23 research outputs found
Recommended from our members
Interior Permanent Magnet Reluctance Machine with Brushless Field Excitation
In a conventional permanent magnet (PM) machine, the air-gap flux produced by the PM is fixed. It is difficult to enhance the air-gap flux density due to limitations of the PM in a series-magnetic circuit. However, the air-gap flux density can be weakened by using power electronic field weakening to the limit of demagnetization of the PMs. This paper presents the test results of controlling the PM air-gap flux density through the use of a stationary brushless excitation coil in a reluctance interior permanent magnet with brushless field excitation (RIPM-BFE) motor. Through the use of this technology the air-gap flux density can be either enhanced or weakened. There is no concern with demagnetizing the PMs during field weakening. The leakage flux of the excitation coil through the PMs is blocked. The prototype motor built on this principle confirms the concept of flux enhancement and weakening through the use of excitation coils
Recommended from our members
Report on Toyota/Prius Motor Torque Capability, Torque Property, No-Load Back EMF, and Mechanical Losses, Revised May 2007
In today's hybrid vehicle market, the Toyota/Prius drive system is currently considered the leader in electrical, mechanical, and manufacturing innovations. It is significant that in today's marketplace, Toyota is able to manufacture and sell the vehicle for a profit. This project's objective is to test the torque capability of the 2004 Prius motor and to analyze the torque properties relating to the rotor structure. The tested values of no-load back electromotive force (emf) and mechanical losses are also presented
Lichenometric dating (lichenometry) and the biology of the lichen genus rhizocarpon:challenges and future directions
Lichenometric dating (lichenometry) involves the use of lichen measurements to estimate the age of exposure of various substrata. Because of low radial growth rates and considerable longevity, species of the crustose lichen genus Rhizocarpon have been the most useful in lichenometry. The primary assumption of lichenometry is that colonization, growth and mortality of Rhizocarpon are similar on surfaces of known and unknown age so that the largest thalli present on the respective faces are of comparable age. This review describes the current state of knowledge regarding the biology of Rhizocarpon and considers two main questions: (1) to what extent does existing knowledge support this assumption; and (2) what further biological observations would be useful both to test its validity and to improve the accuracy of lichenometric dates? A review of the Rhizocarpon literature identified gaps in knowledge regarding early development, the growth rate/size curve, mortality, regeneration, competitive effects, colonization, and succession on rock surfaces. The data suggest that these processes may not be comparable on different rock surfaces, especially in regions where growth rates and thallus turnover are high. In addition, several variables could differ between rock surfaces and influence maximum thallus size, including rate and timing of colonization, radial growth rates, environmental differences, thallus fusion, allelopathy, thallus mortality, colonization and competition. Comparative measurements of these variables on surfaces of known and unknown age may help to determine whether the basic assumptions of lichenometry are valid. Ultimately, it may be possible to take these differences into account when interpreting estimated dates
Whole-genome sequencing reveals host factors underlying critical COVID-19
Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease