Assessing the performance of artificial reefs as substitute habitat for temperate reef fishes: Implications for reef design and placement.

Artificial reefs (ARs) have been advocated and implemented as management tools for recreational fisheries, species conservation and habitat replacement. For ARs to function as substitute habitat for degraded natural reefs, they should perform as close as possible to local natural reefs, however this is seldom investigated. Here we evaluated the performance of new custom-designed reef structures (CDARs) as fish habitat. As a benchmark for their success, we compared fish abundance, diversity and community composition on CDARs to another commonly used AR type (Reef Balls (RBs)) and nearby natural reefs. Fish were monitored on all reef types over two recruitment seasons at three locations in Port Phillip Bay, Australia. Overall, there were no consistent differences in fish density among reef types, although densities on both AR designs were markedly lower than natural reefs at some locations. However, fish species richness on the CDARs was, on average, 2× higher than natural or RB reefs. There were large dissimilarities in fish community composition among reef types across all locations and years. These dissimilarities declined over time with the CDARs becoming more similar to natural communities than to RB reefs. Our results suggest that CDARs can play a role in reef fish conservation where natural reefs are under threat, supporting natural community structure and enhancing local biodiversity. Overall, our findings suggest that location of deployment, rather than design, has a more significant influence on fish abundances on ARs, whereas reef design is an important determinant of species diversity and community structure irrespective of location. ARs represent an important management tool for enhancing fisheries productivity and conservation in areas where reef habitat has been degraded or lost. However, failure to incorporate consideration of reef location and design into future AR deployments may lead to poor performance and failure to achieve restoration or conservation goals.

Diabetes and hypercholesterolemia increase blood-brain barrier permeability and brain amyloid deposition: beneficial effects of the LpPLA2 inhibitor darapladib.

Diabetes mellitus (DM) and hypercholesterolemia (HC) have emerged as major risk factors for Alzheimer's disease, highlighting the importance of vascular health to normal brain functioning. Our previous study showed that DM and HC favor the development of advanced coronary atherosclerosis in a porcine model, and that treatment with darapladib, an inhibitor of lipoprotein-associated phospholipase A2, blocks atherosclerosis progression and improves animal alertness and activity levels. In the present study, we examined the effects of DM and HC on the permeability of the blood-brain barrier (BBB) using immunoglobulin G (IgG) as a biomarker. DMHC increased BBB permeability and the leak of microvascular IgG into the brain interstitium, which was bound preferentially to pyramidal neurons in the cerebral cortex. We also examined the effects of DMHC on the brain deposition of amyloid peptide (Aß42), a well-known pathological feature of Alzheimer's disease. Nearly all detectable Aß42 was contained within cortical pyramidal neurons and DMHC increased the density of Aß42-loaded neurons. Treatment of DMHC animals with darapladib reduced the amount of IgG-immunopositive material that leaked into the brain as well as the density of Aß42-containing neurons. Overall, these results suggest that a prolonged state of DMHC may have chronic deleterious effects on the functional integrity of the BBB and that, in this DMHC pig model, darapladib reduces BBB permeability. Also, the preferential binding of IgG and coincident accumulation of Aß42 in the same neurons suggests a mechanistic link between the leak of IgG through the BBB and intraneuronal deposition of Aß42 in the brain.

Atrial septal defect closure in a patient with "irreversible" pulmonary hypertensive arteriopathy.

The presence of irreversible pulmonary hypertension in patients with atrial septal defect (ASD) is thought to preclude shunt closure. We report the case of a woman with plexiform pulmonary arteriopathy secondary to an ostium secundum ASD who was able to successfully undergo percutaneous shunt closure following therapy with chronic intravenous prostacyclin (Flolan). One year after closure, the patient was weaned off Flolan over a period of 7 months following the institution of oral Bosentan therapy. Our case illustrates how aggressive vasodilator therapy with prostaglandins may be capable of reducing pulmonary artery pressure and permitting shunt closure in a patient once considered to have "inoperable" pulmonary arteriopathy.

Pulmonary pathology of severe acute respiratory syndrome in Toronto.

