September 25 - October 1, 2022: Issue 556

This law makes it illegal for companies to collect third-party data to profile you. But they do anyway

Unsplash, CC BY-SA
Katharine Kemp, UNSW Sydney

A little-known provision of the Privacy Act makes it illegal for many companies in Australia to buy or exchange consumers’ personal data for profiling or targeting purposes. It’s almost never enforced. In a research paper published today, I argue that needs to change.

“Data enrichment” is the intrusive practice of companies going behind our backs to “fill in the gaps” of the information we provide.

When you purchase a product or service from a company, fill out an online form, or sign up for a newsletter, you might provide only the necessary data such as your name, email, delivery address and/or payment information.

That company may then turn to other retailers or data brokers to purchase or exchange extra data about you. This could include your age, family, health, habits and more.

This allows them to build a more detailed individual profile on you, which helps them predict your behaviour and more precisely target you with ads.

For almost ten years, there has been a law in Australia that makes this kind of data enrichment illegal if a company can “reasonably and practicably” request that information directly from the consumer. And at least one major data broker has asked the government to “remove” this law.

The burning question is: why is there not a single published case of this law being enforced against companies “enriching” customer data for profiling and targeting purposes?

Data collection ‘only from the individual’

The relevant law is Australian Privacy Principle 3.6 and is part of the federal Privacy Act. It applies to most organisations that operate businesses with annual revenues higher than A$3 million, and smaller data businesses.

The law says such organisations:

must collect personal information about an individual only from the individual […] unless it is unreasonable or impracticable to do so.

This “direct collection rule” protects individuals’ privacy by allowing them some control over information collected about them, and avoiding a combination of data sources that could reveal sensitive information about their vulnerabilities.

But this rule has received almost no attention. There’s only one published determination of the federal privacy regulator on it, and that was against the Australian Defence Force in a different context.

According to Australian Privacy Principle 3.6, it’s only legal for an organisation to collect personal information from a third party if it would be “unreasonable or impracticable” to collect that information from the individual alone.

This exception was intended to apply to limited situations, such as when:

  • the individual is being investigated for some wrongdoing
  • the individual’s address needs to be updated for delivery of legal or official documents.

The exception shouldn’t apply simply because a company wants to collect extra information for profiling and targeting, but realises the customer would probably refuse to provide it.

Who’s bypassing customers for third-party data?

Aside from data brokers, companies also exchange information with each other about their respective customers to get extra information on customers’ lives. This is often referred to as “data matching” or “data partnerships”.

Companies tend to be very vague about who they share information with, and who they get information from. So we don’t know for certain who’s buying data-enrichment services from data brokers, or “matching” customer data.

Major companies such as Amazon Australia, eBay Australia, Meta (Facebook), 10Play Viacom and Twitter include terms in the fine print of their privacy policies that state they collect personal information from third parties, including demographic details and/or interests.

Google, News Corp, Seven, Nine and others also say they collect personal information from third parties, but are more vague about the nature of that information.

These privacy policies don’t explain why it would be unreasonable or impracticable to collect that information directly from customers.

Consumer ‘consent’ is not an exception

Some companies may try to justify going behind customers’ backs to collect data because there’s an obscure term in their privacy policy that mentions they collect personal information from third parties. Or because the company disclosing the data has a privacy policy term about sharing data with “trusted data partners”.

But even if this amounts to consumer “consent” under the relatively weak standards for consent in our current privacy law, this is not an exception to the direct collection rule.

The law allows a “consent” exception for government agencies under a separate part of the direct collection rule, but not for private organisations.

Data enrichment involves personal information

Many companies with third-party data collection terms in their privacy policies acknowledge this is personal information. But some may argue the collected data isn’t “personal information” under the Privacy Act, so the direct collection rule doesn’t apply.

Companies often exchange information about an individual without using the individual’s legal name or email. Instead they may use a unique advertising identifier for that individual, or “hash” the email address to turn it into a unique string of numbers and letters.

They essentially allocate a “code name” to the consumer. So the companies can exchange information that can be linked to the individual, yet say this information wasn’t connected to their actual name or email.

However, this information should still be treated as personal information because it can be linked back to the individual when combined with other information about them.

At least one major data broker is against it

Data broker Experian Australia has asked the government to “remove” Australian Privacy Principle 3.6 “altogether”. In its submission to the Privacy Act Review in January, Experian argued:

It is outdated and does not fit well with modern data uses.

Others who profit from data enrichment or data matching would probably agree, but prefer to let sleeping dogs lie.

A screenshot shows six different categories of consumer data offered by Experian.
On its website, Experian claims to offer a ‘combination of demographic, geographic, financial and market research data - both online and offline’. Screenshot/Experian

Experian argued the law favours large companies with direct access to lots of customers and opportunities to pool data collected from across their own corporate group. It said companies with access to fewer consumers and less data would be disadvantaged if they can’t purchase data from brokers.

But the fact that some digital platforms impose extensive personal data collection on customers supports the case for stronger privacy laws. It doesn’t mean there should be a data free-for-all.

Our privacy regulator should take action

It has been three years since the consumer watchdog recommended major reforms to our privacy laws to reduce the disadvantages consumers suffer from invasive data practices. These reforms are probably still years away, if they eventuate at all.

The direct collection rule is a very rare thing. It is an existing Australian privacy law that favours consumers. The privacy regulator should prioritise the enforcement of this law for the benefit of consumers.The Conversation

Katharine Kemp, Senior Lecturer, Faculty of Law & Justice, UNSW, UNSW Sydney

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Hilary Mantel was one of the great voices of historical fiction – and so much more

PA Images / Alamy
Dinah Birch, University of Liverpool

Dame Hilary Mantel was a writer of immense skill and originality, and her death represents an incalculable loss to British literature. She will be chiefly remembered for her trilogy on the life of the Tudor politician Thomas Cromwell.

The grace and vigour of these gripping novels transformed our understanding of what historical fiction can do. They were extraordinarily successful. Wolf Hall (2009) and Bring Up the Bodies (2012) both won the Booker Prize (she was the first woman to win the prize more than once), and The Mirror and the Light (2020) was longlisted. I was a member of the jury that awarded the Booker Prize to Bring Up the Bodies, and we were of one mind about the superb quality of that novel.

