Bibliographies thématiques / Genetic risk factor

Littérature scientifique sur le sujet « Genetic risk factor »

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Publié le 7 juillet 2024

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Articles de revues sur le sujet "Genetic risk factor"

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Koch, Linda. « Genetic T2DM risk factor found ». Nature Reviews Endocrinology 10, no 3 (14 janvier 2014) : 128. http://dx.doi.org/10.1038/nrendo.2013.273.

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Reitsma, Pieter H. « Genetic Risk Factors of Thrombosis. » Blood 114, no 22 (20 novembre 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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Sokolova, I. V., D. A. Mustafina, A. G. Sadertdinova, A. N. Zagitova, D. A. Khusnullin, L. G. Sadertdinova et N. A. Mescheryakov. « GENETIC RISK FACTOR FOR IDIOPATHIC SCOLIOSIS ». International Journal of Applied and Fundamental Research (Международный журнал прикладных и фундаментальных исследований), no 1 2023 (2023) : 25–29. http://dx.doi.org/10.17513/mjpfi.13501.

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Ohishi, Mitsuru, Kenshi Fujii, Takazo Minamino, Jitsuo Higaki, Atsushi Kamitani, Hiromi Rakugi, Yi Zhao, Hiroshi Mikami, Tetsuro Miki et Toshio Ogihara. « A potent genetic risk factor for restenosis ». Nature Genetics 5, no 4 (décembre 1993) : 324–25. http://dx.doi.org/10.1038/ng1293-324.

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Senior, Kathryn. « New genetic risk factor for sporadic PD ». Nature Reviews Neurology 5, no 7 (juillet 2009) : 354. http://dx.doi.org/10.1038/nrneurol.2009.79.

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Bertina, Rogier M. « Factor V Leiden and other coagulation factor mutations affecting thrombotic risk ». Clinical Chemistry 43, no 9 (1 septembre 1997) : 1678–83. http://dx.doi.org/10.1093/clinchem/43.9.1678.

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Abstract Five genetic defects have been established as risk factors for venous thrombosis. Three are protein C, protein S, and antithrombin deficiencies, defects in the anticoagulant pathways of blood coagulation. Together they can be found in ∼15% of families with inherited thrombophilia. Their laboratory diagnosis is hampered by the large genetic heterogeneity of these defects. The other two genetic risk factors, resistance to activated protein C associated with the factor V Leiden mutation and increased prothrombin associated with the prothrombin 20210 A allele, are much more prevalent and together can be found in 63% of the thrombophilia families. Because both defects are caused by a single mutation, DNA analysis is the basis of their laboratory diagnosis.
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Cushman, Mary. « Inherited Risk Factors for Venous Thrombosis ». Hematology 2005, no 1 (1 janvier 2005) : 452–57. http://dx.doi.org/10.1182/asheducation-2005.1.452.

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Abstract Venous thrombosis occurs as a consequence of genetic and environmental risk factors. Since the discovery of factor V Leiden, the most common genetic risk factor, there has been intense interest in clarifying the roles of genes and the environment with thrombosis risk. The translation of this risk information to clinical practice is a challenging one in the setting of a rapidly expanding knowledge base that includes application of genetic medicine. There are benefits, but also potential harms, of testing for inherited disorders associated with thrombosis. This paper reviews inherited risk factors for thrombosis and discuss clinical applications of testing.
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Cheekurthy, Alice Jayapradha. « Predisposition of Obesity through Genetic and Non-Genetic Risk Factors ». Journal of Endocrinology Research 2, no 2 (6 février 2021) : 27. http://dx.doi.org/10.30564/jer.v2i2.2767.

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Globally there is an increase in the number of people affected by obesity.This has increased the count of individuals to double,triple, and even quadruple. Obesity is a complex disease that has a genetic, behavioural,socioeconomic, and environmental effect. This raises morbidity and mortality in obesity. It is an important predisposition for diabetes as well as the current pandemic COVID-19. The rationale of this case-control observational study is to identify obese individuals among the diabetic and non-diabetic population. The study includes non - genetic factors like lipid profiles with genetic factors in form of SNP as a predisposition factor. The amplified portion of the ADIPOQ gene sequence revealed the presence of SNPs rs2241767 in 46.3% population and showed increased lipid profile values. It can be concluded that these are important predisposing factors for obesity.
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Schwab, Manfred, Andreas Claas et Larissa Savelyeva. « BRCA2 : a genetic risk factor for breast cancer ». Cancer Letters 175, no 1 (janvier 2002) : 1–8. http://dx.doi.org/10.1016/s0304-3835(01)00752-2.

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EVANS, JEFF. « Major Genetic Risk Factor Is Discovered for Parkinson's ». Clinical Psychiatry News 38, no 2 (février 2010) : 33. http://dx.doi.org/10.1016/s0270-6644(10)70097-7.

