248 research outputs found
Suppression Mechanism of Electron Emission under Fast Cluster Impact on Solids
We have specified the mechanism of suppressed electron emission from surfaces bombarded by fast cluster ions. From key information obtained from a comparison of the electron emissions for insulator KCl and conductor graphite, we concluded that the suppression is predominantly caused by the disturbance of the electron transport by the electric potential generated by moving cluster atoms. The possible shift from suppressed emission to enhanced emission of electrons as cluster speed increases is also discussed in relation to that in the case of cluster stopping power
Chemical Abundances in the Secondary Star of the Black Hole Binary V4641 Sagittarii (SAX J1819.3-2525)
We report on detailed spectroscopic studies performed for the secondary star
in the black hole binary (micro-quasar) V4641 Sgr in order to examine its
surface chemical composition and to see if its surface shows any signature of
pollution by ejecta from a supernova explosion. High-resolution spectra of
V4641 Sgr observed in the quiescent state in the blue-visual region are
compared with those of the two bright well-studied B9 stars (14 Cyg and
Cap) observed with the same instrument. The effective temperature of V4641 Sgr
(10500 200 K) is estimated from the strengths of He~{\sc i} lines, while
its rotational velocity, sin (95 10 km s), is
estimated from the profile of the Mg~{\sc ii} line at 4481 \AA. We obtain
abundances of 10 elements and find definite over-abundances of N (by 0.8 dex or
more) and Na (by 0.8 dex) in V4641 Sgr. From line-by-line comparisons of eight
other elements (C, O, Mg, Al, Si, Ti, Cr, and Fe) between V4641 Sgr and the two
reference stars, we conclude that there is no apparent difference in the
abundances of these elements between V4641 Sgr and the two normal late B-type
stars, which have been reported to have solar abundances. An evolutionary model
of a massive close binary system has been constructed to explain the abundances
observed in V4641 Sgr. The model suggests that the progenitor of the black hole
forming supernova was as massive as ~ 35 Msun on the main-sequence and, after
becoming a ~ 10 Msun He star, underwent "dark" explosion which ejected only N
and Na-rich outer layer of the He star without radioactive Ni.Comment: 13 pages, 14 figures. Accepted for publication in the PASJ:
Publications of the Astronomical Society of Japa
Immediate implant loading following computer-guided surgery
AbstractPurposeThe aim of this study was to develop and apply a new method for easy intraoperative adjustment of a provisional fixed full-arch restoration, in order to allow immediate implant loading following computer-guided surgery, regardless of any implant positioning errors compared to the virtual planning.MethodsIn accordance with the NobelGuide™ protocol, a provisional restoration for immediate loading of six maxillary implants was prepared prior to surgery. Because small shifts between the planned and the actual implant positions were to be expected, the provisional restoration was not fabricated directly on temporary cylinders as a conventional one-piece superstructure, but was divided into two portions: six custom made abutments and a long span fixed restoration which were left unconnected. After implantation, the custom abutments were attached to the six implants to be immediately loaded, and the superstructure was cemented simultaneously to all abutments using dual cure resin cement. After the excess cement was cleaned and polished, the superstructure was then reseated. Passive fit was achieved between implants and the superstructure.ConclusionThe superstructure described in this article can be easily seated and adjusted to accommodate any possible shifts in implant positioning occurring during computer-guided surgery. Through this method uneventful immediate implant loading can be achieved in a reasonable operative time
Acquired dysfibrinogenemia: monoclonal λ-type IgA binding to fibrinogen caused lower functional plasma fibrinogen level and abnormal clot formation
ArticleInternational journal of hematology. 112(1): 96-104. (2020)journal articl
Oxidation behaviour of lattice oxygen in Li-rich manganese-based layered oxide studied by hard X-ray photoelectron spectroscopy
The oxidation/reduction behaviours of lattice oxygen and transition metals in a Li-rich manganese-based layered oxide Li[Li0.25Ni0.20Mn0.55]O1.93 are investigated by using hard X-ray photoelectron spectroscopy (HAX-PES). By making use of its deeper probing depth rather than in-house XPS analyses, we clearly confirm the formation of O- ions as bulk oxygen species in the active material. They are formed on the 1st charging process as a charge compensation mechanism for delithiation and decrease on discharging. In particular, the cation-anion dual charge compensation involving Ni and O ions is suggested during the voltage slope region of the charging process. The Ni ions in the material are considered to increase the capacity delivered by a reversible anion redox reaction with the suppression of O2 gas release. On the other hand, we found structural deterioration in the cycled material. The O- species are still observed but are electrochemically inactive during the 5th charge-discharge cycle. Also, the oxidation state of Ni ions is divalent and inactive, although that of Mn ions changes reversibly. We believe that this is associated with the structural rearrangement occurring after the activation process during the 1st charging, leading to the formation of spinel- or rocksalt-like domains over the sub-surface region of the particles
