Search

We report the observation of four-wave mixing in hydrogenated-amorphous-silicon waveguides. The maximum conversion efficiency is −19 dB for 4.0-mm-long hydrogenated-amorphous-silicon waveguide and 10-GHz repetition pump. The operation bandwidth is estimated to be over 60 nm.

Fibronectin (Fn), which is released from several kinds of cells including alveolar macrophages (AM), is important in inflammatory reactions in the certain lung diseases such as idiopathic pulmonary fibrosis (IPF). Therefore, information on the mechanisms regulating Fn release from AM may be useful for elucidating the pathogenesis of these diseases and developing therapeutic modalities. We supposed that prostaglandin E2 (PGE2), which is known to modulate cellular functions, might be involved in regulation of Fn release, and, accordingly, we measured the release of Fn and PGE2 from AM from normal volunteers (NV), control patients (CP), and patients with IPF. AM from patients with IPF were found to release more Fn than AM from NV (IPF: 250 +/- 58.8/10(6) cells.24 h, NV: 53.0 +/- 7.3 ng/10(6) cells.24 h) and to release less PGE2 than the latter (IPF: 0.48 +/- 0.12 ng/10(6) cells.24 h, NV:1.35 +/- 0.24 ng/10(6) cells.24 h). A negative correlation was found between the contents of Fn and PGE2 in the culture media of AM from NV, CP, and patients with IPF. Lipopolysaccharide, phorbol myristate acetate, and zymosan suppressed Fn release from AM but stimulated their PGE2 release, and these effects were reversed by indomethacin. Exogenous PGE2 (greater than 1 x 10(-8) M) suppressed Fn release. The albumin-antialbumin complex stimulated Fn release but did not affect PGE2 release. These results indicate that Fn release from AM changed in response to various stimuli, and that PGE2 is important in suppressing Fn release from AM, suggesting a negative feedback mechanism of PGE2 in releasing Fn.

We investigated the effects of Dermatophagoides farinae (Df) and interleukin (IL)-2 on the release of eosinophil colony-stimulating factor (Eo-CSF) activity from mononuclear cells (MNC) and lymphocytes of patients with bronchial asthma (BA) who were sensitive to Df to clarify its relationship with IL-5 and granulocyte/macrophage colony-stimulating factor (GM-CSF). MNC and T cells of patients cultured with IL-2 and Df released Eo-CSF activity. These Eo-CSF activities were partially inhibited by anti-IL-5 and anti-GM-CSF antibodies. In 11 of 15 cases studied, MNC from patients produced GM-CSF in response to IL-2. In four of 15 cases studied, MNC from patients produced GM-CSF in response to Df. On culture with IL-2 or Df, the releases of IL-5 into the medium by MNC from individual patients varied. The results indicate that in BA responsiveness of lymphocytes to Df is increased, and suggest that IL-5 and GM-CSF produced by T cells play a role in the induction of eosinophilia and the pathogenesis of BA.

To investigate the mechanism of eosinophilia in patients with eosinophilic pleural effusions, we measured the activities of eosinophil colony-stimulating factor (Eo-CSF) and stimulating factor for eosinophil survival in the eosinophilic pleural fluids of six patients (two with tuberculous pleuritis, two with drug allergy, and one each with chronic eosinophilic pneumonia and pleuritis associated with rheumatoid arthritis). The number of eosinophil colonies formed by the pleural fluid of patients with eosinophilic pleural effusions significantly exceeded that of control patients with noneosinophilic pleural effusions (7.5 +/- 1.9 colonies/10(5) bone marrow cells, n = 6, versus 0.3 +/- 0.1 colonies/10(5) bone marrow cells, n = 6, P < 0.01). Similarly, eosinophil survival evaluated on day 4 of culture with pleural fluid of patients with eosinophilic pleural effusions significantly exceeded that of patients with noneosinophilic pleural effusions (83.9 +/- 9.8% versus 46.1 +/- 11.2%, P < 0.001). Both activities were inhibited mainly by anti-IL-5 antibody and partially by anti-GM-CSF antibody and anti-IL-3 antibody. Mononuclear cells obtained from eosinophilic pleural fluid released the activities of Eo-CSF and stimulating factor for eosinophil survival in vitro. These findings suggest that GM-CSF, IL-5, and IL-3 are important to eosinophil accumulation in pleural cavity as stimulators of proliferation and survival of eosinophils.

Alveolar macrophages are thought to be important in immune or inflammatory reactions. We investigated the role of alveolar macrophages in defense against Pseudomonas aeruginosa infection in the lower respiratory tract. Intratracheal inoculation of formalin-inactivated P. aeruginosa (1 x 10(8)-1 x 10(10) organisms) into normal rats resulted in increase in the number of neutrophils in the bronchoalveolar lavage (BAL) fluid obtained 24 h later. The phagocytic activity of neutrophils for P. aeruginosa was higher than that of alveolar macrophages. These findings indicate that neutrophils are essential for phagocytosis of P. aeruginosa in the lower respiratory tract. On incubation with P. aeruginosa, alveolar macrophages released neutrophil chemotactic factor (NCF) dose-dependently. MDP-Lys(L18), a muramyl dipeptide analog, stimulated alveolar macrophages to phagocytize P. aeruginosa and stimulate the release of NCF from alveolar macrophages in vitro and enhanced the neutrophil response to inoculated P. aeruginosa in vivo. These results indicate that alveolar macrophages are important in initiating the neutrophil-dependent defense system against P. aeruginosa by releasing NCF and that MDP-Lys(L18) can amplify the defense system.

The present study was carried out to differentiate orienting reflexes (OR) from defensive reflexes (DR) using 20 female college students as Ss. All Ss received 5 stimulations of 1 sec weak tone (1000 Hz, 40 dB) and 5 stimulation of 1 sec strong tone (white noise, 100 dB) in a randomized order and time interval. Finger pulse amplitude (PA), finger blood content (BC), heart rate (HR), and palmar skin potential reflex (SPR) were recorded simultaneously. BC decrease, HR deceleration, and negative wave of SPR occurred to weak stimulations, while increase, acceleration, and positive wave occurred to strong stimulations. Both intensities of stimulation produced a decrease in PA. These results were discussed in relation to the autonomic changes involved in OR and DR.