HESI Reading Comprehension #2

What is the meaning of the word generalized in the attached passage?

“When animals get sick, they may change their behaviour, becoming less active, for example. The study’s lead author, Patricia Lopes from the Department of Evolutionary Biology and Environmental Studies at the University of Zurich, says that previous research in wild animals has generally ignored how this change in behaviour may affect social contacts in a group and how, in turn, these changes can impact the transmission of a disease. Sick mice are not avoided, but remove themselves from the group.

To tackle this problem, Patricia Lopes and her colleagues used a novel combination of experimental manipulations of free-living mice, radio frequency tracking of animals, social network analysis and disease modelling. To simulate an infection, mice were injected with lipopolysaccharides (a component of the bacterial cell wall), which results in an immune response and generalized disease symptoms. In a paper published this week in the journal Scientific Reports, the team reveals that sick mice become disconnected from their social groups.

It is known that mice have the ability to detect other sick mice. Therefore, it was surprising to find that the animals in the same social group did not avoid the sick mouse. In fact, they went on interacting with the sick mouse and other mice more or less in the same way as before the experimental infection. “It was the sick mouse that removed itself from the group”, emphasizes Lopes. She suggests that such a change in the behaviour of the sick mouse may protect relatives in the same group from catching the disease, which could be beneficial from an evolutionary perspective.

Speed and extent of disease spread are greatly reduced.

In a further step, the researchers used mathematical models to predict how an infectious disease would spread considering the changes in behaviour of the sick animals. “When we account for the behavioural changes and how they affect social contacts, we find that the speed and the extent of disease spread are greatly reduced,” says Lopes.”

According to the attached passage, why is it important to replace standard implanted defibrillators?

A research team from the University of Bonn has succeeded for the first time in using light stimuli to stop life-threatening cardiac arrhythmia in mouse hearts. Furthermore, as shown in computer simulations at Johns Hopkins University, this technique could also be used successfully for human hearts. The study opens up a whole new approach to the development of implantable optical defibrillators, in which the strong electrical impulses of conventional defibrillators are replaced by gentler, pain-free light impulses. The Journal of Clinical Investigation has now published the results. Ventricular fibrillation! When the heart muscle races and no longer contracts in an orderly fashion, sudden death often follows due to the lack of blood circulation. In such an emergency, a defibrillator helps to restore normal heart activity by means of intense electrical shocks. In patients with a known risk for these arrhythmia, the prophylactic implantation of a defibrillator is the treatment of choice. If ventricular fibrillation is detected, a pulse of electricity is automatically generated, which normalizes the excitation of the heart muscle and saves the person’s life.

“When an implanted defibrillator is triggered, which unfortunately can also happen because of false detection of arrhythmia, it is always a very traumatic event for the patient”, says the head of the study, Junior-Professor Philipp Sasse of the Institute of Physiology I at the University of Bonn. “The strong electrical shock is very painful and can even damage the heart further”. Therefore, Professor Sasse’s team investigated the principles for a pain-free, gentler alternative. As the scientists have now shown, ventricular fibrillation can be stopped by optical defibrillation.

Optical defibrillation requires gene transfer

The team used the new method of “optogenetic” stimulation of mouse hearts, which had genes inserted for so-called channelrhodopsins. These channels are derived from a green algae and change the ion permeability of heart cell membranes when illuminated. When the researchers triggered ventricular fibrillation in the mouse heart, a light pulse of one second applied to the heart was enough to restore normal rhythm. “This is a very important result”, emphasizes lead author Dr. med. Tobias Brügmann of Professor Sasse’s team. “It shows for the first time experimentally in the heart that optogenetic stimulation can be used for defibrillation of cardiac arrhythmia”. It also worked in normal mice that received the channelrhodopsin through injection of a biotechnologically-produced virus. This shows a possible clinical application, because similar viruses have already been used for gene therapy in human patients.”

According to the attached passage, what might instigate the use of light stimuli in future medical applications?

