Author: ModernMedia

Categories : Cancer ExerciseTags :

Physical Exercise Concomitant with Chemotherapy Reduces Nerve Damage

On By ModernMedia
Photo by Mikhail Nilov

Many cancer medications, from chemotherapy to modern immunotherapies, attack the nerves as well as the tumour cells. Some therapies, such as oxaliplatin or vinca alkaloids, leave 70 to 90% of patients complaining of pain, balance issues, or feelings of numbness, burning or tingling. These symptoms can be very debilitating. They can disappear following cancer treatment, but in around 50% they become chronic. Specialists call it chemotherapy-induced peripheral neuropathy, or CIPN for short.

A research team led by sports scientist Dr Fiona Streckmann from the University of Basel and the German Sport University Cologne has now shown that specific exercise, concomitant to cancer therapy, can prevent nerve damage in many cases. The researchers have reported their findings in JAMA Internal Medicine.

Exercise alongside chemo

The study involved 158 cancer patients, both male and female, who were receiving treatment either with oxaliplatin or vinca-alkaloids. The researchers divided the patients at random into three groups. The first was a control group, whose members received standard care. The other two groups completed exercise sessions twice a week for the duration of their chemotherapy, with each session lasting between 15 and 30 minutes. One of these groups carried out exercises that focused primarily on balancing on an increasingly unstable surface. The other group trained on a vibration plate.

Regular examinations over the next five years showed that in the control group around twice as many participants developed CIPN as in either of the exercise groups. In other words, the exercises undertaken alongside chemotherapy were able to reduce the incidence of nerve damage by 50 to 70%. In addition, they increased the patients’ subjectively perceived quality of life, made it less necessary to reduce their dose of cancer medications, and reduced mortality in the five years following chemotherapy.

The participants receiving vinca-alkaloids and performing sensorimotor training, had the largest benefit. 

Ineffective medications

A lot of money has been invested over the years in reducing the incidence of CIPN, explains Streckmann. “This side effect has a direct influence on clinical treatment: for example, patients may not be able to receive the planned number of chemotherapy cycles that they actually need, the dosage of neurotoxic agents in the chemotherapy may have to be reduced, or their treatment may have to be terminated.”

Despite the investments made, there is no effective pharmacological treatment to date: various studies have shown that medications can neither prevent nor reverse this nerve damage. However, according to the latest estimates, USD 17 000 are spent per patient every year in the USA on treating nerve damage associated with chemotherapy. Streckmann’s assumption is that “doctors prescribe medications despite everything, because patients’ level of suffering is so high.”

Study ongoing in children’s hospitals

In contrast, the sports scientist emphasises, the positive effect of exercise has been substantiated, and this treatment is very cheap in comparison. At the moment she and her team are working on guidelines for hospitals, so that they can integrate the exercises into clinical practice as supportive therapy. In addition, since 2023 a study has been ongoing in six children’s hospitals in Germany and Switzerland (Project PrepAIR), which is intended prevent sensory and motor dysfunctions in children receiving neurotoxic chemotherapy.

“The potential of physical activity is hugely underestimated,” says Fiona Streckmann. She very much hopes that the results of the newly published study will lead to more sports therapists being employed in hospitals, in order to better exploit this potential.

Source: University of Basel

Categories : Ethics and Law HospitalsTags :

Court Finds Netcare Failed to Protect Employee Against an Abusive Surgeon

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Operating theatre manager wins her case

Photo by Bill Oxford on Unsplash

By Tania Broughton

The former manager of an operating theatre at Universitas Hospital has successfully sued Netcare for failing to protect her and take action against an abusive surgeon because, she claimed, it was well known that he was a “money spinner” for the company.

Tilana Alida Louw also sued Dr Stephen Paul Grobler but, following his sudden death in June 2022, entered into a confidential settlement agreement with the executor of his estate.

She then pursued her case against Netcare Universitas Hospital.

In a ruling this month, Bloemfontein High Court Judge Ilsa van Rhyn directed Netcare to pay her R300 000 for damages, past and future medical expenses, and to pay part of her costs on a punitive scale.

