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Using neuroimaging techniques and electroencephalography (EEG), Kessler Foundation researchers compared the neural correlates of balance in individuals with traumatic brain injury and matched controls. This study is the first to report EEG-based functional connectivity measures during a balance perturbation task and show the association with white matter integrity in the brain.
The article, “Graph-theoretical analysis of EEG functional connectivity during balance perturbation in traumatic brain injury: A pilot study,” was published online on July 26, 2021 by Human Brain Mapping.The authors are Vikram Shenoy Handiru, PhD, Alaleh Alivar, PhD, Armand Hoxha, MS, Soha Saleh, PhD, Easter S. Suviseshamuthu, PhD, Guang Yue, PhD, and Didier Allexandre, PhD, from the Center for Mobility and Rehabilitation Engineering Research at Kessler Foundation.
Postural instability is an understudied complication of traumatic brain injury that hinders progress in rehabilitation, limits independence, and compromises safety. Despite the impact on the daily lives of individuals and their care partners, little research has been done on the neural mechanisms that contribute to balance function.
For this pilot study, researchers in Dr. Allexandre’s Neuromuscular and Neurophysology Laboratory studied 17 adults with traumatic brain injury and 15 matched controls. Using a computerized posturography platform and EEG, scientists delivered random balance perturbations and measured each participant’s neural and postural responses. Furthermore, a subset of participants had magnetic resonance imaging (MRI) performed at the Rocco Ortenzio Center for Neuroimaging at Kessler Foundation, to measure brain structural integrity using diffusion tensor imaging (DTI).
DTI studies showed widespread structural damage in the traumatic brain injury group, which had poorer balance performance and reduced brain activity and connectivity during balance tasks. The graph-theoretic measures of brain functional connectivity derived from EEG data show an abnormal brain network response during the balance task, an intriguing finding that warrants further investigation.
“Using EEG-based graph measures, we were able to explore the differences in underlying structural and functional mechanisms in individuals with and without traumatic brain injury, which may lead to the identification of a neural biomarker for balance dysfunction,” said lead author Dr. Shenoy Handiru. “Future investigations need to look at how to modulate brain networks affected by brain injury. We hypothesize that postural training may be a way to ‘re-wire’ damaged networks so their function mimics that of the healthy brain, and lead to the desired outcome of improved balance function.”
Funding sources: New Jersey Commission on Brain Injury Research CBIR15MIG004
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By combining computational and experimental approaches, University of Pittsburgh School of Medicine and Prairie View A&M University researchers identified cancer drugs that show promise for treating pulmonary hypertension, or PH, a rare and incurable lung disease.
Published today in Science Advances, the study used a new algorithm to identify candidate cancer drugs for PH. Two of these compounds improved markers of the disease in human cells and rodents. The findings support broader use of this drug-repurposing platform for other non-cancerous conditions that don’t yet have effective treatments.
“Repurposing drugs can cut down the time and cost of developing treatments for rare diseases, which historically don’t receive much investment into research and drug development,” said senior author Stephen Chan, M.D., Ph.D., professor of medicine and director of the Vascular Medicine Institute at Pitt and UPMC. “Pulmonary hypertension is an example of a rare disease where there is an unmet need for new treatments, given its devastating consequences. We developed this pipeline to rapidly predict which drugs are effective for PH and get these treatments to patients faster.”
Pulmonary hypertension is a type of high blood pressure that occurs in the vessels that transport blood from the heart to the lungs. As the disease progresses and the heart must strain harder against these high pressures, it can lead to heart failure, multi-organ dysfunction and death. PH affects people of all ages but hits young women more often than men.
One of these young women is Allison Dsouza, a 24-year-old nurse who not only lives with the condition herself but also treats PH patients in the UPMC Lung Transplant Program. She was diagnosed with PH as a high school senior after she started having trouble walking to her car and doing hobbies like horseback riding. According to Dsouza, she was the sickest patient with the highest lung pressures that her doctors had seen.
