Relevant bibliographies by topics / Angiopoietin

Academic literature on the topic 'Angiopoietin'

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Published: 4 June 2021
Last updated: 11 March 2023

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Journal articles on the topic "Angiopoietin"

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CHANG, Hang, Bao-Wei WANG, Peiliang KUAN, and Kou-Gi SHYU. "Cyclical mechanical stretch enhances angiopoietin-2 and Tie2 receptor expression in cultured human umbilical vein endothelial cells." Clinical Science 104, no. 4 (March 20, 2003): 421–28. http://dx.doi.org/10.1042/cs1040421.

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Endothelial cells are essential for neovascularization. Angiopoietins and Tie receptors are required for a normal vasculature. How cyclical mechanical stretch affects the expression of components of the angiopoietin system is not known. In this study, we investigated the regulation of angiopoietins and Tie receptors by cyclical mechanical stretch in cultured human umbilical vein endothelial cells (HUVECs). HUVECs grown on a flexible membrane base were stretched by vacuum to 20% elongation, at 60cycles/min. The levels of angiopoietin-2 protein began to increase as early as 2h after stretch was initially applied, reached a maximum of 2.7-fold over the control value by 6h. The Tie2 receptor protein showed the same pattern as Ang-2. These increases in angiopoietin-2 and Tie2 receptor proteins at 6h were blocked by the addition (30min before stretch) of the protein kinase C inhibitor Gö6976 (16nM) or the tyrosine kinase inhibitor herbimycin A (24µM). Similar to protein expression, the levels of angiopoietin-2 and Tie2 receptor mRNAs in HUVECs increased 3.1-fold and 2.5-fold respectively after stretch for 6h. These increases were also blocked by Gö6976 or herbimycin A. Cyclical mechanical stretch increased (and Gö6976 or herbimycin A abrogated these increases) the immunohistochemical labelling of angiopoietin-2 and Tie2 receptor after a 6h stretch. The levels of angiopoietin-1 and Tie1 receptor proteins, mRNAs and immunohistochemical staining were unaffected by cyclical mechanical stretch. Thus cyclical mechanical stretch activates the expression of angiopoietin-2 and the Tie2 receptor, but not angiopoietin-1 or the Tie1 receptor, in cultured HUVECs. This mechanical effect is probably mediated by the tyrosine kinase and protein kinase C pathways.
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Tsakogiannis, Dimitris, Asimina Nikolakopoulou, Flora Zagouri, Grigorios Stratakos, Konstantinos Syrigos, Eleni Zografos, Nikolaos Koulouris, and Garyfalia Bletsa. "Update Overview of the Role of Angiopoietins in Lung Cancer." Medicina 57, no. 11 (November 1, 2021): 1191. http://dx.doi.org/10.3390/medicina57111191.

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Angiogenesis is a biological process that involves the formation of new blood vessels from the existing vasculature, and it plays a fundamental role in the development and progression of several types of cancer, including lung cancer. The angiopoietin/Tie2 ligand/receptor system orchestrates vascular integrity. In particular, Angiopoietin-1 activates the endothelial cell (EC)-specific receptor tyrosine kinase,Tie2,which is essential for preserving endothelial quiescence. On the other hand, Angiopoietin-2 acts as an inhibitor of the Angiopoietin-1/Tie2 signaling pathways, thus facilitating the destabilization of quiescent endothelium in cases of inflammation and cancer. Clinical studies have proven that high levels of Angiopoietin-2 indicate the development of non-small-cell lung carcinomas (NSCLC), while high levels of Angiopoietin-2 are strongly related to tumor angiogenesis, lymphangiogenesis, metastasis, and poor prognosis. Interestingly, the association of Angiopoietin-2 levels with the type of surgical approach makes Angiopoietin-2 a valuable factor in selecting the most suitable therapeutic strategy for lung cancer patients. The role of the Angiopoietin-1 and Angiopoietin-4 levels in NSCLC development requires further investigation. The present review focuses on the clinical impact of the Angiopoietin-1, Angiopoietin-2, and Angiopoietin-4 levels in patients diagnosed with NSCLC, emphasizing the interaction between them, and how they affect the development, progression, and metastasis of lung disease. Finally, it estimates the role of angiopoietins levels in the effective therapy of lung cancer patients.
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Sabatino, Laura, Claudia Kusmic, Giuseppina Nicolini, Rosario Amato, Giovanni Casini, Giorgio Iervasi, and Silvana Balzan. "T3 enhances Ang2 in rat aorta in myocardial I/R: comparison with left ventricle." Journal of Molecular Endocrinology 57, no. 3 (October 2016): 139–49. http://dx.doi.org/10.1530/jme-16-0118.

