Relevant bibliographies by topics / Genetic risk factors

Academic literature on the topic 'Genetic risk factors'

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Published: 4 June 2021
Last updated: 15 June 2024

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Journal articles on the topic "Genetic risk factors"

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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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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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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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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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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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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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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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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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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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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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Dissertations / Theses on the topic "Genetic risk factors"

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Kelempisioti, A. (Anthi). "Genetic risk factors for intervertebral disc degeneration." Doctoral thesis, Oulun yliopisto, 2016. http://urn.fi/urn:isbn:9789526211350.

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Abstract Low back pain (LBP) is the leading cause of years lived with disabilities worldwide. Intervertebral disc (IVD) degeneration is a strong contributing factor to LBP. Recent studies have shown that genetic determinants contribute markedly to IVD degeneration but knowledge about the actual genes involved as well as their roles is still limited. The aim of this thesis work was to study genetic factors that may predispose to IVD degeneration. Using both family and case-control association study designs, variants in five genes showed association with IVD degeneration on magnetic resonance imaging (MRI) in a population-based sample and among patients with sciatica due to lumbar disc herniation (LDH). We performed a candidate gene association study of the known variants implicated in IVD degeneration in a Finnish cohort of 538 young individuals with a moderate degree of lumbar IVD degeneration on MRI. We were able to confirm the associations of variants in the IL6, SKT, and CILP genes, which provides further evidence for true associations. Based on our earlier linkage study in Finnish sciatica families, we performed a candidate gene analysis and identified IL17F as a potential candidate gene. To the best of our knowledge this is the first study to observe an association between this gene and discogenic sciatica. Both IL-6 and IL-17 are pro-inflammatory cytokines with elevated expression levels in herniated tissues, which suggest a role in IVD degeneration. Study of the role of genes coding for inflammatory mediators is of interest as it may contribute to the understanding of the overall inflammatory response of the disc. In addition, we reported on the involvement of SKT in the etiology of lumbar disc herniation (LDH) both in Japanese and Finnish case-control samples. Experimental studies in mice have shown that Skt homozygous mutants exhibit disc abnormalities resulting in a kinky tale phenotype. We hypothesized that the human homolog SKT could have long-term importance in the onset of IVD degeneration by making the discs more vulnerable. Finally, through linkage studies and in the subsequent association analyses, the role of CHST3 as a novel risk factor for IVD degeneration was identified. CHST3 encodes an enzyme that catalyzes the sulfation of chondroitin, and mutations in this gene are associated with spondylepiphyseal dysplasia and humerospinal dysostosis. In our study, we identified this gene using genome –wide linkage based on data from a Southern Chinese family and speculated that mild CHST3 reduction caused by the reported susceptibility SNP could result in disc degeneration in adults in conjunction with other risk factors. This thesis provides new information about the genetic background of IVD degeneration and new insights into the etiology of the disease. The specific roles of these genes in the IVD function and pathogenesis of sciatica are not clear however, and need to be elucidated
Tiivistelmä Alaselkäkipu on yksi yleisimmistä sairauksista ja johtava syy työkyvyttömyyteen. Välilevyrappeuma myötävaikuttaa merkittävästi alaselän kipuun. Vaikka aiemmat tutkimukset ovat osoittaneet, että perintötekijöillä on vahva osuus välilevyrappeumaan, altistavat geenit ja niiden rooli tunnetaan huonosti. Tämän tutkimuksen tavoitteena oli arvioida tiettyjen perintötekijöiden osuutta välilevyrappeumassa ja tunnistaa taudille altistava geeni perheaineistossa aiemmin havaitulta kromosomialueelta. Aineistoina tutkimuksessa olivat perheaineistot sekä laajat potilas-kontrolliaineistot suomalaisesta ja aasialaisista väestöistä. Tutkimuksessa osoitimme, että perimän vaihtelut viidessä tutkitussa geenissä altistivat erilaisille välilevyrappeuman taudin muodoille. Tutkimus, jossa analysoimme aiemmin tunnistettuja alttiusgeenejä, vahvisti IL6, SKT ja CILP geenien vaihteluiden osuuden taudin alttiustekijöinä. Tutkimusaineistona oli pohjoissuomalainen syntymäkohortti, jossa välilevyrappeuma oli määritetty magneettikuvauksella (MRI). Suomalaisessa perheaineistossa tehdyn kokogenomin laajuisen kartoituksen pohjalta analysoimme IL17F geenin mahdollisena uutena alttiusgeeninä oireiselle välilevytaudille. Kahdesta geenin variantista koostuva haplotyyppi assosioitui tautiin merkitsevästi. Lisäksi osoitimme, että SKT-geenin tietty muutos altistaa välilevyn pullistumille sekä japanilaisessa että suomalaisessa potilasaineistossa. Hiirikokeissa on havainnoitu, että SKT-geenin homotsygootti mutaatio johtaa välilevy-poikkeamaan, joka edelleen aiheuttaa hiiren poikkeavan häntäilmiasun-. Hypoteesimme oli, että ihmisen SKT -geeni voi myötävaikuttaa välilevypullistuman kehittymiseen altistamalla välilevyt rappeumalle. Edelleen, laajassa usean populaation aineiston käsittävässä tutkimuksessa osoitimme CHST3-geenin muutoksen altistavan välilevyrappeumalle. Peittyvästi periytyvät muutokset tässä geenissä aiheuttavat perinnöllisiä harvinaisia luusairauksia. Tämä väitöstutkimus tarjoaa uutta tietoa välilevyrappeuman geneettisestä taustasta ja auttaa taudin syiden tutkintaa. Geenien rooli välilevyn toiminnassa ja muutosten vaikutus taudin kulkuun vaativat kuitenkin vielä lisätutkimuksia
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Tilley, Louise. "Genetic risk factors in sporadic Alzheimer's disease." Thesis, University of Nottingham, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.311748.

