The eLitmus exam consists of 3 compulsory sections, namely Aptitude, Logical and Verbal. Each section contains 20 questions, and the maximum score per section is 200 marks which adds up to a total of 600 marks. The technical section is no longer part of the eLitmus syllabus. Also check out eLitmus verbal questions in this article.
While there is no official material available for the eLitmus exam, you can attempt eLitmus verbal questions to understand the eLitmus paper pattern and level of difficulty of the questions. Check out the eLitmus Test schedule here.
In the new eLitmus syllabus of 2018, two new sub-topics have been added to the Verbal Reasoning section. Lets take a look at what the verbal syllabus consists of:
To summarize:
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eLitmus Verbal questions are relatively easier than the aptitude questions. The overall difficulty level is easy-intermediate. Lets take a look at a question and how to go about solving it:
1. That jacket would have been looked smart on Anita.
How to solve: Look at the words outside the italics and understand the tense and tone of the statement. Then look at the options and see which option fits. In the end, read the statement with the chosen option again to make sure it sounds right. A similar approach can be used with sentence correction questions as well. Here, the correct answer is D.
Given below are some more eLitmus verbal questions for Verbal section that you can attempt to solve:
1. While the doctor____________Mr. Jones this morning, his son was waiting outside.
Solution: Option b was waiting is in the past continuous tense and the answer needs to match the tense. Hence option b is the correct answer.
2. After Larry __________the film on TV, he decided to buy the book.
Solution: Option a decided is in the past tense and the answer needs to match the tense. Hence option a is the correct answer.
3. Look, it __________, so we can’t goto the beach.
Solution: Option d go is in the present tense and the answer needs to match the tense. Hence option d is the correct answer.
Arrange the sentences A, B, C and D in a proper sequence so as to make a coherent paragraph.
A. Archaeologists believe that the Incas started building this glorious city around 1430, but completely abandoned it once European conquerors arrived.
B. Because of the specific area where it was built, the city is surrounded by the most unique animals and plants, including butterflies which do not live anywhere else in the world.
C. Lying at 8,000 feet above the ground, Machu Picchu is known as The Lost City of the Incas, the indigenous people of South America.
D. No more than 750 people lived in Machu Picchu.
Solution: c. CADB
C is a general statement that opens the paragraph and introduces Machu Pichu. A relies on C (this glorious city) and hence is next. D then gives more information on the topic. B is dependent on “Machu Pichu†being mentioned previously and is hence last in line.
Arrange the sentences A, B, C and D in a proper sequence so as to make a coherent paragraph.
A. A cold front happens when cold air is moving near the surface of Earth, and it pushes warm air up very quickly.
B. Lightning has enough energy to heat the air all around it, and this sudden burst of heat is what causes the noise we know as thunder.
C. This is often the beginning of a thunderstorm. Clouds form, and heavy rains begin falling.
D. Thunderstorms often bring disasters with them, including floods, fires caused by lightning, damage from hailstones or strong winds, and even tornadoes.
Solution: d. ACDB
A is a general statement that starts the explanation of the passage. C then follows and elaborates that what has been described in A is the beginning of a thunderstorm. D further explains what thunderstorms do. B closes the paragraph by explaining how thunder is formed.
Arrange the sentences A, B, C and D in a proper sequence so as to make a coherent paragraph.
A. Summers never get very warm, and the summer season is exceptionally short.
B. The weather is very cold in taiga ecosystems.
C. Storms are severe, bringing biting cold winds.
D. The winter season lasts a long time, and the weather is icy cold.
Solution: B opens the paragraph by introducing Taiga systems. D carries on from the “cold†mentioned in B, and C elaborates further on what happens in the winter. A closes the paragraph by explaining the summer season.
The passage given below is followed by a set of three questions. Choose the best answer to each question.
Cancer biologists have long hoped to discover a single step that determines whether cells become cancerous. By targeting drugs at that step, physicians would be able to stop a cell from becoming cancerous just as a switchman stops a train from going down the wrong track. lt turns out that a gene called p53 – a useless mutant form of which luckless families have passed from parent to child may be that switch.
Not bad for a gene that first broke on the scene in a bad case of mistaken identity. ln 1979, biologists discovered the protein (p53) that the p53 gene makes and in 1982, they isolated the p53 gene. But it seemed to cause, rather than suppress cancer. Few researchers were interested in yet another of those oncogenes. lt was not until 1989 that biologists separately discovered p53’s true colors: it was a tumor killer. Some 2000 biologists dropped the date they brought to the dance and latched onto the new area of research. “Our interest converged on p53’s ability (to suppress cancer) like no other moleculeâ€, recalls an oncologist who showed how rogue molecules can prevent p53 from performing its good deeds.
p53 acts as the cell’s director of damage control. A healthy cell keeps a small number of p53 proteins around, continuously degrading them and replenishing the supply. But if carcinogens damage a cell’s DNA and set it on the path to cancer, the cell switches into high alert. If everything is working right, something signals the p53 to stop degrading “and tells it that it is time to be activeâ€, says molecular biologist Carol Pives of Columbia University. “The p53 supply builds up, p53 starts acting like an office clerk who, discovering a typo in an original document that is about to be copied, turns off the copier until he can fix the typo. p53 turns off the cell’s copying machinery and stops the progression of the cell cycle until the cell can repair its damaged DNA. p53 floats toward the cell’s genes and slips into a specific stretch of DNA triggering expression of genes which make proteins that directly inhibit the growth of the cell. The tumor-to-be is stopped dead. p53 also activates the transcription of proteins involved in DNA repair. Sometimes p53 acts more like a clerk so disgusted with the many typos that he just trashes the document: p53 activates the cell’s suicide software, resulting in apoptosis (programmed cell death.
