Top PDF Genetic evidence for the association between the early growth response 3 (EGR3) gene and schizophrenia.

Genetic evidence for the association between the early growth response 3 (EGR3) gene and schizophrenia.

Genetic evidence for the association between the early growth response 3 (EGR3) gene and schizophrenia.

[6,46,47,48,49]. Induction of EGR3 by BDNF enables EGR3 to control the expression of Gamma-aminobutyric acid receptor (GABAR) [50], which is also a candidate risk gene for the schizophrenia [51]. In addition to being downstream and upstream of susceptibility genes, EGR3 has been linked to a number of miRNAs that have been associated with schizophrenia. MiRNAs are a class of non- coding small RNAs that negatively regulate gene expression in numerous biological processes by promoting mRNA degradation and/or repressing translation through sequence-specific interac- tions with the 3 9 UTRs of target mRNAs [52,53]. The miR-15 family was reported to be significantly up-regulated in the cerebral cortex of schizophrenia patients and was therefore hypothesized to have a biological influence in the cortex of schizophrenia patients by influencing genes involved in cortical structure and neural plasticity [54]. EGR3 is one of the targets genes for miR-15 family as predicated by the Miranda (http:// www.microrna.org/microrna/home.do) and TargetScan (http:// www.targetscan.org/) websites, consistent with the findings of elevated expression of miRNAs and decreased expression of EGR3 in schizophrenia patients. Guo et al. proposed a model highlighting EGR3 and miRNAs involved in signaling pathways and regulatory networks in the nervous system [55]. Further exploration regarding functional relationship between miR-15 family and EGR3 gene involved in the pathogenesis of schizophrenia will be worthwhile.
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Association between the c.910A.G genetic variant of the XRCC1 gene and susceptibility to esophageal cancer in the Chinese Han population

Association between the c.910A.G genetic variant of the XRCC1 gene and susceptibility to esophageal cancer in the Chinese Han population

EC is a common and polygenic malignant cancer caused by complex interactions between genetic and environmental factors. It is a global health problem. A large number of studies have been conducted on genetic variants of candidate genes that play key roles in the pathogenesis of EC (8,14,15). In the present study, the influence of the c.910A.G genetic variant of the XRCC1 gene on EC risk was evaluated by association analysis in 383 EC patients and 387 cancer-free Chinese subjects with Han ethnicity. Our data indicated that the distribu- tions of allele and genotype frequencies in EC patients were significantly different from those of cancer-free controls (all P values ,0.05; Table 2). The genotype GG was statistically associated with increased EC risk compared with genotype AA and AG/AA carriers (all P values ,0.05; Table 3). Compared with allele A, allele G might be an increased genetic risk factor for EC. Results from this study provided more evidence of the role of the XRCC1 gene in the development of EC and suggested that the c.910A.G genetic variant of the XRCC1 gene was statistically associated with EC risk in the Chinese Han population; therefore, this variant could be used as a
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Identification of G1-regulated genes in normally cycling human cells.

Identification of G1-regulated genes in normally cycling human cells.

Next, we examined stress-response gene activity among those known genes which could be considered pertinent to our selection method, gene products associated with mechanical stress. Researchers have identified genes activated under various types of mechanical stress [31–33,44]. Examination of the stress- response gene datasets from the array experiments clearly shows there is no association between stress-response gene activity and the mitotic shake-off method, either in the early time period (2 hours) following selection (shake 2) or throughout the first 14 hours of a new cell cycle (shake 1). We then examined a set of well-characterized genes that were identified as being activated in serum starved cells, in response to serum stimulation [7]. With the exception of CTGF, this gene set did not show any significant increase in gene activity in our experiments (Fig. 4A, B). We suggest that CTGF upregulation is probably not indicative of cellular stress activity. CTGF is a growth factor and one possible explanation to its upregulation late in early G1 (shake 2) is likely due to its involvement in signaling pathways essential for cells to progress in the cell cycle, and particularly beyond G1. The exact role of CTGF in the cell cycle is not completely understood. One study showed that use of anti-sense approach against CTGF reversed angiotensin II-induced renal hypertrophy by releasing renal cells from angiotensin II-induced G0–G1 arrest [49]. In contrast, CTGF was shown to be a mediator of diabetic nephropathy by inducing re-entry into G1 phase [50]. Further, CTGF is an important regulator of fibroblast proliferation in connective tissue in late G1 and into S phase [51]. Clearly the function of CTGF is dependent on cell type or disease state, and our microarray data in unperturbed synchronized cells shows that further experiments are needed to elucidate the function of CTGF in G1 and whether it is required for progression into a new cell cycle.
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Population-specific haplotype association of the postsynaptic density gene DLG4 with schizophrenia, in family-based association studies.

