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Journal articles on the topic 'Genetic risk factors'

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Published: 4 June 2021
Last updated: 15 June 2024

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1

Tuma, Rabiya. "Genetic risk factors." Oncology Times 4, no. 6 (June 2007): 8. http://dx.doi.org/10.1097/01434893-200706000-00012.

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2

Sawikr, Yousef, Khlid G. ALqathafy, and Ibrahim S. Ibrahem. "Biochemical Markers and Genetic Risk Factors in Alzheimer's Disease." International Journal of Research Publication and Reviews 4, no. 12 (December 2, 2023): 890–93. http://dx.doi.org/10.55248/gengpi.4.1223.123328.

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3

Pullicino, Patrick, Steven Greenberg, and Maurizio Trevisan. "Genetic stroke risk factors." Current Opinion in Neurology 10, no. 1 (February 1997): 58–63. http://dx.doi.org/10.1097/00019052-199702000-00012.

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4

Fung, Jenny N., Yadav Sapkota, Dale R. Nyholt, and Grant W. Montgomery. "Genetic Risk Factors for Endometriosis." Journal of Endometriosis and Pelvic Pain Disorders 9, no. 2 (January 2017): 69–76. http://dx.doi.org/10.5301/je.5000273.

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Advances in genetics and genomics are driving progress in understanding genetic risk factors for endometriosis. Genome-wide association scans (GWAS) in endometriosis have identified 11 genomic regions associated with increased risk of disease. Many of the regions contain interesting candidate genes, but the risk alleles may not always act through the obvious candidates. Functional evidence to identify the causal gene(s) will require multiple steps including better mapping precision, genetic studies on gene expression and epigenetic marks, chromatin looping and functional studies. Evidence from gene expression studies in endometrium and chromatin looping experiments implicate CDC42 on chromosome 1, CDKN2B-AS1 on chromosome 9 and VEZT on chromosome 12 as likely causal genes in these regions. Confirming the causal gene(s) in these and other regions will identify the important pathways increasing risk for endometriosis and identify novel targets for interventions to improve diagnosis and treatment.
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5

Roberts, Robert. "Molecular genetics: Cardiac disease and risk-related genes-Genetic risk factors." Clinical Cardiology 18, S4 (September 1995): IV13—IV19. http://dx.doi.org/10.1002/clc.4960181604.

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6

Cardno, A. G., M. C. O’Donovan, and M. J. Owen. "Genetic Risk Factors for Schizophrenia." International Journal of Mental Health 29, no. 3 (September 2000): 13–38. http://dx.doi.org/10.1080/00207411.2000.11449495.

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7

Yamada, Kazuo, and Masayasu Matsumoto. "Genetic Risk Factors of Stroke." Nosotchu 29, no. 6 (2007): 711. http://dx.doi.org/10.3995/jstroke.29.711.

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8

Montagnana, Martina, Elisa Danese, and Giuseppe Lippi. "Genetic risk factors of atherothrombosis." Polish Archives of Internal Medicine 124, no. 9 (July 29, 2014): 474–82. http://dx.doi.org/10.20452/pamw.2409.

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9

Reitsma, Pieter H. "Genetic Risk Factors of Thrombosis." Blood 114, no. 22 (November 20, 2009): SCI—43—SCI—43. http://dx.doi.org/10.1182/blood.v114.22.sci-43.sci-43.

