Dissertationen: „Growth factors“

1

Griffiths, Leigh. „Angiogenic growth factors in tumour growth“. Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312384.

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2

Robertson, James Gray. „Insulin-like growth factors and insulin-like growth factor binding proteins in wounds /“. Title page, contents and abstract only, 1999. http://web4.library.adelaide.edu.au/theses/09PH/09phr6509.pdf.

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3

Wahlgren, Aida. „Growth factors in spermatogenesis /“. Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-579-4/.

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4

Aase, Karin. „On vascular endothelial growth factor B and platelet-derived growth factor C : two members of the VEGF/PDGF family of growth factors /“. Stockholm : Karolinska Univ. Press, 2001. http://diss.kib.ki.se/2001/91-89428-14-5/.

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5

Martinez, Humberto Jose. „Nerve growth factor actions on the brain /“. Access full-text from WCMC, 1989. http://proquest.umi.com/pqdweb?did=744572291&sid=1&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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6

Gillies, 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.

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In order to effect permanent closure in burns patients suffering from full thickness wounds, replacing their skin via split thickness autografting, is essential. Dermal substitutes in conjunction with widely meshed split thickness autografts (+/- cultured keratinocytes) reduce scarring at the donor and recipient sites of burns patients by reducing demand for autologous skin (both surface area and thickness), without compromising dermal delivery at the wound face. Tissue engineered products such as Integra consist of a dermal template which is rapidly remodelled to form a neodermis, at which time the temporary silicone outer layer is removed and replaced with autologous split thickness skin. Whilst provision of a thick tissue engineered dermis at full thickness burn sites reduces scarring, it is hampered by delays in vascularisation which results in clinical failure. The ultimate success of any skin graft product is dependent upon a number of basic factors including adherence, haemostasis and in the case of viable tissue grafts, success is ultimately dependent upon restoration of a normal blood supply, and hence this study. Ultimately, the goal of this research is to improve the therapeutic properties of tissue replacements, through impregnation with growth factors aimed at stimulating migration and proliferation of microvascular endothelial cells into the donor tissue post grafting. For the purpose of my masters, the aim was to evaluate the responsiveness of a dermal microvascular endothelial cell line to growth factors and haemostatic factors, in the presence of the glycoprotein vitronectin. Vitronectin formed the backbone for my hypothesis and research due to its association with both epithelial and, more specifically, endothelial migration and proliferation. Early work using a platform technology referred to as VitroGro (Tissue Therapies Ltd), which is comprised of vitronectin bound BP5/IGF-1, aided keratinocyte proliferation. I hypothesised that this result would translate to another epithelium - endothelium. VitroGro had no effect on endothelial proliferation or migration. Vitronectin increases the presence of Fibroblast Growth Factor (FGF) and Vascular Endothelial Growth Factor (VEGF) receptors, enhancing cell responsiveness to their respective ligands. So, although Human Microvascular Endothelial Cell line 1 (HMEC-1) VEGF receptor expression is generally low, it was hypothesised that exposure to vitronectin would up-regulate this receptor. HMEC-1 migration, but not proliferation, was enhanced by vitronectin bound VEGF, as well as vitronectin bound Epidermal Growth Factor (EGF), both of which could be used to stimulate microvascular endothelial cell migration for the purpose of transplantation. In addition to vitronectin's synergy with various growth factors, it has also been shown to play a role in haemostasis. Vitronectin binds thrombin-antithrombin III (TAT) to form a trimeric complex that takes on many of the attributes of vitronectin, such as heparin affinity, which results in its adherence to endothelium via heparan sulfate proteoglycans (HSP), followed by unaltered transcytosis through the endothelium, and ultimately its removal from the circulation. This has been documented as a mechanism designed to remove thrombin from the circulation. Equally, it could be argued that it is a mechanism for delivering vitronectin to the matrix. My results show that matrix-bound vitronectin dramatically alters the effect that conformationally altered antithrombin three (cATIII) has on proliferation of microvascular endothelial cells. cATIII stimulates HMEC-1 proliferation in the presence of matrix-bound vitronectin, as opposed to inhibiting proliferation in its absence. Binding vitronectin to tissues and organs prior to transplant, in the presence of cATIII, will have a profound effect on microvascular infiltration of the graft, by preventing occlusion of existing vessels whilst stimulating migration and proliferation of endothelium within the tissue.

7

McMurray, Heather Forbes. „Macrophage growth factors in atherogenesis“. Thesis, University of Cambridge, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.306460.

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8

Sowter, Heidi Michelle. „Growth factors in ovarian cancer“. Thesis, Anglia Ruskin University, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.299988.

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9

Martin, 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.

