Body temperature: What is the new normal?
Many researchers have argued that the accumulation of toxic beta-amyloid in the brain causes Alzheimer’s. However, a new study offers some evidence contradicting this sequence.
New research is questioning the predominant hypothesis that a buildup of beta-amyloid causes Alzheimer’s disease.
Alzheimer’s disease affects over 5.5 million people in the United States and millions more around the globe.
Yet, researchers are still at a loss as to why this condition — which is characterized by memory impairment and many other cognitive problems — occurs in the first place. And until they fully understand the cause, investigators will remain unable to devise a cure.
So far, the prevailing hypothesis among experts has been that the excessive accumulation of a potentially toxic protein — beta-amyloid — in the brain causes Alzheimer’s.
Researchers have argued that beta-amyloid plaques disrupt the communication between brain cells, potentially leading to cognitive function problems.
Now, a new study from the University of California San Diego School of Medicine and the Veterans Affairs San Diego Healthcare System suggests that while the buildup of beta-amyloid has associations with Alzheimer’s, it may not actually cause the condition.
In a study paper that appears in the journal Neurology, the researchers explain what led them to reach this conclusion.
“The scientific community has long thought that amyloid drives the neurodegeneration and cognitive impairment associated with Alzheimer’s disease,” says senior author Prof. Mark Bondi.
He notes that “[t]hese findings, in addition to other work in our lab, suggest that this is likely not the case for everyone and that sensitive neuropsychological measurement strategies capture subtle cognitive changes much earlier in the disease process than previously thought possible.”
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What comes first?
In their study, the researchers worked with a total of 747 participants with different levels of cognitive health. All of the study participants agreed to undergo neuropsychological assessments, as well as PET and MRI brain scans.
Of the participants, 305 were cognitively healthy, 289 had mild cognitive impairment, and 153 displayed markers of what the investigators call “objectively-defined subtle cognitive difficulties (Obj-SCD).”
Experts define mild cognitive impairment as a state of cognitive impairment that is more severe than what one would normally experience with age, but not yet severe enough for a dementia diagnosis.
However, mild cognitive impairment does develop into dementia in a significant number of people.
But what are Obj-SCD? In their paper, the investigators define them as “difficulties or inefficiencies on some sensitive cognitive tasks even though the overall neuropsychological profile is in the normal range.”
That is, they are a measurement of experienced, subtle cognitive functioning problems that occur in the absence of any visible signs of brain or psychological issues. To find out whether someone is experiencing Obj-SCD, researchers assess, among other factors, how efficiently that person can learn and retain new information.
Previous research has suggested that individuals with Obj-SCD are at a higher risk of mild cognitive impairment and forms of dementia.
In the current study, Prof. Bondi and the team found that beta-amyloid built up at a faster rate in the participants with Obj-SCD compared with those who were deemed cognitively healthy. Moreover, brain scans of people with Obj-SCD showed that these individuals experienced a thinning of brain matter in a region called the entorhinal cortex.
Past research has shown that the entorhinal cortex decreases in volume in people with Alzheimer’s disease. This is significant because this brain region plays a role in memory and spatial orientation.
The researchers also found that while people with mild cognitive impairment had higher quantities of beta-amyloid in their brains at the beginning of the study, this protein did not seem to build up any faster in these participants than it did in cognitively healthy individuals.
But why do the current findings potentially contradict a decades-old hypothesis about the development of Alzheimer’s? Prof. Bondi explains:
“This work […] suggests that cognitive changes may be occurring before significant levels of amyloid have accumulated. It seems like we may need to focus on treatment targets of pathologies other than amyloid, such as tau, that are more highly associated with the thinking and memory difficulties that impact people’s lives.”
“While the emergence of biomarkers of Alzheimer’s disease has revolutionized research and our understanding of how the disease progresses, many of these biomarkers continue to be highly expensive, inaccessible for clinical use, or not available to those with certain medical conditions,” adds first author Kelsey Thomas, Ph.D.
The new study’s findings could help change that by refocusing the research approach on more subtle markers of Alzheimer’s, such as those assessing for Obj-SCD.
“A method of identifying individuals at risk for progression to [Alzheimer’s disease] using neuropsychological measures has the potential to improve early detection in those who may otherwise not be eligible for more expensive or invasive screening,” says Thomas.
