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A specific combination of targeted therapy and immunotherapy may better help patients with non-small cell lung cancer (NSCLC) overcome inherent immune resistance and reinvigorate anti-tumor activity, according to a new study led by a researcher from The University of Texas MD Anderson Cancer Center.
Results from the Phase II umbrella HUDSON study, published today in Nature Medicine, demonstrated that the anti PD-L1 antibody, durvalumab, coupled with the ATR inhibitor, ceralasertib, provided the greatest clinical benefit of four combinations evaluated.
This pair had an objective response rate (ORR) of 13.9% compared to just 2.6% with the other tested combinations. Median progression-free survival (PFS) was 5.8 months versus 2.7 months for other combinations, while median overall survival (OS) was 17.4 months versus 9.4 months. In patients with ATM alterations, which should sensitize tumors to ATR inhibitors, the ORR increased to 26.1%. Durvalumab-ceralasertib had a manageable safety profile.
“Patients with advanced non-small cell lung cancer face significant challenges when standard-of-care treatments fail,” said corresponding author John Heymach, M.D., Ph.D., chair of Thoracic/Head & Neck Medical Oncology. “For these individuals, options become limited, emphasizing the urgent need for innovative approaches. Our study represents a promising advancement in addressing this unmet need and holds the potential to offer more effective therapeutic strategies to improve outcomes for this population.”
This study enrolled 268 patients with advanced NSCLC who progressed following standard-of-care therapy. The median age of participants was 63-64 years; 58% were male.
Patients on the trial received one of four targeted therapies in combination with durvalumab: ceralasertib (ATR kinase inhibitor), olaparib (PARP inhibitor), danvatirsen (STAT3 antisense oligonucleotide) or oleclumab (anti-CD73 monoclonal antibody).
Tumor molecular characteristics were analyzed before treatment, and patients were categorized into biomarker-matched or -unmatched treatment cohorts based on ATM alterations, homologous recombination repair defects, STK11/LKB1 alterations, or high CD73 expression.
Based on the results, durvalumab plus ceralasertib is now being tested in a randomized Phase III trial for patients with immunotherapy-refractory NSCLC.

People using anabolic steroids could be increasing their underlying risk of a heart condition called atrial fibrillation, a new study has found.
The new research published in the Journal of Physiology conducted by an interdisciplinary consortium of clinicians and researchers led by University of Birmingham and collaborators in Germany.
The team found that male sex hormones, such as testosterone, also called androgenic anabolic steroids (AAS), which are misused for muscle building particularly among in young men can increase the risk of atrial fibrillation in individuals genetically predisposed to heart diseases.
Dr Laura Sommerfeld, Postdoctoral Researcher at the UKE Hamburg, who completed her PhD at the Institute of Cardiovascular Sciences at the University of Birmingham focusing on this work is lead author of the study.
Dr Sommerfeld said: “Our study can significantly contribute to understanding the impact on the heart health of young men who misuse anabolic steroids to increase muscle mass. Recent reports have shown that young men in particular are being targeted on social media such as TikTok being sold testosterone products, but we have shown how the misuse of steroids carries a specific risk that many people will not be aware of.”
Professor Larissa Fabritz, Chair of Inherited Cardiac Conditions at UKE Hamburg and Honorary Chair in the Institute of Cardiovascular Sciences at the University of Birmingham added:
“Heart muscle diseases like ARVC affect young, athletic individuals and can lead to life-threatening heart rhythm disturbances. Atrial fibrillation is a common condition in the general population. Elevated testosterone levels can result in an earlier onset of these diseases.”
The scientists examined potential effects on a condition called arrhythmogenic right ventricular cardiomyopathy (ARVC), which is genetically determined and primarily attributed to disruptions in the formation of cell connections critical for heart muscle stability.

