Upper circulation deck, Mooloomba House, Point Lookout, North Stradbroke Island

View along circulation deck to belvedere (deck) beyond.

Lower studio dining room, Mooloomba House, Point Lookout, North Stradbroke Island

View through courtyard to lower studio dining room, as seen from upper living area.

Lower studio dining room, Mooloomba House, Point Lookout, North Stradbroke Island

View through courtyard to lower studio dining room, as seen from upper living area.

Mooloomba House, Point Lookout, North Stradbroke Island

North elevation, deck below and belvedere above, as seen from path to beach.

Lower studio dining room, Mooloomba House, Point Lookout, North Stradbroke Island

View through courtyard to lower studio dining room, as seen from upper living area.

Internal cladding to north-east facade, Mooloomba House, Point Lookout, North Stradbroke Island

View of internal cladding to north-east facade as seen from dining studio.

Dining studio, Mooloomba House, Point Lookout, North Stradbroke Island

View through courtyard to dining studio as seen from upper living room.

Mooloomba House, Point Lookout, North Stradbroke Island

North elevation, deck below and belvedere above, as seen from path to beach.

Cladding detail, Mooloomba House, Point Lookout, North Stradbroke Island

Detail view of cladding to upper level dining studio.

Determination of Wolbachia genome size by Pulsed-Field Gel Electrophoresis

Genome sizes of six different Wolbachia strains from insect and nematode hosts have been determined by pulsed-field gel electrophoresis of purified DNA both before and after digestion with rare-cutting restriction endonucleases. Enzymes SmaI, ApaI, AscI, and FseI cleaved the studied Wolbachia strains at a small number of sites and were used for the determination of the genome sizes of wMelPop, wMel, and wMelCS (each 1.36 Mb), wRi (1.66 Mb), wBma (1.1 Mb), and wDim (0.95 Mb). The Wolbachia genomes studied were all much smaller than the genomes of free-living bacteria such as Escherichia coli (4.7 Mb), as is typical for obligate intracellular bacteria. There was considerable genome size variability among Wolbachia strains, especially between the more parasitic A group Wolbachia infections of insects and the mutualistic C and D group infections of nematodes. The studies described here found no evidence for extrachromosomal plasmid DNA in any of the strains examined. They also indicated that the Wolbachia genome is circular.

Arterial heparan sulfate proteoglycans inhibit vascular smooth muscle cell proliferation and phenotype change in vitro and neointimal formation in vivo

Purpose: The aim of this study was to determine whether heparan sulfate proteoglycans (HSPGs) from the normal arterial wall inhibit neointimal formation after injury in vivo and smooth muscle cell (SMC) phenotype change and proliferation in vitro. Methods: Arterial HSPGs were extracted from rabbit aortae and separated by anion-exchange chromatography. The effect of HSPGs, applied in a periadventitial gel, on neointimal formation was assessed 14 days after balloon catheter injury of rabbit carotid arteries. Their effect on SMC phenotype and proliferation was measured by point-counting morphometry of the cytoplasmic volume fraction of myofilaments (Vvmyo) and H-3-thymidine incorporation in SMCs in culture. Results: Arterial HSPGs (680 mu g) reduced neointimal formation by 35% at 14 days after injury (P =.029), whereas 2000 mu g of the low-molecular-weight heparin Enoxaparin was ineffective. HSPGs at 34 mu g/mL maintained subconfluent primary cultured SMCs with the same high Vvmyo (52.1% +/- 13.8%) after 5 days in culture as did cells freshly isolated from the arterial wall (52.1% +/- 15.1%). In contrast, 100 mu g/mL Enoxaparin was ineffective in preventing phenotypic change over this time period (Vvmyo 38.9% +/- 14.6%, controls 35.9% +/- 12.8%). HSPGs also inhibited 3H-thymidine incorporation into primary cultured SMCs with an ID50 value of 0.4 mu g/mL compared with a value of 14 mu g/ml; for Enoxaparin (P