The Biology Of Why Coronavirus Is So Deadly

The Biology Of Why Coronavirus Is So Deadly

COVID-19 is caused by a coronavirus called SARS-CoV-2. Coronaviruses belong to a group of viruses that infect animals, from peacocks to whales. They’re named for the bulb-tipped spikes that project from the virus’s surface and give the appearance of a corona surrounding it.

A coronavirus infection usually plays out one of two ways: as an infection in the lungs that includes some cases of what people would call the common cold, or as an infection in the gut that causes diarrhea. COVID-19 starts out in the lungs like the common cold coronaviruses, but then causes havoc with the immune system that can lead to long-term lung damage or death.

SARS-CoV-2 is genetically very similar to other human respiratory coronaviruses, including SARS-CoV and MERS-CoV. However, the subtle genetic differences translate to significant differences in how readily a coronavirus infects people and how it makes them sick.

 

SARS-CoV-2 virus particles (pink dots) on a dying cell. National Institute of Allergy and Infectious Diseases, NIH

 

SARS-CoV-2 has all the same genetic equipment as the original SARS-CoV, which caused a global outbreak in 2003, but with around 6,000 mutations sprinkled around in the usual places where coronaviruses change. Think whole milk versus skim milk.

Compared to other human coronaviruses like MERS-CoV, which emerged in the Middle East in 2012, the new virus has customized versions of the same general equipment for invading cells and copying itself. However, SARS-CoV-2 has a totally different set of genes called accessories, which give this new virus a little advantage in specific situations. For example, MERS has a particular protein that shuts down a cell’s ability to sound the alarm about a viral intruder. SARS-CoV-2 has an unrelated gene with an as-yet unknown function in that position in its genome. Think cow milk versus almond milk.

 

How the virus infects

 

Every coronavirus infection starts with a virus particle, a spherical shell that protects a single long string of genetic material and inserts it into a human cell. The genetic material instructs the cell to make around 30 different parts of the virus, allowing the virus to reproduce. The cells that SARS-CoV-2 prefers to infect have a protein called ACE2 on the outside that is important for regulating blood pressure.

The infection begins when the long spike proteins that protrude from the virus particle latch on to the cell’s ACE2 protein. From that point, the spike transforms, unfolding and refolding itself using coiled spring-like parts that start out buried at the core of the spike. The reconfigured spike hooks into the cell and crashes the virus particle and cell together. This forms a channel where the string of viral genetic material can snake its way into the unsuspecting cell.

An illustration of the SARS-CoV-2 spike protein shown from the side (left) and top. The protein latches onto human lung cells. 5-HT2AR/Wikimedia

SARS-CoV-2 spreads from person to person by close contact. The Shincheonji Church outbreak in South Korea in February provides a good demonstration of how and how quickly SARS-CoV-2 spreads. It seems one or two people with the virus sat face to face very close to uninfected people for several minutes at a time in a crowded room. Within two weeks, several thousand people in the country were infected, and more than half of the infections at that point were attributable to the church. The outbreak got to a fast start because public health authorities were unaware of the potential outbreak and were not testing widely at that stage. Since then, authorities have worked hard and the number of new cases in South Korea has been falling steadily.

 

How the virus makes people sick

 

SARS-CoV-2 grows in type II lung cells, which secrete a soap-like substance that helps air slip deep into the lungs, and in cells lining the throat. As with SARS, most of the damage in COVID-19, the illness caused by the new coronavirus, is caused by the immune system carrying out a scorched earth defense to stop the virus from spreading. Millions of cells from the immune system invade the infected lung tissue and cause massive amounts of damage in the process of cleaning out the virus and any infected cells.

Each COVID-19 lesion ranges from the size of a grape to the size of a grapefruit. The challenge for health care workers treating patients is to support the body and keep the blood oxygenated while the lung is repairing itself.

 

How SARS-CoV-2 infects, sickens and kills people

 

SARS-CoV-2 has a sliding scale of severity. Patients under age 10 seem to clear the virus easily, most people under 40 seem to bounce back quickly, but older people suffer from increasingly severe COVID-19. The ACE2 protein that SARS-CoV-2 uses as a door to enter cells is also important for regulating blood pressure, and it does not do its job when the virus gets there first. This is one reason COVID-19 is more severe in people with high blood pressure.

SARS-CoV-2 is more severe than seasonal influenza in part because it has many more ways to stop cells from calling out to the immune system for help. For example, one way that cells try to respond to infection is by making interferon, the alarm signaling protein. SARS-CoV-2 blocks this by a combination of camouflage, snipping off protein markers from the cell that serve as distress beacons and finally shredding any anti-viral instructions that the cell makes before they can be used. As a result, COVID-19 can fester for a month, causing a little damage each day, while most people get over a case of the flu in less than a week.

At present, the transmission rate of SARS-CoV-2 is a little higher than that of the pandemic 2009 H1N1 influenza virus, but SARS-CoV-2 is at least 10 times as deadly. From the data that is available now, COVID-19 seems a lot like severe acute respiratory syndrome (SARS), though it’s less likely than SARS to be severe.

 

What isn’t known

 

There are still many mysteries about this virus and coronaviruses in general – the nuances of how they cause disease, the way they interact with proteins inside the cell, the structure of the proteins that form new viruses and how some of the basic virus-copying machinery works.

Another unknown is how COVID-19 will respond to changes in the seasons. The flu tends to follow cold weather, both in the northern and southern hemispheres. Some other human coronaviruses spread at a low level year-round, but then seem to peak in the spring. But nobody really knows for sure why these viruses vary with the seasons.

What is amazing so far in this outbreak is all the good science that has come out so quickly. The research community learned about structures of the virus spike protein and the ACE2 protein with part of the spike protein attached just a little over a month after the genetic sequence became available. I spent my first 20 or so years working on coronaviruses without the benefit of either. This bodes well for better understanding, preventing and treating COVID-19.

By Benjamin Neuman, Professor of Biology, Texas A&M University-Texarkana. This article is republished from The Conversation under a Creative Commons license. Read the original article.

The Conversation Thu, 04/02/2020 - 14:02

Categories

Life Sciences

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The Biology Of Why Coronavirus Is So Deadly

COVID-19 is caused by a coronavirus called SARS-CoV-2. Coronaviruses belong to a group of viruses that infect animals, from peacocks to whales. They’re named for the bulb-tipped spikes that project from the virus’s surface and give the appearance of a corona surrounding it.

A coronavirus infection usually plays out one of two ways: as an infection in the lungs that includes some cases of what people would call the common cold, or as an infection in the gut that causes diarrhea. COVID-19 starts out in the lungs like the common cold coronaviruses, but then causes havoc with the immune system that can lead to long-term lung damage or death.

SARS-CoV-2 is genetically very similar to other human respiratory coronaviruses, including SARS-CoV and MERS-CoV. However, the subtle genetic differences translate to significant differences in how readily a coronavirus infects people and how it makes them sick.

 

SARS-CoV-2 virus particles (pink dots) on a dying cell. National Institute of Allergy and Infectious Diseases, NIH

 

SARS-CoV-2 has all the same genetic equipment as the original SARS-CoV, which caused a global outbreak in 2003, but with around 6,000 mutations sprinkled around in the usual places where coronaviruses change. Think whole milk versus skim milk.

Compared to other human coronaviruses like MERS-CoV, which emerged in the Middle East in 2012, the new virus has customized versions of the same general equipment for invading cells and copying itself. However, SARS-CoV-2 has a totally different set of genes called accessories, which give this new virus a little advantage in specific situations. For example, MERS has a particular protein that shuts down a cell’s ability to sound the alarm about a viral intruder. SARS-CoV-2 has an unrelated gene with an as-yet unknown function in that position in its genome. Think cow milk versus almond milk.

 

How the virus infects

 

Every coronavirus infection starts with a virus particle, a spherical shell that protects a single long string of genetic material and inserts it into a human cell. The genetic material instructs the cell to make around 30 different parts of the virus, allowing the virus to reproduce. The cells that SARS-CoV-2 prefers to infect have a protein called ACE2 on the outside that is important for regulating blood pressure.

The infection begins when the long spike proteins that protrude from the virus particle latch on to the cell’s ACE2 protein. From that point, the spike transforms, unfolding and refolding itself using coiled spring-like parts that start out buried at the core of the spike. The reconfigured spike hooks into the cell and crashes the virus particle and cell together. This forms a channel where the string of viral genetic material can snake its way into the unsuspecting cell.

An illustration of the SARS-CoV-2 spike protein shown from the side (left) and top. The protein latches onto human lung cells. 5-HT2AR/Wikimedia

SARS-CoV-2 spreads from person to person by close contact. The Shincheonji Church outbreak in South Korea in February provides a good demonstration of how and how quickly SARS-CoV-2 spreads. It seems one or two people with the virus sat face to face very close to uninfected people for several minutes at a time in a crowded room. Within two weeks, several thousand people in the country were infected, and more than half of the infections at that point were attributable to the church. The outbreak got to a fast start because public health authorities were unaware of the potential outbreak and were not testing widely at that stage. Since then, authorities have worked hard and the number of new cases in South Korea has been falling steadily.

 

How the virus makes people sick

 

SARS-CoV-2 grows in type II lung cells, which secrete a soap-like substance that helps air slip deep into the lungs, and in cells lining the throat. As with SARS, most of the damage in COVID-19, the illness caused by the new coronavirus, is caused by the immune system carrying out a scorched earth defense to stop the virus from spreading. Millions of cells from the immune system invade the infected lung tissue and cause massive amounts of damage in the process of cleaning out the virus and any infected cells.

Each COVID-19 lesion ranges from the size of a grape to the size of a grapefruit. The challenge for health care workers treating patients is to support the body and keep the blood oxygenated while the lung is repairing itself.

 

How SARS-CoV-2 infects, sickens and kills people

 

SARS-CoV-2 has a sliding scale of severity. Patients under age 10 seem to clear the virus easily, most people under 40 seem to bounce back quickly, but older people suffer from increasingly severe COVID-19. The ACE2 protein that SARS-CoV-2 uses as a door to enter cells is also important for regulating blood pressure, and it does not do its job when the virus gets there first. This is one reason COVID-19 is more severe in people with high blood pressure.

SARS-CoV-2 is more severe than seasonal influenza in part because it has many more ways to stop cells from calling out to the immune system for help. For example, one way that cells try to respond to infection is by making interferon, the alarm signaling protein. SARS-CoV-2 blocks this by a combination of camouflage, snipping off protein markers from the cell that serve as distress beacons and finally shredding any anti-viral instructions that the cell makes before they can be used. As a result, COVID-19 can fester for a month, causing a little damage each day, while most people get over a case of the flu in less than a week.

At present, the transmission rate of SARS-CoV-2 is a little higher than that of the pandemic 2009 H1N1 influenza virus, but SARS-CoV-2 is at least 10 times as deadly. From the data that is available now, COVID-19 seems a lot like severe acute respiratory syndrome (SARS), though it’s less likely than SARS to be severe.

 

What isn’t known

 

There are still many mysteries about this virus and coronaviruses in general – the nuances of how they cause disease, the way they interact with proteins inside the cell, the structure of the proteins that form new viruses and how some of the basic virus-copying machinery works.

Another unknown is how COVID-19 will respond to changes in the seasons. The flu tends to follow cold weather, both in the northern and southern hemispheres. Some other human coronaviruses spread at a low level year-round, but then seem to peak in the spring. But nobody really knows for sure why these viruses vary with the seasons.

What is amazing so far in this outbreak is all the good science that has come out so quickly. The research community learned about structures of the virus spike protein and the ACE2 protein with part of the spike protein attached just a little over a month after the genetic sequence became available. I spent my first 20 or so years working on coronaviruses without the benefit of either. This bodes well for better understanding, preventing and treating COVID-19.

By Benjamin Neuman, Professor of Biology, Texas A&M University-Texarkana. This article is republished from The Conversation under a Creative Commons license. Read the original article.

The Conversation Thu, 04/02/2020 - 14:02

Categories

Life Sciences

from ScienceBlogs - Where the world discusses science https://ift.tt/2X2LE7b

COVID-19: The Downside To More Testing Could Be Overflowing Hospitals

COVID-19: The Downside To More Testing Could Be Overflowing Hospitals

"You can’t fight a virus if you don’t know where it is."

These were the words of Director General of the World Health Organisation (WHO), Dr Tedros Adhanom Ghebreyesus, at his briefing on the COVID-19 pandemic in mid-March.

He made the statement in a bid to underscore the need to test many more people as key to containing the spread of the disease.

Ordinarily, that makes sense and I would agree with it. It is the right thing to do in the face of a disease which would show mild to no symptoms in the majority of those that are infected but does not inhibit their ability to infect others.

Countries that follow the WHO view have sought to buy test kits and increase the number of tests conducted daily. Others have been more cautious and have set up guidelines to ensure that they only test people with significant history of risk for COVID-19 or symptoms of the disease.

An aerial view of a new isolation and treatment centre established by the Lagos State government at the main bowl of the state-owned Stadium. Pius Utomi Ekpei/AFP via Getty Images via The Conversation

 

Looking at the various models and the progression of the pandemic, I wish to offer some views on testing and the attendant issues and challenges.

I believe that there are a myriad of factors to consider and that, particularly in Africa, countries have to take them all on board when making their decisions to curtail the spread of the virus.

The factors include the dangers posed by false test results, the fact that testing data is being badly communicated leading to a rise in panic levels and the fact that testing capacity is limited in many countries.

The fear factor

It is quite clear that the world is now dealing with two pandemics instead of one. The first is the virus. The second is fear and, in many cases, outright panic. That is why landlords are kicking out health workers from their houses. That is why we get reports of chloroquine toxicity within 24 hours of US President Donald Trump saying that might be the treatment for COVID-19.

What has panic got to do with testing? Panic is being driven by the way in which the outcome of testing is being communicated. For example, most countries are releasing data about how many more cases there are. But they are not telling their citizens how many of these people have no symptoms at all, or have mild ones.

Knowing how many of those who tested positive were not considered to be in a critical state would be helpful.

The other area in which data is being badly handled, and adding to panic levels, is that countries are reporting new cases on a daily basis. These aren’t necessarily new infections but, rather, new detections. Most are people who already had it and (for whatever reason were able to get tested) were found to be positive. They are people who, just the day before, did not know they had the virus and therefore weren’t provoking fear in others. Also, the number of new confirmed cases alone may not be the best indicator for the challenge the disease poses in a country or community.

