Publisher Health

Adults with high levels of attention-deficit hyperactivity disorder (ADHD) symptoms are more likely to experience anxiety and depression than adults with high levels of autistic traits, according to new research led by psychologists at the University of Bath in the UK.
This study is the first to show that ADHD is more predictive of poor mental health outcomes in adults than other neurodevelopmental conditions, like autism.
Until now, there has been a dearth of information on the effects of ADHD on poor mental health, with far more research focusing on the impact of autism on depression, anxiety and quality of life. As a result, people with ADHD have often struggled to access the clinical care they need to cope with their symptoms.
The authors of the study hope their findings will trigger new research into ADHD and ultimately improve the mental health outcomes for people with the condition. ADHD is a neurodevelopmental condition characterised by inattention and/or hyperactivity and impulsivity. The condition is estimated to affect between 3% and 9% of the population.
Blue Monday
Speaking on Blue Monday (January 16) — the third Monday of January, described by some as the gloomiest day of the year — lead researcher, Luca Hargitai, said: “Scientists have long known that autism is linked to anxiety and depression, but ADHD has been somewhat neglected.

“Researchers have also struggled to statistically separate the importance of ADHD and autism for mental health outcomes because of how frequently they occur together.”
Ms Hargitai, a PhD Researcher at Bath, added: “Our aim was to precisely measure how strongly ADHD personality traits were linked to poor mental health while statistically accounting for autistic traits.”
The new research — a collaborative effort between the Universities of Bath, Bristol and Cardiff, and King’s College London — is published this week in Scientific Reports. It comes in the same month that two British TV personalities — Johnny Vegas and Sue Perkins — have opened up about their recent diagnoses of ADHD.
“The condition affects many people — both children and adults — and the fact that more people are willing to talk about it is to be welcomed,” said Ms Hargitai. “The hope is that with greater awareness will come more research in this area and better resources to support individuals in better managing their mental health.”
Overly active, as though driven by a motor
The study used a large, nationally representative sample of adults from the UK population. All participants completed gold standard questionnaires — one on autistic traits, the other on ADHD traits — responding to statements such as “I frequently get strongly absorbed in one thing” and “How often do you feel overly active and compelled to do things, like you were driven by a motor?”

The researchers found that ADHD traits were highly predictive of the severity of anxiety and depression symptoms: the higher the levels of ADHD traits, the more likely a person is to experience severe mental health symptoms. Through innovative analytical techniques, the study authors further confirmed that having more of an ADHD personality was more strongly linked to anxiety and depression than autistic traits.
These results were replicated in computerised simulations with a 100% ‘reproducibility rate’. This showed, with great confidence, that ADHD traits are almost certainly linked to more severe anxiety and depression symptoms in adults than autistic traits.
Shifting the focus of research and clinical practice
Ms Hargitai said: “Our findings suggest that research and clinical practice must shift some of the focus from autism to ADHD. This may help to identify those most at risk of anxiety and depression so that preventative measures — such as supporting children and adults with the management of their ADHD symptoms — can be put in place earlier to have a greater impact on improving people’s wellbeing.”
According to Dr Punit Shah, senior author and associate professor of Psychology at Bath, another important aspect of the new study is that it advances scientific understanding of neurodevelopmental conditions.
“By addressing the shortcomings of previous research, our work provides fresh information about the complex links between neurodiversity and mental health in adults — an area that is often overlooked.
“Further research is now needed to delve deeper into understanding exactly why ADHD is linked to poor mental health, particularly in terms of the mental processes that might drive people with ADHD traits to engage in anxious and depressive thinking.
“At the moment, funding for ADHD research — particularly psychological research — is lacking. This is especially pronounced when you compare it to the relatively high level of funds directed at autism.
“As the evidence becomes clear that ADHD isn’t just a childhood condition but persists throughout life, we must adjust our research agendas to better understand ADHD in adulthood.”
Commenting on the new findings, Dr Tony Floyd, CEO of ADHD Foundation, The Neurodiversity Foundation, said: “This research demonstrates clear evidence of the increased risks of mental health comorbidities associated with adult ADHD. This is a step towards recognising the broader impact of unmanaged and untreated ADHD. We hope this research will lead to more research being commissioned in this area. We also hope it will result in changes to the design and delivery of health services.
“The cost implications to the NHS of leaving ADHD untreated, and the need to better train health practitioners in both primary and secondary care, are now more apparent. And of course there are other costs too that need to be considered — to the health of UK citizens with ADHD and to their family life, employability and economic wellbeing. These costs are often hidden but they are considerable.
“This research from Bath University will add to the growing national debate and the business case for a national review of health services for ADHD across a person’s lifespan.”

Researchers at University of California San Diego School of Medicine have discovered a molecular pathway critical to the initiation of pancreatic tumors. The mechanism could also contribute to the disease’s high resistance to chemotherapy and its propensity for metastasis.
The study, published on January 16, 2022 in Nature Cell Biology, found that pancreatic tumor-initiating cells must first overcome local ‘isolation stress’ by creating their own tumor-promoting microenvironment, and then recruit surrounding cells into this network. By targeting this tumor-initiating pathway, new therapeutics could limit the progression, relapse and spread of pancreatic cancer.
Pancreatic cancer is one of the most lethal cancers, notoriously resistant to treatment. Almost all patients experience cancer recurrence or metastasis.
In the early stages of tumor formation, cancer cells (those with cancerous mutations, called oncogenes) experience a loss of adhesion to other cells and the extracellular matrix — the web of macromolecules that encase and support all cells. This isolation leads to a local lack of oxygen and nutrients. Most cells do not survive such isolation stress, but a certain group of cells can.
Tumor-initiating cells (TIC) play a major role in the formation, recurrence and metastatic spread of tumors. What sets them apart from other cancer cells is their resilience to these early substandard conditions. Like cacti in a desert, they can adapt to the harsh environment and set the scene for further tumor progression.
“Our goal was to understand what special properties these tumor-initiating cells have and whether we can control the growth and spread of cancer by disrupting them,” said senior study author David Cheresh, PhD, Distinguished Professor and vice chair of the Department of Pathology at UC San Diego School of Medicine and a member of the UC San Diego Moores Cancer Center.

