Conservation in the community: the Kilum-Ijim Forest Project,Cameroon

Thomas, D.H.L., Anders, S. & Penn, N.J. 2000. Conservation in the community: the Kilum-Ijim Forest Project, Cameroon. Ostrich 71 (1 & 2): 157–161.

BirdLife International has worked for ten years in Cameroon's North-West Province to assist the local people and government of Cameroon in achieving the conservation and sutainable management of the last significant remnant of a unique montane forest ecosystem. The Kilum/Ijim forests are almost certainly the last remaining habitat for the conservation of two endemic and threatened bird species, Bannerman's Turaco Tauraco bannermani and Banded Wattle-eye Platytiera laticincta. The forests have no legal designation as formal protected areas but have been conserved through local concern and knowledge of the multiple values of an intact forest ecosystem, backed up by the enforcement of traditional regulations, and support from the project to finding solutions to peoples' land use and natural resource management needs within and outside the forests. The project is now working under the umbrella of a national Biodiversity Conservation and Management Programme in Cameroon, funded by the Global Environment Facility, to establish the Kilum/Ijirn as the first community-managed forest in the country. A brief history and background to the project is presented, with emphasis on lessons learned by BiraLife and the success of current efforts to achieve the conservation of the forests through community management. The issues are discussed in the general context of an integrated conservation and development programme (ICDP).     

Major histocompatibility complex heterozygosity reduces fitness in experimentally infected mice

It is often suggested that heterozygosity at major histocompatibility complex (MHC) loci confers enhanced resistance to infectious diseases (heterozygote advantage, HA, hypothesis), and overdominant selection should contribute to the evolution of these highly polymorphic genes. The evidence for the HA hypothesis is mixed and mainly from laboratory studies on inbred congenic mice, leaving the importance of MHC heterozygosity for natural populations unclear. We tested the HA hypothesis by infecting mice, produced by crossbreeding congenic C57BL/10 with wild ones, with different strains of Salmonella, both in laboratory and in large population enclosures. In the laboratory, we found that MHC influenced resistance, despite interacting wild-derived background loci. Surprisingly, resistance was mostly recessive rather than dominant, unlike in most inbred mouse strains, and it was never overdominant. In the enclosures, heterozygotes did not show better resistance, survival, or reproductive success compared to homozygotes. On the contrary, infected heterozygous females produced significantly fewer pups than homozygotes. Our results show that MHC effects are not masked on an outbred genetic background, and that MHC heterozygosity provides no immunological benefits when resistance is recessive, and can actually reduce fitness. These findings challenge the HA hypothesis and emphasize the need for studies on wild, genetically diverse species.     

Stress impacts telomere dynamics

Telomeres are DNA-protein complexes at the ends of chromosomes that control genomic integrity but appear to become shorter with age and stress. To test whether stress causes telomere attrition, we exposed the offspring of wild-caught house mice (Mus musculus) to stressful conditions and examined the changes in telomere length over six months. We found that females exposed to males and reproductive stress (either with or without crowding) had significantly shorter telomeres than controls, and males exposed to crowding stress had shorter telomeres than males that were not crowded. Our results indicate that stress alters telomere dynamics, causing attrition and hindering restoration, and these effects are sex dependent. Telomeres may thus provide a biomarker for assessing an individual's cumulative exposure or ability to cope with stressful conditions.     

Trophoblast–endothelium signaling involves angiogenesis and apoptosis in a dynamic bioprinted placenta model

Trophoblast invasion and remodeling of the maternal spiral arteries are required for pregnancy success. Aberrant endothelium–trophoblast crosstalk may lead to preeclampsia, a pregnancy complication that has serious effects on both the mother and the baby. However, our understanding of the mechanisms involved in this pathology remains elementary because the current in vitro models cannot describe trophoblast–endothelium interactions under dynamic culture. In this study, we developed a dynamic three-dimensional (3D) placenta model by bioprinting trophoblasts and an endothelialized lumen in a perfusion bioreactor. We found the 3D printed perfusion bioreactor system significantly augmented responses of endothelial cells by encouraging network formations and expressions of angiogenic markers, cluster of differentiation 31 (CD31), matrix metalloproteinase-2 (MMP2), matrix metalloproteinase-9 (MMP9), and vascular endothelial growth factor A (VEGFA). Bioprinting favored colocalization of trophoblasts with endothelial cells, similar to in vivo observations. Additional analysis revealed that trophoblasts reduced the angiogenic responses by reducing network formation and motility rates while inducing apoptosis of endothelial cells. Moreover, the presence of endothelial cells appeared to inhibit trophoblast invasion rates. These results clearly demonstrated the utility and potential of bioprinting and perfusion bioreactor system to model trophoblast–endothelium interactions in vitro. Our bioprinted placenta model represents a crucial step to develop advanced research approach that will expand our understanding and treatment options of preeclampsia and other pregnancy-related pathologies.     