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Al-Chalabi, Ammar. "Genetic risk factors in amytrophic lateral sclerosis." Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321934.

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Burger, Marilize Cornelle. "Genetic risk factors for carpal tunnel syndrome." Doctoral thesis, University of Cape Town, 2014. http://hdl.handle.net/11427/12714.

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Carpal tunnel syndrome (CTS) is a common occupational injury that is caused by an increase in pressure within the carpal tunnel structure which, in turn, causes compression of the median nerve. Although several factors are believed to be associated with increased risk of CTS, the direct causes of this injury remain unknown and it is generally accepted that CTS, with the exception of acutely caused CTS, is a multifactorial condition. Although it is generally accepted that an increase in pressure within the carpal tunnel structure, which contains nine flexor tendons, causes compression of the median nerve, the involvement of these tendons and other connective tissue structures in the aetiology of CTS cannot be excluded. In support of this, pathology of these connective structures have been proposed as being comorbid conditions or a precursor of CTS, cause CTS and/or can lead to an increase in carpal tunnel pressure. Several studies have suggested that specific non-occupational risk factors, such as anatomical, systemic and chronic factors as well as mostly repetition- and force-related occupational risk factors are associated with CTS. Although genetic influences in the aetiology of CTS have been proposed, this area has received little attention. Common DNA sequence variants on the other hand have previously been reported to associate with common exercise-associated tendon, such as chronic Achilles tendinopathy, and ligament injuries. The aim of this thesis was to determine whether common DNA sequence variants within several genes that have been associated or implicated in the aetiology of exercise-related musculoskeletal soft tissue injuries, are associated with altered risk of CTS by using a genetic association case-control study approach.
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Abelson, Anna-Karin. "Genetic Risk Factors for Systemic Lupus Erythematosus : From Candidate Genes to Functional Variants." Doctoral thesis, Uppsala : Universitetsbiblioteket [distributör], 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-9367.

