Competição interespecífica entre o parasitoide exótico Fopius arisanus e o nativo Doryctobracon areolatus (Hymenoptera Braconidae) em Anastrepha fraterculus (Diptera: Tephritidae).

SICONBIOL 2013

A time-domain control signal detection technique for OFDM

Transmission of system-critical control information plays a key role in efficient management of limited wireless network resources and successful reception of payload data information. This paper uses an orthogonal frequency division multiplexing (OFDM) architecture to investigate the detection performance of a time-domain approach used to detect deterministic control signalling information. It considers a type of control information chosen from a finite set of information, which is known at both transmitting and receiving wireless terminals. Unlike the maximum likelihood (ML) estimation method, which is often used, the time-domain detection technique requires no channel estimation and no pilots as it uses a form of time-domain correlation as the means of detection. Results show that when compared with the ML method, the time-domain approach improves detection performance even in the presence of synchronisation error caused by carrier frequency offset

In Defence of Public Higher Education: Knowledge for a Successful Society (The Alternative White Paper for HE)

The present Conservative Government, like the Coalition Government that preceded it, has an ideological predisposition towards the market and its supposed benefits to consumers, but appears to have no vision of Higher Education and its benefits to students and to the whole of society. These wider societal benefits can be summarised under three aspects: * educating the next generation of the population * carrying out research to address social and scientific challenges * maintaining an independent platform for research into society and science to facilitate democratic debate. The last of these, sometimes drawn under the umbrella of ‘academic freedom’, is the basis of the historic contract between Universities and the State. We contend, following the UNESCO Recommendation (1997), that academic freedom must be sufficient to guarantee the independence of scientific inquiry, commentary and teaching. Pressures from funding agencies and the state are usually cited as the principal threats to academic independence. The last decade has seen the rise of a third threat, namely an increasing managerial interference in academic life deriving from the introduction of market imperatives. These three societal benefits are interconnected. Without independent research there can be no scientific independence and no cutting-edge teaching. Without a focus on critique and challenge, students may see ‘education’ as a mere process of accumulating ‘facts’ to meet test criteria. A narrow focus on the acquisition of qualifications undermines the education process itself. Employers have criticised graduate recruits for insufficient creativity, of being rote-taught and thus un-adaptable to a modern business subject to rapid technological change. Importantly, critical skills are necessary to meet the challenge of business and for inclusive democratic engagement. The idea of a University that unites these three aspects is undermined by a new model of Higher Education Institution that sees the investment in human capital only as a private benefit. The Government’s White Paper, Success as a Knowledge Economy, and associated legislative programme, consolidate a fee-loan (or debt-finance) model of funding which puts the costs of higher education onto new graduates and future taxpayers, while reducing taxes for current taxpayers – many of whom directly benefit from publicly-supported higher education, or from its wider public benefits. The Government suggests that it is merely replacing direct public funding with one that places the ‘student at the heart of the system’. But it proposes that public funding should be directed towards the realisation of the private benefits of higher education, and it fails to acknowledge the wider public benefits that higher education affords. In truth, the proposals place the market at the heart of the system and subordinate the student as a consumer of higher education, with loans functioning as a voucher to present at a university of choice (providing that the student has the grades required). It is our view that this new funding model is wrong in principle and deficient in practice. The regulatory framework that is being introduced in its wake will undermine the declared aims to improve teaching quality, to enhance social mobility, and to improve access and achievement. The extension of university title to for-profit providers will also threaten the wider public benefits of higher education, by allowing them to compete as single-function institutions, and giving them access to publicly-supported loans for their students without a guarantee of their longer term stability. This will intensify existing competition and encourage a ‘race to the bottom’. Our defence of an alternative vision of Higher Education takes place in the context of a dismal lack of leadership by the various mission groups representing universities in the sector – for example, Universities UK and the Russell Group – and other bodies responsible for the sector. Their willing advocacy of a fee-loan model of funding (to avoid possible cuts) has abdicated their leadership role in a proper debate on the values of public higher education. This failure to defend the values of the very public higher education they are chartered to provide is in marked contrast to representations made by another group. Lobbyists on behalf of for-profit providers are seeking a supposed ‘level-playing field’ in undergraduate degree provision, despite having no track record of success in the UK, a disastrous record in the USA, and no desire to provide any wider public benefit of their existence. The Government’s position is also in marked contrast to public attitudes. The British Social Attitudes Survey (NatCen) has, before and since the introduction of tuition fee changes, regularly asked questions about public attitudes to higher education and inequality. The majority of the population has consistently opposed high levels of student debt, believed that education has a value beyond simply providing the means to a better job, and maintained that inequality in Britain is an obstacle to the fulfillment of opportunities. Perhaps surprisingly, this commitment to the values of publicly-funded higher education is especially marked among those without graduate-level qualifications. Politicians who argue that the latter resent paying taxes to finance education for ‘middle-class people’ should seek evidence for this assertion. But the ‘debate’ among politicians, members of the BIS secretariat and corporate lobbyists over the issue has been remarkable for its superficial, un-evidenced character. It has also been remarkable for the absence of full public debate (Leach 2016). This Alternative White Paper aims to correct this imbalance. We need a proper debate about the future of UK Higher Education

