Comment on ``Local dimer-adatom stacking fault structures from 3x3 to 13x13 along Si(111)-7x7 domain boundaries''

Zhao et al. [Phys.Rev.B 58, 13824 (1998)] depicted several atomic structures of domain boundaries on a Si(111) surface and criticized the article by the present author and the co-workers. I will point out that their criticism is incorrect and their structure models have no consistency.Comment: 2 pages. Physical Review B, to appea

Adipocytes harbor a glucosylceramide biosynthesis pathway involved in iNKT cell activation

Background: Natural killer T (NKT) cells in adipose tissue (AT) contribute to whole body energy homeostasis. Results: Inhibition of the glucosylceramide synthesis in adipocytes impairs iNKT cell activity. Conclusion: Glucosylceramide biosynthesis pathway is important for endogenous lipid antigen activation of iNKT cells in adipocytes.Significance: Unraveling adipocyte-iNKT cell communication may help to fight obesity-induced AT dysfunction.Overproduction and/or accumulation of ceramide and ceramide metabolites, including glucosylceramides, can lead to insulin resistance. However, glucosylceramides also fulfill important physiological functions. They are presented by antigen presenting cells (APC) as endogenous lipid antigens via CD1d to activate a unique lymphocyte subspecies, the CD1d-restricted invariant (i) natural killer T (NKT) cells. Recently, adipocytes have emerged as lipid APC that can activate adipose tissue-resident iNKT cells and thereby contribute to whole body energy homeostasis. Here we investigate the role of the glucosylceramide biosynthesis pathway in the activation of iNKT cells by adipocytes.UDP-glucose ceramide glucosyltransferase (Ugcg), the first rate limiting step in the glucosylceramide biosynthesis pathway, was inhibited via chemical compounds and shRNA knockdown in vivo and in vitro. beta-1,4-Galactosyltransferase (B4Galt) 5 and 6, enzymes that convert glucosylceramides into potentially inactive lactosylceramides, were subjected to shRNA knock down. Subsequently, (pre)adipocyte cell lines were tested in co-culture experiments with iNKT cells (IFN gamma and 114 secretion).Inhibition of Ugcg activity shows that it regulates presentation of a considerable fraction of lipid self-antigens in adipocytes. Furthermore, reduced expression levels of either B4Galt5 or -6, indicate that B4Galt5 is dominant in the production of cellular lactosylceramides, but that inhibition of either enzyme results in increased iNKT cell activation. Additionally, in vivo inhibition of Ugcg by the aminosugar AMP-DNM results in decreased iNKT cell effector function in adipose tissue.Inhibition of endogenous glucosylceramide production results in decreased iNKT cells activity and cytokine production, underscoring the role of this biosynthetic pathway in lipid self-antigen presentation by adipocytes

STM characterization of the Si-P heterodimer

We use scanning tunneling microscopy (STM) and Auger electron spectroscopy to study the behavior of adsorbed phosphine (PH$_{3}$) on Si(001), as a function of annealing temperature, paying particular attention to the formation of the Si-P heterodimer. Dosing the Si(001) surface with ${\sim}$0.002 Langmuirs of PH$_{3}$ results in the adsorption of PH$_{x}$ (x=2,3) onto the surface and some etching of Si to form individual Si ad-dimers. Annealing to 350$^{\circ}$C results in the incorporation of P into the surface layer to form Si-P heterodimers and the formation of short 1-dimensional Si dimer chains and monohydrides. In filled state STM images, isolated Si-P heterodimers appear as zig-zag features on the surface due to the static dimer buckling induced by the heterodimer. In the presence of a moderate coverage of monohydrides this static buckling is lifted, rending the Si-P heterodimers invisible in filled state images. However, we find that we can image the heterodimer at all H coverages using empty state imaging. The ability to identify single P atoms incorporated into Si(001) will be invaluable in the development of nanoscale electronic devices based on controlled atomic-scale doping of Si.Comment: 6 pages, 4 figures (only 72dpi

Split-off dimer defects on the Si(001)2x1 surface

Dimer vacancy (DV) defect complexes in the Si(001)2x1 surface were investigated using high-resolution scanning tunneling microscopy and first principles calculations. We find that under low bias filled-state tunneling conditions, isolated 'split-off' dimers in these defect complexes are imaged as pairs of protrusions while the surrounding Si surface dimers appear as the usual 'bean-shaped' protrusions. We attribute this to the formation of pi-bonds between the two atoms of the split-off dimer and second layer atoms, and present charge density plots to support this assignment. We observe a local brightness enhancement due to strain for different DV complexes and provide the first experimental confirmation of an earlier prediction that the 1+2-DV induces less surface strain than other DV complexes. Finally, we present a previously unreported triangular shaped split-off dimer defect complex that exists at SB-type step edges, and propose a structure for this defect involving a bound Si monomer.Comment: 8 pages, 7 figures, submitted to Phys. Rev.