[2016] TIME AIMCAT 1714 (19th August to 22nd August)

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This thread is to discuss the AIMCAT 1714 of 2016. Sharing Test taking strategies, scores etc

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The First RC passage. I am really weak in that perticular area. Can anyone guide me on that perticular genre or tell me how to get more comfortable with it.

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varun.007
@varun.007  ·  244 karma

.

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codemercury
@codemercury  ·  18 karma

#

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Why is it descriptive and not analytical? 


DIRECTIONS for questions 19 to 24: The passage given below is followed by a set of six 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. It 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. In 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. It was not until 1989 that biologists separately discovered p53's true colours: it was a tumour 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 molecule”, 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 sets 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 active”, 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 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 growth of the cell. The tumour-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 tumours.

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 harbour 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 tumours 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 tumour-quashing p53. And just one out-of-control cell can give rise to deadly tumour.

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.



 22.The style of the above passage is


a)argumentative

b)descriptive

c)analytical

d)abstruse
 

Converts - SPJIMR, IIFT D, IIM Ranchi, Udaipur, Raipur, Kashipur, NMIMS, SIBM || Joining - SPJIMR
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Deepayan1999
@Deepayan1999SPJIMR Mumbai  ·  1,167 karma

@abhinavkrishnan descriptive

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abhinavkrishnan
@abhinavkrishnan  ·  484 karma

@Deepayan1999 @Apjoshua64 okay. Now I follow d comments n yes agree wid Joshua's explanation (y)

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Anyone solved this? Explanation for the solution?


DIRECTIONS for questions 13 to 15: The passage given below is followed by a set of three questions. Choose the best answer to each question.

Cultural property, or patrimony, laws limit the transfer of cultural property outside the source country's territory, including outright export prohibitions and national ownership laws. Most art historians, archaeologists, museum officials and policymakers portray cultural property laws in general as invaluable tools for counteracting the ugly legacy of Western cultural imperialism.

During the late 19th and early 20th century – an era former Met director Thomas Hoving called "the age of piracy" – American and European art museums acquired antiquities by hook or by crook, from grave robbers or souvenir collectors, bounty from digs and ancient sites in impoverished but art-rich source countries. Patrimony laws were intended to protect future archaeological discoveries against Western imperialist designs.

But as it turns out, those laws may not be an unalloyed good. In country after country, empirical data show that when rigid cultural property laws are put in place, major archaeological excavations and discoveries slow markedly, making source countries – and the world at large – culturally poorer.

I surveyed 90 countries with one or more archaeological sites on UNESCO's World Heritage Site list, and my study shows that in most cases the number of discovered sites diminishes sharply after a country passes a cultural property law. There are 222 archaeological sites listed for those 90 countries. When you look into the history of the sites, you see that all but 21 were discovered before the passage of cultural property laws.

Many variables may cause a drop-off in archaeological discoveries country by country, but statistically speaking, it's nearly impossible that the decline shown in the data isn't also related to the passage of cultural property laws.

Strict cultural patrimony laws are popular in most countries. But the downside may be that they reduce incentives for foreign governments, nongovernmental organizations and educational institutions to invest in overseas exploration because their efforts will not necessarily be rewarded by opportunities to hold, display and study what is uncovered. To the extent that source countries can fund their own archaeological projects, artifacts and sites may still be discovered. But the drop in World Heritage Site discoveries after passage of cultural property laws suggests that external sources aren't as active as they were and domestic funding isn't offsetting the loss.

The survey has far-reaching implications. It suggests that source countries, particularly in the developing world, should narrow their cultural property laws so that they can reap the benefits of new archaeological discoveries, which typically increase tourism and enhance cultural pride. This does not mean these nations should abolish restrictions on foreign excavation and foreign claims to artifacts.

