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ValentinkaMS [17]
3 years ago
15

A moving object has a kinetic energy of 150J and a momentum of 20.3kgxm/s find the speed of the object in m/s

Physics
1 answer:
Irina-Kira [14]3 years ago
5 0

Answer:

v = 14.78m/s

Explanation:

Given

KE = 150J

p = 20.3kgm/s

Required

Determine the object's speed

Kinetic Energy is calculated as:

KE = \frac{1}{2}mv^2

Make m the subject

m = \frac{2KE}{v^2}

Momentum is calculated as:

p = mv

Make m the subject

m = \frac{p}{v}

So, we have:

m = \frac{p}{v} and m = \frac{2KE}{v^2}

Equate both expressions: m = m

\frac{2KE}{v^2} = \frac{p}{v}

Multiply both sides by v

v *  \frac{2KE}{v^2} = \frac{p}{v}*v

\frac{2KE}{v} = p

Make v the subject

v = \frac{2KE}{p}

Substitute KE = 150J and p = 20.3kgm/s

v = \frac{2 * 150}{20.3}

v = \frac{300}{20.3}

v = 14.78m/s

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Explanation:

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Gut microbiota vary greatly amongst laboratory animals, and these differences result in notable differences in experimental results. Mice of the same strain from different vendors have different microbiota profiles (17), and similarly, the same mice housed at different institutions have different microbiota profiles (18, 19). Conversely, inoculating two different inbred mouse strains with the same gut bacteria leads to differences in host gene expression between the two mouse strains (20). Clearly, there is a complex interplay between the genetics of the microbiota and that of the host organism, which has only recently begun to be appreciated.

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Examples in the literature have highlighted the important and unexpected ways in which gut microbiota can affect a variety of experimental parameters. In a series of studies, Vijay-Kumar et al. (13, 21) reported that although TLR5 null animals initially had a colitis phenotype, when these mice were “rederived” and their gut microbiota altered, the colitis phenotype was greatly attenuated, and instead the null animals exhibited metabolic syndrome. In addition, Lathrop et al. put forward a model by which T-cells are educated not only by self/non-self mechanisms, but also by microbiota-derived “non-self” antigens (22). Accordingly, they found that the presence or absence of microbiota determined whether T cells would induce colitis in mice. Finally, Yang et al. reported that when the same knockout mice were housed at two different institutions, they had markedly different microbiota profiles – and the mice at one institution (MIT) were quite susceptible to colitis, whereas mice at the other institution (MHH) failed to develop any significant pathology under the same conditions (19). Unequivocally, altering gut microbiota – even by housing animals at different institutions – can have dramatic effects on the phenotype observed.

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f =800N

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