Publisher Health

Nearly three quarters of a million fewer global cases of dengue occurred in 2020, which could be linked to COVID-19 disruptions limiting human mobility and contact, according to a new study published in Lancet Infectious Diseases.
Researchers from the London School of Hygiene & Tropical Medicine (LSHTM), Beijing Normal University and other international partners, funded by the Medical Research Council, analysed the monthly dengue cases from the World Health Organization (WHO) Weekly reports between 2014 to 2020 from 23 countries — 16 in Latin America and seven in South East Asia, the main regions where dengue is endemic, as well as climate data on air temperature, relative humidity and precipitation.
They found a strong association between school closures and declines in non-residential trips, such as shopping or using public transport, due to COVID-19 and reduced risk of dengue transmission. This indicates that places such as schools and commonly visited public areas could be dengue transmission hot spots and play a key role in spreading the disease.
Further research is needed into how human movement behaviours (the places people visit, how long they spend there and with whom) impact dengue transmission risk. This could help decision makers decide if measures like contact tracing, testing or quarantine could help control the spread of the disease.
Dr Oliver Brady, Associate Professor and MRC Fellow at LSHTM and study senior author, said: “Currently dengue control efforts are focused on or around the households of people who get sick. We now know that, in some countries, we should also be focusing measures on the locations they recently visited to reduce dengue transmission. For all the harm it has caused, this pandemic has given us an opportunity to inform new interventions and targeting strategies to prevent dengue.”
Dengue is a viral infection transmitted by the Aedes species of mosquitoes, which causes flu-like symptoms. It is found in tropical and sub-tropical climates worldwide, and is most common in urban areas.

A large international study has found an important new benchmark for measuring the risk of death for patients undergoing heart surgery, of which there are two million adults a year globally.
Levels of troponin (a type of protein found in heart muscle) have been used for years, through a blood test, to measure the risk of death and serious complications in patients presenting with symptoms of a heart attack. However, this test is not commonly measured after heart surgery.
With limited data on patients undergoing coronary artery bypass grafting or open-heart surgery such as valve repairs and replacements, recommendations by medical experts varied widely (from 10 times to 70 times or more the laboratory normal value) regarding troponin levels that define heart attack and important heart injury after heart surgery.
This study, published in the New England Journal of Medicine today, assessed patients having heart surgery, measured troponin before and daily for the first few days after surgery, and assessed death and the incidence of major vascular complications — such as heart attack, stroke or life-threatening blood clot — after heart surgery.
“We found that the levels of troponin associated with an increased risk of death within 30 days were substantially higher — 200 to 500 times the normal value- than troponin levels that surgical teams are currently told defines the risk of a patient having one of the most common complications after heart surgery — myocardial injury, a heart muscle injury associated with increased deaths,” said the study’s lead investigator, P.J. Devereaux.
He is a senior scientist at the Population Health Research Institute of McMaster University and Hamilton Health Sciences (HHS), a professor of medicine and health research methodology at McMaster University, and a cardiologist at HHS.
The study found that by 30 days after heart surgery, 2.1% of patients had died, and 2.9% had experience a major vascular complication, such as heart attack, stroke, or life-threatening blot clot.
The study involved 15,984 adult patients with an average age just over 63 years undergoing cardiac surgery. Patients were from 12 countries, with more than a third of the countries being outside of North America and Europe.
“This study is a landmark for the health teams taking care of patients after cardiac surgery. For the first time, we have a marker that is fast and reliable for the monitoring of these patients after cardiac surgery,” said André Lamy, a study investigator, PHRI scientist, professor in McMaster’s department of surgery, and heart surgeon at HHS.
“Our findings will help further studies look at the timing of treatments and procedures to improve patient outcomes after heart surgery,” said investigator Richard Whitlock, PHRI scientist and associate chair, research, professor of McMaster’s department of surgery, and heart surgeon and intensive care doctor at HHS.
The VISION Cardiac Surgery study was funded by Canadian Institutes of Health Research, McMaster Surgical Associates, PHRI internal grant award, HHS, Abbott, Ontario Strategy for Patient Oriented Research, and Hamilton Academic Health Sciences Organization.
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Materials provided by McMaster University. Note: Content may be edited for style and length.

