Literatura académica sobre el tema "Heart – Diseases – Genetic aspects"
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Artículos de revistas sobre el tema "Heart – Diseases – Genetic aspects"
Penyaeva, Elena V. "Genetic aspects of Ebstein anomaly and related heart diseases". Annals of the Russian academy of medical sciences 76, n.º 1 (12 de abril de 2021): 67–74. http://dx.doi.org/10.15690/vramn1228.
Texto completoŁój, Magdalena, Magdalena Garncarz y Michał Jank. "Genomic and genetic aspects of heart failure in dogs — A review". Acta Veterinaria Hungarica 60, n.º 1 (1 de marzo de 2012): 17–26. http://dx.doi.org/10.1556/avet.2012.002.
Texto completoEllingwood, Sara S. y Alan Cheng. "Biochemical and clinical aspects of glycogen storage diseases". Journal of Endocrinology 238, n.º 3 (septiembre de 2018): R131—R141. http://dx.doi.org/10.1530/joe-18-0120.
Texto completoSaryeva, Olga P., Ludmila V. Kulida, Elena V. Protsenko y Maria V. Malysheva. "Cardiomyopathy in children – clinical, genetic and morphological aspects". I.P. Pavlov Russian Medical Biological Herald 28, n.º 1 (9 de abril de 2020): 99–110. http://dx.doi.org/10.23888/pavlovj202028199-110.
Texto completoFerrari, Marta y Stefano Stagi. "Autoimmunity and Genetic Syndromes: A Focus on Down Syndrome". Genes 12, n.º 2 (13 de febrero de 2021): 268. http://dx.doi.org/10.3390/genes12020268.
Texto completoProtasoni, Margherita y Massimo Zeviani. "Mitochondrial Structure and Bioenergetics in Normal and Disease Conditions". International Journal of Molecular Sciences 22, n.º 2 (8 de enero de 2021): 586. http://dx.doi.org/10.3390/ijms22020586.
Texto completoProtasoni, Margherita y Massimo Zeviani. "Mitochondrial Structure and Bioenergetics in Normal and Disease Conditions". International Journal of Molecular Sciences 22, n.º 2 (8 de enero de 2021): 586. http://dx.doi.org/10.3390/ijms22020586.
Texto completoPedersen, Maria Weinkouff, Kristian Ambjørn Groth, Kristian Havmand Mortensen, John Brodersen, Claus Højbjerg Gravholt y Niels Holmark Andersen. "Clinical and pathophysiological aspects of bicuspid aortic valve disease". Cardiology in the Young 29, n.º 1 (30 de octubre de 2018): 1–10. http://dx.doi.org/10.1017/s1047951118001658.
Texto completoAlper, Joseph S. "Does the ADA Provide Protection Against Discrimination on the Basis of Genotype?" Journal of Law, Medicine & Ethics 23, n.º 2 (1995): 167–72. http://dx.doi.org/10.1111/j.1748-720x.1995.tb01346.x.
Texto completoLi, Suyi, Feng Li, Shijie Tang y Wenji Xiong. "A Review of Computer-Aided Heart Sound Detection Techniques". BioMed Research International 2020 (10 de enero de 2020): 1–10. http://dx.doi.org/10.1155/2020/5846191.
Texto completoTesis sobre el tema "Heart – Diseases – 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.
Texto completoMakubalo, 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.
Texto completoENGLISH 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.
AFRIKAANSE OPSOMMING: Sien volteks vir opsomming
Fournier, 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.
Texto completoZhian, Samaneh. "Molecular Genetic Analysis of CRELD1 in Patients with Heterotaxy Disorder". PDXScholar, 2011. https://pdxscholar.library.pdx.edu/open_access_etds/410.
Texto completoYako, Yandiswa. "Bioinformatics-based strategies to identify PFHBII-causing and HCM main locus and/or HCM modifying mutations". Thesis, Stellenbosch : University of Stellenbosch, 2004. http://hdl.handle.net/10019.1/16473.
