Year: 2025

Categories : NeurologyTags :

These Newly Discovered Brain Cells Enable us to Remember Objects

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Discovery of ‘ovoid cells’ reshapes our understanding of how memory works, and could open the door to new treatments for Alzheimer’s disease, epilepsy and more.

Ovoid cells. Photo credit: Dr. Mark Cembrowski

Take a look around your home and you’ll find yourself surrounded by familiar comforts – photos of family and friends on the wall, well-worn tekkies by the door, a shelf adorned with travel mementos.

Objects like these are etched into our memory, shaping who we are and helping us navigate environments and daily life with ease. But how do these memories form? And what if we could stop them from slipping away under a devastating condition like Alzheimer’s disease?

Scientists at the University of British Columbia have just uncovered a crucial piece of the puzzle. In a study published in Nature Communications, the researchers have discovered a new type of brain cell that plays a central role in our ability to remember and recognise objects. 

Called ‘ovoid cells,’ these highly-specialised neurons activate each time we encounter something new, triggering a process that stores those objects in memory and allowing us to recognise them months, even years, later.

“Object recognition memory is central to our identity and how we interact with the world,” said Dr Mark Cembrowski, the study’s senior author, and an associate professor of cellular and physiological sciences at UBC and investigator at the Djavad Mowafaghian Centre for Brain Health. “Knowing if an object is familiar or new can determine everything from survival to day-to-day functioning, and has huge implications for memory-related diseases and disorders.”

Hiding in plain sight

Named for the distinct egg-like shape of their cell body, ovoid cells are present in relatively small numbers within the hippocampus of humans, mice and other animals.

Adrienne Kinman, a PhD student in Dr Cembrowski’s lab and the study’s lead author, discovered the cells’ unique properties while analysing a mouse brain sample, when she noticed a small cluster of neurons with highly distinctive gene expression.

“They were hiding right there in plain sight,” said Kinman. “And with further analysis, we saw that they are quite distinct from other neurons at a cellular and functional level, and in terms of their neural circuitry.”

To understand the role ovoid cells play, Kinman manipulated the cells in mice so they would glow when active inside the brain. The team then used a miniature single-photon microscope to observe the cells as the mice interacted with their environment.

The ovoid cells lit up when the mice encountered an unfamiliar object, but as they grew used to it, the cells stopped responding. In other words, the cells had done their jobs: the mice now remembered the objects.

“What’s remarkable is how vividly these cells react when exposed to something new. It’s rare to witness such a clear link between cell activity and behaviour,” said Kinman. “And in mice, the cells can remember a single encounter with an object for months, which is an extraordinary level of sustained memory for these animals.”

New insights for Alzheimer’s disease, epilepsy

The researchers are now investigating the role that ovoid cells play in a range of brain disorders. The team’s hypothesis is that when the cells become dysregulated, either too active or not active enough, they could be driving the symptoms of conditions like Alzheimer’s disease and epilepsy.

“Recognition memory is one of the hallmarks of Alzheimer’s disease – you forget what keys are, or that photo of a person you love. What if we could manipulate these cells to prevent or reverse that?” said Kinman. “And with epilepsy, we’re seeing that ovoid cells are hyperexcitable and could be playing a role in seizure initiation and propagation, making them a promising target for novel treatments.”

For Dr Cembrowski, discovering the highly specialised neuron upends decades of conventional thinking that the hippocampus contained only a single type of cell that controlled multiple aspects of memory.

“From a fundamental neuroscience perspective, it really transforms our understanding of how memory works,” he said. “It opens the door to the idea that there may be other undiscovered neuron types within the brain, each with specialised roles in learning, memory and cognition. That creates a world of possibilities that would completely reshape how we approach and treat brain health and disease.”

Source: University of British Columbia

Categories : Diet and NutritionTags :

Intermittent Fasting could be Unsafe for Teenagers

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Photo by jamie he

A recent study reveals that age plays a significant role in the outcomes of intermittent fasting. Researchers from Technical University of Munich (TUM), LMU Hospital Munich, and Helmholtz Munich discovered that chronic intermittent fasting disrupted the development of insulin-producing beta cells in young mice. The findings, published in Cell Reports, raise concerns about potential risks for humans, especially teenagers.

