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Artykuły w czasopismach na temat "Coronary heart disease – Genetic aspects"
Cambien, François. "1.C.6 New genetic aspects of coronary heart disease". Atherosclerosis 134, nr 1-2 (październik 1997): 6. http://dx.doi.org/10.1016/s0021-9150(97)88138-5.
Pełny tekst źródłaKadykova, O. I. "GENETIC ASPECTS OF DEVELOPMENT AND PROGRESSION OF CONGESTIVE HEART FAILURE IN PATIENTS WITH ISCHEMIC HEART DISEASE AND OBESITY∗". Problems of Endocrine Pathology 57, nr 3 (23.08.2016): 17–21. http://dx.doi.org/10.21856/j-pep.2016.3.02.
Pełny tekst źródłaGolukhova, Elena Z., Aygerim Z. Zholbaeva, Mari G. Arakelyan, Naida I. Bulaeva i Michail M. Minashkin. "Genetic aspects of lone atrial fibrillation in patients without structural heart disease". Annals of the Russian academy of medical sciences 74, nr 4 (5.10.2019): 245–52. http://dx.doi.org/10.15690/vramn1120.
Pełny tekst źródłaGolukhova, E. Z., O. I. Gromova, R. A. Shomahov, N. I. Bulaeva i L. A. Bockeria. "Monogenec Arrhythmic Syndromes: From Molecular and Genetic Aspects to Bedside". Acta Naturae 8, nr 2 (15.06.2016): 62–74. http://dx.doi.org/10.32607/20758251-2016-8-2-62-74.
Pełny tekst źródłaIslam, AKM Monwarul, AKM Mohibullah i Timir Paul. "Cardiovascular Disease in Bangladesh: A Review". Bangladesh Heart Journal 31, nr 2 (28.04.2017): 80–99. http://dx.doi.org/10.3329/bhj.v31i2.32379.
Pełny tekst źródłaCavarretta, Elena, i Giacomo Frati. "MicroRNAs in Coronary Heart Disease: Ready to Enter the Clinical Arena?" BioMed Research International 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/2150763.
Pełny tekst źródłaBerezikova, Ye N., M. G. Pustovetova, S. N. Shilov, A. V. Yefremov, A. T. Teplyakov, I. D. Safronov i Ye N. Samsonova. "Effects of caspase 8 gene polymorphism on the risks for development/course of chronic heart failure". Patologiya krovoobrashcheniya i kardiokhirurgiya 17, nr 2 (10.10.2015): 45. http://dx.doi.org/10.21688/1681-3472-2013-4-45-49.
Pełny tekst źródłaGroznova, O. S., I. M. Miklashevich, V. Yu Voinova, M. A. Shkolnikova, O. N. Tkacheva, E. N. Dudinskaya i I. A. Kovalev. "Biomarkers of early cardiovascular aging". Rossiyskiy Vestnik Perinatologii i Pediatrii (Russian Bulletin of Perinatology and Pediatrics) 64, nr 4 (15.09.2019): 11–18. http://dx.doi.org/10.21508/1027-4065-2019-64-4-11-18.
Pełny tekst źródłaKhaw, Kay-Tee. "Epidemiological aspects of ageing". Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 352, nr 1363 (29.12.1997): 1829–35. http://dx.doi.org/10.1098/rstb.1997.0168.
Pełny tekst źródłaBarton, Matthias, i Masashi Yanagisawa. "Endothelin: 30 Years From Discovery to Therapy". Hypertension 74, nr 6 (grudzień 2019): 1232–65. http://dx.doi.org/10.1161/hypertensionaha.119.12105.
Pełny tekst źródłaRozprawy doktorskie na temat "Coronary heart disease – Genetic aspects"
McCaskie, Pamela Ann. "Multiple-imputation approaches to haplotypic analysis of population-based data with applications to cardiovascular disease". University of Western Australia. School of Population Health, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0160.
Pełny tekst źródłaFournier, Caroline. "Genetic investigation of vascular diseases in the French-Canadian population". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0030/MQ64355.pdf.
Pełny tekst źródłaMakubalo, Zola. "Mutation screening of candidate genes and the development of polymorphic markers residing on chromosome 19q13.3, the progressive familial heart block I gene search area". Thesis, Stellenbosch : Stellenbosch University, 2000. http://hdl.handle.net/10019.1/51838.