The scientists initially confirmed, based on clinical patient data from UHB and elsewhere, that ARVC occurs more frequently and severely in men than in women. In laboratory experiments, they discovered that six weeks of AAS intake, combined with impaired cell connections, could lead to reduced sodium channel function in heart tissue and a slowing of signal conduction within the atria.
Dr Andrew Holmes, co-author and Assistant Professor in the Institute of Clinical Sciences at the University of Birmingham said:
“This work implies that young male individuals with key inherited genetic changes have a greater risk of developing electrical problems in the heart in response to anabolic steroid abuse.”

Antiretroviral therapies (ART) stop HIV replication in its tracks, allowing people with HIV to live relatively normal lives. However, despite these treatments, some HIV still lingers inside cells in a dormant state known as “latency.” If ART is discontinued, HIV will awaken from its dormant state, begin to replicate, and cause acquired immunodeficiency syndrome (AIDS). To create a cure, researchers have been attempting to drive HIV out of latency and target it for destruction.
A new clinical trial led by Cynthia Gay, MD, MPH, associate professor of infectious diseases, David Margolis, MD, the Sarah Kenan Distinguished Professor of Medicine, Microbiology & Immunology, and Epidemiology, and other clinicians and researchers at the UNC School of Medicine suggests that a combination of the drug vorinostat and immunotherapy can coax HIV-infected cells out of latency and attack them.
The immunotherapy was provided by a team led by Catherine Bollard, MD, at the George Washington University, who took white blood cells from the study participants and expanded them in the laboratory, augmenting the cells’ ability to attack HIV-infected cells, before re-infusion at UNC.
Their results, published in the Journal of Infectious Diseases, showed a small dent on the latent reservoir, demonstrating that there is more work to be done in the field.
“We did show that this approach can reduce the reservoir, but the reductions were not nearly large enough, and statistically speaking were what we call a “trend” but not highly statistically significant,” said David Margolis, MD, director of the HIV Cure Center and senior author on the paper. “We need to create better approaches to flush out the virus and attack it when it comes out. We need to keep chipping away at the reservoir until there’s nothing there.”
DNA inside cell nuclei is kept in a tightly packed space by chromosomes, which act as highly organized storage facilities. When you unfurl a chromosome, you’ll find loop-de-loop-like fibers called chromatin. If you keep unfurling, you’ll see long strands of DNA wrapped around scaffold proteins known as histones, like beads on a string. Finally, when the unfurling is complete, you will see the iconic DNA double helix.
Vorinostat works by inhibiting a lock-like enzyme called histone deacetylase. By stopping this mechanism, tiny doors within the chromatin fibers unlock and open up, effectively “waking up” latent HIV from its slumber and making it vulnerable to an immune system attack. As a result, a tiny blip of HIV expression shows up on very sensitive molecular assays.

But the effects of vorinostat are short lived, only lasting a day per dose. For this reason, Margolis and other researchers are trying to find safe and effective ways to administer the drug and keep the chromatin channels open for longer periods of time.
For the study, six participants were given multiple doses of vorinostat. Researchers then extracted immune cells from the participants and expanded the cells that knew how to attack HIV-infected cells.
This immunotherapy method, which has been successful against other viruses such as Epstein-Barr virus and cytomegalovirus, involves giving participants back their expanded immune cells in the hopes that these cells will further multiply in number and launch an all-out attack on the newly exposed HIV-infected cells.
However, in the first part of this study, only one of the six participants saw a drop in their HIV reservoir levels. To test whether the result was simply random or something more, researchers gave three participants their usual dose of vorinostat, but introduced five times the amount of engineered immune cells. All three of the participants had a slight decline in their reservoirs.
But, statistically speaking, the results were not large enough to be definitive.
“This is not the result we wanted, but it is research that needed to be done,” said Margolis. “We are working on improving both latency reversal and clearance of infected cells, and we hope to do more studies as soon as we can, using newer and better approaches.”
Many of the participants in the study have been working with Margolis’s research team for years, sacrificing their own time and blood for research efforts. Their long-term partnership and commitment have been essential for data collection. The data, which follows the size of the viral reservoir in these people over years prior to this study, makes the small changes found more compelling.
“People living with HIV come in a couple of times a year, and we measure residual traces of virus in their blood cells, which doesn’t have any immediate benefit to them,” said Margolis. “It’s a very altruistic action and we couldn’t make any progress without their help.”

