Year: 2025

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VZV Reactivation Is Driving CNS Infections

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Varicella zoster vires (VZV). Credit: NIH/NIAID

The varicella zoster virus (VZV), an infectious virus from the herpes virus family, is primarily known to cause varicella in children and shingles in adults. But lately, this virus has also been reported to trigger severe complications like central nervous system (CNS) infections. Researchers from Fujita Health University, Japan, conducted a comprehensive study spanning 10 years (2013–2022), to identify the VZV-related infections affecting the CNS. Their study reveals a marked increase in adult VZV-related CNS infections, particularly since 2019. The findings were published in the journal Emerging Infectious Diseases.

The study was led by Professor Tetsushi Yoshikawa, along with Hiroki Miura and Ayami Yoshikane from the Department of Pediatrics, Fujita Health University School of Medicine. The researchers analysed cerebrospinal fluid samples of 615 adult patients with suspected CNS infections. VZV DNA was most frequently detected in these patients, with its presence in 10.2% of the cases, and aseptic meningitis being the most common infection.

The data from 2019 to 2022 revealed that there was a noticeable rise in VZV DNA-positive cases, forming a distinct temporal cluster during this period. Professor Yoshikawa highlighted the results of the patient demographic analysis, reporting that “the proportion of aseptic meningitis increased from 50% between 2013 and 2018 to 86.8% between 2019 and 2022.” He further adds, “Similar to the rise in herpes zoster cases through VZV reactivation in the elderly, we believe this increase is also linked to VZV reactivation.”

The universal varicella vaccination, introduced in Japan in 2014, has reduced the natural booster effects from re-exposure to the virus. This potentially accelerates the immunity decline, leading to VZV reactivation, especially in cases like shingles. The researchers highlight the connection between the vaccination and the current scenario, saying, “The increase in VZV-induced CNS infections coincides with changes in varicella vaccination programs and emphasises the need for better preventive strategies.”

Furthermore, the researchers examined trends in VZV-induced CNS infection throughout the observation period using Kulldorff’s circular spatial scan statistics. As a result, it was confirmed that there was an accumulation of VZV-related CNS infections from 2019 to 2022. Although no direct causation was established, six patients did develop CNS infections after receiving COVID-19 vaccines.

“Further studies are needed to understand these interactions,” Yoshikawa notes. None of the eligible patients in this study had received the zoster vaccine, which was introduced in Japan in 2016. Increasing the number of VZV-related CNS infections underscores the importance of zoster vaccination in adults.

The research team stresses the broader implications of their findings, stating that the reactivation of VZV in the CNS is linked to an increased risk of dementia, including Alzheimer’s disease. They hypothesize, “If the prevention of VZV-related aseptic meningitis through herpes zoster vaccination is possible, these vaccinations could play a pivotal role in mitigating these risks of dementia.”

To address the growing concern, the research team advocates expanding public health initiatives to promote zoster vaccination among at-risk populations. “Our research underscores the necessity of proactive measures to prevent not just shingles, but also severe neurological complications associated with VZV,” explains Yoshikawa.

With the rise of the aging population and CNS infections, the study calls for urgent action to evaluate and implement comprehensive vaccination strategies to prevent CNS infections in the future.

Source: Fujita Health University

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A Third of Children Worldwide Forecast to be Obese or Overweight by 2050

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Obesity rates are set to skyrocket, with one in six children and adolescents worldwide forecast to be obese by 2050, according to a new study. But with significant increases predicted within the next five years, the researchers stress urgent action now could turn the tide on the public health crisis.

The research, led by Murdoch Children’s Research Institute (MCRI) and published in The Lancet, found a third of children and adolescents will be overweight (385 million) or obese (360 million) within the next 25 years. The forecast equates to 356 million children aged 5–14 years and 390 million aged 15–24 years with one in six facing obesity.

The global obesity rate for those between 5-24 years old tripled from 1990 to 2021, rising by 244 per cent to 174 million, suggesting that current approaches to curbing increases in obesity have failed a generation of young people. As of 2021, 493 million children and adolescents were overweight or obese.

MCRI Dr Jessica Kerr said if immediate five-year action plans were not developed, the future was bleak for our youth. 

“Children and adolescents remain a vulnerable population within the obesity epidemic,” she said, adding that obesity drives a whole range of diseases. Prevention is key as obesity rarely resolves after adolescence.