Louw was appointed as surgical theatre manager at the hospital in 2005. Her role was to oversee and manage operating theatres and theatre staff and monitor patient care.

At that time, she was warned by the then hospital manager, and others, that Grobler had an “aggressive type personality”.

She said she soon experienced first hand his temper tantrums.

In her claim, she said he had verbally abused her continually, hurling profanities, insults, using blasphemous language and obscenities at her in the presence of other operating theatre staff and even members of the public.

She said Netcare had failed to come to her assistance, in spite of her numerous requests and complaints.

Netcare had also failed to act against Grobler, even though it was common knowledge that he behaved this way.

Louw alleged that Netcare had failed in its legal duty to create a work environment free from verbal abuse and intimidation and to take reasonable care of her safety and protect her from psychological harm.

As a result she was humiliated, degraded and suffered shock, anguish, fear and anxiety. She experienced post-traumatic stress syndrome.

She wanted to be compensated for this. And she wanted Netcare to publish a written apology in a local newspaper.

Netcare defended the action. It denied that it had breached its duty to Louw and said it had taken action against Grobler.

After Louw and her witness, labour law expert Professor Halton Cheadle, testified, Netcare offered to pay her for damages and to apologise.

Louw accepted the financial offer, but she was not happy with the wording of the apology and the scale of costs tendered.

And so the trial continued.

Read the judgment

Judge van Rhyn said Louw had testified that her complaints and those of others had been largely ignored by management.

“She explained that several of the scrub nurses refused to work with Dr Grobler and she would step in and assist him during surgeries. Her sense of duty and pity for the patients, many of them being cancer patients who were in dire need of urgent and timeous surgeries, caused her to bear the brunt and endure the constant abuse.”

Louw had said she and other personnel were “not allowed” to lay complaints against Grobler because he was a “so-called money-spinner for Netcare”.

Cheadle, in his evidence, said given the number of grievances lodged against Grobler and given Netcare’s professed zero-tolerance approach to harassment, a reasonable employer would have warned Grobler about his behaviour after the first complaint and would have terminated his contract at the very least, after the third complaint.

Judge van Rhyn said Netcare’s offer of damages during the trial had been made after Louw had endured years of abuse at the hands of Grobler and eight years of litigation.

“I also agree with argument on behalf of the Plaintiff (Louw) that Netcare evidently allowed its employees to be abused by Dr Grobler for its own financial interests. Netcare was acquainted with Dr Grobler’s disgusting behaviour even prior to her (Louw’s) appointment as the unit manager,” she said.

This conduct was deserving of a punitive costs order, the judge said.

Louw had rejected the proposed apology because it contained the words “we apologise sincerely that you felt that Netcare did not sufficiently support you”.

The judge said she agreed with Louw’s perception that this did not, in its plain and ordinary meaning, convey a sincere regret and remorseful apology.

She said she had been informed during argument that Netcare had published the apology in the local newspaper.

However, she said, she would not make any order regarding the apology, because it would not be lawful in a case which was not based on defamation.

Republished from GroundUp under a Creative Commons Attribution-NoDerivatives 4.0 International License.

Read the original article

Categories : Neurology Pain ManagementTags :

Researchers Figure out How Propofol Makes Patients Lose Consciousness

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Photo by Anna Shvets on Pexels

There are many drugs that anaesthesiologists can use to induce unconsciousness in patients. Exactly how these drugs cause the brain to lose consciousness has been a longstanding question, but MIT neuroscientists have now answered that question for the commonly used drug propofol.

Using a novel technique for analysing neuron activity, the researchers discovered that the drug propofol induces unconsciousness by disrupting the brain’s normal balance between stability and excitability. The drug causes brain activity to become increasingly unstable, until the brain loses consciousness.

“The brain has to operate on this knife’s edge between excitability and chaos. It’s got to be excitable enough for its neurons to influence one another, but if it gets too excitable, it spins off into chaos. Propofol seems to disrupt the mechanisms that keep the brain in that narrow operating range,” says Earl K. Miller, the Picower Professor of Neuroscience and a member of MIT’s Picower Institute for Learning and Memory.