A research team from the University of Bonn has succeeded for the first time in using light stimuli to stop life-threatening cardiac arrhythmia in mouse hearts. Furthermore, as shown in computer simulations at Johns Hopkins University, this technique could also be used successfully for human hearts. The study opens up a whole new approach to the development of implantable optical defibrillators, in which the strong electrical impulses of conventional defibrillators are replaced by gentler, pain-free light impulses. The Journal of Clinical Investigation has now published the results. Ventricular fibrillation! When the heart muscle races and no longer contracts in an orderly fashion, sudden death often follows due to the lack of blood circulation. In such an emergency, a defibrillator helps to restore normal heart activity by means of intense electrical shocks. In patients with a known risk for these arrhythmia, the prophylactic implantation of a defibrillator is the treatment of choice. If ventricular fibrillation is detected, a pulse of electricity is automatically generated, which normalizes the excitation of the heart muscle and saves the person’s life.

“When an implanted defibrillator is triggered, which unfortunately can also happen because of false detection of arrhythmia, it is always a very traumatic event for the patient”, says the head of the study, Junior-Professor Philipp Sasse of the Institute of Physiology I at the University of Bonn. “The strong electrical shock is very painful and can even damage the heart further”. Therefore, Professor Sasse’s team investigated the principles for a pain-free, gentler alternative. As the scientists have now shown, ventricular fibrillation can be stopped by optical defibrillation.

Optical defibrillation requires gene transfer

The team used the new method of “optogenetic” stimulation of mouse hearts, which had genes inserted for so-called channelrhodopsins. These channels are derived from a green algae and change the ion permeability of heart cell membranes when illuminated. When the researchers triggered ventricular fibrillation in the mouse heart, a light pulse of one second applied to the heart was enough to restore normal rhythm. “This is a very important result”, emphasizes lead author Dr. med. Tobias Brügmann of Professor Sasse’s team. “It shows for the first time experimentally in the heart that optogenetic stimulation can be used for defibrillation of cardiac arrhythmia”. It also worked in normal mice that received the channelrhodopsin through injection of a biotechnologically-produced virus. This shows a possible clinical application, because similar viruses have already been used for gene therapy in human patients.”

What is an accurate contrast between traditional implants and light stimuli implants, according to the attached passage?

A research team from the University of Bonn has succeeded for the first time in using light stimuli to stop life-threatening cardiac arrhythmia in mouse hearts. Furthermore, as shown in computer simulations at Johns Hopkins University, this technique could also be used successfully for human hearts. The study opens up a whole new approach to the development of implantable optical defibrillators, in which the strong electrical impulses of conventional defibrillators are replaced by gentler, pain-free light impulses. The Journal of Clinical Investigation has now published the results. Ventricular fibrillation! When the heart muscle races and no longer contracts in an orderly fashion, sudden death often follows due to the lack of blood circulation. In such an emergency, a defibrillator helps to restore normal heart activity by means of intense electrical shocks. In patients with a known risk for these arrhythmia, the prophylactic implantation of a defibrillator is the treatment of choice. If ventricular fibrillation is detected, a pulse of electricity is automatically generated, which normalizes the excitation of the heart muscle and saves the person’s life.

“When an implanted defibrillator is triggered, which unfortunately can also happen because of false detection of arrhythmia, it is always a very traumatic event for the patient”, says the head of the study, Junior-Professor Philipp Sasse of the Institute of Physiology I at the University of Bonn. “The strong electrical shock is very painful and can even damage the heart further”. Therefore, Professor Sasse’s team investigated the principles for a pain-free, gentler alternative. As the scientists have now shown, ventricular fibrillation can be stopped by optical defibrillation.

Optical defibrillation requires gene transfer

The team used the new method of “optogenetic” stimulation of mouse hearts, which had genes inserted for so-called channelrhodopsins. These channels are derived from a green algae and change the ion permeability of heart cell membranes when illuminated. When the researchers triggered ventricular fibrillation in the mouse heart, a light pulse of one second applied to the heart was enough to restore normal rhythm. “This is a very important result”, emphasizes lead author Dr. med. Tobias Brügmann of Professor Sasse’s team. “It shows for the first time experimentally in the heart that optogenetic stimulation can be used for defibrillation of cardiac arrhythmia”. It also worked in normal mice that received the channelrhodopsin through injection of a biotechnologically-produced virus. This shows a possible clinical application, because similar viruses have already been used for gene therapy in human patients.”