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Angiogenesis is important for recovery after tissue damage in myocardial ischemia/reperfusion, and tri-iodothyronine (T3) has documented effects on angiogenesis. The angiopoietins 1/2 and tyrosine kinase receptor represent an essential system in angiogenesis controlling endothelial cell survival and vascular maturation. Recently, in a 3-day ischemia/reperfusion rat model, the infusion of a low dose of T3 improved the post-ischemic recovery of cardiac function. Adopting this model, our study aimed to investigate the effects of T3 on the capillary index and the expression of angiogenic genes as the angiopoietins 1/2 and tyrosine kinase receptor system, in the thoracic aorta and in the left ventricle. In the thoracic aorta, T3 infusion significantly improved the angiogenic sprouting and angiopoietin 2 expression. Instead, Sham-T3 group did not show any significant increment of capillary density and angiopoietin 2 expression. In the area at risk (AAR) of the left ventricle, T3 infusion did not increase capillary density but restored levels of angiopoietin 1, which were reduced in I/R group. Angiopoietin 2 levels were similar to Sham group and unchanged by T3 administration. In the remote zone, T3 induced a significant increment of both angiopoietin 1/2. In conclusion, T3 infusion induced a different response of angiopoietin 1/2 between the ventricle (the AAR and the remote zone) and the thoracic aorta, probably reflecting the different action of angiopoietin 1/2 in cardiomyocytes and endothelial cells. Overall, these data suggest a new aspect of T3-mediated cardioprotection through angiogenesis.
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Khan, Aafaque Ahmad, Varot K. Sandhya, Priyata Singh, Deepak Parthasarathy, Awinav Kumar, Jayshree Advani, Rudrappa Gattu, et al. "Signaling Network Map of Endothelial TEK Tyrosine Kinase." Journal of Signal Transduction 2014 (October 13, 2014): 1–6. http://dx.doi.org/10.1155/2014/173026.

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TEK tyrosine kinase is primarily expressed on endothelial cells and is most commonly referred to as TIE2. TIE2 is a receptor tyrosine kinase modulated by its ligands, angiopoietins, to regulate the development and remodeling of vascular system. It is also one of the critical pathways associated with tumor angiogenesis and familial venous malformations. Apart from the vascular system, TIE2 signaling is also associated with postnatal hematopoiesis. Despite the involvement of TIE2-angiopoietin system in several diseases, the downstream molecular events of TIE2-angiopoietin signaling are not reported in any pathway repository. Therefore, carrying out a detailed review of published literature, we have documented molecular signaling events mediated by TIE2 in response to angiopoietins and developed a network map of TIE2 signaling. The pathway information is freely available to the scientific community through NetPath, a manually curated resource of signaling pathways. We hope that this pathway resource will provide an in-depth view of TIE2-angiopoietin signaling and will lead to identification of potential therapeutic targets for TIE2-angiopoietin associated disorders.
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Abdulmalek, Kefeya, Fathia Ashur, Nadine Ezer, Fengchun Ye, Sheldon Magder, and Sabah N. A. Hussain. "Differential expression of Tie-2 receptors and angiopoietins in response to in vivo hypoxia in rats." American Journal of Physiology-Lung Cellular and Molecular Physiology 281, no. 3 (September 1, 2001): L582—L590. http://dx.doi.org/10.1152/ajplung.2001.281.3.l582.

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In this study, we assessed the effects of in vivo hypoxia on the expression of Tie-2 receptors and angiopoietins in various organs of conscious rats and correlated these effects with the expression of hypoxia-inducible factor-1 (HIF-1). RT-PCR and Southern blotting were used to amplify mRNA expression of angiopoietin-1, -2, and -3, Tie-2, and HIF-1α in tissues of normoxic and hypoxic (fraction of inspired oxygen of 9–10% for either 12 or 48 h) rats. Hypoxia provoked a decline in angiopoietin-1 mRNA and Tie-2 mRNA, protein, and phosphorylation levels in the lung, liver, cerebellum, and heart but not in the kidney and diaphragm. In comparison, hypoxia raised the levels of angiopoietin-2 mRNA in the cerebellum and angiopoietin-3 mRNA in the lung, kidney, and diaphragm. HIF-1α mRNA was abundant in most organs of normoxic rats but was significantly induced in the kidney and diaphragm of hypoxic rats. We conclude that in vivo hypoxia exerts inhibitory effects on the activity of the angiopoietin-1/Tie-2 receptor pathway through reduction of angiopoietin-1 and upregulation of angiopoietin-2 and -3. Induction of angiopoietin-3 in the kidney and diaphragm of hypoxic rats could be mediated through the HIF-1 transcription factor.
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Hildbrand, Patrick, Vincenzo Cirulli, Robyn C. Prinsen, Kent A. Smith, Bruce E. Torbett, Daniel R. Salomon, and Laura Crisa. "The role of angiopoietins in the development of endothelial cells from cord blood CD34+ progenitors." Blood 104, no. 7 (October 1, 2004): 2010–19. http://dx.doi.org/10.1182/blood-2003-12-4219.

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Abstract Circulating endothelial progenitors contribute to neovascularization at sites of injury and tumorigenesis in postnatal life. Yet, the molecular mechanisms initiating the endothelial developmental program of these precursors remain elusive. Here we provide evidence that endothelial development from progenitors circulating in human cord blood requires angiopoietins, a set of growth factors also involved in vascular branching during embryogenesis. We show that cord blood cells with the potential for endothelial development reside in a CD34+CD11b+ subset capable of autonomously producing and binding angiopoietins. Functionally, endogenous angiopoietin-1 regulates initial endothelial cell commitment, whereas angiopoietin-2 enhances expansion of the endothelial cell progeny. These findings suggest a role for angiopoietins as regulators of endothelial development from circulating progenitors and imply a function of angiopoietins at distinct developmental steps in postnatal angiogenesis.
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Morisada, Tohru, Yoshiaki Kubota, Takashi Urano, Toshio Suda, and Yuichi Oike. "Angiopoietins and Angiopoietin-Like Proteins in Angiogenesis." Endothelium 13, no. 2 (January 2006): 71–79. http://dx.doi.org/10.1080/10623320600697989.

