Málo gólů v hokeji? Zkusme prohodit strany

Globální sportovní průmysl je extrémně konkurenceschopný. Zaměřujeme se na lední hokej a navrhujeme reformu, která může potenciálně zvýšit jeho popularitu sportu zvýšením počtu gólů. Reforma optimalizuje logistickou konvenci o používání stran na ledě a laviček mimo led, která ovlivňuje množství útočné hry a dynamiku skórování ve hře skrz střídání hráčů. Pomocí několika empirických přístupů poskytujeme odhady výsledného nárůstu skóre pro všech 11 geograficky různorodých soutěží v našem unikátním datasetu. Jsou poměrně velké a robustní vůči řadě kontrolních testů, což hovoří pro vyzkoušení reformy v některé hokejové lize (nižší úrovně).The global sports industry is extremely competitive. We focus on ice hockey and propose a (largely) costless reform to its operations that can potentially enhance the sport's popularity by increasing the number of goals. The reform optimizes a logistic convention on the use of on-ice sides and off-ice benches, which affects the amount of attacking play and within-game scoring dynamics through the players' substitutions. Using several empirical approaches, we provide estimates of the resulting scoring rise for all 11 geographically diverse competitions in our unique dataset. They are sizeable and robust to a number of checks, making case for trialling the reform in some (lower-tier) ice-hockey league

HNF1B-associated renal and extra-renal disease-an expanding clinical spectrum.

Journal ArticleAuthor version of article submitted to Nature Reviews Nephrology. The definitive version is available from Nature Publishing Group via http://dx.doi.org/10.1038/nrneph.2014.232. First published online 23 Deceember 2014.ReviewHeterozygous mutations in the gene that encodes the transcription factor hepatocyte nuclear factor 1β (HNF1B) represent the most common known monogenic cause of developmental kidney disease. Renal cysts are the most frequently detected feature of HNF1B-associated kidney disease; however, other structural abnormalities, including single kidneys and renal hypoplasia, and electrolyte abnormalities can also occur. Extra-renal phenotypes might also be observed; consequently, HNF1B-associated disease is considered a multi-system disorder. Other clinical features include early-onset diabetes mellitus, pancreatic hypoplasia, genital tract malformations, abnormal liver function and early-onset gout. Heterozygous mutations in the coding region or splice sites of HNF1B, and complete gene deletion, each account for ∼50% of all cases of HNF1B-associated disease, respectively, and often arise spontaneously. There is no clear genotype-phenotype correlation, consistent with haploinsufficiency as the disease mechanism. Data from animal models suggest that HNF1B has an important function during several stages of nephrogenesis; however, the precise signalling pathways remain to be elucidated. This Review discusses the genetics and molecular pathways that lead to disease development, summarizes the reported renal and extra-renal phenotypes, and identifies areas for future research in HNF1B-associated disease.Medical Research Council (MRC)National Institute for Health ResearchWellcome Trus