Recent studies have shown a correlation between elevated interleukin 6 (IL-6) concentrations and the risk of respiratory failure in COVID-19 patients. Therefore, detection of IL-6 at low concentrations permits early diagnosis of worstcase outcome in viral respiratory infections. Here, a versatile biointerface is presented that eliminates nonspecific adhesion and thus enables immunofluorescence detection of IL-6 in whole human plasma or whole human blood during coagulation, down to a limit of detection of 0.5 pg mL −1. The sensitivity of the developed lubricant-infused biosensor for immunofluorescence assays in detecting low molecular weight proteins such as IL-6 is facilitated by i) producing a bioink in which the capture antibody is functionalized by an epoxy-based silane for covalent linkage to the fluorosilanized surface and ii) suppressing nonspecific adhesion by patterning the developed bioink into a lubricant-infused coating. The developed biosensor addresses one of the major challenges for biosensing in complex fluids, namely nonspecific adhesion, therefore paving the way for highly sensitive biosensing in complex fluids. where significantly elevated levels indicate aggressive tumor growth or viral load and poor prognosis in patients. [2,10] Additionally, IL-6 is an important anti-inflammatory cytokine that induces acute responses in chronic inflammatory pathologies. As such, there has been an increasing interest in the use of IL-6 as a biomarker for the diagnosis of early stages of viral infections, cancer, and chronic inflammation. [9-11] A practical IL-6 biosensor should provide a low limit of detection (LOD) (≤5 pg mL −1) and acceptable linear dynamic range (1-100 pg mL −1) in complex fluids, in addition to accuracy, facile operation, and amenable to mass production. [11,12] There are a large number of different IL-6 detection techniques that have been reported in the literature including electrochemical sensors, [13-22] surface plasmon resonance (SPR), [23-25] chemiluminescence immunoassay (CLIA), [26-29] and immunofluorescence assays (IFA), [30-33] Utilizing 0-and 1-D materials such as carbon nanotubes (CNTs), [14,16] nanoparticles and nanowires, [13,19] as well as porous nanoparticles, [15] optical fibers, [32] and microfluidic platforms, [28] have enabled higher sensitivity in IL-6 detection and to date, electrochemical methods have proven to be the most promising candidate for detection of IL-6 at very low concentrations (0.33 pg mL −1 in buffer) with a wide linear dynamic range. [22] While reported IL-6 biosensors have demonstrated satisfactory LODs in buffer or processed serum, their performance in human whole plasma declines significantly, leading to higher LOD's and/or false positive results. In electrochemical sensors, for example, the nonspecific attachment of biological entities in plasma or blood can interfere with the resistivity at the electrodes thereby deteriorating their sensitivity for detection of IL-6 at clinically relevant concentrations. [34] So far, the lowest theoretical LOD fo...

Rapid advances in sensor technologies have facilitated the development of high-performance electronic noses that can detect and discriminate volatile compounds in situ. The research and development of electronic noses has resulted in a new qualitative and semi-quantitative detection approach in the field of clinical diagnostics. Electronic noses have a clear potential to be a non-invasive, simple and rapid but above all accurate early diagnostic screening tool. This review collates existing knowledge of recent advances in electronic nose technologies and applications.

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The hepatic hormone hepcidin is the master regulator of systemic iron homeostasis. Its expression level is adjusted to alterations in iron levels, inflammatory cues, and iron requirements for erythropoiesis. Bone morphogenetic protein 6 (BMP6) contributes to the iron-dependent control of hepcidin. In addition, TGF-␤1 may stimulate hepcidin mRNA expression in murine hepatocytes and human leukocytes. However, receptors and downstream signaling proteins involved in TGF-␤1-induced hepcidin expression are still unclear. Here we show that TGF-␤1 treatment of mouse and human hepatocytes, as well as ectopic expression of TGF-␤1 in mice, increases hepcidin mRNA levels. The hepcidin response to TGF-␤1 depends on functional TGF-␤1 type I receptor (ALK5) and TGF-␤1 type II receptor (T␤RII) and is mediated by a noncanonical mechanism that involves Smad1/5/8 phosphorylation. Interestingly, increasing availability of canonical Smad2/3 decreases TGF-␤1-induced hepcidin regulation, whereas the BMP6-hepcidin signal was enhanced, indicating a signaling component stoichiometry-dependent cross-talk between the two pathways. Although ALK2/ 3-dependent hepcidin activation by BMP6 can be modulated by each of the three hemochromatosis-associated proteins: HJV (hemojuvelin), HFE (hemochromatosis protein), and TfR2 (transferrin receptor 2), these proteins do not control the ALK5-mediated hepcidin response to TGF-␤1. TGF-␤1 mRNA levels are increased in mouse models of iron overload, indicating that TGF-␤1 may contribute to hepcidin synthesis under these conditions. In conclusion, these data demonstrate that a complex regulatory network involving TGF-␤1 and BMP6 may control the sensing of systemic and/or hepatic iron levels.