PH is thought to be triggered by environmental and genetic factors that damage the endothelial cells that line blood vessels, leading to inflammation and abnormal repair that restrict blood flow or cause the loss of the thinnest branches of the lung vessel tree.

Scientists have revealed how bacteria make tiny liquid droplets from proteins to help them survive harsh environments and thus reduce their chances of being killed by antibiotics.
The study reveals how aggresomes — miniscule liquid droplets assembled from several different proteins — form in response to increasing the stress experienced by bacteria, and that these bacteria can form aggresomes that are more successful at surviving these stresses.
The research team, jointly led by scientists at the University of York and Peking University, discovered that environmental stresses were linked to reducing the level of a chemical called ATP — known as the “universal currency of cell energy” — inside bacteria. It is thought that this reduction may affect the solubility of key cellular proteins that encouraged them to assemble into droplets.
The study may help solve the mystery of how certain types of bacteria can both survive extended treatments of antibiotics, and, through mutating their genes, increase the likelihood of forming complete resistance against antibiotics.
By using advanced optical microscopy and computational modelling, the researchers showed that droplet formation is explained by the physics of “liquid-liquid phase separation.”
Scientists say the forces of attraction between molecules in solution drive them together to form semi-stable assemblies that have interesting liquid properties, and, in the case of aggresomes, comprise up to several hundred molecules of different proteins. Molecules within an aggresome remain free to move as in any liquid, and turnover with other molecules outside an aggresome.

Almost all cells regulate their biological processes over a 24-hour period, otherwise called a cell’s circadian rhythm. To do so, cells use a biological clock that cycles different genes on and off throughout the day and night. Scientists already know that our metabolic health can suffer when our biological clock breaks down, due to shift work or sleep disorders, for example. However, it’s unclear how exactly the biological clock of people with type 2 diabetes differs from healthy people.
Now a team of international scientists has shown that the skeletal muscle in people with type 2 diabetes has a different circadian rhythm. They argue that this might arise because of a communication breakdown between a cell’s time keeping molecules and mitochondria, which produce chemical energy for cells.
“The promise of this research is that it may help us to fine tune the timing of interventions and other medications to treat type 2 diabetes, in order to optimize their effectiveness,” says Professor Juleen R. Zierath from Karolinska Institutet and the Novo Nordisk Foundation Center for Basic Metabolic Research (CBMR) at the University of Copenhagen.
A different pattern of daily gene expression
In the study, which was published in Science Advances, the scientists first obtained skeletal muscle cells from people with type 2 diabetes and measured which genes showed cycling behavior over two days and compared them with cells from similar healthy people. They discovered that cells from people with type 2 diabetes had fewer, and some different, cycling genes.
They carried out further experiments using data generated from clinical tests in people with type 2 diabetes and mice, as well as cell-based experiments. These experiments demonstrated that mitochondria communicate with the molecules that keep time in our cells, and that this communication is disrupted in people with type 2 diabetes.
Diabetes treatments may be more effective if timed to the body clock
Some of the most widely used pharmacological treatments for type 2 diabetes affect mitochondria, meaning that they may work differently depending on the time of day they are taken. As a result, these findings highlight the importance of considering cellular rhythms when prescribing treatments for type 2 diabetes.
“Exercise and diet are regularly used treatment interventions for people with type 2 diabetes, and both of these treatments can affect the time-keeping molecules and mitochondria,” says Dr. Brendan Gabriel from the Department of Physiology and Pharmacology at Karolinska Institutet.
Brendan Gabriel is first author on the paper together with Assistant Professor Ali Altintas from CBMR.
“Given that disrupted sleeping patterns are known to be associated with an increased risk of developing type 2 diabetes, our findings provide evidence of how these disruptions may link to the molecular biology within cells,” says Ali Altintas.

New research has revealed that red blood cells function as critical immune sensors by binding cell-free DNA, called nucleic acid, present in the body’s circulation during sepsis and COVID-19, and that this DNA-binding capability triggers their removal from circulation, driving inflammation and anemia during severe illness and playing a much larger role in the immune system than previously thought. Scientists have long known that red blood cells, which are essential in delivering oxygen throughout the body, also interacted with the immune system, but didn’t know whether they directly altered inflammation, until now. The study, led by researchers at the Perelman School of Medicine at the University of Pennsylvania, was published today in Science Translational Medicine.
