Publisher Health

Researchers have found a naturally occurring compound, known as hydroquinine, has bacterial killing activity against several microorganisms.
Antimicrobial resistance has become one of the greatest threats to public health globally. It occurs when bacteria, viruses, fungi and parasites change over time and no longer respond to medicines, making it difficult to treat infections. Because of this, there is a pressing need for the development of new antimicrobial drugs to combat infections.
A new study by scientists from the University of Portsmouth and Naresuan and Pibulsongkram Rajabhat Universities in Thailand explored whether hydroquinine, which is found in the bark of some trees, could inhibit any bacterial strains. Hydroquinine is already known to be an effective agent against malaria in humans, but until now there has been little investigation into its drug-resistant properties.
The findings, published in the Tropical Medicine and Infectious Disease journal, suggest the antimicrobial properties of the organic compound make it a potential candidate for future clinical investigation.
Dr Robert Baldock from the School of Pharmacy and Biomedical Sciences at the University of Portsmouth, said: “Using bacterial killing experiments, we found that hydroquinine was able to kill several microorganisms including the common multidrug-resistant pathogen pseudomonas aeruginosa.
“Characteristically, we also discovered that one of the main mechanisms used by these bacteria to escape killing activity of the drug was upregulated with treatment — indicating a robust response from the bacteria.
“By studying this compound further, our hope is that it may in future offer another line of treatment in combatting bacterial infections.”
Drug-resistant bacteria occur in more than 2.8 million infections and are responsible for 35,000 deaths per year. Common antibiotic-resistant “superbugs” cause diseases including sepsis, urinary tract infections, and pneumonia. Statistics show bloodstream infections with the bacteria — P. aeruginosa are associated with high mortality rates of between 30 and 50%.
The study recommends further investigation into the antimicrobial resistance properties and side effects of hydroquinine.
Dr Jirapas Jongjitwimol from the Department of Medical Technology at Naresuan University added: “Our future research aims to uncover the molecular target of hydroquinine. This would help our understanding of how the compound works against pathogenic bacteria and how it could potentially be used in a clinical setting.”
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Materials provided by University of Portsmouth. Note: Content may be edited for style and length.

When Russian forces invaded Ukraine in February 2022, disruptions in civilian life (particularly to the healthcare system) created a dire situation for Ukrainian children with cancer and blood disorders. In response, the St. Jude Global initiative of St. Jude Children’s Research Hospital banded together with many international partners and formed Supporting Action for Emergency Response in Ukraine (SAFER Ukraine). An account of SAFER Ukraine appears in the September issue of The Lancet Haematology.
SAFER Ukraine partners include non-governmental organizations (NGOs) or foundations such as Fundacja Herosi and Tabletochki Charity Foundation, the Polish Society of Pediatric Oncology and Hematology (PSPOH), the International Society for Pediatric Oncology-Europe, Childhood Cancer International-Europe and government agencies plus many other volunteers and contributors. The effort facilitated the safe evacuation of more than 900 patients and families to reestablish medical care abroad.
“SAFER Ukraine demonstrates the importance of collaborative networks in global health, with participation from individuals, institutions and governments, to facilitate both rapid responses to emergencies and ongoing capacity building to improve patient care and outcomes,” said first and co-corresponding author Asya Agulnik, M.D., M.P.H., St. Jude Department of Global Pediatric Medicine, St. Jude Global Euro Regional Program director and St. Jude Global Critical Care Program director.
A model for international cooperation
The SAFER Ukraine effort provides a proof-of-concept for global health that can be leveraged in future international emergency responses. There were several unique and notable characteristics of SAFER Ukraine that helped the effort be successful. These factors include the patient population, geopolitical context and well-established pre-war collaborations.