Population-specific haplotype association of the postsynaptic density gene DLG4 with schizophrenia, in family-based association studies.

The first two stages were analyzed in a family-based design and the third stage analysis was performed in an unrelated case-control design. The family-based genetic associations were tested using the Family-Based Association Test (FBAT) v2.0.3 program (http:// www.biostat.harvard.edu/˜fbat/) for SNPs, and hbat command in the same program for haplotype based association testing. The computation was performed using the Monte Carlo simulation with 100,000 replications. Correction for multiple testing on the single markers and haplotypes was performed using the false discovery rate method [35], scripted in R (http://www.r-project. org/). In the third stage analysis of the case-control replication cohort, Fisher’s exact test (two-tailed) was used to compare allele frequencies between patients and control subjects. Statistical differences in genotype distributions were evaluated using Pearson’s x 2 test. The linkage disequilibrium (LD) pattern was plotted for genotyped SNPs using Haploview 4.2 (http://www. broadinstitute.org/science/programs/medical-and-population- genetics/haploview/version-42-15-september-2009) and haplo- type analysis was performed using Unphased 3.1.5 (http:// sourceforge.net/projects/unphased/files/unphased-3.1.5.zip/ download) with 10,000 permutations for deriving empirical significance. To detect significant changes in target gene expression levels among the cases and controls, t-test analysis, followed by Bonferroni correction was used. P values of ,0.05 were considered significant in this study.
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Association of PDE4B Polymorphisms with Susceptibility to Schizophrenia: A Meta-Analysis of Case-Control Studies.

Association of PDE4B Polymorphisms with Susceptibility to Schizophrenia: A Meta-Analysis of Case-Control Studies.

What is important, a genome-wide linkage analysis [18] in ethnically homogeneous pedi- grees has provided strong evidence for schizophrenia risk locus on chromosome 1p31.1, to which the nearest schizophrenia candidate gene is PDE4B. Additionally, they identified 14 SNPs of PDE4B gene associated with schizophrenia under a nominal P value of 0.05 [18]. Indeed, there have been accumulating studies investigating association of PDE4B variations with predisposition to schizophrenia across multi-ethnic populations, including Caucasian populations (Europeans [19–21], Caucasian Canadians [22] and Caucasian Americans [23]), Asian populations (Indians [18], Japanese [24], Chinese [25] and Koreans [26]), and African populations (African Americans [23]). The only meta-analysis concerning the association of PDE4B SNPs and schizophrenia was taken in Bae’s study[26], which just combined Korean population in their own study and Japanese population in Numata’s study[24]. Another limita- tion of their meta-analysis is that it merely involves rs1040716 under dominant model and rs599381, rs2180335 and rs472952 under co-dominant model. Therefore, to better facilitate our interpretation of PDE4B SNPs as risk factors for schizophrenia and comprehensively evalu- ate the association between diverse SNPs and schizophrenia, we conducted this meta-analysis of published case-control studies across multi-ethnic populations under multi-genetic models.
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ACE I/D gene polymorphism can't predict the steroid responsiveness in Asian children with idiopathic nephrotic syndrome: a meta-analysis.

ACE I/D gene polymorphism can't predict the steroid responsiveness in Asian children with idiopathic nephrotic syndrome: a meta-analysis.

