Development of a biking index for measuring Mediterranean cities mobility

[EN] The European Union, its member states and local authorities have been working for long time on the design of solutions for future sustainable mobility. The promotion of a sustainable and affordable urban transport contemplates the bicycle as a mean of transport. The reasons for analysing the cycling mobility in urban areas, has its origin in the confrontation with motorized vehicles, as a sustainable response to the environment. In this context of sustainable mobility, the research team has studied the use of bicycles in Mediterranean cities, specifically in coastal tourist areas.  The present work shows the development of a mobility index oriented to the bicycle, transport that competes with the private vehicle. 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Chromosomes 4 and 8 implicated in a genome wide SNP linkage scan of 762 prostate cancer families collected by the ICPCG

BACKGROUND In spite of intensive efforts, understanding of the genetic aspects of familial prostate cancer (PC) remains largely incomplete. In a previous microsatellite‐based linkage scan of 1,233 PC families, we identified suggestive evidence for linkage (i.e., LOD ≥ 1.86) at 5q12, 15q11, 17q21, 22q12, and two loci on 8p, with additional regions implicated in subsets of families defined by age at diagnosis, disease aggressiveness, or number of affected members. METHODS In an attempt to replicate these findings and increase linkage resolution, we used the Illumina 6000 SNP linkage panel to perform a genome‐wide linkage scan of an independent set of 762 multiplex PC families, collected by 11 International Consortium for Prostate Cancer Genetics (ICPCG) groups. RESULTS Of the regions identified previously, modest evidence of replication was observed only on the short arm of chromosome 8, where HLOD scores of 1.63 and 3.60 were observed in the complete set of families and families with young average age at diagnosis, respectively. The most significant linkage signals found in the complete set of families were observed across a broad, 37 cM interval on 4q13–25, with LOD scores ranging from 2.02 to 2.62, increasing to 4.50 in families with older average age at diagnosis. In families with multiple cases presenting with more aggressive disease, LOD scores over 3.0 were observed at 8q24 in the vicinity of previously identified common PC risk variants, as well as MYC , an important gene in PC biology. CONCLUSIONS These results will be useful in prioritizing future susceptibility gene discovery efforts in this common cancer. Prostate 72:410–426, 2012. © 2011 Wiley Periodicals, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/90245/1/21443_ftp.pd

Genome-wide linkage analysis of 1,233 prostate cancer pedigrees from the International Consortium for prostate cancer Genetics using novel sumLINK and sumLOD analyses

Prostate cancer is generally believed to have a strong inherited component, but the search for susceptibility genes has been hindered by the effects of genetic heterogeneity. The recently developed sumLINK and sumLOD statistics are powerful tools for linkage analysis in the presence of heterogeneity

Association analysis of 9,560 prostate cancer cases from the International Consortium of Prostate Cancer Genetics confirms the role of reported prostate cancer associated SNPs for familial disease

Previous GWAS studies have reported significant associations between various common SNPs and prostate cancer risk using cases unselected for family history. How these variants influence risk in familial prostate cancer is not well studied. Here, we analyzed 25 previously reported SNPs across 14 loci from prior prostate cancer GWAS. The International Consortium for Prostate Cancer Genetics (ICPCG) previously validated some of these using a family-based association method (FBAT). However, this approach suffered reduced power due to the conditional statistics implemented in FBAT. Here, we use a case-control design with an empirical analysis strategy to analyze the ICPCG resource for association between these 25 SNPs and familial prostate cancer risk. Fourteen sites contributed 12,506 samples (9,560 prostate cancer cases, 3,368 with aggressive disease, and 2,946 controls from 2,283 pedigrees). We performed association analysis with Genie software which accounts for relationships. We analyzed all familial prostate cancer cases and the subset of aggressive cases. For the familial prostate cancer phenotype, 20 of the 25 SNPs were at least nominally associated with prostate cancer and 16 remained significant after multiple testing correction (p≤1E−3) occurring on chromosomal bands 6q25, 7p15, 8q24, 10q11, 11q13, 17q12, 17q24, and Xp11. For aggressive disease, 16 of the SNPs had at least nominal evidence and 8 were statistically significant including 2p15. The results indicate that the majority of common, low-risk alleles identified in GWAS studies for all prostate cancer also contribute risk for familial prostate cancer, and that some may be contribute risk to aggressive disease

