Notes

An examination of operating puppy contamination via standing up water dangers after a simulated disaster look for scenario.
Central place foragers are expected to offset travel costs between a central place and foraging areas by targeting productive feeding zones. Harbour seals (Phoca vitulina) make multi-day foraging trips away from coastal haul-out sites presumably to target rich food resources, but periodic track points from telemetry tags may be insufficient to infer reliably where, and how often, foraging takes place. To study foraging behaviour during offshore trips, and assess what factors limit trip duration, we equipped harbour seals in the German Wadden Sea with high-resolution multi-sensor bio-logging tags, recording 12 offshore trips from 8 seals. Using acceleration transients as a proxy for prey capture attempts, we found that foraging rates during travel to and from offshore sites were comparable to offshore rates. Offshore foraging trips may, therefore, reflect avoidance of intra-specific competition rather than presence of offshore foraging hotspots. Time spent resting increased by approx. 37 min/day during trips suggesting that a resting deficit rather than patch depletion may influence trip length. Foraging rates were only weakly correlated with surface movement patterns highlighting the value of integrating multi-sensor data from on-animal bio-logging tags (GPS, depth, accelerometers and magnetometers) to infer behaviour and habitat use.An X-band reflectarray antenna using 16 × 12 double square ring elements for satellite communications is proposed in this paper. The feed is a 4 × 3 elements microstrip patch array designed to create edge taper of approximately - 10 dB. A prototype with right-hand circular polarization (RHCP) is manufactured and tested, and the good agreements between simulations and measurements are demonstrated. The good performance is obtained with the aperture efficiency of 40.7% and the 3-dB gain bandwidth of about 10% which is beneficial to nanosatellites.Mutational activation of KRAS promotes the initiation and progression of cancers, especially in the colorectum, pancreas, lung, and blood plasma, with varying prevalence of specific activating missense mutations. Although epidemiological studies connect specific alleles to clinical outcomes, the mechanisms underlying the distinct clinical characteristics of mutant KRAS alleles are unclear. Here, we analyze 13,492 samples from these four tumor types to examine allele- and tissue-specific genetic properties associated with oncogenic KRAS mutations. The prevalence of known mutagenic mechanisms partially explains the observed spectrum of KRAS activating mutations. However, there are substantial differences between the observed and predicted frequencies for many alleles, suggesting that biological selection underlies the tissue-specific frequencies of mutant alleles. Consistent with experimental studies that have identified distinct signaling properties associated with each mutant form of KRAS, our genetic analysis reveals that each KRAS allele is associated with a distinct tissue-specific comutation network. Moreover, we identify tissue-specific genetic dependencies associated with specific mutant KRAS alleles. Overall, this analysis demonstrates that the genetic interactions of oncogenic KRAS mutations are allele- and tissue-specific, underscoring the complexity that drives their clinical consequences.Patients with triple-negative breast cancer (TNBC) who have residual disease after neoadjuvant therapy have a high risk of recurrence. We tested the impact of DNA-damaging chemotherapy alone or with PARP inhibition in this high-risk population. Patients with TNBC or deleterious BRCA mutation (TNBC/BRCAmut) who had >2 cm of invasive disease in the breast or persistent lymph node (LN) involvement after neoadjuvant therapy were assigned 11 to cisplatin alone or with rucaparib. Germline mutations were identified with BROCA analysis. The primary endpoint was 2-year disease-free survival (DFS) with 80% power to detect an HR 0.5. From Feb 2010 to May 2013, 128 patients were enrolled. Median tumor size at surgery was 1.9 cm (0-11.5 cm) with 1 (0-38) involved LN; median Residual Cancer Burden (RCB) score was 2.6. Six patients had known deleterious BRCA1 or BRCA2 mutations at study entry, but BROCA identified deleterious mutations in 22% of patients with available samples. Toxicity was similar in both arms. Despite frequent dose reductions (21% of patients) and delays (43.8% of patients), 73% of patients completed planned cisplatin. Rucaparib exposure was limited with median concentration 275 (82-4694) ng/mL post-infusion on day 3. The addition of rucaparib to cisplatin did not increase 2-year DFS (54.2% cisplatin vs. 64.1% cisplatin + rucaparib; P = 0.29). In the high-risk post preoperative TNBC/BRCAmut setting, the addition of low-dose rucaparib did not improve 2-year DFS or increase the toxicity of cisplatin. Genetic testing was underutilized in this high-risk population.There is limited information about the initiation of triple therapy (TT) in patients with chronic obstructive pulmonary disease (COPD) in primary care. This was an observational, population-based study in patients identified from a primary care electronic medical records database in Catalonia from 2011 to 2015 aimed to identify the use of TT in patients with newly diagnosed COPD. Disodium Cromoglycate A total of 69,668 newly diagnosed patients were identified of whom 11,524 (16.5%) initiated TT, of whom 8626 initiated TT at or immediately after COPD diagnosis. Among them, 72.3% were GOLD A/B, 14.6% were frequent exacerbators, and 7.1% had asthma-COPD overlap (ACO). Variables associated with TT initiation were male sex, older age, previous exacerbations, ACO, a previous treatment regimen containing an inhaled corticosteroid, previous pneumonia, and history of lung cancer. A significant number of COPD patients in Primary Care initiated TT shortly after or even before an established COPD diagnosis.Isotopic measurements of lunar and terrestrial rocks have revealed that, unlike any other body in the solar system, the Moon is indistinguishable from the Earth for nearly every isotopic system. This observation, however, contradicts predictions by the standard model for the origin of the Moon, the canonical giant impact. Here we show that the vanadium isotopic composition of the Moon is offset from that of the bulk silicate Earth by 0.18 ± 0.04 parts per thousand towards the chondritic value. This offset most likely results from isotope fractionation on proto-Earth during the main stage of terrestrial core formation (pre-giant impact), followed by a canonical giant impact where ~80% of the Moon originates from the impactor of chondritic composition. Our data refute the possibility of post-giant impact equilibration between the Earth and Moon, and implies that the impactor and proto-Earth mainly accreted from a common isotopic reservoir in the inner solar system.
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