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Thèses sur le sujet "Genetic risk factor"

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Ruth, Katherine Sarah. « Identification of genetic and non-genetic factors contributing to female reproductive ageing ». Thesis, University of Exeter, 2015. http://hdl.handle.net/10871/19189.

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The aim of my work was to identify additional genetic and non-genetic factors influencing female reproductive ageing in humans. Although approximately 50% of population variation in age at menopause is due to genetics, less than 3% of variation had been accounted for by common genetic variants. Of non-genetic risk factors, only smoking had consistently been found to have a strong effect on age of menopause. In the wider context of female reproduction, our understanding of the role of genetics in determining sex hormone levels was limited. By combining the results of research in these different areas, I hoped to improve our knowledge of the biology of female reproductive ageing. Chapter 1 is an introduction in which I discuss the biology of menopause, describe relationships with health and present current knowledge regarding non-genetic and genetic risk factors influencing menopause age. Chapter 2 is an analysis of the associations between non-genetic risk factors occurring in early life with early menopause. We identified an association between multiple births and early menopause, connecting events pre-birth, when the oocyte pool is formed, with reproductive ageing in later life. Chapter 3 is a genome-wide association study to identify genetic variants associated with levels of nine sex hormone related phenotypes. We highlighted loci of relevance to reproductive function, which suggested overlaps in the genetic basis of hormone regulation. Chapter 4 is a genome-wide association study of menstrual cycle length. We showed that a common genetic variant related to follicle stimulating hormone levels and age at menopause is associated with several reproductive traits including length of menstrual cycle. Chapter 5 is an investigation of the relationship between differences in length of normal FMR1 triplet repeat alleles and timing of menopause. We found no association between the length of normal FMR1 alleles and timing of menopause, contradicting the results of smaller studies and replicating a null result in another large study. Chapter 6 is large genome-wide meta-analysis to identify common and low-frequency genetic variants associated with age at menopause. We identified 44 regions containing 54 independent common signals and two rare missense alleles of large effect. Finally, in Chapter 7 I evaluate how this work has benefitted our knowledge of female reproductive ageing and describe directions for future research.
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Chen, Hong [Verfasser]. « Plasminogen is a genetic risk factor of periodontitis / Hong Chen ». Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2018. http://d-nb.info/1196803110/34.

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Perdigão, Catarina. « The impact of the genetic risk factor BIN1 to Alzheimer’s disease development ». Doctoral thesis, Universidade Nova de Lisboa. Instituto de Tecnologia Quimica e Biológica António Xavier, 2021. http://hdl.handle.net/10362/132008.

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" Alzheimer’s disease (AD) was identified more than a century ago. Yet, there is still no cure and the mechanisms behind the most common form of AD (late-onset, LOAD) are still an open question. BIN1 was the second gene most frequently associated with LOAD. Bin1 depletion has been linked with AD earliest pathomechanisms: increased beta-amyloid (Aβ) accumulation, endosomal abnormalities, and synaptic defects. Sequencing of BIN1 genomic locus identified regulatory and coding variants of BIN1, indicating that Bin1 correct levels and function are essential for a healthy brain. Two coding variants associated with LOAD (rs754834233, Bin1-PL, and rs138047593, Bin1-KR) lead to missense mutations in Bin1 protein. This work aimed to understand whether LOAD mutations in BIN1 result in Bin1 loss of function and contribute to LOAD early mechanisms. "
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Caglayan, Safak [Verfasser]. « SORLA/SORL1 as genetic risk factor in Alzheimer disease / Safak Caglayan ». Berlin : Freie Universität Berlin, 2013. http://d-nb.info/1043480935/34.

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Newsome, Jamie. « Resilience and Vulnerability in Adolescents at Risk for Delinquency : A Behavioral Genetic Study of Differential Response to Risk ». University of Cincinnati / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1367937532.

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Mutize, Tinashe. « DNA methylation : a risk factor for type 2 diabetes mellitus ». Thesis, Cape Peninsula University of Technology, 2016. http://hdl.handle.net/20.500.11838/2388.