Adaptations for both television and stage followed, and it is a tribute to the power of Mantel’s exploration of the ambiguities surrounding Cromwell’s dramatic life that these versions brought many enthusiastic new readers to her novels. She became, relatively late in her life, a literary star.

The popularity of Mantel’s trilogy should not overshadow the remarkable range of her achievement. Her treatment of Thomas Cromwell brought a mass readership, but the accomplishment of her earlier novels had already won critical recognition.

A writer’s life

Mantel graduated from LSE and Sheffield University, and married Gerald McEwan, a geologist, in 1972 (they divorced in 1981, and remarried in 1982). A short spell of employment as a social worker lay behind her first published novel, the darkly comic Every Day is Mother’s Day (1985), and its sequel Vacant Possession (1986).

Book cover
A Place of Greater Safety.

A major historical novel, A Place of Greater Safety (completed in 1979, but not published until 1992) is a characteristically innovative interpretation of the French Revolution. Here, as throughout Mantel’s writing, a far-sighted grasp of the sweep of history and politics was fused with the inward particularities of individual experience.

Mantel had a lyrical sense of the irreducible strangeness of the world, with its vivid moments of beauty and threat, but this was never removed from her understanding of the moral imperatives of our shared responsibilities. She was never a neutral observer of the ebb and flow of history.

Mantel spent extended periods of her life overseas – notably in Botswana and Saudi Arabia – and she was always alert to a world beyond Britain. Eight Months on Ghazzah Street (1988) is a tense account of misunderstandings between westerners and Saudis living in Jeddah. A Change of Climate (1994) draws on her life in Botswana, and the traumatic social divisions she had witnessed in southern Africa.

Book cover

Mantel had an unusually wide and well-informed grasp of social and cultural politics, but she never lost her interest in lives that unfold on the edge of what might be perceived as normality. Fludd (1989), describes a quasi-supernatural stranger whose arrival turns a dismal Catholic community upside down. It is never quite clear who Fludd is, or where he has come from, or whether he is an agent of good or evil.

The Giant, O’Brien (1998), based on the Irish giant Charles Byrne and the Scottish surgeon John Hunter, is in part a rueful reflection on Mantel’s own Irish roots. The legacies of Irish Catholicism also shadow An Experiment in Love (1995), a novel that looks back on the lives of girls of Mantel’s postwar generation - eager to take advantage of new opportunities for education, but still haunted by the constraints of the past.

A rich legacy

The sense that another world exists, its presence flickering just past our everyday vision, underlies all of Mantel’s work. Beyond Black (2005) is an unsettling and brilliantly entertaining account of the life of a medium, who may or may not be a fraud.

Book cover
Giving Up The Ghost.

Giving up the Ghost (2003), a searing memoir, repeatedly returns to the ghosts that stalked her early years – family ghosts, ghosts of unborn children, ghosts of lives that might have taken a different shape. Learning to Talk (2003), published in the same year, is a collection of short stories that turn on the same theme.

These stories are in part autobiographical recollections of Mantel’s childhood in Glossop, as she began to remove herself from the divided world of her family. Here too, it is the sharply observed details that linger – Miss Webster, for instance, the elocution teacher, with her careful accent – “precariously genteel, Manchester with icing”.

More recent short stories have been openly political, and sometimes controversial – notably The Assassination of Margaret Thatcher, the provocative title story in a collection published in 2014.

This shining stream of writing has now come to an end. It’s good to know that Hilary Mantel experienced and enjoyed all the success she had so richly earned, and that we are left with such a rich body of writing to relish and revisit. But the sense of immediate loss is painful. She was a unique and generous talent, and she will be hugely missed.The Conversation

Dinah Birch, Pro-Vice-Chancellor for Cultural Engagement, Professor of English Literature, University of Liverpool

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Youth mental health improves despite COVID pressure

September 2022
The mental health and wellbeing of young Australians has dramatically improved, despite the ongoing COVID-19 pandemic, new analysis from The Australian National University (ANU) shows. 

The findings come from the ANU Centre for Social Research and Methods' COVID Impact Monitoring survey, which has examined the effect of the pandemic on Australians for more than two years and across 12 waves of data collection.  

According to the researchers, the latest survey of more than 3,500 people completed in August 2022 shows Australians aged 18 to 24 are feeling more positive about their lives and their future, and are experiencing less psychological distress. 

"We found a large and significant turnaround in the number of young Australians who said their lives and wellbeing were improving, especially compared to Australians aged 45 to 64," study co-author Professor Nicholas Biddle said.  

"More than two in three, 67.4 per cent, of young Australians said their life had improved in the last 12 months. This was also the age group with the largest improvement in life satisfaction since our April 2022 survey.  

"We also found a five per cent decline in psychological distress among Australians aged 18 to 24. This was the age group reporting the biggest decline in psychological distress."  

Professor Biddle said it was important to note that levels of psychological distress were still above pre-pandemic levels, but much lower than what they were in 2020 and when COVID took a hold in Australia.  

Young Australians also continued to have the most elevated level of psychological distress of any age group compared to pre-COVID levels.   

"However, overall this is really encouraging news," Professor Biddle said. 

"Young people have been the people most dramatically impacted by the COVID-19 pandemic in Australia, especially when it comes to their economic security, future prospects and mental health and wellbeing.  

"So it is heartening to see that the majority of young Australians say there are feeling much better than they were 12 months ago, even though they still face ongoing pandemic pressures."  

The study found that across the board Australians thought their life and wellbeing was improving, with levels of life satisfaction steadily increasing since January 2022.  

Levels of psychological distress among all Australians have also steadily declined between October 2021 and August 2022.  

"In May 2020, roughly half of Australians thought their life was worse, 51.3 per cent, including 6.5 per cent who thought it was much worse," Professor Biddle said.  

