In recent years, a class of drugs known as COX-2 inhibitors has gotten much publicity for the drugsandrsquo; power to relieve inflammation and pain. These drugs are relatively new to the pharmaceutical industry, their mechanisms of action having been discovered only in 1971. That year, John Vane discovered the relationship between nonsteroidal antiinflammatory drugs, such as aspirin, and a group of molecules, called prostaglandins, responsible for producing the sensation of pain in the human body, among other functions.Prostaglandins were first discovered in the 1930s and are now known to be generated by most mammalian tissues in response to external stimuli. Unlike classical hormones that are synthesized in one tissue but act on a distant one, prostaglandins act on the cells that produce them or on cells located close to the prostaglandinsandrsquo; cells of origin.Aspirin alleviates pain by inhibiting the function of an enzyme called cyclooxygenase or COX; this inhibition prevents the production of prostaglandins. The three forms of this enzyme, COX-1, COX-2, and COX-3, all stimulate the production of prostaglandins, but each serves a different purpose. COX-1 functions to protect the stomach from irritating gastric acids. COX-2 functions to induce inflammation in injured tissue and COX-3 functions to control the sensation of pain. Aspirin and other similar drugs, such as naproxen, inhibit both COX-1 and COX-2, sometimes producing or aggravating stomach ulcers in patients who take them.In order to eliminate the side effects of aspirin and related drugs, several pharmaceutical companies in the 1990s developed drugs that inhibited only COX-2. However, side effects almost always cropped up, even after clinical trials that seemed to indicate none. This often occurs because trials are conducted within very limited parameters; once the drug has been approved for mass distribution, however, the number of people taking it and the length of time that it is taken increase dramatically. Several COX-2 drugs that have been popular in recent years fit this pattern: initially successful in clinical trials, subsequent studies showed them to have serious, potentially lethal side effects.Though prostaglandin chemistry and enzymology have been studied for half a century, pinpointing the exact role of the molecules in physiological processes still remains a challenge for researchers. Hence it is not surprising that recent therapeutic attempts to interfere with the formation of certain prostaglandins have produced unexpected side effects. It now seems that the hype surrounding COX-2 drugs may have been premature.Q. The primary purpose of this passage is toa)explain the therapeutic benefits of a new type of pain relieverb)initiate a debate concerning the benefits of COX-2 inhibitorsc)warn the public that clinical trials cannot ensure drug safetyd)describe the impetus for and result of COX-2 inhibitorsandrsquo; introductione)introduceres earch findings to support COX-2 inhibitors over COX-1 inhibitorsCorrect answer is option 'D'. Can you explain this answer?

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In recent years, a class of drugs known as COX-2 inhibitors has gotten much publicity for the drugs’ power to relieve inflammation and pain. These drugs are relatively new to the pharmaceutical industry, their mechanisms of action having been discovered only in 1971. That year, John Vane discovered the relationship between nonsteroidal antiinflammatory drugs, such as aspirin, and a group of molecules, called prostaglandins, responsible for producing the sensation of pain in the human body, among other functions.
Prostaglandins were first discovered in the 1930s and are now known to be generated by most mammalian tissues in response to external stimuli. Unlike classical hormones that are synthesized in one tissue but act on a distant one, prostaglandins act on the cells that produce them or on cells located close to the prostaglandins’ cells of origin.
Aspirin alleviates pain by inhibiting the function of an enzyme called cyclooxygenase or COX; this inhibition prevents the production of prostaglandins. The three forms of this enzyme, COX-1, COX-2, and COX-3, all stimulate the production of prostaglandins, but each serves a different purpose. COX-1 functions to protect the stomach from irritating gastric acids. COX-2 functions to induce inflammation in injured tissue and COX-3 functions to control the sensation of pain. Aspirin and other similar drugs, such as naproxen, inhibit both COX-1 and COX-2, sometimes producing or aggravating stomach ulcers in patients who take them.
In order to eliminate the side effects of aspirin and related drugs, several pharmaceutical companies in the 1990s developed drugs that inhibited only COX-2. However, side effects almost always cropped up, even after clinical trials that seemed to indicate none. This often occurs because trials are conducted within very limited parameters; once the drug has been approved for mass distribution, however, the number of people taking it and the length of time that it is taken increase dramatically. Several COX-2 drugs that have been popular in recent years fit this pattern: initially successful in clinical trials, subsequent studies showed them to have serious, potentially lethal side effects.
Though prostaglandin chemistry and enzymology have been studied for half a century, pinpointing the exact role of the molecules in physiological processes still remains a challenge for researchers. Hence it is not surprising that recent therapeutic attempts to interfere with the formation of certain prostaglandins have produced unexpected side effects. It now seems that the hype surrounding COX-2 drugs may have been premature.

Q. The primary purpose of this passage is to

a)
explain the therapeutic benefits of a new type of pain reliever
b)
initiate a debate concerning the benefits of COX-2 inhibitors
c)
warn the public that clinical trials cannot ensure drug safety
d)
describe the impetus for and result of COX-2 inhibitors’ introduction
e)
introduceres earch findings to support COX-2 inhibitors over COX-1 inhibitors

Correct answer is option 'D'. Can you explain this answer?

