Silicon-based 2 Terminal Tandem Solar Cells with Lattice-Matched Buffer Layers

A novel structure for a Si-based 2-terminal tandem solar cell was proposed. The structure was optimized to get high efficiency considering the realistic material parameters. Gallium arsenide phosphide (GaAs₁₋xPx) and indium gallium phosphide (In₁₋xGaxP) were suggested as a top-cell material. A semi-empirical method was proposed to calculate the absorption coefficients of GaAs₁₋xPx and In₁₋xGaxP at any value of the composition x. The conversion efficiency of the cell was calculated by simulating its voltage-current characteristics. It was shown that an efficiency of 33.1% can be obtained for a GaAs.₇₃P.₂₇/Si cell and 34.2% for an In.₅₇Ga.₄₃P/Si cell. In₁₋xGaxP was shown to be more promising because of its larger absorption coefficient than GaAs₁₋xPx's

Probiotics, Prebiotics, and Biogenics for the Stomach

Recently, many studies concerning probiotics, prebiotics, and biogenics have been performed, whereas only a few are related to the stomach (about 2% as publication number). In this chapter, we focus on recent studies on probiotics, prebiotics, and biogenics for the stomach and also describe our recent research on a novel strain of lactobacillus beneficial to stomach, Lactobacillus johnsonii No.1088 (LJ88). As probiotics for the stomach, some beneficial strains were summarized, and underlying mechanisms of anti-Helicobacter pylori activity were discussed. Prebiotics for the stomach were considered as a future potential target, since no indigenous bacteria beneficial to the stomach have been found to date. As biogenics, some plant-derived candidates were discussed. In this context, recent results on LJ88 lactobacillus were presented. Orally administered LJ88 inhibited H. pylori growth and the increase in the number of gastrin-producing cells, which side effect is caused by triple therapy for H. pylori. LJ88 had no resistance to typical antibiotics, and both living and heat-killed forms of it increased the number of bifidobacteria among human intestinal-microbiota in mice. These results suggest that LJ88 is a lactobacillus beneficial to both stomach and intestine as a probiotic and biogenic

Neural crest contribution to lingual mesenchyme, epithelium and developing taste papillae and taste buds

AbstractThe epithelium of mammalian tongue hosts most of the taste buds that transduce gustatory stimuli into neural signals. In the field of taste biology, taste bud cells have been described as arising from “local epithelium”, in distinction from many other receptor organs that are derived from neurogenic ectoderm including neural crest (NC). In fact, contribution of NC to both epithelium and mesenchyme in the developing tongue is not fully understood. In the present study we used two independent, well-characterized mouse lines, Wnt1-Cre and P0-Cre that express Cre recombinase in a NC-specific manner, in combination with two Cre reporter mouse lines, R26R and ZEG, and demonstrate a contribution of NC-derived cells to both tongue mesenchyme and epithelium including taste papillae and taste buds. In tongue mesenchyme, distribution of NC-derived cells is in close association with taste papillae. In tongue epithelium, labeled cells are observed in an initial scattered distribution and progress to a clustered pattern between papillae, and within papillae and early taste buds. This provides evidence for a contribution of NC to lingual epithelium. Together with previous reports for the origin of taste bud cells from local epithelium in postnatal mouse, we propose that NC cells migrate into and reside in the epithelium of the tongue primordium at an early embryonic stage, acquire epithelial cell phenotypes, and undergo cell proliferation and differentiation that is involved in the development of taste papillae and taste buds. Our findings lead to a new concept about derivation of taste bud cells that include a NC origin

Increased activity of mesenchymal ALK2â BMP signaling causes posteriorly truncated microglossia and disorganization of lingual tissues

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/153778/1/dvg23337.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/153778/2/dvg23337_am.pd

Contribution of Underlying Connective Tissue Cells to Taste Buds in Mouse Tongue and Soft Palate

Taste buds, the sensory organs for taste, have been described as arising solely from the surrounding epithelium, which is in distinction from other sensory receptors that are known to originate from neural precursors, i.e., neural ectoderm that includes neural crest (NC). Our previous study suggested a potential contribution of NC derived cells to early immature fungiform taste buds in late embryonic (E18.5) and young postnatal (P1-10) mice. In the present study we demonstrated the contribution of the underlying connective tissue (CT) to mature taste buds in mouse tongue and soft palate. Three independent mouse models were used for fate mapping of NC and NC derived connective tissue cells: (1) P0-Cre/R26-tdTomato (RFP) to label NC, NC derived Schwann cells and derivatives; (2) Dermo1-Cre/RFP to label mesenchymal cells and derivatives; and (3) Vimentin-CreER/mGFP to label Vimentin-expressing CT cells and derivatives upon tamoxifen treatment. Both P0-Cre/RFP and Dermo1-Cre/RFP labeled cells were abundant in mature taste buds in lingual taste papillae and soft palate, but not in the surrounding epithelial cells. Concurrently, labeled cells were extensively distributed in the underlying CT. RFP signals were seen in the majority of taste buds and all three types (I, II, III) of differentiated taste bud cells, with the neuronal-like type III cells labeled at a greater proportion. Further, Vimentin-CreER labeled cells were found in the taste buds of 3-month-old mice whereas Vimentin immunoreactivity was only seen in the CT. Taken together, our data demonstrate a previously unrecognized origin of taste bud cells from the underlying CT, a conceptually new finding in our knowledge of taste bud cell derivation, i.e., from both the surrounding epithelium and the underlying CT that is primarily derived from NC