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Abstract Abstract SCI-43 Venous thrombosis is a common episodic disease with a steep age gradient. Interactions between various risk factors determine the development of the disease, and the proportion of variance attributable to genetic factors may be as high as 50-60%. There are six (moderately) strong genetic risk factors. First there are heterozygous deficiencies of the natural anticoagulants protein C, protein S, and antithrombin. These deficiency states are quite rare in the general population (in all races) and their genetic architecture is complex with hundreds of documented mutations. The risk for the development of venous thrombosis may be increased 10-20-fold in these deficiency states. There is no consistent evidence that deficiencies of other members of the anticoagulant systems - such as thrombomodulin, EPCR, and heparin co-factor II - are also strong risk factors for venous thrombosis, possibly because these natural anticoagulants are associated with other episodic or chronic diseases. Secondly there are three genetic factors associated with an increase, directly or indirectly, in the procoagulant potential of the coagulation system: blood group non-O, factor V Leiden and prothrombin G20201A. The genetic architecture of these risk factors is extremely simple. The prevalence in the general Caucasian population is modest for prothrombin G20210A and factor V Leiden; in other races these two risk factors are extremely rare. The increase in thrombotic risk is about 3-fold or 7-fold for prothrombin G20210 and Factor V Leiden respectively. Blood group non-O is the most common of the prothrombotic genetic risk factors and approximately doubles the risk of venous thrombosis, and may do so in all races. In addition to these six ‘classical’ risk factors, a growing list of weak genetic risk factors has been discovered. Almost without exception, these weak risk factors are common single nucleotide polymorphisms in coagulation factor genes - e.g. those encoding for fibrinogen, factor XIII, factor IX, et cetera - that have a small effect on gene function, and consequently a small effect on thrombotic risk. This list of weak but common risk factors is expected to grow considerably in the near future as the large-scale genome wide association studies that are currently under way deliver their results. Moreover, deep resequencing studies are expected to start soon, whether based on a candidate gene approach or genome-wide, which will yield unprecedented insight in the extend to which rare genetic variation determines individual thrombotic risk. Disclosures No relevant conflicts of interest to declare.
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10

Theile, M., H. Krause, L. Luebbe, M. Strauss, U. Kiessling, and E. Geissler. "Papovaviruses, possible genetic risk factors." Mutation Research/Environmental Mutagenesis and Related Subjects 147, no. 5 (October 1985): 324. http://dx.doi.org/10.1016/0165-1161(85)90216-x.

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11

Meyle, Kathrine Damm, and Per Guldberg. "Genetic risk factors for melanoma." Human Genetics 126, no. 4 (July 8, 2009): 499–510. http://dx.doi.org/10.1007/s00439-009-0715-9.

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12

Shubina, M. V., K. V. Kopylova, M. V. Smolnikova, N. N. Gorbacheva, and S. Yu Tereshchenko. "Genetic risk factors of headache." Russian Journal of Pain 21, no. 4 (2023): 11. http://dx.doi.org/10.17116/pain20232104111.

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13

Lucas, Sionne E. M., and Kathryn P. Burdon. "Genetic and Environmental Risk Factors for Keratoconus." Annual Review of Vision Science 6, no. 1 (September 15, 2020): 25–46. http://dx.doi.org/10.1146/annurev-vision-121219-081723.

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Keratoconus, a progressive corneal ectasia, is a complex disease with both genetic and environmental risk factors. The exact etiology is not known and is likely variable between individuals. Conditions such as hay fever and allergy are associated with increased risk, while diabetes may be protective. Behaviors such as eye rubbing are also implicated, but direct causality has not been proven. Genetics plays a major role in risk for some individuals, with many large pedigrees showing autosomal inheritance patterns. Several genes have been implicated using linkage and follow-up sequencing in these families. Genome-wide association studies for keratoconus and for quantitative traits such as central corneal thickness have identified several genetic loci that contribute to a cumulative risk for keratoconus, even in people without a family history of the disease. Identification of risk genes for keratoconus is improving our understanding of the biology of this complex disease.
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14

Arai, Hiroyuki. "Genetic Risk Factors in Senile Dementia." Nippon Ronen Igakkai Zasshi. Japanese Journal of Geriatrics 36, no. 4 (1999): 251–55. http://dx.doi.org/10.3143/geriatrics.36.251.

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15

Пивоварова, Д. Д., and Е. В. Машкина. "Genetic risk factors for hepatitis B." Nauchno-prakticheskii zhurnal «Medicinskaia genetika», no. 8(217) (August 31, 2020): 85–86. http://dx.doi.org/10.25557/2073-7998.2020.08.85-86.