Researchers have shed new light on how viral evolution, population immunity, and the co-circulation of other flu viruses shape seasonal flu epidemics.
The research, published today as a Reviewed Preprint in eLife, explores the relationships among evolutionary and epidemiological quantities in influenza, and presents fundamental findings that substantially advance our understanding of the drivers of influenza epidemics, according to the eLife editors. The authors used a rich set of data sources to provide what the editors say is compelling evidence on the roles of genetic distance, influenza subtype dynamics, and epidemiological indicators in predicting flu epidemics. The findings highlight genetic distance and subtype interference as key factors in determining the timing and severity of annual outbreaks.
Influenza viruses continually accumulate genetic changes in two key proteins displayed on their surface — called haemagglutinin (HA) and neuraminidase (NA) — a process known as antigenic drift. Antigenic drift allows the virus to escape immune recognition in people who have been vaccinated or had a previous infection, leaving them exposed to re-infection. Of the two types of influenza viruses that routinely circulate together in humans (influenza A and B), influenza A, and particularly subtype A(H3N2), has the fastest rates of antigenic drift and causes the most severe illness and death.
Amanda Perofsky, the lead author of the study and a research scientist at the Brotman Baty Institute, University of Washington, US, and Fogarty International Center, National Institutes of Health, US, says: “In theory, antigenic drift will lead to more susceptible individuals, which in turn should lead to more flu infections and larger or more severe epidemics. However, prior evidence for this in epidemiological data has been mixed. Mutations in HA are considered to cause the majority of antigenic drift, so surveillance efforts to monitor and predict influenza evolution focus on HA. There has been less focus on NA, even though antibodies against NA also correlate with immunity and influence infection severity. Moreover, outside of flu pandemics, little is known about how different cocirculating influenza subtypes potentially interfere with each other, affecting the size of outbreaks.”
In this study, Perofsky and colleagues from the Fred Hutchinson Cancer Center, the Icahn School of Medicine at Mount Sinai, US Centers for Disease Control and Prevention, and World Health Organization tracked A(H3N2) evolutionary dynamics — measured by both genetic sequences and serological assays — and linked this to epidemiological flu surveillance data in the US over 22 influenza seasons before the COVID-19 pandemic.
They started out by identifying different indicators of flu evolution each season, using HA and NA genetic sequence data from the Global Initiative on Sharing Avian Influenza Data (GISAID) Epiflu database and serological data on immune cross-reactivity between viruses provided by World Health Organization Global Influenza Surveillance and Response System (GISRS) Collaborating Centres in Tokyo, London, Melbourne and Atlanta. They created phylogenetic trees showing lines of evolution of A(H3N2) viruses over time and measured genetic and antigenic distances between viruses circulating in consecutive seasons, to show how far apart the viruses evolved in that timeframe.
Next, the team explored which of these measures of viral ‘fitness’ are most strongly related to variation across A(H3N2) flu outbreaks in different years. When comparing the predictive performance of sequence-based and serological evolutionary metrics, they found that genetic distances based on broad sets of antigenic sites (“epitopes”) in HA and NA had the strongest, most consistent relationship with the disease burden of annual epidemics, rates of virus transmission, and severity of infection, and influenced the dominant subtype of influenza A — A(H3N2) or A(H1N1) — circulating in each season.