“Despite these findings indicating monumental societal failures and a lack of coordinated global action across the entire developmental window to reduce obesity, our results provide optimism that this trajectory can be avoided if action comes before 2030.”

The analysis, released on World Obesity Day, used the 2021 Global Burden of Diseases, Injuries, and Risk Factors Study to estimate the latest overweight and obesity levels and forecasts in 204 countries and territories.

The United Arab Emirates, Cook Islands, Nauru and Tonga are forecast to have the highest prevalence while China, Egypt, India and the US will have the greatest number of children and adolescents with obesity by 2050.

In Australia, children and adolescents have experienced some of the fastest transitions to obesity in the world. Girls are already more likely to be obese than overweight. Overall, by 2050 for those aged 5-24 years, 2.2 million are forecasted to be obese and 1.6 million overweight.

Globally, there will be more boys, 5–14 years, with obesity than being overweight by 2050.

“Without urgent policy reform, the transition to obesity will be particularly rapid in north Africa, the Middle East, Latin America and in the Caribbean, where the rise is concurrent with high population numbers and limited resources,” Dr Kerr said.

“Many regions have historically had to focus on preventing undernutrition and stunting in children. To prevent a public health emergency from this newer threat, an immediate imperative should be creating national surveillance surveys of obesity in children and adolescents in every country.”

Dr Kerr said older adolescent girls, aged 15-24 years entering their reproductive years, were a priority population for intervention.

“Adolescent girls who are obese are a main focus if we are to avoid intergenerational transmission of obesity, chronic conditions and the dire financial and societal costs across future generations,” she said.

“With this age group increasingly being out of school and cared for by adult services, we need to focus interventions at the community and commercial level.”

Source: Murdoch Childrens Research Institute

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Interventions to Eliminate Vertical Transmission of Hepatitis B in Africa

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Researchers at the University of Liverpool have conducted a large-scale analysis that sheds light on the critical steps needed to combat the vertical transmission of chronic hepatitis B virus (HBV) in Africa.

Almost two thirds of all new hepatitis B infections globally occur in Africa. The newly published paper in The Lancet Global Health shows the importance of giving the hepatitis B birth dose vaccine (HepB-BD) within 24 hours of birth, and the potential impact of providing antiviral therapy (antiviral prophylaxis) to mothers during pregnancy. The study estimates for the first time that hepatitis B vertical transmission (passed from mother to baby) could be eliminated in Africa, with increased coverage of these two key interventions.

Chronic hepatitis B is the leading cause of liver cancer and liver cirrhosis in Africa and deaths are rising. Most cases of liver cancer are diagnosed late and are associated with a very poor prognosis in the region. Vertical transmission is one of the commonest routes of infection and is associated with an increased lifetime risk of severe liver disease.

Dr Alexander Stockdale, Senior Clinical Lecturer at the University’s Department of Clinical Infection, Microbiology and Immunology, based at the Malawi-Liverpool-Wellcome Trust Clinical Research Programme, together with Dr Nicholas Riches at Liverpool School of Tropical Medicine, led the comprehensive analysis of more than 113 individual studies which reported on the prevalence of hepatitis B in more than 190 000 women and investigated rates of vertical transmission.

The World Health Organization (WHO) African region faces a significant burden, accounting for 63% of the global total of new infections. This amounted to 771 000 new infections and 272 000 deaths in 2022. Among children under 5 years, the prevalence of HBV stands at 2.5% in the WHO African region – the highest globally.

Dr Alexander Stockdale said: “This study makes the case for investment in birth dose vaccination and maternal antiviral prophylaxis, in view of the exciting potential for elimination of vertical transmission in the WHO African region in our lifetime. Vertical transmission is a key route of new hepatitis B infections. Due to limited implementation of interventions, elimination targets are not currently being met. We project that expanding HepB-BD vaccination coverage to 90% could reduce transmission events by 44%, and adding maternal antiviral prophylaxis for 90% of eligible women could further reduce transmission by 86% and achieve the WHO targets for elimination.”

