84 research outputs found
Source apportionment of fine particulate matter in Houston, Texas: insights to secondary organic aerosols
Online and offline measurements of ambient particulate matter (PM) near the
urban and industrial Houston Ship Channel in Houston, Texas, USA, during May
2015 were utilized to characterize its chemical composition and to evaluate
the relative contributions of primary, secondary, biogenic, and anthropogenic
sources. Aerosol mass spectrometry (AMS) on nonrefractory PM1 (PM  ≤ 
1 µm) indicated major contributions from sulfate (averaging
50 % by mass), organic aerosol (OA, 40 %), and ammonium (14 %).
Positive matrix factorization (PMF) of AMS data categorized OA on average as
22 % hydrocarbon-like organic aerosol (HOA), 29 % cooking-influenced
less-oxidized oxygenated organic aerosol (CI-LO-OOA), and 48 %
more-oxidized oxygenated organic aerosol (MO-OOA), with the latter two
sources indicative of secondary organic aerosol (SOA). Chemical analysis of
PM2.5 (PM  ≤  2.5 µm) filter samples agreed that organic
matter (35 %) and sulfate (21 %) were the most abundant components.
Organic speciation of PM2.5 organic carbon (OC) focused on molecular
markers of primary sources and SOA tracers derived from biogenic and
anthropogenic volatile organic compounds (VOCs). The sources of PM2.5 OC
were estimated using molecular marker-based positive matric factorization
(MM-PMF) and chemical mass balance (CMB) models. MM-PMF resolved nine factors
that were identified as diesel engines (11.5 %), gasoline engines
(24.3 %), nontailpipe vehicle emissions (11.1 %), ship emissions
(2.2 %), cooking (1.0 %), biomass burning (BB, 10.6 %), isoprene
SOA (11.0 %), high-NOx anthropogenic SOA (6.6 %),
and low-NOx anthropogenic SOA (21.7 %). Using available
source profiles, CMB apportioned 41 % of OC to primary fossil sources
(gasoline engines, diesel engines, and ship emissions), 5 % to BB,
15 % to SOA (including 7.4 % biogenic and 7.6 % anthropogenic),
and 39 % to other sources that were not included in the model and are
expected to be secondary.This study presents the first application of in situ AMS-PMF, MM-PMF, and
CMB for OC source apportionment and the integration of these methods to
evaluate the relative roles of biogenic, anthropogenic, and BB-SOA. The three
source apportionment models agreed that  ∼  50 % of OC is associated
with primary emissions from fossil fuel use, particularly motor vehicles.
Differences among the models reflect their ability to resolve sources based
upon the input chemical measurements, with molecular marker-based methods
providing greater source specificity and resolution for minor sources. By
combining results from MM-PMF and CMB, BB was estimated to contribute
11 % of OC, with 5 % primary emissions and 6 % BB-SOA. SOA was
dominantly anthropogenic (28 %) rather than biogenic (11 %) or
BB-derived. The three-model approach
demonstrates significant contributions of anthropogenic SOA to fine PM. More
broadly, the findings and methodologies presented herein can be used to
advance local and regional understanding of anthropogenic contributions to
SOA.</p
The ischemic preconditioning effect of adenosine in patients with ischemic heart disease
<p>Abstract</p> <p>Introduction</p> <p><it>In vivo </it>and <it>in vitro </it>evidence suggests that adenosine and its agonists play key roles in the process of ischemic preconditioning. The effects of low-dose adenosine infusion on ischemic preconditioning have not been thoroughly studied in humans.</p> <p>Aims</p> <p>We hypothesised that a low-dose adenosine infusion could reduce the ischemic burden evoked by physical exercise and improve the regional left ventricular (LV) systolic function.</p> <p>Materials and methods</p> <p>We studied nine severely symptomatic male patients with severe coronary artery disease. Myocardial ischemia was induced by exercise on two separate occasions and quantified by Tissue Doppler Echocardiography. Prior to the exercise test, intravenous low-dose adenosine or placebo was infused over ten minutes according to a randomized, double blind, cross-over protocol. The LV walls were defined as ischemic if a reduction, no increment, or an increment of < 15% in peak systolic velocity (PSV) was observed during maximal exercise compared to the baseline values observed prior to placebo-infusion. Otherwise, the LV walls were defined as non-ischemic.</p> <p>Results</p> <p>PSV increased from baseline to maximal exercise in non-ischemic walls both during placebo (<it>P </it>= 0.0001) and low-dose adenosine infusion (<it>P </it>= 0.0009). However, in the ischemic walls, PSV increased only during low-dose adenosine infusion <it>(P </it>= 0.001), while no changes in PSV occurred during placebo infusion (<it>P </it>= NS).</p> <p>Conclusion</p> <p>Low-dose adenosine infusion reduced the ischemic burden and improved LV regional systolic function in the ischemic walls of patients with exercise-induced myocardial ischemia, confirming that adenosine is a potential preconditioning agent in humans.</p
A palaeoenvironmental reconstruction of the Middle Jurassic of Sardinia (Italy) based on integrated palaeobotanical, palynological and lithofacies data assessment
