Test: Reading Comprehension- 2 - GMAT MCQ

A recent ball-catching experiment conducted in space by astronauts on board a space shuttle has led neuroscientists to conclude that the brain contains an internal model of gravity that is both powerful and persistent. At the same time, the experiment provided evidence that the brain can adapt to environments in which the force of downward acceleration is less pronounced than it is on earth.
The experiment’s outcomes suggested that an individual’s understanding of motion is hard-wired from an earthcentric perspective. In the experiment, the astronauts were asked to catch balls released from a spring-loaded cannon.
Analyzing data gathered from infrared tracking cameras and electrodes placed on the astronauts’ arms, McIntyre, the experiment’s principal designer, noticed that the astronauts’ anticipation of the ball’s motion was slightly off. Though they were able to catch the ball, the astronauts expected the ball to move faster than it did. He theorized that this over-anticipation is due to the fact that the brain expects the force of the earth’s gravity to act on the ball.
The experiment also demonstrates the brain’s ability to adjust to conditions that run counter to its pre-set wiring.
While the astronauts did not adapt to the conditions in space for some time, by day 15 of the experiment, the amplitude of the premature arm movements decreased and a new well-timed arm movement immediately preceded the catch. Upon returning to earth, the astronauts again mis-anticipated the ball’s motion, though this time the ball moved faster than anticipated. However, the astronauts were able to adjust back to the earth’s gravitational effect on the balls much more quickly than they had been able to adapt to the conditions in space.
Many scientists view the findings as a first step in research that could have serious practical benefits. The ability of astronauts to safely explore space and investigate other planets is dependent on understanding the differences between our physical reactions on earth and elsewhere.
On another level, understanding timing processes in the body might lead to the development of treatments for coordination problems experienced by individuals with certain types of brain damage.
Q.
The passage implies which of the following about gravity?

A recent ball-catching experiment conducted in space by astronauts on board a space shuttle has led neuroscientists to conclude that the brain contains an internal model of gravity that is both powerful and persistent. At the same time, the experiment provided evidence that the brain can adapt to environments in which the force of downward acceleration is less pronounced than it is on earth.
The experiment’s outcomes suggested that an individual’s understanding of motion is hard-wired from an earthcentric perspective. In the experiment, the astronauts were asked to catch balls released from a spring-loaded cannon.
Analyzing data gathered from infrared tracking cameras and electrodes placed on the astronauts’ arms, McIntyre, the experiment’s principal designer, noticed that the astronauts’ anticipation of the ball’s motion was slightly off. Though they were able to catch the ball, the astronauts expected the ball to move faster than it did. He theorized that this over-anticipation is due to the fact that the brain expects the force of the earth’s gravity to act on the ball.
The experiment also demonstrates the brain’s ability to adjust to conditions that run counter to its pre-set wiring.
While the astronauts did not adapt to the conditions in space for some time, by day 15 of the experiment, the amplitude of the premature arm movements decreased and a new well-timed arm movement immediately preceded the catch. Upon returning to earth, the astronauts again mis-anticipated the ball’s motion, though this time the ball moved faster than anticipated. However, the astronauts were able to adjust back to the earth’s gravitational effect on the balls much more quickly than they had been able to adapt to the conditions in space.
Many scientists view the findings as a first step in research that could have serious practical benefits. The ability of astronauts to safely explore space and investigate other planets is dependent on understanding the differences between our physical reactions on earth and elsewhere.
On another level, understanding timing processes in the body might lead to the development of treatments for coordination problems experienced by individuals with certain types of brain damage.
Q.
The function of the final paragraph is to

A recent ball-catching experiment conducted in space by astronauts on board a space shuttle has led neuroscientists to conclude that the brain contains an internal model of gravity that is both powerful and persistent. At the same time, the experiment provided evidence that the brain can adapt to environments in which the force of downward acceleration is less pronounced than it is on earth.
The experiment’s outcomes suggested that an individual’s understanding of motion is hard-wired from an earthcentric perspective. In the experiment, the astronauts were asked to catch balls released from a spring-loaded cannon.
Analyzing data gathered from infrared tracking cameras and electrodes placed on the astronauts’ arms, McIntyre, the experiment’s principal designer, noticed that the astronauts’ anticipation of the ball’s motion was slightly off. Though they were able to catch the ball, the astronauts expected the ball to move faster than it did. He theorized that this over-anticipation is due to the fact that the brain expects the force of the earth’s gravity to act on the ball.
The experiment also demonstrates the brain’s ability to adjust to conditions that run counter to its pre-set wiring.
While the astronauts did not adapt to the conditions in space for some time, by day 15 of the experiment, the amplitude of the premature arm movements decreased and a new well-timed arm movement immediately preceded the catch. Upon returning to earth, the astronauts again mis-anticipated the ball’s motion, though this time the ball moved faster than anticipated. However, the astronauts were able to adjust back to the earth’s gravitational effect on the balls much more quickly than they had been able to adapt to the conditions in space.
Many scientists view the findings as a first step in research that could have serious practical benefits. The ability of astronauts to safely explore space and investigate other planets is dependent on understanding the differences between our physical reactions on earth and elsewhere.
On another level, understanding timing processes in the body might lead to the development of treatments for coordination problems experienced by individuals with certain types of brain damage.
Q.
The primary purpose of the passage is to:

A recent ball-catching experiment conducted in space by astronauts on board a space shuttle has led neuroscientists to conclude that the brain contains an internal model of gravity that is both powerful and persistent. At the same time, the experiment provided evidence that the brain can adapt to environments in which the force of downward acceleration is less pronounced than it is on earth.
The experiment’s outcomes suggested that an individual’s understanding of motion is hard-wired from an earthcentric perspective. In the experiment, the astronauts were asked to catch balls released from a spring-loaded cannon.
Analyzing data gathered from infrared tracking cameras and electrodes placed on the astronauts’ arms, McIntyre, the experiment’s principal designer, noticed that the astronauts’ anticipation of the ball’s motion was slightly off. Though they were able to catch the ball, the astronauts expected the ball to move faster than it did. He theorized that this over-anticipation is due to the fact that the brain expects the force of the earth’s gravity to act on the ball.
The experiment also demonstrates the brain’s ability to adjust to conditions that run counter to its pre-set wiring.
While the astronauts did not adapt to the conditions in space for some time, by day 15 of the experiment, the amplitude of the premature arm movements decreased and a new well-timed arm movement immediately preceded the catch. Upon returning to earth, the astronauts again mis-anticipated the ball’s motion, though this time the ball moved faster than anticipated. However, the astronauts were able to adjust back to the earth’s gravitational effect on the balls much more quickly than they had been able to adapt to the conditions in space.
Many scientists view the findings as a first step in research that could have serious practical benefits. The ability of astronauts to safely explore space and investigate other planets is dependent on understanding the differences between our physical reactions on earth and elsewhere.
On another level, understanding timing processes in the body might lead to the development of treatments for coordination problems experienced by individuals with certain types of brain damage.
Q.
According to the passage, research suggests that the brain’s built-in understanding of gravity is

Symptoms of Parkinson’s Disease, such as tremors, are thought to be caused by low dopamine levels in the brain.
Current treatments of Parkinson’s disease are primarily reactionary, aiming to replenish dopamine levels after dopamine-producing neurons in the brain have died.
Without a more detailed understanding of the behavior of dopamine-producing neurons, it has been impossible to develop treatments that would prevent the destruction of these neurons in Parkinson’s patients.
Recent research provides insight into the inner workings of dopamine-producing neurons, and may lead to a new drug treatment that would proactively protect the neurons from decay. By examining the alpha-synuclein protein in yeast cells, scientists have determined that toxic levels of the protein have a detrimental effect on protein transfer within the cell. More specifically, high levels of alphasynuclein disrupt the flow of proteins from the endoplasmic reticulum, the site of protein production in the cell, to the Golgi apparatus, the component of the cell that modifies and sorts the proteins before sending them to their final destinations within the cell. When the smooth transfer of proteins from the endoplasmic reticulum to the Golgi apparatus is interrupted, the cell dies.
With this in mind, researchers conducted a genetic screen in yeast cells in order to identify any gene that works to reverse the toxic levels of alpha-synuclein in the cell.
Researchers discovered that such a gene does in fact exist, and have located the genetic counterpart in mammalian nerve cells, or neurons. This discovery has led to new hopes that drug therapy could potentially activate this gene, thereby suppressing the toxicity of alpha-synuclein in dopamine-producing neurons.
While drug therapy to suppress alpha-synuclein has been examined in yeast, fruitflies, roundworms, and cultures of rat neurons, researchers are hesitant to conclude that such therapies will prove successful on human patients.
Alpha-synuclein toxicity seems to be one cause for the death of dopamine-producing neurons in Parkinson’s patients, but other causes may exist. Most scientists involved with Parkinson’s research do agree, however, that such promising early results provide a basis for further testing.
Q.
It can be inferred from the passage that a yeast cell with toxic levels of alpha-synuclein will die because

Symptoms of Parkinson’s Disease, such as tremors, are thought to be caused by low dopamine levels in the brain.
Current treatments of Parkinson’s disease are primarily reactionary, aiming to replenish dopamine levels after dopamine-producing neurons in the brain have died.
Without a more detailed understanding of the behavior of dopamine-producing neurons, it has been impossible to develop treatments that would prevent the destruction of these neurons in Parkinson’s patients.
Recent research provides insight into the inner workings of dopamine-producing neurons, and may lead to a new drug treatment that would proactively protect the neurons from decay. By examining the alpha-synuclein protein in yeast cells, scientists have determined that toxic levels of the protein have a detrimental effect on protein transfer within the cell. More specifically, high levels of alphasynuclein disrupt the flow of proteins from the endoplasmic reticulum, the site of protein production in the cell, to the Golgi apparatus, the component of the cell that modifies and sorts the proteins before sending them to their final destinations within the cell. When the smooth transfer of proteins from the endoplasmic reticulum to the Golgi apparatus is interrupted, the cell dies.
With this in mind, researchers conducted a genetic screen in yeast cells in order to identify any gene that works to reverse the toxic levels of alpha-synuclein in the cell.
Researchers discovered that such a gene does in fact exist, and have located the genetic counterpart in mammalian nerve cells, or neurons. This discovery has led to new hopes that drug therapy could potentially activate this gene, thereby suppressing the toxicity of alpha-synuclein in dopamine-producing neurons.
While drug therapy to suppress alpha-synuclein has been examined in yeast, fruitflies, roundworms, and cultures of rat neurons, researchers are hesitant to conclude that such therapies will prove successful on human patients.
Alpha-synuclein toxicity seems to be one cause for the death of dopamine-producing neurons in Parkinson’s patients, but other causes may exist. Most scientists involved with Parkinson’s research do agree, however, that such promising early results provide a basis for further testing.
Q.
One function of the third paragraph of the passage is to

Symptoms of Parkinson’s Disease, such as tremors, are thought to be caused by low dopamine levels in the brain.
Current treatments of Parkinson’s disease are primarily reactionary, aiming to replenish dopamine levels after dopamine-producing neurons in the brain have died.
Without a more detailed understanding of the behavior of dopamine-producing neurons, it has been impossible to develop treatments that would prevent the destruction of these neurons in Parkinson’s patients.
Recent research provides insight into the inner workings of dopamine-producing neurons, and may lead to a new drug treatment that would proactively protect the neurons from decay. By examining the alpha-synuclein protein in yeast cells, scientists have determined that toxic levels of the protein have a detrimental effect on protein transfer within the cell. More specifically, high levels of alphasynuclein disrupt the flow of proteins from the endoplasmic reticulum, the site of protein production in the cell, to the Golgi apparatus, the component of the cell that modifies and sorts the proteins before sending them to their final destinations within the cell. When the smooth transfer of proteins from the endoplasmic reticulum to the Golgi apparatus is interrupted, the cell dies.
With this in mind, researchers conducted a genetic screen in yeast cells in order to identify any gene that works to reverse the toxic levels of alpha-synuclein in the cell.
Researchers discovered that such a gene does in fact exist, and have located the genetic counterpart in mammalian nerve cells, or neurons. This discovery has led to new hopes that drug therapy could potentially activate this gene, thereby suppressing the toxicity of alpha-synuclein in dopamine-producing neurons.
While drug therapy to suppress alpha-synuclein has been examined in yeast, fruitflies, roundworms, and cultures of rat neurons, researchers are hesitant to conclude that such therapies will prove successful on human patients.
Alpha-synuclein toxicity seems to be one cause for the death of dopamine-producing neurons in Parkinson’s patients, but other causes may exist. Most scientists involved with Parkinson’s research do agree, however, that such promising early results provide a basis for further testing.
Q.
It can be inferred from the passage that current treatments of Parkinson’s Disease