Published in Science, University of Minnesota Medical School researchers found that blood pressure medications have an unanticipated effect on the brain.
The research team discovered that drugs used to treat blood pressure unexpectedly increase the effect of opioids that the brain naturally produces. This can fine-tune the function of a specific brain circuit and counteract the addictive properties of opiates like fentanyl, which are used to treat pain.
“Our findings suggest a new strategy to boost opioid signaling in the brain in a way that is protective and beneficial, with a very low risk of dependence or addiction,” said Patrick Rothwell, PhD, an assistant professor of neuroscience at the U of M Medical School and Medical Discovery Team on Addiction.
The study focused on angiotensin-converting enzyme (ACE), which has long been known to regulate blood pressure. However, little is known about the function of ACE in the brain.
Based on the study findings, Rothwell recommends further research on ACE inhibitors, a safe class of drugs used to control blood pressure. ACE inhibitors have the potential to be redesigned to treat brain conditions.
This research was funded by Minnesota’s Discovery, Research, and Innovation Economy (MnDRIVE) initiative, and the National Institute on Drug Abuse. The project was led by Brian Trieu, an MD/PhD candidate working in the Rothwell lab.
In collaboration with Dr. Swati More from the Center for Drug Design in the College of Pharmacy, Rothwell and University researchers are creating new ACE inhibitors in order to optimize their effect on brain function. This ongoing effort is supported by a Faculty Research Development Grant from the Office of Academic Clinical Affairs.
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Materials provided by University of Minnesota Medical School. Original written by Kat Dodge. Note: Content may be edited for style and length.

The virus does not infect nerve cells that detect odors, researchers have found. Instead, it attacks nearby supporting cells.Few of Covid-19’s peculiarities have piqued as much interest as anosmia, the abrupt loss of smell that has become a well-known hallmark of the disease. Covid patients lose this sense even without a stuffy nose; the loss can make food taste like cardboard and coffee smell noxious, occasionally persisting after other symptoms have resolved.Scientists are now beginning to unravel the biological mechanisms, which have been something of a mystery: The neurons that detect odors lack the receptors that the coronavirus uses to enter cells, prompting a long debate about whether they can be infected at all.Insights gleaned from new research could shed new light on how the coronavirus might affect other types of brain cells, leading to conditions like “brain fog,” and possibly help explain the biological mechanisms behind long Covid — symptoms that linger for weeks or months after the initial infection.The new work, along with earlier studies, settles the debate over whether the coronavirus infects the nerve cells that detect odors: It does not. But the virus does attack other supporting cells that line the nasal cavity, the researchers found.The infected cells shed virus and die, while immune cells flood the region to fight the virus. The subsequent inflammation wreaks havoc on smell receptors, proteins on the surface of the nerve cells in the nose that detect and transmit information about odors.The process alters the sophisticated organization of genes in those neurons, essentially short-circuiting them, the researchers reported.Their paper significantly advances the understanding of how cells critical to the sense of smell are affected by the virus, despite the fact that they are not directly infected, said Dr. Sandeep Robert Datta, an associate professor of neurobiology at Harvard Medical School, who was not involved in the study.“It’s clear that indirectly, if you affect the support cells in the nose, lots of bad things happen,” Dr. Datta said. “The inflammation in the adjacent cells triggers changes in the sensory neurons that prevent them from working properly.”Indeed, many complications of Covid appear to be caused by the immune system’s friendly fire as it responds to infection by flooding the bloodstream with inflammatory proteins called cytokines, which can damage tissue and organs.“This might be a general principle: that a lot of what the virus is doing to us is a consequence of its ability to generate inflammation,” Dr. Datta said.The new study is based on research carried out at Zuckerman Institute and Irving Medical Center at Columbia University in New York; the New York University Grossman School of Medicine; the Icahn School of Medicine at Mount Sinai in New York; Baylor Genetics in Houston; and the School of Medicine at the University of California, Davis. The research was published online in Cell in early February.The scientists examined golden hamsters and human tissue specimens from 23 patients who succumbed to Covid. After the hamsters were infected with the original coronavirus, scientists tracked the damage to their olfactory systems over time.(How do you know a golden hamster has lost its sense of smell? You don’t feed it for several hours and then bury Cocoa Puffs in its bedding, said Benjamin tenOever, a professor of microbiology at NYU Langone Health and an author of the new research. Hamsters that can smell will find the cereal in seconds.)The virus did not invade neurons, the researchers learned, only the cells that play supporting roles in the olfactory system. But that was enough to alter the function of the nearby neurons, leading to a loss of smell.The Coronavirus Pandemic: Key Things to KnowCard 1 of 3A new U.S. strategy.