To answer these questions, first author Chengsheng Wu, PhD, a postdoctoral fellow in Cheresh’s lab, subjected pancreatic cell lines to various forms of stress, including low oxygen and sugar levels. He then identified which cells could adapt to the harsh conditions and observed which genes and molecules were modified in these cells.
The stress-tolerant tumor-initiating cells showed reduced levels of a tumor-suppressive microRNA, miR-139-5p. This in turn led to the upregulation of lysophosphatidic acid receptor 4 (LPAR4), a G-protein-coupled receptor on the cell surface.
“LPAR4 is not normally found on happy cells, but it gets turned on in stressful environments to help the cells survive, which is particularly advantageous for tumor-initiating cells,” said Cheresh.
The researchers found that LPAR4 expression promoted the production of new extracellular matrix proteins, allowing the solitary cancer cells to start building their own tumor-supporting microenvironment.
The new extracellular matrix was particularly rich in fibronectin, a protein that binds to transmembrane receptors called integrins on surrounding cells. Once the integrins on these cells sensed the fibronectin, they began signaling the cells to express their own tumor-initiating genes. Eventually, these other cells were recruited into the fibronectin matrix laid by the tumor-initiating cells and a tumor started to form.

“Our findings establish a critical role for LPAR4 in pancreatic tumor initiation, and a likely role in other epithelial cancers, such as lung cancer,” said Cheresh. “It is central to tumor-initiating cells’ ability to overcome isolation stress and build their own niche in which tumors can form.”
But isolation stress is not the only way this signaling pathway can be triggered, the researchers said. Chemotherapy drugs are also designed to put cancer cells under stress. Indeed, Cheresh’s team found that treating cultured tumor cells and pancreatic tumors in mice with standard-of-care chemotherapeutics also led to the upregulation of LPAR4. The researchers said this might explain how such tumor cells could develop a stress tolerance and resistance to the drugs.
Further experiments also showed that using integrin antagonists to block cells’ ability to utilize the fibronectin matrix reversed the stress tolerance benefit of LPAR4 expression. Thus, the authors suggest targeting the LPAR4 pathway or disrupting the fibronectin/integrin interaction could be effective in preventing the growth, spread and drug resistance of pancreatic tumors.
“We can think of tumor-initiating cells as being in a transient state that can be induced by different stressors, so our clinical goal would be to prevent oncogenic cells from ever entering this state,” said Cheresh. “Now that we’ve identified the pathway, we can assess all the different ways we can intervene.”
The researchers suggested a new drug targeting this pathway could be used as a prophylactic in patients at high risk of developing the disease, or to prevent new tumors from forming in cancer cases with a high likelihood of metastasis.
Pairing the new drug with existing chemotherapeutics that put stress on mature tumor cells could also mitigate the effects of drug resistance and make cancer treatments more effective, authors said.
“Treating cancer can feel a little like whack-a-mole,” said Cheresh, “but if we have two or three hammers and we know where the moles are going to pop up next, we can beat the game.”
Co-authors include: Taha Rakhshandehroo, Hiromi I. Wettersten, Alejandro Campos, Tami Von Schalscha, Shashi Jain, Ziqi Yu, Jiali Tan, Evangeline Mose, Betzaira G. Childers, Andrew M. Lowy and Sara M. Weis, all at UC San Diego.

A new test that ‘fishes’ for multiple respiratory viruses at once using single strands of DNA as ‘bait’, and gives highly accurate results in under an hour, has been developed by Cambridge researchers.
The test uses DNA ‘nanobait’ to detect the most common respiratory viruses — including influenza, rhinovirus, RSV and COVID-19 — at the same time. In comparison, PCR (polymerase chain reaction) tests, while highly specific and highly accurate, can only test for a single virus at a time and take several hours to return a result.
While many common respiratory viruses have similar symptoms, they require different treatments. By testing for multiple viruses at once, the researchers say their test will ensure patients get the right treatment quickly and could also reduce the unwarranted use of antibiotics.
In addition, the tests can be used in any setting, and can be easily modified to detect different bacteria and viruses, including potential new variants of SARS-CoV-2, the virus which causes COVID-19. The results are reported in the journal Nature Nanotechnology.
The winter cold, flu and RSV season has arrived in the northern hemisphere, and healthcare workers must make quick decisions about treatment when patients show up in their hospital or clinic.
“Many respiratory viruses have similar symptoms but require different treatments: we wanted to see if we could search for multiple viruses in parallel,” said Filip Bošković from Cambridge’s Cavendish Laboratory, the paper’s first author. “According to the World Health Organization, respiratory viruses are the cause of death for 20% of children who die under the age of five. If you could come up with a test that could detect multiple viruses quickly and accurately, it could make a huge difference.”
For Bošković, the research is also personal: as a young child, he was in hospital for almost a month with a high fever. Doctors could not figure out the cause of his illness until a PCR machine became available.