The genetic origin of renal diseases had been a focus of research in the past years; and some investigations found that the genetic alteration could become an early diagnosis indicator to predict the onset of some diseases [32,33,34]. There were some significant evidences showing that the RAS had taken part in the onset of some renal diseases [9,10,11,12]. The level of plasma ACE, constitutively expressed in several types of somatic cells, is linked to an I/D polymorphism of 287 bp in intron 16 of the ACE gene [35,36,37]. D allele and DD homozygous have been reported to be associated with higher plasma ACE level [6,16]. ACE is an important enzyme of RAS which can convert inactive angiotensin I into a vasoactive and aldosterone-stimulating peptide angiotensin II [38,39]. The increased ACE protein expression is responsible for the elevation of plasma angiotensin II level [40]. So, D allele or DD homozygous might be an important molecular marker for early diagnosis of the onset of SRNS or SSNS. Most of the studies, investigating the association between ACE I/D gene polymor- phism and the response to steroid treatment, were performed in Asian children with INS and tried to explore whether the ACE I/ D gene polymorphism could become an early diagnosis indicator to predict the treatment response to steroid. However, data were insufficient. Furthermore, findings on the association of ACE I/D gene polymorphism with the susceptibility of SRNS or SSNS have been controversial since the first investigation was reported. In this study, we investigated whether the ACE I/D gene polymorphism could become a valuable indicator to predict the treatment response to steroid in Asian children with INS and tried to draw a more credible conclusion by meta-analysis.
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Rev. Nutr.  vol.29 número1

Rev. Nutr. vol.29 número1

Genotyping of the rs7895833 (A/G) polymorphism was performed in 200 subjects (100 MetS and 100 non-MetS) by Polymerase Chain Reaction using the Amplification Refractory Mutation System (PCR-ARMS), 43 samples were excluded because they were not amplified. The primers were designed using the Gene Runner software, version 3.05 (Hastings Software, Inc., San Francisco, California, United States). A common reverse primer (5’-CATCTGTGTATCCCC TAGAAAGT-3’) and two forward allele-specific primers that amplify two allele-specific regions were used: A allele - 5’-GGTGGTAAAAGGCCTA CAGGACA-3’, and G allele - 5’-GGTGGTAAAAG GCCTACAGGACG-3’ (299-bp amplicon). Control primers were used for single nucleotide polymerase co-amplification of a portion of the β-globin gene 23 . These primers served as an internal
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Recycled materials for the investment casting process

Recycled materials for the investment casting process

W artykule przedstawiono najprostsz ą metodę wykorzystania materiałów woskowych odpadowych, które w rzeczywisto ci są dobr ą mieszaniną wosków Castylene B405 (około 70%) [2], KC 4017B (około 15%) [3] i A7-FR/60 (około 15%) [4]. W bada- niach zastosowano mieszank ę odpadową po dodaniu do parafiny i stearyny, któr ą porównano z woskiem Blaysona A7-FR/60 oraz stosowan ą w odlewni krajowej mieszanką PSW p (Parafina 70%,

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Genetic variants of EGF and VEGF predict prognosis of patients with advanced esophageal squamous cell carcinoma.

Genetic variants of EGF and VEGF predict prognosis of patients with advanced esophageal squamous cell carcinoma.

The rs4444903 SNP, localized at position 61 in the 59- untranslated region (59UTR) of EGF, has been found to be correlated with production level of EGF measured in peripheral- blood mononuclear cells in-vitro [35]. Meanwhile, rs2010963 at the 59-UTR of VEGF has also been suggested to modulate VEGF level [36]. We then investigated whether the genetic polymor- phisms within the 59UTR were associated with expression levels of EGF or VEGF. We randomly selected 115 subjects from these patients. The levels of EGF and VEGF in the serum of each patient were determined by ELISA. As expected, homozygous GG carriers of rs4444903 showed a trend of increased EGF level compared with AA carriers (Fig. 2A, T-test P = 0.136). However, we did not find an association between the genotypes of rs2010963 and serum VEGF level (Fig. 2B, T-test P = 0.395 for CG vs. GG and P = 0.504 for CC vs. GG). We further observed the impact of EGF and VEGF on the clinical outcome of patients. Kaplan- Meier survival analysis revealed that the group with detectable levels of EGF had a significantly increased risk of death compared to the group with undetectable levels (MST = 36.92 vs. 9.12 months, log-rank P = 0.010, Fig. 2C). A similar result was observed in the VEGF analysis. Patients with detectable VEGF showed an increased risk for poor prognosis (MST = 13.48 vs. 8.85 months, log-rank P = 0.001, Fig. 2D). Finally, the logistic regression model also demonstrated that patients with detectable VEGF exhibited a higher risk of death as well as recurrence ([OR] = 1.89, 95% CI = 1.22–2.92, P = 0.005 for death; [OR] = 1.57, 95% CI = 1.04– 2.38, P = 0.032 for recurrence; see Table S2).
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Carlos Carvalho Niels Arne Dam Jae Won Lee