For example, childhood cancer treatment can be effective but requires precise timing. Patients whose care was interrupted can benefit from a rapid evacuation and relocation to a hospital where they can continue their care. If performed quickly, these patients can receive a substantial survival benefit. The war also galvanized support for Ukraine, with the European Union extending immediate protection and legal status to Ukrainian refugees. That status created the legal and financial framework that ultimately made it possible to refer patients throughout Europe for care. Additionally, St. Jude Global already had partnerships in the region. The rapid repurposing of existing collaborative networks was key to the effort’s success.

A person’s blood type may be linked to their risk of having an early stroke, according to a new meta-analysis led by University of Maryland School of Medicine (UMSOM) researchers. Findings were published today in the journal Neurology. The meta-analysis included all available data from genetic studies focusing on ischemic strokes, which are caused by a blockage of blood flow to the brain, occurring in younger adults under age 60.
“The number of people with early strokes is rising. These people are more likely to die from the life-threatening event, and survivors potentially face decades with disability. Despite this, there is little research on the causes of early strokes,” said study co-principal investigator Steven J. Kittner, MD, MPH, Professor of Neurology at UMSOM and a neurologist with the University of Maryland Medical Center.
He and his colleagues conducted the study by performing a meta-analysis of 48 studies on genetics and ischemic stroke that included 17,000 stroke patients and nearly 600,000 healthy controls who never had experienced a stroke. They then looked across all collected chromosomes to identify genetic variants associated with a stroke and found a link between early-onset stroke — occurring before age 60 — and the area of the chromosome that includes the gene that determines whether a blood type is A, AB, B, or O.
The study found that people with early stroke were more likely to have blood type A and less likely to have blood type O (the most common blood type) — compared to people with late stroke and people who never had a stroke. Both early and late stroke were also more likely to have blood type B compared to controls. After adjusting for sex and other factors, researchers found those who had blood type A had a 16 percent higher risk of having an early stroke than people with other blood types. Those who had blood type O had a 12 percent lower risk of having a stroke than people with other blood types.
“Our meta-analysis looked at people’s genetic profiles and found associations between blood type and risk of early-onset stroke. The association of blood type with later-onset stroke was much weaker than what we found with early stroke,” said study co-principal investigator Braxton D. Mitchell, PhD, MPH, Professor of Medicine at UMSOM.
The researchers emphasized that the increased risk was very modest and that those with type A blood should not worry about having an early-onset stroke or engage in extra screening or medical testing based on this finding.
“We still don’t know why blood type A would confer a higher risk, but it likely has something to do with blood-clotting factors like platelets and cells that line the blood vessels as well as other circulating proteins, all of which play a role in the development of blood clots,” said Dr. Kittner. Previous studies suggest that those with an A blood type have a slightly higher risk of developing blood clots in the legs known as deep vein thrombosis. “We clearly need more follow-up studies to clarify the mechanisms of increased stroke risk,”he added.
In addition to Dr. Kittner and Dr. Mitchell, UMSOM faculty involved in this study included Huichun Xu, MD, PhD, Associate Professor of Medicine; Patrick F. McArdle, PhD, Associate Professor of Medicine; Timothy O’Connor, PhD, Associate Professor of Medicine; James A. Perry, PhD, Assistant Professor of Medicine; Kathleen A. Ryan, MPH, MS, Statistician; John W. Cole, MD, Professor of Neurology; Marc C. Hochberg, MD, MPH, Professor of Medicine; O. Colin Stine, PhD, Professor of Epidemiology and Public Health; and Charles C. Hong, MD, PhD, Melvin Sharoky MD Professor of Medicine.
A limitation of the study was the relative lack of diversity among participants. The data was derived from the Early Onset Stroke Consortium, a collaboration of 48 different studies across North America, Europe, Japan, Pakistan, and Australia. About 35 percent of the participants were of non-European ancestry.
“This study raises an important question that requires a deeper investigation into how our genetically predetermined blood type may play a role in early stroke risk,” said Mark T. Gladwin, MD, Executive Vice President for Medical Affairs, UM Baltimore, and the John Z. and Akiko K. Bowers Distinguished Professor and Dean, University of Maryland School of Medicine. “It points to the urgent need to find new ways to prevent these potentially devastating events in younger adults.”