“Intermittent fasting is known to have benefits, including boosting metabolism and helping with weight loss and heart disease. But until now, its potential side effects weren’t well understood,” says Alexander Bartelt, the Else Kröner Fresenius Professor and Chair of Translational Nutritional Medicine at TUM. In a recently published study, the team shows that intermittent fasting during adolescence could have long-term negative effects on metabolism.

Fasting improves metabolism in older mice, but not in the young

The researchers studied three groups of mice: adolescent, adult, and older animals. The mice remained without food for one day and were fed normally on two days. After ten weeks, insulin sensitivity improved in both the adult and older mice, meaning that their metabolism responded better to insulin produced by the pancreas. This is key to regulating blood sugar levels and preventing conditions like type 2 diabetes.

However, the adolescent mice showed a troubling decline in their beta cell function, the insulin-producing cells of the pancreas. Insufficient insulin production is linked to diabetes and disrupted metabolism. “Intermittent fasting is usually thought to benefit beta cells, so we were surprised to find that young mice produced less insulin after the extended fasting,” explains Leonardo Matta from Helmholtz Munich, one of the study’s lead authors.

Defective beta cells resemble those of type 1 diabetes patients

The researchers used the latest single-cell sequencing to uncover the cause of the beta cell impairment. By examining the blueprint of the pancreas, the team found that the beta cells in the younger mice failed to mature properly. “At some point, the cells in the adolescent mice stopped developing and produced less insulin,” says Peter Weber from Helmholtz Munich, also a lead author. Older mice, whose beta cells were already mature before the fasting began, remained unaffected.

This shows an accumulation of beta cells from the pancreas of an older mouse.
Beta cells from an older mouse.

The team compared their mouse findings to data from human tissues. They found that patients with type 1 diabetes, where beta cells are destroyed by an autoimmune response, showed similar signs of impaired cell maturation. This suggests that the findings from the mouse study could also be relevant to humans.

“Our study confirms that intermittent fasting is beneficial for adults, but it might come with risks for children and teenagers,” says Stephan Herzig, a professor at TUM and director of the Institute for Diabetes and Cancer at Helmholtz Munich. “The next step is digging deeper into the molecular mechanisms underlying these observations. If we better understand how to promote healthy beta cell development, it will open new avenues for treating diabetes by restoring insulin production.”

Source: Technical University of Munich (TUM)

Categories : AgeingTags :

Older Patients can Inadvertently be Put at Risk When Taken off Anticoagulants

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For patients with atrial fibrillation, the risk of stroke or heart attack from stopping anticoagulants usually outweighs the risk of bleeding, according to new findings from the University of Bath.

Clinicians often worry about the dangers of prescribing blood thinning medications to older patients, due to concerns about falls and major bleeding, however this new study suggests that for patients with the common heart condition atrial fibrillation (AF), the health risks of not taking these drugs are significantly higher than the risk of a life-threatening bleed.

AF is associated with a fivefold increase in the risk of stroke. It also increases the risk of heart attacks and death. Anticoagulants are highly effective in managing AF and preventing strokes and other complications.

Older people also tend to fall more frequently, with falls being a leading cause of injury among adults aged 65 and older. These can lead to serious injuries, such as hip fractures and head injuries.

However, the new study, published in Heart, found that contrary to popular medical belief, stopping anticoagulants for patients aged 75 and over does not change the risk of major bleeds. These findings are important for clinicians to factor into their prescribing behaviour, according to the study’s authors.

“Prescribers need to consider the increased risk to patients of coming off anticoagulants, including stroke,” said Dr Anneka Mitchell, who conducted the research from the University of Bath and is a visiting researcher at the University’s Department of Life Sciences.

Rising cases

Cases of AF are rising in all age groups but particularly among people aged 85 years and over. In this age group, the number of people diagnosed with the condition doubled in men from 11.6% to 22.1% between 2000 and 2016, and increased in women from 9.6% to 16.5%. There is no data available to show trends from 2016.

Though there is a large body of evidence to support the use of blood thinners for older people with AF, the new study is believed to be the first to measure patient outcomes when anticoagulant medication is stopped.

Dr Mitchell’s study analysed data from the UK Clinical Practice Research Datalink (a research dataset that includes anonymised patient data from some UK general practices) between 2013 and 2017, focusing on patients aged 75 and older who were newly prescribed anticoagulants.

It found that the risks of stroke and death were three times higher during periods when patients were not receiving anticoagulation therapy. The risk of heart attacks was nearly double compared with periods when patients were treated with anticoagulants.

