164 research outputs found
Ultrafast Interference Imaging of Air in Splashing Dynamics
A drop impacting a solid surface with sufficient velocity will emit many
small droplets creating a splash. However, splashing is completely suppressed
if the surrounding gas pressure is lowered. The mechanism by which the gas
affects splashing remains unknown. We use high-speed interference imaging to
measure the air beneath all regions of a spreading viscous drop as well as
optical absorption to measure the drop thickness. Although an initial air
bubble is created on impact, no significant air layer persists until the time a
splash is created. This suggests that splashing in our experimentally
accessible range of viscosities is initiated at the edge of the drop as it
encroaches into the surrounding gas
Thin Film Formation During Splashing of Viscous Liquids
After impact onto a smooth dry surface, a drop of viscous liquid initially
spreads in the form of a thick lamella. If the drop splashes, it first emits a
thin fluid sheet that can ultimately break up into droplets causing the splash.
Ambient gas is crucial for creating this thin sheet. The time for sheet
ejection, , depends on impact velocity, liquid viscosity, gas pressure
and molecular weight. A central air bubble is trapped below the drop at
pressures even below that necessary for this sheet formation. In addition, air
bubbles are entrained underneath the spreading lamella when the ejected sheet
is present. Air entrainment ceases at a lamella velocity that is independent of
drop impact velocity as well as ambient gas pressure.Comment: 8 pages, 11 figure
Creation of prompt and thin-sheet splashing by varying surface roughness or increasing air pressure
A liquid drop impacting a solid surface may splash by emitting a thin liquid
sheet that subsequently breaks apart or by promptly ejecting droplets from the
advancing liquid-solid contact line. Using high-speed imaging, we show that air
pressure and surface roughness influence both splash mechanisms. Roughness
increases prompt splashing at the advancing contact line but inhibits the
formation of the thin sheet. If the air pressure is lowered, droplet ejection
is suppressed not only during thin-sheet formation but for prompt splashing as
well. The threshold pressure depends on impact velocity, liquid viscosity and
surface roughness
FSVPy: A Python-based Package for Fluorescent Streak Velocimetry (FSV)
Predictive constitutive equations that connect easy-to-measure transport
properties (e.g., viscosity and conductivity) with system performance variables
(e.g., power consumption and efficiency) are needed to design advanced thermal
and electrical systems. In this work, we explore the use of fluorescent
particle-streak analysis to directly measure the local velocity field of a
pressure-driven flow, introducing a new Python package (FSVPy) to perform the
analysis. Fluorescent streak velocimetry (FSV) combines high-speed imaging with
highly fluorescent particles to produce images that contain fluorescent
streaks, whose length and intensity can be related to the local flow velocity.
By capturing images throughout the sample volume, the three-dimensional
velocity field can be quantified and reconstructed. We demonstrate this
technique by characterizing the channel flow profiles of several non-Newtonian
fluids: micellar Cetylpyridinium Chloride solution, Carbopol 940, and
Polyethylene Glycol. We then explore more complex flows, where significant
acceleration is created due to micro-scale features encountered within the
flow. We demonstrate the ability of FSVPy to process streaks of various shapes,
and use the variable intensity along the streak to extract position-specific
velocity measurements from individual images. Thus, we demonstrate that FSVPy
is a flexible tool that can be used to extract local velocimetry measurements
from a wide variety of fluids and flow conditions
Evidence-Based Annotation of Gene Function in Shewanella oneidensis MR-1 Using Genome-Wide Fitness Profiling across 121 Conditions
Most genes in bacteria are experimentally uncharacterized and cannot be annotated with a specific function. Given the great diversity of bacteria and the ease of genome sequencing, high-throughput approaches to identify gene function experimentally are needed. Here, we use pools of tagged transposon mutants in the metal-reducing bacterium Shewanella oneidensis MR-1 to probe the mutant fitness of 3,355 genes in 121 diverse conditions including different growth substrates, alternative electron acceptors, stresses, and motility. We find that 2,350 genes have a pattern of fitness that is significantly different from random and 1,230 of these genes (37% of our total assayed genes) have enough signal to show strong biological correlations. We find that genes in all