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This research investigated if exogenous growth factors (GFs), in particular platelet derived growth factor (PDGF), has an in vivo effect on the healing response of normal healthy bone. The research was orientated to study whether a clinical beneficial effect could be demonstrated. To achieve this two animal models were utilised, namely, a rabbit tibial osteotomy model and an ovine tibial defect and porous implant ingrowth model. The rabbit model comprised of a unilateral V-shaped tibial osteotomy, stabilised with an absorbable intramedullary pin and figure-of-eight tension band suture, with a 3 week survival period. The GFs tested in this model were 3 concentrations of PDGF, a single dose of insulin-like growth factor binding protein (IGF-BP) and a combination of the two. Each osteotomy was injected with a single bolus of collagen (control) or collagen containing GF (treatment) during surgery. After sacrifice tibiae were CT-scanned in situ, harvested and subject to 4-point bend testing. The callus, underlying bone and contralateral bone's greyscales and mechanical testing results were used for comparative analysis. The ovine model consisted of implanting 6 small rectangular shaped titanium alloy porous implants and one empty defect bilaterally in sheep's tibiae, for 4 and 6 weeks. The sheep were injected with tetracycline bone marker at 2 week intervals. The model's characteristics and any positional effects were initially investigated. Followed by an investigation into the influence of various exogenous GFs on the healing response and ingrowth characteristics of bone into the porous implants. The GFs investigated were PDGF, IGF-BP and fibroblast growth factor impregnated into the porous implants in a collagen carrier. Comparative analysis was done on results from 3-point bend testing of the bone/implant interface, image analysis to quantify percentage of bone, from scanning electron microscopy images of implant sections and confocal microscopy images of tibial defect sections. Analyses indicate that the GFs investigated have a direct and quantifiable positive in vivo effect. The more significant finding is that the growth factors have a potent systemic effect. These results were confirmed by both the sheep porous bone plug model and the rabbit tibial osteotomy model used within this research.

10

Olofsson, Susanne. „Design, synthesis, structure, and dynamics of a polypeptide with supersecondary structure a helix-loop-helix dimer /“. Göteborg : Dept. of Organic Chemistry, University of Göteborg, 1994. http://books.google.com/books?id=6AdrAAAAMAAJ.

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11

Porteous, C. „Epidermal growth factor, α-transforming growth factor and breast cancer“. Thesis, University of Aberdeen, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.383650.

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Evidence exists that epidermal growth factor (EGF) and alpha transforming growth factor (αTGF) are important in breast cancer. An inverse relationship between epidermal growth factor receptor (EGF-R) and oestrogen receptor (ER) has been reported by some, (1) but not all workers (2). The aim in this thesis was to develop assays to measure, levels of EGF, and determine EGF-R status in human breast tumours. These results were then correlated with each other, with ER and node status and histological grade (Bloom & Richardson). An additional aim in this thesis was to develop a source of αTGF in conditioned median (CM) from a transformed cell line. After extraction and purification, the αTGF was intended for use as an immunogen to produce a polyclonal antiserum which could be used in either an RIA or ELISA. EGF was measured by a radioimmunoassay (RIA) utilising a rabbit antimouse EGF antiserum. This assay (sensitivity 0.1ng/ml) was demonstrated to have no cross reactivity with αTGF. The EGF-R assay was similar to that described by Sainsbury. (1) In a series of 88 human breast tumours 47 (53.4%) were found to contain extractable EGF. Forty eight (54.5%) were EGF-R positive and 39 (44.3%) were ER positive. A direct relationship between EGF and ER+ ve status was found (p < 0.01). Significantly higher levels of EGF were extracted from ER+ ve tumours (p = 0.049) compared with that from ER-ve tumours. However no relationship between EGF-R and EGF or ER status was found, or between EGF levels and histological grade or node status. A suitable cell line which produced αTGF, was obtained and culture conditions optimised. Alpha-TGF was assayed by a radioreceptor assay which utilised a cell line rich in EGF-R (A431). Extraction of αTGF was based on the principles of molecular grading by gel filtration (Sephadex G50), and ion exchange (Sephadex CM C25). By this process the αTGF was purified and separated it from any EGF present. By this method 20μg of αTGF was produced from 61t of CM. 1) Sainsbury JRC, Farndon JR, Serbet GV, Harris AL. Epidermal-growth-factor-receptors and oestrogen receptors in human breast cancer. Lancet 1985; 1: 364-368. 2) Fitzpatrick SL, Brightwell J, Wattliff JL, Barrows GH, Schultz GS. Epidermal growth factor binding by breast tumour biopsies and relationship to oestrogen receptor and progestin receptor levels. Cancer Res 1984; 44: 3448-3453.

12

Sia, Vicente Y. „Factors affecting church growth in selected Filipino-Chinese churches“. Online full text .pdf document, available to Fuller patrons only, 2004. http://www.tren.com.