The new findings, published in Neuron, could help researchers develop better tools for monitoring patients as they undergo general anaesthesia.

Miller and Ila Fiete, a professor of brain and cognitive sciences, the director of the K. Lisa Yang Integrative Computational Neuroscience Center (ICoN), and a member of MIT’s McGovern Institute for Brain Research, are the senior authors of the new study. MIT graduate student Adam Eisen and MIT postdoc Leo Kozachkov are the lead authors of the paper.

Losing consciousness

Propofol is a drug that binds to GABA receptors in the brain, inhibiting neurons that have those receptors. Other anaesthesia drugs act on different types of receptors, and the mechanism for how all of these drugs produce unconsciousness is not fully understood.

Miller, Fiete, and their students hypothesised that propofol, and possibly other anaesthesia drugs, interfere with a brain state known as “dynamic stability.” In this state, neurons have enough excitability to respond to new input, but the brain is able to quickly regain control and prevent them from becoming overly excited.

Previous studies of how anaesthesia drugs affect this balance have found conflicting results: Some suggested that during anaesthesia, the brain shifts toward becoming too stable and unresponsive, which leads to loss of consciousness. Others found that the brain becomes too excitable, leading to a chaotic state that results in unconsciousness.

Part of the reason for these conflicting results is that it has been difficult to accurately measure dynamic stability in the brain. Measuring dynamic stability as consciousness is lost would help researchers determine if unconsciousness results from too much stability or too little stability.

In this study, the researchers analysed electrical recordings made in the brains of animals that received propofol over an hour-long period, during which they gradually lost consciousness. The recordings were made in four areas of the brain that are involved in vision, sound processing, spatial awareness, and executive function.

These recordings covered only a tiny fraction of the brain’s overall activity, so to overcome that, the researchers used a technique called delay embedding. This technique allows researchers to characterize dynamical systems from limited measurements by augmenting each measurement with measurements that were recorded previously.

Using this method, the researchers were able to quantify how the brain responds to sensory inputs, such as sounds, or to spontaneous perturbations of neural activity.

In the normal, awake state, neural activity spikes after any input, then returns to its baseline activity level. However, once propofol dosing began, the brain started taking longer to return to its baseline after these inputs, remaining in an overly excited state. This effect became more and more pronounced until the animals lost consciousness.

This suggests that propofol’s inhibition of neuron activity leads to escalating instability, which causes the brain to lose consciousness, the researchers say.

Better anesthesia control

To see if they could replicate this effect in a computational model, the researchers created a simple neural network. When they increased the inhibition of certain nodes in the network, as propofol does in the brain, network activity became destabilized, similar to the unstable activity the researchers saw in the brains of animals that received propofol.

“We looked at a simple circuit model of interconnected neurons, and when we turned up inhibition in that, we saw a destabilization. So, one of the things we’re suggesting is that an increase in inhibition can generate instability, and that is subsequently tied to loss of consciousness,” Eisen says.

As Fiete explains, “This paradoxical effect, in which boosting inhibition destabilises the network rather than silencing or stabilising it, occurs because of disinhibition. When propofol boosts the inhibitory drive, this drive inhibits other inhibitory neurons, and the result is an overall increase in brain activity.”

The researchers suspect that other anesthetic drugs, which act on different types of neurons and receptors, may converge on the same effect through different mechanisms – a possibility that they are now exploring.

If this turns out to be true, it could be helpful to the researchers’ ongoing efforts to develop ways to more precisely control the level of anaesthesia that a patient is experiencing. These systems, which Miller is working on with Emery Brown, the Edward Hood Taplin Professor of Medical Engineering at MIT, work by measuring the brain’s dynamics and then adjusting drug dosages accordingly, in real-time.

“If you find common mechanisms at work across different anaesthetics, you can make them all safer by tweaking a few knobs, instead of having to develop safety protocols for all the different anaesthetics one at a time,” Miller says. “You don’t want a different system for every anesthetic they’re going to use in the operating room. You want one that’ll do it all.”

The researchers also plan to apply their technique for measuring dynamic stability to other brain states, including neuropsychiatric disorders.