Dr Stockdale and colleagues have also recently been awarded £3million funding from the National Institute of Health and Care Research to conduct implementation research in Malawi and The Gambia. The NIHR Global Health Research Grant will allow researchers in Malawi, led by Dr Stockdale and in The Gambia, led by Professor Maud Lemoine and Dr Gibril Ndow, to evaluate the effectiveness, safety, feasibility and cost-effectiveness of giving antiviral treatment (tenofovir) to all pregnant women living with chronic hepatitis B to prevent transmission. This study will provide vital evidence on the potential impact of this strategy to guide public health policy in Africa, which has been recognised as a key knowledge gap by the WHO in the 2024 hepatitis B guidelines.

Source: University of Liverpool

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Scientists Discover that GLP-1 is Involved in Cocaine Addiction

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Cocaine use disorder casts a long shadow, trapping individuals in a cycle of dependence and leaving limited options for effective treatment. A new study in Science Advances delves deep into the brain, offering crucial insights into the underlying mechanisms of this complex disorder. By understanding how this intricate circuitry functions, scientists can pave the way for the development of more effective therapies, offering new hope to those struggling with this debilitating disorder.

At the heart of this discovery lies the role of glucagon-like peptide-1 (GLP-1), a hormone known for its involvement in regulating food intake and blood sugar. The study reveals that chronic cocaine use is associated with reduced GLP-1 levels, effects that suggest that increasing central GLP-1 signalling could reduce cocaine seeking.

Further investigation pinpointed a specific brain circuit: GLP-1-producing neurons in the nucleus tractus solitarius (NTS) that project to the ventral tegmental area (VTA), a key brain region involved in reward and motivation. By manipulating this circuit, researchers were able to significantly reduce cocaine-seeking behavior in animal models.

The study also sheds light on the specific cells involved. GLP-1 receptors were found to be primarily located on GABA neurons within the VTA. GABA, an inhibitory neurotransmitter, plays a crucial role in regulating brain activity. Importantly, activating these GLP-1 receptors increases the activity of GABA neurons, which in turn reduces the activity of dopamine neurons, a key neurotransmitter involved in reward and addiction.

“This research provides exciting new insights into the brain mechanisms underlying cocaine seeking,” said Schmidt, the Killebrew-Censits Chair of Undergraduate Education and a Professor of Neuroscience and Pharmacology in the Department of Biobehavioral Health Sciences. “By understanding how GLP-1 signaling influences brain activity in this context, we can potentially develop new GLP-1-based treatments to treat cocaine use disorder.”

This research opens a new chapter in the fight against cocaine use disorder. The findings offer a promising avenue for developing innovative therapies that target this critical brain circuit, potentially offering a lifeline to individuals struggling to break free from the grip of this devastating disorder.

Source: University of Pennsylvania School of Nursing

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Researchers Unravel Menopause Timing, Shedding Light on Ovarian Aging and Fertility

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Female reproductive system. Credit: Scientific Animations CC4.0 BY-SA

Menopause, driven by ovarian aging and the depletion of ovarian reserve, marks the end of a woman’s fertility, and while many aspects of these processes are well understood, the overall dynamics remain unclear. A new study from Rice University researchers, published in Biophysical Journal, introduces a novel approach to unravelling the complex patterns of ovarian aging using stochastic analysis, a mathematical approach that examines systems by evaluating all potential outcomes using random probability.

Led by Anatoly Kolomeisky, professor of chemistry and chemical and biomolecular engineering, the research team has developed a theoretical framework that quantitatively predicts menopause timing. By analysing how ovarian follicles transition through different stages, the researchers’ model explains why menopause occurs and sheds light on individual variability and cross-population differences. These insights could improve fertility planning, inform health care decisions related to hormonal therapies and enhance our understanding of age-related health risks associated with ovarian aging.

“By considering menopause as a sequential process involving random transitions of follicles, we can better understand individual variability and population-wide trends in menopause timing,” Kolomeisky said.

A new theoretical model unlocks the mystery of menopause

The research team hypothesised that ovarian aging follows a stochastic sequential process influenced by follicles transitioning through multiple developmental stages. Unlike previous studies focusing primarily on hormonal and genetic influences, this study employed explicit analytical calculations supported by extensive computer simulations.

The approach allowed researchers to model the gradual depletion of ovarian follicle reserves, providing a detailed quantitative framework that aligns with medical data from diverse populations.

“By applying stochastic analysis, we can move beyond broad observations and develop precise, predictive insights into menopause timing and variability,” Kolomeisky said.