The study was supported by the National Institutes of Health and Department of Veterans Affairs. Researchers from more than 50 institutions worldwide were co-authors on this study.

New research confirms for the first time that ethnicity is a risk factor for developing kidney disease in people with Type 1 diabetes.
The study is one of the largest of its type and is published today in Diabetes Care by researchers from King’s College London. The findings also show people of African-Caribbean heritage and living with diabetes have nearly a 60% greater risk of advanced kidney disease.
Type 1 diabetes is an autoimmune condition that can cause symptoms early in life. Type 2 diabetes is often lifestyle-related and can develop over time. An estimated 10% of people with diabetes have type 1, with 400,000 people living with the condition in the UK. Kidney disease affects nearly 30-40% of people with diabetes, regardless of type.
While it is known that ethnicity is a risk factor for type 2 diabetes and kidney disease, there is little understanding of whether ethnicity is a risk factor for kidney complications of type 1 diabetes. Most previous studies looking at risk factors for kidney disease have been in less diverse or predominantly Caucasian cohorts.
Researchers from King’s College London looked at more than 5,000 people with type 1 diabetes. All people in this cohort had good kidney function and 13% were African-Caribbean. They observed after eight years of follow-up that 260 people had a decline of more than 50% of kidney function and developed stage 4 kidney disease, which is an indicator of severe and advanced kidney disease. Stage 5 is kidney failure when people often need a kidney transplant or dialysis to live.
Findings show that this increased risk for African-Caribbean people is independent of other established risk factors for kidney disease such as blood pressure and glucose control.
Lead author Dr Janaka Karalliedde, from King’s College London, said: “Diabetes-related kidney failure is devastating for people affected and their families. This is the first study in type 1 diabetes to describe the impact of ethnicity on kidney function loss. We observed that African-Caribbean people with type 1 diabetes are at nearly 60% higher risk of losing more than half of their kidney function and that this loss also occurs faster. Further studies are needed to study and understand the exact reasons for this increased risk of kidney disease in African-Caribbean people with type 1 diabetes.”
Hilary Nathan, Director of Policy and Communications at JDRF UK: “This is important research, showing for the first time that people of African-Caribbean heritage have a far higher risk of developing kidney disease because of type 1 diabetes. This research area needs greater funding and focus to help form future approaches to genuinely personalised medicine, so that people from African-Caribbean backgrounds with type 1 diabetes do not have to face undue fear or consequences of traumatic kidney function loss. The study was supported by a research grant from Guy’s and St Thomas Hospital Charity.”
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Materials provided by King’s College London. Note: Content may be edited for style and length.

Scientists working to develop new therapies and treatments for heart failure patients have discovered three proteins that can be injected immediately after a heart attack, which have the potential to preserve heart function following an attack.
Positive preclinical data in Science Translational Medicine, published today, outlines the mechanisms of the three proteins, which have been shown to restore heart function following a heart attack in mice.
Heart failure is the primary cause of death and disability globally, affecting approximately 64 million people worldwide according to the British Heart Foundation. There is currently no effective therapeutic treatment.
Led by Mauro Giacca, Professor of Cardiovascular Sciences at King’s College London, supported by the British Heart Foundation, researchers developed an innovative technology called FunSel that searched for proteins that could protect heart cells against the rapid cell death that typically occurs following a heart attack.
Forcefield Therapeutics, a pioneer of best-in-class therapeutics to retain heart function via protection of cardiomyocytes, which was launched in 2022 backed by leading healthcare investor Syncona, is undertaking the development work to enable clinical trials in patients in the future. The work originated at the International Centre for Genetic Engineering and Biology (ICGEB) and the University of Trieste, Italy.