As the incidence of diabetes continues to increase globally, the fight against this chronic condition continues. New research explains not only what triggers type 2 diabetes but also how to reverse the condition. The findings also shed light on what leads to remission after reversal for some people.
New research looks at the causes of type 2 diabetes and the lifestyle changes that may reverse this condition.
Between 1980 and 2014, the number of people living with diabetes across the world increased from about 108 million to 422 million.
As many as 90% of these individuals have type 2 diabetes.
Pharmacological interventions have done little to stop what some have referred to as the diabetes pandemic.
Lifestyle interventions, however, may succeed where other approaches have failed.
A couple of years ago, Medical News Today reported on the first results of a clinical trial, which showed that intensive weight loss programs could help people with type 2 diabetes achieve remission without taking any medication.
The trial was called the Diabetes Remission Clinical Trial (DiRECT), and one of its co-leaders was Prof. Roy Taylor from Newcastle University in the United Kingdom.
But how does this remission occur, and can it last in the long term? Why do some people achieve lasting remission while for others, the condition returns?
Prof. Taylor set out with his team to answer these questions, using data from the DiRECT trial and applying cutting-edge imaging and blood monitoring techniques.
The researchers published their findings in the journal Cell Metabolism.
MEDICAL NEWS TODAY NEWSLETTER
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Expect in-depth, science-backed toplines of our best stories every day. Tap in and keep your curiosity satisfied.
Enter your email
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Testing the ‘twin cycle hypothesis’
The study aimed to test — and confirm — the so-called twin cycle hypothesis, which Prof. Taylor and team put forth more than a decade ago.
The theory proposed that type 2 diabetes results from the accumulation of fat in the liver, which induces insulin resistance and increases blood sugar production.
These effects, in turn, increase plasma insulin levels, precipitating “a self-reinforcing cycle” in which insulin stimulates fat production.
These increased levels of liver fat cause the lipids to overspill into several tissues, including the pancreas.
Beta-cells, which are responsible for creating insulin, are located in the pancreas. “Long-term exposure to saturated fatty acids is harmful to [beta]-cells,” write the authors.
In the present study, the authors investigated the predictions of the twin cycle hypothesis 2 years into the DiRECT trial.
The researchers wanted to “describe the pathophysiologic processes underlying the recurrence of type 2 diabetes in the group that initially achieved remission but then relapsed back to diabetes.”
To this end, the researchers quantified intra-organ and abdominal fat using cutting-edge MRI scans at 12 and 24 months. They looked at pancreatic and liver fat, specifically.
The analysis included measurements of glucose, HbA1c, high-density lipoprotein (HDL) cholesterol, and triglycerides. The team also analyzed fatty acids, insulin secretion, and beta-cell function.
When liver fat ‘clogs up’ the pancreas
The study revealed that the majority of the trial participants maintained remission over the 2 years but that this was only possible if liver triglycerides and fat in the pancreas remained low.
Specifically, almost 9 out of 10 participants who managed to lose 15 kilograms or more in the DiRECT trial reversed their condition.
After 2 years, more than one-third of these individuals had been free of diabetes and the need for diabetes medication for at least 24 months.
A small group, however, experienced relapse, which was associated with a return to high liver triglycerides and high intrapancreatic fat levels.
Prof. Taylor explains: “We saw that when a person accumulates too much fat, which should be stored under the skin, then it has to go elsewhere in the body. The amount that can be stored under the skin varies from person to person, indicating a ‘personal fat threshold’ above which fat can cause mischief.”
“When fat cannot be safely stored under the skin, it is then stored inside the liver and overspills to the rest of the body, including the pancreas. This ‘clogs up’ the pancreas, switching off the genes [that] direct how insulin should effectively be produced, and this causes type 2 diabetes.”
Prof. Roy Taylor
‘Diet and persistence’ can reverse diabetes
“This means we can now see type 2 diabetes as a simple condition where the individual has accumulated more fat than they can cope with,” continues the author, stressing the hopeful implications of this finding.
“Importantly, this means that through diet and persistence, patients are able to lose the fat and potentially reverse their diabetes. The sooner this is done after diagnosis, the more likely it is that remission can be achieved.”