Key findings uncover menopause timing

The researchers discovered a universal relationship between three critical factors: the initial follicle reserve, the rate of ovarian depletion and the threshold that triggers menopause. Their model also revealed that menopause occurs within a surprisingly narrow age range, a phenomenon that had not yet been fully explained.

“One of the most unexpected findings was the synchronisation of follicular transitions, which may regulate the timing of menopause,” Kolomeisky said. “This suggests that underlying biochemical processes ensure a relatively consistent age of menopause despite individual variations.”

Source: Rice University

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X-Rays in ‘Colour’: Paving the Way for New Era in Medical Imaging

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New X-ray imaging technologies may soon offer a lot more information than the simple black-and-white images we are used to. Photo by Tima Miroshnichenko on Pexels

New technology developed by researchers at the University of Houston could revolutionise medical imaging and lead to faster, more precise and more cost-effective alternatives to traditional diagnostic methods.

For years, doctors have relied on conventional 2D X-rays to diagnose common bone fractures, but small breaks or soft tissue damage like cancers often go undetected. More expensive and time-consuming MRI scans are not always suitable for these tasks in these detection or screening settings. Now, Mini Das, UH professor, has developed a 3D solution.

In a paper featured on the cover of the Journal of Medical Imaging, Das explains how photon counting detectors along with novel algorithms allow for more precise 3D visualisation of different tissues and contrast agents by capturing X-rays at multiple energy levels simultaneously, which helps differentiate materials inside the body.

“There are so many other potential applications for this technology including in materials imaging, baggage scanning for security, imaging for geophysics, and micro- and nano-electronics imaging – it’s very promising.”

Mini Das

“Right now, X-rays used in medical clinics and other industries collect incoming photons as a whole, similar to how white light contains all the colours, but they aren’t separated,” Das says. “So, while they can show differences in density – like distinguishing between bone and soft tissue – they can’t tell us exactly what materials are present.”

Medical and Industrial Applications

The photon counting detectors developed by Das’s team at UH can separate X-ray photons by their energy levels, similar to how a prism splits white light into different colours – and they can help identify specific materials, such as distinguishing between aluminium, plastic, iodine or other contrast agents like gadolinium used in medical imaging.

“This could improve cancer detection, for example,” Das says. “If you inject two different contrast agents – one targeting a tumor and another targeting inflammation – you could see where each one accumulates. Right now, we can see bright areas in an image, but we can’t always tell what they are. This technology would give us a much clearer, quantitative analysis. It would allow us to determine not just what’s inside an object, but what different materials are present and in what quantities.”

However, even with this advanced detection, some materials have similar X-ray properties, so distinguishing more than two or three at once can be a challenge. This is also amplified due to errors in the detectors as they separate photons by energy. But Das is working on a solution to that problem.

“We have developed a method that compensates for these detector distortions by calibrating the detector using known materials,” Das says. “Once corrected, we can use the data along with the proposed novel algorithm, for accurate material decomposition – breaking down an image into its component materials. We do this in a multi-step solution from the same CT data collected improving accuracy.”

Still Work to Do

Before the detectors can be widely used, there is still a lot of work to do. But Das says her team is working with industry partners in Europe to develop larger versions of these novel detectors and optimize their performance.

“We’re still in the research and development phase,” Das says. “Right now, the detectors are small, and we need to refine their measurement accuracy. But once we solve those challenges, we can begin testing in real-world medical and industrial settings. There are so many other potential applications for this technology including in materials imaging, baggage scanning for security, imaging for geophysics, and micro- and nano-electronics imaging – it’s very promising.”

Previously, Das addressed a century-old problem in another innovative area related to the exploration of the wave nature of X-rays to significantly enhance soft material contrast. This research was featured in the prestigious scientific journal Optica last year.

Das’s research is funded through multiple agencies including NSF, CDMRP and NIH. The latest funding from the National Institute of Biomedical Imaging and Bioengineering aims to develop low-dose Micro-CT that utilises multiple novel contrast mechanisms, thereby reducing radiation dose and imaging time which continues to be a significant issue.

Source: University of Houston

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Cold Sore Discovery Reveals an Unexpected Trigger for Flare-ups

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Scientists have a new target to prevent cold sores after University of Virginia researchers discovered an unexpected way the herpes virus re-activates in the body. The finding, published in PNAS, could also have important implications for genital herpes caused by the same virus.