Texto completoENGLISH ABSTRACT: Progressive familial heart block type II (PFHBII) is an inherited cardiac conduction disorder of unknown aetiology, which has been described in a South African family. The disorder was mapped to a 2.9 centimorgan (cM) locus on chromosome 1q32.2-32.3. Clinically, PFHBII manifests cardiac conduction aberrations, that progress to a disease of the heart muscle, dilated cardiomyopathy (DCM). DCM is also reported as an end phase in hypertrophic cardiomyopathy (HCM), another heart muscle disorder. These cardiomyopathies are genetically heterogeneous with some of the genes reported as causes of both disorders. Therefore, genes identified as causes of HCM and DCM were considered plausible candidates for PFHBII mutation analysis. Additionally, this study provided an opportunity to assess potential modifiers of HCM. HCM exhibits marked phenotypic variability, observed within and between families harbouring the same causative mutation. Genes within the PFHBII locus were selected for PCR-SSCP analysis based on homology to genes previously reported as causing conduction system disorders associated with arrhythmias, DCM and/or HCM. Results were confirmed by direct sequencing and association between the detected variants and HCM parameters was assessed using a quantitative transmission disequilibrium test (QTDT). Eleven plausible candidate genes were selected within the PFHBII locus and two of the genes, PFKFB2 and ATF3, that encode for 6-phosphofructo-2,6-bisphosphatase (PFK-2/FBPase-2) and activating transcription factor 3 (ATF3), respectively, were analysed for PFHBII-causing and HCM main locus and/or HCM modifying mutations. Mutation analysis of PFKFB2 and ATF3 in the PFHBII family revealed no PFHBII causal mutation. PFKFB2 and ATF3 were later localised outside the PFHBII locus, and, therefore, were excluded as PFHBII plausible candidates. Further analysis of the two genes for HCM main locus and/or HCM modifying mutations in the HCM panel identified several sequence variants. QTDT analysis of these variants showed no significant association. Completion of the Human Genome Project (HGP) and annotation of new genes within the PFHBII locus allowed the identification of more PFHBII plausible candidate genes. Identification of causal mutations in plausible PFHBII candidate genes will allow molecular diagnosis of PFHBII pathophysiology. Furthermore, identification of both HCM-modifying and HCM-causing genes will give insight into the phenotypic variability noted among South African HCM-affected individuals and into the molecular cause of the disease among individuals with HCM-like clinical features.
AFRIKAANSE OPSOMMING: Progressiewe familiële hartblok tipe II (PFHBII) is ʼn oorgeërfde hart geleidingsiekte van onbekende etiologie wat in ʼn Suid-Afrikaanse familie beskryf is. Die siekte is ʼn 2.9 sentimorgan (cM) lokus op chromosoom 1q32.2-32.3 gekarteer. Klinies presenteer PFHBII met geleidingsfwykings wat uitloop op gedilateerde kardiomiopatie (DCM). DCM word ook gerapporteer as ʼn endfase in hipertrofiese kardiomiopatie (HCM), ʼn ander hartspiersiekte. Die kardiomiopatieë is geneties heterogeen, met ʼn aantal gene wat as oorsaak van altwee siektetoestande gerapporteer word. Daarom is alle gene wat geïdentifiseer is as oorsake van DCM en HCM, as moontlike kandidaatgene vir PFHBII mutasieanaliese beskou. Bykomend het hierdie studie die geleentheid gebied om potensiële modifiseerders van HCM te assesseer. HCM toon beduidende fenotipiese variasie binne en tussen families wat dieselfde siekteveroorsakende mutasie het. Gene binne die PFHBII-lokus is geselekteer vir PCR-SSCP-analiese gebaseer op homologie met gene wat voorheen gerapporteer is om betrokke te wees by geleidingsiesisteemsiektes, geassosieerde arritmieë, DCM en/of HCM. Resultate is bevestig deur volgordebepaling. Assosiasie tusssen ontdekte variante en die siekteparameter is bepaal met ʼn kwantitatiewe transmissie disekwilibrium toets (QTDT). Elf moontlike kandidaatgene in die PFHBII-lokus is geselekteer en twee van die gene, PFKFB2 en ATF3, wat kodeer vir 6-fosfofrukto-2,6-bifosfatase (PFK-2/FBPase-2) en