Author: ModernMedia

Categories : Medical Research & TechnologyTags :

Vibration Technique Controls Strength of Lab-grown Tissues

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Photo by Pawel Czerwinski on Unsplash

Researchers in McGill’s Department of Mechanical Engineering have discovered a safe and low-cost method of engineering living materials such as tissues, organs and blood clots. By simply vibrating these materials as they form, scientists can dramatically influence how strong or, weak they become.

The findings, published in the journal Advanced Functional Materials, could have a range of innovative applications, including in organ transplants, wound healing and regenerative medicine.

Good vibrations

The researchers used a speaker to apply controlled vibration, gently agitating the living materials during formation. By doing so, they found they could influence how cells organized and how strong or weak the final material became.

The technique works across a range of soft cellular materials, including blood clots made from real blood and other human tissues.

Aram Bahmani, study co-author and Yale postdoctoral fellow, conducted the research at McGill as a PhD student with Associate Professor Jianyu Li’s Biomaterials Engineering lab. Bahmani explained that strong, fast-forming blood clots are vital for use in emergencies like traumatic injuries. They’re also useful for people with clotting disorders.

“On the other hand, the same approach could help design clots that break down more easily as necessary, helping to prevent dangerous conditions like stroke or deep vein thrombosis,” he added. “Mechanical nudging allows us to make the material up to four times stronger or weaker, depending on what we need it to do.”

Why previous methods fell short

Earlier approaches to shaping living tissues relied on physical forces like magnets or ultrasound waves. While promising, these methods often fail to replicate the complexity of real tissues, which contain billions of cells and have thick, three-dimensional structures. In addition, they are often limited to specific materials, can damage healthy tissues and sometimes trigger immune responses.

The researchers’ study is the first to show that mechanical agitation, a very simple and widely accessible tool, can control the inner structure and performance of living materials in a “safe, scalable and highly tunable way.”

From the lab bench to living systems

To validate their findings, the team ran a series of tests to measure how vibration affected various cell-laden materials such as blood-based gels, plasma and seaweed-derived alginate. Using imaging and mechanical analysis, they assessed how broadly the method could be applied. Next, they tested the technique in animals.

The results showed that the technique works when applied inside the body, without harming surrounding healthy tissues.

Toward advanced medical technology

Bahmani said he believes the simple method could one day be integrated into advanced medical devices or wound-healing techniques.

“What makes this especially exciting is that our method is non-invasive, low-cost and easy to implement,” he said. “It does not rely on expensive machines or complex chemicals, meaning it could one day be built into portable medical devices, like a hand-held tool to stop bleeding, or a smart bandage that speeds up healing.” 

He noted that the method requires further testing, such as in irregular wounds or in combination with certain medications, before it can be used in real-life medical settings.

“Moving toward clinical use will require miniaturising the devices, optimising settings for different medical scenarios and completing regulatory testing to ensure safety and effectiveness in humans,” he said.

Source: McGill University

Categories : HIVTags :

AIDS Healthcare Foundation (AHF) Celebrates Milestone: 2.5 Million Lives in Care, 1.3 Million in Africa

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Supported by robust advocacy initiatives to achieve policy reform, AHF ensures equitable access to HIV and public health services globally

Dr Penninah Iutung, Executive Vice President of AHF

The AIDS Healthcare Foundation (AHF) (www.AIDSHealth.org) proudly announces a transformative milestone: delivering life-saving HIV prevention, care, and treatment to 2.5 million people across 49 countries, with 1.3 million in 15 African nations (https://apo-opa.co/45zIVFg). This achievement transcends numbers, embodying restored hope, preserved families, and a bold vision for a healthier, equitable world. 

AHF’s contribution to the HIV response that has enabled countries like Malawi to see a remarkable increase in life expectancy from 46 to 67 years over a 25-year period is profound. Children who may have been orphaned due to HIV can now grow up with their parents present, and communities are thriving through access to quality care. This story can be told in several countries, and it reflects AHF’s unwavering commitment to transforming lives and achieving global HIV control. 