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Mayosi, B. M. "Genetic determination of cardiovascular risk factors in families." Thesis, University of Oxford, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249502.

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Maude, Sophia Karen. "An investigation of genetic risk factors for migraine." Thesis, University of Aberdeen, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248576.

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Migraine manifests itself episodically with incidence ranging from one attack in a lifetime to one almost every day. Most migraineurs suffer from typical migraine with or without aura, that is inherited in a complex manner. A small number of migraineurs suffer from FHM, a condition that exhibits Mendelian inheritance. BFNC is another rare episodic disorder that exhibits Mendelian inheritance. In a four generational family the BFNC phenotype was linked to the KCNQ2 gene on chromosome 20q13.3. Blood samples and epidemiological information were collected from 214 migraine probands in the Grampian region. An Access database was created to hold these data which were subsequently input. The database was utilised to extract epidemiological information about the cohort for subsequent analysis. These data were compared to other studies to characterise the severity of the cohort. A total of six polymorphisms were analysed by association analysis for involvement in migraine. The first polymorphism to be analysed was the -141C Ins/Del polymorphism in the DRD2 gene on chromosome 11q22. This polymorphism was analysed by restriction digest. Statistical analysis excluded this polymorphism and the regions encompassed by linkage disequilibrium in the aetiology of migraine. The second and third polymorphisms were located in intron 1 of the ERa gene on chromosome 6q25. These two polymorphisms were identified by restriction digest. Individual and haplotype analysis excluded the involvement of both polymorphisms in the aetiology of migraine. The fourth, fifth and sixth polymorphisms were located in exon 47, exon 23 and exon 8 of the CACNA1A gene on chromosome 19p13. The polymorphisms were analysed by capillary electrophoresis, restriction digest and DASH, respectively. All three polymorphisms were excluded from the aetiology of migraine. A total of 12 hot spot exons were sequenced in the CACNA1A gene in one individual afflicted by FHM and two by HM. No mutations were presented in the exons sequenced.
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Posthumus, Michael. "Genetic risk factors for anterior cruciate ligament ruptures." Doctoral thesis, University of Cape Town, 2009. http://hdl.handle.net/11427/3195.

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The primary aim of this thesis was to identify candidate genes that may be associated with ACL ruptures, and then use a genetic association approach following a case-control study design to identify specific sequence variants (single nucleotide polymorphisms, SNPs) within these candidate genes which may predispose individuals to ACL ruptures. Candidate genes (COL1A1, COL5A1 and COL12A1) were selected based on the biological function of their encoded proteins (type I, type V and type XII collagen respectively) within the basic structural and functional unit of ligaments, namely the collagen microfibril.
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Hughes, Katherine Carlson. "Dietary and Genetic Risk Factors for Parkinson's Disease." Thesis, Harvard University, 2016. http://nrs.harvard.edu/urn-3:HUL.InstRepos:27201728.

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Parkinson’s disease (PD) is the second most common neurodegenerative disease. Motor symptoms typically do not manifest until significant neuronal loss has already occurred, highlighting the need for early detection and prevention. In this dissertation, we sought to improve our understanding of PD epidemiology by studying associations between potential modifiable risk factors, including antioxidant vitamins, dairy products, and urate, and PD risk. We conducted prospective analyses within three large cohort studies: the Nurses’ Health Study, the Health Professionals Follow-up Study, and the Cancer Prevention Study II Nutrition Cohort. Across all analyses, PD cases were identified via biennial questionnaires and confirmed through medical record review by neurologists specializing in movement disorders. In our first two aims, we used Cox proportional hazards models to calculate relative risks of PD according to cumulative average intakes of foods and nutrients of interest. In aim 1, we found no associations between intake of vitamin E, vitamin C, or carotenoids and risk of PD. In our second aim, we found that low fat dairy intake was associated with increased PD risk, and that this association appeared to be driven by an increased risk of PD associated with skim and low-fat milk intake. The results of a meta-analysis including previously conducted prospective investigations of milk intake and PD risk suggested a relative risk of PD comparing extreme milk intake levels of 1.80 (95% CI 1.44-2.25). In our third aim, although a large body of research suggests that higher urate levels could be protective against PD risk and progression, we found that genetic variants in the SLC2A9 gene that influence circulating urate levels were not associated with risk of PD. Our analyses suggest that while antioxidant vitamins are unlikely to alter PD risk, dairy products may represent an important modifiable PD risk factor. Whether dairy products also alter rates of PD progression or conversion from premotor PD to clinical PD are important, answerable questions. Finally, the results of our third analysis suggest that genetic variants associated with plasma urate levels are not associated with PD risk; however, larger studies are needed to confirm these results.
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Ylönen, S. (Susanna). "Genetic risk factors for movement disorders in Finland." Doctoral thesis, Oulun yliopisto, 2019. http://urn.fi/urn:isbn:9789526223988.