Warfarin versus direct oral anticoagulants

Dr Mitchell believes that as well as concern about falls, many clinicians base their decisions to withhold anticoagulants on the historic experience of patients taking the anticoagulant warfarin.

This medication – the only available option for treating AF until 2012 – is associated with a complex medication regimen, along with dietary restrictions and frequent blood-tests, making treatment difficult for many older patients.

Since 2013, however, a new family of drugs called direct oral anticoagulants (DOACs) have become the first line option for most patients. DOACs are as effective and safe as warfarin – sometimes more so – and are far more straightforward to take.

Dr Mitchell said: “For example, apixaban (a DOAC) has a lower risk of significant bleeding than warfarin, so for many older patients with AF, this would be an excellent medication.

“Our findings highlight the critical need for clinicians to carefully consider the risks of stopping anticoagulation therapy in older patients. Despite concerns about bleeding, this study suggests that discontinuing anticoagulation does not significantly affect the risk of major bleeding but does increase the risk of serious events such as stroke and death.”

She added: “Both the risks and benefits of medication must be discussed fully with patients before a medic stops prescribing anticoagulants, so that both doctor and patient are making a shared and informed decision. This study underscores the importance of evaluating the consequences of deprescribing anticoagulants, particularly in older adults who are at higher risk of adverse outcomes.”

Impacting the lives of older patients

Dr Anita McGrogan who led the research team from the Department of Life Sciences at Bath, said: “Older patients were poorly represented in clinical trials that evaluated the efficacy and safety of DOACs before these products were licensed, and those who were included were healthier than many people in the target group for prescribing. Because of this, the safety of these medications for people aged 75-plus was not evaluated, and many chose to avoid prescribing them for older people.

“This study has produced important results that will have an impact on patients in the future. It has filled the information gap by looking at anonymous data on 20 167 people aged over 75 years, collected by GPs. It clearly demonstrates the value of using big data to investigate important clinical questions, especially in vulnerable populations.”

Dr Tomas Welsh, an academic geriatrician at Royal United Hospitals Bath and research & medical director at ReMind, hopes the new research will provide both clinicians and patients with better evidence to inform their decisions regarding anticoagulants. He noted that, until now, clinicians advising patients to stop taking blood thinners were unable to quantify the increased risk of stroke.

“These data help patients and clinicians have a firmer grasp of the risks that they are being exposed to,” he said.

Dr Welsh also stressed that new-generation blood thinners were not always the right course of action for frail, older people.

“Suspending any medication or reducing the use of multiple medications in a frailer older patient is always a nuanced and individual discussion,” he said.

Source: University of Bath

Categories : Metabolic DisordersTags :

Mitochondria may Hold the Key to Curing Diabetes

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Cells with nuclei in blue, energy factories in green and the actin cytoskeleton in red. Credit: NIH

A new study has revealed that abnormalities in mitochondria, the powerhouses of the cell, can affect the development and maturation of pancreatic beta cells, eventually leading to them no longer being able to produced. This opens to the door to possibly restoring their function – and reversing the course of type 2 diabetes.

Mitochondrial defects are associated with the development of diseases such as type 2 diabetes. Several studies have shown that insulin-producing pancreatic β-cells of patients with diabetes have abnormal mitochondria and are unable to generate energy. Yet, these studies were unable to explain why the cells behaved this way.

In a study published in Science, University of Michigan researchers used mice to show that dysfunctional mitochondria trigger a response that affects the maturation and function of β-cells.

“We wanted to determine which pathways are important for maintaining proper mitochondrial function,” said first author Emily M. Walker, PhD, a research assistant professor of internal medicine.

To do so, the team damaged three components that are essential for mitochondrial function: their DNA, a pathway used to get rid of damaged mitochondria, and one that maintains a healthy pool of mitochondria in the cell.

“In all three cases, the exact same stress response was turned on, which caused β-cells to become immature, stop making enough insulin, and essentially stop being β-cells,” Walker said. 

“Our results demonstrate that the mitochondria can send signals to the nucleus and change the fate of the cell.”

The researchers also confirmed their findings in human pancreatic islet cells.

Mitochondrial dysfunction affects several types of cells

Their results prompted the team to expand their search into other cells that are affected during diabetes.  

Losing your β-cells is the most direct path to getting type 2 diabetes. Through our study we now have an explanation for what might be happening and how we can intervene and fix the root cause.”

