Assertion (A): A line of length slightly more than and open circuited at far end is equivalent to an inductive reactance.Reason (R): A line of length slightly more than and short circuited at far end behaves as a capacitive reactance.p> ?->(Show Answer!)

1. Assertion (A): A line of length slightly more than and open circuited at far end is equivalent to an inductive reactance.Reason (R): A line of length slightly more than and short circuited at far end behaves as a capacitive reactance.

Write Comment

Comments

Tags

Show Similar Question And Answers

QA->The impedance in an LCR circuit in which the inductive reactance is equal to the cacacitive reactance:....

QA->A program Graph has ‘start’ and ‘end’ nodes. The total number of paths from start to end is equivalent to the -----------set of test data required to test the software.....

QA->Extreme of old age when a man behaves like a fool....

QA->A is taller than B; B is taller than C; D is taller than E and E is taller than B. Who is the shortest?....

QA->Reboring of an engine cylinder to the next oversize would slightly....

MCQ->Assertion (A): A line of length slightly more than and open circuited at far end is equivalent to an inductive reactance.Reason (R): A line of length slightly more than and short circuited at far end behaves as a capacitive reactance.

....

MCQ->Assertion (A): A line of length and short circuited at far end has an input impedance of infinity.Reason (R): A line of length and short circuited at far end behaves as a parallel resonant circuit.

....

MCQ-> Cells are the ultimate multi-taskers: they can switch on genes and carry out their orders, talk to each other, divide in two, and much more, all at the same time. But they couldn’t do any of these tricks without a power source to generate movement. The inside of a cell bustles with more traffic than Delhi roads, and, like all vehicles, the cell’s moving parts need engines. Physicists and biologists have looked ‘under the hood’ of the cell and laid out the nuts and bolts of molecular engines.The ability of such engines to convert chemical energy into motion is the envy nanotechnology researchers looking for ways to power molecule-sized devices. Medical researchers also want to understand how these engines work. Because these molecules are essential for cell division, scientists hope to shut down the rampant growth of cancer cells by deactivating certain motors. Improving motor-driven transport in nerve cells may also be helpful for treating diseases such as Alzheimer’s, Parkinson’s or ALS, also known as Lou Gehrig’s disease.We wouldn’t make it far in life without motor proteins. Our muscles wouldn’t contract. We couldn’t grow, because the growth process requires cells to duplicate their machinery and pull the copies apart. And our genes would be silent without the services of messenger RNA, which carries genetic instructions over to the cell’s protein-making factories. The movements that make these cellular activities possible occur along a complex network of threadlike fibers, or polymers, along which bundles of molecules travel like trams. The engines that power the cell’s freight are three families of proteins, called myosin, kinesin and dynein. For fuel, these proteins burn molecules of ATP, which cells make when they break down the carbohydrates and fats from the foods we eat. The energy from burning ATP causes changes in the proteins’ shape that allow them to heave themselves along the polymer track. The results are impressive: In one second, these molecules can travel between 50 and 100 times their own diameter. If a car with a five-foot-wide engine were as efficient, it would travel 170 to 340 kilometres per hour.Ronald Vale, a researcher at the Howard Hughes Medical Institute and the University of California at San Francisco, and Ronald Milligan of the Scripps Research Institute have realized a long-awaited goal by reconstructing the process by which myosin and kinesin move, almost down to the atom. The dynein motor, on the other hand, is still poorly understood. Myosin molecules, best known for their role in muscle contraction, form chains that lie between filaments of another protein called actin. Each myosin molecule has a tiny head that pokes out from the chain like oars from a canoe. Just as rowers propel their boat by stroking their oars through the water, the myosin molecules stick their heads into the actin and hoist themselves forward along the filament. While myosin moves along in short strokes, its cousin kinesin walks steadily along a different type of filament called a microtubule. Instead of using a projecting head as a lever, kinesin walks on two ‘legs’. Based on these differences, researchers used to think that myosin and kinesin were virtually unrelated. But newly discovered similarities in the motors’ ATP-processing machinery now suggest that they share a common ancestor — molecule. At this point, scientists can only speculate as to what type of primitive cell-like structure this ancestor occupied as it learned to burn ATP and use the energy to change shape. “We’ll never really know, because we can’t dig up the remains of ancient proteins, but that was probably a big evolutionary leap,” says Vale.On a slightly larger scale, loner cells like sperm or infectious bacteria are prime movers that resolutely push their way through to other cells. As L. Mahadevan and Paul Matsudaira of the Massachusetts Institute of Technology explain, the engines in this case are springs or ratchets that are clusters of molecules, rather than single proteins like myosin and kinesin. Researchers don’t yet fully understand these engines’ fueling process or the details of how they move, but the result is a force to be reckoned with. For example, one such engine is a spring-like stalk connecting a single-celled organism called a vorticellid to the leaf fragment it calls home. When exposed to calcium, the spring contracts, yanking the vorticellid down at speeds approaching three inches (eight centimetres) per second.Springs like this are coiled bundles of filaments that expand or contract in response to chemical cues. A wave of positively charged calcium ions, for example, neutralizes the negative charges that keep the filaments extended. Some sperm use spring-like engines made of actin filaments to shoot out a barb that penetrates the layers that surround an egg. And certain viruses use a similar apparatus to shoot their DNA into the host’s cell. Ratchets are also useful for moving whole cells, including some other sperm and pathogens. These engines are filaments that simply grow at one end, attracting chemical building blocks from nearby. Because the other end is anchored in place, the growing end pushes against any barrier that gets in its way.Both springs and ratchets are made up of small units that each move just slightly, but collectively produce a powerful movement. Ultimately, Mahadevan and Matsudaira hope to better understand just how these particles create an effect that seems to be so much more than the sum of its parts. Might such an understanding provide inspiration for ways to power artificial nano-sized devices in the future? “The short answer is absolutely,” says Mahadevan. “Biology has had a lot more time to evolve enormous richness in design for different organisms. Hopefully, studying these structures will not only improve our understanding of the biological world, it will also enable us to copy them, take apart their components and recreate them for other purpose.”According to the author, research on the power source of movement in cells can contribute to
....