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Abstract Parkinson’s disease and Huntington’s disease are progressive neurodegenerative movement disorders that typically manifest in adulthood. In this study, genetic risk factors contributing to these two movement disorders were investigated in Finnish patients. Patients with early-onset or late-onset Parkinson’s disease as well as population controls were examined. The p.L444P mutation in GBA was found to contribute to the risk of Parkinson’s disease. POLG1 compound heterozygous mutations were detected in two patients with Parkinson’s disease and rare length variants in POLG1 were associated with Parkinson’s disease. Variants in SMPD1, LRRK2 or CHCHD10, previously detected in other populations, were not detected, suggesting that they are rare or even absent in the Finnish population. Patients with Huntington’s disease were investigated for HTT gene haplotypes as well as whether these haplotypes alter the stability of the elongated CAG repeat. Haplogroup A was less common in Finns than in other European populations, whereas it was significantly more common in patients with Huntington’s disease than in the general population. Certain HTT haplotypes as well as the parental gender were found to affect the repeat instability. We found that compound heterozygous mutations in POLG1 were causative of Parkinson’s disease, rare length variants in POLG1 were associated with Parkinson’s disease and GBA p.L444P was significantly more frequent in patients than in the controls, which suggests that these mutations are associated with the development of Parkinson’s disease. The low prevalence of Huntington’s disease in Finland correlates with the low frequency of the disease-associated HTT haplogroup A. Paternal inheritance combined with haplotype A1 increased the risk of repeat expansion. Movement disorders in Finland were found to share some of the same genetic risk factors found in other European populations, but some other recognized genetic variants could not be detected
Tiivistelmä Parkinsonin tauti ja Huntingtonin tauti ovat hermostoa rappeuttavia eteneviä liikehäiriösairauksia, jotka tyypillisesti ilmenevät aikuisiällä. Tässä tutkimuksessa selvitettiin näiden kahden liikehäiriösairauden geneettisiä riskitekijöitä suomalaisilla potilailla. Tutkimme potilaita, joilla oli varhain alkava Parkinsonin tauti tai myöhään alkava Parkinsonin tauti sekä väestökontrolleja. GBA-geenin p.L444P mutaation havaittiin lisäävän Parkinsonin taudin riskiä. Kaksi Parkinsonin tautia sairastavaa potilasta oli yhdistelmäheterotsygootteja haitallisten POLG1-geenin varianttien suhteen ja harvinaiset POLG1 CAG toistojaksovariantit assosioituivat Parkinsonin tautiin. Tutkittuja variantteja SMPD1-, LRRK2- ja CHCHD10-geeneissä ei löydetty tästä aineistosta lainkaan, mikä viittaa siihen, että ne puuttuvat suomalaisesta väestöstä tai ovat harvinaisia. Huntingtonin tautia sairastavilta potilailta tutkittiin HTT-geenin haploryhmiä ja niiden vaikutusta Huntingtonin tautia aiheuttavan pidentyneen toistojakson epästabiiliuteen. Haploryhmä A oli suomalaisessa väestössä harvinainen verrattuna eurooppalaiseen väestöön ja se oli huomattavasti yleisempi Huntingtonin tautipotilailla kuin väestössä. Toistojakson epästabiiliuteen vaikuttivat tietyt HTT-geenin haplotyypit samoin kuin sen vanhemman sukupuoli, jolta pidentynyt toistojakso periytyy. POLG1 yhdistelmäheterotsygoottien katsottiin aiheuttavat Parkinsonin tautia ja harvinaisten POLG1 CAG toistojaksovarianttien todettiin assosioituvan Parkinsonin tautiin Suomessa. GBA p.L444P mutaatio merkittävästi yleisempi Parkinsonin tautipotilailla kuin kontrolleilla, mikä viittaa siihen, että se on Parkinsonin taudin riskitekijä. Huntingtonin tautiin assosioituvan haploryhmä A:n matala frekvenssi selittää taudin vähäistä esiintyvyyttä Suomessa. Paternaalinen periytyminen ja haplotyyppi A1 lisäsivät HTT-geenin toistojakson pidentymisen riskiä. Liikehäiriösairauksilla todettiin Suomessa osittain samanlaisia riskitekijöitä kuin muualla Euroopassa, mutta kaikkia tutkittuja variantteja emme havainneet
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Books on the topic "Genetic risk factors"