-Scott A. Soleimanpour, M.D.

“Diabetes is a multi-system disease – you gain weight, your liver produces too much sugar and your muscles are affected. That’s why we wanted to look at other tissues as well,” said Scott A. Soleimanpour, M.D., director of the Michigan Diabetes Research Center and senior author of the study.

The team repeated their mouse experiments in liver cells and lipid cells and saw that the same stress response was turned on. Both cell types were unable to mature and function properly.

“Although we haven’t tested all possible cell types, we believe that our results could be applicable to all the different tissues that are affected by diabetes,” Soleimanpour said.

Reversing mitochondrial damage could help cure diabetes

Regardless of the cell type, the researchers found that damage to the mitochondria did not cause cell death. 

This observation brought up the possibility that if they could reverse the damage, the cells would function normally.

To do so, they used a drug called ISRIB that blocked the stress response. They found that after four weeks, the β-cells regained their ability to control glucose levels in mice.

“Losing your β-cells is the most direct path to getting type 2 diabetes. Through our study we now have an explanation for what might be happening and how we can intervene and fix the root cause,” Soleimanpour said.

The team is working on further dissecting the cellular pathways that are disrupted and hope that they will be able to replicate their results in cell samples from diabetic patients.

Source: Michigan Medicine – University of Michigan

Categories : Hospitals Respiratory DiseasesTags :

Global Action Needed to Solve the Medical Oxygen Crisis

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Targets for universal access, national roadmaps and more affordable and accessible care are vital to help fill the medical oxygen gap affecting more than half of the world’s population, according to a new global report.

The Lancet Global Health Commission report details for the first time how future investment in strengthening medical oxygen systems could have a huge impact by saving millions of lives and improving pandemic preparedness.

Almost 400 million children and adults require medical oxygen every year. More than five billion people, 60 per cent of the world’s population, don’t have access to safe and affordable medical oxygen services.

The Commission, co-chaired by Makerere University in Uganda, the International Centre for Diarrheal Disease Research (icddr,b) in Bangladesh, Murdoch Children’s Research Institute (MCRI) in Australia, Karolinska Institute in Sweden and the Every Breath Counts Coalition in the US was launched in 2022 against the backdrop of the COVID-19 pandemic. The Commission was tasked with submitting actionable recommendations for governments, industry, global health agencies, donors and the healthcare workforce.

MCRI Dr Hamish Graham said the COVID-19 pandemic had put a spotlight on the longstanding global inequities in accessing medical oxygen.

“Oxygen is required at every level of the healthcare system for children and adults with a wide range of acute and chronic conditions,” he said. Previous efforts, including the major investments in response to the COVID-19 pandemic, largely focused on the delivery of equipment to produce more oxygen, neglecting the supporting systems and people required to ensure it was distributed, maintained, and used safely and effectively.”

Dr Graham said channelling investments into national oxygen plans and bolstering health systems, including wider use of pulse oximeters (a small device that measures how much oxygen is in the blood), would help solve the medical oxygen crisis.

“We urgently need to make high-quality, pulse oximeters more affordable and widely accessible,” he said. Pulse oximeters are available in 54 per cent of general and 83 per cent of tertiary hospitals in low- and middle-income countries, with frequent shortages and equipment breakdowns.

“Concerningly, in these countries the devices are performed for only 20 per cent of patients presenting to general hospitals and almost never for those at primary healthcare facilities. We see the greatest inequities in small and rural government health facilities and across Sub-Saharan Africa.”

Dr Graham said the importance of medical oxygen must also be recognised and integrated into broader national strategies and pandemic preparedness and response planning.

“Governments should bring together public and private sector partners with a stake in medical oxygen delivery, including health, education, industry, energy and transport to design a system and set up a governance structure that supports the new Global Oxygen Alliance (GO₂AL) and replenishing The Global Fund with a strong oxygen access mandate,” he said.

Source: Murdoch Childrens Research Institute

Categories : Diet and Nutrition Mental HealthTags :

Calorie Labels on Menus could Make Eating Disorders Worse

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Calorie labels on restaurant menus are negatively impacting people with eating disorders, according to a new study published in the BMJ Public Health.

The review, which is the first of its kind, is led by researchers at King’s College London. It found that individuals who have been diagnosed with an eating disorder changed their behaviours if presented with a menu featuring calorie labels.