“For the first time,” conclude Prof. Taylor and team in their paper, “we are able to report the underlying physiologic changes during a full cycle of disease reversal and re-emergence.”
In the U.K., the National Health Service (NHS) will roll out a program that will test the weight loss therapy in thousands of people living with type 2 diabetes.
A recent analysis of temperature trends suggests that the average human body temperature has dropped since the 19th century due to physiological changes. The authors of the new study also highlight potential causes of these alterations.
New research suggests that our regular body temperature has dropped over time.
Most of us only take our temperatures when we are worried that we have a fever, as a result of an infection or a cold, for example.
But body temperature can indicate and be influenced by many other factors; lifestyle habits, age, and ambient temperature can all influence how our body disperses heat.
Body temperature is also a marker of metabolic health. Specifically, the authors of the new study explain, human body temperature indicates metabolic rate, which some have linked with longevity and body size.
So what is our normal body temperature? In 1851, a German physician called Carl Reinhold August Wunderlich surveyed 25,000 people in one city and established that 37°C is the standard temperature of the human body.
However, recent analyses and surveys suggest that the average body temperature is now lower.
For instance, a study of more than 35,000 people in the United Kingdom and nearly 250,000 temperature measurements found that 36.6°C is the average oral temperature. Could this discrepancy be a result of changes in measurement tools? Or, do the new findings reflect higher life expectancy and better overall health?
Myroslava Protsiv, then at Stanford University’s Division of Infectious Diseases and Geographic Medicine, in California, and colleagues set out to investigate.
The team hypothesized that “the differences observed in temperature between the 19th century and today are real and that the change over time provides important physiologic clues to alterations in human health and longevity since the Industrial Revolution.”
Their paper appears in the journal eLife.
MEDICAL NEWS TODAY NEWSLETTER
Stay in the know. Get our free daily newsletter
Expect in-depth, science-backed toplines of our best stories every day. Tap in and keep your curiosity satisfied.
Enter your email
Your privacy is important to us
Studying historic trends in body temperature
To test their hypothesis, the researchers analyzed information from three datasets:
The first included data from 1862–1930 obtained from Union Army veterans of the Civil War.
The second dataset was from the United States National Health and Nutrition Examination Survey I, which took place from 1971–1975.
The third dataset was from the Stanford Translational Research Integrated Database Environment, which contains data from people who received healthcare through Stanford between 2007 and 2017.
Overall, the scientists had access to 677,423 temperature measurements, which they integrated, forming a model of change over time.
New normal body temperature is cooler
Some of the researchers’ findings include:
The body temperature of men today is, on average, 0.59°C lower than that of men born in the early 19th century.
Similarly, women’s body temperature dropped by 0.32°C from the 1890s to today.
Overall, the analysis found a 0.03°C decrease in average temperature with every decade.
To check whether the decreases stemmed from advances in thermometer technology, Protsiv and the team looked at changes within datasets, assuming that doctors in each historical period were generally using the same types of thermometers.
The results of the analysis within datasets reflected the changes in the combined data. “Our temperature’s not what people think it is,” says Dr. Julie Parsonnet, a professor of medicine, health research, and policy, and the senior author of the study.
“What everybody grew up learning, which is that our normal temperature is [37°C], is wrong.”
Dr. Julie Parsonnet
However, because gender, time of day, and age can each change our body temperature, the researchers do not advise updating the standard for all U.S. adults.
powered by Rubicon Project
What has caused our temperature to drop?
So why has the average body temperature changed? “Physiologically, we’re just different from what we were in the past,” Dr. Parsonnet says.
“The environment that we’re living in has changed, including the temperature in our homes, our contact with microorganisms, and the food that we have access to.”
“All these things mean that, although we think of human beings as if we’re monomorphic and have been the same for all of human evolution, we’re not the same. We’re actually changing physiologically.”
Furthermore, Dr. Parsonnet believes, the average metabolic rate, which indicates how much energy our bodies use, has declined over time. This decrease could result from a decrease in inflammation.
“Inflammation produces all sorts of proteins and cytokines that rev up your metabolism and raise your temperature,” she says.
Finally, air conditioning and heating have resulted in a more consistent ambient temperature, making it unnecessary to expend energy to maintain the same body temperature.
New research is questioning the predominant hypothesis that a buildup of beta-amyloid causes Alzheimer’s disease.
