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The current sensorless vector-controlled permanent-magnet synchronous motor (PMSM) drive using a single sensor (i.e., speed sensor) is presented in this work. The current sensors are removed, and the estimated currents are used to close the current loop to minimize the drive cost and make it fault-tolerant against current sensor failure. A classical vector-control PMSM drive requires at least three sensors, i.e., two current sensors and one speed/position sensor. This paper presents a new current estimation technique that is free from inverter switching states, an integrator, and differentiator terms. The drive is suitable for retrofit applications, as it does not require any additional hardware. The reference voltages (vds and vqs) are used to estimate the rotor reference frame currents (i.e., iqs and ids). The presented algorithm depends on the stator resistance (Ɍs). The online Ɍs estimation algorithm is used for compensation to overcome the effect of the Ɍs on the estimated currents. The sensitivity analysis for the currents against the speed is verified and presented. The speed loop is closed with actual speed information, which will try to maintain the reference speed under any circumstances. The proposed current sensorless PMSM drive was validated using MATLAB/Simulink and also verified on a hardware prototype. The presented technique was verified for various operation conditions, and some of the extensive results are presented.

Entomopathogenic nematodes (EPNs) have been a useful model for studying wound healing in insects due to their natural mechanism of entering an insect host either through the cuticle or an orifice. While many experiments have shed light on nematode and host behavior, as well as the host immune response, details regarding early nematode entry and proliferative events have been limited. Using high-resolution microscopy, we provide data on the early infection kinetics of Heterorhabditis bacteriophora and its symbiotic bacteria, Photorhabdus luminescens. EPNs appendage themselves to the host and enter through the host cuticle with a drill-like mechanism while leaving their outer sheath behind. EPNs immediately release their symbiotic bacteria in the host which leads to changes in host behavior and septicemia within 6 h while EPNs travel through the host in a predictable manner, congregating in the anterior end of the host. This paper sheds light on the entry and proliferative events of EPN infection, which will further aid in our understanding of wound healing and host immune activation at a high spatiotemporal resolution.

Several insect innate immune mechanisms are activated in response to infection by entomopathogenic nematodes (EPNs). In this review, we focus on the coagulation of hemolymph, which acts to stop bleeding after injury and prevent access of pathogens to the body cavity. After providing a general overview of invertebrate coagulation systems, we discuss recent findings in Drosophila melanogaster which demonstrate that clots protect against EPN infections. Detailed analysis at the cellular level provided insight into the kinetics of the secretion of Drosophila coagulation factors, including non-classical modes of secretion. Roughly, clot formation can be divided into a primary phase in which crosslinking of clot components depends on the activity of Drosophila transglutaminase and a secondary, phenoloxidase (PO)-dependent phase, characterized by further hardening and melanization of the clot matrix. These two phases appear to play distinct roles in two commonly used EPN infection models, namely Heterorhabditis bacteriophora and Steinernema carpocapsae. Finally, we discuss the implications of the coevolution between parasites such as EPNs and their hosts for the dynamics of coagulation factor evolution.

Roof fall is one of the major problems of the bord and pillar coal mines during the depillaring phase. Roof fall not only causes considerable damage to the mining equipment but also to the miners. To keep in view, development of software is essential for the calculation of roof fall risk to reduce the accidents to a certain extent. In this paper, the software has been developed and tested on seam-2, the main panel of RK-5 underground coal mine, Singareni Collieries Company Limited, India and corresponding roof fall risk was calculated. The best combination of the parameters causing roof fall risk was evaluated to reduce the risk.

A personal narrative is presented which explores the author's experience of feeling anxious and helpless when her father was brought in the emergency care.

Zinc (Zn) is an essential trace element; it serves as a cofactor for a great number of enzymes, transcription factors, receptors, and other proteins. Zinc is also an important signaling molecule, which can be released from intracellular stores into the cytosol or extracellular space, for example, during synaptic transmission. Amongst cellular effects of zinc is activation of Kv7 (KCNQ, M-type) voltage-gated potassium channels. Here, we investigated relationships between Kv7 channel inhibition by Ca2+/calmodulin (CaM) and zinc-mediated potentiation. We show that Zn2+ ionophore, zinc pyrithione (ZnPy), can prevent or reverse Ca2+/CaM-mediated inhibition of Kv7.2. In the presence of both Ca2+ and Zn2+, the Kv7.2 channels lose most of their voltage dependence and lock in an open state. In addition, we demonstrate that mutations that interfere with CaM binding to Kv7.2 and Kv7.3 reduced channel membrane abundance and activity, but these mutants retained zinc sensitivity. Moreover, the relative efficacy of ZnPy to activate these mutants was generally greater, compared with the WT channels. Finally, we show that zinc sensitivity was retained in Kv7.2 channels assembled with mutant CaM with all four EF hands disabled, suggesting that it is unlikely to be mediated by CaM. Taken together, our findings indicate that zinc is a potent Kv7 stabilizer, which may protect these channels from physiological inhibitory effects of neurotransmitters and neuromodulators, protecting neurons from overactivity. [ABSTRACT FROM AUTHOR]