This included avoiding restaurants, triggering eating disorder thoughts and paying more attention to calorie labels as identified by eye tracking research.

The research found that some people with eating disorders reported that seeing menu labels reinforced their eating disorder beliefs.

The study evaluated existing research to help build a picture of how nutritional labels on menus impact people with a lived experience of eating disorders or disordered eating. It reviewed 16 studies from the UK, US, Canada and Saudi Arabia which included 8,074 participants in total.

The study highlights that people with eating disorders can feel that eating disorders are perceived as less important in the light of obesity prevention policies.

However, physical health cannot be measured by a single indicator such as weight. Some argue that calorie labels can be seen as a blunt instrument to fix a complicated problem and that people with eating disorders could be losing out.

Food labelling came into force in England in 2022. Restaurants, take-aways and cafes with 250 employees or more must display the calories of the food and drink they sell on menus, online menus and take-away platforms. The measure was an attempt to curb rising obesity levels. The United States and Canada have also made calorie displays mandatory, however, few policies targeting obesity have considered the potential impact on eating disorders.

The eating disorder charity Beat estimates that at least 1.25 million people in the UK have an eating disorder. The number of people admitted to hospital with an eating disorder has risen approximately 7% each year since 2005 – 2006.

Senior author Dr Tom Jewell, Lecturer in Mental Health Nursing at King’s College London, said: “Our study highlights that people with lived experience of eating disorders are frustrated at being left out of the conversation around calorie labels.”

Striking a balance between the positive and harmful impacts of calorie labels on menus is vital in any public health policies.Dr Tom Jewell, Senior author and Lecturer in Mental Health Nursing at King’s College London

“Policymakers should consider the impact on both obesity and eating disorders when making decisions about nutrition labelling. A recent review found that calorie labelling has a modest effect on people’s behaviour but this needs to be counterbalanced with the potential harm it does for people with eating disorders.”

Co-author Dr Nora Trompeter, Research Fellow University College London, said: “Our study provides an important addition to the evidence base around calorie labels.”

Typically, there is a lot of focus on whether policies are effective in reducing obesity, but it is also critical to investigate whether these policies inadvertently harm people with eating disorders.

“Our review also shows that more research is needed to fully understand the impact of calorie labels on individuals with eating disorders. For example, none of the studies included young people.”

Source: King’s College London

Categories : Diet and Nutrition NeurologyTags :

‘Healthy’ Vitamin B12 Levels not Enough to Ward off Neuro Decline

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Meeting the minimum requirement for vitamin B12, needed to make DNA, red blood cells and nerve tissue, may not actually be enough – particularly if for older adults. It may even put them at risk for cognitive impairment, according to a study published in Annals of Neurology.

The research found that older, healthy volunteers, with lower concentrations of B12, but still in the normal range, showed signs of neurological and cognitive deficiency. These levels were associated with more damage to the brain’s white matter – the nerve fibres that enable communication between areas of the brain – and test scores associated with slower cognitive and visual processing speeds, compared to those with higher B12.

The UC San Francisco researchers, led by senior author Ari J. Green, MD, of the Departments of Neurology and Ophthalmology and the Weill Institute for Neurosciences, said that the results raise questions about current B12 requirements and suggest the recommendations need updating.

“Previous studies that defined healthy amounts of B12 may have missed subtle functional manifestations of high or low levels that can affect people without causing overt symptoms,” said Green, noting that clear deficiencies of the vitamin are commonly associated with a type of anaemia. “Revisiting the definition of B12 deficiency to incorporate functional biomarkers could lead to earlier intervention and prevention of cognitive decline.”

Lower B12 correlates with slower processing speeds, brain lesions

In the study, researchers enrolled 231 healthy participants without dementia or mild cognitive impairment, whose average age was 71. They were recruited through the Brain Aging Network for Cognitive Health (BrANCH) study at UCSF.

Their blood B12 amounts averaged 414.8pmol/L, well above the U.S. minimum of 148pmol/L. Adjusted for factors like age, sex, education and cardiovascular risks, researchers looked at the biologically active component of B12, which provides a more accurate measure of the amount of the vitamin that the body can utilize. In cognitive testing, participants with lower active B12 were found to have slower processing speed, relating to subtle cognitive decline. Its impact was amplified by older age. They also showed significant delays responding to visual stimuli, indicating slower visual processing speeds and general slower brain conductivity.

