Serious lesions in Green turtles (Chelonia mydas) afflicted by fatal Spirorchiidiasis found stranded in south and southeastern Brazil.

Several diseases have been reported as affecting endangered wild sea turtle population worldwide, including spirorchiidiasis. This parasitic infection results in serious circulatory disorders in sea turtles, as well as tissue damage due to the presence of spirorchiids eggs. However, few reports of organs severely affected by tissue replacement caused by granulomatous inflammatory processes due to spirorchiidiasis in sea turtles are available. In this regard, this study describes massive lesions in 16 juvenile green turtles from southeastern Brazil presenting no other detectable diseases or injuries, associated to parasitic compression of air spaces, parasitic thyroid atrophy, parasitic encephalic compression and parasitic splenic lymphoid depletion. These rare injuries were categorized as extremely severe, affecting most spirorchiidiasis-infected organs. Spirorchiidiasis was, thus, noted herein as capable of causing a variety of lethal injuries to vital or extremely important organs in sea turtles. Spirorchiidiasis should, therefore, also be considered a potential cause of death in stranded green sea turtle monitoring efforts.

Lack of association between a 3'UTR VNTR polymorphism of dopamine transporter gene (SLC6A3) and ADHD in a Brazilian sample of adult patients.

OBJECTIVE: To investigate a possible association between a 3'UTR VNTR polymorphism of the dopamine transporter gene (SLC6A3) and ADHD in a Brazilian sample of adult patients. METHOD: Study Case-control with 102 ADHD adult outpatients ( DSM-IV criteria) and 479 healthy controls. The primers' sequence used were: 3'UTR-Forward: 5' TGT GGT GAT GGG AAC GGC CTG AG 3' and 3'UTR-Reverse: 5' CTT CCT GGA GGT CAC GGC TCA AGG 3'. Alleles of the 3'UTR were coded according to their number of repeats: 6- repeat 320 bp (allele 6), 8- repeat 400 bp (allele 8), 9- repeat 440 bp (allele 9), 10- repeat 480 bp (allele 10), and 11- repeat 520 bp (allele 11). RESULTS: There were no allelic (χ(2) = 2.67, 5df, p = .75) and genotypic (χ(2) = 7.20, 1 df, p = .61) association between adult ADHD and VNTR 3'UTR polymorphism of SLC6A3. CONCLUSION: Our findings do not support SLC6A3 as marker genetic susceptibility factor in adult ADHD. More comprehensive polymorphism coverage within the SLC6A3 region should be conducted in larger samples, including comparisons in clinical subgroups, and in samples with different ethnic backgrounds.