“Good diagnostics are the key to good treatments,” said Bošković, who is a PhD student at St John’s College, Cambridge. “People show up at hospital in need of treatment and they might be carrying multiple different viruses, but unless you can discriminate between different viruses, there is a risk patients could receive incorrect treatment.”
PCR tests are powerful, sensitive and accurate, but they require a piece of genome to be copied millions of times, which takes several hours.
The Cambridge researchers wanted to develop a test that uses RNA to detect viruses directly, without the need to copy the genome, but with high enough sensitivity to be useful in a healthcare setting.
“For patients, we know that rapid diagnosis improves their outcome, so being able to detect the infectious agent quickly could save their life,” said co-author Professor Stephen Baker, from the Cambridge Institute of Therapeutic Immunology and Infectious Disease. “For healthcare workers, such a test could be used anywhere, in the UK or in any low- or middle-income setting, which helps ensure patients get the correct treatment quickly and reduce the use of unwarranted antibiotics.”
The researchers based their test on structures built from double strands of DNA with overhanging single strands. These single strands are the ‘bait’: they are programmed to ‘fish’ for specific regions in the RNA of target viruses. The nanobaits are then passed through very tiny holes called nanopores. Nanopore sensing is like a ticker tape reader that transforms molecular structures into digital information in milliseconds. The structure of each nanobait reveals the target virus or its variant.

The researchers showed that the test can easily be reprogrammed to discriminate between viral variants, including variants of the virus that causes COVID-19. The approach enables near 100% specificity due to the precision of the programmable nanobait structures.
“This work elegantly uses new technology to solve multiple current limitations in one go,” said Baker. “One of the things we struggle with most is the rapid and accurate identification of the organisms causing the infection. This technology is a potential game changer; a rapid, low-cost diagnostic platform that is simple and can be used anywhere on any sample.”
A patent on the technology has been filed by Cambridge Enterprise, the University’s commercialisation arm, and co-author Professor Ulrich Keyser has co-founded a company, Cambridge Nucleomics, focused on RNA detection with single-molecule precision.
“Nanobait is based on DNA nanotechnology and will allow for many more exciting applications in the future,” said Keyser, who is based at the Cavendish Laboratory. “For commercial applications and roll-out to the public we will have to convert our nanopore platform into a hand-held device.”
“Bringing together researchers from medicine, physics, engineering and chemistry helped us come up with a truly meaningful solution to a difficult problem,” said Bošković, who received a 2022 PhD award from Cambridge Society for Applied Research for this work.
The research was supported in part by the European Research Council, the Winton Programme for the Physics of Sustainability, St John’s College, UK Research and Innovation (UKRI), Wellcome, and the National Institute for Health and Care Research (NIHR) Cambridge Biomedical Research Centre.

Doctors at Queen Mary University of London and Barts Hospital, and Cambridge University Hospital, have led research using a new type of CT scan to light up tiny nodules in a hormone gland and cure high blood pressure by their removal. The nodules are discovered in one-in-twenty people with high blood pressure.
Published today in Nature Medicine, the research solves a 60-year problem of how to detect the hormone producing nodules without a difficult catheter study that is available in only a handful of hospitals, and often fails. The research also found that, when combined with a urine test, the scan detects a group of patients who come off all their blood pressure medicines after treatment.
128 people participated in the study of a new scan after doctors found that their Hypertension (high blood pressure) was caused by a steroid hormone, aldosterone. The scan found that in two thirds of patients with elevated aldosterone secretion, this is coming from a benign nodule in just one of the adrenal glands, which can then be safely removed. The scan uses a very short-acting dose of metomidate, a radioactive dye that sticks only to the aldosterone-producing nodule. The scan was as accurate as the old catheter test, but quick, painless and technically successful in every patient. Until now, the catheter test was unable to predict which patients would be completely cured of hypertension by surgical removal of the gland. By contrast, the combination of a ‘hot nodule’ on the scan and urine steroid test detected 18 of the 24 patients who achieved a normal blood pressure off all their drugs.
The research, conducted on patients at Barts Hospital, Cambridge University Hospital, and Guy’s and St Thomas’s, and Universities of Glasgow and Birmingham, was funded by the National Institute for Health and Care Research (NIHR) and Medical Research Council (MRC) partnership, Barts Charity, and the British Heart Foundation.
Professor Morris Brown, co-senior author of the study and Professor of Endocrine Hypertension at Queen Mary University of London, said: “These aldosterone-producing nodules are very small and easily overlooked on a regular CT scan. When they glow for a few minutes after our injection, they are revealed as the obvious cause of Hypertension, which can often then be cured. Until now, 99% are never diagnosed because of the difficulty and unavailability of tests. Hopefully this is about to change.”
Professor William Drake, co-senior author of the study and Professor of Clinical Endocrinology at Queen Mary University of London, said:”This study was the result of years of hard work and collaboration between centres across the UK. Much of the ‘on the ground’ energy and drive came from the talented research fellows who, in addition to doing this innovative work, gave selflessly of their time and energy during the national pandemic emergency. The future of research in this area is in very safe hands.”
In most people with Hypertension (high blood pressure), the cause is unknown, and the condition requires life-long treatment by drugs. Previous research by the group at Queen Mary University discovered that in 5-10% of people with Hypertension the cause is a gene mutation in the adrenal glands, which results in excessive amounts of the steroid hormone, aldosterone, being produced. Aldosterone causes salt to be retained in the body, driving up the blood pressure. Patients with excessive aldosterone levels in the blood are resistant to treatment with the commonly used drugs for Hypertension, and at increased risk of heart attacks and strokes.

