Recent results of medium wave infrared compressive sensing.

The application of compressive sensing (CS) for imaging has been extensively investigated and the underlying mathematical principles are well understood. The theory of CS is motivated by the sparse nature of real-world signals and images, and provides a framework in which high-resolution information can be recovered from low-resolution measurements. This, in turn, enables hardware concepts that require much fewer detectors than a conventional sensor. For infrared imagers there is a significant potential impact on the cost and footprint of the sensor. When smaller focal plane arrays (FPAs) to obtain large images are allowed, large formats FPAs are unnecessary. From a hardware standpoint, this benefit is independent of the actual level of compression and effective data rate reduction, which depend on the choice of codes and information recovery algorithm. Toward this end, we used a CS testbed for mid-wave infrared (MWIR) to experimentally show that information at high spatial resolution can be successfully recovered from measurements made with a small FPA. We describe the highly parallel and scalable CS architecture of the testbed, and its implementation using a reflective spatial light modulator and a focal plane array with variable pixel sizes. We also discuss the impact of real-world devices and the effect of sensor calibration that must be addressed in practice. Finally, we present preliminary results of image reconstruction, which demonstrate the testbed operation. These results experimentally confirm that high-resolution spatial information (for tasks such as imaging and target detection) can be successfully recovered from low-resolution measurements. We also discuss the potential system-level benefits of CS for infrared imaging, and some of the challenges that must be addressed in future infrared CS imagers designs.

Transgenic expression of human S100A12 induces structural airway abnormalities and limited lung inflammation in a mouse model of allergic inflammation.

BACKGROUND: The calcium-binding protein S100A12 is highly up-regulated in the serum and sputum of patients with allergic asthma and is suggested to be a biomarker and pathologic mediator of asthma. OBJECTIVE: To test the role of S100A12 in mediating airway inflammation in a mouse model of allergic lung inflammation. METHODS: Transgenic (TG) mice that express human S100A12 and wild-type (WT) littermates were sensitized and challenged with ovalbumin (OVA) and assessed for inflammation, lung structure, and function. RESULTS: Following OVA sensitization and challenge, S100A12 TG mice showed reduced peribronchial and perivascular inflammation, mucus production, and eosinophilia as well as attenuated airway responsiveness to contractile agonist compared with WT sensitized and challenged animals. This is explained, at least in part, by remodelled airways in S100A12 TG mice with thinning of the airway smooth muscle. S100A12 exposure induced Fas expression and activation of caspase 3 in cultured airway smooth muscle cells, suggesting that airway smooth muscle abnormalities observed in S100A12 TG mice may be mediated through myocyte apoptosis. CONCLUSION AND CLINICAL RELEVANCE: S100A12 is one of the most abundant proteins found in the airways of human asthmatics, and it was postulated that S100A12 could mediate the inflammatory process. Our study shows for the first time that TG expression of S100A12 in the lung of mice does not exacerbate lung inflammation in a model of OVA-induced allergic inflammation. We speculate that the high levels of S100/calgranulins found in bronchoalveolar lavage fluid of asthmatics and of OVA-treated TG S100A12 mice do not significantly mediate pulmonary inflammation.

CD43 interaction with ezrin-radixin-moesin (ERM) proteins regulates T-cell trafficking and CD43 phosphorylation.

Cell polarization is a key feature of cell motility, driving cell migration to tissues. CD43 is an abundantly expressed molecule on the T-cell surface that shows distinct localization to the migrating T-cell uropod and the distal pole complex (DPC) opposite the immunological synapse via association with the ezrin-radixin-moesin (ERM) family of actin regulatory proteins. CD43 regulates multiple T-cell functions, including T-cell activation, proliferation, apoptosis, and migration. We recently demonstrated that CD43 regulates T-cell trafficking through a phosphorylation site at Ser-76 (S76) within its cytoplasmic tail. Using a phosphorylation-specific antibody, we now find that CD43 phosphorylation at S76 is enhanced by migration signals. We further show that CD43 phosphorylation and normal T-cell trafficking depend on CD43 association with ERM proteins. Interestingly, mutation of S76 to mimic phosphorylation enhances T-cell migration and CD43 movement to the DPC while blocking ERM association, showing that CD43 movement can occur in the absence of ERM binding. We also find that protein kinase CΘ can phosphorylate CD43. These results show that while CD43 binding to ERM proteins is crucial for S76 phosphorylation, CD43 movement and regulation of T-cell migration can occur through an ERM-independent, phosphorylation-dependent mechanism.

Immunobiology of chronic lung allograft dysfunction: new insights from the bench and beyond.

The first successful human lung transplants were performed in the 1980s. Since that time lung transplantation has been a therapeutic modality for end-stage pulmonary diseases. However, chronic rejection, known as obliterative bronchiolitis (OB)/bronchiolitis obliterans syndrome (BOS), is the key reason why the 5-year survival is only 50%, which is significantly worse than most other solid organ transplants. Recent studies have provided exciting advances that are beginning to be translated into findings in humans. This review will highlight the current advances in understanding the mechanisms of OB/BOS in lung transplant recipients.

Microdissection and microcloning of mid-chromosome 4: genetic mapping of 41 microdissection clones.

Available genetic information places the mouse db gene approximately 5 cM distal to Ifa on mid/distal mouse chromosome 4. These data have indicated that there is a relevant paucity of genetic markers that map to this region of chromosome 4. To increase the density of the genetic map on mid-chromosome 4, we have applied the techniques of microdissection and microcloning of the mid-portion of mouse chromosome 4. A total of 47 RFLPs from the microdissection library were used to type the progeny of three C57BL/6J Mus spretus backcrosses. The resulting composite genetic map positions seven known genes, 41 microclones, and three other anonymous markers to a region of approximately 21 cM on mid-chromosome 4 extending from b to Lck. The density of markers in this region of chromosome 4 should be sufficient to initiate the physical mapping of this subchromosomal segment, facilitating efforts to clone the db gene, as well as other uncloned mutant loci in this region of chromosome 4.

Auditory backward recognition masking: effect of interaural phase on masker efficacy.

The effect of interaural phase on pitch and lateralization recognition was examined. Tonal signals were followed by a variable interstimulus interval and an interference tone. Stimuli were presented in a binaural masking-level difference paradigm as a means of manipulating the perceptual location of the signal within the head. In separate tasks, subjects were required to recognize the pitch or location of the signal. The pitch-recognition task resulted in the expected increase in performance as the interstimulus interval increased. There was no effect of interaural phase on pitch-recognition performance. There was no significant effect of interstimulus interval on performance in location recognition. Subjects were proficient at recognizing location of the signal regardless of the interstimulus interval. The data suggest that a strict single-channel interpretation of the preperceptual storage model of backward auditory recognition is inadequate.

Rat adrenal zona fasciculata cell electrophysiological responses to ACTH and gamma-MSH vary with age.

A comparison was made of the resting membrane potential (MP) as well as the MP responses to K+, ACTH and gamma-MSH of superfused adrenocortical, zona fasciculata cells from young (Y) and old (O) male rats. The resting MP of these cells did not vary with age. However, the MP responses to altered extracellular [K+] varied significantly with age. A prolonged biphasic depolarization was observed following ACTH administration; these responses were significantly reduced in O cells. In contrast, stimulation with gamma-MSH did not consistently elicit depolarization in the Y but caused a consistent and prominent depolarization in O cells. These findings suggest that aging is associated with changes in primary membrane events which could explain the reduced ACTH-stimulated steroidogenesis associated with age. Elevated cellular responses to gamma-MSH may contribute to a maintenance of, or increase in, circulating corticosterone levels in aged rats.