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Nanoparticles of MnO with average diameters in the 6-14 nm range have been prepared by the decomposition of manganese cupferronate in the presence of TOPO, under solvothermal conditions. Nanoparticles of NiO with average diameters in the 3-24 nm range have been prepared by the decomposition of nickel cupferronate or acetate under solvothermal conditions. The nanoparticles have been characterized by X-ray diffraction and transmission electron microscopy. Both MnO and NiO nanoparticles exhibit supermagnetism, accompanied by magnetic hysteresis below the blocking temperature (T B). The T B increases with the increase in particle size in the case of NiO, and exhibits the reverse trend in the case of MnO.

Pure CoO nanoparticles in the 4.5-18 nm range have been prepared by the decomposition of Co(ΙΙ) cupferronate in Decalin at 270 °C under solvothermal conditions. The particles have been characterized by X-ray diffraction, transmission electron microscopy, and cognate techniques. The particles are stable because of the organic coating that occurs in situ. The organic coating is readily removed by heating the particles to 260 °C without loss of the nanoparticulate nature. Magnetic measurements reveal the presence of ferromagnetic interactions at low temperatures in the small CoO nanoparticles (<16 nm). The small nanoparticles do not exhibit a distinct antiferromagnetic transition around 300 K as the bulk sample but instead show hysteresis below a blocking temperature of ∼10 K.

Multipotential (MP) differentiation is one characteristic of a tissuespecific stem cell (TSC). Lineage tracing of tracheobronchial basal cells after naphthalene (NA) injury or in the postnatal period demonstrated that basal cells were MP progenitors for Clara-like and ciliated cells. These studies, as well as reports of spatially restricted, label-retaining basal cells, and MP differentiation by human bronchial cells support the hypothesis that a TSC maintained and repaired the tracheobronchial epithelium. However, differences in basal cell phenotype (keratin [K] 51 versus K141), age (postnatal versus adult), health status (normal versus injured), and injury type (acid, detergent, NA) limited comparisons among studies and thus diminished the strength of the TSC argument. The finding that K14 was up-regulated after NA injury was a caveat to our previous analysis of reparative (r)K14-expressing cells (EC). Thus, the present study lineage traced steady-state (s)K14EC and evaluated differentiation potential in the normal and repairing epithelium. We showed that sK14EC were unipotential in the normal epithelium and MP after NA, sK14EC-dervied clones were not restricted to putative TSC niches, sK14EC cells were a direct progenitor for Claralike and ciliated cells, MP-sK14EC clones accumulated over time, and sK14EC-derived Clara-like cells were progenitors for ciliated cells.

Phagocytosis of non-opsonized microorganisms by macrophages initiates innate immune responses for host defense against infection. Cytosolic phospholipase A 2 is activated during phagocytosis, releasing arachidonic acid for production of eicosanoids, which initiate acute inflammation. Our objective was to identify pattern recognition receptors that stimulate arachidonic acid release and cyclooxygenase 2 (COX2) expression in macrophages by pathogenic yeast and yeast cell walls. Zymosan-and Candida albicans-stimulated arachidonic acid release from resident mouse peritoneal macrophages was blocked by soluble glucan phosphate. In RAW264.7 cells arachidonic acid release, COX2 expression, and prostaglandin production were enhanced by overexpressing the ␤-glucan receptor, dectin-1, but not dectin-1 lacking the cytoplasmic tail. Pure particulate (1, 3)-␤-D-glucan stimulated arachidonic acid release and COX2 expression, which were augmented in a Tolllike receptor 2 (TLR2)-dependent manner by macrophage-activating lipopeptide-2. However, arachidonic acid release and leukotriene C 4 production stimulated by zymosan and C. albicans were TLR2-independent, whereas COX2 expression and prostaglandin production were partially blunted in TLR2

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Tissue-specific stem cell (TSC) behavior is determined by the stem cell niche. However, delineation of the TSC-niche interaction requires purification of both entities. We reasoned that the niche could be defined by the location of the TSC. We demonstrate that a single CD49f bright /Sca1 1 /ALDH 1 basal cell generates rare label-retaining cells and abundant label-diluting cells. Label-retaining and labeldiluting cells were located in the rimmed domain of a unique clone type, the rimmed clone. The TSC property of self-renewal was tested by serial passage at clonal density and analysis of clone-forming cell frequency. A single clone could be passaged up to five times and formed only rimmed clones. Thus, rimmed clone formation was a cell-intrinsic property. Differentiation potential was evaluated in air-liquid interface cultures. Homogenous cultures of rimmed clones were highly mitotic but were refractory to standard differentiation signals. However, rimmed clones that were cocultured with unfractionated tracheal cells generated each of the cell types found in the tracheal epithelium. Thus, the default niche is promitotic: Multipotential differentiation requires adaptation of the niche. Because lung TSCs are typically evaluated after injury, the behavior of CD49f bright / Sca1 1 /ALDH 1 cells was tested in normal and naphthalene-treated mice. These cells were mitotically active in the normal and repaired epithelium, their proliferation rate increased in response to injury, and they retained label for 34 days. We conclude that the CD49f bright /Sca1 1 /ALDH 1 tracheal basal cell is a TSC, that it generates its own niche in vitro, and that it participates in tracheal epithelial homeostasis and repair.

The enzymatic properties of cytosolic phospholipase A 2 ␥ (cPLA 2 ␥), an isoform of 85-kDa group IV cPLA 2 ␣ (cPLA 2 ␣) were studied in vitro and when the enzyme was expressed in cells. cPLA 2 The membrane-associated activity is inhibited by the group IV PLA 2 inhibitor methylarachidonyl fluorophosphonate, but not effectively by the group VI PLA 2 inhibitor (E)-6-(bromomethylene)-3-(1-naphthalenyl)-2H-tetrahydropyran-2-one. cPLA 2 ␥ has higher lysophospholipase activity than PLA 2 activity. Purified His-cPLA 2 ␥ does not exhibit phospholipase A 1 activity, but sequentially hydrolyzes fatty acid from the sn-2 and sn-1 positions of phosphatidylcholine. cPLA 2 ␥ overexpressed in HEK293 cells is constitutively active in isolated membranes, releasing large amounts of oleic, arachidonic, palmitic, and stearic acids; however, basal fatty acid release from intact cells is not increased. cPLA 2 ␥ overexpressed in lung fibroblasts from cPLA 2 ␣-deficient mice is activated by mouse serum resulting in release of arachidonic, oleic, and palmitic acids, whereas overexpression of cPLA 2 ␣ results primarily in arachidonic acid release.