Using context clues from the attached passage, determine the meaning of the term ionizing radiation.

For the first time, researchers from the Wellcome Trust Sanger Institute and their collaborators have been able to identify in human cancers two characteristic patterns of DNA damage caused by ionising radiation. These fingerprint patterns may now enable doctors to identify which tumours have been caused by radiation, and investigate if they should be treated differently. Published in Nature Communications today, the results will also help to explain how radiation can cause cancer.

Ionising radiation, such as gamma rays, X-rays and radioactive particles can cause cancer by damaging DNA. However, how this happens, or how many tumours are caused by radiation damage has not been known.

Previous work on cancer had revealed that DNA damage often leaves a molecular fingerprint, known as a mutational signature, on the genome of a cancer cell. The researchers looked for mutational signatures in 12 patients with secondary radiation-associated tumours, comparing these with 319 that had not been exposed to radiation.

Dr Peter Campbell from the Wellcome Trust Sanger Institute who led the study, said: “To find out how radiation could cause cancer, we studied the genomes of cancers caused by radiation in comparison to tumours that arose spontaneously. By comparing the DNA sequences we found two mutational signatures for radiation damage that were independent of cancer type. We then checked the findings with prostate cancers that had or had not been exposed to radiation, and found the same two signatures again. These mutational signatures help us explain how high-energy radiation damages DNA.”

One mutational signature is a deletion where small numbers of DNA bases are cut out. The second is called a balanced inversion, where the DNA is cut in two places, the middle piece spins round, and is joined back again in the opposite orientation. Balanced inversions don’t happen naturally in the body, but high-energy radiation could provide enough DNA breaks at the same time to make this possible.””

According to the attached passage, what is the difference between the two mutations linked to cancer?

For the first time, researchers from the Wellcome Trust Sanger Institute and their collaborators have been able to identify in human cancers two characteristic patterns of DNA damage caused by ionising radiation. These fingerprint patterns may now enable doctors to identify which tumours have been caused by radiation, and investigate if they should be treated differently. Published in Nature Communications today, the results will also help to explain how radiation can cause cancer.

Ionising radiation, such as gamma rays, X-rays and radioactive particles can cause cancer by damaging DNA. However, how this happens, or how many tumours are caused by radiation damage has not been known.

Previous work on cancer had revealed that DNA damage often leaves a molecular fingerprint, known as a mutational signature, on the genome of a cancer cell. The researchers looked for mutational signatures in 12 patients with secondary radiation-associated tumours, comparing these with 319 that had not been exposed to radiation.

Dr Peter Campbell from the Wellcome Trust Sanger Institute who led the study, said: “To find out how radiation could cause cancer, we studied the genomes of cancers caused by radiation in comparison to tumours that arose spontaneously. By comparing the DNA sequences we found two mutational signatures for radiation damage that were independent of cancer type. We then checked the findings with prostate cancers that had or had not been exposed to radiation, and found the same two signatures again. These mutational signatures help us explain how high-energy radiation damages DNA.”

One mutational signature is a deletion where small numbers of DNA bases are cut out. The second is called a balanced inversion, where the DNA is cut in two places, the middle piece spins round, and is joined back again in the opposite orientation. Balanced inversions don’t happen naturally in the body, but high-energy radiation could provide enough DNA breaks at the same time to make this possible.””

Select the best summary of the attached passage.

For the first time, researchers from the Wellcome Trust Sanger Institute and their collaborators have been able to identify in human cancers two characteristic patterns of DNA damage caused by ionising radiation. These fingerprint patterns may now enable doctors to identify which tumours have been caused by radiation, and investigate if they should be treated differently. Published in Nature Communications today, the results will also help to explain how radiation can cause cancer.

Ionising radiation, such as gamma rays, X-rays and radioactive particles can cause cancer by damaging DNA. However, how this happens, or how many tumours are caused by radiation damage has not been known.