Knowing their status now should not cause panic. It should simply inform about the importance of the preventive measures, including testing, to prevent spread of the disease.

Limited resources

Countries are being urged to test as many people as possible in the face of limited test resources. The mainstay polymerase chain reaction test is quite limited and relatively slow. It is also expensive given the requirements even of staff and laboratories.

Enter rapid test kits to the rescue. But there aren’t enough. Even the US doesn’t have enough test kits to meet the demand.

In addition, not all the kits in use have been tested properly. For example, there are reports that thousands of test kits imported by the Spanish health authorities were found to be faulty.

The challenge of a test kit giving false negatives is that the people are told, erroneously, that they do not have the virus. They go away and continue to infect others freely. In the event that they have any symptoms, they are likely to ignore these, and some may become severely ill before seeking care. If they do seek care early, the health care workers may be exposed to COVID-19 thinking that this person had tested negative and could only have some other disease.

A false positive, on the other hand, means that the number of cases reported continues to rise along with the panic created and attendant socio-economic disruption.

The Jack Ma Foundation has donated 20,000 test kits to Nigeria. But what are these among so many? Consider two statistics alongside this number. The population of the country – about 200 million people. And the fact that with 65 confirmed cases (as at the time of writing this), Nigeria is tracking over 4,000 contacts already.

A further complication in Nigeria is that the allocation of available tests kits could become subject to social and political whims. Government officials are scrambling to get tested along with their families and wealthy friends. Unfortunately, the guidelines for determining who to test won’t apply to this category of people. This means that limited resources will be used up.

 

Overwhelming hospitals

 

The fatality rate for COVID-19 has not yet been definitively established. Nevertheless, the fatality rate – particularly among older people – has been one of the major factors stoking fear. It is also one of the reasons hospitals are overwhelmed with COVID-19 positive cases.

This is why the decision to increase testing needs to be made along with ensuring that the facilities are in place to manage the increase in numbers of people identified with COVID-19. Without additional measures, hospitals will simply become overwhelmed, as has happened in the US.

In China, for example, several new health facilities were built in just a few weeks along with the deployment of thousands of health workers to Wuhan, the epicentre of the outbreak in that country. For its part the UK recalled about 10,000 retired health workers and the US is offering visas to health workers who might want to come and work there.

In Nigeria, the approach being taken is similar to that of China. New facilities are being established and equipped to handle COVID-19 cases.

But the strain on the health system must not be underestimated. Admission of a case of a highly infectious disease, like COVID-19, stretches the health system many times over and increases the risk of health care workers being infected. Of course, as the numbers rise, the health care workers are soon overwhelmed and the fatalities could rise along.

 

What needs to be done

 

I would argue that we should not just follow the admonition of the WHO to “test, test, test” without examining it in the context of our local peculiarities. Testing is important but countries should adapt guidelines for testing that work for them, knowing also the dangers of having asymptomatic disease spreaders – that is those who have the virus but aren’t showing any symptoms.

They should also consider reporting confirmed cases along with their clinical status as well as recoveries and discharges (all to encourage reporting of possible cases). The bigger worry is the fatalities and that is what countries must work to avoid.

Lastly, lock downs must be considered – the socio-economic challenges weighed into it – as a means to minimise the spread in the face of limited facilities. This would allow those who might require hospital admissions to show up, while those who don’t will stop spreading the disease while they recover on their own.

By Doyin Odubanjo, Executive Secretary, Nigerian Academy of Science. This article is republished from The Conversation under a Creative Commons license. Read the original article.

The Conversation Mon, 03/30/2020 - 22:25

Categories

Medicine

from ScienceBlogs - Where the world discusses science https://ift.tt/3bGRmQq

COVID-19: The Downside To More Testing Could Be Overflowing Hospitals

"You can’t fight a virus if you don’t know where it is."

These were the words of Director General of the World Health Organisation (WHO), Dr Tedros Adhanom Ghebreyesus, at his briefing on the COVID-19 pandemic in mid-March.

He made the statement in a bid to underscore the need to test many more people as key to containing the spread of the disease.

Ordinarily, that makes sense and I would agree with it. It is the right thing to do in the face of a disease which would show mild to no symptoms in the majority of those that are infected but does not inhibit their ability to infect others.

Countries that follow the WHO view have sought to buy test kits and increase the number of tests conducted daily. Others have been more cautious and have set up guidelines to ensure that they only test people with significant history of risk for COVID-19 or symptoms of the disease.

An aerial view of a new isolation and treatment centre established by the Lagos State government at the main bowl of the state-owned Stadium. Pius Utomi Ekpei/AFP via Getty Images via The Conversation

 

Looking at the various models and the progression of the pandemic, I wish to offer some views on testing and the attendant issues and challenges.

I believe that there are a myriad of factors to consider and that, particularly in Africa, countries have to take them all on board when making their decisions to curtail the spread of the virus.

The factors include the dangers posed by false test results, the fact that testing data is being badly communicated leading to a rise in panic levels and the fact that testing capacity is limited in many countries.

The fear factor

It is quite clear that the world is now dealing with two pandemics instead of one. The first is the virus. The second is fear and, in many cases, outright panic. That is why landlords are kicking out health workers from their houses. That is why we get reports of chloroquine toxicity within 24 hours of US President Donald Trump saying that might be the treatment for COVID-19.

What has panic got to do with testing? Panic is being driven by the way in which the outcome of testing is being communicated. For example, most countries are releasing data about how many more cases there are. But they are not telling their citizens how many of these people have no symptoms at all, or have mild ones.

Knowing how many of those who tested positive were not considered to be in a critical state would be helpful.

The other area in which data is being badly handled, and adding to panic levels, is that countries are reporting new cases on a daily basis. These aren’t necessarily new infections but, rather, new detections. Most are people who already had it and (for whatever reason were able to get tested) were found to be positive. They are people who, just the day before, did not know they had the virus and therefore weren’t provoking fear in others. Also, the number of new confirmed cases alone may not be the best indicator for the challenge the disease poses in a country or community.

Knowing their status now should not cause panic. It should simply inform about the importance of the preventive measures, including testing, to prevent spread of the disease.

Limited resources

Countries are being urged to test as many people as possible in the face of limited test resources. The mainstay polymerase chain reaction test is quite limited and relatively slow. It is also expensive given the requirements even of staff and laboratories.

Enter rapid test kits to the rescue. But there aren’t enough. Even the US doesn’t have enough test kits to meet the demand.

In addition, not all the kits in use have been tested properly. For example, there are reports that thousands of test kits imported by the Spanish health authorities were found to be faulty.

The challenge of a test kit giving false negatives is that the people are told, erroneously, that they do not have the virus. They go away and continue to infect others freely. In the event that they have any symptoms, they are likely to ignore these, and some may become severely ill before seeking care. If they do seek care early, the health care workers may be exposed to COVID-19 thinking that this person had tested negative and could only have some other disease.

A false positive, on the other hand, means that the number of cases reported continues to rise along with the panic created and attendant socio-economic disruption.

The Jack Ma Foundation has donated 20,000 test kits to Nigeria. But what are these among so many? Consider two statistics alongside this number. The population of the country – about 200 million people. And the fact that with 65 confirmed cases (as at the time of writing this), Nigeria is tracking over 4,000 contacts already.

A further complication in Nigeria is that the allocation of available tests kits could become subject to social and political whims. Government officials are scrambling to get tested along with their families and wealthy friends. Unfortunately, the guidelines for determining who to test won’t apply to this category of people. This means that limited resources will be used up.

 

Overwhelming hospitals

 

The fatality rate for COVID-19 has not yet been definitively established. Nevertheless, the fatality rate – particularly among older people – has been one of the major factors stoking fear. It is also one of the reasons hospitals are overwhelmed with COVID-19 positive cases.

This is why the decision to increase testing needs to be made along with ensuring that the facilities are in place to manage the increase in numbers of people identified with COVID-19. Without additional measures, hospitals will simply become overwhelmed, as has happened in the US.

In China, for example, several new health facilities were built in just a few weeks along with the deployment of thousands of health workers to Wuhan, the epicentre of the outbreak in that country. For its part the UK recalled about 10,000 retired health workers and the US is offering visas to health workers who might want to come and work there.

In Nigeria, the approach being taken is similar to that of China. New facilities are being established and equipped to handle COVID-19 cases.

But the strain on the health system must not be underestimated. Admission of a case of a highly infectious disease, like COVID-19, stretches the health system many times over and increases the risk of health care workers being infected. Of course, as the numbers rise, the health care workers are soon overwhelmed and the fatalities could rise along.

 

What needs to be done

 

I would argue that we should not just follow the admonition of the WHO to “test, test, test” without examining it in the context of our local peculiarities. Testing is important but countries should adapt guidelines for testing that work for them, knowing also the dangers of having asymptomatic disease spreaders – that is those who have the virus but aren’t showing any symptoms.

They should also consider reporting confirmed cases along with their clinical status as well as recoveries and discharges (all to encourage reporting of possible cases). The bigger worry is the fatalities and that is what countries must work to avoid.

Lastly, lock downs must be considered – the socio-economic challenges weighed into it – as a means to minimise the spread in the face of limited facilities. This would allow those who might require hospital admissions to show up, while those who don’t will stop spreading the disease while they recover on their own.

By Doyin Odubanjo, Executive Secretary, Nigerian Academy of Science. This article is republished from The Conversation under a Creative Commons license. Read the original article.

The Conversation Mon, 03/30/2020 - 22:25

Categories

Medicine

from ScienceBlogs - Where the world discusses science https://ift.tt/3bGRmQq

'Virtual' Communication During Social Distancing: How We Change When We Know We're Being Seen

'Virtual' Communication During Social Distancing: How We Change When We Know We're Being Seen

Social distancing due to the SARS-CoV-2 virus and the threat of COVID-19 has meant online communication is more popular than ever, with even casual parenting groups discovering the previous enterprise video conferencing tool Zoom.

But how will that affect communications? Have you ever met someone who is stiff in person but great on camera or the other way around? Neuroscientists study brain and behavior and in a recent study found that a person's gaze is altered during tele-communication if they think that the person on the other end of the conversation can see them.

People are very sensitive to the gaze direction of others and even two-day-old infants prefer faces where the eyes are looking directly back at them. The phenomenon known as "gaze cueing," a powerful signal for orienting attention, is a mechanism that likely plays a role in the developmentally and socially important wonder of "shared" or "joint" attention where a number of people attend to the same object or location. The ability to do this is what makes humans unique among primates.

Throughout almost all of human history, conversations were generally conducted face-to-face, so people knew where their conversational partner was looking and vice versa. Now, with virtual communication, that assumption no longer holds - sometimes people communicate with both cameras on while other times only the speaker may be visible. The researchers set out to determine whether being observed affects people's behavior during online communication. 

Co-authors Elan Barenholtz, Ph.D., associate professor of psychology at Florida Atlantic University, and Michael H. Kleiman, Ph.D., a postdoctoral researcher, compared fixation behavior in 173 participants under two conditions: one in which the participants believed they were engaging in a real-time interaction and one in which they knew they were watching a pre-recorded video. 

The researchers wanted to know if face fixation would increase in the real-time condition based on the social expectation of facing one's speaker in order to get attention or if it would lead to greater face avoidance, based on social norms as well as the cognitive demands of encoding the conversation. 

Similarly, they wanted to know where participants would fixate on the face. Would it be the eyes more in the real-time condition because of social demands to make eye contact with one's speaker? Or, in the pre-recorded condition, where the social demands to make eye contact are eliminated, would participants spend more time looking at the mouth in order to encode the conversation, which is consistent with previous studies showing greater mouth fixations during an encoding task. 

Three areas of interest for fixation analyses: full face (purple), eyes (red) and mouth (blue). Credit:  Florida Atlantic University

 

Results of the study showed that participants fixated on the whole face in the real-time condition and significantly less in the pre-recorded condition. In the pre-recorded condition, time spent fixating on the mouth was significantly greater compared to the real-time condition. 

There were no significant differences in time spent fixating on the eyes between the real-time and the pre-recorded conditions. These findings may suggest that participants are more comfortable looking directly at the mouth of a speaker - which has previously been found to be optimal for encoding speech - when they think that no one is watching them. 

To simulate a live interaction, the researchers convinced participants that they were engaging in a real-time, two-way video interaction (it was actually pre-recorded) where they could been seen and heard by the speaker, as well as a pre-recorded interaction where they knew the video was previously recorded and therefore the speaker could not see their behavior. 

"Because gaze direction conveys so much socially relevant information, one's own gaze behavior is likely to be affected by whether one's eyes are visible to a speaker," said Barenholtz. "For example, people may intend to signal that they are paying more attention to a speaker by fixating their face or eyes during a conversation. Conversely, extended eye contact also can be perceived as aggressive and therefore noticing one's eyes could lead to reduced direct fixation of another's face or eyes. Indeed, people engage in avoidant eye movements by periodically breaking and reforming eye contact during conversations."

There was a highly significant tendency for participants engaging in perceived real-time interaction to display greater avoidant fixation behavior, which supports the idea that social contexts draw fixations away from the face compared to when social context is not a factor. When the face was fixated, attention was directed toward the mouth for the greater percentage of time in the pre-recorded condition versus the real-time condition. The lack of difference in time spent fixating the eyes suggests that the additional mouth fixations in the pre-recorded condition did not come at the cost of reduced eye fixation and must have derived from reduced fixations elsewhere on the face. 

Comparisons between total fixation durations of the eyes versus the mouth were calculated for both the real-time and pre-recorded conditions, with the eyes of both conditions being significantly more fixated than the mouth. Gender, age, cultural background, and native language did not have an influence on fixation behavior across conditions. 

"Regardless of the specific mechanisms underlying the observed differences in fixation patterns, results from our study suggest participants were taking social and attentional considerations into account in the real-time condition," said Barenholtz. "Given that encoding and memory have been found to be optimized by fixating the mouth, which was reduced overall in the real-time condition, this suggests that people do not fully optimize for speech encoding in a live interaction."