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In recent years, a class of drugs known as COX-2 inhibitors has gotten...

The first paragraph introduces COX-2 inhibitors and talks briefly about a 1971 discovery linking aspirin to prostaglandins.
Paragraph 2 elaborates on the connections among aspirin, prostaglandins, and the three types of COX enzymes. Paragraph 3 discusses COX-2 inhibitors specifically, both the impetus for creating them and some negative effects. The final paragraph provides caution about the promise of COX-2 inhibitors.
(A) The passage explains the intended benefits behind the development of COX-2 inhibitors, but this is much too narrow to be the main purpose of the passage, particularly when a large part of the passage addresses the negative consequences.
(B) The author does not initiate a “debate.” For a debate, the author must introduce two clear opposing sides. The COX-2 inhibitors were developed to replace the earlier drugs that inhibited both COX-1 and COX-2, but then they were also found to have side effects.
(C) While paragraph 4 states that “Side effects almost always cropped up, even after clinical trials that seemed to indicate none," the author notes this only in the context of explaining the result of COX-2 inhibitors. This is too narrow to be the main purpose of the passage.
(D) CORRECT. This choice reflects the summary above: why COX-2 inhibitors were developed and the result of the drugs' introduction into the marketplace.
(E) This is incorrect because the passage never mentions a drug class of “COX-1 inhibitors.” COX-1 is introduced as an enzyme; it is not a class of drug.

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In recent years, a class of drugs known as COX-2 inhibitors has gotten much publicity for the drugs’ power to relieve inflammation and pain. These drugs are relatively new to the pharmaceutical industry, their mechanisms of action having been discovered only in 1971. That year, John Vane discovered the relationship between nonsteroidal antiinflammatory drugs, such as aspirin, and a group of molecules, called prostaglandins, responsible for producing the sensation of pain in the human body, among other functions.Prostaglandins were first discovered in the 1930s and are now known to be generated by most mammalian tissues in response to external stimuli. Unlike classical hormones that are synthesized in one tissue but act on a distant one, prostaglandins act on the cells that produce them or on cells located close to the prostaglandins’ cells of origin.Aspirin alleviates pain by inhibiting the function of an enzyme called cyclooxygenase or COX; this inhibition prevents the production of prostaglandins. The three forms of this enzyme, COX-1, COX-2, and COX-3, all stimulate the production of prostaglandins, but each serves a different purpose. COX-1 functions to protect the stomach from irritating gastric acids. COX-2 functions to induce inflammation in injured tissue and COX-3 functions to control the sensation of pain. Aspirin and other similar drugs, such as naproxen, inhibit both COX-1 and COX-2, sometimes producing or aggravating stomach ulcers in patients who take them.In order to eliminate the side effects of aspirin and related drugs, several pharmaceutical companies in the 1990s developed drugs that inhibited only COX-2. However, side effects almost always cropped up, even after clinical trials that seemed to indicate none. This often occurs because trials are conducted within very limited parameters; once the drug has been approved for mass distribution, however, the number of people taking it and the length of time that it is taken increase dramatically. Several COX-2 drugs that have been popular in recent years fit this pattern: initially successful in clinical trials, subsequent studies showed them to have serious, potentially lethal side effects.Though prostaglandin chemistry and enzymology have been studied for half a century, pinpointing the exact role of the molecules in physiological processes still remains a challenge for researchers. Hence it is not surprising that recent therapeutic attempts to interfere with the formation of certain prostaglandins have produced unexpected side effects. It now seems that the hype surrounding COX-2 drugs may have been premature.Q. The author mentions that prostaglandins a re generated in response to external stimuli primarily in order to support the contention that

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In recent years, a class of drugs known as COX-2 inhibitors has gotten much publicity for the drugs’ power to relieve inflammation and pain. These drugs are relatively new to the pharmaceutical industry, their mechanisms of action having been discovered only in 1971. That year, John Vane discovered the relationship between nonsteroidal antiinflammatory drugs, such as aspirin, and a group of molecules, called prostaglandins, responsible for producing the sensation of pain in the human body, among other functions.Prostaglandins were first discovered in the 1930s and are now known to be generated by most mammalian tissues in response to external stimuli. Unlike classical hormones that are synthesized in one tissue but act on a distant one, prostaglandins act on the cells that produce them or on cells located close to the prostaglandins’ cells of origin.Aspirin alleviates pain by inhibiting the function of an enzyme called cyclooxygenase or COX; this inhibition prevents the production of prostaglandins. The three forms of this enzyme, COX-1, COX-2, and COX-3, all stimulate the production of prostaglandins, but each serves a different purpose. COX-1 functions to protect the stomach from irritating gastric acids. COX-2 functions to induce inflammation in injured tissue and COX-3 functions to control the sensation of pain. Aspirin and other similar drugs, such as naproxen, inhibit both COX-1 and COX-2, sometimes producing or aggravating stomach ulcers in patients who take them.In order to eliminate the side effects of aspirin and related drugs, several pharmaceutical companies in the 1990s developed drugs that inhibited only COX-2. However, side effects almost always cropped up, even after clinical trials that seemed to indicate none. This often occurs because trials are conducted within very limited parameters; once the drug has been approved for mass distribution, however, the number of people taking it and the length of time that it is taken increase dramatically. Several COX-2 drugs that have been popular in recent years fit this pattern: initially successful in clinical trials, subsequent studies showed them to have serious, potentially lethal side effects.Though prostaglandin chemistry and enzymology have been studied for half a century, pinpointing the exact role of the molecules in physiological processes still remains a challenge for researchers. Hence it is not surprising that recent therapeutic attempts to interfere with the formation of certain prostaglandins have produced unexpected side effects. It now seems that the hype surrounding COX-2 drugs may have been premature.Q. According to the passage, all of the following are true of prostaglandins EXCEPT