Founded in 1987 in Los Angeles as the AIDS Hospice Foundation, AHF has grown into the world’s largest HIV/AIDS service organisation. With over 8000 dedicated staff, AHF delivers expert, compassionate, and non-judgmental care to all, regardless of ability to pay. Supported by robust advocacy initiatives to achieve policy reform, AHF ensures equitable access to HIV and public health services globally. 

AHF President Michael Weinstein shared, “When we began, I never imagined we’d touch 2.5 million lives. This milestone, born of our staff’s courage and our patients’ trust, demands recognition. As George Bernard Shaw said, ‘You see things; and say, Why? But I dream of things that never were and I say, Why not?’ Our dream – delivering exceptional care to all – has become reality. We’ve stayed true to our principles, proving hope can shine in a challenging world. Yet, our journey continues. AHF is tackling STIs, hunger, homelessness, and the global HIV epidemic with relentless resolve. I’m deeply honoured to serve alongside our extraordinary team.” 

“When we launched our first global programs in South Africa and Uganda in 2002, serving 100 clients in each country, we could never have fathomed expanding to 13 more African countries and caring for 1.3 million lives across the continent,” said Dr Penninah Iutung, AHF’s Executive Vice President . “Building on years of advocacy and innovation, AHF Africa now delivers programs that go beyond clinical care to include community-led prevention, equitable access strategies, and pandemic preparedness. These successes reflect the deep collaboration with government and civil society partners that has enabled us to reach the most marginalized, advance equity, and ensure no one is left behind.”  

Dr. Nombuso Madonsela, who leads AHF’s largest country program as AHF South Africa Country Program Director, adds, “Being part of this historic milestone is a privilege. AHF South Africa remains steadfast in championing combination prevention, reducing new infections, and ensuring quality service delivery and support for all in our care. Through our Community Power Voices (CPV), we amplify the stories and triumphs of those living with HIV. Ending HIV is not just a dream, it’s a promise we are determined to keep.” 

Looking forward, AHF is resolute in expanding access, dismantling barriers, and ensuring no one is left behind in the global fight against HIV. This milestone fuels AHF’s mission to push boundaries, innovate solutions, and build a future where HIV is no longer a threat. 

Distributed by APO Group on behalf of AIDS Healthcare Foundation.

Categories : Diet and Nutrition Neurodegenerative DiseasesTags :

Significant Drop in Omega Fatty Acids in Women with Alzheimer’s

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Photo by Aleksander Saks on Unsplash

Analysis of lipid blood levels in women with Alzheimer’s disease has shown noticeable loss of unsaturated fats, such as those that contain omega fatty acids, compared to healthy women.

In men with Alzheimer’s, no significant difference was found in the same lipid molecule composition disease compared to healthy men, which suggests that those lipids have a different role in the disease according to sex. Fats perform important roles in maintaining a healthy brain, so this study could indicate why more women are diagnosed with the disease.

The study, published today in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association by scientists from King’s College London and Queen Mary University London, is the first to reveal the important role lipids could have in the risk for Alzheimer’s between the sexes.

Women are disproportionately impacted by Alzheimer’s Disease and are more often diagnosed with the disease than men after the age of 80. One of the most surprising things we saw when looking at the different sexes was that there was no difference in these lipids in healthy and cognitively impaired men, but for women this picture was completely different. The study reveals that Alzheimer’s lipid biology is different between the sexes, opening new avenues for research.

Dr Cristina Legido-Quigley, Reader in Systems Medicine

The scientists took plasma samples from 841 participants who had Alzheimer’s Disease, mild cognitive impairment and cognitively health controls and and were measured for brain inflammation and damage.

They used mass spectrometry to analyse the 700 individual lipids in the blood. Lipids are a group of many molecules. Saturated lipids are generally considered as ‘unhealthy’ or ‘bad’ lipids, while unsaturated lipid, which sometime contains omega fatty acids, are generally considered ‘healthy’.

Scientists saw a steep increase in lipids with saturation – the ‘unhealthy lipids’ – in women with Alzheimer’s compared to the healthy group. The lipids with attached omega fatty acids were the most decreased in the Alzheimer’s group.

Now, the scientists say there is a statistical indication that there is a causal link between Alzheimer’s Disease and fatty acids. But a clinical trial is necessary to confirm the link.

