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Published10 hours agoShareclose panelShare pageCopy linkAbout sharingImage source, The Washington Post via Getty ImagesBy Chelsea BaileyBBC News, WashingtonA US doctor who provided an abortion to a 10-year-old is facing a disciplinary hearing after speaking to media about the case. Indiana officials say Dr Caitlin Bernard violated her patient’s privacy after she spoke publicly about the girl’s treatment.Her lawyers argue she was acting on her duty to inform the public about the impact of policies like abortion bans. It is not immediately clear what punishment she might face.In July 2022, a month after a US Supreme Court ruling ended the nationwide guarantee to an abortion, the Indianapolis Star published a story detailing Dr Bernard’s account of treating a 10-year-old rape survivor. The child had travelled from neighbouring Ohio to Indiana to receive an abortion. At the time, Ohio law prohibited abortion after six weeks of gestation. The case of the 10-year-old, who was a victim of child abuse, being denied an abortion quickly gained national attention. Pro-choice advocates – including President Joe Biden – used the case as an example of the impact of restrictive abortion bans.Later that month, an Ohio man was charged with raping the 10-year-old girl, who has remained unnamed. Last November, the Indiana State Attorney General’s office filed a complaint alleging that Dr Bernard failed to immediately report the abuse of the child, as required by state law, and to protect patient privacy. She testified that she followed her hospital’s policy by reporting the patient’s abuse to a social worker.”As a physician my role is to provide care for the patient no matter how she winds up in my care, it is not my job to investigate the crime,” she said.A hearing before the state Medical and Licensing Board is being held on Thursday. During the hearing, state officials sought to portray Dr Bernard as an “abortion activist” who shared details about the procedure with the media without first requesting permission from the child’s family. “Trust was violated when (Bernard) sought to further her own agenda,” said Deputy Attorney General Cory Voight of the accusations facing the physician. He said if the board agreed with the state’s complaint, Dr Bernard “has become unfit to practice”. Dr Bernard was at times emotional in her testimony as she discussed treating other underage patients who were victims of abuse and had sought abortions. She said she did not violate her patient’s privacy, or release protected health information in discussing the case with the Indianapolis Star. “I think that it’s incredibly important for people to understand the real-world impacts of the laws in this country, about abortion or otherwise,” Dr Bernard said. “I think that it’s important for people to know what patients will have to go through because of legislation that’s being passed.”At the conclusion of the hearing, members of the medical board are expected to vote on whether Dr Bernard’s conduct merits disciplinary action. Indiana’s state medical licencing board has the ability to suspend or revoke a medical licence or place the physician on probation. The attorney general’s initial complaint requests “appropriate disciplinary action” but stops short of demanding specific punishment. More on this storyMan held for raping US girl who was denied abortionPublished14 July 2022What happens now Roe v Wade has been overturned?Published29 June 2022

Using an artificial intelligence algorithm, researchers at MIT and McMaster University have identified a new antibiotic that can kill a type of bacteria that is responsible for many drug-resistant infections.
If developed for use in patients, the drug could help to combat Acinetobacter baumannii, a species of bacteria that is often found in hospitals and can lead to pneumonia, meningitis, and other serious infections. The microbe is also a leading cause of infections in wounded soldiers in Iraq and Afghanistan.
“Acinetobacter can survive on hospital doorknobs and equipment for long periods of time, and it can take up antibiotic resistance genes from its environment. It’s really common now to find A. baumannii isolates that are resistant to nearly every antibiotic,” says Jonathan Stokes, a former MIT postdoc who is now an assistant professor of biochemistry and biomedical sciences at McMaster University.
The researchers identified the new drug from a library of nearly 7,000 potential drug compounds using a machine-learning model that they trained to evaluate whether a chemical compound will inhibit the growth of A. baumannii.
“This finding further supports the premise that AI can significantly accelerate and expand our search for novel antibiotics,” says James Collins, the Termeer Professor of Medical Engineering and Science in MIT’s Institute for Medical Engineering and Science (IMES) and Department of Biological Engineering. “I’m excited that this work shows that we can use AI to help combat problematic pathogens such as A. baumannii.”
Collins and Stokes are the senior authors of the new study, which appears today in Nature Chemical Biology. The paper’s lead authors are McMaster University graduate students Gary Liu and Denise Catacutan and recent McMaster graduate Khushi Rathod.

Drug discovery
Over the past several decades, many pathogenic bacteria have become increasingly resistant to existing antibiotics, while very few new antibiotics have been developed.
Several years ago, Collins, Stokes, and MIT Professor Regina Barzilay (who is also an author on the new study), set out to combat this growing problem by using machine learning, a type of artificial intelligence that can learn to recognize patterns in vast amounts of data. Collins and Barzilay, who co-direct MIT’s Abdul Latif Jameel Clinic for Machine Learning in Health, hoped this approach could be used to identify new antibiotics whose chemical structures are different from any existing drugs.
In their initial demonstration, the researchers trained a machine-learning algorithm to identify chemical structures that could inhibit growth of E. coli. In a screen of more than 100 million compounds, that algorithm yielded a molecule that the researchers called halicin, after the fictional artificial intelligence system from “2001: A Space Odyssey.” This molecule, they showed, could kill not only E. coli but several other bacterial species that are resistant to treatment.
“After that paper, when we showed that these machine-learning approaches can work well for complex antibiotic discovery tasks, we turned our attention to what I perceive to be public enemy No. 1 for multidrug-resistant bacterial infections, which is Acinetobacter,” Stokes says.