Over 80% of premature deaths caused by small smoke particles in the United States result directly from human-ignited fires. This is the outcome of a study published today in IOP Publishing’s journal Environmental Research Letters.
The new study, led by researchers at the Massachusetts Institute of Technology, analyses the impact of smoke particles on air quality in the United States. Their research shows that human-ignited fires account for more than 67% of small smoke particles called PM2.5 in the United States. These particles are known to degrade air quality, causing respiratory illnesses and premature death.
The level of fire activity in the US is on the rise. The research team estimate that smoke from human-ignited fires was responsible for 20,000 premature deaths in 2018 alone, a year with a high frequency of fire events — a substantial portion of which were associated with human ignitions such as agricultural and human lit fires. This is 270% more than there were in 2003, when there was a low frequency of fire events. The research highlights that during high fire activity years, there are much higher concentrations of smoke PM2.5 in the air.
Dr Therese Carter, lead author of the study, said: “Fires not only threaten human lives, infrastructure, and ecosystems, but they are also a major cause for concern in terms of air quality. High levels of smoke exposure can negatively impact human health resulting in conditions such as respiratory infections, lung cancer, heart disease and even premature births. Our results show that a large and significant portion of harmful smoke particles result directly from human-lit fires.”
The team used the Global Fire Emissions Database to quantify agricultural fire emissions, then classify these fires into two categories: human vs. natural ignition. Applying a chemical transport model, they simulate the concentration of smoke particles across the United States, concluding that a significant portion of PM2.5 in the US results from human-ignited fires and thus has the potential to be managed.
To limit the devastating effects of pollution from small smoke particles, the team recommends an ignition-focused approach. State agencies can implement management plans to restrict the ignition of agricultural fires to periods when weather conditions would minimise health impacts. However, human-ignited wildfires are much harder to manage due to their sporadic and unplanned nature.
Carter concludes, “Now we know that humans can play a pivotal role in reducing PM2.5 concentrations, we should be putting policies, regulations, and management plans in place to reduce human-ignited fires. Efforts to minimise human-ignited fires should be focused on certain regions and ignition types in order to be more successful. Identifying and acknowledging the sources of these particles is the first step in a cleaner, healthier future.”