"By August 2022, only about one in five Australians thought that their life had become worse in the 12 months since August 2021, with only 3.9 per cent thinking that their life had got much worse. 
"And in October 2021, 27.2 per cent of adult Australians reported feeling hopeless at least some of the time. By August 2022, this had declined to 22.3 per cent, a drop of about 981,000 Australia adults. 

"That does not mean that Australia has returned to pre-pandemic levels of wellbeing and mental health. Life satisfaction was lower in August 2022 than it was in October 2019. There are also still more Australians who have high levels of psychological distress.  

"However, wellbeing and mental health outcomes have improved over recent months as lockdown conditions have substantially eased, and despite high case numbers." 

Address the logjam to end the cycle of horror stories: AMA

September 21, 2022
The AMA today renewed its call for reform of public hospital funding, following a week of harrowing media stories highlighting the plight Australians face from an under-funded and under-resourced hospital system.  

AMA President Professor Steve Robson said the horror stories coming out of every state and territory were the result of increased pressure on hospitals and a funding agreement that is “failing the health system and Australians who rely on that system”. 

“Story after story is showing a system buckling under pressure. People are dying waiting to be seen which is unacceptable in a country that prides itself on having a world-class health system," Professor Robson said. 

“NSW is facing record wait times for emergency departments and essential surgery, as ambulance ramping spikes, one in 10 people are leaving the emergency department without receiving care, and more than 18,700 people are overdue for surgery. This is no surprise, given reports of patients stuck in hospital beds for more than five years, waiting for disability or aged care services — beds that are needed to provide hospital care. 

“In QLD, there are reports of patients dying as they wait for ambulances, with one suicidal patient waiting more than two hours for an ambulance and being found dead by paramedics, and another dying as the ambulance arrived nine hours after the call for help.  

“How many more people need to die before we act?” 

Professor Robson said the ACT also has beds taken up by patients who are waiting for disability or aged care services, and while the federal government’s new plan will help address this, more is needed to address systemic hospital issues.   

“As inflation — and therefore the cost of providing care — continues to increase, the dollars   available to provide healthcare will decrease, which was highlighted in a report on Victoria’s health budget over the weekend.” 

The states and territories agree the current funding model is inadequate and have joined the AMA’s call for a permanent 50-50 funding split with the Commonwealth; with SA and TAS re-stating their position this week as they grapple with unprecedented demand and GP shortages. 

“The previous federal government failed to act on an inadequate funding system, and decisive action is needed from the current government to address the issue,” Professor Robson said.  

“We appreciate the decision to extend pandemic-related funding arrangements for another three months, however the health minister’s suggestion yesterday that the current funding agreement should run until 2025 isn’t good enough. Our hospitals were in crisis before COVID-19. The horrific stories we are hearing are simply the result of inadequate funding arrangements.” 

The AMA’s Clear the Hospital Logjam campaign is calling for 50-50 funding between the Commonwealth and states to improve hospital performance, expand capacity, and address avoidable admissions. It also calls for the 6.5 per cent cap on activity to be scrapped, to allow hospitals to meet community demand. 

“Over the next few months, the AMA will be renewing our push for hospital reform through our campaign. We will be advocating for funding to address elective surgery and outpatient appointment wait times, the bed block created by having inadequate aged care and NDIS funding and proposing solutions to the current GP crisis. 

“My hope is that we give hospitals what they need, and soon.  

“Behind every horror story of an avoidable death is someone’s loved one, and all Australians deserve better — it’s time to act.”   

Even mild COVID raises the chance of heart attack and stroke. What to know about the risks ahead

Clare Arnott, George Institute for Global Health; Bruce Neal, George Institute for Global Health, and Jamie Cham, University of Sydney

A concerning report recently published in Nature Medicine suggests even a mild case of COVID can increase the long-term risks of serious cardiovascular diseases such as stroke, heart attack and heart failure. The study highlights our limited understanding of the full consequences of COVID infection and the long-term impact of the COVID pandemic.

Australia has now reported more than 10 million cases of acute COVID infection and more than 14,000 deaths, with at least 600 million more people infected worldwide.

The immediate effects of COVID infection on the heart have been well documented, with myocarditis (inflammation of the heart muscle) an infrequent but potentially lethal complication. But myocarditis only occurs in about 40 people per million infected.

The big concern raised by this fresh study is that medium- to long-term harms on the body’s blood vessel network (the vascular system) may be much more common than that. And it could drive a new pandemic of cardiovascular disease over the coming years.

What they found

The study, led by researchers at Washington University, showed a heightened risk of future cardiovascular events among people who have recovered from COVID.

The authors analysed the health records of around 150,000 US veterans, who are often studied because they are a well-documented group within a discrete health-care system. They compared the rates of cardiovascular disease in veterans who’d experienced a COVID infection against uninfected control groups that included some 10 million people.

Between 30 days and a year after recovery from COVID, survivors were 52% more likely to have a stroke, 63% more likely to have a heart attack, and 72% more likely to develop heart failure. This means that over one year, for every 1,000 people who had COVID, there would be five extra strokes, three extra heart attacks and 12 extra cases of heart failure. There was also evidence of an increased risk of serious blood clots on the lungs.

While these numbers might sound small to some, when scaled to 600 million COVID infections worldwide, the implications are enormous.

One particularly concerning finding was that while those with more severe acute COVID infections had the highest risk of a cardiovascular events over the following year, even those with a mild infection were at increased risk. And that risk was not restricted to those who’d had heart health problems before – it could affect anyone.

Necessary cautions

The study was large and had many strengths. But the findings must be reviewed with a degree of caution. It was an observational study (in which researchers draw inferences from what they see in a population, rather than control variables for an experimental study). So, we can’t be certain the increased risk of heart disease or stroke was definitely caused by the COVID infection. The people infected with COVID were not identical to the people who were uninfected.

That said, the researchers made statistical adjustments and could not identify another explanation for the large increases in risks seen.

It is also likely some people with asymptomatic COVID infection were accidentally included in the control groups. However, the effect of this would have been to underestimate the risks of COVID infection on cardiovascular risk.