Rice University bioengineers have shown they can eradicate advanced-stage ovarian and colorectal cancer in mice in as little as six days with a treatment that could be ready for human clinical trials later this year.
The researchers used implantable “drug factories” the size of a pinhead to deliver continuous, high doses of interleukin-2, a natural compound that activates white blood cells to fight cancer. The drug-producing beads can be implanted with minimally invasive surgery. Each contains cells engineered to produce interleukin-2 that are encased in a protective shell.
The treatment and animal test results are described online today in a Science Advances study co-authored by Omid Veiseh, Amanda Nash and colleagues from Rice, the University of Texas MD Anderson Cancer Center, the University of Virginia and others.
Veiseh, an assistant professor of bioengineering whose lab produced the treatment, said human clinical trials could begin as soon as this fall because one of his team’s key design criteria was helping cancer patients as quickly as possible. The team chose only components that had previously proven safe for use in humans, and it has demonstrated the safety of the new treatment in multiple tests.
“We just administer once, but the drug factories keep making the dose every day, where it’s needed until the cancer is eliminated,” Veiseh said. “Once we determined the correct dose — how many factories we needed — we were able to eradicate tumors in 100% of animals with ovarian cancer and in seven of eight animals with colorectal cancer.”
In the newly published study, researchers placed drug-producing beads beside tumors and within the peritoneum, a sac-like lining that supports intestines, ovaries and other abdominal organs. Placement within this cavity concentrated interleukin-2 within tumors and limited exposure elsewhere.

Researchers at the National Eye Institute (NEI) have discovered that power-producing organelles in the eye’s photoreceptor cells, called mitochondria, function as microlenses that help channel light to these cells’ outer segments where it’s converted into nerve signals. The discovery in ground squirrels provides a more precise picture of the retina’s optical properties and could help detect eye disease earlier. The findings, published today in Science Advances, also shed light on the evolution of vision. NEI is part of the National Institutes of Health.
“We were surprised by this fascinating phenomenon that mitochondria appear to have a dual purpose: their well-established metabolic role producing energy, as well as this optical effect,” said the study’s lead investigator, Wei Li, Ph.D./B.M., who leads the NEI Retinal Neurophysiology Section.
The findings also address a long-standing mystery about the mammalian retina. Despite evolutionary pressure for light to be translated into signals and pass instantly from the retina to the brain, the trip is hardly direct. Once light reaches the retina, it must pass through multiple neural layers before reaching the outer segment of photoreceptors, where phototransduction (the conversion of light’s physical energy into cellular signals) occurs. Photoreceptors are long, tube-like structures divided into inner and outer segments. The last obstacle a photon must traverse before moving from the inner to the outer segment is an unusually dense bundle of mitochondria.
Those bundles of mitochondria would seem to work against the process of vision either by scattering light or absorbing it. So, Li’s team set out to investigate their purpose by studying cone photoreceptors from the 13-lined ground squirrel.
Unlike other animal models used for vision research, the 13-lined ground squirrel’s retina comprises mostly cones, which see color, as opposed to rods that enable night vision. Li’s team studies the 13-lined ground squirrel to better understand the causes of human eye diseases that primarily affect cone photoreceptors.
The researchers used a modified confocal microscope to observe the optical properties of living cone mitochondria exposed to light. Far from scattering light, the tightly packed mitochondria concentrated light along a thin, pencil-like trajectory onto the outer segment. Computational modeling using high-resolution mitochondrial reconstructions corroborated the live-imaging findings.