During the Jurassic, Sardinia was close to continental Europe. Emerged lands started from a single island forming in time a progressively sinking archipelago. This complex palaeogeographic situation gave origin to a diverse landscape with a variety of habitats. Collection- and literature-based palaeobotanical, palynological and lithofacies studies were carried out on the Genna Selole Formation for palaeoenvironmental interpretations. They evidence a generally warm and humid climate, affected occasionally by drier periods. Several distinct ecosystems can be discerned in this climate, including alluvial fans with braided streams (Laconi-Gadoni lithofacies), paralic swamps and coasts (Nurri-Escalaplano lithofacies), and lagoons and shallow marine environments (Ussassai-Perdasdefogu lithofacies). The non-marine environments were covered by extensive lowland and a reduced coastal and tidally influenced environment. Both the river and the upland/hinterland environments are of limited impact for the reconstruction. The difference between the composition of the palynological and palaeobotanical associations evidence the discrepancies obtained using only one of those proxies. The macroremains reflect the local palaeoenvironments better, although subjected to a transport bias (e.g. missing upland elements and delicate organs), whereas the palynomorphs permit to reconstruct the regional palaeoclimate. Considering that the flora of Sardinia is the southernmost of all Middle Jurassic European floras, this multidisciplinary study increases our understanding of the terrestrial environments during that period of time
Subclinical cardiac involvement in myotonic dystrophy manifesting as decreased myocardial Doppler velocities
To assess subendocardial (long-axis) and mid-wall (short-axis) left ventricular (LV) function in patients with type 1 myotonic dystrophy (MD1), with no symptoms or clinical signs of heart disease, to investigate if they have subclinical cardiac involvement, 28 subjects (14 with MD1, and 14 age- and sex-matched normals) had conventional and tissue Doppler echocardiography. Myocardial velocities and timings to peak systolic contractions were measured. LV wall thickness, diameters, and ejection fraction were not different between the groups. 4/14 of the MD1 patients (29%) had global diastolic dysfunction. Both long-axis and short-axis systolic and early diastolic myocardial velocities were lower in patients with MD1, whereas time-to-peak myocardial contraction was longer; mean longitudinal systolic velocity was 5.5+/-1.7 cm/s in patients with MD1, compared with 7.8+/-1.3 cm/s in normal subjects (P<0.001) 10/14 of the patients (71%) had reduced longitudinal systolic function. Longitudinal systolic and diastolic velocities were inversely related to the duration of the QRS complex ( r=-0.86 and r=-0.63 respectively, both P<0.01), but they did not correlate with the CTG-repeat size. Patients with MD1 have subclinical cardiac impairment revealed by measurement of myocardial velocities using tissue Doppler echocardiography
Does chemical cross-linking with NHS esters reflect the chemical equilibrium of protein-protein noncovalent interactions in solution?
Chemical cross-linking in combination with matrix-assisted laser desorption/ionization mass spectrometry (MALDI-MS) has emerged as a powerful tool to study non-covalent protein complexes. Nevertheless, there are still many questions to answer: Does the amount of detected cross-linked complex correlate with the amount of protein complex in solution? In which concentration and affinity range is specific cross-linking possible? In order to answer these questions, we performed systematic cross-linking studies with two complexes using the N8
hydroxysuccinimidyl ester disuccinimidyl suberate (DSS): i) NCoA-1 and mutants of the interacting peptide STAT6Y, covering a KD range of 30 nM to > 25 μM and ii) α-thrombin and basic pancreatic trypsin inhibitor (BPTI), which shows a buffer dependent KD value between 100 and 320 μM. Samples were analyzed by MALDI-MS. For NCoA-1•STAT6Y, a good correlation of the amount of cross-linked species with the calculated fraction of complex present in solution was observed. Thus, chemical cross-linking in combination with MALDI-MS can be used to rank binding affinities. The specificity of complex formation for the mid-affinity range up to about KD ≈ 25 μM could be proven by comparing against a non-binding peptide and by studying the concentration dependence. In order to study in which affinity range specific cross-linking can be applied, the weak α-thrombin•BPTI complex was investigated. Although variations of the sodium concentration can change the dissociation constant up to 3-fold for this interaction, no significant effect on the amount of detected complex was observed at different peptide concentrations. Our interpretation of this result is that the detected complex is not specific, but a nonspecifically cross-linked species. Consequently, chemical cross-linking is not applicable to low-affinity complexes with KD >> 25 μM with the experimental approach used in this study
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