And of course, US veterans are a very particular set of individuals (mostly older, male and white). Even if the effects of COVID on cardiovascular risk are real for them, there must be some uncertainty about whether the same effects would be seen in other populations.

COVID and hearts

The clear, but low, risk of heart disease at the time of COVID infection also provides support for a connection between COVID infection and medium- to long-term heart disease.

Even before the COVID pandemic there was a well-established link between the inflammation caused by infection and the risk of heart attack.

A heart attack occurs when an artery supplying blood to the heart is blocked and the heart muscle is starved of oxygen. This usually happens when rupture of a fatty plaque in the artery causes a blood clot to form. This process is driven by inflammation in the tissues and thickening of the blood, both of which can occur with COVID, and both of which can persist long after the initial infection has resolved.

These data remind us once again of the importance of limiting the spread of the SARS-CoV-2 virus. The best way to reduce COVID-related risks is to prevent COVID infection and reduce the severity of infection. We must maintain high vaccination rates and support infection control measures such as mask wearing in high-risk situations. Ever stronger evidence of the long-term effects of COVID redoubles the importance of these efforts.

Future problems

We rightly feared the respiratory complications of COVID throughout 2020 and 2021 but only now are we appreciating the full impact of the pandemic across other body systems.

Doctors will need to view COVID infection as a new long-term risk factor for cardiovascular disease in much the same way that many other chronic inflammatory conditions such as rheumatoid arthritis are viewed now. We should advocate for fair access to heart disease prevention and treatment in all Australians, particularly those at highest risk such as First Nations people. And most importantly, as patients, we must prioritise our own heart health.

And we’ll need to remain vigilant for the effects of new strains. Over the decades to come we’ll need to plan for the enduring effects of COVID.The Conversation

Clare Arnott, Co-Director of Global Chronic and Complex Diseases, George Institute for Global Health; Bruce Neal, Executive Director, George Institute Australia, George Institute for Global Health, and Jamie Cham, Lecturer, University of Sydney

This article is republished from The Conversation under a Creative Commons license. Read the original article.

I’ve had COVID and am constantly getting colds. Did COVID harm my immune system? Am I now at risk of other infectious diseases?

Pavel Danilyuk/Pexels, CC BY-SA
Lara Herrero, Griffith University

So you’ve had COVID and have now recovered. You don’t have ongoing symptoms and luckily, you don’t seem to have developed long COVID.

But what impacts has COVID had on your overall immune system?

It’s early days yet. But growing evidence suggests there are changes to your immune system that may put you at risk of other infectious diseases.

Here’s what we know so far.

A round of viral infections

Over this past winter, many of us have had what seemed like a continual round of viral illness. This may have included COVID, influenza or infection with respiratory syncytial virus. We may have recovered from one infection, only to get another.

Then there is the re-emergence of infectious diseases globally such as monkeypox or polio.

Could these all be connected? Does COVID somehow weaken the immune system to make us more prone to other infectious diseases?

There are many reasons for infectious diseases to emerge in new locations, after many decades, or in new populations. So we cannot jump to the conclusion COVID infections have given rise to these and other viral infections.

But evidence is building of the negative impact of COVID on a healthy individual’s immune system, several weeks after symptoms have subsided.

What happens when you catch a virus?

There are three possible outcomes after a viral infection:

1) your immune system clears the infection and you recover (for instance, with rhinovirus which causes the common cold)

2) your immune system fights the virus into “latency” and you recover with a virus dormant in our bodies (for instance, varicella zoster virus, which causes chickenpox)

3) your immune system fights, and despite best efforts the virus remains “chronic”, replicating at very low levels (this can occur for hepatitis C virus).

Ideally we all want option 1, to clear the virus. In fact, most of us clear SARS-CoV-2, the virus that causes COVID. That’s through a complex process, using many different parts of our immune system.

But international evidence suggests changes to our immune cells after SARS-CoV-2 infection may have other impacts. It may affect our ability to fight other viruses, as well as other pathogens, such as bacteria or fungi.

How much do we know?

An Australian study has found SARS-CoV-2 alters the balance of immune cells up to 24 weeks after clearing the infection.

There were changes to the relative numbers and types of immune cells between people who had recovered from COVID compared with healthy people who had not been infected.

This included changes to cells of the innate immune system (which provides a non-specific immune response) and the adaptive immune system (a specific immune response, targeting a recognised foreign invader).

Another study focused specifically on dendritic cells – the immune cells that are often considered the body’s “first line of defence”.

Researchers found fewer of these cells circulating after people recovered from COVID. The ones that remained were less able to activate white blood cells known as T-cells, a critical step in activating anti-viral immunity.

Dendritic cells (red) attacking viruses (green)
Fewer dendritic cells (red) were circulating after COVID. Shutterstock

Other studies have found different impacts on T-cells, and other types of white blood cells known as B-cells (cells involved in producing antibodies).

After SARS-CoV-2 infection, one study found evidence many of these cells had been activated and “exhausted”. This suggests the cells are dysfunctional, and might not be able to adequately fight a subsequent infection. In other words, sustained activation of these immune cells after a SARS-CoV-2 infection may have an impact on other inflammatory diseases.

One study found people who had recovered from COVID have changes in different types of B-cells. This included changes in the cells’ metabolism, which may impact how these cells function. Given B-cells are critical for producing antibodies, we’re not quite sure of the precise implications.

Could this influence how our bodies produce antibodies against SARS-CoV-2 should we encounter it again? Or could this impact our ability to produce antibodies against pathogens more broadly – against other viruses, bacteria or fungi? The study did not say.

What impact will these changes have?

One of the main concerns is whether such changes may impact how the immune system responds to other infections, or whether these changes might worsen or cause other chronic conditions.

So more work needs to be done to understand the long-term impact of SARS-CoV-2 infection on a person’s immune system.

For instance, we still don’t know how long these changes to the immune system last, and if the immune system recovers. We also don’t know if SARS-CoV-2 triggers other chronic illnesses, such as chronic fatigue syndrome (myalgic encephalomyelitis). Research into this is ongoing.