To obtain training data for their computational model, the researchers first exposed A. baumannii grown in a lab dish to about 7,500 different chemical compounds to see which ones could inhibit growth of the microbe. Then they fed the structure of each molecule into the model. They also told the model whether each structure could inhibit bacterial growth or not. This allowed the algorithm to learn chemical features associated with growth inhibition.
Once the model was trained, the researchers used it to analyze a set of 6,680 compounds it had not seen before, which came from the Drug Repurposing Hub at the Broad Institute. This analysis, which took less than two hours, yielded a few hundred top hits. Of these, the researchers chose 240 to test experimentally in the lab, focusing on compounds with structures that were different from those of existing antibiotics or molecules from the training data.
Those tests yielded nine antibiotics, including one that was very potent. This compound, which was originally explored as a potential diabetes drug, turned out to be extremely effective at killing A. baumannii but had no effect on other species of bacteria including Pseudomonas aeruginosa, Staphylococcus aureus, and carbapenem-resistant Enterobacteriaceae.
This “narrow spectrum” killing ability is a desirable feature for antibiotics because it minimizes the risk of bacteria rapidly spreading resistance against the drug. Another advantage is that the drug would likely spare the beneficial bacteria that live in the human gut and help to suppress opportunistic infections such as Clostridium difficile.
“Antibiotics often have to be administered systemically, and the last thing you want to do is cause significant dysbiosis and open up these already sick patients to secondary infections,” Stokes says.
A novel mechanism
In studies in mice, the researchers showed that the drug, which they named abaucin, could treat wound infections caused by A. baumannii. They also showed, in lab tests, that it works against a variety of drug-resistant A. baumannii strains isolated from human patients.
Further experiments revealed that the drug kills cells by interfering with a process known as lipoprotein trafficking, which cells use to transport proteins from the interior of the cell to the cell envelope. Specifically, the drug appears to inhibit LolE, a protein involved in this process.
All Gram-negative bacteria express this enzyme, so the researchers were surprised to find that abaucin is so selective in targeting A. baumannii. They hypothesize that slight differences in how A. baumannii performs this task might account for the drug’s selectivity.
“We haven’t finalized the experimental data acquisition yet, but we think it’s because A. baumannii does lipoprotein trafficking a little bit differently than other Gram-negative species. We believe that’s why we’re getting this narrow spectrum activity,” Stokes says.
Stokes’ lab is now working with other researchers at McMaster to optimize the medicinal properties of the compound, in hopes of developing it for eventual use in patients.
The researchers also plan to use their modeling approach to identify potential antibiotics for other types of drug-resistant infections, including those caused by Staphylococcus aureus and Pseudomonas aeruginosa.

New research from Oregon Health & Science University is helping explain why at least five people have become HIV-free after receiving a stem cell transplant. The study’s insights may bring scientists closer to developing what they hope will become a widespread cure for the virus that causes AIDS, which has infected about 38 million people worldwide.
Published today in the journal Immunity, the OHSU-led study describes how two nonhuman primates were cured of the monkey form of HIV after receiving a stem cell transplant. It also reveals that two circumstances must co-exist for a cure to occur and documents the order in which HIV is cleared from the body — details that can inform efforts to make this cure applicable to more people.
“Five patients have already demonstrated that HIV can be cured,” said the study’s lead researcher, Jonah Sacha, Ph.D., a professor at OHSU’s Oregon National Primate Research Center and Vaccine and Gene Therapy Institute.
“This study is helping us home in on the mechanisms involved in making that cure happen,” Sacha continued. “We hope our discoveries will help to make this cure work for anyone, and ideally through a single injection instead of a stem cell transplant.”
The first known case of HIV being cured through a stem cell transplant was reported in 2009. A man who was living with HIV was also diagnosed with acute myeloid leukemia, a type of cancer, and underwent a stem cell transplant in Berlin, Germany. Stem cell transplants, which are also called bone marrow transplants, are used to treat some forms of cancer. Known as the Berlin patient, he received donated stem cells from someone with a mutated CCR5 gene, which normally codes for a receptor on the surface of white blood cells that HIV uses to infect new cells. A CCR5 mutation makes it difficult for the virus to infect cells, and can make people resistant to HIV. Since the Berlin patient, four more people have been similarly cured.
This study was conducted with a species of nonhuman primate known as Mauritian cynomolgus macaques, which the research team previously demonstrated can successfully receive stem cell transplants. While all of the study’s eight subjects had HIV, four of them underwent a transplant with stem cells from HIV-negative donors, and the other half served as the study’s controls and went without transplants.

Of the four that received transplants, two were cured of HIV after successfully being treated for graft-versus-host disease, which is commonly associated with stem cell transplants.
Other researchers have tried to cure nonhuman primates of HIV using similar methods, but this study marks the first time that HIV-cured research animals have survived long term. Both remain alive and HIV-free today, about four years after transplantation. Sacha attributes their survival to exceptional care from Oregon National Primate Research Center veterinarians and the support of two study coauthors, OHSU clinicians who care for people who undergo stem cell transplants: Richard T. Maziarz, M.D., and Gabrielle Meyers, M.D.
“These results highlight the power of linking human clinical studies with pre-clinical macaque experiments to answer questions that would be almost impossible to do otherwise, as well as demonstrate a path forward to curing human disease,” said Maziarz, a professor of medicine in the OHSU School of Medicine and medical director of the adult blood and marrow stem cell transplant and cellular therapy programs in the OHSU Knight Cancer Institute.
The how behind the cure
Although Sacha said it was gratifying to confirm stem cell transplantation cured the nonhuman primates, he and his fellow scientists also wanted to understand how it worked. While evaluating samples from the subjects, the scientists determined there were two different, but equally important, ways they beat HIV.

