32 research outputs found
Coupling to haloform molecules in intercalated C60?
For field-effect-doped fullerenes it was reported that the superconducting
transition temperature Tc is markedly larger for C60.2CHX_3 (X=Cl, Br)
crystals, than for pure C60. Initially this was explained by the expansion of
the volume per C60-molecule and the corresponding increase in the density of
states at the Fermi level in the intercalated crystals. On closer examination
it has, however, turned out to be unlikely that this is the mechanism behind
the increase in Tc. An alternative explanation of the enhanced transition
temperatures assumes that the conduction electrons not only couple to the
vibrational modes of the C60-molecule, but also to the modes of the
intercalated molecules. We investigate the possibility of such a coupling. We
find that, assuming the ideal bulk structure of the intercalated crystal, both
a coupling due to hybridization of the molecular levels, and a coupling via
dipole moments should be very small. This suggests that the presence of the
gate-oxide in the field-effect-devices strongly affects the structure of the
fullerene crystal at the interface.Comment: 4 pages, 1 figure, to be published in PRB (rapid communication
Mott Transition in Degenerate Hubbard Models: Application to Doped Fullerenes
The Mott-Hubbard transition is studied for a Hubbard model with orbital
degeneracy N, using a diffusion Monte-Carlo method. Based on general arguments,
we conjecture that the Mott-Hubbard transition takes place for U/W \propto
\sqrt{N}, where U is the Coulomb interaction and W is the band width. This is
supported by exact diagonalization and Monte-Carlo calculations. Realistic
parameters for the doped fullerenes lead to the conclusion that stoichiometric
A_3 C_60 (A=K, Rb) are near the Mott-Hubbard transition, in a correlated
metallic state.Comment: 4 pages, revtex, 1 eps figure included, to be published in Phys.Rev.B
Rapid Com
Surprises in the Orbital Magnetic Moment and g-Factor of the Dynamic Jahn-Teller Ion C_{60}^-
We calculate the magnetic susceptibility and g-factor of the isolated
C_{60}^- ion at zero temperature, with a proper treatment of the dynamical
Jahn-Teller effect, and of the associated orbital angular momentum, Ham-reduced
gyromagnetic ratio, and molecular spin-orbit coupling. A number of surprises
emerge. First, the predicted molecular spin-orbit splitting is two orders of
magnitude smaller than in the bare carbon atom, due to the large radius of
curvature of the molecule. Second, this reduced spin-orbit splitting is
comparable to Zeeman energies, for instance, in X-band EPR at 3.39KGauss, and a
field dependence of the g-factor is predicted. Third, the orbital gyromagnetic
factor is strongly reduced by vibron coupling, and so therefore are the
effective weak-field g-factors of all low-lying states. In particular, the
ground-state doublet of C_{60}^- is predicted to show a negative g-factor of
\sim -0.1.Comment: 19 pages RevTex, 2 postscript figures include
Modeling the actinides with disordered local moments
A first-principles disordered local moment (DLM) picture within the
local-spin-density and coherent potential approximations (LSDA+CPA) of the
actinides is presented. The parameter free theory gives an accurate description
of bond lengths and bulk modulus. The case of -Pu is studied in
particular and the calculated density of states is compared to data from
photo-electron spectroscopy. The relation between the DLM description, the
dynamical mean field approach and spin-polarized magnetically ordered modeling
is discussed.Comment: 6 pages, 4 figure
Genetic Sharing with Cardiovascular Disease Risk Factors and Diabetes Reveals Novel Bone Mineral Density Loci.