Alzheimer’s disease affects over 5.5 million people in the United States and millions more around the globe.
Yet, researchers are still at a loss as to why this condition — which is characterized by memory impairment and many other cognitive problems — occurs in the first place. And until they fully understand the cause, investigators will remain unable to devise a cure.
So far, the prevailing hypothesis among experts has been that the excessive accumulation of a potentially toxic protein — beta-amyloid — in the brain causes Alzheimer’s.
Researchers have argued that beta-amyloid plaques disrupt the communication between brain cells, potentially leading to cognitive function problems.
Now, a new study from the University of California San Diego School of Medicine and the Veterans Affairs San Diego Healthcare System suggests that while the buildup of beta-amyloid has associations with Alzheimer’s, it may not actually cause the condition.
In a study paper that appears in the journal Neurology, the researchers explain what led them to reach this conclusion.
“The scientific community has long thought that amyloid drives the neurodegeneration and cognitive impairment associated with Alzheimer’s disease,” says senior author Prof. Mark Bondi.
He notes that “[t]hese findings, in addition to other work in our lab, suggest that this is likely not the case for everyone and that sensitive neuropsychological measurement strategies capture subtle cognitive changes much earlier in the disease process than previously thought possible.”
MEDICAL NEWS TODAY NEWSLETTER
Stay in the know. Get our free daily newsletter
Expect in-depth, science-backed toplines of our best stories every day. Tap in and keep your curiosity satisfied.
Enter your email
Your privacy is important to us
What comes first?
In their study, the researchers worked with a total of 747 participants with different levels of cognitive health. All of the study participants agreed to undergo neuropsychological assessments, as well as PET and MRI brain scans.
Of the participants, 305 were cognitively healthy, 289 had mild cognitive impairment, and 153 displayed markers of what the investigators call “objectively-defined subtle cognitive difficulties (Obj-SCD).”
Experts define mild cognitive impairment as a state of cognitive impairment that is more severe than what one would normally experience with age, but not yet severe enough for a dementia diagnosis.
However, mild cognitive impairment does develop into dementia in a significant number of people.
But what are Obj-SCD? In their paper, the investigators define them as “difficulties or inefficiencies on some sensitive cognitive tasks even though the overall neuropsychological profile is in the normal range.”
That is, they are a measurement of experienced, subtle cognitive functioning problems that occur in the absence of any visible signs of brain or psychological issues. To find out whether someone is experiencing Obj-SCD, researchers assess, among other factors, how efficiently that person can learn and retain new information.
Previous research has suggested that individuals with Obj-SCD are at a higher risk of mild cognitive impairment and forms of dementia.
In the current study, Prof. Bondi and the team found that beta-amyloid built up at a faster rate in the participants with Obj-SCD compared with those who were deemed cognitively healthy. Moreover, brain scans of people with Obj-SCD showed that these individuals experienced a thinning of brain matter in a region called the entorhinal cortex.
Past research has shown that the entorhinal cortex decreases in volume in people with Alzheimer’s disease. This is significant because this brain region plays a role in memory and spatial orientation.
The researchers also found that while people with mild cognitive impairment had higher quantities of beta-amyloid in their brains at the beginning of the study, this protein did not seem to build up any faster in these participants than it did in cognitively healthy individuals.
But why do the current findings potentially contradict a decades-old hypothesis about the development of Alzheimer’s? Prof. Bondi explains:
“This work […] suggests that cognitive changes may be occurring before significant levels of amyloid have accumulated. It seems like we may need to focus on treatment targets of pathologies other than amyloid, such as tau, that are more highly associated with the thinking and memory difficulties that impact people’s lives.”
“While the emergence of biomarkers of Alzheimer’s disease has revolutionized research and our understanding of how the disease progresses, many of these biomarkers continue to be highly expensive, inaccessible for clinical use, or not available to those with certain medical conditions,” adds first author Kelsey Thomas, Ph.D.
The new study’s findings could help change that by refocusing the research approach on more subtle markers of Alzheimer’s, such as those assessing for Obj-SCD.
“A method of identifying individuals at risk for progression to [Alzheimer’s disease] using neuropsychological measures has the potential to improve early detection in those who may otherwise not be eligible for more expensive or invasive screening,” says Thomas.