Thalidomide Prevents the Progression of Peritoneal Fibrosis in Mice
Thalidomide is clinically recognized as a therapeutic agent for multiple myeloma and has been known to exert anti-angiogenic actions. Recent studies have suggested the involvement of angiogenesis in the progression of peritoneal fibrosis. The present study investigated the effects of thalidomide on the development of peritoneal fibrosis induced by injection of chlorhexidine gluconate (CG) into the mouse peritoneal cavity every other day for 3 weeks. Thalidomide was given orally every day. Peritoneal tissues were dissected out 21 days after CG injection. Expression of CD31 (as a marker of endothelial cells), proliferating cell nuclear antigen (PCNA), vascular endothelial growth factor (VEGF), α-smooth muscle actin (as a marker of myofibroblasts), type III collagen and transforming growth factor (TGF)-β was examined using immunohistochemistry. CG group showed thickening of the submesothelial zone and increased numbers of vessels and myofibroblasts. Large numbers of VEGF-, PCNA-, and TGF-β-positive cells were observed in the submesothelial area. Thalidomide treatment significantly ameliorated submesothelial thickening and angiogenesis, and decreased numbers of PCNA- and VEGF-expressing cells, myofibroblasts, and TGF-β-positive cells. Moreover, thalidomide attenuated peritoneal permeability for creatinine, compared to the CG group. Our results indicate the potential utility of thalidomide for preventing peritoneal fibrosis
The renin–angiotensin system promotes arrhythmogenic substrates and lethal arrhythmias in mice with non-ischaemic cardiomyopathy
[Aims]The progression of pathological left ventricular remodelling leads to cardiac dysfunction and contributes to the occurrence of malignant arrhythmias and sudden cardiac death. The underlying molecular mechanisms remain unclear, however. Our aim was to examine the role of the renin–angiotensin system (RAS) in the mechanism underlying arrhythmogenic cardiac remodelling using a transgenic mouse expressing a cardiac-specific dominant-negative form of neuron-restrictive silencer factor (dnNRSF-Tg). This mouse model exhibits progressive cardiac dysfunction leading to lethal arrhythmias. [Methods and results]Subcutaneous administration of aliskiren, a direct renin inhibitor, significantly suppressed the progression of pathological cardiac remodelling and improved survival among dnNRSF-Tg mice while reducing arrhythmogenicity. Genetic deletion of the angiotensin type 1a receptor (AT1aR) similarly suppressed cardiac remodelling and sudden death. In optical mapping analyses, spontaneous ventricular tachycardia (VT) and fibrillation (VF) initiated by breakthrough-type excitations originating from focal activation sites and maintained by functional re-entry were observed in dnNRSF-Tg hearts. Under constant pacing, dnNRSF-Tg hearts exhibited markedly slowed conduction velocity, which likely contributes to the arrhythmogenic substrate. Aliskiren treatment increased conduction velocity and reduced the incidence of sustained VT. These effects were associated with suppression of cardiac fibrosis and restoration of connexin 43 expression in dnNRSF-Tg ventricles. [Conclusion]Renin inhibition or genetic deletion of AT1aR suppresses pathological cardiac remodelling that leads to the generation of substrates maintaining VT/VF and reduces the occurrence of sudden death in dnNRSF-Tg mice. These findings demonstrate the significant contribution of RAS activation to the progression of arrhythmogenic substrates
Effect of switching from sevelamer hydrochloride to lanthanum carbonate on metabolic acidosis in dialysis patients
Treatments for hyperphosphatemia in dialysis patients include dietary therapy and oral administration of phosphate binders; however, it has recently been suggested that oral administration of sevelamer hydrochloride, a phosphate binder, may cause metabolic acidosis. Owing to the decreased supply of sevelamer hydrochloride after the Eastern Japan Great Earthquake Disaster on March 11, 2011, hyperphosphatemia patients switched to another phosphate binder, lanthanum carbonate. Here, we retrospectively evaluated the effect of this medication substitution on metabolic acidosis in patients on maintenance hemodialysis. 32 patients, who underwent maintenance hemodialysis at Nagasaki Kidney Center in Japan, were enrolled in our study and followed to evaluate the effect of switching medication on metabolic acidosis at 3 months after switching from sevelamer hydrochloride to lanthanum carbonate. The mean dose of sevelamer hydrochloride prior to the earthquake disaster was 3 g/day, and the mean dose of lanthanum carbonate thereafter was 0.9 g/day. Three months after the medication was changed, the concentration of bicarbonate ion did not increase significantly (p = 0.186), whereas pH and base excess increased significantly (p = 0.007 and p = 0.036, respectively). In this study, although the HCO3 - level was not significantly changed, the pH and base excess were significantly increased. Our findings indicate that lanthanum carbonate ameliorates metabolic acidosis
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