Magnus den Godes, Harald Haardraades og hans sønners sagaer;

Mode of access: Internet.

Sögur Noregs konúnga frá Magnúsi Berfætta til Magnúss Erlíngssonar.

Edited by R. K. Rask.

Truncated recombinant human SP-D attenuates emphysema and type II cell changes in SP-D deficient mice

BACKGROUND: Surfactant protein D (SP-D) deficient mice develop emphysema-like pathology associated with focal accumulations of foamy alveolar macrophages, an excess of surfactant phospholipids in the alveolar space and both hypertrophy and hyperplasia of alveolar type II cells. These findings are associated with a chronic inflammatory state. Treatment of SP-D deficient mice with a truncated recombinant fragment of human SP-D (rfhSP-D) has been shown to decrease the lipidosis and alveolar macrophage accumulation as well as production of proinflammatory chemokines. The aim of this study was to investigate if rfhSP-D treatment reduces the structural abnormalities in parenchymal architecture and type II cells characteristic of SP-D deficiency. METHODS: SP-D knock-out mice, aged 3 weeks, 6 weeks and 9 weeks were treated with rfhSP-D for 9, 6 and 3 weeks, respectively. All mice were sacrificed at age 12 weeks and compared to both PBS treated SP-D deficient and wild-type groups. Lung structure was quantified by design-based stereology at the light and electron microscopic level. Emphasis was put on quantification of emphysema, type II cell changes and intracellular surfactant. Data were analysed with two sided non-parametric Mann-Whitney U-test. MAIN RESULTS: After 3 weeks of treatment, alveolar number was higher and mean alveolar size was smaller compared to saline-treated SP-D knock-out controls. There was no significant difference concerning these indices of pulmonary emphysema within rfhSP-D treated groups. Type II cell number and size were smaller as a consequence of treatment. The total volume of lamellar bodies per type II cell and per lung was smaller after 6 weeks of treatment. CONCLUSION: Treatment of SP-D deficient mice with rfhSP-D leads to a reduction in the degree of emphysema and a correction of type II cell hyperplasia and hypertrophy. This supports the concept that rfhSP-D might become a therapeutic option in diseases that are characterized by decreased SP-D levels in the lung.

The history of Esarhaddon (son of Sennacherib) king of Assyria, B. C. 681-688; tr. from the cuneiform inscriptions upon cylinders and tablets in the British museum collection, together with original texts; a grammatical analysis of each word, explanations of the ideographs by extracts from the bi-lingual syllabaries, and list of eponyms, etc.,

Cuneiform text and English translation on opposite pages.

The life of Gustavus Adolphus, surnamed The Great, King of Sweden /

Mode of access: Internet.

A descriptive catalogue (with remarks and anecdotes never before published in English) of some pictures, of the different schools, purchased for His Majesty the late King of Poland, which will be exhibited early in 1802, at the Great Room, No. 3, in Berners-Street, the third door on the right, from Oxford-Street /

Mode of access: Internet.

The life of Marguerite d'Angouleme, Queen of Navarre, Duchesse d'Alencon and de Berry, sister of Francis I., King of France : From numerous unpublished sources, including MS. documents in the Bibliotheque Imperiale, and the Archives du Royaume de France, and also the private correspondence of Queen Marguerite with Francis I., & c.

Mode of access: Internet.

Gesta regis Henrici Secundi Benedicti abbatis. The chronicle of the reigns of Henry II. and Richard I.A.D. 1169-1192; known commonly under the name of Benedict of Peterborough.

Text in Latin.

3-D reconstruction by extended depth-of-field in failure analysis - Case study II: Fractal analysis of interlaminar fracture in carbon/epoxy composites

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Self-assembly of Pd(II) pyrazolyl complexes to 1-D hydrogen-bonded coordination polymers

This work describes the synthesis and characterization of two novel Pd(II) pyrazolyl complexes of the type [PdX2(HdmPz)(2)](n) {X=SCN- (1), N-3(-) (2); HdmPz=3,5-dimethylpyrazole} that self-assemble through N-H...NCS or N-H...NNN hydrogen bonds to yield infinite one-dimensional chains, as confirmed by single crystal X-ray study on 1. The expected solid state polymeric structure for 2 is slowly broken up in CHCl3 Solution, leading to an equilibrium mixture of cis and trans-[Pd(N-3)(2)(HdmPz)(2)] monomers, as demonstrated by time-dependent IR and NMR studies. (C) 2003 Elsevier B.V. B.V. All rights reserved.

Targeted ablation of the vitamin D receptor: An animal model of vitamin D-dependent rickets type II with alopecia

Vitamin D, the major steroid hormone that controls mineral ion homeostasis, exerts its actions through the vitamin D receptor (VDR). The VDR is expressed in many tissues, including several tissues not thought to play a role in mineral metabolism. Studies in kindreds with VDR mutations (vitamin D-dependent rickets type II, VDDR II) have demonstrated hypocalcemia, hyperparathyroidism, rickets, and osteomalacia. Alopecia, which is not a feature of vitamin D deficiency, is seen in some kindreds. We have generated a mouse model of VDDR II by targeted ablation of the second zinc finger of the VDR DNA-binding domain. Despite known expression of the VDR in fetal life, homozygous mice are phenotypically normal at birth and demonstrate normal survival at least until 6 months. They become hypocalcemic at 21 days of age, at which time their parathyroid hormone (PTH) levels begin to rise. Hyperparathyroidism is accompanied by an increase in the size of the parathyroid gland as well as an increase in PTH mRNA levels. Rickets and osteomalacia are seen by day 35; however, as early as day 15, there is an expansion in the zone of hypertrophic chondrocytes in the growth plate. In contrast to animals made vitamin D deficient by dietary means, and like some patients with VDDR II, these mice develop progressive alopecia from the age of 4 weeks.