Late Monday morning, two police officers drove up a gravel driveway to a mobile home in Benton, Tenn., a tiny town in the foothills of the southern Appalachians, to question Susan Meachen, a 47-year-old homemaker and author of romance novels.She had been expecting them. For a week, she had been the focus of a scandal within the online subculture of self-published romance writers, part of the literary world sometimes known as “Romancelandia.”The police wanted to talk to Ms. Meachen about faking her own death. In the fall of 2020, a post announcing she had died had appeared on her Facebook page, where she had often described her struggles with mental health and complained of poor treatment at the hands of other writers.The post, apparently written by her daughter, led many to assume she had died by suicide. It sent fans and writers into a spiral of grief and introspection, wondering how their sisterhood had turned so poisonous.But she wasn’t dead. Last week, to the shock of her online community, Ms. Meachen returned to her page to say she was back and now “in a good place,” and ready to resume writing under her own name. She playfully concluded: “Let the fun begin.”Other writers, seeing this, were not in the mood for fun. Describing deep feelings of betrayal, they have called for her to be prosecuted for fraud, alleging that she faked her death to sell books or solicit cash donations. They have reported her to the F.B.I. cybercrimes unit and the local sheriff and vowed to shun her and her work. Some have questioned whether she exists in real life.Ms. Meachen does exist. In a series of interviews, she said the online community had become a treacherous place for a person in her mental state, as she struggled to manage a new diagnosis of bipolar disorder.“I think it’s a very dangerous mix-up, especially if you have a mental illness,” she said. “I would log on and get in, and at some point in the day my two worlds would collide, and it would be hard to differentiate between book world and the real world. It was like they would sandwich together.”A text message from Ms. Meachen to Samantha A. Cole, another romance writer in her Facebook group.via FacebookWhen she was first introduced to “the book world,” as she calls it, she was alone at home for long stretches while her husband, a long-haul truck driver, traversed the country.She read romance novels, sometimes plowing through more than one a day. She had always been a reader, despite dropping out of school in the 9th grade to marry. The online romance community was a revelation to her, “like an escape, a timeout, a break from everyday reality,” she said.Over time, though, it began to feel more like quicksand. Over the next three years, she self-published 14 novels and maintained a near-constant social media presence. She was also diagnosed with bipolar disorder, a disease characterized by periods of manic activity that can alternate with deep depression.The book world made her disorder worse, she said. Writing often sent her into a manic state, and conflicts on the fan pages left her seething. She knew she should walk away, and she tried. But she said it was “an addiction”; every time she tried to log off for good, her phone would ping.Dead people don’t postRomance writers’ groups can be fizzy, exhilarating places. There is sexy cover art. There is snappy industry jargon, like HEA (Happily Ever After), Dubcon (dubious consent) and Reverse Harem (a female protagonist with multiple male love interests.)At their best, the groups are a fountain of support for “indie” authors, who self-publish their work and help each other with covers and marketing, which is known as “pimping.” At their worst, they can be “epicenters of nonstop drama,” said Sarah Wendell, the co-founder of the romance blog Smart Bitches, Trashy Books.Ms. Meachen’s fan page, The Ward — a humorous reference to a psychiatric hospital — went in that direction. She complained bitterly about colleagues who, she said, she had helped but had failed to help her in return, and threatened to leave the indie world.“Every day it got to the point I’d rather be dead than to deal with the industry and the people who swear they are friends,” she wrote in September of 2020. “I’ve had some dog eat dog jobs in my life but this one is by far the most vicious with the least amount of money.”Ms. Meachen lives in the tiny town of Benton in the Appalachian foothills in southeastern Tennessee.Jessica Tezak for The New York TimesShe described her psychiatric treatment and alluded to past suicide attempts.“Dear Scary people in my head, I truly understand we’ve been doing your story for over a year,” she wrote. “Waking me up with muscles screaming at me to get up and finish does not motivate me.”Ms. Meachen’s psychiatrist, Dr. Niansen Liu, confirmed, with her permission, that she is under his treatment for bipolar disorder and that she has been prescribed medications for anxiety, depression and psychosis. He would not comment further on her case.Her online friends worried about her, and some reached out to express their concern, but there was a limit to what they could do, said Kimberly Grell, who became friendly with her through writing groups.“She was becoming pretty chaotic,” Ms. Grell said. “It just seemed like every problem that surfaced with her she was in the middle of, and it turned to where she was the victim of it all.”She sympathized with Ms. Meachen’s frustration, though, as it became clear that she might not be able to earn money with her writing.“A lot of people get into this type of business thinking they’re going to make their millions, like Stephen King or James Patterson,” said Ms. Grell, who exited the romance industry last year to sell beaded jewelry. “The reality is, it’s a money pit. You are literally tossing your money into a pit hoping someone will find you.”Ms. Meachen’s husband, Troy, said he came to see the “book world” as a danger to his wife’s welfare.When she sent out samples of her work to other authors, the responses she got were often “really brutal,” he said. When writing, he said, she had periods of mania and psychosis; sometimes, he would come home and “she would talk like a character from a book, like she was the individual she was writing.”He worried that it was too dangerous to leave her alone during the day. “It got to the point where it was like, enough is enough,” he said, comparing the community’s effect on her to a whirlpool. “She was going round and round,” he said, “and the bottom was just right there.”This reached a climax in the fall of 2020, according to Mr. and Ms. Meachen and their 22-year-old daughter, who described the episode on the condition that her name not be used.It had been a rough few weeks. In August, someone had called police because they feared she would harm herself. On September 10, Mr. Meachen was away, hauling a shipment of chemicals. Their daughter stopped by to check on her mother, and found her semiconscious.Ms. Meachen had taken a large dose of Xanax, enough to make her “like a limp noodle,” and was “not cognitive or responsive,” Mr. Meachen said. He instructed their daughter to announce her death online, he said.“I told them that she is dead to the indie world, the internet, because we had to stop her, period,” he said. “She could not stop it on her own. And, even to this day, I’ll take 100 percent of the blame, the accolades, whatever you want to call it.”The post on Meachen’s page said she had died two days earlier. “Author Susan Meachen left this world behind Tuesday night for bigger and better things,” it said. “Please leave us alone we have no desire in this messed-up industry.”A follow-up post appeared on Oct. 23. “Sorry thought everyone on this page knew my mom passed away,” it said. “Dead people don’t post on social media.”Ms. Meachen and her husband of 27 years, Troy. He said he came to see the “book world” as a danger to his wife’s welfare.via Susan Meachen‘I feel majorly gaslit’The news of Ms. Meachen’s death radiated out through the fan pages. Ms. Meachen was well known in the community, and had often reached out to new authors, volunteering to provide cover art or help with marketing.“Susan, I will never, ever forget how kind you were to me,” wrote Sai Marie Johnson, 38, the author of “Embers of Ecstasy,” at the time.“I only wish you would have known I would have talked you through the night, I’d have defended you against your bullies,” she wrote. “I will do everything I can to make a difference so your death is not in vain.”Ms. Johnson, who lives in Oregon, was so upset that she reached out to Ms. Meachen’s daughter online and offered to edit her mother’s last book for free, as a tribute. But the damage had been done, she said: Over the months that followed, many members, disgusted by the Mean Girl-ness of it all, migrated out of the community or deleted their accounts.“It caused a huge shift in this community,” Ms. Johnson said. “There was a lot of drama, but this was the tidal wave. Nobody before had gotten so abused that they wanted to commit suicide.”The subject receded, replaced by other dramas, until Jan. 2, when Ms. Meachen reappeared on her fan page with the news that she was alive.Ms. Meachen did not see it as a particularly big deal. Eager to resume writing under her own name, she had been considering such a move for about a year, she said. She sat down at the computer, she said, and “hit enter before I could talk myself out of it.”“I debated on how to do this a million times and still not sure if it’s right or not,” the post read. “There’s going to be tons of questions and a lot of people leaving the group I’d guess. But my family did what they thought was best for me and I can’t fault them for it.”For the first few hours, the response was muted. Then, as she put it, “all hell broke loose.” Her post was widely shared by Samantha A. Cole, a romance writer from the suburbs of New York City, along with a seething commentary.“I was horrified, stunned, livid, and felt like I’d been kicked in the gut and the chest at the same time,” wrote Ms. Cole, who previously worked as a police officer, and asked to be identified by her pen name to avoid the notice of people she had arrested.More than anything, Ms. Cole said, she was hurt. She had gone into a “major funk” for months over Ms. Meachen’s death, worried that she had not been a good friend. Worse, in the recriminations that followed, Ms. Cole was accused on one fan page of bullying Ms. Meachen, something both women said was untrue.Ms. Cole, who describes herself as “naturally suspicious,” set about documenting Ms. Meachen’s false claims in a series of screen shots and DMs.An excerpt from Ms. Cole’s Facebook page.via FacebookShe provided screenshots showing that Ms. Meachen had appealed to the group for financial help in medical emergencies and noted that she returned to the fan page under a new identity, T.N. Steele, effectively eavesdropping on her own mourners.“It was important to me because the people that had grieved for her death for so long had a right to know that the whole thing was a hoax,” Ms. Cole said. “That’s what led me to do this, my anger and the sense of betrayal. I needed a way to vent.”Many authors who are angry say it is because they know so many people struggling with mental illness themselves, and that it is despicable to falsify suicide for any reason.”“I feel majorly gaslit,” said Ms. Johnson, who, last week, filed a report about the incident to the cybercrimes unit of the F.B.I. She added, “It doesn’t seem like she is apologetic, and she is trying to cast blame on people, trying to get them to accept that she had a mental illness.”As the scandal drew the attention of mainstream media outlets to the romance industry, many of its senior figures drew a weary sigh.“I do not think it is going to help the romance industry’s persona of being a bunch of overly emotional women,” said Clair Brett, the president of the Romance Writers of America.A twinge of remorseMs. Meachen watched from Benton while the online backlash made headlines in Greece and Britain and France; reporters from various countries were appearing in her DMs, which stressed her out.This meant, among other things, that her real-life neighbors might read her novels, which fall on the racier end of the genre’s spectrum. For years, she has carefully separated her two identities — the romance writer and the homebody — but now they were smashing together.She had not heard again from the police and sounded confident that she would not face charges, saying the family had not received substantial donations after her online death announcement; she had offered the detectives access to her bank accounts to prove it. She did admit feeling remorse for the fans who had grieved her loss.“I’m sorry for their mourning, but from a legal standpoint, I did nothing wrong,” she said. “Morally, I might have done something wrong. But legally, there’s nothing wrong.”If Ms. Meachen was on the edges of a literary world before, she is now cast out of it. Her fan page has gone silent. Her inbox is full of angry messages from former friends. Looking back on the whole story, she said she regrets it all, starting with entering the romance groups.“It wasn’t good for me,” she said. “No, it wasn’t. I wish I had never met the book industry whatsoever.”She has set aside her plans to resume writing fiction, for now, to deal with more immediate concerns. Someone is impersonating her on social media, issuing comments about the scandal, she said, and hoax Susans were bouncing around the internet saying God knows what.“That’s what’s so funny about it,” her husband said. “You can be anybody you want to be on the internet.”

