Small piscivores are regarded as important regulators of the composition of coral reef fish communities, but few studies have investigated their predatory ecology or impact on assemblages of juvenile ...fishes. This study investigated the foraging ecology of a common coral reef predator, the dottyback
Pseudochromis fuscus
, using underwater focal animal observations. Observations were conducted at two times of year: the summer, when recruit fishes were an available food item and winter, when remaining juveniles had outgrown vulnerability to
P. fuscus
. During the summer,
P. fuscus
directed 76% of its strikes at invertebrates and 24% at recruiting juvenile fishes. When striking at fishes,
P. fuscus
exhibited two distinct feeding modes: an ambush (26% successful) and a pursuit mode (5% successful). Predator activity in the field peaked at midday, averaging 2.5 captures h
−1
of juvenile fishes. Monitoring of activity and foraging in the laboratory over 24-h periods found that
P. fuscus
was a diurnal predator and was active for 13 h d
−1
during the summer. The number of hours during which foraging was recorded differed greatly among individuals (
n
= 10), ranging from 4 to 13 h. The number of predatory strikes did not increase with standard length, but the success rate and consumption rate of juvenile fishes did increase with size. Estimated hourly mortality on juvenile fish ranged from 0.49 fish h
−1
in small
P. fuscus
individuals (30–39 mm standard length, SL; equating to 6.3 per 13 h day) to 2.4 fish h
−1
in large
P. fuscus
individuals (55–65 mm SL; 30.6 per 13 h day). During the winter,
P. fuscus
struck at invertebrates with a similar rate to the summer period. These observations of the predatory ecology of
P. fuscus
support the hypothesis that in coral reef systems, small piscivores, because of their high metabolism and activity, are probably important regulators of coral reef fish community composition.
The remarkable complexity of soil and its importance to a wide range of ecosystem services presents major challenges to the modeling of soil processes. Although major progress in soil models has ...occurred in the last decades, models of soil processes remain disjointed between disciplines or ecosystem services, with considerable uncertainty remaining in the quality of predictions and several challenges that remain yet to be addressed. First, there is a need to improve exchange of knowledge and experience among the different disciplines in soil science and to reach out to other Earth science communities. Second, the community needs to develop a new generation of soil models based on a systemic approach comprising relevant physical, chemical, and biological processes to address critical knowledge gaps in our understanding of soil processes and their interactions. Overcoming these challenges will facilitate exchanges between soil modeling and climate, plant, and social science modeling communities. It will allow us to contribute to preserve and improve our assessment of ecosystem services and advance our understanding of climate-change feedback mechanisms, among others, thereby facilitating and strengthening communication among scientific disciplines and society. We review the role of modeling soil processes in quantifying key soil processes that shape ecosystem services, with a focus on provisioning and regulating services. We then identify key challenges in modeling soil processes, including the systematic incorporation of heterogeneity and uncertainty, the integration of data and models, and strategies for effective integration of knowledge on physical, chemical, and biological soil processes. We discuss how the soil modeling community could best interface with modern modeling activities in other disciplines, such as climate, ecology, and plant research, and how to weave novel observation and measurement techniques into soil models. We propose the establishment of an international soil modeling consortium to coherently advance soil modeling activities and foster communication with other Earth science disciplines. Such a consortium should promote soil modeling platforms and data repository for model development, calibration and intercomparison essential for addressing contemporary challenges.
•Appropriate portion sizes are important to the prevention of obesity in children.•Large portion sizes promote high meal and total energy intakes.•Response to portion size in children reflects ...biological and social influences.•Parents adopt a variety of strategies around portion size when feeding children.•Evidence-based guidance to support healthy child portion sizes is needed.
Establishing eating habits in early life that include appropriate portion sizes of foods which are nutrient dense and low in energy density is considered important in the prevention of obesity in children. This special supplement presents the proceedings of a symposium focusing on advances in scientific understanding of the development of healthy food portion sizes in children and their families. Recent basic research highlights individual differences in children's responsiveness to portion size as well as potential mechanisms of portion size effects. Quantitative approaches highlight the influence of maternal serving in determining intake, while qualitative approaches seek to elaborate caregiver decisions around child portion sizes at meals and snacks. Family-based environmental interventions for child weight control involving food portion size are outlined. An overview of the overarching issues and roundtable discussion on the forefronts of portion size research are presented as well as policy considerations to promote healthy portion control.