Carlos Carvalho Niels Arne Dam Jae Won Lee

We use a standard sticky-price model to provide evidence on three mechanisms that can reconcile somewhat frequent price changes with large and persistent real e¤ects of monetary shocks. To that end, we estimate a semi-structural model for the U.S. economy that allows for varying degrees of real rigidities, and cross-sectional heterogeneity in price stickiness. The model can extract some information about these two features of the economy from aggregate data, and discriminate between di¤erent distributions of price stickiness. Hence it can also speak to the debate about the role of sales and other temporary price changes in shaping the e¤ects of monetary policy. Employing a Bayesian approach, we combine macroeconomic time-series data with information about empirical distributions of price stickiness derived from micro price data for the U.S. economy. Our estimates point to the presence of both large real rigidities and an important degree of heterogeneity in price stickiness. Moreover, cross-sectional distributions of price stickiness that factor out sales improve the empirical …t of the model. Our results suggest that bridging the gap between micro and macro evidence on nominal price rigidity may require the combination of several mechanisms.
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Bank Privatization and Market Structure of the Banking Industry: Evidence from a Dynamic Structural Model

Bank Privatization and Market Structure of the Banking Industry: Evidence from a Dynamic Structural Model

a Dynamic Structural Model”. We are indebted to Martin Pesendorfer for his support and guidance during this project. We would like to thank Dimitri Szerman for the help with the data and for insightful comments on several versions of this draft. Robinson Silva helped us to organize the data. We also benefited from discussions with Bernardo Guimarães, Bruno Rocha, Emmanuel Guerre, Fabio Pinna, Francesco Caselli, Francisco Costa, Gabriel Garber, Jason Garred, Joachim Groeger, Johannes Spinnewijn, Maitreesh Ghatak, Matthew Gentry, Michael Dickstein, Panle Jia, Pasquale Schiraldi, Pedro Carvalho, Robert Miller and Tim Besley. Fabio gratefully acknowledges the financial support from CAPES (Brazilian Ministry of Education) and Daniel gratefully acknowledges the support from CNPQ (Brazilian Ministry of Science and Technology). The usual disclaimer applies.
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Systematic review of evidence on the association between personality and tinnitus

Systematic review of evidence on the association between personality and tinnitus

Objective: To assess the scientific evidence of the association between tinnitus and personality. Methods: A systematic review of the following databases: PubMed, SciELO, LILACS, and Web of Knowledge. Only studies of patients older than 18 years published in English, Portuguese, or Spanish that established an association between tinnitus and personality were selected. Results: Seventeen of the 77 articles found were selected: 13 cross-sectional studies, two lon- gitudinal studies, one validation study, and one birth cohort study. The samples ranged from 27 to 970 patients.
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Estudos de associação entre transtorno obsessivo-compulsivo e genes candidatos: uma revisão.

Estudos de associação entre transtorno obsessivo-compulsivo e genes candidatos: uma revisão.

Objective: The obsessive compulsive-disorder (OCD) is a psychiatric disorder characterized by the presence of obsessions and compulsions. ,WVSUHYDOHQFHLVRIDSSUR[LPDWHO\LQWKHJHQHUDOSRSXODWLRQ,QWKH last years, genes of the serotoninergic and dopaminergic systems have been investigated as these neurotransmitters are probably involved in the pathophysiology of the OCD. This article aims at revising the results of studies of association between candidate genes and OCD. Methods: Review of the literature in the Medline database until August of 2006, using the key words: obsessive-compulsive disorder, OCD and/or gene(s), polymorphism(s), genetics. Results: A series of studies presented negative results when comparing OCD patients and controls. Nevertheless, positive results have been observed, when studying among OCD patients, distinct clinical features (gender, age of beginning, dimension and/or severity of the obsessive and/or compulsive symptoms, presence of tics). Conclusion: For the advance of genetic studies in OCD, it would be necessary to identify homogeneous subgroups of OCD patients. Based on these subgroups, LWPD\EHSRVVLEOHWRGH¿QHUHOLDEOHHQGRSKHQRW\SHVWKDWFRXOGOHDGWRD more rational search for genes possibly involved in OCD pathogenesis. Key words: obsessive-compulsive disorder, genes, polymorphism.
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Early trauma, attachment experiences and comorbidities in schizophrenia

