19 research outputs found
Titanium and titanium oxides at the K- and L-edges: validating theoretical calculations of X-ray absorption and X-ray emission spectra with measurements
Using well-calibrated experimental data we validate theoretical X-ray
absorption spectroscopy (XAS) as well as X-ray emission spectroscopy (XES)
calculations for titanium (Ti), titanium oxide (TiO), and titanium dioxide
(TiO) at the Ti K- and L-edges as well as O K-edge. XAS and XES in
combination with a multi-edge approach offer a detailed insight into the
electronic structure of materials since both the occupied and unoccupied
states, are probed. The experimental results are compared with ab initio
calculations from the OCEAN package which uses the Bethe-Salpeter equation
(BSE) approach. Using the same set of input parameters for each compound for
calculations at different edges, the transferability of the OCEAN calculations
across different spectroscopy methods and energy ranges is validated. Thus, the
broad applicability for analysing and interpreting the electronic structure of
materials with the OCEAN package is shown
a controlled multicenter study with assessment of echocardiographic reference values, and the frequency of dilatation and aneurysm in Marfan syndrome
Background Echocardiographic upper normal limits of both main pulmonary artery
(MPA) diameters (MPA-d) and ratio of MPA to aortic root diameter (MPA-r) are
not defined in healthy adults. Accordingly, frequency of MPA dilatation based
on echocardiography remains to be assessed in adults with Marfan syndrome
(MFS). Methods We enrolled 123 normal adults (72 men, 52 women aged 42 ± 14
years) and 98 patients with MFS (42 men, 56 women aged 39 ± 14 years) in a
retrospective cross-sectional observational controlled study in four tertiary
care centers. We defined outcome measures including upper normal limits of
MPA-d and MPA-r as 95 quantile of normal persons, MPA dilatation as diameters
> upper normal limits, MPA aneurysm as diameters >4 cm, and indication for
surgery as MPA diameters >6 cm. Results MPA diameters revealed normal
distribution without correlation to age, sex, body weight, body height, body
mass index and body surface area. The upper normal limit was 2.6 cm (95%
confidence interval (CI) =2.44-2.76 cm) for MPA-d, and 1.05 (95% CI =
.86–1.24) for MPA-r. MPA dilatation presented in 6 normal persons (4.9%) and
in 68 MFS patients (69.4%; P < .001), MPA aneurysm presented only in MFS (15
patients; 15.3%; P < .001), and no patient required surgery. Mean MPA-r were
increased in MFS (P 1.05 were equally frequent in 7
normal persons (5%) and in 8 MFS patients (10.5%; P = .161). MPA-r related to
aortic root diameters (P = .042), reduced left ventricular ejection fraction
(P = .006), and increased pulmonary artery systolic pressures (P = .040). No
clinical manifestations of MFS and no FBN1 mutation characteristics related to
MPA diameters. Conclusions We established 2.6 cm for MPA-d and 1.05 for MPA-r
as upper normal limits. MFS exhibits a high prevalence of MPA dilatation and
aneurysm. However, patients may require MPA surgery only in scarce
circumstances, most likely because formation of marked MPA aneurysm may
require LV dysfunction and increased PASP
The main pulmonary artery in adults : a controlled multicenter study with assessment of echocardiographic reference values, and the frequency of dilatation and aneurysm in Marfan syndrome
BACKGROUND: Echocardiographic upper normal limits of both main pulmonary artery (MPA) diameters (MPA-d) and ratio of MPA to aortic root diameter (MPA-r) are not defined in healthy adults. Accordingly, frequency of MPA dilatation based on echocardiography remains to be assessed in adults with Marfan syndrome (MFS). METHODS: We enrolled 123 normal adults (72 men, 52 women aged 42 ± 14 years) and 98 patients with MFS (42 men, 56 women aged 39 ± 14 years) in a retrospective cross-sectional observational controlled study in four tertiary care centers. We defined outcome measures including upper normal limits of MPA-d and MPA-r as 95 quantile of normal persons, MPA dilatation as diameters > upper normal limits, MPA aneurysm as diameters >4 cm, and indication for surgery as MPA diameters >6 cm. RESULTS: MPA diameters revealed normal distribution without correlation to age, sex, body weight, body height, body mass index and body surface area. The upper normal limit was 2.6 cm (95% confidence interval (CI) =2.44-2.76 cm) for MPA-d, and 1.05 (95% CI = .86–1.24) for MPA-r. MPA dilatation presented in 6 normal persons (4.9%) and in 68 MFS patients (69.4%; P < .001), MPA aneurysm presented only in MFS (15 patients; 15.3%; P < .001), and no patient required surgery. Mean MPA-r were increased in MFS (P < .001), but ratios >1.05 were equally frequent in 7 normal persons (5%) and in 8 MFS patients (10.5%; P = .161). MPA-r related to aortic root diameters (P = .042), reduced left ventricular ejection fraction (P = .006), and increased pulmonary artery systolic pressures (P = .040). No clinical manifestations of MFS and no FBN1 mutation characteristics related to MPA diameters. CONCLUSIONS: We established 2.6 cm for MPA-d and 1.05 for MPA-r as upper normal limits. MFS exhibits a high prevalence of MPA dilatation and aneurysm. However, patients may require MPA surgery only in scarce circumstances, most likely because formation of marked MPA aneurysm may require LV dysfunction and increased PASP
A Plasmodium Actin-depolymerizing Factor That Binds Exclusively to Actin Monomers
ADF/cofilins (AC) are essential F- and G-actin binding proteins that modulate microfilament turnover. The genome of Plasmodium falciparum, the parasite causing malaria, contains two members of the AC family. Interestingly, P. falciparum ADF1 lacks the F-actin binding residues of the AC consensus. Reverse genetics in the rodent malaria model system suggest that ADF1 performs vital functions during the pathogenic red blood cell stages, whereas ADF2 is not present in these stages. We show that recombinant PfADF1 interacts with monomeric actin but does not bind to actin polymers. Although other AC proteins inhibit nucleotide exchange on monomeric actin, the Plasmodium ortholog stimulates nucleotide exchange. Thus, PfADF1 differs in its biochemical properties from previously known AC proteins and seems to promote turnover exclusively by interaction with actin monomers. These findings provide important insights into the low cytosolic abundance and unique turnover characteristics of actin polymers in parasites of the phylum Apicomplexa
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Pivotal and distinct role for Plasmodium actin capping protein alpha during blood infection of the malaria parasite
Accurate regulation of microfilament dynamics is central to cell growth, motility and response to environmental stimuli. Stabilizing and depolymerizing proteins control the steady-state levels of filamentous (F-) actin. Capping protein (CP) binds to free barbed ends, thereby arresting microfilament growth and restraining elongation to remaining free barbed ends. In all CPs characterized to date, alpha and beta subunits form the active heterodimer. Here, we show in a eukaryotic parasitic cell that the two CP subunits can be functionally separated. Unlike the beta subunit, the CP alpha subunit of the apicomplexan parasite Plasmodium is refractory to targeted gene deletion during blood infection in the mammalian host. Combinatorial complementation of Plasmodium berghei CP genes with the orthologs from Plasmodium falciparum verified distinct activities of CP alpha and CP alpha/beta during parasite life cycle progression. Recombinant Plasmodium CP alpha could be produced in Escherichia coli in the absence of the beta subunit and the protein displayed F-actin capping activity. Thus, the functional separation of two CP subunits in a parasitic eukaryotic cell and the F-actin capping activity of CP alpha expand the repertoire of microfilament regulatory mechanisms assigned to CPs