The international acute lymphoblastic leukemia (ALL) study was designed to prospectively define the optimal therapy for adults 60 years of age or younger with newly diagnosed ALL. All patients ...received identical induction therapy, and 91% achieved complete remission (CR). Patients 50 years of age or younger with a compatible sibling were assigned to undergo allogeneic transplantation; the others were randomly assigned to autologous transplantation or to consolidation/maintenance therapy for 2.5 years. Patients who did not achieve CR after induction had an overall survival rate of 5% compared with 45% for patients who achieved CR. Factors at diagnosis predictive of overall survival and disease-free survival were age (P = .001), white blood cell count less than 30 × 109/L for B lineage or less than 100 × 109/L for T lineage (P = .001) and immunophenotype, T lineage versus B lineage (P = .001). The data demonstrate that achieving CR with induction therapy is indispensable for long-term survival in adult patients with ALL. Furthermore, with a response rate greater than 90%, the induction regimen was highly efficacious as remission-inducing therapy. This large database has validated several previously identified independent prognostic factors in ALL, such as age, white blood cell count at presentation, cytogenetics, and immunophenotype. However, the achievement of CR within 4 weeks does not appear to be an independent prognostic factor.
Background and purpose: Large conductance calcium‐ and voltage‐activated potassium (BK) channels are encoded by a single gene that displays extensive pre‐mRNA splicing. Here we exploited a membrane ...potential assay to investigate the sensitivity of different BK splice variants to elevations in intracellular free calcium and their inhibition by the BK channel blocker paxilline.
Experimental approach: Murine BK channel splice variants were expressed in human embryonic kidney 293 cells and their properties analysed in response to ionomycin‐induced calcium influx in both fluorescent membrane potential (fluorescent‐imaging plate reader) and patch clamp electrophysiological assays. The dose‐dependent inhibition of distinct splice variants by the BK channel‐specific blocker paxilline was also investigated.
Key results: Ionomycin‐induced calcium influx induced a robust hyperpolarization of human embryonic kidney 293 cells expressing distinct BK channel splice variants: stress regulated exon (STREX), e22 and ZERO. Splice variant expression resulted in membrane hyperpolarization that displayed a rank order of potency in response to calcium influx of STREX > e22 > ZERO. The BK channel inhibitor paxilline exhibited very similar potency on all three splice variants with IC50s in membrane potential assays of 0.35 ± 0.04, 0.37 ± 0.03 and 0.70 ± 0.02 µmol·L−1 for STREX, ZERO and e22 respectively.
Conclusions and implications: BK channel splice variants can be rapidly discriminated using membrane potential based assays, based on their sensitivity to calcium. BK channel splice variants are inhibited by the specific blocker paxilline with similar IC50s. Thus, paxilline may be used in functional assays to inhibit BK channel function, irrespective of the variant expressed.
We describe and benchmark a new quantum charge-coupled device (QCCD) trapped-ion quantum computer based on a linear trap with periodic boundary conditions, which resembles a race track. The new ...system successfully incorporates several technologies crucial to future scalability—including electrode broadcasting, multilayer rf routing, and magneto-optical trap (MOT) loading—while maintaining, and in some cases exceeding, the gate fidelities of previous QCCD systems. The system is initially operated with 32 qubits, but future upgrades will allow for more. We benchmark the performance of primitive operations, including an average state preparation and measurement error of 1.6(1)×10^{-3}, an average single-qubit gate infidelity of 2.5(3)×10^{-5}, and an average two-qubit gate infidelity of 1.84(5)×10^{-3}. The system-level performance of the quantum processor is assessed with mirror benchmarking, linear cross-entropy benchmarking, a quantum volume measurement of QV=2^{16}, and the creation of 32-qubit entanglement in a GHZ state. We also tested application benchmarks, including Hamiltonian simulation, QAOA, error correction on a repetition code, and dynamics simulations using qubit reuse. We also discuss future upgrades to the new system aimed at adding more qubits and capabilities.
Asthma is a heterogeneous disease driven by diverse immunologic and inflammatory mechanisms.
Using transcriptomic profiling of airway tissues, we sought to define the molecular phenotypes of severe ...asthma.
The transcriptome derived from bronchial biopsies and epithelial brushings of 107 subjects with moderate to severe asthma were annotated by gene set variation analysis using 42 gene signatures relevant to asthma, inflammation, and immune function. Topological data analysis of clinical and histologic data was performed to derive clusters, and the nearest shrunken centroid algorithm was used for signature refinement.
Nine gene set variation analysis signatures expressed in bronchial biopsies and airway epithelial brushings distinguished two distinct asthma subtypes associated with high expression of T-helper cell type 2 cytokines and lack of corticosteroid response (group 1 and group 3). Group 1 had the highest submucosal eosinophils, as well as high fractional exhaled nitric oxide levels, exacerbation rates, and oral corticosteroid use, whereas group 3 patients showed the highest levels of sputum eosinophils and had a high body mass index. In contrast, group 2 and group 4 patients had an 86% and 64% probability, respectively, of having noneosinophilic inflammation. Using machine learning tools, we describe an inference scheme using the currently available inflammatory biomarkers sputum eosinophilia and fractional exhaled nitric oxide levels, along with oral corticosteroid use, that could predict the subtypes of gene expression within bronchial biopsies and epithelial cells with good sensitivity and specificity.