Validation of prostate cancer risk-related loci identified from genome-wide association studies using family-based association analysis: evidence from the International Consortium for Prostate Cancer Genetics (ICPCG)

Multiple prostate cancer (PCa) risk-related loci have been discovered by genome-wide association studies (GWAS) based on case–control designs. However, GWAS findings may be confounded by population stratification if cases and controls are inadvertently drawn from different genetic backgrounds. In addition, since these loci were identified in cases with predominantly sporadic disease, little is known about their relationships with hereditary prostate cancer (HPC). The association between seventeen reported PCa susceptibility loci was evaluated with a family-based association test using 1,979 hereditary PCa families of European descent collected by members of the International Consortium for Prostate Cancer Genetics, with a total of 5,730 affected men. The risk alleles for 8 of the 17 loci were significantly over-transmitted from parents to affected offspring, including SNPs residing in 8q24 (regions 1, 2 and 3), 10q11, 11q13, 17q12 (region 1), 17q24 and Xp11. In subgroup analyses, three loci, at 8q24 (regions 1 and 2) plus 17q12, were significantly over-transmitted in hereditary PCa families with five or more affected members, while loci at 3p12, 8q24 (region 2), 11q13, 17q12 (region 1), 17q24 and Xp11 were significantly over-transmitted in HPC families with an average age of diagnosis at 65 years or less. Our results indicate that at least a subset of PCa risk-related loci identified by case–control GWAS are also associated with disease risk in HPC families

HOXB13 is a susceptibility gene for prostate cancer: results from the International Consortium for Prostate Cancer Genetics (ICPCG)

Prostate cancer has a strong familial component but uncovering the molecular basis for inherited susceptibility for this disease has been challenging. Recently, a rare, recurrent mutation (G84E) in HOXB13 was reported to be associated with prostate cancer risk. Confirmation and characterization of this finding is necessary to potentially translate this information to the clinic. To examine this finding in a large international sample of prostate cancer families, we genotyped this mutation and 14 other SNPs in or flanking HOXB13 in 2,443 prostate cancer families recruited by the International Consortium for Prostate Cancer Genetics (ICPCG). At least one mutation carrier was found in 112 prostate cancer families (4.6%), all of European descent. Within carrier families, the G84E mutation was more common in men with a diagnosis of prostate cancer (194 of 382, 51%) than those without (42 of 137, 30%), P=9.9×10−8 [odds ratio 4.42 (95% confidence interval 2.56–7.64)]. A family-based association test found G84E to be significantly over-transmitted from parents to affected offspring (P=6.5×10−6). Analysis of markers flanking the G84E mutation indicates that it resides in the same haplotype in 95% of carriers, consistent with a founder effect. Clinical characteristics of cancers in mutation carriers included features of high-risk disease. These findings demonstrate that the HOXB13 G84E mutation is present in ~5% of prostate cancer families, predominantly of European descent, and confirm its association with prostate cancer risk. While future studies are needed to more fully define the clinical utility of this observation, this allele and others like it could form the basis for early, targeted screening of men at elevated risk for this common, clinically heterogeneous cancer.Electronic supplementary materialThe online version of this article (doi:10.1007/s00439-012-1229-4) contains supplementary material, which is available to authorized users

Association analysis of 9,560 prostate cancer cases from the International Consortium of Prostate Cancer Genetics confirms the role of reported prostate cancer associated SNPs for familial disease

