Patterns of Loss and Regeneration of Tropical Dry Forest in Madagascar: The Social Institutional Context

Loss of tropical forests and changes in land-use/land-cover are of growing concern worldwide. Although knowledge exists about the institutional context in which tropical forest loss is embedded, little is known about the role of social institutions in influencing regeneration of tropical forests. In the present study we used Landsat images from southern Madagascar from three different years (1984, 1993 and 2000) and covering 5500 km(2), and made a time-series analysis of three distinct large-scale patterns: 1) loss of forest cover, 2) increased forest cover, and 3) stable forest cover. Institutional characteristics underlying these three patterns were analyzed, testing the hypothesis that forest cover change is a function of strength and enforcement of local social institutions. The results showed a minor decrease of 7% total forest cover in the study area during the whole period 1984–2000, but an overall net increase of 4% during the period 1993–2000. The highest loss of forest cover occurred in a low human population density area with long distances to markets, while a stable forest cover occurred in the area with highest population density and good market access. Analyses of institutions revealed that loss of forest cover occurred mainly in areas characterized by insecure property rights, while areas with well-defined property rights showed either regenerating or stable forest cover. The results thus corroborate our hypothesis. The large-scale spontaneous regeneration dominated by native endemic species appears to be a result of a combination of changes in precipitation, migration and decreased human population and livestock grazing pressure, but under conditions of maintained and well-defined property rights. Our study emphasizes the large capacity of a semi-arid system to spontaneously regenerate, triggered by decreased pressures, but where existing social institutions mitigate other drivers of deforestation and alternative land-use

Temporal allocation of foraging effort in female Australian fur seals (Arctocephalus pusillus doriferus)

Across an individual\u27s life, foraging decisions will be affected by multiple intrinsic and extrinsic drivers that act at differing timescales. This study aimed to assess how female Australian fur seals allocated foraging effort and the behavioural changes used to achieve this at three temporal scales: within a day, across a foraging trip and across the final six months of the lactation period. Foraging effort peaked during daylight hours (57% of time diving) with lulls in activity just prior to and after daylight. Dive duration reduced across the day (196 s to 168 s) but this was compensated for by an increase in the vertical travel rate (1500–1600 m•h−1) and a reduction in postdive duration (111–90 s). This suggests physiological constraints (digestive costs) or prey availability may be limiting mean dive durations as a day progresses. During short trips (<2.9 d), effort remained steady at 55% of time diving, whereas, on long trips (>2.9 d) effort increased up to 2–3 d and then decreased. Dive duration decreased at the same rate in short and long trips, respectively, before stabilising (long trips) between 4–5 d. Suggesting that the same processes (digestive costs or prey availability) working at the daily scale may also be present across a trip. Across the lactation period, foraging effort, dive duration and vertical travel rate increased until August, before beginning to decrease. This suggests that as the nutritional demands of the suckling pup and developing foetus increase, female effort increases to accommodate this, providing insight into the potential constraints of maternal investment in this specie

Evaluation of kynurenine pathway metabolism in Toxoplasma gondii-infected mice: Implications for schizophrenia

Toxoplasma gondii, an intracellular protozoan parasite, is a major cause of opportunistic infectious disease affecting the brain and has been linked to an increased incidence of schizophrenia. In murine hosts, infection with T. gondii stimulates tryptophan degradation along the kynurenine pathway (KP), which contains several neuroactive metabolites, including 3-hydroxykynurenine (3-HK), quinolinic acid (QUIN) and kynurenic acid (KYNA). As these endogenous compounds may provide a mechanistic connection between T. gondii and the pathophysiology of schizophrenia, we measured KP metabolites in both the brain and periphery of T. gondii-treated C57BL/6 mice 8 and 28 days post-infection. Infected mice showed early decreases in the levels of tryptophan in the brain and serum, but not in the liver. These reductions were associated with elevated levels of kynurenine, KYNA, 3-HK and QUIN in the brain. In quantitative terms, the most significant increases in these KP metabolites were observed in the brain at 28 days post-infection. Notably, the anti-parasitic drugs pyrimethamine and sulfadiazine, a standard treatment of toxoplasmosis, significantly reduced 3-HK and KYNA levels in the brain of infected mice when applied between 28 and 56 days post-infection. In summary, T. gondii infection, probably by activating microglia and astrocytes, enhances the production of KP metabolites in the brain. However, during the first two months after infection, the KP changes in these mice do not reliably duplicate abnormalities seen in the brain of individuals with schizophrenia