Metabolic diseases affect male reproduction and induce signatures in gametes that may compromise the offspring health

The most prevalent diseases worldwide are non-communicable such as obesity and type 2 diabetes. Noteworthy, the prevalence of obesity and type 2 diabetes is expected to steadily increase in the next decades, mostly fueled by bad feeding habits, stress, and sedentarism. The reproductive function of individuals is severely affected by abnormal metabolic environments, both at mechanical and biochemical levels. Along with mechanical dysfunctions, and decreased sperm quality (promoted both directly and indirectly by metabolic abnormalities), several studies have already reported the potentially harmful effects of metabolic disorders in the genetic and epigenetic cargo of spermatozoa, and the epigenetic inheritance of molecular signatures induced by metabolic profile (paternal diet, obesity, and diabetes). The inheritance of epigenetic factors towards the development of metabolic abnormalities means that more people in reproductive age can potentially suffer from these disorders and for longer periods. In its turn, these individuals can also transmit this (epi)genetic information to future generations, creating a vicious cycle. In this review, we collect the reported harmful effects related to acquired metabolic disorders and diet in sperm parameters and male reproductive potential. Besides, we will discuss the novel findings regarding paternal epigenetic inheritance, particularly the ones induced by paternal diet rich in fats, obesity, and type 2 diabetes. We analyze the data attained with in vitro and animal models as well as in long-term trans generational population studies. Although the findings on this topic are very recent, epigenetic inheritance of metabolic disease has a huge societal impact, which may be crucial to tackle the `fat epidemic' efficiently

Measurements of inclusive W and Z cross sections in pp collisions at √s = 7 TeV The CMS collaboration

Measurements of inclusive W and Z boson production cross sections in pp collisions at √s = 7 TeV are presented, based on 2.9 pb-1 of data recorded by the CMS detector at the LHC. The measurements, performed in the electron and muon decay channels, are combined to give σ(pp → WX) × B(W → l?) = 9.95 ± 0.07 (stat.) ± 0.28 (syst.) ± 1.09 (lumi.) nb and σ(pp → ZX) × B(Z → l +l-) = 0.931 ± 0.026 (stat.) ± 0.023 (syst.) ± 0.102 (lumi.) nb, where l stands for either e or μ. Theoretical predictions, calculated at the next-to-next-to-leading order in QCD using recent parton distribution functions, are in agreement with the measured cross sections. Ratios of cross sections, which incur an experimental systematic uncertainty of less than 4%, are also reported

Study of W boson production in PbPb and pp collisions at root s(NN)=2.76 TeV

A measurement is presented of W-boson production in PbPb collisions carried out at a nucleon-nucleon (NN) centre-of-mass energy sNN of 2.76 TeV at the LHC using the CMS detector. In data corresponding to an integrated luminosity of 7.3 μb -1, the number of W→μν μ decays is extracted in the region of muon pseudorapidity |η μ|<2.1 and transverse momentum pTμ>25 GeV/c. Yields of muons found per unit of pseudorapidity correspond to (159±10(stat.)±12(syst.))×10 -8 W + and (154±10(stat.)±12(syst.))×10 -8 W - bosons per minimum-bias PbPb collision. The dependence of W production on the centrality of PbPb collisions is consistent with a scaling of the yield by the number of incoherent NN collisions. The yield of W bosons is also studied in a sample of pp interactions at s=2.76 TeV corresponding to an integrated luminosity of 231 nb -1. The individual W + and W - yields in PbPb and pp collisions are found to agree, once the neutron and proton content in Pb nuclei is taken into account. Likewise, the difference observed in the dependence of the positive and negative muon production on pseudorapidity is consistent with next-to-leading-order perturbative QCD calculations. © 2012 CERN