 

sb admin Mon, 03/30/2020 - 17:25

Categories

Brain and Behavior

from ScienceBlogs - Where the world discusses science https://ift.tt/2ylzZpP

'Virtual' Communication During Social Distancing: How We Change When We Know We're Being Seen

Social distancing due to the SARS-CoV-2 virus and the threat of COVID-19 has meant online communication is more popular than ever, with even casual parenting groups discovering the previous enterprise video conferencing tool Zoom.

But how will that affect communications? Have you ever met someone who is stiff in person but great on camera or the other way around? Neuroscientists study brain and behavior and in a recent study found that a person's gaze is altered during tele-communication if they think that the person on the other end of the conversation can see them.

People are very sensitive to the gaze direction of others and even two-day-old infants prefer faces where the eyes are looking directly back at them. The phenomenon known as "gaze cueing," a powerful signal for orienting attention, is a mechanism that likely plays a role in the developmentally and socially important wonder of "shared" or "joint" attention where a number of people attend to the same object or location. The ability to do this is what makes humans unique among primates.

Throughout almost all of human history, conversations were generally conducted face-to-face, so people knew where their conversational partner was looking and vice versa. Now, with virtual communication, that assumption no longer holds - sometimes people communicate with both cameras on while other times only the speaker may be visible. The researchers set out to determine whether being observed affects people's behavior during online communication. 

Co-authors Elan Barenholtz, Ph.D., associate professor of psychology at Florida Atlantic University, and Michael H. Kleiman, Ph.D., a postdoctoral researcher, compared fixation behavior in 173 participants under two conditions: one in which the participants believed they were engaging in a real-time interaction and one in which they knew they were watching a pre-recorded video. 

The researchers wanted to know if face fixation would increase in the real-time condition based on the social expectation of facing one's speaker in order to get attention or if it would lead to greater face avoidance, based on social norms as well as the cognitive demands of encoding the conversation. 

Similarly, they wanted to know where participants would fixate on the face. Would it be the eyes more in the real-time condition because of social demands to make eye contact with one's speaker? Or, in the pre-recorded condition, where the social demands to make eye contact are eliminated, would participants spend more time looking at the mouth in order to encode the conversation, which is consistent with previous studies showing greater mouth fixations during an encoding task. 

Three areas of interest for fixation analyses: full face (purple), eyes (red) and mouth (blue). Credit:  Florida Atlantic University

 

Results of the study showed that participants fixated on the whole face in the real-time condition and significantly less in the pre-recorded condition. In the pre-recorded condition, time spent fixating on the mouth was significantly greater compared to the real-time condition. 

There were no significant differences in time spent fixating on the eyes between the real-time and the pre-recorded conditions. These findings may suggest that participants are more comfortable looking directly at the mouth of a speaker - which has previously been found to be optimal for encoding speech - when they think that no one is watching them. 

To simulate a live interaction, the researchers convinced participants that they were engaging in a real-time, two-way video interaction (it was actually pre-recorded) where they could been seen and heard by the speaker, as well as a pre-recorded interaction where they knew the video was previously recorded and therefore the speaker could not see their behavior. 

"Because gaze direction conveys so much socially relevant information, one's own gaze behavior is likely to be affected by whether one's eyes are visible to a speaker," said Barenholtz. "For example, people may intend to signal that they are paying more attention to a speaker by fixating their face or eyes during a conversation. Conversely, extended eye contact also can be perceived as aggressive and therefore noticing one's eyes could lead to reduced direct fixation of another's face or eyes. Indeed, people engage in avoidant eye movements by periodically breaking and reforming eye contact during conversations."

There was a highly significant tendency for participants engaging in perceived real-time interaction to display greater avoidant fixation behavior, which supports the idea that social contexts draw fixations away from the face compared to when social context is not a factor. When the face was fixated, attention was directed toward the mouth for the greater percentage of time in the pre-recorded condition versus the real-time condition. The lack of difference in time spent fixating the eyes suggests that the additional mouth fixations in the pre-recorded condition did not come at the cost of reduced eye fixation and must have derived from reduced fixations elsewhere on the face. 

Comparisons between total fixation durations of the eyes versus the mouth were calculated for both the real-time and pre-recorded conditions, with the eyes of both conditions being significantly more fixated than the mouth. Gender, age, cultural background, and native language did not have an influence on fixation behavior across conditions. 

"Regardless of the specific mechanisms underlying the observed differences in fixation patterns, results from our study suggest participants were taking social and attentional considerations into account in the real-time condition," said Barenholtz. "Given that encoding and memory have been found to be optimized by fixating the mouth, which was reduced overall in the real-time condition, this suggests that people do not fully optimize for speech encoding in a live interaction."

 

sb admin Mon, 03/30/2020 - 17:25

Categories

Brain and Behavior

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How To Spot Coronavirus Fake News

How To Spot Coronavirus Fake News

The proliferation of fake news about the COVID-19 pandemic has been labelled a dangerous “infodemic”. Fake news spreads faster and more easily today through the internet, social media and instant messaging. These messages may contain useless, incorrect or even harmful information and advice, which can hamper the public health response and add to social disorder and division.

Confusingly some fake news also contains a mixture of correct information, which makes it difficult to spot what is true and accurate. Fake news may also be shared by trusted friends and family, including those who are doctors and nurses. They might not have read the full story before sharing or just glanced over it. Before you decide to share, make sure to read stories properly and follow some checks to determine the accuracy.

If the story appears to claim a much higher level of certainty in its advice and arguments than other stories, this is questionable. People will be seeking certainty in a time of high uncertainty, anxiety and panic. So it is only natural to more readily accept information that resolves, reassures and provides easy solutions – unfortunately, often in a false way.

Similarly, if a story is more surprising or upsetting than other stories it is worth double-checking, as fake news will try to grab your attention by being more exaggerated than real stories.

What to look out for

• Source. Question the source. References have been made to “Taiwanese experts” or “Japanese doctors” or “Stanford University” during the outbreak. Check on official websites if stories are repeated there. If a source is “a friend of a friend”, this is a rumour unless you also know the person directly.

• Logo: Check whether any organisation’s logo used in the message looks the same as on the official website.

• Bad English: Credible journalists and organisations are less likely to make repeated spelling and grammar mistakes. Also, anything written entirely in capital letters or containing a lot of exclamation marks should raise your suspicions.

• Pretend social media accounts: Some fake accounts mimic the real thing. For example, the unofficial Twitter handle @BBCNewsTonight, which was made to look like the legitimate @BBCNews account, shared a fake story about the actor Daniel Radcliffe testing positive for coronavirus. Media platforms try to remove or flag fake accounts and stories as well as verify real ones. Look out for what their policies are to try to do this.

• Over-encouragement to share: Be wary if the message presses you to share – this is how viral messaging works.

• Use fact-checking websites: Websites such as APFactCheck and Full Fact highlight common fake news stories. You can also use a search engine to look up the title of the article to see if it has been identified as fake news by the mainstream media.

Who to trust

The best sources to go to for health information about COVID-19 are your government health websites and the World Health Organization website. Primary sources are generally better than news articles.

Even government messaging and the mainstream media can get things wrong, but they are more trustworthy than unverified sources on social media and viral messaging. For instance, The Conversation is a more trusted source because all content is written by academics who are experts in their fields.

A time of high uncertainty. How Hwee Young/EPA

Charlatans have been promoting false preventions and cures for people to spend their money on. For example, the New York attorney general has had to send cease and desist notices for claims that toothpaste, dietary supplements and creams will prevent and cure COVID-19.

The effects can also be more serious than losing some cash. Iran has reported at least 44 people died from alcohol poisoning after drinking bootleg alcohol in a misguided attempt to cure COVID-19.

Unfortunately, the most basic and correct advice given so far does not offer a miracle or special insight. Wash your hands often (use hand sanitisers if you cannot), avoid touching your face, and sneeze or cough into the crook of your elbow or a tissue (and throw it away in a bag-lined bin). Avoid crowds and public places, keep a sensible distance from people, and do not travel unless absolutely necessary. Now many governments are introducing measures including travel bans and quarantines that need to be followed to protect the health of everyone, especially the most vulnerable.

We can all get caught out. Think twice about the messages currently circulating and help guide your family and friends to decide what to trust.

By Samantha Vanderslott, Postdoctoral Researcher in Social Sciences, University of Oxford. This article is republished from The Conversation under a Creative Commons license. Read the original article.

sb admin Fri, 03/20/2020 - 12:16

Categories

Social Sciences

from ScienceBlogs - Where the world discusses science https://ift.tt/2IZPzcP

How To Spot Coronavirus Fake News

The proliferation of fake news about the COVID-19 pandemic has been labelled a dangerous “infodemic”. Fake news spreads faster and more easily today through the internet, social media and instant messaging. These messages may contain useless, incorrect or even harmful information and advice, which can hamper the public health response and add to social disorder and division.

Confusingly some fake news also contains a mixture of correct information, which makes it difficult to spot what is true and accurate. Fake news may also be shared by trusted friends and family, including those who are doctors and nurses. They might not have read the full story before sharing or just glanced over it. Before you decide to share, make sure to read stories properly and follow some checks to determine the accuracy.

If the story appears to claim a much higher level of certainty in its advice and arguments than other stories, this is questionable. People will be seeking certainty in a time of high uncertainty, anxiety and panic. So it is only natural to more readily accept information that resolves, reassures and provides easy solutions – unfortunately, often in a false way.

Similarly, if a story is more surprising or upsetting than other stories it is worth double-checking, as fake news will try to grab your attention by being more exaggerated than real stories.

What to look out for

• Source. Question the source. References have been made to “Taiwanese experts” or “Japanese doctors” or “Stanford University” during the outbreak. Check on official websites if stories are repeated there. If a source is “a friend of a friend”, this is a rumour unless you also know the person directly.

• Logo: Check whether any organisation’s logo used in the message looks the same as on the official website.

• Bad English: Credible journalists and organisations are less likely to make repeated spelling and grammar mistakes. Also, anything written entirely in capital letters or containing a lot of exclamation marks should raise your suspicions.

• Pretend social media accounts: Some fake accounts mimic the real thing. For example, the unofficial Twitter handle @BBCNewsTonight, which was made to look like the legitimate @BBCNews account, shared a fake story about the actor Daniel Radcliffe testing positive for coronavirus. Media platforms try to remove or flag fake accounts and stories as well as verify real ones. Look out for what their policies are to try to do this.

• Over-encouragement to share: Be wary if the message presses you to share – this is how viral messaging works.

• Use fact-checking websites: Websites such as APFactCheck and Full Fact highlight common fake news stories. You can also use a search engine to look up the title of the article to see if it has been identified as fake news by the mainstream media.

Who to trust

The best sources to go to for health information about COVID-19 are your government health websites and the World Health Organization website. Primary sources are generally better than news articles.

Even government messaging and the mainstream media can get things wrong, but they are more trustworthy than unverified sources on social media and viral messaging. For instance, The Conversation is a more trusted source because all content is written by academics who are experts in their fields.

A time of high uncertainty. How Hwee Young/EPA

Charlatans have been promoting false preventions and cures for people to spend their money on. For example, the New York attorney general has had to send cease and desist notices for claims that toothpaste, dietary supplements and creams will prevent and cure COVID-19.

The effects can also be more serious than losing some cash. Iran has reported at least 44 people died from alcohol poisoning after drinking bootleg alcohol in a misguided attempt to cure COVID-19.

Unfortunately, the most basic and correct advice given so far does not offer a miracle or special insight. Wash your hands often (use hand sanitisers if you cannot), avoid touching your face, and sneeze or cough into the crook of your elbow or a tissue (and throw it away in a bag-lined bin). Avoid crowds and public places, keep a sensible distance from people, and do not travel unless absolutely necessary. Now many governments are introducing measures including travel bans and quarantines that need to be followed to protect the health of everyone, especially the most vulnerable.

We can all get caught out. Think twice about the messages currently circulating and help guide your family and friends to decide what to trust.

By Samantha Vanderslott, Postdoctoral Researcher in Social Sciences, University of Oxford. This article is republished from The Conversation under a Creative Commons license. Read the original article.

sb admin Fri, 03/20/2020 - 12:16

Categories

Social Sciences

from ScienceBlogs - Where the world discusses science https://ift.tt/2IZPzcP

Coronavirus Isn't a Pandemic, But That Doesn't Change Its Relative Risk

Coronavirus Isn't a Pandemic, But That Doesn't Change Its Relative Risk

Is the coronavirus a pandemic, and does that matter? 4 questions answered

The new coronavirus has now affected more than 20,000 people in China and claimed more lives as of Feb. 4 than the SARS epidemic from 2002 to 2004. Hong Kong has reported its first death. Some public health officials have said the outbreak is likely to soon be a pandemic, but the World Health Organization said Feb. 4 that it isn’t, yet.

Just what is a pandemic anyway? An epidemiologist and public health researcher explains.

1. What is a pandemic?

When a disease outbreak, or epidemic, crosses international boarders and spreads across a wide region, we public health professionals typically call it a pandemic. The term “pandemic” tells us that the outbreak is occurring in many places but says nothing about its severity.

Because of their wide geographic distribution, pandemics usually affect a large number of people. While we usually think of pandemics in relation to serious, life-threatening diseases, even outbreaks of mild diseases could cross borders and become pandemics.

2. Does it matter if it is or isn’t called a pandemic?

Calling an outbreak a pandemic is simply a reflection of where the disease is spreading. The terminology doesn’t change anything about the severity of the disease or how we are responding.

Since the day the outbreak was identified, health officials worldwide have been taking steps to isolate ill people to try and prevent any spread and quarantine people who have traveled to certain areas of China. The World Health Organization declared it to be a Public Health Emergency of International Concern Jan. 30, which improves information sharing and coordination throughout the world.

These actions will continue no matter what it is called.

Flight attendants check temperatures of passengers aboard an Air China flight from Melbourne to Beijing on Feb. 4, 2020. AP Photo/Andy Wong

3. Would it being a pandemic put me at greater risk?

Your risk wouldn’t changed simply because of a change in terminology. Though the virus has been identified in 23 countries as of Feb. 4, over 99% of the cases have occurred in China.

Local transmission outside of China has generally been limited to people who had direct contact with ill travelers from China. In a cluster reported from Germany, several employees of a company were infected by a co-worker who returned from travel to China, and one of the employees infected one of their children. This clearly shows that person-to-person spread is possible, but it doesn’t mean that the disease is spreading extensively in the community.