When relating genetic distance in HA versus NA to A(H3N2) epidemiology, antigenic drift of H3 (the HA antigen of the A(H3N2) virus) was more strongly linked to epidemic size, viral transmissibility, the age distribution of cases, and the number of excess deaths caused by the A(H3N2) virus, while antigenic drift of N2 (the NA antigen of the A(H3N2) virus) was more strongly linked to the intensity of epidemics (the “sharpness” of the epidemic curve) and greater prevalence of A(H3N2) cases relative to A(H1N1) cases in the population. Increased drift in N2 was also associated with fewer days from epidemic onset to peak incidence (a measure of the speed of the epidemic).
“The direct link between NA antigenic drift and A(H3N2) incidence patterns was a surprising and key result from our study,” says Perofsky. “We expected HA to exhibit stronger associations with seasonal incidence, given that it elicits a stronger immune response than NA.”
Taken together, the authors’ results showed that greater antigenic drift in both HA and NA was linked to larger, more intense epidemics, higher transmission, a greater dominance of the A(H3N2) subtype, and more cases in adults than children.
Finally, the team applied machine learning models to assess the relative importance of viral evolution, prior population immunity, the co-circulation of other flu viruses, and vaccine coverage and effectiveness in predicting regional A(H3N2) epidemic dynamics. Using one of the models (called a random forest) they could accurately predict regional epidemic size, peak incidence, and subtype dominance patterns of seasonal outbreaks that occurred between 1997 and 2019. Surprisingly, they found that the incidence of A(H1N1) was more predictive of A(H3N2) epidemics than viral evolution, suggesting that interactions between different viral subtypes — that is, subtype interference — play a key role in influenza type A infection dynamics.
“Our study shows that influenza epidemic dynamics are shaped in part by the virus’ antigenic drift in both surface proteins, and that genetic sequence indicators of antigenic drift were more informative than serological (or antibody) data for predicting epidemics in the timeframe analysed,” concludes senior author Cécile Viboud, a staff scientist at Fogarty International Center, National Institutes of Health, US. “Our work is the first to link NA antigenic drift to epidemic burden, timing, and the age distribution of infections. The connection between NA drift and seasonal incidence further highlights the importance of monitoring evolution of both HA and NA to inform the selection of strains for annual flu vaccines and epidemic forecasting efforts.”

Type 2 diabetes alters the behavior of discs in the vertebral column, making them stiffer, and also causes the discs to change shape earlier than normal. As a result, the disc’s ability to withstand pressure is compromised. This is one of the findings of a new study in rodents from a team of engineers and physicians from the University of California San Diego, UC Davis, UCSF and the University of Utah.
Low back pain is a major cause of disability, often associated with intervertebral disc degeneration. People with Type 2 diabetes face a higher risk of low back pain and disc-related issues. Yet the precise mechanisms of disc degeneration remain unclear.
Investigating the biomechanical properties of the intervertebral disc is crucial for understanding the disease and developing effective strategies for managing low back pain. The research team was co-led by Claire Acevedo, a faculty member in the Department of Mechanical and Aerospace Engineering at the University of California San Diego, and Aaron Fields, faculty in the Department of Orthopaedic Surgery at UC San Francisco.
“These findings provide novel insight into the potential mechanisms underlying diabetes-related disc tissue damage and may inform the development of preventative and therapeutic strategies for this debilitating condition,” the researchers write.
The study emphasizes that nanoscale deformation mechanisms of collagen fibrils accommodate compressive loading of the intervertebral disc. In the context of type 2 diabetes, these mechanisms are compromised, resulting in collagen embrittlement. These findings provide novel insight into the potential mechanisms underlying diabetes-related disc tissue damage and may inform the development of preventative and therapeutic strategies for this debilitating condition.
Researchers employed synchrotron small-angle x-ray scattering (SAXS), an experimental technique that looks at collagen fibril deformation and orientation at the nanoscale. They wanted to explore how alterations in collagen behavior contribute to changes in the disc’s ability to withstand compression.
They compared discs from healthy rats to those from rats with Type 2 diabetes (UC Davis rat model). The healthy rats showed that collagen fibrils rotate and stretch when discs are compressed, allowing the disc to dissipate energy effectively.

