Design and Analysis of a LWIR Detector Electronics for Space Applications

µBolometers based on a-Si technology provide a marketable performance while at the same time requiring only moderate resources in terms of cooling requirements. The PICO1024 is a high resolution (1024x768 pixels) infrared image sensor for thermography applications. It makes use of LYNRED latest, state of the art, 17 µm pixel pitch technology. The PICO1024 sensor is a 2-dimensional detector array sensitive to infrared radiation in the long wave spectral range (LWIR) from 8 to 14 m. It uses microbolometer technology to convert infrared radiation into electronic signal for use in thermal imaging cameras. Starting from an analysis of the Capacitance Trans-Impedance Amplifier (CTIA) the front-end electronics architecture is described and analyzed. This includes transient and AC Spice simulations as well as an analysis of the readout signal chain noise performance. The paper also presents a possible replacement of key components (ADC, opamp) by low power, high performance space qualified IEEE parts. An instrument concept presents the implementation of the PICO1024 into a thermal infrared multi-spectral imager for an Io mission

Nitric oxide synthase 2 is required for conversion of pro-fibrogenic inflammatory CD133+ progenitors into F4/80+ macrophages in experimental autoimmune myocarditis

Aims Experimental autoimmune myocarditis (EAM) model mirrors important mechanisms of inflammatory dilated cardiomyopathy (iDCM). In EAM, inflammatory CD133+ progenitors are a major cellular source of cardiac myofibroblasts in the post-inflammatory myocardium. We hypothesized that exogenous delivery of macrophage-colony-stimulating factor (M-CSF) can stimulate macrophage lineage differentiation of inflammatory progenitors and, therefore, prevent their naturally occurring myofibroblast fate in EAM. Methods and results EAM was induced in wild-type (BALB/c) and nitric oxide synthase 2-deficient (Nos2−/−) mice and CD133+ progenitors were isolated from inflamed hearts. In vitro, M-CSF converted inflammatory CD133+ progenitors into nitric oxide-producing F4/80+ macrophages and prevented transforming growth factor-β-mediated myofibroblast differentiation. Importantly, only a subset of heart-infiltrating CD133+ progenitors expresses macrophage-specific antigen F4/80 in EAM. These CD133+/F4/80hi cells show impaired myofibrogenic potential compared with CD133+/F4/80− cells. M-CSF treatment of wild-type mice with EAM at the peak of disease markedly increased CD133+/F4/80hi cells in the myocardium, and CD133+ progenitors isolated from M-CSF-treated mice failed to differentiate into myofibroblasts. In contrast, M-CSF was not effective in converting CD133+ progenitors from inflamed hearts of Nos2−/− mice into macrophages, and M-CSF treatment did not result in increased CD133+/F4/80hi cell population in hearts of Nos2−/− mice. Accordingly, M-CSF prevented post-inflammatory fibrosis and left ventricular dysfunction in wild-type but not in Nos2−/− mice. Conclusion Active and NOS2-dependent induction of macrophage lineage differentiation abrogates the myofibrogenic potential of heart-infiltrating CD133+ progenitors. Modulating the in vivo differentiation fate of specific progenitors might become a novel approach for the treatment of inflammatory heart disease

Local and systemic inflammation after implantation of a novel iron based porous degradable bone replacement material in sheep model

Despite the high potential of healthy bone to regenerate, the reconstruction of large bone defects remains a challenge. Due to the lack of mechanical stability of existing bone substitutes, recently developed degradable metallic alloys are an interesting alternative providing higher load-bearing capabilities. Degradable iron-based alloys therefore might be an attractive innovation. To test the suitability of a newly-designed iron-based alloy for such applications, an animal experiment was performed. Porous iron-based degradable implants with two different densities and a control group were tested. The implants were positioned in the proximal tibia of Merino sheep. Over a period of 6 and 12~months, blood and histological parameters were monitored for signs of inflammation and degradation. In the histological evaluation of the implants` environment we found degraded alloy particles, but no inflammatory reaction. Iron particles were also found within the popliteal lymph nodes on both sides. The serum blood levels of phosphorus, iron and ferritin in the long term groups were elevated. Other parameters did not show any changes. Iron-based degradable porous bone replacement implants showed a good biocompatibility in this experiment. For a clinical application, however, the rate of degradation would have to be significantly increased. Biocompatibility would then have to be re-evaluated

AC and Transient Magnetic Emissions of the JUICE Ganymede Laser Altimeter

We report here on qualification and calibration test results constraining the AC magnetic emissions of the JUICE Ganymede Laser Altimeter (GALA) in the frequency range from 0.1 Hz to 50 kHz. The GALA instrument is intended to be launched in 2023 onboard ESA's JUICE spacecraft. It shall map the planetary surfaces of the Jovian moons Europa, Callisto, and Ganymede. The highest AC magnetic emissions are generated at the pulse repetition frequency of 30 Hz and their harmonics by the pump diode laser current pulses with an amplitude of 200 A and a width of 50 to 60 µs and by the load currents of the capacitor reservoirs that drive these current pulses. Additional signatures arise from currents caused by software processes