This analysis demonstrates the usefulness of a transcriptomics-driven approach to phenotyping that segments patients who may benefit the most from specific agents that target T-helper cell type 2-mediated inflammation and/or corticosteroid insensitivity.
Neonatal surgical mortality has steadily fallen over the last five decades. Improved survival does not appear to be related to the introduction of new operative procedures. Most of the basic ...procedures were developed by 1960. Eight developments appear to be responsible: (1) The growth of pediatric surgery resulted in widespread availability of neonatal surgeons and dissemination of knowledge about newborn surgical emergencies. (2) The parallel growth of pediatric anesthesia, beginning in 1946, provided specialized intraoperative management of the neonate. (3) Understanding neonatal physiology is the key to successful management; major advances occurred between 1950 and 1970. (4) New inventions revolutionized patient care; the transistor (1947) made it possible for medical devices to sense, amplify and control physiologic responses and opened the communication and computer age. (5) Neonatal mechanical ventilation had a prohibitive mortality and was seldom utilized; the development of CPAP and a continuous flow ventilator in the 1970s allowed safe ventilatory support. (6) Total parenteral nutrition (1968) prevented starvation that frequently affected infants with major anomalies. (7) The effective treatment of infection began with the clinical use of penicillin (1941); antibiotics have reduced mortality but infants suffering from the septic syndrome have a prohibitive mortality; cytokine, proinflammatory agent research, and the development of anti-inflammatory and blocking agents in the 1980s have not affected mortality. (8) The establishment of newborn intensive care units (1960) provided an environment, equipment, and staff for effective physiologic management.
Inflammatory lung diseases are highly complex in respect of pathogenesis and relationships between inflammation, clinical disease and response to treatment. Sophisticated large-scale analytical ...methods to quantify gene expression (transcriptomics), proteins (proteomics), lipids (lipidomics) and metabolites (metabolomics) in the lungs, blood and urine are now available to identify biomarkers that define disease in terms of combined clinical, physiological and patho-biological abnormalities. The aspiration is that these approaches will improve diagnosis, i.e. define pathological phenotypes, and facilitate the monitoring of disease and therapy, and also, unravel underlying molecular pathways. Biomarker studies can either select predefined biomarker(s) measured by specific methods or apply an "unbiased" approach involving detection platforms that are indiscriminate in focus. This article reviews the technologies presently available to study biomarkers of lung disease within the 'omics field. The contributions of the individual 'omics analytical platforms to the field of respiratory diseases are summarised, with the goal of providing background on their respective abilities to contribute to systems medicine-based studies of lung disease.
Although several studies link high levels of IL-6 and soluble IL-6 receptor (sIL-6R) to asthma severity and decreased lung function, the role of IL-6 trans-signaling (IL-6TS) in asthmatic patients is ...unclear.
We sought to explore the association between epithelial IL-6TS pathway activation and molecular and clinical phenotypes in asthmatic patients.
An IL-6TS gene signature obtained from air-liquid interface cultures of human bronchial epithelial cells stimulated with IL-6 and sIL-6R was used to stratify lung epithelial transcriptomic data (Unbiased Biomarkers in Prediction of Respiratory Disease Outcomes U-BIOPRED cohorts) by means of hierarchical clustering. IL-6TS–specific protein markers were used to stratify sputum biomarker data (Wessex cohort). Molecular phenotyping was based on transcriptional profiling of epithelial brushings, pathway analysis, and immunohistochemical analysis of bronchial biopsy specimens.
Activation of IL-6TS in air-liquid interface cultures reduced epithelial integrity and induced a specific gene signature enriched in genes associated with airway remodeling. The IL-6TS signature identified a subset of patients with IL-6TS–high asthma with increased epithelial expression of IL-6TS–inducible genes in the absence of systemic inflammation. The IL-6TS–high subset had an overrepresentation of frequent exacerbators, blood eosinophilia, and submucosal infiltration of T cells and macrophages. In bronchial brushings Toll-like receptor pathway genes were upregulated, whereas expression of cell junction genes was reduced. Sputum sIL-6R and IL-6 levels correlated with sputum markers of remodeling and innate immune activation, in particular YKL-40, matrix metalloproteinase 3, macrophage inflammatory protein 1β, IL-8, and IL-1β.
Local lung epithelial IL-6TS activation in the absence of type 2 airway inflammation defines a novel subset of asthmatic patients and might drive airway inflammation and epithelial dysfunction in these patients.
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