J-85 jet engine noise measured in the ONERA S1 wind tunnel and extrapolated to far field

Noise from a J-85 turbojet with a conical, convergent nozzle was measured in simulated flight in the ONERA S1 Wind Tunnel. Data are presented for several flight speeds up to 130 m/sec and for radiation angles of 40 to 160 degrees relative to the upstream direction. The jet was operated with subsonic and sonic exhaust speeds. A moving microphone on a 2 m sideline was used to survey the radiated sound field in the acoustically treated, closed test section. The data were extrapolated to a 122 m sideline by means of a multiple-sideline source-location method, which was used to identify the acoustic source regions, directivity patterns, and near field effects. The source-location method is described along with its advantages and disadvantages. Results indicate that the effects of simulated flight on J-85 noise are significant. At the maximum forward speed of 130 m/sec, the peak overall sound levels in the aft quadrant were attentuated approximately 10 dB relative to sound levels of the engine operated statically. As expected, the simulated flight and static data tended to merge in the forward quadrant as the radiation angle approached 40 degrees. There is evidence that internal engine or shock noise was important in the forward quadrant. The data are compared with published predictions for flight effects on pure jet noise and internal engine noise. A new empirical prediction is presented that relates the variation of internally generated engine noise or broadband shock noise to forward speed. Measured near field noise extrapolated to far field agrees reasonably well with data from similar engines tested statically outdoors, in flyover, in a wind tunnel, and on the Bertin Aerotrain. Anomalies in the results for the forward quadrant and for angles above 140 degrees are discussed. The multiple-sideline method proved to be cumbersome in this application, and it did not resolve all of the uncertainties associated with measurements of jet noise close to the jet. The simulation was complicated by wind-tunnel background noise and the propagation of low frequency sound around the circuit

The evolving SARS-CoV-2 epidemic in Africa: Insights from rapidly expanding genomic surveillance

INTRODUCTION Investment in Africa over the past year with regard to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) sequencing has led to a massive increase in the number of sequences, which, to date, exceeds 100,000 sequences generated to track the pandemic on the continent. These sequences have profoundly affected how public health officials in Africa have navigated the COVID-19 pandemic. RATIONALE We demonstrate how the first 100,000 SARS-CoV-2 sequences from Africa have helped monitor the epidemic on the continent, how genomic surveillance expanded over the course of the pandemic, and how we adapted our sequencing methods to deal with an evolving virus. Finally, we also examine how viral lineages have spread across the continent in a phylogeographic framework to gain insights into the underlying temporal and spatial transmission dynamics for several variants of concern (VOCs). RESULTS Our results indicate that the number of countries in Africa that can sequence the virus within their own borders is growing and that this is coupled with a shorter turnaround time from the time of sampling to sequence submission. Ongoing evolution necessitated the continual updating of primer sets, and, as a result, eight primer sets were designed in tandem with viral evolution and used to ensure effective sequencing of the virus. The pandemic unfolded through multiple waves of infection that were each driven by distinct genetic lineages, with B.1-like ancestral strains associated with the first pandemic wave of infections in 2020. Successive waves on the continent were fueled by different VOCs, with Alpha and Beta cocirculating in distinct spatial patterns during the second wave and Delta and Omicron affecting the whole continent during the third and fourth waves, respectively. Phylogeographic reconstruction points toward distinct differences in viral importation and exportation patterns associated with the Alpha, Beta, Delta, and Omicron variants and subvariants, when considering both Africa versus the rest of the world and viral dissemination within the continent. Our epidemiological and phylogenetic inferences therefore underscore the heterogeneous nature of the pandemic on the continent and highlight key insights and challenges, for instance, recognizing the limitations of low testing proportions. We also highlight the early warning capacity that genomic surveillance in Africa has had for the rest of the world with the detection of new lineages and variants, the most recent being the characterization of various Omicron subvariants. CONCLUSION Sustained investment for diagnostics and genomic surveillance in Africa is needed as the virus continues to evolve. This is important not only to help combat SARS-CoV-2 on the continent but also because it can be used as a platform to help address the many emerging and reemerging infectious disease threats in Africa. In particular, capacity building for local sequencing within countries or within the continent should be prioritized because this is generally associated with shorter turnaround times, providing the most benefit to local public health authorities tasked with pandemic response and mitigation and allowing for the fastest reaction to localized outbreaks. These investments are crucial for pandemic preparedness and response and will serve the health of the continent well into the 21st century

Far-Field Pressure Estimation of a plate from the Interpolated Acceleration Distribution

International audienc

Humanisation de la réponse à la Fièvre Hémorragique Ebola en Guinée: approche anthropologique (Conakry/Guéckédou mars-juillet 2014)

Il s'agit ici d'un document ayant servi à la fois de rapport d'activité des auteurs et de plate forme de formation et de sensibilisation des acteurs de la réponse à l'épidémie de maladie à virus Ebola en Guinée diffusé à compter de juillet 2014.Rapport de mission conjoint de Julienne Anoko et Alain Epelboin en Guinée lors de l'épidémie de maladie à virus Ebol

