RC Practice Test - 2

Which of these is a short gist of what the author wants to say?

Directions: Answer the given question based on the following passage:

The back-to-school season is upon us, and once again, parents across the country have loaded their kids’ backpacks up with snack packs and school supplies. It’s a good moment to reflect on what else we should be giving our kids as they head off to school.
American parents are feeling particularly anxious about that question this year. The educational process feels more than ever like a race, one that starts in pre-preschool and doesn’t end until your child is admitted to the perfect college. There is a lot of advice out there on how best to help our kids thrive, but after surveying the research, I believe that most parents are more worried than they need to be about their children’s grades, test scores and IQ. And what we don’t think about enough is how to help our children build their character — how to help them develop skills like perseverance, grit, optimism, conscientiousness, and self-control, which together arguably do more to determine success than S.A.T. scores or I.Q.
In fact, there’s growing evidence that our anxiety about our children’s school performance may actually be holding them back from learning some of these valuable skills. If you’re concerned solely with a child’s G.P.A., then you will likely choose to minimize the challenges that child faces in school. With real challenge comes the risk of real failure. And in an ultra-competitive academic environment, the idea of failure — even a small, temporary failure — can be very scary, to students and parents alike.
But experiencing failure and adversity, researchers have found, is a critical part of building character. Recent research by a team of psychologists led by Mark Seery of the University at Buffalo, State University of New York, found that adults who had experienced little or no adversity growing up were actually less happy and confident than those who had experienced a few significant setbacks in childhood. Overcoming those obstacles, the researchers hypothesized, “could teach effective coping skills, help engage social support networks, create a sense of mastery over past adversity,  foster beliefs in the ability to cope successfully.
By contrast, when we protect our children from every possible adversity — when we call their teachers to get an extension on a paper; when we intervene in the sandbox to make sure everyone is sharing their toys; when we urge them to choose only those subjects they’re good at  — we are denying them those same character-building experiences. As the psychologists Madeline Levine and Dan Kindlon have written, that can lead to difficulties in adolescence and young adulthood, when overprotected young people finally confront real problems on their own and don’t know how to overcome them.

Which of these is an effective counter argument to the author's argument that character building skills are more necessary for children than intelligence building skills?

Directions: Answer the given question based on the following passage:

The back-to-school season is upon us, and once again, parents across the country have loaded their kids’ backpacks up with snack packs and school supplies. It’s a good moment to reflect on what else we should be giving our kids as they head off to school.
American parents are feeling particularly anxious about that question this year. The educational process feels more than ever like a race, one that starts in pre-preschool and doesn’t end until your child is admitted to the perfect college. There is a lot of advice out there on how best to help our kids thrive, but after surveying the research, I believe that most parents are more worried than they need to be about their children’s grades, test scores and IQ. And what we don’t think about enough is how to help our children build their character — how to help them develop skills like perseverance, grit, optimism, conscientiousness, and self-control, which together arguably do more to determine success than S.A.T. scores or I.Q.
In fact, there’s growing evidence that our anxiety about our children’s school performance may actually be holding them back from learning some of these valuable skills. If you’re concerned solely with a child’s G.P.A., then you will likely choose to minimize the challenges that child faces in school. With real challenge comes the risk of real failure. And in an ultra-competitive academic environment, the idea of failure — even a small, temporary failure — can be very scary, to students and parents alike.
But experiencing failure and adversity, researchers have found, is a critical part of building character. Recent research by a team of psychologists led by Mark Seery of the University at Buffalo, State University of New York, found that adults who had experienced little or no adversity growing up were actually less happy and confident than those who had experienced a few significant setbacks in childhood. Overcoming those obstacles, the researchers hypothesized, “could teach effective coping skills, help engage social support networks, create a sense of mastery over past adversity,  foster beliefs in the ability to cope successfully.
By contrast, when we protect our children from every possible adversity — when we call their teachers to get an extension on a paper; when we intervene in the sandbox to make sure everyone is sharing their toys; when we urge them to choose only those subjects they’re good at  — we are denying them those same character-building experiences. As the psychologists Madeline Levine and Dan Kindlon have written, that can lead to difficulties in adolescence and young adulthood, when overprotected young people finally confront real problems on their own and don’t know how to overcome them.

Which of these activities will the author prefer the parents encourage their children to do?