As the incidence of diabetes continues to increase globally, the fight against this chronic condition continues. New research explains not only what triggers type 2 diabetes but also how to reverse the condition. The findings also shed light on what leads to remission after reversal for some people.
New research looks at the causes of type 2 diabetes and the lifestyle changes that may reverse this condition.
Between 1980 and 2014, the number of people living with diabetes across the world increased from about 108 million to 422 million.
As many as 90% of these individuals have type 2 diabetes.
Pharmacological interventions have done little to stop what some have referred to as the diabetes pandemic.
Lifestyle interventions, however, may succeed where other approaches have failed.
A couple of years ago, Medical News Today reported on the first results of a clinical trial, which showed that intensive weight loss programs could help people with type 2 diabetes achieve remission without taking any medication.
The trial was called the Diabetes Remission Clinical Trial (DiRECT), and one of its co-leaders was Prof. Roy Taylor from Newcastle University in the United Kingdom.
But how does this remission occur, and can it last in the long term? Why do some people achieve lasting remission while for others, the condition returns?
Prof. Taylor set out with his team to answer these questions, using data from the DiRECT trial and applying cutting-edge imaging and blood monitoring techniques.
The researchers published their findings in the journal Cell Metabolism.
MEDICAL NEWS TODAY NEWSLETTER
Stay in the know. Get our free daily newsletter
Expect in-depth, science-backed toplines of our best stories every day. Tap in and keep your curiosity satisfied.
Enter your email
Your privacy is important to us
Testing the ‘twin cycle hypothesis’
The study aimed to test — and confirm — the so-called twin cycle hypothesis, which Prof. Taylor and team put forth more than a decade ago.
The theory proposed that type 2 diabetes results from the accumulation of fat in the liver, which induces insulin resistance and increases blood sugar production.
These effects, in turn, increase plasma insulin levels, precipitating “a self-reinforcing cycle” in which insulin stimulates fat production.
These increased levels of liver fat cause the lipids to overspill into several tissues, including the pancreas.
Beta-cells, which are responsible for creating insulin, are located in the pancreas. “Long-term exposure to saturated fatty acids is harmful to [beta]-cells,” write the authors.
In the present study, the authors investigated the predictions of the twin cycle hypothesis 2 years into the DiRECT trial.
The researchers wanted to “describe the pathophysiologic processes underlying the recurrence of type 2 diabetes in the group that initially achieved remission but then relapsed back to diabetes.”
To this end, the researchers quantified intra-organ and abdominal fat using cutting-edge MRI scans at 12 and 24 months. They looked at pancreatic and liver fat, specifically.
The analysis included measurements of glucose, HbA1c, high-density lipoprotein (HDL) cholesterol, and triglycerides. The team also analyzed fatty acids, insulin secretion, and beta-cell function.
When liver fat ‘clogs up’ the pancreas
The study revealed that the majority of the trial participants maintained remission over the 2 years but that this was only possible if liver triglycerides and fat in the pancreas remained low.
Specifically, almost 9 out of 10 participants who managed to lose 15 kilograms or more in the DiRECT trial reversed their condition.
After 2 years, more than one-third of these individuals had been free of diabetes and the need for diabetes medication for at least 24 months.
A small group, however, experienced relapse, which was associated with a return to high liver triglycerides and high intrapancreatic fat levels.
Prof. Taylor explains: “We saw that when a person accumulates too much fat, which should be stored under the skin, then it has to go elsewhere in the body. The amount that can be stored under the skin varies from person to person, indicating a ‘personal fat threshold’ above which fat can cause mischief.”
“When fat cannot be safely stored under the skin, it is then stored inside the liver and overspills to the rest of the body, including the pancreas. This ‘clogs up’ the pancreas, switching off the genes [that] direct how insulin should effectively be produced, and this causes type 2 diabetes.”
Prof. Roy Taylor
‘Diet and persistence’ can reverse diabetes
“This means we can now see type 2 diabetes as a simple condition where the individual has accumulated more fat than they can cope with,” continues the author, stressing the hopeful implications of this finding.
“Importantly, this means that through diet and persistence, patients are able to lose the fat and potentially reverse their diabetes. The sooner this is done after diagnosis, the more likely it is that remission can be achieved.”