“In diabetic rats, the way vertebral discs dissipate energy under compression is significantly impaired: diabetes reduces the rotation and stretching of collagen fibrils, indicating a compromised ability to handle pressure,” the researchers write.
Further analysis showed that the discs from diabetic rats exhibited a stiffening of collagen fibrils, with a higher concentration of non-enzymatic cross-links. This increase in collagen cross-linking, induced by hyperglycemia, limited plastic deformations via fibrillar sliding. These findings highlight that fibril reorientation, straightening, stretching, and sliding are crucial mechanisms facilitating whole-disc compression. Type 2 diabetes disrupts these efficient deformation mechanisms, leading to altered whole-disc biomechanics and a more brittle (low-energy) behavior.
The team published their findings in the December 2023 issue of PNAS Nexus.
This research was supported by the Research Allocation Committee at UCSF (A.J.F.), the Core Center for Musculoskeletal Biology and Medicine at UCSF (A.J.F.), the University of California Office of the President (P.J.H.), the National Institutes of Health (R01 DK095980, R01 HL107256, R01 HL121324, P30 AR066262, R01 AR070198), the University of Utah (J.L.R.), and the Advanced Light Source (ALS07392; T.N.A., C.A.).

Extracted from the core of sandalwood trees (santalum album tree), sandalwood oil has been used for many centuries by several cultures throughout the world for perfume, soaps, incense and candles. With its earthy sweet scent, this essential oil also is used in the food industry and topically in various cosmetic preparations.
Importantly, this natural oil is known for its health benefits and medicinal applications from antibacterial to anticancer because of its phytochemical constituents. In addition to containing esters, free acids, aldehydes, ketones and santenone, sandalwood oil primarily (90 percent or more) constitutes santalol — equal amounts of two compounds, alpha and beta-santalol.
Now, researchers from Florida Atlantic University’s Schmidt College of Medicine and collaborators are the first to demonstrate in vivo the chemo-preventive properties of alpha-santalol against prostate cancer development using a transgenic mouse model.
Results of the study, published in the journal Phytomedicine Plus, showed that administration of alpha-santalol decreased the incidence of prostate tumors by decreasing cell proliferation and inducing apoptosis, without causing weight loss or any noticeable side effects. Apoptosis, or programmed cell death, is a method the body uses to get rid of unneeded or abnormal cells such as cancer cells.
Findings revealed that the area occupied by normal tissue in alpha-santalol-treated mice was 53 percent compared to 12 percent in control mice. This suggests that administering alpha-santalol protected the normal tissue and delayed progression from prostatic intraepithelial neoplasia, a precancerous condition, to poorly differentiated carcinoma, a high-grade form of cancer where cancer cells and tissue look very abnormal. These results are significant because mortality in prostate cancer patients is mainly attributable to advanced stages of the disease.
In prior studies, the researchers demonstrated the efficacy of alpha-santalol in suppressing growth and inducing apoptotic cell death in cultured human prostate cancer cells. Based on these observations, they selected a genetically engineered mouse model that resembles many features similar to human prostate cancer, eliciting different lesion grades and cancer progression.
“Although our cellular studies provided important mechanistic insights, relevant in vivo models are vital for developing novel chemo-preventive agents for clinical use and to determine if alpha-santalol offers protection against prostate cancer development,” said Ajay Bommareddy, Ph.D., senior author and an associate professor of pharmacology in the Department of Biomedical Science, FAU Schmidt College of Medicine. “Prior to this new study, alpha-santalol’s in vivo efficacy against prostate cancer development had not yet been established.”
Additional findings of the current study showed alpha-santalol reduced the incidence of visible prostate tumors compared to control-treated mice. Only 11 percent in the treated group developed prostate tumors whereas more than half in the control group developed the tumors. The differences in urogenital and prostate weights were statistically significantly different in alpha-santalol-treated mice compared with controls. The average wet weight of urogenital tract in alpha-santalol treated mice was about 74.28 percent lower compared with control mice. Similarly, the average wet weight of the prostate gland was lower by 52.9 percent compared with control mice.