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Cordeiro, Ana Lúcia, António Figueiredo, Inês Tomada, Henrique de Almeida, and Delminda Neves. "Characterization of the Expression of Ang1, Ang2, and Tie2 in the Corpus Cavernosum of the Rat during Aging." Microscopy and Microanalysis 16, no. 6 (October 25, 2010): 699–709. http://dx.doi.org/10.1017/s1431927610094006.

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AbstractAging is the single most significant risk factor for erectile dysfunction (ED), leading to structural modification of cavernous tissue and altering expression of vascular growth factors. The angiopoietin/Tie2 system has been recently considered as a potential target for therapy of vascular disorders, including ED. Hence, the aim of this study was to analyze expression of angiopoietin1 (Ang1), angiopoietin2 (Ang2), and their receptor Tie2 in corpus cavernosum (CC) of rat during aging (6, 12, 18, and 24 months). The expression of Ang1, Ang2, and Tie2 was studied by immunohistochemistry and immunofluorescence, followed by semiquantification after Western blotting. Both Ang1 and Ang2 were localized mainly in perivascular smooth muscle and endothelial cells, while Tie2 was strictly detected at the vascular endothelium. A significant decrease in Ang2's expression was observed at 12 months when compared with 6-month-old rats, a tendency that reverses in older animals. No significant differences were demonstrated for Ang1 or Tie2, which is consistent with their constitutive expression in CC. The ratios Ang1/Tie2 and Ang2/Tie2 were also calculated and both decrease during aging, while no marked variation was observed for Ang1/Ang2. Our results suggest that the angiopoietin/Tie2 system participate in the vascular maintenance and remodeling of the CC during aging.
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Person, Anthony, Wendy Xiong, Christian Erickson, Kate Shields, Jun Li, Ming BI, Guoping Wu, and Vassili Kalabokis. "Angiopoietins and angiopoietin-like proteins bind to LILRA/B receptors and activate innate immune responses in human monocytes (INC1P.405)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 54.26. http://dx.doi.org/10.4049/jimmunol.194.supp.54.26.

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Abstract Angiopoietins and Angiopoietin-like (ANGPTL) proteins are secreted glycoproteins that play multiple roles in angiogenesis, lipid metabolism, hematopoietic stem cell expansion, and inflammation. Unlike Angiopoietins, which are known to signal through the tyrosine kinase Tie1 or Tie2 receptors, ANGPTL proteins have long been considered orphan ligands. Recently, ANGPTL1, 2, 5, and 7 were shown to bind to human leukocyte immunoglobulin like receptor B2 (LILRB2), resulting in enhancement of human haematopoietic stem cell proliferation and expansion. Leukocyte immunoglobulin-like receptors (LILRs) also named ILTs, LIRs and CD85s, are a family of immunomodulatory molecules that are expressed on professional APCs and regulate their functional properties to influence immune activation and inhibition. While the MHC class I complexes have been identified as the physiological ligands for many LILR members, the direct interaction between LILRs and ANGPTLs has suggested a new signaling mechanism for those two groups of molecules. We have tested Angiopoietins and ANGPTL proteins in binding studies with the LILRA and LILRB family members, and identified additional LILR family members as potential receptors of Angiopoietin-1 and several ANGPTL proteins. We find correlations between these newly described interactions of Angiopoietins and ANGPTL proteins with LILR family members and their abilities to activate innate immune responses in human monocytes.
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Blecharz, Kinga G., Dietmar Frey, Tobias Schenkel, Vincent Prinz, Gloria Bedini, Susanne M. Krug, Marcus Czabanka, et al. "Autocrine release of angiopoietin-2 mediates cerebrovascular disintegration in Moyamoya disease." Journal of Cerebral Blood Flow & Metabolism 37, no. 4 (July 21, 2016): 1527–39. http://dx.doi.org/10.1177/0271678x16658301.

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Moyamoya disease is a rare steno-occlusive cerebrovascular disorder often resulting in hemorrhagic and ischemic strokes. Although sharing the same ischemic stimulus with atherosclerotic cerebrovascular disease, Moyamoya disease is characterized by a highly instable cerebrovascular system which is prone to rupture due to pathological neovascularization. To understand the molecular mechanisms underlying this instability, angiopoietin-2 gene expression was analyzed in middle cerebral artery lesions obtained from Moyamoya disease and atherosclerotic cerebrovascular disease patients. Angiopoietin-2 was significantly up-regulated in Moyamoya vessels, while serum concentrations of soluble angiopoietins were not changed. For further evaluations, cerebral endothelial cells incubated with serum from these patients in vitro were applied. In contrast to atherosclerotic cerebrovascular disease serum, Moyamoya disease serum induced an angiopoietin-2 overexpression and secretion, accompanied by loss of endothelial integrity. These effects were absent or inverse in endothelial cells of non-brain origin suggesting brain endothelium specificity. The destabilizing effects on brain endothelial cells to Moyamoya disease serum were partially suppressed by the inhibition of angiopoietin-2. Our findings define brain endothelial cells as the potential source of vessel-destabilizing factors inducing the high plasticity state and disintegration in Moyamoya disease in an autocrine manner. We also provide new insights into Moyamoya disease pathophysiology that may be helpful for preventive treatment strategies in future.
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Dissertations / Theses on the topic "Angiopoietin"

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Tausch, Kathrin. "Expression von Angiopoietin-1 und Angiopoietin-2 im Endometrium und in Endometriosegewebe." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=971973113.

