Present state of diseases and other signs of reef deterioration at seven coral reefs at Los Roques Archipelago National Park, Venezuela

This work was aimed to determine the incidence of coral diseases in six different reef sites at the Parque Nacional Archipiélago de Los Roques, Venezuela: Arrecife de herradura, Arrecife costanero, both at Dos Mosquises Sur Key, Boca de Cote, Carenero, Crasquí and Pelona de Rabusquí. Each reef was surveyed by using ten 10 m2-band transects (10 x 1 m), placed parallel to the long axis of the reef within a depth gradient ranging from 1 to 9 m depth. All healthy and injured corals, along each band transect, were counted and identified to species level. Additionally, all diseases and recent mortality that were still identifiable on each colony were also recorded. The occurrence of diseased colonies and other signs of reef decline between localities were compared by means of a Chi2 test. The absolute, relative and mean incidence was estimated for each disease and other signs of damage observed for all coral species surveyed at each site. The overall incidence of coral diseases was low for all the localities surveyed, only 6.04% of the 3 344 colonies observed, showed signs of diseases. The most important diseases recorded were the Yellow-Blotch Disease (YBD) and Dark Spots Disease (DSD) with 2.1% +/- 1.52 y 2.1% +/- 2.54, respectively. Significant differences were found in the incidence of coral diseases between reef sites (Chi2 p < 0.05). Finally, the occurrence of colonies injured by parrotfish bites and pomacentrids was higher compared with the incidence of coral diseases for all the reefs surveyed. In conclusion, currently the proportion of healthy colonies at Los Roques coral reefs is higher than the percentage of both diseased and injured colonies.     

Prehistoric tuberculosis in america: adding comments to a literature review

Tuberculosis is a prehistoric American human disease. This paper reviews the literature and discusses hypotheses for origins and epidemiological patterns of prehistoric tuberculosis. From the last decades, 24 papers about prehistoric tuberculosis were published and 133 cases were reviewed. In South America most are isolated case studies, contrary to North America where more skeletal series were analyzed. Disease was usually located at the deserts of Chile and Peru, Central Plains in USA, and Lake Ontario in Canada. Skeletal remains represent most of the cases, but 16 mummies have also been described. Thirty individuals had lung disease, 19 of them diagnosed by the ribs. More then 100 individuals had osseous tuberculosis and 26 also had it in other organs. As today, transmission of the infection and establishment of the disease were favored by cultural and life-style changes such as sedentarization, crowding, undernutrition, use of dark and insulated houses, and by the frequency of interpersonal contacts. The papers confirm that despite previous perceptions, tuberculosis seems to have occurred in America for millennia. It only had epidemiological expression when special conditions favored its expansion. Occurring as epidemic bursts or low endemic disease, it had differential impact on groups or social segments in America for at least two millennia.     

Structure and biogenesis of the capsular F1 antigen from Yersinia pestis: preserved folding energy drives fiber formation

Most gram-negative pathogens express fibrous adhesive virulence organelles that mediate targeting to the sites of infection. The F1 capsular antigen from the plague pathogen Yersinia pestis consists of linear fibers of a single subunit (Caf1) and serves as a prototype for nonpilus organelles assembled via the chaperone/usher pathway. Genetic data together with high-resolution X-ray structures corresponding to snapshots of the assembly process reveal the structural basis of fiber formation. Comparison of chaperone bound Caf1 subunit with the subunit in the fiber reveals a novel type of conformational change involving the entire hydrophobic core of the protein. The observed conformational change suggests that the chaperone traps a high-energy folding intermediate of Caf1. A model is proposed in which release of the subunit allows folding to be completed, driving fiber formation.     

The effects of a mutant connexin 26 on epidermal differentiation

To elucidate the mode of action of dominant mutant connexins in causing inherited skin diseases, transgenic mice were produced that express the true Vohwinkel syndrome-associated mutant Cx26 (D66H), from a keratin 10 promoter, specifically in the suprabasal epidermal keratinocytes. Following birth, the transgenic mice developed keratoderma similar to that of human carriers of Cx26 (D66H). Expression of the transgene resulted in a loss of Cx26 and Cx30 at intercellular junctions of epidermal keratinocytes and accumulation of these connexins in the cytoplasm. Injection of primary mouse keratinocytes with Lucifer Yellow showed no difference in terms of dye spreading between transgenic and non transgenic keratinocytes in vitro. Expression of the mutant Cx26 (D66H) did not interfere with the formation of the epidermal water barrier during late embryonic development. Attempts to produce transgenic mice expressing the wild type form of Cx26 from the K10 promoter failed to produce viable animals although transgenic embryos were recovered at days 9 and 12 of gestation, suggesting that the transgene might be embryonic lethal.     