“This method is pretty powerful, and I think it’s going to be very exciting to apply it to different brain states, different types of anaesthetics, and also other neuropsychiatric conditions like depression and schizophrenia,” Fiete says.

Source: MIT

Categories : Diet and Nutrition Metabolic DisordersTags :

Caution Advised in Following High-protein ‘Paleo’ Diets

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Photo by Jose Ignacio Pompe on Unsplash

High-protein diets, known as ‘‘Paleolithic diets’’, are popular. Using mouse models, scientists at the University of Geneva (UNIGE) have studied their impact. While effective in regulating weight and stabilizing diabetes, these diets are not without risks. Excess protein greatly increases ammonium production, overwhelming the liver. Excess ammonium can cause neurological disorders and, in severe cases, lead to coma. These results, published in the Journal of Biological Chemistry, suggest caution when following these diets.

While current treatments help control the progression of the type 2 diabetes, they do not cure it. Losing weight is often an essential part of the treatment.

‘‘Diets rich in animal and/or plant proteins, known as Paleolithic diets, can be used to stabilise type 2 diabetes and regulate weight,’’ explains Pierre Maechler, full professor at the Department of Cell Physiology and Metabolism at the UNIGE Faculty of Medicine, who led this research. These diets are inspired by the meat-based diets of pre-agricultural time. ‘‘But what impact do they have on the body? Are they harmless? That’s what we set out to find out.’’

Liver under Pressure

Ammonium is a normal waste product of protein breakdown, essentially eliminated in the liver by the enzyme glutamate dehydrogenase (GDH). In the event of protein overload, the GDH enzyme comes under pressure. To study the impact of high-protein diets, Pierre Maechler’s team fed healthy mice and mice lacking the GDH enzyme in their liver a diet with a protein content mimicking the so-called Paleolithic diet.

Scientists observed that in healthy mice, although excess protein increased ammonium production, the liver managed this excess due to the action of the GDH enzyme, which detoxifies ammonium before it can cause damage. ‘‘In contrast, in mice lacking the GDH enzyme, the liver is unable to eliminate the excess of toxic ammonium derived from proteins. No need to wait for weeks or months; a change of diet lasting a few days is enough to observe major consequences,’’ explains Karolina Luczkowska, a former PhD student at the Department of Cell Physiology and Metabolism at the UNIGE Faculty of Medicine, and the study’s first author.

Caution is Advised

These results suggest that in case of dysfunctional GDH enzyme, high-protein diets may cause a harmful excess of ammonium. Ammonium not eliminated by the liver can cause severe disorders, particularly neurological ones. A blood test could assess GDH activity to avoid overloading the metabolism with proteins in people whose GDH enzyme is deficient. ‘‘It is therefore important to be well informed before following a high-protein diet,’’ concludes Pierre Maechler.

Source: Université de Genève

Categories : PaediatricsTags :

Siblings of Autistic Children have Higher Risk of Autism

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Photo by Ben Wicks on Unsplash

Siblings of autistic children have a 20% chance of being autistic themselves – about seven times higher than the rate in infants with no autistic siblings, according to new research published in Pediatrics.

The study, by UC Davis MIND Institute distinguished professor Sally Ozonoff and the Baby Siblings Research Consortium, is based on a large, diverse group of families at research sites across the United States, Canada, and the United Kingdom. It confirms the same research group’s 2011 findings about the likelihood of autism in siblings, and adds news information suggesting it is more common, not less, in historically underrepresented groups.

Increasing autism rates prompt new study

“The rate of autism diagnosis in the general community has been steadily increasing since our previous paper was published,” Ozonoff explained. Ozonoff has studied the recurrence of autism in families for decades.

The latest estimates from the Centers for Disease Control and Prevention show that about 1 in 36 children has autism.  In 2011, the estimate was 1 in 68.

Ozonoff noted that there have also been changes in autism diagnostic criteria over the past decade. In addition, there is a growing awareness of autism in girls.

“So, it was important to understand if these had any impact on the likelihood of autism recurrence within a family,” she said.

The 2011 paper found a recurrence rate of 18.7%, while the new paper found a rate of 20.2% – a small but not significant increase.