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Neuschl, Elvira. "Einfluss von Angiopoietin-1 und Angiopoietin-2 auf die Angiogenese im Ratten-Gliommodell." [S.l.] : [s.n.], 2006. http://deposit.ddb.de/cgi-bin/dokserv?idn=979987113.

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Drenkhahn, Merle. "Expression von Angiopoietin-1 und Angiopoietin-2 im ektopen Endometrium auf der Chorioallantoismembran." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=976803968.

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Gardizi, Masyar [Verfasser]. "Angiopoietin-1 und Angiopoietin-2 als Serummarker für das Maligne Melanom / Masyar Gardizi." Köln : Deutsche Zentralbibliothek für Medizin, 2013. http://d-nb.info/1046472232/34.

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Moss, Andrew James. "Engineering novel angiopoietin receptor ligands." Thesis, University of Leicester, 2011. http://hdl.handle.net/2381/27654.

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Angiopoietin-1 is a multimeric glycoprotein which signals through the vascular endothelial Tie2 receptor to protect against inflammation and leakage, an effect antagonised by the selectively upregulated antagonist angiopoietin-2. In many pathologies this destabilisation by angiopoietin-2 is excessive or inappropriate, and here angiopoietin-1 has a promising role in therapeutic application. However angiopoietin-1 is difficult to purify and administer, its large multimeric structure rendering it prone to aggregation and insolubility. In this work the abilities of two small heptameric Tie2 binding peptides, VTSRGNV and NLLMAAS, multimerised using the established oligomeric scaffold cartilage oligomeric matrix protein (COMP), to bind and activate Tie2 were investigated. cDNAs for synthetic ligands were created by PCR, and protein synthesis was carried out in mammalian and bacterial expression systems. Ligands were expressed as stable, soluble pentamers and tetramers which showed similar abilities to bind Tie2 in vitro. Both ligands activated Tie2 similarly in Eahy926 and HUVEC endothelial cells. Both ligands were also able to activate two important downstream signalling mediators of Tie2 in HUVECs, namely Akt and ERK, in a dose-dependent fashion. However, the kinetics of ERK appeared different between the two ligands, implying possible differences in signalling of the two ligands through Tie2. This work is proof of principle and is among the first work to demonstrate that Tie2 binding elements other than the ang1 FRD can be used to activate Tie2. Additionally, kinetics work suggests that the two ligands, presumed to bind to different areas on Tie2, might induce slightly different patterns of receptor activation.
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Alves, Brunna Eulálio 1979. "Avaliação de moduladores do aumento da permeabilidade microvascular e sua correlação com a evolução clínica na sepse em pacientes onco-hematológicos neutropênicos febris." [s.n.], 2011. http://repositorio.unicamp.br/jspui/handle/REPOSIP/309168.

