Renewable power for lean desktops in media applications

An integration of solar microgeneration to supply a low-power IT desktop, using the Power over Ethernet standards IEEE 802.3af/at as a low power distribution network avoiding transformer losses from DC generation to mains power AC and back to low-voltage DC and hence maximising efficiency. The resulting design points to applications in media technology where reducing grid power consumption is critical for improving sustainability, or where there are supply constraints, and indicates new directions in how we manage and consume power for IT devices

Pathways to social inequality

Social inequality is now pervasive in human societies, despite the fact that humans lived in relatively egalitarian, small-scale societies across most of our history. Prior literature highlights the importance of environmental conditions, economic defensibility, and wealth transmission for shaping early Holocene origins of social inequality. However, it remains untested whether the mechanisms that drive the evolution of inequality in recent human societies follow a similar trajectory. We conduct the first global analysis of pathways to inequality within modern human societies using structural equation modeling. Our analytical approach demonstrates that environmental conditions, resource intensification, and wealth transmission mechanisms impact various forms of social inequality via a complex web of causality. We further find that subsistence practices have a direct impact on some institutionalized forms of inequality. This work identifies drivers of social inequality in the modern world and demonstrates the application of structural equation modeling methods to investigate complex relationships between elements of human culture

The competing effects of sulfide saturation versus degassing on the behavior of the chalcophile elements during the differentiation of hydrous melts

There is a lack of consensus regarding the roles of sulfide saturation versus volatile degassing on the partitioning of Cu and Ag during differentiation and eruption of convergent margin magmas. Because of their oxidized character, volatile-rich magmas from the Eastern Manus Back-arc Basin (EMBB) only reach sulfide saturation following magnetite-driven reduction of the melt: the so-called ‘‘magnetite crisis.’’ If sulfide saturation typically precedes volatile saturation, the magnetite crisis will limit the proportion of Cu and Ag that can partition from the melt into an exsolving volatile-rich phase, which may contribute to the sporadic occurrence of magmatic-hydrothermal ore deposits at convergent margins. However, it is unclear whether the magnetite crisis is a common or rare event during differentiation of volatile-rich magmas. We report major and trace element data for submarine volcanic glasses from the Tonga arc-proximal Valu Fa Ridge (VFR; SW Pacific). Cu-Se-Ag systematics of samples erupting at the southern VFR suggest magnetite fractionation-triggered sulfide saturation. The similarity in chalcophile element systematics of the southern VFR and EMBB samples is unlikely to be coincidental, and may indicate that the magnetite crisis is a common event during differentiation of hydrous melts. However, unlike many convergent margin magmas, it is unlikely that the evolving VFR and EMBB were saturated in a S-bearing volatile phase prior to magnetite fractionation. Hence, the metal-depleting magnetite crisis may be restricted to back-arc basin magmas that do not degas volatiles prior to magnetite fractionation and potentially convergent margin magmas fractionating at high pressures in the continental crust

Africa-specific human genetic variation near <i>CHD1L</i> associates with HIV-1 load

HIV-1 remains a global health crisis1, highlighting the need to identify new targets for therapies. Here, given the disproportionate HIV-1 burden and marked human genome diversity in Africa2, we assessed the genetic determinants of control of set-point viral load in 3,879 people of African ancestries living with HIV-1 participating in the international collaboration for the genomics of HIV3. We identify a previously undescribed association signal on chromosome 1 where the peak variant associates with an approximately 0.3 log10-transformed copies per ml lower set-point viral load per minor allele copy and is specific to populations of African descent. The top associated variant is intergenic and lies between a long intergenic non-coding RNA (LINC00624) and the coding gene CHD1L, which encodes a helicase that is involved in DNA repair4. Infection assays in iPS cell-derived macrophages and other immortalized cell lines showed increased HIV-1 replication in CHD1L-knockdown and CHD1L-knockout cells. We provide evidence from population genetic studies that Africa-specific genetic variation near CHD1L associates with HIV replication in vivo. Although experimental studies suggest that CHD1L is able to limit HIV infection in some cell types in vitro, further investigation is required to understand the mechanisms underlying our observations, including any potential indirect effects of CHD1L on HIV spread in vivo that our cell-based assays cannot recapitulate

Author Correction: Africa-specific human genetic variation near CHD1L associates with HIV-1 load.

Correction to: Nature https://doi.org/10.1038/s41586-023-06370-4 Published online 2 August 2023In the version of the article originally published, the “Acknowledgements” section was missing the following funding statement: “This work was supported in part by IAVI funded by the United States Agency for International Development (USAID). The full list of IAVI donors is available at http://www.iavi.org. The contents of this manuscript are the responsibility of the authors and do not necessarily reflect the views of USAID or the US Government”. This has now been added to the HTML and PDF versions of the article

Africa-specific human genetic variation near CHD1L associates with HIV-1 load.

HIV-1 remains a global health crisis1, highlighting the need to identify new targets for therapies. Here, given the disproportionate HIV-1 burden and marked human genome diversity in Africa2, we assessed the genetic determinants of control of set-point viral load in 3,879 people of African ancestries living with HIV-1 participating in the international collaboration for the genomics of HIV3. We identify a previously undescribed association signal on chromosome 1 where the peak variant associates with an approximately 0.3 log10-transformed copies per ml lower set-point viral load per minor allele copy and is specific to populations of African descent. The top associated variant is intergenic and lies between a long intergenic non-coding RNA (LINC00624) and the coding gene CHD1L, which encodes a helicase that is involved in DNA repair4. Infection assays in iPS cell-derived macrophages and other immortalized cell lines showed increased HIV-1 replication in CHD1L-knockdown and CHD1L-knockout cells. We provide evidence from population genetic studies that Africa-specific genetic variation near CHD1L associates with HIV replication in vivo. Although experimental studies suggest that CHD1L is able to limit HIV infection in some cell types in vitro, further investigation is required to understand the mechanisms underlying our observations, including any potential indirect effects of CHD1L on HIV spread in vivo that our cell-based assays cannot recapitulate