Lattice-point enumerators of ellipsoids

Minkowski's second theorem on successive minima asserts that the volume of a 0-symmetric convex body K over the covolume of a lattice \Lambda can be bounded above by a quantity involving all the successive minima of K with respect to \Lambda. We will prove here that the number of lattice points inside K can also accept an upper bound of roughly the same size, in the special case where K is an ellipsoid. Whether this is also true for all K unconditionally is an open problem, but there is reasonable hope that the inductive approach used for ellipsoids could be extended to all cases.Comment: 9 page

Ionic liquids for carbon dioxide capture and conversion

Ionic liqs. (ILs) are defined as org. compds. consisting entirely of ions and are characterized by m.ps. below 100 °C, with many of them being liq. at room temp. (RTILs). ILs feature often unique property profiles, which can be tuned by design, such as viscosity, d., soly., cond. or high thermal and chem. stability, just to name the most important ones. With these versatile properties they may have a major impact on many promising applications. In this context, our focus is on CO2 capture. The current process to capture CO2 is based on highly corrosive, volatile and smelly aq. amine

Properties of Thirteen Viruses and Virus Variants Obtained from Eight Isolates of the Wheat Take-All Fungus, Gaeumannomyces graminis var. tritici.

The properties of polyhedral double-stranded ( s)RNA virus particles obtained from eight isolates of the wheat take-all fungus, Gaeumannomyces graminis var. tritici, have been investigated. Thirteen viruses and virus variants were distinguished and these were classified into three groups on the basis of serological and physical properties of the virus particles; viruses in a group were related serologicaUy to other members of the same group, but unrelated serologically to members of other groups. Group I viruses had particles of diam. 35 nm sedimenting at 109 to 126S; the virus capsid contained one polypeptide species, mol. wt. 54 × l03 to 60 × 103 and virus dsRNA consisted of two to four components, mol. wt. 1.0 x 10 6 tO I-3 X 106. Group II viruses had particles of diam. 35 nm sedimenting at 133 to 140S; the virus capsid contained one polypeptide species, tool. wt. 68 × 103 to 73 x 103 and virus dsRNA consisted of two to four components with mol. wt. 1.39 × 106 to 1.60 × l06. Group III viruses had particles of diam. 40 nm sedimenting at 159 to 163S; the viru

The amount of keratinized mucosa may not influence peri-implant health in compliant patients: A retrospective 5-year analysis

AIM (a) To investigate the influence of the keratinized mucosa (KM) on peri-implant health or disease and (b) to identify a threshold value for the width of KM for peri-implant health. MATERIALS AND METHODS The total dataset was subsampled, that is one implant was randomly chosen per patient. In 87 patients, data were extracted at baseline (prosthesis insertion) and 5 years including the width of mid-buccal KM, bleeding on probing, probing depth, plaque index and marginal bone level (MB). Spearman correlations with Holm adjustment for multiple testing were used for potential associations. RESULTS Depending on the definition of peri-implant diseases, the prevalence of peri-implantitis ranged from 9.2% (bleeding on probing threshold: <50% or ≥50%) to 24.1% (threshold: absence or the presence). The prevalence of peri-implant mucositis was similar, irrespective of the definition (54%-55.2%). The width of KM and parameters for peri-implant diseases demonstrated negligible (Spearman correlation coefficients: -0.2 < ρ < 0.2). No threshold value was detected for the width of mid-buccal KM in relation to peri-implant health. CONCLUSION The width of KM around dental implants correlated to a negligible extent with parameters for peri-implant diseases. No threshold value for the width of KM to maintain peri-implant health could be identified