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Orientador: Erich Vinicius de Paula
Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
Made available in DSpace on 2018-08-18T13:46:04Z (GMT). No. of bitstreams: 1 Alves_BrunnaEulalio_D.pdf: 4762678 bytes, checksum: 34eea414d90830a52ed9c9b044538888 (MD5) Previous issue date: 2011
Resumo: Pacientes portadores de neoplasia hematológica e neutropenia febril representam um grupo de risco elevado de sepse e choque séptico. Nas últimas décadas, estratégias terapêuticas alvo-específicas para a sepse não modificaram de forma significativa a sobrevida dos pacientes e o tratamento permanece baseado em antibioticoterapia e cuidados de suporte, com altas taxas de mortalidade. A quebra da barreira endotelial é um evento fundamental na fisiopatologia do choque séptico e a compreensão dos mecanismos envolvidos neste evento tem o potencial de auxiliar na identificação de novos biomarcadores de gravidade e de novos alvos terapêuticos para estes pacientes. Estudos recentes demonstraram a participação do fator de crescimento do endotélio vascular (VEGF-A), do seu receptor solúvel (sFlt-1) e das angiopoietinas 1 e 2, proteínas envolvidas na angiogênese e na regulação da integridade da barreira endotelial na fisiopatogenia do choque séptico em pacientes não oncológicos internados em unidade de terapia intensiva. Neste trabalho, avaliamos prospectivamente a cinética do VEGF-A, do sFlt-1 e das angiopoietinas 1 e 2 durante as 48 horas inicias da neutropenia febril em 41 pacientes portadores de neoplasia hematológica submetidos a quimioterapia intensiva ou a regime de condicionamento para transplante de células progenitoras hematopoiéticas, através da dosagem dos mesmos por ensaio imuno-enzimático. Exploramos também a associação dos níveis séricos destes biomarcadores com a gravidade da sepse através da correlação com o MASCC, um índice desenvolvido para identificar pacientes com neutropenia febril de baixo risco, e com o SOFA, um escore de avaliação de disfunção orgânica em pacientes com sepse, ambos amplamente aceitos. A evolução para choque séptico foi associada a níveis significativamente maiores de VEGF-A, sFlt-1 e angiopoietina-2 48 horas após o início da neutropenia febril quando comparado aos valores em pacientes com sepse não complicada e a estimativa da acurácia diagnóstica sugere a capacidade de discriminar os pacientes que evoluíram com choque séptico. Estes biomarcadores também apresentaram correlação com os escores gravidade, sugerindo a relevância biológica da associação. Em conclusão, nossos achados sugerem que a avaliação destes biomarcadores em pacientes com neutropenia febril deve ser avaliada em estudos com maior número de pacientes, quanto ao seu potencial de incorporação na prática clínica. Além disso, os resultados reforçam o potencial terapêutico da intervenção nestas vias para o tratamento da sepse
Abstract: Patients with hematologic malignancy and neutropenia represent a group at high risk of sepsis and septic shock. In recent decades, target-specific therapeutic strategies for sepsis did not change significantly the survival of patients and treatment is still based on antibiotic therapy and supportive care, with high mortality rates. The breakdown of the endothelial barrier is a key event in the pathophysiology of septic shock and understanding of the mechanisms involved in this event has the potential to assist in the identification of new biomarkers and severity of new therapeutic targets for these patients. Recent studies have demonstrated the involvement of endothelial growth factor (VEGF-A), its soluble receptor (sFlt-1) and angiopoietins 1 and 2, proteins involved in angiogenesis and in regulation of endothelial barrier integrity in the pathogenesis of shock septic patients without cancer admitted to the intensive care unit. In this study, we prospectively evaluated the kinetics of VEGF-A, sFlt-1 and angiopoietins 1 and 2 during the initial 48 hours of febrile neutropenia in 41 patients with hematological malignancy undergoing intensive chemotherapy or conditioning regimen for stem cell transplantation hematopoietic cells by the same dosage by enzyme immunoassay. We also explored the association of serum levels of these biomarkers with the severity of sepsis through correlation with the MASCC, an index developed to identify patients with febrile neutropenia at low risk, and the SOFA score for assessment of organ dysfunction in patients with sepsis, both widely accepted. Progression to septic shock was associated with significantly higher levels of VEGF-A, sFlt-1 and angiopoietin-2 48 hours after the onset of febrile neutropenia when compared to values in patients with uncomplicated sepsis and the estimation of diagnostic accuracy suggests the ability to discriminate among patients who developed septic shock. These biomarkers also correlated with the severity scores, suggesting the biological relevance of the association
Doutorado
Clinica Medica
Doutor em Clínica Médica
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Ward, Emma Gwenllian. "Characterisation of the human angiopoietin genes." Thesis, University of Leeds, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.413277.

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Pietilä, R. (Riikka). "Angiopoietin 1 and 2-regulated Tie2 receptor translocation in endothelial cells and investigation of Angiopoietin-2 splice variant 443." Doctoral thesis, Oulun yliopisto, 2015. http://urn.fi/urn:isbn:9789526207971.