“Anemia is common, affecting about a quarter of the world’s population. Acute inflammatory anemia is often seen early after an infection such as parasitic infections that cause malaria,” said senior author Nilam Mangalmurti, MD, an assistant professor of Medicine at Penn. “For a long time we haven’t known why people, when they are critically ill from sepsis, trauma, COVID-19, a bacterial infection, or parasite infection, develop an acute anemia. These findings explain one of the mechanisms for the development of acute inflammatory anemia for the first time.”
Toll-like receptors (TLRs) are a class of proteins that play a key role in the immune system by activating immune responses like cytokine production. This study examined the red blood cells of about 50 sepsis patients and 100 COVID-19 patients and found that, during these illnesses, red blood cells express an increased amount of the specific TLR protein called TLR9 on their surface.
Results showed that when the red blood cells bind too much inflammation-causing nucleic acid, they lose their normal structure, causing the body to not recognize them anymore. This leads immune cells, called macrophages, to ‘eat’ them, taking them out of circulation in the body. When this happens it causes the immune system to become activated in otherwise unaffected organs, creating inflammation. This mechanistic discovery opens the door to research on how to block this specific receptor and create targeted therapies for autoimmune diseases, infectious diseases, and a whole host of inflammatory illnesses associated with acute anemia.
“Right now when patients in the ICU become anemic, which is almost all of our critically ill patients, the standard is to give them blood transfusions, which has long been known to be accompanied by a host of issues including acute lung injury and increased risk of death,” Mangalmurti said. “Now that we know more about the mechanism of anemia, it allows us to look at new therapies for treating acute inflammatory anemia without transfusions, such as blocking TLR9 on the red blood cells. Targeting this TLR9 may also be a way to dampen some of the innate immune activation without blocking this receptor in immune cells, which are very important for the host when fighting a pathogen or injury.”
Mangalmurti says that this DNA-binding discovery could also have implications for research into using red blood cells in diagnostics. For example, whether a physician could take red blood cells from a patient with pneumonia, sequence the nucleic acid that has been soaked up from the infection, and identify the specific kind of pathogen to better determine what kind of antibiotic to prescribe.
Mangalmurti and fellow researchers are studying whether this is a valid option in diagnosing infection in critically ill patients and if this DNA-binding mechanism by red blood cells is a universal mechanism of anemia in parasitic infections.
The research was funded by the National Institutes of Health (R01 HL126788, R01 AI 091595, UM1 AI126620) and the Office of the Assistant Secretary of Defense for Health Affairs through the Peer Reviewed Medical Research Program.
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In a paper published today in the journal Science Translational Medicine, researchers at the Schroeder Arthritis Institute, part of University Health Network (UHN) in Toronto, have made a discovery that could lead to new treatments for axial spondyloarthritis (SpA), a painful and debilitating form of arthritis which affects 1-2% of Canadians and causes inflammation in the spine, joints, eyes, gut and skin.
“We currently have very few therapeutic options for the majority of patients living with SpA and this is a devastating disease that directly impacts quality of life,” says Dr. Nigil Haroon, a rheumatologist, Co-Director of the spondylitis program and senior author on the paper.
“Although several treatments including biologic drugs have been approved for SpA, 40-50 % of patients do not respond to any treatments and develop severe pain and abnormal new bone formation,” says Dr. Akihiro Nakamura, first author on the paper and a spondylitis fellow and PhD candidate in Dr. Haroon’s lab. “So, there is a desperate need to find new treatments that are effective and cover all of the clinical symptoms of SpA.”
The study focuses on the role of the Macrophage migration inhibitory factor (MIF), which functions as a protein that induces an inflammatory or immune response in the body. Until now, the role that MIF plays in the disease progression of SpA was unknown.