Symptoms of Parkinson’s Disease, such as tremors, are thought to be caused by low dopamine levels in the brain.
Current treatments of Parkinson’s disease are primarily reactionary, aiming to replenish dopamine levels after dopamine-producing neurons in the brain have died.
Without a more detailed understanding of the behavior of dopamine-producing neurons, it has been impossible to develop treatments that would prevent the destruction of these neurons in Parkinson’s patients.
Recent research provides insight into the inner workings of dopamine-producing neurons, and may lead to a new drug treatment that would proactively protect the neurons from decay. By examining the alpha-synuclein protein in yeast cells, scientists have determined that toxic levels of the protein have a detrimental effect on protein transfer within the cell. More specifically, high levels of alphasynuclein disrupt the flow of proteins from the endoplasmic reticulum, the site of protein production in the cell, to the Golgi apparatus, the component of the cell that modifies and sorts the proteins before sending them to their final destinations within the cell. When the smooth transfer of proteins from the endoplasmic reticulum to the Golgi apparatus is interrupted, the cell dies.
With this in mind, researchers conducted a genetic screen in yeast cells in order to identify any gene that works to reverse the toxic levels of alpha-synuclein in the cell.
Researchers discovered that such a gene does in fact exist, and have located the genetic counterpart in mammalian nerve cells, or neurons. This discovery has led to new hopes that drug therapy could potentially activate this gene, thereby suppressing the toxicity of alpha-synuclein in dopamine-producing neurons.
While drug therapy to suppress alpha-synuclein has been examined in yeast, fruitflies, roundworms, and cultures of rat neurons, researchers are hesitant to conclude that such therapies will prove successful on human patients.
Alpha-synuclein toxicity seems to be one cause for the death of dopamine-producing neurons in Parkinson’s patients, but other causes may exist. Most scientists involved with Parkinson’s research do agree, however, that such promising early results provide a basis for further testing.
Q.
According to the passage, which of the following represents the chronology of a typical protein life in a healthy yeast cell?

The single-celled parasite known as Toxoplasma gondii infects more than half of the world’s human population without creating any noticeable symptoms. Once inside the human body, Toxoplasma rapidly spreads to the heart and other organs. It can even penetrate the tight barrier that normally protects the brain from most pathogens.
Yet, the blood of infected persons carries very few freefloating Toxoplasma cells. Scientists have long been puzzled by this ability of Toxoplasma to parasitize the human body without triggering an immune response and without an appreciable presence in the bloodstream.
Recent research, however, has shed light on the ways in which Toxoplasma achieves its remarkable infiltration of the human body.
Though there are few individual Toxoplasma cells coursing freely in the blood of an infected person, scientists have discovered that the parasite is quite common in certain cells, known as dendritic cells, involved in the human immune system. Dendritic cells are found in the digestive tract and frequently come into contact with the various pathogens that enter the human body through food and water. When the dendritic cells encounter pathogens, they travel to lymph nodes and relay this information to other immune cells that then take action against the reported pathogen. Scientists have found, however, that Toxoplasma is capable of hijacking dendritic cells, forcing them from their usual activity and using them as a form of transportation to infect the human body quickly. Without this transport mechanism, Toxoplasma could not reach the better-protected areas of the body.
Toxoplasma invades the human body through consumption of the undercooked meat of infected animals, primarily pigs and chickens. Other animals, such as cats, can become infected as well. In fact, cats are a necessary component in the reproductive cycle of Toxoplasma, since the animal’s intestines are the parasite’s sole breeding ground.
Toxoplasma creates egg-like cysts, known as oocysts, in the cats’ intestines. These oocysts are shed in the cats’ droppings and contaminate ground water and soil, eventually finding their way into the food chain. Because Toxoplasma must somehow find its way into a new host cat in order to reproduce, it cannot kill its current host.
Instead, it waits for the host, usually a small rodent, to be eaten by a cat, thus providing Toxoplasma the opportunity to reproduce.
Q.
It can be inferred from the passage that which of the following statements is true of dendritic cells in the human body?

The single-celled parasite known as Toxoplasma gondii infects more than half of the world’s human population without creating any noticeable symptoms. Once inside the human body, Toxoplasma rapidly spreads to the heart and other organs. It can even penetrate the tight barrier that normally protects the brain from most pathogens.
Yet, the blood of infected persons carries very few freefloating Toxoplasma cells. Scientists have long been puzzled by this ability of Toxoplasma to parasitize the human body without triggering an immune response and without an appreciable presence in the bloodstream.
Recent research, however, has shed light on the ways in which Toxoplasma achieves its remarkable infiltration of the human body.
Though there are few individual Toxoplasma cells coursing freely in the blood of an infected person, scientists have discovered that the parasite is quite common in certain cells, known as dendritic cells, involved in the human immune system. Dendritic cells are found in the digestive tract and frequently come into contact with the various pathogens that enter the human body through food and water. When the dendritic cells encounter pathogens, they travel to lymph nodes and relay this information to other immune cells that then take action against the reported pathogen. Scientists have found, however, that Toxoplasma is capable of hijacking dendritic cells, forcing them from their usual activity and using them as a form of transportation to infect the human body quickly. Without this transport mechanism, Toxoplasma could not reach the better-protected areas of the body.
Toxoplasma invades the human body through consumption of the undercooked meat of infected animals, primarily pigs and chickens. Other animals, such as cats, can become infected as well. In fact, cats are a necessary component in the reproductive cycle of Toxoplasma, since the animal’s intestines are the parasite’s sole breeding ground.
Toxoplasma creates egg-like cysts, known as oocysts, in the cats’ intestines. These oocysts are shed in the cats’ droppings and contaminate ground water and soil, eventually finding their way into the food chain. Because Toxoplasma must somehow find its way into a new host cat in order to reproduce, it cannot kill its current host.
Instead, it waits for the host, usually a small rodent, to be eaten by a cat, thus providing Toxoplasma the opportunity to reproduce.
Q.
According to the passage, all of the following are true of Toxoplasma gondii EXCEPT