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Abstract Angiopoietins 1 and 2 (Ang1 and Ang2) are the ligands of the Angiopoietin/Tie signalling system, which is a binary pathway offering mechanisms for healthy vessels to reach and maintain their quiescence but also to rapidly respond to activating stimuli leading to a remodelling of endothelium. The latter is linked to disease settings such as inflammation and cancer where endothelial cell (EC) integrity is compromised and is often related to an increase in Ang2 expression. This study focused on the mechanisms enabling Ang1 to mediate both EC stability and migration and molecular and cellular determinants for ligand-specific functions of Ang2 and its isoform Ang2443. The findings revealed that Ang1 induces differential signalling depending on whether it anchors and activates Tie2 in cell-cell junctions in quiescent ECs, or in cell-matrix contacts in mobile ECs, thus leading to cellular phenotypes characteristic of resting and mobile ECs, respectively. In the second part of the thesis Ang2-Tie2 specific cell-extracellular matrix (ECM) contact sites were studied. Formation of Ang2/Tie2 EC-ECM contact sites was dependent on the collagen I and IV matrices, low Ang2 oligomerization state, α2β1-integrins, and intact microtubules. In the third part of the thesis the comparison of Ang2 mRNA splice variant Ang2443 with full length Ang2 (Ang2FL) revealed both redundant and ligand form–specific effects, expression of Ang2443443 increased the amount of monomeric ligand forms due to proteolytic processing and promoted transendothelial migration of cancer cells in vitro. On the other hand, both Ang2443 and Ang2FL were stored in endothelial Weibel-Palade bodies (WPBs), similarly induced Ang2-specific Tie2 cellular redistribution, and were mostly comparable in developmental angio- and lymphangiogenesis
Tiivistelmä Angiopoietiinit 1 ja 2 (Ang1 ja Ang2) ovat Ang/Tie signalointireitin kasvutekijöitä. Ang1 kasvutekijää tarvitaan sydämen ja verisuoniston sikiöaikaiseen kehittymiseen, se vähentää Tie2 reseptorin kautta verisuonten läpäisevyyttä, mutta edistää myös yksittäisten endoteelisolujen liikkumista. Saman Tie2 signalointireitin toisen kasvutekijän Ang2:n ilmeneminen johtaa verisuonten läpäisevyyden kasvuun tulehduksessa, uusien verisuonten muodostumiseen syöpäkasvaimissa ja syöpäsolujen leviämiseen elimistössä. Väitöskirjatutkimuksessa selvitettiin niitä solutason mekanismeja, joilla Ang1 kykenee välittämään sekä endoteelisolujen tiiviyttä että liikkumista. Lisäksi tutkittiin niitä molekyyli- ja solutason mekanismeja, joilla Ang2 ja sen isomuoto Ang2443 välittävät kasvutekijäspesifisiä vaikutuksiaan. Väitöskirjassa osoitettiin että Tie2 reseptori paikantuu verisuonten endoteelisoluissa Ang1 sitoutumisen seurauksena joko solu-soluliitoksiin, tai yksittäisissä endoteelisoluissa solu-soluväliaine rajapinnalle. Tie2:n siirtyminen solu-soluliitoksiin aktivoi soluissa signalointireittejä, jotka ovat tyypillisiä normaaleille tiiviille verisuonille ja solu-soluväliaineliitoksissa liikkuville endoteelisoluille tyypillisiä piirteitä. Väitöskirjatyön toisessa osassa tutkittiin Ang2:lle ominaisia vaikutuksia ja Ang2-Tie2 kompleksin paikantumista erityisiin solu-soluväliaineliitoksiin. Tämä oli riippuvaista Ang2:n oligomerisaatiosta, kollageenisoluväliaineesta, α2β1-integriinistä ja normaalista mikrotubulusverkostosta. Väitöskirjatyön kolmannessa osassa osoitettiin että Ang2443 isomuodolla on sekä yhteisiä että isomuotospesifisiä piirteitä verrattuna kokopitkään Ang2:een (Ang2FL). Liukoinen Ang2443, mutta ei Ang2FL, esiintyi yleisesti monomeerisenä ligandimuotona proteiinin multimerisaatio-osan pilkkomisen seurauksena. Ang2443 lisäsi myös syöpäsolujen liikkumista endoteelisolujen läpi. Toisaalta sekä Ang2443 että Ang2FL varastoitiin endoteelisoluissa Weibel-Palade varastokappaleisin, ne välittivät samanlaista Tie2 reseptorin paikantumista endoteelisoluissa ja toimivat pääsääntöisesti samanlaisina kasvutekijöinä veri- ja imusuonten kehityksen aikana hiiressä
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Li, Shihhui. "Angiopoietin-like protein 4 in bovine physiology." Thesis, Kansas State University, 2011. http://hdl.handle.net/2097/13107.

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Master of Science
Department of Animal Sciences and Industry
Barry Bradford
Angiopoietin-like protein 4 (ANGPTL4) is a 55-kDa secreted glycoprotein which is an important factor for regulation of energy and lipid metabolism. Plasma ANGPTL4 has the ability to inhibit lipoprotein lipase (LPL) function by preventing it from catalyzing hydrolysis of lipoprotein triglyceride, which contributes to ANGPTL4’s ability to decrease fat storage. Furthermore, research in mice suggests that gut microbes suppress gastrointestinal ANGPTL4 production, and that decreased plasma ANGPTL4 concentrations promote fat storage. In our previous work, we found that bovine ruminal epithelial cells expressed ANGPTL4 to a greater extent than liver hepatocytes, which are usually considered the predominant source of circulating ANGPTL4. Therefore, 3 studies were conducted to evaluate the hypothesis that ruminal expression and plasma concentrations of ANGPTL4 could be influenced by alterations in ruminal fermentation. The first and second studies utilized dietary treatments intended to alter ruminal fermentability. Diets with relatively low or high forage content were fed to 12 non-lactating dairy cows (study 1) and 8 beef cattle (study 2) prior to collection of ruminal fluid and ruminal tissue samples. The results suggested that increasing the dietary concentrate decreased ruminal expression of ANGPTL4 but did not significantly alter plasma ANGPTL4 concentrations. The third study was designed to assess whether effects of diet fermentability on ruminal ANGPTL4 synthesis are mediated by changes in volatile fatty acid concentrations. In this study, 6 lactating cows were infused with acetate, propionate, or butyrate in a Latin square design. Results showed that ANGPTL4 expression was not significantly altered by volatile fatty acid infusions, but that expression was correlated with ruminal pH and total volatile fatty acid concentration. The mechanism by which ANGPTL4 regulates intracellular lipid metabolism also remains unclear. Although ANGPTL4 is known to associate with β1 and β5 integrins, it is unknown if these extracellular matrix proteins mediate the effects of ANGPTL4 in adipose tissue or muscle. The objective of the last experiment was to detect the ANGPTL4 receptor or mediator in muscle satellite cells and adipose tissue. We successfully expressed recombinant bovine ANGPTL4 with a cell free glycoprotein synthesis system. However, we did not detect the ANGPTL4–receptor complex following exposure to bovine adipose tissue explants or cultured bovine muscle satellite cells. Overall, these research projects determined that the ruminal ANGPTL4 production is influenced by fermentation, but it remains unclear whether fermentation products or direct host/microbe interactions are responsible. Finally, it will be important to identify the ANGPTL4 receptor or mediator to better understand the downstream regulatory mechanisms involved in mediating the metabolic effects of ANGPTL4.
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Long, David Andrew. "Angiopoietin growth factors in models of kidney disease." Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.401031.