Early trauma, attachment experiences and comorbidities in schizophrenia

Methods: Twenty patients diagnosed with schizophrenia according to criteria from the Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5) underwent retrospective symptom assessment and careful assessment of the number and manner of childhood caregiver changes. The Diagnostic Interview for Psychosis and Affective Disorders (DI-PAD) was used to assess symptoms related to schizophrenia (positive and negative symptoms), depression and mania. Anxiety disorder comorbidities were assessed by the Liebowitz Social Anxiety Scale (LSAS), Yale-Brown Obsessions and Compulsions Scale (Y-BOCS) and Panic and Schizophrenia Interview (PaSI). Experience in Close Relationships – Relationship Structures (ECR-RS) and Early Trauma Inventory Self Report-Short Form (ETISR-SF) were used to assess attachment patterns and traumatic history, respectively. Results: Moderate and significant correlations between attachment patterns and early trauma showed that greater severity of anxious attachment was predicted by a higher frequency of total early traumas (Spearman ρ = 0.446, p = 0.04), mainly general traumas (ρ = 0.526, p = 0.017; including parental illness and separation, as well as natural disaster and serious accidents). Among the correlations between early trauma and comorbid symptoms, panic attacks occurring before the onset of schizophrenia showed significant and positive correlations with ETISR-SF total scores and the sexual trauma subscale.
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Association between ST8SIA2 and the Risk of Schizophrenia and Bipolar I Disorder across Diagnostic Boundaries.

Association between ST8SIA2 and the Risk of Schizophrenia and Bipolar I Disorder across Diagnostic Boundaries.

In the present study, we found suggestive associations between ST8SIA2 and schizophrenia and BD-I in the Korean population. Through fine mapping of the gene with tag SNPs and additional candidate SNPs, we identified 14 associated variants with at least a nominal level of significance in a diagnostic group, however none of them survived after multiple testing correc- tion; these association trends were strongest in the combined schizophrenia and BD-I group. The strongest association was observed between rs11637898 and schizophrenia and BD-I under the dominant model, and the association with combined schizophrenia and the BD-I group remained significant after correcting for multiple testing. These results are consistent with a previous study of the Australian population revealing an association trend between several SNPs in ST8SIA2 and BD [15]. Two of these SNPs (rs11637898 and rs2168351) over- lapped with SNPs showing association signals in the present study. Consistency between the two studies was also observed for two more pairs of SNPs with high linkage disequilibrium, i.e., rs4777980–rs11074070 and rs8037133–rs3784735. Fig 2 presents the relative positions of the ST8SIA2 SNPs that have been studied in schizophrenia and/or BD.
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Association between the Growth Hormone Receptor Exon 3 Polymorphism and Metabolic Factors in Korean Patients with Acromegaly

Association between the Growth Hormone Receptor Exon 3 Polymorphism and Metabolic Factors in Korean Patients with Acromegaly

this study was described as following; first, a diagnosis of ac- romegaly was established by documenting an elevated IGF-1 level in combination with failure of GH to suppress after oral glucose to below 0.3 µg/L [15] and second, patients was con- firmed by pathological examination of surgically resected tis- sues. We excluded patients with any medication which can af- fect their obese state (e.g., oral pills, herbal medication, lipid lowering agents). All patients agreed to participate in the Ko- rean Genomic Cohort Study and provided written informed consent for the investigation. The study protocol was approved by the Institutional Review Board of Kyungpook National University Hospital.
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Genetic Variations in Pattern Recognition Receptor Loci Are Associated with Anti-TNF Response in Patients with Rheumatoid Arthritis.

Genetic Variations in Pattern Recognition Receptor Loci Are Associated with Anti-TNF Response in Patients with Rheumatoid Arthritis.