Human Genome Replication Proceeds through Four Chromatin States

International audienceAdvances in genomic studies have led to significant progress in understanding the epigenetically controlled interplay between chromatin structure and nuclear functions. Epigenetic modifications were shown to play a key role in transcription regulation and genome activity during development and differentiation or in response to the environment. Paradoxically, the molecular mechanisms that regulate the initiation and the maintenance of the spatio-temporal replication program in higher eukaryotes, and in particular their links to epigenetic modifications, still remain elusive. By integrative analysis of the genome-wide distributions of thirteen epigenetic marks in the human cell line K562, at the 100 kb resolution of corresponding mean replication timing (MRT) data, we identify four major groups of chromatin marks with shared features. These states have different MRT, namely from early to late replicating, replication proceeds though a transcriptionally active euchromatin state (C1), a repressive type of chromatin (C2) associated with polycomb complexes, a silent state (C3) not enriched in any available marks, and a gene poor HP1-associated heterochromatin state (C4). When mapping these chromatin states inside the megabase-sized U-domains (U-shaped MRT profile) covering about 50% of the human genome, we reveal that the associated replication fork polarity gradient corresponds to a directional path across the four chromatin states, from C1 at U-domains borders followed by C2, C3 and C4 at centers. Analysis of the other genome half is consistent with early and late replication loci occurring in separate compartments, the former correspond to gene-rich, high-GC domains of intermingled chromatin states C1 and C2, whereas the latter correspond to gene-poor, low-GC domains of alternating chromatin states C3 and C4 or long C4 domains. This new segmentation sheds a new light on the epigenetic regulation of the spatio-temporal replication program in human and provides a framework for further studies in different cell types, in both health and disease

Epigenetic regulation of the human genome: coherence between promoter activity and large-scale chromatin environment

International audienceIncreasing knowledge of chromatin structure in various cell types raises the challenge of deciphering the contribution of epigenetic modifications to the regulation of nuclear functions in mammals. In a recent study, we have analysed the genome-wide distributions of thirteen epigenetic marks in the human cell line K562 at 100 kb resolution of Mean Replication Timing (MRT) data. Using classical clustering techniques, we have shown that the combinatorial complexity of these epigenetic data can be reduced to four predominant chromatin states that replicate at different periods of the S-phase. C1 is an early replicating transcriptionally active euchromatin state, C2 a mid-S repressive type of chromatin associated with Polycomb complexes, C3 a silent chromatin with lack of chromatin marks that replicates later than C2 but before C4, a HP1-associated heterochromatin state that replicates at the end of S-phase. These four chromatin states display remarkable similarities with those recently reported in fly, worm and plants at higher ∼ 1 kb resolution of gene expression data. Here, we extend our integrative analysis of epigenetic data in the K562 human cell line to this smaller scale by focusing on gene promoters (±3 kb around transcription start sites). We show that these promoters can similarly be classified into four main chromatin states: P1 regroups all the marks of transcriptionally active chromatin and corresponds to CpG rich promoters of highly expressed genes; P2 is notably associated with the histone modification H3K27me3 that is the mark of a polycomb repressed chromatin state; P3 corresponds to promoters that are not enriched for any available marks as the signature of a ‘null’ or ‘black’ silent heterochromatin state and P4 characterizes the few gene promoters that contain only the constitutive heterochromatin histone modification H3K9me3. When investigating the coherence between promoter activity (P1, P2, P3 or P4) and the large-scale chromatin environment (C1, C2, C3 or C4), we find that the higher the gene density in a considered 100 kb-window, the higher (resp. the lower) the probability of a P1 active promoter (resp. silent P2, P3 and P4 promoters) to be surrounded by an open euchromatin C1 (resp. facultative C2, black C3 or HP1-associated C4 heterochromatin) environment. From large to small scales, it is mainly C4 and to a lesser extent C3 heterochromatin environments both corresponding to gene poor regions, that strongly conditions promoters to belong to the inactive P3 and P4 classes. If C1 (resp. C2) environment surrounds a majority of corresponding active P1 (resp. P2) promoters, it also contains a non-negligible proportion of inactive P2 and P3 (resp. active P1 and inactive P3) promoters. When further investigating the large-scale organization of human genes with respect to ‘master’ replication origins that were shown to border megabase-sized U-shaped MRT domains, we reveal some significant enrichment of highly expressed P1 genes in a closed neighbourhood of these early initiation zones consistently with the gradient of chromatin states observed from C1 at U-domain borders followed by C2, C3 and C4 at U-domain centers. On the contrary to P2 promoters that are mainly found in the C2 environment at finite distance (∼200–300 kb) from U-domain borders, the inactive P3 and P4 promoters are distributed rather homogeneously inside U-domains. The generalization of our study to different cell types including ES, somatic and cancer cells is likely to provide new insight on the global reorganization of replication domains during differentiation (or disease) in relation to coordinated changes in chromatin environment and gene expression

Modelling adipocytes size distribution

International audienceAdipocytes are cells whose task is to store excess energy as lipid droplets in their cytoplasm. Adipocytes can adapt their size according to the lipid amount to be stored. Adipocyte size variation can reach one order of magnitude inside the same organism which is unique among cells. A striking feature in adipocytes size distribution is the lack of characteristic size since typical size distributions are bimodal. Since energy can be stored and retrieved and adipocytes are responsible for these lipid fluxes, we propose a simple model of size-dependent lipid fluxes that is able to predict typical adipocytes size distribution

Gene content in the four prevalent chromatin states of H1hesc and K562 cell lines.

<p>For each chromatin state the following information is given: (i) the total number of promoters per chromatin state, (ii) the density of promoters per Mb, (iii) the mean level of expression per chromatin state in RPKM (Materials and Methods), (iv) the median level of expression per chromatin state in RPKM, (v) the mean gene length per chromatin state in kb.</p><p>Gene content in the four prevalent chromatin states of H1hesc and K562 cell lines.</p

Epigenetic marks enrichment in specific MRT U-domains of H1hesc and Nhdfad.

<p>(A) Mean coverage of H2AZ enriched intervals with respect to the distance to the closest U-domain border specific to the cell line. The different colors correspond to specific U-domains of Nhdfad (black), specific U-domains of H1hesc whose border is in EC1 or EC2 (red) and specific U-domains of H1hesc whose border is in EC4 (blue). (B), (C) and (D) are as (A) for respectively CTCF, NANOG anf OCT4. Note that in (C) and (D) coverage are per thousand.</p