To clarify the mechanisms of altered bone repair in the diabetic state, we investigated RANK, RANKL and OPG expression by immunohistochemistry and RT-PCR in the fracture sites of rats that were either healthy or made diabetic by alloxan. Histomorphometric analysis of the fracture site at 7 days after fracture revealed that diabetic rats (db) have significantly less hard tissue formation at the fracture site, compared to controls. The number of RANK, RANKL and OPG positive cells was decreased in the db group; however, the RANKL/OPG ratio was similar in controls and db at this time. At day 14, numbers of RANKL and OPG positive cells and the mRNA expression for these markers were higher in the control group than in db (P = 0.008). The RANKL/OPG ratio in the db group was greater than in controls. Our results demonstrate an imbalance of RANKL/OPG expression associated with diabetes that may contribute to the delay of fracture repair during the course of diabetes.

Life-prolonging antiretroviral therapy remarkably reduces viral load, but it does not eradicate the virus. An important obstacle preventing virus clearance is the presence of latent virion reservoirs in the host. However, new promising antiviral approaches are emerging, and a number of host cell factors involved in the disease progression and control of HIV-1 replication have been recently discovered. For instance, the RNA interference (RNAi) mechanism, besides many functions conserved throughout evolution, works as a defence mechanism against noxious transcripts which may provide a new tool to block viral replication. The recent definition of basic RNAi mechanisms, as well as the discovery of micro RNAs (microRNAs) encoded by the host cell genome and by HIV-1, also suggest that RNAi may be involved in the control of HIV replication.

Aerobic and facultative bacteria belonging to the Enterobacteriaceae, Pseudomonadaceae, Bacillaceae, Corynebacteriaceae and Streptococcaceae families have been isolated from corroded metallic structures of a hydroelectric power unit in the Amazon region of Brazil. In addition to anamorphic dematiaceous and moniliaceous fungi, members of the archeobacteria kingdom were also detected in the same samples. Scanning electron micrographs of metal bars cultivated with consortia of the isolated microorganisms depicted suggestiveimagesofbiofilmformationandcorrodedmetallicstructuresquestioningthepossibleroleofthese microorganismsinthe corrosion activity. We also found Amazonian medicinal plants exhibiting inhibitory activity against some of the isolated microorganisms. Our new findings need additional studies to confirm the participation of some isolated microorganisms in the process of metallic degradationdespiteourmainquestionifarethereparticularmicroorganismsinvolvedinthecorrosionprocess?orif physicochemical conditions would favor the development of a particular microbiota and consequently the corrosion process would result from its metabolism?Thereforewehypothesizethatanymicroorganismcouldbepotentiallyinvolvedinthegenesisofcorrosionprocess.Thisis thefirstreportintheliteraturedealingwithmicrobiologicallyinducedcorrosionintheAmazonregionwhichisespecially characterized by its high humidity and elevated temperature all year round.

Feline Leukemia virus (FeLV) is a pathogenic retrovirus endemic among domestic cats, remaining a serious disease since its discovery in 1964. RNA interference (RNAi) is a process in which double-stranded RNA induces the post-transcriptional sequencespecific degradation of homologous messenger RNA. At present, RNAi technology is regarded as a potential strategy for the treatment of various diseases as it can be used to inhibit the expression of desired peptides/proteins. This study aimed to apply RNAi technology to inhibit the replication of FeLV. We examined the effect of vector-mediated transfer and expression of FeLV specific short hairpin RNA (shRNA) against p27 protein expression and replication of FeLV in a feline T-cell line chronically infected with FeLV (3201-EECC). Three shRNA homologous to the FeLV gag gene were synthesized, cloned and transfected into a feline fibroblastic cell line (CrFK) expressing FeLV which efficiently reduced FeLV p27 protein expression, consequently decreasing and inhibiting the viral replication in a chronically FeLV infected feline T-cell line (3201-EECC). The expression of shRNA against FeLV gag gene showed markedly lower p27 levels and viral replication in both cell lines, 3201-EECC and CrFK. These results provide useful information to pave the road for the development of a gene therapy strategy to control FeLV and related pathogenic retrovirus infections in the future.