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Uri, Goldbourt, De Faire Ulf, and Berg Kåre, eds. Genetic factors in coronary heart disease. Dordrecht: Kluwer Academic, 1994.

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Petrakis, Peter L. Alcoholism, and inherited disease. Rockville, Md: U.S. Dept. of Health and Human Services, Public Health Service, Alcohol, Drug Abuse, and Mental Health Administration, National Institute on Alcohol Abuse and Alcoholism, 1985.

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Kåre, Berg, ed. Genetic approaches of coronary heart disease and hypertension. Berlin: Springer-Verlag, 1991.

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Offit, Kenneth. Clinical cancer genetics: Risk counseling and management. New York: Wiley-Liss, 1998.

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Introduction to risk calculation in genetic counselling. Oxford: Oxford University Press, 1991.

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Genetic susceptibility to cancer. Boston: Kluwer Academic, 1998.

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A, Levin Morris, and Strauss Harlee S, eds. Risk assessment in genetic engineering. New York: McGraw-Hill, 1991.

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J, Alberts Mark, ed. Genetics of cerebrovascular disease. Armonk, NY: Futura Pub. Co., 1999.

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Ovarian cancer: The signs, symptoms, treatments, and genetic risk factors. [United States]: Fort Press, 2010.

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Introduction to risk calculation in genetic counseling. 2nd ed. Oxford [England]: Oxford University Press, 1999.

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Book chapters on the topic "Genetic risk factors"

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Thiriet, Marc. "Genetic Risk Factors." In Biomathematical and Biomechanical Modeling of the Circulatory and Ventilatory Systems, 595–676. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-89315-0_7.

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Hetherington, J. "Genetic Risk Factors for Glaucoma." In Pathogenesis and Risk Factors of Glaucoma, 67–75. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-60203-0_8.

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Hollingworth, Paul, and Julie Williams. "Genetic Risk Factors for Dementia." In The Handbook of Alzheimer's Disease and Other Dementias, 195–234. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444344110.ch6.

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Li, Donghui. "Risk Factors and Genetic Predisposition." In Pancreatic Cancer: A Multidisciplinary Approach, 23–31. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-05724-3_2.

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Spitz, Margaret R. "Risk factors and genetic susceptibility." In Head and Neck Cancer, 73–87. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-2023-8_4.

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Waldinger, Marcel D. "Risks Factors in Premature Ejaculation: The Genetic Risk Factor." In Premature Ejaculation, 111–23. Milano: Springer Milan, 2012. http://dx.doi.org/10.1007/978-88-470-2646-9_9.