Funsel, a protein ‘search engine’ screens a library of human proteins to identify those with therapeutic potential, in an unbiased manner (unconstrained by the bias that researchers typically bring to drug development). Starting from a library of over 1,000 proteins, it identified three, (Chrdl1, Fam3c and Fam3b) which have been shown to prevent cardiac damage in mice after a heart attack and preserve cardiac function over time.

The risk of children being orphaned per COVID-19 death is highest in the poorest countries and those where people of reproductive age have the highest rates of non-communicable diseases, according to a new study published this week in the open-access journal PLOS Global Public Health by Callum Lowe of Australian National University and colleagues.
Due to the higher COVID-19 mortality risk among adults than children, and the propensity of the SARS-CoV-2 virus to quickly spread throughout a household, there is the possibility that children will survive a COVID-19 infection while their parents or caregivers will not. In this study, the researchers used a previously developed COVID-19 orphanhood calculator to predict the total orphans per COVID-19 death for 139 countries. The calculator integrated information on fertility rates and pandemic mortality by age and sex. Information on other factors, including vaccine coverage and sociodemographics was also available at the country level.
The team found that the risk of orphaned children (those who have lost at least one of their parents or caregivers) was much higher in countries below median GDP per capita (1.56 orphans per COVID-19 death) compared to countries above median GDP (0.09 orphans per death). The increased risk of orphans was specifically associated with greater poverty prevalence (B = 2.32, p

Pain is an important alarm system that alerts us to tissue damage and prompts us to withdraw from harmful situations. Pain is expected to subside as injuries heal, but many patients experience persistent pain long after recovery. Now, a new study published in Science Translational Medicine points to possible new treatments for chronic pain with a surprising link to lung cancer. The work was spearheaded by an international team of researchers at IMBA — Institute of Molecular Biotechnology of the Austrian Academy of Sciences, Harvard Medical School, and Boston Children’s Hospital. Their findings of the research, conducted in laboratory mouse models, open up multiple therapeutic opportunities that could allow the world to improve chronic pain management and eclipse the opioid epidemic.
Acute pain is an important danger signal. By contrast, chronic pain is based on persistent injury and can even be experienced in the absence of a stimulus, injury, or disease. Despite the hundreds of millions of people affected, chronic pain is among the least well-managed areas of healthcare. To improve how persistent pain is managed and considering the raging opioid crisis, it is paramount to develop novel drugs based on a fundamental understanding of the underlying mechanisms. “We had previously shown that sensory neurons produce a specific metabolite, BH4, which then drives chronic pain, such as neuropathic pain or inflammatory pain,” says project lead and co-corresponding author Shane Cronin, a staff scientist in the Penninger lab at IMBA and a former postdoc in the Woolf lab at Harvard Medical School and F.M. Kirby Neurobiology Center, Boston Children’s Hospital. “The concentrations of BH4 correlated very well with the pain intensity. So, we naturally thought that this was a great pathway to target.”
To identify drugs that reduce BH4 levels in pain neurons, the researchers performed a “phenotypic screen” of 1000 target-annotated, FDA-approved medications. This approach allowed the scientists to start their search using medications that are currently in use for various indications, and to identify undescribed, off-target analgesic properties. Among the first findings of this hypothesis-driven search, the team was able to link the previously observed analgesic effects of several drugs, including clonidine and capsaicin, to the BH4 pathway.
“However, our phenotypic screen also allowed us to ‘repurpose’ a surprising drug,” says Cronin. The drug ‘fluphenazine’, an antipsychotic, has been used to treat schizophrenia. “We found that fluphenazine blocks the BH4 pathway in injured nerves. We also demonstrated its effects in chronic pain following nerve injury in vivo.” The researchers also found that the effective analgesic dose of fluphenazine in their experiments in the mouse model is comparable to the low end of the doses safely indicated for schizophrenia in humans.