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13

Kampman, Kimberly A. „The insulin-like growth factors in intrauterine growth retarded swine /“. The Ohio State University, 1992. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487759914760326.

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14

Kind, Karen Lee. „Insulin-like growth factors and growth of the fetal sheep /“. Title page, contents and abstract only, 1995. http://web4.library.adelaide.edu.au/theses/09PH/09phk525.pdf.

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15

Brinkworth, Craig Steven. „The primary and secondary structure determination of bioactive amphibian peptides : a thesis submitted for the degree of Doctor of Philosophy“. Title page, contents and abstract only, 2003. http://web4.library.adelaide.edu.au/theses/09PH/09phb8586.pdf.

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"May 2003." Includes a list of publications by the author (journal articles related to thesis); and , copies of journal articles co-authored by the author. Includes bibliographical references (leaves 226-242) The solution structures of three peptides: Ala4Lys14-citopin 1.1 (amphipathic đ-helix); Gly15Gly19-caerin 1.1 (a less defined đ-helix); and, frenatin 3.1 (amphipathic đ-helix with a flexible c-terminal end) are presented in a discussion about structure/activity relationship

16

Rodekohr, Chad L. Bozack Michael J. Flowers George T. „Material factors influencing metallic whisker growth“. Auburn, Ala, 2008. http://repo.lib.auburn.edu/EtdRoot/2008/FALL/Mechanical_Engineering/Dissertation/Rodekohr_Chad_16.pdf.

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17

Zhang, Echo Ge. „Angiogenic growth factors in human placentation“. Thesis, University of Cambridge, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621333.

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18

Gifford, Roy. „Factors Contributing to Sustainable Brand Growth“. Case Western Reserve University School of Graduate Studies / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=case1488372404181176.

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19

Tam, Y. M. „The relationships of growth with nutrition and serum growth factors in early life /“. Hong Kong : University of Hong Kong, 1999. http://sunzi.lib.hku.hk/hkuto/record.jsp?B2152712X.

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20

Zern, Blaine Joseph. „A biocompatible, heparin-binding polycation for the controlled delivery of growth factors“. Diss., Atlanta, Ga. : Georgia Institute of Technology, 2009. http://hdl.handle.net/1853/28145.

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Thesis (M. S.)--Biomedical Engineering, Georgia Institute of Technology, 2009.
Committee Chair: Wang, Yadong; Committee Member: Barker, Thomas; Committee Member: Boyan, Barbara; Committee Member: Chaikof, Elliot; Committee Member: Meredith, J. Carson; Committee Member: Prausnitz, Mark.

21

Tran, Nhat-Thang. „La citrulline, un nouvel agent en thérapeutique pour le retard de croissance intra-utérin (RCIU) ? : impact sur le placenta, la croissance fœtale et questions ouvertes sur la supplémentation néo-natale dans un modèle animal de RCIU“. Thesis, Nantes, 2016. http://www.theses.fr/2016NANT1011/document.

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Le retard de croissance intra-utérin (RCIU) reste une complication fréquente de la grossesse et expose non seulement à une mortalité néonatale plus élevée, mais également au risque d'un cortège de pathologies chroniques (cardio-métaboliques) à l'âge adulte. Étant un fardeau important pour la santé publique dans le monde entier, il n'existe pas encore à ce jour de traitement curatif autre qu'une extraction plus. précoce avec éventuellement une prématurité. Une étude récente de notre équipe a montré que l'administration de citrulline pendant la gestation améliore la croissance et la synthèse protéique fœtales dans un modèle de RCIU induit chez la rate par la restriction sévère en protéines. L'objectif de ce travail de thèse était donc d'explorer les mécanismes d'action de la supplémentation en citrulline pendant la période périnatale (gestation et allaitement) dans le même modèle. Notre première partie de ce travail confirme que la citrulline stimule la croissance en nous montrant que la supplémentation anténatale en citrulline agit dès le milieu de la gestation sur des gènes codant pour des facteurs de croissance, d’angiogenèse et de transporteurs d'acides aminés pour aboutir à une efficacité placentaire renforcée jusqu'à la fin de la gestation fœtale. Dans la deuxième partie, nous n'avons pas mis en évidence d'effet bénéfique de cette supplémentation postnatale chez des ratons nés dénutris, puis soumis à un régime déséquilibré riche en fructose, ni en termes de croissance, ni sur le métabolisme glucido-lipidique à l'âge adulte jeune. La vigilance impose davantage d'explorations mécanistiques avant d'envisager une étude translationnelle clinique à ce stade sensible de développement qu'est la période néonatale. En revanche, dans le cas de la période gestationnelle, nos résultats incitent à réfléchir à la mise en place d'essais cliniques pertinents pour cette pathologie de la croissance fœtale
Intra-uterine growth restriction (IUGR) remains a common pregnancy-related complication resulting not only in a significant neonatal mortality, but in an increased risk of chronic cardio-metabolic diseases in adulthood as well. This condition represents a serious burden to public health across the world due to lack of a curative treatment except early cessation of gestation with induced prematurity. Developing alternative strategies aimed towards targeted therapy would thus be highly desirable. In recent studies, we showed that citrulline supplementation during gestation in rats under severe dietary protein restriction enhanced fetal growth and protein synthesis. The objective of this work was to further investigate the mechanisms mediating the effect of citrulline during the perinatal period, i.e. gestation and nursing in the same model. In the first part, we confirmed that citrulline improved fetal growth, and further demonstrated that citrulline activated placental genes coding for growth factors, angiogenesis and amino acid transporters early from mid-gestation, resulting in improved fetal weight. However, in the second part of the current work, we failed to observe any beneficial effect of neonatal citrulline supplementation neither on growth, nor on the prevention of alterations of glucose and lipid metabolism in IUGR rats that were later exposed to an unbalanced, fructose-enriched diet. Therefore, further explorations are needed for a better mechanistic understanding before postnatal citrulline supplementation can be considered in translational trials. Otherwise, the results obtained in the gestational period in this work suggest clinical trails should be envisioned for prenatal citrulline supplementation in targeted populations of patients