What we do know is that having a healthy immune system and being vaccinated (when a vaccine has been developed) is critically important to have the best chance of fighting any infection.The Conversation

Lara Herrero, Research Leader in Virology and Infectious Disease, Griffith University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Did my computer say it best?

September 20, 2022
With autocorrect and auto-generated email responses, algorithms offer plenty of assistance to help people express themselves. But new research from the University of Georgia shows people who rely on algorithms for assistance with language-related, creative tasks didn't improve their performance and were more likely to trust low-quality advice.

Aaron Schecter, an assistant professor in management information systems at the Terry College of Business, had his study "Human preferences toward algorithmic advice in a word association task" published this month in Scientific Reports. His co-authors are Nina Lauharatanahirun, a biobehavioural health assistant professor at Pennsylvania State University, and recent Terry College Ph.D. graduate and current Northeastern University assistant professor Eric Bogert.

The paper is the second in the team's investigation into individual trust in advice generated by algorithms. In an April 2021 paper, the team found people were more reliant on algorithmic advice in counting tasks than on advice purportedly given by other participants.

This study aimed to test if people deferred to a computer's advice when tackling more creative and language-dependent tasks. The team found participants were 92.3% more likely to use advice attributed to an algorithm than to take advice attributed to people.

"This task did not require the same type of thinking (as the counting task in the prior study) but in fact we saw the same biases," Schecter said. "They were still going to use the algorithm's answer and feel good about it, even though it's not helping them do any better."

Using an algorithm during word association
To see if people would rely more on computer-generated advice for language-related tasks, Schecter and his co-authors gave 154 online participants portions of the Remote Associates Test, a word association test used for six decades to rate a participant's creativity.

"It's not pure creativity, but word association is a fundamentally different kind of task than making a stock projection or counting objects in a photo because it involves linguistics and the ability to associate different ideas," he said. "We think of this as more subjective, even though there is a right answer to the questions."

During the test, participants were asked to come up with a word tying three sample words together. If, for example, the words were base, room and bowling, the answer would be ball.

Participants chose a word to answer the question and were offered a hint attributed to an algorithm or a hint attributed to a person and allowed to change their answers. The preference for algorithm-derived advice was strong despite the question's difficulty, the way the advice was worded, or the advice's quality.

Participants taking the algorithm's advice were also twice as confident in their answers as people who used the person's advice. Despite their confidence in their answers, they were 13% less likely than those who used human-based advice to choose correct answers.

"I'm not going say the advice was making people worse, but the fact they didn't do any better yet still felt better about their answers illustrates the problem," he said. "Their confidence went up, so they're likely to use algorithmic advice and feel good about it, but they won't necessarily be right.

Should you accept autocorrect when writing an email?
"If I have an autocomplete or autocorrect function on my email that I believe in, I might not be thinking about whether it's making me better. I'm just going to use it because I feel confident about doing it."

Schechter and colleagues call this tendency to accept computer-generated advice without an eye to its quality as automation bias. Understanding how and why human decision-makers defer to machine learning software to solve problems is an important part of understanding what could go wrong in modern workplaces and how to remedy it.

"Often when we're talking about whether we can allow algorithms to make decisions, having a person in the loop is given as the solution to preventing mistakes or bad outcomes," Schecter said. "But that can't be the solution if people are more likely than not to defer to what the algorithm advises."

Eric Bogert, Nina Lauharatanahirun, Aaron Schecter. Human preferences toward algorithmic advice in a word association task. Scientific Reports, 2022; 12 (1) DOI: 10.1038/s41598-022-18638-2

Genetic variants linked to congenital urinary tract obstruction in males

September 20, 2022
Genetic variation affecting developmental genes not previously linked to urethral development may contribute to a congenital condition that is the most common cause of kidney failure in young males, a new study suggests.

The discovery may help scientists better understand what causes a rare condition called posterior urethral valves (PUV), which affects 1 in 4,000 males and leads to blockages in the urethra and a build up of urine in the bladder which can then damage the kidneys. About one-third of individuals with this condition develop kidney failure before age 30. Affected individuals often undergo surgery to remove the blockages, but most continue to have urinary tract problems even after surgery. Therefore, new insights about the condition's cause are required to better understand how the urinary tract develops in health and disease and potentially inform new treatment approaches in the future.

"PUV does not follow a Mendelian pattern of inheritance, where each parent contributes one of two possible alleles for a trait, and scientists have not identified a single gene cause," explains lead author Dr Melanie Chan, who conducted the study as a Clinical Research Fellow at the UCL Department of Renal Medicine, London, UK. "This suggests that the genetic basis of this condition is more complex."

To identify the genetic causes, Chan and colleagues analysed the genomes of 132 unrelated males with PUV and 23,727 individuals without the condition who had been recruited to the UK's 100,000 Genomes Project. They included individuals with diverse genetic ancestry, including people of South Asian, African and European descent. They found two genetic variants associated with the risk of PUV. One was a common genetic variant located on chromosome 12q24.21 and the other was a rare genetic variant on chromosome 6p21.1. They confirmed the link between these two genetic differences and the disease in a separate group of individuals of European descent that included 395 males with PUV and 4,152 individuals without the condition.

The team then mapped the variation on 12q24.21 to a gene called TBX5, which contributes to turning other genes on or off. They also mapped the 6p21.1 variation to a gene called PTK7, which plays an essential role in cell development. When they looked at cells from developing human embryos, they found that the proteins encoded by the genes are active in the developing urinary tract. This discovery suggests that alterations in these proteins may interfere with normal urethra development.

Finally, they showed that structural changes in chromosomes, including flipped sections of DNA or other changes that alter the regulation of gene expression, were also linked to PUV.

"Our study is the first to identify rare and common genetic variation strongly associated with PUV, as well as structural variations in chromosomes that may contribute to the disease," says Dr Chan. "It provides new insights on what causes this poorly understood disorder."

The authors add that the small number of individuals included in this genetic analysis reduces its statistical power to detect very rare genetic variations linked with PUV. Additionally, they say more studies are needed to verify how exactly these genetic changes cause PUV.