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In recent years, a class of drugs known as COX-2 inhibitors has gotten much publicity for the drugs’ power to relieve inflammation and pain. These drugs are relatively new to the pharmaceutical industry, their mechanisms of action having been discovered only in 1971. That year, John Vane discovered the relationship between nonsteroidal antiinflammatory drugs, such as aspirin, and a group of molecules, called prostaglandins, responsible for producing the sensation of pain in the human body, among other functions.Prostaglandins were first discovered in the 1930s and are now known to be generated by most mammalian tissues in response to external stimuli. Unlike classical hormones that are synthesized in one tissue but act on a distant one, prostaglandins act on the cells that produce them or on cells located close to the prostaglandins’ cells of origin.Aspirin alleviates pain by inhibiting the function of an enzyme called cyclooxygenase or COX; this inhibition prevents the production of prostaglandins. The three forms of this enzyme, COX-1, COX-2, and COX-3, all stimulate the production of prostaglandins, but each serves a different purpose. COX-1 functions to protect the stomach from irritating gastric acids. COX-2 functions to induce inflammation in injured tissue and COX-3 functions to control the sensation of pain. Aspirin and other similar drugs, such as naproxen, inhibit both COX-1 and COX-2, sometimes producing or aggravating stomach ulcers in patients who take them.In order to eliminate the side effects of aspirin and related drugs, several pharmaceutical companies in the 1990s developed drugs that inhibited only COX-2. However, side effects almost always cropped up, even after clinical trials that seemed to indicate none. This often occurs because trials are conducted within very limited parameters; once the drug has been approved for mass distribution, however, the number of people taking it and the length of time that it is taken increase dramatically. Several COX-2 drugs that have been popular in recent years fit this pattern: initially successful in clinical trials, subsequent studies showed them to have serious, potentially lethal side effects.Though prostaglandin chemistry and enzymology have been studied for half a century, pinpointing the exact role of the molecules in physiological processes still remains a challenge for researchers. Hence it is not surprising that recent therapeutic attempts to interfere with the formation of certain prostaglandins have produced unexpected side effects. It now seems that the hype surrounding COX-2 drugs may have been premature.Q. The passage suggest which the following about COX2 inhibitors?

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Read the passage and answer the question given below.The sensation of pain cannot accurately be described as “located” at the point of an injury, or, for that matter, in any one place in the nerves or brain. Rather, pain signals—and pain relief—are delivered through a highly complex interacting circuitry.When a cell is injured, a rush of prostaglandins sensitizes nerve endings at the injury. Prostaglandins are chemicals produced in and released from virtually all mammalian cells when they are injured: these are the only pain signals that do not originate in the nervous system. Aspirin and other similar drugs (such as indomethacin and ibuprofen) keep prostaglandins from being made by interfering with an enzyme known as prostaglandin synthetase, or cyclooxygenase. The drugs’ effectiveness against pain is proportional to their success in blocking this enzyme at the site of injury.From nerve endings at the injury, pain signals move to nerves feeding into the spinal cord. The long, tubular membranes of nerve cells carry electrical impulses. When electrical impulses get to the spinal cord, a pain-signaling chemical known as substance P is released there. Substance P then excites nearby neurons to send impulses to the brain. Local anesthetics such as novocaine and xylocaine work by blocking the electrical transmission along nerves in a particular area. They inhibit the flow of sodium ions through the membranes, making the nerves electrically quiescent; thus no pain signals are sent to the spinal cord or to the brain.Recent discoveries in the study of pain have involved the brain itself—the supervising organ that notices pain signals and that sends messages down to the spinal cord to regulate incoming pain traffic. Endorphins—the brain’s own morphine—are a class of small peptides that help to block pain signals within the brain itself. The presence of endorphins may also help to explain differences in response to pain signals, since individuals seem to differ in their ability to produce endorphins. It now appears that a number of techniques for blocking chronic pain—such as acupuncture and electrical stimulation of the central brain stem—involve the release of endorphins in the brain and spinal cord.Q. According to the passage, which of the following is one of the first things to occur when cells are injured?

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A pharmaceutical company developed a new diuretic reported to cause fewer side effects than their old diuretic, which was still being manufactured. Duringthe first year that both were sold, the earlier medication far outsold the new one; the manufacturer thus concluded that reducing side effects was not the customers primary consideration.Q. Which of the following, if true, would most seriously weaken the manufacturer’s conclusion?