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Berg, K. "Genetic Risk Factors for Atherosclerotic Disease." In Human Genetics, 326–35. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71635-5_40.

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Combarros, Onofre. "Genetic Risk Factors for Alzheimer’s Disease." In Neurodegenerative Diseases, 49–64. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-6380-0_4.

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Tsang, Kin-Lun, Zhe-Hui Feng, Hong Jiang, Shu-Leong Ho, and David B. Ramsden. "Genetic Risk Factors in Parkinson’s Disease." In Mapping the Progress of Alzheimer’s and Parkinson’s Disease, 251–57. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-0-306-47593-1_42.

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Baker, Jessica H., Lauren Janson, Sara E. Trace, and Cynthia M. Bulik. "Genetic Risk Factors for Eating Disorders." In The Wiley Handbook of Eating Disorders, 367–78. Chichester, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781118574089.ch28.

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Conference papers on the topic "Genetic risk factors"

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Petersen, Gloria M. "Abstract IA03: Genetic and non-genetic risk factors of pancreatic cancer." In Abstracts: AACR Special Conference on Pancreatic Cancer: Advances in Science and Clinical Care; May 12-15, 2016; Orlando, FL. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.panca16-ia03.

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Francis-Lyon, Patricia, Shashank Belvadi, and Fu-Yuan Cheng. "Detection and characterization of interactions of genetic risk factors in disease." In Python in Science Conference. SciPy, 2013. http://dx.doi.org/10.25080/majora-8b375195-007.

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Cimino, Silvia. "Genetic Factors In Families: Parental Psychopathological Risk And Offspring’s Develompmental Oucomes." In 11th International Conference on Education and Educational Psychology. European Publisher, 2020. http://dx.doi.org/10.15405/epiceepsy.20111.35.

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Hernandez Cordero, A. I., X. Li, S. Milne, C. X. Yang, Y. Bossé, P. Joubert, W. Timens, et al. "Integrative Genomic Analysis Highlights Potential Genetic Risk Factors for Covid-19." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a3765.

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Fialkovska, Anastasiia, and Svetlana Ilchenko. "The genetic risk factors for developing chronic bronchitis in adolescent smokers." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa5387.

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Gunther, Max L., James C. Jackson, Pratik Pandharipande, Alessandro Morandi, Maureen Hahn, Josh Buckholtz, Brett English, et al. "Genetic Risk Factors For Long-Term Cognitive Impairment After Critical Illness." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6718.

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Xu, Yu, Chonghao Wang, Zeming Li, Yunpeng Cai, Ouzhou Young, Aiping Lyu, and Lu Zhang. "A machine learning model for disease risk prediction by integrating genetic and non-genetic factors." In 2022 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2022. http://dx.doi.org/10.1109/bibm55620.2022.9994925.

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Guy, Attia, Levinberg Roee, Arad Erez, Ilan Davidov, and Ludmila Sidorenko. "New Biotechnological Opportunities to Assess the Influence of Lifestyle Factors in Obesity." In 12th International Conference on Electronics, Communications and Computing. Technical University of Moldova, 2022. http://dx.doi.org/10.52326/ic-ecco.2022/bme.05.