MRIs revealed a higher volume of lesions in the participants’ white matter, which may be associated with cognitive decline, dementia or stroke.

While the study volunteers were older adults, who may have a specific vulnerability to lower levels of B12, co-first author Alexandra Beaudry-Richard, MSc, said that these lower levels could “impact cognition to a greater extent than what we previously thought, and may affect a much larger proportion of the population than we realize.” Beaudry-Richard is currently completing her doctorate in research and medicine at the UCSF Department of Neurology and the Department of Microbiology and Immunology at the University of Ottawa.

“In addition to redefining B12 deficiency, clinicians should consider supplementation in older patients with neurological symptoms even if their levels are within normal limits,” she said. “Ultimately, we need to invest in more research about the underlying biology of B12 insufficiency, since it may be a preventable cause of cognitive decline.”

Source: University of California – San Francisco

Categories : General InterestTags :

Dating is Not Broken, but the Trajectories of Relationships have Changed

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Despite many societal changes, including technology such as dating apps and young adults waiting longer to get married, two surveys of college students conducted 10 years apart showed that their expectations about romantic relationships have remained remarkably consistent, according to a new study led from the University of Illinois Urbana-Champaign

According to some popular culture writers and online posts by discouraged singles lamenting their inability to find romantic partners, dating is “broken,” fractured by the social isolation created by technology, pandemic lockdowns and potential partners’ unrealistic expectations.

Yet two studies of college students conducted a decade apart found that their ideas about romantic relationships have remained much the same, although the trajectories of their relationships have changed somewhat, according to study leader Brian Ogolsky, a professor of human development and family studies at the University of Illinois Urbana-Champaign.

“College students in our study did not share this perception of dating as a broken system, despite many massive cultural shifts during this decade,” Ogolsky said. “Their perspectives on relationships today aren’t that different from what they were 10 years ago — or even 10 years before that. Instead, young adults are taking more diverse and multifaceted pathways through romantic partnering and considering a broader range of outcomes.”

Ogolsky surveyed college students ages 18-29 in 2012 and in early 2022, asking them to describe their thoughts and experiences about the typical initiation and progression of romantic relationships.

Published in the journal Personal Relationships, the study was co-written by Jennifer L. Hardesty, a professor in the same department; psychology professor Kiersten Dobson of McMaster University; and U. of I. graduate students Matthew Rivas-Koehl and Ghada Kawas.

More than 250 students were surveyed, about half of whom said they had romantic partners at the time.

Based upon participants’ responses, the researchers identified four stages of romantic relationships. The first stage, which they called “flirtationship,” may occur online or in person and involves the first sparks of attraction, fanning those embers through flirtation and exploring common interests.

If the attraction and level of interest are mutual, the individuals test the waters for “relationship potential” — the second stage in relationship development — by spending increased time together, with a heavy focus on communicative activities that probe whether the relationship should move forward. Study participants repeatedly mentioned friendship as an important basis for romantic partnerships, and they most often mentioned dating in reference to this stage, the data indicated.

“Young adults clearly distinguish dating from being in a relationship,” Ogolsky said. “In our study, we used the term ‘relationship development’ to describe the activities we were investigating, but it became clear that participants did not view early behaviors as part of being in a relationship per se. Instead, they viewed flirting and even dating as part of a broader pattern of interpersonal interaction that may or may not eventually lead to the formation of a relationship.”

If romance does blossom and the union progresses to the third stage — being in a relationship — defining their union becomes important to the partners, such as labeling their status as “official” and identifying themselves as significant others, the researchers said.

Although those in the first study were less likely to mention sexual activity, students in both studies were more likely to talk about it in the context of defining the relationship. And the researchers found that the majority of the students in both studies implied an expectation of exclusivity and monogamy from committed relationships.

Although many studies on young adults’ relationships have focused on hookup culture — casual sex without commitment — only nine of those in the more recent study mentioned it. And the researchers hypothesized that college students may use the term when referring to sexual activity in any context, even that which occurs within a predefined relationship.

Ogolsky said it was during the third stage that the greatest differences emerged between the two groups of students’ beliefs. Those in the 2012 study were more likely to believe that the typical relationship path was for partners to become engaged after becoming official. However, those in the 2022 study rarely mentioned engagement, saying instead that commitment proceeds in more diverse pathways such as moving in together.

