We use the Eastern Cordillera of Colombia as an example in early stages of inversion orogen showing still modest values of shortening. The style of deformation recorded in this orogenic chain seems to be strongly influenced by two main factors. The first is the pre-compression geometry of the rift basin, conditioning the strong heterogeneity imparted by a trough filled with Jurassic to Neocomian sediments limited by Precambrian and Palaeozoic high-angle walls. The second factor is the orientation of the stress regime with respect to the main normal faults during the inversion. If the stress field is of pure compression, the normal faults are not extensively inverted and the deformation is accommodated mainly in terms of footwall shortcuts. On the other hand, in transpressive regimes the inversion of the former normal faults is more common and the footwall shortcuts are not dominant structures. No significant lateral variations in tectonic shortening are found in the Eastern Cordillera. Finally we emphasize the role of buckle folds in the internal parts of the inversion orogens and give a cautionary note when interpreting these structures in terms of fault-related folding using the well-documented example of the Soapaga fault area.

Background: Most of the effects of statins can be explained by pleiotropic effects independent of their lowering of serum cholesterol; in some cases, these effects have been shown to be a result of the role of statins in the prenylation of cellular proteins, some of which are involved in the life cycle of animal viruses. This study evaluated the potential antiviral activity of lovastatin (LOV) against dengue virus (DENV) infection of epithelial and endothelial cells (VERO cells, epithelial cells derived from African green monkey kidney, and HMEC-1 cells, human dermal microvascular endothelial cells). Methods: To evaluate its potential antiviral effects, LOV was used before, during and after inoculation of cell cultures with DENV. Results: Before and after viral inoculation, LOV caused a reduction in virus yield (80% for HMECs and 25% for VERO cells). However, with LOV treatment after inoculation induced a marked increase (2- to 9-fold) in viral-positive RNA while the amount of viral protein increased only by 13–23%. A moderate reduction (1 log unit) in viral titer occurred concurrent with the increase in DENV genomic RNA and protein within the cells. Conclusions: According to our results, LOV appears to have a greater effect on viral assembly than on replication, resulting in the cellular presence of viral genomic RNA and proteins that fail to take the normal assembly pathway.

Several studies have shown that the dentin-resin interface is unstable due to poor infiltration of resin monomers into the demineralized dentin matrix. This phenomenon is related to the incomplete infiltration of the adhesive system into the network of exposed collagen fibrils, mainly due to the difficulty of displacement and subsequent replacement of trapped water between interfibrillar spaces, avoiding adequate hybridization within the network of collagen fibrils. Thus, unprotected fibrils are exposed to undergo denaturation and are susceptible to cyclic fatigue rupture after being subjected to repetitive loads during function. The aqueous inclusions within the hybrid layer serve as a functional medium for the hydrolysis of the resin matrix, giving rise to the activity of esterases and collagenolytic enzymes, such as matrix metalloproteinases, which play a fundamental role in the degradation process of the hybrid layer. Achieving better interdiffusion of the adhesive system in the network of collagen fibrils and the substrate stability in the hybrid layer through different strategies are key events for the interfacial microstructure to adequately function. Hence, it is important to review the factors related to the mechanisms of degradation and stabilization of the hybrid layer to support the implementation of new materials and techniques in the future. The enzymatic degradation of collagen matrix, together with resin leaching, has led to seeking strategies that inhibit the endogenous proteases, cross-linking the denudated collagen fibrils and improving the adhesive penetration removing water from the interface. Some of dentin treatments have yielded promising results and require more research to be validated. A longer durability of adhesive restorations could resolve a variety of clinical problems, such as microleakage, recurrent caries, postoperative sensitivity, and restoration integrity.

The clinical findings of a pregnant woman from Colombia with a triple co-infection caused by dengue, chikungunya, and Zika viruses are described. Weekly obstetric ultrasounds from 14.6 to 29 weeks of gestation were normal. She remains under follow-up and management according to the standard guidelines for the management of Zika virus-infected pregnant women.

BackgroundIt has been reported that treatment of DENV-infected cultures with Lovastatin (LOV), can affect viral assembly. The objective of this study was to evaluate the effect of LOV on the survival rate and viremia levels of DENV-2-infected AG129 mice.Methodology/Principal FindingsMice were inoculated with 1×106 plaque-forming units (PFU/ml) of DENV-2 and treated with LOV (200 mg/kg/day). Pre-treatment with one or three doses of LOV increased the survival rate compared to untreated mice (7.3 and 7.1 days, respectively, compared to 4.8 days). Viremia levels also decreased by 21.8% compared to untreated mice, but only in the group administered three doses prior to inoculation. When LOV was administered after viral inoculation, the survival rate increased (7.3 days in the group treated at 24 hpi, 6.8 days in the group treated at 48 hpi and 6.5 days in the group treated with two doses) compared to the untreated group (4.8 days). Interestingly, the serum viral titer increased by 24.6% in mice treated at 48 hpi with a single dose of LOV and by 21.7% in mice treated with two doses (at 24 and 48 hpi) of LOV compared to untreated mice. Finally histopathological changes in the liver and spleen in infected and untreated mice included massive extramedullary erythropoiesis foci and inflammatory filtration, and these characteristics were decreased or absent in LOV-treated mice.Conclusions/SignificanceOur results suggest that the effect of LOV on viremia depends on the timing of treatment and on the number of doses administered. We observed a significant increase in the survival rate in both schemes due to a delay in the progression of the disease. However, the results obtained in the post-treatment scheme must be handled carefully because this treatment scheme increases viremia and we do not know how this increase could affect disease progression in humans.