The discovery from UVA’s Anna Cliffe, PhD, and colleagues seems to defy common sense. She and her team found that the slumbering herpes virus will make a protein to trigger the body’s immune response as part of its escape from dormancy. You’d think this would be bad for the virus – that activating the body’s antiviral defences would be like poking a bear. But, instead, it’s the opposite: The virus hijacks the antiviral process in infected neurons to make the type of comeback nobody wants.

“Our findings identify the first viral protein required for herpes simplex virus to wake up from dormancy, and, surprisingly, this protein does so by triggering responses that should act against the virus,” said Cliffe of UVA’s Department of Microbiology, Immunology and Cancer Biology. “This is important because it gives us new ways to potentially prevent the virus from waking up and activating immune responses in the nervous system that could have negative consequences in the long term.”

Herpes Simplex Virus-Associated Disease

Cold sores are caused primarily by herpes simplex virus 1 (HSV-1), one of two forms of the herpes virus. HSV-1 is very contagious, and worldwide more than 60% of people under 50 (more than 3.8 billion) have been infected, the World Health Organization estimates.

In addition to causing cold sores, herpes simplex virus 1 can also cause genital herpes, a condition most often associated with HSV-1’s cousin, herpes simplex virus 2. Now, however, there are more new cases of genital herpes in the United States caused by HSV-1 than HSV-2. Notably, the UVA researchers found that herpes simplex virus 2 also makes this same protein and may use a similar mechanism to reactivate. So UVA’s new discovery may also lead to new treatments for genital herpes. 

In addition to cold sores and genital herpes, HSV-1 can also cause viral encephalitis (brain inflammation) and has been linked to the development of Alzheimer’s disease.

Once HSV-1 makes its way into our bodies, it stays forever. Our immune systems can send it into hiding, allowing infected people to be symptom free. But stress, other infections and even sunburns are known to cause it to flare. UVA’s new discovery adds another, surprising way it can spring back into action.

The researchers found that while the virus can make a protein called UL12.5 to reactivate, the protein was not needed in the presence of another infection. The scientists believe this is because the infections trigger certain “sensing pathways” that act as the home security system for neurons. Detection of a pathogen alone may be sufficient to trigger the herpes virus to begin replicating, the scientists believe, even in instances of “abortive infections” – when the immune system contains the new pathogen before it can replicate.

“We were surprised to find that HSV-1 doesn’t just passively wait for the right conditions to reactivate – it actively senses danger and takes control of the process,” researcher Patryk Krakowiak said. “Our findings suggest that the virus may be using immune signals as a way to detect cellular stress – whether from neuron damage, infections or other threats – as a cue to escape its host and find a new one.” 

With the new understanding of how herpes flares can be triggered, scientists may be able to target the protein to prevent them, the researchers say. 

“We are now following up on this work to investigate how the virus is hijacking this response and testing inhibitors of UL12.5 function,” Cliffe said. “Currently, there are no therapies that can prevent the virus from waking up from dormancy, and this stage was thought to only use host proteins. Developing therapies that specifically act on a viral protein is an attractive approach that will likely have fewer side effects than targeting a host protein.” 

Source: University of Virginia Health System

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New Study Supports Caution on Corticosteroids Use in Lupus Heart Condition

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Human heart. Credit: Scientific Animations CC4.0

A new study of more than 2900 patients provides evidence that it’s likely best to use as little corticosteroid medicine as possible when treating people who have lupus pericarditis, a common heart complication of the autoimmune disease Systemic Lupus Erythematosus (SLE).

This study, funded by the National Institutes of Health’s (NIH) National Heart, Lung, and Blood Institute (NHLBI) and led by Johns Hopkins Medicine cardiologists and rheumatologists who led the study say their analysis of data affirms that using steroids to curb heart inflammation and other painful symptoms for lupus patients is also a risk factor for recurring pericarditis,.  

Results of this study were published in JAMA Network Open.

The American Heart Association defines pericarditis as inflammation of the pericardium, the twin-layered sac-like structure surrounds the heart to hold it in place and help protect it. Pericarditis typically presents as chest pain that can be exacerbated by lying flat and improved by leaning forward. This pain can last anywhere from a few days to several months. Treatment options for pericarditis include use of colchicine, an anti-inflammatory medication that prevents the recurrence of pericarditis, and corticosteroids.