Previous work on cancer had revealed that DNA damage often leaves a molecular fingerprint, known as a mutational signature, on the genome of a cancer cell. The researchers looked for mutational signatures in 12 patients with secondary radiation-associated tumours, comparing these with 319 that had not been exposed to radiation.

Dr Peter Campbell from the Wellcome Trust Sanger Institute who led the study, said: “To find out how radiation could cause cancer, we studied the genomes of cancers caused by radiation in comparison to tumours that arose spontaneously. By comparing the DNA sequences we found two mutational signatures for radiation damage that were independent of cancer type. We then checked the findings with prostate cancers that had or had not been exposed to radiation, and found the same two signatures again. These mutational signatures help us explain how high-energy radiation damages DNA.”

One mutational signature is a deletion where small numbers of DNA bases are cut out. The second is called a balanced inversion, where the DNA is cut in two places, the middle piece spins round, and is joined back again in the opposite orientation. Balanced inversions don’t happen naturally in the body, but high-energy radiation could provide enough DNA breaks at the same time to make this possible.””

What can be inferred from the attached passage about study participants with balanced inversion mutations?

For the first time, researchers from the Wellcome Trust Sanger Institute and their collaborators have been able to identify in human cancers two characteristic patterns of DNA damage caused by ionising radiation. These fingerprint patterns may now enable doctors to identify which tumours have been caused by radiation, and investigate if they should be treated differently. Published in Nature Communications today, the results will also help to explain how radiation can cause cancer.

Ionising radiation, such as gamma rays, X-rays and radioactive particles can cause cancer by damaging DNA. However, how this happens, or how many tumours are caused by radiation damage has not been known.

Previous work on cancer had revealed that DNA damage often leaves a molecular fingerprint, known as a mutational signature, on the genome of a cancer cell. The researchers looked for mutational signatures in 12 patients with secondary radiation-associated tumours, comparing these with 319 that had not been exposed to radiation.

Dr Peter Campbell from the Wellcome Trust Sanger Institute who led the study, said: “To find out how radiation could cause cancer, we studied the genomes of cancers caused by radiation in comparison to tumours that arose spontaneously. By comparing the DNA sequences we found two mutational signatures for radiation damage that were independent of cancer type. We then checked the findings with prostate cancers that had or had not been exposed to radiation, and found the same two signatures again. These mutational signatures help us explain how high-energy radiation damages DNA.”

One mutational signature is a deletion where small numbers of DNA bases are cut out. The second is called a balanced inversion, where the DNA is cut in two places, the middle piece spins round, and is joined back again in the opposite orientation. Balanced inversions don’t happen naturally in the body, but high-energy radiation could provide enough DNA breaks at the same time to make this possible.””

According to the attached passage, how is cancer derived from ionizing radiation different from other types of cancer?

For the first time, researchers from the Wellcome Trust Sanger Institute and their collaborators have been able to identify in human cancers two characteristic patterns of DNA damage caused by ionising radiation. These fingerprint patterns may now enable doctors to identify which tumours have been caused by radiation, and investigate if they should be treated differently. Published in Nature Communications today, the results will also help to explain how radiation can cause cancer.

Ionising radiation, such as gamma rays, X-rays and radioactive particles can cause cancer by damaging DNA. However, how this happens, or how many tumours are caused by radiation damage has not been known.

Previous work on cancer had revealed that DNA damage often leaves a molecular fingerprint, known as a mutational signature, on the genome of a cancer cell. The researchers looked for mutational signatures in 12 patients with secondary radiation-associated tumours, comparing these with 319 that had not been exposed to radiation.

Dr Peter Campbell from the Wellcome Trust Sanger Institute who led the study, said: “To find out how radiation could cause cancer, we studied the genomes of cancers caused by radiation in comparison to tumours that arose spontaneously. By comparing the DNA sequences we found two mutational signatures for radiation damage that were independent of cancer type. We then checked the findings with prostate cancers that had or had not been exposed to radiation, and found the same two signatures again. These mutational signatures help us explain how high-energy radiation damages DNA.”