aktiveringstranskripsiefaktor 3 (ATF3) respektiewelik, is vir PFHBII-oorsakende en HCMhooflokus en/of HCM-modifiseerende mutasies ondersoek. Mutasie-analiese van PFKFB2 en ATF3 in die PFHBII-familie het nie ʼn siekteveroorsakende mutasie onthul/uitgelig nie. PFKFB2 en ATF3 is later buite die PFHBII-lokus geplaas en dus ook as moontlike PFHBII-kandidate uitgesluit. Verdere ondersoek van díe twee gene vir HCM-hooflokus en/of HCM-modifiserende mutasies in die HCM-paneel het ʼn aantal volgorde variante geïdentifiseer. QTDT-analiese van die variante het geen beduidende assosiasies aangetoon nie. Voltooiing van die Menslike Genoom Projek (HGP) en annotasie van nuwe gene in die PFHBIIlokus het tot die identifikasie van verdere moontlike PFHBII-kandidaatgene gelei. Identifikase van siekte-veroorsaakende mutasies in die moontlike PFHBII-kandidaatgene sal die molekulêre diagnose van PFHBII toelaat en insig in die patofisiologie van die siekte gee. Verder, identifikasie van beide HCM-veroorsakende of HCM-modifiserende gene kan insig gee in die fenotipiese varieerbaarheid wat onder Suid-Afrikaanse HCM-geaffekteerde individue waargeneem word en ook in die molekulêre oorsake van die siekte in individue met HCMsoortige kliniese kenmerke.
Chan, Kin-wang y 陳健宏. "Study of the in vivo role of TSPYL2 in transgenic mice". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B38225049.
Texto completoPocathikorn, 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.
Texto completoKuek, 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.
Texto completoSznajer, Yves. "Etude des manifestations cardiovasculaires chez les patients présentant un syndrome de Noonan porteurs de mutation au sein du gène PTPN11: rôles des gènes de la voie de signalisation des MAP kinases pour les syndromes apparentés". Doctoral thesis, Universite Libre de Bruxelles, 2009. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210210.
Texto completoAfin d’appréhender les implications possibles du gène PTPN11 dans la survenue des cardiopathies chez les patients porteurs de ces deux syndromes, nous avons conduit une étude chez 272 patients au syndrome de Noonan et une étude chez 19 patients porteurs du syndrome LEOPARD. Parmi la cohorte de patients atteints du syndrome de Noonan, 104 ont été diagnostiqués porteurs d’une mutation du gène (38%). Une prévalence de survenue de cardiopathies affectant les structures droites du cœur se dégage chez les patients identifiés porteurs d’une mutation avec une différence significative pour la SVP, une tendance est relevée pour le canal atrio-ventriculaire et la communication inter-auriculaire de type Ostium Secundum. L’absence de mutation est corrélée avec la survenue de cardiomyopathie hypertrophique et de cardiopathies du cœur gauche. Parmi les patients atteints du syndrome LEOPARD, il n’existe pas de différence statistiquement significative pour les patients porteurs d’une mutation ou non et/ou pour une cardiopathie particulière.
Toutes les mutations identifiées du gène PTPN11 sont des mutations ‘faux-sens’. Ce gène appartient à la famille des gènes codant pour une protéine tyrosyl phosphatase, SHP-2, ne possédant pas de récepteur trans-membranaire. Cette phosphatase est impliquée dans la voie de signalisation cellulaire des MAP (‘Mitogen-activated protein’) kinases dont l’expression est ubiquitaire et inclut le coeur. Depuis nos travaux, le concept de syndrome « neuro-cardio-facio-cutané » est établi puisque, à ce jour, 9 gènes (SOS1, RAF1, BRAF, KRAS, NRAS, HRAS, NF1, SPRED1 et SHOC2), tous impliqués dans la voie de signalisation RAS (voie des MAP kinases) sont identifiés. Un spectre phénotypique existe avec des signes communs mais aussi distinctifs chez les patients présentant le syndrome de Noonan, le syndrome LEOPARD, le syndrome de Costello, le syndrome Cardio-Facio-Cutané (CFC), le syndrome « Noonan-NF1 », le syndrome de Legius et le syndrome « Noonan/Multiple Giant Cell Lesion ». Nous rapportons enfin l’observation d’une patiente atteinte du syndrome CFC et porteuse d’une mutation (p.R257Q) au sein du gène BRAF ayant développé une cardiomyopathie hypertrophique.