“This should reassure providers who are counseling families and monitoring development. It should also help families plan for and support future children,” Ozonoff said.

A larger, more diverse study

The new study included data from 1605 infants at 18 research sites. All infants had an older autistic sibling.

“This study was much larger than the first and included more racially diverse participants,” Ozonoff said. The original study included 664 children.

Researchers followed the children from as early as six months of age for up to seven visits. Trained clinicians assessed the children for autism at age three using the Autism Diagnostic Observation Schedule (ADOS-2), a well-validated tool. The data were gathered from 2010 to 2019.

Sex of first autistic child, multiple autistic siblings key factors

Researchers found that the sex of the first autistic child influenced the likelihood that autism would recur within a family.

“If a family’s first autistic child was a girl, they were 50% more likely to have another child with autism than if their first autistic child was a boy,” Ozonoff said. “This points to genetic differences that increase recurrence likelihood in families who have an autistic daughter.”  

The researchers also found that a child with multiple autistic siblings has a higher chance of autism (37%) than a child with only one sibling on the spectrum (21%).

The sex of the infant was also associated with the likelihood of familial recurrence. If the later-born infant was a boy, they were almost twice as likely as a girl to be diagnosed themselves.

“The familial recurrence rate if the new baby was a boy was 25%, whereas it was 13% if the new baby was a girl,” Ozonoff explained. “This is in line with the fact that boys are diagnosed with autism about four times as often as girls in general.”

Race, maternal education level influence recurrence

The researchers found that race and the mother’s education level were likely factors as well. In non-white families, the recurrence rate was 25%. In white families, the recurrence rate was about 18%. In families where the mother had a high school education or less, recurrence was 32%. With some college, the rate was 25.5%, and with a college degree the rate was 19.7%. When the mother had a graduate degree, it dropped to 16.9%.

“These findings are new – and critical to replicate,” Ozonoff explained. “They do mirror the recent CDC findings that autism is more prevalent in children of historically underrepresented groups.” She noted that this reversed a longtime trend of lower prevalence in those groups. 

Most importantly, said Ozonoff, if these findings are replicated, they may indicate that there are social determinants of health that may lead to higher rates of autism in families. She emphasized that this study was not designed to answer those critical questions, and more research is needed.

Tracking outcomes

Unlike the first study, the researchers also tracked families who dropped out of the three-year study to see if their outcomes differed from those who did. “We wondered whether families who stayed in the study may have had children who were more affected — making them more worried about their development,” she explained.

That could have biased the estimates of recurrence to be higher than they really were. The current study showed that was not the case.

“So, now we have two large, independent studies that report familial recurrence in the same range,” Ozonoff said. “This reinforces how important it is that providers closely monitor the siblings of autistic children for delays in social development or communication. This is especially true in families who have reduced access to care, because early diagnosis and intervention are critical.”

Categories : CancerTags :

Why are Some Cancers Resistant Even Before the First Treatment?

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Squamous cancer cell being attacked by cytotoxic T cells. Image by National Cancer Institute on Unsplash

In cancer, it is well known that small numbers of drug-resistant cells likely exist in tumours even before they’re treated. In something of a paradox, before treatment, these mutants have been repeatedly shown to have lower fitness than the surrounding ancestor cells from which they arose. It leads to a scenario that seems to break Darwin’s rules. Why is it that these least-fit cells survive?

In a new study published in PRX Life, researchers at Case Western Reserve University and Cleveland Clinic reveal a fascinating discovery: interactions between these mutants and their ancestors, like two species in an ecosystem, may hold the key to understanding this paradox.

Their findings suggest these ecological interactions play a pivotal role in reducing the costs of resistance, providing a path to survival for preexisting resistance. And not just in lung cancer, but across various biomedical contexts where drug resistance is a challenge, including other cancers, pathogens and even parasites.

The study

Combining computer simulations and analytical results, the study establishes a mathematical framework to examine the impact of these ecological interactions on the evolutionary dynamics of resistance.

“This is a really exciting finding because it settles some fundamental disagreements between classical population genetics and theoretical ecology,” said the study’s principal investigator Jacob Scott, staff physician-scientist at Cleveland Clinic and an associate professor of physics and medicine at Case Western Reserve.

