Magnetic moments' arrangement in Fe layers deposited from acetone based electrolyte

The acetone based electrolyte was used for electrodeposition of iron layers on the copper substrate. Two types of surfaces of the deposited layer can be obtained: shiny or black. Magnetic properties of the near-surface regions were studied by the conversion electron MÄossbauer spectroscopy. The conversion electron MÄossbauer spectra revealed apparent dependence of magnetic moments' arrangement on the deposition time. Those results were compared with the magnetization measurements. Composition of black coating was examined by the X-ray photoelectron spectroscopy measurements

The impact of pulmonary regurgitation on right ventricular size and function in patients with repaired tetralogy of Fallot and additional haemodynamic abnormalities

Purpose: Right ventricular (RV) outflow tract obstruction (RVOTO) was demonstrated to be protective against RV dilatation in patients with repaired tetralogy of Fallot and chronic pulmonary regurgitation (PR). We hypothesised that the presence of additional haemodynamic abnormalities (more than mild tricuspid regurgitation, residual ventricular septal defect) reduces this protective association. Accordingly, we aimed to assess the impact of PR on RV size and function in this population. Material and methods: Consecutive patients with additional haemodynamic abnormalities after tetralogy of Fallot (TOF) repair, who had undergone cardiovascular magnetic resonance, were included. Results: Out of 90 patients studied, 18 individuals (mean age 32.5 ± 10.7 years, 72.2% males) met the inclusion criteria. There were no differences in RV volumes and ejection fraction between patients with and without RVOTO. Neither PR fraction (PRF) nor PR volume (PRV) correlated with RV end-diastolic volume (r = 0.36; p = 0.15 and r = 0.37; p = 0.14, respectively, for PRF and PRV) or RV end-systolic volume (r = 0.2; p = 0.42 and r = 0.19; p = 0.45, respectively, for PRF and PRV). Similarly, no significant correlations were observed between PRF or PRV and RV ejection fraction (r = –0.04; p = 0.87 and r = –0.03; p = 0.9, respectively). Conclusions: Additional haemodynamic abnormalities are associated with the abolition of the protective effect of RVOTO on RV size. There was no significant relationship between measures of PR and RV volumes in patients after TOF repair with concomitant haemodynamic abnormalities. These abnormalities acted as confounding factors in the assessment of the impact of pulmonary regurgitation on RV size and function

The Complex Story of American Debt

This report explores a key element of wealth: household debt. Debt is sometimes acquired for mobility-enhancing purposes, such as to pay for college or purchase a home. But debt can also serve as a stopgap for families to cover regular expenses or deal with financial emergencies, especially if their savings are not sufficient. The type and amount of debt that households carry contribute to their wealth and their overall financial health

Assessment of genotype imputation methods

Several methods have been proposed to impute genotypes at untyped markers using observed genotypes and genetic data from a reference panel. We used the Genetic Analysis Workshop 16 rheumatoid arthritis case-control dataset to compare the performance of four of these imputation methods: IMPUTE, MACH, PLINK, and fastPHASE. We compared the methods' imputation error rates and performance of association tests using the imputed data, in the context of imputing completely untyped markers as well as imputing missing genotypes to combine two datasets genotyped at different sets of markers. As expected, all methods performed better for single-nucleotide polymorphisms (SNPs) in high linkage disequilibrium with genotyped SNPs. However, MACH and IMPUTE generated lower imputation error rates than fastPHASE and PLINK. Association tests based on allele "dosage" from MACH and tests based on the posterior probabilities from IMPUTE provided results closest to those based on complete data. However, in both situations, none of the imputation-based tests provide the same level of evidence of association as the complete data at SNPs strongly associated with disease

A genome-wide association study of antidepressant-induced mania

Antidepressant-induced mania (AIM) is a side effect of antidepressant treatment that is characterized by mania or hypomania after the start of medication. It is likely polygenic, but its genetic component remains largely unexplored. We aim to conduct the first genome-wide association study of AIM in 814 bipolar disorder patients of European ancestry. We report no significant findings from our single-marker or gene-based analyses. Our polygenic risk score analyses also did not yield significant results with bipolar disorder, antidepressant response, or lithium response. Our suggestive findings on the hypothalamic-pituitary-adrenal axis and the opioid system in AIM require independent replications

Molecular Mechanism of Capacitative Calcium Entry Deficits in Familial Alzheimer’s Disease

Poster PresentationPresenilin (PS) is the catalytic subunit of the gamma-secretase which is responsible for the cleavage of amyloid precursor protein to form beta amyloid (Aβ). Mutations in PS associated with familial Alzheimer’s disease (FAD) increase the Aβ plaques formation in the brain and cause neurodegeneration. Apart from this, FAD-linked PS mutations have been demonstrated to disrupt intracellular calcium (Ca2+) regulation. Accumulating evidence suggests that Ca2+ disruption may play a proximal role in the AD pathogenesis. Mutant PS exaggerated Ca2+ release from the endoplasmic reticulum (ER). It also attenuated Ca2+ entry through the capacitative Ca2+ entry (CCE) pathway, yet, the mechanism is not fully understood. Using a human neuroblast cell line SH-SY5Y and Ca2+ imaging technique, we observed CCE deficits in FAD-linked PS1-M146L retroviral infected cell. The attenuation of CCE in PS1 mutant cells was not mediated by the down-regulation of STIM1 and Orai1 expression, the known essential molecular players in the CCE pathway. Instead, we identified a molecular interaction between PS and STIM1 proteins by immunoprecipitation. On the other hand, immunofluorescence staining showed a significant reduction in puncta formation after ER Ca2+ depleted by thapsigargin in cells infected with PS1-M146L as compared to the wild type PS1 infected cells. Taken together, our results suggest a molecular mechanism for the CCE deficits in FAD associated with PS1 mutations. The interaction of mutant PS1 with STIM1 exerts a negative impact on its oligomerization and/or its interaction with Orai1. Our results may suggest molecular targets for the development of therapeutic agents that help to treat the disease.published_or_final_versio