Dr Legido-Quigley added: “Our study suggests that women should make sure they are getting omega fatty acids in their diet – through fatty fish or via supplements. However, we need clinical trials to determine if shifting the lipid composition can influence the biological trajectory of Alzheimer’s Disease.”

Dr Asger Wretlind, first author of the study from the School of Cancer & Pharmaceutical Sciences, said: “Scientists have known for some time that more women than men are diagnosed with Alzheimer’s disease. 

Although this still warrants further research, we were able to detect biological differences in lipids between the sexes in a large cohort, and show the importance of lipids containing omegas in the blood, which has not been done before. The results are very striking and now we are looking at how early in life this change occurs in women.

Dr Asger Wretlind, School of Cancer & Pharmaceutical Sciences

Source: King’s College London

Categories : Cancer Diet and NutritionTags :

Animal Protein Not Linked to Higher Mortality Risk, Study Finds

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Photo by Jose Ignacio Pompe on Unsplash

Eating animal-sourced protein foods is not linked to a higher risk of death and may even offer protective benefits against cancer-related mortality, new research finds.   

The study, published in Applied Physiology, Nutrition, and Metabolism, analysed data from nearly 16 000 adults aged 19 and older using the National Health and Nutrition Examination Survey (NHAMES III). 

Researchers examined how much animal and plant protein people typically consume and whether those patterns were associated with their risk of dying from heart disease, cancer or any cause.  

They found no increased risk of death associated with higher intake of animal protein. In fact, the data showed a modest but significant reduction in cancer-related mortality among those who ate more animal protein.  

“There’s a lot of confusion around protein – how much to eat, what kind and what it means for long-term health. This study adds clarity, which is important for anyone trying to make informed, evidence-based decisions about what they eat,” explains Stuart Phillips, Professor and Chair of the Department of Kinesiology at McMaster University, who supervised the research.  

To ensure reliable results, the team employed advanced statistical methods, including the National Cancer Institute (NCI) method and multivariate Markov Chain Monte Carlo (MCMC) modelling, to estimate long-term dietary intake and minimize measurement error.   

“It was imperative that our analysis used the most rigorous, gold standard methods to assess usual intake and mortality risk. These methods allowed us to account for fluctuations in daily protein intake and provide a more accurate picture of long-term eating habits,” says Phillips.   

The researchers found no associations between total protein, animal protein or plant protein and risk of death from any cause, cardiovascular disease, or cancer. When both plant and animal protein were included in the analysis, the results remained consistent, suggesting that plant protein has a minimal impact on cancer mortality, while animal protein may offer a small protective effect. 

Observational studies like this one cannot prove cause and effect; however, they are valuable for identifying patterns and associations in large populations. Combined with decades of clinical trial evidence, the findings support the inclusion of animal proteins as part of a healthy dietary pattern.  

“When both observational data like this and clinical research are considered, it’s clear both animal and plant protein foods promote health and longevity,” says lead researcher Yanni Papanikolaou, MPH, president, Nutritional Strategies. 

This research was funded by the National Cattlemen’s Beef Association (NCBA), a contractor to the Beef Checkoff. NCBA was not involved in the study design, data collection and analysis or publication of the findings.  

This article was first published on Brighter World. Read the original article.

Categories : Metabolic Disorders NeurologyTags :

New Research Shows that Macrophages Help Prevent the Development of Neuropathy

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Source: Pixabay CC0

An increase in high-fat, high-fructose foods in people’s diets has contributed to a dramatic increase in type 2 diabetes. This, in turn, has led to an increase in peripheral neuropathy. About half of people with type 2 diabetes are affected, and of these, about half experience severe neuropathic pain.

The damage begins as axons from sensory neurons begin to retract and disappear from the tissues they innervate. New research from the lab of Clifford Woolf, MB, BCh, PhD, director of the F.M. Kirby Neurobiology Center at Boston Children’s Hospital, reveals that months before the damage occurs, immune cells flood into peripheral nerves in an apparent attempt to protect them. This surprising insight, published in Nature, could lead to strategies to prevent peripheral neuropathy or at least minimize and slow the onset of the damage.