The study also highlights the clinical relevance of these findings by genetically engineering common resistance mechanisms observed in non-small-cell lung cancer, a disease notorious for preexisting resistance to targeted therapies.

Each genetically engineered cancer cell line experienced a benefit from being with its ancestor, in the group’s evolutionary game assay when cultured with their treatment sensitive ancestor, just as the new theory predicted, bringing closure to the paradox.

“Our findings offer an attractive new hypothesis for why treatment resistance is so common: The resistant cells are saved from extinction by the other cells surrounding them through an ecological mechanism,” said Jeff Maltas, the study’s lead author and a post-doctoral fellow at Case Western Reserve. “These results provide a novel treatment strategy: designing treatments that disrupt the ecological interaction that allows resistance to gain a foothold in the first place, rather than developing new drugs for increasingly resistant populations.”

The hope is that this multidisciplinary research may lead to innovative approaches to fighting cancer and infectious diseases, the researchers said.

Source: Case Western Reserve University

Categories : Metabolic DisordersTags :

New Method Could Boost GLP-1 Agonists While Reducing Side Effects

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Photo by I Yunmai on Unsplash

By modulating a network of proteins found in the central nervous system, the effectiveness and reduce the side effects of glucagon-like peptide (GLP)-1 agonists.

The study, published in the Journal of Clinical Investigation, focused on two proteins called melanocortin 3 and melanocortin 4 found primarily on the surface of neurons in the brain that play a central role in regulating feeding behaviour and maintaining the body’s energy balance.

Melanocortin 3 and melanocortin 4 impact everything from sensing long-term energy stores to processing signals from the gut regarding short-term fullness, or satiety, said U-M physiologist Roger Cone, who led the study.

The GLP-1 agonist class, which includes semaglutides and tirzepatides, has received substantial attention recently for their effectiveness in treating not only type 2 diabetes, but also obesity, heart disease and potentially addiction. They work by mimicking a natural satiation hormone, triggering the brain to reduce feeding behaviour.

“So the obvious question for us was: How do these GLP-1 drugs, which work by manipulating satiety signals, function when we prime the melanocortin system?” said Cone, professor of molecular and integrative physiology at the U-M Medical School and director of the U-M Life Sciences Institute where his lab is located.

Working in mouse models, Cone and his colleagues tested the effects of several hormones that reduce food intake. They compared the results in normal mice with mice that genetically lacked the MC3R protein, in mice that were given chemicals to block the activity of MC3R, and in mice that were given a drug to increase the activity of MC4R. (Because MC3R is a natural negative regulator of MC4R, meaning it decreases the activity of MC4R, blocking MC3R and increasing MC4R activity has similar effects.)

In all cases, Naima Dahir, first author of the study and a postdoctoral research fellow in Cone’s lab, and colleagues found that adjusting the melanocortin system – either by inhibiting MC3R or increasing MC4R activity – made the mice more sensitive to GLP-1 drugs and other hormones that affect feeding behaviour. The mice that were given a GLP-1 drug in combination with an MC4R agonist or MC3R antagonist showed up to five times more weight loss and reduced feeding than mice receiving only the GLP-1 drugs.

“We found that activating the central melanocortin system hypersensitises animals to the effects of not just GLP-1s, but to every anti-feeding hormone we tested,” Cone said.

The researchers also measured activity in parts of the brain thought to trigger nausea in response to GLP-1 drugs and observed no increased activation when GLP-1 drugs were combined with alterations to the melanocortin system. In contrast, priming of the melanocortin neurons significantly increased GLP-1 drug activation of neurons in hypothalamic feeding centres in the brain.

The findings indicate that pairing the existing GLP-1 drugs with an MC4R agonist could increase sensitivity to the desired effects of the drugs by up to fivefold, without increasing unwanted side effects. Ultimately, this approach could enable patients who are sensitive to the side effects to take a lower dose, or could improve the results in patients who have not responded to the existing drug dosages. Further drug development and clinical testing are needed before this can occur.

While this research has been conducted only in mouse models, Cone is optimistic that the results will translate well to humans.