Directions: Answer the given question based on the following passage:

The back-to-school season is upon us, and once again, parents across the country have loaded their kids’ backpacks up with snack packs and school supplies. It’s a good moment to reflect on what else we should be giving our kids as they head off to school.
American parents are feeling particularly anxious about that question this year. The educational process feels more than ever like a race, one that starts in pre-preschool and doesn’t end until your child is admitted to the perfect college. There is a lot of advice out there on how best to help our kids thrive, but after surveying the research, I believe that most parents are more worried than they need to be about their children’s grades, test scores and IQ. And what we don’t think about enough is how to help our children build their character — how to help them develop skills like perseverance, grit, optimism, conscientiousness, and self-control, which together arguably do more to determine success than S.A.T. scores or I.Q.
In fact, there’s growing evidence that our anxiety about our children’s school performance may actually be holding them back from learning some of these valuable skills. If you’re concerned solely with a child’s G.P.A., then you will likely choose to minimize the challenges that child faces in school. With real challenge comes the risk of real failure. And in an ultra-competitive academic environment, the idea of failure — even a small, temporary failure — can be very scary, to students and parents alike.
But experiencing failure and adversity, researchers have found, is a critical part of building character. Recent research by a team of psychologists led by Mark Seery of the University at Buffalo, State University of New York, found that adults who had experienced little or no adversity growing up were actually less happy and confident than those who had experienced a few significant setbacks in childhood. Overcoming those obstacles, the researchers hypothesized, “could teach effective coping skills, help engage social support networks, create a sense of mastery over past adversity,  foster beliefs in the ability to cope successfully.
By contrast, when we protect our children from every possible adversity — when we call their teachers to get an extension on a paper; when we intervene in the sandbox to make sure everyone is sharing their toys; when we urge them to choose only those subjects they’re good at  — we are denying them those same character-building experiences. As the psychologists Madeline Levine and Dan Kindlon have written, that can lead to difficulties in adolescence and young adulthood, when overprotected young people finally confront real problems on their own and don’t know how to overcome them.

Which of these can be compared to the human genome after the new finding?

Directions: Answer the given question based on the following passage:

Junk. Barren. Non-functioning. Dark matter. That’s how scientists had described the 98% of human genome that lies between our 21,000 genes, ever since our DNA was first sequenced about a decade ago. The disappointment in those descriptors was intentional and palpable.
It had been believed that the human genome — the underpinnings of the blueprint for the talking, empire-building, socially evolved species that we are — would be stuffed with sophisticated genes, coding for critical proteins of unparalleled complexity. But when all was said and done, and the Human Genome Project finally determined the entire sequence of our DNA in 2001, researchers found that the 3 billion base pairs that comprised our mere 21,000 genes made up a paltry 2% of the entire genome. The rest, geneticists acknowledged with unconcealed embarrassment, was an apparent biological wasteland.
But it turns out they were wrong. In an impressive series of more than 30 papers published in several journals, including Nature, Genome Research, Genome Biology, Science and Cell, scientists now report that these vast stretches of seeming “junk” DNA are actually the seat of crucial gene-controlling activity — changes that contribute to hundreds of common diseases. The new data come from the Encyclopaedia of DNA Elements project, or ENCODE, a $123 million endeavor begun by the National Human Genome Research Institute (NHGRI) in 2003, which includes 442 scientists in 32 labs around the world.
ENCODE has revealed that some 80% of the human genome is biochemically active. “What is remarkable is how much of the genome is doing at least something. It has changed my perception of the genome,” says Ewan Birney, ENCODE’s lead analysis coordinator from the European Bioinformatics Institute.
Rather than being inert, the portions of DNA that do not code for genes contain about 4 million so-called gene switches, transcription factors that control when our genes turn on and off and how much protein they make, not only affecting all the cells and organs in our body, but doing so at different points in our lifetime. Somewhere amidst that 80% of DNA, for example, lie the instructions that coax an uncommitted cell in a growing embryo to form a brain neuron, or direct a cell in the pancreas to churn out insulin after a meal, or guide a skin cell to bud off and replace a predecessor that has sloughed off.
“What we learned from ENCODE is how complicated the human genome is, and the incredible choreography that is going on with the immense number of switches that are choreographing how genes are used,” Eric Green, director of NHGRI, told reporters during a teleconference discussing the findings. “We are starting to answer fundamental questions like what are the working parts of the human genome, parts list of the human genome and what those parts do.”

Which of the following best describes the purpose of the author in the passage?