In Situ-Targeting of Dendritic Cells with Donor-Derived Apoptotic Cells Restrains Indirect Allorecognition and Ameliorates Allograft Vasculopathy

Chronic allograft vasculopathy (CAV) is an atheromatous-like lesion that affects vessels of transplanted organs. It is a component of chronic rejection that conventional immuno-suppression fails to prevent, and is a major cause of graft loss. Indirect allo-recognition through T cells and allo-Abs are critical during CAV pathogenesis. We tested whether the indirect allo-response and its impact on CAV is down-regulated by in situ-delivery of donor Ags to recipient's dendritic cells (DCs) in lymphoid organs in a pro-tolerogenic fashion, through administration of donor splenocytes undergoing early apoptosis. Following systemic injection, donor apoptotic cells were internalized by splenic CD11chi CD8α+ and CD8− DCs, but not by CD11cint plasmacytoid DCs. Those DCs that phagocytosed apoptotic cells in vivo remained quiescent, resisted ex vivo-maturation, and presented allo-Ag for up to 3 days. Administration of donor apoptotic splenocytes, unlike cells alive, (i) promoted deletion, FoxP3 expression and IL-10 secretion, and decreased IFN-γ-release in indirect pathway CD4 T cells; and (ii) reduced cross-priming of anti-donor CD8 T cells in vivo. Targeting recipient's DCs with donor apoptotic cells reduced significantly CAV in a fully-mismatched aortic allograft model. The effect was donor specific, dependent on the physical characteristics of the apoptotic cells, and was associated to down-regulation of the indirect type-1 T cell allo-response and secretion of allo-Abs, when compared to recipients treated with donor cells alive or necrotic. Down-regulation of indirect allo-recognition through in situ-delivery of donor-Ag to recipient's quiescent DCs constitutes a promising strategy to prevent/ameliorate indirect allorecognition and CAV

Recent acquisition of Helicobacter pylori by Baka Pygmies

Both anatomically modern humans and the gastric pathogen Helicobacter pylori originated in Africa, and both species have been associated for at least 100,000 years. Seven geographically distinct H. pylori populations exist, three of which are indigenous to Africa: hpAfrica1, hpAfrica2, and hpNEAfrica. The oldest and most divergent population, hpAfrica2, evolved within San hunter-gatherers, who represent one of the deepest branches of the human population tree. Anticipating the presence of ancient H. pylori lineages within all hunter-gatherer populations, we investigated the prevalence and population structure of H. pylori within Baka Pygmies in Cameroon. Gastric biopsies were obtained by esophagogastroduodenoscopy from 77 Baka from two geographically separated populations, and from 101 non-Baka individuals from neighboring agriculturalist populations, and subsequently cultured for H. pylori. Unexpectedly, Baka Pygmies showed a significantly lower H. pylori infection rate (20.8%) than non-Baka (80.2%). We generated multilocus haplotypes for each H. pylori isolate by DNA sequencing, but were not able to identify Baka-specific lineages, and most isolates in our sample were assigned to hpNEAfrica or hpAfrica1. The population hpNEAfrica, a marker for the expansion of the Nilo-Saharan language family, was divided into East African and Central West African subpopulations. Similarly, a new hpAfrica1 subpopulation, identified mainly among Cameroonians, supports eastern and western expansions of Bantu languages. An age-structured transmission model shows that the low H. pylori prevalence among Baka Pygmies is achievable within the timeframe of a few hundred years and suggests that demographic factors such as small population size and unusually low life expectancy can lead to the eradication of H. pylori from individual human populations. The Baka were thus either H. pylori-free or lost their ancient lineages during past demographic fluctuations. Using coalescent simulations and phylogenetic inference, we show that Baka almost certainly acquired their extant H. pylori through secondary contact with their agriculturalist neighbors

Analysis of Inducible Nitric Oxide Synthase Gene Polymorphisms in Vitiligo in Han Chinese People

Background: Vitiligo is a chronic depigmented skin disorder with regional melanocytes depletion. The pathogenesis was not completely clarified. Recently, more and more evidence suggested that polymorphisms of some genes are associated with vitiligo risk. Here, we want to examine the association between the inducible nitric oxide synthase (iNOS) gene polymorphisms and the risk of vitiligo in Chinese populations. Methods and Principal Findings: In a hospital-based case-control study of 749 patients with vitiligo and 763 age- and sexmatched healthy controls, three polymorphisms of iNOS gene were genotyped by using the PCR-restriction fragment length polymorphism (PCR-RFLP) and mutagenically separated PCR (MS-PCR) methods, respectively. We found the iNOS-954 polymorphism was associated with a significantly higher risk of vitiligo (adjusted OR = 1.36, 95 % CI = 1.02–1.81). Furthermore, this association is more pronounced in vulgaris vitiligo, active vitiligo and vitiligo without other autoimmune diseases in the stratification study. Analysis of haplotypes showed increased risk for the C-1173C-954CEx16+14 (OR = 1.44, 95% CI = 1.01–1.74). In addition, the serum iNOS activity is significantly associated with iNOS-954 combined genotype (GC+CC) and is much higher in vitiligo patients than in the controls (P,0.01). Logistic regression analysis of iNOS activity showed increased risk between higher activity and iNOS-954 GRC variant genotype carriers (Ptrend,0.001). Conclusions and Significance: INOS gene polymorphisms may play an important role in the genetic susceptibility to th