The severe acute respiratory syndrome (SARS) pandemic in Toronto resulted in a large number of autopsies on its victims. We describe the pulmonary pathology of patients who died in the 2003 Toronto outbreak. Autopsy material from the lungs of 20 patients who died between March and July 2003 were characterized by histology, molecular biology, and immunohistochemistry for cytokeratins, thyroid transcription factor-1, CD68, Epstein-Barr virus, cytomegalovirus, and human herpes simplex viruses. Matched controls were obtained from patients who died of other causes over the same interval. The mean duration of illness was 27 days (range 5-108 days). Post-mortem lung tissues from 19 of 20 patients with probable SARS were positive for SARS-associated coronavirus by RT-PCR. Histologically, all patients showed varying degrees of exudative and proliferative phase acute lung injury, evidenced in conventional and immunohistochemical stains by edema, inflammatory infiltrate, pneumocyte hyperplasia, fibrinous exudates, and organization. Eight of 20 patients showed predominantly a diffuse alveolar damage pattern of acute lung injury, six showed predominantly an acute fibrinous and organizing pneumonia pattern, and the remainder showed an admixture of the two patterns. Squamous metaplasia and scattered multinucleate giant cells were present in most cases. Vascular fibrin thrombi were a common finding and were often associated with pulmonary infarcts. Special stains demonstrated vascular endothelial damage of both small- and mid-sized pulmonary vessels. Two cases were complicated by invasive fungal disease consistent with Aspergillosis, and another by coinfection with cytomegalovirus. Our findings indicate that the lungs of patients who die of SARS are almost always positive for the SARS-associated coronavirus by RT-PCR, and may show features of both diffuse alveolar damage and acute fibrinous and organizing pneumonia patterns of acute injury. Cases of SARS may be complicated by coexistent infections and therapy-related lung injury.

Bilateral lung transplantation for metastatic leiomyosarcoma.

As increased experience is gained in the field of lung transplantation, novel applications for this life saving therapy will evolve. We have described a case of bilateral lung transplantation in a young patient with respiratory failure secondary to metastatic leiomyosarcoma that was limited to the lungs. While lung transplantation for malignancy remains a controversial area, this case illustrates that lung transplantation can provide improved quality and quantity of life for highly selected patients with malignant disease.

Rapidly progressive pulmonary fibrosis in a patient treated with danazol for idiopathic thrombocytopenic purpura.

The case of a patient that developed pulmonary fibrosis two months after initiation of danazol for treatment of idiopathic thrombocytopenic purpura is described. Bilateral pneumothoraxes and pneumomediastinum complicated the rapidly fatal pulmonary fibrosis. An association between danazol therapy and the development of pulmonary fibrosis is suspected. There is only one other case report with this connection in the literature.

De novo pulmonary capillary hemangiomatosis occurring rapidly after bilateral lung transplantation.

A 45-year-old woman experienced diffuse bilateral pulmonary capillary hemangiomatosis within 3 months after bilateral lung transplantation. The donor was a 41-year-old man with excellent lung function and without histologic or macroscopic pulmonary lesions at the time of retrieval. This case supports the theory that persistent infection or inflammation may be an inciting factor in uncontrolled angiogenesis, leading ultimately to diffuse pulmonary capillary hemangiomatosis.

Phosphoinositide 3-kinase regulates beta2-adrenergic receptor endocytosis by AP-2 recruitment to the receptor/beta-arrestin complex.

Internalization of beta-adrenergic receptors (betaARs) occurs by the sequential binding of beta-arrestin, the clathrin adaptor AP-2, and clathrin. D-3 phosphoinositides, generated by the action of phosphoinositide 3-kinase (PI3K) may regulate the endocytic process; however, the precise molecular mechanism is unknown. Here we demonstrate that betaARKinase1 directly interacts with the PIK domain of PI3K to form a cytosolic complex. Overexpression of the PIK domain displaces endogenous PI3K from betaARK1 and prevents betaARK1-mediated translocation of PI3K to activated beta2ARs. Furthermore, disruption of the betaARK1/PI3K interaction inhibits agonist-stimulated AP-2 adaptor protein recruitment to the beta2AR and receptor endocytosis without affecting the internalization of other clathrin dependent processes such as internalization of the transferrin receptor. In contrast, AP-2 recruitment is enhanced in the presence of D-3 phospholipids, and receptor internalization is blocked in presence of the specific phosphatidylinositol-3,4,5-trisphosphate lipid phosphatase PTEN. These findings provide a molecular mechanism for the agonist-dependent recruitment of PI3K to betaARs, and support a role for the localized generation of D-3 phosphoinositides in regulating the recruitment of the receptor/cargo to clathrin-coated pits.