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Thesis (MSc (Biomedical Technology))--Cape Peninsula University of Technology, 2016.
The early detection of individuals who are at risk of developing type 2 diabetes mellitus (T2DM) would decrease the morbidity and mortality associated with this disease. DNA methylation, the most widely studied epigenetic mechanism, offers unique opportunities in this regard. Aberrant DNA methylation is associated with disease pathogenesis and is observed during the asymptomatic stage of disease. DNA methylation has therefore attracted increasing attention as a potential biomarker for identifying individuals who have an increased risk of developing T2DM. The identification of high risk biomarkers for T2DM could facilitate risk stratification and lifestyle interventions, which could ultimately lead to better ways to prevent, manage and control the T2DM epidemic that is rampant worldwide. The aim of the study was to investigate global DNA methylation as a potential risk factor for T2DM by studying the association between the global DNA methylation levels and hyperglycaemic states. A cross-sectional, quantitative study design, involving 564 individuals of mixed ancestry descent, residing in Bellville South, South Africa was used. Participants were classified as normal, pre-diabetic (impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT)) or diabetic (screen detected diabetic and known diabetics) according to WHO criteria of 1998. DNA was extracted from whole blood using the salt extraction method. The percentage global DNA methylation was measured by an enzyme-linked immunosorbent assay (ELISA). The association between global DNA methylation and hyperglycaemia, as well as other biochemical markers of T2DM was tested in a robust linear regression analysis adjusted for age, gender and smoking.
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Kirin, Mirna. « Genetic analysis of retinal traits ». Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/9619.

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Retina is a unique site in the human body where the microcirculation can be imaged directly and non-invasively, allowing us to study in vivo the structure and pathology of the human microcirculation. Retinal images can be quantitatively assessed with computerized imaging techniques, enabling us to measure several different quantitative traits derived from the retinal vasculature. Arterial and venular calibres are the most extensively studied traits of the retinal microvasculature and numerous epidemiological studies demonstrated promising associations with systemic and ocular diseases as well as with disease markers. However, there has been a lack of research into pathophysiological processes leading to retinal vascular signs, and how they link retinal microcirculation with coronary and cerebral microvasculature change. Information about genetic determinants underlying retinal vascular structure is therefore important for understanding the processes leading to microvascular pathophysiology. Two genome wide association studies have been published so far revealing four loci associated with retinal venular calibre and one locus with arteriolar calibre. Here the results from the genome-wide association analysis of 10 different retinal vessel traits in two population based cohorts are presented. Retinal images were measured in non-mydriatic fundus images from 808 subjects in the Orkney Complex Disease Study (ORCADES) and 390 subjects from the Croatian island of Korcula, using the semi-automated retinal vasculature measurement programme SIVA and VAMPIRE. Using pairwise estimates of kinship based on genomic sharing, heritability was calculated for each trait. Estimates of tortuosity measure and fractal dimensions present first published reports of heritability estimates for those traits. In addition correlation analysis with systemic risk factor was also completed, confirming already published results as well as revealing some new associations. A genome wide association analysis of retinal arteriolar width revealed a genome wide significant hit (1.8x10-7) in a region of chromosome 2q32 (within TTN gene). Replication was sought in a further independent Scottish population (LBC) and additional 400 retinal images were graded. The result did not replicate, however the direction of the effect was consistent and a larger sample size is required. Analysis of the remaining traits did not yield genome wide significant result,s and will also require larger sample sizes. Genetic analysis of a binary retinal trait was also explored in a case control study of retinal detachment, which is an important cause of vision loss. A two-stage genetic association discovery phase followed by a replication phase in a combined total of 2,833 RRD cases and 7,871 controls was carried out. None of the SNPs tested in the discovery phase reached the threshold for association. Further testing was carried out in independent case-control series from London (846 cases) and Croatia (120 cases). The combined meta-analysis identified one association reaching genome-wide significance for rs267738 (OR=1.29, p=2.11x10-8), a missense coding SNP and eQTL for CERS2 encoding the protein ceramide synthase 2. Additional genetic risk score, pathway analysis and genetic liability analysis were also carried out.
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Mahlman, M. (Mari). « Genetic background and antenatal risk factors of bronchopulmonary dysplasia ». Doctoral thesis, Oulun yliopisto, 2018. http://urn.fi/urn:isbn:9789526219530.