Even if an outbreak is spreading worldwide, how it is spreading locally and how people respond is what determines your risk.

4. So what happens next?

Public and global health experts and health care workers will continue to respond to this outbreak as they have for the last month. Doctors and nurses in the community will continue to quickly identify ill people and test them for the coronavirus. Sick people will be isolated so that they don’t spread their illness to their family, friends or co-workers. Public health officials will track the spread of this outbreak and will use that information to prevent the spread of the disease in the community.

The next move is up to the virus.

By Brian Labus, Assistant Professor of Epidemiology and Biostatistics, University of Nevada, Las Vegas. Labus received past funding from the Centers for Disease Control and Prevention for disease surveillance activities while working at the local health department. This article is republished from The Conversation under a Creative Commons license. Read the original article.

 

The Conversation Fri, 02/14/2020 - 10:41

Categories

Medicine

from ScienceBlogs - Where the world discusses science https://ift.tt/2SOJ2WG

Coronavirus Isn't a Pandemic, But That Doesn't Change Its Relative Risk

Is the coronavirus a pandemic, and does that matter? 4 questions answered

The new coronavirus has now affected more than 20,000 people in China and claimed more lives as of Feb. 4 than the SARS epidemic from 2002 to 2004. Hong Kong has reported its first death. Some public health officials have said the outbreak is likely to soon be a pandemic, but the World Health Organization said Feb. 4 that it isn’t, yet.

Just what is a pandemic anyway? An epidemiologist and public health researcher explains.

1. What is a pandemic?

When a disease outbreak, or epidemic, crosses international boarders and spreads across a wide region, we public health professionals typically call it a pandemic. The term “pandemic” tells us that the outbreak is occurring in many places but says nothing about its severity.

Because of their wide geographic distribution, pandemics usually affect a large number of people. While we usually think of pandemics in relation to serious, life-threatening diseases, even outbreaks of mild diseases could cross borders and become pandemics.

2. Does it matter if it is or isn’t called a pandemic?

Calling an outbreak a pandemic is simply a reflection of where the disease is spreading. The terminology doesn’t change anything about the severity of the disease or how we are responding.

Since the day the outbreak was identified, health officials worldwide have been taking steps to isolate ill people to try and prevent any spread and quarantine people who have traveled to certain areas of China. The World Health Organization declared it to be a Public Health Emergency of International Concern Jan. 30, which improves information sharing and coordination throughout the world.

These actions will continue no matter what it is called.

Flight attendants check temperatures of passengers aboard an Air China flight from Melbourne to Beijing on Feb. 4, 2020. AP Photo/Andy Wong

3. Would it being a pandemic put me at greater risk?

Your risk wouldn’t changed simply because of a change in terminology. Though the virus has been identified in 23 countries as of Feb. 4, over 99% of the cases have occurred in China.

Local transmission outside of China has generally been limited to people who had direct contact with ill travelers from China. In a cluster reported from Germany, several employees of a company were infected by a co-worker who returned from travel to China, and one of the employees infected one of their children. This clearly shows that person-to-person spread is possible, but it doesn’t mean that the disease is spreading extensively in the community.

Even if an outbreak is spreading worldwide, how it is spreading locally and how people respond is what determines your risk.

4. So what happens next?

Public and global health experts and health care workers will continue to respond to this outbreak as they have for the last month. Doctors and nurses in the community will continue to quickly identify ill people and test them for the coronavirus. Sick people will be isolated so that they don’t spread their illness to their family, friends or co-workers. Public health officials will track the spread of this outbreak and will use that information to prevent the spread of the disease in the community.

The next move is up to the virus.

By Brian Labus, Assistant Professor of Epidemiology and Biostatistics, University of Nevada, Las Vegas. Labus received past funding from the Centers for Disease Control and Prevention for disease surveillance activities while working at the local health department. This article is republished from The Conversation under a Creative Commons license. Read the original article.

 

The Conversation Fri, 02/14/2020 - 10:41

Categories

Medicine

from ScienceBlogs - Where the world discusses science https://ift.tt/2SOJ2WG

9 Ways to Debunk Coronavirus Myths Without it Backfiring

9 Ways to Debunk Coronavirus Myths Without it Backfiring

The spread of misinformation about the novel coronavirus, now known as COVID-19, seems greater than the spread of the infection itself.

The World Health Organisation (WHO), government health departments and others are trying to alert people to these myths.

But what’s the best way to tackle these if they come up in everyday conversation, whether that’s face-to-face or online? Is it best to ignore them, jump in to correct them, or are there other strategies we could all use?

Public health officials expect misinformation about disease outbreaks where people are frightened. This is particularly so when a disease is novel and the science behind it is not yet clear. It’s also the case when we still don’t know how many people are likely to become sick, have a life-threatening illness or die.

Yet we can all contribute to the safe control of the disease and to minimizing its social and economic impacts by addressing misinformation when we encounter it.

To avoid our efforts backfiring, we need to know how to do this effectively and constructively.

 

Be patient when addressing myths. And keep it brief. shutterstock.com

What doesn’t work

Abundant research shows what doesn’t work. Telling people not to panic or their perceptions and beliefs are incorrect can actually strengthen their commitment to their incorrect views.

Over-reactions are common when new risks emerge and these over-reactions will pass. So, it’s often the best choice to not engage in the first place.

What can I do?

If you wish to effectively counter misinformation, you need to pay more attention to your audience than to the message you want to convey. See our tips below.

Next, you need to be trusted.

People only listen to sources they trust. This involves putting in the time and effort to make sure your knowledge is correct and reliable; discussing information fairly (what kind of information would make you change your own mind?); and being honest enough to admit when you don’t know, and even more importantly, when you are wrong.

Here’s how all this might work in practice.

1. Understand how people perceive and react to risks

We all tend to worry more about risks we perceive to be new, uncertain, dreaded, and impact a large group in a short time – all features of the new coronavirus.

Our worries increase significantly if we do not feel we, or the governments acting for us, have control over the virus.

2. Recognize people’s concerns

People can’t process information unless they see their worries being addressed.

So instead of offering facts (“you won’t catch coronavirus from your local swimming pool”), articulate their worry (“you’ve caught colds in swimming pools before, and now you’re worried someone might transmit the virus before they know they are infected”).

Being heard helps people re-establish a sense of control.

3. Be aware of your own feelings

Usually when we want to correct someone, it’s because we’re worried about the harms their false beliefs will cause.

But if we are emotional, what we communicate is not our knowledge, but our disrespect for the other person’s views. This usually produces a defensive reaction.

Manage your own outrage first before jumping in to correct others. This might mean saving a discussion for another day.

4. Ask why someone is worried

If you ask why someone is worried, you might discover your assumptions about that person are wrong.

Explaining their concerns to you helps people explore their own views. They might become aware of what they don’t know or of how unlikely their information sounds.

5. Remember, the facts are going to change

Because there is still considerable uncertainty about how severe the epidemic will be, information and the government’s response to it is going to change.

So you will need to frequently update your own views. Know where to find reliable information.

For instance, state and federal health departments, the WHO and the US Centers for Disease Control websites provide authoritative and up-to-date information.

6. Admit when you’re wrong

Being wrong is likely in an uncertain situation. If you are wrong, say so early.

If you asked your family or employees to take avoidance measures you now realise aren’t really necessary, then admit it and apologize. This helps restore the trust you need to communicate effectively the next time you need to raise an issue.

7. Politely provide your own perspective

Phrases like, “here’s why I am not concerned about that” or “I actually feel quite confident about doing X or Y” offer ways to communicate your knowledge without attacking someone else’s views.

You can and should be explicit about what harms you worry misinformation can cause. An example could be, “I’m worried that avoiding Chinese restaurants will really hurt their business. I’m really conscious of wanting to support Chinese Australians right now.”

8. On social media, model the behavior you want to see

It’s harder to be effective on social media, where outrage, not listening, is common. Often your goal might be to promote a reasoned, civil discussion, not to defend one particular belief over another. Use very reliable links.

9. Don’t make it worse online

Your online comment can unintentionally reinforce misinformation, for example by giving it more prominence. Check the Debunking Handbook for some strategies to avoid this.

Make sure your posts or comments are polite, specific, factual and very brief.

Acknowledging common values or points of connection by using phrases such as “I’m worried about my grandmother, too”, or by being supportive (“It’s so great that you’re proactive about looking after your staff”), can help.

Remember why this is important

The ability to respond to emergencies rests on having civil societies. The goal is to keep relationships constructive and dialogue open – not to be right.

By Claire Hooker, Senior Lecturer and Coordinator, Health and Medical Humanities, University of Sydney. This article is republished from The Conversation under a Creative Commons license. Read the original article.

The Conversation Wed, 02/12/2020 - 23:22

Categories

Social Sciences

from ScienceBlogs - Where the world discusses science https://ift.tt/2OLGtDN

9 Ways to Debunk Coronavirus Myths Without it Backfiring

The spread of misinformation about the novel coronavirus, now known as COVID-19, seems greater than the spread of the infection itself.

The World Health Organisation (WHO), government health departments and others are trying to alert people to these myths.

But what’s the best way to tackle these if they come up in everyday conversation, whether that’s face-to-face or online? Is it best to ignore them, jump in to correct them, or are there other strategies we could all use?

Public health officials expect misinformation about disease outbreaks where people are frightened. This is particularly so when a disease is novel and the science behind it is not yet clear. It’s also the case when we still don’t know how many people are likely to become sick, have a life-threatening illness or die.

Yet we can all contribute to the safe control of the disease and to minimizing its social and economic impacts by addressing misinformation when we encounter it.

To avoid our efforts backfiring, we need to know how to do this effectively and constructively.

 

Be patient when addressing myths. And keep it brief. shutterstock.com

What doesn’t work

Abundant research shows what doesn’t work. Telling people not to panic or their perceptions and beliefs are incorrect can actually strengthen their commitment to their incorrect views.

Over-reactions are common when new risks emerge and these over-reactions will pass. So, it’s often the best choice to not engage in the first place.

What can I do?

If you wish to effectively counter misinformation, you need to pay more attention to your audience than to the message you want to convey. See our tips below.

Next, you need to be trusted.

People only listen to sources they trust. This involves putting in the time and effort to make sure your knowledge is correct and reliable; discussing information fairly (what kind of information would make you change your own mind?); and being honest enough to admit when you don’t know, and even more importantly, when you are wrong.

Here’s how all this might work in practice.

1. Understand how people perceive and react to risks

We all tend to worry more about risks we perceive to be new, uncertain, dreaded, and impact a large group in a short time – all features of the new coronavirus.

Our worries increase significantly if we do not feel we, or the governments acting for us, have control over the virus.

2. Recognize people’s concerns

People can’t process information unless they see their worries being addressed.

So instead of offering facts (“you won’t catch coronavirus from your local swimming pool”), articulate their worry (“you’ve caught colds in swimming pools before, and now you’re worried someone might transmit the virus before they know they are infected”).

Being heard helps people re-establish a sense of control.

3. Be aware of your own feelings

Usually when we want to correct someone, it’s because we’re worried about the harms their false beliefs will cause.

But if we are emotional, what we communicate is not our knowledge, but our disrespect for the other person’s views. This usually produces a defensive reaction.

Manage your own outrage first before jumping in to correct others. This might mean saving a discussion for another day.

4. Ask why someone is worried

If you ask why someone is worried, you might discover your assumptions about that person are wrong.

Explaining their concerns to you helps people explore their own views. They might become aware of what they don’t know or of how unlikely their information sounds.

5. Remember, the facts are going to change

Because there is still considerable uncertainty about how severe the epidemic will be, information and the government’s response to it is going to change.

So you will need to frequently update your own views. Know where to find reliable information.

For instance, state and federal health departments, the WHO and the US Centers for Disease Control websites provide authoritative and up-to-date information.

6. Admit when you’re wrong

Being wrong is likely in an uncertain situation. If you are wrong, say so early.

If you asked your family or employees to take avoidance measures you now realise aren’t really necessary, then admit it and apologize. This helps restore the trust you need to communicate effectively the next time you need to raise an issue.

7. Politely provide your own perspective

Phrases like, “here’s why I am not concerned about that” or “I actually feel quite confident about doing X or Y” offer ways to communicate your knowledge without attacking someone else’s views.

You can and should be explicit about what harms you worry misinformation can cause. An example could be, “I’m worried that avoiding Chinese restaurants will really hurt their business. I’m really conscious of wanting to support Chinese Australians right now.”

8. On social media, model the behavior you want to see

It’s harder to be effective on social media, where outrage, not listening, is common. Often your goal might be to promote a reasoned, civil discussion, not to defend one particular belief over another. Use very reliable links.

9. Don’t make it worse online

Your online comment can unintentionally reinforce misinformation, for example by giving it more prominence. Check the Debunking Handbook for some strategies to avoid this.

Make sure your posts or comments are polite, specific, factual and very brief.

Acknowledging common values or points of connection by using phrases such as “I’m worried about my grandmother, too”, or by being supportive (“It’s so great that you’re proactive about looking after your staff”), can help.

Remember why this is important

The ability to respond to emergencies rests on having civil societies. The goal is to keep relationships constructive and dialogue open – not to be right.

By Claire Hooker, Senior Lecturer and Coordinator, Health and Medical Humanities, University of Sydney. This article is republished from The Conversation under a Creative Commons license. Read the original article.

The Conversation Wed, 02/12/2020 - 23:22

Categories

Social Sciences

from ScienceBlogs - Where the world discusses science https://ift.tt/2OLGtDN

Coronavirus Is Not Passed From Mother to Child Late In Pregnancy

Coronavirus Is Not Passed From Mother to Child Late In Pregnancy

After a newborn (born to a mother infected with the 2019 novel coronavirus disease (COVID-19) testing positive for COVID-19 infection within 36 hours of birth, there were concerns about whether the virus could be contracted in the womb. A new study finds that COVID-19 does not pass to the child while in the womb. The women in the small study were from Wuhan, China, in the third trimester of pregnancy and had pneumonia caused by COVID-19. However, it only included women who were late in their pregnancy and gave birth by caesarean section. 

There were two cases of fetal distress but all nine pregnancies resulted in live births. That symptoms from COVID-19 infection in pregnant women were similar to those reported in non-pregnant adults, and no women in the study developed severe pneumonia or died.

