Property rights of landholders in non-captive wildlife and prospects for conservation

In order to reduce the rate of human-induced biodiversity loss of wild species, it has become increasingly important to stem this loss on private and tribal lands and to find effective policies to do this. Some writers believe that granting landholders commercial property rights in wildlife might be effective in dealing with this matter and result in the sustainable use of wildlife. This paper explores this view using economic theory. In doing so, it takes into account the total economic valuation concept. While granting of commercial property rights is found to be effective for conserving some species, it is predicted to be a complete failure as a means of conserving other species. In addition, particular attention is given to the economics of the utilisation and conservation of non-captive fugitive (or mobile) wildlife. The economic theory involved is contrasted and compared with that for the exploitation of open-access resources.

Inducible nitric oxide synthase-deficient mice show exacerbated inflammatory process and high production of both Th1 and Th2 cytokines during paracoccidioidomycosis

Paracoccidioidomycosis, the major systemic mycosis in Latin America, is caused by fungus Paracoccidioides brasiliensis. To analyze the influence of inducible nitric oxide synthase (iNOS) in this disease, iNOS-deficient (iNOS(-/-)) and wild-type (WT) mice were infected intravenously with P. brasiliensis 18 isolate. We found that, unlike WT mice, iNOS(-/-) mice did not control fungal proliferation, and began to succumb to infection by day 50 after inoculation of yeast cells. Typical inflammatory granulomas were found in WT mice, while, iNOS(-/-) mice presented incipient granulomas with intense inflammatory process and necrosis. Additionally, splenocytes from iNOS(-/-) mice did not produce nitric oxide, however, their proliferative response to Con-A was impaired, just like infected WT mice. Moreover, infected iNOS(-/-) mice presented a mixed pattern of immune response, releasing high levels of both Th1 (IL-12, IFN-gamma and TNF-alpha) and Th2 (IL-4 and IL-10) cytokines. These data suggest that the enzyme iNOS is a resistance factor during paracoccidioidomycosis by controlling fungal proliferation, by influencing cytokines production, and by appeasing the development of a high inflammatory response and consequently formation of necrosis. However, iNOS-derived nitric oxide seems not being the unique factor responsible for immunosuppression observed in infections caused by P. brasiliensis. (c) 2008 Elsevier Masson SAS. All rights reserved.

Role of preoptic opioid receptors in the body temperature reduction during hypoxia

Evidence indicates that endogenous opioids play a role in body temperature (Tb) regulation in mammals but no data exist about the involvement of the specific opioid receptors, mu, kappa and delta, in the reduction of Tb induced by hypoxia. Thus, we investigated the participation of these opioid receptors in the anteroventral preoptic region (AVPO) in hypoxic decrease of Th. To this end, Th of unanesthetized Wistar rats was monitored by temperature data loggers before and after intra-AVPO microinjection of the selective kappa-opioid receptor antagonist nor-binaltorphimine dihydrochloride (nor-BNI; 0.1 and 1.0 mu g/100 nL/animal), the selective mu-opioid receptor antagonist D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH(2) cyclic (CTAP; 0.1 and 1.0 mu g/100 nL/animal), and the selective delta-opioid receptor antagonist Naltrindole (0.06 and 0.6 mu g/100 nL/animal) or saline (vehicle, 100 nu animal), during normoxia and hypoxia (7% inspired O(2)). Under normoxia, no effect of opioid antagonists on Th was observed. Hypoxia induced Th to reduce in vehicle group, a response that was inhibited by the microinjection intra-AVPO of nor-BNI. In contrast, CTAP and Naltrindole did not change Th during hypoxia but caused a longer latency for the return of Th to the normoxic values just after low O(2) exposure. Our results indicate the kappa-opioid receptor in the AVPO is important for the reduction of Th during hypoxia while the mu and delta receptors are involved in the increase of Th during normoxia post-hypoxia. (C) 2009 Elsevier B.V. All rights reserved.