Recent progress in high-power GaInAsP lasers

The high-power characteristics (180 mW, CW) and reliability of 1.48-μm Fabry-Perot laser diodes are studied for V-grooved inner stripe lasers grown by liquid phase epitaxy on p-type substrate (VIPS lasers). Their potential as pumping sources of erbium-doped fiber amplifiers is reported, and their power saturation behavior at several wavelengths is discussed. Aging tests were conducted at high power levels of up to 75% CW maximum power (P_max) at -40, 25, and 70°C. The ageing power reached more than 200 mW at -40°C; however, no significant degradation was observed at any temperature level. At 25°C the median lifetime is estimated to be 60000 h, and stable operation is observed at the highest aging level (to date) of 200 mW for up to 1600 h at -40°C     

CD23 deficient mice develop allergic airway hyperresponsiveness following sensitization with ovalbumin

The low affinity receptor for IgE (CD23) is reported to regulate immune and inflammatory events and as a result, it may have a role in the development of allergic airway inflammation and hyperresponsiveness (AHR). To test this hypothesis CD23-deficient mice were studied following different modes of allergic sensitization. Mice were actively sensitized either intraperitoneally with ovalbumin (OA)/alum or via the airways (10 days exposure to OA aerosol with no adjuvant). Passive sensitization was performed by intravenous injections of OA-specific IgE. Airway responsiveness, serum IgE and IgG levels were assessed together with airway inflammation. Passive sensitization followed by airway challenges resulted in increased OA-specific lgG and IgE in the serum of wild-type mice only, while both the CD23+/+ and CD23-/- groups developed tracheal smooth muscle hyperresponsiveness to electrical field stimulation, indicating that IgE/CD23-mediated immune functions may not be necessary for the development of allergic changes. Active sensitization of both CD23-/- and CD23+/+ mice resulted in increased serum levels of OA-specific IgE and lgG, airway eosinophilia and significant AHR when compared with nonsensitized mice. The genetic deficiency of CD23-/- mice not only failed to prevent but was associated with a significant increase of these responses. These results indicate that CD23 may not be essential for the development of allergen-induced AHR and further, that its presence may have some inhibitory effects on the allergic response.     

Differential expression of CD40 ligand on T cell subsets. Implications for different roles of CD45RA+ and CD45RO+ cells in IgE production

Physical contact between human T lymphocytes and B lymphocytes is required for the induction of IgE production. In the present study, we examined the abilities of CD45RA+ and CD45RO+ human T cell subsets to provide help for IgE production by human peripheral blood B cells in the presence of IL-4. Purified peripheral CD45RA+ T cells are much better inducers of IgE synthesis than are CD45RO+ T cells. Activation of CD45RA+ T cells, but not CD45RO+ T cells, via the TCR/CD3 complex is sufficient to confer the ability to provide IgE help, suggesting that an inducible T cell surface molecule plays an important role in this system. The CD40 ligand, an inducible T cell surface molecule, is expressed at higher levels on CD45RA+ T cells as compared with CD45RO+ T cells following CD3-stimulation. Blocking of the CD40-CD40 ligand interaction in vitro by the addition of a soluble form of B cell CD40 Ag completely blocks IgE production induced by CD45RA+ T cells. Finally, the in vitro conversion of CD45RA+ T cells to the CD45RO+ phenotype is accompanied by a loss in the ability of these cells to express the CD40 ligand in response to anti-CD3 stimulation as well as a loss in their ability to provide IgE help. These results suggest that both CD45 subsets may play significant and distinct roles in the induction of IgE production under physiologic conditions: CD45RO+ T cells provide IL-4 and the CD45RA+ subset provides the second signal via the CD40 ligand.     

