Accumulation and activation of inflammatory cells in the lung characterize the acute respiratory distress syndrome (ARDS). However, the precise mechanism for lung epithelial and endothelial cell damage remains unknown. Based on evidence that rapid apoptosis caused by CD8(+) cytolytic T cells can induce pathological cell death, we hypothesized that this mechanism may also participate in the acute lung injury, and attempted to evaluate apoptosis-related factors in bronchoalveolar lavage fluid (BALF) from ARDS patients. Quantitative polymerase chain reaction (PCR) analysis revealed that the messenger ribonucleic acids (mRNAs) for several apoptosis molecules, such as perforin, granzyme A, granzyme B, FasL, and Fas were highly upregulated in the acute phase of ARDS following sepsis. In contrast, low or negligible mRNA expression of these molecules was detected in patients with normal lung function, in septic patients without lung injury (septic non-ARDS), and in patients in the late phase of septic ARDS (late ARDS). While the genes of the classic proinflammatory cytokines interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), IL-6, and IL-8, and inducible nitric oxide synthase (iNOS) were upregulated in septic non-ARDS or late ARDS patients, expressions of these genes in the acute phase of septic ARDS were most distinct. The immunofluorescence flow cytometry showed that only the lymphocyte population in BALF from acute phase of septic ARDS patients expressed perforin and granzyme. The level of soluble FasL in the BALF increased only in the acute ARDS patients. These results thus suggested that the dual apoptosis pathway, perforin/granzyme and FasL/Fas system, is likely to be another participant for the pathogenesis of acute lung injury.
The antiferroquadrupolar ordering in DyB2C2 has been investigated using the x-ray resonant scattering technique. The dependence of the intensities of two superlattice peaks on temperature, azimuthal angle, and energy of the incident x-rays was measured. The results show that the antiferroquadrupole ordering, which accompanies a structural phase transition, exists below TQ = 25 K. A structural model for the antiferroquadrupole ordering, for which the propagation vectors are (0,0,1/2) and (0,1,1/2), is presented.
The D022-type (Al3Ti-type) phase in the Mn–Ga system is ferrimagnetic; the spin direction is parallel to the tetragonal c axis. The Curie temperature is about 765 K (for δ=0.67), near the decomposition temperature. We have prepared the D022-type alloys by annealing the quenched ingots of the high-temperature phase (γMn phase) at 400 or 300 °C for a long time. The preparation becomes much easier if the ingots are powdered by filing before the annealing. The single-phase specimens of Mn3−δGa were obtained in the composition range 0.15≤δ≤1.06. The coercivity of some specimens was so large that we measured the magnetization curve in high magnetic fields up to 150 kOe. The room-temperature values of saturation magnetization, remanent magnetization, and coercivity of the powder sample of the alloy with δ=0.67 are 50 emu/g, 25 emu/g, and 13.5 kOe, respectively. We have also studied the effect of magnetic annealing during the transition from the γMn phase to the D022-type phase and the effect of the addition of Fe to Mn3−δGa of the D022-type phase.
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