University of Houston, associate professor of electrical and computer engineering Bhavin R. Sheth and former student Adam Jones, have introduced a groundbreaking approach to sleep stage classification that could replace the current gold standard in sleep testing, the cumbersome polysomnography, which uses a myriad of wires and is performed in a clinic. Their new procedure, which can be performed at home by the user, uses a single-lead electrocardiography-based deep learning neural network.
If you’ve ever had a problem sleeping, and ended up in a sleep lab, you know the polysomnography test is anything but restful. With a multitude of leads — sensors and wires — dangling from every part of your body, you are asked to sleep, which is a state difficult to reach without such encumbrance, nearly impossible with it.
But what if the number of those electrodes — attached from your scalp to your heart — was reduced to simply two?
“We have successfully demonstrated that our method achieves expert-level agreement with the gold-standard polysomnography without the need for expensive and cumbersome equipment and a clinician to score the test,” reports Sheth in Computers in Biology and Medicine. “This advancement challenges the traditional reliance on electroencephalography (or EEG) for reliable sleep staging and paves the way for more accessible, cost-effective sleep studies.”
Even more, by enabling access to high-quality sleep analysis outside clinical settings, Adam and Bhavin’s research holds the potential to expand the reach of sleep medicine significantly.
Reliable classification of sleep stages is crucial in sleep medicine and neuroscience research for providing valuable insights, diagnoses and understanding of brain states. Although commercial devices like the Apple Watch, Fitbit and Oura Ring track sleep, their performance is well below that of polysomnography.
The electrocardiography-based model was trained on 4000 recordings from subjects 5-90 years old. They showed that the model is robust and performs just as well as a clinician scoring polysomnography.

“Our method significantly outperforms current research and commercial devices that do not use EEG and achieves gold-standard levels of agreement using only a single lead of electrocardiography data,” said Sheth, who is also a member of the UH Center for NeuroEngineering and Cognitive Systems.
“It makes less-expensive, higher-quality studies accessible to a broader community, enabling improved sleep research and more personalized, accessible sleep-related healthcare interventions.”
To that end Jones made the complete source code freely available for researchers, clinicians and anyone else interested at https://cardiosomnography.com
The collaboration also includes Laurent Itti at the University of Southern California.

Researchers discovered that temperatures in different face regions are associated with various chronic illnesses, such as diabetes and high blood pressure. These temperature differences are not easily perceptible by one’s own touch but can instead be identified using specific AI-derived spatial temperature patterns that require a thermal camera and a data-trained model. The results appear July 2 in the journal Cell Metabolism. With further research, doctors could one day use this simple and non-invasive approach for early detection of diseases.
“Aging is a natural process,” says Jing-Dong Jackie Han, the paper’s corresponding author at Peking University in Beijing. “But our tool has the potential to promote healthy aging and help people live disease-free.”
The team had previously used 3D facial structure to predict people’s biological age, which indicates how well the body is aging. Biological age is closely related to the risk of diseases, including cancer and diabetes. They were curious if other features of the face, such as temperature, could also predict aging rate and health status.
Han and her colleagues analyzed facial temperatures of more than 2,800 Chinese participants between the ages of 21 and 88. Then, the researchers used the information to train AI models that could predict a person’s thermal age. They identified several key facial regions where the temperatures were significantly related to age and health, including the nose, eyes and cheeks.
The team found the temperature of the nose decreases with age at a rate faster than other parts of the face, meaning people with warmer noses have a younger thermal age. At the same time, temperatures around the eyes tend to increase with age.
The team also found that people with metabolic disorders such as diabetes and fatty liver disease had faster thermal aging. They tended to have higher eye area temperatures than their healthy counterparts of the same age. People with elevated blood pressure also had higher cheek temperatures.

By analyzing participants’ blood samples, the team revealed that the increase in temperatures around the eyes and cheeks was mainly because of an increase in cellular activities related to inflammation, such as repairing damaged DNAs and fighting infections. The increase in these activities led to a rise in temperatures in certain facial regions.
“The thermal clock is so strongly associated with metabolic diseases that previous facial imaging models were not able to predict these conditions,” Han says.
Due to this connection, the team set out to test if exercise could influence thermal age. They asked 23 participants to jump rope for at least 800 times daily for two weeks. To the team’s surprise, these participants reduced their thermal age by five years after just two weeks of exercise.
Next, the team wants to explore if they can use thermal facial imaging to predict other diseases, such as sleeping disorders or cardiovascular problems.
“We hope to apply thermal facial imaging in clinical settings, as it holds significant potential for early disease diagnosis and intervention,” Han says.