“Another difference we found pertained to integrating romantic partners into one’s social circle,” Ogolsky said. “For the students in 2012, this process centered around introducing a new partner to family members. However, those in the more recent study viewed it as integrating the partner into one’s broader social networks of friends as well as family members.”

In the fourth relationship stage — called “commitment or bust” — Ogolsky said that participants described arriving at an eventual crossroads, where the partners either decide to marry or enter into another type of long-term legal commitment or go their separate ways.

Surprisingly, despite the rapid growth in social media, dating apps and other platforms for meeting potential partners that proliferated across the decade between the two surveys, technology did not play as big a role in the minds of the participants as expected, Ogolsky said.

“When we ask people about relationship prototypes, they’re not talking about technology,” he said. “They’re thinking about relationships in broad strokes. And we found it interesting that the centerpiece of relationships was not dating apps, artificial intelligence or robots or all the other things we may have predicted 25 or 40 years ago.”

Source: University of Illinois at Urbana-Champaign, News Bureau

Categories : Antibiotics Metabolic DisordersTags :

Diabetes Can Drive the Evolution of Antibiotic Resistance

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Staphylococcus aureus is a leading cause of antibiotic resistance associated infections and deaths. It is also the most prevalent bacterial infection among those with diabetes mellitus, a chronic condition that affects blood sugar control and reduces the body’s ability to fight infections.

Microbiologists at the UNC School of Medicine have just shown that people with diabetes are more likely to develop antibiotic-resistant strains of Staph, too. Their results, which were published in Science Advances, show how the diabetic microbial environment produces resistant mutations, while hinting at ways antibiotic resistance can be combatted in this patient population.

“We found that antibiotic resistance emerges much more rapidly in diabetic models than in non-diabetic models of disease,” said Brian Conlon, PhD, associate professor of immunology. “This interplay between bacteria and diabetes could be a major driver of the rapid evolution and spread of antibiotic resistance that we are seeing.”

 Staph feeds off the high levels of blood glucose in diabetes, allowing it to reproduce more rapidly. The bacterium can also grow without consequence, as diabetes also impairs the immune system’s ability to destroy cells and control infection.

As the numbers of bacteria increase in a diabetic infection, so does the likelihood of resistance. Random mutations appear and some build up resistance to external stressors, like antibiotics. Once a resistant mutant is present in a diabetic infection, it rapidly takes over the population, using the excess glucose to drive its rapid growth.

“Staphylococcus aureus is uniquely suited to take advantage of this diabetic environment,” said Lance Thurlow, PhD, assistant professor of microbiology and immunology. “Once that resistant mutation happens, you have excess glucose and you don’t have the immune system to clear the mutant and it takes over the entire bacterial population in a matter of days.”

Conlon, an expert on antibiotic treatment failure, and Thurlow, an expert on Staph pathogenesis in diabetes, have long been interested in comparing the effectiveness of antibiotics in a model with and without diabetes. Using their connections within the Department of Microbiology and Immunology, the researchers brought their labs together to perform a study with antibiotics in a diabetic mouse model of S. aureus infection.

First, the team prepared a mouse model with bacterial infection in the skin and soft tissue. The mouse models were divided into two groups: one half was given a compound that selectively kills cells in the pancreas, rendering them diabetic, and the other half was not given the compound. Researchers then infected both diabetic and non-diabetic models with S. aureus and treated them with rifampicin, an antibiotic where resistance evolves at a high rate.

After five days of infection, it was time to observe the results.

Conlon and Thurlow were quick to notice that the rifampicin had practically no effect in diabetic models. So, they took some samples to investigate. Researchers were shocked to find that the bacteria had evolved to become resistant to rifampicin, with the infection harboring over a hundred million rifampicin resistant bacteria. There were no rifampicin resistant bacteria in the non-diabetic models.

Their new findings have left Conlon and Thurlow with many questions; however, they are certain that the evolution of antibiotic resistance in people with diabetes could spell trouble for the population at large.

And, even more surprisingly, the mutation had taken over the entire infection in just four days. They next inoculated diabetic and non-diabetic models with Staphylococcus aureus as before, but this time supplemented with a known number of rifampicin resistant bacteria. Again, these bacteria rapidly took over the diabetic infection, but remained as only a sub-population in non-diabetic models after 4 days rifampicin treatment.