First, the transplanted donor stem cells helped kill the recipients’ HIV-infected cells by recognizing them as foreign invaders and attacking them, similar to the process of graft-versus-leukemia that can cure people of cancer.
Second, in the two subjects that were not cured, the virus managed to jump into the transplanted donor cells. A subsequent experiment verified that HIV was able to infect the donor cells while they were attacking HIV. This led the researchers to determine that stopping HIV from using the CCR5 receptor to infect donor cells is also needed for a cure to occur.
The researchers also discovered that HIV was cleared from the subjects’ bodies in a series of steps. First, the scientists saw that HIV was no longer detectable in blood circulating in their arms and legs. Next, they couldn’t find HIV in lymph nodes, or lumps of immune tissue that contain white blood cells and fight infection. Lymph nodes in the limbs were the first to be HIV-free, followed by lymph nodes in the abdomen.
The step-wise fashion by which the scientists observed HIV being cleared could help physicians as they evaluate the effectiveness of potential HIV cures. For example, clinicians could focus on analyzing blood collected from both peripheral veins and lymph nodes. This knowledge may also help explain why some patients who have received transplants initially have appeared to be cured, but HIV was later detected. Sacha hypothesizes that those patients may have had a small reservoir of HIV in their abdominal lymph nodes that enabled the virus to persist and spread again throughout the body.
Sacha and colleagues continue to study the two nonhuman primates cured of HIV. Next, they plan to dig deeper into their immune responses, including identifying all of the specific immune cells involved and which specific cells or molecules were targeted by the immune system.
This research is supported by the National Institutes of Health (grants AI112433, AI129703, P51 OD011092) and the Foundation for AIDS Research (grant 108832), and the Foundation for AIDS Immune Research. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
In our interest of ensuring the integrity of our research and as part of our commitment to public transparency, OHSU actively regulates, tracks and manages relationships that our researchers may hold with entities outside of OHSU. In regard to this research, Dr. Sacha has a significant financial interest in CytoDyn, a company that may have a commercial interest in the results of this research and technology. Review?details of OHSU’s conflict of interest program?to find out more about how we manage these business relationships.
All research involving animal subjects at OHSU must be reviewed and approved by the university’s?Institutional Animal Care and Use Committee (IACUC). The IACUC’s priority is to ensure the health and safety of animal research subjects. The IACUC also reviews procedures to ensure the health and safety of the people who work with the animals. No live animal work may be conducted at OHSU without IACUC approval.
REFERENCE: Helen Wu, Kathleen Busman-Sahay, Whitney C. Weber, Courtney M. Waytashek, Carla D. Boyle, Katherine Bateman, Jason S. Reed, Joseph M. Hwang, Christine Shriver-Munsch, Tonya Swanson, Mina Northrup, Kimberly Armantrout, Heidi Price, Mitch Robertson-LeVay, Samantha Uttke, Mithra R. Kumar, Emily J. Fray, Sol Taylor-Brill, Stephen Bondoc, Rebecca Agnor, Stephanie L. Junell, Alfred W. Legasse, Cassandra Moats, Rachele M. Bochart, Joseph Sciurba, Benjamin N. Bimber, Michelle N. Sullivan, Brandy Dozier, Rhonda P. MacAllister, Theodore R. Hobbs, Lauren D. Martin, Angela Panoskaltsis-Mortari, Lois M.A. Colgin, Robert F. Silciano, Janet D. Silciano, Jacob D. Estes, Jeremy V. Smedly, Michael K. Axthelm, Gabrielle Meyers, Richard T. Maziarz, Benjamin J. Burwitz, Jeffrey J. Stanton, Jonah B. Sacha, Allogeneic immunity clears latent virus following allogenic stem cell transplantation in SIV-infected antiretroviral therapy-suppressed macaques, Immunity, May 25, 2023, DOI: 10.1016/j.immuni.2023.04.019.