Directions: Answer the given question based on the following passage:

Junk. Barren. Non-functioning. Dark matter. That’s how scientists had described the 98% of human genome that lies between our 21,000 genes, ever since our DNA was first sequenced about a decade ago. The disappointment in those descriptors was intentional and palpable.
It had been believed that the human genome — the underpinnings of the blueprint for the talking, empire-building, socially evolved species that we are — would be stuffed with sophisticated genes, coding for critical proteins of unparalleled complexity. But when all was said and done, and the Human Genome Project finally determined the entire sequence of our DNA in 2001, researchers found that the 3 billion base pairs that comprised our mere 21,000 genes made up a paltry 2% of the entire genome. The rest, geneticists acknowledged with unconcealed embarrassment, was an apparent biological wasteland.
But it turns out they were wrong. In an impressive series of more than 30 papers published in several journals, including Nature, Genome Research, Genome Biology, Science and Cell, scientists now report that these vast stretches of seeming “junk” DNA are actually the seat of crucial gene-controlling activity — changes that contribute to hundreds of common diseases. The new data come from the Encyclopaedia of DNA Elements project, or ENCODE, a $123 million endeavor begun by the National Human Genome Research Institute (NHGRI) in 2003, which includes 442 scientists in 32 labs around the world.
ENCODE has revealed that some 80% of the human genome is biochemically active. “What is remarkable is how much of the genome is doing at least something. It has changed my perception of the genome,” says Ewan Birney, ENCODE’s lead analysis coordinator from the European Bioinformatics Institute.
Rather than being inert, the portions of DNA that do not code for genes contain about 4 million so-called gene switches, transcription factors that control when our genes turn on and off and how much protein they make, not only affecting all the cells and organs in our body, but doing so at different points in our lifetime. Somewhere amidst that 80% of DNA, for example, lie the instructions that coax an uncommitted cell in a growing embryo to form a brain neuron, or direct a cell in the pancreas to churn out insulin after a meal, or guide a skin cell to bud off and replace a predecessor that has sloughed off.
“What we learned from ENCODE is how complicated the human genome is, and the incredible choreography that is going on with the immense number of switches that are choreographing how genes are used,” Eric Green, director of NHGRI, told reporters during a teleconference discussing the findings. “We are starting to answer fundamental questions like what are the working parts of the human genome, parts list of the human genome and what those parts do.”

Which of these is true according to the contents of the passage?

Directions: Answer the given question based on the following passage:

Women have to get their reproducing done early. The menopause curtails it, and even before that a woman’s fertility falls significantly over the years. Men—those who can find willing partners, at least—do not suffer in quite the same way, as many stories of celebrity elder fathers testify. But perhaps such ageing Lotharios should think twice, for evidence is accumulating that their offspring are at greater-than-average risk of genetic disease.
The latest study to this effect has just been published in Nature by Kari Stefansson and his colleagues at deCODE Genetics, a genetic-analysis company based in Reykjavik that was founded to take advantage of Iceland’s excellent medical records and its unique genealogical history. Recent immigrants apart, the relationship of almost everybody on the island to everybody else is known back as far as the first census, in 1703. In many cases it is known back to the first human settlement of the island, in 874.
Dr Stefansson’s study does not reach as far back as that. He and his colleagues examined 78 trios of father, mother and child who are all still alive. In some cases they looked at grandchildren as well. Their goal was to examine the number of new mutations—traits not found in the normal body cells of either parent—in children.
The average answer is about 63. That number, however, varies widely—and the main factor involved in this variation is the age of the father. Mothers transmitted an average of 14 mutations to their children, regardless of age. Fathers showed a much wider range: 20-year-olds passed on an average of 29 mutations; 30-year-olds (the average age of fatherhood in Dr Stefansson’s sample) passed on 49; and 40-year-olds passed 69.
That it is the father, rather than the mother, who causes this effect is probably because a woman’s eggs are created early on, when she is still in her mother’s womb, and are then put into what is, in effect, physiological deep-freeze until they are required for ovulation. Sperm, by contrast, are made continuously throughout life, and each division of their precursor cells brings risk of a misinterpretation of the DNA, and thus a mutation.
Dr Stefansson’s work adds to an existing body of research on the effect of paternal age. Previous studies have linked older fathers with higher rates of schizophrenia and autism in their offspring. In April three teams of researchers identified specific mutations that increase the chance of autism; all three observed that the risk of such mutations in a child rose with his father’s age at conception. But Dr Stefansson and his team are the first to measure the impact of older fathers so precisely.
Modern genomics made their task easier. After sequencing the genomes of each of the people involved, tallying the new mutations in the children was simply a matter of comparing the sequences of the parents with those of their offspring. Though both mother and father contribute to a child’s DNA, their contributions come in large, identifiable blocks. If a mutation is seen, its parentage is thus obvious.
There is, of course, the question of how much this matters, for most mutations have little effect—and a rare few, the stuff of evolution, are actually beneficial. According to Alexey Kondrashov of the University of Michigan, an expert on the matter who wrote an article in Nature to accompany Dr Stefansson’s study, about 10% of mutations are damaging. This means that for the average baby, six of Dr Stefansson’s 63 mutations are probably up to no good.
In Iceland, the average age of fathers at conception has risen from 28 in 1980 to 33 in 2011. Over the same period Dr Stefansson estimates that the number of new mutations in Iceland’s newborns jumped by more than 17%.

