Vaccines can be made over 25% more effective by adding left-handed chiral gold nanoparticles as adjuvants, according to a study by an international collaboration in which Brazilian researchers took part. An article reporting the results is published in Nature.
Three research groups collaborated on the study, one affiliated with the University of Michigan in the United States, and another with Jiangnan University in China. The Brazilian group was led by André Farias de Moura, a professor in the Chemistry Department at the Federal University of São Carlos (UFSCar) and a researcher with the Center for Development of Functional Materials (CDMF), one of the Research, Innovation and Dissemination Centers (RIDCs) funded by FAPESP.
The study did not involve COVID-19 vaccines because it began well before the pandemic. The researchers used vaccines developed to combat a specific influenza virus strain. While this is not the strain that is currently circulating in Brazil, in principle the results can be generalized for any type of vaccine, evidently with case-by-case complementary studies. The reason is that left-handed chiral gold nanoparticles are not the active ingredient, but an adjuvant that potentiates the recipient's immune response.
"The key to understanding the contribution of these nanoparticles is the concept of chirality, which applies to an object or system that can't be superimposed on its own mirror image," Moura told Agência FAPESP.
The number of Americans with visual impairment or blindness is expected to jump to more than 8 million by the year 2050, according to research lead by the USC Gayle and Edward Roski Eye Institute conducted back in 2016.
With the youngest baby boomers reaching 65 years old by 2029, age-related eye diseases and conditions are expected to swell during what's being called the "silver tsunami".
According to medical experts, it's safe to say many of those cases will be caused by retinal degenerative diseases, the progressive degeneration of the light-sensitive photoreceptors in your retina.
Based on these estimates, there is an unmet need for new technologies that treat vision loss due to diseases of photoreceptor degeneration.
While there are no successful non-invasive therapeutics currently available for the treatment of vision loss, researchers at USC have come up with a new idea to address this growing problem.
Currently, ophthalmologists use electronic technology to directly stimulate retinal neurons by implanting electrode devices inside the eye, a technique that requires expensive and invasive surgery.
The research team in the USC Viterbi School of Engineering's Department of Biomedical Engineering is exploring a non-surgical solution that could restore sight by using another of the five senses.
Before being accidentally introduced to the New World by the 16th century slave trade, the yellow fever mosquito was a species native only to Africa. Highly adaptable, it has since become an invasive species in North America, but researchers at The Ohio State University may have found a way to squash the pesky population in its juvenile stages.
Recently published in the journal Insects, a new paper describes how mosquitoes have evolved a natural resistance to some chemical insecticides, and offers an alternative called carbon black, a type of carbon-based nanoparticles, or CNPs.
Study co-author and an associate professor of entomology at Ohio State, Peter Piermarini described CNPs as "microscopic" materials made out of organic elements. The study used a modified version of carbon black called Emperor 1800, which is often used to coat automobiles black. While CNPs are a relatively new scientific development, they have been considered as new tools to control various insect and pest infestations, he said.
"If we can learn more about how carbon black works and how to use it safely, we could design a commercially available nanoparticle that is highly effective against insecticide-resistant mosquitoes," Piermarini said.
For many of us, Google Maps has become an indispensable daily tool: We pop open a web browser and instantly access a powerful map where we can get directions, zoom in and pan, overlay features like traffic and terrain, and search for specific landmarks. But what if there were a tool with similar functionality to explore an entirely different kind of map? What if we had a Magic School Bus-esque ability to dive deep into the details of tissues that make up the human body?
This is precisely the idea behind Minerva, a software tool developed by Harvard Medical School researchers in the Laboratory of Systems Pharmacology in the Department of Systems Biology in the Blavatnik Institute at HMS.
Minerva, available online to anyone, is named after the Roman goddess of wisdom. It allows users to access in-depth maps of tissue samples gathered during research, ranging from cancerous tumors to heart muscle in distress. On each map, users can zoom and pan, overlay features such as immune cells, and explore noteworthy areas. The maps also incorporate the expertise of scientists and medical doctors who can create narratives to guide users through the samples.
The researchers hope that as Minerva's library of tissue samples grows, the tool will be used by other scientists, scientific journals, clinicians, trainees, medical students, or anyone who is simply curious, thus allowing scientific information—and scientific expertise—to be shared more broadly.
University of Calgary researchers have identified a new oxygen sensing mechanism in a small population of spinal cord neurons capable of protecting the brain and other vital organs from low oxygen (hypoxia). As blood oxygenation decreases mammals mount a cardiorespiratory response and prioritize oxygen supply to vital organs. The team discovered the kick-start to that rescue response are spinal oxygen sensors (SOS) that trigger activation of the sympathetic and respiratory nervous system.