Pericarditis occurs in 15% to 30% of patients with SLE, a chronic autoimmune disease that causes the body’s immune system to attack its own tissues. “It is well known that, in the general population, one fifth of patients who experience pericarditis end up experiencing one or more recurrences. Surprisingly, even though pericarditis is the most common cardiac complication of Lupus, we could not find any information on recurrent of pericarditis in this patient population,” says Dr Luigi Adamo, MD, PhD, director of Cardiac Immunology at Johns Hopkins University and co-senior author of this study.

Researchers set out to address this gap in knowledge and examine the risk factors contributing to the recurrence.

For the new analysis, researchers used data gathered among the Hopkins Lupus Cohort, a large ongoing study group that includes information on 2,931 patients diagnosed with SLE between 1988 to 2023 and the investigators focused on data from 590 patients also diagnosed with pericarditis. Pericarditis in the data set was identified using the Safety of Estrogens in Lupus Erythematosus National Assessment – SLE Disease Activity Index (SELENA-SLEDAI), a standard tool in the assessment of SLE clinical activity.   

Study results showed that 20% of patients with Lupus who experienced pericarditis had a recurrence. Recurrent pericarditis was most prevalent among patients within the first year of pericarditis onset, with recurrence decreasing in the following years. Younger patients and those with uncontrolled disease were at greater risk of recurrence. It was noted that oral prednisone therapy, a tool frequently used to treat pericarditis in patients with autoimmune diseases, was associated with a higher chance of pericarditis recurrence in patients with SLE.

“The cardiology literature has shown that use of corticosteroids increases the risk of recurrent pericarditis in the general population. Nevertheless, steroids are very frequently used by rheumatologists to treat lupus pericarditis. Therefore, the findings from this study underscore the importance of minimising oral corticosteroid use in patients with lupus and indicate the need for alternative strategies.” said Andrea Fava, MD, a rheumatologist who specialises in care of patients with lupus and co-senior author of the study.

Source: Johns Hopkins Medicine

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Do Starchy Carbs Cause Cavities?

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It’s common knowledge that sugar causes cavities, but new research provides evidence that – depending on your genetic makeup – starches could also be a contributing factor.

The study, published in Microorganisms, explores the response of the oral microbiome to starch, finding that the number of copies of a particular gene, AMY1, in combination with starch, alters the complex composition of bacteria that play a role in oral health.

“Most people have been warned that if you eat a bunch of sugar, make sure you brush your teeth,” said Angela Poole, senior author and assistant professor of molecular nutrition in the College of Agriculture and Life Sciences and the College of Human Ecology. “The takeaway finding here is that depending on your AMY1 copy number, you may want to be just as vigilant about brushing your teeth after eating those digestible starches.”

Researchers, including first author Dorothy Superdock, PhD ’23, collected saliva samples from 31 subjects with a range of AMY1 copy numbers – copies of the AMY1 gene in the DNA – and added starch to the cultured samples, or biofilms, to see how the bacterial makeup changed. They found that, in general, the diversity of bacteria decreased when starch was added. For those samples with high numbers of AMY1, the starch significantly reduced the proportions of two bacteria, Atopobium and Veillonella, while Streptococcus appeared to increase.

All three bacteria are associated with tooth decay or gum disease, Poole said.

“Some increased and some decreased, so it’s not so straightforward as saying, ‘The whole thing is good or bad,’” Poole said. “It’s an interaction, but it looks like the AMY1 copy number, as well as which species are present in people’s mouths when they eat starch, is affecting the risk for developing these diseases.”

AMY1 codes for the salivary amylase enzyme, which helps break down starch in the mouth. Previous studies have associated AMY1 with cavities and periodontal disease. Poole, in prior studies, found that a high AMY1 copy number is associated with higher levels of the species Porphyromonas endodontalis, which is strongly associated with periodontitis and gum disease.

But how the salivary amylase enzyme interacts with its main substrate, starch, to alter the oral microbiome and increase disease risk was unclear.

“That’s what we wanted to know in this experiment,” Poole said. “What’s going on in the mouth if someone eats starch, and is the answer different if their copy number is high or if it’s low? What we found was that there are other bacteria involved in these processes and that the changes depended on AMY1.”

The researchers also found evidence that the oral microbiome has co-evolved in response to increasing copies of AMY1, which is found in higher numbers in populations where there’s a long history of agriculture and starch consumption. In the pool of 31 samples, taken locally in Ithaca, the AMY1 number ranged from two to 20 copies.