Immune cells prevent nerve damage

A team led by Sara Hakim, PhD, a graduate student in the lab, created a mouse model of diabetes induced by a high-fat, high-fructose diet. The model showed that these mice developed all the major features of diabetes within eight to 12 weeks of starting the diet. At about six months, axons in the skin began to degenerate, indicating the presence of neuropathy.

“Diabetic neuropathy takes years, or even decades to develop in humans,” says Hakim, who is now at Vertex. “By using a mouse model in which symptoms slowly develop over months, we were able to catch the progression of the disease over time, and observe those early protective responses when the body is still trying to fight the disease.”

The researchers suspected that peripheral neuropathy is caused by the immune system, so used single-cell sequencing to detect changes in immune cells near sensory neuron axons in peripheral nerves.

One type of immune cell residing in nerves, a pro-inflammatory macrophage, began producing chemokines. These signaling molecules recruited a second population of circulating macrophages, which began infiltrating the nerve 12 weeks after the mice began the diet – as sensory symptoms were starting to appear but before nerve degeneration was seen.

Previously, macrophages were thought to have a pathogenic role in diabetes and were mainly reacting to axon loss. But Hakim, Woolf, and colleagues observed just the opposite.

“To our great surprise, when we blocked infiltration of macrophages into the nerve, neuropathy started getting worse, not better,” says Woolf. “The macrophages were protective. They slowed down the onset of neuropathy and reduced its impact.”

Potential strategies for peripheral neuropathy

The Woolf Lab is now exploring how the infiltrating macrophages protect against peripheral neuropathy. The next step would be to find a way to induce and sustain this protection and identify biomarkers that would flag those people with diabetes who are at risk.

One potential protective strategy might involve accelerating the recruitment of macrophages into nerves; another might involve mimicking their protective function by harnessing compounds they secrete, such as galectin 3.

“Since we could profile the cells and identify what genes they are expressing, we found a number of signalling molecules known to be protective,” says Woolf. “We can now go through that list and check to see which are most active.”

The latest work reinforces the idea that pain isn’t just a disease of neurons, but results from interactions between the nervous system and the immune system. In a study last year, the Woolf Lab discovered thousands of molecular interactions between pain-sensing neurons and different types of immune cells.

Now, the plot is thickening with this example of immune cells acting to prevent painful nerve damage. “We’ve now revealed a novel, slower protective effect of the immune system,” Woolf says.

Source: Boston Children’s Hospital

Categories : Cancer NeurologyTags :

Researchers Find TBI Link to Development of Malignant Brain Tumours

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Coup and contrecoup brain injury. Credit: Scientific Animations CC4.0

New research led by investigators at Mass General Brigham suggests a link between a history of traumatic brain injury (TBI) and risk of developing a malignant brain tumour. By evaluating data from 2000–2024 of more than 75 000 people with a history of mild, moderate or severe TBI, the team found the risk of developing a malignant brain tumour was significantly higher compared to people without a history of TBI. The results were published in JAMA Network Open.

“I see these results as alarming,” said co-senior author and corresponding author Saef Izzy, MD, FNCS, FAAN, a neurologist and head of the Immunology of CNS Injury Program at Brigham and Women’s Hospital, a founding member of the Mass General Brigham healthcare system. “Our work over the past five years has shown that TBI is a chronic condition with lasting effects. Now, evidence of a potential increased risk of malignant brain tumours adds urgency to shift the focus from short-term recovery to lifelong vigilance.

“Alongside our earlier findings linking TBI and cardiovascular disease, this underscores the importance of long-term monitoring for anyone with a history of TBI.”

The team divided the severity of TBI between mild, moderate and severe, with participants suffering from incidents ranging from car accidents to falls. In the two categories of moderate and severe, 0.6% of people (87 out of 14 944) developed brain tumours within 3-to-5 years after the TBI, which was a higher percentage than controls. Mild cases of TBI, such as those caused by concussions, were not associated with an increased risk of tumour. The aim of the study was not to establish a cause-and-effect link between moderate-to-severe TBI and malignant tumours, but rather to explore whether an association exists. Determining causality and understanding the underlying mechanisms will require a dedicated translational study in the future.

