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Growth factors and beta-tricalcium phosphate in the treatment of periodontal intraosseous defects: A systematic review and meta-analysis of randomised controlled trials.
Cãlin, C, Pãtraşcu, I
Archives of oral biology. 2016;:44-54
Abstract
OBJECTIVE To evaluate the effectiveness at different points in time, of recombinant human platelet-derived growth factor-BB (rhPDGF-BB) coated onto a beta-tricalcium phosphate (β-TCP) carrier compared to β-TCP alone, or to recombinant human growth/differentiation factor-5 (rhGDF-5) adsorbed onto a β-TCP scaffold in intraosseous periodontal defects. DESIGN A digital search for randomised controlled trials (RCTs) was conducted on MEDLINE/PubMed. The quality of reporting and the risk of bias of the included RCTs were assessed using the CONSORT guidelines and the Cochrane risk of bias tool. The difference between the means of the outcomes at baseline and at follow-up for each group was tested using the Student's t-test for paired samples. The difference between the means of the outcome changes at follow-up between groups was analysed using the Student's t-test for two independent samples. Prior to each analysis a test of homogeneity of variances (Ansari-Bradley) was performed. RESULTS From 11 articles assessed for eligibility, 5 RCTs were included in this review. The risk of bias was considered to be low in 2 articles, medium in 1 study and high in 2 studies. CONCLUSIONS In the treatment of periodontal intraosseous defects the application of rhPDGF-BB/β-TCP improved all outcomes when compared to β-TCP at 6 months follow-up. Either rhPDGF-BB/β-TCP or rhGDF-5/β-TCP seemed to provide similar results in terms of probing pocket depth (PPD) reduction and clinical attachment level (CAL) gain. The application of rhGDF-5/β-TCP resulted in a more pronounced reduction in gingival recession (GR) depth at 6 months follow-up compared to rhPDGF-BB/β-TCP.
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Associations Between Fetal Imprinted Genes and Maternal Blood Pressure in Pregnancy.
Petry, CJ, Sanz Marcos, N, Pimentel, G, Hayes, MG, Nodzenski, M, Scholtens, DM, Hughes, IA, Acerini, CL, Ong, KK, Lowe, WL, et al
Hypertension (Dallas, Tex. : 1979). 2016;(6):1459-1466
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Abstract
In addition to maternal genes and environmental exposures, variation in fetal imprinted genes could also affect maternal blood pressure during pregnancy. Our objective was to test the associations between polymorphic variants in 16 imprinted genes and maternal mean arterial blood pressures in 1160 DNA trios from 2 established birth cohorts (the Cambridge Baby Growth and Wellbeing Studies) and seek replication in 1367 Hyperglycemia and Adverse Pregnancy Outcome Study participants. Significant univariate associations, all independent of fetal sex, were observed in the Cambridge cohorts, including FAM99A rs1489945 transmitted from the mother (P=2×10-4), DLK1 rs10139403 (mother; P=9×10-4), DLK1 rs12147008 (mother; P=1×10-3), H19 rs217222 (father; P=1×10-3), SNRPN rs1453556 (father; P=1×10-3), IGF2 rs6356 (father; P=1×10-3), and NNAT rs6066671 (father; P=1×10-3). In meta-analysis including additional independent Hyperglycemia and Adverse Pregnancy Outcome Study data, the association with maternally transmitted fetal DLK1 rs10139403 reached genome-wide significance (P=6.3×10-10). With the exception of fetal rs1489945 and rs217222, all of other associations were unidirectional and most were statistically significant. To further explore the significance of these relationships, we developed an allele score based on the univariate findings. The score was strongly associated with maternal blood pressure at 31 weeks (P=4.1×10-8; adjusted r2=5.6%) and 37 weeks of pregnancy (P=1.1×10-4; r2=3.6%), and during the last 2 weeks before parturition (P=1.1×10-10; r2=8.7%). It was also associated with gestational hypertension (odds ratio, 1.54 [range, 1.14-2.09] per allele; P=0.005; 45 cases and 549 controls). These data support the concept that fetal imprinted genes are related to the development of gestational hypertension.
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Linkage disequilibrium screening for multiple sclerosis implicates JAG1 and POU2AF1 as susceptibility genes in Europeans.
, , Ban, M, Booth, D, Heard, R, Stewart, G, Goris, A, Vandenbroeck, K, Dubois, B, Laaksonen, M, Ilonen, J, et al
Journal of neuroimmunology. 2006;(1-2):108-16
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Abstract
By combining all the data available from the Genetic Analysis of Multiple sclerosis in EuropeanS (GAMES) project, we have been able to identify 17 microsatellite markers showing consistent evidence for apparent association. As might be expected five of these markers map within the Major Histocompatibility Complex (MHC) and are in LD with HLA-DRB1. Individual genotyping of the 12 non-MHC markers confirmed association for three of them--D11S1986, D19S552 and D20S894. Association mapping across the candidate genes implicated by these markers in 937 UK trio families revealed modestly associated haplotypes in JAG1 (p=0.019) on chromosome 20p12.2 and POU2AF1 (p=0.003) on chromosome 11q23.1.