Their new findings have left Conlon and Thurlow with many questions; however, they are certain that the evolution of antibiotic resistance in people with diabetes could spell trouble for the population at large. Antibiotic-resistant strains of bacteria spread from person to person in the same ways as other bacteria and viruses do – in the air, on doorknobs, and the food that we eat – which makes preventing these types of infections a major priority.

So, what can be done to prevent it? Well, the Conlon and Thurlow labs showed that reducing blood sugar levels in diabetic models (through administration of insulin) deprived bacteria of their fuel, keeping their numbers at bay, and reducing the chances of antibiotic-resistant mutations from occurring. Their findings suggest that controlling blood sugar through insulin use could be key in preventing antibiotic resistance.

“Resistance and its spread are not only associated with the prescription of drugs, but also the health status of those that are taking antibiotics,” said Conlon. “Controlling blood glucose then becomes really important. When we gave our mice insulin, we were able to bring their blood sugar back to normal and we didn’t get this rapid proliferation of resistant bacteria.”

Now, Conlon and Thurlow are expanding their efforts to study the evolution of resistance in humans (with and without diabetes) and other antibiotic-resistant bacteria of interest, including Enterococcus faecalis, Pseudomonas aeruginosa, and Streptococcus pyogenes. Recognizing how large a role the host plays a role in the evolution of antibiotic resistance, the researchers plan to perform similar studies in patients undergoing chemotherapy and recent transplant recipients to see if those populations are also prone to antibiotic resistant infections.

Source: University of North Carolina Health Care

Categories : Neurodegenerative Diseases PaediatricsTags :

More Sunshine as a Baby Linked to Less Disease Activity for Children with MS

On By ModernMedia
Photo by Anders Jilden on Unsplash

Getting at least 30 minutes of daily summer sun in the first year of life may mean a lower relapse risk for children who are diagnosed with multiple sclerosis (MS) later, according to a study published in Neurology® Neuroimmunology & Neuroinflammation, an official journal of the American Academy of Neurology. The study also found if a child’s biological mother had at least 30 minutes of daily sun during the second trimester of pregnancy, the child had a lower risk of MS relapses.

The study does not prove that sun lowers relapse risk for children with MS, it only shows an association. “It is important not to spend too much time in the sun without sun protection, however greater exposure to sun has been tied in previous research to a lower risk of developing MS in childhood,” said Gina Chang, MD, MPH, of The Children’s Hospital of Philadelphia and member of the American Academy of Neurology. “It’s encouraging that our study found that greater sun exposure during early development may also be beneficial in helping to reduce disease activity in children who are later diagnosed with MS.”

For the study, researchers looked at health records from 18 MS clinics across the United States to identify 334 children and young people with childhood-onset MS age four to 21. Participants were within four years of experiencing their first symptoms. The median follow-up time was 3.3 years. To determine sun exposure, participants’ parents or guardians completed questionnaires that asked how much time the participant and their biological mother had spent in the sun at various periods of life, what kind of clothing they typically wore and how often they used sunscreen.

Of the total group, 206, or 62%, experienced at least one relapse during the study. Relapses were defined as new or returning symptoms lasting for at least 24 hours and separated by at least 30 days from the last MS attack, without a fever or infection. They found that of 75 participants who had 30 minutes to an hour of daily summer sun during their first year of life, 34 children, or 45%, had a relapse.

Of the 182 participants who had less than 30 minutes of daily summer sun during their first year of life, 118 children, or 65%, had a relapse. After adjusting for factors such as tobacco exposure in the first year of life, season of birth, the type of MS medication taken and use of sun protection such as sunscreen, hats and clothing, researchers found that 30 or more minutes of daily summer sun during the first year of life was associated with a 33% lower risk of relapse compared to less than 30 minutes of daily summer sun.

Researchers also looked at sun exposure for the biological mothers of the children. They found that 30 minutes or more of daily sun during the second trimester of pregnancy was associated with a 32% reduced risk of relapse for their child with MS.

“Our findings suggest that sun exposure in early childhood may have long-lasting benefits on the progression of childhood-onset MS,” said Chang. “Future studies should look at how time in the sun at other time periods before and after MS diagnosis affects disease course, to better guide sun exposure recommendations for children with MS and to help design potential clinical trials.” A limitation of the study was that it relied on participants’ parents or guardians reporting their sun exposure and use of sun protection, which they may not have remembered accurately.

Source: American Academy of Neurology