In this study, researchers observed that the expression of MIF and its receptor CD74, is increased in the blood and tissues of pre-clinical models. They also found that human neutrophils (a type of white blood cell that induces the immune system’s response) from SpA patients secreted higher concentrations of MIF, compared to healthy individuals. This, in turn, drives other cells to cause more inflammation.
“What this means is that if the body has been exposed to a trigger, too much MIF could be produced in susceptible individuals that could then lead to a diagnosis of SpA later in life. If we can block the excess production of MIF early, we may be able to induce disease remission and prevent disability and mortality linked to SpA,” explains Dr. Haroon.

FAYETTEVILLE, N.C. — One humid day this summer, Brian Long, a senior executive at the chemical company Chemours, took a reporter on a tour of the Fayetteville Works factory.Mr. Long showed off the plant’s new antipollution technologies, designed to stop a chemical called GenX from pouring into the Cape Fear River, escaping into the air and seeping into the ground water.There was a new high-tech filtration system. And a new thermal oxidizer, which heats waste to 2,000 degrees. And an underground wall — still under construction — to keep the chemicals out of the river. And more.“They’re not Band-Aids,” Mr. Long said. “They’re long-term, robust solutions.”A Chemours executive, Brian Long, at Fayetteville Works.Ed Kashi for The New York TimesYet weeks later, North Carolina officials announced that Chemours had exceeded limits on how much GenX its Fayetteville factory was emitting. This month, the state fined the company $300,000 for the violations — the second time this year the company has been penalized by the state’s environmental regulator.GenX is part of a family of chemicals called per- and polyfluoroalkyl substances, or PFAS. They allow everyday items — frying pans, rain jackets, face masks, pizza boxes — to repel water, grease and stains. Exposure to the chemicals has been linked to cancer and other serious health problems.To avoid responsibility for what many experts believe is a public health crisis, leading chemical companies like Chemours, DuPont and 3M have deployed a potent mix of tactics.They have used public charm offensives to persuade regulators and lawmakers to back off. They have engineered complex corporate transactions to shield themselves from legal liability. And they have rolled out a conveyor belt of scantly tested substitute chemicals that sometimes turn out to be just as dangerous as their predecessors.“You don’t have to live near Chemours or DuPont or 3M to have exposure to these things,” said Linda S. Birnbaum, the former head of the National Institute of Environmental Health Sciences. “It is in the water. It is in our food. It’s in our homes and in our house dust. And depending where you live, it may be in our air.”Contaminants in the GroundwaterSince 2018, potentially unsafe levels of PFAS have been found in the groundwater of more than 4,000 residential parcels near the Chemours factory in Fayetteville, N.C., according to the state’s environmental regulator. High concentrations of GenX, a type of PFAS, were found in 232 of those parcels. More than 4,000 homes qualify for under-sink treatment systems because of the contamination.

She documented her last months with ovarian cancer on Twitter while raising funds to support students from backgrounds that are underrepresented in the sciences.Nadia Chaudhri, a neuroscientist with terminal ovarian cancer who used her final months to raise money for graduate students of diverse backgrounds and to educate the public about her disease through a widely followed social media chronicle, died on Oct. 5 at a hospital in Montreal. She was 43.Her husband, Moni Orife, confirmed her death.Dr. Chaudhri, a professor at Concordia University in Montreal, was in palliative care at Royal Victoria Hospital when she wrote on Twitter in August that she would be embarking on a walk-a-thon: pacing her hospital floor each day in a fund-raising appeal for minority, female, L.G.B.T.Q. and other students from underrepresented backgrounds who are pursuing scientific research at the university. Her own research centered on the neural basis of drug and alcohol addiction.Her campaign raised funds for the Nadia Chaudhri Wingspan Award, which was established in her honor and announced by Concordia in May. She had previously raised money with a GoFundMe campaign to sponsor students from diverse backgrounds to attend the annual conference of the nonprofit Research Society on Alcoholism.In the announcement of the award, Dr. Chaudhri recalled the discrimination she had experienced as a Pakistani woman in graduate school. “When I gave talks or presentations, people often commented on my accent instead of my science,” she said.Through her walk-a-thon and her large and active Twitter following, the fund surpassed $635,000 in mid-October. Paul Chesser, the university’s vice president for fund-raising, said small donors had led the way: nearly 9,000 from 60 countries, forming a rare grass roots effort in institutional fund-raising.