Human evolution in Polynesia

The number of eastern Polynesian females required to found the Maori population of Aotearoa (New Zealand) has been recalculated. Our estimates use computer simulations that incorporate realistic sigmoid population growth models and include previously published and new mitochondrial DNA (mtDNA) 3' hypervariable region 1 sequences from M?ori (N = 109) and other eastern Polynesian (N = 125) volunteers. Approximately 190 (170-230) women are estimated to have been present in the founding waka (canoes). This new figure is more than double the previous estimate (Murray-McIntosh et al. 1998). Our claim for a large Maori founding population fits well with M?ori oral history and has additional support from M?ori paleodemography studies based on fertility estimates (Brewis et al. 1990; Pool 1991). An increasing body of data, including our own, supports the concept of planned multiple settlement voyages to Aotearoa by Polynesian navigators, leading us to suggest that theories for an "accidental discovery" of Aotearoa can now be completely disregarded. Four rare and novel M?ori mtDNA haplotypes have been identified in the present study, but we are unable to assign the immediate origin of M?ori to an exact Pacific island "homeland" because these haplotypes are not currently known elsewhere in Polynesia. We also discuss briefly the ultimate origin of all Polynesians (including M?ori) in a wider context. In general, we support the emerging consensus for Pacific origins most closely encapsulated by the "slow boat" model (Oppenheimer and Richards 2001a). Previously "competing" models for the settlement of Oceania are seen as extremes in a continuum of possibilities with the slow boat representing an "intermediate" model. We suggest that a complete account is now close, incorporating data from all relevant interdisciplinary fields to provide a "synthetic total evidence theory."     

NK cells stimulate proliferation of T and NK cells through 2B4/CD48 interactions

Few studies have addressed the consequences of physical interactions between NK and T cells, as well as physical interactions among NK cells themselves. We show in this study that NK cells can enhance T cell activation and proliferation in response to CD3 cross-linking and specific Ag through interactions between 2B4 (CD244) on NK cells and CD48 on T cells. Furthermore, 2B4/CD48 interactions between NK cells also enhanced proliferation of NK cells in response to IL-2. Overall, these results suggest that NK cells augment the proliferation of neighboring T and NK cells through direct cell-cell contact. These results provide new insights into NK cell-mediated control of innate and adaptive immunity and demonstrate that receptor/ligand-specific cross talk between lymphocytes may occur in settings other than T-B cell or T-T cell interactions.     

Response of tree biomass and wood litter to disturbance in a Central Amazon forest

We developed an individual-based stochastic-empirical model to simulate the carbon dynamics of live and dead trees in a Central Amazon forest near Manaus, Brazil. The model is based on analyses of extensive field studies carried out on permanent forest inventory plots, and syntheses of published studies. New analyses included: (1) growth suppression of small trees, (2) maximum size (trunk base diameter) for 220 tree species, (3) the relationship between growth rate and wood density, and (4) the growth response of surviving trees to catastrophic mortality (from logging). The model simulates a forest inventory plot, and tracks recruitment, growth, and mortality of live trees, decomposition of dead trees (coarse litter), and how these processes vary with changing environmental conditions. Model predictions were tested against aggregated field data, and also compared with independent measurements including maximum tree age and coarse litter standing stocks. Spatial analyses demonstrated that a plot size of ~10 ha was required to accurately measure wood (live and dead) carbon balance. With the model accurately predicting relevant pools and fluxes, a number of model experiments were performed to predict forest carbon balance response to perturbations including: (1) increased productivity due to CO₂ fertilization, (2) a single semi-catastrophic (10%) mortality event, (3) increased recruitment and mortality (turnover) rates, and (4) the combined effects of increased turnover, increased tree growth rates, and decreased mean wood density of new recruits. Results demonstrated that carbon accumulation over the past few decades observed on tropical forest inventory plots (~0.5 Mg C ha^–1 year^–1) is not likely caused by CO₂ fertilization. A maximum 25% increase in woody tissue productivity with a doubling of atmospheric CO₂ only resulted in an accumulation rate of 0.05 Mg C ha^–1 year^–1 for the period 1980–2020 for a Central Amazon forest, or an order of magnitude less than observed on the inventory plots. In contrast, model parameterization based on extensive data from a logging experiment demonstrated a rapid increase in tree growth following disturbance, which could be misinterpreted as carbon sequestration if changes in coarse litter stocks were not considered. Combined results demonstrated that predictions of changes in forest carbon balance during the twenty-first century are highly dependent on assumptions of tree response to various perturbations, and underscores the importance of a close coupling of model and field investigations.     

The effective mutation rate at Y chromosome short tandem repeats, with application to human population-divergence time

We estimate an effective mutation rate at an average Y chromosome short-tandem repeat locus as 6.9x10-4 per 25 years, with a standard deviation across loci of 5.7x10-4, using data on microsatellite variation within Y chromosome haplogroups defined by unique-event polymorphisms in populations with documented short-term histories, as well as comparative data on worldwide populations at both the Y chromosome and various autosomal loci. This value is used to estimate the times of the African Bantu expansion, the divergence of Polynesian populations (the Maoris, Cook Islanders, and Samoans), and the origin of Gypsy populations from Bulgaria.     

