Abstract
Fisheries management is commonly based on the outputs of single-species stock assessment models. While such models are appropriate for tactical issues such as quota setting, they typically ...omit explicit trophic interactions between different parts of the ecosystem. To successfully manage multiple fisheries in the same ecosystem, we need to understand how fishing one species may indirectly affect other species. In this paper, we used a simulation model of the southern Benguela ecosystem, built in the Atlantis framework, to explore fisheries interaction effects. We first measured the impact of fishing different stocks individually at FMSY, the hypothetical level of fishing effort which produces maximum sustainable yield (MSY) in a single-species modelling context. We then applied FMSY to all stocks simultaneously and compared the simultaneous yield with the sum of yields from the individual applications of FMSY. Contrary to expectations, the total catch was higher under the simultaneous scenario. We explored our results by studying the influences of trophic interaction between species at different levels of the foodweb, and found that our overall result was driven by two key factors: volumetric dominance of small pelagic fish in the total catch, and asymmetric influences of competition and predation between piscivorous and planktivorous species. The simultaneous increase in fishing pressure across multiple species in the model led to increased effective carrying capacity for small pelagic species (due to reduced competition), but reduced carrying capacity for piscivorous species (due to reduced small pelagic prey). This work has important implications for the design of tactical multispecies models for use in ecosystem-based fisheries management.
We present the discovery of KELT-24 b, a massive hot Jupiter orbiting a bright (V = 8.3 mag, K = 7.2 mag) young F-star with a period of 5.6 days. The host star, KELT-24 (HD 93148), has a Teff = K, a ...mass of M* = M , a radius of R* = 1.506 0.022 R , and an age of Gyr. Its planetary companion (KELT-24 b) has a radius of RP = 1.272 0.021 RJ and a mass of MP = MJ, and from Doppler tomographic observations, we find that the planet's orbit is well-aligned to its host star's projected spin axis ( ). The young age estimated for KELT-24 suggests that it only recently started to evolve from the zero-age main sequence. KELT-24 is the brightest star known to host a transiting giant planet with a period between 5 and 10 days. Although the circularization timescale is much longer than the age of the system, we do not detect a large eccentricity or significant misalignment that is expected from dynamical migration. The brightness of its host star and its moderate surface gravity make KELT-24b an intriguing target for detailed atmospheric characterization through spectroscopic emission measurements since it would bridge the current literature results that have primarily focused on lower mass hot Jupiters and a few brown dwarfs.
We announce the discovery of KELT-12b, a highly inflated Jupiter-mass planet transiting the mildly evolved, V = 10.64 host star TYC 2619-1057-1. We followed up the initial transit signal in the ...KELT-North survey data with precise ground-based photometry, high-resolution spectroscopy, precise radial velocity measurements, and high-resolution adaptive optics imaging. Our preferred best-fit model indicates that the host star has = 6279 51 K, = 3.89 0.05, Fe/H = , = , and = 2.37 0.17 . The planetary companion has = 0.95 0.14 , = , = , and density = g cm−3, making it one of the most inflated giant planets known. Furthermore, for future follow-up, we report a high-precision time of inferior conjunction in of 2,457,083.660459 0.000894 and period of days. Despite the relatively large separation of ∼0.07 au implied by its ∼5.03-day orbital period, KELT-12b receives significant flux of erg s−1 cm−2 from its host. We compare the radii and insolations of transiting gas giant planets around hot ( K) and cool stars, noting that the observed paucity of known transiting giants around hot stars with low insolation is likely due to selection effects. We underscore the significance of long-term ground-based monitoring of hot stars and space-based targeting of hot stars with the Transiting Exoplanet Survey Satellite to search for inflated gas giants in longer-period orbits.
Vascular Health in Kawasaki Disease Selamet Tierney, Elif Seda, MD; Gal, Dana, BA; Gauvreau, Kimberly, ScD ...
Journal of the American College of Cardiology,
09/2013, Letnik:
62, Številka:
12
Journal Article
Recenzirano
Odprti dostop
Objectives The objective of our study was to compare the indices of vascular health in Kawasaki disease (KD) patients to those of control subjects. Background The literature on peripheral vascular ...health after KD is conflicting. Methods Subjects were patients 11 to 29 years of age with the onset of KD >12 months before the study visit (n = 203) and healthy control subjects (n = 50). We measured endothelial function (using the Endothelial Pulse Amplitude Testing index), intima-media thickness (IMT) of the right common carotid artery (RCCA) and the left common carotid artery (LCCA), and fasting lipid profile and C-reactive protein (CRP). KD patients were classified according to their worst-ever coronary artery (CA) status: group I, always normal CAs (n = 136, 67%); group II, CA z -scores ≥2 but <3 (n = 20, 10%); group III, CA aneurysm z -scores ≥3 but <8 mm (n = 40, 20%); and group IV, giant CA aneurysm, defined as ≥8 mm (n = 7, 3%). Results At a median of 11.6 years (range, 1.2 to 26 years) after KD onset, compared with controls, KD patients had a higher peak velocity in the LCCA (p = 0.04) and higher pulsatility index of both the RCCA and LCCA (p = 0.006 and p = 0.05, respectively). However, there were no differences in the Endo-PAT index or carotid IMT or stiffness. The mean IMT of the LCCA tended to differ across the KD subgroups and control group (p = 0.05), with a higher mean in group IV. Otherwise the KD subgroups and control group had similar vascular health indexes. Conclusions In contrast to some earlier reports, our study of North American children and young adults demonstrated that KD patients whose maximum CA dimensions were either always normal or mildly ectatic have normal vascular health indexes, providing reassurance regarding peripheral vascular health in this population.
