2,020 research outputs found
Lunar science prior to Apollo 11
Evolutional aspects and geological interpretations in lunar scienc
Quantitative estimation of plant characteristics using spectral measurement: A survey of the literature
There are no author-identified significant results in this report
Gram-negative bacterial molecules associate with Alzheimer disease pathology.
ObjectiveWe determined whether Gram-negative bacterial molecules are associated with Alzheimer disease (AD) neuropathology given that previous studies demonstrate Gram-negative Escherichia coli bacteria can form extracellular amyloid and Gram-negative bacteria have been reported as the predominant bacteria found in normal human brains.MethodsBrain samples from gray and white matter were studied from patients with AD (n = 24) and age-matched controls (n = 18). Lipopolysaccharide (LPS) and E coli K99 pili protein were evaluated by Western blots and immunocytochemistry. Human brain samples were assessed for E coli DNA followed by DNA sequencing.ResultsLPS and E coli K99 were detected immunocytochemically in brain parenchyma and vessels in all AD and control brains. K99 levels measured using Western blots were greater in AD compared to control brains (p < 0.01) and K99 was localized to neuron-like cells in AD but not control brains. LPS levels were also greater in AD compared to control brain. LPS colocalized with Aβ1-40/42 in amyloid plaques and with Aβ1-40/42 around vessels in AD brains. DNA sequencing confirmed E coli DNA in human control and AD brains.ConclusionsE coli K99 and LPS levels were greater in AD compared to control brains. LPS colocalized with Aβ1-40/42 in amyloid plaques and around vessels in AD brain. The data show that Gram-negative bacterial molecules are associated with AD neuropathology. They are consistent with our LPS-ischemia-hypoxia rat model that produces myelin aggregates that colocalize with Aβ and resemble amyloid-like plaques
Analysis of the pulsar P-Ṗ distribution
A new technique for the systematic evaluation of models of pulsar period evolution on the basis of a complete observational sample is outlined and applied to the existing incomplete sample. Possible selection effects are discussed. It is concluded that the simple law for the rate of change of period P, Ṗ ∝ P^(2−n) is incompatible with the assumption of stationarity and pulsar ‘death’ at large periods, if n > 2. Models with n < 2, or with n ≳ 2.5 and torque decay on a time-scale of 1 Myr are consistent with the data. Another possibility is that the beaming fraction decreases by a factor ∼5 as a pulsar slows down. A new procedure for deriving a rigorous lower limit to the creation rate of pulsars within the sample is presented, and it is shown that most pulsars appear to be born with large values of Ṗ
Timing the millisecond pulsars in 47 Tucanae
In the last 10 years 20 millisecond pulsars have been discovered in the
globular cluster 47 Tucanae. Hitherto, only 3 of these had published timing
solutions. Here we improve upon these 3 and present 12 new solutions. These
measurements can be used to determine a variety of physical properties of the
pulsars and of the cluster. The 15 pulsars have positions determined with
typical uncertianties of only a few milliarcsec and they are all located within
1.2 arcmin of the cluster centre. We have also measured the proper motions of 5
of the pulsars, which are consistent with the proper motion of 47 Tuc based on
Hipparcos data. The period derivatives measured for many of the pulsars are
dominated by the dynamical effects of the cluster gravitational field, and are
used to constrain the surface mass density of the cluster. All pulsars have
characteristic ages T > 170 Myr and magnetic fields B < 2.4e9 Gauss, and the
average T > 1 Gyr. We have measured the rate of advance of periastron for the
binary pulsar J0024-7204H, implying a total system mass 1.4+-0.8 solar masses.Comment: 17 pages, 11 included figures, accepted for publication in MNRA
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Gender-specific changes in energy metabolism and protein degradation as major pathways affected in livers of mice treated with ibuprofen.
Ibuprofen, an inhibitor of prostanoid biosynthesis, is a common pharmacological agent used for the management of pain, inflammation and fever. However, the chronic use of ibuprofen at high doses is associated with increased risk for cardiovascular, renal, gastrointestinal and liver injuries. The underlying mechanisms of ibuprofen-mediated effects on liver remain unclear. To determine the mechanisms and signaling pathways affected by ibuprofen (100 mg/kg/day for seven days), we performed proteomic profiling of male mice liver with quantitative liquid chromatography tandem mass spectrometry (LC-MS/MS) using ten-plex tandem mass tag (TMT) labeling. More than 300 proteins were significantly altered between the control and ibuprofen-treated groups. The data suggests that several major pathways including (1) energy metabolism, (2) protein degradation, (3) fatty acid metabolism and (4) antioxidant system are altered in livers from ibuprofen treated mice. Independent validation of protein changes in energy metabolism and the antioxidant system was carried out by Western blotting and showed sex-related differences. Proteasome and immunoproteasome activity/expression assays showed ibuprofen induced gender-specific proteasome and immunoproteasome dysfunction in liver. The study observed multifactorial gender-specific ibuprofen-mediated effects on mice liver and suggests that males and females are affected differently by ibuprofen
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