“For the first time,” conclude Prof. Taylor and team in their paper, “we are able to report the underlying physiologic changes during a full cycle of disease reversal and re-emergence.”
In the U.K., the National Health Service (NHS) will roll out a program that will test the weight loss therapy in thousands of people living with type 2 diabetes.
A recent analysis of temperature trends suggests that the average human body temperature has dropped since the 19th century due to physiological changes. The authors of the new study also highlight potential causes of these alterations.
New research suggests that our regular body temperature has dropped over time.
Most of us only take our temperatures when we are worried that we have a fever, as a result of an infection or a cold, for example.
But body temperature can indicate and be influenced by many other factors; lifestyle habits, age, and ambient temperature can all influence how our body disperses heat.
Body temperature is also a marker of metabolic health. Specifically, the authors of the new study explain, human body temperature indicates metabolic rate, which some have linked with longevity and body size.
So what is our normal body temperature? In 1851, a German physician called Carl Reinhold August Wunderlich surveyed 25,000 people in one city and established that 37°C is the standard temperature of the human body.
However, recent analyses and surveys suggest that the average body temperature is now lower.
For instance, a study of more than 35,000 people in the United Kingdom and nearly 250,000 temperature measurements found that 36.6°C is the average oral temperature. Could this discrepancy be a result of changes in measurement tools? Or, do the new findings reflect higher life expectancy and better overall health?
Myroslava Protsiv, then at Stanford University’s Division of Infectious Diseases and Geographic Medicine, in California, and colleagues set out to investigate.
The team hypothesized that “the differences observed in temperature between the 19th century and today are real and that the change over time provides important physiologic clues to alterations in human health and longevity since the Industrial Revolution.”
Their paper appears in the journal eLife.
MEDICAL NEWS TODAY NEWSLETTER
Stay in the know. Get our free daily newsletter
Expect in-depth, science-backed toplines of our best stories every day. Tap in and keep your curiosity satisfied.
Enter your email
Your privacy is important to us
Studying historic trends in body temperature
To test their hypothesis, the researchers analyzed information from three datasets:
The first included data from 1862–1930 obtained from Union Army veterans of the Civil War.
The second dataset was from the United States National Health and Nutrition Examination Survey I, which took place from 1971–1975.
The third dataset was from the Stanford Translational Research Integrated Database Environment, which contains data from people who received healthcare through Stanford between 2007 and 2017.
Overall, the scientists had access to 677,423 temperature measurements, which they integrated, forming a model of change over time.
New normal body temperature is cooler
Some of the researchers’ findings include:
The body temperature of men today is, on average, 0.59°C lower than that of men born in the early 19th century.
Similarly, women’s body temperature dropped by 0.32°C from the 1890s to today.
Overall, the analysis found a 0.03°C decrease in average temperature with every decade.
To check whether the decreases stemmed from advances in thermometer technology, Protsiv and the team looked at changes within datasets, assuming that doctors in each historical period were generally using the same types of thermometers.
The results of the analysis within datasets reflected the changes in the combined data. “Our temperature’s not what people think it is,” says Dr. Julie Parsonnet, a professor of medicine, health research, and policy, and the senior author of the study.
“What everybody grew up learning, which is that our normal temperature is [37°C], is wrong.”
Dr. Julie Parsonnet
However, because gender, time of day, and age can each change our body temperature, the researchers do not advise updating the standard for all U.S. adults.
powered by Rubicon Project
What has caused our temperature to drop?
So why has the average body temperature changed? “Physiologically, we’re just different from what we were in the past,” Dr. Parsonnet says.
“The environment that we’re living in has changed, including the temperature in our homes, our contact with microorganisms, and the food that we have access to.”
“All these things mean that, although we think of human beings as if we’re monomorphic and have been the same for all of human evolution, we’re not the same. We’re actually changing physiologically.”
Furthermore, Dr. Parsonnet believes, the average metabolic rate, which indicates how much energy our bodies use, has declined over time. This decrease could result from a decrease in inflammation.
“Inflammation produces all sorts of proteins and cytokines that rev up your metabolism and raise your temperature,” she says.
Finally, air conditioning and heating have resulted in a more consistent ambient temperature, making it unnecessary to expend energy to maintain the same body temperature.
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