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Background. Obesity results from a malfunction of the body's weight-control mechanisms, which may be influenced by environmental changes. Essentially, the obesity risk relies on two significant interdependent factors: genetic variations (single-nucleotide polymorphisms, haplotypes) and environmental risk exposure. Due to new biotechnologies over 127 potential genes for obesity have been identified, and evidence supports the function of 22 genes in at least five distinct groups. Gene and environment interactions mean that the synergy between genotype and environment is neither additive or multiplicative. The application of innovative methods for both genotype and lifestyle variables should be emphasized. Aim of study: Investigate variable data of lifestyle factors in obese people with genetic predisposition and without in order to figure out the trigger risks which transform the predisposition into obesity. Material and methods: This is a descriptive study. A questionnaire was elaborated. It was developed based on the data of new biotechnological analysis of metabolic changes in obese humans. 142 individuals were included. 82 obese individuals, 42 with genetic predisposition and 40 without, and 60 healthy probands were interviewed. Further followed a comparative statistical analysis. Results: Obese probands were found with higher levels of disability compare those without, cardiovascular events higher compared with healthy probnads, disability level and smoking habits had significantly correlation in obese with genetic predisposition. On the other hand, health probands were found in higher level of anxiety compared obese people with genetic predisposition. Conclusions: All the lifestyle aspects which lead to an increased central nervous overactivity disturb significantly the metabolism and are critical risk factors for people with genetic predisposition relate to the pathogenesis of obesity. that might lead to high disability level associated comorbid states and high risk of cardiovascular events.
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Makey, T. V., and P. M. Marozik. "GENETIC FACTORS OF PREPOSITION TO BONE FRACTURES IN ATHLETES." In SAKHAROV READINGS 2021: ENVIRONMENTAL PROBLEMS OF THE XXI CENTURY. International Sakharov Environmental Institute, 2021. http://dx.doi.org/10.46646/sakh-2021-1-287-290.

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A retrospective study was carried out, which included professional athletes. The athletes were divided into two groups, depending on the presence of bone fractures in the anamnesis. DNA isolated from the buccal epithelium was used as a biological material. Two informative genetic markers were identified that statistically increase the risk of stress fractures in the study group. The most significant differences between the studied groups in the distribution of genotype and allele frequencies were found for the rs7975232 variants of the VDR gene and rs42517 of the COL1A2 gene. The results indicate the important role of these loci in the pathogenesis of fractures. Identification of unfavorable variants of allelic combinations makes it possible to assess the individual risk of bone fractures.
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Comeau, Mary E., Hannah C. Ainsworth, Miranda C. Marion, Timothy D. Howard, and Carl D. Langefeld. "GG-05 Predictive ability of SLE genetic risk factors varies across ethnicities." In LUPUS 21ST CENTURY 2018 CONFERENCE, Abstracts of the Fourth Biannual Scientific Meeting of the North and South American and Caribbean Lupus Community, Armonk, New York, USA, September 13 – 15, 2018. Lupus Foundation of America, 2018. http://dx.doi.org/10.1136/lupus-2018-lsm.92.

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Reports on the topic "Genetic risk factors"

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Sarma, Aruna. Genetic and Hormonal Risk Factors for Cancer in African American Men. Fort Belvoir, VA: Defense Technical Information Center, May 2006. http://dx.doi.org/10.21236/ada455088.

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Mack, Thomas M. Genetic Abnormalities in Breast Cancer Tumors and Relationships to Environmental and Genetic Risk Factors Using Twins. Fort Belvoir, VA: Defense Technical Information Center, October 1995. http://dx.doi.org/10.21236/ada303152.

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Mack, Thomas M. Genetic Abnormalities in Breast Cancer Tumors and Relationships to environmental and Genetic Risk Factors Using Twins. Fort Belvoir, VA: Defense Technical Information Center, October 1999. http://dx.doi.org/10.21236/ada393066.

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Sarma, Aruna V. Genetic and Hormonal Risk Factors for Prostate Cancer in African American Men. Fort Belvoir, VA: Defense Technical Information Center, May 2005. http://dx.doi.org/10.21236/ada442683.

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Cao, Xianling, Xuanyou Zhou, Naixin Xu, Songchang Chang, and Chenming Xu. Association of IL-4 and IL-10 Polymorphisms with Preterm Birth Susceptibility: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0044.