During the corona epidemic many of us became amateur mathematicians. How quickly would the number of hospitalized patients rise, and when would herd immunity be achieved? Professional mathematicians were challenged as well, and a researcher at University of Copenhagen became inspired to solve a 30-year-old problem in computer science. The breakthrough has just been published in th Journal of the ACM (Association for Computing Machinery).
“Like many others, I was out to calculate how the epidemic would develop. I wanted to investigate certain ideas from theoretical computer science in this context. However, I realized that the lack of solution to the old problem was a showstopper,” says Joachim Kock, Associate Professor at the Department of Mathematics, University of Copenhagen.
His solution to the problem can be of use in epidemiology and computer science, and potentially in other fields as well. A common feature for these fields is the presence of systems where the various components exhibit mutual influence. For instance, when a healthy person meets a person infected with COVID, the result can be two people infected.
Smart method invented by German teenager
To understand the breakthrough, one needs to know that such complex systems can be described mathematically through so-called Petri nets. The method was invented in 1939 by German Carl Adam Petri (by the way at the age of only 13) for chemistry applications. Just like a healthy person meeting a person infected with COVID can trigger a change, the same may happen when two chemical substances mix and react.
In a Petri net the various components are drawn as circles while events such as a chemical reaction or an infection are drawn as squares. Next, circles and squares are connected by arrows which show the interdependencies in the system.

A simple version of a Petri net for COVID infection. The starting point is a non-infected person. “S” denotes “susceptible.” Contact with an infected person (“I”) is an event which leads to two persons being infected. Later another event will happen, removing a person from the group of infected. Here, “R” denotes “recovered” which in this context could be either cured or dead. Either outcome would remove the person from the infected group.
Computer scientists regarded the problem as unsolvable
In chemistry, Petri nets are applied for calculating how the concentrations of various chemical substances in a mixture will evolve. This manner of thinking has influenced the use of Petri nets in other fields such as epidemiology: we are starting out with a high “concentration” of un-infected people, whereafter the “concentration” of infected starts to rise. In computer science, the use of Petri nets is somewhat different: the focus is on individuals rather than concentrations, and the development happens in steps rather than continuously.
What Joachim Kock had in mind was to apply the more individual-oriented Petri nets from computer science for COVID calculations. This was when he encountered the old problem:
“Basically, the processes in a Petri net can be described through two separate approaches. The first approach regards a process as a series of events, while the second approach sees the net as a graphical expression of the interdependencies between components and events,” says Joachim Kock, adding:
“The serial approach is well suited for performing calculations. However, it has a downside since it describes causalities less accurately than the graphical approach. Further, the serial approach tends to fall short when dealing with events that take place simultaneously.”

“The problem was that nobody had been able to unify the two approaches. The computer scientists had more or less resigned, regarding the problem as unsolvable. This was because no-one had realized that you need to go all the way back and revise the very definition of a Petri net,” says Joachim Kock.
Small modification with large impact
The Danish mathematician realized that a minor modification to the definition of a Petri net would enable a solution to the problem:
“By allowing parallel arrows rather than just counting them and writing a number, additional information is made available. Things work out and the two approaches can be unified.”
The exact mathematical reason why this additional information matters is complex, but can be illustrated by an analogy:
“Assigning numbers to objects has helped humanity greatly. For instance, it is highly practical that I can arrange the right number of chairs in advance for a dinner party instead of having to experiment with different combinations of chairs and guests after they have arrived. However, the number of chairs and guests does not reveal who will be sitting where. Some information is lost when we consider numbers instead of the real objects.”
Similarly, information is lost when the individual arrows of the Petri net are replaced by a number.
“It takes a bit more effort to treat the parallel arrows individually, but one is amply rewarded as it becomes possible to combine the two approaches so that the advantages of both can be obtained simultaneously.”
The circle to COVID has been closed
The solution helps our mathematical understanding of how to describe complex systems with many interdependencies, but will not have much practical effect on the daily work of computer scientists using Petri nets, according to Joachim Kock:
“This is because the necessary modifications are mostly back-compatible and can be applied without need for revision of the entire Petri net theory.”
“Somewhat surprisingly, some epidemiologists have started using the revised Petri nets. So, one might say the circle has been closed!”
Joachim Kock does see a further point to the story:
“I wasn’t out to find a solution to the old problem in computer science at all. I just wanted to do COVID calculations. This was a bit like looking for your pen but realizing that you must find your glasses first. So, I would like to take the opportunity to advocate the importance of research which does not have a predefined goal. Sometimes research driven by curiosity will lead to breakthroughs.”