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Abstract Advances over the past few decades in ante- and neonatal care have led to the survival of a growing number of premature infants of extremely low gestational age. However, the occurrence of serious diseases, particularly those affecting the most immature infants, remains high. Bronchopulmonary dysplasia (BPD), a chronic lung disease of premature infants, is one such disease. Our current understanding of the molecular pathogenesis of BPD is incomplete; consequently, there are few preventive and therapeutic options for BPD. Moreover, it is challenging to predict the risk of BPD. Previous studies of BPD in twins revealed that the heritability of BPD is quite high. However, the individual genes that predispose premature infants to BPD are largely unknown. The aim of this study was to identify and study genes associated with BPD in order to investigate its pathogenesis. An additional aim was to add to knowledge of the risk of BPD in newborn premature infants, with an emphasis on twins. A candidate gene study found no consistent association between common polymorphisms of vascular endothelial growth factor receptor 2 and BPD. A second candidate gene study noted an association between the gene encoding Kit ligand and BPD. A genome-wide association study found a suggestive association between a locus close to the gene encoding C-reactive protein (CRP) and BPD, and in subsequent analyses, plasma levels of CRP during the first week of life predicted BPD. Finally, a nationwide register study found that the risk of BPD was lower in twins than in singletons. The results of this study add to what is known of the genetics and pathogenesis of BPD. They also provide new data on the risk of BPD, which may be used to improve early identification of infants for whom the risk of developing BPD is high
Tiivistelmä Ennenaikaisen syntymän ja keskoslasten hoidon kehittymisen myötä yhä useammat huomattavan epäkypsinä syntyneet lapset jäävät henkiin. Samalla erityisesti juuri näitä lapsia uhkaavien sairauksien esiintyvyys on pysynyt korkeana. Bronkopulmonaalinen dysplasia (BPD, keskosen krooninen keuhkosairaus) on yksi näistä sairauksista. BPD:n molekyylitasoinen tautimekanismi on vielä osin tuntematon, eikä BPD:tä tehokkaasti estävää tai siitä parantavaa hoitoa ole. Myös BPD riskin arvioiminen vastasyntyneen keskoslapsen kohdalla on vaikeaa. BPD on huomattavan perinnöllinen tauti. BPD:lle altistavista geeneistä on kuitenkin vasta vähän tietoa. Tämän tutkimuksen tavoitteena oli lisätä tietoa BPD:n tautimekanismista tutkimalla BPD:lle altistavia geenejä. Lisäksi tutkimuksessa tarkasteltiin BPD:n esiintyvyyttä ja syntymää edeltäviä riskitekijöitä erityisesti kaksosten osalta. Ehdokasgeenitutkimuksessa verisuonten endoteelikasvutekijää koodaava geeni ei assosioitunut toistuvasti BPD:hen. Kit ligandia koodaava geeni sen sijaan assosioitui. Koko genomin assosiaatiotutkimuksessa C-reaktiivista proteiinia (CRP) koodaavan geenin lähistöltä löydettiin BPD:hen mahdollisesti assosioituva alue. Lisäksi ensimmäisen viikon CRP-arvojen osoitettiin ennakoivan myöhemmin kehittyvää BPD:tä. BPD-riskin todettiin olevan matalampi kaksi- kuin yksisikiöisistä raskauksista syntyneillä lapsilla. Tutkimuksen tulokset lisäävät tietoa BPD:n perinnöllisyydestä ja sitä kautta BPD:n tautimekanismista. Tutkimus toi myös uutta tietoa BPD:n riskitekijöistä parantaen vastasyntyneen keskoslapsen BPD-riskin arviota
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Bayoumy, Nervana M. K. « Genetic analysis of plasma von Willebrand factor antigen levels as a risk factor for arterial and venous thrombosis ». Thesis, University of Aberdeen, 2006. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU223247.

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We carried out the first genome-wide linkage analysis in British families for VWF levels. ABO and VWF loci were specifically examined. The results showed that VWF levels are highly heritable 42% ( P>0.000001) with age and C-reactive protein (CRP) the main covariates. The ABO locus was strongly associated with VWF levels ( P=2x10-18), but linkage was modest (LOD = 1.6). VWF gene marker showed no significant association or linkage with phenotype. Genome-wide linkage analysis, conditioned on age and ABO genotypes, revealed regions with potential linkage. Highlighted regions were on chromosomes 2 and 3 (LOD = 1.78 & 1.08 respectively) and two areas on chromosome 12 (LOD = 1.5 & 1.3). Inflammatory biomarkers concentrations were also investigated. Heritabilities of CRP and tumour necrosis factor-alpha (TNF-alpha) were significantly high 38% and 47% respectively, while interleukin-6 was not heritable. VWF levels showed significant genetic correlation with CRP. As ABO group has a major role in determining VWF levels, if the VWF stroke association is causal, blood groups should be associated with stroke (Mendelian Randomisation). ABO genotype frequencies in stroke patients were investigated by a case-control study (503 objectively diagnosed cases and 327 controls). Non-O groups were not significantly over-represented in stroke cases (OR 1.1, CI95 0.83--1.47). Monte Carlo method, taking into account ABO effect on VWF levels, showed no association between ABO genotypes and stroke risk. This was reinforced by the findings of the systematic review we conducted on ABO groups and stroke. In contrast to results obtained from venous TE systematic review, where almost a two fold increased risk was found with non-O groups vs. O group.
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Polasek, Ozren. « Investigating the role of human genome-wide heterozygosity as a health risk factor ». Thesis, University of Edinburgh, 2009. http://hdl.handle.net/1842/4799.

