A 21-cm power spectrum at 48 MHz, using the Owens Valley Long Wavelength Array

The Large-aperture Experiment to detect the Dark Age (LEDA) was designed to measure the 21-cm signal from neutral hydrogen at Cosmic Dawn, $z \approx$15-30. Using observations made with the $\approx$ 200 m diameter core of the Owens Valley Long Wavelength Array (OVRO-LWA), we present a 2-D cylindrical spatial power spectrum for data at 43.1-53.5 MHz ($z_{\rm median}\approx 28$) incoherently integrated for 4 hours, and an analysis of the array sensitivity. Power from foregrounds is localized to a "wedge" within $k_\perp, k_\parallel$ space. After calibration of visibilities using 5 bright compact sources including VirA, we measure $\Delta^2(k) \approx 2 \times 10^{12}\ \mathrm{mK}^2$outside the foreground wedge, where an uncontaminated cosmological signal would lie, in principle. The measured$\Delta^2(k)$is an upper limit that reflects a combination of thermal instrumental and sky noise, and unmodelled systematics that scatter power from the wedge, as will be discussed. By differencing calibrated visibilities for close pairs of frequency channels, we suppress foreground sky structure and systematics, extract thermal noise, and use a mix of coherent and incoherent integration to simulate a noise-dominated power spectrum for a 3000 h observation and$z = $16-37. For suitable calibration quality, the resulting noise level,$\Delta^2(k) \approx 100$mK$^2$(k = 0.3 Mpc$^{-1}$), would be sufficient to detect peaks in the 21-cm spatial power spectrum due to early Ly-$\alpha$ and X-ray sources, as predicted for a range of theoretical model parameters.Comment: 16 pages, 11 figures. Accepted for MNRAS; replaced with accepted versio

Biennial report of the Fish Commission of the State of Oregon to the Governor and the Thirty-Third Legislative Assembly : 1925

December 1, 1922 - November 30, 1924

Decomposition of radiational effects of model feedbacks

Three separate doubled CO/sub 2/ experiments with the statistical dynamic model are used to illustrate efforts to study the climate dynamics, feedbacks, and interrelationships of meteorological parameters by decomposing and isolating their individual effects on radiation transport

Biennial report of the Fish Commission of the State of Oregon to the Govenor and the Fortieth Legislative Assembly : 1939

July 1, 1936 - June 30, 1938

Biennial report of the Fish Commission of the State of Oregon to the Governor and the Forty-Second Legislative Assembly : 1943

July 1, 1940 - June 30, 1942

Biennial report of the Fish Commission of the State of Oregon to the Governor and the Forty-First Legislative Assembly : 1941

July 1, 1938 - June 30, 1940

Folyóirat vagy gyűjteményes kötet? (Csokonai Diétai Magyar Múzsája)

BACKGROUND: The complex interplay between viral replication and host immune response during infection remains poorly understood. While many viruses are known to employ anti-immune strategies to facilitate their replication, highly pathogenic virus infections can also cause an excessive immune response that exacerbates, rather than reduces pathogenicity. To investigate this dichotomy in severe acute respiratory syndrome coronavirus (SARS-CoV), we developed a transcriptional network model of SARS-CoV infection in mice and used the model to prioritize candidate regulatory targets for further investigation. RESULTS: We validated our predictions in 18 different knockout (KO) mouse strains, showing that network topology provides significant predictive power to identify genes that are important for viral infection. We identified a novel player in the immune response to virus infection, Kepi, an inhibitory subunit of the protein phosphatase 1 (PP1) complex, which protects against SARS-CoV pathogenesis. We also found that receptors for the proinflammatory cytokine tumor necrosis factor alpha (TNFα) promote pathogenesis, presumably through excessive inflammation. CONCLUSIONS: The current study provides validation of network modeling approaches for identifying important players in virus infection pathogenesis, and a step forward in understanding the host response to an important infectious disease. The results presented here suggest the role of Kepi in the host response to SARS-CoV, as well as inflammatory activity driving pathogenesis through TNFα signaling in SARS-CoV infections. Though we have reported the utility of this approach in bacterial and cell culture studies previously, this is the first comprehensive study to confirm that network topology can be used to predict phenotypes in mice with experimental validation

