Calculations of the Knight Shift Anomalies in Heavy Electron Materials

We have studied the Knight shift $K(\vec r, T)$ and magnetic susceptibility $\chi(T)$ of heavy electron materials, modeled by the infinite U Anderson model with the NCA method. A systematic study of $K(\vec r, T)$ and $\chi(T)$ for different Kondo temperatures $T_0$ (which depends on the hybridization width $\Gamma$) shows a low temperature anomaly (nonlinear relation between $K$ and $\chi$) which increases as the Kondo temperature $T_0$ and distance $r$ increase. We carried out an incoherent lattice sum by adding the $K(\vec r)$ of a few hundred shells of rare earth atoms around a nucleus and compare the numerically calculated results with the experimental results. For CeSn_3, which is a concentrated heavy electron material, both the ^{119}Sn NMR Knight shift and positive muon Knight shift are studied. Also, lattice coherence effects by conduction electron scattering at every rare earth site are included using the average-T matrix approximation. Also NMR Knight shifts for YbCuAl and the proposed quadrupolar Kondo alloy Y_{0.8}U_{0.2}Pd_{3} are studied.Comment: 31 pages of RevTex, 22 Postscript figures, submmitted to PRB, some figures are delete

Origin of myofibroblasts in liver fibrosis

Most chronic liver diseases of all etiologies result in progressive liver fibrosis. Myofibroblasts produce the extracellular matrix, including type I collagen, which constitutes the fibrous scar in liver fibrosis. Normal liver has little type I collagen and no detectable myofibroblasts, but myofibroblasts appear early in experimental and clinical liver injury. The origin of the myofibroblast in liver fibrosis is still unresolved. The possibilities include activation of endogenous mesenchymal cells including fibroblasts and hepatic stellate cells, recruitment from the bone marrow, and transformation of epithelial or endothelial cells to myofibroblasts. In fact, the origin of myofibroblasts may be different for different types of chronic liver diseases, such as cholestatic liver disease or hepatotoxic liver disease. This review will examine our current understanding of the liver myofibroblast

Pathogens and host immunity in the ancient human oral cavity.

Calcified dental plaque (dental calculus) preserves for millennia and entraps biomolecules from all domains of life and viruses. We report the first, to our knowledge, high-resolution taxonomic and protein functional characterization of the ancient oral microbiome and demonstrate that the oral cavity has long served as a reservoir for bacteria implicated in both local and systemic disease. We characterize (i) the ancient oral microbiome in a diseased state, (ii) 40 opportunistic pathogens, (iii) ancient human-associated putative antibiotic resistance genes, (iv) a genome reconstruction of the periodontal pathogen Tannerella forsythia, (v) 239 bacterial and 43 human proteins, allowing confirmation of a long-term association between host immune factors, 'red complex' pathogens and periodontal disease, and (vi) DNA sequences matching dietary sources. Directly datable and nearly ubiquitous, dental calculus permits the simultaneous investigation of pathogen activity, host immunity and diet, thereby extending direct investigation of common diseases into the human evolutionary past