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Aim The aim of this study was to investigate the most commonly used approaches to measure individual genome-wide heterozygosity (IGWH) and to investigate whether IGWH can be considered as a health risk factor or a protective factor in humans. Methods This study was based on two samples from isolated communities of Croatian Adriatic islands, with a total of 1,930 adult examinees from Islands of Vis (N=986) and Korcula (N=944). Examinees were genotyped with a total of 302,662 single nucleotide polymorphisms. Heterozygosity was estimated using five commonly calculated methods. Results Correlation coefficients between different heterozygosity methods were generally in the range of 0.7-0.8. A worsening in some phenotypic traits, including cholesterol and triglycerides as well as increased odds for osteoporosis and metabolic syndrome was recorded in cases of IGWH reduction. Nevertheless, in these cases heterozygosity explained a relatively low amount of variance, generally in range of 0.4-0.6% of total trait variance. Conclusion However, these results were significant in Vis Island sample, while in the replication sample, Korcula Island, most of the associations were not significant, possibly due to the overall lower amount of inbreeding and higher heterozygosity in Korcula Island sample. The results warrant further research in order to provide more information on the extent and importance of individual genome-wide heterozygosity, which might have an important role in communities which experience consanguinity on a greater scale. Two main shortcomings of the study include possible lack of power to detect inbreeding depression and the need to replicate the results in other populations.
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Livres sur le sujet "Genetic risk factor"

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

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

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

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

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

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Garte, Seymour J. Genetic susceptibility to cancer. Boston : Kluwer Academic, 1998.

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Symposium on Phenotypic Variation in Populations : Relevance to Risk Assessment (1986 Brookhaven National Laboratory). Phenotypic variation in populations : Relevance to risk assessment. New York : Plenum Press, 1988.

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

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Young, Ian D. Introduction to risk calculation in genetic counseling. 2e éd. Oxford [England] : Oxford University Press, 1999.

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Chapitres de livres sur le sujet "Genetic risk factor"

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

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Astermark, Jan. « Genetic and Environmental Risk Factors for Factor VIII Inhibitor Development ». Dans Textbook of Hemophilia, 48–52. Oxford, UK : John Wiley & Sons, Ltd, 2014. http://dx.doi.org/10.1002/9781118398258.ch6.

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Berg, Kåre. « Lp(a) Lipoprotein : A Monogenic Risk Factor for Cardiovascular Disease ». Dans Genetic factors in coronary heart disease, 275–87. Dordrecht : Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1130-0_18.

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Friedlander, Yechiel. « Familial Clustering of Coronary Heart Disease : A Review of its Significance and Role as a Risk Factor for the Disease ». Dans Genetic factors in coronary heart disease, 37–53. Dordrecht : Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1130-0_3.

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Gonchar, Alexander, Maxim Ameliyanovich, Kristina Zhur, Irma Mosse et Konstantin Mosse. « Molecular-Genetic Analysis of Genetic Predisposition to Myocardial Infarction and Comparison of Risk Factor Population Rates in Different Countries ». Dans Radiobiology and Environmental Security, 111–25. Dordrecht : Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-1939-2_11.

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Poirier, Judes. « Apolipoprotein E4 : From synaptic remodeling to genetic risk factor in both familial and sporadic Alzheimer’s disease ». Dans Alzheimer : 100 Years and Beyond, 289–94. Berlin, Heidelberg : Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/978-3-540-37652-1_37.

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Zheng, Wei. « Genetic Polymorphisms in the Transforming Growth Factor-β Signaling Pathways and Breast Cancer Risk and Survival ». Dans Methods in Molecular Biology, 265–77. Totowa, NJ : Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-492-0_11.

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Thiriet, Marc. « Genetic Risk Factors ». Dans 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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Kronenberg, Florian. « Lipoprotein(a) ». Dans Prevention and Treatment of Atherosclerosis, 201–32. Cham : Springer International Publishing, 2021. http://dx.doi.org/10.1007/164_2021_504.

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AbstractLipoprotein(a) [Lp(a)] is an atherogenic lipoprotein with a strong genetic regulation. Up to 90% of the concentrations are explained by a single gene, the LPA gene. The concentrations show a several-hundred-fold interindividual variability ranging from less than 0.1 mg/dL to more than 300 mg/dL. Lp(a) plasma concentrations above 30 mg/dL and even more above 50 mg/dL are associated with an increased risk for cardiovascular disease including myocardial infarction, stroke, aortic valve stenosis, heart failure, peripheral arterial disease, and all-cause mortality. Since concentrations above 50 mg/dL are observed in roughly 20% of the Caucasian population and in an even higher frequency in African-American and Asian-Indian ethnicities, it can be assumed that Lp(a) is one of the most important genetically determined risk factors for cardiovascular disease.Carriers of genetic variants that are associated with high Lp(a) concentrations have a markedly increased risk for cardiovascular events. Studies that used these genetic variants as a genetic instrument to support a causal role for Lp(a) as a cardiovascular risk factor are called Mendelian randomization studies. The principle of this type of studies has been introduced and tested for the first time ever with Lp(a) and its genetic determinants.There are currently no approved pharmacologic therapies that specifically target Lp(a) concentrations. However, some therapies that target primarily LDL cholesterol have also an influence on Lp(a) concentrations. These are mainly PCSK9 inhibitors that lower LDL cholesterol by 60% and Lp(a) by 25–30%. Furthermore, lipoprotein apheresis lowers both, Lp(a) and LDL cholesterol, by about 60–70%. Some sophisticated study designs and statistical analyses provided support that lowering Lp(a) by these therapies also lowers cardiovascular events on top of the effect caused by lowering LDL cholesterol, although this was not the main target of the therapy. Currently, new therapies targeting RNA such as antisense oligonucleotides (ASO) or small interfering RNA (siRNA) against apolipoprotein(a), the main protein of the Lp(a) particle, are under examination and lower Lp(a) concentrations up to 90%. Since these therapies specifically lower Lp(a) concentrations without influencing other lipoproteins, they will serve the last piece of the puzzle whether a decrease of Lp(a) results also in a decrease of cardiovascular events.
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Thimm, F., et G. Fleckenstein-Grün. « Potentiation of the Age-Dependent Ca Uptake into Coronary Arteries of Rats by the Risk Factor Genetic Hypertension ». Dans Advances in Experimental Medicine and Biology, 489–93. Boston, MA : Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0333-6_62.