A previous study showed veterans of the Iraq and Afghanistan wars who suffered TBI experienced an increased risk of brain tumours, but previous studies on civilian populations showed conflicting results. The collaborative team of researchers used an international disease classifying system known as ICD codes to exclude anyone in the study with a history of brain tumour, benign tumours, and risk factors such as radiation exposure.

Previous neurotrauma studies from Mass General Brigham have looked at patients with a history of TBI and found an association with the emergence of anxiety, depression, and other psychiatric, neurological, and cardiovascular diseases, but the current study focuses on malignant tumour development.

Future imaging studies could draw a connection between the location of the TBI and where tumours developed in the brains of participants. The team would like to further study patients with repeated injuries, such as falls. 

“While there is an increased risk of tumour from TBI, the overall risk remains low. Still, brain tumour is a devastating disease and often gets detected in later stages,” said lead author Sandro Marini, MD, a neurologist at Mass General Brigham. “Now, we’ve opened the door to monitor TBI patients more closely.”

Source: Mass General Brigham

Categories : GastrointestinalTags :

Research Uncovers Why IBD Causes Blood Clots – and How to Prevent Them

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Irritable bowel syndrome. Credit: Scientific Animations CC4.0

Rates of inflammatory bowel disease are rising, and there’s currently no cure. IBD can also be deadly: up to 8% of people with the disease develop blood clots, which can lead to heart attack and stroke. New research has uncovered why blood clotting malfunctions in IBD – and identified drugs that normalise blood clotting in human cells and animal models of IBD.

“We think we can leverage these findings to reduce inflammation and the risk of blood clots,” says senior author Aaron Petrey, PhD, assistant professor of microbiology and immunology at University of Utah Health, associate director of the U’s Molecular Medicine Program.  “This could be lifesaving.”
 
The results are published in Blood.

Clotting with the brakes off

Most research into IBD has focused on immune cells. But blood cells called platelets are another key contributor to IBD symptoms. In healthy people, platelets clump together into clots in response to injuries to stop bleeding, and don’t form clots otherwise. But in patients with IBD, platelets are on a hair trigger, ready to form clots at the slightest provocation.

Surprisingly, platelets from IBD patients weren’t clotting via the normal pathways that trigger clotting, says first author Rebecca Mellema, PhD, pathology postdoc. “It’s completely independent of what we would expect.”

“There’s an innate mechanism by blood vessels to tell platelets to stay quiet and not form a clot yet,” Petrey explains. “Once there’s injury or inflammation, that signal can switch over and tell them to form a clot. That’s the process that’s broken in IBD patients.”

IBD platelets appear to clot more often because they don’t have enough of a key protein called layilin, the researchers found. In healthy people, layilin acts as a molecular brake for clotting: it senses the difference between healthy and injured blood vessels and prevents platelets from clotting as long as blood vessels are intact.

But when the researchers deleted the layilin gene in mice, the brakes came off. Without layilin, platelets were extra sticky, forming clots when they shouldn’t.

The researchers also found that platelets from IBD patients only had about 60% of the layilin protein that they should, leaving them constantly on the verge of clotting. 

A promising drug target

Layilin prevents unwanted clotting by tamping down the activity of a clot-triggering molecule called Rac1. In mice without the layilin gene – and in people with IBD – Rac1 is always a little bit too active, which means platelets are too prone to forming clots.

But there’s good news. Drugs that prevent Rac1 activity are already in clinical trials for other conditions, and the researchers’ results suggest that these Rac1 inhibitors could be powerful therapeutics for IBD.

One Rac1 inhibitor reduced excessive clotting in human platelets in a dish. The inhibitor also decreased the level of tissue damage in the gut in a mouse model of IBD.

Promisingly, the drug decreased clotting in platelets from IBD patients even more strongly than it affected healthy cells. “We have shown a hyperactivation pathway in resting IBD patient platelets, but they’re also incredibly sensitive to treatment, moreso than those from a healthy person,” Mellema says.

Normalizing Rac1 activity might not only reduce the risk of heart attack and stroke—it could also help alleviate day-to-day IBD symptoms, the researchers say. Excessive clotting can block blood flow in the gut and make inflammation worse, which means that preventing clotting could reduce inflammation.