Prostate cancer is the second leading cause of cancer death in men in the United States. An estimated 288,300 new cases were diagnosed in American men last year with about 34,700 estimated deaths.
Current treatment methods for prostate cancer include androgen ablation, chemotherapy, radiotherapy and radical prostatectomy, but are ineffective against advanced prostate cancers. Early detection and local therapy have resulted in improved outcomes but has been challenging with the management of advanced stages.
“Identifying agents that have the ability to selectively target cancerous cells and delay onset and progression of prostate cancer is greatly needed,” said Bommareddy. “Additional studies are essential to systemically explore the feasibility of alpha-santalol as a promising chemo-preventive and anti-tumor agent against human prostate cancer development and to elucidate the mechanisms surrounding the role of pro-apoptotic and antiapoptotic proteins.”
Study co-authors are John Oberlin Jr., PharmD; Kaitlyn Blankenhorn, PharmD; Sarah Hughes, PharmD; Erica Mabry, PharmD; Aaron Knopp, PharmD; Adam L. VanWert, PharmD, Ph.D., all with the Wilkes University Nesbitt School of Pharmacy; Chandradhar Dwivedi, Ph.D., South Dakota State University; Isaiah Pinkerton, a graduate of Wilkes University; and Linda Gutierrez, M.D., Wilkes University.

A group of international mycology experts led by Professor Dr Oliver A. Cornely at the University of Cologne has jointly drafted a guideline for the diagnosis and treatment of cryptococcosis, which aims at improving infection management and thus the survival rate of patients. Cryptococcosis is a fungal infection of mainly the lungs that might lead to meningitis. The article ‘Global guideline for the diagnosis and management of cryptococcosis’ was published in the journal The Lancet Infectious Diseases.
Cryptococcosis, especially cryptococcal meningitis (CM) as the most fatal form, is responsible for a high fatality rate among patients. It is one of the most widespread invasive fungal infections in the world and is a major threat particularly to people suffering from immunodeficiencies. For example, around one million cases of cryptococcal meningoencephalitis are diagnosed worldwide every year in people with HIV alone, and more than 600,000 people die from the disease each year. Patients who have undergone a bone marrow transplant or organ transplant are also at high risk of infection. It is transmitted through the inhalation of spores from soil. Other organs are then also infected via the bloodstream. The lungs, brain, skin and bones are most frequently affected.
“Invasive fungal infections are often difficult to recognize in everyday work in clinics because they occur so rarely. However, it is particularly important for patients at risk to be treated quickly and appropriately,” said Cornely from Department I of Internal Medicine at University Hospital Cologne and Director of the Institute of Translational Research at the University of Cologne’s CECAD Cluster of Excellence for Aging Research. “At the same time, we must not forget that the conditions for recognizing the infection at an early stage are not equally good everywhere in the world and that resources are sometimes very limited. There are many countries with a high number of cases that are poorly equipped in this respect. As part of our Global Guideline Programme, we would like to contribute to improving this situation.”
The cryptococcosis guideline is designed to support medical staff in handling invasive fungal infections. It is intended to provide practical guidance and support in decision-making and thus improve clinical approaches, diagnosis, management, and aftercare for the benefit of patients.
The project was carried out by the mycological societies ECMM (European Confederation of Medical Mycology) and ISHAM (International Society for Human and Animal Mycology) in collaboration with the ASM (American Society for Microbiology). “More than 70 other international specialist institutions were involved in developing this new guideline. This is a great help for our scientific work and shows how great the interest, but also the need for such recommendations is,” explained Cornely. Authors from 22 countries contributed to this guideline. Dr Christina Chang from Monash University in Melbourne, Australia, and Professor Dr John Robert Perfect from Duke University in Durham, USA, were in charge of the project.
Invasive fungal infections are emergencies. However, as a single pathogen often only occurs very rarely, it is often only discovered late. But patients’ lives depend on rapid detection and well-practised procedures. Since 2017, University Hospital Cologne has been home to one of the European Centres of Excellence recognized by the ECMM. At the centre, patients have access to modern testing procedures and treatment options. In addition, the experts under the direction of Professor Cornely serve as advisory contacts for colleagues in Germany and abroad.