Uvod U uvodu se objašnjava da krvne grupe predstavljaju nepromjenljive biološke karakteristike koje se po Mendelovim zakonima, faktorima nasljeđa, genima, prenose s generacije na generaciju (nalaze se na: eritrocitima, leukocitima, trombocitima i na proteinima plazme). Suština podjele na krvne grupe sastoji se u tome što eritrociti pokazuju izoantigenske osobine, sadržavajući mnoge antigene koji se pomoću antitijela mogu dokazati. Pored podjele na ABO grupe, postoji i rhesus faktor (Rh faktor), koji je dobio naziv po Rhesus majmunu kod kojega je i prvi put otkriven. Svi ljudi se dijele na Rh+ (rh pozitivne) i Rh- (rh negativne). Ljudi sa Rh+ krvlju stvaraju rhesus protein, dok ga ljudi sa Rh- krvlju ne stvaraju. Kod trudnoće, Rh faktor se nasljeđuje. Ako je majka Rh-, postoji šansa od 50% do 100% da će dijete biti Rh+ (pod uvjetom da je otac Rh+). Tijekom poroda, plodova krv može doći u kontakt sa krvlju iz posteljice te se može pokrenuti stvaranje imunog odgovora kod majke. Majka će poslje poroda stvoriti antitijela i trajno će biti imunizirana. Cilj Cilj ovog rada je ukazati na važnost određivanja Rh(D) antigena kod trudnica u svrhu izbjegavanja ozbiljnih zdravstvenih posljedica za majku i plod. Izvori podataka i metode U svakom laboratoriju postoji točno određeni protokol koji se mora slijediti kod određivanja Rh(D) antigena, a važno je pravilno i potpuno pridržavati se pravila. Kako bi se izbjegla imunizacija trudnica testiranja se moraju provoditi u propisanim vremenskim razmacima sukladno navedenom protokolu. Ukoliko se ipak razvije imunizacija, na laboratoriju je da istu pravovremeno dijagnosticira a kada dođe vrijeme za intervenciju da poduzmu potrebne korake u daljnjem liječenju. U dijagnostici se moramo služiti najboljom dostupnom opremom i metodama, a sve u svrhu uspješnog praćenja i liječenja trudnica i novorođenčadi. Zaključak Određivanje Rh(D) antigena jedan je od imprerativa prenatalne dijagnostike. Samo testiranje je neinvazivno i potpuno sigurno za plod, a koristi od testiranja su mnogobrojne i velike. Bolesti koje uzrokuje Rh(D) imunizacija majke ozbiljne su sa čak mogućim smrtnim ishodom za plod i zato je bitno da se Rh(D)antigen majke odredi na vrijeme i da se daljnja trudnoća vodi u skladu sa rhesus faktorom majke. Jedino tako možemo pravovremeno reagirati ako dođe do porasta titra antitijela tijekom trudnoće, a tako možda i spasiti život djeteta i omogućiti sigurne naredne trudnoće pacijentice.Introduction The introduction explains that blood types are immutable biological characteristics which, according to Mendel's laws, heritage factors, genes, passed from generation to generation (found at: erythrocytes, leukocytes, platelets and plasma proteins). The essence of the division of the blood is to show that the erythrocytes isogenese properties, comprising, many antigens using the antibodies can be demonstrated. In addition to the division of the ABO groups, there is Rhesus factor (Rh factor), which is named after the Rhesus monkey with whom he first discovered. All people are divided into Rh + (Rh positive) and Rh (Rh negative). People with Rh + blood created rhesus protein, while people with Rh blood does not create. In pregnancy, Rh factor is inherited. If the mother is Rh, there is a chance of 50% to 100% that the baby will be Rh + (providing that the father Rh +). During childbirth, the blood of mother may come in contact with blood from the placenta and can be initiated the creation of an immune response in the mother. Mother after giving birth can create antibodies and will be permanent immunized. Objective The objective of this paper is to point out the importance of determining the Rh (D) antigen in pregnant women to prevent serious health consequences for the mother and fetus. Sources of information and methods In each laboratory there is a specific protocol that must be followed in determining the Rh (D) antigen, and it is important to properly and fully comply with the rules. To avoid immunization of pregnant women testing must be carried out at prescribed intervals in accordance with said protocol. If, however, spread immunization, the laboratory is that the same timely diagnosed and when the time comes for the intervention to take the necessary steps to further treatment. The diagnostics have to use the best available equipment and methods all in favour of successful monitoring and treatment of pregnant women and newborns. Conclusion Determination of Rh (D) antigen is one of the imperatives of prenatal diagnosis. The testing is non-invasive and completely safe for the fetus, and the benefits of testing are numerous and large. Diseases caused by Rh (D) immunization of mothers are serious with even potentially fatal to the fetus, and therefore it is important that the Rh (D) antigen mothers determine the time and that further pregnancies are conducted in accordance with the Rhesus factor mother. The only way we can react if there is an increase in the antibody during pregnancy, and so you might as well save the life of a child and enable secure subsequent pregnancies of the patient