Estimation of norovirus removal performance in a coagulation-rapid sand filtration process by using recombinant norovirus VLPs

Norovirus (NV) is an important human pathogen that causes epidemic acute nonbacterial gastroenteritis worldwide. Because of the lack of a cell culture system or an animal model for this virus, studies of drinking water treatment such as separation and disinfection processes are still hampered. We successfully estimated NV removal performance during a coagulation-rapid sand filtration process by using recombinant NV virus-like particles (rNV-VLPs) morphologically and antigenically similar to native NV. The behaviors of two widely accepted surrogates for pathogenic waterborne viruses, bacteriophages Qβ and MS2, were also investigated for comparison with that of rNV-VLPs. Approximately 3-log₁₀ removals were observed for rNV-VLPs with a dose of 40 μM-Al or -Fe, as polyaluminum chloride at pH 6.8 or ferric chloride at pH 5.8, respectively. Smaller removal ratios were obtained with alum and ferric chloride at pH 6.8. The removal performance for MS2 was somewhat larger than that for rNV-VLPs, meaning that MS2 is not recommended as an appropriate surrogate for native NV. By comparison, the removal performance for Qβ was similar to, or smaller than, that for rNV-VLPs. However, the removal performances for rNV-VLPs and Qβ differed between the coagulation process and the following rapid sand filtration process. Therefore, Qβ also is not recommended as an appropriate surrogate for native NV.     

Transform-limited optical short-pulse generation at high repetitionrate over 40 GHz from a monolithic passive mode-locked DBR laser diode

The fabrication of monolithic InP-based passively mode-locked distributed-Bragg-reflector (DBR) laser is reported. An optical short-pulse train with a duration of 3.5 ps was generated at a repetition rate of over 40 GHz. The time-bandwidth product was 0.43, and it was very close to the transform-limited value of a Gaussian waveform. Peak power of 60 mW has been achieved. This laser is promising as an optical source for a high-bit-rate soliton transmission system     

High-power aging tests of 1.3 and 1.5 ?m VIPS lasers

1.3 and 1.5 ?m VIPS lasers were tested under high-power aging levels up to 130 mW. The output powers of the lasers were enhanced by AR/HR-coating of facets and optimisation of cavity lengths. Aging power levels were 75% of ?Pmaxand were up to 130mW at 25°C and up to 90 mW at 70°C for 1.3?m VIPS lasers. The median lifetimes were estimated to be 150,000 h at 25°C and 60,000 h at 70°C. For the 1.5?m VIPS lasers, the aging power levels were up to 90 mW at 25°C and up to 50 mW at 70°C. Median lifetimes of about 60,000 h and 45,000 h for 25 and 70°C aging tests, respectively, were achieved.     

Reliability of 1.3 ?m V-grooved inner-stripe laser diodes under high-power operation

Aging tests of 1.3 ?m laser diodes were performed under extremely high power levels up to 85% of the maximum CW output powers. We have verified high reliability under high power levels as high as 75% of the maximum CW output powers at room temperature. The median lifetime is estimated to be 7×104 h at 75% of the maximum CW output power.     

Antiinterleukin-5 antibody prevents airway hyperresponsiveness in a murine model of airway sensitization

Eosinophils play a central role in the inflammatory response associated with bronchial asthma. We studied the involvement of eosinophils in the development of airway hyperresponsiveness (AHR) in a mouse model of allergic airway sensitization. Sensitization of BALB/c mice to OVA via the airways induced allergen-specific T-cell responses, IgE production, immediate cutaneous hypersensitivity (ICH), and increased airway reactivity. Airway sensitization was associated with eosinophil infiltration of the airways and increased production of interleukin-5 (IL-5) in cultures of peribronchial lymph node cells. Treatment of OVA-challenged animals with anti-IL-5 antibody during the sensitization protocol completely abolished the infiltration of eosinophils into the lung tissue and prevented the development of AHR without affecting levels of allergen-specific IgE, cutaneous hypersensitivity and allergen-specific T cell responses. These findings demonstrate that infiltration of lung tissue by eosinophils, triggered by increased IL-5 production, is a major factor in the development of AHR in this mouse model of airway sensitization.