New research has demonstrated, for the first time, that a wearable brain scanner can measure brain function whilst people are standing and walking around. This breakthrough could help better understand and diagnose a range of neurological problems that affect movement, including Parkinson’s Disease, stroke and concussion.
To enable this novel technology, researchers from the University of Nottingham’s School of Physics have developed a new design of magnetic field control system. This allows a much greater degree of subject movement than has ever been possible previously. The results have been published in NeuroImage.
The unique wearable brain scanner system uses small LEGO-brick-sized sensors — called optically pumped magnetometers (OPMs) — to measure magnetic fields generated by cellular activity in the brain — a technique called Magnetoencephalography, or MEG. These sensors are incorporated into a lightweight helmet. The unique design means the system can be adapted to fit anyone, from newborns to adults, and sensors can be placed much closer to the head, dramatically enhancing data quality. This is a step change from conventional brain scanners that are large and fixed and require the patient to stay very still during scanning.
However, OPMs must operate at precisely zero magnetic field to become sensitive enough to measure brain signals, this means they must be operated inside a magnetically shielded room (MSR). This room must contain additional equipment that allows precise control of magnetic fields at a level 50,000 times smaller than the Earth’s magnetic field. Existing solutions to this problem used complex wire patterns to generate cancellation fields over small, fixed regions. This allowed people to move their heads whilst seated, but was unable to allow ambulatory movement.
The Nottingham team have now designed a ‘matrix coil’ system formed from multiple simple square coils. The coil currents can be reconfigured in real time to compensate magnetic fields over a moving region that can be flexibly placed within the coils, giving much greater scope for people to move during a scan.
Niall Holmes, Research Fellow from the University of Nottingham, has led this study and said: “By using the matrix coils to allow greater movement we can, for the first time, realise many scanning scenarios that would have previously been considered impossible, but that have the potential to significantly expand our understanding of exactly what is happening in the brain during movement, neurodevelopment and in a range of neurological issues.”
Professor Matt Brookes leads MEG research in Nottingham and said: “Just 5 years ago, the idea of acquiring high resolution images of human brain electrophysiology whilst people walk around a room would have seemed like something from science fiction. The matrix coil has made this a reality! The applications span a huge area, from basic neuroscientific questions like how do young children learn to walk, to clinical challenges like why are older people prone to falling. It’s incredible to think how far this technology has come, and even more incredible to imagine where it’s going.”
The University launched the spin-out company Cerca Magnetics in 2020 to bring OPM-MEG research systems to the market. The wearable system has been installed in a number of research institutions across the globe, including Young Epilepsy’s Health and Research Centre in the UK. The team are currently working towards gaining clinical approval of the Cerca System to bring it closer to being used in clinical settings.
Niall adds: “We are excited to work with Cerca to incorporate this new coil design into the commercial systems and to see what new studies will be enabled by our work.”
The work is part of the UK Quantum Technologies Programme and was funded by the Engineering and Physics Research Council alongside the National Institutes of Health and the Wellcome Trust.

Some mammals and birds have a clever way to preserve energy and heat by going into torpor, during which their body temperature and metabolic rate drop to allow them to survive potentially fatal conditions in the environment, such as extreme cold or lack of food. While a similar condition was proposed for scientists making flights to space in the 1960s or for patients with life-threatening health conditions, safely inducing such a state remains elusive.
Hong Chen, an associate professor at Washington University in St. Louis, and a multidisciplinary team induced a torpor-like state in mice by using ultrasound to stimulate the hypothalamus preoptic area in the brain, which helps to regulate body temperature and metabolism. In addition to the mouse, which naturally goes into torpor, Chen and her team induced torpor in a rat, which does not. Their findings, published May 25, 2023, in Nature Metabolism, show the first noninvasive and safe method to induce a torpor-like state by targeting the central nervous system.
Chen, associate professor of biomedical engineering in the McKelvey School of Engineering and of radiation oncology at the School of Medicine, and her team, including Yaoheng (Mack) Yang, a postdoctoral research associate, created a wearable ultrasound transducer to stimulate the neurons in the hypothalamus preoptic area. When stimulated, the mice showed a drop in body temperature of about 3 degrees C for about one hour. In addition, the mice’s metabolism showed a change from using both carbohydrates and fat for energy to only fat, a key feature of torpor, and their heart rates fell by about 47%, all while at room temperature.
The team also found that as the acoustic pressure and duration of the ultrasound increased, so did the depth of the lower body temperature and slower metabolism, known as ultrasound-induced hypothermia and hypometabolism (UIH).
“We developed an automatic closed-loop feedback controller to achieve long-duration and stable ultrasound-induced hypothermia and hypometabolism by controlling of the ultrasound output,” Chen said. “The closed-loop feedback controller set the desired body temperature to be lower than 34C, which was previously reported as critical for natural torpor in mice. This feedback-controlled UIH kept the mouse body temperature at 32.95C for about 24 hours and recovered to normal temperature after ultrasound was off.”
To learn how ultrasound-induced hypothermia and hypometabolism is activated, the team studied the dynamics of the activity of neurons in the hypothalamus preoptic area in response to ultrasound. They observed a consistent increase in neuronal activity in response to each ultrasound pulse, which aligned with the changes in body temperature in the mice.
“These findings revealed that UIH was evoked by ultrasound activation of hypothalamus preoptic area neurons,” Yang said. “Our finding that transcranial stimulation of the hypothalamus preoptic area was sufficient to induce UIH revealed the critical role of this area in orchestrating a torpor-like state in mice.”
Chen and her team also wanted to find the molecule that allowed these neurons to activate with ultrasound. Through genetic sequencing, they found that ultrasound activated the TRPM2 ion channel in the hypothalamus preoptic area neurons. In a variety of experiments, they showed that TRPM2 is an ultrasound-sensitive ion channel and contributed to the induction of UIH.
In the rat, which does not naturally go into torpor or hibernation, the team delivered ultrasound to the hypothalamus preoptic area and found a decrease in skin temperature, particularly in the brown adipose tissue region, as well as about a 1 degree C drop in core body temperature, resembling natural torpor.
This multidisciplinary team consists of Jonathan R. Brestoff, MD, PhD, assistant professor of pathology & immunology at the School of Medicine; Alexxai V. Kravitz, associate professor of psychiatry, of anesthesiology and of neuroscience at the School of Medicine, and Jianmin Cui, professor of biomedical engineering in the McKelvey School of Engineering, all at Washington University in St. Louis. The team also includes Michael R. Bruchas, professor of anesthesiology and of pharmacology at the University of Washington.
“UIH has the potential to address the long sought-after goal of achieving noninvasive and safe induction of the torpor-like state, which has been pursued by the scientific community at least since the 1960s,” Chen said. “Ultrasound stimulation possesses a unique capability to noninvasively reach deep brain regions with high spatial and temporal precision in animal and human brains.”
This work was supported by the National Institutes of Health (R01MH116981, UG3MH126861, R01EB027223, and R01EB030102). JRB is supported by NIH (DP5 OD028125) and Burroughs Wellcome Fund (CAMS #1019648).