Methodology for estimating the abundance of rare animals: seabird nesting on north east Herald Cay

We discuss the problem of estimating the number of nests of different species of seabirds on North East Herald Cay based on the data from a 1996 survey of quadrats along transects and data from similar past surveys. We consider three approaches based on different plausible models, namely a conditional negative binomial model that allows for additional zeroes in the data, a weighting approach (based on a heteroscedastic regression model), and a transform-both-sides regression approach. We find that the conditional negative binomial approach and a linear regression approach work well but that the transform-both-sides approach should not be used. We apply the conditional negative binomial and linear regression approaches with poststratification based on data quality and availability to estimate the number of frigatebird nests on North East Herald Cay.     

Activation of osteoclasts by interleukin-1: divergent responsiveness in osteoclasts formed in vivo and in vitro

Recently, it has been found that osteoclasts are induced and activated by osteoblastic cells through expression of receptor activator NF-kB ligand (RANKL), and that soluble recombinant RANKL, with M-CSF, can replace the need for osteoblastic cells in osteoclast formation. We exploited this opportunity to compare the responsiveness of osteoclast-like cells (OCL) formed in vitro in the absence of osteoblasts, with that of osteoclasts ex vivo. We found that while OCL responded to several hormones and cytokines like ex vivo osteoclasts, their responsiveness to interleukin-1 (IL-1) was fundamentally different: IL1 directly stimulated actin ring formation in OCL, but had no effect on actin rings or survival in osteoclasts ex vivo unless osteoblastic cells were present. This difference could not be attributed to the use of plastic culture substrates for OCL formation, nor to osteoblastic contamination, and did not seem to be mediated by the macrophages that form in OCL cultures. To understand the mechanisms by which IL-1 induces bone loss, it will need to be determined whether or not IL-1-responsive OCLs have a counterpart in vivo. Whichever is the case, our data suggest that the behavior of osteoclasts formed in culture will not always predict that of osteoclasts in vivo.     

Direct NK cell-mediated lysis of syngenic dorsal root ganglia neurons in vitro

In contrast to extensive studies on the role of T and B lymphocytes in the pathogenesis of autoimmune diseases of the nervous system, little is known about NK cells and their potential role in the destruction of neural tissue. NK cells have been implicated in the selective death of sympathetic neurons resident in the superior cervical ganglia of rats after exposure to the drug guanethidine. This observation suggests that NK cells may function as principle effectors in immunological diseases of the nervous system. However, the direct mechanism of action of NK cells in this model is not known. In particular, it is not known whether NK cells can kill autologous neurons directly. The aim of the present study was to examine whether NK cells can kill directly dorsal root ganglia neurons cultured in vitro. We demonstrate that C57BL/6 (B6)-derived dorsal root ganglia neurons can be killed directly by syngenic IL-2-activated NK cells, and that this nerve cell lysis is dependent on the expression of perforin in the NK cells. NK cells were less effective in destroying neurons grown in the presence of glial cells. These observations indicate a potential role for NK cells in nerve cell degeneration in inflammatory diseases of the nervous system.     

The role of osteopontin in the development of granulomatous lesions in lung

Osteopontin (OPN) has been shown to be expressed by cells in granulomas of various origins, but whether it plays a functional role in granuloma formation is not known. Here we used a cardiomyopathic hamster (TO2) model, to test the hypothesis that OPN contributes functionally to granuloma development. We immunized cardiomyopathic and normal hamsters by subcutaneous injection of bovine serum albumin in complete Freund's adjuvant, and assessed various tissues for both OPN RNA expression and granuloma formation. Cardiomyopathic hamsters expressed OPN, and formed granulomatous lesions, in heart tissue in both immunized and untreated animals. In addition, immunization induced expression of OPN in lung and lymph nodes of cardiomyopathic (but not normal) hamsters, and also induced granuloma formation in these organs. To test whether OPN expression could play a functional role in inducing granulomas, we produced an adenoviral vector containing the murine OPN gene, and introduced this vector intratracheally into the lungs of normal hamsters. The OPN-containing vector, but not the control vector, induced pulmonary granuloma formation. These studies provided direct in vivo evidence that OPN can contribute functionally to the formation of granulomatous lesions, and suggest that OPN expression may be a common factor involved in formation of granulomas of various origin.     

A review of molecular recognition technologies for detection of biological threat agents

The present review summarizes the state of the art in molecular recognition of biowarfare agents and other pathogens and emphasizes the advantages of using particular types of reagents for a given target (e.g. detection of bacteria using antibodies versus nucleic acid probes). It is difficult to draw firm conclusions as to type of biorecognition molecule to use for a given analyte. However, the detection method and reagents are generally target-driven and the user must decide on what level (genetic versus phenotypic) the detection should be performed. In general, nucleic acid-based detection is more specific and sensitive than immunological-based detection, while the latter is faster and more robust. This review also points out the challenges faced by military and civilian defense components in the rapid and accurate detection and identification of harmful agents in the field. Although new and improved sensors will continue to be developed, the more crucial need in any biosensor may be the molecular recognition component (e.g. antibody, aptamer, enzyme, nucleic acid, receptor, etc.). Improvements in the affinity, specificity and mass production of the molecular recognition components may ultimately dictate the success or failure of detection technologies in both a technical and commercial sense. Achieving the ultimate goal of giving the individual soldier on the battlefield or civilian responders to an urban biological attack or epidemic, a miniature, sensitive and accurate biosensor may depend as much on molecular biology and molecular engineering as on hardware engineering. Fortunately, as this review illustrates, a great deal of scientific attention has and is currently being given to the area of molecular recognition components. Highly sensitive and specific detection of pathogenic bacteria and viruses has increased with the proliferation of nucleic acid and immuno-based detection technologies. If recent scientific progress is a fair indicator, the future promises remarkable new developments in molecular recognition elements for use in biosensors with a vast array of applications.