In addition, the screen uncovered a novel and unexpected molecular link between the BH4 pathway and EGFR/KRAS signaling, a pathway involved in multiple cancers. Blocking EGFR/KRAS signaling reduced pain sensitivity by decreasing the levels of BH4. The genes of EGFR and KRAS are the two most frequently mutated genes in lung cancer, which prompted the researchers to look at BH4 in lung cancer. Surprisingly, by deleting an important enzyme, GCH1, in the BH4 pathway, the mouse models of KRAS-driven lung cancer developed fewer tumors and survived much longer. Hence, the researchers uncovered a common signaling pathway for chronic pain and lung cancer through EGFR/KRAS and BH4, thus opening up new avenues of treatment for both conditions.
“Chronic pain is currently subjected to often ineffective palliative treatments. Furthermore, effective painkillers such as opioids can lead, if used inappropriately, to severe addiction. It is therefore critical to find and develop new and repurposed drugs to treat chronic pain,” says co-corresponding author Clifford Woolf, professor of neurology and neurobiology at Harvard Medical School and director of the F.M. Kirby Neurobiology Center at Boston Children’s Hospital.
One intriguing aspect of the study is the mechanistic link between pain and lung cancer. “The same triggers that drive tumor growth appear to be also involved in setting the path to chronic pain, often experienced by cancer patients. We also know that sensory nerves can drive cancer, which could explain the vicious circuit of cancer and pain,” adds co-corresponding author Josef Penninger, IMBA group leader and founding director, who is currently also the director of the Life Sciences Institute at the University of British Columbia (UBC), Vancouver, Canada. “Understanding these cross-talks is therefore not only critical for cancer treatments but might also help to improve the quality of life for cancer patients towards less pain.”

Cilia are tiny, hair-like structures on cells throughout our bodies that beat rhythmically to serve a variety of functions when they are working properly, including circulating cerebrospinal fluid in brains and transporting eggs in fallopian tubes.
Defective cilia can lead to disorders including situs inversus — a condition where a person’s organs develop on the side opposite of where they usually are.
Researchers know about many of cilia’s roles, but not exactly how they beat in the first place. This knowledge would be a step toward better understanding, and ultimately being able to treat, cilia-related diseases.
A team of McKelvey School of Engineering researchers at Washington University in St. Louis, led by Louis Woodhams, senior lecturer, and Philip V. Bayly, the Lee Hunter Distinguished Professor and chair of the Department of Mechanical Engineering & Materials Science, have developed a mathematical model of the cilium in which beating arises from a mechanical instability due to steady forces generated by the cilium motor protein, dynein.
Results of the research appeared on the cover of the August issue of Journal of the Royal Society Interface.
Bayly’s lab has been working with cilia as a model to study vibration, wave motion and instability in mechanical and biomedical systems. As intricate nanomachines in their own right, cilia could inspire similarly propelled machines that can do useful tasks on the tiniest scales, maybe even for chemical sensing or drug delivery in the human body.
The new model will allow the team to explore what happens when the motor protein exerts different forces, or when internal structures are more or less stiff, as a result of genetic or environmental factors.
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Materials provided by Washington University in St. Louis. Original written by Beth Miller. Note: Content may be edited for style and length.

Since the start of the COVID-19 pandemic, images of the coronavirus, SARS-CoV-2, have been seared in our minds. But the way we picture the virus, typically as a sphere with spikes, is not strictly accurate. Microscope images of infected tissues have revealed that coronavirus particles are actually ellipsoidal, displaying a wide variety of squashed and elongated shapes.
Now, a global research team, including scientists from Queen’s University, Canada, and the Okinawa Institute of Science and Technology (OIST), Japan, have modeled how the different elliptical shapes affect the way these viral particles rotate within fluids, impacting how easily the virus can be transmitted. The study was published recently in Physics of Fluids.
“When coronavirus particles are inhaled, these particles move around within the passageways in the nose and lungs,” said Professor Eliot Fried, who leads the Mechanics and Materials Unit at OIST. “We are interested in studying to what extent they are mobile in these environments.”