22

Pascal, M. M. „The role of transforming growth factor beta and other growth factors in the development of diabetic retinopathy“. Thesis, University of Aberdeen, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.593270.

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The present study showed that TFG-β mRNA and protein expression is regulated by glucose concentration in HREC. Maximal secreted protein levels and mRNA were produced at a concentration of 15 mM and the majority of the TGF-β is found in an active form in these cells. These results were novel and specific as HREC have not been shown before to express TFG-β in response to glucose. TGF-β appears to be central to a wide range of pathological features involved in the disease and this first study highlights a possible important role for TGF-β in the mechanism of induction of microvascular abnormalities in the retina. It could also play a role as a key mediator of the high glucose induced effects in DR, as is the case in the kidney. Glucose dependent changes in TGF-β receptors expression and signalling intermediates were also examined in HREC. These studies indicate that glucose is able to regulate both TGF-β expression and the receptor numbers of affinity but it is apparent that there is no simple correlation between secreted TGF-β and receptor number or affinity or expression. Protein kinase C isoforms protein expression did not change relatively to glucose but various isoforms were expressed at different intensities in endothelial cells and TGF-β signalling cascade involves a MAPK independent pathway. TGF-β expression in the ganglion cell layer demonstrated a neurotrophic role for TGF-β, whereas VEGF expression did not seem to correlate spatially or temporally with angiogenesis. We suggest that both systemic cells (PBLs) and endothelial cells are able to secrete a wide range of growth factors when activated by glucose. These factors, along with other ones (platelet derived growth factor or insulin like growth factor type 1), may act in synergy to produce an imbalance in growth factor levels which could lead to angiogenesis and therefore contribute to the pathogenesis of PDR.

23

Östlund, Eva. „Growth factors and vasoactive substances in intrauterine growth restriction and preeclampsia /“. Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-5046-6/.

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24

Chung, Seung-Wook. „Modeling and analysis of the transforming growth factor beta signaling pathway“. Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 115 p, 2008. http://proquest.umi.com/pqdweb?did=1597632591&sid=15&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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25

Kiefer, Julie Christine. „Analysis of myogenic regulatory factors and insulin-like growth factors in early somite myogenesis /“. Thesis, Connect to this title online; UW restricted, 2001. http://hdl.handle.net/1773/9227.

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26

Sites, Emily. „Proposed Roles for Sox Transcription Factors and Growth Factor Receptors in NF1“. University of Cincinnati / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1226071241.

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27

Ekman, 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.

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28

Tam, Y. M., und 譚月明. „The relationships of growth with nutrition and serum growth factors inearly life“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B44569798.

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29

Ødegård, Rønnaug A. „Preeclampsia - maternal risk factors and fetal growth“. Doctoral thesis, Norwegian University of Science and Technology, Department of Cancer Research and Molecular Medicine, 2002. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-484.

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Preeclampsia is a complex and variable maternal disturbance that ranges from a dramatic onset at early gestation to slowly developing symptoms towards term. Hypertension and renal involvement with proteinuria are cardinal signs, which are often accompanied by fluid retention, blood-clotting dysfunction, and reduced organ perfusion. HELLP (haemolysis, elevated liver enzymes, and low platelet count) syndrome is regarded as a variant of preeclampsia, and the fulminante disease, eclampsia, includes convulsions. Preeclampsia is the main cause of maternal and fetal morbidity and mortality in western countries (1, 2), and in Nordic countries, 17 percent of maternal deaths have been ascribed to preeclampsia (2). Antenatal care in Norway includes on average 12 doctor/midwife consultations per pregnancy (3), and since blood pressure monitoring and urinary testing are main aims of the consultations, preeclampsia is a pregnancy complication that also generates substantial societal costs.