The single-celled parasite known as Toxoplasma gondii infects more than half of the world’s human population without creating any noticeable symptoms. Once inside the human body, Toxoplasma rapidly spreads to the heart and other organs. It can even penetrate the tight barrier that normally protects the brain from most pathogens.
Yet, the blood of infected persons carries very few freefloating Toxoplasma cells. Scientists have long been puzzled by this ability of Toxoplasma to parasitize the human body without triggering an immune response and without an appreciable presence in the bloodstream.
Recent research, however, has shed light on the ways in which Toxoplasma achieves its remarkable infiltration of the human body.
Though there are few individual Toxoplasma cells coursing freely in the blood of an infected person, scientists have discovered that the parasite is quite common in certain cells, known as dendritic cells, involved in the human immune system. Dendritic cells are found in the digestive tract and frequently come into contact with the various pathogens that enter the human body through food and water. When the dendritic cells encounter pathogens, they travel to lymph nodes and relay this information to other immune cells that then take action against the reported pathogen. Scientists have found, however, that Toxoplasma is capable of hijacking dendritic cells, forcing them from their usual activity and using them as a form of transportation to infect the human body quickly. Without this transport mechanism, Toxoplasma could not reach the better-protected areas of the body.
Toxoplasma invades the human body through consumption of the undercooked meat of infected animals, primarily pigs and chickens. Other animals, such as cats, can become infected as well. In fact, cats are a necessary component in the reproductive cycle of Toxoplasma, since the animal’s intestines are the parasite’s sole breeding ground.
Toxoplasma creates egg-like cysts, known as oocysts, in the cats’ intestines. These oocysts are shed in the cats’ droppings and contaminate ground water and soil, eventually finding their way into the food chain. Because Toxoplasma must somehow find its way into a new host cat in order to reproduce, it cannot kill its current host.
Instead, it waits for the host, usually a small rodent, to be eaten by a cat, thus providing Toxoplasma the opportunity to reproduce.
Q.
The second paragraph performs which of the following functions in the passage?

The single-celled parasite known as Toxoplasma gondii infects more than half of the world’s human population without creating any noticeable symptoms. Once inside the human body, Toxoplasma rapidly spreads to the heart and other organs. It can even penetrate the tight barrier that normally protects the brain from most pathogens.
Yet, the blood of infected persons carries very few freefloating Toxoplasma cells. Scientists have long been puzzled by this ability of Toxoplasma to parasitize the human body without triggering an immune response and without an appreciable presence in the bloodstream.
Recent research, however, has shed light on the ways in which Toxoplasma achieves its remarkable infiltration of the human body.
Though there are few individual Toxoplasma cells coursing freely in the blood of an infected person, scientists have discovered that the parasite is quite common in certain cells, known as dendritic cells, involved in the human immune system. Dendritic cells are found in the digestive tract and frequently come into contact with the various pathogens that enter the human body through food and water. When the dendritic cells encounter pathogens, they travel to lymph nodes and relay this information to other immune cells that then take action against the reported pathogen. Scientists have found, however, that Toxoplasma is capable of hijacking dendritic cells, forcing them from their usual activity and using them as a form of transportation to infect the human body quickly. Without this transport mechanism, Toxoplasma could not reach the better-protected areas of the body.
Toxoplasma invades the human body through consumption of the undercooked meat of infected animals, primarily pigs and chickens. Other animals, such as cats, can become infected as well. In fact, cats are a necessary component in the reproductive cycle of Toxoplasma, since the animal’s intestines are the parasite’s sole breeding ground.
Toxoplasma creates egg-like cysts, known as oocysts, in the cats’ intestines. These oocysts are shed in the cats’ droppings and contaminate ground water and soil, eventually finding their way into the food chain. Because Toxoplasma must somehow find its way into a new host cat in order to reproduce, it cannot kill its current host.
Instead, it waits for the host, usually a small rodent, to be eaten by a cat, thus providing Toxoplasma the opportunity to reproduce.
Q.
Which of the following is the most likely outcome for Toxoplasma cells that invade the human body?

The single-celled parasite known as Toxoplasma gondii infects more than half of the world’s human population without creating any noticeable symptoms. Once inside the human body, Toxoplasma rapidly spreads to the heart and other organs. It can even penetrate the tight barrier that normally protects the brain from most pathogens.
Yet, the blood of infected persons carries very few freefloating Toxoplasma cells. Scientists have long been puzzled by this ability of Toxoplasma to parasitize the human body without triggering an immune response and without an appreciable presence in the bloodstream.
Recent research, however, has shed light on the ways in which Toxoplasma achieves its remarkable infiltration of the human body.
Though there are few individual Toxoplasma cells coursing freely in the blood of an infected person, scientists have discovered that the parasite is quite common in certain cells, known as dendritic cells, involved in the human immune system. Dendritic cells are found in the digestive tract and frequently come into contact with the various pathogens that enter the human body through food and water. When the dendritic cells encounter pathogens, they travel to lymph nodes and relay this information to other immune cells that then take action against the reported pathogen. Scientists have found, however, that Toxoplasma is capable of hijacking dendritic cells, forcing them from their usual activity and using them as a form of transportation to infect the human body quickly. Without this transport mechanism, Toxoplasma could not reach the better-protected areas of the body.
Toxoplasma invades the human body through consumption of the undercooked meat of infected animals, primarily pigs and chickens. Other animals, such as cats, can become infected as well. In fact, cats are a necessary component in the reproductive cycle of Toxoplasma, since the animal’s intestines are the parasite’s sole breeding ground.
Toxoplasma creates egg-like cysts, known as oocysts, in the cats’ intestines. These oocysts are shed in the cats’ droppings and contaminate ground water and soil, eventually finding their way into the food chain. Because Toxoplasma must somehow find its way into a new host cat in order to reproduce, it cannot kill its current host.
Instead, it waits for the host, usually a small rodent, to be eaten by a cat, thus providing Toxoplasma the opportunity to reproduce.
Q.
The author mentions “pigs and chickens” in the final paragraph in order to