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Books on the topic "Angiopoietin"

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Nourhaghighi, Nima. Altered expression of angiopoietins after cerebral trauma. Ottawa: National Library of Canada, 2001.

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Ramsden, James Daniel. Angiopoietins in goitre: Candidates for anti-angiogenic gene therapy? Birmingham: University of Birmingham, 2002.

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Haninec, Alexandra Lynn. The effects of liver-specific angiopoietin-1 overexpression on the portal microcirculation and lymphatic network. 2004.

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Kugathasan, Lakshmi. Role of the angiopoietin/Tie2 system in a rodent model of hypoxia-induced pulmonary arterial hypertension. 2004.

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Book chapters on the topic "Angiopoietin"

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Kiss, Elina A., and Pipsa Saharinen. "Anti-angiogenic Targets: Angiopoietin and Angiopoietin Receptors." In Tumor Angiogenesis, 227–50. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-33673-2_4.

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Kiss, Elina A., and Pipsa Saharinen. "Anti-angiogenic Targets: Angiopoietin and Angiopoietin-Receptors." In Tumor Angiogenesis, 1–24. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-31215-6_4-1.

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Clément, Lionel C. "Angiopoietin-Like 4 (Angptl4) in MCNS." In Molecular Mechanisms in the Pathogenesis of Idiopathic Nephrotic Syndrome, 25–43. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55270-3_3.

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Kersten, Sander. "Angiopoietin-Like Proteins and Lipid Metabolism." In Cellular Lipid Metabolism, 237–49. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-00300-4_9.

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Thurston, Gavin, John S. Rudge, Ella Ioffe, Nicholas Papadopoulos, Christopher Daly, Srilatha Vuthoori, Thomas Daly, Stanley J. Wiegand, and George D. Yancopoulos. "The anti-inflammatory actions of angiopoietin-1." In Mechanisms of Angiogenesis, 233–45. Basel: Birkhäuser Basel, 2005. http://dx.doi.org/10.1007/3-7643-7311-3_16.

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Stöltzing, O., S. A. Ahmad, W. Liu, M. R. McCarty, E. Fan, C. D. Bucana, and L. M. Ellis. "Inhibition von Tumor-Angiogenese und Gefäßpermeabilität durch Angiopoietin-1." In Zurück in die Zukunft, 486–87. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-55611-1_305.

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Stöltzing, Oliver, S. A. Ahmad, W. Liu, M. F. McCarty, F. Fan, C. D. Bucana, and L. M. Ellis. "Inhibition von Tumor-Angiogenese und Gefäßpermeabilität durch Angiopoietin-1." In Deutsche Gesellschaft für Chirurgie, 95–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-19024-7_27.

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Yip, Fanny L. T., Cherie Y. K. Wong, and Timothy Y. Y. Lai. "Agents Targeting Angiopoietin/Tie Pathway in Diabetic Macular Edema." In Diabetic Macular Edema, 63–68. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-7307-9_7.

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Naumnik, W., B. Naumnik, K. Niewiarowska, M. Ossolinska, and E. Chyczewska. "Angiogenic Axis Angiopoietin-1 and Angiopoietin-2/Tie-2 in Non-Small Cell Lung Cancer: A Bronchoalveolar Lavage and Serum Study." In Neurobiology of Respiration, 341–48. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6627-3_46.

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Reiss, Yvonne, Alexander Scholz, and Karl H. Plate. "The Angiopoietin—Tie System: Common Signaling Pathways for Angiogenesis, Cancer, and Inflammation." In Endothelial Signaling in Development and Disease, 313–28. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2907-8_13.

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Conference papers on the topic "Angiopoietin"

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Bhatraju, P., K. Hisert, M. L. Aitken, C. Goss, W. C. Liles, and W. A. Altemeier. "Higher Plasma Concentrations of Angiopoietin-1 and Angiopoietin-1/Angiopoietin-2 in Adults with Cystic Fibrosis Compared to Healthy Age Matched Controls." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2575.

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Lee, Yang Deok, Yongseon Cho, Dong Jib Na, Min Soo Han, Sung Kyu Lee, Haing Woon Baik, and Jung Joo Hwang. "The Role Of VEGF, Angiopoietin-1 And Angiopoietin-2 In Scrub Typhus Complicated With Interstitial Pneumonia." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a1804.

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Das, Anusuya, Harry Asada, Doug Lauffenburger, and Roger Kamm. "A Stochastic Field/Agent Model of Angiogenesis." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-204115.

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Abstract:
Angiogenesis is the formation of blood vessels from an existing vessel or a monolayer of endothelial cells. It is crucial during the processes of tissue and organ maintenance, wound healing, and development and also plays a crucial role in tumor growth. An understanding of this process is also critical from a tissue engineering perspective. Several biochemical factors such as VEGF, Angiopoietin I (Ang I), Angiopoietin II (Ang II), PLGF, PDGF, TNF α, TGF β, α-FGF, β-FGF, ENA/VASP [1] and biomechanical factors such as extracellular matrix (ECM) stiffness, interstitial flow, shear stress affect the formation of capillaries. While some of them are proangiogenic, others are anti-angiogenic. A balance in these factors is decisive to the characteristics of the capillaries formed.
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Wada, Y., M. Sudo, T. Kuroda, M. Nakano, and I. Narita. "OP0048 The utility of serum angiopoietin-1 and angiopoietin-2 in patients with anti-neutrophil cytoplasmic autoantibody-associated vasculitis." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.1310.

