutation experiments. Additionally, activate NF-kappaB sites activated by IL-1 were detected at the LBP promoter. By mutation experiments of the promoter furthermore were found differentially active glucocorticoid response elements (GREs). The promoter contains GREs enhancing the activity as well as inhibitory ones. The enhancing effect towards LBP expression by Dex was mediated by IL-6. Dex stimulated the expression of the IL-6 receptor and therefore upregulated the IL-6 pathway. Transforming Growth Factor (TGF)-beta is able to inhibit LBP expression in stimulated cells. An AP-1 binding site was identified mediating inhibitory TGF-beta effects towards LBP promoter activity. Furthermore it was shown that a growth factor independence (Gfi)-1 binding site localized near the AP-1 site is essential for mediating the TGF-beta inhibitory effect. The relevancy of the Gfi-1 site fore mediating TGF-beta effects indicates a novel mechanism for understanding inhibitory TGF-beta effects at the transcriptional level. In summary the complex regulation of LBP were elucidate which may help to eventually develop novel intervention strategies for acute phase, sepsis, and septic shock.
Pelletier, Sanja [Verfasser], Yves [Gutachter] Garnier, and Angela [Gutachter] Kribs. "Differenzierte Therapie der drohenden spontanen Frühgeburt bei Einlingsschwangerschaften unter Berücksichtigung des phosphorylierten insulin-like growth-factor binding protein-1 (phIGFBP-1) im Zervikalsekret und der sonographisch gemessenen Zervixlänge Eine multizentrische prospektive Kohortenstudie : eine multizentrische prospektive Kohortenstudie / Sanja Pelletier ; Gutachter: Yves Garnier, Angela Kribs." Köln : Deutsche Zentralbibliothek für Medizin, 2021. http://d-nb.info/1229194835/34.
Full textCunha, Angela Francisca Trinconi da. "Avaliação dos fatores de crescimento insulinóides IGF-1 e IGFBP-3 em mulheres com alto risco para câncer de mama." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/5/5139/tde-04112010-141608/.
Full textINTRODUCTION: The rising incidence of breast cancer, a disease that is increasingly affecting young women, has aroused a great deal of interest in early diagnosis and the search for a more efficient and minimally aggressive treatment. Likewise, the population at high risk for breast cancer has been growing, and it is now the focus of research efforts in the struggle to prevent neoplasia. Inspired by Peyrat, who was the first to associate breast cancer with insulin-like growth factor type 1 (IGF-1), several authors have taken on the challenge, and the international literature now leans towards a direct relationship, albeit still controversial, between IGF-1 and breast cancer in premenopause. The IGF binding protein 3 (IGFBP-3) has also been added to the list of cancer-causing agents, but its mechanism of action has not shown to be clearly regular. Targeting a population at high risk for breast cancer for histopathologic or familial reasons, and guided by the mathematical calculations of Gail and Tyrer-Cuzick, this thesis aimed at evaluating the relationship between IGF-1 and IGFB-3 in Brazilian female outpatients at the Mastology Sector of the Gynecology Discipline of the Department of Obstetrics and Gynecology of the School of Medicine of the University of São Paulo. METHODS: Transverse study to compare the serum levels of IGF-1 and IGFBP- 3 measured by the chemiluminescent immunometric method. The patients were divided into 3 different groups: women with untreated breast cancer (n=51), women with a population-based risk of breast cancer (n=66), and women at high risk for breast cancer (n=108). The comparison factors were age, menopausal state, and body mass index. RESULTS: 1) there were no differences among the groups with respect to BMI; 2) but there were statistically significant differences among the groups regarding mean age, and the younger women were those at a higher risk for breast cancer (p<0.001); 3) as for menopausal state, the groups were significantly different, and the postmenopausal women were prevalent among the patients with breast cancer (58.8%; p<0.001); 4) no statistically significant relationship was found between the IGF-1 percentage and the median, the IGFBP-3 percentage and the median, or the IGF-1 and IGFBP-3 ratio and the median in any of the groups; 5) measurements did not vary according to the determinant reason for high breast cancer risk (familial or histopathologic); 6) statistically significant changes in the variables under consideration did not take place, even after subdivision of the high-risk group (lifelong risk between 20% and 29% X lifelong risk over 29%). CONCLUSION: The serum levels of IGF-I and IGFBP-3 showed no variation among women with breast cancer, at high risk for cancer, or with populationbased risk
Zhang, Fan. "Receptor-operated signaling pathways in normal and diabetic pancreatic islet cell function /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7357-006-0/.
Full textBradburn, Jennifer Elizabeth. "Reactive species promotion of head and neck squamous cell carcinoma." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1166555968.
Full textGiroto, Alan Brunholi. "Adição de proteína plasmática a associada à prenhez (PAPP-A) durante a maturação in vitro aumenta o IGF-1 biodisponível e modula o perfil transcricional de complexos cumulus-oócitos e embriões bovinos." Universidade do Oeste Paulista, 2018. http://bdtd.unoeste.br:8080/jspui/handle/jspui/1091.
