The structure of triphenylgermanium hydroxide

C18H~6GeO, Mr = 320.9, triclinic, Pi, a = 15.408 (6), b = 19.974 (7), c = 23.264 (11) A, a = 107.78 (4), 13 = 1.03.54 (4), y= 101.51 (3) °, V = 6338 (5)/~3, Z = 16, Dx = 1.34 g cm -3, a(Mo Ka) = 0.71073A, /z = 19.1cm-1, F(000)=2624, T= 293 K, R = 0.055 for 6846 observed reflections. The eight independent molecules in the asymmetric unit form two independent O--H...O hydrogen-bonded tetramers with the O atoms in a flattened tetrahedral arrangement [hydrogen-bond distances in the range 2.609 (11) to 2.657 (11)A]. The Ge atoms are tetrahedrally coordinated with mean Gc O 1.791 (7) and Gc C 1.931 (8) A

Keloids and Hypertrophic Scars: Update and Future Directions

Summary: The development of cutaneous pathological scars, namely, hypertrophic scars (HSs) and keloids, involves complex pathways, and the exact mechanisms by which they are initiated, evolved, and regulated remain to be fully elucidated. The generally held concepts that keloids and HSs represent “aberrant wound healing” or that they are “characterized by hyalinized collagen bundles” have done little to promote their accurate clinicopathological classification or to stimulate research into the specific causes of these scars and effective preventative therapies. To overcome this barrier, we review here the most recent findings regarding the pathology and pathogenesis of keloids and HSs. The aberrations of HSs and keloids in terms of the inflammation, proliferation, and remodeling phases of the wound healing process are described. In particular, the significant roles that the extracellular matrix and the epidermal and dermal layers of skin play in scar pathogenesis are examined. Finally, the current hypotheses of pathological scar etiology that should be tested by basic and clinical investigators are detailed. Therapies that have been found to be effective are described, including several that evolved directly from the aforementioned etiology hypotheses. A better understanding of pathological scar etiology and manifestations will improve the clinical and histopathological classification and treatment of these important lesions

[8,8-(PPh3)2-9-(OEt)-8,7-RhSB9H9].0.95(CH2Cl2)

9-Ethoxy-8,8-di(triphenylphosphine)-9,10- tz H-8-rhoda-7-thia-nido-undecaborane( l O) dichloromethane solvate, C38Ha4B9OP2RhS.0.95(CH2C12), Mr = 891.7, triclinic, Pi, a = 10.271 (4), b = 11.401 (3), c = 19.426 (4)/~, a = 74.86 (2), 13 = 88.51 (3), y = 83.51 (3) °, V= 2182 (2)/~3, Z= 2, Dx = 1.357 g cm-3, graphite-monochromated Mo Ka radiation, a = 0.71073 A, /z = 6.5 cm-1, F(000) = 912, T= 294 K, R = 0.038 for 3984 observed reflections. The title compound contains an l 1-atom RhSB9 nido-structured cage with Rh and S atoms adjacent in the open RhSB3 face. An ethoxy group is bonded to the B atom adjacent to Rh in the open face with Rh--B9 2.119 (6) and B9--O 1.387 (9)A. The phosphine ligands are bonded to the Rh atom with one Rh--P bond [2.278 (2)A] trans to the S atom and the other [2.417 (1) A] located perpendicular to the open face of the cage

Recent Decisions

Comments on recent decisions by Louis Albert Hafner, Patrick F. Coughlin, George J. Murphy, Benedict R. Danko, John E. Lindberg, William J. O\u27Connor, Mark Harry Berens, Joseph M. Gaydos, William G. Greif, Lawrence S. May, Jr., Charles James Perrin, Arthur L. Beaudette, F. Richard Kramer, Kenneth N. Obrecht, William T. Huston, and Maurice J. Moriarty

Chronically KIT-Stimulated Clonally-Derived Human Mast Cells Show Heterogeneity in Different Tissue Microenvironments

Human mast cell precursors arise in the bone marrow and circulate to different tissue microenvironments, where they develop distinct phenotypes that may be characterized by differential expression of the serine protease, chymase. The growth and development of mast cells is stimulated by mast cell growth factor, which is also known as kit ligand because its obligate receptor is KIT, the protein product of the c-KIT proto-oncogene. The in vivo influence of the KIT-kit ligand axis on the phenotype of human mast cells has not been determined. We used immunohistochemistry to detect in situ expression of tryptase and chymase by mast cells of a patient with urticaria pigmentosa and aggressive systemic mastocytosis, whose pathologic mast cells are clonally derived and chronically stimulated by KIT because they all contain the same point mutation causing constitutive activation of KIT. Mast cells in both spleen and skin expressed tryptase, but only in the skin did a majority of mast cells express chymase. We conclude that chronic stimulation of the KIT-kit ligand axis does not irrevocably commit mast cells to a chymase-positive or chymase-negative phenotype. These findings suggest that factors other than kit ligand predominate in determining mast cell phenotype