Abstract:Fragmented populations are usually exposed to the negative effects of reduced gene flow, genetic drift and population differentiation. These effects result in the collective loss of genetic variation, thereby reducing the probability of population adaptation to new environmental conditions and increasing the risk of extinction. Forest fragments commonly exhibit suboptimal site conditions, which can result in enhanced clonal reproduction, and a potential reduction in clonal diversity due to increased selfing and inbreeding depression. The clonal diversity, genetic diversity and structure of Heliconia angusta (Heliconiaceae) were assessed using AFLP-markers. We analysed six patches in the continuous forest (Atlantic rain forest, State of Rio de Janeiro) and eight patches (155 leaf samples in total) in five nearby forest fragments (age of oldest fragment: c. 50 y; size range: < 5–100 ha). Clonal diversity (Pd) of patches was slightly, yet significantly, lower in forest fragments compared with continuous forest. Measures of genetic diversity of patches in forest fragments did not differ from those in the continuous forest. A STRUCTURE analysis did not show any clear clustering of patches in the continuous forest and forest fragments. Our results suggest that H. angusta has not yet suffered from the anticipated negative effects of fragmentation.
BackgroundPreterm newborns typically require supplemental oxygen but hyperoxic conditions also damage the premature lung. Oxygen-induced lung damages are mainly studied in newborn mouse models using oxygen concentrations above 75% and looking at short-term effects. Therefore, we aimed at the investigation of long-term effects and their dependency on different oxygen concentrations.MethodsNewborn mice were exposed to moderate vs. severe hyperoxic air conditions (50 vs. 75% O2) for 14 days followed by a longer period of normoxic conditions. Lung-related parameters were collected at an age of 60 or 120 days.ResultsSevere hyperoxia caused lower alveolar density, enlargement of parenchymal air spaces and fragmented elastic fibers as well as higher lung compliance with peak airflow limitations and higher sensitivity to ventilation-mediated damages in later life. However, these long-term lung structural and functional changes did not restrict the voluntary physical activity. Also, they were not accompanied by ongoing inflammatory processes, increased formation of reactive oxygen species (ROS) or altered expressions of antioxidant enzymes (superoxide dismutases, catalase) and lung elasticity-relevant proteins (elastin, pro-surfactant proteins) in adulthood. In contrast to severe hyperoxia, moderate hyperoxia was less lung damaging but also not free of long-term effects (higher lung compliance without peak airflow limitations, increased ROS formation).ConclusionsSevere but not moderate neonatal hyperoxia causes emphysematous lungs without persisting oxidative stress and inflammation in adulthood. As the existing fragmentation of the elastic fibers seems to play a pivotal role, it indicates the usefulness of elastin-protecting compounds in the reduction of long-term oxygen-related lung damages.
The receptor for advanced glycation end-products (RAGE) is an immunoglobulin superfamily cell adhesion molecule predominantly expressed in the lung, but its pulmonary importance is incompletely understood. Since RAGE alters the respiratory mechanics, which is also challenged by endurance running activity, we studied the RAGE-dependent effect of higher running activity on selected lung parameters in a long-term animal model using wild-type (WT) and RAGE knockout (RAGE-KO) mice. Higher long-term running activity of mice was ensured by providing a running wheel for 8 months. Recording the running activity revealed that RAGE-KO mice are more active than WT mice. RAGE-KO caused an increased lung compliance which additionally increased after long-term running activity with minor limitation of the expiratory flow, whereas the respiratory mechanics of WT mice remained constant. Although RAGE-KO mice had a less dense alveolar-capillary barrier for immune cells, higher long-term running activity led only in WT mice to more leukocyte infiltrations in the lung tissue and aggregations of lymphoid cells in the airways. In this regard, WT mice of the activity group were also more sensitive to ventilation-mediated airway damages. In contrast to RAGE-KO mice of the activity group, lungs of WT mice did not show an increase in the cAMP response element-binding protein, a transcription factor regulating many pro-survival genes. Our findings suggest an important role of RAGE in the physical capability due to its effect on the lung compliance as well as RAGE as a mediator of airway damages caused by higher long-term running activity.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.