Experimental observations and numerical modeling of lipid-shell microbubbles with calcium-adhering moieties for minimally-invasive treatment of urinary stones

A novel treatment modality incorporating calcium-adhering microbubbles has recently entered human clinical trials as a new minimally-invasive approach to treat urinary stones. In this treatment method, lipid-shell gas-core microbubbles can be introduced into the urinary tract through a catheter. Lipid moities with calcium-adherance properties incorporated into the lipid shell facilitate binding to stones. The microbubbles can be excited by an extracorporeal source of quasi-collimated ultrasound. Alternatively, the microbubbles can be excited by an intraluminal source, such as a fiber-optic laser. With either excitation technique, calcium-adhering microbubbles can significantly increase rates of erosion, pitting, and fragmentation of stones. We report here on new experiments using high-speed photography to characterize microbubble expansion and collapse. The bubble geometry observed in the experiments was used as one of the initial shapes for the numerical modeling. The modeling showed that the bubble dynamics strongly depends on bubble shape and stand-off distance. For the experimentally observed shape of microbubbles, the numerical modeling showed that the collapse of the microbubbles was associated with pressure increases of some two-to-three orders of magnitude compared to the excitation source pressures. This in-vitro study provides key insights into the use of microbubbles with calcium-adhering moieties in treatment of urinary stones

Investigating Dunedin whistlers using volcanic lightning

Whistlers detected at Dunedin, New Zealand are an anomaly: there is little lightning around Dunedin's conjugate point yet whistlers appear in relatively large numbers. These surplus whistlers have consequently inspired investigations into their origins. Dunedin's lightning-sparse conjugate point lies in the Aleutian Islands, a region populated with active volcanoes. Their presence has allowed us to perform a novel analysis: the correlation of whistlers to volcanic lightning. We report on our investigation, which successfully yielded the first observations of "volcanic whistlers." It was found that the single July 2008 Mount Okmok eruption had an impressive effect on the number of whistlers at Dunedin. The eruptions at Mount Redoubt in 2009 also caused a sporadic flow of whistlers in Dunedin

Exposure to ultrafine carbon particles at levels below detectable pulmonary inflammation affects cardiovascular performance in spontaneously hypertensive rats

<p>Abstract</p> <p>Background</p> <p>Exposure to particulate matter is a risk factor for cardiopulmonary disease but the underlying molecular mechanisms remain poorly understood. In the present study we sought to investigate the cardiopulmonary responses on spontaneously hypertensive rats (SHRs) following inhalation of UfCPs (24 h, 172 μg·m^-3), to assess whether compromised animals (SHR) exhibit a different response pattern compared to the previously studied healthy rats (WKY).</p> <p>Methods</p> <p>Cardiophysiological response in SHRs was analyzed using radiotelemetry. Blood pressure (BP) and its biomarkers plasma renin-angiotensin system were also assessed. Lung and cardiac mRNA expressions for markers of oxidative stress (hemeoxygenase-1), blood coagulation (tissue factor, plasminogen activator inhibitor-1), and endothelial function (endothelin-1, and endothelin receptors A and B) were analyzed following UfCPs exposure in SHRs. UfCPs-mediated inflammatory responses were assessed from broncho-alveolar-lavage fluid (BALF).</p> <p>Results</p> <p>Increased BP and heart rate (HR) by about 5% with a lag of 1–3 days were detected in UfCPs exposed SHRs. Inflammatory markers of BALF, lung (pulmonary) and blood (systemic) were not affected. However, mRNA expression of hemeoxygenase-1, endothelin-1, endothelin receptors A and B, tissue factor, and plasminogen activator inhibitor showed a significant induction (~2.5-fold; p < 0.05) with endothelin 1 being the maximally induced factor (6-fold; p < 0.05) on the third recovery day in the lungs of UfCPs exposed SHRs; while all of these factors – except hemeoxygenase-1 – were not affected in cardiac tissues. Strikingly, the UfCPs-mediated altered BP is paralleled by the induction of renin-angiotensin system in plasma.</p> <p>Conclusion</p> <p>Our finding shows that UfCPs exposure at levels which does not induce detectable pulmonary neutrophilic inflammation, triggers distinct effects in the lung and also at the systemic level in compromised SHRs. These effects are characterized by increased activity of plasma renin-angiotensin system and circulating white blood cells together with moderate increases in the BP, HR and decreases in heart rate variability. This systemic effect is associated with pulmonary, but not cardiac, mRNA induction of biomarkers reflective of oxidative stress; activation of vasoconstriction, stimulation of blood coagulation factors, and inhibition of fibrinolysis. Thus, UfCPs may cause cardiovascular and pulmonary impairment, in the absence of detectable pulmonary inflammation, in individuals suffering from preexisting cardiovascular diseases.</p