Living in an almshouse can boost the longevity of its residents by as much as two-and-a-half years compared to their counterparts in the general population, according to a new Bayes Business School report.
Almshouses provide affordable community housing for local people in housing need. They are generally designed around a courtyard to provide a ‘community spirit’, that is synonymous with the almshouse movement. They offer independent living but provide friendship and support when needed.
Analysing up to 100 years’ worth of residents’ records from various almshouses in England, the research suggests that living in these communities can reduce the negative impact on health and social wellbeing which is commonly experienced by the older population in lower socioeconomic groups, particularly those individuals who are living in isolation.
The results are very encouraging. They show that, for several of the almshouses included in the study, residents can expect to live as long as wealthier members of the general population despite coming from the most deprived quintile. This shows that the disparity in longevity and health outcomes could be mitigated even after reaching retirement age, provided a suitable social infrastructure can be put in place.
The report, authored by Professor Ben Rickayzen, Dr David Smith, Dr Anastasia Vikhanova and Alison Benzimra, concludes that almshouses could help the Government’s aims to reduce inequalities in mortality, which are observed between socioeconomic groups, by reducing the social isolation experienced by many in the older population.
Titled ‘Almshouse Longevity Study — Can living in an almshouse lead to a longer life?’, the report’s key findings are: Residents in almshouses in England receive a longevity boost relative to people of the same socioeconomic group from the wider population. The best-performing almshouses in the study so far have shown a longevity boost which increases life expectancy to that of a life in the second-highest socioeconomic quintile — a remarkable outcome. As an example, the authors estimate that a 73-year-old male entering an almshouse such as The Charterhouse today would receive a longevity boost of 2.4 years (an extra 15% of future lifetime at the point of joining) compared to his peers from the same socioeconomic group, and 0.7 years when compared to an average 73-year-old from the general population. This longevity boost could be due to both the strong sense of community and social belonging within almshouses which lead to better physical and mental health. Enhanced wellbeing helps to mitigate loneliness which is endemic in older age groups.Professor Ben Rickayzen, Professor of Actuarial Science at Bayes Business School, said:

“It is well known that, on average, the lower a person’s socioeconomic status, the lower their life expectancy. However, intriguingly, our research has found that this doesn’t have to be the case. We discovered that many almshouse residents receive a longevity boost when compared to their peers of the same socioeconomic status from the wider population.
“More research is needed to ascertain exactly what factors cause almshouse residents to have a longer life; however, we postulate that it is the sense of the community that is the most powerful ingredient. For example, a common theme within the almshouses included in the study is that they encourage residents to undertake social activities and responsibilities on behalf of their fellow residents. This is likely to increase their sense of belonging and give them a greater sense of purpose in their everyday lives while mitigating against social isolation.
“We would encourage the Government to invest in retirement communities, such as almshouses, which would be in keeping with their overarching levelling up agenda. While this agenda is commonly associated with enhancing equality on a regional basis, it is important that levelling up should also aim to combat health inequalities experienced by people from lower socioeconomic groups across the country. There is an opportunity to improve the Government’s levelling up agenda by incorporating the best features of communal living into their social housing policy. This should make a significant difference to the quality of life experienced by the older population across the UK.
“The findings from this research are important as they could offer solutions to the social care problems currently being experienced in the UK.”
Alison Benzimra, a co-author of the report and Head of Research at United St Saviour’s Charity, said:
“Many almshouse trustees and staff members anecdotally believe that almshouse living is beneficial for residents. The results from this study demonstrate that the community spirit provided by almshouses does in fact result in longer life expectancy. These findings are encouraging to those living and working in the almshouse community and provide the motivation to continue to explore what it is about almshouses’ physical design and support services that result in positive outcomes for older residents. This study strengthens the case that this historic form of housing is addressing the evolving needs of older people living in our modern-day society.”

Nick Phillips, CEO, The Almshouse Association, said:
“We are delighted to read this report. It is further evidence that the almshouse model — 1,000 years after its inception — seems to be adding something special to the lives of residents. There is a growing body of research that is suggesting this model of community housing seems to be right for the future. This must now beg the question, where are the philanthropists to lead this robust charity housing model into the next century?”
Susan Kay, Chief Executive of Dunhill Medical Trust, said:
“It’s been great to support this piece of work and to see it take its place in the wider body of work about the characteristics of age-friendly living spaces and supportive communities. A one-hundred-year life is now a realistic expectation and we need to build on this learning to create the homes and communities that will be so important for the health and wellbeing of us all.”
Nigel Hulme, a resident of the United St Saviour’s Charity almshouse, explained how much living in the almshouse has helped him in his later years:
“Moving to Hopton’s Gardens has been a godsend. To have a roof over my head has helped me to deal with my addiction issues, and having the support from the staff and my neighbours has made my recovery possible.”
The study was sponsored by the Dunhill Medical Trust and the Justham Trust and was supported by The Almshouse Association