“Nadia’s legacy is forever entrenched in many, many ways here on campus,” Mr. Chesser said.Dr. Chaudhri in 2014. She learned she had ovarian cancer in May 2020. “Do not dismiss your pain or malaise,” she wrote to her Twitter followers. “Find the expert doctors.”Moni OrifeHer Twitter feed drew more than 150,000 followers and was the backbone of her money-raising efforts. Many of her followers said they were inspired by her frankness about her illness and cited her bravery.“I’ve been so moved by your story, Nadia, and your kindness and spirit are just something I don’t think I’ve ever seen in such abundance before,” one Twitter user wrote. “I will carry you in my heart for as long as I live.”Dr. Chaudhri, in turn, connected closely with her Twitter following. Addressing donors, she wrote, “You are making my final days incredibly special & meaningful.”In May she wrote of how she was preparing to tell her 6-year-old son about her terminal diagnosis. “Today is the day I tell my son that I’m dying from cancer,” she said. “Let me howl with grief now so that I can comfort him.”Dr. Chaudhri produced creative work while in the hospital. She sent some donors copies of a short story she wrote about growing up in Karachi, Pakistan. She painted, posting vibrant artwork depicting flowers and nature scenes, some inspired by pictures her followers had sent her and some featuring her husband and son.She also used her Twitter platform to call for more research into ovarian cancer. “The bottom line is that ovarian cancer research is underfunded,” she wrote in September. “We also need more awareness of symptoms because early detection improves prognosis dramatically.”Dr. Chaudhri urged women to pay attention to their health. “Do not dismiss your pain or malaise,” she wrote in one thread recounting her diagnosis. “Find the expert doctors.”She was found to have ovarian cancer in May 2020. The cancer resisted treatment, she said, and she was admitted to palliative care in August this year.Nadia Chaudhri was born in Karachi on Jan. 25, 1978. Her mother, Susan (Metcalf) Chaudhri, was an occupational therapist. Her father, Abdul Shakoor Chaudhri, was an orthopedic surgeon.Nadia attended Karachi Grammar School in Pakistan. She went to the United States for college, earning a Bachelor of Science degree in the biological foundations of behavior from Franklin & Marshall College in Pennsylvania in 1999. She was the first woman to win the college’s Williamson Medal for academic and extracurricular achievement.She attended the University of Pittsburgh and received a Ph.D. in neuroscience in 2005, writing her thesis on the science of cigarette addiction. She had a postdoctoral fellowship from 2005 to 2009 at the Ernest Gallo Clinic and Research Center at the University of California, San Francisco.She married Mr. Orife in 2009. Their son, Reza Orife, was born in 2015. In addition to her husband and son, she is survived by her mother and her sister, Amina.Dr. Chaudhri joined the Concordia University faculty in 2010 as an assistant professor in the department of psychology and was placed at the head of her own lab. She earned tenure as an associate professor in 2014. Less than a month before she died, Concordia promoted her to full professor.

Cerebral blood flow (CBF), which supplies oxygen and nutrients to our brain, is a crucial indicator of brain health. Information from CBF can, therefore, help us diagnose brain disorders. While this information is usually obtained from speckle imaging, the technique cannot provide information on both flow speed and direction. Now, scientists from GIST take things to the next level with a new technique that quantitatively estimates CBF in real time at high speeds.
The brain is arguably the most crucial aspect of our existence. Our brain health governs how well we function. In turn, our brain health is determined by the blood supply to our brain via “cerebral blood flow” (CBF), which regulates the supply of oxygen and nutrients and removes metabolic by-products. An imbalance in CBF can lead to brain disorders such as headache, seizures, Alzheimer’s disease (AD), and stroke.
