Proteus 3 Phase Spd

[Prisc Chandola]

Iam looking to design a driver circuit that can run 33v AC induction motor through 48V Battery for Electric Vehicle.The motor tag is attached. I have seen 33v AC induction for the first time.

I was able to design 3 phase half bridge driver on proteus but as proteus does not have induction motor I can not test it. Also, I dont have much experience in power electronics. Can anybody guide me how I can control the speed and direction of this motor using Arduino ?

Your circuit looks interesting however I cannot read it nor determine what parts you used. It appears you use N channel devices for both upper and lower FETs. This causes me to assume the driver chip has a charge pump to drive the gate of the upper FET or a higher voltage supply. I would suggest you spend some time understanding 3 phase circuits and how they work. This link will help you get started. How a Three-Phase Motor Works Sciencing

You should be able to model a 3ph motor in proteus, it will be a combination of resistors and inductors basically.

The cosO of 0.86 should help.

Tom...

PS, The resolution of the circuit diagram is not high enough to read component labels. Did you export the diagram as a jpg or did you screen grab?

Yes I am aware that PWM is modulated to produce a current/voltage that is sinusoidal due to the motor impedance, but does the OP know that.

Think a UNO would be pushing to do this job in modulated PWM form.

Hi all! There's here a note about the implementation of a V/f control for an induction motor. You may want to use the attached simulation model to see how it works: V/f control of an induction machine - imperix power electronics

Hope it helps!

Matt

The site is secure.

The ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

In concert with the development of novel beta-lactams and broad-spectrum cephalosporins, bacterially encoded beta-lactamases have evolved to accommodate the new agents. This study was designed to identify, at the sequence level, the genes responsible for the extended-spectrum-beta-lactamase (ESBL) phenotypes of Escherichia coli, Klebsiella pneumoniae, and Proteus mirabilis isolates collected during the global tigecycline phase 3 clinical trials. PCR assays were developed to identify and clone the bla(TEM), bla(SHV), bla(OXA), and bla(CTX) genes from clinical strains. Isolates were also screened for AmpC genes of the bla(CMY), bla(ACT), bla(FOX), and bla(DHA) families as well as the bla(KPC) genes encoding class A carbapenemases. E. coli, K. pneumoniae, and P. mirabilis isolates with ceftazidime MICs of > or =2 microg/ml were designated possible ESBL-producing pathogens and were then subjected to a confirmatory test for ESBLs by use of Etest. Of 272 unique patient isolates, 239 were confirmed by PCR and sequencing to carry the genes for at least one ESBL, with 44% of the positive isolates harboring the genes for multiple ESBLs. In agreement with current trends for ESBL distribution, bla(CTX-M)-type beta-lactamase genes were found in 83% and 71% of the ESBL-positive E. coli and K. pneumoniae isolates, respectively, whereas bla(SHV) genes were found in 41% and 28% of the ESBL-positive K. pneumoniae and E. coli isolates, respectively. Ninety-seven percent of the E. coli and K. pneumoniae isolates were tigecycline susceptible (MIC(90) = 2 microg/ml), warranting further studies to define the therapeutic utility of tigecycline against strains producing ESBLs in a clinical setting.

SUMMARY: Three phases of Proteus vulgaris, A, B and C, are distinguishable by cellular and colonial morphology, and to some extent serologically. Phase A is the modal form of freshly-isolated strains; it has a uniform bacillary morphology, swarms intermittently on nutrient agar, and forms stable suspensions in 085% saline. Phase B strains, though possessing flagella, are usually non-motile, non-swarming, and highly pleomorphie; usually form unstable suspensions. Phase C strains are uniformly filamentous, motile, often swarm in a continuous film, and stability in saline varies with the strain.

The somatic surface of phase A strains is characterized by a dominant type-specific antigen, and traces of a non-specific and a possibly strain-specific antigen. In phase B strains the type-specific antigen is largely lost, and the other two antigens dominate the surface. The antigenic surface of phase C strains does not differ markedly from that of phase A.