Paper II, III, IV and V reproduced with permission of Elsevier, sciencedirect.com

30

Jondell, Assbring Malin. „What factors affect economic growth in China?“ Thesis, Södertörns högskola, Institutionen för livsvetenskaper, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:sh:diva-16828.

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The objective of this thesis is to find out what factors have been the main sources of economic growth in China in 2003 and 2010. It also aims to find out whether the Solow model can be used to explain growth in China, if factors of growth are the same in rich and poor regions, whether the factors are the same in 2003 and 2010 and if the results are in line with previous research. The theoretical framework is the Solow model. Empirical tests are performed using econometrics, and therefore this thesis has a quantitative approach. Factors used are growth in GDP per capita which is tested against investments, household savings, the level of GDP per capita, population growth, healthcare and education. The results show that the Solow model can explain economic growth in China. Investments, the level of GDP per capita and population growth are the factors most significant to growth. In poor regions, both investments and population growth are more significant than in rich regions, whereas healthcare is more significant in rich regions. Investments and population growth also have a smaller impact in 2010 than 2003. Healthcare is more significant in 2010 and than 2003, and education is only significant in 2010. Previous research shows a wide range of results, and the results of investments and population growth are consistent with those.

31

Kehinde, Elijah Oladunni. „Regulation of prostatic carcinoma by growth factors“. Thesis, University of Leicester, 1997. http://hdl.handle.net/2381/29556.

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The present study was designed to test the hypothesis that non-androgenic growth factor inhibitors have a role to play in the management of patients with metastatic hormone-resistant prostate cancer.;The effects of the growth factor inhibitors, Somatostatin 201-995 (SMS 201-995), Estramustine phosphate (EMP) alone and in combinations on the cellular proliferation of established human prostate cancer cell lines LNCaP, DU145 and PC3 and on cells obtained by primary culture from patients with various stages of prostate cancer were assessed using 3H thymidine incorporation assay.;Suramin (0-270 ug/ml), SMS 201-995 (0-20 ug/ml), and EMP (0-50 ug/ml) produced dose dependent growth inhibition on both hormone dependent (LNCaP) and hormone independent (PC3) prostate cancer cells and cells obtained by primary culture of prostate cancer epithelial cells. Suramin and EMP combination produced statistically significant synergism on established prostate cancer cell lines, but not on prostate cancer cells obtained by primary culture.;In a preliminary clinical trial, patients with metastatic hormone-resistant prostate cancer were randomised into two treatment groups, Group A received EMP (280 mg twice daily) while Group B received EMP (280 mg twice daily) and low dose intravenous Suramin (1 gm weekly for 6 weeks). There were 6 patients in each treatment group. The control group, made up of 6 patients, continued on maximal androgen blockade namely castration and Flutamide (250 mg three times daily) or Cyproterone acetate (100 mg three times daily). At the end of 6 months of treatment, there was statistical significant reduction of serum levels of prostate specific antigen and better pain control for patients on EMP and Suramin compared to patients who received EMP alone (P < 0.01) or patients on EMP and Suramin compared to controls (P < 0.001) (Kruskal-Wallis test).;Suramin, a non-androgen growth factor inhibitor has been shown in this study to produce significant in vitro and in vivo inhibition of the proliferation of prostate cancer cells. Its use as a novel chemotherapeutic agent for hormone-resistant prostate cancer patients alone or in combination with EMP deserves further study.

32

Patel, Ambreen. „Fibroblast growth factors and retinal cell genesis“. Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0025/MQ48033.pdf.

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33

Balch, Samora Julie. „Factors regulating arteriolar tone during microvascular growth“. Morgantown, W. Va. : [West Virginia University Libraries], 2007. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=5423.

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Thesis (Ph. D.)--West Virginia University, 2007.
Title from document title page. Document formatted into pages; contains xxiii, 251 p. : ill. Vita. Includes abstract. Includes bibliographical references.

34

Brigstock, David Roger. „Heparin-binding growth factors from porcine uterus“. Thesis, University of Cambridge, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.279306.

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35

Ng, Ping-yi Doris, und 吳冰怡. „Psycho-spiritual factors of stress-related growth“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B50700777.