All mothers in the study were aged between 26-40 years. None of them had underlying health conditions, but one developed gestational hypertension from week 27 of her pregnancy, and another developed pre-eclampsia at week 31. Both patients’ conditions were stable during pregnancy. The nine women in the study had typical symptoms of COVID-19 infection, and were given oxygen support and antibiotics. Six of the women were also given antiviral therapy. In the study, the medical records of nine pregnant women who had pneumonia caused by COVID-19 infection were retrospectively reviewed. Infection was lab-confirmed for all women in the study, and the authors studied the nine women’s symptoms.

(A) Patient 1: left-sided patchy consolidation and multiple bilateral ground-glass opacities. (B) Patient 2: subpleural patchy consolidation in the right lung and slightly infiltrated shadows around left bronchus. (C) Patient 3: bilateral multiple ground-glass opacities, prominent on the left. (D) Patient 4: left-sided patchy ground-glass opacity. (E) Patient 5: multiple ground-glass opacities bilaterally. (F) Patient 6: bilateral clear lung fields with no obvious ground-glass opacities. (G) Patient 7: right-sided subpleural patchy consolidation. (H) Patient 8: multiple bilateral ground-glass opacities, prominent on the right. (I) Patient 9: multiple bilateral ground-glass opacities.

In addition, samples of amniotic fluid, cord blood, neonatal throat swabs and breast milk were taken for six of the nine cases [2] and tested for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Importantly, the samples of amniotic fluid, cord blood, and neonatal throat swabs were collected in the operating room at the time of birth to guarantee that samples were not contaminated and best represented intrauterine conditions. All nine pregnancies resulted in live births, and there were no cases of neonatal asphyxia. Four women had pregnancy complications (two had fetal distress and two had premature rupture of membrane), and four women had preterm labor which was not related to their infection and occurred after 36 gestational weeks. Two of the prematurely born newborns had a low birth weight.

The authors note that their findings are similar to observations of the severe acute respiratory syndrome (SARS) virus in pregnant women, where there was no evidence of the virus being passed from mother to child during pregnancy or birth. The findings are based on a limited number of cases, over a short period of time, and the effects of mothers being infected with the virus during the first or second trimester of pregnancy and the subsequent outcomes for their offspring are still unclear, as well as whether the virus can be passed from mother to child during vaginal birth.

Dr Jie Qiao (who was not involved in the study) of Peking University Third Hospital, China,compares the effects of the virus to those of SARS, and says: “Previous studies have shown that SARS during pregnancy is associated with a high incidence of adverse maternal and neonatal complications, such as spontaneous miscarriage, preterm delivery, intrauterine growth restriction, application of endotracheal intubation, admission to the intensive care unit, renal failure, and disseminated intravascular coagulopathy. However, pregnant women with COVID-19 infection in the present study had fewer adverse maternal and neonatal complications and outcomes than would be anticipated for those with SARS-CoV-1 infection. Although a small number of cases was analysed and the findings should be interpreted with caution, the findings are mostly consistent with the clinical analysis done by Zhu and colleagues of ten neonates born to mothers with COVID-19 pneumonia."

sb admin Wed, 02/12/2020 - 13:03

Categories

Life Sciences

from ScienceBlogs - Where the world discusses science https://ift.tt/39qNFx1

Coronavirus Is Not Passed From Mother to Child Late In Pregnancy

After a newborn (born to a mother infected with the 2019 novel coronavirus disease (COVID-19) testing positive for COVID-19 infection within 36 hours of birth, there were concerns about whether the virus could be contracted in the womb. A new study finds that COVID-19 does not pass to the child while in the womb. The women in the small study were from Wuhan, China, in the third trimester of pregnancy and had pneumonia caused by COVID-19. However, it only included women who were late in their pregnancy and gave birth by caesarean section. 

There were two cases of fetal distress but all nine pregnancies resulted in live births. That symptoms from COVID-19 infection in pregnant women were similar to those reported in non-pregnant adults, and no women in the study developed severe pneumonia or died.

All mothers in the study were aged between 26-40 years. None of them had underlying health conditions, but one developed gestational hypertension from week 27 of her pregnancy, and another developed pre-eclampsia at week 31. Both patients’ conditions were stable during pregnancy. The nine women in the study had typical symptoms of COVID-19 infection, and were given oxygen support and antibiotics. Six of the women were also given antiviral therapy. In the study, the medical records of nine pregnant women who had pneumonia caused by COVID-19 infection were retrospectively reviewed. Infection was lab-confirmed for all women in the study, and the authors studied the nine women’s symptoms.

(A) Patient 1: left-sided patchy consolidation and multiple bilateral ground-glass opacities. (B) Patient 2: subpleural patchy consolidation in the right lung and slightly infiltrated shadows around left bronchus. (C) Patient 3: bilateral multiple ground-glass opacities, prominent on the left. (D) Patient 4: left-sided patchy ground-glass opacity. (E) Patient 5: multiple ground-glass opacities bilaterally. (F) Patient 6: bilateral clear lung fields with no obvious ground-glass opacities. (G) Patient 7: right-sided subpleural patchy consolidation. (H) Patient 8: multiple bilateral ground-glass opacities, prominent on the right. (I) Patient 9: multiple bilateral ground-glass opacities.

In addition, samples of amniotic fluid, cord blood, neonatal throat swabs and breast milk were taken for six of the nine cases [2] and tested for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Importantly, the samples of amniotic fluid, cord blood, and neonatal throat swabs were collected in the operating room at the time of birth to guarantee that samples were not contaminated and best represented intrauterine conditions. All nine pregnancies resulted in live births, and there were no cases of neonatal asphyxia. Four women had pregnancy complications (two had fetal distress and two had premature rupture of membrane), and four women had preterm labor which was not related to their infection and occurred after 36 gestational weeks. Two of the prematurely born newborns had a low birth weight.

The authors note that their findings are similar to observations of the severe acute respiratory syndrome (SARS) virus in pregnant women, where there was no evidence of the virus being passed from mother to child during pregnancy or birth. The findings are based on a limited number of cases, over a short period of time, and the effects of mothers being infected with the virus during the first or second trimester of pregnancy and the subsequent outcomes for their offspring are still unclear, as well as whether the virus can be passed from mother to child during vaginal birth.

Dr Jie Qiao (who was not involved in the study) of Peking University Third Hospital, China,compares the effects of the virus to those of SARS, and says: “Previous studies have shown that SARS during pregnancy is associated with a high incidence of adverse maternal and neonatal complications, such as spontaneous miscarriage, preterm delivery, intrauterine growth restriction, application of endotracheal intubation, admission to the intensive care unit, renal failure, and disseminated intravascular coagulopathy. However, pregnant women with COVID-19 infection in the present study had fewer adverse maternal and neonatal complications and outcomes than would be anticipated for those with SARS-CoV-1 infection. Although a small number of cases was analysed and the findings should be interpreted with caution, the findings are mostly consistent with the clinical analysis done by Zhu and colleagues of ten neonates born to mothers with COVID-19 pneumonia."

sb admin Wed, 02/12/2020 - 13:03

Categories

Life Sciences

from ScienceBlogs - Where the world discusses science https://ift.tt/39qNFx1

To Reduce Risk of Coronavirus and Flu, Wash Your Hands

To Reduce Risk of Coronavirus and Flu, Wash Your Hands

A new study finds an easy way to reduce the spread of many infectious diseases, from coronavirus to influenza; washing hands more frequently in just 10 airports. 

Though the findings were published in late December, just before the recent coronavirus outbreak in Wuhan, China, the study's authors say that its results would apply to any such disease and are relevant to the current outbreak. The methods included epidemiological and data-based simulations.

People can be surprisingly casual about washing their hands, even in crowded locations like airports where people from many different locations are touching surfaces such as chair armrests, check-in kiosks, security checkpoint trays, and restroom doorknobs and faucets. Based on data from previous research, the team estimates that on average, only about 20 percent of people in airports have clean hands -- meaning that they have been washed with soap and water, for at least 15 seconds, within the last hour or so. The other 80 percent are potentially contaminating everything they touch with whatever germs they may be carrying.

Use soap and water in airports. And everywhere else. 

 

"Seventy percent of the people who go to the toilet wash their hands afterwards, and of those that do, only 50 percent use soap. Others just rinse briefly in some water. That figure, combined with estimates of exposure to the many potentially contaminated surfaces that people come into contact with in an airport, leads to the team's estimate that about 20 percent of travelers in an airport have clean hands.

Improving handwashing at all of the world's airports to triple that rate, so that 60 percent of travelers to have clean hands at any given time, would have the greatest impact, potentially slowing global disease spread by almost 70 percent, the researchers found. Deploying such measures at so many airports and reaching such a high level of compliance may be impractical, but the new study suggests that a significant reduction in disease spread could still be achieved by just picking the 10 most significant airports based on the initial location of a viral outbreak. Focusing handwashing messaging in those 10 airports could potentially slow the disease spread by as much as 37 percent, the researchers estimate.

They arrived at these estimates using detailed epidemiological computer models that involved data on worldwide flights including duration, distance, and interconnections; estimates of wait times at airports; and studies on typical rates of interactions of people with various elements of their surroundings and with other people.

Even small improvements in hygiene could make a noticeable dent. Increasing the prevalence of clean hands in all airports worldwide by just 10 percent, which the researchers think could potentially be accomplished through education, posters, public announcements, and perhaps improved access to handwashing facilities, could slow the global rate of the spread of a disease by about 24 percent, they found.

The researchers used data from previous studies on the effectiveness of handwashing in controlling transmission of disease, so these data would have to be calibrated in the field to obtain refined estimates of the slow-down in spreading of a specific outbreak.

sb admin Tue, 02/11/2020 - 21:03

Categories

Medicine

from ScienceBlogs - Where the world discusses science https://ift.tt/39tkrxy

To Reduce Risk of Coronavirus and Flu, Wash Your Hands

A new study finds an easy way to reduce the spread of many infectious diseases, from coronavirus to influenza; washing hands more frequently in just 10 airports. 

Though the findings were published in late December, just before the recent coronavirus outbreak in Wuhan, China, the study's authors say that its results would apply to any such disease and are relevant to the current outbreak. The methods included epidemiological and data-based simulations.

People can be surprisingly casual about washing their hands, even in crowded locations like airports where people from many different locations are touching surfaces such as chair armrests, check-in kiosks, security checkpoint trays, and restroom doorknobs and faucets. Based on data from previous research, the team estimates that on average, only about 20 percent of people in airports have clean hands -- meaning that they have been washed with soap and water, for at least 15 seconds, within the last hour or so. The other 80 percent are potentially contaminating everything they touch with whatever germs they may be carrying.

Use soap and water in airports. And everywhere else. 

 

"Seventy percent of the people who go to the toilet wash their hands afterwards, and of those that do, only 50 percent use soap. Others just rinse briefly in some water. That figure, combined with estimates of exposure to the many potentially contaminated surfaces that people come into contact with in an airport, leads to the team's estimate that about 20 percent of travelers in an airport have clean hands.

Improving handwashing at all of the world's airports to triple that rate, so that 60 percent of travelers to have clean hands at any given time, would have the greatest impact, potentially slowing global disease spread by almost 70 percent, the researchers found. Deploying such measures at so many airports and reaching such a high level of compliance may be impractical, but the new study suggests that a significant reduction in disease spread could still be achieved by just picking the 10 most significant airports based on the initial location of a viral outbreak. Focusing handwashing messaging in those 10 airports could potentially slow the disease spread by as much as 37 percent, the researchers estimate.

They arrived at these estimates using detailed epidemiological computer models that involved data on worldwide flights including duration, distance, and interconnections; estimates of wait times at airports; and studies on typical rates of interactions of people with various elements of their surroundings and with other people.

Even small improvements in hygiene could make a noticeable dent. Increasing the prevalence of clean hands in all airports worldwide by just 10 percent, which the researchers think could potentially be accomplished through education, posters, public announcements, and perhaps improved access to handwashing facilities, could slow the global rate of the spread of a disease by about 24 percent, they found.

The researchers used data from previous studies on the effectiveness of handwashing in controlling transmission of disease, so these data would have to be calibrated in the field to obtain refined estimates of the slow-down in spreading of a specific outbreak.

sb admin Tue, 02/11/2020 - 21:03

Categories

Medicine

from ScienceBlogs - Where the world discusses science https://ift.tt/39tkrxy

First Artificial Enzyme From Two Non-Biological Groups Created

First Artificial Enzyme From Two Non-Biological Groups Created

Scientists have used an unnatural amino acid and a catalytic copper complex to create a new, artificial enzyme. 

Enzymes are natural catalysts that operate under mild conditions. This makes them an attractive alternative for industrial chemical catalysis, which may require high temperature and pressure and toxic solvents or metals. However, not all chemical reactions can be catalyzed by natural enzymes. Modifying existing enzymes is one option but University of Groningen Chemistry Professor Gerard Roelfes believes that creating new enzymes could be another valuable option.

For this study, they added a copper complex to a protein that had no enzymatic properties and inserted an unnatural amino acid into the protein. Together with the copper, a side chain of the amino acid was able to catalyze the required reaction. This technique could replace standard chemical catalysis and make chemistry more energy-efficient and therefore cleaner.

The structure of the LmrR protein (green), with the two added catalytic groups binding to their substrates. Image:  Reuben Leveson-Gower

"Natural enzymes evolved to catalyse specific reactions. Adapting requires a kind of devolving of the enzyme. That is why we pioneered the creation of new, unnatural enzymes," Roelfes says. In 2018, they created a non-enzymatic protein, the bacterial transcription factor LmrR, which could form non-biological hydrazone structures after the insertion of the unnatural amino acid p aminophenylalanine. This was the first enzyme created using an unnatural amino acid as a catalytic group.

This time, they used the same LmrR protein and added two abiological catalytic components to it: one was the same unnatural amino acid p aminophenylalanine and the other a copper-containing complex. Both can activate the reaction partners for the classic Michael addition reaction, which is widely used in organic chemistry to create carbon-carbon bonds. "But they both have to be in the right position to efficiently and selectively catalyse this reaction,' says Roelfes. "Just adding both components to a test tube would not work: 'In fact, they cancel each other out when they come too close."