Antibiotics are chemical substances that kill or inhibit the growth of bacteria. The success of antibiotics against disease-causing bacteria is one of modern medicine’s great achievements. However, many bacteria harmful to humans have developed ways to circumvent the effects of antibiotics, and many infectious diseases are now much more difficult to treat than they were just a few decades ago. Antibiotic resistance is an especially difficult problem for hospitals with critically ill patients who are less able to fight off infections without the help of antibiotics.
Bacteria can develop antibiotic resistance because they have the ability to adapt quickly to new environmental conditions. Most commonly, bacteria share with each other genetic material called resistance plasmids; these shared plasmids, which contain the genetic code enabling antibiotic resistance, can spread throughout a bacterial population to create a strain of resistant bacteria. Less commonly, a natural mutation that enables antibiotic resistance takes place within the chromosome of the bacteria, and the resulting strain of bacteria can reproduce and become dominant via natural selection. In the absence of human involvement, however, bacteria in the wild rarely develop resistance to antibiotics.
In the United States, animals raised on industrial-scale factory farms are routinely administered low levels of antibiotics in their feed not as a cure for ongoing maladies, but primarily as a growth-enhancing agent to produce more meat and also as a prophylactic measure to compensate for overcrowded and unsanitary conditions.
Currently, several antibiotics that are used in human medical treatment are administered non-therapeutically to healthy livestock and poultry. Examples include tetracycline, penicillin and erythromycin. This long-term non-therapeutic feeding of antibiotics to animals creates the ideal conditions for the development of antibioticresistant bacteria, as it kills the susceptible bacteria while leaving the resistant strains to reproduce and flourish.
Europe is far ahead of the United States in the responsible use of antibiotics: On January 1, 2006, the European Union banned the feeding of all antibiotics to livestock for nontherapeutic purposes. This sweeping policy follows a 1998 ban on the non-therapeutic use of four medically-important antibiotics on animals. The time has come for the United States to follow Europe’s lead.
Q.
Based on the information in the passage, to which of the following practices would the author most likely be opposed?

Antibiotics are chemical substances that kill or inhibit the growth of bacteria. The success of antibiotics against disease-causing bacteria is one of modern medicine’s great achievements. However, many bacteria harmful to humans have developed ways to circumvent the effects of antibiotics, and many infectious diseases are now much more difficult to treat than they were just a few decades ago. Antibiotic resistance is an especially difficult problem for hospitals with critically ill patients who are less able to fight off infections without the help of antibiotics.
Bacteria can develop antibiotic resistance because they have the ability to adapt quickly to new environmental conditions. Most commonly, bacteria share with each other genetic material called resistance plasmids; these shared plasmids, which contain the genetic code enabling antibiotic resistance, can spread throughout a bacterial population to create a strain of resistant bacteria. Less commonly, a natural mutation that enables antibiotic resistance takes place within the chromosome of the bacteria, and the resulting strain of bacteria can reproduce and become dominant via natural selection. In the absence of human involvement, however, bacteria in the wild rarely develop resistance to antibiotics.
In the United States, animals raised on industrial-scale factory farms are routinely administered low levels of antibiotics in their feed not as a cure for ongoing maladies, but primarily as a growth-enhancing agent to produce more meat and also as a prophylactic measure to compensate for overcrowded and unsanitary conditions.
Currently, several antibiotics that are used in human medical treatment are administered non-therapeutically to healthy livestock and poultry. Examples include tetracycline, penicillin and erythromycin. This long-term non-therapeutic feeding of antibiotics to animals creates the ideal conditions for the development of antibioticresistant bacteria, as it kills the susceptible bacteria while leaving the resistant strains to reproduce and flourish.
Europe is far ahead of the United States in the responsible use of antibiotics: On January 1, 2006, the European Union banned the feeding of all antibiotics to livestock for nontherapeutic purposes. This sweeping policy follows a 1998 ban on the non-therapeutic use of four medically-important antibiotics on animals. The time has come for the United States to follow Europe’s lead.
Q.
Based on the information in the passage, which of the following statements can be inferred?

Antibiotics are chemical substances that kill or inhibit the growth of bacteria. The success of antibiotics against disease-causing bacteria is one of modern medicine’s great achievements. However, many bacteria harmful to humans have developed ways to circumvent the effects of antibiotics, and many infectious diseases are now much more difficult to treat than they were just a few decades ago. Antibiotic resistance is an especially difficult problem for hospitals with critically ill patients who are less able to fight off infections without the help of antibiotics.
Bacteria can develop antibiotic resistance because they have the ability to adapt quickly to new environmental conditions. Most commonly, bacteria share with each other genetic material called resistance plasmids; these shared plasmids, which contain the genetic code enabling antibiotic resistance, can spread throughout a bacterial population to create a strain of resistant bacteria. Less commonly, a natural mutation that enables antibiotic resistance takes place within the chromosome of the bacteria, and the resulting strain of bacteria can reproduce and become dominant via natural selection. In the absence of human involvement, however, bacteria in the wild rarely develop resistance to antibiotics.
In the United States, animals raised on industrial-scale factory farms are routinely administered low levels of antibiotics in their feed not as a cure for ongoing maladies, but primarily as a growth-enhancing agent to produce more meat and also as a prophylactic measure to compensate for overcrowded and unsanitary conditions.
Currently, several antibiotics that are used in human medical treatment are administered non-therapeutically to healthy livestock and poultry. Examples include tetracycline, penicillin and erythromycin. This long-term non-therapeutic feeding of antibiotics to animals creates the ideal conditions for the development of antibioticresistant bacteria, as it kills the susceptible bacteria while leaving the resistant strains to reproduce and flourish.
Europe is far ahead of the United States in the responsible use of antibiotics: On January 1, 2006, the European Union banned the feeding of all antibiotics to livestock for nontherapeutic purposes. This sweeping policy follows a 1998 ban on the non-therapeutic use of four medically-important antibiotics on animals. The time has come for the United States to follow Europe’s lead.
Q.
Which of the following best describes what the phrase “prophylactic measure” in the third paragraph means?