But senior author Professor Daniel Gale, the St Peter's Chair of Nephrology at the UCL Department of Renal Medicine, says the study demonstrates the importance of including people with diverse genetic backgrounds in genome-wide studies of rare conditions. Too often, he noted, genetic studies may consist of only European populations, making them less likely to identify genetic variants that might be important in other groups.

"Increasing diversity in genetic studies is both scientifically and ethically beneficial," Professor Gale says. "It increases the power of studies to find and verify rare genetic variants and allows detection of genetic variants disproportionately affecting individuals with Asian, African, or other non-European ancestries. It also helps to ensure that people across the world benefit more equally from treatment advances driven by genetic discoveries."

Melanie Mai Yee Chan, Omid Sadeghi-Alavijeh, Filipa M Lopes, Alina C Hilger, Horia C Stanescu, Catalin D Voinescu, Glenda M Beaman, William G Newman, Marcin Zaniew, Stefanie Weber, Yee Mang Ho, John O Connolly, Dan Wood, Carlo Maj, Alexander Stuckey, Athanasios Kousathanas, Robert Kleta, Adrian S Woolf, Detlef Bockenhauer, Adam P Levine, Daniel P Gale. Diverse ancestry whole-genome sequencing association study identifies TBX5 and PTK7 as susceptibility genes for posterior urethral valves. eLife, 2022; 11 DOI: 10.7554/eLife.74777

Zebrafish to help in search for MS drugs

September 20, 2022
The zebrafish should be known to many aquarium enthusiasts mainly because of its striking pigmentation. However, the characteristic black-blue stripes, to which the animal owes its name, only form over time. Its eyelash-sized larvae, on the other hand, are still more or less transparent. Many developmental processes in their bodies can therefore be observed under the light microscope. For this reason, they now serve as a model organism for research groups around the globe.

"At the University of Bonn, for example, we are investigating how zebrafish repair defective nerve tissue," explains Prof. Dr. Benjamin Odermatt from the Institute of Anatomy at the University Hospital Bonn. "We are also interested in this because many genes involved in this process also exist in a similar form in humans." In principle, agents that boost these repair genes in fish could thus also work in humans. However, the differences between the genetic makeup of fish and humans are often significant. The larvae are therefore sometimes of limited use in the search for new drugs.

Fish gene replaced by human gene
"We therefore took a different approach," explains Prof. Dr. Evi Kostenis from the Institute of Pharmaceutical Biology at the University of Bonn. " For a human gene known to play a role in the repair of nerve cells we looked for its counterpart in zebrafish. Then we excised this counterpart in the fish and replaced it with the human version." The new genetic material took over the function of the original zebrafish gene. "If we now find a substance that boosts the repair processes in the fish with the human gene, there is a good chance that this will also be the case in humans," says the scientist, who is also a member of the Transdisciplinary Research Area "Life and Health" at the University of Bonn.

The researchers demonstrated that this replacement works in their pilot study on the so-called GPR17 receptor. In humans, its overactivation can lead to diseases such as multiple sclerosis (MS). Nerve cells communicate by means of electrical signals. Their extensions are surrounded by a kind of insulating layer, a lipid-like substance called myelin. It prevents short circuits and also significantly speeds up the transmission of stimuli. This protective sheath is produced by specialized cells named oligodendrocytes. These resemble a microscopic octopus: many long arms extend from their cell body, most of which consist of myelin. Like an insulating tape, these wrap themselves around the nerve cell processes during brain development. Normally, the protective layer lasts a lifetime.

Insulating tape dispenser remain in immature state
In multiple sclerosis, however, the body's own immune system destroys the myelin layer. This results in neurological disorders, for example in speech, vision or walking. But normally there is a supply of immature oligodendrocytes in the brain for repair work. When damage occurs, they mature and patch up the hole. In multiple sclerosis, this mechanism is disrupted -- many of the cellular insulating tape donor cells remain in their immature state. The GPR17 receptor seems to bear the main blame for this: if it is activated by a molecular signal, it slows down the maturation of the oligodendrocytes.

"Zebrafish also have a GPR17 receptor," explains Dr. Jesus Gomeza, who led the study with Kostenis and Odermatt. "And there it also regulates how many oligodendrocytes mature." The researchers now replaced part of the receptor gene with its human counterpart -- namely, the very structure responsible for receiving molecular signals. "We were able to show that this new mosaic gene functions normally in the fish larvae," says Gomeza. A molecule that inhibits the human GPR17 receptor in the test tube also cranked up the formation of mature oligodendrocytes in the modified fish.

In the search for new active ingredients, substances are first tested in cell cultures. Only individual, very promising candidates are then tested in mice or other animal models. But even if they work there, tests in humans still often end soberingly. "Humanized zebrafish larvae allow many substances to be screened quickly, and with a high chance of success, since the target genes originate from humans," explains Benjamin Odermatt. "From our point of view, this is a very promising avenue for drug development."

Felix Häberlein, Enrico Mingardo, Nicole Merten, Nina-Katharina Schulze Köhling, Philip Reinoß, Katharina Simon, Anna Japp, Bhuvaneswari Nagarajan, Ramona Schrage, Cecile Pegurier, Michel Gillard, Kelly R. Monk, Benjamin Odermatt, Evi Kostenis, Jesus Gomeza. Humanized zebrafish as a tractable tool for in vivo evaluation of pro-myelinating drugs. Cell Chemical Biology, 2022; DOI: 10.1016/j.chembiol.2022.08.007

Octopuses prefer certain arms when hunting and adjust tactics to prey

September 20, 2022
Famous for their eight arms, octopuses leverage all of their appendages to move, jet through the water and capture prey. But their movements can look awkward and seemingly unplanned at times, more closely resembling aliens than earthly creatures.

"Normally when you look at an octopus for a short while, nothing is repeatable. They squirm around… and just look weird in their exploratory movements," said Trevor Wardill, an assistant professor in the College of Biological Sciences who studies octopuses and other cephalopods.

