Universality of the thermodynamic Casimir effect

Recently a nonuniversal character of the leading spatial behavior of the thermodynamic Casimir force has been reported [X. S. Chen and V. Dohm, Phys. Rev. E {\bf 66}, 016102 (2002)]. We reconsider the arguments leading to this observation and show that there is no such leading nonuniversal term in systems with short-ranged interactions if one treats properly the effects generated by a sharp momentum cutoff in the Fourier transform of the interaction potential. We also conclude that lattice and continuum models then produce results in mutual agreement independent of the cutoff scheme, contrary to the aforementioned report. All results are consistent with the {\em universal} character of the Casimir force in systems with short-ranged interactions. The effects due to dispersion forces are discussed for systems with periodic or realistic boundary conditions. In contrast to systems with short-ranged interactions, for $L/\xi \gg 1$ one observes leading finite-size contributions governed by power laws in $L$ due to the subleading long-ranged character of the interaction, where $L$ is the finite system size and $\xi$ is the correlation length.Comment: 11 pages, revtex, to appear in Phys. Rev. E 68 (2003

Physical activity attenuates the influence of FTO variants on obesity risk: A meta-analysis of 218,166 adults and 19,268 children

Background: The FTO gene harbors the strongest known susceptibility locus for obesity. While many individual studies have suggested that physical activity (PA) may attenuate the effect of FTO on obesity risk, other studies have not been able to confirm this interaction. To confirm or refute unambiguously whether PA attenuates the association of FTO with obesity risk, we meta-analyzed data from 45 studies of adults (n = 218,166) and nine studies of children and adolescents (n = 19,268). Methods and Findings: All studies identified to have data on the FTO rs9939609 variant (or any proxy [r2>0.8]) and PA were invited to participate, regardless of ethnicity or age of the participants. PA was standardized by categorizing it into a dichotomous variable (physically inactive versus active) in each study. Overall, 25% of adults and 13% of children were categorized as inactive. Interaction analyses were performed within each study by including the FTO×PA interaction term in an additive model, adjusting for age and sex. Subsequently, random effects meta-analysis was used to pool the interaction terms. In adults, the minor (A-) allele of rs9939609 increased the odds of obesity by 1.23-fold/allele (95% CI 1.20-1.26), but PA attenuated this effect (pinteraction= 0.001). More specifically, the minor allele of rs9939609 increased the odds of obesity less in the physically active group (odds ratio = 1.22/allele, 95% CI 1.19-1.25) than in the inactive group (odds ratio = 1.30/allele, 95% CI 1.24-1.36). No such interaction was found in children and adolescents. Concl

Flora fanerogâmica da Serra Negra, Minas Gerais, Brasil

O presente estudo teve como objetivo caracterizar a flora fanerogâmica da região da Serra Negra localizada no sul da Zona da Mata de Minas Gerais, entre os municípios de Lima Duarte, Rio Preto, Santa Bárbara do Monte Verde e Olaria. Embora considerada de importância biológica alta, esta região não possui nenhum registro anterior de dados florísticos, o que levou ao desenvolvimento deste levantamento, durante o período de 2003 a 2010. A vegetação é caracterizada por um mosaico de formações florestais e campestres onde se destacam os campos rupestres e florestas nebulares em altitudes que variam de 1300 a ca. 1700 m. Um total de 1033 espécies foi encontrado, distribuídas em 469 gêneros e 121 famílias sendo as mais representativas Orchidaceae (115 spp.), Asteraceae 54 spp.), Melastomataceae (56 spp.), Myrtaceae (53 spp.), Fabaceae, Poaceae e Rubiaceae (48 spp. cada), Bromeliaceae (43 spp.), Solanaceae (38 spp.) e Piperaceae (33 spp). Novos registros e endemismos para a flora mineira foram encontrados e 58 espécies estão citadas na lista de espécies ameaçadas de Minas Gerais

Meta-analysis of type 2 Diabetes in African Americans Consortium

Type 2 diabetes (T2D) is more prevalent in African Americans than in Europeans. However, little is known about the genetic risk in African Americans despite the recent identification of more than 70 T2D loci primarily by genome-wide association studies (GWAS) in individuals of European ancestry. In order to investigate the genetic architecture of T2D in African Americans, the MEta-analysis of type 2 DIabetes in African Americans (MEDIA) Consortium examined 17 GWAS on T2D comprising 8,284 cases and 15,543 controls in African Americans in stage 1 analysis. Single nucleotide polymorphisms (SNPs) association analysis was conducted in each study under the additive model after adjustment for age, sex, study site, and principal components. Meta-analysis of approximately 2.6 million genotyped and imputed SNPs in all studies was conducted using an inverse variance-weighted fixed effect model. Replications were performed to follow up 21 loci in up to 6,061 cases and 5,483 controls in African Americans, and 8,130 cases and 38,987 controls of European ancestry. We identified three known loci (TCF7L2, HMGA2 and KCNQ1) and two novel loci (HLA-B and INS-IGF2) at genome-wide significance (4.15 × 10(-94)<P<5 × 10(-8), odds ratio (OR)  = 1.09 to 1.36). Fine-mapping revealed that 88 of 158 previously identified T2D or glucose homeostasis loci demonstrated nominal to highly significant association (2.2 × 10(-23) < locus-wide P<0.05). These novel and previously identified loci yielded a sibling relative risk of 1.19, explaining 17.5% of the phenotypic variance of T2D on the liability scale in African Americans. Overall, this study identified two novel susceptibility loci for T2D in African Americans. A substantial number of previously reported loci are transferable to African Americans after accounting for linkage disequilibrium, enabling fine mapping of causal variants in trans-ethnic meta-analysis studies.Peer reviewe

Novel Loci for Adiponectin Levels and Their Influence on Type 2 Diabetes and Metabolic Traits : A Multi-Ethnic Meta-Analysis of 45,891 Individuals

J. Kaprio, S. Ripatti ja M.-L. Lokki työryhmien jäseniä.Peer reviewe

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease