RESUMO
Concurrent sound associated with very bright meteors manifests as popping, hissing, and faint rustling sounds occurring simultaneously with the arrival of light from meteors. Numerous instances have been documented with -11 to -13 brightness. These sounds cannot be attributed to direct acoustic propagation from the upper atmosphere for which travel time would be several minutes. Concurrent sounds must be associated with some form of electromagnetic energy generated by the meteor, propagated to the vicinity of the observer, and transduced into acoustic waves. Previously, energy propagated from meteors was assumed to be RF emissions. This has not been well validated experimentally. Herein we describe experimental results and numerical models in support of photoacoustic coupling as the mechanism. Recent photometric measurements of fireballs reveal strong millisecond flares and significant brightness oscillations at frequencies ≥40 Hz. Strongly modulated light at these frequencies with sufficient intensity can create concurrent sounds through radiative heating of common dielectric materials like hair, clothing, and leaves. This heating produces small pressure oscillations in the air contacting the absorbers. Calculations show that -12 brightness meteors can generate audible sound at ~25 dB SPL. The photoacoustic hypothesis provides an alternative explanation for this longstanding mystery about generation of concurrent sounds by fireballs.
RESUMO
A 100X magnification, ± 2.5° field of view micro-concentrating optical system has been developed for a microsystems-enabled photovoltaic (MEPV) prototype module using 250 µm diameter multi-junction "stacked" PV cells.
RESUMO
IL-2-deficient mice develop a lymphoproliferative and autoimmune disease characterized by autoimmune hemolytic anemia (AHA) and inflammatory bowel disease. We have previously reported that IL-2 is necessary for optimal up-regulation of CTLA-4, an inducible negative regulator of T cell activation. In this study, we have tested the hypothesis that reduced expression of CTLA-4 in IL-2-deficient T cells contributes to the pathogenesis of disease in IL-2-deficient mice. Expression of CTLA-4 as a transgene completely prevented lymphoaccumulation and AHA in IL-2-deficient mice. The normalization of T cell numbers was due to inhibition of expansion of conventional CD4+CD25- T cells rather than to rescue of the numbers or function of CD4+CD25+ regulatory T cells, suggesting that CTLA-4 expression on conventional T cells plays a role in maintaining normal T cell homeostasis. In addition, the inhibitory effect of the CTLA-4 transgene on T cell expansion was at least in part independent of CD28 expression. Our results suggest that deficient CTLA-4 expression on conventional T cells contributes to the pathophysiology of the lymphoproliferative disease and AHA in IL-2-deficient mice. Thus, restoring CTLA-4 expression in T cells may be an attractive strategy to control clinical autoimmune diseases in which CTLA-4 expression is reduced.
Assuntos
Antígenos de Diferenciação/biossíntese , Antígenos de Diferenciação/genética , Regulação da Expressão Gênica/imunologia , Interleucina-2/deficiência , Interleucina-2/genética , Ativação Linfocitária/genética , Transgenes/imunologia , Anemia Hemolítica Autoimune/genética , Anemia Hemolítica Autoimune/imunologia , Anemia Hemolítica Autoimune/prevenção & controle , Animais , Células Apresentadoras de Antígenos/imunologia , Antígenos CD , Antígenos de Diferenciação/fisiologia , Antígenos CD28/fisiologia , Linfócitos T CD4-Positivos/imunologia , Linfócitos T CD4-Positivos/metabolismo , Linfócitos T CD4-Positivos/patologia , Antígeno CTLA-4 , Morte Celular/genética , Morte Celular/imunologia , Inibidores do Crescimento/biossíntese , Inibidores do Crescimento/genética , Inibidores do Crescimento/fisiologia , Contagem de Linfócitos , Camundongos , Camundongos Knockout , Camundongos Transgênicos , Receptores de Interleucina-2/biossíntese , Esplenomegalia/genética , Esplenomegalia/imunologia , Esplenomegalia/prevenção & controle , Subpopulações de Linfócitos T/imunologia , Subpopulações de Linfócitos T/metabolismo , Subpopulações de Linfócitos T/patologiaRESUMO
Natural engagement of CTLA-4 on host B7 limits T cell activation. We hypothesized that therapeutic cross-linking of CTLA-4 in vivo may further inhibit T cell function and prevent allograft rejection. However, none of the currently available CTLA-4-binding reagents have ligating properties when injected in vivo. The observation that surface-immobilized anti-CTLA-4 mAb inhibits T cell activation in vitro prompted us to develop a membrane-bound single-chain anti-CTLA-4 Ab (7M). To model whether tissue expression of 7M could suppress allograft rejection, we examined the ability of H-2L(d)-specific TCR-transgenic T cells to reject 7M-expressing allogeneic tumor cells injected s.c. Expression of 7M significantly inhibited allogeneic rejection in mice that received CTLA-4(+/+) but not CTLA-4(-/-) T cells. Furthermore, CTLA-4(+/+) T cells that had encountered 7M-expressing tumors in vivo acquired defects in cytokine production and cytotoxicity. Thus, deliberate ligation of CTLA-4 in vivo potently inhibits allogeneic T cell responses.