“The melanocortin system is highly conserved in humans,” he said. “Everything we’ve observed in the mouse over the past decades studying these proteins has also been found in humans, so I suspect that these results would also be translatable to patients.”

Source: University of Michigan

Categories : Respiratory DiseasesTags :

Respiratory Bacteria ‘Turns off’ Immune System to Survive

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Scanning electron microscope image of bacteria responsible for Haemophilus influenzae type B infections. Photographer Alain Grillet. Copyright Sanofi Pasteur

Researchers from The University of Queensland have identified how a common bacterium is able to manipulate the human immune system during respiratory infections and cause persistent illness.

The research, led by Professor Ulrike Kappler from UQ’s School of Chemical and Molecular Biosciences, studied the virulence mechanisms of Haemophilus influenzae, a bacterium that plays a significant role in worsening respiratory tract infections.

“These bacteria are especially damaging to vulnerable groups, such as those with cystic fibrosis, asthma, the elderly, and Indigenous communities,” Professor Kappler said.

“In some conditions, such as asthma and chronic obstructive pulmonary disease, they can drastically worsen symptoms.

“Our research shows the bacterium persists by essentially turning off the body’s immune responses, inducing a state of tolerance in human respiratory tissues.”

Professor Kappler said the bacterium had a unique ability to ‘talk’ to and deactivate the immune system, convincing it there was no threat.

The researchers prepared human nasal tissue in the lab, growing it to resemble the surfaces of the human respiratory tract, then monitored gene expression changes over a 14-day ‘infection’.

They found limited production of inflammation molecules over time, which normally would be produced within hours of bacteria infecting human cells.

“We then applied both live and dead Haemophilus influenzae, showing the dead bacteria caused a fast production of the inflammation makers, while live bacteria prevented this,” Professor Kappler said.

“This proved that the bacteria can actively reduce the human immune response.”

Co-author and paediatric respiratory physician Emeritus Professor Peter Sly from UQ’s Faculty of Medicine, said the results show how Haemophilus influenzae can cause chronic infections, essentially living in the cells that form the surface of the respiratory tract.

“This is a rare behaviour that many other bacteria don’t possess,” Emeritus Professor Sly said.

“If local immunity drops, for example during a viral infection, the bacteria may be able to ‘take over’ and cause a more severe infection.”

The findings will lead to future work towards new treatments to prevent these infections by helping the immune system to recognise and kill these bacteria.

“We’ll look at ways of developing treatments that enhance the immune system’s ability to detect and eliminate the pathogen before it can cause further damage,” Professor Kappler said.

The research was published in PLOS Pathogens.

Source: University of Queensland

Categories : COVID Diet and NutritionTags :

American Diets got (Briefly) Healthier During the COVID Pandemic

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Photo by Jonathan Borba

American diets may have gotten healthier and more diverse in the months following the start of the COVID-19 pandemic, according to a new study led by Penn State researchers.

The study, published in PLOS ONE, found that as states responded to the pandemic with school closures and other lockdown measures, citizens’ diet quality improved by up to 8.5% and food diversity improved by up to 2.6%.

Co-author Edward Jaenicke, professor of agricultural economics in the College of Agricultural Sciences, said the findings provide a snapshot of what Americans’ diet and eating habits might look like in the nearly complete absence of restaurant and cafeteria eating.

“When dine-in restaurants closed, our diets got a little more diverse and a little healthier,” Jaenicke said. “One post-pandemic lesson is that we now have some evidence that any future shifts away from restaurant expenditures, even those not caused by the pandemic, could improve Americans’ food diversity and healthfulness.”

Prior to the pandemic, the researchers said, the average US diet was considered generally unhealthy. According to the Dietary Guidelines for Americans, eating patterns in the US have remained far below the guidelines’ recommendations, with only slight improvements in the population’s average Healthy Eating Index score between 2005 and 2016.

Also, before the pandemic, the research team was in the midst of a grant-funded project that asked how people would feed themselves after a giant global catastrophe, such as an asteroid strike or nuclear war. In particular, Jaenicke’s team was tasked with investigating how consumers and food retailers might behave during such a disaster.