High loading of polygenic risk for ADHD in children with comorbid aggression

Objective: Although attention deficit hyperactivity disorder (ADHD) is highly heritable, genome-wide association studies (GWAS) have not yet identified any common genetic variants that contribute to risk. There is evidence that aggression or conduct disorder in children with ADHD indexes higher genetic loading and clinical severity. The authors examine whether common genetic variants considered en masse as polygenic scores for ADHD are especially enriched in children with comorbid conduct disorder. Method: Polygenic scores derived from an ADHD GWAS meta-analysis were calculated in an independent ADHD sample (452 case subjects, 5,081 comparison subjects). Multivariate logistic regression analyses were employed to compare polygenic scores in the ADHD and comparison groups and test for higher scores in ADHD case subjects with comorbid conduct disorder relative to comparison subjects and relative to those without comorbid conduct disorder. Association with symptom scores was tested using linear regression. Results: Polygenic risk for ADD, derived from the meta-analysis, was higher in the independent ADHD group than in the comparison group. Polygenic score was significantly higher in ADHD case subjects with conduct disorder relative to ADHD case subjects without conduct disorder. ADHD polygenic score showed significant association with comorbid conduct disorder symptoms. This relationship was explained by,the aggression items. Conclusions: Common genetic variation is relevant to ADHD, especially in individuals with comorbid aggression. The findings suggest that the previously published ADHD GWAS meta-analysis contains weak but true associations with common variants, support for which falls below genome-wide significance levels. The findings also highlight the fact that aggression in ADHD indexes genetic as well as clinical severity

Expression analyses of the mitochondrial complex I 75-kDa subunit in early onset schizophrenia and autism spectrum disorder: increased levels as a potential biomarker for early onset schizophrenia

Searching for a peripheral biological marker for schizophrenia, we previously reported on elevated mitochondrial complex I 75-kDa subunit mRNA-blood concentrations in early onset schizophrenia (EOS). The aim of this study was to further evaluate the utility of this gene as a potential marker for schizophrenia. Both—schizophrenia and autism—are suggested to be neuronal maldevelopmental disorders with reports of mitochondrial dysfunction and increased oxidative stress. Therefore we have investigated the expression levels of mitochondrial complex I 75-kDa subunit mRNA in whole blood of children with autistic spectrum disorder (ASD) and a group of adolescent acute first-episode EOS patients in comparison to matched controls. We have found that compared to the respective controls only the group of EOS patients—and not the ASD group—showed a significantly altered expression of the complex I 75-kDa subunit mRNA. Although further studies are necessary to test for the specificity of this marker, our findings point to the potential use of the mitochondrial complex I as a biomarker for schizophrenia

Effective detection of human leukocyte antigen risk alleles in celiac disease using tag single nucleotide polymorphisms.

Background: The HLA genes, located in the MHC region on chromosome 6p21.3, play an important role in many autoimmune disorders, such as celiac disease (CD), type 1 diabetes (T1D), rheumatoid arthritis, multiple sclerosis, psoriasis and others. Known HLA variants that confer risk to CD, for example, include DQA1*05/DQB1*02 (DQ2.5) and DQA1*03/ DQB1*0302 (DQ8). To diagnose the majority of CD patients and to study disease susceptibility and progression, typing these strongly associated HLA risk factors is of utmost importance. However, current genotyping methods for HLA risk factors involve many reactions, and are complicated and expensive. We sought a simple experimental approach using tagging SNPs that predict the CD-associated HLA risk factors. Methodology: Our tagging approach exploits linkage disequilibrium between single nucleotide polymorphism (SNPs) and the CD-associated HLA risk factors DQ2.5 and DQ8 that indicate direct risk, and DQA1*0201/DQB1*0202 (DQ2.2) and DQA1*0505/DQB1*0301 (DQ7) that attribute to the risk of DQ2.5 to CD. To evaluate the predictive power of this approach, we performed an empirical comparison of the predicted DQ types, based on these six tag SNPs, with those executed with current validated laboratory typing methods of the HLA-DQA1 and -DQB1 genes in three large cohorts. The results were validated in three European celiac populations. Conclusion: Using this method, only six SNPs were needed to predict the risk types carried by .95% of CD patients. We determined that for this tagging approach the sensitivity was .0.991, specificity .0.996 and the predictive value .0.948. Our results show that this tag SNP method is very accurate an