Solvable Optimal Velocity Models and Asymptotic Trajectory

In the Optimal Velocity Model proposed as a new version of Car Following Model, it has been found that a congested flow is generated spontaneously from a homogeneous flow for a certain range of the traffic density. A well-established congested flow obtained in a numerical simulation shows a remarkable repetitive property such that the velocity of a vehicle evolves exactly in the same way as that of its preceding one except a time delay $T$. This leads to a global pattern formation in time development of vehicles' motion, and gives rise to a closed trajectory on $\Delta x$-$v$ (headway-velocity) plane connecting congested and free flow points. To obtain the closed trajectory analytically, we propose a new approach to the pattern formation, which makes it possible to reduce the coupled car following equations to a single difference-differential equation (Rondo equation). To demonstrate our approach, we employ a class of linear models which are exactly solvable. We also introduce the concept of ``asymptotic trajectory'' to determine $T$ and $v_B$ (the backward velocity of the pattern), the global parameters associated with vehicles' collective motion in a congested flow, in terms of parameters such as the sensitivity $a$, which appeared in the original coupled equations.Comment: 25 pages, 15 eps figures, LaTe

Augmentation of smad‐dependent BMP signaling in neural crest cells causes craniosynostosis in mice

Craniosynostosis describes conditions in which one or more sutures of the infant skull are prematurely fused, resulting in facial deformity and delayed brain development. Approximately 20% of human craniosynostoses are thought to result from gene mutations altering growth factor signaling; however, the molecular mechanisms by which these mutations cause craniosynostosis are incompletely characterized, and the causative genes for diverse types of syndromic craniosynostosis have yet to be identified. Here, we show that enhanced bone morphogenetic protein (BMP) signaling through the BMP type IA receptor (BMPR1A) in cranial neural crest cells, but not in osteoblasts, causes premature suture fusion in mice. In support of a requirement for precisely regulated BMP signaling, this defect was rescued on a Bmpr1a haploinsufficient background, with corresponding normalization of Smad phosphorylation. Moreover, in vivo treatment with LDN‐193189, a selective chemical inhibitor of BMP type I receptor kinases, resulted in partial rescue of craniosynostosis. Enhanced signaling of the fibroblast growth factor (FGF) pathway, which has been implicated in craniosynostosis, was observed in both mutant and rescued mice, suggesting that augmentation of FGF signaling is not the sole cause of premature fusion found in this model. The finding that relatively modest augmentation of Smad‐dependent BMP signaling leads to premature cranial suture fusion suggests an important contribution of dysregulated BMP signaling to syndromic craniosynostoses and potential strategies for early intervention.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/98343/1/jbmr1857.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/98343/2/jbmr1857-0008-sm-SupplFigS8.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/98343/3/jbmr1857-0004-sm-SupplFigS4.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/98343/4/jbmr1857-0009-sm-SupplFigS9.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/98343/5/jbmr1857-0005-sm-SupplFigS5.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/98343/6/jbmr1857-0001-sm-SupplFigS1.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/98343/7/jbmr1857-0006-sm-SupplFigS6.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/98343/8/jbmr1857-0002-sm-SupplFigS2.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/98343/9/jbmr1857-0007-sm-SupplFigS7.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/98343/10/jbmr1857-0003-sm-SupplFigS3.pd

Multiple roles of PPAR alpha in brown adipose tissue under constitutive and cold conditions

Peroxisome proliferator-activated receptor alpha (PPAR alpha) is a member of the nuclear receptor family, regulating fatty acid degradation in many organs. Two-dimensional SDS-PAGE of brown adipose tissue (BAT) from PPAR alpha-null mice produced a higher-density spot. Proteomic analysis indicated that the protein was pyruvate dehydrogenase beta (PDH beta). To observe PDH beta regulation in BAT, the organ was stimulated by long-term cold exposure, and the activities of associated enzymes were investigated. Histological and biochemical analyses of BAT showed a significant decrease in the triglyceride content in wild-type mice and some degree of decrease in PPAR alpha-null mice on cold exposure. Analyses of molecules related to glucose metabolism showed that the expression of PDH beta is under PPAR alpha-specific regulation, and that glucose degradation ability may decrease on cold exposure. In contrast, analyses of molecules related to fatty acid metabolism showed that numerous PPAR alpha/gamma target molecules are induced on cold exposure, and that fatty acid degradation ability in wild-type mice is markedly enhanced and also increases to same degree in PPAR alpha-null mice on cold exposure. Thus, this study proposes novel and multiple roles of PPAR alpha in BAT.ArticleGENES TO CELLS. 15(2):91-100 (2010)journal articl

Identification and characterization of neural crest-derived cells in adult periodontal ligament of mice

Cells derived from the neural crest (NC) contribute to the development of several adult tissues, including tooth and periodontal tissue. Here, two transgenic lines, Wnt1-Cre/ZEG and P0-Cre/ZEGwere analyzed to determine the fate and distribution of neural crest cells (NCCs) in adult mouse periodontal ligament (PDL)