Stem cells from the human stomach can be converted into cells that secrete insulin in response to rising blood sugar levels, offering a promising approach to treating diabetes, according to a preclinical study from researchers at Weill Cornell Medicine.
In the study, which appeared April 27 in Nature Cell Biology, the researchers showed that they could take stem cells obtained from human stomach tissue and reprogram them directly — with strikingly high efficiency — into cells that closely resemble pancreatic insulin-secreting cells known as beta cells. Transplants of small groups of these cells reversed disease signs in a mouse model of diabetes.
“This is a proof-of-concept study that gives us a solid foundation for developing a treatment, based on patients’ own cells, for type 1 diabetes and severe type 2 diabetes,” said study senior author Dr. Joe Zhou, a professor of regenerative medicine and a member of the Hartman Institute for Therapeutic Organ Regeneration at Weill Cornell Medicine.
Insulin is a hormone that regulates blood glucose levels — without it, blood glucose becomes too high, causing diabetes and its many complications. An estimated 1.6 million Americans have type 1 diabetes, which results from an autoimmune attack that destroys beta cells in the pancreas. At least several million other Americans lack sufficient beta cells due to severe type 2 diabetes. Current treatments in such cases include manual and wearable-pump injections of insulin, which have multiple drawbacks including pain, potentially inefficient glucose control, and the necessity of wearing cumbersome equipment.
Biomedical researchers aim to replace beta-cell function in a more natural way, with transplants of human cells that work as beta cells do: automatically sensing blood sugar levels and secreting insulin as needed. Ideally, such transplants would use patients’ own cells, to avoid the problem of transplant rejection.
Dr. Zhou has been working toward this goal for more than 15 years. In early experiments as a postdoctoral researcher, he discovered that ordinary pancreatic cells could be turned into insulin-producing beta-like cells by forcing the activation of three transcription factors — or proteins that control gene expression — resulting in the subsequent activation of genes required for the development of normal beta cells. In a 2016 study, again in mice, he and his team showed that certain stem cells in the stomach, called gastric stem cells, are also highly sensitive to this three-factor activation method.
“The stomach makes its own hormone-secreting cells, and stomach cells and pancreatic cells are adjacent in the embryonic stage of development, so in that sense it isn’t completely surprising that gastric stem cells can be so readily transformed into beta-like insulin-secreting cells,” Dr. Zhou said.
Attempts to reproduce these results using human gastric stem cells, which can be removed from patients relatively easily in an outpatient procedure called endoscopy, were slowed by various technical hurdles. However, in the new study, led by first author Dr. Xiaofeng Huang, an instructor of molecular biology in medicine at Weill Cornell Medicine, the researchers at last achieved success.
After turning human gastric stem cells into beta-like cells, the team grew the cells in small clusters called organoids and found that these organ-like pieces of tissue quickly became sensitive to glucose, responding with secretions of insulin. When transplanted into diabetic mice, the beta-like organoids functioned largely as real pancreatic beta cells would, secreting insulin in response to rises in blood glucose, and thereby keeping blood glucose levels steady. The transplants also kept working for as long as the researchers monitored them — six months — suggesting good durability.
Dr. Zhou said that he and his lab still need to optimize their method in various ways before it can be considered for clinical use. Necessary improvements include methods to increase the scale of beta-cell production for transplants to humans, and modifications of the beta-like cells to make them less vulnerable to the type of immune attack that initially wipes out beta cells in type 1 diabetes patients.
Ultimately, the researchers hope to develop a technique enabling the relatively easy harvesting of gastric stem cells from patients, followed by the transplant, weeks later, of insulin-secreting organoids that regulate blood sugar levels without the need for further medication.

Exploring diverse ancestry is a critical factor in furthering medical research.
A new study published in Nature Genetics from researchers in the Department of Biomedical Informatics (DBMI) at the University of Colorado School of Medicine, in partnership with the University of California San Francisco and Stanford University, is the largest of its kind that focuses on ancestry correlations with biomedical traits and the first study to examine the role of genetic variants across diverse ancestries in regulating gene expression.
“We’re trying to understand how genetic variability around the world allows us to gain a deeper understanding of the relationship between genetics and RNA levels and then protein levels and physiology,” says DBMI associate professor and study co-senior author Chris Gignoux, PhD. “The genome and gene expression each on their own only tells us so much. Having these layers coming together helps us a lot more.”
Gignoux describes the genetic control of gene expression as a dial that controls the amount of the gene that gets transcribed into RNA and protein levels, ultimately impacting function in various ways.
The study analyzed whole genome and RNA sequencing from African American and Latino children. Researchers say their findings demonstrate the importance of measuring gene expression across multiple populations because those gene expressions can vary greatly depending on ancestry and enable new discoveries that may also reduce health care disparities for historically underrepresented populations.
Gignoux’s lab used data from The National Heart, Lung, and Blood Institute-funded Trans-Omics for Precision Medicine (TOPMed) consortium and the National Human Genome Research Institute-funded Population Architecture using Genomics and Epidemiology (PAGE) Study. They analyzed whole genome and RNA sequencing data from 2,733 African American and Hispanic/Latino children, exploring ancestry and heterozygosity-related differences in the genetic architecture of whole blood gene expression.
“The ultimate goal was that we learn by looking at gene expression patterns in populations that came from the same ethnic group,” Gignoux explains. “Individuals from across Latin America do not reflect one homogeneous population, so that was part of the reason why it was important to not just look at Hispanics in one group, but to highlight what we can learn from studying Mexican Americans and Puerto Ricans, specifically. We’re able to leverage some of that diversity to understand some of these patterns.”
Because ethnicity is a sociopolitical identity, understanding the relationship between genetics and ancestry is quite complex and can vary greatly between individuals. This is true even within certain populations such as individuals of Puerto Rican descent.
Historically, there’s been a deficit in genetics research focused on people of non-European descent, but knowing more about the relationship between genetic variability and gene expression can inform deeper research into many different health issues.
That’s been proven true in examples such as the medical community’s knowledge of heart attacks, which for decades only focused on men. With more research, it became apparent that risk factors and symptoms look much different in women.
Without studying diverse populations, it’s nearly impossible to know a disease might present in another group of people. The work done by Gignoux and his fellow researchers, including researchers from the various communities represented, may help inform more discoveries that are significant to diverse populations, just like identifying different risk factors women face with heart attacks.
“We’re not going to know what we don’t know unless we look, and that has the potential to impact how we think about individuals’ risk factors for a number of different conditions and traits,” Gignoux says. “It’s also important to look in the right kind of ways and develop the methodologies so that we can leverage these kinds of diversity-focused efforts. The hope is that as these kinds of initiatives move forward in genetic and non-genetic disciplines there’s an opportunity to improve our understanding of biomedical traits for anyone who walks into the clinic.”

