Power scaling, vascular branching patterns, and the golden ratio

The Golden Ratio (a ratio of ~1.618:1) appears repeatedly in nature including structural and functional traits of organisms (e.g. Fibonacci spirals of snail shells and certain seed heads), the spiraled shape of galaxies and hurricanes, and even in much cultural architecture and art. In the mid-19th century, branching structures in plant and animal vascular systems were found to follow the Golden Ratio; that is, successive branches in the vascular systems of plants and animals tend to follow a length ratio of about 1.618:1. Here we present a model that uses this empirical evidence as a branching ratio in theoretical vascular systems. We then use a defined mass of the model system as a predictor of log-log scaling of terminal units. In this model, log terminal units and log mass scale similarly with that of other models as well as empirical evidence, but with more parsimony and a perspective not yet offered among all available models of allometric scaling. This model invites novel and broad hypotheses on the influence of the Golden Ratio on power scaling in organisms

Below the Line: an Analysis of Income Poverty in New Zealand, 1984 - 1998

The economic and social reforms between 1984 and 1999 led to claims of increasing economic hardship, a widening income distribution and adverse consequences on living standards from higher housing costs. This article provides a systematic discussion of those claims, based on an analysis of Statistics New Zealand annual Household Economic Survey. Using a focus group determined poverty line, the paper explores who was poor in 1998, as well as commenting on trends in poverty between 1984 and 1998, on both the basis of disposable income and when this poverty measure is adjusted for relative housing costs. Trends in the incidence and severity of poverty depend crucially on whether an absolute or relative approach is taken to adjusting the poverty line through time. Key Words: Poverty, focus groups, income distribution, trends

Lowering the bar: options for the automotive industry to achieve 80g/km CO2 by 2020 in Europe

Transport is the fastest growing sector for greenhouse gas emissions in the EU. In 2007, transport accounted for 28% of the EU’s overall emissions and passenger cars are responsible for over half of these. Recognising the problem, European Commission President José Manuel Barroso has singled out the transport sector, alongside the power sector, as a priority area for climate action during his second term in office. Executive summary: In April 2010, the European Commission proposed a European strategy on clean and energy efficient vehicles. The Commission recognised that “Ambitious emission targets will be crucial in driving innovations in the long-term and will take account of their contribution to achieving the overall level of greenhouse gas reduction needed in the transport sector.” Under EU legislation adopted in 2009, the average new passenger car sold in 2015 should comply with a CO2 target of 130 grammes per kilometre (g/km). By 2020, the target is 95g/km. A review of this legislation is scheduled no later than the end of 2012, to agree the modalities of how carmakers should reach the 2020 target. The first studies have been carried out for the European Commission into the feasibility of the 95g/km target as well as others. These studies have focused on technology improvements as a solitary means of achieving the reduction, ignoring other means such as lowering performance and a shift toward smaller cars. Unsurprisingly, a target of 85g/km has been identified as “the maximum attainable target under the assumptions in the study,” (AEA 2009: 23). Greenpeace has commissioned a separate study to demonstrate the feasibility of reaching an even lower target of 80g/km by 2020. This target would increase the emissions savings from the legislation to 100 million tons (Mt) CO2 by 2020, instead of 80 Mt CO2 saved with a target of 95g/km by 2020, according to earlier research carried out for Greenpeace. The study is released as EU ministers discuss the regulatory framework, as part of the European strategy on clean and energy efficient vehicles

CD32-Expressing CD4 T Cells Are Phenotypically Diverse and Can Contain Proviral HIV DNA.

Efforts to both characterize and eradicate the HIV reservoir have been limited by the rarity of latently infected cells and the absence of a specific denoting biomarker. CD32a (FcγRIIa) has been proposed to be a marker for an enriched CD4 T cell HIV reservoir, but this finding remains controversial. Here, we explore the expression of CD32 on CD3+CD4+ cells in participants from two primary HIV infection studies and identify at least three distinct phenotypes (CD32low, CD32+CD14+, and CD32high). Of note, CD4 negative enrichment kits remove the majority of CD4+CD32+ T cells, potentially skewing subsequent analyses if used. CD32high CD4 T cells had higher levels of HLA-DR and HIV co-receptor expression than other subsets, compatible with their being more susceptible to infection. Surprisingly, they also expressed high levels of CD20, TCRαβ, IgD, and IgM (but not IgG), markers for both T cells and naïve B cells. Compared with other populations, CD32low cells had a more differentiated memory phenotype and high levels of immune checkpoint receptors, programmed death receptor-1 (PD-1), Tim-3, and TIGIT. Within all three CD3+CD4+CD32+ phenotypes, cells could be identified in infected participants, which contained HIV DNA. CD32 expression on CD4 T cells did not correlate with HIV DNA or cell-associated HIV RNA (both surrogate measures of overall reservoir size) or predict time to rebound viremia following treatment interruption, suggesting that it is not a dominant biomarker for HIV persistence. Our data suggest that while CD32+ T cells can be infected with HIV, CD32 is not a specific marker of the reservoir although it might identify a population of HIV enriched cells in certain situations

CD32-Expressing CD4 T Cells Are Phenotypically Diverse and Can Contain Proviral HIV DNA.