Phytoplankton and light limitation in the Southern Ocean: Learning from high-nutrient high-chlorophyll areas

Most of the Southern Ocean is a high-nutrient, low-chlorophyll (HNLC) area. There are exceptions to this situation downstream of some of the islands, where iron from the islands or surrounding shallow plateau fertilizes the mixed layer and causes a phytoplankton bloom in spring and summer. The main locations where this occurs are downstream of the South Georgia, Crozet, and Kerguelen islands. Data on mixed layer depths from Argo float profiles together with Sea-viewing Wide Field-of-view Sensor chlorophyll a (chl a) and photosynthetically available radiation from these high-nutrient, high-chlorophyll (HNHC) areas are combined to study the effects of mixed layer-averaged light availability on phytoplankton concentrations in areas where iron limitation has been lifted. The results of this analysis are then transferred to HNLC areas to assess the potential importance of light limitation through the year. We conclude that light limitation does not significantly constrain the annual integrated standing stock of chl a in the HNLC Southern Ocea

Genome-wide association study identifies a variant in HDAC9 associated with large vessel ischemic stroke

Genetic factors have been implicated in stroke risk but few replicated associations have been reported. We conducted a genome-wide association study (GWAS) in ischemic stroke and its subtypes in 3,548 cases and 5,972 controls, all of European ancestry. Replication of potential signals was performed in 5,859 cases and 6,281 controls. We replicated reported associations between variants close to PITX2 and ZFHX3 with cardioembolic stroke, and a 9p21 locus with large vessel stroke. We identified a novel association for a SNP within the histone deacetylase 9(HDAC9) gene on chromosome 7p21.1 which was associated with large vessel stroke including additional replication in a further 735 cases and 28583 controls (rs11984041, combined P = 1.87×10−11, OR=1.42 (95% CI) 1.28-1.57). All four loci exhibit evidence for heterogeneity of effect across the stroke subtypes, with some, and possibly all, affecting risk for only one subtype. This suggests differing genetic architectures for different stroke subtypes

Length of carotid stenosis predicts peri-procedural stroke or death and restenosis in patients randomized to endovascular treatment or endarterectomy.

BACKGROUND: The anatomy of carotid stenosis may influence the outcome of endovascular treatment or carotid endarterectomy. Whether anatomy favors one treatment over the other in terms of safety or efficacy has not been investigated in randomized trials. METHODS: In 414 patients with mostly symptomatic carotid stenosis randomized to endovascular treatment (angioplasty or stenting; n = 213) or carotid endarterectomy (n = 211) in the Carotid and Vertebral Artery Transluminal Angioplasty Study (CAVATAS), the degree and length of stenosis and plaque surface irregularity were assessed on baseline intraarterial angiography. Outcome measures were stroke or death occurring between randomization and 30 days after treatment, and ipsilateral stroke and restenosis ≥50% during follow-up. RESULTS: Carotid stenosis longer than 0.65 times the common carotid artery diameter was associated with increased risk of peri-procedural stroke or death after both endovascular treatment [odds ratio 2.79 (1.17-6.65), P = 0.02] and carotid endarterectomy [2.43 (1.03-5.73), P = 0.04], and with increased long-term risk of restenosis in endovascular treatment [hazard ratio 1.68 (1.12-2.53), P = 0.01]. The excess in restenosis after endovascular treatment compared with carotid endarterectomy was significantly greater in patients with long stenosis than with short stenosis at baseline (interaction P = 0.003). Results remained significant after multivariate adjustment. No associations were found for degree of stenosis and plaque surface. CONCLUSIONS: Increasing stenosis length is an independent risk factor for peri-procedural stroke or death in endovascular treatment and carotid endarterectomy, without favoring one treatment over the other. However, the excess restenosis rate after endovascular treatment compared with carotid endarterectomy increases with longer stenosis at baseline. Stenosis length merits further investigation in carotid revascularisation trials