Researchers at Wilmer Eye Institute, Johns Hopkins Medicine say they have evidence that an experimental drug may prevent or slow vision loss in people with diabetes. The results are from a study that used mouse as well as human retinal organoids and eye cell lines. Eye conditions that cause vision loss are common complications of diabetes, affecting nearly 8 million Americans — a statistic likely to almost double by 2040, according to the National Institutes of Health.
The team focused on models of two common diabetic eye conditions: proliferative diabetic retinopathy and diabetic macular edema, both of which affect the retina, the light-sensing tissue at the back of the eye that also transmits vision signals to the brain. In proliferative diabetic retinopathy, new blood vessels overgrow on the retina’s surface, causing bleeding or retinal detachments and profound vision loss. In diabetic macular edema, blood vessels in the eye leak fluid, leading to swelling of the central retina, damaging the retinal cells responsible for central vision.
Results of the study, published May 25 in the Journal of Clinical Investigation, show that a compound called 32-134D, previously shown to slow liver tumor growth in mice, prevented diabetic retinal vascular disease by decreasing levels of a protein called HIF, or hypoxia-inducible factor. Doses of 32-134D also appeared to be safer than another treatment that also targets HIF and is under investigation to treat diabetic eye disease.
Current treatment for both proliferative diabetic retinopathy and diabetic macular edema includes eye injections with anti-vascular endothelial growth factor (anti-VEGF) therapies. Anti-VEGF therapies can halt the growth and leakiness of blood vessels in the retina in patients with diabetes. However, these treatments aren’t effective for many patients, and may cause side effects with prolonged use, such as increased internal eye pressure or eye tissue damage.
Akrit Sodhi, M.D., Ph.D., an author of the new study, says that in general, the idea of inhibiting HIF, a fundamental protein in the body, has raised concerns about toxicity to many tissues and organs. But when his team screened a library of HIF inhibitor drugs and conducted extensive testing, “We came to find that the drug examined in this study, 32-134D, was remarkably well tolerated in the eyes and effectively reduced HIF levels in diseased eyes,” says Sodhi, associate professor of ophthalmology and the Branna and Irving Sisenwein Professor of Ophthalmology at the Johns Hopkins University School of Medicine and the Wilmer Eye Institute.
HIF, a type of protein known as a transcription factor, has the ability to switch certain genes, including vascular endothelial growth factor (VEGF), on or off throughout the body. In the eye, elevated levels of HIF cause genes like VEGF to increase blood vessel production and leakiness in the retina, contributing to vision loss.
To test 32-134D, researchers dosed multiple types of human retinal cell lines associated with the expression of proteins that promote blood vessel production and leakiness. When they measured genes regulated by HIF in cells treated with 32-134D, they found that their expression had returned to near-normal levels, which is enough to halt new blood vessel creation and maintain blood vessels’ structural integrity.
Researchers also tested 32-134D in two different adult mouse models of diabetic eye disease. In both models, injections were administered into the eye. Five days post-injection, the researchers observed diminished levels of HIF, and also saw that the drug effectively inhibited the creation of new blood vessels or blocked vessel leakage, therefore slowing progression of the animals’ eye disease. Sodhi and his team said they also were surprised to find that 32-134D lasted in the retina at active levels for about 12 days following a single injection without causing retinal cell death or tissue wasting.
“This paper highlights how inhibiting HIF with 32-134D is not just a potentially effective therapeutic approach, but a safe one, too,” says Sodhi. “People facing diabetic eye disease and vision loss include our family members, friends, co-workers — this is a disease that impacts a large group of people. Having safer therapies is critical for this growing population of patients.”
Sodhi says that further studies in animal models are needed before moving to clinical trials.
Additional authors involved in this study are Jing Zhang, Deepti Sharma, Aumreetam Dinabandhu, Jaron Sanchez, Brooks Puchner Applewhite, Kathleen Jee, Monika Deshpande, Ming-Wen Hu, Chuanyu Guo, Jiang Qian, Shaima Salman, Yousang Hwand and Gregg Semenza of the Johns Hopkins University School of Medicine; Miguel Flores-Bellver and Maria Valeria Canto-Soler of University of Colorado School of Medicine; Nicole Anders and Michelle Rudek of the Johns Hopkins Sidney Kimmel Comprehensive Cancer Center; and Silvia Montaner of the University of Maryland.
Funding for this work was supported by NIH grants (R01EY029750, R01EY032104, EY001765, P30 CA006973, 1S10RR026824, UL1 TR003098); the TEDCO Maryland Innovation Initiative, the Research to Prevent Blindness, Inc. Special Scholar Award; the Sybil B. Harrington Stein Innovations Award; an unrestricted grant to the Wilmer Eye Institute, Johns Hopkins University School of Medicine and the University of Colorado; the Armstrong Family Foundation; the CellSight Development Fund; the Doni Solich Family Chair in Ocular Stem Cell Research; and the Branna Irving Sisenwein Professorship in Ophthalmology.