Researchers show for the first time that engineered human plasma B cells can be used to treat a disease — specifically leukemia — in a humanized animal model. The results mark a key step in the realization of ePCs as therapies to treat cancer, auto-immune disorders, and protein deficiency disorders. The results appear July 2 in the journal Molecular Therapy.
“We hope that this proof-of-concept study is the first of many applications of engineered plasma B cells, and eventually will lead to a single-shot therapeutic,” says senior study author Richard James (@ScienceRicker) of the Seattle Children’s Research Institute. “Because engineered plasma B cells can live for a very long time, greater than 10 years, they could be used as a long-term source of many biologic drugs.”
Immunotherapies that recruit cytotoxic T cells to kill cancer cells, such as bispecific antibodies, have contributed to improved survival rates for patients with B cell acute lymphoblastic leukemia (B-ALL). Blinatumomab is a bispecific antibody that received FDA approval in 2014 for the treatment of patients with relapsed/refractory B-ALL, but a limitation of blinatumomab is that it requires continuous high-dose intravenous infusions to maintain activity. This intensive regimen poses challenges for patients because frequent bag changes prove inconvenient, and the use of ports increases the risk of infection.
“Bispecific non-immunoglobulin therapies pose stability challenges in patients, necessitating three courses of 20-day steady-state infusion,” James says. “Enhanced drug delivery methods for bispecific antibodies like blinatumomab could improve patient adherence and bolster treatment efficacy.”
“We think that the first application of engineered plasma B cells will be to produce drugs that are difficult for patients to use,” James says. “In this study, we wanted to demonstrate proof of concept and efficacy for engineered B cell therapies.”
Toward that goal, James and his team developed a gene-editing strategy for the generation of ePCs that produce large quantities of bispecifics to target B-ALL or acute myeloid leukemia. The combined findings demonstrated that ePCs secreting bispecifics can promote T cell-driven killing of primary human cells and human leukemic cell lines.
“One challenge we encountered was that the bispecific antibody used for killing tumor cells can also bind the engineered plasma B cells because they express the same target protein,” James says. “To overcome this challenge, we deleted the protein target of the antibody, CD19, when we were making the engineered cells. We were surprised that deletion of CD19 did not hinder manufacturing of engineered plasma B cells.”
In addition, the researchers discovered that plasma cells secreting anti-CD19 bispecific antibodies elicited antitumor activity, as demonstrated with acute lymphoblastic leukemia patient-derived xenografts in immunodeficient mice co-engrafted with autologous T cells. Notably, the steady-state concentration of anti-CD19 bispecifics in serum one month after cell delivery and tumor eradication was comparable to that observed in patients treated with continuous infusion of blinatumomab.

Based on the results, the researchers propose that ePC strategies could increase the functional half-life of bispecifics in patients with acute leukemias and other diseases where treatment half-life is limiting or where plasma cell local delivery could enhance therapeutic efficacy.
The results suggest that prolonged clinically relevant levels of bispecific and perhaps other biologics can be achieved via a single administration of ePCs. The robust levels of bispecific achieved by ePCs compare favorably to those observed by other bispecific-secreting cell products, including macrophages and T cells. According to the authors, these findings support further development of ePCs for use as a durable delivery system for the treatment of acute leukemias and potentially other cancers.
“We created engineered plasma B cells capable of continuously producing bispecific antibodies throughout the treatment period after only one injection,” James says. “These cells effectively eliminated tumors to a comparable extent as the clinical drug. The key takeaway is that engineered plasma B cells can provide long-lasting drug production in vivo.”
However, ePC bispecifics should be carefully evaluated for several possible toxicities if used clinically. Persistent on-target, off-tumor toxicity to normal bystander B cells is common in patients receiving B cell-targeted therapeutics. “In addition, for treatment of a B cell malignancy, it may be difficult to engineer a patient’s own B cells to be used as the therapy because there is a risk that some of the B cells will be cancerous,” James says. “We did not test whether we can use a different person’s B cells to produce the bispecific antibody. Studies using such allogeneic products will likely need to be done before this specific therapy can be used to treat B cell cancers.”
As noted by the authors, further studies in humanized mice and non-human primates are warranted to fully understand the activity, longevity, and tissue localization of ePCs. “In the short term, we plan to test whether engineered plasma B cells that produce bispecific antibodies are effective in other B cell-mediated diseases, including autoimmunity. These tests will initially be conducted in animal models. Additionally, we are developing engineered plasma B cells to produce other therapeutic drugs, such as those needed in protein deficiency diseases such as hemophilia. Finally, we are exploring additional applications of engineered B cells, including modifying other immune cells to either enhance or suppress the immune system.”

