Solubility Limits of Α'-SiAION Solid Solutions in the System Si,Al,Y/N,O

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/66438/1/j.1151-2916.1991.tb06797.x.pd

Structural basis for tetraspanin functions as revealed by the cryo-EM structure of uroplakin complexes at 6-Å resolution

Tetraspanin uroplakins (UPs) Ia and Ib, together with their single-spanning transmembrane protein partners UP II and IIIa, form a unique crystalline 2D array of 16-nm particles covering almost the entire urothelial surface. A 6 Å–resolution cryo-EM structure of the UP particle revealed that the UP tetraspanins have a rod-shaped structure consisting of four closely packed transmembrane helices that extend into the extracellular loops, capped by a disulfide-stabilized head domain. The UP tetraspanins form the primary complexes with their partners through tight interactions of the transmembrane domains as well as the extracellular domains, so that the head domains of their tall partners can bridge each other at the top of the heterotetramer. The secondary interactions between the primary complexes and the tertiary interaction between the 16-nm particles contribute to the formation of the UP tetraspanin network. The rod-shaped tetraspanin structure allows it to serve as stable pilings in the lipid sea, ideal for docking partner proteins to form structural/signaling networks

Subsolidus phase relationships in the systems Re---Al---O---N (Where Re = Rare Earth Elements)

Subsolidus phase relationships in the systems R---Al---O---N (where Re = Ce, Pr, Nd, and Sm) were determined. A family of lanthanum aluminium oxynitrides, ReAl12O18N, with magnetoplumbite structure occurs, where the rare earth elements have large ionic radii ranging from La to Eu. The lattice parameters of these compounds were determined, and the results indicated that all these compounds have nearly the same value of a = 5.564 A, C = 22.00 A, and c/a = 3.96 A.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/29008/1/0000037.pd

Subsolidus phase relationships in part of the system Si, Al, Ca/N, O

Subsolidus phase relationships in the region bounded by Si3N4, SiO2, CaSiO3, 2CaO.Al2O3.SiO2, CaO.Al2O3, Al2O3 and [beta]'-Si2Al4O4N4([beta]60) have been studied. A new quinary phase with composition near to CaO. 1[middle dot]33Al2O3.0[middle dot]67Si2N2O (designated as S-phase) and a complete series of solid solution between S-phase and CaO.2Al2O3 were found. Fourteen compatible tetrahedra, of which five contain S-phase, occur in the region explored. They are as follows: X1-SiO2-anorthite-mullite; X1-anorthite-mullite-Al2O3; X1-anorthite-Al2O3-[beta]60; X1-anorthite-[beta]60-Si3N4; X1-anorthite-Si3N4-Si2N2O; X1-anorthite-Si2N2O-SiO2; anorthite-Si2N2O-SiO2-CaSiO3; anorthite-Si2N2O-CaSiO3-gehlenite; anorthite-Si2N2O-gehlenite-Si3N4; S-anorthite-Al2O3-[beta]60; S-Al2O3-CaO.2Al2O3-gehlenite; S-Al2O3-gehlenite-anorthite; S-gehlenite-anorthite-Si3N4; S-anorthite-Si3N4-[beta]60.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/27507/1/0000551.pd

A survivin gene signature predicts aggressive tumor behavior

Gene signatures that predict aggressive tumor behavior at the earliest stages of disease, ideally before overt tissue abnormalities, are urgently needed. To search for such genes, we generated a transgenic model of survivin, an essential regulator of cell division and apoptosis overexpressed in cancer. Transgenic expression of survivin in the urinary bladder did not cause histologic abnormalities of the urothelium. However, microarray analysis revealed that survivin-expressing bladders exhibited profound changes in gene expression profile affecting extracellular matrix and inflammatory genes. Following exposure to a bladder carcinogen, N-butyl-N-(4-hydroxybutyl) nitrosamine (OH-BBN), survivin transgenic animals exhibited accelerated tumor progression, preferential incidence of tumors as compared with premalignant lesions, and dramatically abbreviated survival. Conversely, transgenic expression of a survivin Thr34--\u3eAla dominant-negative mutant did not cause changes in gene expression or accelerated tumor progression after OH-BBN treatment. Therefore, survivin expression induces global transcriptional changes in the tissue microenvironment that may promote tumorigenesis. Detection of survivin or its associated gene signature may provide an early biomarker of aggressive tumor behavior before the appearance of tissue abnormalities

Proximal location of mouse prostate epithelial stem cells: a model of prostatic homeostasis

Stem cells are believed to regulate normal prostatic homeostasis and to play a role in the etiology of prostate cancer and benign prostatic hyperplasia. We show here that the proximal region of mouse prostatic ducts is enriched in a subpopulation of epithelial cells that exhibit three important attributes of epithelial stem cells: they are slow cycling, possess a high in vitro proliferative potential, and can reconstitute highly branched glandular ductal structures in collagen gels. We propose a model of prostatic homeostasis in which mouse prostatic epithelial stem cells are concentrated in the proximal region of prostatic ducts while the transit-amplifying cells occupy the distal region of the ducts. This model can account for many biological differences between cells of the proximal and distal regions, and has implications for prostatic disease formation

Cellular basis of urothelial squamous metaplasia: roles of lineage heterogeneity and cell replacement

Although the epithelial lining of much of the mammalian urinary tract is known simply as the urothelium, this epithelium can be divided into at least three lineages of renal pelvis/ureter, bladder/trigone, and proximal urethra based on their embryonic origin, uroplakin content, keratin expression pattern, in vitro growth potential, and propensity to keratinize during vitamin A deficiency. Moreover, these cells remain phenotypically distinct even after they have been serially passaged under identical culture conditions, thus ruling out local mesenchymal influence as the sole cause of their in vivo differences. During vitamin A deficiency, mouse urothelium form multiple keratinized foci in proximal urethra probably originating from scattered K14-positive basal cells, and the keratinized epithelium expands horizontally to replace the surrounding normal urothelium. These data suggest that the urothelium consists of multiple cell lineages, that trigone urothelium is closely related to the urothelium covering the rest of the bladder, and that lineage heterogeneity coupled with cell migration/replacement form the cellular basis for urothelial squamous metaplasia