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Actes de conférences sur le sujet "Genetic risk factor"

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Kulkarni, S., X. Zhou, M. Nesline, C. Murekeyisoni, N. Watroba, M. Berry, W. Davis, C. Ambrosone et Y. Zheng. « Genetic Susceptibility as a Possible Risk Factor for Breast Cancer. » Dans Abstracts : Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009 ; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-6067.

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MOTSINGER, ALISON A., BRIAN S. DONAHUE, NANCY J. BROWN, DAN M. RODEN et MARYLYN D. RITCHIE. « RISK FACTOR INTERACTIONS AND GENETIC EFFECTS ASSOCIATED WITH POST-OPERATIVE ATRIAL FIBRILLATION ». Dans Proceedings of the Pacific Symposium. WORLD SCIENTIFIC, 2005. http://dx.doi.org/10.1142/9789812701626_0054.

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Dooper, Marten. « Nitric oxide synthase genetic variant is a risk factor for suicidal behaviour ». Dans 35th ECNP Congress, sous la direction de Christina Dalla. Baarn, the Netherlands : Medicom Medical Publishers, 2022. http://dx.doi.org/10.55788/c63a9364.

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Ferreira, Nancy, Darley Ferreira et Thais Ferreira. « GENETIC EVALUATION OF MICROCALCIFICATIONS AS A PROGNOSTIC FACTOR ». Dans Abstracts from the Brazilian Breast Cancer Symposium - BBCS 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s2101.

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Introduction: Breast cancer is the most recurring type of cancer among women, with reduced mortality at an initial stage of lesion. From a radiological perspective, perceived microcalcifications may be associated with histological findings such as proliferative injuries with or without atypical features and ductal carcinoma in situ. Currently, percutaneous and vacuum biopsies allow for the correlation between anatomoradiological and identification of previous lesions and those that offer the risk of cancer. No biomarker has been established to predict the risk of cancer in women diagnosed with benign mammary disease. Doing so could strengthen the possibility of stratifying the individual risk of benign injuries for cancer. The platelet-derived growth factor receptor A (PDGFRA) plays its part in tumor oncogenesis, angiogenesis, and metastasis, and its activation is found in some kinds of cancer. In contrast, DNA methylation standards are initial changes to the development of cancer and may be helpful in its early identification, being regulated by a family of enzymes called DNMTs (DNA methyltransferase). Methods: The aim of this study was to evaluate the profile of BI-RADS® 4 and 5 mammary microcalcification women carriers and determine the level of the gene expression of possible molecular markers in 37 patients with mammary microcalcification (paraffin blocks) and 26 patients with breast cancer (fresh in RNA later tissue) cared for at the Hospital Barão de Lucena’s Mastology Ambulatory. Anatomoradiological aspects along with clinical findings have been evaluated , and percentage rates have been calculated. The PDGFRA and DNMTs (DMNT3a) gene expressions have been established using quantitative polymerase chain reaction (qPCR), with the use of β-actin as reference gene. Discussion: In the patients with mammary microcalcification, the average age was 55.9; predominantly whiteskinned subjects (p<0.014). Most of them were mothers (p<0.001), and the average menarche age was 13. The subgroups that presented greater significance were patients classified BI-RADS® in category IV (67.6%) and histological findings of nonproliferative lesion (p<0.001). Lesions of the ductal carcinoma in situ type (100%) presented positive estrogen and progesterone receptors, and 94.6% have undergone sectorectomy surgery by prior needling (p<0.001). The most damaged breast was the left one (62.2%), and the most affected quadrant was the top lateral one (59.5%) (p<0.001). There was no family history in 83.8% of the cases. In the tested microcalcification samples, it was not possible to observe the expression of PDGFRA. Nevertheless, 15 out of 37 patients with microcalcification showed an increase in the gene expression of DMNT3a, most of them greater than Luminal and triple-negative cancer types. Conclusion: The data presented here highlight the improvement on the description of BI-RADS® 4 subclassification in order to better conduct the clinical decision and also demonstrated the potential of DNMTs evaluation in microcalcification samples as a strategy to access the understanding about the role of these molecules in the breast cancer development.
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Surniyantoro, H. N. E., et N. R. Hidayati. « Preliminary study in genetic polymorphism of hOGG1 and risk factor for thyroid cancer in Indonesia ». Dans PROCEEDINGS OF THE INTERNATIONAL CONFERENCE AND SCHOOL ON PHYSICS IN MEDICINE AND BIOSYSTEM (ICSPMB) : Physics Contribution in Medicine and Biomedical Applications. AIP Publishing, 2021. http://dx.doi.org/10.1063/5.0047941.