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Psycho-religious factors of posttraumatic growth (PTG) had been widely studied, yet only a few studies had examined the psycho-spiritual factors with stress-related growth (SRG). In order to measure spirituality locally, Study One explored the validity of the Spiritual Transcendence Scale (STS) (Piedmont, 2004) in a 415 adult students sample. Results of the study supported the internal consistency reliability of the overall STS and its concurrent validity with the Religious subscale of the Social Axioms Scale (Leung, Lam, Bond, Conway, Gornick, Amponash et al., 2012) and the Faith Maturity Scale (short-form) (Hui, Ng, Mok, Lau, & Cheung, 2011). Contrary to our prediction, the three-factor structure of the original STS was not supported in Hong Kong population. In accord with previous studies on psycho-religious factors of PTG (for example, Stanton, Bower & Low, 2006), age, gender, personality and spirituality were hypothesized to predict SRG in context of academic stress in Study Two. A total of 182 adult student samples were recruited. Results of the study only supported that spirituality as well as extraverted and agreeable in personalities predicted SRG, but not the other measured variables. Besides, age was the only variable moderated the relationship between academic stress and SRG as hypothesized. Last but not least, consistent with previous studies by Kleim and Ehlers (2010) and our hypothesis, a curvilinear relationship between SRG and depressive symptom was supported. Findings of the present study shed light to clinicians about the conceptualization of SRG and direction for potential psychological treatment.
published_or_final_version
Clinical Psychology
Master
Master of Social Sciences

36

Blostein, Ashley C. „Effects of running on hormonal growth factors“. Virtual Press, 1993. http://liblink.bsu.edu/uhtbin/catkey/865946.

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To determine the influence of running on certain blood-born parameters that are involved in bone metabolism, serum levels of calcium, alkaline phosphatase (ALP, a marker of bone formation), growth hormone (hGH), and parathyroid hormone (PTH), were analyzed in 10 male subjects following a 40 min. run at 70% VO2max. Each trial was preceeded by 1 day of inactivity, a 8-12 hr. fast, and drawing of a baseline blood sample by venipuncture. All other blood samples were taken via an indwelling catheter which was inserted in an antecubital vein immediately following the completion of the exercise bout. When the catheter was in place, an "immediate post" sample was drawn. Subsequent samples were taken at 1, 2, 3, 4, 5, 10, 15, 20, 30, 45, and 60 min. after the immediate post sample. Analysis of serum calcium concentrations demonstrated that levels were significantly elevated by 12% following exercise, going from a fasted level of 9.7 ± .53 mg/dl to post-exercise levels of 11.8 ± .73 mg/dl. Serum calcium remained elevated during the first 4 min. following exercise. By 5 min. post-exercise, calcium levels dropped to levels that were significantly lower than the post-exercise sample. However, serum alkaline phosphatase did not change significantly following exercise, as the values remained within normal range throughout the experimental period. Concentrations tended to decrease over time but were not significantly lower than the preor post-exercise levels by the end of the sampling period. Serum concentrations of hGH were more than doubled following a single bout of exercise, going from 4.0 ± 0.98 ng/ml before exercise to 8.8 ± 1.6 ng/ml immediately post-exercise. Following this initial rise, hGH progressively declined and returned to baseline values by 30 min. post-exercise. The concentrations of PTH did not change significantly following exercise. The postexercise sample tended to be higher than baseline values but were not significantly different. The results presented here indicate that an exercise bout 40 min. at 70% V02max results in an elevation of serum calcium and hGH, but does not alter PTH secretion or ALP activity. The data presented in this study indicate that the temporary rise in calcium following exercise is unrelated to PTH. It is hypothesized that the increase in calcium that we observed is attributable to lactate accumulation that would result from an exercise bout of this nature. The buildup of lactic acid and drop in pH causes a dissolution of the crystaline calcium hydroxyapatite compartment of the skeleton, thus causing an increase in ionized calcium. It is not known whether a single bout of exercise can influence hormonal secretion to a sufficient degree to affect bone density, but the hormonal changes demonstrated here could be involved in long-term effects of training.
School of Physical Education

37

Lannigan, Alison Kerr. „Tyrosine kinase growth factors in gastric cancer“. Thesis, University of Glasgow, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.394975.

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38

FERNANDES, CRISTIANO AUGUSTO COELHO. „LINEAR GROWTH BAYESIAN MODEL USING DISCOUNT FACTORS“. PONTIFÍCIA UNIVERSIDADE CATÓLICA DO RIO DE JANEIRO, 1985. http://www.maxwell.vrac.puc-rio.br/Busca_etds.php?strSecao=resultado&nrSeq=9308@1.

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CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO
O objetivo principal desta dissertação é descrever e discutir o Modelo Bayesiano de Crescimento Linear Sazonal, formulação Estados múltiplos, utilizando descontos. As idéias originais deste modelo foram desenvolvidas por Ameen e Harrison. Na primeira parte do trabalho (capítulos 2 e 3) apresentamos idéias bem gerais sobre Séries Temporais e os principais modelos da literatura. A segunda parte (capítulos 4, 5 e 6) é dedicada à Estatística Bayesiana (conceitos gerais), ao MDL na sua formulação original, e ao nosso modelo de interesse. São apresentadas algumas sugestões operacionais e um fluxograma de operação do modelo, com vistas a uma futura implementação computacional.
The aim of this thesis is to discuss in details the Multiprocess Linear Grawth Bayesian Model for seasonal and/or nonseasonal series, using discount factors. The original formulation of this model was put forward recently by Ameen and Harrison. In the first part of the thesis (chapters 2 and 3) we show some general concepts related to time series and time series modelling, whereas in the second (chapters 4, 5 and 6) we formally presented / the Bayesian formulation of the proposed model. A flow chart and some optional parameter setings aiming a computational implementation is also presented.

