The Dynamics and Social Organization of Tropical Deforestation in Northwest Ecuador, 1983-1995

This paper examines the regional dynamics and natural resource use strategies related to the deforestation of tropical rain forests west of the Ecuadorian Andes for the period 1983–1995. Research was based on regional level analysis of remotely sensed and secondary data and local level analysis of the ways local populations use the resources at their disposal. The process observed departs significantly from what has been described in the literature for Latin America and should be seen as a window into a broader environmental process occurring in most tropical forests on the Pacific side of northern South America. Deforestation in the Northwest Ecuador is primarily related to a complex productive structure, made up a countless number of timber producers and middlemen, ranging from fully informal to fully formal, and from small scale to large scale. A key finding is that local traditional populations play a critical role through productive coalitions between small primary producers and large timber firms. These have been shaped by the articulation of local conditions with external markets, settlement processes, and the convergence of local populations in an economic system which relies on the unsustainable exploitation of natural resources. If deforestation rates in Northwest Ecuador remain at current levels, forests in the region will disappear completely within 30–35 years, a fate that is likely to be the same for most tropical rain forests west of the tropical Andes.     

The black-tailed marmoset (Callithrix argentata melanura) recorded from paraguay

The black-tailed marmoset (Callithrix argentata melanura) occurs in central-western Brazil and adjacent parts of Bolivia, and is the only member of the genus (Callithrix) to occur naturally outside Brazil. Data presented in this paper extend the range of this marmoset at least 200 km to the southwest into yet another country, Paraguay.     

Nominal association with CHRNA4 variants and nicotine dependence

Nicotine binds to nicotinic acetylcholine receptors and studies in animal models have shown that α4β2 receptors mediate many behavioral effects of nicotine. Human genetics studies have provided support that variation in the gene that codes for the α4 subunit influences nicotine dependence (ND), but the evidence for the involvement of the β2 subunit gene is less convincing. In this study, we examined the genetic association between variation in the genes that code for the α4 (CHRNA4) and β2 (CHRNB2) subunits of the nicotinic acetylcholine receptor and a quantitative measure of lifetime DSM‐IV ND symptom counts. We performed this analysis in two longitudinal family‐based studies focused on adolescent antisocial drug abuse: the Center on Antisocial Drug Dependence (CADD, N = 313 families) and Genetics of Antisocial Drug Dependence (GADD, N = 111 families). Family‐based association tests were used to examine associations between 14 single nucleotide polymorphisms (SNPs) in CHRNA4 and CHRNB2 and ND symptoms. Symptom counts were corrected for age, sex and clinical status prior to the association analysis. Results, when the samples were combined, provided modest evidence that SNPs in CHRNA4 are associated with ND. The minor allele at both rs1044394 (A; Z = 1.988, P = 0.047, unadjusted P‐value) and rs1044396 (G; Z = 2.398, P = 0.017, unadjusted P‐value) was associated with increased risk of ND symptoms. These data provide suggestive evidence that variation in the α4 subunit of the nicotinic acetylcholine receptor may influence ND liability.     

Provisional assignment of TPI, GPI, and PEPD to Chinese hamster autosomes 8 and 9: a cytogenetic basis for functional haploidy of an autosomal linkage group in CHO cells

Concordant segregation analysis of Chinese hamster (Cricetulus griseus) isozymes and chromosomes segregating from interspecific somatic cell hybrids made with mouse C11D cells revealed the locations of GPI and PEPD on chromosome 9 and TPI on chromosome 8 in both euploid Chinese hamster and CHO cells. The patterns of electrophoretically detectable shift mutants of these loci in CHO cells were consistent with the observed presence of two normally banded chromosome 8's and monosomy for chromosome 9. These findings and the isolation of three independent, null PEPD mutants in only 527 ethyl methansulfonate-exposed clones indicate that the high frequency of recovery of recessive drug resistant mutants in CHO cells may be due not only to haploidy caused by deletions and monosomy but also by great sensitivity of certain loci to particular mutagens.