"Understanding how the central nervous system regulates oxygen supply is of considerable scientific and medical importance," say Dr. Nicole Barioni, Ph.D., first author on the study. "Hypoxia can lead to cognitive decline, memory impairment and in extreme circumstances such as heart attack, stroke or sudden infant death syndrome (SIDS), can be fatal."
The study, published in Science Advances, is the first to definitively demonstrate the existence of spinal oxygen sensors. The result of eight years of research by Barioni and principal investigator, Dr. Richard Wilson, Ph.D.
There's no safe way to get a close-up view of the human heart as it goes about its work: you can't just pop it out, take a look, then slot it back in. Scientists have tried different ways to get around this fundamental problem: they've hooked up cadaver hearts to machines to make them pump again, attached lab-grown heart tissues to springs to watch them expand and contract. Each approach has its flaws: reanimated hearts can only beat for a few hours; springs can't replicate the forces at work on the real muscle. But getting a better understanding of this vital organ is urgent: in America, someone dies of heart disease every 36 seconds, according to the Centers for Disease Control and Prevention.
Now, an interdisciplinary team of engineers, biologists, and geneticists has developed a new way of studying the heart: they've built a miniature replica of a heart chamber from a combination of nanoengineered parts and human heart tissue. There are no springs or external power sources—like the real thing, it just beats by itself, driven by the live heart tissue grown from stem cells. The device could give researchers a more accurate view of how the organ works, allowing them to track how the heart grows in the embryo, study the impact of disease, and test the potential effectiveness and side effects of new treatments—all at zero risk to patients and without leaving a lab.
Purdue University researchers in the College of Pharmacy and College of Engineering are developing a patent-pending treatment that could impact millions of American lives each year.
The Centers for Disease Control and Prevention reports that at least 1.7 million American adults develop sepsis annually; almost 270,000 die as a result. One in three patients who die in a hospital has sepsis. Sepsis occurs when the body's immune response to an infection or injury goes unchecked. Chemicals or proteins released into the blood lead to leaky blood vessels, inflammation and widespread blood clots. These conditions lead to impaired blood flow, which can cause organ damage and death.
Yoon Yeo leads a Purdue team developing biocompatible nanoparticles that treat sepsis systemically through intravenous injection. Yeo is a professor and the associate department head of industrial and physical pharmacy in the College of Pharmacy. She also is a professor in the Weldon School of Biomedical Engineering. The research was published in the Aug. 2021 issue of Science Advances.
Children with Dravet syndrome, a severe form of epilepsy that begins in infancy, experience seizures, usually for their entire life. They are at high risk of sudden unexpected death in epilepsy (SUDEP) and can also develop intellectual disability and autism. Available treatments typically fail to improve these symptoms.
Now, a group of scientists at Gladstone Institutes led by Lennart Mucke, MD, reports new findings in the journal Science Translational Medicine that could guide the development of better therapeutic strategies for Dravet syndrome and related conditions.
The researchers had previously discovered, in a mouse model of Dravet syndrome, that genetically removing the protein tau from the entire body during embryonic development reduces epilepsy, SUDEP, and autism-like behaviors. In the new study, they pinpoint the key cell type in the brain in which tau levels must be reduced to avoid these problems. They also show that lowering tau is still effective in mice when the intervention is delayed until after their birth.
"Our findings provide new insights into the cellular mechanisms by which tau reduction prevents abnormal overexcitation in the brain," says Mucke, director of the Gladstone Institute of Neurological Disease. "They are also encouraging from a therapeutic perspective, since in humans, initiating treatment after birth is still more feasible than treating embryos in the womb."
Currently available therapies to treat multiple sclerosis (MS) lack precision and can lead to serious side effects. Researchers at Karolinska Institutet in Sweden have now developed a method for identifying the immune cells involved in autoimmune diseases, and have identified four new target molecules of potential significance for future personalized treatment of MS. The results, which are published in Science Advances, have been obtained in collaboration with KTH Royal Institute of Technology and Region Stockholm.
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system that usually develops between the ages of 20 and 40. The disease is driven by immune cells that mistakenly attack the tissue surrounding neurons in the brain and spinal cord. MS causes neurological symptoms such as sensory disorders, difficulties with walking and balance and impaired vision. There is currently no cure, only treatments that reduce relapse rates and alleviate symptoms.