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Machado, Kayla L. „Management factors affecting calf growth and health“. Thesis, Virginia Tech, 2011. http://hdl.handle.net/10919/76914.

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Two calf feeding trends are emerging in the dairy industry in the United States. Large herds often find it economical to feed pasteurized waste milk; while smaller herds are embracing technological advancements by utilizing automated calf milk feeders. Housing of calves varies depending on feeding mechanism. Calves fed using autofeeders are grouped together but large herds often find it more labor efficient to house calves individually in elevated wooden crates or polyethylene hutches. Two studies were conducted. The objective of the first field study was to evaluate the influence of diet and housing type on growth and morbidity in 84 Holstein heifer calves in a 2 by 2 factorial experimental design. Calves were housed in either polyethylene hutches or elevated wooden crates with slatted floors. Diets consisted of pasteurized waste milk or the same waste milk supplemented to provide approximately 454 g of milk replacer solids containing 25% protein and 10% fat (LOL Balancer). Calves were randomly placed in 1 of 4 treatment groups 48 h after birth and monitored until weaning (~60 d of age). Body weights and hip heights were measured at time of enrollment and weaning. Milk samples of pasteurized waste milk were obtained five times weekly to measure standard bacteriological plate count, fat, protein and total solids content. All calves were fed 3.3 L of liquid diet via bottle at 0730 and 1530 h. Calves were monitored daily for respiratory and digestive illness and treated according to established protocols. Pasteurized waste milk contained 332,171 ° 733,487 cfu/ mL, 3.51 ° 0.59% fat, 3.13 ° 0.30% protein, and 11.64 ° 1.05% total solids. Housing (P = 0.02) and diet (P = 0.01) affected weight gain, but there was no interaction. Least squares average daily gain for crate and hutches were 0.52 ° 0.024 and 0.59 ° 0.024 kg/d. Least squares average daily gain for waste milk and balancer diets were 0.52 ° 0.024 and 0.60 ° 0.024 kg/d, respectively. Housing or diet did not affect hip height growth/d (0.196 ° 0.007 cm). Health of the calves was not affected by diet or housing. Supplementing waste milk with balancer or housing calves in hutches resulted in higher weight gain. The objective of the second study was to evaluate management, and sanitation and consistency of liquid delivered to calves via automated feeders. Ten herds in Virginia and North Carolina with sophisticated (FÃ¶rster-Technik, Germany) and basic (Biotic Industries Inc., TN, USA) machines completed a 60-question survey concerning calf and autofeeder management. Duplicate milk replacer samples were obtained to measure sanitation, dry matter, and temperature of milk in the autofeeder at the time of the survey. Six dairies from the original 10 were visited monthly for 3 mo for continued evaluation of sanitation, dry matter, and temperature of milk replacer from the autofeeder. Seven herds utilizing basic machines had a mean SPC of 6,925,000 ° 7,371,000 cfu/ml. The mean dry matter and temperature readings were 12.0 ° 2.1 Brix and 38.8 ° 6.7 °C, respectively. Three dairies that used sophisticated autofeeders had a mean SPC of 1,339,000 ° 2,203,000 cfu/ml. Mean dry matter and temperature readings were 10.37 ° 1.68 Brix and 38.6 ° 6.76°C, respectively. Dairies were also categorized based on management strategies. Producers that purchased autofeeders to manipulate feeding rates, refocus labor to sanitation, and care and well-being of calves, or for technological advancements were successful at rearing calves via autofeeders. Dairy producers who purchased an autofeeder to explore feeding options were not as successful because proper time and management was not dedicated to care of calves or to maintenance of the autofeeder.
Master of Science

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Bracken, Cynthia J. „Factors controlling ovarian follicular growth in sows /“. free to MU campus, to others for purchase, 2003. http://wwwlib.umi.com/cr/mo/fullcit?p3115527.

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41

Jäckle, Markus [Verfasser]. „Microscopic factors influencing dendrite growth / Markus Jäckle“. Ulm : Universität Ulm, 2020. http://d-nb.info/1222595966/34.

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Hesselager, Göran. „A short thesis about growth factors in gliomas /“. Uppsala : Acta Universitatis Upsaliensis Univ.-bibl. [distributör], 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3445.