The copper-containing complex attaches itself to the doughnut-shaped LmrR protein through supramolecular bonds. Its position is determined by the interaction with the protein. They determined where the p-aminophenylalanine should be inserted into the protein to create an active site. The catalytic part of this amino acid is an aniline side chain. They knew the potential utility of this aniline side chain for catalysis and envisioned that it would be possible to combine it with copper catalysis. When the novel enzyme was constructed, the adapted protein turned out to be a very selective catalyst for the Michael addition.

sb admin Mon, 02/10/2020 - 13:34

Categories

Technology

from ScienceBlogs - Where the world discusses science https://ift.tt/37h3Onb

First Artificial Enzyme From Two Non-Biological Groups Created

Scientists have used an unnatural amino acid and a catalytic copper complex to create a new, artificial enzyme. 

Enzymes are natural catalysts that operate under mild conditions. This makes them an attractive alternative for industrial chemical catalysis, which may require high temperature and pressure and toxic solvents or metals. However, not all chemical reactions can be catalyzed by natural enzymes. Modifying existing enzymes is one option but University of Groningen Chemistry Professor Gerard Roelfes believes that creating new enzymes could be another valuable option.

For this study, they added a copper complex to a protein that had no enzymatic properties and inserted an unnatural amino acid into the protein. Together with the copper, a side chain of the amino acid was able to catalyze the required reaction. This technique could replace standard chemical catalysis and make chemistry more energy-efficient and therefore cleaner.

The structure of the LmrR protein (green), with the two added catalytic groups binding to their substrates. Image:  Reuben Leveson-Gower

"Natural enzymes evolved to catalyse specific reactions. Adapting requires a kind of devolving of the enzyme. That is why we pioneered the creation of new, unnatural enzymes," Roelfes says. In 2018, they created a non-enzymatic protein, the bacterial transcription factor LmrR, which could form non-biological hydrazone structures after the insertion of the unnatural amino acid p aminophenylalanine. This was the first enzyme created using an unnatural amino acid as a catalytic group.

This time, they used the same LmrR protein and added two abiological catalytic components to it: one was the same unnatural amino acid p aminophenylalanine and the other a copper-containing complex. Both can activate the reaction partners for the classic Michael addition reaction, which is widely used in organic chemistry to create carbon-carbon bonds. "But they both have to be in the right position to efficiently and selectively catalyse this reaction,' says Roelfes. "Just adding both components to a test tube would not work: 'In fact, they cancel each other out when they come too close."

The copper-containing complex attaches itself to the doughnut-shaped LmrR protein through supramolecular bonds. Its position is determined by the interaction with the protein. They determined where the p-aminophenylalanine should be inserted into the protein to create an active site. The catalytic part of this amino acid is an aniline side chain. They knew the potential utility of this aniline side chain for catalysis and envisioned that it would be possible to combine it with copper catalysis. When the novel enzyme was constructed, the adapted protein turned out to be a very selective catalyst for the Michael addition.

sb admin Mon, 02/10/2020 - 13:34

Categories

Technology

from ScienceBlogs - Where the world discusses science https://ift.tt/37h3Onb

FHR4: Age-Related Macular Degeneration Breakthrough

FHR4: Age-Related Macular Degeneration Breakthrough

Almost 2 million Americans have age-related macular degeneration (AMD), where the cells in the retina, which is the layer of tissue in the back of the eye, break down, causing central vision to become blurry. Over time, 100,000 of those will become blind.

An international team of scientists has identified a protein, FHR4, which is strongly linked to AMD when its levels are raised in the blood. The findings were confirmed in 484 patient and 522 control samples from two independent collections across Europe. FHR4 is one of a group of proteins that regulate the complement system and the genes encoding these proteins are tightly clustered on chromosome 1, the largest human chromosome.

Analyses of eyes donated for research after life also revealed the FHR4 protein was present in the AMD-affected parts of the eye and FHR4 was shown by the team to activate part of the immune system -called the complement system; over activation is a major causal factor of AMD.

Credit: NIH

When the team investigated a set of genetic variants across the human genome, they found that genetic variants in this region on chromosome 1 determined the levels of FHR4 in the blood. And they found that the same genetic variants were associated with AMD.

"We have shown that genetically determined higher blood FHR4 levels leads to more FHR4 in the eye which in turn increases the risk of the uncontrolled immune system response that drives the disease," said Professor Paul Bishop from the University of Manchester. "So apart from improving understanding of how AMD is caused, this work provides a way of predicting risk of the disease by simply measuring blood levels of FHR4."

sb admin Fri, 02/07/2020 - 11:52

Categories

Brain and Behavior

from ScienceBlogs - Where the world discusses science https://ift.tt/31zqwWp

FHR4: Age-Related Macular Degeneration Breakthrough

Almost 2 million Americans have age-related macular degeneration (AMD), where the cells in the retina, which is the layer of tissue in the back of the eye, break down, causing central vision to become blurry. Over time, 100,000 of those will become blind.

An international team of scientists has identified a protein, FHR4, which is strongly linked to AMD when its levels are raised in the blood. The findings were confirmed in 484 patient and 522 control samples from two independent collections across Europe. FHR4 is one of a group of proteins that regulate the complement system and the genes encoding these proteins are tightly clustered on chromosome 1, the largest human chromosome.

Analyses of eyes donated for research after life also revealed the FHR4 protein was present in the AMD-affected parts of the eye and FHR4 was shown by the team to activate part of the immune system -called the complement system; over activation is a major causal factor of AMD.

Credit: NIH

When the team investigated a set of genetic variants across the human genome, they found that genetic variants in this region on chromosome 1 determined the levels of FHR4 in the blood. And they found that the same genetic variants were associated with AMD.

"We have shown that genetically determined higher blood FHR4 levels leads to more FHR4 in the eye which in turn increases the risk of the uncontrolled immune system response that drives the disease," said Professor Paul Bishop from the University of Manchester. "So apart from improving understanding of how AMD is caused, this work provides a way of predicting risk of the disease by simply measuring blood levels of FHR4."

sb admin Fri, 02/07/2020 - 11:52

Categories

Brain and Behavior

from ScienceBlogs - Where the world discusses science https://ift.tt/31zqwWp

CRISPR Immune Cells Not Only Survive, They Thrive After Infusion Into Cancer Patients

CRISPR Immune Cells Not Only Survive, They Thrive After Infusion Into Cancer Patients

In the first-ever (sanctioned) investigational use of multiple edits to the human genome, a study found that cells edited in three specific ways and then removed from patients and brought back into the lab setting were able to kill cancer months after their original manufacturing and infusion.

This is the first U.S. clinical trial to test the gene editing approach in humans, and the publication of this new data today follows on the initial report last year that researchers were able to use CRISPR/Cas9 technology to successfully edit three cancer patients' immune cells. The ongoing study is a cooperative between Tmunity Therapeutics, the Parker Institute for Cancer Immunotherapy, and the University of Pennsylvania. 

Patients on this trial were treated by Edward A. Stadtmauer, MD, section chief of Hematologic Malignancies at Penn, co-lead author on the study. The approach in this study is closely related to CAR T cell therapy, in which patient immune cells are engineered to fight cancer, but it has some key differences. Just like CAR T, researchers in this study began by collecting a patient's T cells from blood. However, instead of arming these cells with a receptor against a protein such as CD19, the team first used CRISPR/Cas9 editing to remove three genes. The first two edits removed a T cell's natural receptors so they can be reprogrammed to express a synthetic T cell receptor, allowing these cells to seek out and destroy tumors. The third edit removed PD-1, a natural checkpoint that sometimes blocks T cells from doing their job. 

Once the three genes are knocked out, a fourth genetic modification was accomplished using a lentivirus to insert the cancer-specific synthetic T cell receptor, which tells the edited T cells to target an antigen called NY-ESO-1. Previously published data show these cells typically survive for less than a week, but this new analysis shows the edited cells used in this study persisted, with the longest follow up at nine months. 

Several months after the infusion, researchers drew more blood and isolated the CRISPR-edited cells for study. When brought back into the lab setting, the cells were still able to kill tumors. 

The CRISPR-edited T cells used in this study are not active on their own like CAR T cells. Instead, they require the cooperation of a molecule known as HLA-A*02:01, which is only expressed in a subset of patients. This means that patients had to be screened ahead of time to make sure they were a match for the approach. Participants who met the requirements received other clinically-indicated therapy as needed while they waited for their cells to be manufactured. Once that process was completed, all three patients received the gene-edited cells in a single infusion after a short course of chemotherapy. Analysis of blood samples revealed that all three participants had the CRISPR-edited T cells take root and thrive in the patients. While none responded to the therapy, there were no treatment-related serious adverse events. 

CRISPR technology has not previously been tested in humans in the U.S. so the research team had to move through a comprehensive and rigorous series of institutional and federal regulatory approval steps, including approval by the National Institutes of Health's Recombinant DNA Research Advisory Committee and review by the U.S. Food and Drug Administration, as well as Penn's institutional review board and institutional biosafety committee. The entire process required more than two years.

 Researchers say these new data will open the door to later stage studies to investigate and extend this approach to a broader field beyond cancer, several of which are already planned at Penn.

sb admin Thu, 02/06/2020 - 14:52

Categories

Life Sciences

from ScienceBlogs - Where the world discusses science https://ift.tt/39bFNiI

CRISPR Immune Cells Not Only Survive, They Thrive After Infusion Into Cancer Patients

In the first-ever (sanctioned) investigational use of multiple edits to the human genome, a study found that cells edited in three specific ways and then removed from patients and brought back into the lab setting were able to kill cancer months after their original manufacturing and infusion.

This is the first U.S. clinical trial to test the gene editing approach in humans, and the publication of this new data today follows on the initial report last year that researchers were able to use CRISPR/Cas9 technology to successfully edit three cancer patients' immune cells. The ongoing study is a cooperative between Tmunity Therapeutics, the Parker Institute for Cancer Immunotherapy, and the University of Pennsylvania. 

Patients on this trial were treated by Edward A. Stadtmauer, MD, section chief of Hematologic Malignancies at Penn, co-lead author on the study. The approach in this study is closely related to CAR T cell therapy, in which patient immune cells are engineered to fight cancer, but it has some key differences. Just like CAR T, researchers in this study began by collecting a patient's T cells from blood. However, instead of arming these cells with a receptor against a protein such as CD19, the team first used CRISPR/Cas9 editing to remove three genes. The first two edits removed a T cell's natural receptors so they can be reprogrammed to express a synthetic T cell receptor, allowing these cells to seek out and destroy tumors. The third edit removed PD-1, a natural checkpoint that sometimes blocks T cells from doing their job. 

Once the three genes are knocked out, a fourth genetic modification was accomplished using a lentivirus to insert the cancer-specific synthetic T cell receptor, which tells the edited T cells to target an antigen called NY-ESO-1. Previously published data show these cells typically survive for less than a week, but this new analysis shows the edited cells used in this study persisted, with the longest follow up at nine months. 

Several months after the infusion, researchers drew more blood and isolated the CRISPR-edited cells for study. When brought back into the lab setting, the cells were still able to kill tumors. 

The CRISPR-edited T cells used in this study are not active on their own like CAR T cells. Instead, they require the cooperation of a molecule known as HLA-A*02:01, which is only expressed in a subset of patients. This means that patients had to be screened ahead of time to make sure they were a match for the approach. Participants who met the requirements received other clinically-indicated therapy as needed while they waited for their cells to be manufactured. Once that process was completed, all three patients received the gene-edited cells in a single infusion after a short course of chemotherapy. Analysis of blood samples revealed that all three participants had the CRISPR-edited T cells take root and thrive in the patients. While none responded to the therapy, there were no treatment-related serious adverse events. 

CRISPR technology has not previously been tested in humans in the U.S. so the research team had to move through a comprehensive and rigorous series of institutional and federal regulatory approval steps, including approval by the National Institutes of Health's Recombinant DNA Research Advisory Committee and review by the U.S. Food and Drug Administration, as well as Penn's institutional review board and institutional biosafety committee. The entire process required more than two years.

 Researchers say these new data will open the door to later stage studies to investigate and extend this approach to a broader field beyond cancer, several of which are already planned at Penn.

sb admin Thu, 02/06/2020 - 14:52

Categories

Life Sciences

from ScienceBlogs - Where the world discusses science https://ift.tt/39bFNiI

Rural health report card - three reasons for higher mortality

Rural health report card - three reasons for higher mortality

A recent paper, "Higher U.S. Rural Mortality Rates Linked To Socioeconomic Status, Physician Shortages, And Lack Of Health Insurance," published in Health Affairs Journal, seeks to explain differences in rural and urban people when it comes to mortality, but also rank states using county level data on outcomes and health care access.

The study focused on five explanatory variables within each county: socioeconomic (e.g., poverty status, access to housing and education, employment), uninsured rates, the supply of and access to primary care physicians, the percentage of racial or ethnic groups and the number of rural and urban residents.

However, after compiling all of the data, the researchers believed that only three of their explanatory variables were applicable: socioeconomic deprivation, percentage of uninsured and the primary care physician supply. Those three variables were linked to 81.8% of the total variance of mortality. Correlation is not necessarily causation but it is well known that people who claim their supplements and organic food and fitness crazes led to their better health often leave out that a lot of issues correlate with greater wealth. It isn't the special label on the food making people live longer, it is the other trappings of wealth. The percentage of racial and ethnic groups and the number of rural or urban residents were not significantly associated with mortality even though the percentage of African Americans was positively associated with mortality. After adjustments for socioeconomic deprivation, uninsured rates and supply-access to primary care physicians were factored in, the percentage of African Americans was no longer significantly associated with mortality. They used the rural-urban continuum codes put out by the USDA to break down and divide by counties, and because the health data tends to be by counties, they feel like the data are better matched.

"We're not saying that African Americans across the country don't have higher rates of mortality because they absolutely do," said Scott Phillips, editor in chief for theTexas Tech University Health Sciences Center Rural Health Quarterly magazine and a co-author to the study. "What we are saying, and what we discovered with this study, is that other disparities that African Americans face, particularly socioeconomic status and access to care, account for the higher African American mortality rates across the country."

The study also showed the percentage of Hispanic Americans is negatively associated with mortality, another facet of the "Hispanic paradox", an epidemiological confounder showing that Hispanic Americans tend to have health outcomes that are comparable to or better than whites even though Hispanic Americans on average tend to have lower socioeconomic status.