Which of these could be a good title for the passage?

Directions: Answer the given question based on the following passage:

The back-to-school season is upon us, and once again, parents across the country have loaded their kids’ backpacks up with snack packs and school supplies. It’s a good moment to reflect on what else we should be giving our kids as they head off to school.
American parents are feeling particularly anxious about that question this year. The educational process feels more than ever like a race, one that starts in pre-preschool and doesn’t end until your child is admitted to the perfect college. There is a lot of advice out there on how best to help our kids thrive, but after surveying the research, I believe that most parents are more worried than they need to be about their children’s grades, test scores and IQ. And what we don’t think about enough is how to help our children build their character — how to help them develop skills like perseverance, grit, optimism, conscientiousness, and self-control, which together arguably do more to determine success than S.A.T. scores or I.Q.
In fact, there’s growing evidence that our anxiety about our children’s school performance may actually be holding them back from learning some of these valuable skills. If you’re concerned solely with a child’s G.P.A., then you will likely choose to minimize the challenges that child faces in school. With real challenge comes the risk of real failure. And in an ultra-competitive academic environment, the idea of failure — even a small, temporary failure — can be very scary, to students and parents alike.
But experiencing failure and adversity, researchers have found, is a critical part of building character. Recent research by a team of psychologists led by Mark Seery of the University at Buffalo, State University of New York, found that adults who had experienced little or no adversity growing up were actually less happy and confident than those who had experienced a few significant setbacks in childhood. Overcoming those obstacles, the researchers hypothesized, “could teach effective coping skills, help engage social support networks, create a sense of mastery over past adversity,  foster beliefs in the ability to cope successfully.
By contrast, when we protect our children from every possible adversity — when we call their teachers to get an extension on a paper; when we intervene in the sandbox to make sure everyone is sharing their toys; when we urge them to choose only those subjects they’re good at  — we are denying them those same character-building experiences. As the psychologists Madeline Levine and Dan Kindlon have written, that can lead to difficulties in adolescence and young adulthood, when overprotected young people finally confront real problems on their own and don’t know how to overcome them.

Which of these options tells about what the author will write if he were to continue writing the passage after the last paragraph?

Directions: Answer the given question based on the following passage:

The back-to-school season is upon us, and once again, parents across the country have loaded their kids’ backpacks up with snack packs and school supplies. It’s a good moment to reflect on what else we should be giving our kids as they head off to school.
American parents are feeling particularly anxious about that question this year. The educational process feels more than ever like a race, one that starts in pre-preschool and doesn’t end until your child is admitted to the perfect college. There is a lot of advice out there on how best to help our kids thrive, but after surveying the research, I believe that most parents are more worried than they need to be about their children’s grades, test scores and IQ. And what we don’t think about enough is how to help our children build their character — how to help them develop skills like perseverance, grit, optimism, conscientiousness, and self-control, which together arguably do more to determine success than S.A.T. scores or I.Q.
In fact, there’s growing evidence that our anxiety about our children’s school performance may actually be holding them back from learning some of these valuable skills. If you’re concerned solely with a child’s G.P.A., then you will likely choose to minimize the challenges that child faces in school. With real challenge comes the risk of real failure. And in an ultra-competitive academic environment, the idea of failure — even a small, temporary failure — can be very scary, to students and parents alike.
But experiencing failure and adversity, researchers have found, is a critical part of building character. Recent research by a team of psychologists led by Mark Seery of the University at Buffalo, State University of New York, found that adults who had experienced little or no adversity growing up were actually less happy and confident than those who had experienced a few significant setbacks in childhood. Overcoming those obstacles, the researchers hypothesized, “could teach effective coping skills, help engage social support networks, create a sense of mastery over past adversity,  foster beliefs in the ability to cope successfully.
By contrast, when we protect our children from every possible adversity — when we call their teachers to get an extension on a paper; when we intervene in the sandbox to make sure everyone is sharing their toys; when we urge them to choose only those subjects they’re good at  — we are denying them those same character-building experiences. As the psychologists Madeline Levine and Dan Kindlon have written, that can lead to difficulties in adolescence and young adulthood, when overprotected young people finally confront real problems on their own and don’t know how to overcome them.

What is the tone of the author in the passage?