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Batai, Ken, Ebony Shah et Rick A. Kittles. « Abstract B14 : Population genetics analysis of prostate cancer GWAS SNPs to evaluate West African genetic ancestry as a risk factor ». Dans Abstracts : Sixth AACR Conference : The Science of Cancer Health Disparities ; December 6–9, 2013 ; Atlanta, GA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7755.disp13-b14.

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Allam, Ines, Aldjia Lamri, Sihem Oulacrouz, Mohamed Saidani et Reda Djidjik. « P85 The IRF5 (rs729302) polymorphism is a genetic risk factor for systemic lupus erythematosus in Algerian patients ». Dans 12th European Lupus Meeting. Lupus Foundation of America, 2020. http://dx.doi.org/10.1136/lupus-2020-eurolupus.130.

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Anghel, Lucretia, Dumitru Ursu, Simona Mitincu Caramfil, Cristina Stefanescu, Stefana Maria Moisa, Anamaria Ciubara et Liliana Baroiu. « THE LINK BETWEEN LIPIDIC PROFILE, DEPRESSION AND CARDIOVASCULAR DISEASE ». Dans The European Conference of Psychiatry and Mental Health "Galatia". Archiv Euromedica, 2023. http://dx.doi.org/10.35630/2022/12/psy.ro.17.

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The purpose of this study was to identify the connection between cardiovascular disease and depression taking lipid profile as a common risk factor in the occurrence of both pathologies. Materials and methods: 100 patients were examined for 3 months, admitted to the internal medicine department of St. Andrew's Emergency Hospital in Galati. Anamnesis was collected; electrocardiogram, objective examination and lipid profile were performed. The Hamilton scale (HDRS-17) was used to assess depression. Results: In patients with depression, an increased prevalence of dyslipidaemia and obesity was detected, especially in women. Of 10 women with mild and severe depression, all had altered lipid profile, obesity or overweight and increased risk of cardiovascular disease. Conclusions: Although it is claimed that depression would be an individual risk factor for the occurrence of an adverse cardiac event, the comprehensive pathophysiological approach allows the identification of risk factors for both CVD and depression as being largely common. Therefore, a coexistence relationship is created. The other possible situations may arise due to the involvement of individual protective factors and genetic vulnerability. As a result, treatment of depression may reduce risk of cardiovascular event in some cases.
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Smyk, W., R. Hall, S. Weber, F. Grünhage, F. Lammert et M. Krawczyk. « Common genetic variant c.711A>T in the hepatobiliary phospholipid translocator ABCB4 as risk factor for liver fibrosis ». Dans 36. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3402121.

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Finlen Copeland, Catherine, Francine L. Kelly, Laurie D. Snyder et Scott M. Palmer. « Clinical And Genetic Predictors Of Pulmonary Aspergillus Infection, A Major Risk Factor For Bronchiolitis Obliterans Syndrome After Lung Transplantation ». Dans 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.a2570.

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Rapports d'organisations sur le sujet "Genetic risk factor"

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

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Cao, Xianling, Xuanyou Zhou, Naixin Xu, Songchang Chang et 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, avril 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. Genetics Risk Factor for Prostate Cancer. Fort Belvoir, VA : Defense Technical Information Center, janvier 2004. http://dx.doi.org/10.21236/ada422932.

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

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Eshed-Williams, Leor, et Daniel Zilberman. Genetic and cellular networks regulating cell fate at the shoot apical meristem. United States Department of Agriculture, janvier 2014. http://dx.doi.org/10.32747/2014.7699862.bard.