People exposed to more green space during the first year of the COVID-19 pandemic reported significantly less depression and anxiety, according to new University of Colorado Boulder research published March 2 in the journal PLOS One.
The study also found that, at a time when mental health problems soared due to financial woes, supply shortages and nonstop news coverage of the virus, people sought solace in the great outdoors, with one-third spending more time there than they did pre-COVID.
“This research shows how critical it is to keep parks and green spaces open in times of crisis,” said senior author Colleen Reid, an assistant professor of geography in the Institute for Behavioral Science. “It also shows that, as a public health measure, more effort should be made to put in green spaces and make them accessible.”
For the study, the authors presented about 1,200 Denver-area residents with a 30-minute survey gauging their mental health and their perceptions of green space near their home, including: how much there was, whether they could see it, whether it was accessible, how much they used it and its quality. They also collected aerial satellite imagery to objectively quantify greenery in respondents’ neighborhoods.
The survey ran from November 2019 to January 2021.
Once COVID-19 emerged and lockdowns ensued, Reid added additional questions, providing a rare opportunity to also look at how the pandemic influenced mental health over time and what was most stressful about it.

In a world first discovery, South Australian researchers have identified a genetic mutation responsible for a lymphatic disorder that may cause stillbirth or severe, chronic disease in affected children.
An anomaly in the development of lymphatic vessels in unborn children, leading to fluid accumulating in the heart, lungs and other organs, has been uncovered by scientists from the Centre for Cancer Biology (CCB) based at the University of South Australia (UniSA) and SA Pathology.
The findings are published today in the journal Science Translational Medicine.
CCB Director Professor Natasha Harvey says a genetic study of six families affected by stillbirth or lymphoedema revealed the link between a mutated protein coding gene called MDFIC and fluid accumulation in vital organs and tissues.
This has demonstrated that MFDIC is important for controlling the growth and development of the lymphatic vessels in the fetus for the first time.
The Centre for Cancer Biology collaborated with scientists and clinical teams from the Women’s and Children’s Hospital, University of Adelaide, Belgium, Germany, the United States and Iran to make the breakthrough.

Women who enter menopause very early, before age 40, were found to be more likely to develop dementia of any type later in life compared to women who begin menopause at the average menopause-onset age of 50 to 51 years, according to preliminary research to be presented at the American Heart Association’s Epidemiology, Prevention, Lifestyle & Cardiometabolic Health Conference 2022. The meeting will be held in-person in Chicago and virtually Tuesday, March 1 — Friday, March 4, 2022,.
“Our study found that women who enter menopause very early were at greater risk of developing dementia later in life,” said Wenting Hao, M.D., a Ph.D. candidate at Shandong University in Jinan, China. “Being aware of this increased risk can help women practice strategies to prevent dementia and to work with their physicians to closely monitor their cognitive status as they age.”
Dementia involves serious changes in the brain that impair a person’s ability to remember, make decisions and use language. Alzheimer’s disease is the most common type of dementia, while the second most common is vascular dementia, which is the result of disruptions in blood flow to brain cells caused by strokes or plaque build-up in arteries supplying blood to the brain. Both of these types of dementia are more common with age. Diseases affecting specific parts of the brain can also lead to dementia, and a person can have dementia due to more than one disease process.
In the current study, the researchers analyzed the potential relationship between age at menopause onset and the diagnosis of dementia from any cause. Health data was examined for 153,291 women who were an average age of 60 years when they became participants in the UK Biobank (between 2006 and 2010) were examined. The UK Biobank is a large biomedical database that includes genetic and health information on a half million people living in the United Kingdom.
The investigators identified the diagnosis of all types of dementia including Alzheimer’s disease, vascular dementia and dementias from other causes. They calculated risk of occurrence in terms of the age at which the women reported having entered menopause, compared with the women who began menopause at average age of menopause onset, which is 50-51 years (51 years is the average age for menopause onset among women in the U.S.). The results were adjusted for factors including age at last exam, race, educational level, cigarette and alcohol use, body mass index, cardiovascular disease, diabetes, income and leisure and physical activities.
The analysis found: Women who entered menopause before the age of 40 were 35% more likely to have been diagnosed with dementia. Women who entered menopause before the age of 45 were 1.3 times more likely to have been diagnosed with dementia before they were 65 years old (called presenile or early-onset dementia). Women who entered menopause at age 52 or older had similar rates of dementia to those women who entered menopause at average age of menopause onset, which is the age of 50-51 years.Although post-menopausal women are at greater risk of stroke than pre-menopausal women, and stroke can disrupt blood flow to the brain and may result in vascular dementia, in this study the researchers did not find an association between age at menopause and the risk of vascular dementia.