Directions: Answer the given question based on the following passage:

Women have to get their reproducing done early. The menopause curtails it, and even before that a woman’s fertility falls significantly over the years. Men—those who can find willing partners, at least—do not suffer in quite the same way, as many stories of celebrity elder fathers testify. But perhaps such ageing Lotharios should think twice, for evidence is accumulating that their offspring are at greater-than-average risk of genetic disease.
The latest study to this effect has just been published in Nature by Kari Stefansson and his colleagues at deCODE Genetics, a genetic-analysis company based in Reykjavik that was founded to take advantage of Iceland’s excellent medical records and its unique genealogical history. Recent immigrants apart, the relationship of almost everybody on the island to everybody else is known back as far as the first census, in 1703. In many cases it is known back to the first human settlement of the island, in 874.
Dr Stefansson’s study does not reach as far back as that. He and his colleagues examined 78 trios of father, mother and child who are all still alive. In some cases they looked at grandchildren as well. Their goal was to examine the number of new mutations—traits not found in the normal body cells of either parent—in children.
The average answer is about 63. That number, however, varies widely—and the main factor involved in this variation is the age of the father. Mothers transmitted an average of 14 mutations to their children, regardless of age. Fathers showed a much wider range: 20-year-olds passed on an average of 29 mutations; 30-year-olds (the average age of fatherhood in Dr Stefansson’s sample) passed on 49; and 40-year-olds passed 69.
That it is the father, rather than the mother, who causes this effect is probably because a woman’s eggs are created early on, when she is still in her mother’s womb, and are then put into what is, in effect, physiological deep-freeze until they are required for ovulation. Sperm, by contrast, are made continuously throughout life, and each division of their precursor cells brings risk of a misinterpretation of the DNA, and thus a mutation.
Dr Stefansson’s work adds to an existing body of research on the effect of paternal age. Previous studies have linked older fathers with higher rates of schizophrenia and autism in their offspring. In April three teams of researchers identified specific mutations that increase the chance of autism; all three observed that the risk of such mutations in a child rose with his father’s age at conception. But Dr Stefansson and his team are the first to measure the impact of older fathers so precisely.
Modern genomics made their task easier. After sequencing the genomes of each of the people involved, tallying the new mutations in the children was simply a matter of comparing the sequences of the parents with those of their offspring. Though both mother and father contribute to a child’s DNA, their contributions come in large, identifiable blocks. If a mutation is seen, its parentage is thus obvious.
There is, of course, the question of how much this matters, for most mutations have little effect—and a rare few, the stuff of evolution, are actually beneficial. According to Alexey Kondrashov of the University of Michigan, an expert on the matter who wrote an article in Nature to accompany Dr Stefansson’s study, about 10% of mutations are damaging. This means that for the average baby, six of Dr Stefansson’s 63 mutations are probably up to no good.
In Iceland, the average age of fathers at conception has risen from 28 in 1980 to 33 in 2011. Over the same period Dr Stefansson estimates that the number of new mutations in Iceland’s newborns jumped by more than 17%.

What could be a criticism levelled against the way the passage is written?

Directions: Answer the given question based on the following passage:

Women have to get their reproducing done early. The menopause curtails it, and even before that a woman’s fertility falls significantly over the years. Men—those who can find willing partners, at least—do not suffer in quite the same way, as many stories of celebrity elder fathers testify. But perhaps such ageing Lotharios should think twice, for evidence is accumulating that their offspring are at greater-than-average risk of genetic disease.
The latest study to this effect has just been published in Nature by Kari Stefansson and his colleagues at deCODE Genetics, a genetic-analysis company based in Reykjavik that was founded to take advantage of Iceland’s excellent medical records and its unique genealogical history. Recent immigrants apart, the relationship of almost everybody on the island to everybody else is known back as far as the first census, in 1703. In many cases it is known back to the first human settlement of the island, in 874.
Dr Stefansson’s study does not reach as far back as that. He and his colleagues examined 78 trios of father, mother and child who are all still alive. In some cases they looked at grandchildren as well. Their goal was to examine the number of new mutations—traits not found in the normal body cells of either parent—in children.
The average answer is about 63. That number, however, varies widely—and the main factor involved in this variation is the age of the father. Mothers transmitted an average of 14 mutations to their children, regardless of age. Fathers showed a much wider range: 20-year-olds passed on an average of 29 mutations; 30-year-olds (the average age of fatherhood in Dr Stefansson’s sample) passed on 49; and 40-year-olds passed 69.
That it is the father, rather than the mother, who causes this effect is probably because a woman’s eggs are created early on, when she is still in her mother’s womb, and are then put into what is, in effect, physiological deep-freeze until they are required for ovulation. Sperm, by contrast, are made continuously throughout life, and each division of their precursor cells brings risk of a misinterpretation of the DNA, and thus a mutation.
Dr Stefansson’s work adds to an existing body of research on the effect of paternal age. Previous studies have linked older fathers with higher rates of schizophrenia and autism in their offspring. In April three teams of researchers identified specific mutations that increase the chance of autism; all three observed that the risk of such mutations in a child rose with his father’s age at conception. But Dr Stefansson and his team are the first to measure the impact of older fathers so precisely.
Modern genomics made their task easier. After sequencing the genomes of each of the people involved, tallying the new mutations in the children was simply a matter of comparing the sequences of the parents with those of their offspring. Though both mother and father contribute to a child’s DNA, their contributions come in large, identifiable blocks. If a mutation is seen, its parentage is thus obvious.
There is, of course, the question of how much this matters, for most mutations have little effect—and a rare few, the stuff of evolution, are actually beneficial. According to Alexey Kondrashov of the University of Michigan, an expert on the matter who wrote an article in Nature to accompany Dr Stefansson’s study, about 10% of mutations are damaging. This means that for the average baby, six of Dr Stefansson’s 63 mutations are probably up to no good.
In Iceland, the average age of fathers at conception has risen from 28 in 1980 to 33 in 2011. Over the same period Dr Stefansson estimates that the number of new mutations in Iceland’s newborns jumped by more than 17%.