When it comes to managing blood sugar levels, most people think about counting carbs. But new research from the University of British Columbia shows that, for some, it may be just as important to consider the proteins and fats in their diet.
The study, published today in Cell Metabolism, is the first large-scale comparison of how different people produce insulin in response to each of the three macronutrients: carbohydrates (glucose), proteins (amino acids) and fats (fatty acids).
The findings reveal that production of the blood sugar-regulating hormone insulin is much more dynamic and individualized than previously thought, while showing for the first time a subset of the population who are hyper-responsive to fatty foods.
“Glucose is the well-known driver of insulin, but we were surprised to see such high variability, with some individuals showing a strong response to proteins, and others to fats, which had never been characterized before,” said senior author Dr. James Johnson, a professor of cellular and physiological sciences at UBC. “Insulin plays a major role in human health, in everything from diabetes, where it is too low, to obesity, weight gain and even some forms of cancer, where it is too high. These findings lay the groundwork for personalized nutrition that could transform how we treat and manage a range of conditions.”
For the study, the researchers conducted tests on pancreatic islets from 140 deceased male and female donors across a wide age range. The islets were exposed to each of the three macronutrients, while the researchers measured the insulin response alongside 8,000 other proteins.
Although most donors’ islet cells had the strongest insulin response to carbohydrates, approximately nine per cent responded strongly to proteins, while another eight per cent of the donor cells were more responsive to fats than any other nutrient — even glucose.
“This research challenges the long-held belief that fats have negligible effects on insulin release in everyone,” says first author Dr. Jelena Kolic, a research associate in the Johnson lab at UBC. “With a better understanding of a person’s individual drivers of insulin production, we could potentially provide tailored dietary guidance that would help people better manage their blood sugar and insulin levels.”
The research team also examined a subset of islet cells from donors who had Type 2 diabetes. As expected, these donor cells had a low insulin response to glucose. However, the researchers were surprised to see that their insulin response to proteins remained largely intact.

“This really bolsters the case that protein-rich diets could have therapeutic benefits for patients with Type 2 diabetes and highlights the need for further research into protein-stimulated insulin secretion,” said Dr. Kolic.
The team conducted a comprehensive protein and gene expression analysis on the pancreatic islet cells, providing insights into the molecular and cellular characteristics that shape insulin production. In the future, the researchers say it could be possible use genetic testing to determine which macronutrients are likely to trigger a person’s insulin response.
As a next step, the researchers hope to expand their work into clinical studies that would test insulin responsiveness to the trio of macronutrients in a real-world setting, and to begin developing personalized nutrition approaches based on the findings.
This research was supported by the Canadian Institutes for Health Research and JDRF Canada. The researchers would like to thank the organ donors and their families for their gift that enabled this research, made through the Human Organ Procurement and Exchange program and Trillium Gift of Life Network.