The specific type of movement that the scientists modeled is known as rotational diffusivity, which determines the rate at which the particles rotate as they move through fluid (in the coronavirus’ case, droplets of saliva). Particles which are smoother and more hydrodynamic encounter less drag resistance from the fluid and rotate faster. For coronavirus particles, this rotational speed affects how well the virus can attach to and infect cells.
“If the particles rotate too much, they might not spend enough time interacting with the cell to infect it, and if they rotate too little, they might not be able to interact in the necessary way,” explained Prof. Fried.
In the study, the scientists modeled both prolate and oblate ellipsoids of revolution. These shapes differ from spheres (which have three axes of identical length) in just one of their axes, with prolate shapes having one longer axis, whilst oblate shapes have one shorter axis. Taken to the extreme, prolate shapes elongate into rod-like shapes, whilst oblate shapes squash into coin-like shapes. But for coronavirus particles, the differences are more subtle.
The scientists also made the model the most realistic yet, by adding the spike proteins onto the surface of the ellipsoids. Previous research from Queen’s University and OIST showed that the presence of triangular-shaped spike proteins lowers the speed at which the coronavirus particles rotate, potentially increasing their ability to infect cells.
Here, the scientists modelled the spike proteins in a simpler way — with each spike protein represented by a single sphere on the surface of the ellipsoids.
“We then figured out the arrangement of the spikes on the surface of each ellipsoidal shape by assuming that they all contain the same charge,” explained Dr. Vikash Chaurasia, a postdoctoral researcher in the OIST Mechanics and Materials Unit. “Spikes with identical charges repel each other and prefer to be as far from each other as possible. They therefore end up evenly distributed across the particle in a way that minimizes this repulsion.”
In their model, the researchers found that the more a particle differs from a spherical shape, the slower it rotates. This could mean that the particles are better able to align and attach to cells.
The model is still simplistic, the researchers acknowledge, but it brings us one step closer to understanding the transport properties of the coronavirus and could help pin down one of the factors key to its infective success.

According to ARRS’ American Journal of Roentgenology (AJR), fully automated and normalized body composition analysis of abdominal CT has promise to augment traditional cardiovascular risk prediction models.
“Visceral fat area from fully automated and normalized analysis of abdominal CT examinations predicts subsequent myocardial infarction or stroke in Black and White patients, independent of traditional weight metrics, and should be considered as an adjunct to BMI in risk models,” wrote first author Kirti Magudia, MD, PhD, currently from the department of radiology at Duke University School of Medicine.
Dr. Magudia and colleagues’ retrospective study numbered 9,752 outpatients (5,519 women, 4,233 men; 890 self-reported Black, 8,862 self-reported White; mean age, 53.2 years) who underwent routine abdominal CT at Brigham and Women’s Hospital or Massachusetts General Hospital from January-December 2012, sans a major cardiovascular or oncologic diagnosis within 3 months of examination. Fully automated deep learning body composition analysis was performed at the L3 vertebral level to determinate three body composition areas: skeletal muscle area, visceral fat area, and subcutaneous fat area. Subsequent myocardial infarction or stroke was established via electronic health records.
Ultimately, after normalization for age, sex, and race, visceral fat area derived from routine CT was associated with risk of myocardial infarction (HR 1.31 [1.03-1.67], p=.04 for overall effect) and stroke (HR 1.46 [1.07-2.00], p=.04 for overall effect) in multivariable models in Black and White patients; normalized weight, BMI, skeletal muscle area, and subcutaneous fat area were not.
Noting that their large study demonstrates a pipeline for body composition analysis and age-, sex-, and race-specific reference values to add prognostic utility to clinical practice, “we anticipate that fully automated body composition analysis using machine learning could be widely adopted to harness latent value from routine imaging studies,” the authors of this AJR article concluded.
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