A California two-spot octopus hunts a shrimp in an experiment, striking with its second arm. Credit: Wardill Lab, University of Minnesota

For a new study in Current Biology, Wardill and colleagues investigated whether octopuses preferred certain arms over others when hunting, rather than using each arm equally. A better understanding of how they use their arms will aid efforts to develop next-generation highly manipulative soft robots.

The research team studied the California two-spot octopus, which live for about two years and grow to the size of tennis balls. Octopus arms are numbered on each side of its body, starting at the center. Researchers dropped different types of prey, including crabs and shrimp, into the tanks and recorded video as the octopuses, who were hiding in ornamental SpongeBob "dens" with one eye facing outward, lunged for the snack. Because crabs move slowly while shrimp can flick their tails to escape quickly, each type of prey potentially requires different hunting tactics.

The researchers found:
  • Octopuses used arms on the same side as the eye viewing the prey.
  • No matter what type of prey came by, each octopus attacked using the second arm from the middle.
  • When hunting crabs, octopuses pounced on the prey with a cat-like movement, leading with the second arm.
  • When hunting shrimp, the octopuses were more careful to avoid spooking the prey. They led with the second arm and after it made contact with the shrimp, they used neighbouring arms one and three to secure it.
Flavie Bidel, the lead author and a postdoctoral researcher in the lab, was shocked at how predictably octopuses began prey capture with the second arm. For creatures whose movement appears unpredictable, the hunting behaviour was actually exceedingly repeatable. One of the next steps is to study how neurons facilitate the arm movements.

"Octopuses are extremely strong. For them, to grasp and open a door is trivial, given their dexterity. If we can learn from octopuses, then we can apply that to making an underwater vehicle or soft robot application," said Wardill. Underwater vehicles inspired by octopuses could play a crucial role in deep ocean exploration.

Funding and support for this work was provided by the Office of Naval Research. The Wardill lab is based in the Ecology, Evolution and Behavior Department in CBS.

Flavie Bidel, Natalie C. Bennett, Trevor J. Wardill. Octopus bimaculoides’ arm recruitment and use during visually evoked prey capture. Current Biology, 2022; DOI: 10.1016/j.cub.2022.08.080

World first achievement in diabetes research: WSU

September 20, 2022
Distinguished Professor David Simmons has become the first ‘diabetes in pregnancy’ researcher to receive three prestigious honours in the field: the Norbert Freinkel Award, Joseph Hoet Award and, most recently, the Jørgen Pederson Award Lecture.

Professor Simmons, from Western Sydney University’s Translation Health Research Institute and Macarthur Clinical School, said that while it was a great honour to receive global recognition of his work, the accolades were simply a reflection of his passion for trying to curb the impact of diabetes on both pregnant women and the community more generally.

“I have seen first-hand the life-changing and devastating effects that poorly managed diabetes can have during pregnancy both for women and our youngest children. This condition demands the best of our research, resources and collaborations and I am honoured to be contributing to finding solutions to reduce the impact of this disease,” said Professor Simmons.

“The impact of diabetes on our community, our ‘diabetes epidemic’, is equally devastating, yet there is hope. I have seen – during more than 30 years as an endocrinologist – community-based solutions work in programs throughout the world and will continue to promote the power of community in combatting this deadly disease.”

For the prestigious Jørgen Pedersen Award, Professor Simmons presented a lecture at the annual meeting of the Diabetic Pregnancy Study Group (DPSG) in Madrid last week. The award is presented to someone chosen by the DPSG Board in recognition of outstanding contributions (including scientific publications and presentations) to the understanding and treatment of diabetes and pregnancy.

In 2020, Professor Simmons was the recipient of American Diabetes Association Norbert Freinkel Award, where he presented the Norbert Freinkel Award Lecture. The lecture is given in memory of Professor Norbert Freinkel to honour a researcher who has made outstanding contributions to the field of diabetes and pregnancy.

In addition to these two prestigious ‘diabetes in pregnancy’ awards, Professor Simmons is also the recipient of the Joseph Hoart Award, presented to a leading figure who highly contributes to the field of prevention of diabetes and its complications.

With over 350 peer review publications and research collaborations in Sweden, Europe, UK, USA, New Zealand, China and Australia, Professor Simmons is renowned for instilling in his teams a dedication to achieving results, working in collaboration and ensuring his research can be easily understood by the communities it impacts.

Professor Simmons is a Distinguished Professor of Medicine at the Western Sydney University Macarthur Clinical School, Head of the Campbelltown Hospital Endocrinology Department, Chair of the Campbelltown Hospital Clinical Council, Director of the Diabetes Obesity and Metabolism Translation Unit (DOMTRU) and Co-Director of the Diabetes Obesity and Metabolism Clinical Academic Group of the Sydney Partnership for Health, Education, Research and Enterprise (SPHERE).

Malaria spike linked to amphibian die-off

September 20, 2022
Dozens of species of frogs, salamanders and other amphibians quietly disappeared from parts of Latin America in the 1980s and 2000s, with little notice from humans, outside of a small group of ecologists. Yet the amphibian decline had direct health consequences for people, according to a study from the University of California, Davis.

The study, published in the journal Environmental Research Letters, links an amphibian die-off in Costa Rica and Panama with a spike in malaria cases in the region. At the spike's peak, up to 1 person per 1,000 annually contracted malaria that normally would not have had the amphibian die-off not occurred, the study found.

The Panamanian golden frog is endemic to Panama and is among the species whose populations collapsed following the deadly fungal pathogen "Bd." (Brian Gratwicke, Wikimedia Commons)

"Stable ecosystems underpin all sorts of aspects of human wellbeing, including regulating processes important for disease prevention and health," said lead author Michael Springborn, a professor in the UC Davis Department of Environmental Sciences and Policy. "If we allow massive ecosystem disruptions to happen, it can substantially impact human health in ways that are difficult to predict ahead of time and hard to control once they're underway."

A natural experiment
From the early 1980s to the mid-1990s, a deadly fungal pathogen called Batrachochytrium dendrobatidis, or "Bd," travelled across Costa Rica, devastating amphibian populations. This amphibian chytrid fungus continued its path eastward across Panama through the 2000s. Globally, the pathogen led to the extinction of at least 90 amphibian species, and to the decline of at least 500 additional species.

