LEADER 01649aam 2200457I 450 001 9910711399703321 005 20151113033707.0 024 8 $aGOVPUB-C13-c81324c5d6bac8eadda1a3ad170730eb 035 $a(CKB)5470000002482029 035 $a(OCoLC)929068344 035 $a(EXLCZ)995470000002482029 100 $a20151113d2009 ua 0 101 0 $aeng 181 $2rdacontent 182 $2rdamedia 183 $2rdacarrier 200 10$aFDS wall flows part I $estraight channels /$fRandall J. McDermott 210 1$aGaithersburg, MD :$cU.S. Dept. of Commerce, National Institute of Standards and Technology,$d2009. 215 $a1 online resource 225 1 $aNIST technical note ;$v1640 300 $a2009. 300 $aContributed record: Metadata reviewed, not verified. Some fields updated by batch processes. 300 $aTitle from PDF title page. 320 $aIncludes bibliographical references. 517 $aFDS wall flows part I 606 $aEddies$xMathematical modlels 606 $aTurbulent boundary layer$xMathematical modlels 606 $aWalls$xFires and fire prevention$xMathematical modlels 615 0$aEddies$xMathematical modlels. 615 0$aTurbulent boundary layer$xMathematical modlels. 615 0$aWalls$xFires and fire prevention$xMathematical modlels. 700 $aMcDermott$b Randall J$01386482 701 $aMcDermott$b Randall J$01386482 712 02$aUnited States.$bNational Bureau of Standards. 801 0$bNBS 801 1$bNBS 801 2$bGPO 906 $aBOOK 912 $a9910711399703321 996 $aFDS wall flows part I$93515491 997 $aUNINA LEADER 04858nam 2200433z- 450 001 9910137086803321 005 20210212 035 $a(CKB)3710000000824762 035 $a(oapen)https://directory.doabooks.org/handle/20.500.12854/60753 035 $a(oapen)doab60753 035 $a(EXLCZ)993710000000824762 100 $a20202102d2015 |y 0 101 0 $aeng 135 $aurmn|---annan 181 $ctxt$2rdacontent 182 $cc$2rdamedia 183 $acr$2rdacarrier 200 00$aTestis cancer: Genes, environment, hormones 210 $cFrontiers Media SA$d2015 215 $a1 online resource (86 p.) 225 1 $aFrontiers Research Topics 311 08$a9782889196722 311 08$a2889196720 330 $aTesticular cancer (TC) is the most common cancer in males aged 20-40 years, with a worldwide incidence of 7.5 per 100,000, but the rates vary considerably between countries and ethnic groups and there is evidence also for an increasing incidence in last decades. About 95% of all TCs are represented by testicular germ cell tumors (TGCTs), which include seminoma and non-seminoma histological types. It is generally assumed that the development of TGCT is under endocrine control. In particular, unbalanced androgen/estrogen levels and/or activity are believed to represent the key events for TGCT development and progression. Furthermore, recent evidence has suggested genetic association of TGCT with variations in genes involved in hypothalamic-pituitary-testicular axis and steroidogenic enzymes. This recent evidence expands the current knowledge on the role of genetic contribution in testicular cancer susceptibility, and supports the hypothesis that variations in hormone metabolism genes might change the hormonal environment implicated in testicular carcinogenesis. Therefore, hormonal carcinogenesis is an important and controversial area of current research in TGCT, and further attention is given to genetic factors influencing hormone-related cancer risk. The genetic component to TGCT is in general strong. In fact, although environmental factors clearly contribute to TGCT development (and probably to its increasing incidence in some geographical areas), the proportion of TGCT susceptibility accounted for by the genetic effects is estimated at 25%. TGCT has high familial risks compared with most other cancer types that are generally no more than two-fold: brothers of individuals with TGCT have an 8- to 12-fold increased risk of disease, and sons of affected individuals have a 4- to 6-fold increased risk. Despite this strong familial relative risk, early results from linkage studies identified a limited relationship with genetic factors, suggesting that TGCT is a genetically complex trait. However, more recently, four genome-wide association studies (GWAS) from the UK and USA have reported association of TGCTs with six new loci (KITLG, SPRY4, BAK1, DMRT1, TERT, and ATF7IP). The strongest association for TGCT susceptibility was found for SNPs in KITLG (ligand for the membrane-bound receptor tyrosine kinase KIT) gene with a greater than 2.5-fold increased risk of disease per major allele, which is the highest reported for any cancer to date. These studies are being now replicated by other researches and attention is given to the relationship between these genetic variations, TGCT risk and frequently associated anomalies of the reproductive tract, such as cryptorchidism and infertility. Finally, over the past few decades, TCGT research has focused also on external environmental causes acting mainly as endocrine disrupters of androgen and oestrogen pathways, even during the foetal development of the testis. It is well known that the testicular dysgenesis syndrome (TDS) hypothesis, proposed ten years ago, suggests that disturbed testicular development in fetal life may result in one or more of four disorders postnatally, named cryptorchidism, hypospadias, poor semen quality, and TGCT. These four disorders are therefore considered as one clinical entity and are linked together by epidemiological and pathophysiological relations. The relative contribution of genetics and environment in TGCT development, and the interactions between endocrine disruptors and variations in genes involved in hormonal carcinogenesis is therefore another interesting area of research. 517 $aTestis cancer 606 $aMedicine and Nursing$2bicssc 610 $acancer genetics 610 $aCryptorchidism 610 $aEndocrine Disruptors 610 $aGerm cell tumor 610 $aKITLG 610 $atestis cancer 615 7$aMedicine and Nursing 700 $aFerlin$b Alberto$4auth$01839608 702 $aForesta$b Carlo$4auth 906 $aBOOK 912 $a9910137086803321 996 $aTestis cancer: Genes, environment, hormones$94418881 997 $aUNINA