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In recent years, a class of drugs known as COX-2 inhibitors has gotten much publicity for the drugs’ power to relieve inflammation and pain. These drugs are relatively new to the pharmaceutical industry, their mechanisms of action having been discovered only in 1971. That year, John Vane discovered the relationship between nonsteroidal antiinflammatory drugs, such as aspirin, and a group of molecules, called prostaglandins, responsible for producing the sensation of pain in the human body, among other functions.Prostaglandins were first discovered in the 1930s and are now known to be generated by most mammalian tissues in response to external stimuli. Unlike classical hormones that are synthesized in one tissue but act on a distant one, prostaglandins act on the cells that produce them or on cells located close to the prostaglandins’ cells of origin.Aspirin alleviates pain by inhibiting the function of an enzyme called cyclooxygenase or COX; this inhibition prevents the production of prostaglandins. The three forms of this enzyme, COX-1, COX-2, and COX-3, all stimulate the production of prostaglandins, but each serves a different purpose. COX-1 functions to protect the stomach from irritating gastric acids. COX-2 functions to induce inflammation in injured tissue and COX-3 functions to control the sensation of pain. Aspirin and other similar drugs, such as naproxen, inhibit both COX-1 and COX-2, sometimes producing or aggravating stomach ulcers in patients who take them.In order to eliminate the side effects of aspirin and related drugs, several pharmaceutical companies in the 1990s developed drugs that inhibited only COX-2. However, side effects almost always cropped up, even after clinical trials that seemed to indicate none. This often occurs because trials are conducted within very limited parameters; once the drug has been approved for mass distribution, however, the number of people taking it and the length of time that it is taken increase dramatically. Several COX-2 drugs that have been popular in recent years fit this pattern: initially successful in clinical trials, subsequent studies showed them to have serious, potentially lethal side effects.Though prostaglandin chemistry and enzymology have been studied for half a century, pinpointing the exact role of the molecules in physiological processes still remains a challenge for researchers. Hence it is not surprising that recent therapeutic attempts to interfere with the formation of certain prostaglandins have produced unexpected side effects. It now seems that the hype surrounding COX-2 drugs may have been premature.Q. The primary purpose of this passage is toa)explain the therapeutic benefits of a new type of pain relieverb)initiate a debate concerning the benefits of COX-2 inhibitorsc)warn the public that clinical trials cannot ensure drug safetyd)describe the impetus for and result of COX-2 inhibitors’ introductione)introduceres earch findings to support COX-2 inhibitors over COX-1 inhibitorsCorrect answer is option 'D'. Can you explain this answer?