functional categories have phenotypes, including hundreds of hypotheticals, and that potentially redundant genes (over 50% amino acid identity to another gene in the genome) are also likely to have distinct phenotypes. Using fitness patterns, we were able to propose specific molecular functions for 40 genes or operons that lacked specific annotations or had incomplete annotations. In one example, we demonstrate that the previously hypothetical gene SO_3749 encodes a functional acetylornithine deacetylase, thus filling a missing step in S. oneidensis metabolism. Additionally, we demonstrate that the orphan histidine kinase SO_2742 and orphan response regulator SO_2648 form a signal transduction pathway that activates expression of acetyl-CoA synthase and is required for S. oneidensis to grow on acetate as a carbon source. Lastly, we demonstrate that gene expression and mutant fitness are poorly correlated and that mutant fitness generates more confident predictions of gene function than does gene expression. The approach described here can be applied generally to create large-scale gene-phenotype maps for evidence-based annotation of gene function in prokaryotes
Basic science232. Certolizumab pegol prevents pro-inflammatory alterations in endothelial cell function
Background: Cardiovascular disease is a major comorbidity of rheumatoid arthritis (RA) and a leading cause of death. Chronic systemic inflammation involving tumour necrosis factor alpha (TNF) could contribute to endothelial activation and atherogenesis. A number of anti-TNF therapies are in current use for the treatment of RA, including certolizumab pegol (CZP), (Cimzia ®; UCB, Belgium). Anti-TNF therapy has been associated with reduced clinical cardiovascular disease risk and ameliorated vascular function in RA patients. However, the specific effects of TNF inhibitors on endothelial cell function are largely unknown. Our aim was to investigate the mechanisms underpinning CZP effects on TNF-activated human endothelial cells. Methods: Human aortic endothelial cells (HAoECs) were cultured in vitro and exposed to a) TNF alone, b) TNF plus CZP, or c) neither agent. Microarray analysis was used to examine the transcriptional profile of cells treated for 6 hrs and quantitative polymerase chain reaction (qPCR) analysed gene expression at 1, 3, 6 and 24 hrs. NF-κB localization and IκB degradation were investigated using immunocytochemistry, high content analysis and western blotting. Flow cytometry was conducted to detect microparticle release from HAoECs. Results: Transcriptional profiling revealed that while TNF alone had strong effects on endothelial gene expression, TNF and CZP in combination produced a global gene expression pattern similar to untreated control. The two most highly up-regulated genes in response to TNF treatment were adhesion molecules E-selectin and VCAM-1 (q 0.2 compared to control; p > 0.05 compared to TNF alone). The NF-κB pathway was confirmed as a downstream target of TNF-induced HAoEC activation, via nuclear translocation of NF-κB and degradation of IκB, effects which were abolished by treatment with CZP. In addition, flow cytometry detected an increased production of endothelial microparticles in TNF-activated HAoECs, which was prevented by treatment with CZP. Conclusions: We have found at a cellular level that a clinically available TNF inhibitor, CZP reduces the expression of adhesion molecule expression, and prevents TNF-induced activation of the NF-κB pathway. Furthermore, CZP prevents the production of microparticles by activated endothelial cells. This could be central to the prevention of inflammatory environments underlying these conditions and measurement of microparticles has potential as a novel prognostic marker for future cardiovascular events in this patient group. Disclosure statement: Y.A. received a research grant from UCB. I.B. received a research grant from UCB. S.H. received a research grant from UCB. All other authors have declared no conflicts of interes
Measuring performance on the Healthcare Access and Quality Index for 195 countries and territories and selected subnational locations: A systematic analysis from the Global Burden of Disease Study 2016
Background A key component of achieving universal health coverage is ensuring that all populations have access to
quality health care. Examining where gains have occurred or progress has faltered across and within countries is
crucial to guiding decisions and strategies for future improvement. We used the Global Burden of Diseases, Injuries,
and Risk Factors Study 2016 (GBD 2016) to assess personal health-care access and quality with the Healthcare Access
and Quality (HAQ) Index for 195 countries and territories, as well as subnational locations in seven countries, from
1990 to 2016.