Antibiotics are chemical substances that kill or inhibit the growth of bacteria. The success of antibiotics against disease-causing bacteria is one of modern medicine’s great achievements. However, many bacteria harmful to humans have developed ways to circumvent the effects of antibiotics, and many infectious diseases are now much more difficult to treat than they were just a few decades ago. Antibiotic resistance is an especially difficult problem for hospitals with critically ill patients who are less able to fight off infections without the help of antibiotics.
Bacteria can develop antibiotic resistance because they have the ability to adapt quickly to new environmental conditions. Most commonly, bacteria share with each other genetic material called resistance plasmids; these shared plasmids, which contain the genetic code enabling antibiotic resistance, can spread throughout a bacterial population to create a strain of resistant bacteria. Less commonly, a natural mutation that enables antibiotic resistance takes place within the chromosome of the bacteria, and the resulting strain of bacteria can reproduce and become dominant via natural selection. In the absence of human involvement, however, bacteria in the wild rarely develop resistance to antibiotics.
In the United States, animals raised on industrial-scale factory farms are routinely administered low levels of antibiotics in their feed not as a cure for ongoing maladies, but primarily as a growth-enhancing agent to produce more meat and also as a prophylactic measure to compensate for overcrowded and unsanitary conditions.
Currently, several antibiotics that are used in human medical treatment are administered non-therapeutically to healthy livestock and poultry. Examples include tetracycline, penicillin and erythromycin. This long-term non-therapeutic feeding of antibiotics to animals creates the ideal conditions for the development of antibioticresistant bacteria, as it kills the susceptible bacteria while leaving the resistant strains to reproduce and flourish.
Europe is far ahead of the United States in the responsible use of antibiotics: On January 1, 2006, the European Union banned the feeding of all antibiotics to livestock for nontherapeutic purposes. This sweeping policy follows a 1998 ban on the non-therapeutic use of four medically-important antibiotics on animals. The time has come for the United States to follow Europe’s lead.
Q.
The passage is primarily concerned with

Antibiotics are chemical substances that kill or inhibit the growth of bacteria. The success of antibiotics against disease-causing bacteria is one of modern medicine’s great achievements. However, many bacteria harmful to humans have developed ways to circumvent the effects of antibiotics, and many infectious diseases are now much more difficult to treat than they were just a few decades ago. Antibiotic resistance is an especially difficult problem for hospitals with critically ill patients who are less able to fight off infections without the help of antibiotics.
Bacteria can develop antibiotic resistance because they have the ability to adapt quickly to new environmental conditions. Most commonly, bacteria share with each other genetic material called resistance plasmids; these shared plasmids, which contain the genetic code enabling antibiotic resistance, can spread throughout a bacterial population to create a strain of resistant bacteria. Less commonly, a natural mutation that enables antibiotic resistance takes place within the chromosome of the bacteria, and the resulting strain of bacteria can reproduce and become dominant via natural selection. In the absence of human involvement, however, bacteria in the wild rarely develop resistance to antibiotics.
In the United States, animals raised on industrial-scale factory farms are routinely administered low levels of antibiotics in their feed not as a cure for ongoing maladies, but primarily as a growth-enhancing agent to produce more meat and also as a prophylactic measure to compensate for overcrowded and unsanitary conditions.
Currently, several antibiotics that are used in human medical treatment are administered non-therapeutically to healthy livestock and poultry. Examples include tetracycline, penicillin and erythromycin. This long-term non-therapeutic feeding of antibiotics to animals creates the ideal conditions for the development of antibioticresistant bacteria, as it kills the susceptible bacteria while leaving the resistant strains to reproduce and flourish.
Europe is far ahead of the United States in the responsible use of antibiotics: On January 1, 2006, the European Union banned the feeding of all antibiotics to livestock for nontherapeutic purposes. This sweeping policy follows a 1998 ban on the non-therapeutic use of four medically-important antibiotics on animals. The time has come for the United States to follow Europe’s lead.
Q.
According to the passage, which of the following describes how bacteria can develop antibiotic resistance?

In the early to mid-1980s, a business practice known as a “leveraged buyout” became popular as a method for companies to expand without having to spend any of their own assets. The leveraged buyout was not without its problems, however, and in time it came to represent in the public imagination not only corporate ingenuity and success, but also excess and greed. Many of the main corporate figures of the 1980s saw spectacular rises and, perhaps inevitably, spectacular falls as they abused the leveraged buyout as a means to extraordinary financial gain.
A leveraged buyout entails one company purchasing another using the assets of the purchased company as the collateral to secure the funds needed to buy that company. The leveraged buyout allows companies to take on debt that their own assets would have been insufficient to secure in order to finance expansion. The benefit of the leveraged buyout is obvious: companies with insufficient funds can still expand to compete with larger competitors. The drawbacks, however, became apparent only after the fact: the purchased company must perform extraordinarily well in order to generate the capital to pay off the loans that made the purchase possible in the first place. When the purchased company underperforms, the buyer must somehow find the money to pay off the loans. If such funds are not obtained, the buyer may be forced to sell off the company, or parts thereof, for less than the purchase price. In these cases, the buyer is still responsible for repaying the debt that is not covered by the sale price. Many of these deals resulted in the evisceration of the purchased companies, as subparts were sold to pay down the loans and employees were laid off to reduce costs and increase profits.
The most famous leveraged buyout is probably the 1988 purchase of RJR Nabisco by Kohlberg Kravis Roberts (“KKR”). The purchase price for the corporate giant RJR Nabisco was $25 billion, almost all of which was borrowed money. The takeover was “hostile,” meaning that RJR Nabisco resisted any overtures from potential buyers. KKR ultimately succeeded by buying a controlling interest in RJR Nabisco, thereby obtaining voting control over the company. By the mid-1990s, though, KKR had seen a reversal of fortune and was forced to sell off RJR Nabisco in order to relieve itself of the crushing debt load.
The 1980s were the heyday of the leveraged buyout, as lending institutions were willing to loan money for these ventures. When the deals turned out to be much riskier in life than on paper, the lenders turned away from the buyouts and returned to the notion that borrowers must possess adequate collateral of their own.
Q.
The primary purpose of the passage is to