Somitogenesis Clock-Wave Initiation Requires Differential Decay and Multiple Binding Sites for Clock Protein

Somitogenesis is a process common to all vertebrate embryos in which repeated blocks of cells arise from the presomitic mesoderm (PSM) to lay a foundational pattern for trunk and tail development. Somites form in the wake of passing waves of periodic gene expression that originate in the tailbud and sweep posteriorly across the PSM. Previous work has suggested that the waves result from a spatiotemporally graded control protein that affects the oscillation rate of clock-gene expression. With a minimally constructed mathematical model, we study the contribution of two control mechanisms to the initial formation of this gene-expression wave. We test four biologically motivated model scenarios with either one or two clock protein transcription binding sites, and with or without differential decay rates for clock protein monomers and dimers. We examine the sensitivity of wave formation with respect to multiple model parameters and robustness to heterogeneity in cell population. We find that only a model with both multiple binding sites and differential decay rates is able to reproduce experimentally observed waveforms. Our results show that the experimentally observed characteristics of somitogenesis wave initiation constrain the underlying genetic control mechanisms

Long-COVID cognitive impairments and reproductive hormone deficits in men may stem from GnRH neuronal death

BACKGROUND: We have recently demonstrated a causal link between loss of gonadotropin-releasing hormone (GnRH), the master molecule regulating reproduction, and cognitive deficits during pathological aging, including Down syndrome and Alzheimer's disease. Olfactory and cognitive alterations, which persist in some COVID-19 patients, and long-term hypotestosteronaemia in SARS-CoV-2-infected men are also reminiscent of the consequences of deficient GnRH, suggesting that GnRH system neuroinvasion could underlie certain post-COVID symptoms and thus lead to accelerated or exacerbated cognitive decline. METHODS: We explored the hormonal profile of COVID-19 patients and targets of SARS-CoV-2 infection in post-mortem patient brains and human fetal tissue. FINDINGS: We found that persistent hypotestosteronaemia in some men could indeed be of hypothalamic origin, favouring post-COVID cognitive or neurological symptoms, and that changes in testosterone levels and body weight over time were inversely correlated. Infection of olfactory sensory neurons and multifunctional hypothalamic glia called tanycytes highlighted at least two viable neuroinvasion routes. Furthermore, GnRH neurons themselves were dying in all patient brains studied, dramatically reducing GnRH expression. Human fetal olfactory and vomeronasal epithelia, from which GnRH neurons arise, and fetal GnRH neurons also appeared susceptible to infection. INTERPRETATION: Putative GnRH neuron and tanycyte dysfunction following SARS-CoV-2 neuroinvasion could be responsible for serious reproductive, metabolic, and mental health consequences in long-COVID and lead to an increased risk of neurodevelopmental and neurodegenerative pathologies over time in all age groups. FUNDING: European Research Council (ERC) grant agreements No 810331, No 725149, No 804236, the European Union Horizon 2020 research and innovation program No 847941, the Fondation pour la Recherche Médicale (FRM) and the Agence Nationale de la Recherche en Santé (ANRS) No ECTZ200878 Long Covid 2021 ANRS0167 SIGNAL, Agence Nationale de la recherche (ANR) grant agreements No ANR-19-CE16-0021-02, No ANR-11-LABEX-0009, No. ANR-10-LABEX-0046, No. ANR-16-IDEX-0004, Inserm Cross-Cutting Scientific Program HuDeCA, the CHU Lille Bonus H, the UK Medical Research Council (MRC) and National Institute of Health and care Research (NIHR)

Quantification of Circadian Rhythms in Single Cells

Bioluminescence techniques allow accurate monitoring of the circadian clock in single cells. We have analyzed bioluminescence data of Per gene expression in mouse SCN neurons and fibroblasts. From these data, we extracted parameters such as damping rate and noise intensity using two simple mathematical models, one describing a damped oscillator driven by noise, and one describing a self-sustained noisy oscillator. Both models describe the data well and enabled us to quantitatively characterize both wild-type cells and several mutants. It has been suggested that the circadian clock is self-sustained at the single cell level, but we conclude that present data are not sufficient to determine whether the circadian clock of single SCN neurons and fibroblasts is a damped or a self-sustained oscillator. We show how to settle this question, however, by testing the models' predictions of different phases and amplitudes in response to a periodic entrainment signal (zeitgeber)