The drug, Kisunla, made by Eli Lilly, is the latest in a new class of treatments that could modestly slow cognitive decline in initial stages of the disease but also carry safety risks.The Food and Drug Administration on Tuesday approved a new drug for Alzheimer’s disease, the latest in a novel class of treatments that has been greeted with hope, disappointment and skepticism.The drug, donanemab, to be sold under the brand name Kisunla, was shown in studies to modestly slow the pace of cognitive decline in early stages of the disease. It also had significant safety risks, including swelling and bleeding in the brain.Kisunla, made by Eli Lilly, is similar to another drug, Leqembi, approved last year. Both are intravenous infusions that attack a protein involved in Alzheimer’s, and both can slow the unfolding of dementia by several months. Both also carry similar safety risks. Leqembi, made by Eisai and Biogen, is given every two weeks; Kisunla is given monthly.Kisunla has a significant difference that may appeal to patients, doctors and insurers: Lilly says patients can stop the drug after it clears the protein, amyloid, which clumps into plaques in the brains of people with Alzheimer’s.“Once you’ve removed the target that you’re going after, you then can stop dosing,” said Anne White, an executive vice president of Lilly and president of its neuroscience division. She said that this could reduce the overall cost and inconvenience of the treatment as well as the risk of side effects.The company said that 17 percent of patients receiving donanemab in the 18-month-long clinical trial were able to discontinue the drug at six months, 47 percent stopped within a year and 69 percent stopped within 18 months. Their cognitive decline continued to slow even after they stopped. The company is evaluating how long that slowing will continue past the duration of the trial, said Dr. John Sims, a medical director at Lilly.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

A research team led by Prof. GUO Yusong, Associate Professor of the Division of Life Science at the Hong Kong University of Science and Technology (HKUST), recently made a novel discovery related to the coronavirus (SARS-CoV-2) that causes COVID-19. The team identified new host factors that interact with the receptor binding domain of the SARS-CoV-2 spike protein to promote viral entry. This finding offers valuable mechanistic insights and potential therapeutic strategies against SARS-CoV-2 infection.
It is generally believed that SARS-CoV-2 enters host cells through the interaction between its spike protein’s receptor-binding domain (CoV2-RBD) and the host cell receptor ACE2, facilitating viral invasion. However, most evidence is based on the overexpression of ACE2 to promote viral entry, with few studies conducted on whether completely knocking out ACE2 inhibits viral entry. To address this, the HKUST research team, led by Prof. Guo, in collaboration with research teams from the University of Hong Kong (HKU) and the Hong Kong Polytechnic University (PolyU), has identified other novel surface-located host factors, apart from ACE2, that also bind to CoV2-RBD using the GST pull-down method.
The experiment demonstrates that among the factors, one in particular called SH3BP4, regulates the internalization of CoV2-RBD and mediates the entry of SARS-CoV-2 pseudovirus in a manner that is dependent on integrins and the clathrin, but not on ACE2, implying that SH3BP4 promotes viral entry via the endocytic pathway. Many identified factors, including SH3BP4, ADAM9, and TMEM2, show a stronger affinity for CoV2-RBD compared to the RBD of the less infectious SARS-CoV, indicating their specific usage for SARS-CoV-2. Moreover, this study uncovers factors that preferentially bind to the RBD of the SARS-CoV-2 Delta variant, potentially enhancing its entry.
“These findings identify novel host cell surface factors involved in the invasion of SARS-CoV-2 and highlight the crucial role of integrins in mediating viral internalization, establishing new research foundations for treating COVID-19,” Prof. Guo said.
The study was recently published in the international academic journal, Journal of Biological Chemistry. The research team also consists of Prof. CHEN Honglin from Department of Microbiology at HKU; and Prof. YAO Zhongping, from Department of Applied Biology and Chemical Technology at PolyU; and their team members.