In this cohort of RA patients, there were marked clinical differences between the seroposi- tive and seronegative subgroups (fraction of smokers, erosive status, age, baseline tender joint count, pain and patient global score), and this could potentially cause confounding. However, additional multivariate regression analysis adjusting for these potential confounders did not markedly change the significance levels or effect sizes for the RF status-stratified analyses of CARD8 (rs2043211), IFNGR2 (rs17882748), IL12B (rs6887695), IL18 (rs187238, rs360719), TLR5 (rs5744174) or TLR1 (rs4833095) (S6 Table).
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REVIEW_AN INTERDISCIPLINARY APPROACH TO THE RELATIONSHIP BETWEEN MASS-MEDIA AND DEMOCRACY IN POST-COMMUNIST ROMANIA

REVIEW_AN INTERDISCIPLINARY APPROACH TO THE RELATIONSHIP BETWEEN MASS-MEDIA AND DEMOCRACY IN POST-COMMUNIST ROMANIA

The events of 1989 helped Romanian mass-media to escape from the prison of censorship and conformism, of imposed but also self-imposed servitude. The changes happening in the political area also brought along a revolution of communication means. But not all was nice and good since in the new political framework, which featured a democracy in search of its own identity, the evolution of the mass-media also experienced such phenomena as the monopolisation of the public space, the cartelisation of the mass-media or the usage of media trusts as tools serving political interests.
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IGF-1, IGFBP-1, and IGFBP-3 polymorphisms predict circulating IGF levels but not breast cancer risk: findings from the Breast and Prostate Cancer Cohort Consortium (BPC3).

IGF-1, IGFBP-1, and IGFBP-3 polymorphisms predict circulating IGF levels but not breast cancer risk: findings from the Breast and Prostate Cancer Cohort Consortium (BPC3).

IGF-1 has been shown to promote proliferation of normal epithelial breast cells, and the IGF pathway has also been linked to mammary carcinogenesis in animal models. We comprehensively examined the association between common genetic variation in the IGF1, IGFBP1, and IGFBP3 genes in relation to circulating IGF-I and IGFBP-3 levels and breast cancer risk within the NCI Breast and Prostate Cancer Cohort Consortium (BPC3). This analysis included 6,912 breast cancer cases and 8,891 matched controls (n = 6,410 for circulating IGF-I and 6,275 for circulating IGFBP-3 analyses) comprised primarily of Caucasian women drawn from six large cohorts. Linkage disequilibrium and haplotype patterns were characterized in the regions surrounding IGF1 and the genes coding for two of its binding proteins, IGFBP1 and IGFBP3. In total, thirty haplotype- tagging single nucleotide polymorphisms (htSNP) were selected to provide high coverage of common haplotypes; the haplotype structure was defined across four haplotype blocks for IGF1 and three for IGFBP1 and IGFBP3. Specific IGF1 SNPs individually accounted for up to 5% change in circulating IGF-I levels and individual IGFBP3 SNPs were associated up to 12% change in circulating IGFBP-3 levels, but no associations were observed between these polymorphisms and breast cancer risk. Logistic regression analyses found no associations between breast cancer and any htSNPs or haplotypes in IGF1, IGFBP1, or IGFBP3. No effect modification was observed in analyses stratified by menopausal status, family history of breast cancer, body mass index, or postmenopausal hormone therapy, or for analyses stratified by stage at diagnosis or hormone receptor status. In summary, the impact of genetic variation in IGF1 and IGFBP3 on circulating IGF levels does not appear to substantially influence breast cancer risk substantially among primarily Caucasian postmenopausal women.
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The Concept of Early Vascular Ageing – An Update in 2015

The Concept of Early Vascular Ageing – An Update in 2015

Arterial ageing is a process that can be quantiied, at least to some degree, by measurement of pulse wave velocity along the aorta, the largest elastic artery, as a marker of arterial stifness. In recent years the new concept of early vascular ageing (EVA) has been developed by a group of mostly European researchers and some reviews have been published. Based on a lecture given at the European Association for the Study of Diabetes (EASD) Meeting in Vienna 2014, this review was written to describe recent developments in research dedicated to EVA and new emerging aspects found in studies of families at high cardiovascular (CV) risk. This brings new perspectives related to genetics, telomere biology, and the role of gut microbiota. Even if EVA has been described in general terms there is still no unifying deinition available and no direct treatment, only recommendations for conventional CV risk factor control. However, a new intervention study (SPARTE) is ongoing in France with a randomised design to treat arterial stifness in patients with hypertension versus conventional treatment strategies. Results are expected in a few years and will be of importance in deining the role of arterial stifness, a core feature of EVA, as a target for treatment.
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