Cancers often release molecules into the bloodstream that pathologically alter the liver, shifting it to an inflammatory state, causing fat buildup and impairing its normal detoxifying functions, according to a study from investigators at Weill Cornell Medicine. This discovery illuminates one of cancer’s more insidious survival mechanisms and suggests the possibility of new tests and drugs for detecting and reversing this process.
In the study, published May 24 in Nature, the researchers found that a wide variety of tumor types growing outside the liver remotely reprogram the liver to a state resembling fatty liver disease via secretion of extracellular vesicles and particles (EVPs) containing fatty acids. The scientists found evidence of this process in animal models of cancer and in the livers of human cancer patients.
“Our findings show that tumors can lead to significant systemic complications including liver disease, but also suggest that these complications can be addressed with future treatments,” said study co-senior author Dr. David Lyden, the Stavros S. Niarchos Professor in Pediatric Cardiology and a professor of pediatrics and of cell and developmental biology at Weill Cornell Medicine.
For the past two decades, Dr. Lyden, who is also a member of the Gale and Ira Drukier Institute for Children’s Health and the Sandra and Edward Meyer Cancer Center at Weill Cornell Medicine, and his research group have been studying the systemic effects of cancers. These effects reflect specific strategies cancers use to secure their survival and speed their progression. In their work published in 2015, for example, the team discovered that pancreatic cancers secrete molecules encapsulated in extracellular vesicles, that travel through the bloodstream, are taken up by the liver, and prepare the organ to support the outgrowth of new, metastatic tumors.
In the new study, the researchers uncovered a different set of liver changes caused by distant cancer cells which they observed in animal models of bone, skin and breast cancer that metastasize to other organs but not to the liver. The study’s key finding is that these tumors induce accumulation of fat molecules in liver cells, consequently reprogramming the liver in a way that resembles the obesity- and alcohol-related condition known as fatty liver disease.
The team also observed that reprogrammed livers have high levels of inflammation, marked by elevated level of tumor necrosis factor-α (TNF-α), and low levels of drug-metabolizing enzymes called cytochrome P450, which break down potentially toxic molecules, including many drug molecules. The observed reduction in cytochrome P450 levels could explain why cancer patients often become less tolerant of chemotherapy and other drugs as their illness progresses.

The researchers traced this liver reprogramming to EVPs that are released by the distant tumors and carry fatty acids, especially palmitic acid. When taken up by liver-resident immune cells called Kupffer cells, the fatty acid cargo triggers the production TNF-α, which consequently drives fatty liver formation.
Although the researchers principally used animal models of cancers in the study, they observed similar changes in the livers of newly diagnosed pancreatic cancer patients who later developed non-liver metastases.
“One of our more striking observations was that this EVP-induced fatty liver condition did not co-occur with liver metastases, suggesting that causing fatty liver and preparing the liver for metastasis are distinct strategies that cancers use to manipulate liver function,” said co-first author Dr. Gang Wang, a postdoctoral associate in the Lyden laboratory. Dr. Jianlong Li, a scientific collaborator in the Lyden laboratory, is also a co-first author of the study.
The scientists suspect that the fatty liver condition benefits cancers in part by turning the liver into a lipid-based source of energy to fuel cancer growth.
“We see in liver cells not only an abnormal accumulation of fat but also a shift away from the normal processing of lipids, so that the lipids that are being produced are more advantageous to the cancer,” said co-senior author Dr. Robert Schwartz, associate professor of medicine in the Division of Gastroenterology and Hepatology and a member of the Meyer Cancer Center at Weill Cornell Medicine and a hepatologist at NewYork-Presbyterian/Weill Cornell Medical Center.
That may not be the only benefit that cancers derive from this liver alteration. “There are also crucial molecules involved in immune cell function, but their production is altered in these fatty livers, hinting that this condition may also weakens anti-tumor immunity,” said co-senior author Dr. Haiying Zhang, assistant professor of cell and developmental biology in pediatrics at Weill Cornell Medicine.
The researchers were able to mitigate these systemic effects of tumors on the livers by implementing strategies such as blocking tumor-EVP release, inhibiting the packaging of palmitic acid into tumor EVPs, suppressing TNF-α activity, or eliminating Kupffer cells in the experimental animal models. The researchers are further investigating the potential of implementing these strategies in human patients to block these remote effects of tumors on the liver, and exploring the possibility of utilizing the detection of palmitic acid in tumor EVPs circulating in the blood as a potential warning sign of advanced cancer.