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В работе в качестве материала для исследования были использованы образцы ДНК, выделенные из крови 99 людей в возрасте от 20 до 80 лет, из них 47 человек инфицированы вирусом гепатита В и 52 человека без вирусной нагрузки. По результатам исследования установлено, что аллель А полиморфизма rs1800450 гена MBL2 ассоциирован с высоким риском развития гепатита В, а наличие генотипа GG снижает такой риск; взаимодействие полиморфных вариантов гена STAT3 с генотипом GG гена MBL2 снижает риск развития гепатита В. DNA samples extracted from the blood of 99 people aged 20 to 80 years were used as the material for our research. Among these people 47 were infected with HBV and 52 were not. The reseach found that the allele A of the rs1800450 polymorphism of the MBL2 gene is associated with a high risk of hepatitis B, and the presence of the GG genotype reduces this risk; interaction of polymorphic variants of the STAT3 gene with a GG genotype of the MBL2 gene reduces the risk of hepatitis B.
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16

Skrzypa, Marzena, Natalia Potocka, Halina Bartosik-Psujek, and Izabela Zawlik. "Genetic risk factors of Alzheimer’s disease." European Journal of Clinical and Experimental Medicine 17, no. 1 (2019): 57–66. http://dx.doi.org/10.15584/ejcem.2019.1.10.

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17

Sahin-Tóth, Miklós, Péter Hegyi, and Miklós Tóth. "Genetic risk factors in chronic pancreatitis." Orvosi Hetilap 149, no. 36 (September 1, 2008): 1683–88. http://dx.doi.org/10.1556/oh.2008.28441.

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A hasnyálmirigy idült gyulladásos megbetegedését a mirigyszövet pusztulása, emésztési zavarok, krónikus fájdalom jellemzi, és cukorbetegség kísérheti. A betegséggel kapcsolatos genetikai tényezőket két csoportra oszthatjuk: 1. olyan génmutációk, amelyek önmagukban a betegség kialakulásához vezetnek, ezek elsősorban a kationos tripszinogén génjét érintik és igen ritkák, illetve 2. olyan génmutációk, amelyek hajlamosítanak a betegség kialakulására és egyéb kockázati tényezőkkel együtt okozzák a betegséget. Ezek tehát genetikai rizikófaktoroknak tekinthetők. Ilyen génmutációkat az utóbbi 10 évben ismertünk meg, előfordulásuk gyakori, ezért etiológiai jelentőségük is nagy. Az esetek többségében komplex módon öröklődnek, a betegek egyszerre több génben is hordozhatnak különböző mértékű kockázatot jelentő mutációt, és ezek hatásukban összeadódva, környezeti tényezőkkel társulva vezetnek a betegség kialakulásához. A mutációk okozta genetikai hajlam biokémiai hátterében a tripszin pancreason belüli fokozott ectopiás aktiválódása, illetve a tripszininaktiválásért felelős védőmechanizmusok elégtelen működése állhat.
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18

Millichap, J. Gordon. "Genetic Risk Factors for Perinatal Stroke." Pediatric Neurology Briefs 27, no. 2 (February 1, 2013): 10. http://dx.doi.org/10.15844/pedneurbriefs-27-2-2.

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19

Ye-Jee, Shim, and Lee Kun-Soo. "Genetic Risk Factors of Hemophilia A." Journal of Genetic Medicine 7, no. 1 (June 30, 2010): 1–8. http://dx.doi.org/10.5734/jgm.2010.7.1.1.

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20

Vaikhanskaya, T. G., L. N. Sivitskaya, O. D. Levdansky, T. V. Kurushko, and N. G. Danilenko. "Genetic risk factors for dilated cardiomyopathy." Russian Journal of Cardiology 26, no. 10 (November 22, 2021): 4628. http://dx.doi.org/10.15829/1560-4071-2021-4628.