One mutational signature is a deletion where small numbers of DNA bases are cut out. The second is called a balanced inversion, where the DNA is cut in two places, the middle piece spins round, and is joined back again in the opposite orientation. Balanced inversions don’t happen naturally in the body, but high-energy radiation could provide enough DNA breaks at the same time to make this possible.””

Which of the following ideas is not found in the attached passage?

For the first time, researchers from the Wellcome Trust Sanger Institute and their collaborators have been able to identify in human cancers two characteristic patterns of DNA damage caused by ionising radiation. These fingerprint patterns may now enable doctors to identify which tumours have been caused by radiation, and investigate if they should be treated differently. Published in Nature Communications today, the results will also help to explain how radiation can cause cancer.

Ionising radiation, such as gamma rays, X-rays and radioactive particles can cause cancer by damaging DNA. However, how this happens, or how many tumours are caused by radiation damage has not been known.

Previous work on cancer had revealed that DNA damage often leaves a molecular fingerprint, known as a mutational signature, on the genome of a cancer cell. The researchers looked for mutational signatures in 12 patients with secondary radiation-associated tumours, comparing these with 319 that had not been exposed to radiation.

Dr Peter Campbell from the Wellcome Trust Sanger Institute who led the study, said: “To find out how radiation could cause cancer, we studied the genomes of cancers caused by radiation in comparison to tumours that arose spontaneously. By comparing the DNA sequences we found two mutational signatures for radiation damage that were independent of cancer type. We then checked the findings with prostate cancers that had or had not been exposed to radiation, and found the same two signatures again. These mutational signatures help us explain how high-energy radiation damages DNA.”

One mutational signature is a deletion where small numbers of DNA bases are cut out. The second is called a balanced inversion, where the DNA is cut in two places, the middle piece spins round, and is joined back again in the opposite orientation. Balanced inversions don’t happen naturally in the body, but high-energy radiation could provide enough DNA breaks at the same time to make this possible.””

What is the purpose of the attached passage?

The SRF initiated coronary heart disease research in 1965 and its first project was a literature review published in the New England Journal of Medicine in 1967. The review focused on fat and cholesterol as the dietary causes of coronary heart disease and downplayed sugar consumption as also a risk factor. SRF set the review’s objective, contributed articles to be included and received drafts, while the SRF’s funding and role were not disclosed, according to the article.

“This historical account of industry efforts demonstrates the importance of having reviews written by people without conflicts of interest and the need for financial disclosure,” note the authors, who point out the NEJM has required authors to disclose all conflicts of interest since 1984. There also is no direct evidence that the sugar industry wrote or changed the NEJM review manuscript and evidence that that the industry shaped its conclusions is circumstantial, the authors acknowledge.

Limitations of the article include that the papers and documents used in the research provide only a small view into the activities of one sugar industry trade group. The authors did not analyze the role of other organizations, nutrition leaders or food industries. Key figures in the historical episode detailed in this article could not be interviewed because they have died.

“This study suggests that the sugar industry sponsored its first CHD [coronary heart disease] research project in 1965 to downplay early warning signs that sucrose consumption was a risk factor in CHD. As of 2016, sugar control policies are being promulgated in international, federal, state and local venues. Yet CHD risk is inconsistently cited as a health consequence of added sugars consumption. Because CHD is the leading cause of death globally, the health community should ensure that CHD risk is evaluated in future risk assessments of added sugars. Policymaking committees should consider giving less weight to food industry-funded studies, and include mechanistic and animal studies as well as studies appraising the effect of added sugars on multiple CHD biomarkers and disease development,” the article concludes.

What is the meaning of the word disclosed in the attached passage?

The SRF initiated coronary heart disease research in 1965 and its first project was a literature review published in the New England Journal of Medicine in 1967. The review focused on fat and cholesterol as the dietary causes of coronary heart disease and downplayed sugar consumption as also a risk factor. SRF set the review’s objective, contributed articles to be included and received drafts, while the SRF’s funding and role were not disclosed, according to the article.