Pełny tekst źródłaENGLISH ABSTRACT: Progressive familial heart block type I (PFHBI) is a cardiac ventricular conduction disorder of unknown cause associated with risk of sudden death, which has been described in several South African families. Clinically, PFHBI is characterised by right bundle branch block on ECG, which may progress to complete heart block, necessitating pacemaker implantation. The disease shows an autosomal dominant pattern of inheritance with evidence of genetic anticipation. Using genetic linkage analysis, the PFHBI-causative gene was mapped to a 10 eentimorgan (cM) gene-rich area of chromosome (C) 19q13.3, which has, subsequently, been reduced to 7cM by fine mapping with polymorphic dinucleotide (CA)n short tandem repeat (STR) markers. Several attractive candidate genes, including muscle glycogen synthase (GSY 1) and histidine-rich calcium binding protein (HRC), lie within this region. The aim of the present study was two-fold: 1) to identify and characterise tetranucleotide (AAAT)n STRs within the PFHBI critical region that could be developed as polymorphic markers for use in genetic fine mapping and 2) to screen selected regions of GSY 1and HRC, positional candidate genes, for the presence ofPFHBI-causing mutation(s). Cosmids harbouring CI9q13.3 insert DNA were screened for the presence of (AAAT)n STRs by dot blot and Southern blot hybridisation using a radiolabelled (AAAT)lO oligonucleotide probe. To characterise the harboured (AAAT)n STRs, the positively hybridising fragments identified by Southern blot were sub-cloned, sequenced and primers designed from the unique repeat-flanking sequences. These primers were used to genotype the (AAAT)n repeat locus to assess its polymorphic nature in a panel of unrelated individuals. Alternatively, vectorette PCR, a rapid method of identifying repeat sequences and obtaining the flanking sequences in large inserts, was employed to develop polymorphic markers from the positively hybridising clones. Selected exons of GSY1 and HRC were screened for the presence of potentially disease-causing mutations by PCR-SSCP analysis and direct sequencing, respectively, in PFHBI-affected and unaffected family members. Of the available cosmid clones that gave strong signals on dot blot and Southern blot hybridisation, three, 29395, 24493 and 20381, were located within the critical PFHBI area and were used for marker development. An interrupted (AAAT)n repeat motif (n less than 5) was identified in cosmid 29395, however, the repeat locus was not polymorphic in the tested population. No (AAAT)n motif, single or repeated was observed in the partial sequence of the sub-cloned fragment of cosmid 24493. Using vectorette peR, no repeated (AAAT)n motif was identified on sequencing the generated products in either cosmid 24493 or 2038l. However, diffuse single AAAT motifs were detected in both cosmids. Exons 4, 5, 11, 12 and 16 of GSY 1, containing domains that are conserved across species, and the conserved eterminus- encoding exons 2-6 of HRC were selected for screening for potential PFHBI-causing mutation(s). However, no sequence variations were detected. The interrupted (AAAT)n repeat identified in cosmid 29395 was not polymorphic, which confirmed reports that complex repeats, especially those containing AAAT motifs of less than 6 repeats, are not polymorphic. One possible explanation for the absence of a repeated AAAT motif in cosmids 24493 and 20381, which both gave positive hybridisation signals, is that the low annealing temperature of the AfT -rich repeat-anchored primers used in vectorette peR may have resulted in transient annealing to the diffuse single AAAT motifs detected on sequencing. The screened regions of candidate genes GSYI and HRC were excluded from carrying the disease-causing mutation(s). The availability of new sequence data generated by the Human Genome Project will influence future strategies to identify the PFHBI gene. Electronic searches will allow identification of STR sequences for development of polymorphic markers and gene annotation will allow selection of new candidate genes for mutation screening.
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Kuek, Conchita Maria. "Hereditary haemochromatosis and the C282Y genotype : implications in diagnosis and disease". University of Western Australia. School of Surgery and Pathology, 2003. http://theses.library.uwa.edu.au/adt-WU2004.0024.
Pełny tekst źródłaPocathikorn, Anothai. "Low density lipoprotein receptor-related protein (LRP) and its mRNA : influence of genetic polymorphisms, a fat load and statin therapy". University of Western Australia. School of Surgery and Pathology, 2006. http://theses.library.uwa.edu.au/adt-WU2006.0117.
Pełny tekst źródłaZdravkovic, Slobodan. "Coronary heart disease in Swedish twins : quantitative genetic studies /". Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-771-5/.
Pełny tekst źródłaMeng, Weihua. "Investigation of the genetic basis of coronary heart disease". Thesis, Queen's University Belfast, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.501377.
Pełny tekst źródłaDunn, Jeremy. "Genetic influences on the premature development of coronary heart disease". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/mq24837.pdf.
Pełny tekst źródłaNet, J. B. van der. "Towards genetic prediction of coronary heart disease in familial hypercholesterolemia". [S.l.] : Rotterdam : [The Author] ; Erasmus University [Host], 2009. http://hdl.handle.net/1765/14566.
Pełny tekst źródłaSarwar, Nadeem. "Emerging molecular and genetic risk factors for coronary heart disease". Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611549.
Pełny tekst źródłaKsiążki na temat "Coronary heart disease – Genetic aspects"
The Apoe gene diet: A breakthrough in lowering cholesterol, weight, and the risk of cardiovascular and Alzheimer's disease through knowledge of your body's genes. Santa Rosa, CA: Elite Books, 2007.
Znajdź pełny tekst źródłaMcDonald, Pamela. Apo e gene diet. Livermore, CA: WingSpan Press, 2006.
Znajdź pełny tekst źródłaGoldbourt, Uri, Ulf de Faire i Kåre Berg, red. Genetic factors in coronary heart disease. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1130-0.