Unlike established anti-clotting drugs, the researchers say, Rac1 inhibitors shouldn’t lead to an increased risk of dangerous bleeding, which is a serious concern for IBD patients with chronic inflammation. Blocking Rac1 won’t interfere with other, independent pathways that can trigger platelet clotting, so the cells should still be able to form needed clots in response to injury. 

“We’re targeting a pathway that is not pre-activated in healthy people,” Petrey says. “So we can address that step of the pathway, and if there’s a significant injury, the platelets can overcome that inhibition.”

Other groups had been looking into the potential of Rac1 inhibitors to reduce inflammation in IBD. The new work emphasises the potential of these drugs to address multiple symptoms. “Paying more attention to what we can do to address these blood clotting risks could significantly improve patient lives,” Petrey says.

Source: University of Utah Health

Categories : GeneticsTags :

Like Likes Like: Partner Preferences May Be Explained by Genetics 

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Couple or siblings? New study may explain why we prefer partners who are similar to us. Photo by Daniil Onischenko on Unsplash

It is no secret that people are often drawn to romantic partners who seem similar to themselves. This tendency, called assortative mating, has been established in humans (Horwitz et al., 2023; Luo, 2017) as well as other species. Fish, for example, demonstrate the behaviour frequently (Jiang et al., 2013).  

Assortative mating has also recently been in focus on social media with the viral Siblings or Dating game, where people guess whether two individuals who look alike are related or a couple. 

The idea is well-founded in academic research. Humans have been observed to select partners with similar physical, personality, and demographic traits (Horwitz et al., 2023), which can impact the genetics of populations – creating subgroups that emphasise the presence of shared traits (Abdellaoui et al., 2015).  

But selecting a partner like ourselves may not be solely determined by personal choice. A new study soon to be published in Psychological Science suggests that assortative mating can be explained relatively simply by looking at the inheritance of preferred traits and corresponding preferences for those traits. 

Coauthors Kaitlyn Harper and Brendan Zietsch from the University of Queensland describe this scenario simply: If you are tall, you may have inherited tallness from one parent (say, your mother) and the preference for tallness in a romantic partner from your other parent (in this case, your father). The combination of those inherited traits means that you exist in the world as a tall person and are attracted to tall people.  

The idea that preference for a particular trait could lead to genetic correlations has been discussed in previous research but is a newer concept for evolutionary psychology, especially in the context of assortative mating.  

“The pieces were there, but they hadn’t been connected in this way before,” Harper said. “Agent-based modelling helped us connect the dots – by simulating populations, we could see that assortative mating naturally emerged without the need for additional assumptions or processes.” 

She added that this research wouldn’t have been possible without an interdisciplinary mindset. 

“The mechanism itself is familiar in evolutionary biology, but it wasn’t thought of as an explanation for assortative mating,” she said. “Making that connection only became possible when we looked across the two disciplines.” 

To test this theory, the authors ran an agent-based model where partners are chosen according to heritable traits and preferences over 100 generations. They included models with and without selection pressure on the number of offspring within each generation to assess how the theory stands up under more naturalistic conditions.  

They found that even with up to 10 preferences for traits in a partner, clear genetic correlations formed between traits and preferences for those traits, which resulted in the agents choosing partners similar to themselves. Models with selection pressure generated less-stable correlations, which the authors attribute to reduced variance in traits.  

“The power of this finding is in its parsimony – it shows that a phenomenon which has puzzled researchers for decades can be understood through an explanation that was hiding in plain sight,” Harper said. “And because the mechanism is so general, it can also apply to assortative mating in animals, where many of the explanations proposed for humans wouldn’t make sense.” 

Source: Association for Psychological Science

Categories : Cardiovascular DiseaseTags :

High-salt Diet Causes Brain Inflammation, Raising Blood Pressure

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Credit: Pixabay CC0

A new study from McGill University finds that a high-salt diet triggers brain inflammation that drives up blood pressure.