“This historical account of industry efforts demonstrates the importance of having reviews written by people without conflicts of interest and the need for financial disclosure,” note the authors, who point out the NEJM has required authors to disclose all conflicts of interest since 1984. There also is no direct evidence that the sugar industry wrote or changed the NEJM review manuscript and evidence that that the industry shaped its conclusions is circumstantial, the authors acknowledge.

Limitations of the article include that the papers and documents used in the research provide only a small view into the activities of one sugar industry trade group. The authors did not analyze the role of other organizations, nutrition leaders or food industries. Key figures in the historical episode detailed in this article could not be interviewed because they have died.

“This study suggests that the sugar industry sponsored its first CHD [coronary heart disease] research project in 1965 to downplay early warning signs that sucrose consumption was a risk factor in CHD. As of 2016, sugar control policies are being promulgated in international, federal, state and local venues. Yet CHD risk is inconsistently cited as a health consequence of added sugars consumption. Because CHD is the leading cause of death globally, the health community should ensure that CHD risk is evaluated in future risk assessments of added sugars. Policymaking committees should consider giving less weight to food industry-funded studies, and include mechanistic and animal studies as well as studies appraising the effect of added sugars on multiple CHD biomarkers and disease development,” the article concludes.

According to the attached passage, what is the primary concern regarding CHD studies conducted in 1965?

The SRF initiated coronary heart disease research in 1965 and its first project was a literature review published in the New England Journal of Medicine in 1967. The review focused on fat and cholesterol as the dietary causes of coronary heart disease and downplayed sugar consumption as also a risk factor. SRF set the review’s objective, contributed articles to be included and received drafts, while the SRF’s funding and role were not disclosed, according to the article.

“This historical account of industry efforts demonstrates the importance of having reviews written by people without conflicts of interest and the need for financial disclosure,” note the authors, who point out the NEJM has required authors to disclose all conflicts of interest since 1984. There also is no direct evidence that the sugar industry wrote or changed the NEJM review manuscript and evidence that that the industry shaped its conclusions is circumstantial, the authors acknowledge.

Limitations of the article include that the papers and documents used in the research provide only a small view into the activities of one sugar industry trade group. The authors did not analyze the role of other organizations, nutrition leaders or food industries. Key figures in the historical episode detailed in this article could not be interviewed because they have died.

“This study suggests that the sugar industry sponsored its first CHD [coronary heart disease] research project in 1965 to downplay early warning signs that sucrose consumption was a risk factor in CHD. As of 2016, sugar control policies are being promulgated in international, federal, state and local venues. Yet CHD risk is inconsistently cited as a health consequence of added sugars consumption. Because CHD is the leading cause of death globally, the health community should ensure that CHD risk is evaluated in future risk assessments of added sugars. Policymaking committees should consider giving less weight to food industry-funded studies, and include mechanistic and animal studies as well as studies appraising the effect of added sugars on multiple CHD biomarkers and disease development,” the article concludes.

According to the attached passage, what is an important part of any reliable body of research or trial?

The SRF initiated coronary heart disease research in 1965 and its first project was a literature review published in the New England Journal of Medicine in 1967. The review focused on fat and cholesterol as the dietary causes of coronary heart disease and downplayed sugar consumption as also a risk factor. SRF set the review’s objective, contributed articles to be included and received drafts, while the SRF’s funding and role were not disclosed, according to the article.

“This historical account of industry efforts demonstrates the importance of having reviews written by people without conflicts of interest and the need for financial disclosure,” note the authors, who point out the NEJM has required authors to disclose all conflicts of interest since 1984. There also is no direct evidence that the sugar industry wrote or changed the NEJM review manuscript and evidence that that the industry shaped its conclusions is circumstantial, the authors acknowledge.

Limitations of the article include that the papers and documents used in the research provide only a small view into the activities of one sugar industry trade group. The authors did not analyze the role of other organizations, nutrition leaders or food industries. Key figures in the historical episode detailed in this article could not be interviewed because they have died.

