An adapative filter for the reduction of cardiogenic oscillation on esophageal pressure signals

in pulmonary monitoring the processing and interpretation of esophageal pressure signals is often complicated by strong cardiogenic oscillations (CGO). In this paper, we descibe an adaptative filter that reduces CGO based on simultaneous recordings of the electrocardiogram. The algorithm is tested in a computer simulation and on patients data. In simulation, a reduction of the mean squared errors introduced by the CGO by 87% is achieved. In patients data, the filter reduces the power in Pes in a ± 0.25Hz band around the hearth rate by 76

In vivo measurements of changes in respiratory mechanics with age in mice deficient in surfactant protein D

Mice deficient in surfactant protein D [SP-D (-/-)] develop progressive emphysema with age, associated with loss of parenchymal tissue, subpleural fibrosis, and accumulation of abnormal elastin fibers. We measured the changes in lung function, partitioned into components for the airways and lung parenchyma, occurring with age in SP-D (-/-) mice at three ages (n=8 per group) (5, 8, and 13 wk). Impedance spectra between 0.25 and 19.625 Hz were calculated and a model, consisting of an airway compartment [airway resistance (Raw) and inertance (Iaw)] and a constant-phase tissue compartment [coefficients of tissue damping (G) and elastance (H)], was fitted to the data. Hysteresivity was calculated as G/H. Adult values of Raw, G, and H are reached by 8 wk of age in wild-type controls. Raw and H were lower at all ages in SP-D (-/-) compared with the wild-type controls (p=0.006 and 0.029, respectively), and a similar trend was seen in G (p=0.060). The patterns of change in respiratory mechanics were similar in both SP-D (+/+) and (-/-) groups. There were no changes in hysteresivity with age and no differences between wild-type and SP-D (-/-) mice. These data demonstrate that the changes in lung structure in SP-D (-/-) mice are reflected in the mechanical properties of both airway and lung parenchyma measured in vivo

Mouse Invariant Monoclonal Antibody NKT14: A Novel Tool to Manipulate iNKT Cell Function <i>In Vivo</i>

<div><p>Invariant Natural Killer T (iNKT) cells are a T cell subset expressing an invariant T Cell Receptor (TCR) that recognizes glycolipid antigens rather than peptides. The cells have both innate-like rapid cytokine release, and adaptive-like thymic positive selection. iNKT cell activation has been implicated in the pathogenesis of allergic asthma and inflammatory diseases, while reduced iNKT cell activation promotes infectious disease, cancer and certain autoimmune diseases such as Type 1 diabetes (T1D). Therapeutic means to reduce or deplete iNKT cells could treat inflammatory diseases, while approaches to promote their activation may have potential in certain infectious diseases, cancer or autoimmunity. Thus, we developed invariant TCR-specific monoclonal antibodies to better understand the role of iNKT cells in disease. We report here the first monoclonal antibodies specific for the mouse invariant TCR that by modifying the Fc construct can specifically deplete or activate iNKT cells <i>in vivo</i> in otherwise fully immuno-competent animals. We have used both the depleting and activating version of the antibody in the NOD model of T1D. As demonstrated previously using genetically iNKT cell deficient NOD mice, and in studies of glycolipid antigen activated iNKT cells in standard NOD mice, we found that antibody mediated depletion or activation of iNKT cells respectively accelerated and retarded T1D onset. In BALB/c mice, ovalbumin (OVA) mediated airway hyper-reactivity (AHR) was abrogated with iNKT cell depletion prior to OVA sensitization, confirming studies in knockout mice. Depletion of iNKT cells after sensitization had no effect on AHR in the conducting airways but did reduce AHR in the lung periphery. This result raises caution in the interpretation of studies that use animals that are genetically iNKT cell deficient from birth. These activating and depleting antibodies provide a novel tool to assess the therapeutic potential of iNKT cell manipulation.</p></div