We report the discovery of KELT-18b, a transiting hot Jupiter in a 2.87-day orbit around the bright (V = 10.1), hot, F4V star BD+60 1538 (TYC 3865-1173-1). We present follow-up photometry, ...spectroscopy, and adaptive optics imaging that allow a detailed characterization of the system. Our preferred model fits yield a host stellar temperature of K and a mass of , situating it as one of only a handful of known transiting planets with hosts that are as hot, massive, and bright. The planet has a mass of , a radius of , and a density of , making it one of the most inflated planets known around a hot star. We argue that KELT-18b's high temperature and low surface gravity, which yield an estimated ∼600 km atmospheric scale height, combined with its hot, bright host, make it an excellent candidate for observations aimed at atmospheric characterization. We also present evidence for a bound stellar companion at a projected separation of ∼1100 au, and speculate that it may have contributed to the strong misalignment we suspect between KELT-18's spin axis and its planet's orbital axis. The inferior conjunction time is 2457542.524998 0.000416 (BJDTDB) and the orbital period is 2.8717510 0.0000029 days. We encourage Rossiter-McLaughlin measurements in the near future to confirm the suspected spin-orbit misalignment of this system.
We announce the discovery of KELT-16b, a highly irradiated, ultra-short period hot Jupiter transiting the relatively bright (visual magnitude equals 11.7) star TYC 2688-1839-1/KELT-16. A global ...analysis of the system shows KELT-16 to be an F7V star with effective temperature equal to 6236 plus or minus 54 degrees Kelvin, log g (sub asterisk) equal to 4.253 from plus 0.031 to minus 0.036, Fe/H equal to minus 0.002 from plus 0.086 to minus 0.085, mass (sub asterisk) equal to 1.211 from plus 0.043 to minus 0.046 times the solar mass, and radius (sub asterisk) equal to 1.360 from plus 0.064 o minus 0.053 times the solar radius. The planet is a relatively high-mass inflated gas giant with planetary mass equal to 2.75 from plus 0.016 to minus 0.15 times Jupiter's mass, planetary radius equal to 1.415 from plus 0.084 to minus 0.067 times Jupiter's radius, density planetary rho equal to 1.20 plus or minus 0.18 grams per cubic centimeter, surface gravity, log planetary gravity equal to 3.530 from plus 0.042 to minus 0.049, and equatorial temperature equal to 2453 from plus 55 to minus 47 degrees Kelvin. The best-fitting linear ephemeris is T(sub C) equal to 22457247.24791 plus or minus 0.00019 BJD (sub TDB) and P equal to 0.9689951 plus or minus 0.0000024 day. KELT-16b joins WASP-18b, -19b, -43b, -103b, and HATS-18b as the only giant transiting planets with periodicity P less than 1 day. Its ultra-short period and high irradiation make it a benchmark target for atmospheric studies by the Hubble Space Telescope, Spitzer, and eventually the James Webb Space Telescope. For example, as a hotter, higher-mass analog of WASP-43b, KELT-16b may feature an atmospheric temperature-pressure inversion and day-to-night temperature swing extreme enough for TiO to rain out at the terminator. KELT-16b could also join WASP-43b in extending tests of the observed mass-metallicity relation of the solar system gas giants to higher masses. KELT-16b currently orbits at a mere approximately 1.7 Roche radii from its host star, and could be tidally disrupted in as little as a few times 10 (sup 5) years (for a stellar tidal quality factor of Q (sup prime) (sub asterisk) equal to 10 (sup 5). Finally, the likely existence of a widely separated bound stellar companion in the KELT-16 system makes it possible that Kozai-Lidov (KL) oscillations played a role in driving KELT-16b inward to its current precarious orbit.