Efforts to both characterize and eradicate the HIV reservoir have been limited by the rarity of latently infected cells and the absence of a specific denoting biomarker. CD32a (FcγRIIa) has been proposed to be a marker for an enriched CD4 T cell HIV reservoir, but this finding remains controversial. Here, we explore the expression of CD32 on CD3+CD4+ cells in participants from two primary HIV infection studies and identify at least three distinct phenotypes (CD32low, CD32+CD14+, and CD32high). Of note, CD4 negative enrichment kits remove the majority of CD4+CD32+ T cells, potentially skewing subsequent analyses if used. CD32high CD4 T cells had higher levels of HLA-DR and HIV co-receptor expression than other subsets, compatible with their being more susceptible to infection. Surprisingly, they also expressed high levels of CD20, TCRαβ, IgD, and IgM (but not IgG), markers for both T cells and naïve B cells. Compared with other populations, CD32low cells had a more differentiated memory phenotype and high levels of immune checkpoint receptors, programmed death receptor-1 (PD-1), Tim-3, and TIGIT. Within all three CD3+CD4+CD32+ phenotypes, cells could be identified in infected participants, which contained HIV DNA. CD32 expression on CD4 T cells did not correlate with HIV DNA or cell-associated HIV RNA (both surrogate measures of overall reservoir size) or predict time to rebound viremia following treatment interruption, suggesting that it is not a dominant biomarker for HIV persistence. Our data suggest that while CD32+ T cells can be infected with HIV, CD32 is not a specific marker of the reservoir although it might identify a population of HIV enriched cells in certain situations

Early and nonreversible decrease of CD161++ /MAIT cells in HIV infection

HIV infection is associated with immune dysfunction, perturbation of immune-cell subsets and opportunistic infections. CD161++ CD8+ T cells are a tissue-infiltrating population that produce IL17A, IL22, IFN, and TNFα, cytokines important in mucosal immunity. In adults they dominantly express the semi-invariant TCR Vα7.2, the canonical feature of mucosal associated invariant T (MAIT) cells and have been recently implicated in host defense against pathogens. We analyzed the frequency and function of CD161++ /MAIT cells in peripheral blood and tissue from patients with early stage or chronic-stage HIV infection. We show that the CD161++ /MAIT cell population is significantly decreased in early HIV infection and fails to recover despite otherwise successful treatment. We provide evidence that CD161++ /MAIT cells are not preferentially infected but may be depleted through diverse mechanisms including accumulation in tissues and activation-induced cell death. This loss may impact mucosal defense and could be important in susceptibility to specific opportunistic infections in HIV

Evidence for HIV-1 cure after CCR5 Δ32/Δ32 allogeneic haemopoietic stem-cell transplantation 30 months post analytical treatment interruption : a case report

The London patient (participant 36 in the IciStem cohort) underwent allogeneic stem-cell transplantation with cells that did not express CCR5 (CCR5 Δ32/Δ32); remission was reported at 18 months after analytical treatment interruption (ATI). Here, we present longer term data for this patient (up to 30 months after ATI), including sampling from diverse HIV-1 reservoir sites. We used ultrasensitive viral load assays of plasma, semen, and cerebrospinal fluid (CSF) samples to detect HIV-1 RNA. In gut biopsy samples and lymph-node tissue, cell-copy number and total HIV-1 DNA levels were quantified in multiple replicates, using droplet digital PCR (ddPCR) and quantitative real-time PCR. We also analysed the presence of intact proviral DNA using multiplex ddPCR targeting the packaging signal (ψ) and envelope (env). We did intracellular cytokine staining to measure HIV-1-specific T-cell responses. We used low-sensitive and low-avidity antibody assays to measure the humoral response to HIV-1. We predicted the probability of rebound using a mathematical model and inference approach. HIV-1 viral load in plasma remained undetectable in the London patient up to 30 months (last tested on March 4, 2020), using an assay with a detection limit of 1 copy per mL. The patient's CD4 count was 430 cells per μL (23·5% of total T cells) at 28 months. A very low-level positive signal for HIV-1 DNA was recorded in peripheral CD4 memory cells at 28 months. The viral load in semen was undetectable in both plasma (lower limit of detection [LLD] <12 copies per mL) and cells (LLD 10 copies per 10 6 cells) at 21 months. CSF was within normal parameters at 25 months, with HIV-1 RNA below the detection limit (LLD 1 copy per mL). HIV-1 DNA by ddPCR was negative in rectum, caecum, and sigmoid colon and terminal ileum tissue samples at 22 months. Lymph-node tissue from axilla was positive for the long-terminal repeat (33 copies per 10 6 cells) and env (26·1 copies per 10 6 cells), negative for ψ and integrase, and negative by the intact proviral DNA assay, at 27 months. HIV-1-specific CD4 and CD8 T-cell responses have remained absent at 27 months. Low-avidity Env antibodies have continued to decline. Mathematical modelling suggests that the probability of remission for life (cure) is 98% in the context of 80% donor chimerism in total HIV target cells and greater than 99% probability of remission for life with 90% donor chimerism. The London patient has been in HIV-1 remission for 30 months with no detectable replication-competent virus in blood, CSF, intestinal tissue, or lymphoid tissue. Donor chimerism has been maintained at 99% in peripheral T cells. We propose that these findings represent HIV-1 cure. Wellcome Trust and amfAR (American Foundation for AIDS Research)

The Australia Telescope 20GHz Survey: Hardware, Observing Strategy, and Scanning Survey Catalog

The Australia Telescope 20GHz (AT20G) survey is a large area (2{\pi} sr), sensitive (40mJy), high frequency (20GHz) survey of the southern sky. The survey was conducted in two parts: an initial fast scanning survey, and a series of more accurate follow-up observations. The follow-up survey catalog has been presented by Murphy et al. 2010. In this paper we discuss the hardware setup and scanning survey strategy as well as the production of the scanning survey catalog.Comment: 32 pages, 20 figures, accepted for publication in experimental astronom