Staff member

Metal Oxide (MOX) gas sensors rely on chemical reactions that occur efficiently at high temperatures, resulting in too-demanding power requirements for certain applications. Operating the sensor under a Pulsed-Temperature Operation (PTO), by which the sensor heater is switched ON and OFF periodically, is a common practice to reduce the power consumption. However, the sensor performance is degraded as the OFF periods become larger. Other research works studied, generally, PTO schemes applying waveforms to the heater with time periods of seconds and duty cycles above 20%. Here, instead, we explore the behaviour of PTO sensors working under aggressive schemes, reaching power savings of 99% and beyond with respect to continuous heater stimulation. Using sensor sensitivity and the limit of detection, we evaluated four Ultra Low Power (ULP) sensors under different PTO schemes exposed to ammonia, ethylene, and acetaldehyde. Results show that it is possible to operate the sensors with total power consumption in the range of microwatts. Despite the aggressive power reduction, sensor sensitivity suffers only a moderate decline and the limit of detection may degrade up to a factor five. This is, however, gas-dependent and should be explored on a case-by-case basis since, for example, the same degradation has not been observed for ammonia. Finally, the run-in time, i.e., the time required to get a stable response immediately after switching on the sensor, increases when reducing the power consumption, from 10 minutes to values in the range of 10–20 hours for power consumptions smaller than 200 microwatts.

JTD Keywords: Robot sensing systems, Temperature sensors, Heating systems, Gas detectors, Power demand, Sensitivity, Electronic nose, gas sensors, low-power operation, machine olfaction, pulsed-temperature operation, temperature modulation

Background: Patients with acutely decompensated cirrhosis (AD) may or may not develop acute-on-chronic liver failure (ACLF). ACLF is characterized by high-grade systemic inflammation, organ failures (OF) and high short-term mortality. Although patients with AD cirrhosis exhibit distinct clinical phenotypes at baseline, they have low short-term mortality, unless ACLF develops during follow-up. Because little is known about the association of profile of systemic inflammation with clinical phenotypes of patients with AD cirrhosis, we aimed to investigate a battery of markers of systemic inflammation in these patients. Methods: Upon hospital admission baseline plasma levels of 15 markers (cytokines, chemokines, and oxidized albumin) were measured in 40 healthy controls, 39 compensated cirrhosis, 342 AD cirrhosis, and 161 ACLF. According to EASL-CLIF criteria, AD cirrhosis was divided into three distinct clinical phenotypes (AD-1: Creatinine<1.5, no HE, no OF; AD-2: creatinine 1.5–2, and or HE grade I/II, no OF; AD-3: Creatinine<1.5, no HE, non-renal OF). Results: Most markers were slightly abnormal in compensated cirrhosis, but markedly increased in AD. Patients with ACLF exhibited the largest number of abnormal markers, indicating “full-blown” systemic inflammation (all markers). AD-patients exhibited distinct systemic inflammation profiles across three different clinical phenotypes. In each phenotype, activation of systemic inflammation was only partial (30% of the markers). Mortality related to each clinical AD-phenotype was significantly lower than mortality associated with ACLF (p < 0.0001 by gray test). Among AD-patients baseline systemic inflammation (especially IL-8, IL-6, IL-1ra, HNA2 independently associated) was more intense in those who had poor 28-day outcomes (ACLF, death) than those who did not experience these outcomes. Conclusions: Although AD-patients exhibit distinct profiles of systemic inflammation depending on their clinical phenotypes, all these patients have only partial activation of systemic inflammation. However, those with the most extended baseline systemic inflammation had the highest the risk of ACLF development and death.

JTD Keywords: ACLF, Acute decompensation, Cirrhosis, Organ dysfunction, Organ failure, Signature

Lateral segregation of cell membranes is accepted as a primary mechanism for cells to regulate a diversity of cellular functions. In this context, lipid rafts have been conceptualized as organizing principle of biological membranes where underlying cholesterol-mediated selective connectivity must exist even at the resting state. However, such a level of nanoscale compositional connectivity has been challenging to prove. Here we used single-molecule near-field scanning optical microscopy to visualize the nanolandscape of raft ganglioside GM1 after tightening by its ligand cholera toxin (CTxB) on intact cell membranes. We show that CTxB tightening of GM1 is sufficient to initiate a minimal raft coalescence unit, resulting in the formation of cholesterol-dependent GM1 nanodomains <120 nm in size. This particular arrangement appeared independent of cell type and GM1 expression level on the membrane. Simultaneous dual color high-resolution images revealed that GPI anchored and certain transmembrane proteins were recruited to regions proximal (<150 nm) to CTxB-GM1 nanodomains without physical intermixing. Together with in silico experiments, our high-resolution data conclusively demonstrate the existence of raft-based interconnectivity at the nanoscale. Such a linked state on resting cell membranes constitutes thus an obligatory step toward the hierarchical evolution of large-scale raft coalescence upon cell activation.

JTD Keywords: Cholera toxin, Membrane heterogeneity, Near-field scanning optical microscopy, Raft ganglioside GM1, Single-molecule detection