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43

Smith, Cheryl A. „Skeletal muscle injury, fibrosis and transforming growth factor-[beta]“. Morgantown, W. Va. : [West Virginia University Libraries], 2000. http://etd.wvu.edu/templates/showETD.cfm?recnum=1744.

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Thesis (Ph. D.)--West Virginia University, 2000.
Title from document title page. Document formatted into pages; contains xii, 146 p. : ill. (some col.). Includes abstract. Includes bibliographical references.

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Sköld, Mattias. „On VEGF and related factors in neurotrauma /“. Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-986-2/.

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Moenner, Michel. „Étude du mécanisme d'action des facteurs de croissance "Fibroblast Growth Factors" (FGF)“. Paris 12, 1988. http://www.theses.fr/1988PA120010.

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Pour les deux types cellulaires etudies, il apparait que le signal mitogene induit par la formation du complexe fgf-recepteurs est independant de l'activation du cycle des polyphosphoinositides et de l'activation de la proteine kinase c

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Moenner, Michel. „Etude du mécanisme d'action des facteurs de croissance "fibroblast growth factors", FGF“. Grenoble 2 : ANRT, 1988. http://catalogue.bnf.fr/ark:/12148/cb376165817.

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47

Harrison-Woolrych, Mira. „Studies of peptide growth factors in uterine fibroids“. Thesis, University of Southampton, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295533.

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48

Gu, Ye. „Homo & heterodimeric TGF-[beta] family growth factors“. Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610106.

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49

Firman, David Mark. „Leaf growth and senescence of the potato“. Thesis, University of Cambridge, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.330197.

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50

Chim, Shek Man. „Identification and characterization of novel secreted factors involved in bone remodeling“. University of Western Australia. School of Surgery, 2009. http://theses.library.uwa.edu.au/adt-WU2010.0110.

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[Truncated abstract] Bone remodeling is an important process to maintain mechanical integrity. It is accomplished by two important steps, bone resorption followed by new bone formation. Osteoclasts and osteoblasts are the principal cells in bone resorption and bone formation, respectively. A multitude of local and systemic factors regulates this process by controlling the cellular activities in bone remodeling compartments (BRC). An imbalance of osteoblastic bone formation and osteoclastic bone destruction will result in the development of skeletal diseases. Recent studies suggested that angiogenesis is closely associated with bone remodeling. The vasculature in bone is important for skeletal development, growth and repair. During endochondral ossification, cartilage is invaded by blood vessels which bring in osteoblast and osteoclast precursor cells, nutrients, growth factors and differentiation factors. During fracture repair, it has been demonstrated that mature osteoclasts produce heparanase which can degrade heparin sulfate proteoglycans, a major component in extracellular matrix (ECM). The process leads to the release of heparin-binding growth factors including vascular endothelial growth factor (VEGF), a potent angiogenic factor which contributes largely to local angiogenesis. In recent studies, endothelial cells have been found to produce bone morphogenetic protein (BMP)-2 and BMP-4 when they are subjected to mechanical stimuli, or a hypoxia environment. Conversely, inhibition of angiogenesis has been shown to prevent fracture healing. In a distraction osteogenesis model, either inhibition of angiogenesis or disruption of the mechanical environment prevents normal osteogenesis and results in fibrous nonunion. .... A total of 42 mice from F1 and F2 generations were genotyped as transgene positive. Preliminary analysis using radiography did not reveal any difference between the gross structures of transgenic and wild type mice. Interestingly, the preliminary histology revealed a decrease in trabecular bone and an increase of lipid space in metaphysis of transgenic mice overexpressing EGFL6. However, further studies will need to be carried out to investigate the role of EGFL6 in angiogenesis and adipogenesis using a transgenic mice model. This will be a prime focus of future work. Collectively, the results presented in this thesis have identified EGFL6, a member of the EGF-like family, as a potential angiogenic factor which may play an important role in bone remodeling. EGFL6 has been found to be expressed highly in calvarial osteoblasts and upregulated during primary murine osteoblast differentiation. EGFL6 has been 8 characterized to be a secreted homomeric complex. More importantly, EGFL6 has been shown to induce angiogenic activity in endothelial cell migration, tube formation and in vivo chick embryo chorioallantoic membrane assay. Furthermore, conditioned medium containing the EGFL6 recombinant protein was shown to induce phosphorylation of ERK in endothelial cells. Inhibition of ERK impaired EGFL6-induced ERK activation and endothelial cell migration. Taken together these studies raise the possibility that EGFL6 has a potential role in angiogenesis, and mediates a paracrine mechanism of cross-talk between vascular endothelial cells and osteoblasts during osteogenesis. An understanding of this process offers the potential to facilitate the development of therapeutic treatments for bone disease.

Dissertationen zum Thema „Growth factors“

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