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In recent years, a class of drugs known as COX-2 inhibitors has gotten much publicity for the drugs’ power to relieve inflammation and pain. These drugs are relatively new to the pharmaceutical industry, their mechanisms of action having been discovered only in 1971. That year, John Vane discovered the relationship between nonsteroidal antiinflammatory drugs, such as aspirin, and a group of molecules, called prostaglandins, responsible for producing the sensation of pain in the human body, among other functions.Prostaglandins were first discovered in the 1930s and are now known to be generated by most mammalian tissues in response to external stimuli. Unlike classical hormones that are synthesized in one tissue but act on a distant one, prostaglandins act on the cells that produce them or on cells located close to the prostaglandins’ cells of origin.Aspirin alleviates pain by inhibiting the function of an enzyme called cyclooxygenase or COX; this inhibition prevents the production of prostaglandins. The three forms of this enzyme, COX-1, COX-2, and COX-3, all stimulate the production of prostaglandins, but each serves a different purpose. COX-1 functions to protect the stomach from irritating gastric acids. COX-2 functions to induce inflammation in injured tissue and COX-3 functions to control the sensation of pain. Aspirin and other similar drugs, such as naproxen, inhibit both COX-1 and COX-2, sometimes producing or aggravating stomach ulcers in patients who take them.In order to eliminate the side effects of aspirin and related drugs, several pharmaceutical companies in the 1990s developed drugs that inhibited only COX-2. However, side effects almost always cropped up, even after clinical trials that seemed to indicate none. This often occurs because trials are conducted within very limited parameters; once the drug has been approved for mass distribution, however, the number of people taking it and the length of time that it is taken increase dramatically. Several COX-2 drugs that have been popular in recent years fit this pattern: initially successful in clinical trials, subsequent studies showed them to have serious, potentially lethal side effects.Though prostaglandin chemistry and enzymology have been studied for half a century, pinpointing the exact role of the molecules in physiological processes still remains a challenge for researchers. Hence it is not surprising that recent therapeutic attempts to interfere with the formation of certain prostaglandins have produced unexpected side effects. It now seems that the hype surrounding COX-2 drugs may have been premature.Q. The primary purpose of this passage is toa)explain the therapeutic benefits of a new type of pain relieverb)initiate a debate concerning the benefits of COX-2 inhibitorsc)warn the public that clinical trials cannot ensure drug safetyd)describe the impetus for and result of COX-2 inhibitors’ introductione)introduceres earch findings to support COX-2 inhibitors over COX-1 inhibitorsCorrect answer is option 'D'. Can you explain this answer? for GMAT 2024 is part of GMAT preparation. The Question and answers have been prepared according to the GMAT exam syllabus. Information about In recent years, a class of drugs known as COX-2 inhibitors has gotten much publicity for the drugs’ power to relieve inflammation and pain. These drugs are relatively new to the pharmaceutical industry, their mechanisms of action having been discovered only in 1971. That year, John Vane discovered the relationship between nonsteroidal antiinflammatory drugs, such as aspirin, and a group of molecules, called prostaglandins, responsible for producing the sensation of pain in the human body, among other functions.Prostaglandins were first discovered in the 1930s and are now known to be generated by most mammalian tissues in response to external stimuli. Unlike classical hormones that are synthesized in one tissue but act on a distant one, prostaglandins act on the cells that produce them or on cells located close to the prostaglandins’ cells of origin.Aspirin alleviates pain by inhibiting the function of an enzyme called cyclooxygenase or COX; this inhibition prevents the production of prostaglandins. The three forms of this enzyme, COX-1, COX-2, and COX-3, all stimulate the production of prostaglandins, but each serves a different purpose. COX-1 functions to protect the stomach from irritating gastric acids. COX-2 functions to induce inflammation in injured tissue and COX-3 functions to control the sensation of pain. Aspirin and other similar drugs, such as naproxen, inhibit both COX-1 and COX-2, sometimes producing or aggravating stomach ulcers in patients who take them.In order to eliminate the side effects of aspirin and related drugs, several pharmaceutical companies in the 1990s developed drugs that inhibited only COX-2. However, side effects almost always cropped up, even after clinical trials that seemed to indicate none. This often occurs because trials are conducted within very limited parameters; once the drug has been approved for mass distribution, however, the number of people taking it and the length of time that it is taken increase dramatically. Several COX-2 drugs that have been popular in recent years fit this pattern: initially successful in clinical trials, subsequent studies showed them to have serious, potentially lethal side effects.Though prostaglandin chemistry and enzymology have been studied for half a century, pinpointing the exact role of the molecules in physiological processes still remains a challenge for researchers. Hence it is not surprising that recent therapeutic attempts to interfere with the formation of certain prostaglandins have produced unexpected side effects. It now seems that the hype surrounding COX-2 drugs may have been premature.Q. The primary purpose of this passage is toa)explain the therapeutic benefits of a new type of pain relieverb)initiate a debate concerning the benefits of COX-2 inhibitorsc)warn the public that clinical trials cannot ensure drug safetyd)describe the impetus for and result of COX-2 inhibitors’ introductione)introduceres earch findings to support COX-2 inhibitors over COX-1 inhibitorsCorrect answer is option 'D'. Can you explain this answer? covers all topics & solutions for GMAT 2024 Exam. Find important definitions, questions, meanings, examples, exercises and tests below for In recent years, a class of drugs known as COX-2 inhibitors has gotten much publicity for the drugs’ power to relieve inflammation and pain. These drugs are relatively new to the pharmaceutical industry, their mechanisms of action having been discovered only in 1971. That year, John Vane discovered the relationship between nonsteroidal antiinflammatory drugs, such as aspirin, and a group of molecules, called prostaglandins, responsible for producing the sensation of pain in the human body, among other functions.Prostaglandins were first discovered in the 1930s and are now known to be generated by most mammalian tissues in response to external stimuli. Unlike classical hormones that are synthesized in one tissue but act on a distant one, prostaglandins act on the cells that produce them or on cells located close to the prostaglandins’ cells of origin.Aspirin alleviates pain by inhibiting the function of an enzyme called cyclooxygenase or COX; this inhibition prevents the production of prostaglandins. The three forms of this enzyme, COX-1, COX-2, and COX-3, all stimulate the production of prostaglandins, but each serves a different purpose. COX-1 functions to protect the stomach from irritating gastric acids. COX-2 functions to induce inflammation in injured tissue and COX-3 functions to control the sensation of pain. Aspirin and other similar drugs, such as naproxen, inhibit both COX-1 and COX-2, sometimes producing or aggravating stomach ulcers in patients who take them.In order to eliminate the side effects of aspirin and related drugs, several pharmaceutical companies in the 1990s developed drugs that inhibited only COX-2. However, side effects almost always cropped up, even after clinical trials that seemed to indicate none. This often occurs because trials are conducted within very limited parameters; once the drug has been approved for mass distribution, however, the number of people taking it and the length of time that it is taken increase dramatically. Several COX-2 drugs that have been popular in recent years fit this pattern: initially successful in clinical trials, subsequent studies showed them to have serious, potentially lethal side effects.Though prostaglandin chemistry and enzymology have been studied for half a century, pinpointing the exact role of the molecules in physiological processes still remains a challenge for researchers. Hence it is not surprising that recent therapeutic attempts to interfere with the formation of certain prostaglandins have produced unexpected side effects. It now seems that the hype surrounding COX-2 drugs may have been premature.Q. The primary purpose of this passage is toa)explain the therapeutic benefits of a new type of pain relieverb)initiate a debate concerning the benefits of COX-2 inhibitorsc)warn the public that clinical trials cannot ensure drug safetyd)describe the impetus for and result of COX-2 inhibitors’ introductione)introduceres earch findings to support COX-2 inhibitors over COX-1 inhibitorsCorrect answer is option 'D'. Can you explain this answer?.