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Aim. To study the diagnostic significance of genetic testing in patients with dilated cardiomyopathy (DCM), identify predictors of life-threatening ventricular tachyarrhythmias (VTAs) and assess adverse clinical outcomes in different genetic groups.Material and methods. The study included 126 unrelated patients with verified DCM as follows: 70 (55,6%) probands with criteria for familial DCM and 56 (44,4%) individuals with a probable hereditary component. All patients (age, 43,1±11,3 years; men, 92 (73%); left ventricular ejection fraction, 30,6±8,43%; left ventricular enddiastolic diameter, 68,3±8,36 mm; follow-up period — median, 49 months) receive a complex of diagnostic investigations, including genetic screening using nextgeneration sequencing, followed by verification of variants by the Sanger method.Results. Pathogenic and likely pathogenic genetic variants were found in 61 (48,4%) of 126 patients with DCM. The dominant mutations were titin-truncating variants (TTNtvs), identified in 16 individuals (12,7%), and variants of lamin A/C (LMNA), identified in 13 probands (10,3%). Mutations in the other 19 genes were found in 32 (25,4%) patients. The following primary endpoints were assessed: sudden cardiac death (SCD), episodes of VTA (sustained ventricular tachycardia/ventricular fibrillation) and appropriate shocks of implanted cardiac resynchronization therapy (CRT)/cardioverter defibrillators (CVD) devices. As a result of ROC analysis, the following independent risk factors for SCD were identified: mutations in the LMNA gene (AUC, 0,760; p=0,0001) and non-sustained ventricular tachycardia (cut-off heart rate ≥161 bpm: AUC, 0,788; p=0,0001). When comparing the phenotypes and genotypes of DCM, TTNtv genotype was associated with a lower prevalence of complete left bundle branch block (χ2=7,46; p=0,024), a lower need for CRT/CVD implantation (χ2=5,70; p=0,017) and more rare episodes of sustained ventricular tachycardia/ventricular fibrillation (χ2=30,1; p=0,0001) compared with LMNA carriers. Kaplan-Meier analysis showed the worst prognosis in carriers of LMNA mutations both in relation to life-threatening VTA (log rang χ2=88,5; p=0,0001) and in achieving all unfavorable outcomes (χ2=27,8; p=0,0001) compared with groups of genenegative individuals, carriers of TTNtv and other genotypes.Conclusion. The phenotypes of DCM with TTNtv did not significantly differ in the incidence of VTAs and adverse outcomes compared with the gene-negative group and other genotypes (with the exception of LMNA). The contribution of the associations of LMNA mutations with VTAs on prognosis was confirmed, which shows the important role of LMNA genotype diagnosis for SCD risk stratification in patients with DCM.
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21

Sato, Naoyuki. "Non-genetic risk factors for dementia." Rinsho Shinkeigaku 52, no. 11 (2012): 968–70. http://dx.doi.org/10.5692/clinicalneurol.52.968.

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22

Krausz, Csilla, and Claudia Giachini. "Genetic Risk Factors in Male Infertility." Archives of Andrology 53, no. 3 (January 2007): 125–33. http://dx.doi.org/10.1080/01485010701271786.

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23

Stewart, L. L., L. L. Field, S. Ross, and R. G. MacArthur. "Genetic Risk Factors in Diabetic Retinopathy." Retina 14, no. 3 (1994): 289. http://dx.doi.org/10.1097/00006982-199414030-00030.

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24

Papakostas, Thanos D., Margaux A. Morrison, Anne Marie Lane, Caroline Awh, Margaret M. DeAngelis, Evangelos S. Gragoudas, and Ivana K. Kim. "Genetic Risk Factors for Radiation Vasculopathy." Investigative Opthalmology & Visual Science 59, no. 3 (March 23, 2018): 1547. http://dx.doi.org/10.1167/iovs.17-22791.