“This study suggests that the sugar industry sponsored its first CHD [coronary heart disease] research project in 1965 to downplay early warning signs that sucrose consumption was a risk factor in CHD. As of 2016, sugar control policies are being promulgated in international, federal, state and local venues. Yet CHD risk is inconsistently cited as a health consequence of added sugars consumption. Because CHD is the leading cause of death globally, the health community should ensure that CHD risk is evaluated in future risk assessments of added sugars. Policymaking committees should consider giving less weight to food industry-funded studies, and include mechanistic and animal studies as well as studies appraising the effect of added sugars on multiple CHD biomarkers and disease development,” the article concludes.

In the attached passage, what is the meaning of this phrase?

“…The sugar industry sponsored its first CHD research project in 1965 to downplay early warning signs that sucrose consumption was a risk factor in CHD.”

The SRF initiated coronary heart disease research in 1965 and its first project was a literature review published in the New England Journal of Medicine in 1967. The review focused on fat and cholesterol as the dietary causes of coronary heart disease and downplayed sugar consumption as also a risk factor. SRF set the review’s objective, contributed articles to be included and received drafts, while the SRF’s funding and role were not disclosed, according to the article.

“This historical account of industry efforts demonstrates the importance of having reviews written by people without conflicts of interest and the need for financial disclosure,” note the authors, who point out the NEJM has required authors to disclose all conflicts of interest since 1984. There also is no direct evidence that the sugar industry wrote or changed the NEJM review manuscript and evidence that that the industry shaped its conclusions is circumstantial, the authors acknowledge.

Limitations of the article include that the papers and documents used in the research provide only a small view into the activities of one sugar industry trade group. The authors did not analyze the role of other organizations, nutrition leaders or food industries. Key figures in the historical episode detailed in this article could not be interviewed because they have died.

“This study suggests that the sugar industry sponsored its first CHD [coronary heart disease] research project in 1965 to downplay early warning signs that sucrose consumption was a risk factor in CHD. As of 2016, sugar control policies are being promulgated in international, federal, state and local venues. Yet CHD risk is inconsistently cited as a health consequence of added sugars consumption. Because CHD is the leading cause of death globally, the health community should ensure that CHD risk is evaluated in future risk assessments of added sugars. Policymaking committees should consider giving less weight to food industry-funded studies, and include mechanistic and animal studies as well as studies appraising the effect of added sugars on multiple CHD biomarkers and disease development,” the article concludes.

Given its use in the attached passage, what is the meaning of the word prevalence?

More people are eating gluten-free, although the prevalence of celiac disease appears to have remained stable in recent years, according to an article published online by JAMA Internal Medicine. Hyun-seok Kim, M.D., M.P.H., of the Rutgers New Jersey Medical School, Newark, and coauthors analyzed data from the National Health and Nutrition Examination Surveys (NHANES) 2009 to 2014. There were 22,278 individuals over the age of 6 who participated in the surveys who underwent blood tests for celiac for whom information about prior diagnosis of celiac disease and adherence to a gluten-free diet was collected in a direct interview.

Overall, 106 (0.69 percent) individuals had a celiac disease diagnosis and 213 (1.08 percent) were identified as adhering to a gluten-free diet although they didn’t have celiac disease, according to the results reported in a research letter.

Those numbers correlated to an estimated 1.76 million people with celiac disease and 2.7 million people who adhere to a gluten-free diet even though they don’t have celiac disease in the United States.

While the prevalence of celiac disease appears to have remained steady overall (0.70 percent in 2009-2010, 0.77 percent in 2011-2012 and 0.58 percent in 2013-2014), adherence to a gluten-free diet by people without celiac disease has increased over time (0.52 percent in 2009-2010, 0.99 percent in 2011-2012 and 1.69 percent in 2013-2014), the authors report.

The two trends may be related because decreased gluten consumption could be contributing to the plateau in celiac disease, according to the report.

Limitations of the study include the small numbers of people participating in NHANES who were identified as having a diagnosis of celiac disease and as adhering to a gluten-free diet without celiac disease.

The report concludes the growing interest in a gluten-free diet by people without celiac disease could be due to a variety of factors, including public perception that it may be healthier, the growing availability of gluten-free products, and a self-diagnosis of gluten sensitivity by some individuals.”