 

Rural residency does not negatively affect mortality but it does favor lower mortality - except in these western states

The results indicate that rural dwellers would have lived longer than their urban counterparts had their socioeconomic conditions and access to health care been similar. 

Now the authors want to further analyze the three states that proved to be exceptions to those findings: Colorado, Montana and Wyoming. Those three contiguous states in the Mountain West have higher urban mortality than rural mortality.

sb admin Wed, 02/05/2020 - 10:38

Categories

Medicine

from ScienceBlogs - Where the world discusses science https://ift.tt/394Bbea

Rural health report card - three reasons for higher mortality

A recent paper, "Higher U.S. Rural Mortality Rates Linked To Socioeconomic Status, Physician Shortages, And Lack Of Health Insurance," published in Health Affairs Journal, seeks to explain differences in rural and urban people when it comes to mortality, but also rank states using county level data on outcomes and health care access.

The study focused on five explanatory variables within each county: socioeconomic (e.g., poverty status, access to housing and education, employment), uninsured rates, the supply of and access to primary care physicians, the percentage of racial or ethnic groups and the number of rural and urban residents.

However, after compiling all of the data, the researchers believed that only three of their explanatory variables were applicable: socioeconomic deprivation, percentage of uninsured and the primary care physician supply. Those three variables were linked to 81.8% of the total variance of mortality. Correlation is not necessarily causation but it is well known that people who claim their supplements and organic food and fitness crazes led to their better health often leave out that a lot of issues correlate with greater wealth. It isn't the special label on the food making people live longer, it is the other trappings of wealth. The percentage of racial and ethnic groups and the number of rural or urban residents were not significantly associated with mortality even though the percentage of African Americans was positively associated with mortality. After adjustments for socioeconomic deprivation, uninsured rates and supply-access to primary care physicians were factored in, the percentage of African Americans was no longer significantly associated with mortality. They used the rural-urban continuum codes put out by the USDA to break down and divide by counties, and because the health data tends to be by counties, they feel like the data are better matched.

"We're not saying that African Americans across the country don't have higher rates of mortality because they absolutely do," said Scott Phillips, editor in chief for theTexas Tech University Health Sciences Center Rural Health Quarterly magazine and a co-author to the study. "What we are saying, and what we discovered with this study, is that other disparities that African Americans face, particularly socioeconomic status and access to care, account for the higher African American mortality rates across the country."

The study also showed the percentage of Hispanic Americans is negatively associated with mortality, another facet of the "Hispanic paradox", an epidemiological confounder showing that Hispanic Americans tend to have health outcomes that are comparable to or better than whites even though Hispanic Americans on average tend to have lower socioeconomic status.

 

Rural residency does not negatively affect mortality but it does favor lower mortality - except in these western states

The results indicate that rural dwellers would have lived longer than their urban counterparts had their socioeconomic conditions and access to health care been similar. 

Now the authors want to further analyze the three states that proved to be exceptions to those findings: Colorado, Montana and Wyoming. Those three contiguous states in the Mountain West have higher urban mortality than rural mortality.

sb admin Wed, 02/05/2020 - 10:38

Categories

Medicine

from ScienceBlogs - Where the world discusses science https://ift.tt/394Bbea

Coronavirus: Less Hype, More Perspective, Worry About The Flu Instead

Coronavirus: Less Hype, More Perspective, Worry About The Flu Instead

With a new infectious disease outbreak on our doorstep, we might ask ourselves: are we reacting to the coronavirus in a way that is proportional to the threat?

The problem is that when it comes to infectious disease epidemics, we have a strong tendency to overreact emotionally and under-react behaviorally. The overreaction aspect may be attributable to the fact that we are primed to fear infectious diseases appearing suddenly within our population, in the same way that we are evolutionarily prepared to fear snakes and spiders.

Most of us fear snakes and spiders without ever having been harmed by them. Compare that with automobiles, which harm many more of us, yet are only feared by a small number who have been in accidents themselves. In the same way, we fear infectious disease outbreaks much more readily and intensely than we fear diabetes epidemics.

The amygdala (in red) is largely responsible for fear learning. (Shutterstock)

From the perspective of the brain, the amygdala is largely responsible for fear learning, a process by which fear responses become attached to formerly neutral cues that are now viewed as signifying something genuinely threatening.

This explains fearful emotional responses to a formerly innocuous sneezing sound in a crowded subway train. Such amygdala-driven learning more readily occurs when the threat in question is an infectious disease than, say, a chronic disease epidemic of a much larger scale that poses an authentic personal threat.

Déjà vu

In 2003, SARS infected more than 8,000 people worldwide and caused 774 deaths. In Canada, 438 people were infected and 44 died. Those figures yield about a 10 per cent death rate for SARS. To be sure, it was a lethal virus, and it spread at an alarming rate with tragic consequences, particularly in places where infection protocols were not enacted quickly and decisively.

Now, 17 years later, we are facing a very similar-looking threat from another coronavirus, again originating in China, and quickly spreading around the globe. The mortality rate is difficult to estimate so early, but signs so far suggest a mortality rate similar to or lower than SARS.

A man wearing a protective mask carries flowers at Women’s College Hospital in Toronto during the SARS outbreak in March 2003. THE CANADIAN PRESS/Kevin Frayer

In just over a week, mass travel restrictions are been enacted overseas, and governments (appropriately) are advising against travelling to the epicentre of the outbreak, the city of Wuhan, China.

Highly alarming stories and images are circulating on social media depicting an epidemic out of control, about to overtake North America. Netflix even just launched a (very) hastily prepared docu-series on the horrors of infectious disease epidemics (just like coronavirus). If that isn’t a sign of the coming apocalypse, I’m not sure what is.

Viral information

The world seems riveted to media content pertaining to the coronavirus outbreak. From many perspectives, this is not surprising.

We respond quickly and intensely to information about infectious disease threats, even in faraway places or if they’re unlikely to have an impact on us. A reader’s attention is captured by the topic even when the coverage itself is intentionally not sensationalistic. I would read a responsibly written Ebola article over an excitingly written heart disease article any day.

In this age of social media, sharing is an individual choice and one made almost reflexively. In our brains, this relatively unconscious level of processing is disproportionately in the domain of the amygdala and largely unimpeded by higher cortical centres known to be implicated in thoughtful deliberation.

Sensationalized news and misinformation about infectious diseases can spread quickly through social media. (Shutterstock)

The tendency to share emotionally evocative images and text is even more unchecked than in conventional media. This results in selective spread of highly sensationalistic content via social media, and motivation for media outlets to shape their offerings to be more sensational. An old dynamic on steroids.

There is also a trend evident in some media outlets to intentionally counter this. All of us, when we catch ourselves, can recognize and limit our indulgence of overly sensationalistic content and reactions, including when it comes to infectious disease outbreaks.

Word to the wise

What should we do while we wait for things to unfold? My advice, if I were a physician dispensing it, would be to encourage people to pay attention to official information as much as possible, the Public Health Agency of Canada, for example, or its provincial counterparts. It will be there, and will be up to date and accurate for the most part.

The behavioural advice is relatively straightforward: wash your hands often, cover your mouth (with your arm) when you cough, avoid touching your face (surprisingly difficult to do consistently) and, for now, avoid travelling to Wuhan.

Read more: Coronavirus: Fear of a pandemic, or a pandemic of fear?

The situation is more complicated in mainland China, where the state-controlled media is struggling to compete with social media sharing, in part because of lack of trust. One advantage that the Chinese government does enjoy, however, is the ability to quickly and decisively implement top-down actions to limit disease spread.

So really, there are very different challenges for capitalist and communist countries when attempting to stem the flow of infectious disease epidemics.

Food for thought

Long story short, don’t lose sight of the larger picture in terms of risks in everyday life.

Spending too much time watching television while snacking on potato chips is probably riskier than shaking hands. But maybe avoid both for now, just to be safe.

And to end where I began — recalling how SARS overtook our collective consciousness in 2003 — it’s important to also remember that five times more deaths are attributable to the seasonal flu every year. If there is an infection we should fear, could it be that one? Or should we stop fearing infections altogether?

By Peter Hall, Professor, School of Public Health and Health Systems, University of Waterloo. Hall receives funding from the Natural Sciences and Engineering Research Council of Canada (NSERC), the Canadian Institutes of Health Research (CIHR) and the Social Sciences and Humanities Research Council of Canada (SSHRC). This article is republished from The Conversation under a Creative Commons license. Read the original article.

The Conversation Tue, 02/04/2020 - 13:05

Categories

Medicine

from ScienceBlogs - Where the world discusses science https://ift.tt/36Wn7SK

Coronavirus: Less Hype, More Perspective, Worry About The Flu Instead

With a new infectious disease outbreak on our doorstep, we might ask ourselves: are we reacting to the coronavirus in a way that is proportional to the threat?

The problem is that when it comes to infectious disease epidemics, we have a strong tendency to overreact emotionally and under-react behaviorally. The overreaction aspect may be attributable to the fact that we are primed to fear infectious diseases appearing suddenly within our population, in the same way that we are evolutionarily prepared to fear snakes and spiders.

Most of us fear snakes and spiders without ever having been harmed by them. Compare that with automobiles, which harm many more of us, yet are only feared by a small number who have been in accidents themselves. In the same way, we fear infectious disease outbreaks much more readily and intensely than we fear diabetes epidemics.

The amygdala (in red) is largely responsible for fear learning. (Shutterstock)

From the perspective of the brain, the amygdala is largely responsible for fear learning, a process by which fear responses become attached to formerly neutral cues that are now viewed as signifying something genuinely threatening.

This explains fearful emotional responses to a formerly innocuous sneezing sound in a crowded subway train. Such amygdala-driven learning more readily occurs when the threat in question is an infectious disease than, say, a chronic disease epidemic of a much larger scale that poses an authentic personal threat.

Déjà vu

In 2003, SARS infected more than 8,000 people worldwide and caused 774 deaths. In Canada, 438 people were infected and 44 died. Those figures yield about a 10 per cent death rate for SARS. To be sure, it was a lethal virus, and it spread at an alarming rate with tragic consequences, particularly in places where infection protocols were not enacted quickly and decisively.

Now, 17 years later, we are facing a very similar-looking threat from another coronavirus, again originating in China, and quickly spreading around the globe. The mortality rate is difficult to estimate so early, but signs so far suggest a mortality rate similar to or lower than SARS.

A man wearing a protective mask carries flowers at Women’s College Hospital in Toronto during the SARS outbreak in March 2003. THE CANADIAN PRESS/Kevin Frayer

In just over a week, mass travel restrictions are been enacted overseas, and governments (appropriately) are advising against travelling to the epicentre of the outbreak, the city of Wuhan, China.

Highly alarming stories and images are circulating on social media depicting an epidemic out of control, about to overtake North America. Netflix even just launched a (very) hastily prepared docu-series on the horrors of infectious disease epidemics (just like coronavirus). If that isn’t a sign of the coming apocalypse, I’m not sure what is.

Viral information

The world seems riveted to media content pertaining to the coronavirus outbreak. From many perspectives, this is not surprising.

We respond quickly and intensely to information about infectious disease threats, even in faraway places or if they’re unlikely to have an impact on us. A reader’s attention is captured by the topic even when the coverage itself is intentionally not sensationalistic. I would read a responsibly written Ebola article over an excitingly written heart disease article any day.

In this age of social media, sharing is an individual choice and one made almost reflexively. In our brains, this relatively unconscious level of processing is disproportionately in the domain of the amygdala and largely unimpeded by higher cortical centres known to be implicated in thoughtful deliberation.

Sensationalized news and misinformation about infectious diseases can spread quickly through social media. (Shutterstock)

The tendency to share emotionally evocative images and text is even more unchecked than in conventional media. This results in selective spread of highly sensationalistic content via social media, and motivation for media outlets to shape their offerings to be more sensational. An old dynamic on steroids.

There is also a trend evident in some media outlets to intentionally counter this. All of us, when we catch ourselves, can recognize and limit our indulgence of overly sensationalistic content and reactions, including when it comes to infectious disease outbreaks.

Word to the wise

What should we do while we wait for things to unfold? My advice, if I were a physician dispensing it, would be to encourage people to pay attention to official information as much as possible, the Public Health Agency of Canada, for example, or its provincial counterparts. It will be there, and will be up to date and accurate for the most part.

The behavioural advice is relatively straightforward: wash your hands often, cover your mouth (with your arm) when you cough, avoid touching your face (surprisingly difficult to do consistently) and, for now, avoid travelling to Wuhan.

Read more: Coronavirus: Fear of a pandemic, or a pandemic of fear?

The situation is more complicated in mainland China, where the state-controlled media is struggling to compete with social media sharing, in part because of lack of trust. One advantage that the Chinese government does enjoy, however, is the ability to quickly and decisively implement top-down actions to limit disease spread.

So really, there are very different challenges for capitalist and communist countries when attempting to stem the flow of infectious disease epidemics.

Food for thought

Long story short, don’t lose sight of the larger picture in terms of risks in everyday life.

Spending too much time watching television while snacking on potato chips is probably riskier than shaking hands. But maybe avoid both for now, just to be safe.

And to end where I began — recalling how SARS overtook our collective consciousness in 2003 — it’s important to also remember that five times more deaths are attributable to the seasonal flu every year. If there is an infection we should fear, could it be that one? Or should we stop fearing infections altogether?

By Peter Hall, Professor, School of Public Health and Health Systems, University of Waterloo. Hall receives funding from the Natural Sciences and Engineering Research Council of Canada (NSERC), the Canadian Institutes of Health Research (CIHR) and the Social Sciences and Humanities Research Council of Canada (SSHRC). This article is republished from The Conversation under a Creative Commons license. Read the original article.

The Conversation Tue, 02/04/2020 - 13:05

Categories

Medicine

from ScienceBlogs - Where the world discusses science https://ift.tt/36Wn7SK

Fireflies Face Extinction Threat Due To Pesticides, Habitat Loss, And Light Pollution

Fireflies Face Extinction Threat Due To Pesticides, Habitat Loss, And Light Pollution

The International Union for the Conservation of Nature, a coalition of activist groups which recently charged that climate change is contributing to exploitation of women, is now arguing that various factors are causing 2,000 species of fireflies to go extinct. 

They came to the conclusion by surveying affiliates to ask them what is driving fireflies to extinction. 