Which of these options accurately encapsulates the essence of the passage?

Directions: Answer the given question based on the following passage:

Junk. Barren. Non-functioning. Dark matter. That’s how scientists had described the 98% of human genome that lies between our 21,000 genes, ever since our DNA was first sequenced about a decade ago. The disappointment in those descriptors was intentional and palpable.
It had been believed that the human genome — the underpinnings of the blueprint for the talking, empire-building, socially evolved species that we are — would be stuffed with sophisticated genes, coding for critical proteins of unparalleled complexity. But when all was said and done, and the Human Genome Project finally determined the entire sequence of our DNA in 2001, researchers found that the 3 billion base pairs that comprised our mere 21,000 genes made up a paltry 2% of the entire genome. The rest, geneticists acknowledged with unconcealed embarrassment, was an apparent biological wasteland.
But it turns out they were wrong. In an impressive series of more than 30 papers published in several journals, including Nature, Genome Research, Genome Biology, Science and Cell, scientists now report that these vast stretches of seeming “junk” DNA are actually the seat of crucial gene-controlling activity — changes that contribute to hundreds of common diseases. The new data come from the Encyclopaedia of DNA Elements project, or ENCODE, a $123 million endeavor begun by the National Human Genome Research Institute (NHGRI) in 2003, which includes 442 scientists in 32 labs around the world.
ENCODE has revealed that some 80% of the human genome is biochemically active. “What is remarkable is how much of the genome is doing at least something. It has changed my perception of the genome,” says Ewan Birney, ENCODE’s lead analysis coordinator from the European Bioinformatics Institute.
Rather than being inert, the portions of DNA that do not code for genes contain about 4 million so-called gene switches, transcription factors that control when our genes turn on and off and how much protein they make, not only affecting all the cells and organs in our body, but doing so at different points in our lifetime. Somewhere amidst that 80% of DNA, for example, lie the instructions that coax an uncommitted cell in a growing embryo to form a brain neuron, or direct a cell in the pancreas to churn out insulin after a meal, or guide a skin cell to bud off and replace a predecessor that has sloughed off.
“What we learned from ENCODE is how complicated the human genome is, and the incredible choreography that is going on with the immense number of switches that are choreographing how genes are used,” Eric Green, director of NHGRI, told reporters during a teleconference discussing the findings. “We are starting to answer fundamental questions like what are the working parts of the human genome, parts list of the human genome and what those parts do.”

Which of these is a good title for the passage?

Directions: Answer the given question based on the following passage:

Women have to get their reproducing done early. The menopause curtails it, and even before that a woman’s fertility falls significantly over the years. Men—those who can find willing partners, at least—do not suffer in quite the same way, as many stories of celebrity elder fathers testify. But perhaps such ageing Lotharios should think twice, for evidence is accumulating that their offspring are at greater-than-average risk of genetic disease.
The latest study to this effect has just been published in Nature by Kari Stefansson and his colleagues at deCODE Genetics, a genetic-analysis company based in Reykjavik that was founded to take advantage of Iceland’s excellent medical records and its unique genealogical history. Recent immigrants apart, the relationship of almost everybody on the island to everybody else is known back as far as the first census, in 1703. In many cases it is known back to the first human settlement of the island, in 874.
Dr Stefansson’s study does not reach as far back as that. He and his colleagues examined 78 trios of father, mother and child who are all still alive. In some cases they looked at grandchildren as well. Their goal was to examine the number of new mutations—traits not found in the normal body cells of either parent—in children.
The average answer is about 63. That number, however, varies widely—and the main factor involved in this variation is the age of the father. Mothers transmitted an average of 14 mutations to their children, regardless of age. Fathers showed a much wider range: 20-year-olds passed on an average of 29 mutations; 30-year-olds (the average age of fatherhood in Dr Stefansson’s sample) passed on 49; and 40-year-olds passed 69.
That it is the father, rather than the mother, who causes this effect is probably because a woman’s eggs are created early on, when she is still in her mother’s womb, and are then put into what is, in effect, physiological deep-freeze until they are required for ovulation. Sperm, by contrast, are made continuously throughout life, and each division of their precursor cells brings risk of a misinterpretation of the DNA, and thus a mutation.
Dr Stefansson’s work adds to an existing body of research on the effect of paternal age. Previous studies have linked older fathers with higher rates of schizophrenia and autism in their offspring. In April three teams of researchers identified specific mutations that increase the chance of autism; all three observed that the risk of such mutations in a child rose with his father’s age at conception. But Dr Stefansson and his team are the first to measure the impact of older fathers so precisely.
Modern genomics made their task easier. After sequencing the genomes of each of the people involved, tallying the new mutations in the children was simply a matter of comparing the sequences of the parents with those of their offspring. Though both mother and father contribute to a child’s DNA, their contributions come in large, identifiable blocks. If a mutation is seen, its parentage is thus obvious.
There is, of course, the question of how much this matters, for most mutations have little effect—and a rare few, the stuff of evolution, are actually beneficial. According to Alexey Kondrashov of the University of Michigan, an expert on the matter who wrote an article in Nature to accompany Dr Stefansson’s study, about 10% of mutations are damaging. This means that for the average baby, six of Dr Stefansson’s 63 mutations are probably up to no good.
In Iceland, the average age of fathers at conception has risen from 28 in 1980 to 33 in 2011. Over the same period Dr Stefansson estimates that the number of new mutations in Iceland’s newborns jumped by more than 17%.

All of the following are true according to the passage except

Directions: Answer the given question based on the following passage:

Junk. Barren. Non-functioning. Dark matter. That’s how scientists had described the 98% of human genome that lies between our 21,000 genes, ever since our DNA was first sequenced about a decade ago. The disappointment in those descriptors was intentional and palpable.
It had been believed that the human genome — the underpinnings of the blueprint for the talking, empire-building, socially evolved species that we are — would be stuffed with sophisticated genes, coding for critical proteins of unparalleled complexity. But when all was said and done, and the Human Genome Project finally determined the entire sequence of our DNA in 2001, researchers found that the 3 billion base pairs that comprised our mere 21,000 genes made up a paltry 2% of the entire genome. The rest, geneticists acknowledged with unconcealed embarrassment, was an apparent biological wasteland.
But it turns out they were wrong. In an impressive series of more than 30 papers published in several journals, including Nature, Genome Research, Genome Biology, Science and Cell, scientists now report that these vast stretches of seeming “junk” DNA are actually the seat of crucial gene-controlling activity — changes that contribute to hundreds of common diseases. The new data come from the Encyclopaedia of DNA Elements project, or ENCODE, a $123 million endeavor begun by the National Human Genome Research Institute (NHGRI) in 2003, which includes 442 scientists in 32 labs around the world.
ENCODE has revealed that some 80% of the human genome is biochemically active. “What is remarkable is how much of the genome is doing at least something. It has changed my perception of the genome,” says Ewan Birney, ENCODE’s lead analysis coordinator from the European Bioinformatics Institute.
Rather than being inert, the portions of DNA that do not code for genes contain about 4 million so-called gene switches, transcription factors that control when our genes turn on and off and how much protein they make, not only affecting all the cells and organs in our body, but doing so at different points in our lifetime. Somewhere amidst that 80% of DNA, for example, lie the instructions that coax an uncommitted cell in a growing embryo to form a brain neuron, or direct a cell in the pancreas to churn out insulin after a meal, or guide a skin cell to bud off and replace a predecessor that has sloughed off.
“What we learned from ENCODE is how complicated the human genome is, and the incredible choreography that is going on with the immense number of switches that are choreographing how genes are used,” Eric Green, director of NHGRI, told reporters during a teleconference discussing the findings. “We are starting to answer fundamental questions like what are the working parts of the human genome, parts list of the human genome and what those parts do.”

What is the author’s attitude towards the new findings?