Bone Mineral Density (BMD) is a highly heritable trait, but genome-wide association studies have identified few genetic risk factors. Epidemiological studies suggest associations between BMD and several traits and diseases, but the nature of the suggestive comorbidity is still unknown. We used a novel genetic pleiotropy-informed conditional False Discovery Rate (FDR) method to identify single nucleotide polymorphisms (SNPs) associated with BMD by leveraging cardiovascular disease (CVD) associated disorders and metabolic traits. By conditioning on SNPs associated with the CVD-related phenotypes, type 1 diabetes, type 2 diabetes, systolic blood pressure, diastolic blood pressure, high density lipoprotein, low density lipoprotein, triglycerides and waist hip ratio, we identified 65 novel independent BMD loci (26 with femoral neck BMD and 47 with lumbar spine BMD) at conditional FDR < 0.01. Many of the loci were confirmed in genetic expression studies. Genes validated at the mRNA levels were characteristic for the osteoblast/osteocyte lineage, Wnt signaling pathway and bone metabolism. The results provide new insight into genetic mechanisms of variability in BMD, and a better understanding of the genetic underpinnings of clinical comorbidity
Genome-wide association and Mendelian randomisation analysis provide insights into the pathogenesis of heart failure
Heart failure (HF) is a leading cause of morbidity and mortality worldwide. A small proportion of HF cases are attributable to monogenic cardiomyopathies and existing genome-wide association studies (GWAS) have yielded only limited insights, leaving the observed heritability of HF largely unexplained. We report results from a GWAS meta-analysis of HF comprising 47,309 cases and 930,014 controls. Twelve independent variants at 11 genomic loci are associated with HF, all of which demonstrate one or more associations with coronary artery disease (CAD), atrial fibrillation, or reduced left ventricular function, suggesting shared genetic aetiology. Functional analysis of non-CAD-associated loci implicate genes involved in cardiac development (MYOZ1, SYNPO2L), protein homoeostasis (BAG3), and cellular senescence (CDKN1A). Mendelian randomisation analysis supports causal roles for several HF risk factors, and demonstrates CAD-independent effects for atrial fibrillation, body mass index, and hypertension. These findings extend our knowledge of the pathways underlying HF and may inform new therapeutic strategies
Educational expansion and inequalities in mortality - A fixed-effects analysis using longitudinal data from 18 European populations
The aim of this paper is to empirically evaluate whether widening educational inequalities in mortality are related to the substantive shifts that have occurred in the educational distribution. Data on education and mortality from 18 European populations across several decades were collected and harmonized as part of the Demetriq project. Using a fixed-effects approach to account for time trends and national variation in mortality, we formally test whether the magnitude of relative inequalities in mortality by education is associated with the gender and age-group specific proportion of high and low educated respectively. The results suggest that in populations with larger proportions of high educated and smaller proportions of low educated, the excess mortality among intermediate and low educated is larger, all other things being equal. We conclude that the widening educational inequalities in mortality being observed in recent decades may in part be attributed to educational expansion
Expression of CD45RB functionally distinguishes intestinal T lymphocytes in inflammatory bowel disease.
The importance of CD45RB expression on T cells was already shown in mice where CD45RB(high) expression determines pathogenic potential. In this study, we analyzed the expression of CD45RA, CD45RB, and CD45RO on CD4(+) T lymphocytes in the intestinal mucosa and in the circulation of patients with inflammatory bowel disease (IBD). In addition, we studied the cytokine profile of these cells. In the circulation, virtually all CD4(+)CD45RB(high) T cells expressed the naive marker CD45RA, and circulating CD4(+)CD45RB(low) cells expressed the memory marker CD45RO in IBD patients and a control patient population. In contrast, the intestinal CD4(+) CD45RB(high) T cells are in normal controls for 90% CD45RO(+). However, in IBD, 27.7% [Crohn's disease (CD)] and 49% [ulcerative colitis (UC)] of the intestinal CD4(+) CD45RB(high) T cells are CD45RA(+). This special CD4CD45RA(+) T cell in IBD can be found in the lamina propria as well as in lymphoid follicles (confocal laser-scanning microscopy). The CD4(+)CD45RB(high) T lymphocytes produce significantly less interleukin (IL)-10 and IL-4 and produce more tumor necrosis factor alpha than CD45RB(low) T lymphocytes in control patients. CD4(+)CD45RB(low) T cells from IBD patients produced less IL-10 than CD4(+)CD45RB(low) T lymphocytes of controls, and interferon-gamma production by both T lymphocyte subsets was decreased in IBD. These data indicate that CD and UC are characterized by an influx of CD4(+)CD45RB(high) T lymphocytes. These CD4(+)CD45RB(high) T lymphocytes seem to be important in the pathogenesis of IBD, as they produce more proinflammatory cytokines and less anti-inflammatory cytokines compared with CD4(+)CD45RB(low) T lymphocytes