Threshold for optimal administration of plerixafor in autologous peripheral blood stem cell collections through CD34+ cell monitoring based on the experience from two Japanese university hospitals.

Plerixafor was introduced to Japan in 2017 as a stem cell mobilization enhancement reagent, but the threshold for its use remains unclear. In this study, we assessed 57 patients treated with plerixafor (33 patients with multiple myeloma (MM) and 24 with malignant lymphoma (ML) and 152 patients without plerixafor administration. When CD34+ cell pre-counts were between 5.5 and 20 cells/µL in MM or 6 and 21 cells/µL in ML, the CD34+ cell count increased significantly, attaining the highest yield in response to plerixafor (achievement rate by one leukapheresis is 93.3% and 91.7% in MM and ML, at P < .001 and P = .012, respectively). In case the CD34+ cell pre-count was less than 5.5 cells/µL, an increase of at least 7 cells/µL from baseline by plerixafor was the necessary condition to achieve successful collection through a two-time leukapheresis. Monitoring CD34+ cell numbers might improve the collection efficiency and reduce the cost.

Platelet-activating factor (PAF) induced cytokine production and otitis media with effusion (OME) in the rat middle ear.

OBJECTIVES: We examined the effect of platelet-activating factor (PAF) on IL-8 production in cultured rat middle ear epithelial cells (RMECs), and the concentrations of cytokine, PAF, and PAF-acetylhydrolase (PAF-AH) were also examined in the PAF-induced experimental OME (otitis media with effusion) of rats. METHODS: Using an enzyme-linked immunospecific assay, we measured the levels of cytokines in the cultured RMECs and the PAF-induced OME of rats. The PAF was quantitated by the platelet-aggregating activity and the PAF-AH was measured by radioimmunoassay. RESULTS: Both PAF and C-PAF, which is a stable analogue of PAF, significantly induced production of IL-8 in the RMECs in a dose-dependent manner. The PAF-induced IL-8 production was abolished by co-incubation with WEB2170, a specific PAF receptor antagonist. The concentrations of the cytokines and PAF in the PAF-induced OME of rats were higher on day 1 and the PAF and cytokine levels seemed to correspond well with the persistence of OME. CONCLUSION: PAF may stimulate the local production of cytokines and may induce OME in the middle ear.

Optical microscopy and in situ Raman scattering of single crystalline ethylene hydrate and binary methane-ethylene hydrate at high pressures.

Visual observations through a microscope and in situ Raman measurements have been made for single crystalline ethylene hydrate (EH) and binary methane-ethylene hydrate (MEH) at pressures up to 3.7 GPa and room temperature. Both hydrates showed pressure-induced phase transitions at 1.6, 2.0, and 3.0 GPa for EH and at 1.7, 2.1, and 3.3 GPa for MEH. The cubic sI phase of EH and MEH remains stable up to 1.6 and 1.7 GPa, respectively, which are more widely ranging values than the values for the methane hydrate sI phase. In this sI phase of binary MEH, the cage occupancies by methane and ethylene molecules are investigated from Raman spectra. Above P = 3.0 GPa for EH and 3.3 GPa for MEH, they decomposed by associating with the formation of the polyethylene.

Experimental otitis media with effusion induced by leukotriene D4.

OBJECTIVE: inflammatory mediators such as prostaglandins (PGs), leukotrienes (LTs), and platelet-activating factor (PAF) have been identified in human middle ear effusions (MEEs), as well as in the experimentally induced MEEs of animals. However, the exact function of LTs in the middle ear cavity is still unknown. In this study, the role of LTs was investigated using an experimental model in which OME was induced by LTD4. METHODS: to examine whether leukotrienes (LTs) induce otitis media with effusion (OME), 2x10(-6), 2x10(-5), 1x10(-4) and 2x10(-4) M of LTD4 was injected into the rat ear. The severity of OME was assessed based on the histological findings. The concentrations of IL1-beta, TNF-alpha, and GRO/CINC-1 in MEE were also measured. Additionally the therapeutic efficacy of a specific LTs antagonist, pranlukast on experimental OME was investigated. RESULTS: all ears developed middle ear effusion (MEE) within 24 h and about 50% of the animals continued to demonstrate MEE for 14 days in the 1x10(-4) and 2x10(-4) M groups. The cytokine levels seemed to correspond well with the persistence of OME. The oral administration of a specific LTs antagonist, pranlukast, was found to alleviate the experimental OME. CONCLUSION: these findings suggest that LTs appear to plays an important role in the pathogenesis of OME.