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Bready, James V., Kyung Lee, Rick Jacobsen, Kevin Graham, Juan Estrada, Stephen A. Kaufman, Dongyin Yu, Angela Coxon, and Jon Oliner. "Abstract 1022: Development and preclinical testing of AMG 780, a fully human antibody targeting angiopoietin 1 (Ang1) and angiopoietin 2 (Ang2)." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1022.

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Hall, Kelly, Michael Flister, Lisa Volk, Shannon Curry, Andrew Wilber, and Sophia Ran. "Abstract 2354: Angiopoietin-2 role in breast cancer metastasis." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2354.

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Mofarrahi, M., G. Danialou, and SN Hussain. "Regulation of Skeletal Muscle Regeneration by Angiopoietin-1 (Ang-1)." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a6134.

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Plate, Karl H., Alexander Scholz, Patrick Harter, Michel Mittelbronn, Paul van Slyke, Dan Dumont, and Yvonne Reiss. "Abstract B70: Targeting the Tie2/angiopoietin signaling pathway in glioblastoma." In Abstracts: AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment; February 26 — March 1, 2014; San Diego, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.chtme14-b70.

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Peplinski, B., B. A. Houston, D. A. Bluemke, S. M. Kawut, T. M. Kolb, R. A. Kronmal, J. A. C. Lima, et al. "Angiopoietin Associations Across the Cardiovascular Disease Spectrum: The Mesa Angiogenesis Study." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a4239.

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Faller, Simone, Sashko G. Spassov, Kornelia Zimmermann, Karl M. Strosing, and Alexander Hoetzel. "Hydrogen Sulphide Mediates Protection In Hyperoxic Lung Injury Via Angiopoietin 2." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1333.

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Reports on the topic "Angiopoietin"

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Carter, Bradford W. HER2 Regulation of Angiopoietin-2: A Mechanistic Factor in Metastasis. Fort Belvoir, VA: Defense Technical Information Center, October 2001. http://dx.doi.org/10.21236/ada398722.

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Carter, Bradford W. HER2 Regulation of Angiopoietin-2: A Mechanistic Factor in Metastasis. Fort Belvoir, VA: Defense Technical Information Center, October 2004. http://dx.doi.org/10.21236/ada431916.

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Carter, Bradford W. HER2 Regulation of Angiopoietin-2: A Mechanistic Factor in Metastasis. Fort Belvoir, VA: Defense Technical Information Center, October 2002. http://dx.doi.org/10.21236/ada411717.

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Carter, W. B. HER2 Regulation of Angiopoietin-2: A Mechanistic Factor in Metastasis. Fort Belvoir, VA: Defense Technical Information Center, October 2003. http://dx.doi.org/10.21236/ada425178.

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Carter, W. B., and Douglas Turner. HER2 Regulation of Angiopoietin-2: A Mechanistic Factor in Metastasis. Fort Belvoir, VA: Defense Technical Information Center, October 2006. http://dx.doi.org/10.21236/ada469358.

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Aleksandrov, V. A., A. V. Aleksandrov, L. N. Shilova, G. Y. Osmanova, and N. V. Aleksandrova. EFFECT OF ANGIOPOIETIN-LIKE PROTEIN TYPE 4 ON OSTEOPOROTIC DISORDERS IN RHEUMATOID ARTHRITIS PATIENTS WITH METABOLIC SYNDROME. DOI CODE, 2021. http://dx.doi.org/10.18411/wco-iof-esceo-2021-460.

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Aleksandrov, V. A., A. V. Aleksandrov, L. N. Shilova, G. Y. Osmanova, N. V. Aleksandrova, and I. A. Zborovskaya. ROLE OF ANGIOPOIETIN-LIKE PROTEINS TYPES 3 AND 4 IN PREDICTING AXIAL FRACTURE RISK IN PATIENTS WITH RHEUMATOID ARTHRITIS. DOI CODE, 2021. http://dx.doi.org/10.18411/wco-iof-esceo-2021-462.

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Witte, Marlys H. Progression of Inflammatory Bowel Disease to Cancer: Is the Patient Better Off without Lymphatic Vessels or Nodes (or Angiopoietin 2)? Fort Belvoir, VA: Defense Technical Information Center, December 2013. http://dx.doi.org/10.21236/ada606012.

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Witte, Marlys H. Progression of Inflammatory Bowel Disease to Cancer: Is the Patient Better Off without Lymphatic Vessels or Nodes (or Angiopoietin 2)? Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada577348.

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Aleksandrov, V. A., A. V. Aleksandrov, L. N. Shilova, and N. V. Aleksandrova. Diagnostic role of angiopoietin-like protein type 3 in assessing the activity of resorptive processes in bone tissue in women with rheumatoid arthritis. Ljournal, 2020. http://dx.doi.org/10.18411/wco-iof-esceo-2020-309.

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