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25

Morgan, Laleh, Jackie Cooper, Hugh Montgomery, Steve Humphries, and Neil Kitchen. "Genetic Risk Factors for Subarachnoid Hemorrhage." Neurosurgery 61, no. 1 (July 1, 2007): 197. http://dx.doi.org/10.1227/01.neu.0000279889.51914.3a.

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26

Friedman, D., S. Thompson, Y. Yasui, G. Bunin, T. Rebbeck, K. Nichols, J. Potter, and A. Meadows. "Genetic risk factors for second malignancy." Journal of Pediatric Hematology/Oncology 22, no. 4 (July 2000): 368. http://dx.doi.org/10.1097/00043426-200007000-00028.

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27

Jones, Nick. "Genetic risk factors for sporadic ALS." Nature Reviews Neurology 5, no. 11 (November 2009): 579. http://dx.doi.org/10.1038/nrneurol.2009.172.

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28

Wilson, WA, and AE Gharavi. "Genetic Risk Factors for aPL Syndrome." Lupus 5, no. 5 (October 1996): 398–403. http://dx.doi.org/10.1177/096120339600500513.

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MHC class II alleles and C4 deficiency alleles have been variably associated with aPL syndrome, but the extensive linkage disequilibrium among many of these alleles has made it difficult to assign a causal role for any of them. Interethnic studies of these and other alleles in large cohorts of subjects would help to clarify the roles of these alleles in aPL syndrome.
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29

Sato, Hideki, Norio Tanahashi, Daisuke Ito, Hidenori Hattori, Mitsuru Murata, and Norihiro Suzuki. "Genetic risk factors for cerebral infarction." Nosotchu 27, no. 4 (2005): 585–89. http://dx.doi.org/10.3995/jstroke.27.585.

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30

Zdoukopoulos, Nikos, and Elias Zintzaras. "Genetic Risk Factors for Placental Abruption." Epidemiology 19, no. 2 (March 2008): 309–23. http://dx.doi.org/10.1097/ede.0b013e3181635694.

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31

Corral, J., JA Iniesta, R. Gonza-Conejero, ML Lozano, J. Rivera, and V. Vicente. "Migraine and prothrombotic genetic risk factors." Cephalalgia 18, no. 5 (June 1998): 257–60. http://dx.doi.org/10.1046/j.1468-2982.1998.1805257.x.

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32

Bonaïti-Pellié, C. "Genetic risk factors in colorectal cancer." European Journal of Cancer Prevention 8 (December 1999): S33. http://dx.doi.org/10.1097/00008469-199912001-00005.

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33

Hamsten, A. "Genetic determination of haemostatic risk factors." Atherosclerosis 144 (May 1999): 14–15. http://dx.doi.org/10.1016/s0021-9150(99)80050-1.

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34

Feltkamp, T. E. W., Lucien A. Aarden, Cees J. Lucas, Cor L. Verweij, and René R. P. de Vries. "Genetic risk factors for autoimmune diseases." Immunology Today 20, no. 1 (January 1999): 10–12. http://dx.doi.org/10.1016/s0167-5699(98)01347-4.

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35

Gyllensten, U., A. Beskow, M. Moberg, and J. Rønnholm. "Genetic risk factors for cervical cancer." European Journal of Cancer 37 (April 2001): S140. http://dx.doi.org/10.1016/s0959-8049(01)81012-1.

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36

Altukhova, OB, MI Churnosov, and OP Lebedeva. "Genetic Risk Factors of Large Myomas." Journal of Minimally Invasive Gynecology 22, no. 6 (November 2015): S157. http://dx.doi.org/10.1016/j.jmig.2015.08.593.

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37

Billingsley, K. J., S. Bandres-Ciga, S. Saez-Atienzar, and A. B. Singleton. "Genetic risk factors in Parkinson’s disease." Cell and Tissue Research 373, no. 1 (March 13, 2018): 9–20. http://dx.doi.org/10.1007/s00441-018-2817-y.