According to folklore, silver bullets kill werewolves, but in the real world, researchers want to harness this metal to fight another deadly foe: bacteria. Recently, scientists have tried to develop a silver coating for implantable medical devices to protect against infection, but they've had limited success. In a study in ACS Central Science, one team describes a new, long-acting silver-ion releasing coating that, in rats, prevents bacteria from adhering to implants and then kills them.
Sometimes medical care requires surgeons to implant a device, such as a tube to drain a wound or the bladder, or to deliver medication directly into the blood. However, bacteria can attach to and collect on the surfaces of these devices, creating a risk for dangerous infections. Researchers have been working to develop bacteria-repelling coatings, including those containing silver, which is known to kill microbes. However, their efforts have faced numerous challenges: Silver can also be toxic to human cells, and it's difficult to make a coating that continually releases small amounts of the metal over long periods, for example. Dirk Lange and Jayachandran Kizhakkedathu wanted to identify a formula that could overcome these and other difficulties.
At least 5 million people in Germany suffer from liver disease. Fibrosis, the pathological proliferation of connective tissue, plays an important role in many complications of chronic liver problems. Activated hepatic stellate cells (HSCs) are massively involved in this tissue remodeling. An international research team led by Professor Dr. Ingmar Mederacke, Managing Senior Physician at the Department of Gastroenterology, Hepatology and Endocrinology at the Hannover Medical School (MHH) has now found an approach to lower the activation of HSCs and reduce the associated development of liver fibrosis. The work has been published in the journal Science Translational Medicine.
Hepatic stellate cells produce connective tissue
Liver fibrosis and the end-stage of liver fibrosis, cirrhosis, are a significant medical problem for which there are as yet no suitable drugs. The best-known causes include chronic alcohol consumption, infection with hepatitis viruses, but also medication or a fatty liver. The pathogenic stimuli damage the liver cells, the so-called hepatocytes. They die and thus trigger an inflammatory reaction. Until now, it was not known how this inflammatory process activates the hepatic stellate cells. The HSCs are located in the blood vessel walls in the immediate vicinity of the hepatocytes, where they mainly store vitamin A when at rest. However, when they are activated, they transform into myofibroblasts and produce abnormally large amounts of connective tissue.
The global effort against tuberculosis, a disease which takes 1.5 million lives annually, presents some cause for optimism, according to an expert from the Hackensack Meridian Center for Discovery and Innovation (CDI) and a colleague from the Harvard T.H. Chan School of Public Health.
The paper "Anti-tuberculosis treatment strategies and drug development: challenges and priorities" is authored by Véronique Dartois, a member of the CDI, and her colleague Eric J. Rubin, of Harvard, and appears in the latest issue of Nature Reviews Microbiology.
The two experts assess the last decade-plus of progress in developing new drug regimens, as well as the discoveries made toward cracking the scientific riddle of the stubborn bacterial disease which disproportionately affects the developing world.
"For now, big challenges remain, but change has already come and there is cause for optimism with a healthy dose of realism," the authors write.
The paper states that multi-drug regimens—the current one-size-fits-all strategy for drug-susceptible TB takes six months under medical supervision—has saved millions of lives.
Science has also reached an "exciting juncture"—where global health authorities are on the cusp of establishing a four-month regimen of drugs in a different combination, and a new 3-drug regimen that cures multidrug resistant TB in six months, both of which could further battle back against this worldwide scourge. Furthermore, crucial partnerships like the TB Drug Accelerator, of which the two authors are part, have made significant advances in understanding how the available drugs work, what new treatments are promising, and the biological problems of the Mycobacterium tuberculosis organism itself.
Osteoarthritis is a wear-and-tear disorder marked by bone thickening and cartilage degeneration, an excruciatingly painful disability and a major cause of impaired mobility as people age. But scientists have begun viewing this form of arthritis differently with a deeper understanding of the disorder's causes and an eye toward personalized medicine as a treatment option.
Although for decades medical experts have focused on problems such as the pain caused by bone thickening and the disappearance of cartilage, scientists conducting research in Homburg, Germany at the Institute of Experimental Orthopedics and Osteoarthritis Research, say bone malalignment may play a critical role in osteoarthritis. In a novel clinical study, medical scientists demonstrate how the alignment problem can contribute to osteoarthritis—and they also suggest that correcting it can protect cartilage and reverse its degeneration.
"Although osteoarthritis, a leading cause of disability, has been associated with joint malalignment, scientific translational evidence for this link is lacking," wrote Dr. Tamás Oláh, first author of a research paper in Science Translational Medicine.