In the early to mid-1980s, a business practice known as a “leveraged buyout” became popular as a method for companies to expand without having to spend any of their own assets. The leveraged buyout was not without its problems, however, and in time it came to represent in the public imagination not only corporate ingenuity and success, but also excess and greed. Many of the main corporate figures of the 1980s saw spectacular rises and, perhaps inevitably, spectacular falls as they abused the leveraged buyout as a means to extraordinary financial gain.
A leveraged buyout entails one company purchasing another using the assets of the purchased company as the collateral to secure the funds needed to buy that company. The leveraged buyout allows companies to take on debt that their own assets would have been insufficient to secure in order to finance expansion. The benefit of the leveraged buyout is obvious: companies with insufficient funds can still expand to compete with larger competitors. The drawbacks, however, became apparent only after the fact: the purchased company must perform extraordinarily well in order to generate the capital to pay off the loans that made the purchase possible in the first place. When the purchased company underperforms, the buyer must somehow find the money to pay off the loans. If such funds are not obtained, the buyer may be forced to sell off the company, or parts thereof, for less than the purchase price. In these cases, the buyer is still responsible for repaying the debt that is not covered by the sale price. Many of these deals resulted in the evisceration of the purchased companies, as subparts were sold to pay down the loans and employees were laid off to reduce costs and increase profits.
The most famous leveraged buyout is probably the 1988 purchase of RJR Nabisco by Kohlberg Kravis Roberts (“KKR”). The purchase price for the corporate giant RJR Nabisco was $25 billion, almost all of which was borrowed money. The takeover was “hostile,” meaning that RJR Nabisco resisted any overtures from potential buyers. KKR ultimately succeeded by buying a controlling interest in RJR Nabisco, thereby obtaining voting control over the company. By the mid-1990s, though, KKR had seen a reversal of fortune and was forced to sell off RJR Nabisco in order to relieve itself of the crushing debt load.
The 1980s were the heyday of the leveraged buyout, as lending institutions were willing to loan money for these ventures. When the deals turned out to be much riskier in life than on paper, the lenders turned away from the buyouts and returned to the notion that borrowers must possess adequate collateral of their own.
Q.
The passage provides support for which of the following statements?

In the early to mid-1980s, a business practice known as a “leveraged buyout” became popular as a method for companies to expand without having to spend any of their own assets. The leveraged buyout was not without its problems, however, and in time it came to represent in the public imagination not only corporate ingenuity and success, but also excess and greed. Many of the main corporate figures of the 1980s saw spectacular rises and, perhaps inevitably, spectacular falls as they abused the leveraged buyout as a means to extraordinary financial gain.
A leveraged buyout entails one company purchasing another using the assets of the purchased company as the collateral to secure the funds needed to buy that company. The leveraged buyout allows companies to take on debt that their own assets would have been insufficient to secure in order to finance expansion. The benefit of the leveraged buyout is obvious: companies with insufficient funds can still expand to compete with larger competitors. The drawbacks, however, became apparent only after the fact: the purchased company must perform extraordinarily well in order to generate the capital to pay off the loans that made the purchase possible in the first place. When the purchased company underperforms, the buyer must somehow find the money to pay off the loans. If such funds are not obtained, the buyer may be forced to sell off the company, or parts thereof, for less than the purchase price. In these cases, the buyer is still responsible for repaying the debt that is not covered by the sale price. Many of these deals resulted in the evisceration of the purchased companies, as subparts were sold to pay down the loans and employees were laid off to reduce costs and increase profits.
The most famous leveraged buyout is probably the 1988 purchase of RJR Nabisco by Kohlberg Kravis Roberts (“KKR”). The purchase price for the corporate giant RJR Nabisco was $25 billion, almost all of which was borrowed money. The takeover was “hostile,” meaning that RJR Nabisco resisted any overtures from potential buyers. KKR ultimately succeeded by buying a controlling interest in RJR Nabisco, thereby obtaining voting control over the company. By the mid-1990s, though, KKR had seen a reversal of fortune and was forced to sell off RJR Nabisco in order to relieve itself of the crushing debt load.
The 1980s were the heyday of the leveraged buyout, as lending institutions were willing to loan money for these ventures. When the deals turned out to be much riskier in life than on paper, the lenders turned away from the buyouts and returned to the notion that borrowers must possess adequate collateral of their own.
Q.
The author mentions the RJR Nabisco case most probably in order to emphasize which of the following points?

To remain financially sound, health insurance companies must charge higher rates to insure people considered a higher risk. Lacking complete information about individuals, insurers are forced to set a standard rate, based on the average risk of the group, for a particular segment of the population. Consumers in poor health are willing to pay for the insurance, knowing that it will cover their higher-than-average health-care costs. In contrast, healthy consumers often decide to forgo the insurance, reasoning that it is less expensive to pay out-of-pocket for their lower-than-average health-care costs. The result, called “adverse selection,” is that the riskier members of a group will comprise the group of insurance applicants, potentially leading to a market failure in which insurance companies cannot afford to offer insurance at any price.
Among people over age sixty-five, even the wealthy can have difficulty obtaining fairly priced medical insurance, simply because of their age. However, those who blame so-called insurance company greed and discrimination against the elderly are ignoring the reality of adverse selection. Younger people generally obtain health insurance through their employers’ group insurance plan.
Employer’s plans obligate all employees to enroll in the plan and effectively pre-screen for general health, as a minimum health level is required to hold a job. Insurance companies can therefore charge a lower premium, based on the lower average risk of the employee pool, without worrying that healthy employees will opt out of the plan.
Consumers over sixty-five, typically not employed and thus seeking insurance individually, are necessarily more vulnerable to market failure stemming from adverse selection.
Q.
It can be inferred from the passage that unemployed people

