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Changes in extracellular potassium ([K + ] e ) modulate neuronal networks via changes in membrane potential, voltage-gated channel activity, and alteration to transmission at the synapse. Given the limited extracellular space in the central nervous system, potassium clearance is crucial. As activity-induced potassium transients are rapidly managed by astrocytic Kir4.1 and astrocyte-specific Na + /K + -ATPase, any neurotransmitter/neuromodulator that can regulate their function may have indirect influence on network activity. Neuromodulators differentially affect cortical/thalamic networks to align sensory processing with differing behavioral states. Given serotonin (5HT), norepinephrine (NE), and acetylcholine (ACh) differentially affect spike frequency adaptation and signal fidelity ("signal-to-noise") in somatosensory cortex, we hypothesize that [K + ] e may be differentially regulated by the different neuromodulators to exert their individual effects on network function. This study aimed to compare effects of individually applied 5HT, NE, and ACh on regulating [K + ] e in connection to effects on cortical-evoked response amplitude and adaptation in male mice. Using extracellular field and K + ion-selective recordings of somatosensory stimulation, we found that differential effects of 5HT, NE, and ACh on [K + ] e regulation mirrored differential effects on amplitude and adaptation. 5HT effects on transient K + recovery, adaptation, and field post-synaptic potential amplitude were disrupted by barium (200 µM), whereas NE and ACh effects were disrupted by ouabain (1 µM) or iodoacetate (100 µM). Considering the impact [K + ] e can have on many network functions; it seems highly efficient that neuromodulators regulate [K + ] e to exert their many effects. This study provides functional significance for astrocyte-mediated buffering of [K + ] e in neuromodulator-mediated shaping of cortical network activity., (© 2020 Wiley Periodicals, Inc.)

Piston gauges or pressure balances are important primary standards for the realization of the SI unit of pressure, the pascal. Because of their long-term stability, they are also used as secondary or working standards in the dissemination of the pressure scale. The National Institute of Standards and Technology (NIST) operates and maintains a calibration service for these devices, and has recently undertaken a modernization effort. Following a preliminary investigation into the feasibility of using transducers as instantaneous in-situ transfer standards, we now present the results of a near fully automated calibration system. This effort includes the design, building, and validation of an automated gas-handling manifold, and the development of a new software suite. The new system demonstrates an expanded uncertainty on the order of 1 in 10 5 , comparable to the traditional system, but offers a five-fold decrease in calibration turnaround time.

Background: Cigarette smoking (CS) is the main risk factor for the development of chronic obstructive pulmonary disease (COPD) and most COPD exacerbations are caused by respiratory infections including influenza. Influenza infections are more severe in smokers. The mechanism of the increased risk and severity of infections in smokers is likely multifactorial, but certainly includes changes in immunologic host defenses., Methods: We investigated retinoic acid-inducible protein I (RIG-I) and interferon (IFN) induction by influenza A virus (IAV) in human bronchial epithelial cells (HBEC) isolated from smokers or nonsmokers. Subcultured HBEC cells were infected with A/Puerto Rico/8/1934 (PR8) IAV at an MOI of 1. After 24 h of infection, cells and supernatants were collected for qRT-PCR, immunoblot or ELISA to determine RIG-I, Toll-like receptor3 (TLR3) and IFN expression levels., Results: IAV exposure induced a vigorous IFN-β, IFN-λ 1 and IFN-λ 2/3 antiviral response in HBEC from nonsmokers and significant induction of RIG-I and TLR3. In cells from smokers, viral RIG-I and TLR3 mRNA induction was reduced 87 and 79 % compared to the response from nonsmokers. CS exposure history was associated with inhibition of viral induction of the IFN-β, IFN-λ1 and IFN-λ 2/3 mRNA response by 85, 96 and 95 %, respectively, from that seen in HBEC from nonsmokers. The demethylating agent 5-Aza-2-deoxycytidine reversed the immunosuppressive effects of CS exposure in HBEC since viral induction of all three IFNs was restored. IFN-β induction of RIG-I and TLR3 was also suppressed in the cells from smokers., Conclusion: Our results suggest that active smoking reduces expression of antiviral cytokines in primary HBEC cells. This effect likely occurs via downregulation of RIG-I and TLR3 due to smoke-induced epigenetic modifications. Reduction in lung epithelial cell RIG-I and TLR3 responses may be a major mechanism contributing to the increased risk and severity of viral respiratory infections in smokers and to viral-mediated acute exacerbations of COPD.

Clinical, pathological, and necropsy findings are recorded from two cases of endocarditis due to Erysipelothrix insidiosa, one in a 53-year-old grocer and the other in a 56-year-old housewife. The possible sources of infection are suggested.