But Oláh and a team of researchers launched a two-pronged approach to the problem demonstrating in both animal research and in a human case study that relieving a troublesome misalignment of the joint can help alleviate pain and restore the shock-absorbing role of cartilage in the knee. They report that malalignment of a joint can cause excessive pressure to be placed on it in a manner similar to a condition known as varus malalignment, more commonly known as bow-leggedness. People with severe forms of that condition can suffer cartilage loss and impaired mobility.
New research in mice raises the prospects for development of post-concussion therapies that could ward off cognitive decline and depression, two common conditions among people who have experienced a moderate traumatic brain injury.
The study in mice clarified the role of specific immune cells in the brain that contribute to chronic inflammation. Using a technique called forced cell turnover, researchers eliminated these cells in the injured brains of mice for a week and then let them repopulate for two weeks.
"It's almost like hitting the reset button," said senior study author Jonathan Godbout, professor of neuroscience in The Ohio State University College of Medicine.
Compared to brain-injured mice recovering naturally, mice that were given the intervention showed less inflammation in the brain and fewer signs of thinking problems 30 days after the injury.
Though temporarily clearing away these cells, called microglia, in humans isn't feasible, the findings shed light on pathways to target that could lower the brain's overall inflammatory profile after a concussion, potentially reducing the risk for behavioral and cognitive problems long after the injury.
"In a moderate brain injury, if the CT scan doesn't show damage, patients go home with a concussion protocol. Sometimes people come back weeks, months later with neuropsychiatric issues. It's a huge problem affecting millions of people," said Godbout, faculty director of Ohio State's Chronic Brain Injury Program and assistant director of basic science in the Institute for Behavioral Medicine Research.
University of Texas at Dallas researchers have developed a rapid virus test using gold particles and lasers that promises to deliver results as accurate as lab tests in a fraction of the time.
The technology, called digital plasmonic nanobubble detection—or Diamond for short—is 150 times more accurate than standard rapid tests, according to a study published in Nature Communications last month. Its accuracy is comparable to polymerase chain reaction (PCR) tests, which take hours to perform.
The team of UTD scientists that authored the study, led by associate professor of mechanical engineering Dr. Zhenpeng Qin, tested Diamond against respiratory syncytial virus, although the researchers say the technology can be used to detect other prominent viruses, like COVID-19 and influenza.
A team of researchers from the French health care company Sanofi, working with the National Institutes of Health and the National Cancer Institute in the U.S., has developed two new vaccines against Epstein-Barr infections. In their paper published in the journal Science Translational Medicine, the group describes attributes of the two vaccines and their effectiveness in mouse models.
Epstein-Barr viral infections are known to cause mononucleosis and have also been associated with several other conditions including certain cancers. In January, it was found to be a likely cause of multiple sclerosis. Prior research has shown that approximately 95% of adults in the world today have been infected by the virus. For that reason, researchers have been working on a vaccine to protect people from infection, but thus far, none have worked as hoped. In this new effort, the researchers working on these two new vaccines believe they have made a breakthrough.
The work involved developing nanoparticle-based vaccines that target the glycoproteins that mediate entry of the virus into both B cells and epithelial cells. The idea is that this will help the immune system target the viruses and kill them. The vaccines are called gH/gL+gp350D123 and gH/gL/gp42+gp350D123. More specifically, the researchers developed single chain-chain proteins that would fuse to bacterial ferritin and, in the process, would self-assemble into nanoparticles.
Researchers have identified distinct differences among the cells comprising a tissue in the retina that is vital to human visual perception. The scientists from the National Eye Institute (NEI) discovered five subpopulations of retinal pigment epithelium (RPE)—a layer of tissue that nourishes and supports the retina's light-sensing photoreceptors. Using artificial intelligence, the researchers analyzed images of RPE at single-cell resolution to create a reference map that locates each subpopulation within the eye. A report on the research published in Proceedings of the National Academy of Sciences.
"These results provide a first-of-its-kind framework for understanding different RPE cell subpopulations and their vulnerability to retinal diseases, and for developing targeted therapies to treat them," said Michael F. Chiang, M.D., director of the NEI, part of the National Institutes of Health.
"The findings will help us develop more precise cell and gene therapies for specific degenerative eye diseases," said the study's lead investigator, Kapil Bharti, Ph.D., who directs the NEI Ocular and Stem Cell Translational Research Section.