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Review question / Objective: The aim of our systematic review and meta-analysis was to summarize the effects of IL-4 and IL-10 gene polymorphism and clarify their possible association with PTB. Condition being studied: World Health Organization (WHO) defines preterm birth (PTB) as babies born alive before 37 weeks of pregnancy are completed. The new estimates show that the prevalence of PTB during 2014 ranged from 8.7% to13.4% of all live births, about 15 million preterm babies born each year. Besides, PTB is the leading cause of death worldwide for children below 5 years of age. Babies born preterm are at an increased risk of short-term and long-term complications attributed to immaturity of multiple organ systems, such as cerebral palsy, intellectual disabilities, vision and hearing impairments, and impaired cognitive development. PTB has become a worldwide public health problem, but its etiology remains unclear. Accumulating evidence shows that PTB is a syndrome that can be attributed to a variety of pathological processes(5). Inflammatory diseases and genetic background are known risk factors for PTB, many studies had shown that genetic variations in proinflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-1 α (IL-1 α) are associated with increased risk of PTB, but the relationship between genetic polymorphism in anti-inflammatory cytokines and risk of PTB remains controversial.
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Gelmann, Edward P. Genetic Risk Factor for Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, January 2005. http://dx.doi.org/10.21236/ada434784.

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Gelmann, Edward P. Genetic Risk Factor for Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, January 2003. http://dx.doi.org/10.21236/ada414867.

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Gelmann, Edward P. Genetics Risk Factor for Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, January 2004. http://dx.doi.org/10.21236/ada422932.

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Seale, Maria, Natàlia Garcia-Reyero, R. Salter, and Alicia Ruvinsky. An epigenetic modeling approach for adaptive prognostics of engineered systems. Engineer Research and Development Center (U.S.), July 2021. http://dx.doi.org/10.21079/11681/41282.

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Prognostics and health management (PHM) frameworks are widely used in engineered systems, such as manufacturing equipment, aircraft, and vehicles, to improve reliability, maintainability, and safety. Prognostic information for impending failures and remaining useful life is essential to inform decision-making by enabling cost versus risk estimates of maintenance actions. These estimates are generally provided by physics-based or data-driven models developed on historical information. Although current models provide some predictive capabilities, the ability to represent individualized dynamic factors that affect system health is limited. To address these shortcomings, we examine the biological phenomenon of epigenetics. Epigenetics provides insight into how environmental factors affect genetic expression in an organism, providing system health information that can be useful for predictions of future state. The means by which environmental factors influence epigenetic modifications leading to observable traits can be correlated to circumstances affecting system health. In this paper, we investigate the general parallels between the biological effects of epigenetic changes on cellular DNA to the influences leading to either system degradation and compromise, or improved system health. We also review a variety of epigenetic computational models and concepts, and present a general modeling framework to support adaptive system prognostics.
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Corkum, Eleanor, Tiffanie Perrault, and Erin C. Strumpf. Improving Breast Cancer Diagnosis Pathways in Quebec. CIRANO, October 2023. http://dx.doi.org/10.54932/qsho2261.

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Delays in breast cancer diagnosis can worsen the severity of illness and reinforce inequalities. This report analyzes Quebec’s capabilities and performance along the diagnosis pathway, gathering information from the scientific literature on cancer care, government reports, and expert interviews. The first section outlines which types of breast cancer data Quebec collects, and how data availability impacts the measurement of performance indicators. The second section discusses how socio-economic factors and unclear guidelines for patients outside Quebec’s organized screening program create barriers to diagnosis. We also explore how Quebec’s lack of standardized and integrated care and its outdated cancer registry can create further delays and inefficiencies. The final section of the report compares innovations in breast cancer diagnosis in Quebec to those in Alberta and Ontario, where diagnostic delays are shorter. This comparison suggests that Quebec should include high-risk individuals in its screening program, create personalized screening recommendations, update available imaging and genetic testing technologies, and modernize communication methods. Relevant research and initiatives seeking to increase screening adherence among groups with low screening rates are also discussed. Overall, this paper highlights tangible strategies to shorten and streamline the breast cancer diagnosis interval, and points the reader to key resources for further investigation.
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