Methods Drawing from established methods and updated estimates from GBD 2016, we used 32 causes from which
death should not occur in the presence of effective care to approximate personal health-care access and quality by
location and over time. To better isolate potential effects of personal health-care access and quality from underlying
risk factor patterns, we risk-standardised cause-specific deaths due to non-cancers by location-year, replacing the local
joint exposure of environmental and behavioural risks with the global level of exposure. Supported by the expansion
of cancer registry data in GBD 2016, we used mortality-to-incidence ratios for cancers instead of risk-standardised
death rates to provide a stronger signal of the effects of personal health care and access on cancer survival. We
transformed each cause to a scale of 0–100, with 0 as the first percentile (worst) observed between 1990 and 2016, and
100 as the 99th percentile (best); we set these thresholds at the country level, and then applied them to subnational
locations. We applied a principal components analysis to construct the HAQ Index using all scaled cause values,
providing an overall score of 0–100 of personal health-care access and quality by location over time. We then compared
HAQ Index levels and trends by quintiles on the Socio-demographic Index (SDI), a summary measure of overall
development. As derived from the broader GBD study and other data sources, we examined relationships between
national HAQ Index scores and potential correlates of performance, such as total health spending per capita.
Findings In 2016, HAQ Index performance spanned from a high of 97·1 (95% UI 95·8–98·1) in Iceland, followed by
96·6 (94·9–97·9) in Norway and 96·1 (94·5–97·3) in the Netherlands, to values as low as 18·6 (13·1–24·4) in
the Central African Republic, 19·0 (14·3–23·7) in Somalia, and 23·4 (20·2–26·8) in Guinea-Bissau. The pace of
progress achieved between 1990 and 2016 varied, with markedly faster improvements occurring between 2000 and
2016 for many countries in sub-Saharan Africa and southeast Asia, whereas several countries in Latin America and
elsewhere saw progress stagnate after experiencing considerable advances in the HAQ Index between 1990 and 2000.
Striking subnational disparities emerged in personal health-care access and quality, with China and India having
particularly large gaps between locations with the highest and lowest scores in 2016. In China, performance ranged
from 91·5 (89·1–93·6) in Beijing to 48·0 (43·4–53·2) in Tibet (a 43·5-point difference), while India saw a 30·8-point
disparity, from 64·8 (59·6–68·8) in Goa to 34·0 (30·3–38·1) in Assam. Japan recorded the smallest range in
subnational HAQ performance in 2016 (a 4·8-point difference), whereas differences between subnational locations
with the highest and lowest HAQ Index values were more than two times as high for the USA and three times as high
for England. State-level gaps in the HAQ Index in Mexico somewhat narrowed from 1990 to 2016 (from a 20·9-point
to 17·0-point difference), whereas in Brazil, disparities slightly increased across states during this time (a 17·2-point
to 20·4-point difference). Performance on the HAQ Index showed strong linkages to overall development, with high
and high-middle SDI countries generally having higher scores and faster gains for non-communicable diseases.
Nonetheless, countries across the development spectrum saw substantial gains in some key health service areas from
2000 to 2016, most notably vaccine-preventable diseases. Overall, national performance on the HAQ Index was
positively associated with higher levels of total health spending per capita, as well as health systems inputs, but these
relationships were quite heterogeneous, particularly among low-to-middle SDI countries.
Interpretation GBD 2016 provides a more detailed understanding of past success and current challenges in improving
personal health-care access and quality worldwide. Despite substantial gains since 2000, many low-SDI and middle-
SDI countries face considerable challenges unless heightened policy action and investments focus on advancing access to and quality of health care across key health services, especially non-communicable diseases. Stagnating or
minimal improvements experienced by several low-middle to high-middle SDI countries could reflect the complexities
of re-orienting both primary and secondary health-care services beyond the more limited foci of the Millennium
Development Goals. Alongside initiatives to strengthen public health programmes, the pursuit of universal health
coverage hinges upon improving both access and quality worldwide, and thus requires adopting a more comprehensive
view—and subsequent provision—of quality health care for all populations.info:eu-repo/semantics/publishedVersio
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