For people with paralysis caused by neurologic injury or disease — such as ALS (also known as Lou Gehrig’s disease), stroke, or spinal cord injury — brain-computer interfaces (BCIs) have the potential to restore communication, mobility, and independence by transmitting information directly from the brain to a computer or other assistive technology.
Although implanted brain sensors, the core component of many brain-computer interfaces, have been used in neuroscientific studies with animals for decades and have been approved for short term use (

Hormone Replacement Therapy (HRT) could help prevent Alzheimer’s Dementia among women at risk of developing the disease — according to University of East Anglia research.
The study shows that HRT use is associated with better memory, cognition and larger brain volumes in later life among women carrying the APOE4 gene — the strongest risk factor gene for Alzheimer’s disease.
The research team found that HRT was most effective when introduced early in the menopause journey during perimenopause.
Prof Anne-Marie Minihane, from UEA’s Norwich Medical School and director of the Norwich Institute for Healthy Aging at UEA, led the study in collaboration with Prof Craig Ritchie at the University of Edinburgh.
Prof Minihane said: “We know that 25 per cent of women in the UK are carriers of the APOE4 gene and that almost two thirds of Alzheimer’s patients are women.
“In addition to living longer, the reason behind the higher female prevalence is thought to be related to the effects of menopause and the impact of the APOE4 genetic risk factor being greater in women.

“We wanted to find out whether HRT could prevent cognitive decline in at-risk APOE4 carriers.”
The research team studied data from 1,178 women participating in the European Prevention of Alzheimer’s Dementia initiative — which was set up to study participants’ brain health over time.
The project spanned 10 countries and tracked participants’ brains from ‘healthy’ to a diagnosis of dementia in some. Participants were included if they were over 50 and dementia-free.
The research team studied their results to analyse the impact of HRT on women carrying the APOE4 genotype.
Dr Rasha Saleh, also from UEA’s Norwich Medical School, said: “We found that HRT use is associated with better memory and larger brain volumes among at-risk APOE4 gene carriers. The associations were particularly evident when HRT was introduced early — during the transition to menopause, known as perimenopause.

“This is really important because there have been very limited drug options for Alzheimer’s disease for 20 years and there is an urgent need for new treatments.
“The effects of HRT in this observation study, if confirmed in an intervention trial, would equate to a brain age that is several years younger.”
Prof Anne Marie Minihane said: “Our research looked at associations with cognition and brain volumes using MRI scans. We did not look at dementia cases, but cognitive performance and lower brain volumes are predictive of future dementia risk.
Prof Michael Hornberger, from UEA’s Norwich Medical School, said: : “It’s too early to say for sure that HRT reduces dementia risk in women, but our results highlight the potential importance of HRT and personalised medicine in reducing Alzheimer’s risk.
“The next stage of this research will be to carry out an intervention trial to confirm the impact of starting HRT early on cognition and brain health. It will also be important to analyse which types of HRT are most beneficial,” he added.
Prof Craig Ritchie, from the University of Edinburgh, said: “This important finding from the EPAD Cohort highlights the need to challenge many assumptions about early Alzheimer’s disease and its treatment, especially when considering women’s brain health. An effect on both cognition and brain changes on MRI supports the notion that HRT has tangible benefit. These initial findings need replication however in other populations.”