Asymmetric limb malformations in a new transgene insertional mutant,footless

Six to eight copies of a transgene integrated into mouse chromosome 15 resulting in a new transgene insertional mutant, Footless, presenting with malformations of the limbs, kidney, and soft palate. Homozygotes possess a unique asymmetric pattern of limb truncations. Posterior structures from the autopod and zeugopod of the hindlimbs are missing with left usually more severely affected than right. In contrast, anterior structures are missing from the right forelimbs. The left forelimb is usually normal except for the absence of the distal telephalanges and nails. These structures are absent on all formed digits. In situ hybridization assays examined the expression of Shh, dHand, Msx2, Fgf8, En1, and Lmx1b in mutant limb buds and indicated normal establishment of the anterior/posterior and dorsal/ventral axes of the developing limbs. However, dysmorphology of the apical ectodermal ridge was observed in the mutant limb buds.     

Structure-activity relationships of the peptide deformylase inhibitor BB-3497: modification of the methylene spacer and the P1' side chain

Structural modifications to the peptide deformylase inhibitor BB-3497 are described. In this paper, we describe the initial SAR around this lead for modifications to the methylene spacer and the P1' side chain. Enzyme inhibition and antibacterial activity data revealed that the optimum distance between the N-formyl hydroxylamine metal binding group and the P1' side chain is one unsubstituted methylene unit. Additionally, lipophilic P1' side chains that closely mimic the methionine residue in the substrate provided compounds with the best microbiological profile.     

Interrelationship of indices of body composition and zinc status in 11-yr-old New Zealand children

Serum zinc and hair zinc concentrations of some New Zealand children aged 11 yr, were examined in relation to selected anthropometric indices. Serum zinc concentrations (n=453) in boys and girls were similar and were unrelated to anthropometric indices and hair zinc concentrations. Mean hair zinc concentration (n=620) of the girls was higher than that for the boys (2.95±0.49 vs 2.46±0.47 μmol/g; p<0.001). Correlation analysis demonstrated that, for the boys, all the studied anthropometric indices, with the exception of height, were significantly related to hair zinc concentration and that the confounding effects of mid-parent height and the timing of the adolescent growth spurt was small. Results for the girls were similar but less significant. Dichotomizing the hair zinc results divided both the boys and girls into two groups: those with hair zinc <2.44 μmol/g were heavier (girls, 39.0 vs 35.2 kg; boys, 36.6 vs 34.7 kg) and fatter (mid-upper-arm fat area: girls, 15.2 vs 12.0 cm²; boys, 11.1 vs 9.5 cm²) compared to their counterparts with hair zinc >2.44 μmol/g. The results demonstrate that in these healthy New Zealand children, those with lower hair zinc concentrations are fatter and heavier than their high-hair-zinc counterparts.     

Intracellular Signal Triggered by Cholera Toxin in Saccharomyces boulardii and Saccharomyces cerevisiae

As is the case for Saccharomyces boulardii, Saccharomyces cerevisiae W303 protects Fisher rats against cholera toxin (CT). The addition of glucose or dinitrophenol to cells of S. boulardii grown on a nonfermentable carbon source activated trehalase in a manner similar to that observed for S. cerevisiae. The addition of CT to the same cells also resulted in trehalase activation. Experiments performed separately on the A and B subunits of CT showed that both are necessary for activation. Similarly, the addition of CT but not of its separate subunits led to a cyclic AMP (cAMP) signal in both S. boulardii and S. cerevisiae. These data suggest that trehalase stimulation by CT probably occurred through the cAMP-mediated protein phosphorylation cascade. The requirement of CT subunit B for both the cAMP signal and trehalase activation indicates the presence of a specific receptor on the yeasts able to bind to the toxin, a situation similar to that observed for mammalian cells. This hypothesis was reinforced by experiments with ¹²⁵I-labeled CT showing specific binding of the toxin to yeast cells. The adhesion of CT to a receptor on the yeast surface through the B subunit and internalization of the A subunit (necessary for the cAMP signal and trehalase activation) could be one more mechanism explaining protection against the toxin observed for rats treated with yeasts.     

Nitric Oxide Prevents Alveolar Senescence and Emphysema in a Mouse Model

N^ω-nitro-L-arginine methyl ester (L-NAME) treatment induces arteriosclerosis and vascular senescence. Here, we report that the systemic inhibition of nitric oxide (NO) production by L-NAME causes pulmonary emphysema. L-NAME-treated lungs exhibited both the structural (alveolar tissue destruction) and functional (increased compliance and reduced elastance) characteristics of emphysema development. Furthermore, we found that L-NAME-induced emphysema could be attenuated through both genetic deficiency and pharmacological inhibition of plasminogen activator inhibitor-1 (PAI-1). Because PAI-1 is an important contributor to the development of senescence both in vitro and in vivo, we investigated whether L-NAME-induced senescence led to the observed emphysematous changes. We found that L-NAME treatment was associated with molecular and cellular evidence of premature senescence in mice, and that PAI-1 inhibition attenuated these increases. These findings indicate that NO serves to protect and defend lung tissue from physiological aging.