Except when it doesn’t. Even good genes can go bad, and most often, the p53 gene goes bad by undergoing a mutation, typically a spelling mistake. One of the 2362 chemical ‘letters’ (designated A, T, G and C) that make up the p53 gene changes into another letter. The p53 protein that the gene makes is garbled too. And proteins are not very forgiving of errors. A single wrong letter in a crucial part of the p53 gene produces a protein with a wrong molecule; the protein is now not able to suppress tumors.
The Li-Fraumeni families inherit their p53 mutations. If the sperm or egg from which a baby grew held a mutant p53, then every single cell in her body will also harbor a mutant copy. In theory, inheriting only one mutant p53 gene, from one parent, should not be a problem as long as the child inherits a healthy p53 gene from the other parent. The healthy copy should make enough p53 to keep tumors at bay. But p53 doesn’t work that way.
First of all, each cell with one bad p53 gene is only one mutation away from completely lacking the function of this critical gene. That mutation can occur when the cell makes a spelling mistake as it copies its gene before dividing into two cells. Then the cell has lost its primary defense against cancer. A single mutant gene is enough to leave a cell with no healthy tumor-quashing p53. And just one out-of-control cell can give rise to the deadly tumor.
But even a cell whose healthy p53 gene stays that way can be in trouble. The p53 proteins made by the genes, both good and bad, get together in groups of four to form a sinuous ribbon-like complex. If the mutant gene is churning out mutant proteins, then each four-ribbon tangle likely has a mutant among its strands. That is enough to keep the p53 ribbon from doing its job.
Question 1
What does the author wish to imply when he says, “It turns out that a gene called p53 may be that switch†(para 1)?
Solution: Option A
By targeting drugs at that single step (that determines whether cells become cancerous), physicians would be able to stop a cell from becoming cancerous just as a switch-man stops a train from going down the wrong track. It turns out that a gene called p53 may be that switch.
Option A: From a careful reading of the third para (p53 acts as the cell’s director of damage control. A healthy cell …… sets it on the path to cancer, the cell switches into high alert …….the tumor-to-be is stopped dead) and the fourth para (Except when it doesn’t the p53 gene goes bad by undergoing a mutation………. protein with a wrong molecule not able to suppress tumours), we can say that choice A is the correct description of how p53 can serve as a switch in keeping a cell normal or taking it down the cancerous path. So, choice A is the answer.
Option B: Choice B is out of scope and is not an implication. We only know from the passage that until 1989 biologists thought that p53 caused cancer but in 1989 biologists discovered that p53 was a tumor killer. Hence choice B is incorrect.
Option C: Choice C is not the answer. The passage clearly explains the role of p53 in suppressing tumors. We cannot say that treating cancer depends on pure luck. “p53 is the gene whose useless mutant form, luckless families passed from parent to child†may seem misleading as far as the ‘luck’ factor is concerned.
Question 2:
When the author says, “Some 2000 biologists dropped the date they brought to the dance†(para 2), “the date†most likely refers to:
Solution: Option D
It was not until 1989 that biologists separately discovered p53’s true colors: it was a tumor killer. Some 2000 biologists dropped the date they brought to the dance and latched onto the new area of research. One can infer that the term “date†refers to the previous research subject.
Option A: The term “date†does not refer to the year 1989. The year 1989 cannot be dropped if one considers the given context. Hence choice A is not correct.
Option B: One of the previous research subjects of the biologists (before 1989) was the seeming ability of p53 to cause cancer. (Few researchers were interested in yet another one of those oncogenes). (We do not know if all the 2000 biologists were interested only in the subject of p53’s ability to cause cancer). The ability of p53 to kill tumors is the new research area of cancer biologists from 1989 onwards. So choice B is not true.
Option C: The contemporary research subject of the biologists cannot be the “date†that was dropped. The “date†that was dropped has to be the “older†or “previous†research subject of cancer biologists. Hence choice C is fundamentally wrong. Also, the current research subject of the biologists is to address the ability of p53 to kill tumors and not primarily the ability of rogue molecules to prevent p53 from suppressing cancer (though the latter can also be a related area of research). Hence choice C is not the answer.
Option D: Choice D is the answer. “erstwhile†means In the pastâ€. The term “date†refers to the previous research subject wrt p53 for biologists.
Therefore Option(D) is the correct answer.
Question 3:
According to one biologist, the p53 gene is analogous to an office clerk, in all of the following aspects EXCEPT?
Solution: Option C
The answer to this question lies in para 3. The molecular biologist Carol Pives of Columbia University likens the p53 gene to an office clerk. The p53 supply builds up, p53 starts acting like an office clerk who, discovering a typo in an original document that is about to be copied turns off the copier until he can fix the typo
Option A: p53 turns off the cell’s copying machinery and stops the progression of the cell cycle until the cell can repair its damaged DNA. So choice A is true and is not the answer.
Option B: The penultimate sentence of para 3 states that p53 may activate the transcription of proteins involved in DNA repair. Hence choice B is true and is not the answer.
Option C: The passage does not say that an office clerk is prone to committing typing errors. The fact that the p53 gene can make a garbled protein if there is a spelling mistake in one of its chemical letters (A, T, G, and C) has been discussed in para 4. But this statement is not related to the question and therefore choice C is the answer.
Option D: The last sentence of para 3 also likens p53 to an office clerk. Sometimes p53 acts more like a clerk so disgusted with the many typos that he just trashes the document: p53 activates the cell’s suicide software, resulting in apoptosis or programmed cell death.
So, choice D is not the answer. (Apoptosis is the “last resort†to avoid the proliferation of cells containing abnormal DNA.)
Check out the video below for more eLitmus verbal questions for verbal section with answer explanations!