Vision begins when light hits the rod and cone photoreceptors that line the retina in the back of the eye. Once activated, photoreceptors send signals through a complex network of other retinal neurons that converge at the optic nerve before traveling to various centers in the brain. The RPE sits beneath the photoreceptors as a monolayer, one cell deep.
Age and disease can cause metabolic changes in RPE cells that can lead to photoreceptor degeneration. The impact on vision from these RPE changes varies dramatically by severity and where the RPE cells reside within the retina. For example, late-onset retinal degeneration (L-ORD) affects mostly peripheral retina and, therefore, peripheral vision. Age-related macular degeneration (AMD), a leading cause of vision loss, primarily affects RPE cells in the macula, which is crucial for central vision.
(EurekAlert) Historically, there has been racial inequity when it comes to primary care appointments, which are vital for managing and preventing chronic disease. But as COVID-19 struck the United States in 2020 and telemedicine availability rose sharply, gaps in access disappeared for Black patients at Penn Medicine, new research shows. And even once “normal” in-office appointments returned, the historic inequities stayed erased, indicating that telemedicine wasn’t just a stopgap solution but a potential long-term tool for equity. These findings, from researchers at the Perelman School of Medicine at the University of Pennsylvania, were published in Telemedicine and e-Health.
“We looked through the entire year of 2020, not just the first half of the year when telemedicine was the only option for many people, and the appointment completion gap between Black and non-Black patients closed,” said the study’s senior author, Krisda Chaiyachati, MD, an assistant professor Medicine at Penn Medicine and the physician lead for Value-based Care and Innovation at Verily. “Offering telemedicine, even though it was for a crisis, appears to have been a significant step forward toward addressing long-standing inequities in healthcare access.”
COVID-19’s sudden onset in early 2020 resulted in a telemedicine boom. Use of it had typically been narrow, largely as a result of regulations and hesitancy among payers, but emergency provisions allowed health care entities to quickly conduct appointments via phone or computer. There was some concern that these developments, while good for preventing the spread of COVID, might adversely impact racial and ethnic groups who have been historically underserved by health care.
That’s why Chaiyachati – who headed Penn Medicine’s virtual visit service, Penn Medicine OnDemand, through most of the pandemic – and his fellow researchers decided to focus on whether Black patients at Philadelphia-area practices were able to see their primary care providers as often in 2020 as they had in 2019, and then compare those numbers to non-Black patients (which, in this population, mainly consists of white, non-Hispanic people). Data from roughly 1 million appointments in each year were analyzed.
US scientists say Sarin gas blamed for Gulf War syndrome
Source: BBC
US scientists say they have discovered what caused thousands of soldiers who served in the 1991 Gulf War to fall sick with mysterious symptoms. They have pinned the blame on the nerve agent sarin, which was released into the air when caches of Iraqi chemical weapons were bombed. Many veterans have complained of a range of debilitating symptoms which developed after their service. But for decades the cause of Gulf War Syndrome has remained elusive.
Sarin is usually deadly, but lead researcher Dr Robert Haley said the gas that soldiers were exposed to in Iraq was diluted, and so not fatal. "But it was enough to make people ill if they were genetically predisposed to illness from it." Dr Haley said the key to whether somebody fell ill was a gene known as PON1, which plays an important role in breaking down toxic chemicals in the body.
His team found veterans with a less effective version of the PON1 gene were more likely to become sick. The latest study - largely funded by the US government - involved more than 1,000 randomly-selected American Gulf War veterans. Dr Haley, of the University of Texas Southwestern Medical Center, said: "This is the most definitive study. "We believe it will stand up to any criticism. And we hope our findings will lead to treatment that will relieve some of the symptoms."
For the first time, researchers have successfully used bacteriophages—viruses that kill bacteria—to treat an antibiotic-resistant mycobacterial lung infection, clearing the way for a young National Jewish Health patient with cystic fibrosis to receive a life-saving lung transplant. The successful use of phages to treat a Mycobacterium abscessus lung infection was reported in a case study published today in the journal Cell.
"We had tried unsuccessfully for years to clear the mycobacterial infection with a variety of antibiotics," said Jerry Nick, MD, lead author on the study and director of the Adult Cystic Fibrosis Program at National Jewish Health. "When we used the bacteria's own natural enemies, we were able to clear the infection which resulted in a successful lung transplant."
"I am so grateful for the effort, persistence and creativity of all the people who were involved in my treatment," said Jarrod Johnson, recipient of the lung transplant. "I thought I was going to die. They have literally saved my life."
