Laboratory Testing of Precast Paving Notch System, RB01-005, 2008

The Iowa State University (ISU) Bridge Engineering Center (BEC) performed full-scale laboratory testing of the proposed paving notch replacement system. The objective of the testing program was to verify the structural capacity of the proposed precast paving notch system and to investigate the feasibility of the proposed solution. This report describes the laboratory testing procedure and discusses its results

Nouba De Ochak Sabahna V ; Nouba De Ochak Fi Dauha Ti Lazhar VI / Troupe El Hadj Abdelslam Errbati, chant [acc. voc. et instr.]

[Traditions. Afrique du Nord. Maroc]

Materiales para una flora de las algas del NE de España, V a, Bacillariophyta

En las páginas siguientes se estudian las diatomeas contenidas en una serie de recolecciones que no han sido utilizadas en la preparación de trabajos de tipo regional publicados anteriormente, aunque una parte de estos materiales inéditos se aprovechó para un estudio sobre la vegetación de las aguas dulces de Cataluña (Vegetatio, vol. i, págs. 258-284, 1949), en el que se pueden encontrar algunas referencias complementarias sobre ecología y biocenología de las especies.

Aportación a la Flora Bentónica de las Islas Baleares, V.

Los numerosos trabajos sobre fitobentos marino de las islas Baleares fueron recopilados en los catálogos florísticos de RIBERA & GÓMEZ (Collect. Bot. (Barcelona) 15: 377-406. 1984; Collect. Bot. (Barcelona) 16:25-41.1985). Posteriormente, debido a la realización de numerosos estudios bentónicos de la zona, se han publicado adiciones a dicho catálogo (PERICAS, Boll. Soc. Hist. Nat. Balears: 139-146.1984; BALLESTEROS, Bull. Inst. Cat. Hist. Nat. 51 (See. Bot, 5): 31-33. 1984; BALLESTEROS, Fol. Bot. Mise. 6: 65-70. 1989; RULL LLUCH, GÓMEZ GARRETA and RIBERA Collect. Bot. (Barcelona) 15: 377-406. 1987; CREMADES Anales Jard. Bot. Madrid 46 (1): 149-152. 1989; CREMADES A nales Jard. Bot. Madrid 46 (1): 341-343. 1989).

De vegetations notulae, V

Asplenio (onopteridis)-quercetum ilicis

Role of the V-ATPase in regulation of the vacuolar fission-fusion equilibrium.

Like numerous other eukaryotic organelles, the vacuole of the yeast Saccharomyces cerevisiae undergoes coordinated cycles of membrane fission and fusion in the course of the cell cycle and in adaptation to environmental conditions. Organelle fission and fusion processes must be balanced to ensure organelle integrity. Coordination of vacuole fission and fusion depends on the interactions of vacuolar SNARE proteins and the dynamin-like GTPase Vps1p. Here, we identify a novel factor that impinges on the fusion-fission equilibrium: the vacuolar H(+)-ATPase (V-ATPase) performs two distinct roles in vacuole fission and fusion. Fusion requires the physical presence of the membrane sector of the vacuolar H(+)-ATPase sector, but not its pump activity. Vacuole fission, in contrast, depends on proton translocation by the V-ATPase. Eliminating proton pumping by the V-ATPase either pharmacologically or by conditional or constitutive V-ATPase mutations blocked salt-induced vacuole fragmentation in vivo. In living cells, fission defects are epistatic to fusion defects. Therefore, mutants lacking the V-ATPase display large single vacuoles instead of multiple smaller vacuoles, the phenotype that is generally seen in mutants having defects only in vacuolar fusion. Its dual involvement in vacuole fission and fusion suggests the V-ATPase as a potential regulator of vacuolar morphology and membrane dynamics.

Atopic dermatitis-like disease and associated lethal myeloproliferative disorder arise from loss of Notch signaling in the murine skin.

BACKGROUND: The Notch pathway is essential for proper epidermal differentiation during embryonic skin development. Moreover, skin specific loss of Notch signaling in the embryo results in skin barrier defects accompanied by a B-lymphoproliferative disease. However, much less is known about the consequences of loss of Notch signaling after birth. METHODOLOGY AND PRINCIPAL FINDINGS: To study the function of Notch signaling in the skin of adult mice, we made use of a series of conditional gene targeted mice that allow inactivation of several components of the Notch signaling pathway specifically in the skin. We demonstrate that skin-specific inactivation of Notch1 and Notch2 simultaneously, or RBP-J, induces the development of a severe form of atopic dermatitis (AD), characterized by acanthosis, spongiosis and hyperkeratosis, as well as a massive dermal infiltration of eosinophils and mast cells. Likewise, patients suffering from AD, but not psoriasis or lichen planus, have a marked reduction of Notch receptor expression in the skin. Loss of Notch in keratinocytes induces the production of thymic stromal lymphopoietin (TSLP), a cytokine deeply implicated in the pathogenesis of AD. The AD-like associated inflammation is accompanied by a myeloproliferative disorder (MPD) characterized by an increase in immature myeloid populations in the bone marrow and spleen. Transplantation studies revealed that the MPD is cell non-autonomous and caused by dramatic microenvironmental alterations. Genetic studies demontrated that G-CSF mediates the MPD as well as changes in the bone marrow microenvironment leading to osteopenia. SIGNIFICANCE: Our data demonstrate a critical role for Notch in repressing TSLP production in keratinocytes, thereby maintaining integrity of the skin and the hematopoietic system.

[Voyage en Italie : 1824-1830]. , Palais Maccarani. Maison de Sixte V : [deux plans de rez-de-chaussée] : [dessin] / h. L. [Henri Labrouste]

Référence bibliographique : Weigert, 578

Notch signaling is a direct determinant of keratinocyte growth arrest and entry into differentiation.

The role of Notch signaling in growth/differentiation control of mammalian epithelial cells is still poorly defined. We show that keratinocyte-specific deletion of the Notch1 gene results in marked epidermal hyperplasia and deregulated expression of multiple differentiation markers. In differentiating primary keratinocytes in vitro endogenous Notch1 is required for induction of p21WAF1/Cip1 expression, and activated Notch1 causes growth suppression by inducing p21WAF1/Cip1 expression. Activated Notch1 also induces expression of 'early' differentiation markers, while suppressing the late markers. Induction of p21WAF1/Cip1 expression and early differentiation markers occur through two different mechanisms. The RBP-Jkappa protein binds directly to the endogenous p21 promoter and p21 expression is induced specifically by activated Notch1 through RBP-Jkappa-dependent transcription. Expression of early differentiation markers is RBP-Jkappa-independent and can be induced by both activated Notch1 and Notch2, as well as the highly conserved ankyrin repeat domain of the Notch1 cytoplasmic region. Thus, Notch signaling triggers two distinct pathways leading to keratinocyte growth arrest and differentiation.