The evolutionary roots of our environmental problems: toward a Darwinian ecology

It is widely acknowledged that we need to stabilize population growth and reduce our environmental impact; however, there is little consensus about how we might achieve these changes. Here I show how evolutionary analyses of human behavior provide important, though generally ignored, insights into our environmental problems. First, I review increasing evidence that Homo sapiens has a long history of causing ecological problems. This means that, contrary to popular belief, our species' capacity for ecological destruction is not simply due to "Western" culture. Second, I provide an overview of how evolutionary research can help to understand why humans are ecologically destructive, including the reasons why people often overpopulate, overconsume, exhaust common-pool resources, discount the future, and respond maladaptively to modern environmental hazards. Evolutionary approaches not only explain our darker sides, they also provide insights into why people cherish plants and animals and often support environmental and conservation efforts (e.g., Wilson's "biophilia hypothesis"). Third, I show how evolutionary analyses of human behavior offer practical implications for environmental policy, education, and activism. I suggest that education is necessary but insufficient because people also need incentives. Individual incentives are likely to be the most effective, but these include much more than narrow economic interests (e.g., they include one's reputation in society). Moralizing and other forms of social pressure used by environmentalists to bring about change appear to be effective, but this idea needs more research. Finally, I suggest that integrating evolutionary perspectives into the environmental sciences will help to break down the artificial barriers that continue to divide the biological and social sciences, which unfortunately obstruct our ability to understand ourselves and effectively address our environmental problems.     

Bcl-xL/Bcl-2 coordinately regulates apoptosis, cell cycle arrest and cell cycle entry

Bcl-x(L) and Bcl-2 inhibit both apoptosis and proliferation. In investigating the relationship between these two functions of Bcl-x(L) and Bcl-2, an analysis of 24 Bcl-x(L) and Bcl-2 mutant alleles, including substitutions at residue Y28 previously reported to selectively abolish the cell cycle activity, showed that cell cycle delay and anti-apoptosis co-segregated in all cases. In determining whether Bcl-2 and Bcl-x(L) act in G(0) or G(1), forward scatter and pyronin Y fluorescence measurements indicated that Bcl-2 and Bcl-x(L) cells arrested more effectively in G(0) than controls, and were delayed in G(0)-G(1) transition. The cell cycle effects of Bcl-2 and Bcl-x(L) were reversed by Bad, a molecule that counters the survival function of Bcl-2 and Bcl-x(L). When control and Bcl-x(L) cells of equivalent size and pyronin Y fluorescence were compared, the kinetics of cell cycle entry were similar, demonstrating that the ability of Bcl-x(L) and Bcl-2 cells to enhance G(0) arrest contributes significantly to cell cycle delay. Our data suggest that cell cycle effects and increased survival both result from intrinsic functions of Bcl-2 and Bcl-x(L).     

Myc is an essential negative regulator of platelet-derived growth factor beta receptor expression

Platelet-derived growth factor BB (PDGF BB) is a potent mitogen for fibroblasts as well as many other cell types. Interaction of PDGF BB with the PDGF beta receptor (PDGF-betaR) activates numerous signaling pathways and leads to a decrease in receptor expression on the cell surface. PDGF-betaR downregulation is effected at two levels, the immediate internalization of ligand-receptor complexes and the reduction in pdgf-betar mRNA expression. Our studies show that pdgf-betar mRNA suppression is regulated by the c-myc proto-oncogene. Both constitutive and inducible ectopic Myc protein can suppress pdgf-betar mRNA and protein. Suppression of pdgf-betar mRNA in response to Myc is specific, since expression of the related receptor pdgf-alphar is not affected. We further show that Myc suppresses pdgf-betar mRNA expression by a mechanism which is distinguishable from Myc autosuppression. Analysis of c-Myc-null fibroblasts demonstrates that Myc is required for the repression of pdgf-betar mRNA expression in quiescent fibroblasts following mitogen stimulation. In addition, it is evident that the Myc-mediated repression of pdgf-betar mRNA levels plays an important role in the regulation of basal pdgf-betar expression in proliferating cells. Thus, our studies suggest an essential role for Myc in a negative-feedback loop regulating the expression of the PDGF-betaR.