Full textMade available in DSpace on 2018-08-30T12:23:36Z (GMT). No. of bitstreams: 1 Alan Brunholi Giroto.pdf: 1342184 bytes, checksum: eec4738d5199b553c1a6ae446589328b (MD5) Previous issue date: 2018-05-25
In this study we aimed to evaluate how PAPP-A addition during in vitro maturation affected the IGF-1 quantification, transcript abundance related to cumulus oocyte complexes (COCs) and blastocysts quality, embryonic yield, as well as post-warming survival. We matured COCs through a 24 h treatment of TCM199 serum-free medium, either with PAPP-A supplementation (100 ng/mL; PAPP-A group) or without (control). Maturation medium was collected for IGF-1 quantification, and matured COCs were used for in vitro fertilization and culturing. The PAPP-A group exhibited 1.27 times higher IGF-1 concentrations than control. A comparison of in vitro embryo production across the groups found no difference in cleavage rate, embryonic yield, and survival, 3 and 24 h post-cryopreservation. In PAPP-A oocytes, only TXNRD1 was up-regulated. However, in PAPP-A cumulus cells, VNN1 and HDAC2 were up-regulated, while AGPAT1, AGPAT9, FASN, CASP3, EGFR, HAS2, IMPDH1, and MTIF3 were down-regulated. Finally, in PAPP-A blastocysts, CPT2, CASP9, DNMT3A, TFAM, and KRT8 were up-regulated, while ATF4, CASP3, and IFITM3 were down-regulated. We concluded that PAPP-A addition increased IGF-1 but did not influence embryonic yield and survival. Nevertheless, elevated IGF-1 could improve embryo competence through modulating expression of genes involved with lipid metabolism, oocyte competence and apoptosis in COCs and blastocysts.
A protéina sérica associada à prenhez (PAPP-A) é capaz de modular a biodisponibilidade do IGF-1 (fator de crescimento semelhante à insulina tipo 1) pela quebra das ligação com as proteínas de ligação do IGF (IGFBPs). O objetivo foi avaliar como a adição da PAPP-A durante a maturação in vitro (MIV) afetou a biodisponibilidade de IGF-1, a abundância de transcritos nos oócitos e células do cumulus e blastocistos, a produção embrionária e a sobrevivência pós aquecimento. Foi realizada a MIV de 24 h em complexos cumulus oócitos (CCOs – 20/grupo) oriundos de abatedouro, em meio TCM199 livre de soro, com adição de PAPP-A (100 ng/mL; grupo PAPP-A) ou sem (controle). O IGF-1 foi quantificado no meio de maturação e os CCOs maturados foram utilizados na fertilização e cultivo in vitro. Oócitos e células do cúmulus foram separados; e blastocistos foram congelados para a realização da expressão gênica. Taxa de clivagem e produção de blastocistos foram calculados como porcentagem e transformados para arco seno. Dados de expressão gênica foram normalizados com a média do grupo de controle. Os resultados foram analisados por test t, porém a criopreservação embrionária foi testada por Qui-quadrado (JMP software, SAS). Diferenças foram consideradas significativas quando p ≤ 0,05. O grupo PAPP-A apresentou 27% mais concentração de IGF-1 biodisponível. Na produção in vitro de embriões, não encontrou-se diferença na taxa de clivagem, produção e sobrevivência embrionária. Apenas o gene TXNRD1 mostrou maior expressão nos oócitos do grupo PAPP-A. No entanto, nas células do cumulus PAPP-A, o VNN1 e HDAC2 apresentaram maior expressão, enquanto os genes AGPAT1, AGPAT9, FASN, CASP3, EGFR, HAS2, IMPDH1 e MTIF3 apresentaram menor expressão. Nos blastocistos PAPP-A, os genes CPT2, CASP9, DNMT3A, TFAM e KRT8 apresentaram maior expressão, enquanto os genes ATF4, CASP3 e IFITM3 apresentaram menor expressão. Em conclusão, a adição de PAPP-A durante a MIV aumentou o IGF-1 biodisponível, mas não influenciou a produção e a sobrevivência embrionária após desvitrificação. No entanto, o aumento do IGF-1 biodisponível pode melhorar a competência embrionária através da modulação da expressão gênica em oócitos, células do cúmulus e blastocistos.
Zabihi, Sheller. "Fetal Outcome in Experimental Diabetic Pregnancy." Doctoral thesis, Uppsala University, Department of Medical Cell Biology, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8739.
Full textWomen with pregestational diabetes have a 2-5 fold increased risk of giving birth to malformed babies compared with non-diabetic women. Diabetes-induced oxidative stress in maternal and embryonic tissues has been implicated in the teratogenic process. The malformations are likely to be induced before the seventh week of pregnancy, when the yolk sac is partly responsible for the transfer of metabolites to the embryo, and the uterine blood flow to the implantation site determines the net amount of nutrients available to the conceptus. We aimed to evaluate the effect on embryogenesis caused by a diabetes-induced disturbance in yolk sac morphology, uterine blood flow or altered maternal antioxidative status in conjunction with a varied severity of the maternal diabetic state.
We investigated to which extent maternal diabetes with or without folic acid (FA) supplementation affects mRNA levels and protein distribution of ROS scavenging enzymes (SOD, CAT, GPX), vascular endothelial growth factor-A (Vegf-A), folate binding protein-1 (Folbp-1), and apoptosis associated proteins (Bax, Bcl-2, Caspase-3) in the yolk sacs of rat embryos on gestational days 10 and 11. We found that maternal diabetes impairs, and that FA supplementation restores, yolk sac vessel morphology, and that maternal diabetes is associated with increased apoptotic rate in embryos and yolk sacs, as well as impaired SOD gene expression. We assessed uterine blood flow with a laser-Doppler-flow-meter and found increased blood flow to implantation sites of diabetic rats compared with controls. Furthermore, resorbed and malformed offspring showed increased and decreased blood flow to their implantation sites, respectively. In mice with genetically altered CuZnSOD levels, maternal diabetes increased embryonic dysmorphogenesis irrespective of CuZnSOD expression. We thus found the maternal diabetic state to be a major determinant of diabetic embryopathy and that the CuZnSOD status exerts a partial protection for the embryo in diabetic pregnancy.