Scientists at the National Institutes of Health (NIH) have uncovered a brain circuit in primates that rapidly detects faces. The findings help not only explain how primates sense and recognize faces, but could also have implications for understanding conditions such as autism, where face detection and recognition are often impaired from early childhood. The newly discovered circuit first engages an evolutionarily ancient part of the brain called the superior colliculus, which can then trigger the eyes and head to turn for a better look. This better view enables different brain areas in the temporal cortex to engage in more complex facial recognition. The study was published in the journal Neuron.
“Quick recognition of faces is a key skill in humans and other primates,” said Richard Krauzlis, Ph.D., of NIH’s National Eye Institute (NEI) and senior author of the study. “This newly discovered circuit explains how we’re able to quickly detect and look at faces, even if they first show up in the peripheral visual field where visual acuity is poor. This circuit could be what spotlights faces to help the brain learn to recognize individuals and understand complex facial expressions, helping us acquire important social interaction skills.”
In adult primates, the brain develops specialized regions of the temporal cortex called “face patches” that provide the ability to recognize and distinguish individuals by their facial features. However, facial recognition depends on fine details provided by the eye’s high acuity central vision; for us to recognize a face, we first have to look directly at it.
When babies are born, they lack the high acuity vision needed to see the fine details of faces, and the face-specific areas of the cortex don’t develop until later. Even so, babies generally orient and look at faces very early in life, suggesting that another process is in play.
These observations left scientists with several questions, including: how does the brain shift the eyes towards a face to better see fine details? What provides this face preference before the brain’s “face patches” develop? And how do the brain’s “face patches” develop the ability to understand faces in the first place?
Krauzlis and colleagues hypothesized that the superior colliculus — known to detect objects — could provide the missing link. Part of the midbrain, it tells the rest of the brain if something is present somewhere — not what the object is, but simply that it is there. It functions extremely quickly and connects directly to the motor parts of the brain, directing movements of the eyes towards objects of interest, or flinching out of the way of an object in the peripheral vision.
To test whether the superior colliculus might aid in face detection specifically, co-first authors Gongchen Yu, Ph.D., and Leor Katz, Ph.D., assembled a collection of images, including faces, biological non-face objects, like hands and arms, and other items like fruit or human-made objects. They then showed these images to adult monkeys in the monkeys’ peripheral visual field and recorded neuronal responses in the superior colliculus.

Previous studies had suggested that the detection of objects by the superior colliculus was object-agnostic, meaning that this part of the brain was just noting the presence or absence of something, without any differentiation of what that thing might be. However, in this study, Krauzlis and colleagues found that within 40 milliseconds, more than half the neurons they measured responded more strongly to images of faces compared to other types of objects. Some additional neurons eventually displayed preferences for other types of objects, but not until 100 milliseconds. In other words, the face-specific detection was much faster than detection of other objects, and was preferred by a large proportion of the measured neurons.
The researchers were also able to determine that, while the superior colliculus can receive visual information directly from the eye, this object detection process instead requires input from the early part of the visual cortex first.
Since the superior colliculus also reconnects back to the visual cortex later on in the visual processing pathway, the scientists suspect that this circuit provides a mechanism to highlight the importance of certain objects.
“We believe this face-preference circuit may actually drive the development of the brain’s more advanced facial recognition processes,” said Krauzlis. “If so, deficits in this face preference in the superior colliculus might play a role in autism.”
This study was funded by the NEI Intramural Program. In addition to co-lead authors Yu and Katz, Christian Quaia, Ph.D., and Adam Messinger, Ph.D., also contributed to the research.

The US government has given $176 million to Moderna to develop an mRNA-based pandemic influenza vaccine that would work against bird flu.

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The insects seem to know which injuries to treat as they engage in a behavior that seems almost human.The life of a Florida carpenter ant can be brutal. These half-inch ants are territorial and have violent bouts with ants from rival colonies in the Southeast.Combat can leave the ants with leg injuries. But as scientists recently discovered, these ants have evolved an effective wound treatment: amputation.In the journal Current Biology, on Tuesday, researchers report that the ants bite off the injured limbs of their nest mates to prevent infection. Although other ant species are known to tend to the wounds of their injured, typically by licking them clean, this is the first time that an ant species has been known to use amputation to treat an injury.The ants in the study performed amputations on only certain leg injuries, suggesting that they are methodical in their surgical practices. Aside from humans, no other animal is known to conduct such amputations. The prevalence of the behavior among Florida carpenter ants raises questions about their intelligence and their ability to feel pain.In early 2020, Dany Buffat, a graduate student at the University of Würzburg in Germany, was observing a colony of Florida carpenter ants in his lab when he noticed something strange. “One ant was biting off another ant’s leg,” said Mr. Buffat, who is now a biologist at the University of Lausanne in Switzerland and is an author of the study. His adviser at Würzburg didn’t believe him at first.“But then he showed me a video and I knew immediately that we were onto something,” the adviser, Erik Frank, said.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.