Reforms embedded in the Inflation Reduction Act will bring savings to seniors this year. Already some lawmakers are aiming to repeal the changes.Steve Lubin spent a lot last year on insulin to control his Type 2 diabetes.A retired nurse in Philadelphia, Mr. Lubin relies on Medicare for health coverage, including a Part D plan to cover drug expenses. Yet his out-of-pocket costs kept mounting, including a deductible of $480, monthly supplies of two forms of insulin, and higher prices once he entered the “coverage gap.” His total insulin tab in 2022: $1,582.So Mr. Lubin, 68, was cheering for the sprawling federal Inflation Reduction Act, which among other provisions called for capping insulin prices for Part D beneficiaries at $35 a month, with no deductible. He signed petitions circulated by the American Diabetes Association and the Pennsylvania Health Access Network asking Congress to vote yes.“My income is definitely down from when I was working, and the expenses go up,” he said. “It’s difficult.”But Mr. Lubin also supported the bill because, after working in an intensive care unit for years, he had seen patients suffer the serious consequences of diabetes when they could not afford their prescriptions.“You’d take their history and find out that they were rationing their insulin or couldn’t take it at all,” he recalled.In August, Congress passed the bill, and President Biden signed it. Mr. Lubin’s out-of-pocket insulin costs for 2023 will fall to $630. The legislation establishes other requirements to lower drug prices for Medicare beneficiaries, about three-quarters of whom have Part D plans.“It’s one of the biggest changes to the way Medicare deals with prescription drugs,” said David Lipschutz, associate director of the Center for Medicare Advocacy. “It signals lawmakers’ willingness to take on a very powerful lobby.”Some provisions took effect on Jan. 1; others will phase in over several years. “Collectively, these represent substantial out-of-pocket cost savings, especially for those who use expensive drugs,” said Juliette Cubanski, deputy director of the Kaiser Family Foundation’s Medicare policy program. They could also bolster Medicare by reducing its spending.Beneficiaries will see three significant changes in 2023.The first is the $35 monthly cap on insulin, which will affect more than a million insulin users who have Part D through Medicare Advantage plans or free-standing plans purchased along with traditional Medicare.From 2007 to 2020, beneficiaries’ aggregate out-of-pocket insulin costs quadrupled, even though the number of users only doubled. They spent an average $54 a month on insulin in 2020, according to a Kaiser Family Foundation analysis.The cap will save average users at least 35 percent and applies immediately, without requiring them to first pay the Part D deductible, which amounts to $505 in 2023. About 10 percent of Part D insulin users, like Mr. Lubin, paid more than $1,300 out of pocket in 2020 and will save much more.Although all Part D plans must cap the cost, they aren’t required to offer every form or brand of insulin.“People should make extra sure their plan isn’t dropping their insulin from the formulary,” Dr. Cubanski said.But Medicare’s open enrollment period ended on Dec. 7, and its online cost comparison tool doesn’t reflect changes mandated by the new law, which was passed after Part D plans had already set prices.“People might have made different choices if they’d had more information,” Dr. Cubanski said.So Medicare has begun a one-time special enrollment period through the end of 2023, allowing insulin users to drop, add or change Part D plans. Beneficiaries have to call the 1-800-MEDICARE number to make a switch. Counselors at State Health Insurance Assistance Programs can also help with the decision.In the second major change, adult vaccines covered by Part D, typically offered at pharmacies, are now free, without deductibles or co-pays, just as the flu and pneumonia vaccines (covered by Part B) have been.That will in particular improve access to the shingles vaccine, the most expensive adult vaccine. In 2018, the Kaiser Family Foundation reported, Part D enrollees paid $57 per dose out of pocket — and each recipient needs two doses.Although shingles risk rises with age, only 46 percent of adults over age 65 had been vaccinated by 2020, the Centers for Disease Control and Prevention reported. Rates were much lower among Black and Hispanic older adults.“It’s disappointing because this is a spectacularly effective vaccine,” said Dr. William Schaffner, an infectious disease specialist at Vanderbilt University Medical Center. Shingrix, the current vaccine, is about 90 percent effective, and a new study has found that its protection persists a decade after vaccination.A serious disease in itself, shingles can also cause the lingering nerve pain called post-herpetic neuralgia. “It varies from being annoying to being absolutely life-changing,” Dr. Schaffner said.With Shingrix available at pharmacies without charge, “the receptivity to vaccination for older adults will increase substantially, especially among underserved populations,” he predicted.Also free: hepatitis A and hepatitis B vaccinations, and Tdap, which protects against tetanus, diphtheria and pertussis (whooping cough).The third major change: When prices for drugs covered under Part D, and some under Part B, increase faster than the inflation rate, the law now requires drug manufacturers to pay rebates or face stiff penalties.Although those rebates will go to Medicare, not to individuals, “if you’re responsible for a portion of a drug’s cost and there are limits on how much that can increase, in theory your costs should decrease,” Mr. Lipschutz said.It will take months for Medicare to determine which price increases will prompt rebates and how much the rebates will amount to. But the Congressional Budget Office has estimated that this provision will save Medicare more than $56 billion over 10 years.Medicaid has employed a similar strategy since 1990. “It definitely has an effect on keeping spending in check,” Dr. Cubanski said. “The hope is that it will have the same effect for Medicare.”The changes in subsequent years will be more dramatic.In 2025, Medicare will set a $2,000 annual limit on out-of-pocket spending for Part D beneficiaries. “Nowadays, a lot of drugs can cost $500 or $1,000 a month,” Dr. Cubanski said. “Or maybe you take 10 medications, and that adds up to high out-of-pocket costs.”A kind of cap will take effect even sooner, in 2024. That’s when Medicare will eliminate the 5 percent co-pay that beneficiaries are responsible for once they pass the catastrophic expenditure threshold, effectively limiting out-of-pocket costs to about $3,250. The $2,000 cap takes hold the following year. Access to low-income subsidies will broaden, as well.Probably the most significant policy change is that the new law requires Medicare to begin bargaining with drug manufacturers, “the first time the federal government is not just allowed but required to negotiate prices on behalf of Medicare beneficiaries,” Dr. Cubanski said.Starting in 2026, the prices of 10 brand-name drugs covered by Part D, selected from those with the highest Medicare spending, will reflect those negotiations. The drugs must have been on the market for several years with no generic or biosimilar competitors.Medicare will provide negotiated prices for 15 additional drugs the following year, another 15 in 2028 and 20 each year thereafter. Negotiated prices for selected Part B drugs will be available in 2028.Given the thousands of covered drugs, “it’s a pretty modest proposal when it comes to restraining the cost,” Mr. Lipschutz said. Nevertheless, he added, “the pharmaceutical industry is likely to try to undermine this law — it will be looking for loopholes and escape hatches.”Republicans in Congress, nearly all of whom voted against the Inflation Reduction Act, have already introduced legislation to repeal the measures intended to lower drug prices, and supporters are braced for court challenges, too.But for now, the law is in effect. “It can give people peace of mind,” Dr. Cubanski said. “They won’t go bankrupt or go into medical debt to afford the prescriptions they need.”