Low-energy photon-photon collisions to two loops revisited

In view of ongoing experimental activities to determine the pion polarizabilities, we have started to recalculate the available two-loop expressions in the framework of chiral perturbation theory, because they have never been checked before. We make use of the chiral Lagrangian at order p^6 now available, and of improved techniques to evaluate the two-loop diagrams. Here, we present the result for the neutral pions. The cross section for the reaction gamma+gamma->pi0+pi0 agrees with the earlier calculation within a fraction of a percent. We present analytic results for the dipole and quadrupole polarizabilities, and compare the latter with a recent evaluation from data on gamma+gamma->pi0+pi0.Comment: 28 pages, 7-eps figures, 1 tabl

A new family of matrix product states with Dzyaloshinski-Moriya interactions

We define a new family of matrix product states which are exact ground states of spin 1/2 Hamiltonians on one dimensional lattices. This class of Hamiltonians contain both Heisenberg and Dzyaloshinskii-Moriya interactions but at specified and not arbitrary couplings. We also compute in closed forms the one and two-point functions and the explicit form of the ground state. The degeneracy structure of the ground state is also discussed.Comment: 15 pages, 1 figur

Nucleon Axial Form Factor from Lattice QCD

Results for the isovector axial form factors of the proton from a lattice QCD calculation are presented for both point-split and local currents. They are obtained on a quenched $16^{3} \times 24$ lattice at $\beta= 6.0$ with Wilson fermions for a range of quark masses from strange to charm. We determine the finite lattice renormalization for both the local and point-split currents of heavy quarks. Results extrapolated to the chiral limit show that the $q^2$ dependence of the axial form factor agrees reasonably well with experiment. The axial coupling constant $g_A$ calculated for the local and the point-split currents is about 6\% and 12\% smaller than the experimental value respectively.Comment: 8 pages, 5 figures (included in part 2), UK/93-0

Measurement of spin correlation in ttbar production using dilepton final states

We measure the correlation between the spin of the top quark and the spin of the anti-top quark in (ttbar -> W+ W- b bbar -> l+ nu b l- nubar bbar) final states produced in ppbar collisions at a center of mass energy sqrt(s)=1.96 TeV, where l is an electron or muon. The data correspond to an integrated luminosity of 5.4 fb-1 and were collected with the D0 detector at the Fermilab Tevatron collider. The correlation is extracted from the angles of the two leptons in the t and tbar rest frames, yielding a correlation strength C= 0.10^{+0.45}_{-0.45}, in agreement with the NLO QCD prediction within two standard deviations, but also in agreement with the no correlation hypothesis.Comment: 10 pages, 3 figures, submitted to PL

Measurement of the ttbar production cross section using dilepton events in ppbar collisions

We present a measurement of the ttbar production cross section sigma(ttbar) in ppbar collisions at sqrt{s} = 1.96 TeV using 5.4 fb-1 of integrated luminosity collected with the D0 detector. We consider final states with at least two jets and two leptons (ee, emu, mumu), and events with one jet for the the emu final state as well. The measured cross section is sigma(ttbar)= 7.36 +0.90-0.79 (stat + syst) pb. This result combined with the cross section measurement in the lepton + jets final state yields sigma(ttbar)=7.56 +0.63-0.56 (stat + syst) pb, which agrees with the standard model expectation. The relative precision of 8% of this measurement is comparable to the latest theoretical calculations.Comment: 9 pages, published in Phys. Lett.

DNAH5 mutations are a common cause of primary ciliary dyskinesia with outer dynein arm defects

Rationale: Primary ciliary dyskinesia (PCD) is characterized by recurrent airway infections and randomization of left-right body asymmetry. To date, autosomal recessive mutations have only been identified in a small number of patients involving DNAI1 and DNAH5, which encode outer dynein arm components. Methods: We screened 109 white PCD families originating from Europe and North America for presence of DNAH5 mutations by haplotype analyses and/or sequencing. Results: Haplotype analyses excluded linkage in 26 families. In 30 PCD families, we identified 33 novel (12 nonsense, 8 frameshift, 5 splicing, and 8 missense mutations) and two known DNAH5 mutations. Weobserved clustering of mutationswithin five exons harboring 27 mutant alleles (52%) of the 52 detected mutant alleles. Interestingly, 6 (32%) of 19 PCD families with DNAH5 mutations from North America carry the novel founder mutation 10815delT. Electron microscopic analyses in 22 patients with PCD with mutations invariably detected outer dynein arm ciliary defects. High-resolution immunofluorescence imaging of respiratory epithelial cells from eight patients with DNAH5 mutations showed mislocalization of mutant DNAH5 and accumulation at the microtubule organizing centers. Mutant DNAH5 was absent throughout the ciliary axoneme in seven patients and remained detectable in the proximal ciliary axoneme in one patient carrying compound heterozygous splicing mutations at the 3′-end (IVS75-2A>T, IVS76+5G>A). In a preselected subpopulation with documented outer dynein arm defects (n = 47), DNAH5 mutations were identified in 53% of patients. Conclusions: DNAH5 is frequently mutated in patients with PCD exhibiting outer dynein arm defects and mutations cluster in five exons

Methodology and implementation of the WHO European Childhood Obesity Surveillance Initiative (COSI)