Ces travaux de cohortes de patients au phénotype du syndrome de Noonan, du syndrome LEOPARD et cette dernière description d’une patiente au syndrome CFC ont permis de participer à la découverte de l’implication d’une voie de signalisation cellulaire dont l’origine génétique est maintenant démontrée. Les résultats de nos travaux réalisés depuis 2002 auront permis, avec les équipes travaillant sur le même sujet, d’orienter les investigations et les nouveaux projets de recherche qui étudient spécifiquement le rôle du gène PTPN11 dans l’embryologie du cœur. Les études des orthologues (zebrafish, murin et Drosophila) porteurs à l’état hétérozygote d’une mutation du gène PTPN11 permettent d’intégrer les anomalies phénotypiques et cardiaques observées. Ces études permettent de postuler les effets cellulaires produits par les mutations chez les patients atteints du syndrome de Noonan et chez les patients atteints du syndrome LEOPARD engendrant in vitro une activation de la phosphatase (effet « gain de fonction ») pour les premiers ou une réduction de l’activité phosphatase (« dominant négatif ») mais engendrant un effet gain de fonction in vivo. Nous discutons les connaissances acquises, les compréhensions obtenues et intégrées et traçons enfin les perspectives offertes par ces travaux.
Doctorat en Sciences médicales
info:eu-repo/semantics/nonPublished
Rondelet, Benoît. "Médiation humorale de l'hypertension artérielle pulmonaire dans un modèle de cardiopathie congénitale à shunt systémo-pulmonaire chez le porcelet en croissance". Doctoral thesis, Universite Libre de Bruxelles, 2008. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210373.
Texto completoLibros sobre el tema "Heart – Diseases – Genetic aspects"
Kåre, Berg y Nora Audrey Hart 1936-, eds. Cardiovascular diseases: Genetics, epidemiology, and prevention. New York: Oxford University Press, 1991.
Buscar texto completoAlexander, Akhmedov y Moe Gordon W, eds. Post-genomic cardiology. Amsterdam: Elsevier/AP, Academic Press is an imprint of Elsevier, 2014.
Buscar texto completoDanieli, Gian Antonio. Genetics and genomics for the cardiologist. Dordrecht: Kluwer Academic Pub., 2002.
Buscar texto completoMuenke, Maximilian, Paul S. Kruszka, Craig A. Sable y John W. Belmont. Congenital heart disease: Molecular genetics, principles of diagnosis and treatment. Basel: Karger, 2015.
Buscar texto completoJ, Goldenthal Michael, Moe Gordon W y SpringerLink (Online service), eds. Aging and the Heart: A Post-Genomic View. Boston, MA: Springer Science+Business Media, LLC, 2008.
Buscar texto completoThe 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.
Buscar texto completoMcDonald, Pamela. Apo e gene diet. Livermore, CA: WingSpan Press, 2006.
Buscar texto completoMothers, babies and disease in later life. London: BMJ Pub. Group, 1994.
Buscar texto completoKaslow, Richard A. Genetic susceptibility to infectious diseases. New York: Oxford University Press, 2007.
Buscar texto completoSociety of General Physiologists. Symposium. Ion channels and genetic diseases. New York: Rockefeller University Press, 1995.
Buscar texto completoCapítulos de libros sobre el tema "Heart – Diseases – Genetic aspects"
Meregalli, Paola G., Hanno L. Tan y Arthur A. M. Wilde. "Brugada Syndrome: Clinical and Genetic Aspects". En Electrical Diseases of the Heart, 469–95. London: Springer London, 2013. http://dx.doi.org/10.1007/978-1-4471-4881-4_28.