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38

Franco, Rendrik F., and Pieter H. Reitsma. "Genetic risk factors of venous thrombosis." Human Genetics 109, no. 4 (September 1, 2001): 369–84. http://dx.doi.org/10.1007/s004390100593.

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39

Burlingame, Janet, Hyeong Jun Ahn, John Chen, and Johann Urschitz. "579: Genetic risk factors for preeclampsia." American Journal of Obstetrics and Gynecology 208, no. 1 (January 2013): S247. http://dx.doi.org/10.1016/j.ajog.2012.10.745.

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40

Hinney, Anke, Susann Friedel, Helmut Remschmidt, and Johannes Hebebrand. "Genetic Risk Factors in Eating Disorders." American Journal of PharmacoGenomics 4, no. 4 (2004): 209–23. http://dx.doi.org/10.2165/00129785-200404040-00001.

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41

Tilley, L., K. Morgan, and N. Kalsheker. "Genetic risk factors in Alzheimer's disease." Molecular Pathology 51, no. 6 (December 1, 1998): 293–304. http://dx.doi.org/10.1136/mp.51.6.293.

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42

Sharabitdinova, Gulshad Gafurkhanovna. "GENETIC RISK FACTORS FOR CARDIOVASCULAR DISEASE." Theoretical & Applied Science 59, no. 03 (March 30, 2018): 240–43. http://dx.doi.org/10.15863/tas.2018.03.59.41.

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43

Zöller, Bengt, Peter J. Svensson, Björn Dahlbäck, Christina Lind-Hallden, Christer Hallden, and Johan Elf. "Genetic risk factors for venous thromboembolism." Expert Review of Hematology 13, no. 9 (August 23, 2020): 971–81. http://dx.doi.org/10.1080/17474086.2020.1804354.

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Kwinta, Przemko, Mirosław Bik-Multanowski, Zofia Mitkowska, Tomasz Tomasik, Magdalena Legutko, and Jacek Józef Pietrzyk. "Genetic Risk Factors of Bronchopulmonary Dysplasia." Pediatric Research 64, no. 6 (December 2008): 682–88. http://dx.doi.org/10.1203/pdr.0b013e318184edeb.

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45

Djordjevic, Valentina, Marija Stankovic, Vesna Brankovic-Sreckovic, Ljiljana Rakicevic, Tatjana Damnjanovic, Nebojsa Antonijevic, and Dragica Radojkovic. "Prothrombotic Genetic Risk Factors in Stroke." Clinical and Applied Thrombosis/Hemostasis 18, no. 6 (January 23, 2012): 658–61. http://dx.doi.org/10.1177/1076029611432136.

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Whitcomb, David C. "Genetic Risk Factors for Pancreatic Disorders." Gastroenterology 144, no. 6 (May 2013): 1292–302. http://dx.doi.org/10.1053/j.gastro.2013.01.069.

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Opal, S., S. Garg, J. Jain, and I. Walia. "Genetic factors affecting dental caries risk." Australian Dental Journal 60, no. 1 (February 26, 2015): 2–11. http://dx.doi.org/10.1111/adj.12262.

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48

KOHARA, K., Y. TABARA, T. NAGAI, J. NAKURA, and T. MIKI. "Genetic risk factors for arterial stiffness." American Journal of Hypertension 18, no. 5 (May 2005): A82. http://dx.doi.org/10.1016/j.amjhyper.2005.03.228.

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49

Stewart, L. L., L. L. Field, S. Ross, and R. G. McArthur. "Genetic risk factors in diabetic retinopathy." Diabetologia 36, no. 12 (December 1993): 1293–98. http://dx.doi.org/10.1007/bf00400808.

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50

Spek, C. Arnold, and Pieter H. Reitsma. "Genetic Risk Factors for Venous Thrombosis." Molecular Genetics and Metabolism 71, no. 1-2 (September 2000): 51–61. http://dx.doi.org/10.1006/mgme.2000.3051.

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