Genome-wide association studies (GWAS) have identified >500 common variants associated with quantitative metabolic traits, but in aggregate such variants explain at most 20-30% of the heritable ...component of population variation in these traits. To further investigate the impact of genotypic variation on metabolic traits, we conducted re-sequencing studies in >6,000 members of a Finnish population cohort (The Northern Finland Birth Cohort of 1966 NFBC) and a type 2 diabetes case-control sample (The Finland-United States Investigation of NIDDM Genetics FUSION study). By sequencing the coding sequence and 5' and 3' untranslated regions of 78 genes at 17 GWAS loci associated with one or more of six metabolic traits (serum levels of fasting HDL-C, LDL-C, total cholesterol, triglycerides, plasma glucose, and insulin), and conducting both single-variant and gene-level association tests, we obtained a more complete understanding of phenotype-genotype associations at eight of these loci. At all eight of these loci, the identification of new associations provides significant evidence for multiple genetic signals to one or more phenotypes, and at two loci, in the genes ABCA1 and CETP, we found significant gene-level evidence of association to non-synonymous variants with MAF<1%. Additionally, two potentially deleterious variants that demonstrated significant associations (rs138726309, a missense variant in G6PC2, and rs28933094, a missense variant in LIPC) were considerably more common in these Finnish samples than in European reference populations, supporting our prior hypothesis that deleterious variants could attain high frequencies in this isolated population, likely due to the effects of population bottlenecks. Our results highlight the value of large, well-phenotyped samples for rare-variant association analysis, and the challenge of evaluating the phenotypic impact of such variants.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Abstract 706
While the JAK2 V617F mutation and several other genetic alterations have been identified in myeloproliferative neoplasms (MPNs), a comprehensive delineation of the genomic changes ...underlying these diseases has been lacking. Chronic MPNs such as primary myelofibrosis (PMF) exhibit a propensity for transformation to secondary acute myeloid leukemia (sAML), for which the prognosis is poor. In this era of targeted therapies, a deeper understanding of the genetic complexity and clonal architecture of these diseases is essential.
We describe a woman who first presented with splenomegaly, pancytopenia, and leukoerythroblastosis at the age of 51. A bone marrow biopsy demonstrated severe fibrosis, consistent with a diagnosis of PMF. Cytogenetics were normal. Bone marrow samples were banked at that time. The patient had an excellent response to treatment with thalidomide, ultimately achieving a complete hematologic remission, but was eventually switched to lenalidomide due to neuropathy. Seven years after initial PMF diagnosis, the patient transformed to sAML. A bone marrow biopsy revealed 49% blasts, and cytogenetics were normal. Testing for JAK2 V617F was positive. Bone marrow samples were again banked. The patient received induction chemotherapy with IDA-FLAG and attained a complete remission, followed by consolidation chemotherapy with four cycles of high-dose cytarabine. Subsequently, the patient declined bone marrow transplantation. Approximately 1.5 years after sAML diagnosis, the patient again developed pancytopenia with leukoerythroblastosis, consistent with relapsed/residual PMF, but with no evidence of sAML relapse. Lenalidomide was restarted at that time. Approximately 2.5 years after sAML diagnosis, the patient remains alive with transfusion-dependent anemia and thrombocytopenia.
Whole genome sequencing (WGS) was performed on bone marrow samples banked at PMF and sAML diagnosis, with skin included as a germline surrogate. Haploid coverage of 63.9x (PMF), 60.2x (sAML), and 37.5x (skin) was obtained. A total of 38 high confidence (HC) tier 1 (coding and splice site) single nucleotide variants (SNVs) were identified in the PMF and/or sAML samples but not in the skin. Six of these somatic SNVs were in genes previously known to be involved in MPNs and/or sAML. Both the PMF and sAML samples were predominantly homozygous for JAK2 V617F. Copy-neutral loss of heterozygosity in the first 8.7 Mb of chromosome 9 was identified, confirming uniparental disomy involving JAK2 V617F. U2AF1 was mutated in both the PMF and sAML phases. A mutation in MYB was detected in the PMF but not sAML sample, suggesting the presence of a clone that may have contributed to PMF development, but that was dispensable for transformation. A minor subclone at the PMF stage containing a nonsense mutation in ASXL became substantially enriched upon transformation, illustrating the clonal complexity within a predominantly JAK2 V617F-positive bone marrow. Mutations in IDH1 and RUNX1 were observed in sAML but not PMF, indicating they were likely acquired subsequent to the ASXL1 mutation and also contributed specifically to transformation. These findings suggest that transformation to sAML in this patient was largely driven by the combination of mutations in ASXL1, IDH1, and RUNX1, with possible contribution from a small number of additional mutations.
To fully define the clonal hierarchy of PMF transformed to sAML in this patient, deep sequencing validation of all tier 1 SNVs, all tier 2–3 HC SNVs, and all putative indels and structural variants identified by WGS is currently in progress. This includes putative mutations in several novel genes that may be pathogenic. A sample banked during sAML remission (two years after sAML diagnosis) has also been included in the validation sequencing. This will enable us to determine whether any residual mutations/clones may be identifiable in this particular patient, which has implications for potential future relapse. This study illustrates the capacity of WGS to identify the critical genetic drivers of MPN pathogenesis, and to define the basis for clonal evolution in MPNs and sAML.
No relevant conflicts of interest to declare.
To investigate the genetic changes associated withAML relapse, and to determine whether clonal evolution contributes to relapse, we performed whole-genome sequencing of primary tumour-relapse pairs ...andmatched skin samples fromeight patients, including unique patient identifier (UPN) 933124, whose primary tumourmutations were previously reported3. Assuming that all the mutations detected are heterozygous in the primary tumour sample (with a malignant cellular content at 93.72% for the primary bone marrow sample, see Supplementary Information), we were able to calculate the fraction of total malignant cells in each clone.
Celotno besedilo
Dostopno za:
DOBA, IJS, IZUM, KILJ, KISLJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
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