Texto completoMilewicz, Dianna M. "Genetic Aspects of Congenital Heart Disease". En Cardiovascular Medicine, 2599–605. London: Springer London, 2007. http://dx.doi.org/10.1007/978-1-84628-715-2_127.
Texto completoHerzum, M., S. A. Huber y B. Maisch. "Coxsackie B3 Myocarditis: Genetic Aspects of Different Immunopathogenic Mechanisms in BALB/c and DBA/2 Mice. Antigenic Specificity of Heart-Reactive Antibodies in DBA/2 Mice". En New Concepts in Viral Heart Disease, 188–94. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73610-0_18.
Texto completoTester, David J. y Michael J. Ackerman. "Genetic Testing". En Electrical Diseases of the Heart, 315–32. London: Springer London, 2013. http://dx.doi.org/10.1007/978-1-4471-4978-1_20.
Texto completoJensen, Bjarke y Antoon F. M. Moorman. "Evolutionary Aspects of Cardiac Development". En Congenital Heart Diseases: The Broken Heart, 109–17. Vienna: Springer Vienna, 2016. http://dx.doi.org/10.1007/978-3-7091-1883-2_10.
Texto completoFahed, Akl C. "Genetic Thoracic Aortic Diseases". En Adult Congenital Heart Disease in Clinical Practice, 431–44. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67420-9_30.
Texto completoGaricochea, Bernardo y Rodrigo Santa Cruz Guindalini. "Practical Aspects of Genetic Counseling: Genetic Tests to Identify Risks". En Breast Diseases, 191–97. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-13636-9_21.
Texto completoFalchetti, Alberto, Francesca Giusti, Loredana Cavalli, Tiziana Cavalli y Maria Luisa Brandi. "Genetic Aspects of Hereditary Hyperparathyroidism". En Handbook of Parathyroid Diseases, 229–43. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4614-2164-1_14.
Texto completoWeder, Alan B. "Pathogenesis of Hypertension: Genetic and Environmental Factors". En Atlas of Heart Diseases, 1–33. London: Current Medicine Group, 2001. http://dx.doi.org/10.1007/978-1-4684-6909-7_1.
Texto completoTextoris, Julien y Marc Leone. "Genetic Aspects of Uncommon Diseases". En Uncommon Diseases in the ICU, 3–11. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-04576-4_1.
Texto completoActas de conferencias sobre el tema "Heart – Diseases – Genetic aspects"
Bhavani Shankar, Pagalla y Yarlagadda Divya Vani. "Conceptual Glance of Genetic Algorithms in the Detection of Heart Diseases". En 2021 International Conference on Advances in Electrical, Computing, Communication and Sustainable Technologies (ICAECT). IEEE, 2021. http://dx.doi.org/10.1109/icaect49130.2021.9392604.
Texto completoSavarapu, Pradeep Raj, M. Shankar, Shilpa Itnal, Ram Kumar Madupu, CMAK Zeelan Basha y E. Sreedevi. "Advanced prediction of Heart diseases using Artificial Neural Network and Genetic Algorithm". En 2021 5th International Conference on Computing Methodologies and Communication (ICCMC). IEEE, 2021. http://dx.doi.org/10.1109/iccmc51019.2021.9418459.
Texto completoLiu, Chengcheng. "Strategies on healthy urban planning and construction for challenges of rapid urbanization in China". En 55th ISOCARP World Planning Congress, Beyond Metropolis, Jakarta-Bogor, Indonesia. ISOCARP, 2019. http://dx.doi.org/10.47472/subf4944.
Texto completoKol, Emre. "Dimensions of Health Tourism in Turkey". En 2nd International Conference on Business, Management and Finance. Acavent, 2019. http://dx.doi.org/10.33422/2nd.icbmf.2019.11.767.
Texto completoRahmawati, Dian. "Psychososial Stimulation in Stunting and Non Stunting Firms". En The 7th International Conference on Public Health 2020. Masters Program in Public Health, Universitas Sebelas Maret, 2020. http://dx.doi.org/10.26911/the7thicph.03.24.
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