A team of scientists from Wake Forest University School of Medicine and the University of Southern California (USC) have demonstrated the first successful use of a neural prosthetic device to recall specific memories.
The findings appear online in Frontiers in Computational Neuroscience.
This groundbreaking research was derived from the Wake Forest and USC team’s 2018 study led by Robert Hampson, Ph.D., professor of regenerative medicine, translational neuroscience and neurology at Wake Forest University School of Medicine, that showed the successful implementation of a prosthetic system that uses a person’s own memory patterns to facilitate the brain’s ability to encode and recall memory.
In the previous study, the team’s electronic prosthetic system was based on a multi-input multi-output (MIMO) nonlinear mathematical model, and the researchers influenced the firing patterns of multiple neurons in the hippocampus, a part of the brain involved in making new memories.
In this study, researchers built a new model of processes that assists the hippocampus in helping people remember specific information. When the brain tries to store or recall information such as, “I turned off the stove” or “Where did I put my car keys?” groups of cells work together in neural ensembles that activate so that the information is stored or recalled. Using recordings of the activity of these brain cells, the researchers created a memory decoding model (MDM) which let them decode what neural activity is used to store different pieces of specific information. The neural activity decoded by the MDM was then used to create a pattern, or code, which was used to apply neurostimulation to the hippocampus when the brain was trying to store that information.
“Here, we not only highlight an innovative technique for neurostimulation to enhance memory, but we also demonstrate that stimulating memory isn’t just limited to a general approach but can also be applied to specific information that is critical to a person,” said Brent Roeder, Ph.D., a research fellow in the department of translational neuroscience at Wake Forest University School of Medicine and the study’s corresponding author.
The team enrolled 14 adults with epilepsy who were participating in a diagnostic brain-mapping procedure that used surgically implanted electrodes placed in various parts of the brain to pinpoint the origin of their seizures. Participants underwent all surgical procedures, post-operative monitoring and neurocognitive testing at one of the three sites participating in this study including Atrium Health Wake Forest Baptist Medical Center, Keck Hospital of USC in Los Angeles and Rancho Los Amigo National Rehabilitation Center in Downey, California.

The team delivered MDM electrical stimulation during visual recognition memory tasks to see if the stimulation could help people remember images better. They found that when they used this electrical stimulation, there were significant changes in how well people remembered things. In about 22% of cases, there was a noticeable difference in performance.
When they looked specifically at participants with impaired memory function, who were given the stimulation on both sides of their brain, almost 40% of them showed significant changes in memory performance.
“Our goal is to create an intervention that can restore memory function that’s lost because of Alzheimer’s disease, stroke or head injury,” Roeder said. “We found the most pronounced change occurred in people who had impaired memory.”
Roeder said he hopes the technology can be refined to help people live independently by helping them recall critical information such as whether medication has been taken or whether a door is locked.
“While much more research is needed, we know that MDM-based stimulation has the potential to be used to significantly modify memory,” Roeder said.
This research is built on more than 20 years of preclinical research on memory codes led by Sam Deadwyler, Ph.D., emeritus professor of physiology and pharmacology at Wake Forest University School of Medicine, along with Hampson (now a member of the Wake Forest Institute of Regenerative Medicine), and the USC team led by biomedical engineers Theodore Berger, Ph.D., and Dong Song, Ph.D.
The preclinical work applied the same type of stimulation to restore and facilitate memory in animal models using the MIMO system, which was developed at USC.
The research was funded by the U.S. Defense Advanced Research Projects Agency (DARPA).