Observing local CBF during neural activity could, therefore, help unravel the origins of brain disorders. Speckle imaging, a technique based on the analysis of large number of short exposures, is particularly popular in this regard because it is non-invasive, label-free, simple, and provides high time resolution. However, it cannot provide information on both blood flow direction and speed, making it difficult to analyze and monitor changes in blood flow.
In a recent study,researchers led by Prof. Euiheon Chung from the Gwangju Institute of Science and Technology (GIST) in Korea came up with an innovative solution to this problem. The team developed a technique called “optical speckle image velocimetry” (OSIV) that creates an absolute flow map in real time with information on both speed and direction and a superior time resolution. Prof. Chung explains, “We intended to create a new technique that, unlike its predecessors, allows for a quantitative analysis of CBF and does not require complex mathematical modeling for flow measurements.” This paper was made available online on 13 August 2021 and was published in Volume 8, Issue 8 of the journal Optica.
OSIV utilizes particle image velocimetry and speckle cross-correlations to detect blood flow velocities up to 7 mm/s and can measure flow maps at up to 190 Hz. To put OSIV to the test, the team used it to image blood flow during a stroke in a mouse brain in vivo, obtaining quantitative flow measurements without needing a tracer or a high-speed camera.
The technique can be successfully deployed to diagnose healthy and diseased brains. “Our study can be used to understand the vascular mechanisms and test new drugs for treating vascular-related diseases such as stroke, AD, and diabetes,” speculates Prof. Chung, excitedly.
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A multi-institutional research team has designed nanoparticles that can communicate with and slow the development of cancer cells. The work — detailed in a newly published paper in Advanced Materials — has uncovered a novel framework for the potential development of drug-free cancer therapies.
Led by scientists at the Advanced Science Research Center at the Graduate Center, CUNY (CUNY ASRC), the research team was able to design nanoparticles that are activated to self-assemble when they encounter cancer cells and send messages to instruct the cells to slow their growth. Because the nanoparticles communicate only with the cancer cells, the surrounding healthy cells aren’t impacted.
“Cancer cells take up materials from their environment, and they also secrete factors that help them degrade surrounding tissue in order to spread and metastasize,” said Richard Huang, lead author of the paper, a Ph.D. student at the Graduate Center, CUNY (GC CUNY), and a researcher with the CUNY ASRC Nanoscience Initiative and the Center for Discovery and Innovation at CUNY’s City College of New York (CCNY). “We made particles that respond to both of these characteristics by aggregating into clusters that are actively taken up by cancer cells. Once inside, they appear to be able to reduce the cancer cells’ metabolic activity and consequently reduce their growth.”
One reason the progression of cancer is difficult to control is that the cells secrete an abnormally large amount of the matrix metalloproteinase-9 (MMP-9) enzyme, which breaks down the collagen that holds together healthy tissue. The research team was able to use this feature against the cancer cells. This is achieved by designing nanoparticles that when triggered by MMP-9, begin assembling to large aggregates in the cells’ vicinity. The cells engulf these aggregates, and their size causes physical distress to the cancer cells and reduces their ability to proliferate and survive.
One highlight of the study is that the researchers were able to use confocal reflection microscopy to visualize the nanoparticle aggregates inside the cancer cells in real-time. “This label-free, live imaging technique allowed us to have a closer look at when and where the aggregates were formed, and how the cancer cells respond to the particles at the sub-cellular level,” said Ye He, director of the Live Imaging and Bioenergetics Facility in the CUNY ASRC Neuroscience Initiative.
“Through this research, we wanted to determine whether it’s possible to make use of relatively simple peptide design to create nanoparticles that could produce robust self-assembly in biological media and have an impact on cancer cells,” said Rein Ulijn, director of the CUNY ASRC Nanoscience Initiative and the study’s principal investigator. “While this is early-stage research, the findings provide exciting possibilities for a drug-free therapeutic treatment that could be extremely useful for cancer patients who have developed drug resistance and for extending the lives of people with metastatic cancer.”
Further studies are needed to fully access the therapeutic potential of the team’s discovery.
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