Rapid survey protocol that provides dynamic information on reef condition to managers of the Great Barrier Reef.

Managing to support coral reef resilience as the climate changes requires strategic and responsive actions that reduce anthropogenic stress. Managers can only target and tailor these actions if they regularly receive information on system condition and impact severity. In large coral reef areas like the Great Barrier Reef Marine Park (GBRMP), acquiring condition and impact data with good spatial and temporal coverage requires using a large network of observers. Here, we describe the result of ~10 years of evolving and refining participatory monitoring programs used in the GBR that have rangers, tourism operators and members of the public as observers. Participants complete Reef Health and Impact Surveys (RHIS) using a protocol that meets coral reef managers' needs for up-to-date information on the following: benthic community composition, reef condition and impacts including coral diseases, damage, predation and the presence of rubbish. Training programs ensure that the information gathered is sufficiently precise to inform management decisions. Participants regularly report because the demands of the survey methodology have been matched to their time availability. Undertaking the RHIS protocol we describe involves three ~20 min surveys at each site. Participants enter data into an online data management system that can create reports for managers and participants within minutes of data being submitted. Since 2009, 211 participants have completed a total of more than 10,415 surveys at more than 625 different reefs. The two-way exchange of information between managers and participants increases the capacity to manage reefs adaptively, meets education and outreach objectives and can increase stewardship. The general approach used and the survey methodology are both sufficiently adaptable to be used in all reef regions.

The pyrimido-pyrimidine derivatives, dipyridamole, mopidamol and RA-642, prevent from retinal vascular defects in experimental diabetes mellitus.

We compared the effects of dipyridamole, RA-642, and mopidamol on platelet activity and thromboxane/prostacyclin balance in relation to the degree of retinal vascularization in a model of experimental streptozotocin-induced diabetes in rats. After 3 months, collagen-induced platelet aggregation in whole blood was 25% higher in diabetic animals than in nondiabetics. Dipyridamole inhibited 43% platelet aggregation, mopidamol 39%, and RA-642 36%. Platelet production of thromboxane B2 was 87% higher in untreated diabetic rats. Mopidamol and RA-642 produced a 46% and 41% inhibition of thromboxane B2. Dipyridamole did not inhibited thromboxane B2 synthesis. Aortic production of 6-keto-PGF1 alpha was 43% lower in untreated diabetic animals and showed no change after treatment with either mopidamol or RA-642. In contrast, dipyridamole caused a 90% increase in aortic production of prostacyclin. Computerized analysis of retinal vascularization showed that untreated diabetic rats had a 81% decrease in the area occupied by peroxidase-labelled vessels as compared with nondiabetics. Treatment with dipyridamole, mopidamol, and RA-642 caused 2.5-fold, 2.8-fold and four-fold increases, respectively, in the percentage of retinal surface occupied by peroxidase-labelled vessels. Differences in retinal vascularization between diabetic animals given RA-642 and nondiabetic controls were negligible.

Effects of ditazol on the vascular retinal pattern in experimental diabetes in rats.

Platelets from diabetic patients are hypersensitive to aggregating agents. An imbalance in thromboxane/prostacyclin synthesis has been postulated as an antecedent to the development of diabetic retinopathy. We studied 3-month streptozotocin-diabetic rats (SDR) treated with 200 mg/kg/day p.o. of ditazol, an antiplatelet drug that inhibits thromoboxane formation. Thromboxane B2 (TxB2) production was higher and 6-keto-PGF1 alpha synthesis lower in SDR than nondiabetic rats (NDR). In treated animals, ditazol inhibited platelet aggregation by 66%, and TxB2 production by 58%, and increased vascular 6-keto-PGF 1 alpha by 45%. Furthermore, 13% of the retinal surface was covered by peroxidase-labelled vessels in NDR, 2.1% in nontreated SDR, and 8.9% in SDR treated with ditazol. We postulate that ditazol may prevent or reduce diabetic retinopathy.

The pyrimido-pyrimidine derivatives, dipyridamole and RA-642, reduce opacification of crystalline lens in diabetic rats.

We assessed the effect of dipyridamole, RA-642 and mopidamol, on lenticular opacities in a model of experimental diabetic cataracts in rats. All three pyrimido-pyrimidine derivatives caused a statistically significant reduction of opacification in crystalline lens as compared with untreated diabetic animals. The production of superoxide anions (phenazine methosulphate [PMS]-induced nitroblue tetrazolium [NBT] reduction) showed a decrease of 81.6%, 78.9% and 1.8% in lens tissue homogenates from rats treated with dipyridamole, RA-642 and mopidamol, respectively. Dipyridamole and RA-642 produced a statistically significant inhibition (50% and 64.8%, respectively) of lipid peroxidation (ferrous sulphate and ascorbic acid [FeAs]-induced malondialdehyde [MDA] production) as compared with the group of untreated diabetic rats. Mopidamol did not exert any inhibitory effect on lipid peroxidation. There was a statistically significant correlation between opacification of lens and PMS-induced NBT reduction and FeAs-induced MDA production. We conclude that the protective effect of dipyridamole and RA-642 from free radical damage to crystalline lens in the model of experimental diabetes used in this study, is the result of the antioxidant action of these compounds. The effect exerted by mopidamol, however, suggest a possible complementary effect of the pyrimido-pyrimidine derivatives through interaction with other mechanisms (e.g., the sorbitol pathway) implicated in the development of cataracts.

[Histopathology of mucoceles infiltrated with steroids]. / Histopatología de mucoceles infiltrados con esteroides

The authors have had the opportunity to treat eight cases of lip mucocele with intralesional infiltration of Triamcinolone Acetonide (Kenacort). In three cases there was complete regression of the lesion after a variable period of time between the first and the fourth infiltration. In five cases the results were negative. The patients who reacted positively to treatment were followed-up for a year afterwards.