13.Which of the following, if true, would most weaken the author’s claim that the decline in archaeological discoveries is due to the passage of cultural property laws?


a)Cultural property laws are present only in the developed countries.

b)Cultural property laws in most of the countries came into existence only recently.

c)Cultural property laws are beneficial to the local archaeologists but not to foreign ones.

d)Cultural property laws prohibit foreign ownership of cultural artefacts. 

Converts - SPJIMR, IIFT D, IIM Ranchi, Udaipur, Raipur, Kashipur, NMIMS, SIBM || Joining - SPJIMR
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MBAaspirant2
@MBAaspirant2  ·  1,556 karma

B is the only one which gives some insight into weakening of author's claim - coming into existence recently would not make it a reason for declining discoveries in the past. D is a straight forward information given in the passage, so this would be a neutral statement, rather doesn't provide any reasoning. In A and C, presence of cultural property laws on any one source i.e. developed or non local, might escalate the discoveries through some other source, so this cannot be concluded or would be dicey to say. Hence, B seems to be an apt reasoning.

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Deepayan1999
@Deepayan1999SPJIMR Mumbai  ·  1,167 karma

 @MBAaspirant2  ok, right, time's explanation here seems to be a bit weird. got confused with that. :D

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 AIMCAT 1714

  VARC -50  :(

  DILR - 41   :(

  QA -  80 

  OA - 171 

CAT 2015 : 98.09 | CAT 2016
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AIMCAT 1714

VARC - 76(99.71)

DILR - 40(98.45)

QA - 44(90.49)

OA - 160(99.45)

AIR 79

CAT'16-99.62 NMAT-230 SNAP-99.845 XAT'17-97.122 CET'17-99.82(so close yet so far)
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1714

VARC - 65(98.34)

DILR - 37(95.38)

QA - 53(97.66)

OA - 155(99.28)

Aur kab tak 150-160 mein hi bhatak ta hua aatma jaisa ghumta rahunga!😑

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AIMCAT 1714

Well my score hasn't improved much it is still 140...

My percentile this time has escalated to 98.28%ile..-- Okay, i have got 95-97 bfore....

My rank 245---- this is quantum jump frm prev 500-700s....

plz read patiently coz I am not showing off my improvement here, I am bit concerned bcoz d no. of ppl who hve given dis AIMCAT has come down to 14k from 16-18k before....

And i m more worried whether the good guys from top have stopped giving AIMCAT......anyone if knows anything about this could please comment???

IIFT , XAT'17 -bombed, CAT'16- 98.43 %ile, calls- IIMK || Converted MDI PGPM
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ashrutgarg
@ashrutgargIIM Udaipur  ·  50 karma

Ok thanx...knowig this was a bit relaxing :P... I thought it to be otherwise. :D

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jmayer10
@jmayer10MDI Gurgaon  ·  1,616 karma

@abhinavkrishnan : "Worry kam karo, bas AIMCAT pelte raho" (y)

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Aimcat 1714 

 Varc 96 :(  

Dilr 99.96 

Qa 99.71

Oa 99.93 

Air 10

Time to fill the final gap....
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3214nayan
@3214nayan  ·  123 karma

_____/\________ SIRJEEE


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Aimcat 1714


Varc 99.99 

Dilr 99.79

Qa 98.77


Oa 99.99

Air 2 


Cat '16 - 100, Cat '17 - 100 | Two attempts | Repo - https://goo.gl/qna7zb
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jmayer10
@jmayer10MDI Gurgaon  ·  1,616 karma

Maje hi to le rha h @avi81293 bhai. Btw, is your D.O.B 8th december 1993? :wink

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avi81293
@avi81293  ·  1,017 karma

@jmayer10 haha yeah

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AIMCAT 1714


VARC 54  (94.54 %ile) 🙈 

LRDI  42  (97.82 %ile)

QA    47   (95.33 %ile) 🙈  damn again u silly mistakes

OA   143  (98.56 %ile) 

AIR  205  

Mandevian for Life 😄 
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