To remain financially sound, health insurance companies must charge higher rates to insure people considered a higher risk. Lacking complete information about individuals, insurers are forced to set a standard rate, based on the average risk of the group, for a particular segment of the population. Consumers in poor health are willing to pay for the insurance, knowing that it will cover their higher-than-average health-care costs. In contrast, healthy consumers often decide to forgo the insurance, reasoning that it is less expensive to pay out-of-pocket for their lower-than-average health-care costs. The result, called “adverse selection,” is that the riskier members of a group will comprise the group of insurance applicants, potentially leading to a market failure in which insurance companies cannot afford to offer insurance at any price.
Among people over age sixty-five, even the wealthy can have difficulty obtaining fairly priced medical insurance, simply because of their age. However, those who blame so-called insurance company greed and discrimination against the elderly are ignoring the reality of adverse selection. Younger people generally obtain health insurance through their employers’ group insurance plan.
Employer’s plans obligate all employees to enroll in the plan and effectively pre-screen for general health, as a minimum health level is required to hold a job. Insurance companies can therefore charge a lower premium, based on the lower average risk of the employee pool, without worrying that healthy employees will opt out of the plan.
Consumers over sixty-five, typically not employed and thus seeking insurance individually, are necessarily more vulnerable to market failure stemming from adverse selection.
Q.
The author refers to “greed and discrimination” in the second paragraph of the passage in order to

To remain financially sound, health insurance companies must charge higher rates to insure people considered a higher risk. Lacking complete information about individuals, insurers are forced to set a standard rate, based on the average risk of the group, for a particular segment of the population. Consumers in poor health are willing to pay for the insurance, knowing that it will cover their higher-than-average health-care costs. In contrast, healthy consumers often decide to forgo the insurance, reasoning that it is less expensive to pay out-of-pocket for their lower-than-average health-care costs. The result, called “adverse selection,” is that the riskier members of a group will comprise the group of insurance applicants, potentially leading to a market failure in which insurance companies cannot afford to offer insurance at any price.
Among people over age sixty-five, even the wealthy can have difficulty obtaining fairly priced medical insurance, simply because of their age. However, those who blame so-called insurance company greed and discrimination against the elderly are ignoring the reality of adverse selection. Younger people generally obtain health insurance through their employers’ group insurance plan.
Employer’s plans obligate all employees to enroll in the plan and effectively pre-screen for general health, as a minimum health level is required to hold a job. Insurance companies can therefore charge a lower premium, based on the lower average risk of the employee pool, without worrying that healthy employees will opt out of the plan.
Consumers over sixty-five, typically not employed and thus seeking insurance individually, are necessarily more vulnerable to market failure stemming from adverse selection.
Q.
The primary purpose of the passage is to

To remain financially sound, health insurance companies must charge higher rates to insure people considered a higher risk. Lacking complete information about individuals, insurers are forced to set a standard rate, based on the average risk of the group, for a particular segment of the population. Consumers in poor health are willing to pay for the insurance, knowing that it will cover their higher-than-average health-care costs. In contrast, healthy consumers often decide to forgo the insurance, reasoning that it is less expensive to pay out-of-pocket for their lower-than-average health-care costs. The result, called “adverse selection,” is that the riskier members of a group will comprise the group of insurance applicants, potentially leading to a market failure in which insurance companies cannot afford to offer insurance at any price.
Among people over age sixty-five, even the wealthy can have difficulty obtaining fairly priced medical insurance, simply because of their age. However, those who blame so-called insurance company greed and discrimination against the elderly are ignoring the reality of adverse selection. Younger people generally obtain health insurance through their employers’ group insurance plan.
Employer’s plans obligate all employees to enroll in the plan and effectively pre-screen for general health, as a minimum health level is required to hold a job. Insurance companies can therefore charge a lower premium, based on the lower average risk of the employee pool, without worrying that healthy employees will opt out of the plan.
Consumers over sixty-five, typically not employed and thus seeking insurance individually, are necessarily more vulnerable to market failure stemming from adverse selection.
Q.
Which of the following best describes the function of the first paragraph within the passage as a whole?

To remain financially sound, health insurance companies must charge higher rates to insure people considered a higher risk. Lacking complete information about individuals, insurers are forced to set a standard rate, based on the average risk of the group, for a particular segment of the population. Consumers in poor health are willing to pay for the insurance, knowing that it will cover their higher-than-average health-care costs. In contrast, healthy consumers often decide to forgo the insurance, reasoning that it is less expensive to pay out-of-pocket for their lower-than-average health-care costs. The result, called “adverse selection,” is that the riskier members of a group will comprise the group of insurance applicants, potentially leading to a market failure in which insurance companies cannot afford to offer insurance at any price.
Among people over age sixty-five, even the wealthy can have difficulty obtaining fairly priced medical insurance, simply because of their age. However, those who blame so-called insurance company greed and discrimination against the elderly are ignoring the reality of adverse selection. Younger people generally obtain health insurance through their employers’ group insurance plan.
Employer’s plans obligate all employees to enroll in the plan and effectively pre-screen for general health, as a minimum health level is required to hold a job. Insurance companies can therefore charge a lower premium, based on the lower average risk of the employee pool, without worrying that healthy employees will opt out of the plan.
Consumers over sixty-five, typically not employed and thus seeking insurance individually, are necessarily more vulnerable to market failure stemming from adverse selection.
Q.
The passage states which of the following about the cost of health-care?

Many musicologists consider jazz the only purely American form of music. Others, however, argue that jazz is rooted in a history similar to that of America itself, a history of confluence.
The immigration of Europeans and the slave trade of West Africans to America resulted in a convergence of cultures, traditions, and art forms, including music. Jazz, first played in New Orleans in the early 1900s, borrowed heavily from the European musical scale and harmonic system. Jazz ensembles were built predominantly on European instruments, such as the trumpet, trombone, saxophone, and piano. The West African influence on jazz was manifested primarily in its performance. Scatting, a technique used by jazz vocalists to mimic the sounds of instruments, had its origin in West African vocal traditions.
The emphasis on improvisation in jazz music, in addition to group participation, also came from West African music.
Proponents of the argument that jazz is purely American often point to its genesis in New Orleans as evidence for this perspective. The irony, however, is that the essence of America lies in the plurality of its roots. To deny the rich and complex history of jazz, and the true origins of the art form, is in effect denying the very aspects of the art form that make it undeniably American.
Q.
It can be inferred from the passage that the author would be less inclined to label jazz an American art form if which of the following were true?