Establishment of the WHO European Childhood Obesity Surveillance Initiative (COSI)has resulted in a surveillance system which provides regular, reliable, timely, andaccurate data on children's weight status—through standardized measurement ofbodyweight and height—in the WHO European Region. Additional data on dietaryintake, physical activity, sedentary behavior, family background, and schoolenvironments are collected in several countries. In total, 45 countries in the EuropeanRegion have participated in COSI. The first five data collection rounds, between 2007and 2021, yielded measured anthropometric data on over 1.3 million children. In COSI,data are collected according to a common protocol, using standardized instrumentsand procedures. The systematic collection and analysis of these data enables inter-country comparisons and reveals differences in the prevalence of childhood thinness,overweight, normal weight, and obesity between and within populations. Furthermore,it facilitates investigation of the relationship between overweight, obesity, and poten-tial risk or protective factors and improves the understanding of the development ofoverweight and obesity in European primary-school children in order to supportappropriate and effective policy responses.The authors gratefully acknowledge support through a grant from the Russian Government in the context of the WHO European Office for the Prevention and Control of NCDs. The ministries of health of Austria, Croatia, Greece, Italy, Malta, Norway, and the Russian Federation provided financial support for the meetings at which the protocol, data collection procedures, and analyses were discussed. Data collection in countries was made possible through funding from the following: Albania: WHO through the Joint Programme on Children, Food Security and Nutrition “Reducing Malnutrition in Children,” funded by the Millennium Development Goals Achievement Fund, and the Institute of Public Health. Austria: Federal Ministry of Labor, Social Affairs, Health and Consumer Protection of Austria. Bulgaria: Ministry of Health, National Center of Public Health and Analyses, and WHO Regional Office for Europe. Bosnia and Herzegovina: WHO country office support for training and data management. Croatia: Ministry of Health, Croatian Institute of Public Health, and WHO Regional Office for Europe. Czechia: Ministry of Health of the Czech Republic, grant number 17-31670A and MZCR—RVO EU 00023761. Denmark: Danish Ministry of Health. Estonia: Ministry of Social Affairs, Ministry of Education and Research (IUT 42-2), WHO Country Office, and National Institute for Health Development. Finland: Finnish Institute for Health and Welfare. France: Santé publique France (the French Agency for Public Health). Georgia: WHO. Greece: International Hellenic University and Hellenic Medical Association for Obesity. Hungary: WHO Country Office for Hungary. Ireland: Health Service Executive. Italy: Ministry of Health. Kazakhstan: Ministry of Health of the Republic of Kazakhstan, WHO, and UNICEF. Kyrgyzstan: World Health Organization. Latvia: Ministry of Health and Centre for Disease Prevention and Control. Lithuania: Science Foundation of Lithuanian University of Health Sciences and Lithuanian Science Council and WHO. Malta: Ministry of Health. Montenegro: WHO and Institute of Public Health of Montenegro. North Macedonia: Government of North Macedonia through National Annual Program of Public Health and implemented by the Institute of Public Health and Centers of Public Health; WHO country office provides support for training and data management. Norway: the Norwegian Ministry of Health and Care Services, the Norwegian Directorate of Health, and the Norwegian Institute of Public Health. Poland: National Health Programme, Ministry of Health. Portugal: Ministry of Health Institutions, the National Institute of Health, Directorate General of Health, Regional Health Directorates, and the kind technical support from the Center for Studies and Research on Social Dynamics and Health (CEIDSS). Romania: Ministry of Health. Russian Federation: WHO. San Marino: Health Ministry, Educational Ministry, and Social Security Institute and Health Authority. Serbia: WHO and the WHO Country Office (2015-540940 and 2018/873491-0). Slovakia: Biennial Collaborative Agreement between WHO Regional Office for Europe and Ministry of Health SR. Slovenia: Ministry of Education, Science and Sport of the Republic of Slovenia within the SLOfit surveillance system. Spain: Spanish Agency for Food Safety and Nutrition. Sweden: Public Health Agency of Sweden. Tajikistan: WHO Country Office in Tajikistan and Ministry of Health and Social Protection. Turkmenistan: WHO Country Office in Turkmenistan and Ministry of Health. Turkey: Turkish Ministry of Health and World Bank.info:eu-repo/semantics/publishedVersio

Sexually dimorphic DNA-methylation in cardiometabolic health: A systematic review

Sex is a major determinant of cardiometabolic risk. DNA methylation (DNAm), an important epigenetic mechanism that differs between sexes, has been associated with cardiometabolic diseases. Therefore, we aimed to systematically review studies in adults investigating sex-specific associations of DNAm with intermediate cardiometabolic traits and incident cardiovascular disease including stroke, myocardial infarction (MI) and coronary heart disease (CHD). Five bibliographic databases were searched from inception to 15 July 2019. We selected 35 articles (based on 30 unique studies) from 17,023 references identified, with a total of 14,020 participants of European, North American or Asian ancestry. Four studies reported sex differences between global DNAm and blood lipid levels and stroke risk. In 25 studies that took a genome wide or candidate gene approach, DNAm at 31 gene sites was associated with sex differences in cardiometabolic diseases. The identified genes were PLA2G7, BCL11A, KDM6A, LIPC, ABCG1, PLTP, CETP, ADD1, CNN1B, HOOK2, GFBP-7,PTPN1, GCK, PTX3, ABCG1, GALNT2, CDKN2B, APOE, CTH, GNASAS, INS, PON1, TCN2, CBS, AMT, KDMA6A, FTO, MAP3K13, CCDC8, MMP-2 and ER-α. Prioritized pathway connectivity analysis associated these genes with biological pathways such as vitamin B12 metabolism, statin pathway, plasma lipoprotein, plasma lipoprotein assembly, remodeling and clearance and cholesterol metabolism. Our findings suggest that DNAm might be a promising molecular strategy for understanding sex differences in the pathophysiology of cardiometabolic diseases and that future studies should investigate the effects of sex on epigenetic mechanisms in cardiometabolic risk. In addition, we emphasize the gap between the translational potential and the clinical utilization of cardiometabolic epigenetics