MCQ-> Analyse the following passage and provide appropriate answers for the follow. Popper claimed, scientific beliefs are universal in character, and have to be so if they are to serve us in explanation and prediction. For the universality of a scientific belief implies that, no matter how many instances we have found positive, there will always be an indefinite number of unexamined instances which may or may not also be positive. We have no good reason for supposing that any of these unexamined instances will be positive, or will be negative, so we must refrain from drawing any conclusions. On the other hand, a single negative instance is sufficient to prove that the belief is false, for such an instance is logically incompatible with the universal truth of the belief. Provided, therefore, that the instance is accepted as negative we must conclude that the scientific belief is false. In short, we can sometimes deduce that a universal scientific belief is false but we can never induce that a universal scientific belief is true. It is sometimes argued that this 'asymmetry' between verification and falsification is not nearly as pronounced as Popper declared it to be. Thus, there is no inconsistency in holding that a universal scientific belief is false despite any number of positive instances; and there is no inconsistency either in holding that a universal scientific belief is true despite the evidence of a negative instance. For the belief that an instance is negative is itself a scientific belief and may be falsified by experimental evidence which we accept and which is inconsistent with it. When, for example, we draw a right-angled triangle on the surface of a sphere using parts of three great circles for its sides, and discover that for this triangle Pythagoras' Theorem does not hold, we may decide that this apparently negative instance is not really negative because it is not a genuine instance at all. Triangles drawn on the surfaces of spheres are not the sort of triangles which fall within the scope of Pythagoras' Theorem. Falsification, that is to say, is no more capable of yielding conclusive rejections of scientific belief than verification is of yielding conclusive acceptances of scientific beliefs. The asymmetry between falsification and verification, therefore, has less logical significance than Popper supposed. We should, though, resist this reasoning. Falsifications may not be conclusive, for the acceptances on which rejections are based are always provisional acceptances. But, nevertheless, it remains the case that, in falsification, if we accept falsifying claims then, to remain consistent, we must reject falsified claims. On the other hand, although verifications are also not conclusive, our acceptance or rejection of verifying instances has no implications concerning the acceptance or rejection of verified claims. Falsifying claims sometimes give us a good reason for rejecting a scientific belief, namely when the claims are accepted. But verifying claims, even when accepted, give us no good and appropriate reason for accepting any scientific belief, because any such reason would have to be inductive to be appropriate and there are no good inductive reasons.According to Popper, the statement "Scientific beliefs are universal in character" implies that....

MCQ->A line of length slightly less than and short circuited at far end behaves as....