It may be possible to identify the presence of an aggressive brain tumor in children by studying their cerebrospinal fluid, according to new research led by Johns Hopkins Kimmel Cancer Center investigators.
Comparing cerebrospinal fluid samples from 40 patients with medulloblastoma — the most common malignant brain tumor in children, accounting for 10% to 15% of pediatric central nervous system tumors — and from 11 healthy children without the disease, investigators identified 110 genes, 10 types of RNA — the machinery that translates proteins — called circular RNAs, 14 lipids and several metabolites that were expressed differently between the two groups. While these details were not specific enough to distinguish among the four subtypes of medulloblastoma, they could be used to identify the presence of cancer versus normal fluid.
A description of the work was published Feb. 24 in the journal Acta Neuropathologica Communications.
“We believe this is the first comprehensive, integrated molecular analysis of the cerebrospinal fluid in medulloblastoma patients,” says senior study author Ranjan Perera, Ph.D., director of the Center for RNA Biology at Johns Hopkins All Children’s Hospital (JHACH) in St. Petersburg, Florida. Perera is also a senior scientist at the JHACH Cancer & Blood Disorders Institute and an associate professor of oncology at the Johns Hopkins University School of Medicine. He has a secondary affiliation with the JHACH Institute for Fundamental Biomedical Research.
“Our study provides proof of principle that all three molecular approaches — studying RNA, lipids and metabolites — can be successfully applied to cerebrospinal fluid samples, not only to differentiate medulloblastoma patients from those without the disease, but also to provide new insights into the pathobiology of the disease,” Perera adds.
“This study provides data for novel biomarkers to detect and track medulloblastoma, which are very much needed to enable improved patient outcomes,” says Chetan Bettegowda, M.D., Ph.D., Jennison and Novak Families Professor of Neurosurgery at Johns Hopkins. “This work also forms the theoretical basis for examining similar biomarkers for other types of brain cancers and other neurological disorders.”
Current diagnosis is based on clinical assessment, imaging and biopsies from tumor tissue. There is an unmet need for diagnostic tests to detect the disease sensitively during the initial presentation and especially during any recurrences, because recurrences are not always seen on magnetic resonance imaging (MRI), Perera says.
Liquid biopsy — the molecular analysis of biofluids — is a minimally invasive method that shows promise for disease detection and monitoring by measuring circulating tumor cells, DNA, RNA or other substances in the urine, cerebrospinal fluid and blood samples. Because cerebrospinal fluid bathes the brain and spinal cord, it was considered a way to provide a window to tumors arising in the central nervous system and disseminating in the fluid, Perera says.
During the study, Perera and colleagues used gene sequencing, metabolic and lipid profiling laboratory techniques to tease out the differences in RNA, metabolites and lipids in cerebrospinal fluid samples from patients with medulloblastoma and healthy controls. Patients with medulloblastoma were found to have a unique RNA metabolic and lipid landscape in their fluid that might be helpful for diagnosis and monitoring, and that reflects biological changes consistent with the presence of medulloblastoma in the central nervous system, Perera says. The metabolite and lipid profiles both contained indicators of tumor hypoxia — a condition in which tumor cells were deprived of oxygen.
More studies in larger patient populations are necessary to confirm the findings, Perera says. The analysis provides several biomarkers that can be studied further.
The work was supported in part by the Schamroth Project funded by Ian’s Friends Foundation, the Hough Family Foundation, Susan and Robb Hough, and the National Cancer Institute (grant 1R37CA230400).
In addition to Perera and Bettegowda, study co-authors were Bongyong Lee, Rudramani Pokhrel, Menglang Yuan, Stacie Stapleton, George Jallo and Charles Eberhart of Johns Hopkins; Iqbal Mohamad and Timothy Garrett of the University of Florida College of Medicine in Gainesville and Rabi Murad of the Sanford Burnham Prebys Medical Discovery Institute in La Jolla, California.