Shortly after the mass die-off of amphibians in Costa Rica and Panama, both countries experienced a spike in malaria cases.

Some frogs, salamanders and other amphibians eat hundreds of mosquito eggs each day. Mosquitoes are a vector for malaria. Scientists wondered, could the crash in amphibians have influenced the rise in malaria cases?

To find out, the researchers combined their knowledge of amphibian ecology, newly digitized public health record data, and data analysis methods developed by economists to leverage this natural experiment.

"We've known for a while that complex interactions exist between ecosystems and human health, but measuring these interactions is still incredibly hard," said co-author Joakim Weill, a Ph.D. candidate at UC Davis when the study was conducted. "We got there by merging tools and data that don't usually go together. I didn't know what herpetologists studied before collaborating with one!"

The results show a clear connection between the time and location of the spread of the fungal pathogen and the time and location of increases in malaria cases. The scientists note that while they cannot fully rule out another confounding factor, they found no evidence of other variables that could both drive malaria and follow the same pattern of die-offs.

Tree cover loss was also associated with an increase in malaria cases, but not nearly to the same extent as the loss of amphibians. Typical levels of tree canopy loss increase annual malaria cases by up to 0.12 cases per 1,000 people, compared to 1 in 1,000 for the amphibian die-off.

Trade threats
Researchers were motivated to conduct the study by concerns about the future spread of similar diseases through international wildlife trade. For instance, Batrachochytrieum salamandrivorans, or "Bsal," similarly threatens to invade ecosystems through global trade markets.

Springborn said measures that could help prevent the spread of pathogens to wildlife include updating trade regulations to better target species that host such diseases as our knowledge of threats evolve.

"The costs of putting those protective measures in place are immediate and evident, but the long-term benefits of avoiding ecosystem disruptions like this one are harder to assess but potentially massive, as this paper shows," Springborn said.

Additional co-authors include Karen Lips of University of Maryland, Roberto Ibáñez of Smithsonian Tropical Research Institute in Panamá, and Aniruddha Ghosh of UC Davis and the Alliance of Biodiversity International and CIAT in Kenya.

The study was funded by the National Science Foundation and the UC Davis institute of the Environment.

Michael R Springborn, Joakim A Weill, Karen R Lips, Roberto Ibáñez, Aniruddha Ghosh. Amphibian collapses increased malaria incidence in Central America. Environmental Research Letters, 2022; 17 (10): 104012 DOI: 10.1088/1748-9326/ac8e1d

UNSW: T cells use force to destroy cancer cells

September 15, 2022
As a part of our immune defences, cytotoxic T cells -- or killer T cells -- seek out and destroy cells that are infected or cancerous. This process is essential for the body's defence against diseases.

These specialised immune cells are armed with lytic granules containing two key components for immune attack: perforin (proteins that punch holes in the target cells) and granzymes (which gain access via these holes and ultimately kill disease-causing cells).

T cells snuggle up to targeted diseased cells and form an intimate junction between the two, called the 'cytotoxic immunological synapse'.

A research team at UNSW Sydney's EMBL Australia Node in Single Molecule Science in the School of Biomedical Sciences has found that mechanical forces generated by T cells influence how effectively perforin can punch through tumour cell membranes. In a paper published today in Developmental Cell, they describe the cell interactions and the integration of forces at both the front and rear of the cell.

The researchers detected physical forces within T cells that propel lytic granules toward the immunological synapse where their payloads are released. These forces also enable T cells to grab onto regions of the cancer cell membrane where the membranes of both immune and target cells are pulled and manipulated.

"It was very exciting to discover that, in addition to its mechanical tension and biochemical configuration, the shape of the target cell membrane plays an important role in T cell mediated cancer cell killing," said Dr Daryan Kempe at UNSW Medicine & Health who co-led the research.

By stretching and bending the membranes of tumour cells in a certain direction, T cells made it easier for perforin to punch through, but only if the membranes were bent in the right direction.

Bias towards outwardly curved cell membranes
Using human melanoma cell lines, the researchers demonstrated that perforin preferentially perforated outwardly curved tumour cell membranes, rather than inwardly curved ones. The authors think that this bias ensures that the killer payload is deliver to its intended recipient, and could also be another level of protection for the T cells from their own assault.

"As the granules arrive, their contents will be emptied at this region of the membrane that is very highly curved. That there was a bias between positively curved and negatively curved membranes was completely unexpected," said EMBL Australia Group Leader, Associate Professor Maté Biro at UNSW Medicine & Health, who was senior author and team leader.

Measuring the mechanical properties of cells
A/Prof. Maté Biro said that most of the experiments relied on delicate biophysical assays with cancer cell lines, and T cells isolated from healthy blood donors and mice. They used high precision microfluidic pumps, computer-controlled micromanipulators and micropipettes in which the pressure could be controlled independently.

"This technique really allows us to tease apart the whole integrated process because it is such a controlled method. One micropipette picks up a T cell and another picks up a tumour cell, and we bring them into contact on a microscope.

"We image the entire cytotoxic process. At the same time, because we control and know the exact pressure inside each of the micropipettes, we can also measure the mechanical properties of the cells as they are interacting and engaging in the process," said A/Prof. Biro.

This study adds to the understanding of fundamental mechanisms involved in how T cells destroy disease-causing or compromised cells in our bodies. Knowing that mechanical forces are also at play when pore-formers, like perforin, punch through target cells could also help researchers investigating how these proteins work at the molecular level.

Matt A. Govendir, Daryan Kempe, Setareh Sianati, James Cremasco, Jessica K. Mazalo, Feyza Colakoglu, Matteo Golo, Kate Poole, Maté Biro. T cell cytoskeletal forces shape synapse topography for targeted lysis via membrane curvature bias of perforin. Developmental Cell, 2022; DOI: 10.1016/j.devcel.2022.08.012

Disclaimer: These articles are not intended to provide medical advice, diagnosis or treatment.  Views expressed here do not necessarily reflect those of Pittwater Online News or its staff.