The research, led by Masha Prager-Khoutorsky in collaboration with an interdisciplinary team at McGill and the Research Institute of the McGill University Health Centre, suggests the brain may be a missing link in certain forms of hypertension traditionally attributed to the kidneys.

“This is new evidence that high blood pressure can originate in the brain, opening the door for developing treatments that act on the brain,” said Prager-Khoutorsky, associate professor in McGill’s Department of Physiology.

Hypertension affects two-thirds of people over 60 and contributes to 10 million deaths worldwide each year. Often symptomless, the condition increases the risk of heart disease, stroke and other serious health problems.

About one-third of patients don’t respond to standard medications, which primarily target the blood vessels and kidneys based on the long-standing view that hypertension begins there. The study, published in the journal Neuron, suggests the brain may also be a key driver of the condition, particularly in treatment-resistant cases.

How salt disrupts the brain

To mimic human eating patterns, rats were given water containing two per cent salt, comparable to a daily diet high in fast food and items like bacon, instant noodles and processed cheese.

The high-salt diet activated immune cells in a specific brain region, causing inflammation and a surge in the hormone vasopressin, which raises blood pressure. Researchers tracked these changes using cutting-edge brain imaging and lab techniques that only recently became available.

“The brain’s role in hypertension has largely been overlooked, in part because it’s harder to study,” Prager-Khoutorsky said. “But with new techniques, we’re able to see these changes in action.”

The researchers used rats instead of the more commonly studied mice because rats regulate salt and water more like humans. That makes the findings more likely to apply to people, noted Prager-Khoutorsky.

Next, the scientists plan to study whether similar processes are involved in other forms of hypertension.

Source: McGill University

Categories : Metabolic Disorders NeurologyTags :

The Neurons Responsible for Day-to-day Blood Glucose Regulation

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Photo by Anna Shvets

The brain controls the release of glucose in a wide range of stressful circumstances, including fasting and low blood sugar levels.

However, less attention has been paid to its role in day-to-day situations.

In a study published in Molecular Metabolism, University of Michigan researchers have shown that a specific population of neurons in the hypothalamus help the brain maintain blood glucose levels under routine circumstances.

Over the past five decades, researchers have shown that dysfunction of the nervous system can lead to fluctuations in blood glucose levels, especially in patients with diabetes.

Some of these neurons are in the ventromedial nucleus of the hypothalamus, a region of the brain that controls hunger, fear, temperature regulation and sexual activity.

“Most studies have shown that this region is involved in raising blood sugar during emergencies,” said Alison Affinati, MD, PhD, assistant professor of internal medicine and member of Caswell Diabetes Institute.

“We wanted to understand whether it is also important in controlling blood sugar during day-to-day activities because that’s when diabetes develops.”

The group focused on VMHCckbr neurons, which contain a protein called the cholecystokinin b receptor.

They used mouse models in which these neurons were inactivated.

By monitoring the blood glucose levels, the researchers found that VMHCckbr neurons play an important role in maintaining glucose during normal activities, including the early part of the fasting period between the last meal of the day and waking up in the morning.

“In the first four hours after you go to bed, these neurons ensure that you have enough glucose so that you don’t become hypoglycaemic overnight,” Affinati said.

To do so, the neurons direct the body to burn fat through a process called lipolysis.

The fats are broken down to produce glycerol, which is used to make sugar.

When the group activated the VMHCckbr neurons in mice, the animals had increased glycerol levels in their bodies.

These findings could explain what happens in patients with prediabetes, since they show an increase in lipolysis during the night.

The researchers believe that in these patients, the VMHCckbr neurons could be overactive, contributing to higher blood sugar.

These nerve cells, however, only controlled lipolysis, which raises the possibility that other cells might be controlling glucose levels through different mechanisms.

“Our studies show that the control of glucose is not an on-or-off switch as previously thought,” Affinati said.

“Different populations of neurons work together, and everything gets turned on in an emergency. However, under routine conditions, it allows for subtle changes.”

The team is working to understand how all the neurons in the ventromedial nucleus co-ordinate their functions to regulate sugar levels during different conditions, including fasting, feeding and stress.

They are also interested in understanding how the brain and nervous system together affect the body’s control of sugar, especially in the liver and pancreas.

Source: University of Michigan