Directions: Answer the given question based on the following passage:

Junk. Barren. Non-functioning. Dark matter. That’s how scientists had described the 98% of human genome that lies between our 21,000 genes, ever since our DNA was first sequenced about a decade ago. The disappointment in those descriptors was intentional and palpable.
It had been believed that the human genome — the underpinnings of the blueprint for the talking, empire-building, socially evolved species that we are — would be stuffed with sophisticated genes, coding for critical proteins of unparalleled complexity. But when all was said and done, and the Human Genome Project finally determined the entire sequence of our DNA in 2001, researchers found that the 3 billion base pairs that comprised our mere 21,000 genes made up a paltry 2% of the entire genome. The rest, geneticists acknowledged with unconcealed embarrassment, was an apparent biological wasteland.
But it turns out they were wrong. In an impressive series of more than 30 papers published in several journals, including Nature, Genome Research, Genome Biology, Science and Cell, scientists now report that these vast stretches of seeming “junk” DNA are actually the seat of crucial gene-controlling activity — changes that contribute to hundreds of common diseases. The new data come from the Encyclopaedia of DNA Elements project, or ENCODE, a $123 million endeavor begun by the National Human Genome Research Institute (NHGRI) in 2003, which includes 442 scientists in 32 labs around the world.
ENCODE has revealed that some 80% of the human genome is biochemically active. “What is remarkable is how much of the genome is doing at least something. It has changed my perception of the genome,” says Ewan Birney, ENCODE’s lead analysis coordinator from the European Bioinformatics Institute.
Rather than being inert, the portions of DNA that do not code for genes contain about 4 million so-called gene switches, transcription factors that control when our genes turn on and off and how much protein they make, not only affecting all the cells and organs in our body, but doing so at different points in our lifetime. Somewhere amidst that 80% of DNA, for example, lie the instructions that coax an uncommitted cell in a growing embryo to form a brain neuron, or direct a cell in the pancreas to churn out insulin after a meal, or guide a skin cell to bud off and replace a predecessor that has sloughed off.
“What we learned from ENCODE is how complicated the human genome is, and the incredible choreography that is going on with the immense number of switches that are choreographing how genes are used,” Eric Green, director of NHGRI, told reporters during a teleconference discussing the findings. “We are starting to answer fundamental questions like what are the working parts of the human genome, parts list of the human genome and what those parts do.”

Which of these is the central idea of the passage?

Directions: Answer the given question based on the following passage:

Women have to get their reproducing done early. The menopause curtails it, and even before that a woman’s fertility falls significantly over the years. Men—those who can find willing partners, at least—do not suffer in quite the same way, as many stories of celebrity elder fathers testify. But perhaps such ageing Lotharios should think twice, for evidence is accumulating that their offspring are at greater-than-average risk of genetic disease.
The latest study to this effect has just been published in Nature by Kari Stefansson and his colleagues at deCODE Genetics, a genetic-analysis company based in Reykjavik that was founded to take advantage of Iceland’s excellent medical records and its unique genealogical history. Recent immigrants apart, the relationship of almost everybody on the island to everybody else is known back as far as the first census, in 1703. In many cases it is known back to the first human settlement of the island, in 874.
Dr Stefansson’s study does not reach as far back as that. He and his colleagues examined 78 trios of father, mother and child who are all still alive. In some cases they looked at grandchildren as well. Their goal was to examine the number of new mutations—traits not found in the normal body cells of either parent—in children.
The average answer is about 63. That number, however, varies widely—and the main factor involved in this variation is the age of the father. Mothers transmitted an average of 14 mutations to their children, regardless of age. Fathers showed a much wider range: 20-year-olds passed on an average of 29 mutations; 30-year-olds (the average age of fatherhood in Dr Stefansson’s sample) passed on 49; and 40-year-olds passed 69.
That it is the father, rather than the mother, who causes this effect is probably because a woman’s eggs are created early on, when she is still in her mother’s womb, and are then put into what is, in effect, physiological deep-freeze until they are required for ovulation. Sperm, by contrast, are made continuously throughout life, and each division of their precursor cells brings risk of a misinterpretation of the DNA, and thus a mutation.
Dr Stefansson’s work adds to an existing body of research on the effect of paternal age. Previous studies have linked older fathers with higher rates of schizophrenia and autism in their offspring. In April three teams of researchers identified specific mutations that increase the chance of autism; all three observed that the risk of such mutations in a child rose with his father’s age at conception. But Dr Stefansson and his team are the first to measure the impact of older fathers so precisely.
Modern genomics made their task easier. After sequencing the genomes of each of the people involved, tallying the new mutations in the children was simply a matter of comparing the sequences of the parents with those of their offspring. Though both mother and father contribute to a child’s DNA, their contributions come in large, identifiable blocks. If a mutation is seen, its parentage is thus obvious.
There is, of course, the question of how much this matters, for most mutations have little effect—and a rare few, the stuff of evolution, are actually beneficial. According to Alexey Kondrashov of the University of Michigan, an expert on the matter who wrote an article in Nature to accompany Dr Stefansson’s study, about 10% of mutations are damaging. This means that for the average baby, six of Dr Stefansson’s 63 mutations are probably up to no good.
In Iceland, the average age of fathers at conception has risen from 28 in 1980 to 33 in 2011. Over the same period Dr Stefansson estimates that the number of new mutations in Iceland’s newborns jumped by more than 17%.