According to survey respondents, habitat loss is the most most critical threat to firefly survival, followed by light pollution and pesticide use.

"Lots of wildlife species are declining because their habitat is shrinking," said Professor Sara Lewis of Tufts University, "so it wasn't a huge surprise that habitat loss was considered the biggest threat. Some fireflies get hit especially hard when their habitat disappears because they need special conditions to complete their life cycle. For instance, one Malaysian firefly [Pteroptyx tener], famous for its synchronized flash displays, is a mangrove specialist." 

Lampyris noctiluca, female glow-worm. Image: Jason Steel - www.jason-steel.co.uk

One surprising result that emerged from the survey was their naming light pollution as the second most serious threat. Given the IUCN demographic, pesticides would have been the smart prediction. Yet artificial light at night has grown exponentially during the last century. Many fireflies rely on bioluminescence to find and attract their mates, and it is hypothesized that too much artificial light can interfere with these courtship exchanges. Switching to LEDs is better for climate change but not light pollution, and since environmentalists have driven astronomy out of the U.S. mainland, those limits on limit pollution have now gone unchecked.

Pesticides round out the top three dangers listed by the activists. Though pesticide exposure is unknown, if it happens it is most likely in the larval stages, since juvenile fireflies spend up to two years living below ground or under water. Insecticides such as organophosphates and neonicotinoids kill pests, but IUCN members insist they also have yet unknown off-target effects on beneficial insects. Though that hasn't been shown, some papers claim that commonly used insecticides are harmful to fireflies. 

A few studies have quantified firefly population declines, such as those seen in the tourist-attracting synchronous fireflies of Malaysia, and the glowworm Lampyris noctiluca in England. Otherwise it is just anecdotal reports which suggest that many other firefly species across a wide range of habitats have also suffered recent declines. 

sb admin Mon, 02/03/2020 - 14:26

Categories

Environment

from ScienceBlogs - Where the world discusses science https://ift.tt/2v3KH2I

Fireflies Face Extinction Threat Due To Pesticides, Habitat Loss, And Light Pollution

The International Union for the Conservation of Nature, a coalition of activist groups which recently charged that climate change is contributing to exploitation of women, is now arguing that various factors are causing 2,000 species of fireflies to go extinct. 

They came to the conclusion by surveying affiliates to ask them what is driving fireflies to extinction. 

According to survey respondents, habitat loss is the most most critical threat to firefly survival, followed by light pollution and pesticide use.

"Lots of wildlife species are declining because their habitat is shrinking," said Professor Sara Lewis of Tufts University, "so it wasn't a huge surprise that habitat loss was considered the biggest threat. Some fireflies get hit especially hard when their habitat disappears because they need special conditions to complete their life cycle. For instance, one Malaysian firefly [Pteroptyx tener], famous for its synchronized flash displays, is a mangrove specialist." 

Lampyris noctiluca, female glow-worm. Image: Jason Steel - www.jason-steel.co.uk

One surprising result that emerged from the survey was their naming light pollution as the second most serious threat. Given the IUCN demographic, pesticides would have been the smart prediction. Yet artificial light at night has grown exponentially during the last century. Many fireflies rely on bioluminescence to find and attract their mates, and it is hypothesized that too much artificial light can interfere with these courtship exchanges. Switching to LEDs is better for climate change but not light pollution, and since environmentalists have driven astronomy out of the U.S. mainland, those limits on limit pollution have now gone unchecked.

Pesticides round out the top three dangers listed by the activists. Though pesticide exposure is unknown, if it happens it is most likely in the larval stages, since juvenile fireflies spend up to two years living below ground or under water. Insecticides such as organophosphates and neonicotinoids kill pests, but IUCN members insist they also have yet unknown off-target effects on beneficial insects. Though that hasn't been shown, some papers claim that commonly used insecticides are harmful to fireflies. 

A few studies have quantified firefly population declines, such as those seen in the tourist-attracting synchronous fireflies of Malaysia, and the glowworm Lampyris noctiluca in England. Otherwise it is just anecdotal reports which suggest that many other firefly species across a wide range of habitats have also suffered recent declines. 

sb admin Mon, 02/03/2020 - 14:26

Categories

Environment

from ScienceBlogs - Where the world discusses science https://ift.tt/2v3KH2I

AI Will Revolutionize DNA Evidence – Once We Can Trust The Results

AI Will Revolutionize DNA Evidence – Once We Can Trust The Results

DNA evidence often isn’t as watertight as many people think. Sensitive techniques developed over the past 20 years mean that police can now detect minute traces of DNA at a crime scene or on a piece of evidence. But traces from a perpetrator are often mixed with those from many other people that have been transferred to the sample site, for example via a handshake. And this problem has led to people being wrongly convicted.

Scientists have developed algorithms to separate this DNA soup and to measure the relative amounts of each person’s DNA in a sample. These “probabilsitic genotyping” methods have enabled forensic investigators to indicate how likely it is that an individual’s DNA was included in a mixed sample found at the crime scene.

And now, more sophisticated artificial intelligence (AI) techniques are being developed in an attempt to extract DNA profiles and try to work out whether a DNA sample came directly from someone who was at the crime scene, or whether it had just been innocently transferred.

But if this technology is successful, it could introduce a new problem, because it’s currently impossible to understand exactly how this AI reaches its conclusions. And how can we trust technology to provide vital evidence if we can’t interrogate how it produced that evidence in the first place? It has the potential to open the way to even more miscarriages of justice and so this lack of transparency may be a barrier to the technology’s use in forensic investigations.

Similar challenges emerged when DNA analysis software was first developed a decade ago. Evidence derived from DNA mixture software very quickly ran into challenges from defense teams (including that of OJ Simpson), who were concerned that the prosecution should demonstrate that the software was correctly validated.

How accurate were the results, and what was the known error rate? How exactly did the software work and could it accommodate defense hypotheses? Were the results really so dependable that a jury could safely convict?

It is a fundamental tenet of the law that evidence must be open to scrutiny. The jury cannot rely on bald assertions (claims made without evidence), no matter who makes them and what expertise they have. But the owners of the software argued it was their protected intellectual property and how it worked shouldn’t be made public.

A battle ensued that involved the use of novel court procedures to allow defense teams to privately examine how the software worked. Finally, the courts were persuaded that full access to the source code was needed, not least to test hypotheses other than those put forward by the prosecution.

AI can predict whether someone was actually at the site of a DNA sample. Gorodenkoff/Shutterstock

But the software hasn’t completely solved the issues of DNA mixtures and small, degraded samples. We still don’t know definitively if the DNA in a sample came directly from a person or was transferred there. This is complicated by the fact that different people shed DNA at different rates – a phenomenon known as their “shedder status”.

For example, a sample taken from a murder weapon could contain more DNA from someone who hasn’t touched it than from the person who actually committed the murder. People have been charged with serious offences because of this.

Add the fact that DNA is transferred at different rates across different surfaces and in different environmental conditions and it may become almost impossible to know exactly where DNA in a sample came from. This problem of “transfer and persistence” threatens to seriously undermine forensic DNA.

As a result, experiments are underway to find ways of more accurately quantifying DNA transfer in different circumstances. And AI has the potential to analyse the data from these experiments and use it to indicate the origin of DNA in a sample.

But AI-based software has an even greater transparency problem than probabilistic genotyping software did, and one that’s currently fundamental to the way it works. The exact way the software works isn’t just a commercial secret – it’s unclear even to the software developers.

Transparency issues

AI uses mathematical algorithms to complete tasks such as matching a facial expression to a particular set of emotions. But, crucially, it is able to learn through a process of trial and error and gradually manipulates its underlying algorithms in order to become more efficient.

It’s this process of manipulation and change that isn’t always transparent. The software makes its changes incredibly rapidly according to its own indecipherable logic. It can derive fantastically efficient results but we can’t say how it did so. It acts like a black box that takes inputs and gives outputs, but whose inner workings are invisible. Programmers can go through a clearer development process but it is slower and less efficient.

This transparency issue affects many broader applications of AI. For example, it makes it very difficult to correct AI systems whose decisions display a racial or gender bias, such those used to sift through employee resumes, or to target police resources.

And the advent of AI-driven DNA analysis will add a further dimension to the problems already encountered. Defence lawyers could rightly challenge the use of this technology, even if its use is limited to intelligence gathering rather than providing prosecution evidence. Unless transparency problems are addressed at an early stage, the obstacles to AI use in the forensic field could prove insurmountable.

How might we go about tackling these challenges? One option may be to opt for the less efficient, constrained forms of AI. But if the purpose of AI is to do the tasks we are less capable of or less willing to do ourselves, then reducing efficiency may be a poor solution. Whichever form of AI we opt to use, within an adversarial system of criminal justice there must be the potential for review, to reverse-engineer all automated decisions, and for third parties to provide unambiguous validation.

Ultimately, this is not merely a technical issue, but an urgent ethical problem that goes to the heart of our criminal justice systems. At stake is the right to a fair, open and transparent trial. This is a fundamental requirement that must be addressed before the headlong rush of technological advancement carries us past the point of no return.

By Karen Richmond, Postdoctoral research fellow, University of Strathclyde . This article is republished from The Conversation under a Creative Commons license. Read the original article.

sb admin Wed, 01/29/2020 - 13:23

Categories

Technology

from ScienceBlogs - Where the world discusses science https://ift.tt/2S0I7SQ

AI Will Revolutionize DNA Evidence – Once We Can Trust The Results

DNA evidence often isn’t as watertight as many people think. Sensitive techniques developed over the past 20 years mean that police can now detect minute traces of DNA at a crime scene or on a piece of evidence. But traces from a perpetrator are often mixed with those from many other people that have been transferred to the sample site, for example via a handshake. And this problem has led to people being wrongly convicted.

Scientists have developed algorithms to separate this DNA soup and to measure the relative amounts of each person’s DNA in a sample. These “probabilsitic genotyping” methods have enabled forensic investigators to indicate how likely it is that an individual’s DNA was included in a mixed sample found at the crime scene.

And now, more sophisticated artificial intelligence (AI) techniques are being developed in an attempt to extract DNA profiles and try to work out whether a DNA sample came directly from someone who was at the crime scene, or whether it had just been innocently transferred.

But if this technology is successful, it could introduce a new problem, because it’s currently impossible to understand exactly how this AI reaches its conclusions. And how can we trust technology to provide vital evidence if we can’t interrogate how it produced that evidence in the first place? It has the potential to open the way to even more miscarriages of justice and so this lack of transparency may be a barrier to the technology’s use in forensic investigations.

Similar challenges emerged when DNA analysis software was first developed a decade ago. Evidence derived from DNA mixture software very quickly ran into challenges from defense teams (including that of OJ Simpson), who were concerned that the prosecution should demonstrate that the software was correctly validated.

How accurate were the results, and what was the known error rate? How exactly did the software work and could it accommodate defense hypotheses? Were the results really so dependable that a jury could safely convict?

It is a fundamental tenet of the law that evidence must be open to scrutiny. The jury cannot rely on bald assertions (claims made without evidence), no matter who makes them and what expertise they have. But the owners of the software argued it was their protected intellectual property and how it worked shouldn’t be made public.

A battle ensued that involved the use of novel court procedures to allow defense teams to privately examine how the software worked. Finally, the courts were persuaded that full access to the source code was needed, not least to test hypotheses other than those put forward by the prosecution.

AI can predict whether someone was actually at the site of a DNA sample. Gorodenkoff/Shutterstock

But the software hasn’t completely solved the issues of DNA mixtures and small, degraded samples. We still don’t know definitively if the DNA in a sample came directly from a person or was transferred there. This is complicated by the fact that different people shed DNA at different rates – a phenomenon known as their “shedder status”.

For example, a sample taken from a murder weapon could contain more DNA from someone who hasn’t touched it than from the person who actually committed the murder. People have been charged with serious offences because of this.

Add the fact that DNA is transferred at different rates across different surfaces and in different environmental conditions and it may become almost impossible to know exactly where DNA in a sample came from. This problem of “transfer and persistence” threatens to seriously undermine forensic DNA.

As a result, experiments are underway to find ways of more accurately quantifying DNA transfer in different circumstances. And AI has the potential to analyse the data from these experiments and use it to indicate the origin of DNA in a sample.

But AI-based software has an even greater transparency problem than probabilistic genotyping software did, and one that’s currently fundamental to the way it works. The exact way the software works isn’t just a commercial secret – it’s unclear even to the software developers.

Transparency issues

AI uses mathematical algorithms to complete tasks such as matching a facial expression to a particular set of emotions. But, crucially, it is able to learn through a process of trial and error and gradually manipulates its underlying algorithms in order to become more efficient.

It’s this process of manipulation and change that isn’t always transparent. The software makes its changes incredibly rapidly according to its own indecipherable logic. It can derive fantastically efficient results but we can’t say how it did so. It acts like a black box that takes inputs and gives outputs, but whose inner workings are invisible. Programmers can go through a clearer development process but it is slower and less efficient.

This transparency issue affects many broader applications of AI. For example, it makes it very difficult to correct AI systems whose decisions display a racial or gender bias, such those used to sift through employee resumes, or to target police resources.

And the advent of AI-driven DNA analysis will add a further dimension to the problems already encountered. Defence lawyers could rightly challenge the use of this technology, even if its use is limited to intelligence gathering rather than providing prosecution evidence. Unless transparency problems are addressed at an early stage, the obstacles to AI use in the forensic field could prove insurmountable.

How might we go about tackling these challenges? One option may be to opt for the less efficient, constrained forms of AI. But if the purpose of AI is to do the tasks we are less capable of or less willing to do ourselves, then reducing efficiency may be a poor solution. Whichever form of AI we opt to use, within an adversarial system of criminal justice there must be the potential for review, to reverse-engineer all automated decisions, and for third parties to provide unambiguous validation.

Ultimately, this is not merely a technical issue, but an urgent ethical problem that goes to the heart of our criminal justice systems. At stake is the right to a fair, open and transparent trial. This is a fundamental requirement that must be addressed before the headlong rush of technological advancement carries us past the point of no return.

By Karen Richmond, Postdoctoral research fellow, University of Strathclyde . This article is republished from The Conversation under a Creative Commons license. Read the original article.

sb admin Wed, 01/29/2020 - 13:23

Categories

Technology

from ScienceBlogs - Where the world discusses science https://ift.tt/2S0I7SQ