Browse Microbiology's dedicated article collection exploring competitive mechanisms bacteria use to thrive in their niches, including the molecular characterization of toxins or secretion systems and the investigation of interbacterial competition at the organismal level.

MR/P fimbriae of uropathogenic Proteus mirabilis undergo invertible element-mediated phase variation whereby an individual bacterium switches between expressing fimbriae (phase ON) and not expressing fimbriae (phase OFF). Under different conditions, the percentage of fimbriate bacteria within a population varies and could be dictated by either selection (growth advantage of one phase) or signaling (preferentially converting one phase to the other in response to external signals). Expression of MR/P fimbriae increases in a cell-density dependent manner in vitro and in vivo. However, rather than the increased cell density itself, this increase in fimbrial expression is due to an enrichment of fimbriate bacteria under oxygen limitation resulting from increased cell density. Our data also indicate that the persistence of MR/P fimbriate bacteria under oxygen-limiting conditions is a result of both selection (of MR/P fimbrial phase variants) and signaling (via modulation of expression of the MrpI recombinase). Furthermore, the mrpJ transcriptional regulator encoded within the mrp operon contributes to phase switching. Type 1 fimbriae of Escherichia coli, which are likewise subject to phase variation via an invertible element, also increase in expression during reduced oxygenation. These findings provide evidence to support a mechanism for persistence of fimbriate bacteria under oxygen limitation, which is relevant to disease progression within the oxygen-restricted urinary tract.

I'm simulating a basic low-pass RC filter in Proteus, and I need to find the phase shift of the output at varying frequencies. I've plotted a frequency response graph which shows the phase against frequency, but it doesn't show specific values. I can get rough values by just looking at the graph, but I need a precise answer.Can anyone show me a way to actually calculate the phase shift of the output? (Using Proteus, MATLAB, or just a calculation if possible)

Edit: I've tried a couple of calculations that I've seen while researching this, but I believe that the phase should be 0 at 10Hz, and neither calculation gives me that.I tried: arctan(fRC) and -arctan(f/20)

If this is a theoretical exercise you can get precise values from the simulation, or from mathematical theory. For example, take the values used to generate that plot, and curve-fit or interpolate them.

But if you intend to actually build the thing, you'll have to use real components, with real tolerances, and the actual phase shift will be consequent on them, however accurately you calculated the theoretical value.

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

Catheter-associated urinary tract infections (CAUTIs) are the most common health care-associated infections worldwide and are frequently polymicrobial. Proteus mirabilis is one of the leading causes of CAUTIs and is the most commonly isolated species from polymicrobial CAUTIs. Few studies have focused on polymicrobial interactions during UTIs, but there is evidence that P. mirabilis can significantly affect the ability of other species to establish a UTI and that other species modulate P. mirabilis pathogenicity.

P. mirabilis is exquisitely committed to survival within the host urinary tract, as this species has the greatest number of distinct fimbrial types of any sequenced organism, possesses the ability to generate and utilize an abundant nitrogen source in a nitrogen-limited environment, encodes at least 21 putative systems for iron acquisition in an iron-limited environment and produces an immunoglobulin A protease to evade the host humoral immune response.

To reach the urinary tract, P. mirabilis uses swarming motility to migrate across the catheter surface. This unique type of motility also facilitates migration of non-motile species colonizing the catheter.

Regulation of swarm cell differentiation and swarming motility is highly complex and involves the integration of several signals, including the presence of a surface, cell membrane integrity and composition, nutritional status and the presence or absence of specific amino acids. In addition to these signals, conditions that favour the expression of any of 14 distinct fimbriae for adherence cause a reciprocal decrease in the expression of flagella to reduce motility.

The urease of P. mirabilis promotes polymicrobial infection and bacterial persistence within the urinary tract. Crystalline biofilms and urinary stones that are formed as a result of urease activity facilitate bacterial entry to the urinary tract by obstructing urine flow and may also provide protection from the host immune respons, as well as from antimicrobial agents. The ammonia produced by the action of urease also has the potential to enhance the persistence of some bacterial species, whereas the resulting increase in pH has a detrimental effect on the persistence of other species.

3a8082e126