“The populations that historically had greater access to starch tend to have more copies,” Poole said, “which makes sense from a practical standpoint, because it would have given you a survival advantage when food is scarce, to be able to break down those starches more efficiently.”

In saliva samples with a high AMY1 copy number, the researchers saw increased populations of bacteria, like Streptococcus, that feed off the starch’s sugars.

“If someone has a high copy number, they break down starch efficiently, and bacteria that like those sugars are going to grow more in that person’s mouth,” Poole said. “So you can have species behave differently based on the different substrates. It’s pretty incredible – how we adapt and these microbes turn around and adapt, too.”

Source: Cornell University

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Not Just for Respiration: Lungs Also Produce Blood Cells

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Credit: Scientific Animations CC4.0

For many years, scientists assumed that blood production took place in the bone marrow, providing the 200 billion blood cells needed per day. But now, researchers at UCSF are showing it’s also happening in the lungs. 

They found haematopoietic stem cells (HSCs) in human lung tissue that make red blood cells, as well as megakaryocytes, which produce the platelets that form blood clots. The findings appear in the journal Blood.

The work, which was supported by the National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health (NIH), suggests the lungs could be a potent source for life-saving stem cell transplants.

“For decades, bone marrow transplants have been a lynchpin in the treatment of cancers like leukemia,” said Mark Looney, MD, professor of medicine and laboratory medicine at UCSF and senior author of the paper. “The lung HSCs could prove to be a second and significant reservoir of these precious stem cells.”

From mouse to human

In 2017, the UCSF team found cells in the mouse lung making 50% of the mouse’s platelets. 

They also discovered lung stem cells in mice that made all the constituents of blood, including red blood cells, megakaryocytes and several types of immune cells.

Looney’s group wanted to prove this was also happening in people. So, they obtained donated samples of lung, bone marrow and blood, and compared what they found in each tissue.

Screening a golf-ball-sized volume of lung tissue, the scientists found stem cells in the lung that strongly resembled the well-known HSCs of bone marrow. Surprisingly, the HSCs were found at similar rates in both lung and bone marrow. 

“The lung HSCs weren’t one-offs – they were a reliable presence in the lungs,” said Catharina Conrad, MD, PhD, postdoctoral scholar in Looney’s lab and first author of the paper. “But we still needed to know that they were actually capable of making blood.”

So, the scientists coaxed lung and bone marrow HSCs to mature in petri dishes and found the lung HSCs were productive just like the bone marrow HSCs.

“Both types of HSCs thrived in our gold-standard stem cell experiment, but the lung HSC colonies made more red blood cells and megakaryocytes, while the bone marrow colonies tended to make more immune cells,” Looney said.

The human lung HSCs also could restore bone marrow in HSC-deficient mice. The discovery confirmed Looney’s earlier discovery that the mouse lung and bone marrow complemented one another in producing blood, even sending stem cells to restore one another.

“We think these HSCs could be a reservoir of haematopoiesis in a particular organ, in this case the lung, that gets activated whenever the body needs more of any part of the blood, whether it’s platelets, red blood cells or immune cells,” Looney said.

Getting to know the new HSC in town

To show that the lung HSCs truly resided in the lung, and weren’t just escapees from the bone marrow, Conrad and Looney looked for the HSCs in human lung tissue samples.

They found them between blood vessels in an arrangement that was reminiscent of what’s seen in bone marrow.

“They really seem to live there and aren’t just passing through,” Conrad said. 

Lastly, the team analysed the output of routine bone marrow transplants, which today begin with a blood draw from a donor followed by a screen for stem cells. 

Remarkably, nearly a fifth of the stem cells isolated for bone marrow transplant carried the signature of lung HSCs – suggesting that cells in “bone marrow transplants” aren’t only from bone marrow.

There’s a lot more to learn about the lung HSCs. Could the different pools of HSCs serve different therapeutic roles in medicine? Why do the lungs themselves need to make blood?

“The lungs are critical to blood circulation, so it’s tantalising to see the lung HSCs as an emergency reservoir for red blood cell and platelet production,” Looney said. “Now that we know they exist, it opens up a lot of new opportunities for a therapy, hematopoietic stem cell transplantation, that is very commonly used for patients with the need.”

Source: EurekAlert!