We have investigated electronic band structure of a transparent conducting oxide, Nb-doped anatase TiO2 (TNO), by means of first-principles band calculations and photoemission measurements. The band calculations revealed that Nb 4d orbitals are strongly hybridized with Ti 3d ones to form a d-nature conduction band, without impurity states in the in-gap region, resulting in high carrier density exceeding 1021 cm-3 and excellent optical transparency in the visible region. Furthermore, we confirmed that the results of valence band and core-level photoemission measurements are consistent with prediction by the present band calculations.

Fibroblast growth factors (FGFs) and receptors (FGFRs) are expressed in the developing lung and appear to be major regulators of lung growth and differentiation. By using mesenchyme‐free lung epithelial cultures we show that FGF‐1 (aFGF) and FGF‐7 (KGF) produce different effects in the developing lung. FGF‐1 stimulates epithelial proliferation that results in bud formation (branching), while FGF‐7 promotes epithelial proliferation that leads to formation of cyst‐like structures. In addition, FGF‐7 stimulates epithelial differentiation, stimulating expression of SP‐A and SP‐B mRNA throughout the explant, and inducing formation of focal areas of highly differentiated cells. The FGF‐1 effects on differentiation are limited to induction of surfactant protein SP‐B mRNA at the tips of the explant. The FGF‐induced patterns of growth appear to correlate with the distribution of epithelial FGFRs mRNAs; FGFR‐2 IIIb (KGFR) is diffusely expressed in the day 11 lung epithelium, while FGFR‐4 appears in distal but not in proximal sites. We propose that cyst‐like structures may result from FGF‐7 binding to the uniformly distributed FGFR‐2‐IIIb. Lung bud formation may be regulated by FGF‐1 and/or other ligands binding to FGFR‐2 and a distally located FGFR, such as FGFR‐4, leading to an increasing binding and activation of FGFRs at the tips of the explant. Thus, in the embryonic lung epithelium, growth effects of FGFs appear to be dependent on location of FGFRs, while effects on differentiation are ligand‐dependent. Dev. Dyn. 208:398–405, 1997. © 1997 Wiley‐Liss, Inc.

Cell proliferation is an essential requirement for epithelial expansion and tubular branching; however, little is known of how these events are coupled during morphogenesis. We have previously shown that, in the absence of mesenchyme, fibroblast growth factor 1 (FGF‐1) elicits budding of the mouse lung epithelium cultured in a basement membrane matrix. Although bud formation seems to be the manifestation of a localized response of lung epithelial cells to FGF‐1, it is unclear whether budding results from induction of differential rates of cell proliferation within the epithelium. We performed continuous labeling and pulse‐chase experiments in FGF‐1‐treated mesenchyme‐free lung epithelial cultures at distinct stages of bud induction using bromodeoxyuridine (BrdU), to determine when and to what extent cell proliferation contributes to bud formation. When explants were incubated with BrdU either before bud induction (0–18 hr in culture) or at the onset of budding (24–30 hr), labeled nuclei were found distributed throughout the entire explant. In contrast, BrdU incubation after the onset of budding (30–48 hr) resulted in labeling concentrated in the budding areas, and a decrease of labeling toward the proximal region of the explant, between buds. These results demonstrate that differential rates of cell proliferation between bud and nonbud areas do not appear until when buds are almost completely formed. Thus, in the developing lung epithelium in vitro, bud outgrowth is not triggered by induction of localized cell proliferation. Dev. Dyn. 1998;213:228–235. © 1998 Wiley‐Liss, Inc.

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Mouse submandibular epithelium shows branching morphogenesis in mesenchyme-free conditions when covered with a basement membrane matrix (Matrigel) in medium supplemented with epidermal growth factor. In the present study, the role of laminin-1 (LN1), a major glycoprotein of Matrigel, in this culture system was defined. When the epithelium was cultured in a LN1-nidogen gel, the epithelium showed much branching, comparable to that observed with Matrigel. By electron microscopy, only a felt-like matrix was formed on the epithelial surface in the LN1-nidogen gel cultures, while an organized basal lamina structure was formed on the epithelial surface in direct or transfilter recombination cultures with mesenchyme. Next, the epithelium covered with Matrigel was cultured in medium containing either biologically active peptides from LN1, IKVAV-including peptide (2097-2108), AG10 (2183-2194), AG32 (2370-2381) or AG73 (2719-2730) from the alpha1 chain, or YIGSR-including peptide (926-933) from the beta1 chain. Only AG73 (RKRLQVQLSIRT from the alpha1 chain carboxyl-terminal globular domain) inhibited the epithelial branching in Matrigel. These results suggest that LN1-nidogen can support the branching morphogenesis of submandibular epithelium even if LN1-nidogen is not assembled into an intact basal lamina, and that the AG73 sequence is an important site on LN1, which interacts with submandibular epithelial cells.