Pełny tekst źródłaMothers, babies and disease in later life. London: BMJ Pub. Group, 1994.
Znajdź pełny tekst źródłaBerg, Kare, Victor Bulyzhenkov, Yves Christen i Pierre Corvol, red. Genetic Approaches to Coronary Heart Disease and Hypertension. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76891-0.
Pełny tekst źródłaS, Leon Arthur, red. Coronary heart disease: A behavorial perspective. Champaign, Ill: Research Press, 1992.
Znajdź pełny tekst źródłaBudnick, Herbert N. Heart to heart: A guide to the psychological aspects of heart disease. Santa Fe, NM: Health Press, 1991.
Znajdź pełny tekst źródłaThompson, David R. Counselling the coronary patient and partner. Harrow: Scutari Press, 1990.
Znajdź pełny tekst źródłaKris-Etherton, P. M. Trans fatty acids and coronary heart disease risk. Washington, D.C: ILSI Press, 1995.
Znajdź pełny tekst źródłaMogadam, Michael. Choosing foods for a healthy heart. Yonkers, N.Y: Consumer Reports Books, 1993.
Znajdź pełny tekst źródłaCzęści książek na temat "Coronary heart disease – Genetic aspects"
Erdmann, Jeanette, i Maria Loreto Muñoz Venegas. "The Genetics of Coronary Heart Disease". W Genetic Causes of Cardiac Disease, 141–68. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-27371-2_4.
Pełny tekst źródłaLemmer, Björn, i Klaus Witte. "Chronopharmacological aspects of coronary heart disease". W Developments in Cardiovascular Medicine, 295–308. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-009-1577-0_19.
Pełny tekst źródłaDhawan, Jatinder. "Coronary Heart Disease and Related Diseases". W Genetic Disorders of the Indian Subcontinent, 447–66. Dordrecht: Springer Netherlands, 2004. http://dx.doi.org/10.1007/978-1-4020-2231-9_22.
Pełny tekst źródłaGoldbourt, Uri. "Genetic Variation and Nutrition". W Genetic factors in coronary heart disease, 397–408. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1130-0_28.
Pełny tekst źródłaSchonfeld, Gustav, i Elaine S. Krul. "Genetic Defects in Lipoprotein Metabolism". W Genetic factors in coronary heart disease, 239–66. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1130-0_16.
Pełny tekst źródłaArcavi, Lidia. "Genetic variation and cardiac pharmacotherapy". W Genetic factors in coronary heart disease, 409–24. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1130-0_29.
Pełny tekst źródłaRao, D. C., i George P. Vogler. "Assessing Genetic and Cultural Heritabilities". W Genetic factors in coronary heart disease, 71–81. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1130-0_5.
Pełny tekst źródłaMilewicz, Dianna M. "Genetic Aspects of Congenital Heart Disease". W Cardiovascular Medicine, 2599–605. London: Springer London, 2007. http://dx.doi.org/10.1007/978-1-84628-715-2_127.
Pełny tekst źródłaShiomi, Masashi, i Yoshio Watanabe. "Rabbit Models in Genetic Research in Atherosclerosis". W Genetic factors in coronary heart disease, 115–24. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1130-0_8.
Pełny tekst źródłaAustin, Melissa A. "Low Density Lipoprotein Subclass Phenotypes". W Genetic factors in coronary heart disease, 105–13. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1130-0_7.
Pełny tekst źródłaStreszczenia konferencji na temat "Coronary heart disease – Genetic aspects"
Murthy, H. S. Niranjana, i M. Meenakshi. "Dimensionality reduction using neuro-genetic approach for early prediction of coronary heart disease". W 2014 International Conference on Circuits, Communication, Control and Computing (I4C). IEEE, 2014. http://dx.doi.org/10.1109/cimca.2014.7057817.
Pełny tekst źródłaUzbekova, Nelly, Sergey Kityan i Nodira Badalbaeva. "USE OF PLETHYSMOGRAPHY IN THE ASSESSMENT OF THE ARTERIAL WALL IN PERSONS WITH CORONARY HEART DISEASE". W THEORETICAL AND PRACTICAL ASPECTS OF MODERN SCIENTIFIC RESEARCH. European Scientific Platform, 2021. http://dx.doi.org/10.36074/logos-30.04.2021.v2.43.
Pełny tekst źródłaFalk, E. A. "UNSTABLE ANGINA PECTORIS: PATHOLOGIC ASPECTS". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643711.
Pełny tekst źródłaDenisova, Tatyana P., Lidia I. Malinova i Igor A. Malinov. "Physical and mathematical aspects of blood-glucose- and insulin-level kinetics in patients with coronary heart disease and high risk of its development". W Saratov Fall Meeting 2000, redaktor Valery V. Tuchin. SPIE, 2001. http://dx.doi.org/10.1117/12.431540.
Pełny tekst źródłaVengrenyuk, Yuliya, Theodore J. Kaplan, Luis Cardoso, Gwendalyn J. Randolph i Sheldon Weinbaum. "Biomechanical Modeling of Atherosclerotic Lesions in ApoE Deficient Mice". W ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206571.
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