Solutions for In recent years, a class of drugs known as COX-2 inhibitors has gotten much publicity for the drugs’ power to relieve inflammation and pain. These drugs are relatively new to the pharmaceutical industry, their mechanisms of action having been discovered only in 1971. That year, John Vane discovered the relationship between nonsteroidal antiinflammatory drugs, such as aspirin, and a group of molecules, called prostaglandins, responsible for producing the sensation of pain in the human body, among other functions.Prostaglandins were first discovered in the 1930s and are now known to be generated by most mammalian tissues in response to external stimuli. Unlike classical hormones that are synthesized in one tissue but act on a distant one, prostaglandins act on the cells that produce them or on cells located close to the prostaglandins’ cells of origin.Aspirin alleviates pain by inhibiting the function of an enzyme called cyclooxygenase or COX; this inhibition prevents the production of prostaglandins. The three forms of this enzyme, COX-1, COX-2, and COX-3, all stimulate the production of prostaglandins, but each serves a different purpose. COX-1 functions to protect the stomach from irritating gastric acids. COX-2 functions to induce inflammation in injured tissue and COX-3 functions to control the sensation of pain. Aspirin and other similar drugs, such as naproxen, inhibit both COX-1 and COX-2, sometimes producing or aggravating stomach ulcers in patients who take them.In order to eliminate the side effects of aspirin and related drugs, several pharmaceutical companies in the 1990s developed drugs that inhibited only COX-2. However, side effects almost always cropped up, even after clinical trials that seemed to indicate none. This often occurs because trials are conducted within very limited parameters; once the drug has been approved for mass distribution, however, the number of people taking it and the length of time that it is taken increase dramatically. Several COX-2 drugs that have been popular in recent years fit this pattern: initially successful in clinical trials, subsequent studies showed them to have serious, potentially lethal side effects.Though prostaglandin chemistry and enzymology have been studied for half a century, pinpointing the exact role of the molecules in physiological processes still remains a challenge for researchers. Hence it is not surprising that recent therapeutic attempts to interfere with the formation of certain prostaglandins have produced unexpected side effects. It now seems that the hype surrounding COX-2 drugs may have been premature.Q. The primary purpose of this passage is toa)explain the therapeutic benefits of a new type of pain relieverb)initiate a debate concerning the benefits of COX-2 inhibitorsc)warn the public that clinical trials cannot ensure drug safetyd)describe the impetus for and result of COX-2 inhibitors’ introductione)introduceres earch findings to support COX-2 inhibitors over COX-1 inhibitorsCorrect answer is option 'D'. Can you explain this answer? in English & in Hindi are available as part of our courses for GMAT. Download more important topics, notes, lectures and mock test series for GMAT Exam by signing up for free.