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The shoot apical meristem establishes plant architecture by continuously producing new lateral organs such as leaves, axillary meristems and flowers throughout the plant life cycle. This unique capacity is achieved by a group of self-renewing pluripotent stem cells that give rise to founder cells, which can differentiate into multiple cell and tissue types in response to environmental and developmental cues. Cell fate specification at the shoot apical meristem is programmed primarily by transcription factors acting in a complex gene regulatory network. In this project we proposed to provide significant understanding of meristem maintenance and cell fate specification by studying four transcription factors acting at the meristem. Our original aim was to identify the direct target genes of WUS, STM, KNAT6 and CNA transcription factor in a genome wide scale and the manner by which they regulate their targets. Our goal was to integrate this data into a regulatory model of cell fate specification in the SAM and to identify key genes within the model for further study. We have generated transgenic plants carrying the four TF with two different tags and preformed chromatin Immunoprecipitation (ChIP) assay to identify the TF direct target genes. Due to unforeseen obstacles we have been delayed in achieving this aim but hope to accomplish it soon. Using the GR inducible system, genetic approach and transcriptome analysis [mRNA-seq] we provided a new look at meristem activity and its regulation of morphogenesis and phyllotaxy and propose a coherent framework for the role of many factors acting in meristem development and maintenance. We provided evidence for 3 different mechanisms for the regulation of WUS expression, DNA methylation, a second receptor pathway - the ERECTA receptor and the CNA TF that negatively regulates WUS expression in its own domain, the Organizing Center. We found that once the WUS expression level surpasses a certain threshold it alters cell identity at the periphery of the inflorescence meristem from floral meristem to carpel fate [FM]. When WUS expression highly elevated in the FM, the meristem turn into indeterminate. We showed that WUS activate cytokinine, inhibit auxin response and represses the genes required for root identity fate and that gradual increase in WUCHEL activity leads to gradual meristem enlargement that affect phyllotaxis. We also propose a model in which the direction of WUS domain expansion laterally or upward affects meristem structure differently. We preformed mRNA-seq on meristems with different size and structure followed by k-means clustering and identified groups of genes that are expressed in specific domains at the meristem. We will integrate this data with the ChIP-seq of the 4 TF to add another layer to the genetic network regulating meristem activity.
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Chejanovsky, Nor, Diana Cox-Foster, Victoria Soroker et Ron Ophir. Honeybee modulation of infection with the Israeli acute paralysis virus, in asymptomatic, acutely infected and CCD colonies. United States Department of Agriculture, décembre 2013. http://dx.doi.org/10.32747/2013.7594392.bard.

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Honey bee (Apis mellifera) colony losses pose a severe risk to the food chain. The IAPV (Israeli acute paralysis virus) was correlated with CCD, a particular case of colony collapse. Honey bees severely infected with IAPV show shivering wings that progress to paralysis and subsequent death. Bee viruses, including IAPV, are widely present in honey bee colonies but often there are no pathological symptoms. Infestation of the beehive with Varroa mites or exposure to stress factors leads to significant increase in viral titers and fatal infections. We hypothesized that the honey bee is regulating/controlling IAPV and viral infections in asymptomatic infections and this control is broken through "stress" leading to acute infections and/or CCD. Our aims were: 1. To discover genetic changes in IAPV that may affect tissue tropism in the host, and/or virus infectivity and pathogenicity. 2. To elucidate mechanisms used by the host to regulate/ manage the IAPV-infection in vivo and in vitro. To achieve the above objectives we first studied stress-induced virus activation. Our data indicated that some pesticides, including myclobutanil, chlorothalonil and fluvalinate, result in amplified viral titers when bees are exposed at sub lethal levels by a single feeding. Analysis of the level of immune-related bee genes indicated that CCD-colonies exhibit altered and weaker immune responses than healthy colonies. Given the important role of viral RNA interference (RNAi) in combating viral infections we investigated if CCD-colonies were able to elicit this particular antiviral response. Deep-sequencing analysis of samples from CCD-colonies from US and Israel revealed high frequency of small interfering RNAs (siRNA) perfectly matching IAPV, Kashmir bee virus and Deformed wing virus genomes. Israeli colonies showed high titers of IAPV and a conserved RNAi pattern of targeting the viral genome .Our findings were further supported by analysis of samples from colonies experimentally infected with IAPV. Following for the first time the dynamics of IAPV infection in a group of CCD colonies that we rescued from collapse, we found that IAPV conserves its potential to act as one lethal, infectious factor and that its continuous replication in CCD colonies deeply affects their health and survival. Ours is the first report on the dominant role of IAPV in CCD-colonies outside from the US under natural conditions. We concluded that CCD-colonies do exhibit a regular siRNA response that is specific against predominant viruses associated with colony losses and other immune pathways may account for their weak immune response towards virus infection. Our findings: 1. Reveal that preventive measures should be taken by the beekeepers to avoid insecticide-based stress induction of viral infections as well as to manage CCD colonies as a source of highly infectious viruses such as IAPV. 2. Contribute to identify honey bee mechanisms involved in managing viral infections.
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