Human settlement of East Polynesia earlier, incremental, and coincident with prolonged South Pacific drought

The timing of human colonization of East Polynesia, a vast area lying between Hawai‘i, Rapa Nui, and New Zealand, is much debated and the underlying causes of this great migration have been enigmatic. Our study generates evidence for human dispersal into eastern Polynesia from islands to the west from around AD 900 and contemporaneous paleoclimate data from the likely source region. Lake cores from Atiu, Southern Cook Islands (SCIs) register evidence of pig and/or human occupation on a virgin landscape at this time, followed by changes in lake carbon around AD 1000 and significant anthropogenic disturbance from c. AD 1100. The broader paleoclimate context of these early voyages of exploration are derived from the Atiu lake core and complemented by additional lake cores from Samoa (directly west) and Vanuatu (southwest) and published hydroclimate proxies from the Society Islands (northeast) and Kiribati (north). Algal lipid and leaf wax biomarkers allow for comparisons of changing hydroclimate conditions across the region before, during, and after human arrival in the SCIs. The evidence indicates a prolonged drought in the likely western source region for these colonists, lasting c. 200 to 400 y, contemporaneous with the phasing of human dispersal into the Pacific. We propose that drying climate, coupled with documented social pressures and societal developments, instigated initial eastward exploration, resulting in SCI landfall(s) and return voyaging, with colonization a century or two later. This incremental settlement process likely involved the accumulation of critical maritime knowledge over several generations

Effects of the synthetic estrogen 17 alpha-ethinylestradiol on the life-cycle of the fathead minnow (pimephales promelas)

A fish full life-cycle (FFLC) study was conducted for 17α-ethinylestradiol (EE2) using the fathead minnow, Pimephales promelas. Newly fertilized embryos

Memory B cell reconstitution following allogeneic haematopoietic stem cell transplantation is an EBV-associated transformation event

Allogeneic stem cell transplantation (allo-HSCT) provides a unique opportunity to track Epstein-Barr virus (EBV) infection in the context of the reconstituting B-cell system. Although many allo-HSCT recipients maintain low or undetectable levels of EBV DNA posttransplant, a significant proportion exhibit elevated and rapidly increasing EBV loads which, if left untreated, may lead to potentially fatal EBV-associated posttransplant lymphoproliferative disease. Intriguingly, this high-level EBV reactivation typically arises in the first 3 months posttransplant, at a time when the peripheral blood contains low numbers of CD27(+) memory cells which are the site of EBV persistence in healthy immunocompetent donors. To investigate this apparent paradox, we prospectively monitored EBV levels and B-cell reconstitution in a cohort of allo-HSCT patients for up to 12 months posttransplant. In patients with low or undetectable levels of EBV, the circulating B-cell pool consisted predominantly of transitional and naive cells, with a marked deficiency of CD27(+) memory cells which lasted >12 months. However, among patients with high EBV loads, there was a significant increase in both the proportion and number of CD27(+) memory B cells. Analysis of sorted CD27(+) memory B cells from these patients revealed that this population was preferentially infected with EBV, expressed EBV latent transcripts associated with B-cell growth transformation, had a plasmablastic phenotype, and frequently expressed the proliferation marker Ki-67. These findings suggest that high-level EBV reactivation following allo-HSCT may drive the expansion of latently infected CD27(+) B lymphoblasts in the peripheral blood

Memory B-cell reconstitution following allogeneic hematopoietic stem cell transplantation is an EBV-associated transformation event

Allogeneic stem cell transplantation (allo-HSCT) provides a unique opportunity to track Epstein-Barr virus (EBV) infection in the context of the reconstituting B cell system. While many allo-HSCT recipients maintain low or undetectable levels of EBV DNA post-transplant, a significant proportion exhibit elevated and rapidly increasing EBV loads which, if left untreated, may lead to potentially fatal EBV-associated post-transplant lymphoproliferative disease. Intriguingly this high level EBV reactivation typically arises in the first three months post-transplant, at a time when the peripheral blood contains low numbers of CD27(+) memory cells which are the site of EBV persistence in healthy immunocompetent donors. To investigate this apparent paradox, we prospectively monitored EBV levels and B cell reconstitution in a cohort of allo-HSCT patients for up to 12 months post-transplant. In patients with low or undetectable levels of EBV, the circulating B cell pool consisted predominantly of transitional and naïve cells, with a marked deficiency of CD27(+) memory cells which lasted more than twelve months. However, amongst patients with high EBV loads, there was a significant increase in both the proportion and number of CD27(+) memory B cells. Analysis of sorted CD27(+) memory B cells from these patients revealed that this population was preferentially infected with EBV, expressed EBV latent transcripts associated with B cell growth transformation, had a plasmablastic phenotype and frequently expressed the proliferation marker Ki-67. These findings suggest that high level EBV reactivation following allo-HSCT may drive the expansion of latently infected CD27(+) B lymphoblasts in the peripheral blood.</p