New research from Drexel University’s Center for Weight, Eating and Lifestyle Science (WELL Center), examined how often people experiencing binge eating are also using cannabis recreationally, and whether patients who use cannabis experience more severe eating disorder symptoms or symptoms of struggling with mental health.
While there has been a great deal of research on the impact of cannabis on eating habits, less is known about the effects of cannabis use on individuals with a binge eating disorder. Binge eating is the experience of feeling out of control when eating or unable to stop eating. Cannabis may play a particular role in maintaining binge eating as research suggests cannabis can increase how pleasurable or rewarding people find high sugar or high fat foods.
Recently published in Experimental and Clinical Psychopharmacology, the research found more than 23% of the 165 study participants reported using cannabis in the past three months — either “once or twice” or “monthly.” These participants were individuals seeking treatment for binge eating and reported their cannabis and alcohol use as part of that process.
“Distinguishing the relationship between cannabis use, eating disorder severity and other psychiatric symptoms in binge eating patients is necessary for informing screening and clinical recommendations,” said lead author Megan Wilkinson, a doctoral student in Drexel’s College of Arts and Sciences.
While study participants who used cannabis reported “a strong desire or urge to use cannabis” and they also drank alcohol more frequently and reported more problems related to their alcohol use; the research team noted that participants with binge eating disorders who used cannabis did not have more severe eating disorder or depression symptoms.
“Both alcohol and cannabis can impact an individual’s appetite and mood. Our finding that patients with binge eating who use cannabis also drink more alcohol may suggest that these individuals are at a higher risk for binge eating, given the compounded effects on appetite and mood from these substances,” said Wilkinson. “Treatments for binge eating should explore how substance use affects hunger, mood, and eating for patients.”
Participants also completed surveys and interviews about their binge eating, other eating disorder symptoms and depression. The research team compared individuals who reported cannabis use to individuals who did not report cannabis use to see if there were statistically significant differences in their alcohol use, eating disorder symptoms, or depression symptoms.
The findings indicate that a notable subset of the participants with binge eating disorders use cannabis and experience strong desires or urges to use cannabis. Additionally, using cannabis appears to be related to drinking patterns and problems with drinking (e.g., needing more alcohol to feel intoxicated, inability to control drinking) for patients with binge eating.
“We hope this research is helpful for clinicians treating patients with binge eating, as it can provide them with updated information about the prevalence of cannabis use in their patients,” said Wilkinson. “We recommend that clinicians screen for cannabis and alcohol use in all their patients and assess any potential problems the patient may be experiencing related to their substance use.”
Wilkinson also noted that updated research on cannabis use in patients with binge eating will be required regularly due to changing social norms and laws related to cannabis in the United States. Next, Wilkinson and her colleagues are planning to explore the ways that cannabis use may impact hunger and mood for patients with binge eating, and therefore potentially exacerbate their binge eating symptoms.

Breast cancer is on the rise, but new tools for early detection could save lives.
In Journal of Vacuum Science & Technology B, by AIP Publishing, researchers from the University of Florida and National Yang Ming Chiao Tung University in Taiwan reported successful results from a hand-held breast cancer screening device that can detect breast cancer biomarkers from a tiny sample of saliva. Their biosensor design uses common components, such as widely available glucose testing strips and the open-source hardware-software platform Arduino.
“Imagine medical staff conducting breast cancer screening in communities or hospitals,” author Hsiao-Hsuan Wan said. “Our device is an excellent choice because it is portable — about the size of your hand — and reusable. The testing time is under five seconds per sample, which makes it highly efficient.”
The device uses paper test strips treated with specific antibodies that interact with the targeted cancer biomarkers. A saliva sample is placed on the strip, and pulses of electricity are sent to electrical contact points on the biosensor device. These pulses cause the biomarkers to bind to the antibodies and alter the charge and capacitance over the electrode. This produces a change in the output signal, which can be measured and translated into digital information about how much biomarker is present.
The design is revolutionary compared to its alternatives. Mammograms, ultrasounds, and MRIs are costly and invasive and require large, specialized equipment, present low-dose radiation exposure, and can take days or weeks to return test results.
“In many places, especially in developing countries, advanced technologies like MRI for breast cancer testing may not be readily available,” Wan said. “Our technology is more cost-effective, with the test strip costing just a few cents and the reusable circuit board priced at $5. We are excited about the potential to make a significant impact in areas where people might not have had the resources for breast cancer screening tests before.”
The biosensor requires just a drop of saliva, and it can provide accurate test results even if the concentration of the cancer biomarker in the sample is only one quadrillionth of a gram, or one femtogram, per milliliter.
“The highlight for me was when I saw readings that clearly distinguished between healthy individuals and those with cancer,” Wan said. “We dedicated a lot of time and effort to perfecting the strip, board, and other components. Ultimately, we’ve created a technique that has the potential to help people all around the world.”