Here you can find the meaning of In recent years, a class of drugs known as COX-2 inhibitors has gotten much publicity for the drugs’ power to relieve inflammation and pain. These drugs are relatively new to the pharmaceutical industry, their mechanisms of action having been discovered only in 1971. That year, John Vane discovered the relationship between nonsteroidal antiinflammatory drugs, such as aspirin, and a group of molecules, called prostaglandins, responsible for producing the sensation of pain in the human body, among other functions.Prostaglandins were first discovered in the 1930s and are now known to be generated by most mammalian tissues in response to external stimuli. Unlike classical hormones that are synthesized in one tissue but act on a distant one, prostaglandins act on the cells that produce them or on cells located close to the prostaglandins’ cells of origin.Aspirin alleviates pain by inhibiting the function of an enzyme called cyclooxygenase or COX; this inhibition prevents the production of prostaglandins. The three forms of this enzyme, COX-1, COX-2, and COX-3, all stimulate the production of prostaglandins, but each serves a different purpose. COX-1 functions to protect the stomach from irritating gastric acids. COX-2 functions to induce inflammation in injured tissue and COX-3 functions to control the sensation of pain. Aspirin and other similar drugs, such as naproxen, inhibit both COX-1 and COX-2, sometimes producing or aggravating stomach ulcers in patients who take them.In order to eliminate the side effects of aspirin and related drugs, several pharmaceutical companies in the 1990s developed drugs that inhibited only COX-2. However, side effects almost always cropped up, even after clinical trials that seemed to indicate none. This often occurs because trials are conducted within very limited parameters; once the drug has been approved for mass distribution, however, the number of people taking it and the length of time that it is taken increase dramatically. Several COX-2 drugs that have been popular in recent years fit this pattern: initially successful in clinical trials, subsequent studies showed them to have serious, potentially lethal side effects.Though prostaglandin chemistry and enzymology have been studied for half a century, pinpointing the exact role of the molecules in physiological processes still remains a challenge for researchers. Hence it is not surprising that recent therapeutic attempts to interfere with the formation of certain prostaglandins have produced unexpected side effects. It now seems that the hype surrounding COX-2 drugs may have been premature.Q. The primary purpose of this passage is toa)explain the therapeutic benefits of a new type of pain relieverb)initiate a debate concerning the benefits of COX-2 inhibitorsc)warn the public that clinical trials cannot ensure drug safetyd)describe the impetus for and result of COX-2 inhibitors’ introductione)introduceres earch findings to support COX-2 inhibitors over COX-1 inhibitorsCorrect answer is option 'D'. Can you explain this answer? defined & explained in the simplest way possible. Besides giving the explanation of In recent years, a class of drugs known as COX-2 inhibitors has gotten much publicity for the drugs’ power to relieve inflammation and pain. These drugs are relatively new to the pharmaceutical industry, their mechanisms of action having been discovered only in 1971. That year, John Vane discovered the relationship between nonsteroidal antiinflammatory drugs, such as aspirin, and a group of molecules, called prostaglandins, responsible for producing the sensation of pain in the human body, among other functions.Prostaglandins were first discovered in the 1930s and are now known to be generated by most mammalian tissues in response to external stimuli. Unlike classical hormones that are synthesized in one tissue but act on a distant one, prostaglandins act on the cells that produce them or on cells located close to the prostaglandins’ cells of origin.Aspirin alleviates pain by inhibiting the function of an enzyme called cyclooxygenase or COX; this inhibition prevents the production of prostaglandins. The three forms of this enzyme, COX-1, COX-2, and COX-3, all stimulate the production of prostaglandins, but each serves a different purpose. COX-1 functions to protect the stomach from irritating gastric acids. COX-2 functions to induce inflammation in injured tissue and COX-3 functions to control the sensation of pain. Aspirin and other similar drugs, such as naproxen, inhibit both COX-1 and COX-2, sometimes producing or aggravating stomach ulcers in patients who take them.In order to eliminate the side effects of aspirin and related drugs, several pharmaceutical companies in the 1990s developed drugs that inhibited only COX-2. However, side effects almost always cropped up, even after clinical trials that seemed to indicate none. This often occurs because trials are conducted within very limited parameters; once the drug has been approved for mass distribution, however, the number of people taking it and the length of time that it is taken increase dramatically. Several COX-2 drugs that have been popular in recent years fit this pattern: initially successful in clinical trials, subsequent studies showed them to have serious, potentially lethal side effects.Though prostaglandin chemistry and enzymology have been studied for half a century, pinpointing the exact role of the molecules in physiological processes still remains a challenge for researchers. Hence it is not surprising that recent therapeutic attempts to interfere with the formation of certain prostaglandins have produced unexpected side effects. It now seems that the hype surrounding COX-2 drugs may have been premature.Q. The primary purpose of this passage is toa)explain the therapeutic benefits of a new type of pain relieverb)initiate a debate concerning the benefits of COX-2 inhibitorsc)warn the public that clinical trials cannot ensure drug safetyd)describe the impetus for and result of COX-2 inhibitors’ introductione)introduceres earch findings to support COX-2 inhibitors over COX-1 inhibitorsCorrect answer is option 'D'. Can you explain this answer?, a detailed solution for In recent years, a class of drugs known as COX-2 inhibitors has gotten much publicity for the drugs’ power to relieve inflammation and pain. These drugs are relatively new to the pharmaceutical industry, their mechanisms of action having been discovered only in 1971. That year, John Vane discovered the relationship between nonsteroidal antiinflammatory drugs, such as aspirin, and a group of molecules, called prostaglandins, responsible for producing the sensation of pain in the human body, among other functions.Prostaglandins were first discovered in the 1930s and are now known to be generated by most mammalian tissues in response to external stimuli. Unlike classical hormones that are synthesized in one tissue but act on a distant one, prostaglandins act on the cells that produce them or on cells located close to the prostaglandins’ cells of origin.Aspirin alleviates pain by inhibiting the function of an enzyme called cyclooxygenase or COX; this inhibition prevents the production of prostaglandins. The three forms of this enzyme, COX-1, COX-2, and COX-3, all stimulate the production of prostaglandins, but each serves a different purpose. COX-1 functions to protect the stomach from irritating gastric acids. COX-2 functions to induce inflammation in injured tissue and COX-3 functions to control the sensation of pain. Aspirin and other similar drugs, such as naproxen, inhibit both COX-1 and COX-2, sometimes producing or aggravating stomach ulcers in patients who take them.In order to eliminate the side effects of aspirin and related