“At first, the most impactful events we could study using actual, real-world data were hurricanes and other natural disasters,” Jaenicke said. “But then, along came the COVID-19 pandemic, and we realised that this event was an opportunity to study the closest thing we had to a true global catastrophe.”

For the study, the researchers analyzed data from the NielsenIQ Homescan Consumer Panel on grocery purchases, which includes 41,570 nationally representative U.S. households. Data consisted of the quantity and price paid for every universal product code each family purchased during the study period.

Data was gathered from both before the pandemic hit and after the pandemic led to schools, restaurants and other establishments temporarily closing. Because states did not respond to the pandemic simultaneously, the researchers designated each household’s post-pandemic period as the weeks following the date that their county of residence closed schools in 2020.

Jaenicke noted that this allowed the team to show a true causal effect of the pandemic school closures, which generally occurred around the same time that restaurants and other eateries also closed.

“To establish causality, an individual household’s pre- and post-pandemic food purchases were first compared to the same household’s food purchases from one year earlier,” Jaenicke said. “This way, we controlled for the food-purchasing habits, preferences and idiosyncrasies of individual households.”

The researchers found that in the two to three months following pandemic-based school closures (roughly March to June 2020) there were modest increases in Americans’ food diversity, defined as how many different categories of food a person eats over a period of time.

They also found larger, temporary increases in diet quality, meaning the foods purchased were healthier. This was measured by how closely a household’s purchases adhered to the U.S. Department of Agriculture’s (USDA) Thrifty Food Plan, which was designed to meet the requirements of the recommended healthy diet according to the Dietary Guidelines for Americans.

These patterns were found across households with many different demographics; however, those households with young children, lower incomes and without a car exhibited smaller increases in these measures.

“During the COVID-19 pandemic, dine-in restaurants closed, schools and school cafeterias closed, and many supermarket shelves were empty,” Jaenicke said. “Since about 50% of Americans’ food dollars are spent on ‘away from home’ food from restaurants and cafeterias, the pandemic was a major shock to the food system.”

The researchers said there are several possible explanations for these findings. First, because other studies have found that food from restaurants is often less healthy than food made at home, the dramatic decrease of meals eaten at and purchased from restaurants during the pandemic could have contributed to an increase of food diversity and healthfulness at home.

Second, they said it was possible that a global pandemic triggered some consumers to become more health conscious and contributed to them buying healthier, more diverse groceries. Third, because the pandemic caused widespread disruptions to the supply chain, it’s possible that when familiar products were sold out, consumers shifted to newer ones that led to increased diversity and healthfulness.

Finally, school and business closures may have led to many households having more time to cook and prepare foods than they had before, while others – like those with small children – may have had less free time than pre-pandemic.

Jaenicke said that in the future, additional studies could continue to explore how different disasters affect purchasing and eating habits.

Douglas Wrenn, associate professor of environmental and resource economics at Penn State, and Daniel Simandjuntak, research associate at Newcastle University, were also co-authors on the study.

Open Philanthropy helped support this research.

Source: University of Pennsylvania

Categories : Diseases, Syndromes and Conditions Environmental EffectsTags :

Does Air Pollution Affect Lupus Risk?

On By ModernMedia
Photo by Kouji Tsuru on Pexels

New research published in Arthritis & Rheumatology indicates that chronic exposure to air pollutants may increase the risk of developing lupus, an autoimmune disease that affects multiple organs.

For the study, investigators analysed data on 459 815 participants from the UK Biobank. A total of 399 lupus cases were identified during a median follow-up of 11.77 years. Air pollutant exposure was linked with a greater likelihood of developing lupus. Individuals with a high genetic risk and high air pollution exposure had the highest risk of developing lupus compared with those with low genetic risk and low air pollution exposure.

“Our study provides crucial insights into the air pollution contributing to autoimmune diseases. The findings can inform the development of stricter air quality regulations to mitigate exposure to harmful pollutants, thereby reducing the risk of lupus,” said co–corresponding author Yaohua Tian, PhD, of the Huazhong University of Science and Technology, in China.

Source: Wiley