drugs, several pharmaceutical companies in the 1990s developed drugs that inhibited only COX-2. However, side effects almost always cropped up, even after clinical trials that seemed to indicate none. This often occurs because trials are conducted within very limited parameters; once the drug has been approved for mass distribution, however, the number of people taking it and the length of time that it is taken increase dramatically. Several COX-2 drugs that have been popular in recent years fit this pattern: initially successful in clinical trials, subsequent studies showed them to have serious, potentially lethal side effects.Though prostaglandin chemistry and enzymology have been studied for half a century, pinpointing the exact role of the molecules in physiological processes still remains a challenge for researchers. Hence it is not surprising that recent therapeutic attempts to interfere with the formation of certain prostaglandins have produced unexpected side effects. It now seems that the hype surrounding COX-2 drugs may have been premature.Q. The primary purpose of this passage is toa)explain the therapeutic benefits of a new type of pain relieverb)initiate a debate concerning the benefits of COX-2 inhibitorsc)warn the public that clinical trials cannot ensure drug safetyd)describe the impetus for and result of COX-2 inhibitors’ introductione)introduceres earch findings to support COX-2 inhibitors over COX-1 inhibitorsCorrect answer is option 'D'. Can you explain this answer? has been provided alongside types of In recent years, a class of drugs known as COX-2 inhibitors has gotten much publicity for the drugs’ power to relieve inflammation and pain. These drugs are relatively new to the pharmaceutical industry, their mechanisms of action having been discovered only in 1971. That year, John Vane discovered the relationship between nonsteroidal antiinflammatory drugs, such as aspirin, and a group of molecules, called prostaglandins, responsible for producing the sensation of pain in the human body, among other functions.Prostaglandins were first discovered in the 1930s and are now known to be generated by most mammalian tissues in response to external stimuli. Unlike classical hormones that are synthesized in one tissue but act on a distant one, prostaglandins act on the cells that produce them or on cells located close to the prostaglandins’ cells of origin.Aspirin alleviates pain by inhibiting the function of an enzyme called cyclooxygenase or COX; this inhibition prevents the production of prostaglandins. The three forms of this enzyme, COX-1, COX-2, and COX-3, all stimulate the production of prostaglandins, but each serves a different purpose. COX-1 functions to protect the stomach from irritating gastric acids. COX-2 functions to induce inflammation in injured tissue and COX-3 functions to control the sensation of pain. Aspirin and other similar drugs, such as naproxen, inhibit both COX-1 and COX-2, sometimes producing or aggravating stomach ulcers in patients who take them.In order to eliminate the side effects of aspirin and related drugs, several pharmaceutical companies in the 1990s developed drugs that inhibited only COX-2. However, side effects almost always cropped up, even after clinical trials that seemed to indicate none. This often occurs because trials are conducted within very limited parameters; once the drug has been approved for mass distribution, however, the number of people taking it and the length of time that it is taken increase dramatically. Several COX-2 drugs that have been popular in recent years fit this pattern: initially successful in clinical trials, subsequent studies showed them to have serious, potentially lethal side effects.Though prostaglandin chemistry and enzymology have been studied for half a century, pinpointing the exact role of the molecules in physiological processes still remains a challenge for researchers. Hence it is not surprising that recent therapeutic attempts to interfere with the formation of certain prostaglandins have produced unexpected side effects. It now seems that the hype surrounding COX-2 drugs may have been premature.Q. The primary purpose of this passage is toa)explain the therapeutic benefits of a new type of pain relieverb)initiate a debate concerning the benefits of COX-2 inhibitorsc)warn the public that clinical trials cannot ensure drug safetyd)describe the impetus for and result of COX-2 inhibitors’ introductione)introduceres earch findings to support COX-2 inhibitors over COX-1 inhibitorsCorrect answer is option 'D'. Can you explain this answer? theory, EduRev gives you an ample number of questions to practice In recent years, a class of drugs known as COX-2 inhibitors has gotten much publicity for the drugs’ power to relieve inflammation and pain. These drugs are relatively new to the pharmaceutical industry, their mechanisms of action having been discovered only in 1971. That year, John Vane discovered the relationship between nonsteroidal antiinflammatory drugs, such as aspirin, and a group of molecules, called prostaglandins, responsible for producing the sensation of pain in the human body, among other functions.Prostaglandins were first discovered in the 1930s and are now known to be generated by most mammalian tissues in response to external stimuli. Unlike classical hormones that are synthesized in one tissue but act on a distant one, prostaglandins act on the cells that produce them or on cells located close to the prostaglandins’ cells of origin.Aspirin alleviates pain by inhibiting the function of an enzyme called cyclooxygenase or COX; this inhibition prevents the production of prostaglandins. The three forms of this enzyme, COX-1, COX-2, and COX-3, all stimulate the production of prostaglandins, but each serves a different purpose. COX-1 functions to protect the stomach from irritating gastric acids. COX-2 functions to induce inflammation in injured tissue and COX-3 functions to control the sensation of pain. Aspirin and other similar drugs, such as naproxen, inhibit both COX-1 and COX-2, sometimes producing or aggravating stomach ulcers in patients who take them.In order to eliminate the side effects of aspirin and related drugs, several pharmaceutical companies in the 1990s developed drugs that inhibited only COX-2. However, side effects almost always cropped up, even after clinical trials that seemed to indicate none. This often occurs because trials are conducted within very limited parameters; once the drug has been approved for mass distribution, however, the number of people taking it and the length of time that it is taken increase dramatically. Several COX-2 drugs that have been popular in recent years fit this pattern: initially successful in clinical trials, subsequent studies showed them to have serious, potentially lethal side effects.Though prostaglandin chemistry and enzymology have been studied for half a century, pinpointing the exact role of the molecules in physiological processes still remains a challenge for researchers. Hence it is not surprising that recent therapeutic attempts to interfere with the formation of certain prostaglandins have produced unexpected side effects. It now seems that the hype surrounding COX-2 drugs may have been premature.Q. The primary purpose of this passage is toa)explain the therapeutic benefits of a new type of pain relieverb)initiate a debate concerning the benefits of COX-2 inhibitorsc)warn the public that clinical trials cannot ensure drug safetyd)describe the impetus for and result of COX-2 inhibitors’ introductione)introduceres earch findings to support COX-2 inhibitors over COX-1 inhibitorsCorrect answer is option 'D'. Can you explain this answer? tests, examples and also practice GMAT tests.

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